Who are humans' closest relatives, after primates? This question here addresses the controversy of whether humans are more closely related to bonobos or chimps.

My question is - which group of animals are are closest relatives, beyond primates? Or which group of animals are all primates most closely related to?

Short answer

It is a flying lemur (there exist only 2 species). Flying lemurs and primates are together a sister clade to treeshrews.

Easy source of information

Have a look at the post The best free and most up to date phylogenetic tree on the internet?.

In short, you can have a look at onezoom.org, tolweb.org or opentreeoflife.org by yourself!

Tree of life of placental mammals

Here is a screenshot coming from tolweb.org.

In this tree, there are polytomies showing everything that is unknown. This tree was last updated in 1995 and there are also clades that we now know were misplaced including the bats (as commented by @NoahSnyder). It is not handy to make a good screenshot from onezoom.org or opentreeoflife.org so I just welcome you to explore the tree of life by yourself on onezoom.org or opentreeoflife.org to get a better representation of the reality.

Tree of Supraprimates

Supraprimates (=Euarchontoglires) include all primates and a few of the most related clades. Stealing the tree from @Gwenn's answer, here is the tree of Supraprimates

[

Here is the original tree from Janecka et al. (2007)

Here we see that flying lemurs (=Dermoptera) is a sister clade of primates (ignoring the extinct plesiadapiformes) and treeshrews (=Scandentia) are a sister clade of flying lemurs and primates together. Below I briefly talk about these three clades and about their position on the phylogenetic tree.

Flying lemurs

Flying lemurs is a small clade that contains only two extant species, both found in the family of colugos. Note that flying lemurs are not lemurs (which is confusing). Here is what a flying lemur look like

The position of flying lemurs on the phylogenetic tree has always been quite uncertain. In the tolweb.org screenshot above, flying lemurs (=Dermoptera) is a sister clade to bats (=Chiroptera) and together they are sister clade to treeshrews and primates. However, Janecka et al. (2007) placed flying lemurs as the sister clade to primates. Together flying lemurs and primates are a sister clade to tree shrews.

Tree shrews

Treeshrews is a clade of 20 species native from southeast Asia. Before, the era of phylogenetic comparisons, treeshrews were mistakenly thought to be part of the Insectivora.

Extinct clade of Plesiadapiforms

Although they are represented above as a sister clade of primates, it is possible that they the fossil we found are just individuals coming from the lineage giving rise to primates. As such, they would not be a clade aside from primates. Below is an artistic representation of what they may have looked like.

Introduction on phylogenetic trees

As the question is quite introductory, I presume you might want to improve your understanding of phylogenetic trees. You might want to make sure, you understand what a monophyletic group (=clade) is and understand why a chimpanzee and a human are both equally related to any species of treeshrews.

Here are two sources of information for you:

Understanding Evolution (UC Berkeley) > The history of life
This answer on Biology.SE


Is it possible to build a hive for bumblebee or hornet People commonly build hives for honey bees and it works . Is it also possible to build a hive for a bumblebees or hornets ? Should it have any special shape or form or is it just impossible ?

Yes, it is very common practice and there are many instructions and plans for beehives/nests available online, there are some for wasps


Why is this spider wound in such a dense web? I saw this thing yesterday on my window curtain, and I've been wondering what this is.
It looks like a dense network of spider web, and the spider inside it is visible. I thought the spider was dead, but I saw the spider making very small movements inside it. So, that made me more curious to know what it is.

From the look of the spider outline, it looks to have short legs and is dark. A yellow sac spider is quite light-coloured and has long legs. Yellow sacs and clubionids will sometimes make themselves a sac for resting or eating or molting or laying eggs. Yours is probably a jumping spider, and here is a youtube timelapse video of a jumping spider laying eggs while inside its own protective sac:
https://www.youtube.com/watch?v=yoqMNX0RWuc


How is information sent from the skin to the brain? Say you have a needle, and you poke a very specific area on your left thumb.
A signal gets sent from that nerve up your spine and into your brain.

How does the brain know exactly where this signal has come from to such accuracy?

Does each nerve in every conceivable part of the body have a unique path that goes up the spine and into the brain, so that's how the brain knows where it came from?
Or does the nerve encode the signal as data which travels up a generic nerve, and the brain decodes the information, which contains the "address" of the particular spot that was stimulated? If this is the case, how are the data encoded? Binary?

The accuracy of sensation is actually quite variable depending on the region of our body. Highly innervated areas such as our fingers have a higher degree of accuracy than sparsely innervated areas such as our legs.

There is a simple experiment you can do to illustrate this. Close your eyes and then get a friend to lightly and slowly run their finger from your wrist, up towards the bend in your elbow on the inside of your arm. Try to guess at what point the reach the joint of your elbow.

In terms of how the brain knows where it came from,  there is part of your brain called the sensory cortex. This sensory cortex has a pattern that corresponds to areas of the body. This pattern is known as a the sensory homunculus (google images will find this). As signals pass up the various different spinal pathways and into the brain they are sent up to this sensory area and the appropriate region of the homunculus is stimulated thereby giving the sensation in the appropriate body area.

Interestingly in some brain surgery a patient may be kept conscious so that these areas can be directly stimulated by electric current and the patient will experience sensations.

There is also a matching area, called the motor cortex, which corresponds to movement rather than sensation.

The above is a simplified version of what goes on and there is lots more detail which would be covered in neuroanatomy books


Historical recovery from mass extinction events Is there a way to generally characterize how species "regrew" after the various mass extinction events happening periodically from 450 Ma to 65 Ma.  Would the surviving species just start back where they had left off and evolve willy-nilly as if the destroyed 50% or 70% of biodiverse species had never existed?  Or would the biome in some way have the capacity to regrow something resembling the former order based just on the remaining species.  This is probably a whopper of a dumb question, my apologies in advance.

I think the concept of adaptive radiation is what you may be thinking about, since adaptive radiations have been observed following historic mass extinctions.

When organisms are placed in environments with low diversity (either due to mass extinction or the recent creation of the environment) they can undergo adaptive radiation.  This generally occurs when there are lots of unoccupied niches in the environment - essentially there are lots of potential ways to make a living that are not being exploited by an existing organism.

In this situation, any organism with a heritable trait that was able to utilize a niche better than other organisms would have a selective advantage and would increase in frequency.  Over time this process can result in new species of organisms.

There is nothing really different about adaptive radiation and the normal process of evolution and speciation except that in an environment with lots of unoccupied niches, the probability of having a trait that gives you a selective advantage is greater so speciation occurs at a faster rate.

It is the normal processes of evolution and speciation that give the biome the capacity to increase diversity based on the remaining species.


Do plants need O₂ to consume energy they've stored via sugar? This question came up as I work my way through the answers to another question I just asked.

My understanding is that plant photosynthesis looks something like this (though with lots more going on under the hood):

$$\ce{6 CO_2 + 6H_2O + light -> C_6 H_{12} O_6 (sugar) + 6 O_2}$$

(source)
and that the primary functions of the sugar are to store and transport energy. If that's true, then there's something fishy about the familiar view that plants need CO2 to breathe and produce O2, while animals need O2 and produce CO2. Doesn't a plant need just as much O2 as an animal would when it (the plant) gets around to consuming the sugar it has produced? Doesn't consumption of the sugar take you back to the original reactants?

Plants need sugar not only for energy but also for synthesizing essential metabolites and building blocks including cellulose (used in cell wall), glycoproteins and 5-carbon sugars for nucleotides.

As already mentioned by canadianer, plants respire by oxidizing sugars. This happens mostly during the night. However photosynthesis also produces ATP and therefore plants are not strictly dependent on respiration for energy. Moreover the fixed carbon in the form of starch makes up an energy reserve (like fats and glycogen in animals).


Photosynthetic Pigments vs. Chloroplasts What is the difference between Photosynthetic Pigments and Chloroplasts? I know plants have both but Prokaryotes (Bacteria and Archeae) only have the former.

Photosynthetic pigments are the chemicals which take part in photosynthesis, in particular they are they ones which absorb photons and fluoresce (emit photons of a different wavelength) or emit electrons. Pigments are molecules, and chlorophyll is a key example. These pigments are required for photosynthesis to take place, as they generate the electrons which create the electrochemical gradients which power photosynthesis, thus all photosynthetic organisms will have photosynthetic pigments of some kind.

Chloroplasts are membrane-bound organelles in plant cells, made up of many hundreds of thousands of molecules including pigments. Plant photosynthesis takes place on their internal membrane, the thylakoid. Specifically, the thylakoid membrane of chloroplasts is the membrane across which the aforementioned electrochemical gradients are created in plants.

Chloroplasts originated from a free-living bacterium, probably a cyanobacterium, entering a eukaryotic cell. So prokaryotes don't have them because the chloroplast endosymbiosis event was one way in which plants diverged from their non-plant ancestors. So you can think of a cyanobacterium as a free-living chloroplast - they have their own internal membranes similar to the thylakoid across which electrochemical gradients are created for photosynthesis. Conversely, you can think of a chloroplast as a small cyanobacterium living symbiotically inside a plant cell.


Can someone identify these fungi? Found them in Gujarat, India.
Found growing among potted plants

This may be Clitocyte odora commonly known as aniseed toadstool.

They can be found growing in small groups along the side of tree roots.

it is widespread in the temperate zones, occurring in Asia, Europe, and North America

Young specimens have a light blue texture on the cap which fades to grey in age. The gills and stem are white with no ring.

Reference


How does laughing gas (N₂O) work? Laughing gas (N2O), well, makes people laugh.

How does just a gas make us do that, there has to be some hormones at work...

So, I wanted to know how this works?  What is the mechanism?

This information is all strictly for Entonox - a brand of analgesic gas comprising 50% Oxygen (O2) and 50% Nitrous Oxide (N2O), Laughing Gas.  This mixture is known as 'Gas and Air' and is in very common use.

The active ingredient in Entonox is of course the nitrous oxide, so the discussion of the mechanism below refers solely to the N2O as you asked for.

Nitrous oxide enters the blood by diffusion from the alveoli whilst it is being inhaled, but does not bind with haemoglobin.  It is fat soluble so quickly moves into cells, including synapse ends in the brain.  Because of the stability of the compound, N2O is not metabolised by the body so has its effect as that molecule, then is eliminated by diffusion out of the lungs once inhalation has ceased (taking roughly 2 minutes for on and offset).

According to the material that BOC pharmaceuticals provide, the exact mechanism of the analgesia is not fully understood.  It is known, however, to induce "inconsistent changes in the basal levels of thalamic nuclei".

N2O inhibits NMDA receptors in the brain whilst simultaneously encouraging the stimulation of the parasympathetic GABA receptors.  This eventually produces an anaesthetic effect.  It is also understood that N2O promotes the release of endogenous opioid neurotransmitters ('natural painkillers' e.g. endorphins) that specifically activate descending pain pathways.  This inhibits the transmission of pain.  In this way the analgesia provided by nitrous oxide is antinociceptive (literally pain reducing) rather than a generalised limbic depressor.

However, nitrous oxide also positively effects potassium ion channels too [ref] - reducing the chance of an action potential being generated in affected neurons.  Research into this area of the effects of N2O is ongoing.

Euphoria is a common side effect of N2O usage, hence the name laughing gas.  This is as part of wider emotional changes that can occur when nitrous oxide is being administered.  For example, some people instead of laughing become scared or in other cases extremely aggressive towards those nearby. The emotional excitement may result in depressive or manic behaviour even to the point of psychosis and hallucinations especially in those who have a preexisting vulnerability to mental illness. The precise mechanism for these disinhibiting is again not fully understood.

Whilst it seems a lot of the answers are missing, the course I'm taking this information from is available online at Discover Entonox - modules 8-10 have relevance to this question.  It's free to register and view the materials, they're all nicely narrated with diagrams etc.


Questions regarding a particular paper With respect to the following paper:

Automated identification of protein-ligand interaction features using Inductive Logic Programming: a hexose binding case study

I have a few questions:

in page 2, in the table, what does 501 mean in GLC-501(I searched for GLC-501 in PDB,couldnt find anything)
in page 3, in the table, the cavity center column has got two entries, what does that mean? does one entry belong to the protein and another entry to the ligand(left for protein and right for ligand)??

501 denotes 501st residue in the corresponding PDB entry — 1BDG. See here
A single protein can have multiple cavities (see here) and the multiple entries denote centres of different cavities.


Protein - one polypeptide molecule or a collection of molecules? I'm struggling a bit in Bio 111 with confusing terminology between the terms "chain" and "molecule". I understand the primary structure of a protein is a chain of amino acids connected by peptide (covalent) bonds - easily a molecule. And the secondary helix structure could be a single molecule/polypeptide chain. Up to this point, chain = molecule. But a beta-pleated secondary structure would have to be two or more chains (molecules) connected by hydrogen bonds. No? Or is a beta-pleated sheet considered one molecule? One chain?

This sort of question is easily answered by consulting and carefully reading an introductory biochemistry text, like this section of Berg et al. on line. However, as the diagrams of β-sheets can be confusing, I will summarize.

The amino acids linked by covalent peptide bonds produce a protein molecule in the form of a single polypeptide chain.
This polypeptide chain folds into a specific shape in three-dimensional space, its conformation being maintained by weak non-covalent interactions — ionic bonds, hydrogen bonds and Van der Walls interactions. (Often referred to as protein tertiary structure.) Proteins that have a roughly spheroidal shape (rather than being long and extended) are referred to as globular proteins.
Often the three-dimensional structure has large regular components (often referred to as secondary structure) because of the potential for repeated hydrogen bonding between the CO and NH of the repeating peptide bonds.

Molecular diagrams to illustrate the type of secondary structure known as the β-sheet generally show just a section of the polypeptide chain for clarity, as in the left-hand illustration from Berg et al., below:

This may give the impression that two separate chains are involved†, but cartoon representations such as the one on the right (also from the same section of Berg et al.) show that for globular proteins this is not so.

In the diagram the flat blue arrows represent β-strands that are hydrogen-bonded to one another to form a twisted barrel-shaped β-sheet. The yellow ‘rope’ between the arrows represents the continuation of the chain in the non-sheet areas of the structure.

So the possibility for confusion arises primarily from the difficulty of showing the detailed pattern of hydrogen bonding in the whole of a large protein. (Although it may also arise from the fact that it is easiest to illustrate β-sheets using the diagrams of silk fibroin — historically the first to be described — in which the sheets are very regular and flat. To an extent this is misleading as the right-hand side of my diagram indicates.)

†Footnote

Fibrous proteins, such as silk, exist in which β-sheets are formed between many different chains. The identification of the individual chains can be made unequivocally, e.g. on the basis of the gene sequence, and it is clear that the higher-order structure is composed of many individual molecules. In smaller higher-order structures, e.g. tetramers of globular proteins held together by weak non-covalent interactions, the semantic question of whether a molecule can be made up of several individual chains arises. In my opinion, this question is best ignored, unless one is studying the biophysical chemistry of proteins.


Do diurnal birds of prey recognize each other by their appearance? Just what the title states.

I recognize people around me by their facial appearance to begin with, then by their little idiosyncracies; this applies perhaps to most other humans too. We rely pretty heavily on vision - perhaps because we are a primarily diurnal species gifted with the ability to distinguish colour. But then, so are birds of prey e.g. eagle, kite ...

Do diurnal birds of prey identify each other by their appearance?

Having seen some nature documentaries about Penguins identifying their offspring using sound alone (even in flocks of hundreds of thousands of other birds), my immediate impression was that sound is likely to be more important with regard to recognizing individuals of the same species.

This is corroborated by Melissa Mayntz, a bird enthusiast, who has written a great account on birds use of their 5 senses (Understanding Bird Senses).

To summarize, she explains that whilst sight is a birds most important sense in terms of hunting and avoiding being hunted, their hearing is is their second most important sense and they use this to identify individuals;

  Birds hear a smaller frequency range than humans, but they have much more acute sound recognition skills. Birds are especially sensitive to pitch, tone and rhythm changes and use those variations to recognize other individual birds, even in a noisy flock.


What is the maximum altitude where humans can survive? What is the highest altitude that a human can survive without being pressurized?  Let's assume that oxygen and heat/insulation are not the limiting factors?
Why I asked.

Short answer
Between 62,000 and 63,500 feet (18,900 and 19,350 meters) blood begins to boil at body temperature. This altitude, referred to as the Armstrong limit, is generally considered to be the absolute limit compatible with life. At this point, humans cannot survive without pressurization measures.

Background
Atmospheric pressure drops at higher altitudes. As you go higher into the atmosphere, gases start to expand due to the lower atmospheric pressure. This is what causes your ears to pop when driving up in the mountains or when an airjet lifts off. At altitudes higher than 10,000 feet (3.5 km) people unaccustomed to the reduced atmospheric pressure may become short of breath or experience dizziness. At altitudes above 20,000 ft (6.1 km) supplemental oxygen is required to support life and at 34,000 ft (10.4 km), 100% oxygen is necessary to equal the partial pressure of oxygen in sea level air. Above 40,000 ft (12.2 km), 100% oxygen must be administered pressurized (NASA).

Altitudes above 50,000 ft (15.2 km) are considered near-space and man requires a pressurized suit to be safe. At 55,000 ft (16.8 km), atmospheric pressure is so low that water vapor in the body starts to boil at ambient temperatures, causing the skin to inflate. At 63,000 ft (19.2 km) blood at normal body temperature (98 F / 37oC) starts to boil. At altitudes above 65,000 ft atmospheric pressure approaches that of space, i.e., a vacuum (NASA).

Between 62,000 and 63,500 ft (18.9 - 19.4 km), blood at body temperature (37oC) begins to boil. This is the point beyond which humans absolutely cannot survive in an unpressurized environment. This point is named the Armstrong limit, after Harry George Armstrong, who founded the U.S. Air Force’s Department of Space Medicine in 1947. On Earth, the Armstrong limit is somewhere between 62,000 and 63,500 feet (18.9 and 19,4 km), or about 12 miles.

As a reference, the highest point on earth is the peak of the Mt. Everest at 29,000 ft (8,8 km).

Above the Armstrong limit, water in the soft tissues of your body vaporizes, causing gross swelling, though the tight seal of your skin would prevent you from actually bursting apart. Your eyes, likewise, would refrain from exploding, but continued escape of gas and water vapor leads to rapid cooling of the mouth and airways (Goslin, 2008).

Water and dissolved gas in the blood forms bubbles in the major veins, which travel throughout the circulatory system and block blood flow. After about one minute circulation effectively stops. The lack of oxygen to the brain renders you unconscious in less than 15 seconds, eventually killing you. When the pressure gets very low there is just not enough oxygen, which is thought to be the first and most important concern (Goslin, 2008).

Note that under conditions of near-vacuum, death is not instantaneous. At one three-hundred-eightieth of atmospheric pressure at sea level, dogs were shown to survive up to 90 seconds. During their exposure they weren't in a great state (the dogs were bloated, ice covered their tongue, and many more horrible facts to be read in (Goslin, 2008)). Monkeys were even shown to cope for 3.5 minutes under these conditions.

Reference
- Goslin, Sci Am February 2008


Real-time PCR delay in Cq due to insertion SNP in primer I am collecting evidence, even anecdotal, how does single nucleotide deletion or insertion in primer region affect the outcome of real-time PCR.
I am most interested in how much there is a delay in Cq (treshold cycle value) if compared to perfectly matched primer. But if you do not have Cq data, I also collect "Yes or No" answers, saying, whether there was amplification or no amplification.

I am interested specifically in insertion or deletion mismatches. (For substitution mismatches, there is a lot of data.)

I will appreciate any published or unpublished evidence.

As @WYSIWYG pointed out, having the indel difference in the 3' end can be informative, but I'm having a harder time finding evidence in the middle of the primer.  Putting the mutation/indel at the 3' end will change the ΔCT.  To do it well, you need wide coverage on your mutation site.

I think that it is possible that there could be a difference with a mismatch in the middle of a primer, but it wouldn't be as obvious as if it were closer to the 3' end.  Unless there was some serious reason why you couldn't put it there (ie Tm below 45 on the reference) that sounds like poor primer design.

I will note I am certainly not a qPCR expert, and I don't think the question has been directly researched (as you surmised).  Again when I've looked for Indels before (was doing some interesting stuff with HLA types...) we used larger primers for the qPCR.

If this doesn't answer your question satisfactory, is there an initial reference you would have us look at?  I imagine things like good quenching and other factors could pull out some significance when comparing two templates (one with indel one without), but again, it's kind of odd to put the mutation in the middle.

Edit to comments:
1: I think the Cq delay is going to depend on things like length, sequence, and mutation.  There may be a grand scheme formula/algorithm to predict the delay, but I don't know of one, and I couldn't find it if it does exist.  Most of the graphs and differences I've seen have been big enough that it convinced me that it was significant.  I don't know if this is like flow where you can sit and argue all day about the biological relevance of 40% to 30% of a particular group.

2: Sorry I didn't have time to come in and give an adequate summery of them.  They are, as you pointed out, tangential to what you're trying to do, but do in fact address the problem through their methods.  I will attempt a better summery as I have time (I've got a grant on I'm trying to get done by Tuesday, so probably after that).  If you have any clarifications to the question to add, please do.

3: This may have grown from the general perception that it was needed, and that I aim for the highest Tm I can generally manage without structure problems being introduced.  I also have the luxury of not needing to worry over the cost of ulta-mers.  It also could have come from history of working in BACs years ago.  Longer primers always increased my success rates when I was knocking out cassettes.


Is an antivenom venomous? What happens when someone takes an anti-venom for an animal they weren't bit by, either for incorrect identification of the animal they were bit by or if they weren't bit at all?

I am looking for the immune system reaction, and possibly why it reacts as it does.

Although it is fancy to think of antivenom as a poison for the poison, technically it is a poison only for the poison!

Antivenom is developed in horses (equine) by hyperimmunizing them against the particular venom at a non-lethal dose, followed by collecting the serum. Venoms are complex and have many enzymes and hence are proteins. So, antivenoms are just antibodies against the venom proteins.

Moreover, the antivenoms are classified into monovalent and polyvalent. This signifies whether the sera was prepared by hyperimmunizing the animal with the venom of a single species or many common venomous snake species together.

Usually, a snake bite is an emergency and the victim or the attendants rarely identify the snakes (In our place, patients sometimes to our surprise, even bring the killed snake to the casualty!). Hence, to avoid confusion polyvalent sera are used.

I've written all this just to make an impression that polyvalent sera also carry antibodies against the wrong snake too, but at the end of the day, it's the right antibody that does the job.

As mentioned in the comments, apart from occasional anaphylactic reactions or serum sickness, they are pretty safe (cost/benefit) to use.


What is the distribution of the number of heterozygotes in finite populations? Consider a bi-allelic locus with alleles A and a. We denote the frequency of the A allele by $p$. Assuming absence of selection and panmixia, the expected number of heterozygotes is $2p(1-p)N$, where $N$ is the population size. We can also calculate the expected number of AA and aa individuals.

What is the joint probability distribution of the number of AA, Aa and aa individuals?

It is a multinomial (trinomial) distribution with $N$ trials, $p_{AA}=p^2$, $p_{Aa}=2p(1-p)$, and $p_{aa}=(1-p)^2$. The probability to get exactly $n_{AA}$ AA genotypes, $n_{Aa}$ Aa genotypes and $n_{aa}=N-n_{AA}-n_{Aa}$ aa genotypes is

$$P\left(N_{AA} = n_{AA}, N_{Aa} = n_{Aa}\right) = \frac{N!}{n_{AA}!n_{Aa}!n_{aa}!}p^{2n_{AA}}\left(2p(1-p)\right)^{n_{Aa}}(1-p)^{2n_{aa}}.$$


What does the MAF/MinorAlleleCount mean? I'm not sure why reporting the second most frequent allele is helpful?
what is the Major allele?

[W]hat is the Major allele [frequency]?

If the Minor Allele Frequency is $p$, then, for a bi-allelic locus, the major allele frequency is obviously $1-p$.

  [W]hy reporting the second most frequent allele is helpful?

Most polymorphic loci of interest are bi-allelic. Hence, the MAF is an indication of genetic diversity. One could similarly report the expected heterozygosity instead ($2p(1-p)$).

It is common to consider only loci with a MAF greater than a certain value. There may be different reasons for that. Here are possible two reasons.

Sequencing errors

When sequencing your sample, errors are being made. Sure, error rate is pretty good (see this table from Molecular Ecology) but error still do exist. A polymorphic locus with a minor allele count of less than, says, 3 alleles might well just be caused by sequencing errors.

To avoid considering as polymorphic loci that are in reality not polymorphic, we often just disregard any data with MAF is below a given threshold.

$F_{ST}$

$F_{ST}$ is a measure of genetic differentiation among population. When computed on loci with low MAF, the statistic is biased (Beaumont and Nichols, 1996). Hence, it is usual to only consider loci with a MAF greater than an arbitrary threshold before computing $F_{ST}$


Why do reptiles still move even after death? I saw a video in which a decapitated snake head still tried to bite.

I also saw a video in which a man was hit by the moving tail of a dead crocodile.

So why do reptiles move even after death?

http://en.wikipedia.org/wiki/Reptile

In warm-blooded animals, our high metabolisms are a significant disadvantage when being decapitated. Just a few minutes without oxygen and a mammal's brain is caput—the result of a massive cascading cellular die-off. Not so with cold-blooded reptiles. Their slow metabolism sustains their internal organs for far longer than a mammals causing them to completely die far more slowly. Essentially, cutting off their heads only makes them "mostly dead".


What's the correct name for the war of sexes in evolution? I'm searching for the correct term for the part of the selfish gene evolution regarding sexes. In nature, this means the evolution of the traits such as the ducks' adaptation to "trap" the drakes' penises in order to restrict the male from attending to other females.

Sexual Conflict is the word you are looking for!

Sexual Conflict occurs whenever the optimal mating strategy for the female and the male differ. For example, in Drosophila, it is beneficial for a male to mate as much as possible, while it is beneficial for a female to mate only a few times.


What are multiallelic genes? Is there a clear detailed description for multiallelic genes? Are they simply genes that are more than two alleles?

More than two alternative forms (alleles)of a gene in a population occupying the same locus on a chromosome or its homologue is known as multiple alleles.

Multiple alleles arise due to mutations of gene.A gene can mutate several times by producing a series of alternative expressions.Different alleles in a series show dominant-recessive relation or may show co-dominance or incomplete dominance among themselves.

In Drosophila,a large number of multiple alleles are known.One of them is the series of wing abnormality ranging in size from normal wings to no wings.The normal wing is wild type.The extreme expression with no wings I.e is just stumps is due to one allele 'vg',in homozygous condition .

For reference.
http://eagri.tnau.ac.in/eagri50/GBPR111/lec04.pdf


How to define a 'trait' objectively? I'm coming across an increasing number of papers that use trait-based approaches for risk assessment, like this one . This paper defines a trait as follows:

  Traits are the physiological, morphological, and ecological attributes
  of species or other taxonomic entities, which describe their physical
  characteristics, ecological niche, and functional role within an
  ecosystem.

I've wondered about using this sort of approach during some analyses of invasiveness potential in vector insects before and it's likely to come up during a systematic literature review I'm coordinating, but I'm concerned that devising my own trait classification system is likely to introduce confirmation bias into a study. Is there either a recognised methodology for trait definition, or alternatively some sort of accepted list or classification of traits that I could use, to minimise the chances of this? Is there a generally-accepted method to correct for phylogenetic correlation?

I've tried Google but the results mostly appear to be about trait theory, which is an approach used in psychology to study human personality.

I think you this paper is what you need. The many concepts of trait are discussed in the functional ecology background. But basically, a "trait" can be defined as

  " 'Functional traits’ are defined as morpho-physiophenological
  traits which impact fitness indirectly via their effects on growth, reproduction and survival, the three components of individual performance." (Violle et al. 2007)

Which are not so different from the definition you posted.
Some organisms have an improved methodology to collect and measure traits, like plants. But this is not common to all organisms.
As for the method to correct for phylogenetic correlation, this is a whole different field called Phylogenetic Comparative Methods. To choose the method you need to know the kind of data you have and the question being asked.


Why do toenails grow much slower than fingernails? As the title suggests, I've noticed that my fingernail grow much faster than my toenails. For instance, I usually trim my fingernails every two week or so, but for toenails the number would be about 6 to 8 weeks.
A bit of research revealed this wikipedia article:

In mammals, the length and growth rate of nails is related to the length of the terminal phalanges (outermost finger bones). Thus, in humans, the nail of the index finger grows faster than that of the little finger; and fingernails grow up to four times faster than toenails. [12]
In humans, nails grow at an average rate of 3 mm (0.12 in) a month.[13] Fingernails require three to six months to regrow completely, and toenails require 12 to 18 months. Actual growth rate is dependent upon age, sex, season, exercise level, diet, and hereditary factors. Nails grow faster in the summer than in any other season.[14]

But correlation does not imply causation, so why should the growth rate of nails depend on the  length of the terminal phalanges? Then why do babies grow nail much faster? I wasn't satisfied by its answer, so I looked a bit more where I found this other article. They had two possible candidates:

because hands are physically closer to the heart than are feet, fingers get better blood circulation and consequently better access to oxygen and nutrients.

Fingernails experience almost constant trauma through tapping, typing, bumping, and other seemingly insignificant actions. These persistent minor traumas stimulate fingernail growth. Toes, on the other hand, are not exposed to nearly as much trauma as they are usually bundled up safely inside socks and shoes. Similarly, fingernails on a person's right hand grow faster in right-handed people than on their left hand and vice-versa.

However they don't give actual experimental results. So my question is which of the above is the real cause of this difference in the growth rate of nails; or simply why toenails grow much slower than fingernails?

P.S. The season dependence and the lefthand-righthand asymmetry were news to me; it would be really nice if the answer explains them as well.

Going on the abstract of a study by J.P. Pessan, et al., fluoride intake, as well as "the fact that toenails are less prone to environmental contamination," constitutes a lesser need for growth in toenails than that in fingernails. Also, fluorine being a crucial component in maintaining the solidity of bones, the body may redirect more fluorine that is ingested by various means, to the hands than to the feet, due to the arguably more necessary functions of the hands (in that they are used them for agile and precise motions that tend to influence our survival), meaning less growth in toenails as evidenced in the first citation.


Studying the epigenetic variability, can I use SNPs? So, I'm trying to study the effects of epigenetic variability on the brain structure. Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region? I don't have environmental data, just the SNP information.

Since epigenetics refers to the variations in the gene expression without changing the DNA sequence, I don't really understand if there could be a connection.

Any help would be appreciated, thank you!

Starting from what appears to be your main question:

  Can I use SNPs associated with a gene's higher expression to compute the likelihood of that gene being expressed in the brain region?

I would strongly advise against using SNPs determine if genes are expressed (at all) in a given tissue.For one thing SNPs that affect expression (then often called eQTLs) will usually only have small +- effects on expression instead of switching it on/off and also have that effect in many/all cell types. Unless an (individual) SNP has clearly described /and validated effects on gene expression in a specific tissue/brain region, you should assume it has global effects.

Now, luckily for you gene expression in different cell types, tissues etc is a relatively well studied area and there are resources for gene expression in the brain available (brain atlas is probably closest to what you might look for).
You can uses these resources to determine which genes are expressed in your regions of interest and from there on check if SNPs associated with these genes correlate with certain structural brain features you are interest in.

One more thing you note:
The title of your questions (as well es comments) mention that you are interested in epigenetics. Neither gene expression nor SNPs/eQTLS are diretcly linked to epigenetics, so if this is your actual focus you should also look for availbale ChIP-seq data or similar and also include this into your analysis (correlation of SNPs with epigenetic marks is difficult but not impossible)


Chart of intra-species genetic diversity across species / phyla? I am looking for information on how genetic diversity within a species (not between species) differs between taxa. In other words: Is the "spread" in the genetic pool, if measured, for instance, in terms of single-nucleotide polymorphism (SNP), generally bigger / smaller for some groups of species than for others?

My ad-hoc idea is that species with a stronger phenotypic difference between individuals, like homo, should probably have a higher genetic diversity (higher rate of SNP) than those with lesser phenotypic variation, like, say, Orthoptera (grasshoppers etc.). But I couldn't find any statistics or research on this topic.

I am especially interested in data on far-related taxa. Ideally this would be a chart with comparative data for Sponges, Annelids, Arthropoda, Fish, Mammals (single representatives of these groups), or even Plants, Fungi, Archeae, Bacteria …

I do not look for information on the actual genome sequences, nor on biodiversity, but specifically on the genetic diversity within species from different phyla.

This is my first question here, thanks for you help!

You can look at the Heterozygous SNP rates in genome-sequenced species, which is a measure of within species diversity.

You have an example in Figure 4 here:
https://genomebiology.biomedcentral.com/track/pdf/10.1186/s13059-016-1090-1

You can see in the figure that endangered species are plotted (most of them with poor genetic diversity).

Also, I am afraid that your starting hypothesis is not very good. Our species is very poor in genetic diversity and has little phenotypic variation. The human species went through several major bottlenecks during his evolutionary history that reduced their diversity. Even gorillas or giant pandas are more diverse than humans. You have a bias because you are human and are good at differentiating individuals from your own species.

Also a single representative from each group won't suffice as the differences can be huge inside a group. Additionally phenotypic variation is hard to measure in certain groups.

Sorry for being a bit negative


What DNA does a self-fertile plant's seedling have? Some plants are said to be self-fertile. An example is Prunus tomentosa.

Assuming that no cross-pollination happened with other plants, if a self-fertile plant such as prunus tomentosa produces a seedling, what DNA will the seedling have? Is the seedling's DNA an exact copy of the parent plant's DNA, or do the genes get rearranged?

Selfing (aka self-fertilizing) differs from cloning. When selfing occurs, the offspring is not an exact copy of the parent. When cloning occurs, the offspring is an exact copy (except for a few mutations) of the parent.

Selfing implies that an individual will produce two gametes (typically a spermatozoid and an ovule but that might be a bit more complicated) and these two gametes are fusing to give the zygote (egg or offspring if you prefer).

As a consequence, when selfing, meiosis is occurring (and therefore segregation and recombination) so that the offspring is not an exact clone of the parent but rather some kind of a rearrangement of the parent genome (with a few mutations of course).


PEG-silane treatment: why incubate for 18 hours at 60 degrees Celsius? I am conducting a biochemistry-related experiment and I have been unable to understand a step which is commonly performed.
My aim in this step is to apply a PEG (Polyethylene glycol) silane layer.

After immersing indium tin oxide (ITO) slides in a PEG-concentration, the slides are incubated for 18 hours at a temperature of 60 degrees Celsius.

Can you tell me why the incubation is performed? And why for 18 hours and at 60 degrees Celsius?

Thanks a lot in advance!!

The binding of proteins (and cells) to glass (or silicon) surfaces can be prevented by coating the glass with polyethylene glycol (PEG) groups. PEG-silane is a reagent used to create this coating.

PEG-silane (the image shows a methoxy- version) (image taken from here; no connection)  will coat glass surfaces because the silane portion (right hand end of the structure shown) will react with -OH groups on the glass surface.

I can't help with the part of the question about time and temperature of incubation, but it seems longer and hotter than protocols I have seen. Perhaps the indium tin oxide (ITO) coating on the slides has something to do with it?


Chorophyll and photosynthesis in plants with coloured leaves Do plants that have only coloured leaves (e.g. ‘ornamental’ plants) contain chlorophyll and perform photosynthesis?

If they don’t, how do they obtain energy and metabolic intermediates?

Most of ornamental (often variegated ) plants do performs photosynthesis. They do have chlorophyll even if their color is not green. They have non-green color due to various different pigments. These extra color has their own functions like blocking harsh sunlight or protection from insects (Karageorgou and Manetas 2006).

In many non-green plants carotenoid content is way higher than chlorophyll. One of the main functions of these carotenoids is to expand the range of wavelength where photosynthesis can happen (Hashimoto et al 2016). This is especially important for such plants living in low light conditions or other stress factors are dominant.

Some comparison of content in different color leafs of Acer saccharum is enlisted in table below. Image is taken from (Junker and Ensminger 2016)

Photosynthetic activity of such plants can be measured by chlorophyll fluorescence techniques (Borek et al 2016). Photosynthesis performance of many of these plants (like Actinidia kolomikta) is actually properly maintained (Wang et al 2016) and does not have high Photosynthetic Cost.

Just to extend this answer for little general information, plants without any chlorophyll (like Cuscuta europaea) are often parasitic plants and they need host to survive and get nutrients.


The membrane folds of dendritic cells Dendritic cells have a larger surface area due to extended dendrites (membrane folding into itself). Do other mammalian cells (with functions other than immunological) present these membrane folds?

Yes, these include:

neurons
melanocytes
Merkel cells

In all cases, as you suggested, their function is to extend the surface area of the parent cell. In the case of neurons, the role of dendrites, which receive the vast majority of synapses, is to maximise the number of synapses the cell receives from different pre-synaptic partners (Chklovskii et al. 2002, Chklovksii 2004). In melanocytes, they are used to transfer melanin to keratinocytes. In Merkel cells, they are again used in order to form synapse-like connections with neurons (Mihara et al. 1979).

The word originates from the Greek δένδρον, which means 'tree'. Dendritic structures are found throughout in nature, including in...trees, where presumably they are used to maximise exposure to sunlight. Theoretical studies on the formation of dendritic arborisations in neurons indicate that they are governed by at least these factors: i) repulsion between dendrites (Wen et al. 2009), ii) minimisation of dendritic volume used (Tamori 1993), possibly through resource competition (Graham and van Ooyen 2004). It is an intuitively attractive idea to think that similar processes govern dendrite-like formation in the other biological systems described above as well.

References
- Chklovskii, D. B., Schikorski, T., & Stevens, C. F. (2002). Wiring Optimization in Cortical Circuits. Neuron, 34(3), 341–347. https://doi.org/10.1016/S0896-6273(02)00679-7
- Chklovskii, D. B. (2004). Synaptic Connectivity and Neuronal Morphology: Two Sides of the Same Coin, Neuron, 43(5), 609-617. https://doi.org/10.1016/j.neuron.2004.08.012
- Graham, B. P., & van Ooyen, A. (2004). Transport limited effects in a model of dendritic branching. Journal of Theoretical Biology, 230(3), 421–432. https://doi.org/10.1016/j.jtbi.2004.06.007
- Mihara M., Hashimoto K., Ueda K., Kumakiri M. (1979). The Specialized Junctions between Merkel Cell and Neurite: An Electron Microscopic Study, Journal of Investigative Dermatology, 73(5), 325-334. https://doi.org/10.1111/1523-1747.ep12550322.
- Tamori, Y. (1993). Theory of dendritic morphology. Physical Review E, 48(4), 3124–3129. https://doi.org/10.1103/PhysRevE.48.3124
- Wen, Q., Stepanyants, A., Elston, G. N., Grosberg, A. Y., & Chklovskii, D. B. (2009). Maximization of the connectivity repertoire as a statistical principle governing the shapes of dendritic arbors. Proceedings of the National Academy of Sciences, 106(30), 12536–12541. https://doi.org/10.1073/pnas.0901530106


Mechanism of Tear Gas (chloropicrin/Trichloro methane) Tear gas (CCl3NO2) makes people cry, and crying doesn't seem to be a simple procedure. There has to be a triggering process somewhere. Can someone explain its mechanism / how it works?

The general belief is that these agents are irritants which do not have a very specific effect.  That is to say that there is no specific cell or biological function that they set off, but that they irritate the cells, so the cells respond by putting up general defenses to insulate themselves from the noxious chemicals.

Mucous and tears wash away the compounds.  I'm sure there are all sorts of things going on, but its hard to be more specific.  For instance, onions have many sulfhydryl (-SH) compounds,  many many of them.  In particular propanethial s-oxide causes the tears we get when we cut an onion. This compound is very reactive and reacts with all sorts of proteins and disrupts the membrane, etc.  Its perhaps an example of a specific irritant that is so reactive that it creates tears.

An example of a specific reaction would perhaps be capsaicin.  There is a specific protein that is a heat receptor and the chemical capsaicin activates it, causing the feeling of heat/warmth.

Tear gas and mustard gas appear to fall into the former category, which are chemicals so reactive that they just tear into the cell, damaging all sorts of things in there.


How can space travel affect women’s fertility? From Time:

  The reasoning behind the prerequisite, according to officials, is that
  spaceflight could potentially harm the women's fertility.

How can space travel affect a woman’s fertility?

The most obvious issue is exposure to radiation. Once you're beyond the earth's atmosphere and magnetic field you are exposed to much higher levels of radiation from cosmic rays and solar flares. It's also possible that microgravity (weightlessness) could have effects on the reproductive system, but this isn't well studied yet.

However, given the source you link to to (a nine year old article speculating on why China required female astronaut candidates to be wives and mothers), this may simply be a medical rationalization for a political decision. Radiation can damage male fertility too, and the effect of microgravity on the male reproductive system is also not well understood.


What is the mass of carbon dioxide absorbed by an oak tree in one year? I want to understand the environmental impact of oak trees due to absorption carbon dioxide. So my question is, what is the mass of carbon dioxide absorbed by an oak tree in one year?

Re: Bryan Krause's comment, measurements per hectare are common. However, if you can just estimate average trees per hectare, then it works out. But it still likely depends on the local climate, ecology etc. It also varies across the life term of the tree.
Some estimates have been made, such as in this paper (see Table 4), for Quercus rubra and 2 other hardwood species. They estimate that for the most mature trees, Q. rubra stores ~20 Mg/hectare total biomass, of which approximately half is carbon.
This is a little more than twice the biomass of the 8-year-old tree, so if we just linearly interpolate we could say that a hectare of oak stores ~1 Mg C per year. There are some problems with this- for example, older trees are likely to store much more than that, but it is not clear exactly how much variation there is over the course of an oak's life, and also there is likely variation between the sites in the study.
It is also clear that the other species measured, e.g. American chestnut, are more effective carbon sinks than oaks as young trees.
See the paper or this pop science article on the subject for more information. THere are also a number of papers citing that paper that may be interesting, such as this, this, and this.


help identifying marine item found on beach Need help identifying this hard waxy egg like item found on beach in Destin, FL (USA).  It feels waxy and semi hard. Also smells like squid or real fishy. it is also semi transparent with dark tan looking tie on inside

Larger versions of pictures shown below:

You've found a swim bladder. Swim bladders are largely made from collagen, so when they're dried out on beaches they feel tough and rigid.

Swim bladders differ in shape between species. As an example, the swim bladders of oyster toadfish are similarly-shaped to the one you have found, but that general shape isn't uncommon, so it could have come from many other species.


Nuclear vs Cytoplasmic Fluorescence When staining transciption factor proteins with fluorescent antibodies (Alexa, etc.), why are the fluorescence signals stronger in the nucleus as compared to fluorescence signals in the cytoplasm (in context of transcription factor-activation?)
Is it simply spatial localization, that more fluoresence-marked proteins are at the same place, or are there other factors related?

Yes, your hypothesis is correct. There are more of them.

A few terms need clarifying here, just in case...

First, fluorescence is due to the property of a dye that can be conjugated to the antibody. Different fluorophores have different properties, some are more efficient than others. Some display strong "solvatochromism", i.e. they are happier in the hydrophobic environment (brighter and red shifted).

Second, DNA is stained not with an antibody but with the UV fluorophore DAPI, which shines brighter in DNA —same thing with ethidium bromide and Sybr Safe.

Now, if you are labelling a TF and they ought to be in the nucleus you definitely will have a brighter signal as you suggest. There will be a way-ever-so slight difference as the environment is less aqueous, but the nucleus is not that packed as on pictures.


How are germ cells not reduced in number? If germ cells produce haploid daughter cells by meiosis and are thereby "consumed" (where there was a germ cell there are then 4 daughter cells), where do the germ cells come from?  I asked my biology teacher if they undergo mitosis prior to meiosis, but she said they don't and proceeded to give an unclear answer.  Is this true?  If so, are they regenerated from somatic cells elsewhere in the body?

My question basically is - if the germ cells of, say, the testes are dividing by meiosis to produce sperm, where are the germ cells coming from so that the testes don't shrink and ultimately disappear as they're converted completely into sperm?

In case of gametogenesis (let us talk about spermatogenesis) gametes are formed from meiotic division of Primary spermatocytes.

In Primates Primary spermatocytes are cells that that are formed from mitotic division of B spermatogonia (which is another class of germ cells) which inturn are formed from mitosis of Ap spermatogonia which arise from mitotic division of Ad spermatogonia.  Ad spermatogonia are inturn formed from Primordial germ cells (see below for details).

Ad spermatogonia are dark A type spermatogonia, reserve stem cells  which occasionally divde to renew itself and Ap spermatogonia are pale A type spermatogonia, renewing stem cells.

  Why the testis doesn't run out of germ cells? (adaptation of your key question)

The reserved  Ad spermatogonia and renewal of both  Ad and  Ap spermatogonia are responsible for the continuous cycles of spermatogenesis.

  This process starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. (wikipedia)

The process of spermatogenesis in human:

In non-primates like mice it is little different, the following diagram should explain it:

Note:

Germ cells are cells that give rise to gametes ( present at any level of gametogenesis).
Primordial germ cells are embryonic cells that originate from a different location (outside the gonads) and migrate into the gonads during the course of embryonic development to divide into germ cells.
In females, oogenesis also involve production of germ cells (cells of primary follicles) from PGCs through mitosis but the primary follicles produced is fixed, doesn't increase after birth so at a definite age of 40-45 gametogenesis stops.

Further reading:

Stem Cells in Reproductive Medicine by  Carlos Simón, Antonio Pellicer, Renee Reijo Pera
A paper


A question on ImageQuantTL I am confused about using the ImageQuantTL application as a tool to analyse the Urea Gel. My problem is that I am not sure if the 'shape' for calculation should be the same for all samples (like on picture A) or as close to the band as possible (like on picture B)? And what about the background subtraction? The `Image Rectangle/Ellipse' option says:

  Uses the average pixel intensity in a defined rectangular or elliptical area of the image. To define the area for background calculation, select the background shape in the navigator and then drag with the mouse. Background areas are identified by a broken colored border, and are numbered in the sequence in which they are created. If you have defined several background areas, select the area to use in the Parameters tab.

Does it mean that the shape for the background subtraction not necessarily has to be exactly the same size as the shape for the band? (See Figure C.) I attach some pictures for your convenience.

Thank you very much for any help.

I would definitely go for option A. If you are assuming that the staining in band 6 is all due to whatever you are measuring, there is no reason to think that the signal at the top of lane 1 is not meaningful.

That said, this type of measures is only semi-quantitative, so being too "picky" in how you choose your region probably won't really increase the precision of your result. If you want to get a quantitative measure I am afraid you will have to turn to some other technique.

Finally note that the area obviously means a lot if you are looking at total intensity of the bands, rather than average intensity.


A good textbook on Neuroscience I want to start learning Neuroscience. Can someone give me an advice about a nice textbook for beginners? I'm particularly interested in the application of Neuroscience in programming and AI development. Thanks in advance.

If you are interested in computational neuroscience, I recommend Dayan and Abbott's book: http://www.amazon.com/gp/aw/d/0262541858/ref=redir_mdp_mobile/181-1988504-8834745. This is not a book on neuroscience, not AI, although this particular book has more math than the other introductory neuroscience textbooks I've seen.


What is this African bug? This is an arthropod I found in an apparently abandoned mongoose burrow in the Maasai Mara game reserve, Kenya:

That was the best photo I could get of it. From what I could tell, it had six legs and very long antennae, so I'm guessing it's an insect. It was vaguely orthopteran-like and had striped/banded legs with a dark dorsal side.

Does anyone have any idea what this could be? Even if the species can't be discerned, I'd appreciate knowing what clade this critter belongs to.

Based on the long legs and long antennae, I'd say you're correct that it's an orthopteran, very likely a cricket or one of its allies (i.e., suborder Ensifera).
Within this subgenus, the most likely candidate families are either the "true crickets" (Gryllidae) or "camel crickets" (Rhaphidophoridae).
Your photo is not nearly good enough to begin making more informed specific guesses. However, If I had to guess, it could possibly be a cricket in the genus Phaeophilacris, which are striped-leg crickets found in Africa.

See inaturalist for incidence of this genus in Africa.

You can see some photos of Phaeophilacris Bredoides here, with a few photos copied below:

 Source
You can read an interesting paper about communication in this genus here1

 1. Heinzel, H.G. and Dambach, M., 1987. Travelling air vortex rings as potential communication signals in a cricket. Journal of Comparative Physiology A, 160(1), pp.79-88.


What is the significance of running an uncut plasmid on electrophoresis gel? What is the significance of running an uncut plasmid on electrophoresis gel?
In this case we are talking about inserting a gene into plasmid, which then goes under PCR and then electrophoresis.

It is used to determine whether the unused/excess amount of plasmid has contaminated the  final solution of the desired recombinant DNA  or not.
Electrophoresis is performed on the "Blank"(uncut) plasmid to define its bands.If the electrophoresis result contains the bands of both "blank" and recombinant DNA , it shows that your solution is not 100% pure.


What species is this grey insect with red antennae and mouthparts? I’m very curious to know whether this is a type of ant or not, I only see 6 legs. Found in Tampa, Florida near Tarpon Springs.

It's some type of Reduviidae, or assassin bug - possibly a juvenile wheel bug.  Here's a few pictures of Floridan assassin bugs I've found just browsing the net:

Tagged as unidentified Reduviidae from Tallahassee

Tagged as assassin bug

Tagged as a Wheel Bug

Tagged as a wheel bug nymph

Bottom line:
Not an ant, for sure: it's almost certainly in the family of Reduviidae, possibly the subspecies of Arilus cristatus.


Why do snails come out after the rain? Many times, when there is rain after a long time, snails come out afterwards, and you can see snails and slugs everywhere! I have two questions:

Why do they come out after the rain?
Where are they usually found, not after a rain?

Note that I do emphasize when there is a rain "after a long time"

Snails are similar to amphibians in that they breathe through their skin (though they also have gills or lungs). Under dry conditions, they seek cover to combat dessication. But when it rains, they "come out," just like many amphibians.

I should qualify the first sentence to say SOME snails. There are aquatic snails and terrestrial snails (which I'm sure you're referring to). Aquatic snails generally have gills, while most terrestrial snails have a single lung (I think).

Slugs, like snails, are generally found in moist areas and can often be seen after a rain.

I don't know of a single reference that pulls it all together, but this is a good place to start...

The Living World of Molluscs


Why is there smooth muscle in our bronchioles? Having muscle tissue in our bronchioles that can constrict seems like a poor choice for tissue. Why would our airway want to ever close up? Wouldn't it be more beneficial for our bronchioles to just remain open?

There are at least two things to consider.

First, ability to limit airflow is a defense mechanism for animal. Imagine getting into area of some sort of toxic evaporation, e.g. CO2 cloud near volcano , then it makes sense to decrease delivery of toxin via lungs to minimum. As I understand, that is what an allergic asthma attack. (Sorry for not providing good enough source of that)

Secondly, you are incorrect in assuming that normal state is "dilated". Dilation of branchioles is sympathetic ("fight-and-fly") response of the nervous system to something like danger, that requires short-term boost in energy production. That is, by default, your airflow is limited. Probably, to limit amount of energy you effectively burn via oxygenation. But most importantly, you leave yourself a reserve in terms of oxygen supply for critical moments.

Some more information you might find here.


What is the most difficult feature to explain evolutionarily? I wonder what are examples of organs/structures/behaviours/cooperation that evolutionary biologists themselves find most difficult to explain -- to explain how they could appear evolutionarily -- within known mutation rates, generation frequency, and known time frames.
Excluding issue of appearance of life itself.

Knowing rates of mutation and generation cycle (and population size), it would be possible to estimate time needed for appearance of new feature.

Thus it would be possible to spot counter-examples, such examples that are probabilistically beyond possibility to appear in given evolutionary time. Are such examples known ?

I might be naive, but I think some rare behavioral trait can be a candidate, behavior that does not trigger even once in a lifetime of organism, on average, that triggers really rarely.

To answer your question directly, there are a number of examples which creationists like to bring up, such as woodpecker's tongue which is wrapped around its brain or the archer fish which shoots down insects with water and has to adjust it's aim for refractive difference between water and air. These features supposedly 'couldn't have evolved' but of course one's disbelief doesn't make anything true or untrue. This is what Dawkins calls 'argument from personal incredulity'.

Let me also point out a few evolutionary counter arguments to such reasoning.

The presence of selection radically changes what is 'likely' or 'possible' to happen. For example, you wouldn't argue that it's highly improbable that the stones on the beach are ordered by size, if you know that the action of waves orders them in a certain way. Dawkins' weasel (http://en.wikipedia.org/wiki/Weasel_program) also demonstrates this principle.

Another Dawkins' argument is that, contrary to what creationists claim, complex features such as eye don't have to be completely functional to be useful. In the early history of life, when no organism had eyes, any simple system which could distinguish light from darkness could provide a huge advantage to its owner. The simple system can then evolve to a more complex one to provide a competitive edge etc.

Finally, evolution happens over time scales we cannot grasp. We don't have a good feeling of what billions of years of small changes which are selected for can add up to.


What determines whether a substance can diffuse across the blood-brain-barrier? What determines whether a chemical substance is able to cross the blood-brain-barrier via passive, transmembrane diffusion?  What structurally differentiates these chemicals?

Short answer
The two most important factors that favor passive diffusion across the blood-brain-barrier (BBB) are:

high lipid solubility;
low molecular weight.

And to a lesser extent:

absence of charge;
low affinity for BBB proteins;
not being a substrate for the efflux pumps present in the BBB.

Background

The blood-brain-barrier (BBB) is principally formed by the endothelial cells in the capillaries of the central nervous system (CNS), as depicted in Fig. 1. Outside the CNS, the endothelial cells lining the capillaries allow for relatively free diffusion of substances from and to the blood via transcellular diffusion. In other words, substances can diffuse relatively freely to and from the blood via the extracellular space between the endothelial cells. In contrast, endothelial cells in the capillaries in the CNS are coupled via tight junctions, which prevents most compounds from diffusing into the extracellular space in between the cells (Fig. 1). Therefore, for compounds to enter the brain, they have to diffuse into the endothelial cells and back out again into the brain. This means they have to diffuse from the aqueous milieu in the blood, through the lipid-rich cell membrane and back into an aqueous solution in the extracellular space in the brain (source: University of Texas).

Blood-brain-barrier. source: RIT

Most drugs cross the blood-brain-barrier (BBB) by transmembrane diffusion, which is mainly dependent on whether the drug is able to meld into the cell membrane. A low molecular weight and high degree of lipid solubility favor this mechanism. However, a drug taken up by the membranes in the BBB must eventually dissolve into the aqueous environment of the brain's interstitial fluid to take effect. As a result, a substance that is too lipid soluble collects in the lipid portion, but is not able to leave the BBB. I.e., it enters the BBB, but doesn't cross it.

Moreover, lipid solubility also favors uptake by the peripheral tissues; this, in turn, lowers the concentration of the drug in blood.

Thus, while lipid solubility can increase transport rate across the BBB, it can also lower the amount of the drug presented to the BBB.

Factors in addition to lipid solubility include charge, tertiary structure and degree of protein binding. Chief among these secondary factors, however, is molecular weight. The best approximation of the influence of size on BBB penetration is that it is inversely related to the square route of molecular weight. Few substances over 500 Da cross the BBB. In addition, lipid-soluble substances with molecular weights over 400 Da can be substrates for P-glycoprotein, a major brain-to-blood efflux pump located at the BBB, which prevents or greatly retards a large number of small, lipid soluble molecules from entering the CNS. However, Peptides and proteins with molecular weights in excess of 600 Da are known to cross the BBB in amounts sufficient to affect CNS function, such as the enkephalins. The largest substance found to date to cross the BBB by the mechanism of transmembrane diffusion is cytokine-induced neutrophil chemoattractant-1 at 7.8 kDa (Banks, 2009).

Note that some parts of the brain do not feature a BBB, including but not limited to, the pituitary, area postrema and pineal gland. Many of these areas participate in hormonal control. These structures hence need to be in contact with the blood stream to sense the presence of hormones and other compounds (source: University of Texas).

Reference
- Banks, BMC Neurol (2009); 9(Suppl 1): S3


What is the difference between copy number changes with and without allelic imbalance? I require some clarification on copy number aberrations (structural gain and loss in chromosomes). From what I understand, gain/loss per se can be divided into two types.

Consider two alleles, A and B at the same locus on homologous chromosomes.

Allelic Balance: in one type of structural gain/loss, there is no resulting allelic imbalance; examples:

AB ==> AABB (duplication),
AB => -- (loss).

Allelic Imbalance: in the other type of structural gain/loss, there is resulting allelic imbalance; examples:

AB ==> AAB (duplication of A),
AB => -B (deletion LOH),
AB ==> BB (copy-neutral LOH).

First, is what I have described above correct?

Second, if it is correct, what is the biology underpinning these copy number aberration types? Are the mechanisms responsible for bringing about allelically-imbalanced CN change distinct from the mechanisms for bringing about allelically-balanced CN change? What are these mechanisms?

NB. I'm confining this to just copy number-related allelic imbalance.

Allelic imbalance is a pretty broad phenomenon difference in the expression of two alleles.  As such you have listed would probably cause allelic imbalance, but it could be the result of methylation or even differences in RNA sequences between the alleles which say interfere with post translational splicing say.

In the case of copy number variations, if a copy number region (which is often a higly repetitive sequence in the genome and not a gene duplication) might interfere or not interfere with gene regulation. In cancer cells large segments of the genome may be copied or cut out though, so in that case the mechanism you put forth may be important.


Does a queen wasp sting also have poison? Last night I got sting by a wasp and because of the time of the year I suppose it is a queen. But usually it swells and hurts for a day after it, but this time nothing happened only that I woke up of the sting which hurt a little for a short time, but in the morning I couldn't find any signs of the sting.

Now is this because of the poison is worked out because it could be a pretty 'old'  new wasp queen and her enzymes like histamines and aptoxine are got too old? Or do queen wasps not use/have poison or less? Or is it my body that just reacted different?

Yes, all female wasps are expected to have venom. In the case of social wasps, which I am inferring is what stung you, all female wasps are equally potent as they're morphologically the same. [This opens the question of how could you say this was a queen wasp.] The only difference between a wasp worker and a queen is that a worker is forced to fly around and forage by the queen so it doesn't have the time and energy to invest into laying eggs.

The following paper discusses this: http://dx.doi.org/10.1590/S1519-566X2008000600011

However, not all individuals are the same, both wasps and people, so you may have been stung by a rather weakened wasp/species to which you're not particularly sensitive.

I'd like to recommend the following paper which isn't about wasps, but discusses fundamental venom composition differences between fire ant workers and queens.

Fire Ant Queen Venom is Fire Ants' Secret Weapon
This is the DOI reference: http://dx.doi.org/10.1016/j.toxicon.2018.11.428

(Free Version)
This is the DOI reference: https://doi.org/10.1101/454637

Contrary to wasps, most species of ants present a marked caste specialisation, meaning queens are quite different from workers. However, they still produce (and deliver) venom.

Thanks for your account!


Is it possible for an organism that is polypoloid with an odd number of sets of chromosomes (e.g. 5 sets) to be fertile? Is this possible, since there is five sets, there would be an unequal separation of homologous chromosomes during anaphase I of meiosis?

Yes, it is possible. There seems however to always come up with a cost in fertility eventually of the order of 2/3!

You should have a look at Ramsey and Schemske 1998. I don't remember it well enough to make a good summary (maybe someone else could do that?!) but it is a classical article. Here is a sentence from their abstract

  In contrast to the common claim that triploids are sterile, our results indicate that the triploid bridge pathway can contribute significantly to autopolyploid formation regardless of the mating system, and to allopolyploid formation in outcrossing taxa.


What is this bizarre insect? Well, a friend of mine sent me this picture of an creepy insect. I'm wondering if the picture is photoshoped or if it is real. It is said the insect lives in Indonesia, but I'm not sure.

Can anyone identify this? Thanks.

This is a Creatonotos gangis

This nice arctiine moth was described by Linnaeus in 1763.
The species  lives in South East Asia and parts of Australia.

C. gangis went viral earlier this year because of a post in The independent where they wrote about a facebook video on the species... I don't know if this is the same video that was popular at facebook, but take a look:

https://www.youtube.com/watch?v=hn1ms8qfqzM

Furthermore, I can tell you that those weird tentacles are in fact scent organs which secrete pheromones in order to attract sexual mates. And also, their larvae cause huge problems because they eat pomegranade leaves


Neuron connectivity- how are they connected physically If Neurons are only connected through synapse and there is no physical connection,  how are they just suspended in brain layers?

Neurons are suspended, as you say, in an extracellular matrix. Brain tissues are a little bit more specific. Here I quote a few summaries from literature to answer and give your a perspective on your basic question. In bold I highlight important statements which differentiate the brain's ECM from the ECM found elsewhere in the body.

  Barros, Franco & Müller, 2011: An astonishing number of extracellular matrix glycoproteins are
  expressed in dynamic patterns in the developing and adult nervous
  system. Neural stem cells, neurons, and glia express receptors that
  mediate interactions with specific extracellular matrix molecules.
  Functional studies in vitro and genetic studies in mice have provided
  evidence that the extracellular matrix affects virtually all aspects
  of nervous system development and function. Here we will summarize
  recent findings that have shed light on the specific functions of
  defined extracellular matrix molecules on such diverse processes as
  neural stem cell differentiation, neuronal migration, the formation of
  axonal tracts, and the maturation and function of synapses in the
  peripheral and central nervous system.

  Ruoslahti, 1996: The extracellular matrix of the adult brain
  tissue has a unique composition. The striking feature of this matrix
  is the prominence of lecticans, proteoglycans that contain a lectin
  domain and a hyaluronic acid-binding domain. Hyaluronic acid and
  tenascin family adhesive/anti-adhesive proteins are also abundant.
  Matrix proteins common in other tissues are nearly absent in adult
  brain. The brain extracellular matrix appears to have trophic effects
  on neuronal cells and affect neurite outgrowth. The unique composition
  of this matrix may be responsible for the resistance of brain tissue
  toward invasion by tumors of non-neuronal origin.

  Dityatev et al. 2010: The extracellular matrix (ECM) of the
  central nervous system is well recognized as a migration and diffusion
  barrier that allows for the trapping and presentation of growth
  factors to their receptors at the cell surface. Recent data highlight
  the importance of ECM molecules as synaptic and perisynaptic scaffolds
  that direct the clustering of neurotransmitter receptors in the
  postsynaptic compartment and that present barriers to reduce the
  lateral diffusion of membrane proteins away from synapses. The ECM
  also contributes to the migration and differentiation of stem cells in
  the neurogenic niche and organizes the polarized localization of ion
  channels and transporters at contacts between astrocytic processes and
  blood vessels. Thus, the ECM contributes to functional
  compartmentalization in the brain.


What's the physical meaning of Svedberg unit? Sedimentation coefficients, using a centrifuge, are expressed using Svedberg unit (symbol S, sometimes Sv). Wikipedia states that $S = 10^{-13}$ sec but I also saw in a book that actually $S = 10^{-13}$ sec/$\text{rad}^2$. Which of these is correct?

I know that a 50S ribosome has higher molecular weight than a 30S ribosome and for that reason the 50S would travel faster (on a test tube placed in the centrifuge) than a 30S, but if substitute S by $10^{-13}$ sec, for me it's a little bit-non intuitive, because 50S would be $50\cdot{10^-13}$ sec (and that is greater than $30\cdot{10^-13}$ sec), which means it takes more time to travel? Obviously not, so what's the physical meaning of time in this situation?

In response to Alan Boyd:

"In other words, at 1x g a 1S particle will travel at $10^{-13} m\cdot s^{-1}$" or $10^{-12}$?
Indeed 5.5h is a reasonable value but I still cannot understand the significance of the ratio between velocity and acceleration which corresponds to Svedberg units (in seconds).
Maybe $50\cdot{10^-13}$ sec is the time that our ribosome takes to reach the terminal velocity in the fluid? That would make some sense, for example, if I drop an unfolded A4 paper to the ground the time it will take to reach terminal velocity will be lower than the time a A4 folded paper will take to reach it's specific terminal velocity, which is higher than the velocity from the unfolded A4 paper, because the area is larger (the friction force acting on it will be very high) which is consistent with the observations that are made (in centrifugation objects with larger surface area will travel at a slower terminal velocity). What do you think ?

Wikipedia:

  The sedimentation coefficient is the ratio of the speed of a substance in a centrifuge to its acceleration in comparable units. A substance with a sedimentation coefficient of 26S (26×10−13 s) will travel at 26 micrometers per second (26×10−6 m/s) under the influence of an acceleration of a million gravities (107 m/s2). Centrifugal acceleration is given as rω2; where r is the radial distance from the rotation axis and ω is the angular velocity in radians per second.

In other words, at 1x g a 1S particle will travel at 10-13 m s-1 = 0.1 pm s-1

Particles with higher values of S will travel proportionately faster, and increasing g force will also increase sedimentation rate.

Let's look at the example of a 50S ribosome at 100 000 g:

rate of sedimentation = 10-13 x 105 x 50 m per sec = 50 x 10-8 m s-1

So how long to travel 10 cm = 10-2 m?

=10-2/(50 x 1010-8) s

= approximately 5.5 h, which seems about right.


What effect has changing pH and salt concentration on protein complexes? I'm struggling to find peer reviewed literature that explains the effect of changing the pH and the salt concentration on protein/protein complexes in solution. What effect does the pH and the salt concentration have and what is the physical basis behind this?

The formation of protein complexes or aggregates in aqueous buffers is determined by a number of factors: physical properties of the protein itself, pH, temperature, type and concentration of the used cosolvent (salt). Solutes are often roughly divided by type into chaotropes ('disorder-making'), which destabilise protein structures and kosmotropes ('order-making'), which stabilize them. [1, 2]

Chaotropic salts interfere with intramolecular interactions mediated by non-covalent forces such as hydrogen bonds, van der Waals forces, and hydrophobic interactions, which, at high cosolvent concentrations, results in protein denaturation.

Kosmotropic salts, on the other hand, cause water molecules to favorably interact, which also stabilizes intermolecular interactions in proteins. The salt molecules readily interact with water from the protein's hydratation shell and remove it from the protein surface, which produces thermodynamically unfavourable interactions that are reduced when proteins associate to form complexes. With increase in salt concentration the protein precipitation (salting out) increases.

Both cations and anions have been ranked separately by their capacity to precipitate proteins, to form a Hofmeister series [3, 4] (first set in 1888 but still hotly debated), e.g.:

SO42− > H2PO4− > CH3COO− > Cl− > Br−

At large salt concentrations protein solubility is given by the empirical Cohn equation [6]:

lnS = α − βc

where S is the protein solubility, c is the salt's ionic strength, α and β are empirical constants characteristic of particular salt.

Salting-out agents are very widely used in protein purification (to concentrate proteins eg. with ammonium sulfate), chromatography or crystalization.

The influence of pH on protein-protein interactions in solution works through altering of the electrostatic properties of protein surfaces. At pH equal to the protein's isoelectric point (pI), where its net charge is neutral, charge repulsions of similar molecules are relatively low and many proteins will aggregate. Very low and very high pH will case proteins to denature; during digestion, for instance, proteins are in extremely low and then extremly high pH that exposes their backbones for enzymatic degradation.

For more information, please refer to:

Martin Chaplin, Kosmotropes and Chaotropes, http://www.lsbu.ac.uk/water/kosmos.html
Zangi R. Can salting-in/salting-out ions be classified as chaotropes/kosmotropes? J Phys Chem B. 2010 Jan 14;114(1):643-50.
Pace CN, Treviño S, Prabhakaran E, Scholtz JM. Protein structure, stability and solubility in water and other solvents. Philos Trans R Soc Lond B Biol Sci. 2004 Aug 29;359(1448):1225-34; discussion 1234-5.
Shimizu S, McLaren WM, Matubayasi N. The Hofmeister series and protein-salt interactions. J Chem Phys. 2006 Jun 21;124(23):234905.
Zhang Y, Cremer PS. Interactions between macromolecules and ions: The Hofmeister series. Curr Opin Chem Biol. 2006 Dec;10(6):658-63. Epub 2006 Oct 10.
Ruckenstein E, Shulgin IL. Effect of salts and organic additives on the solubility of proteins in aqueous solutions. Adv Colloid Interface Sci. 2006 Nov 16;123-126:97-103. Epub 2006 Jun 30.


Is the thecal sac ectoderm? The thecal sac, or dural sac, is the membranous sheath of dura mater that surrounds the spinal cord and the cauda equina. The thecal sac contains the cerebrospinal fluid in which the spinal cord 'floats'.

Is the dura matter ectoderm? I know neural crest and such is ectoderm. But the meninges, in particular the dura, where do they come from?

The dura mater is formed by the mesoderm. The mesoderm is the middle layer of the early trilaminar embryo. The three germ layers are the ectoderm, mesoderm and endoderm, formed by gastrulation. The middle germ layer forms connective tissues and muscle throughout the body, with the exception of the head region, where some of these structures have a neural crest (ectoderm) origin. Connective tissues include cartilage, bone, blood, blood vessel endothelium and dermis, but also the dura mater. The muscles include cardiac, skeletal and smooth muscle (fig. 1).

Fig. 1. Germ layers. Source: UNSW

Source
- UNSW


What is the difference between neurotransmitters acting as neurotransmitters and hormones? My main confusion is what differentiates the action of a transmitter substance as a neurotransmitter and as a hormone. For example, when norepinephrine is being talked about as transmitter substance that modulates brain responsiveness and information processing, it's a neurotransmitter. But when norepinephrine is involved in the functions of the autonomic nervous system (ANS), does it work as a hormone or a neurotransmitter?

Quoting from Physiology of Behavior, by N. Carlson, 2013 edition:

  "Neurons in the central nervous system contain a1- and a2-adrenergic
  receptors and b1- and b2-adrenergic receptors. All four kinds of
  receptors are also found in various organs of the body besides the
  brain and are responsible for the effects of epinephrine and
  norepinephrine when they act as hormones outside the central nervous
  system."

So does that mean that whenever norepinephrine works outside the CNS, it works as a hormone?

This figure from Campbell (2011), chapter 45, is very didactic and may clarify this nomenclature for you.

The processes of interest here are a, d and e:

The definition of hormone (in animals) is quite simple: a signaling molecule released in the bloodstream. That's the process a in the figure.

On the other hand, a neurotransmitter is released in the synapse, acting locally. That's the process d in the figure.

However, some nerve cells release their signaling molecule in the bloodstream (process e in the figure). Unlike the synaptic signaling, this molecule can act on a target cell at great distance.

So, despite the fact that we're talking about the very same molecule (norepinephrine in your example), in that last process this molecule is technically speaking a hormone, not a neurotransmitter anymore.

Source: Reece, J., Reece, J. and Campbell, N. (2011). Campbell biology. Boston: Pearson Learning Solutions.


What would be the molar concentration of human DNA in a normal human cell? A diploid human cell has 46 chromosomes. A haploid cell has DNA approximately 3.2 billion bases long. What is the molar concentration of DNA in the cell then? How would we calculate?

I will assume that be "molar concentration of DNA", you mean "molar concentration of nucleotides".

Cell size

Assuming a cell with a radius of 0.05 nm (nanometer). Assuming a perfect sphere, the volume of such sphere is $5.24\cdot 10^{-4} nm^3 = 5.24\cdot 10^{-11} L$.

Of course, cell volume varies a lot among different cell types. The final result will drastically depend upon the cell volume considered (Thanks to @Roland fo highlighting that in the comment).

Number of nucleotides

In the nucleus

The haploid genome size is about $3.2\cdot 10^9$ nucleotides. The whole genome is therefore $6.4\cdot 10^9$ nucleotides. As there are two DNA strands at each haploid genome, we have to further multiply by two to get $1.28\cdot 10^{10}$ nucleotides. Note that this number could be lower at other moment of the life cycle. What I am computing here is the maximal number of nucleotides per nucleus

In the mitochondria

There are about 1500 mitochondria per cell. Each mitochondria contains about 16,000 nucleotides resulting in a total of $2.4\cdot 10^7$ nucleotidesin mitochondria per cell.

mitochondria + nucleus

$2.4\cdot 10^7 + 1.28\cdot 10^{10} ≈ 1.28\cdot 10^{10}$. That is mtDNA is negligible.

In the mols

The Avogadro number is about $6 \cdot 10 ^{23}$. Hence, there are $\frac{1.28\cdot 10^{10}}{6\cdot 10^{23}} = 3.2\cdot 10^{-14}$ mols of nucleotides per cell.

Molarity

Molarity is defined is defined as the number of mols per liter. It is therefore

$$\frac{3.2\cdot 10^{-14}}{5.24\cdot 10^{-11}} ≈ 0.0006M$$


Safe parameters for external nerve stimulation using electrical impulses Introduction

I've recently stumbled upon David Eagleman's TED talk on the concept of sensory substitution and addition. Being the most inspiring thing I've seen on the internet for the last few months I've decided to give it a try and mix it with some of my coding/electronics projects.

I've settled on using electrical impulses over electrode pads to feed sensory data onto a patch of skin, instead of vibro-motors as it is more energy efficient. That being said, when planning on running electrical current through me 24/7, safety obviously comes first.

[edit]
I am targeting the lower back or the side of the hips as these parts have the least contact with the environment and won't make you look goofy. In the long run this would probably have to run on dry skin to avoid the "wrinkling effect", caused when staying in water for too long.

Questions

Main unknowns I want to sort out are:

What is the range of perceivable voltage and current that can be safely  fed through the skin without causing any damage to the nerves or any other part of the body?
Is there a risk of permanent damage or reduction of sensitivity of nerves when exposed to an electrical current for a prolonged time? Any way to circumvent this problem?
What "resolution" or input density can I hope to achieve, before signal becomes "blurry" because of cross-talk?

Nice question(s). I will go through them in sequence.

Safe current limits. With regard to electrical stimuli it is current density that determines safety limits. Therefore, in medical devices, it is not a matter of what is a safe maximum current level, but what is the maximum safe current level given the surface of the electrode? And in terms of skin stimulation, it is not the safety limit that is the bottle neck, but the maximum tolerable current density, which is around 0.5 mA/cm2 (Prausnitz, 1996). Higher stimuli result in pain sensations. This is one of the reasons why the BrainPort device is used on the tongue; the moist surface reduces impedance and hence the currrent needed to elicit a tactile response.
Permanent damage. As said, the tolerable sensation limit is more of an issue (a must-read in this regard is Kaczmareck et al., 1991).
Acuity. The best-possible tactile "resolution" is generally expressed in terms of tactile acuity. Tactile acuity varies across body sites, and unfortunately it is about the worst on the thigh (45 mm) and the back (40 mm). A much cited picture on tactile acuities is the following from Weinstein (1968):

These acuities represent the distance in which 2 simultaneously presented, static pressure points need to be spaced to be just noticeable (the so called two-point discrimination threshold). Although your proposed electric stimuli are different from pressure stimuli, these reported values in the figure (40 - 45 mm) give an impression on the inter-electrode distance needed. From my own work I can confirm the ~40 mm using vibratory stimuli. The unfavorable acuity of the back and external bodily skin in general was also one of the rasons to put the electrode grid of the BrainPort on the tongue, which has excellent tactile acuity.

References
 - Kaczmareck et al. IEEE Trans Biomed Eng 1991;38:1-16
 - Prausnitz, Adv Drug Delivery Rev 1996;18:395-425
 - Weinstein S. 1968. In: Kenshalo. The Skin Senses:195-222. Springfield, IL: Thomas


Why can't bacteriophages survive inside the human body thus negating the possibility of using them against bacteria? I read about the therapeutic uses of bacteriophages in Pelczar's Microbiology. It was written that it is reasonable to think that bacteriophages could be used to kill pathogenic bacteria. However, the book also clearly stated that after a lot of research it was found that bacteriophages can't be used to kill bacteria in the human body because they can't survive inside the human body. But no reason was given why.

This question cannot be answered, because the assumption behind your question is wrong. I haven't found a source to claim that bacteriophages cannot survive in the human body. Bacteriophages can and are, in fact, used as a treatment against human bacterial infections, it's called "phage therapy" (1,2,3).

This is, nevertheless, a rather uncommon procedure for a number of reasons:

Availability: Compared to antibiotics, which you can easily get from any doctor/pharmacy, phage therapy requires special facilities, because very specific phages need to be produced for each disease.
Safety and regulation: Virus handling requires special safety measures and using them in humans requires a lot of paperwork, safety tests and clinical trials.
Money: Due to the reasons above, phage therapy is a lot more expensive than antibiotics.
Lack of research: Thanks to the availability of antibiotics there was no urgent need to develop the application of phage therapy. We know comparably little about how the immune system might react to bacteriophages in the blood or bacterial toxins released by lysed bacteria. We haven't found a way to e.g. quickly engineer bacteriophages for diseases.

With a growing concern about multi-drug resistant bacteria, developing new ways to combat diseases has become more important. Maybe phage therapy will be one way to deal with this more regularly in the future.


Is egg white lysozyme different from bacterial lysozyme? Someone told me that microbial lysozyme has effect on gram negative bacteria but egg white lysozyme only affect gram positive bacteria. Is it true?

PubMed query: "lysozyme"[Title] returns 8673 papers (many of which contain useful data about the activities of bacterial- and chicken-type lysozyme/muramidase against Gram-positive and Gram-negative bacteria).

For example, Gajda & Bugla-Płoskońska (2014, Postepy Hig Med Dosw 21, 1501-1515) write:

  Lysozyme (LZ, muramidase, N-acetylmuramylhydrolase) is a protein occuring in animals, plants, bacteria and viruses.

  Lysozyme hydrolyzes the β-1,4 glycosidic bonds between N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) of cell
  wall peptidoglycan (PG) in Gram-positive and Gram-negative
  bacteria.

  In the animal kingdom, three muramidase types have been
  identified: the c-type (chicken type), the g-type (goose-type) and the
  i-type (invertebrates).

  Muramidase shows bactericidal activity mainly against Gram-positive bacteria. Cytolytic activity against cells of Gram-negative bacteria
  has not been proved.

Lysozyme hydrolyzes bacterial cell walls, which is why its muramidase activity is more effective against Gram-positive than Gram-negative bacteria, for the former have thicker cell walls. Whether or not there is any difference in the effectiveness between the bacterial- and chicken-type lysozyme can be found in the papers; i have not read them.

But one of the 8673 papers is titled Hen egg white lysozyme permeabilizes Escherichia coli outer and inner membranes (Derde et al., 2013, J Agric Food Chem. 16: 9922-9929).

The quick-and-dirty answer to the question, is it true that bacterial lysozyme affects Gram-negative bacteria but hen-egg (chicken-type) lysozyme only affects Gram-positive bacteria? is: No.

The 'slow-and-clean' answer can be found in those 8673 papers.


Pump to separate protein/DNA instead of electrophoresis? I know that DNA molecules or proteins can be separated in electrophoresis because the electrical charge is used to pull the DNA through the gel. So instead of using electrical, can I using physical impact like pumping ?

If you tried to set up a system in which movement of DNA molecules through a gel matrix was driven by pumping buffer, the gel would become compressed. I am old enough to remember running vertical agarose gel electrophoresis overnight, and these gels would collapse under normal pressure to about 2/3rds of their initial height. A gel porous enough to give useful separation of DNA molecules just isn't strong enough to withstand pumping.


Why will world population keep growing if all women have only 2.1 children Why is it that, even if we were going to immediately agree that every women will not have more than 2.1 children on average, the world population would continue to grow for another 60 years? I've learned that a TFR of 2.1 means the population is at 0 growth rate. I guessed the answer was the population-lag effect, but since we are assuming that ALL women immediately have only 2.1 children on average, wouldn't there be a 0 population growth immediately and not after 60 years? Thanks in advance!

As you mention, the population-lag effect is responsible for this. From The Wikipedia article on TFR: http://en.wikipedia.org/wiki/Total_fertility_rate#Population-lag_effect

  A population that has recently dropped below replacement-level
  fertility will continue to grow, because the recent high fertility
  produced large numbers of young couples who would now be in their
  childbearing years.

Thus, even if the current TFR implies long-term stability, the recent history of TFR values will continue to affect birth rates, and thus population growth/decrease, in the future.

Imagine that you have a stable population, with static birth and death rates. Now imagine that the birth rate during a single year for some reason doubles before dropping back to normal the next year, thus transiently increasing TFR. Now, it is easy to see that when the newly born, larger-than-normal generation reaches reproductive age, the population will increase again because the birth rate will increase in proportion with the size of the generation, while the death rate is unaffected until the enlarged generation reaches old age and starts dying off. Later, the population will decrease to its long-term stable level, which will be larger than before the TFR spike.