In which phenomena does one gene pair hide the effect of other unit? This question was asken in an exam,

The answer they are saying is "Epistasis". But I think "Dominance" fits better,  because it is not mentioned whether genes of same allele are to be considered or different allele. Also it is not told whether genes in same locus are being talked of or different.

Please give some reference if you can. I know only school level biology. I do not know even in detail what allele and locus are. As far as I could understand from wikipedea and other sources I think "Dominance" is correct.

The definition of "gene", according to The American Heritage Science Dictionary is:

"A segment of DNA, occupying a specific place on a chromosome, that is the basic unit of heredity. Genes act by directing the production of RNA, which determines the synthesis of proteins that make up living matter and are the catalysts of all cellular processes. The proteins that are determined by genetic DNA result in specific physical traits, such as the shape of a plant leaf, the coloration of an animal's coat, or the texture of a person's hair. Different forms of genes, called alleles, determine how these traits are expressed in a given individual. Humans are thought to have about 35,000 genes, while bacteria have between 500 and 6,000. See also dominant, recessive. See Note at Mendel."

So, when the question refers to genes, it must be referring to two different genes on two different loci. If the question was referring to alleles of the same gene on the same locus, the correct answer would be dominance, but since it is referring to two different genes, the answer is epistasis.


Euthyrodism and goitre I read in Tortora and Derrickson that goitre is associated with euthyrodism.

How is that possible?

In this context, euthyroidism refers to the amount of hormone present.

What is a goiter:

  The term “goiter” simply refers to the abnormal enlargement of the thyroid gland. It is important to know that the presence of a goiter does not necessarily mean that the thyroid gland is malfunctioning. A goiter can occur in a gland that is producing too much hormone (hyperthyroidism), too little hormone (hypothyroidism), or the correct amount of hormone (euthyroidism). A goiter indicates there is a condition present which is causing the thyroid to grow abnormally.

See also here and here for more of the same info.

ETA: According to this:

  Chronic lymphocytic thyroiditis (CLT), also known as Hashimoto thyroiditis, is an autoimmune, inflammatory process that causes up to 55% to 65% of all euthyroid goitres...

Although, as the link I already gave above state, regular ol' iodine deficiency can still cause euthyroid goiter.


Is a fat-soluble vitamin a lipid? I read in a chemistry book that a steroid is a class of lipids, and that the fat-soluble vitamins like vitamin D are part of steroids. So is a fat-soluble vitamin a lipid?
This makes me confused as the lipid nutrients seems to contain vitamins which make another type of nutrients.

Yes steroids are a class of lipids which include cholesterol and sex-hormones such as testosterone and estrogen. Only vitamin-D belongs to the class of steroids.

Vitamins A, E and K are isoprenoids. In fact even steroids are synthesized from simple isoprenoids. You can refer to a standard biochemistry book to understand steroid biosynthesis pathway.

There are other classes of lipids too, such as fatty acids, phospholipids, ceramides etc.

Yes all fat-soluble vitamins are lipids. This is the definition of Lipids from the IUPAC goldbook:

  A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

Both fats and fat-soluble vitamins are nutrients but are functionally different. Fats provide energy whereas vitamins perform regulatory activity and are required in little amounts in the diet compared to essential fatty acids.


Mitotic crossover happens in G1? I was reading this article in wikipedia and came across this :

  It has been suggested that recombination takes place during G1, when
  the DNA is in its 2-strand phase, and replicated during DNA synthesis.

If For example - allele A is present on 1 and a is present on 1' and recombination happens such that a is present on 1 and A on 1' and then both get duplicated during S phase.

So how are the daughter cells going to be different from one another and from the mother cell in terms of phenotype? (obviously the alleles around these alleles are going to change)

How can this result in twin spotting in drosophila or any other trait occurring due to coming together of homozygous alleles by mitotic crossovers ?

First off this is called genetic mosaicism and indeed mitotic recombination is a contribution factor.

Mitotic crossover events involve the exchange, by homologous recombination, of regions of chromosomes. 60% of homologous recombination events might occur during G1 and 40% of those event occurs after chromosomes are replicated (see this paper). For twin spotting to occur, you need the homologous recombination to happen on replicated chromosomes (i.e. you need 4 chromatids).

For you question on twin spotting. The following picture illustrates well what are the outcomes of homologous recombination involving two alleles and replicated chromosomes (each line being a chromatid).

If the cell is heterozygous (normal phenotype) for the two recessive alleles, here called y and sn (respectively the "yellow" and "singed bristles" alleles), then two recombination scenarios are possible and differs based on where the recombination occurred. Note that y+ and sn+ are the wild-type alleles and carrying those alleles do not provoke a particular phenotype. The phenotype of the resulting daughter cells are:

Twin spots: Yellow but not singed spots (y/sn+) and singed but not yellow spots (y+/sn) for recombination after the y/sn locus
Single yellow spots: Yellow but not singed spots (y/sn+) and no spots (y+/sn+) for recombination between y and sn

Here the actual picture of what happens:

Therefore this should make clear why daughter cells can show phenotypes that differ from the original parent cell, i.e. the combination of alleles (especially for recessive ones) changes after mitotic crossover events. The twin spot phenotype in Drosophila melanogaster is an excellent example for illustrating that.


PedigreeAnalysis Genetics Hello! I need help with this exercise question. I am not really sure which pedigree diagram is autosomal and which is not. But, is question b 1/2. Can someone give an explanation? Thanks very much in advance? Appreciate any help!!

According to the key given, the one shaded black on the right is autosomal and one on the left is sex linked.

Yes, the answer to b is half because Maria is XhX ans Peter is XY and so the probability of the child having this disease is 1/2.


Why do I smell flowers after sneezing? Often when I sneeze, I smell flowers for a few seconds afterwards.

I've done some searching on the internet, and apparently it's something that is at least not entirely uncommon, although the exact smell description seems to differ. It's sometimes also referred to as a 'honey sneeze'.

Just to be clear, there are no flowers anywhere in sight when I sneeze.

Biology has never been a field of study of mine, but the scientist in me finds it fascinating. I've yet to come across any real explanation for this phenomenon, only guesses.

Does anyone know what causes this, or can you at least give a somewhat likely explanation?

Edit:
When I sneeze through my mouth, I do not get the same smell sensation.

This will be a hypothetical answer for the moment, so take it with a grain of salt until I can find sources or someone else does:

My best (educated) guess would be that the smell is there all the time, and when you sneeze you reset what's currently being "ignored" (in that you are not aware of it, though it is being sensed) by your brain momentarily. The source of the smell may be up in the air - it could be cologne/perfume, fabric softener residue on your clothes, what you ate for breakfast and are currently digesting, the bar of soap in the kitchen, etc. - but I haven't heard of "scent illusions" before.

One very quirky way of possibly testing that out is to remove yourself from your regular environment, sniff some ground coffee beans for half a minute, and then re-enter your home or smell your clothes to see if any of the scents match up with what you do smell when you sneeze.

My apologies that this isn't a thoroughly-sourced answer, but hopefully it acts as a good starting point.


Ways to distinguish between purifying selection and selective sweep When looking a population genomic data, regions of low diversity (lower than expected; such as in a region of high recombination) can indicate either purifying selection of deleterious mutations or a selective sweep of an adaptive mutation. What are some ways one can tell which one occurred?

One way I've heard of is to use an outgroup that did not live through the same events as the main group. If the outgroup also has low diversity, it means nonsynonymous mutations in that region are deleterious regardless of events, and so those homogeneous regions likely underwent purifying selection. If the outgroup has high diversity in those regions, the main group likely went through a selective sweep.

What are other ways to distinguish between the two?

Welcome to Biology.SE!

I actually recently went through the literature on this and similar subject, so I'll be happy to answer.

The answer will not be easy to formulate as a number of authors are working and arguing on the question. I will try to give a quick overview of methods.

Definitions: Background selection and selective sweep

First off, let's use the correct terms. As you decribed, both positive and purifying selection is reducing genetic diversity at nearby loci. When the reduction in genetic diversity is caused by positive selection, we call the process selective sweep . When the reduction in genetic diversity is caused by purifying selection, we call the process background selection.

What affect background selection?

Recombination rate
Strength of selection.

For a given neutral locus at distance $r$ centimorgans from a locus under purifying selection, the selective coefficient $s$ that is causing the highest decrease in genetic diversity is $s=r$ (Nordborg 1997).

Mutation rate
population structure

What affect a selective sweep?

Strength of selection
population structure
Number of loci involved under adaptation
Whether adaptation comes from de novo mutation or standing genetic variation

By the way, you might want to have a look at the terms 'soft sweep' vs 'hard sweep' in relationship to the two last elements of the above list and in relation to local adaptation.

How to disentangle Background selection from selective sweep?

There are a number of technics but again all of that is a work-in-progress. I would like to classify these methods into three themes.

Environmental covariate

This first element talks about disentangling local selection from background selection. It is maybe not exactly what you asked for but this discussion often comes to center stage in the literature talking about both.

If we assume to know the environmental variable causing the adaptation, then you can compare divergence between population present in different environments and those present in the same environment. If loss of genetic diversity is caused by local selection, then divergence should be higher between population occurring in difference environments. If loss of genetic diversity is caused by background selection, then all populations will show similar divergence. Bayesian Technics such as BayEnv2 (Gunther and Coop 2013) take advantage of this technic.

Among lineages comparisons

By comparing related species, it is possible to find out regions of low genetic diversity. If all related lineage show similar loss of genetic diversity irrespective to the existence of an adaptive event, then the loss of genetic diversity is likely caused by background selection.

From such methods (but I might not totally understand them, I should read the paper again), some authors (such as McVicker 2009) have build B-map and recently implemented in BayeScan (Huber et al. 2016; BayeScan is an Fst outlier method to detect local adaptation), that is map of the genome of the intensity of background selection measured by the B-value introduced by Charlesworth (history of the term reviewed in Charlesworth 2012)

Allele-Frequency-Spectrum

Both background selection and a selective sweep affect the Allele-Frequency-Spectrum as to cause an excess of rare alleles (Tajima's D < 0). However, the strength of the effect and the detailed effect on the Allele-Frequency-Spectrum is not quite the same and some authors have suggested to use such differences to disentangle the two.

Reading suggestions

There is a lot to read on the subject. I would recommend the recent special issue in Molecular Ecology DETECTING SELECTION IN NATURAL POPULATIONS including the review Haasl and Payseur 2016.


Is it correct that the nicotinic acetylcholine receptor has nothing to do with Dopamin? As I know Dopamine is almost exclusively produced via metabotropic receptors, is it possible for a nicotinic ACH receptor to influence a dopamineric neuron?
Can a nicotinic ACH receptor cause a dopamineric synapse to create dopamine?

Unfortunately I can't find anything about it.

Edit: rephrasing my question:  Do 2-neural systems exist where neuron A has a nACH-R and neuron B has a dopamineric receptor? And do dopamineric nikotinic ACH-R exist (receptors which react to dopamine)?

Let's simplify your question with correct terminology: you have a presynaptic neuron and a post-synaptic neuron. The presynaptic neuron can release multiple signals (neurotransmitters) into the synaptic space, or cleft. The postsynaptic neuron can be equipped with multiple sensors (receptors) that are specific to detect certain signals.

The signal and the sensor don't have to match, although this is costly if it's poorly tuned. Most neurons that are entirely unresponsive are pruned. Darwinian selection makes circuits much more efficient than what pure chance alone would produce, but remember that nature can be quite imperfect and stochastic.

However, you can have neurons that have a dopamine sensor (receptor) and provide an acetylcholine signal (neurotransmitter) and vice versa.

Acetylcholonergic and dopaminergic neurons can be connected. Here is an example.

Also, most people forget that neurons not only form chemical synapses but electrical synapses as well. That means the circuitry does not rely on ligands and receptors.


Mithradates - Developing immunity to poison? According to legend, Mithridates studiously researched and examined all known toxins and experimented with potential remedies by using prisoners as his guinea pigs. Supposedly, Mithridates’ toils paid off because numerous ancient authors, including Pliny the Elder, claimed that he created and regularly ingested a universal antidote for all identified toxins, and it became known as mithridate (mithridatium).

It was said that he was pretty much ingesting small amounts of poison to develop an immunity to it.

Whether universal poison or ingesting each type one by one, is this possible to build up your body to resist or be immune to poison/venom/toxins in general?

Welcome to SE. Edit: The answer is in two parts based on the mechanism of action of the toxin. Courtesy: @David and @jamesqf

Immunity

The white blood cells in the body are responsible for recognizing self or non-self peptides and form the adaptive compartment of the immune system. The B lymphocytes have a receptor that can bind to various peptides. Upon recognition of foreign peptides in the body, they go through a reaction (somatic hypermutation) to become further specific to the foreign peptide. They also differentiate into Plasma cells which can now secret another protein (antibodies) which neutralizes the foreign peptide.

Small amounts, which are non-lethal, but in enough concentration to drive the B cell reaction creates an immunological "memory". This memory allows a faster response to the same peptide compared to the reaction. This in order allows the body to withstand a higher concentration of toxic peptide, which otherwise would have been lethal as its being neutralized.

Vaccines work on a principle very close to this.

Homeostasis

Every toxin interacts which some biological process and drives it out of balance. The body actively tries to restore the balance by some means.

For example, if a ligand is depleted the body can increase the number of receptors to counter the effect and vice versa.

By ingesting small amounts of toxins body can adjust the equilibrium by very small amount at a time adjusting the concentration of relevant ligands or receptors.

Again, the person who has been through this process can withstand a higher dosage of the toxin compared to a person who hasn't.


Is there any way the food industry can benefit from biofilms? I realize all of the disadvantages, but I am wondering if the food industry can actually benefit from the formation of biofilms.

inf3rno's comment provides a great example, in the production of vinegar (Food Safety Magazine):

  In the production of some fermented foods, biofilms are an essential element for optimum production. During the production of vinegar, acetic acid bacteria are allowed to grow on wood chips. The biofilm that is formed helps make the conversion of substrate to acid more efficient.

This paper, Biofilms in the Food Environment (Czaczyk & Myszka, 2014) also provides examples of biofilm use in industrial food production (on page 75, 14th page in the linked PDF):

  Bioreactors
  with biofilms (biofilms represent a natural form of cell immobilization) are used to obtain acetic acid, citric acid, ethanol, and polysaccharides.

You can also check out Chapter 7 of this book of the same name, Biofilms in the Food Environment, for more information, if you're interested. It's not available for free online but you may be able to find it in a library.


How do steroids travel in the bloodstream? Cholesterol, which is hydrophobic, cannot simply travel in the bloodstream, and instead is enclosed in lipoprotein (LDL, HDL). Steroids, which are derived from cholesterol, are also hydrophobic (right?). So how do they travel in the bloodstream? If they are enclosed by anything, what is the molecular mechanism of their entering the target cell?

Steroid hormones are transported in an inactive form bound to proteins in the bloodstream. Androgens and estrogen are bound to Sex hormone-binding globulin (SHBG), while glucocorticoids and progestins are bound to transcortin.

References:

Transport of steroid hormones: binding of 21 endogenous steroids to
both testosterone-binding globulin and corticosteroid-binding
globulin in human plasma.
Plasma protein-mediated transport of steroid and thyroid hormones.
The Functions of Corticosteroid-Binding Globulin and Sex
Hormone-Binding Globulin: Recent Advances


Is it necessary for spiders to both wrap the prey in silk, and inject them with venom? I stumbled upon the following paragraph on the Wiki page about Argiope bruennichi:

  When a prey item is first caught in the web, Argiope bruennichi will
  quickly immobilise its prey by wrapping it in silk. The prey is then
  bitten and then injected with a paralysing venom and a
  protein-dissolving enzyme.

On hindsight, it seems a bit redundant to do both those things. If prey is caught in the web, which is rather sticky and therefore restricts its movement, isn't it possible for the spider to go right ahead and inject venom?

Or on the other hand, if it wraps and immobilises the prey in silk, wouldn't it be more logical to then leave it to die, from some sort of evolutionary standpoint of wanting to saving energy and resources?

Nice question!

Based on some previous observations on other web spiders, I belive that these "redundant" behaviors are selected to avoid prey scapes, and are not trully redundant if we remenber that some preys are able to evade even if wraped. Some beetles can find a way out from the web, moving their strong legs with projections, eventually some silk lines are cut. Also beetles are more protected against bites then are other bugs, since many are under their natural armor.

Other possible explanation** :some bees, ants and wasps produces chemical signals when in trouble, attracting their sisters. From the spider point of view, this could be a way to get more food. But too many of these insects could possibly destroy the web, only because their are numerous. Obviously these are speculations.

Also, some wasps prey on web spiders. If the wasp eventually touches the web and entangles itself, now the wrap/bite strategy turns in defensive way, maybe with the "danger turns dinner" bonus.

 I did not search too much, but probably someone has alread tested some of these possibilities. Also, I read once that some spiders can treat distinct preys in distinct ways, even releasing some undesirable bugs from the web.

** This bee-wasp-ants-hypothesis is not based on observation, only on knowlodge about insects and spiders.


Is breathing in deodorant fumes dangerous for my brain? I noticed that I sometimes get dizzy when I accidentaly breathe in too much Axe. Also, I find the smell of alchohol rich deodorants quite unpleasant. But, I was wondering, is it actually dangerous? Can some chemical (alchohol) pass the blood-brain barrier and hurt my brain? Can it hurt other organs? It might be that I'm just dizzy because of the lack of oxygen...

You can definitely absorb alcohols by breathing them in.  But doing do is far less efficient than drinking alcohol, so you don't have anything to worry about on that front.

To address your concern we have to answer two questions: how much alcohol is transfered per unit time and is there a local dosing effect due to proximity to the blood brain barrier.

It is probably pretty obvious that while alcohol evaporates rapidly compared to water, it still takes quite awhile. Imagine trying to inhale a glass of whiskey. You would get a serious headache but 30 minutes in you would still have an almost full glass of whiskey and no alcohol buzz. For an amusing anecdote relating how hard it is to get drunk off of inhaling even from a machine designed for it, see here

As to the second point - Fortunately, the blood brain barrier is a two way street for alcohol, which means that you can't get drunk in your brain if you don't have high levels of alcohol in your bloodstream. The two would dialyze into a reasonably balanced equilibrium.


Do insects with compound eyes have depth perception? Do insects with compound eyes have depth perception? They fly as if they do, but their eyes are so close together it seems like the image would be 2 dimensional.

"1001 questions answered about insects" by Alexander Barrett and Elsie Broughton Klots includes the following passage:

  Do insects have depth perception? Depth perception of some sort is important to an animal who has to catch its prey; fortunately most
  insects have it to a degree.  Although they do not have binocular
  vision that can be compared with man's, it is true that when one eye
  is covered their depth perception is markedly affected.  The criterion
  of depth seems to depend on the angle of simultaneous stimulation of
  two corresponding points of the retina of the two eyes.

However it does not mention compound eyes specifically.

There may be other methods of obtaining a perception of distance rather than the binocular vision seen in humans.  This paper suggests that there is 'clear evidence' that  some insects perceive depth by moving their head to artificially create parallax, which they can then recognise and interpret as depth and distance.  They cite the Praying Mantis as an example, which does have compound eyes.


Can a pathogen be totally resistant to the human immune system? Can a pathogenic organism be totally resistant to the human immune system? For the purpose of this question, the organism in question must cause a disease.

Examples of organisms that would qualify as totally resistant:

Pathogenic organisms that are completely undetected by the immune system while the disease that they cause runs its course.

Pathogenic organisms that, even if detected, are completely invulnerable to the immune system. For instance, macrophages and other immune cells would not be able to destroy even one cell of such an organism.

Is it possible for such a pathogen to exist? Are there any such pathogens?
(For the purpose of this question, the HIV and diseases that only manifest in immuno-compromised individuals do not count)

I can't think of any pathogenic organisms that are completely resistant to the immune system. Some bacteria that cause chronic diseases (e.g. tuberculosis) are relatively resistant, and a handful of viruses (e.g. spumaviruses) are relatively invisible, but the nature of pathogen transmission would mean that completely resistant organisms would spread through a population pretty fast and we'd know about it.

Pathogenic prion agents, like scrapie and Creutzfeld-Jacob disease, are essentially invisible to the immune system, and can be transmitted; but they aren't pathogenic organisms. They might be the closest to your description though.


When has an organism evolved enough to be called a new species? Imagine that we take a population of horses, split them in half and place them in completely different environments. The two species will evolve separate from each other and because the environment is different, the outcome of evolution will be different.

But at what point can you say that these horses have evolved into two different species?

(I do know that they would probably go extinct if we conducted this exact experiment, but this experiment is just to give an example)

I think LuketheDuke's answer is an oversimplification of the biological species concept (possibly resulting from the dictionary having a poor definition). The definition he gives is one of many which are in current use, and is made redundant by many types of organism.

It is important to recognise that because reproduction is not the same process in all organisms, genetic differentiation between individuals occurs in different ways for different groups.

Let's take the definition given in LuketheDuke's answer...

  The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.

Under this definition, lions and tigers (see ligers and tiglons, which are sterile hybrids between the two) would be considered one species, as would donkeys and horses (see mules and hinnys, again sterile hybrids). There are hundreds of other examples of pairs of animal species which can hybridise to produce sterile offspring.

However, these animal hybrids usually only take place with human intervention, by delibrate breeding efforts. Thus we could extend the previous definition to include them...

  The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild.

That last part takes care of the ligers and tiglons. But what if we consider plants? Under the definition I just gave, most grasses (around 11,000 species) would have to be considered as one species. In the wild, most grasses will freely pollinate related species and produce hybrid seed, which germinates. You might then think we could just modify the definition to specify that the offspring must be fertile (i.e. able to reproduce with one another)...

  The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild to produce fertile progeny.

Unfortunately, the situation is still more complicated (we've barely started!). Often wild hybridisation events between plants lead to healthy, fertile offspring. In fact common wheat (Triticum aestivum) is a natural hybrid between three related species of grass. The offspring are able to breed freely with one another.

Perhaps we could account for this by taking into account whether the populations usually interbreed, and whether they form distinct populations...

  The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of populations or meta-populations of related individuals that resemble one another, are able to breed among themselves, but do tend not to breed freely with members of another species in the wild to produce fertile progeny.

This accounts for the grasses, but it still leaves a messy area when you have a hybridisation which establishes - until the hybrid population is segregated away from the parent populations it is unclear whether they still count as the same species.

We could probably live with this situation, except for the fact that bacteria refuse to conform to it at all. Bacteria of the same species, or even very different species, can freely transfer genes from one to the other in conjugation, which combined with fission can result in perfectly replicable hybrids. This is such a common occurence that it breaks even the 'tend to' part of the previous definition, and members of a population can be doing this almost constantly, which negates the segregation requirement.

Richard Dawkins had a go at defining around this, by stating that...

  two organisms are conspecific if and only if they have the same number of chromosomes and, for each chromosome, both organisms have the same number of nucleotides

This partly gets around the bacterial problem and means that bacteria which result from conjugation are a new species. Unfortunately under this definition we might as well not ever bother trying to classify bacteria as billions of new species would be created every day - something which the medical profession might have something to say about. This definition would also mean that those with genetic diseases like trisomy 21 are not human. The final nail in the coffin of this attempt is that there are many species, including frogs and plants, which are very certainly considered a single species by taxonomists but which have some variety in the presence of small accessory chromosomes, which occur in different combinations between individuals.

Let's consider one last option. We now live in the era of genomics where data about genomes of thousands of organisms is accumulating rapidly. We could try to use that data to build a species definition based upon similarity at the nucleotide level. This is often used for bacteria, by considering organisms with less than 97% nucleotide similarity to be different species.

The major point I've been trying to make, though, is that species is not a natural concept. Humans need to be able to classify organisms in order to be able to structure our knowledge about them and make it accessible to people trying to link ideas together. But the natural world doesn't care about our definitions. Ultimately the species concept is different for different groups of organisms and will continue to change over time as our analytical methods and the requirements of our knowledge change. Note that I've deliberately skipped over many historical species concept ideas.

The direct answer to your horse question is "it depends how you want to define a horse".


if sperm contains only 50% of someone's DNA how can it be used to identify someone? Is DNA so unique that 50% of it is enough to identify a single person?

The comment from @User137 pretty much gets it: the mix of all sperm cells in even a small sample will contain the whole genome on average. So in the hair example in the comments above, there are probably a good number of dead cells hanging onto the hair, enough for analysis. Meiosis will redistribute the DNA sequences inherited from mom and dad randomly, so each sperm is in theory a unique patchwork of that person's genome, but overall the genome will be covered well. Single-cell work, on the other hand, is technically very challenging.

[edit: here is an article describing methods for low-input analysis of forensic samples. Unfortunately paywalled.]

To directly answer the OP on uniqueness: absolutely a single sperm is that unique for each person, in principle. There are lots and lots of genetic variants in each human, and everyone represents a unique mix. It is estimated that 1/1000 places in the genome of each person differ from any other person, on average (for substitutions). there are 3*10^9 places in the genome for this to be the case, which gives you a very large number of differences, ASSUMING that you can actually ascertain all those differences. [edit: for a discussion of these stats see here.]

The technical problem with forensics is that often they only look at a few places in the genome (microsatellites usually), because it is relatively expensive and hard even with recent technology to look at more than that in any detail. This leads to the non-trivial possibility of misidentification with the standard battery of loci. This possibility never goes away entirely, but it becomes very small with more data. I am not a forensic scientist, possibly they have gotten more comprehensive or the methods have changed in recent times.

[edit: here is a document that has what appears to be a readable introduction to DNA forensics, including technical discussions of some drawbacks of marker panels used by for instance the FBI of the USA.]


Why don't housekeeping genes have TATA Box regions in their promoter sequences? Housekeeping genes are genes that are continuously transcribed. Like all other genes they have promoter sequences, but they don't have TATA box sequences that are used to specify from where transcription is going to begin.

Why don't housekeeping genes have a TATA Box in their promoter sequences?

Two possible answers:

First, TATA boxes has been found to cause increased "noise" in gene expression, such that the expression of genes that have a TATA box is highly variable. See this review for example.

A different set of results suggests (here) that TATA acts only as an amplifier of expression.

Regardless of whether TATA amplifies expression or also increases expression variance, this is not suited for housekeeping genes, which generally have low and constant expression.


What is the name of this big tree with look of banyan branches? Location is India, Tree is so huge & some branches are hanging like Banyan.

Its Hanging Branches look:

& Finally its leaf:

So what is it then?


Is Valerian extract a diuretic or an antidiuretic? I am trying to determine if valepotriates (valerian extract) is a diuretic or an antidiuretic. Some individuals take valerian as an herbal supplement for anxiety disorders. Some individuals claim that valerian extract can act as a diuretic, while others claim that it is an anti-diuretic. I am trying to determine which it is - diuretic or antidiuretic?

There is one study that I can find that has been cited in the medical literature that examines individuals taking valerian extract for generalized anxiety disorder. In this paper, there do not appear to be any claims that valerian has any diuretic or anti-diuretic properties. However, that's not to say that those properties don't exist. Additionally, there is no indication that the extract is associated with hyponatremia or hypernatremia, which are two other signs of disorders affecting salt/water balance. Overall, it sounds like if there is a diuretic or anti-diuretic effect of valerian, it is not well-described (yet).


What is the name of this bird from Tanzania? I took this picture in late 2018 in Tanzania. The Birds of East Africa book does not include it and I've been unable to identify it looking on the web. Can someone help me identify it, please. Thank you!

That looks like a knob-billed duck.
Their range includes Sub-Saharan Africa, India, and Southeast Asia.

Picture source


What is the difference between conditional and inducible activation? In the modern genetically modified animal models, there are not only constitutive mutations which start producing proteins already in the embryo, but also mutations which can be turned on later. I've seen the terms "conditional activation" and "inducible activation" used, especially in the context of Cre-Lox recombination.

Are they used interchangeably, or is there a difference? If they are different, what is the difference?

If I'm looking at a mouse name, like K-Ras+/G12V;Elas-tTA/tetO-Cre;p16Ink4a/19Arflox/lox, how can I recognize which of the two it is?

In my opinion the terms inducible and conditional are synonyms. Together with the term constitutive they refer to how transcription takes place, that is, the second phase in the central dogma that states that genetic information is propagated from replication to transcription to translation. The proteins that are produced during translation by ribosomes can have a feedback effect on replication and transcription.

When proteins bind to the promoter region of genes, they can induce or inhibit transcription. If a gene is preceded by a promoter region that always promotes transcription, it is said that the gene has a constitutive promoter. If the gene is transcribed conditionally, it may refer to proteins having to bind to the promoter region so that transcription can take place. There could be inverse situations and I believe the Cre/Lox technology is an example of such a situation.

Take the following as an example. A gene could be lethal meaning that if the protein it encodes is expressed it will kill the cell. It could have a promoter that promotes expression if a protein with an inhibitory effect is not bound to the promoter. Suppose I have these cells in a culture plate and I add some compound to the culture plate. The compound diffuses into the cells and binds to the inhibitory protein that is bound to the promoter region. With this binding of the compound to the protein that is in turn bound to the promoter region, the protein loses its ability to bind to the promoter region and inhibition of transcription is uplifted. Transcription then continues and expression of the lethal protein takes place after which the cell dies.

This could be used in practice as follow: if you were selling seeds to farmers, you would want them to buy seeds next year again, so you want the plant not to be able to produce viable seeds.

Coming back to your question, if you want to know more about the mice in question, you should contact the breeder as nomenclatures differ. See this article on interpreting mouse genetic nomenclature:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039125/


How can histidine be classified both as positively charged and hydrophobic? I saw the chart in this post Histidine aromaticity. Since I'm not allowed to comment and post a question instead of an answer, I have to ask my question in a separate thread.

How can histidine be classified both as positively charged and hydrophobic?

As @wysiwig stated, Histidine is not hydrophobic. Depending on the pH different parts of the molecule can carry charges, see the image below (from here):

The nitrogen atoms can be protonated in an acidic environment, the carboxylgroup will loose it proton in a basic environment. All these forms are transferred into each other, when the pH changes.


What is the protein sequence taken as input in the Path-A prediction system Considering the Path-A based metabolic pathway prediction (http://nar.oxfordjournals.org/content/34/suppl_2/W714.short). It uses machine learning for pathway prediction. Suppose that the input was a protein sequence of a query organism. I do not understand what these protein sequences are? Are these the enzymes for the reactions?

  The basic algorithm has two inputs: a set of protein sequences from the query organism and a set of model pathways, one for each target pathway.

Not necessarily, they can be enzymes, but they include a lot more (the whole proteome).

It takes a FASTA format file containing a set of query protein sequences from a single organism (a partial or complete proteome) and identifies those sequences that are likely to participate in any of its supported metabolic pathways
Path-A predicts the pathways supported by arbitrary sets of proteins, using validated prediction techniques based on sequence alignment and machine learning.


Would boiling water kill microorganisms in clothing that had feces spilled on it? Lets say there is a piece of clothing that had a small amount of human feces that spilled on it.

Would placing that clothing in boiling water destroy the microorganisms on that clothing?

Using boiling water alone will not destroy all the toxic compounds found within faeces. One example is skatole, this is found in faeces and is partially responsible for the foul smell faeces gives off. By laundry I assume you mean laundry detergent? If so, it would depend on the detergent being used.

I hope this answered your question :)


Why is gastrin not acing paracrine manner primarily, when it acts mainly on cells nearby its release? Gastrin is released by G cells and stimulates Parietal cells to secrete hydrochloric acid. Why is it not acting in a paracrine fashion instead of endocrine?

Paracrine signalling would mean not merely that gastrin is signalling the same organ, but that it is signalling nearby cells in the same organ - so that a few parietal cells close by respond, while the others perhaps would ignore the signal because maybe the paracrine signal would be degraded.  While the distinction is not absolute - there are shades of gray in all these things - blood gastrin tests are commonly done and medically relevant ( https://medlineplus.gov/ency/article/003697.htm ).  Because you can look at gastrin level as a whole-body characteristic, it is certainly appropriate to call it an endocrine signal.

Though their role is less emphasized, bear in mind that there are gastrin-producing G cells in the duodenum as well, and gastrin affects other digestive organs.


The Identity of this Lepidopteron I snapped this picture on a walk in the Pacific Northwest last week, and, being new to entomology, cannot manage to identify whether this is a moth or a butterfly.

It seems to have the coloring of a moth, yet it was out around 4-5 PM, with the sun still shining brightly. Its antenna look like a butterfly's, but its face (particularly the eyes) seems to be that of a moth. The wings are folded up like a butterfly (in another picture of the lepidoptera), but they look quite drab for a butterfly. Any help?

This looks like the Satyr Comma or Polygonia satyrus.

Characteristic of this species is a dark border near the tops of wings, fading near the bottom. They are common across the Western United States and Southern Canada.

For more information on this species, try this link and this link.

To differentiate between moths and butterflies you can look at the anntenae. Butterflies often have a bulb at the end whereas moth antennae are feathery or saw-edged.


Is there any recent evidence for the aquatic ape theory of human evolution? The aquatic ape theory suggests that many features that distinguish humans from their nearest evolutionary relatives emerged because the ancestors of humans underwent a period when they were adapting to an aquatic or semiaquatic way of life, but returned to terrestrial life before having become fully adapted to the aquatic environment.  Is there any new evidence of this?

The Aquatic Ape theory has never gained wide acceptance. This is because it has never had strong evidential support.

The features supposedly supporting the hypothesis only do so under an extremely superficial analysis (e.g. the argument for bipedalism), frequently actually occur in other non-aquatic mammals (e.g. hairlessness in naked mole rats and rhinos, a descended larynx in red deer), show no sign of having arisen at similar times in the human evolutionary record (e.g. encephalisation evolved far later than bipedalism and bipedalism vastly predates hairlessness) and lack fossil evidence of having evolved near aquatic environments.


The biggest underground living animal It's easy to find information about the biggest animals at land / at sea / in the air. But what was the biggest underground-living animal that ever existed?

No animals that were forced to live underground (e.g. pit ponies)
The animal should live at least 95% of its life under the earth (e.g. foxes)

There are two possible answers:

By length
By mass

My first guess was a mole

Microchaetus rappi
Microchaetus rappi, the African giant earthworm, is a large earthworm in the Microchaetidae family, the largest of the segmented worms (commonly called earthworms). It averages about 1.36 m (4.5 ft) in length, but can reach a length of as much as 6.7 m (22 ft) and can weigh over 1.5 kg (3.3 lb).(https://en.wikipedia.org/wiki/Microchaetus_rappi)

Giant Gippsland earthworm
These giant earthworms average 1 metre (3.3 ft) long and 2 centimetres (0.79 in) in diameter and can reach 3 metres (9.8 ft) in length; however, their body is able to expand and contract making them appear much larger. On average they weigh about 200 grams (0.44 lb). They have a dark purple head and a blue-grey body, and about 300 to 400 body segments.(https://en.wikipedia.org/wiki/Giant_Gippsland_earthworm)


Is there any possible way to take a DNA test without using blood in humans? Is there any possible way to take a DNA test without the need to draw blood in humans? Any information will be useful for me.

Yes, we don't have to use blood to extract DNA for testing.
There are many resource we can use include: hair, buccal swabs and urine. And it seems hair can provide good quality of genome DNA.

Here is the paper you may interested: A Simple Method of Genomic DNA Extraction from Human Samples for PCR-RFLP Analysis


Largest extinct clade? What is the largest (by large I mean most general) clade of organisms that has gone extinct?

domain > kingdom > phylum > class > order > family > genus > species

So, for example, an extinct kingdom would be larger than an extinct class.

Semantics aside, I think the OP wants a group of animals which are  grouped together as related and which are extinct.  I propose trilobites.  They are no more but at one time they ruled the earth.

from https://en.wikipedia.org/wiki/Trilobite

  Trilobites ( /ˈtraɪləˌbaɪt, ˈtrɪ-, -loʊ-/;[2][3] meaning "three
  lobes") are a fossil group of extinct marine arachnomorph arthropods
  that form the class Trilobita. Trilobites form one of the earliest
  known groups of arthropods. The first appearance of trilobites in the
  fossil record defines the base of the Atdabanian stage of the Early
  Cambrian period (521 million years ago), and they flourished
  throughout the lower Paleozoic era before beginning a drawn-out
  decline to extinction when, during the Devonian, all trilobite orders
  except the Proetids died out. Trilobites disappeared in the mass
  extinction at the end of the Permian about 252 million years ago. The
  trilobites were among the most successful of all early animals,
  roaming the oceans for over 270 million years.[4]


Could a sperm be altered to contain a female's genetics? While discussing with a friend a while back on the likelihood a futanari (a woman with both fully developed and functioning sets of genitalia) existing in real life, we got into a discussion of whether a child could carry the genetics over from 2 months.

Currently (to my knowledge), for a female same-sex couple to conceive a child and for both women to be involved, one would donate an egg, the other actually gives birth, and the sperm is donated by a third party. However, this means that the child will carry over the genetics of one women in the couple and the unknown male.

I am wondering if there is a way for sperm to contain the genetic information so that way both women in a same-sex relationship could be genetically related to the child.

You might be interested in this article. In this study they created haploid ES cells from artificially activating an unfertilized oocyte and growing the haploid cells. These cells, when introduced in the ICM, give rise to viable chimeras.

In another study, haploid androgenetic ES cells were created by injecting a sperm into an enucleated oocyte. These cells also are capable of creating offspring when fused with another oocyte. [See this post also]

Also, since these cells can be cultured, they can be genetically modified. However, they undergo spontaneous diploidization and lose reproductive potential after a few rounds of division. This is related to the alteration of epigenetic status of these cells on certain imprinted loci. Others have also indicated the importance of both paternal and maternal imprinting in the viability of embryos which might be a problem in oocyte-oocyte derived hES cell fusions (See cross references). [Check this article too].

It can be concluded that oocyte$-$oocyte-hES fusions are not observed because of same imprint status (Also mentioned by Chris in the comments). AD-hES also lose their paternal imprints on prolonged culture (but retain maternal imprints). It is to be ascertained if paternal imprints are more unstable compared to maternal imprints under these conditions. It may be possible to optimize the culture conditions such that oocyte derived hES lose their maternal marks: would that lead to incorporation of paternal marks post-fusion is debatable.


How to make GABA pass the blood brain barrier? I thought of methylating GABA at the gamma amino group in order to make it pass the blood brain barrier, but would it work?

The goal is to make a sedative. Like GHB or benzodiazepines (I know that benzos have a totally different structure)

Any ideas on how to make GABA  pass the blood brain barrier?

Short answer
Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse.

Background

Given that you ask

  ...how to make GABA pass the blood brain barrier?

I assume that

You wish to elevate GABA by exogenously administering a compound;
That compound has to cross the blood-brain barrier (BBB) and physically turn into GABA;
A drug indirectly elevating GABA through unknown (e.g., GHB) or known mechanisms (Gabapentin) does not suffice your needs.
If you are happy with indirect actions, the links above will help you out. Now on to the real stuff :-)

GABA (Fig. 1) has 3 hydrophylic groups that may prevent it to cross the blood-brain barrier (BBB), namely a hydroxyl-, a keto- and an amine-group. The BBB generally only permits passive entry of small hydrophobic molecules. The amino-group in turn is also prone to de-amination by mono-amino oxidase inhibitors.

An often-used method to get drugs into the brain is shielding of pesky hydrophilic and/or fragile chemical groups by certain molecules that are irreversibly bound to them. A well-known example of shielding a fragile amino-group is the B-methylation of phenetylamine compounds into their amphetamine analogues. Alpha-amination to a methamphetamine further stabilizes the essential amino-group. Amphetamines and methamphetamines are way more stable in the brain than their phenetylamine precursors and likely enter the BBB also more swiftly because they are more hydrophobic by shielding the amino group (Shulgin, 1990).

However, those methyl groups are irreversibly bound, so it's not an option here, as apparently you wish to increase GABA, and not an active derivative of it.

Now, another way is using a Trojan horse method (Pardridge, 2006); by reversibly shielding the essential amine group the drug can enter the brain, where it is converted back to its original compound. Picamilon does the job here. Smarter Nootropics say;

  First developed in the early 1970s in the Soviet Union, picamilon (alongside phenibut) is an “enhanced” form of GABA that is capable of crossing the blood brain barrier when taken as a supplement.Inside the brain, picamilon is rapidly hydrolyzed into its constituent parts; niacin and GABA. Niacin helps to enhance brain blood flow through its vasodilatory properties [].

Fig. 1. GABA and Picamilon. source: Smarter Nootropics

Reference
- Pardridge, Discov Med (2006); 6(34):139-43
- Shulgin, PIHKAL, Transform Press, U.S. (1990)


Adding the Propionyl-CoA Pathway to E.coli So I'm trying to simulate the production of 3-Hydroxypropionic Acid with E.coli via the Propionyl-CoA Pathway.
However I'm not really sure how the production in the pathway goes.
I got the following picture:

If I understand it correctly the pathway goes:
Acetyl-Coa--> Propionate --> Propionyl-CoA --> .... --> 3-HP
When adding these reactions in Cobra are the stoichiometric coefficients always just 1?

Source of the figure:
Luo H, Zhou D, Liu X, Nie Z, Quiroga- Sánchez DL, Chang Y (2016) Production of 3- Hydroxypropionic Acid via the Propionyl-CoA Pathway Using Recombinant Escherichia coli Strains. PLoS ONE 11(5): e0156286. doi:10.1371/journal. pone.0156286

If I understand it correctly the pathway goes: Acetyl-CoA --> Propionate --> Proprionyl-CoA --> ... --> 3-HP

Not exactly. The first reaction is:
$propionate + acetyl\textrm-CoA \rightarrow propionyl\textrm-CoA + acetate$
The CoA group is transferred from acetate to propionate. The following reactions are an oxidation to acryloyl-CoA and a subsequent hydration to 3-HP-CoA. Lastly the CoA group is transferred back to acetate.

Propionate is a 3 carbon molecule and so is 3-HP. So stoechiometric coefficients of 1 seem logical.


Relative concentration of enzyme vs reaction product I was reading a paper in which a recombinant protein (His-6 tagged) is expressed in E Coli (BL21 DE3). The yield of the enzyme isolated from the culture is reported as 10-30 mg per L of bacterial culture. (After purification by Ni-affinity Chromatography)

First, is this a reasonable concentration for an enzyme? I thought it was rather high.

Second, when they measure the concentration of the product of the enzymatic reaction that was found to be merely 1-3 mg/Litre of bacterial culture.

Is this typical or unusual for the product concentration to be an order of magnitude smaller than the enzyme concentration? I assumed that since enzymes were in catalytic amounts they ought to be at lower concentrations?

PS. They use SDS-PAGE followed by the Bradford method for determining the protein titres. How accurate is the Bradford method?

Remember that the concentrations you report are in mass units rather than mole units. If the protein has a mass of 40,000 Da, reasonable for many proteins, then 20 mg/liter means $0.5$ x $10^{-6}$ mol/liter. A typical small-mass product of an enzyme reaction might have a mass about 200, so its apparently lower mass concentration of 2 mg/liter is $10$ x $10^{-6}$ mol/liter, 20 times higher than the enzyme concentration in terms of numbers of molecules per liter. The mole or molecule ratios are what you should think about in terms of catalytic function.

Furthermore, from what you provide we don't know whether the enzyme was produced under circumstances that allowed it to express its activity; there may have been limitations on substrate availability, presence of inhibitors that would be removed in later purification, and so forth. In this scenario, evidently to obtain enzyme for downstream use, the emphasis is typically on getting large amounts of the specific enzyme regardless of whether some reaction product is formed. I don't find the enzyme concentration particularly high for something that the investigators are trying to over-express as in this case.

The Bradford reaction is a mainstay of standard biochemistry, as it's simple and straightforward. Different proteins can bind the reagent to somewhat different extents, so there is a second-order issue of whether the protein used for the standard curve and that being measured are similar enough in that respect. In practice, what's important is to provide enough information in the methods that are described so that someone could repeat the work to determine the relation between the Bradford measurement and some other more accurate method for this particular protein.


When performing mutagenesis for an assay, how do you decide on the sample size of individuals to be mutated such that all genes are covered? If I want to study, say, gustatory response of salmons to a bile acid, I need to mutagenize a sample of salmon males. However, given that there are many genes involved in this response, what is minimum no. of salmons I should mutagenize, such that ALL the genes involved have some mutations?

I have searched quite a lot for some statistical method that tells me this, but to my surprise I haven't found any.

Don't think about mutagenized animals, think about mutagenized genomes. Depending on when the mutagenesis is carried out, and how efficient it is, a very small number of males could give rise to thousands of mutagenized F1 progeny, each carrying a uniquely mutagenized genome. That is the number to focus on. Typically, in fruit flies and soil nematodes the animals are hit "pretty hard" such that each F1 is carrying hundreds, if not thousands, of mutated sites, randomly throughout the genome. The trade-off is to not mutagenize them so much that they suffer a drastic decrease in fertility or viability, while at the same time minimizing the number of F2 homozygotes you have to screen for phenotypes.

In C. elegans exposed to 50 mM ethylmethane sulfonate for 4 hr, you might reasonably hope to recover 1 loss-of-function mutation after screening 2,000 mutagenized F1 genomes.

Are there good genetic markers along all of the salmon chromosomes?  If you are only interested in recovering dominant mutations then you can screen the F1 directly (however dominant alleles tend to be much rarer than recessive alleles, and interpretation of dominant phenotypes is challenging without lots of good genetic tools, like duplications and deficiencies). Otherwise you will have to mate the F1 to obtain male and female F2 and then set up brother-sister matings so that you can score the F3 for phenotypes of interest.

None of these numbers would apply to salmon because the genome is much larger, and unless someone has already done a dose-response curve on the optimal mutagenic dose for salmon, you would need to do that first.


Bipolar disorder genetics My understanding is that bipolar disorder is polygenic.

1) Does one need to have all the genes for bipolar disorder in order to have the disease?

2) Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

Does one need to have all the genes for bipolar disorder in order to have the disease?

No. In genome-wide association studies (GWAS) of psychiatric conditions, it is a constant finding that the associated variants each influence the probability/risk. The effects of all known variants can then be summed up to a polygenic score (PGS). A person with higher PGS is more likely than someone with a low PGS. But some people with low PGS (i.e. people who don't have "all the genes") still get the condition, it is just not as frequent as people with high PGS.

Another reason why we can say 'no' to this question is through findings of quantitative genetics studies. These estimate the heritability of certain traits. For the answer to be 'yes', the heritability would have to be one ($h^2 = 1$). However, as far as I know, there are no known psychiatric conditions that have heritabilities of one. Some high (e.g. $h^2\approx 0.8$), yes, but not one.

It's also worth mentioning that there is probably no sharp line between having bipolar disorder and not having it. It's a medical diagnosis that is useful but rough. Most likely, all of us have a little "bipolar" in us. I think it's probably most useful to view it as a spectrum.

  Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

This is not known and it may not even be a well-defined question. We don't know all the variants that affect the risk of bipolar disorder (or most other polygenic disorders). So we cannot say for sure.

Some 'omnigenetic' hypotheses propose that all genetic variants have some effect on all traits. Some effects are just smaller and some larger. In this case, the expression 'all the genes for X' may be technically meaningless.


Do identical twins have the same fingerprint? When there is every thing same from their genes to their phenotype so then why they don't have same fingerprints?

Identical twins have, despite the name, neither identic fingerprints nor identic genetic fingerprints.

Fingerprints: According to the papers listed below the fingerprints show higher similarities (the "structure" is the same), but they can be distinguished and are not the same.

On the similarity of identical twin fingerprints
Can identical twins be discriminated based on their fingerprints?

Genetic Fingerprint: Although identic (or monozygotic) twins share the same DNA, they are not the same and can still be distinguished with a DNA fingerprint, if enough regions are analyzed. The difference comes from small mutations (so called "single nucleotide polymorphisms", one base mutations) which occur in each of us individually. The other difference comes from epigenetic modifications of our genome (basically adding methyl groups to our DNA) which are also not the same between identic twins (there is an interesting video on this on Youtube). However, when using standard forensic kits it is usually not possible to discriminate between identical twins. Differences are detected with whole genome sequencing.

Have a look at these publications:

Identical Twins' Genes Are Not Identical
Finding the needle in the haystack: Differentiating “identical” twins
in paternity testing and forensics by ultra-deep next generation
sequencing
Epigenetic contributors to the discordance of monozygotic twins.


difference between motifs, domains, patterns, signatures and profiles I can't get clear the difference between those terms, I see them a lot while browsing on Prosite, Pfam, Expasy e.t.c.
However, I can find documentation about them, but It still not clear what the difference is between those terms. I think it's something like:

motifs: Short residu stretch, not an indication of homology
domain: Could contain motifs, howevever most of the time is bigger, it can be used to identify homology if two proteins share a domain.

However I can't fit the patterns and profiles in this list.

Looking at the documentation you provide, I think that I can provide definitions for those terms as defined by EXPASY. Note that those definitions may just be an in-house system that EXPASY uses that you can't generalize to other databases for instance.
First, in section I.C of the documentation, they write "The use of protein sequence patterns (or motifs) to determine the function(s) of proteins is becoming very rapidly one of the essential tools of sequence analysis."
So it looks like for them patterns = motifs and motifs = patterns. Note again that "pattern" appears to be a somewhat informal term. I would certainly say that it is confusing that they use them as synonyms, but they do at least define them as such.
Second, I think that they are using the word "profile" in a very narrow technical sense, with regard to the way that they detect homology between proteins. The standard way to detect homology between proteins is using programs called Hidden Markov Models (HMMs). In section II.B, they write "A profile or weight matrix (the two terms are used synonymously here)...". So a profile is really just a weight matrix derived from a HMM that can be applied to any given alignment to figure out whether or not it matches homology. They go on to give an example of how this weight matrix is applied.
In simple terms, how the HMM works is that you give it a bunch of sequences that you know belong to the same family, and it will try to learn the frequencies of amino acids at each position and what order they come in. This model of the amino acid frequencies is the weight matrix they talk about. Then you make sure that the HMM works well (gives high scores for proteins in the same family, low scores for proteins in different families), and then you can apply the program to try to find new homologs.
Hope that answers the Q.


How compatible are mammalian digestive systems? I'm interested in what kinds of nutrients mammals extract from food and would like to know how similar are the outputs of these systems.

For example, if it is possible to successfully replace one mammal's digestive system with another mammal's one (all the connections are correct). Would the recipient survive or experience some form of malnutrition resulting in death?

I think this would depend entirely on the diet of the host and donor mammal.

Assuming they are of similar size and diet, I don't see any reason why this wouldn't work. The gut tends to absorb more or less everything in the food.

If the diet of the two mammals differed significantly, I could see some problems with eating the correct foods. Herbivores with the significantly shorter carnivore gut would have trouble killing and eating things without carnivore teeth/claws/what have you, and the plants would not provide enough nutrition on their own. Rabbits, for instance, have a two-pass digestive system, so in order to use a rabbit gut the mammal would have to eat their own feces regularly. (Rabbits have digestive bacteria in their colon, but grass has to travel to the colon and then back 'upstream' to the absorptive part of the gut. So this is achieved by going around again.)


Help identify this worm-like thing Many instances of this worm-like creature were found in a water system for a mountain cabin in the Sierra Nevada mountains of the US, in late June / early July.  The water system collects water from an enclosed spring.  Can you help identify this creature?

Clues:

The worms have two "points" on their heads.
They can stretch out and be long and thin, or when poked (or are resting) they contract into a small blob.
Here is a picture of a single worm with markings shown.

Here is a picture of a few worms, somewhat contracted.

Here is a movie of them moving, in natural light.
Here is a movie of them moving, with backlight.
Here are pictures of their undersides and their internal structures.

Whenever I pull some out of the water and put them into a tupperware with the same water, they only survive for around 24 hours, after which they seem to disintegrate.  Here is a picture of about 20 of the worms after about 24 hours, the bulk of them have halfway-decomposed and form a heap in the upper right.  After another day it'll just look like debris in the water, you wouldn't even recognize that there were worms in it.  There is a piece of bacon in there because some suggested putting it there to test if they were leeches, but this disintegration happens repeatably and regardless of the bacon; please ignore the bacon.

Someone suggested that they are trematodes, but there are no snails, frogs, or other creatures in the storage and collection sections of the water system;  we have looked very closely.  There may be something within a 30-foot section of pipe, but we doubt it.

Can you help us identify this creature?  Even just possible families of creatures or general categories would be helpful for us.

I am not too sure but this looks like Polycelis sierrensis.

Though it is apparent that the worm in your pictures is a tricladid planarian, I was not too sure about the species and the geographical distribution.

However, from the Smithsonian list of freshwater planarians in North America, I deduced that this should be Polycelis sierrensis which is found in California and Nevada (Kenk ,1973).

The EOL page on this species also concurs with the geographical distribution. Moreover, the shape and dimensions of the worm, as described in EOL, matches with that of the ones you have got.

I could not find a picture of P. sierrensis but this is how a general Polycelis looks like:


What type of insect is this? I'm naturally thinking this is a bee, but I cannot find it anywhere in any insect identifiers. I caught this picture on top of my doorway, it's about 1 1/2 inches in length, and its torso seems to be coated in a layer of hair, and the rest of its body is narrow. The thick layer of hair may or may not be accurate, I didn't want to get too close to it, but that's how it appeared at least.

What is this?

PS - Found in Kentucky, and I'm not sure why one pic shows wings and the other one doesn't...

From the general body plan, it looks like it's probably a robber fly. Here's a page of specifically Kentucky robber flies – it's possible yours could be a Bearded Robber Fly.


How host defends against S. pneumoniae capsule? The host response involves at least phagocytosis and probably localised acute inflammatory response at least after the colonisation.

I am thinking how the host can defend against pneumolysin which helps the streptococcus pneumoniae invasion.

How can the host defend against Streptococcus pneumoniae capsule?

According to the two papers listed below, this is mostly done by a neutrophilic inflammatory response. The response is regulated by mechanisms of the innate immune system and is mediated by receptor like TLR2, TLR4 and SIGN-R1.

Role of Dectin-2 in the host defense against Streptococcus
pneumoniae infection
Dectin-2-dependent NKT cell activation and serotype-specific antibody
production in mice immunized with pneumococcal polysaccharide
vaccine.

There are a few papers which go deeper (reviews, so you will probably have to go through the reference lists):

Mechanisms of host defense against infection with Streptococcus
pneumoniae.

This paper mentions specific antibodies later on in the reaction and finally the opsonization by immune cells.

These two papers tal specifically about pneumolysin:

Pneumococcal virulence factors and host immune responses to them.
Pneumolysin as a vaccine and drug target in the prevention and
treatment of invasive pneumococcal disease.


Can the negative afterimage appear only if there is light or is it possible in darkness? Reading the following paragraph:

  After staring at the red and blue shamrock, you saw a green and
  yellow afterimage. Opponent-process theory proposes that as you stared
  at the red and blue shamrock, you were using the red and blue portions
  of the opponent-process cells. After a period of 60 to 90 seconds of
  continuous staring, you expended these cells' capacity to fire action
  potentials. In a sense, you temporarily "wore out" the red and blue
  portions of these cells. Then you looked at a blank sheet of white
  paper. Under normal conditions, the while light would excite all of
  the opponent-process cells. Recall that white light contains all
  colors of light. But, given the exhausted state of your
  opponent-process cells, only parts of them were capable of firing
  action potentials. In this example, the green and yellow parts of the
  cells were ready to fire. The light reflected off of the white paper
  could excite only the yellow and green parts of the cells, so you saw
  a green and yellow shamrock.

  (Ellen Pastorino & Susann Doyle-Portillo, What Is Psychology? Essentials, 2010)

I've been wondering:

Can the negative afterimage appear only if there is light or is it possible in darkness?

In other words does the red color make the ganglion continue working even when there is no image and the afterimage appears green or is more light required in order for the afterimage to appear?

Glutamate release from photoreceptors is inhibited by incident photons (ref). During photobleaching, assume that the effect of an incident photon drops to zero. The implication then is that if all light is removed subsequent to selective photobleaching, there will be no difference in activation between bleached photoreceptors and unbleached photoreceptors. This observation suggests that no afterimage will be visible in darkness.

But there might be rebound effects or other effects of light adaptation that will result in a perceivable afterimage in darkness. Certainly there are hallucinatory visual patterns than can be generated cortically, suggesting that a cortical afterimage could be generated in darkness.


How should you choose from the various methods of constrained ordination? I have a bacterial OTU matrix from various sample points and times. So for each sample I have the sequence counts across the various OTUs that they were assigned to.

I also have a corresponding matrix of abiotic variables including temperature, pH and the concentrations of a range of nutrient compounds. This data was collected at the same time as the bacterial OTUs.

This is a tutorial written by the people behind the R package 'vegan', it offers three separate types of constrained ordination. I just don't understand what the differences are between these and what would suit my data-set best. There is not much advice out there at all for this sort of thing so any help would be appreciated.

You might want to check out Mike Palmer's webpage on ordination, specifically the constrained ordination section: http://ordination.okstate.edu/

The main difference between constrained ordination techniques is the distances that are preserved. Redundancy analysis (RDA) preserves Euclidean distances, so in order to use it, you need to transform your OTU table with an appropriate transformation (e.g., Hellinger), after which a Euclidean distance calculation is appropriate. It also works best identifying linear relationships between environmental variables and species responses. Canonical correspondence analysis (CCA) preserves the chi-squared distance, which tends to emphasize common taxa, and looks for unimodal responses to environmental gradients. Distance-based redundancy analysis (dbRDA) accepts any distance matrix, allowing you to use non-metric distances, and then looks for linear relationships with distances and environmental variables.

Before applying these metrics, you'll need to understand their advantages and limitations, and then you'll need to make a decision about which combination of constrained ordination techniques and distance metrics are best for answering your questions. This is something you'll need to justify yourself, based on your own question, because different approaches are better at emphasizing different aspects of your data. I strongly suggest you study a copy of Legendre and Legendre (2012) for more information about these methods.


Mathematical models of gene editing using CRISPR One confusing thing I have found when reading articles about possible CRISPR based gene therapy treatments in humans is that there is vey little discussion about what percentage of your cells will actually have their DNA edited, the rate at which the editing takes place, and how to quantitatively estimate how many edited cells would be needed to "cure" a specific disease.  (It's not so confusing how edits could be made to a small embryo, what's confusing is what is actually possible for grown patients)

Can someone provide a few basic facts that calibrate what is currently possible and what is needed.

For instance, is it currently possible to edit more than 50% of the cells of an adult  nematode (or more complicated organism) using CRISPR?  How long does it take (minutes, hours, days, weeks).

For the current list of human diseases that are possible targets for gene therapy, how many cells need to be edited for one of those diseases to be "cured" (hundreds, thousands, billions, etc)

But in general is there a name for the mathematical models that try to predict how many cells will end up being edited, how those edited cells will multiply and replace diseased tissue,  and how many edits are needed to generate a concentration of missing protein for a treatment to be successful?

cheers!

There are several probabilities that you need to take into account.

The efficiency of DNA transformation of CRISPR encoding DNA and
target DNA into the host cell (varies between cell types and
transformation agent).
Efficiency of cutting by CRISPR at target site. (varies by DNA compaction - which varies by site and cell type, and guide RNA)
Number and cutting efficiency at off targeting sites.
Efficiency of degradation of free DNA by cellular antiviral systems
(varies between cell types)
Efficiency of DNA repair machinery to fix dsDNA breaks. (thus removing CRISPR cut sites. Varies by cell type)
Efficiency of recombination machinery (homologous
recombination and microhomologous recombination) (which is used to
insert new DNA sequence).
Probability of NHEJ damaging target site. (which can delete the CRISPR cut site)

Too many things to count.

However to give you some idea. The efficiency of CRISPR making a correctly targeted knock in for DT40 (chicken lymphoma) is  ~1% of all resistant colonies (ie colonies that have taken up the DNA seq used to make the knock in), when lipofectamine reagents are use. Lipofectamin trasfromation efficiency varies depending on the size of the transformed DNA, host cell type and plating density. So for a 5kb construct that transformation efficiency varies between 30%-50%.

CRISPR is nearly 100% efficient in yeast cells, ie all knock in cells are correctly targeted. This is likely due to the high levels of HR in yeast


How did dolphins acquire their dorsal fin? I had been thinking bout atavism when I saw a picture of a dolphin. I had seen it before, but suddenly the dorsal fin startled me.

How did this dorsal fin evolve? Is it some atavism from eons ago, a revived feature, or a new development altogether? (Strong evidence of the former would be if the genes ruling dorsal fins in fish and dolphins would be similar.)

I've seen this How and why did mammals go back to the oceans?, but it doesn't ask nor explain about the dorsal fin.

Short answer
I reckon that the dorsal fin of sea-faring mammals are a new development altogether.

Background
The presence of a dorsal fin is one of the defining characteristics of fishes like sharks. Mammals that returned to the sea generally lack a dorsal fin.

However, killer whales and dolphins, while being mammals, indeed do have dorsal fins. In contrast to the dorsal fin in fish, these structures do not have bones (Fig. 1). Instead, the dorsal fins of mammals are made up of dense tissue, somewhat like a ridge of thick, folded skin. Hence, it is not a 'revived structure' that was 'activated' from a latent state in mammals.

Hence, given that mammals returned to sea later in evolution and lacked a dorsal fin on land, I would deduce from these data that dorsal fins are an example of convergent evolution where analogous structures with a similar function (like in fishes, the dorsal fin acts as a stabilizer or a rudder in mammals (source: The National Marine Life Center) develop from unrelated bodily structures. Hence the genes involved may, and likely are, different.

Fig. 1. Dorsal fins of a killer whale (left) and in a fish (a redhorse on the right). sources: Sea World and Mosxostoma


Why does evolution not make our life longer? Why does evolution not make life longer for humans or any other species?

Wouldn't evolution favour a long life?

Why do we age is a classical question in Evolutionary Biology. There are several things to consider when we think of how genes that cause disease, aging, and death to evolve.

One explanation for the evolution of aging is the mutation accumulation (MA) hypothesis. This hypothesis by P. Medawar states that mutations causing late life deleterious (damaging) effects can build up in the genome more than diseases that cause early life disease. This is because selection on late acting mutations is weaker. Mutations that cause early life disease will more severely reduce the fitness of its carrier than late acting mutations. For example, if we said in an imaginary species that all individuals cease to reproduce at 40 years old and a mutation arises that causes a fatal disease at 50 years old then selection can not remove it from the population - carriers will have as many children as those who do not have the gene. Under the mutation accumulation hypothesis it is then possible for mutations to drift through the population.

Another hypothesis which could contribute to aging is the antagonistic pleiotropy (AP) hypothesis of G.C. Williams. Pleiotropy is when genes have more than one effect, such genes tend to cause correlations between traits, height and arm length probably have many of the same genes affecting them, otherwise there would be no correlation between arm length and height (though environment and linkage can also cause these patterns)... Back to AP as an explanation for aging, if a gene improves fitness early in life, but causes late life disease it can spread through the population via selection. The favourable early effect spreads well because of selection and, just as with MA, selection can not "see" the late acting disease.

Under both MA and AP the key point is that selection is less efficient at removing late acting deleterious mutations, and they may spread more rapidly thanks to beneficial early life effects. Also if there is extrinsic mortality (predation etc.) then the effect of selection is also weakened on alleles that affect late life. The same late-life reduction in the efficacy of selection also slows the rate at which alleles increasing lifespan spread.

A third consideration is the disposable-soma model, a description by T. Kirkwood of life-history trade-offs which might explain why aging and earlier death could be favoured. The idea is that individuals have a limited amount of resources available to them - perhaps because of environmental constraints or ability to acquire/allocate the resources. If we then assume that individuals have to use their energy for two things, staying alive via repair and maintenance (somatic-maintenance) and making offspring (reproductive-investment), then any energy devoted to one will take away from the other. If an individual carries a gene that makes it devote all of its energy to somatic maintenance then its fitness will be very low (probably 0!) and that gene will not spread. If the level of maintenance required to live forever costs more energy than an individual can spare without suffering from low fitness (very likely) or can even acquire and efficiently convert in the first place (also very likely) then high-maintenance alleles will not spread (and aging & death will continue to occur).

To go a little further, it is common for sexes to age differently (this is what I work on) and one possible explanation is that the sexes favour different balances of the trade off between somatic-maintenance and reproductive investment, this can lead to conflict over the evolution of genes affecting this balance and slow the rates of evolution to sex specific optima. This paper provides a good review of the area.

To summarise, evolution has not managed to get rid of death via genetic disease etc. (intrinsic mortality) because the effect is only weakly selected against, and those alleles may provide some early life benefit, and resource limitation may also reduce the potential to increase lifespan due to trade-offs with reproductive effort. Adaptive evolution is not about the survival of the fittest but the reproduction of the fittest - the fittest allele is the one which spreads the most effectively.

EDIT: Thanks to Remi.b for also pointing out some other considerations.

Another thought is that of altruistic aging - aging for the good of the population (the population is likely to contain related individuals, you are related to all other humans to some degree). In this model aging is an adaptive process (unlike in MA where it is just a consequence of weak selection). By dying an individual makes space for it's offspring/relatives to survive (because resources are then less likely to limit populations). This will stop excessive population growth which could lead to crashes in the population and so, by dying earlier, an individual promotes the likelihood that its progeny will survive. Arguments of altruistic sacrifice are often hard to promote but recent work suggests that this is a more plausible model than once thought.

Evolvabilty theories also suggest that aging is an adaptive process. These suggest that populations, composed of a mixture of young and old, have biases in how well adapted the members of the population are - where younger individuals are better adapted (because they were produced more recently it is likely that the environment is similar to the environment they are favoured in). Thus by removing the less well adapted individuals from a population via senescence and freeing up resources for younger better adapted individuals, a population evolves more rapidly towards it optimal state.


What is the smallest pressure differential that humans can detect? While cooking dinner under an extractor on its lowest setting, I noticed that none of the steam (referenced by the amount of fogging on a nearby window, compared to the absence of the fan, was effectively zero) was going anywhere else but through it.

However, placing my hand under the hood, I couldn't feel a difference in pressure. This is most likely due to two things: my hand smoothly transitioned from "normal" atmospheric pressure to the "adjusted" pressure near the hood, and the hood area is quite wide, so that extraction is done over the significant area not covered by my hand and hence less pressure applied.

But it got me thinking, and a literature check revealed nothing helpful so far, as to what is the smallest pressure differential detectable by the skin of the human body?

I would prefer to exclude anything related to hearing, as this is a well-researched area but tells us nothing about the other 99.9% of what is directly exposed to atmospheric pressure changes. Answers that cover particular parts of the body beyond skin and ears (for example, the eyes) are appreciated but only additional.

Short answer
The sensitivity to pressure differences highly depends on the study setup used. A paper resembling the conditions in your kitchen experiment concludes that the just noticeable difference ranges from 19 to 35 kPa.
Background
The smallest difference that can be perceived between two stimulus levels is called the just noticeable difference, or JND. The issue with determining pressure difference JNDs is that it may be dependent on many things. To name a few important factors are the place on the body and the type of stimulus used. The fingertips and tongue are among the most sensitive parts of the body, while the back is way less sensitive to mechanical stimulation. The type of stimulus may also dramatically affect the findings, because vibratory stimuli are sensed by other types of mechanoreceptors than static pressure stimuli.
Having said that, I found a paper describing an experiment that resembled your kitchen experiment pretty well . The authors used air puffs applied to the fingertips. They used an apparatus where the nozzle could be adjusted to accommodate different aperture sizes. The authors tested 10 normal, right handed controls and used a standard 2 alternative forced choice (2AFC) task applied as a method of constant stimuli. Personally I would have adopted an adaptive 2AFC task, but both methods are valid. The authors conclude that

Subject-averaged pressure JND values ranged from 19.4 – 24.7 kPa, with no statistical differences observed between aperture sizes.

Reference
- 33rd Bianchi et al., Annual International Conference of the IEEE EMBS Boston, Massachusetts USA, August 30 - September 3, 2011


How do a particular arrangement of atoms become self aware? At the simplest level, we're all just atoms, animals, plants and humans alike. But what I don't understand, is how a particular arrangement of atoms such as us can become self aware, and be able to not only understand our environment, but manipulate it to our will? How is that even possible?

You are skipping too many steps.
$Atom \rightarrow \color{red}{molecule \rightarrow structure \rightarrow cell} \rightarrow organ \rightarrow organism$
The following is a proposed speculation regarding the steps in red on the above:

How life originated and how the first cell came into being are matters of speculation, since these events cannot be reproduced in the laboratory. It was first suggested in the 1920s that simple organic molecules could form and spontaneously polymerize into macromolecules under the conditions thought to exist in primitive Earth's atmosphere. At the time life arose, the atmosphere of Earth is thought to have contained little or no free oxygen, instead consisting principally of $CO_2$ and $N_2$ in addition to smaller amounts of gases such as $H_2$, $H_2S$, and $CO$. Such an atmosphere provides reducing conditions in which organic molecules, given a source of energy such as sunlight or electrical discharge, can form spontaneously. The spontaneous formation of organic molecules was first demonstrated experimentally in the 1950s, when Stanley Miller (then a graduate student) showed that the discharge of electric sparks into a mixture of $H_2$, $CH_4$, and $NH_3$, in the presence of water, led to the formation of a variety of organic molecules, including several amino acids.

Although Miller's experiments did not precisely reproduce the conditions of primitive Earth, they clearly demonstrated the plausibility of the spontaneous synthesis of organic molecules, providing the basic materials from which the first living organisms arose.
The next step in evolution was the formation of macromolecules. The monomeric building blocks of macromolecules have been demonstrated to polymerize spontaneously under plausible prebiotic conditions. Heating dry mixtures of amino acids, for example, results in their polymerization to form polypeptides. But the critical characteristic of the macromolecule from which life evolved must have been the ability to replicate itself. Only a macromolecule capable of directing the synthesis of new copies of itself would have been capable of reproduction and further evolution.
Of the two major classes of informational macromolecules in present-day cells (nucleic acids and proteins), only the nucleic acids are capable of directing their own self-replication. Nucleic acids can serve as templates for their own synthesis as a result of specific base pairing between complementary nucleotides. A critical step in understanding molecular evolution was thus reached in the early 1980s, when it was discovered in the laboratories of Sid Altman and Tom Cech that RNA is capable of catalyzing a number of chemical reactions, including the polymerization of nucleotides. RNA is thus uniquely able both to serve as a template for and to catalyze its own replication. Consequently, RNA is generally believed to have been the initial genetic system, and an early stage of chemical evolution is thought to have been based on self-replicating RNA molecules—a period of evolution known as the RNA world. Ordered interactions between RNA and amino acids then evolved into the present-day genetic code, and DNA eventually replaced RNA as the genetic material.
The first cell is presumed to have arisen by the enclosure of self-replicating RNA in a membrane composed of phospholipids.

Phospholipids are the basic components of all present-day biological membranes, including the plasma membranes of both prokaryotic and eukaryotic cells. The key characteristic of the phospholipids that form membranes is that they are amphipathic molecules, meaning that one portion of the molecule is soluble in water and another portion is not. Phospholipids have long, water-insoluble (hydrophobic) hydrocarbon chains joined to water-soluble (hydrophilic) head groups that contain phosphate. When placed in water, phospholipids spontaneously aggregate into a bilayer with their phosphate-containing head groups on the outside in contact with water and their hydrocarbon tails in the interior in contact with each other. Such a phospholipid bilayer forms a stable barrier between two aqueous compartments—for example, separating the interior of the cell from its external environment.
The enclosure of self-replicating RNA and associated molecules in a phospholipid membrane would thus have maintained them as a unit, capable of self-reproduction and further evolution. RNA-directed protein synthesis may already have evolved by this time, in which case the first cell would have consisted of self-replicating RNA and its encoded proteins.

Source: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9841/


How are arms different than legs? Ok, this is a bit of a tangent question, but it came up yesterday and I didn't know the answer:
How are arms and legs defined physiologically? For example, we say humans have two arms and two legs, while cats have four legs, and some monkeys (appear) to have four arms (although I guess they could be legs too). It's really unclear to me how we make these distinctions.

So:

What is the physiological definition of both "arm" and "leg"? How are they different?

I think that's more of a matter of linguistics rather than any scientific/physiological reason. For instance, in Portuguese, you wouldn't call legs to a cat or a dog's limbs. You would say they have 4 "patas" (roughly translated as "paws"). And calling them legs, in Portuguese at least, would be weird.

When veterinary doctors refer to animal limbs, they usually use anterior and posterior limbs. In fact, anatomically speaking, anterior limbs in cats and dogs (and probably in other animals too) have more in common with human arms (upper limbs) that with their own posterior limbs.

Also, as rg255 commented, maybe the reason behind the colloquial nomenclature is quite simple...

To (miss)quote Nancy Sinatra:

  These "legs" are made for walking

  And that's just what they'll do


Examples of references for mathematical approaches in bioinformatics that are applicable to linguistics? Do you have any classic references for mathematical approaches in bioinformatics that are applicable to linguistics (or vice versa)?

EDIT
I am mainly interested in approaches to reconstruct the history of languages, the rate of language mutation, phylogenies of languages, etc.

There are a number of more recent papers dealing with phylogenetic methods in reconstructing language history as well, including work by Colin Renfrew and Quentin Atkinson.

Here are two recent high-profile papers. Unfortunately, both are still behind paywalls, but even reading the list of papers they cite / that cite them would be a great way to answer your question.

 Bouchard-Côté A, Hall D, Griffiths TL, Klein D. 2013. Automated reconstruction of ancient languages using probabilistic models of sound change. Proceedings of the National Academy of Sciences 110: 4224–4229.
 Gray RD, Drummond AJ, Greenhill SJ. 2009. Language phylogenies reveal expansion pulses and pauses in Pacific settlement. Science 323: 479–483.

Maybe not quite as high-profile, but available online, one of my classmates did his (superb) undergraduate thesis as a Biology/Linguistics double major in exactly this topic. I think it could be a very useful place to start, although there have certainly been developments in the field in the last six years:

 Saunders, A. 2006. Linguistic Phylogenetics of the Austronesian Family: a performance review of methods adapted from biology.

See also the wikipedia page Quantitative Comparative Linguistics, this Stanford how-to, and this interesting article Linguistic Phylogenies Are Not the Same as Biological Phylogenies.


Orangish-coloured insect living in wood chips Can anyone Identify this organism?

I dug it up in a pile of 5 year old wood chips in Cleveland, Tennessee, United States. It is about 4 inches long.

That is the pupa of a unicorn beetle, Dynastes tityus. https://arthurevans.wordpress.com/2010/09/15/453/


What allows grass eaters to digest cellulose? Scientists are saying that it was a small step for the Panda to move from a meat diet to a grass diet. The article only refers to differences in the Panda's skull, presumably for better chewing.

I've also heard that the Japanese are able to digest Nori because they have the right gut biome because Nori has been part of their diet and the appropriate bacteria has developed over time.

Does that suggest that if the cellulose of bamboo and other grasses were pre-chewed by mechanical means and the right bacteria were introduced into the human gut that we would likewise be able to digest grasses?

Related story

No there is something else missing besides bacteria

humans often already have the right bacteria but they don't digest most of the cellulose they ingest because digesting cellulose with bacteria is SLOW. Too slow to keep up with normal mammalian digestion. You need a specialized gut that  either has a large complex stomach to keep recycling the cellulose in the system (foregut fermenters) or has large storage chambers to keep the cellulose a long time and allow it to be digested slowly (hindgut fermentation).

humans have neither. To make matters worse Humans have huge caloric needs compared to other animals of the same size. Brains are calorie hogs and our brains are so large they consume 1/4 of all our calories. That is 3 pounds of our mass consumes a quarter of all the calories we eat. honestly without the advent of cooking (which drastically improves the caloric availability of food) human brains could never have reached the size they did.

Further reading

More further reading