What (if any) is the shortest evolutionary process observed by humans? So when I think of evolutionary processes, I think of it taking millions of years to happen. Like how humans evolved from monkeys or birds evolved from dinosaurs (I know that is super-duper simplified). Or how humans have parts that we don't need or use (the appendix, for example), but we don't have any records of a time when it was. But I wonder if there have been any evolutionary processes that happened on a human timescale or if we have evidence of something evolving in, say, thousands of years instead of millions? I think this would be interesting to learn about.

Definition of evolution

The whole problem boils down to the definition of the term "evolution". Typically, evolution is defined as a change in allele frequency over time. See wikipedia > allele if needed.

Answer with definition "evolution = change in allele frequency over time"

Using this definition, any event of death or birth is an evolutionary event. As such, in the human species, there are about 6 evolutionary events per second! This number will vary a lot among species / lineage of course.

Do you want to consider another definition?

If you are willing to use another definition, I am happy to investigate how common are events matching this definition. Please make sure to clearly define the term so as to leave out possibility for subjective appreciation. If you need inspiration for definitions, you might want to have a look at this post.

Sidenote: Evolutionary experiments

You might be interest in evolutionary experiments. An evolutionary experiment consists at putting individuals in a lab, let them breed under some circumstances and let them evolve. Of course, doing such experiment with elephants would be pointless as the generation time is so long. Common species that we use for such experiments include E.coli, S. cervisae (yeast) and D. melanogaster (fruit fly). Some of these experiments can be as short as a few days while others have been running for decades.

Somewhat related posts

How come most animals never seem to evolve over millenia?
Evolutionary chronology - if any, which species have evolved in the last 100 years
Why don't we keep evolving until we are super-human?

For a very introductive source of information in evolutionary biology, you can have a look at the website that @BryanKrause recommended: evo101


How to produce correct epithet of a species named in the honor of a person? I want to name a new diatom species in the honor of Prof. Vodyanitskiy. What will be the species epithet: "vodyanitskiya", or other? Are there any rules that regulates how the end of such epithets is changed?

You should check the article 60 of ICN: http://www.iapt-taxon.org/nomen/main.php?page=art60

See in particular Recommendation 60C about specific epithet, and in the specific case, the rule 60C.1 (specific epithet derived from a person name).

You can use the genitive case (as Plant of Vodyanitskiy) as in rule (a), which is independent of generic name, so  if the professor is male: X. vodyanitskiyi, and she is female: X. vodyanitskiyae.
or as adjective (so inflected according the genera), in rule (c): X. vodyanitskiyana, X. vodyanitskiyanus, X. vodyanitskiyanum

Note: there are other rules to have a valid published name, and it is recommended to explain why you choose such name. In additional to the ICN code, there is the companion book: The code decoded. A user's guide to the International Code of Nomenclature for algae, fungi, and plants(Regnum Vegetabile 155), by Nicolas Turland


Worm compost cannot have cooked food I live in the Netherlands and it is getting fashionable to compost with worms. After investigating a few websites I noticed that most websites suggested that I cannot feed the worms leftovers from citrus fruits. This seems logical. I then started noticing that people advise against feeding the worms cooked food.

I'm no biologist but I cannot imagine a reason why cooked food is bad for the worms. Could anybody explain why this might be in layman’s terms?

There are a few reasons for not feeding cooked foods to worms (Eisenia spp.) in a smaller household size worm farm. It's not because the food is cooked but what it often contains.

The earthworm used in vermiculture is usually Eisenia fetida (red wigglers) though other Eisenia species are sometimes used. All Eisenia are epigeic species meaning they live in the junction of decomposing organic matter (such as leaf litter, aging manure, rotted fallen trees) and their natural food is decaying plant matter and bacteria that are also digesting the organic matter. They don't make use of small dead animals (meat and fat).

In large scale commercial vermiculture operations, leftover and past-due-date foods from restaurants, institutions, nursing homes and schools are used along with plant matter and carboard and paper. I'm not sure how they balance cooked foods but possibly much less is used than plant matter.

The fact food is cooked isn't the problem but what's in it and/or what happens to it when added to the bin. If you have leftover vegetables and fruit that's been cooked with no added salt, it's perfectly acceptable. A certain amount of sweetened cooked fruit is also fine as the worms will eat that too. But ready-made foods usually have preservatives, salt, fats and spices added. Either worms won't eat it, leading to odour caused by mouldy rotten food, or it can make them unthrifty and even killing off your worms if it's fed them repeatedly.

Fats and meat along with cheeses and dairy products will also not be eaten so shouldn't be used. Sites about vermiculture say onions and garlic can 'burn' the worms skin which is the problem with citrus fruit. They can be used but in very small amounts and should be mixed well with their other food.

Vermicomposting for Business, Farms, Institutions & Municipalities

Wormy FACTS and Interesting Tidbits about Eisenia fedita


Resting membrane potential in cells My textbook says “Among K+, Na+ and Cl-, K+ contributes to the resting membrane potential the most, because it has the greatest permeability across the membrane.”

I agree with this, but I’m just curious: why is the equilibrium potential of Cl- (-75mV) closer to the resting membrane potential (-70mV) than that of K+ (-90mV)?

This is only true because the chloride concentration happens to be slightly less negative than potassium, therefore the weighted (by permeability) average of all the other ions is near the reversal potential for chloride.

Even if you assume the permeability of every ion except sodium and potassium is zero (i.e., if chloride doesn't contribute at all), you will end up with a resting potential near chloride's reversal potential.


Does a piezoelectric organic substance exist? that contracts rapidly, in 10 seconds or less, by .5mm or more, when bombarded by electrons as from a cathode ray tube? or expands? could either be living tissue or dead organic matter.  thanks!

I think your question is a bit specific, but piezoelectric organic substances do exist. There was a paper in nature that researchers at Berkeley published.

Please see the following journal article:
http://www.nature.com/nnano/journal/v7/n6/full/nnano.2012.69.html#affil-auth

Also see the following public article:
http://www.extremetech.com/extreme/129389-berkeley-scientists-turn-harmless-virus-into-piezoelectric-generator


How do you compare unpaired biological replicates? I have done proteomics and I have obtained genes with ratios. As an small example you can see my data below

Gene    Control1     Control2   Control3    Treated1    Treated2    Treated3
pps-1   324680000   211350000   356350000   269770000   258080000   292830000
R11A8.7 477490000   610780000   539550000   533590000   530810000   578290000
ugt-21  105080000   103430000   74137000    78915000    42381000    31415000
spp-18  1042800000  615030000   332720000   538340000   448280000   412310000

Now My question is that I have Three controls and Three Treated, Control has two biological replicate and Treated has two biological replicate

I am trying to find the pathways which the list of my genes activate it. I use IPA which is a tool for pathway analysis

How can I calculate the fold change for it? If I use the 6 values, IPA will give me 6 different results and then interpretation will lead me to hell.

I appreciate any help.

Calculating fold change is pretty straightforward but you cannot do one on one comparison because they (control and treated) are not really paired (same sample). That's why IPA gives you six results (FC for each pair). However, you can calculate fold change between two genes because they are from the same sample. Note that fold changes are quite dangerous and can lead to misinterpretation of data (for example 1/2 would be same as 100/200). You should use them cautiously.

I think, in this case, you can simply apply a t-test. This will tell you if your two groups i.e. treated and control are significantly different from each other. You would not be calculating fold changes here. If you had more number of groups then you can go for one-way ANOVA.

I am not sure what output you really want after the analysis but I think the main goal is to say that control is different from treated.

Since you have multiple genes (variables) you can either go for a multivariate t-test, which will tell you if the control is overall different from treated, or many univariate tests which will tell you how each gene differs between the two groups. There are some methods such as Bonferroni correction which can be used to improve the prediction of multivariate tests.

When you have established that a certain gene is differentially expressed, using t-test, you can report the fold change of the averages.


Book on yeast reproduction, evolution and on the use of yeast as model organism I am looking for a good book in:

Yeast reproduction

mating types
Recombination
mating type determination mechanism

Yeast evolution
Yeast as model organism and its use in experimental biology

It should include common technics used to work with yeast. For example: We can add a plasmid in order to fool yeast and let them think they have another mating type than the actually have.

Note: I am mostly interested in Saccharomyces cerevisiae of course.

Here is my list, in no particular order.

Methods in Yeast Genetics

Some other yeast books at CSHL

Fred Sherman's primer, available free at various sites including here.

The Freiburg manual here

The timeless classics (link to volume 3 but see all volumes)

The YeastBook is an attempt to build a current encyclopaedia to replace the previous item on my list.

The Saccharomyces genome database, probably the best organism-specific resource ever.


Separate DNA fragments with very different size (oligo and lambda-DNA) I am running a ligation reaction to one of the sticky ends of lambda-DNA.

The oligo for the ligation is 25 bp (10x excess), whereas lambda-DNA is 48 kbp. I would like to recover the lambda-DNA and discard the unreacted excess oligo.
Given their vastly different molecular weights, they should be easy to separate, but I could not find a standard methodology online.

I do not want to run gel and my total sample volume is 0.5 mL. There are some filtration columns that may work, but the input volume is only 25 uL (I have 20 times that).

I don't have to get rid of all the oligo, having slightly more lambda-DNA than oligo at the end would suffice.

Which simple protocol may work in this case?

A spin column might work for your purposes since you can do multiple rounds of binding if your volume is too large to bind in a single pass, but for DNA of that size a lot will be irreversibly stuck to the column.  See for example the protocol for the Monarch® PCR & DNA Cleanup Kit.

Consequently I would recommend just doing an ethanol precipitation, which favors recovery of longer DNA molecules (see for example this protocol).


Why is trypsin digestion required for proteomic studies? I know that trypsin is used for proteomic studies, but I do not understand why trypsin digestion is necessary/important.

Trypsin digestion allows you to cut proteins into smaller polypeptides, masses of which can be determined by mass spectrometry and then translated back into possible amino acid sequences. Trypsin cleaves after specific amino acids. Altogether, this allows you to identify proteins.


How does sexual reproduction generate more genetic variation? I'm curious as to why sexual reproduction generates genetic variation. For me, the term genetic variation is a little ambiguous. The way I understand it, it's the number of alleles at a locus in a population or "group" of organisms.

But sexual reproduction only "reshuffles" alleles, and doesn't generate new ones (most of the time, at least). So why does it create genetic variation?

Thank you for reading.

There are two questions here. 1) What is genetic variance? It is actually clearly defined. 2) How does sexual reproduction generate more genetic variation?

  What is genetic variance?

Assuming bi-allelic loci, just assign a value of 0 to one allele and 1 to the other allele. Then compute the variance! Average this value over all loci. Done! Have a look at any intro book in quantitative genetic for more info (see here)

  How does sexual reproduction generate more genetic variation?

You are right "sexual reproduction only "reshuffles" alleles, and doesn't generate new ones". It is a common misconception that sexual reproduction generate genetic variation. The details of whether it does or it does not depends upon the detailed distribution of dominance coefficient and distribution of epistatic effects.

There has been a lot of work on the subject and it is not an easy work to summarize it. Sally Otto does a great job to summarize this misconception in her speech On the Evolution of Sex and the Advantages of Recombination. You should definitely have a look at it.

Note however, in some species that preforms both asexual and sexual selection, it happens that sexual selection is coupled with higher mutation rate than asexual selection. In such cases, sexual selection does indeed increase genetic variance but only so because of tis correlated effect on mutation rate.


Why is DNA replication not 100% accurate I've been reading about DNA mismatch repair (MMR) and how this process improves DNA fidelity. However, I was wondering, what is stopping MMR from correcting all mistakes in the daughter DNA with 100% fidelity? Why is the error rate still around 1 in 10^9 base pairs? Is it because the MMR proteins aren't present in cells in a high enough concentration? What would you have to change about this process to achieve 100% fidelity?

Nothing is 100% precise - any measurement or process allow for some error, the only difference is how often such errors occur (i.e., the probability of an error). These wildely range in biology - e.g., it is about 1 per $10^4$ in HIV replication, but only 1 per $10^9$ for human DNA (due to the repair mechanisms).
Note that $1$ in $10^9$ for human DNA means pretty much that there is about 1 error per each copying of the genome (which has the size of about $3\times10^9$). One could therefore still pose a question of why the error rate is so high? E.g., Human body consists of about $15\times10^{12}$ cells. Thus, if the error rate were about 1 per $10^{22}$($\approx 3\times10^9$ by $15\times10^{12}$), we could have human organisms consisting of the cells with identical DNA.
The answer to this is that errors are not necessarily bad: the copying errors are the source of the mutations driving the evolution! Note also that many of the errors have no effect at all on the well-being of the organism. Thus, it is fair to say that the existing error rates were selected by the evolution for assuring the appropriate rate of the evolutionary change/adaptation, without causing immediate harm to the organism. (One could even speculate that 1 error per genome copy is the appropriate rate across the organisms, but for a moment I cannot support this assertion by references).


Are nutrients absorbed in human esophagus? Following this question regarding absorption in human oral cavity (sadly not yet fully answered), I'm curious if any nutrient absorption occurs during the descent of food through the esophagus.

And if so, what requirements must a nutrient meet for that.

For several reasons, I seriously doubt that this has been studied extensively.

There is a good reason to study absorption through oral mucosa because a drug or glucose can be held there by people who needing rapid absorption of a drug (e.g. sublingual nitroglycerine) or by people who may be unable to swallow (e.g. a hypoglycemic individual who has lost consciousness). Where there is a reason to know, there is a reason to study something.

The esophagus, on the other hand, is normally an area of rapid transport (a pill, or a fluid, for instance, is in the esophagus less than 10 seconds). While it's assumed that some pregastric absorption through the esophagus occurs and might be beneficial to avoid a "first pass" metabolism of the drug by the liver, there is no good method to keep a drug in the esophagus. With that in mind, absorption from the sublingual mucosa (where a pill might be held) is more valuable than what might get absorbed in as little as 6 seconds in transit to the stomach. From that point, it will spend significant amounts of time in the stomach, the various sections of the small intestine, and the large intestine.

Absorption of drugs from the rectum has been studied, because it can be used, once again, as a method of drug delivery when another route for whatever reason cannot,

Esophageal motility disorders occur, so studies of esophageal function are common. But as the esophagus is never normally the place for absorption of nutrients, there is no reason to study it except for the sake of satisfying pure curiosity. Studies take time, involve volunteers (or paid recipients), risk, and money. Pure curiosity is a reason to study something. But to get the all the previously mentioned factors to come together and fund a study, the reason usually outweighs pure curiosity.

Esophageal scintigraphy: reproducibility and normal ranges
Oesophageal transit of a radionuclide solid bolus in normals
DRUG ABSORPTION BY SUBLINGUAL AND RECTAL ROUTES


How is photosynthesis observed? How is photosynthesis observed?

Say I have plants A and B, and I want to find how fast they are able to turn carbon dioxide into oxygen. How would I experiment this?
Say I have one plant A, which has two kinds of leafs B and C. I hypothesize the B-leafs produce oxygen faster than the C-leafs. What kind of experiment could I set up to test this?

Not sure, this what you need, but here you can find a detailed description of how photosynthesis efficiency can be measured in the field, with a list of modern devices. In short, it's about measuring the uptake of CO2 and release of H2O of individual leaves.


Can mushrooms spontaneously die? These are called mushrooms I believe, had been growing on my door for a few weeks. It's monsoon here. Last night I took a picture of it and it looked like this . Today when I woke up it became like this: . All this within 12 hours. I'm pretty sure nobody touched the fungus so I'm inclined to believe this was spontaneous.

There are several fungi that autodigest  their lamellae  to release spores. Yours seems to be one of them. Due to the black liquid they release during autodigestion, they have the common name inkcap.

As an example, read this Wikipedia article about Coprinus for more details.


Can I pellet DNA back from dissolved state? I have a dissolved plasmid pellet in water. Can I pellet it again by centrifuging it at 13000 rpm? If not, why?

No, you cannot pellet dissolved DNA with ultracentrifugation.

Yes, you can recover a pellet with additional treatments, similarly to how you got it in the first place; only instead of your input being homogenized cells, or tissue, or extract, or whatever you used to obtain your DNA, it would now just be your aqueous solution of DNA.

For instance, you may have performed a TRIzol extraction to separate your DNA into an aqueous phase, prior to spinning it through mini prep columns to elute your purified DNA in water. You could perform the procedure again and you'd have your pellet once more after the final alcohol (ethanol or isopropanol) precipitation step.

The key idea with pelleting DNA (or any nucleic acid) is to make it insoluble; this is achieved with by using alcohols and salts. If it is soluble, nucleic acids cannot 'come out of solution' to form a pellet.


Did researchers evolve multicellular yeast or did they just turn on multicellularity? In this new paper "Experimental evolution of multicellularity" found via Ars Technica the researchers describe having developed multicellularity and apoptosis within 60 days from a unicellular yeast species.

Is it possible that what they have done is merely turn on an ability of that species that evolved previously and just lay dormant?  Do we know that that yeast species and all its ancestors were never multicellular?  The paper doesn't even mention the possiblity of this.

You're right:

  Within the Fungi, simple linear multicellularity of hyphae occurs in all major clades (see below), but only Ascomycota and Basidomycota display more complex two- and three- dimensional multicellularity in the form of sexual spore- producing fruiting bodies. In both of these groups, reversals to unicellular lifeforms have occurred, for example, Saccharomyces and many other related yeasts in the Saccharomycotina (Ascomycota) or Cryptococcus albidus and related species in the hymenomycete clade of Basidiomycota (de Hoog et al. 2000, p. 130).

Medina, M., A. G. Collins, J. W. Taylor, J. W. Valentine, J. H. Lipps, L. A. Amaral Zettler and M. L. Sogin (2003). "Phylogeny of Opisthokonta and the evolution of multicellularity and complexity in Fungi and Metazoa." International Journal of Astrobiology 2(3): 203-211. doi:10.1017/S1473550403001551
(PDF)

Update: The authors responded to criticism like this on The Loom, here's an excerpt:

  Our yeast are not utilizing ‘latent’ multicellular genes and reverting back to their wild state. The initial evolution of snowflake yeast is the result of mutations that break the normal mitotic reproductive process, preventing daughter cells from being released as they normally would when division is complete. Again, we know from knockout libraries that this phenotype can be a consequence of many different mutations. This is a loss of function, not a gain of function. You could probably evolve a similar phenotype in nearly any microbe (other than bacteria, binary fission is a fundamentally different process). We find that it is actually much harder to go back to unicellularity once snowflake yeast have evolved, because there are many more ways to break something via mutation than fix it.


What is the name of this fruit? I have attached a photo. I know the Nepali name for this fruit but not its common name in English and its scientific names. In Nepal we call it as 'lahare Aanp' (meaning Climber Mango). This fruit is a climber type like cucumber.

Does anybody know its common name in English and its scientific name?

This is a passionfruit. It comes from a plant whose scientific name is Passiflora edulis.

It's indeed a climber, as you can see:

Finally, a curiosity about the name passion fruit. The fruit is called passion fruit because the flower is called passion flower. This is the flower:

But why it is called passion flower? Passion here has nothing to do with sexual love or desire, the common meaning of "passion", but with the suffering of Jesus.

Some say that it's because the flower resembles (?) the crown of thorns placed in Jesus' head. Other say that it symbolises Jesus' wounds. In fact, in portuguese we call it "flor das cinco chagas", or flower of the five wounds.

EDIT: thanks to @AlanBoyd's comment, you can see that its connections with Christianity are way more complex: https://en.wikipedia.org/wiki/Passiflora#Etymology_and_names

Post Scriptum (not related to the question): this plant is native to Brazil, and I had a couple of specimens in my yard. One of the most interesting things about passionfruits in Brazil is that it attracts an insect that we call "percevejo do maracujá", or passionfruit bug in a very free translation. Its scientific name is Diactor bilineatus, and it's one of the most beautiful insects to me. I loved to see them feeding on my passionfruits. This is the adult on a passionfruit (where you normally find them), and the nymph is even more colourful:


What do nerves have to do with feeling nervous? I was thinking about how when people say: "Nerve cells don't regenerate" (which is, apparently, not true at least for some kinds of nerves) and "You're making me nervous" they might not refer to the same "nerves".

What makes a person "feel nervous"? Does it have anything to do with nervous system?

Bonus question: How did people come up with the thought that nerve cells don't regenerate?

As buzrw's first comment states, most nervousness is primarily a sympathetic nervous system response.

There are also neurotransmitter imbalances involved with anxiety, especially in anxiety disorders.  The NT are dopamine, serotonin, and norepinephrine.

I want to clarify buzrw's comment on nerve cell regeneration, as I am unsure if he is stating it's proven to exist or to not exist.  "Primary neurons are not readily mitotic..." makes me think it's the latter.

Neuroregeneration is proven. Mayo Clinic has good information here and this is a well-phrased simplified answer here.

It is more commonly seen in peripheral nervous system, as the central nervous system has limited capabilities to regenerate.  Mostly it is regrowth of severed axons of  cells, and differs between different nerve cell types.  There are other types of regeneration as well.  They involve many physiological processes we're only starting to understand, such as the role of neuroligin.  Without getting too technical, there is a lot that can be done to help stimulate and guide the regrowth of some neural damage, but there are still chasms in our knowledge in the fields of neurology and psychiatry.


Non-fatal / low-harm measurement of Drosophila traits I am trying to generate some candidate traits to measure in a fitness assay of wildtype outbred (lab population) flies. The key trait I will measure is lifespan.

I am looking for some additional traits which can be measured from the same flies as those in the lifespan assay without harming or killing the fly in the process. For example, I could measure wings using a technique devised by the Houle Lab called WingMachine. I think I could also do some other measures with the same equipment, leg length etc.

The traits should also be present in both sexes (can be monomorphic or dimorphic) and quick to measure; I'm aiming for 200-250 measures/collections/images a day. Traits that can be measured properly in a fly which has died of old age would also work. Traits can be morphological, behavioral etc..

What other traits can be done like this?

You could do negative geotaxis (climbing) assay, (larval or adult) locomotion assays, % brain vacuolisation (after the flies die), maze tests. There are probably much more but these are all I can think of that are no-lethal and can be applied to males and females and some larval work too.

You could maybe consider doing starvation assays and longevity in some of your populations.


How much cost would artificial pollination add to common products (fruits etc.)? I've read about ecosystem services and their possible valuation - statements like "honeybee pollination service in the US is worth 1.6 billion dollars".

Is data available on how this would affect the cost a consumer pays for a given product? For example if the humans must do all pollination of fruits themselves, how would that affect the retail cost of these fruit?

The cost would increase; either because pollination services are not provided and the supply is decreased; or because the cost to producers goes up as they must pay for artificial pollination. See the extremely detailed analysis in Winfree et al.

edit

I imagine what you're actually asking for is a $ figure "per apple". This depends on the location, crop, market, etc., but just for a ballpark, if I'm reading the supplementary tables in Allsop et al correctly, the replacement value of insect pollination to apples in the Western Cape of South Africa would represent a 6%-25% increase in production cost (and, if the producers pass that along to the consumers, an equal increase in the cost to consumer).

 Allsopp MH, de Lange WJ, Veldtman R. 2008. Valuing insect pollination services with cost of replacement. PLoS ONE 3: e3128–e3128.
 Winfree, Gross, Kremen. 2011. Valuing pollination services to agriculture. Ecol Econ 71: 9–9. [behind paywall, but posted free here]


Help identifying organism I would like help identifying this "crab".
I looked through 32 pages of crabs on this resource http://species-identification.org/ but none of them look like this little animal found in the waters of Madeira.
They move fast and are something in between a spider and a crab.

It is definitely a crab - not anything spider. I originally thought it was a Sally Lightfoot Crab (a common crab on Madeira from the family of shore crabs) but I agree on your comment that it is more likely a Nimble Spray Crab (of the Flat Crab genus) as the specimen in your photo seemed a lot flatter than a shore crab (but I wasn't sure if it was just the shape of the rock).
The Wikipedia article on this species says that these are also referred to as another kind of Sally Lightfoot crab, and the fact that these are in a different taxonomic family from the other ones (the shore crabs) is a topic of debate.

They are observed in the coastal Atlantic and considered native to Madeira, but have recently spread into the Mediterranean

You can view a gallery of almost 200 photos of these crabs on iNaturalist.


How often does bacterial transformation happen? I have been reading:

  M. Dröge, A. Pühler, W. Selbitschka, "Horizontal gene transfer among bacteria in terrestrial and aquatic habitats as assessed by microcosm and field studies", Biol. Fertil. Soils (1999) 29 pp221–245  [PDF]

I am not a biologist and am trying to get a feeling for how often prokaryotes make changes to their chromosomal DNA.

How often is plasmid DNA successfully incorporated into chromosomal DNA?

I would like to estimate either the number of gene changes (or, failing this, base pair changes) that a bacterium makes per unit time. Or, equivalently, the mean time between such changes.

Transformation underpins a lot of lab modern projects.

This will be a very unsatisfying answer, and this wikipedia entry explains why. The time, and success, of bacterial transformation of competent cells varies greatly depending on a few things mainly:

the length of nucleic acid sequence for insertion (or more accurately, the plasmid)
the species of target organism (or more accurately, the genotype of the target organism)
a host of other things

With a specific plasmid and organism you would be able to get a more satisfying answer, but I imagine the answer would even differ from lab to lab.

I worked with a microbiologist that provided me with a protein as a part of my honours project, and I can give you a broad impression I got from them: it does not happen often. Sometimes none of the cultures you are trying to transform will incorporate the new sequence into their genome, other times the cloning process goes very well and all your cultures will be transformed successfully. For our project, valid colonies only presented after a week with reasonable success (more than half the attempts were successful). But you don't know if the transformation worked until way after the first transformation happened.

The mechanisms behind this are grossly understudied. If we take some thing B. subtilis, arguably the most academically studied organism in the field of transformation, it can take up the DNA as food or incorporate it into its genome but nobody knows exactly how this happens at a molecular level (Chen & Dubnau, 2004)

Chen, I., & Dubnau, D. (2004). DNA uptake during bacterial transformation. Nature Reviews. Microbiology, 2(3), 241–9


definition of tempo and mode in evolution I am reading Punctuated Equilibria: The Tempo and Mode of Evolution Reconsidered, which mentions the "tempo" and "mode" of evolution. I'm not familiar with the related literature and when I google the concept, what I got is something like:

  One general topic, suggested by the word "tempo," has to do with "evolutionary rates..., their acceleration and deceleration, the conditions of exceptionally slow or rapid evolutions, and phenomena suggestive of inertia and momentum." A group of related problems, implied by the word "mode," involves "the study of the way, manner, or pattern of evolution, a study in which tempo is a basic factor, but which embraces considerably more than tempo''

This is as elusive as a definition can be. A clear definition should be something like "tempo is ...."

So what are the definitions of mode and tempo in evolution?

Actually, we can go right to the source on this: George Gaylord Simpson's Tempo and Mode in Evolution (1944).

Tempo is the rate of evolution. Simpson was a paleontologist, so he was trying to answer questions like "what is the percent change in the size of this tooth per million years?" He has a chapter estimating these rates for various characters in horses, which have a very good North American fossil record.

Mode encompasses the mechanisms responsible for evolution and their patterns. Simpson was working at the time of the Modern Synthesis (the wikipedia page is decent and brief enough on the topic, about which books are written), coming from the perspective of a paleontologist trying to reconcile genetic evolution with the macroevolutionary patterns he was seeing in the fossil record.

Simpson was really the first paleontologist to look at fossils in a quantitative way, trying to understand of connections between microevolutionary processes and macroevolutionary patterns. He even co-authored one of the first quantitative and statistical methods books for "organismal" biologists: Quantitative Zoology.

Specifically, of tempo, he says (p. xvii):

  "...evolutionary rates under natural conditions, their acceleration and deceration, the conditions of exceptionally slow or rapid evolutions, and phenomena suggestive of inertia and momentum."

Of mode, he says (p. xviii)

  "...the study of the way, manner, or pattern of evolution, a study in which tempo is a basic factor, but which embraces considerably more than tempo. The purpose is to determine how populations became genetically and morphologically differentiated, to see how they passed from one way of living to another or failed to do so, to examine the figurative outline of the stream of life and the circumstances surrounding each characteristic element in that pattern."

Mode basically encompasses all the processes of evolution. Tempo is the subset of mode that concerns how fast evolution is (or is not) happening.

The great thing is that 70 years after Simpson's book, biologists are still trying to understand tempo and mode of evolution.


How to measure the length of mitochondria from z stack fluorescent microscopy image? I have been working on yeast cells to analyse the effect of DNA damaging agents on mitochondrial structure. I have imaged my culture treated with MMS for a period of 6 hours and while observing the images, I suspect there is fragmentation of mitochondria in later point of time. So, I am wondering if I can get measurements of mitochondria using z stack images.

ImageJ is usually the standard software to measure cell characteristics, a little bit of a learning curve but there is a large suite of analysis methods and image adjustments/filters.


How does one predict how large of an effect on antigenic drift a substitution in the amino acid sequence of a surface protein of influenza has? I know that some amino acid substitutions are more effective in causing antigenic drift than other substitutions based on their location in the 3d structure of the HA protein (proximity to the receptor binding site).

I would like to be able to determine using a program whether a virus will be dominant based on multiple factors including genetic difference from the previously dominant virus. How can one know how much bigger of an effect one AA substitution will have on the antigenicity of a virus compared to another?

Any help is much appreciated.

Your understanding of influenza antigenic drift is, unfortunately, hypersimplified and mostly wrong. In particular, your notion that some mutations are more important for antigenic drift because of their effects on structure is at best oversimplified.

Rather than spend many paragraphs reviewing the complex patterns involved, I'd suggest you start by carefully reading papers from people who have correlated antigenic drift with sequence change, such as

Sequence-Based Antigenic Change Prediction by a Sparse Learning Method Incorporating Co-Evolutionary Information
Using Sequence Data To Infer the Antigenicity of Influenza Virus
Mapping the Antigenic and Genetic Evolution of Influenza Virus
The genomic and epidemiological dynamics of human influenza A virus
Selection of antigenically advanced variants of seasonal influenza viruses
Antibody landscapes after influenza virus infection or vaccination
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

This is a field that a lot of extremely smart people have been looking at extremely closely for many years; all the simple approaches have been tried already.


What is the function of epiglottis? The last time I came across this question was when I was in high school. And the explanation I was given is that epiglottis works like a valve, it prevents foods from getting into the windpipe. Still, if I google the majority of the top results agree with this answer.
Recently I got interested in rabbit anatomy after I bought a pair as pets. I learned they are "obligate nose breathers due to their epiglottis positioned rostrally to the soft palate". Then I tried to revise my understanding of epiglottis and that let to some sources that claim that epiglottis is not essential for swallowing. For example:

  It was at one time thought that the epiglottis acted as " the lid of
  the larynx"; it was supposed that during deglutition it fell back like
  a flap over the laryngeal aperture in order to prevent ingress of food
  or water. This erroneous view as dispelled by Stuart, who proved that
  during swallowing the epiglottis actually moved forwards, to be
  squeezed between the base of the tongue and the rest of the larynx.
  This view cannot be disputed by anyone capable of judging, and the
  truth of it is borne out when observing a patient whose epiglottis has
  been almost entirely destroyed by lupus, but whose powers of
  swallowing remains unaffected.

Negus, VE (1927). "The Function of the Epiglottis". Journal of Anatomy.

  Controversy has continued for well over 100 years regarding the role
  of the epiglottis in deglutition. We describe the effect of isolated
  epiglottectomy on swallowing success in a case series of 3 adult human
  subjects with isolated epiglottectomy due to trauma, surgery, or
  cancerous erosion. The patients were 42, 51, and 70 years of age, and
  swallowing was analyzed objectively with videofluoroscopy. All
  subjects exhibited successful swallowing with all food types: thin
  liquid, puree, and solid food. Specifically, the patient with
  traumatic epiglottectomy exhibited rapid swallowing success, the
  patient with surgical epiglottectomy exhibited a short period of
  dysphagia due to postoperative edema, followed by swallowing success,
  and the patient with epiglottectomy due to cancerous erosion of the
  entire epiglottis exhibited long-term adaptation, with successful
  swallowing maintained. We conclude that the epiglottis is not
  essential for successful swallowing in humans, because individuals
  can readily adapt to isolated epiglottectomy and avoid tracheal
  aspiration.

Leder, Steven B et al. “Epiglottis is not essential for successful swallowing in humans.” The Annals of otology, rhinology, and laryngology vol. 119,12 (2010): 795-8.

Judging from google searches and Wikipedia entry on the topic it seems the dominant view is: epiglottis prevents food from getting into the trachea. But many research like the ones  I have mentioned above says that people can swallow without epiglottis. How to make sense of these apparently contradictory claims?

Edit: My question is not the same as the question suggested. The suggested question seeks the function of "hyoepiglottic ligament" which is a ligament that connects epiglottis "to the upper border of the body of the hyoid bone". My question is related to the function of epiglottis itself in the background of contradictory claims found in the literature.

You are right, The main function of the epiglottis is to seal off the windpipe during eating, so that food is not accidentally inhaled.(quote from here).

It's a flat shield of cartilage, which is obviously an efficient valve, It's a valve between the trachea and the esophagus.

It lets lions to eat a pound of meat without choking on their prey. It lets humans drink tea without coughing on their buddies.

Information stating that it's "possible" to eat without an epiglottis doesn't imply that it's "efficient and safe", and contradicts medical interventions where they use a piece of ear cartilage to build a new epiglottis.

Survival didn't encourage the "possibility to eat"... it has made animals very robust and efficient at it. Herbivores can spend most of their day eating, and are often attacked while they are eating and drinking. Carnivores also have reasons for efficient swallowing, big carnivores can eat many pounds of meat very fast while fending off competition from hyenas and other predators.

Sleep apnea patients have their epiglottis modified to give room to breathe at night, and they risk choking and aspiration for a while, although they can adapt because they keep some of the cartilage, so they still have a valve.

Different animals have different breathing habits, with some being obligate nose breathers, including human babies of under 6 months and up to 6 years. That's because the epiglottis either contacts the trachea or it leaves space there.


Comparative effectiveness of antibiotics against colonies and growing bacteria Appropriate antibiotics usually eliminate bacteria. However are the same antibiotics as effective against bacteria that have grown to form a colony?

It depends on the kind of antibiotic. Some antibiotic are bacteriostatic  i.e. they primarily stop the growth while some are bactericidal i.e. they kill the living bacterial cells. Some antibiotics can have mixed effects. Bacteriostatic antibiotics would not be very efficient in eliminating a colony.

Apart from the mechanism of action, there can be other factors that would dictate the efficacy of the antibiotic; these can all be considered under pharmacokinetics/pharmacodynamics:

Degradation/clearance rate of antibiotic
Rate of diffusion of antibiotic inside the bacterial colony (this rate would be less when the cells are inside a big colony compared to when they are disperse).
Community organization and dynamics inside the colony (like user137 said in their comment, certain biofilms can be more resistant to antibiotics)


Skull size of Homo naledi I want to 3D print the skull of the newly discovered Homo naledi.

The printing data can be found here: http://morphosource.org/index.php/Detail/MediaDetail/Show/media_id/7300

Where can I find the exact size of the skull so that I get a 1:1 copy? Google was of no help.

From my research, I can deduce that the cranial volume for males is

  560 cm3 (34 cu in)

and

  465 cm3 (28.4 cu in) for females

Note: These skulls are approximately half the volume of modern human skulls average Homo erectus skulls are

  900 cm3 (55 cu in)

I don't think you would need the area for 3-D printing, but you can use the volume!


Why does drinking milk lead to increased fractures? Milk has always been associated with strong bones due to the high amount of protein and calcium in it. Yet reading it up on wikipedia,

  A study published in The BMJ that followed more than 45,000 men and 61,000 women in Sweden age 39 and older had similar results. Milk consumption in adults was associated with no protection for men, and an increased risk of fractures in women. The risk of any bone fracture increased 16 percent in women who drank three or more glasses daily, and the risk of a broken hip increased 60 percent. It was also associated with an increased risk of death in both sexes.

My question is:

Why did this happen? Can someone explain the biological reason of this observation?

Even though milk really does provide large amount of calcium and proteins yet isn't is contradictory that the fracture rates increase?

This is the aforementioned study.

Michaëlsson, K.; et al. (2014). "Milk intake and risk of mortality and fractures in women and men: cohort studies". The BMJ. 349: g6015. doi:10.1136/bmj.g6015.

The authors suggest a reason in their abstract:

  Given the observational study designs with the inherent possibility of residual confounding and reverse causation phenomena, a cautious interpretation of the results is recommended.

There are variables they haven't measured that lead to the observed patterns. A simple one is that the respondees to the initial survey are self-selected (they return the survey). What if milk-drinkers are more likely to respond? Even if the base rate of fractures remains the same, then there will be an apparent association of fracture with milk consumption.

They also discuss physiological reasons, which is the subject of a different answer.


Why is the human ear most sensitive to 4000 Hz tones? Human hearing sensitivity is dependent on frequency, which can be visualized by equal-loudness (iso-loudness) contour plots. An example is given below (Taken from here).

This plot shows that a tone with around a 4 kHz frequency (minima above) needs the least amount of actual energy in order to be percieved well as compared with a tone of any other frequency, while on the other hand it shows that tones of frequencies below 100 Hz and above 19 kHz need to have a lot of energy for us to percieve it.

My question is, how does one explain the clearly uniform/persistent fluctuations in these iso-loudness contours? Why are our ears most sensitive to 4 kHz tones, and why is there a "shoulder" in the contours at about 7 kHz? My first guess would be for proper perception of human speech - but the characteristic frequency of human speech is around 80 - 260 Hz!

EDIT:
My question is similar to this previous question, but it is a bit different in detail (they are only concerned with the overall dip, whereas I'm concerned with the dip, the shoulder, etc.). Moreover, that question has no accepted answer.

The frequency-selectivity of loudness perception was first shown in the 1930s, when Fletcher and Munson published a set of curves showing the ear's sensitivity to loudness compared to frequency. These equal-loudness curves, as shown in the question above, are now known as Fletcher-Munson equal-loudness contours.

One straightforward physical explanation is the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.

The evolutionary reason why 4 kHz, and not, e.g. 0.5 or 8 kHz, is difficult to pinpoint. First I can clarify some misconceptions in the question, before getting back to the question proper:

Firstly, you mention that the "characteristic frequency" of a human voice is between 80 and 250 Hz. You are referring to the fundamental frequency; the characteristic frequency is a measure used in electrophysiology to determine the frequency-specificity of inner-ear neural structures.
Secondly, the fundamental frequency does not determine the frequency-selectivity of speech understanding. A useful picture is given below in Fig. 1, which shows which frequencies convey which speech components.

Fig 1. Frequency dependence of speech components. source: The Essential Guide to Hearing Loss

It becomes aparent from Fig. 1 that consonants (f, s, h etc.) are higher pitched than vowels (a, o, u etc.). Arguably, consonants convey most of the word information. Indeed, speech understanding is generally less affected by removing the vowels than by removing the consonants. One may deduce from all this that high-frequency hearing (say 2 - 8 kHz) is most important to understanding speech.

And then, to get back to your evolutionary motivation behind the Fletcher-Munson equal-loudness contours, it may, purely hypothetically be so, that our ancestors with a middle-ear resonance around 4 kHz were advantaged over those that had resonances elsewhere in the audible frequency range, if any, because of an enhanced perception of the spoken word. But this is entirely and purely speculative and remains an unreferenced statement for which I do not wish to be held repsonsible in any way :-)


What is this lightning-fast tiny spider? Saw this spider as I was taking a shower. It moves really fast. This I noticed when it moved away (from the center of this splendid pattern) to repair its web.
Location: West Bengal, India.
It appears to be almost 1.5 cm in length.

Many web-dwelling spiders are lightning-quick in their own web (even if they are slow/clumsy walkers outside of their web) so that doesn't help in identification.
Hard to tell from the photo, but it appears to be Cyclosa ginnaga
A better image of the specimen would help identify.
edit after comment:
Here is a gallery of observations (currently 50 of them) of cyclosa ginnaga: https://inaturalist.ca/observations?place_id=any&subview=grid&taxon_id=360502
All those observations were made in South-East Asia or Australia.
You could also look at Cyclosa Insulana with similar range:
https://inaturalist.ca/taxa/560706-Cyclosa-insulana/browse_photos?quality_grade=any
But I think the length of abdomen in your photo more closely resembles C.ginnaga, and also the observations of C.ginnaga more consistently show a spiral in the thick webbing while C.insulana tends to be more random.
And here is a breakdown of the cyclosa genus broken down into specific species if you want to browse other possibilities:
https://inaturalist.ca/taxa/127360-Cyclosa/browse_photos?quality_grade=any&grouping=taxon_id


True examples of common variation due to Mendelian Inheritance Classic examples of mendelian inheritance are genetic diseases such as sickle-cell anemia, Tay-Sachs, cystic fibrosis, and xeroderma pigmentosa. For some of these diseases, it is believed that they evolved because the genes gave a beneficial effect that outweighed the rare occurrence of the disease (e.g sickle cell and protection against malaria).

However, all of these are examples of uncommon phenotypes, usually less than 1% of the relevant population (where it is most common) has those diseases. I'm interested in examples of mendelian inheritance where variation is common (all of the relevant phenotypes have, say, >5% frequency or something like that).

Consider eye color. In European populations both blue and brown eyes are common phenotypes. Many people have probably experienced a typical high-school class of biology, where this was introduced as an example of mendelian inheritance with brown eyes being dominant and blue eyes being recessive. However, modern studies (for example, genome-wide association studies) show that things like eye, hair and skin color are all polygenic traits. See for example (Sulem, ..., Stefansson, 2007).

Throughout the years I've heard of other traits that some said were examples of mendelian inheritance. Being able to roll the tongue, for example. This question was inspired by this recent question where absence of teeth (Hypodontia) was taught to the OP as an example of a dominant trait. The current answer says that hypodontia is probably an example of a polygenic trait that interacts with certain environmental effects. This got me wondering whether there even are examples of common mendelian variation.

I don't quite know the best way to phrase it, but my question is the following:

  Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

Take eye color as an example again. By common, I mean that both blue eyes and brown eyes are common (over, say, 5% in for example Sweden). On the other hand, for example Tay-Sachs disease occurs only about 1 in 3,500 among Ashkenazi Jews where it is most common, according to Wikipedia. Way less than even 1%.

Preferably I want it to be verified by modern genomic studies (such as GWAS) that it is an example of mendelian inheritance. If such an example does not exist, then I will accept any answer that provides modern, relevant scientific literature that explores this topic. For example, it might explain why we would not expect to see common variation due to mendelian inheritance.

Earwax consistency is an example of a monogenic trait with dimorphic phenotypes in humans -- "wet" and "dry" -- where both phenotypes are globally common, though allele ratios are highly variable between human populations.  The population genetics and molecular basis of this trait are discussed at length by Dr. John H. McDonald as part of a series on the myths of human genetics (archived version here).  I reformat his discussion in my answer.

In The dimorphism in human normal cerumen, Matsunaga summarizes 30 years of research into the earwax of Japanese families, with two major observations:

Dry earwax parents never have wet earwax children, suggesting the genetics underlying the wet phenotype are dominant to those underlying the dry phenotype.
Because the allele for wet earwax is relatively rare in the sampled families, it is likely that most wet earwax parents are heterozygotes.  Following from this, if the trait is monogenic with two allele variants, we expect a 3:1 ratio of wet to dry children in wet × wet parent crosses, and a 1:1 ratio of wet to dry children wet × dry parent crosses.  Indeed, this is observed.

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 35 & 12 \\ \hline
\text{w×d} & 205 & 195 \\ \hline
\text{d×d} & 0 & 634 \\ \hline
\end{array}$$

These results were later corroborated in Native Americans --
Cerumen in American Indians: Genetic Implications of Sticky and Dry Types

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 32 & 6 \\ \hline
\text{w×d} & 20 & 9 \\ \hline
\text{d×d} & 0 & 42 \\ \hline
\end{array}$$

And in a different Japanese cohort --
Distribution and inheritance of earwax types: a study on inhabitants in Awa District, Chiba Prefecture

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 27 & 3 \\ \hline
\text{w×d} & 137 & 109 \\ \hline
\text{d×d} & 0 & 345 \\ \hline
\end{array}$$

In the early 2000s, the molecular basis of human earwax consistency was elucidated in three major publications.

Toshida et al. mapped a single locus on chromosome 16
Yoshiura et al. identified a SNP at position 538 in the coding region of ABCC11.  At this site, G corresponds to a wet earwax phenotype, whereas A leads to a dry earwax phenotype.  A less common allele representing a deletion of 27 nucleotides in exon 29 also yields a dry phenotype.
Toyoda et al. found that the 538G>A transition encodes arginine in place of glycine, resulting in a loss of glycosylation in the mutant protein, leading to deficient cellular localization, rapid degradation, and loss of function.

To directly address your question,

  Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

I point you to the tables above, as well as Table 1 from Cerumen Phenotypes in Certain
Populations of Eurasia and Africa, which shows that the frequency of the dry allele ranges from 59% to 89% across diverse human populations --

To conclude, human earwax consistency is a dimorphic trait controlled by a single gene, where both phenotypes are common across human populations.


Sex differences in response to food deprivation This question was inspired by a casual conversation with friends the other night. Some of us had noted that women tend to eat smaller meals more often (snacks, fruits etc) while men eat larger portions more infrequently. Also, several of the women said to be sensitive to food withdrawal, getting very hungry after a few hours and experiencing low blood sugar symptoms (even fainting in one case) if not eating regularly, for example if skipping lunch. Men (including myself) seemed to be less affected, often skipping meals without noticing.

This was a highly unscientific investigation with a tiny sample size :)  just based on our personal stories and friends we know. It could, of course, reflect attitude/perception/habits rather than actual biological differences. It should also be said that not everybody agreed -- some men also stated that they felt sensitive to food withdrawal. But there are of course known differences in metabolism between the sexes, so it doesn't seem entirely implausible. It might also be related to different body mass, muscle mass, etc.

So my question: is there any scientific evidence that women and men react differently to short-term food withdrawal? Here short-term would be, say, up to 24 hours, as when skipping breakfast and/or lunch. Are there any data on differences in blood glucose levels after food withdrawal, for example?

There are very few studies about the gender-based differences in response to food deprivation in humans (or at least I didn't find many such reports).

In one of the papers, Sodersten et al conducted a research on 30 (17 women and 13 men) high school-aged subjects. After a short-term fast (skipping 2 successive meals), males consumed much more food while women actually ate less, when compared with their respective baseline quantity of meal. They suggested an inherent difficulty for women to compensate a period of fasting by increasing their food intake. They, thus, concluded that fasting might be more risky for women than men as this may start them down a self-sustaining pattern of reduced calorie intake. You can see the reference from Yamada's Textbook of Gastroenterology.

In another study, Soeters et al, 2007 showed that after a period of fasting for 38 hours, women had low plasma glucose levels than men, although they have higher amount of free fatty acids in plasma. They suggest that women are somehow protected from free fatty acid-induced insulin resistance, probably because they prevent myocellular accumulation of ceramide.

A yet another study, by Wu et al, 2011, touches upon the point that the relation between kilojoules consumed and kilojoules utilized is different in men and women. They also state that women consume less kilojoules per kilogram lean mass and store more fats in their body, especially during gestation period, as compared to men (I'm obviously not comparing the gestation period). This finding can, in a way, support the observations by Sodersten et al (see first paragraph).

If you want a more detailed report, you can have a look at this report from United Nations University (old website) by Sara R. Millman and Laurie F. DeRose. They discuss in detail why and how women and children are considered the vulnerable groups in times of long-term food deprivation since they are more likely to express hunger and have more serious probable consequences of hunger in times of food scarcity.

If you can expand your terms a little bit, there are (comparatively) many such studies on rats and other animals. For example, Sarookhani et al, 2014 measure the effects of food deprivation on formalin-induced nociceptive behaviors and $\beta$-endorphin and testosterone concentration in rats. You can find many such studies quite easily. However, I'll keep searching and adding more related studies on humans here.


Is the book "Bioinformatics for Geneticists" outdated? I am going to be working with genetics data in my organization's data warehouse next year and helping our biotechnology department.  I work in academic research, but I have very little genomics background.  I was able to find the book called "Bioinformatics for Geneticists" (Edited by Michael R. Barnes & Ian C. Gray) at a used book store for a couple dollars.  It looks like it was published in 2003.  Do you think this book is too outdated, or would I still get a good introduction to the subject?  If you think it's too outdated, what book(s) do you recommend?

I haven't read through all of it, but from the second edition, which I found available online here, it seems to me that it might be a good introduction, but (as expected from the publishing date) it is really missing out on all the next generation sequencing stuff. Which is important, not only because it is my favourite field.

I am not sure what you want to get from it? You say you have little genomics background, but then you got a book that expects you to know the genetics, but explains the bioinformatics.
There's a basic description of the background of sequencing at the NIH website, maybe that helps.


Large congregation of birds? This year in October, I saw a lot of robins, male and female, finches and chickadees, and geese flying south.

Surprisingly I didn't see many juveniles from previous broods. My guess is that juveniles are harder to see.

And the robins were flying above me, looking for worms below me, and most ended up in tall shrubs. The finches stayed in place longer than the robins.

So why this big congregation of birds when it is still going to be relatively warm for most of the fall(which it ended up being)?

I live in ohio where it usually gets down to -4 in January and 90+ during the summer.

So, we typically think about migrating birds as living somewhere (North) and then traveling South for the winter. This way of thinking is actually not accurate according to a number of ornithologists, including many I used to work with/for. Thy suggest that the birds live in the South and migrate North to breed and to avoid overcrowding of Southern locales. (Though see this article that found support for the more often assumed N-to-S direction of migration). If 'South' is in fact their 'home,' then perhaps they will venture there regardless of weather patterns. However, perhaps neither of these thoughts applies to short-range migrators like robins.

Also, many birds migrate during the dark hours of the night, so I wonder if the birds you saw were even migrating, per se, or just moving about regionally.


Personal Genomic Data Samples a quick question. I am looking for complete personal genomic data of human individuals. The only requirement for the genomic data is that it contains the complete set of SNPs of a human individual. So far I found only one, a hispanic female.

Are there any similar personal genomic data available on the web?
Any database I can access with a collection of SNPs per individual?

Here is the link to the 1000 Genomes project, all the data is available for download. They already have a comprehensive list of SNPs as well.
It is not the only project around but it is definitely the one with more accurate data on so many genomes right now.


Why are large amounts of DNA required for analysis? I know PCR is used to create large amounts of copies of genes and that it's a scientific breakthrough but want to understand why. Why do we need large amounts of DNA to be able to analyse it, to utilise it. Isn't a single DNA molecule enough?

Firstly, A DNA sample obtained from a cell or whatever is never going to contain just the DNA sequence you want but will instead contain the entire genomic DNA, plasmids, RNA sequences and whatnot. By using PCR you can selectively multiply the amount of desired DNA sequence while the undesired sequences do not get copied. Keep the PCR going long enough and the amount of undesirable DNA versus the desired DNA sequence is going to become negligible. At that point you can do whatever experiment you want with your DNA sample and be reasonably sure that whatever result you get is caused entirely by your DNA sequence of interest.

Secondly, even if you could isolate a single DNA molecule what would you do with it? You couldn't determine its length by gel electrophoresis as a single DNA molecule wouldn't make a visible band and building it into a plasmid will most likely fail as you only get 1 chance. You probably wouldn't even be able to tell you had a DNA molecule as machines in your everyday lab aren't sensitive enough to detect a single DNA molecule.

Thirdly, having a large quantity of DNA allows you to perform different experiments from the same sample. Most DNA analysis methods I know of are destructive in that the DNA used cannot be reused for another experiment, so a large enough quantity of DNA to perform all planned experiments without having to obtain a new sample (and introduce all kinds of potential problems) is useful.

So, in summary, PCR allows us to filter the desired DNA sequence from a sample, perform meaningful analysis on this sequence and lets us use one sample for multiple experiments. There might be even more advantages to PCR that I have missed but these the ones that sprung to mind.


What is a good non-fluorescent DNA dye? Can anyone suggest a dye which specifically targets DNA, but is not fluorescent? We plan to mark DNA before observing it with RAMAN-Spectroscopy. Because of the weak signal, even a low emission would disturb the reading.

One option is to use biotin labelling. Most molecular biology supply companies do kits for this, and supply biotinylated nucleotides.


What are ECT parameters? ECT or shock treatment is used to treat psychological disorders. How much voltage,  current and duration is used for this? Wikipedia mentions a treatment of 0.8 Ampere for 5 seconds.

Peterchev et al. (2010) reports

  The current amplitude is [... ] held fixed at the device maximum (e.g., 800 mA or 900 mA)...

and that

  [constant-voltage devices are] now obsolete

The total stimulus duration as I understand is a pulse train of a few seconds (Peterchev, 2010). The duration of total treatment is about 20 minutes in the treatment room and up to an hour including recovery (source: Hopkins Hospital).

Note that the total stimulus duration depends on the total amount of injected charge. This in turn depends on stimulus frequency, stimulus shape, frequency and so forth (Fig. 1). For an excellent overview see (Peterchev et al., 2010).

Fig. 1. Sample ECT waveforms: (a) sine wave, (b) biphasic pulses with indicated parameter definitions, and (c) monophasic pulses (Peterchev et al., 2010)

Reference
- Peterchev et al., J ECT (2010); 26(3): 159–74


Why is hyper pigmentation the common aftermath of skin lesions and abrasions? I'm aware that melanocytes produce melanin, giving color to the skin, but why are these cells recruited or overactive when healing skin abrasions, lesions and sores when T-cells and inflammatory cytokines of the immune response help with healing. I'm just wondering why the production of color is associated with the healing of the wound and if it proves beneficial, or if it just a side effect so to speak.

EDIT: In this study, it explains the recruitment of melanocytes after the initially response of innate immune cells and inflammatory cytokines, however, it does not delve into how this is beneficial to the cell.
[source]

The upper layer of the skin (or the epidermis) is formed mostly by keratinocytes and some melanocytes (about 30-40 times more keratinocytes) and also fibroblasts (although they are not shown here). The melanocytes are found in the basal cell layer at the border between epidermis and dermis as shown in the figure below (from here):

The melanocytes spread out their dendrites between the keratinocytes and transport the melanosomes (pigment containing vacuoles) to them to pigment these cells. This is a highly regulated process and depends strongly on the interaction between keratinocytes and melanocytes.

In the so-called paracrine pathway the keratinocytes secret substances which regulate the production of melanin. These are for example alpha-MSH or ACTH, which stimulate the melanocytes to produces more melanin.

This regulation is the key to the hyperpigmentation. During the proliferation or the inflammation chemokines and hormones are produced (and secreted) in the skin which stimulate keratinocytes and fibroblasts. These are for example the keratinocyte growth factor (KGF), as well as the chemokines IL1-alpha and TNF-alpha. This stimulation leads to the production of ACTH (and derived peptides) by the keratinocytes and the secretion of stem cell factor (SCF) and hepatocyte growth factor (HGF) by the fibroblasts which all induce pigmentation. The chemokine secretion is also enhanced from the keratinocytes by KGF. If you are interested in a deeper view at this topic, have a look at reference 1 (and the references in the paper). Reference 2 goes deeper into the regulation of the paracrine signalling.

In an injury (especially in larger areas of the skin) a lot of cells are damaged and need to be replaced. This functions via cell division but also via the migration of cells into the affected area. This is described by the paper you link - here melanocytes and melanoblasts (melanocyte stem cells which can divide and then differentiate into melanocytes) migrate into the injured region to replace the destroyed melanocytes.

References:

Mechanisms underlying post- inflammatory hyperpigmentation: lessons
from solar lentigo
Hepatocyte Growth Factor Establishes Autocrine and Paracrine
Feedback Loops for the Protection of Skin Cells after UV Irradiation


Can Anyone Identify This Insect? I keep seeing these bugs on a wall in my house in Istanbul (Turkey) walking up and down generally during evening and night. They are about 1 mm long and have a brownish color. I see more of them through late hours. Does anyone know what they are called?

Those are collembolans. Common name, springtails. Do you have a potted plant nearby? They are completely harmless.

Here is an example:

(picture from bugguide.net


A free book/resource for learning genetics? I took an undergrad class in genetics. I felt it was not too intensive and I do not feel prepared for grad school (if I can manage to get in.)

Does anyone know of a preferably free resource for learning genetics?

I know the field is very large, but I would like to be competent in the field, considering I also want to learn more about genomics as well. And I figure one must first have a fundamental understanding of either computer science or biology to be successful in genomics, both of which I lack.

As you said, the question is pretty broad. Genetics is a big gigantic field and it is quite hard to know what you are exactly looking for. If you could refine into one of the subfields (molecular genetics, population genetics, phylogenetics, etc..) it would be much easier to give you better advice. As you talk about both biology and bioinformatics, it might be worth to specify whether you are looking for learning more in fundamental genetics or learning more in the methodologies to analyse genetic data.

Principles of Genetics

You may want in an introductory class in genetics. Here is a course on MIT Open CourseWare, but it may be too easy for you.

Bioinformatics

You may want to take a bioinformatics course. There are so many bioinformatics course online that there is a wikipedia page to list them (there).

Side skills

Programming

You may just want to learn to code in R, Python, Perl or Shell script (to cite few examples). You'll find tons of beginner tutorial online.

Statistics

Or you might want to learn more about statistics. KhanAcademy has a very good (but very introductory) statistics class.


Is the tomato a very very close relative of the pepper? I ask because if you look at a tomato, the way it grows on a vine, its color, the texture, and make up of its skin and internal structure it seems very much like a pepper.  The only thing I can think it lacks that a pepper has is any amount of spice.  I wouldn't be surprised to learn that it has trace amounts of capsaicin.

There are different unrelated plants called "pepper" in English. Black pepper (species of the Piper genus), as indicated by Chris, is not related to tomato and doesn't "look alike".

I guess the OP meant actually a different plant (Capsicum genus), to which the common bell pepper (Capsicum annuum) belongs. This one is similar to tomato and they both belong to Solanaceae, the same subfamily Solanoideae, but different tribes: tomato is classified in Solaneae and Capsicum in Capsiceae.

In this study you can see, how distant phylogenetically the two genera are. Currently accepted classification generally reflects phylogeny, and there are three more tribes that are closer to Capsiceae, to which Solaneae is nevertheless a close relative.

The most striking morphological difference between Capsicum and Solanum is that the first one is characterized by hollow fruits, while tomato and other Solanum species have fleshy berry-like fruits.

EDIT: It's actually not a difficult task for one's imagination to see that the two types of fruit are structurally very similar. In reality a pepper-structured tomato cultivar is known, and even quantitative trait loci underlying this morphological trait were already found.


How do neurons receive the ions needed for creating electrical pulses? I really wonder how ions are transported into the brain and the neurons for creating electrical potentials - how do ions get from our digestive system to the neurons? Or are the ions just freely released into the brain like hormones? Or are they transmitted during neural signalling somehow (via neurotransmitters maybe)?

Short answer
The sodium-potassium pump in the epithelial cells lining the brain capillaries pumps Na+ and K+ into the brain.

Background
The blood-brain-barrier is formed by the endothelial cells lining the capillaries in the brain. Not many compounds can pass this lining, especially not when they are hydrophilic, such as charged metal ions. However, as you rightfully state, somehow these metal ions, and especially Na+ and K+ need to get access to the brain because they are crucial for membrane potentials and action potentials, and hence for neuronal survival and function. And indeed they can, albeit the exchange between blood plasma and brain is slow compared with other tissues.

Intravenously administered K+, for example, exchanges with muscle K+ in 1 hr, but K+ exchange in brain is only half completed in 24 to 36 hr. Na+ exchange is somewhat faster, with half-exchange into brain occurring in 3 to 8 hr. Despite its relatively slow entry into the brain, Na+ exchange across the blood—brain barrier appears to occur by mediated transport. This occurs, in part, through brain capillary Na+,K+-ATPase (the sodium-potassium pump). The Na+,K+-ATPase in the brain also may mediate removal of interstitial fluid K+ from the brain and thereby aid in brain K+ homeostasis.

Reference
- Laterra et al. In: Siegel et al. eds. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th ed. Philadelphia: Lippincott-Raven; 1999


Explanation for hyenas asymmetric legs length Hyenas seem to have disproportionately short hind legs. It may be the opposite, maybe the front ones lengthened to raise their heads even higher than their already long necks do. In any case, this trait is not seen in any other cursorial animal (that I know), asymmetry is not a good Ally in the long run. So why?

First most animals have limbs of different lengths. consider a house cat at full extension its hind limbs are much longer than the forelimbs.

The relative length of the limbs means almost nothing functionally, it is the relative length of the gait, or the distance the limbs can swing that is important, a longer less flexible limb may swing the same distance as a shorter but more flexible limb. Source

When the limbs have very different gaits you end up with hoppers or so called pendulum runners like rabbits and kangaroo or they do not fully utilize the possible arc of one limb like gorilla this second one pops up when ground travel is not the primary means of locomotion. Hyena do fall in either category their limbs are close enough for a normal gait.

Hyena limbs are not as different in length as many people think, the massive neck and shoulder muscles make the front limbs look taller than they are in many photographs, but yes they are longer. The heavy musculature plus the longer forelimbs are all adaptation to make the animal stronger with more leverage, better able to rip apart a carcass and crush bones. They do not need the massive hind limbs of the large cats becasue they do not "pounce", you see the same adaptation in the so called "Fanged Cats" or saber tooth cats they have massive forelimbs. More importantly the massive muscles on the shoulder and neck make the forelimbs less flexible so to get the same arc swing out of the limb, it has to be longer.


Does my brain have limited learning capacity or memory? Lately in my free time I like to read books, articles etc etc.. What I have discovered, or maybe it is an illusion(lack of concentration or something), is that I usually forget most of the material that I read about, and have lost my ability to remember names of objects, planets or whatever I read about. Does that mean that I am over-reading or that my brain has limited memory/learning capacity? I should also mention that I have an IT job, which you know requires high concentration throughout the day.

Short answer is yes, the brain has a limited capacity. It's a large but limited physical system with numerous but countable connection, it follows that it must have a limited capacity.

Learning wise, we usually say we learned something when we can recall it at will. I'm not sure I agree with that definition, but if this were the case, learning would be intimately related with memory capacity, so the answer would also have to be yes.

All this without taking into account energy consumption and metabolism which would impose also further limitations, e.g. I bet you that if you switch the activities around and start reading in the morning and try to work at night your work would suffer but your retention capability would improve (just a guess). Now, is all this relevant? I can't say, we (humans) might be working already at full capacity, in this case it would be relevant, or we could be very far away from this theoretical limit and all this is moot.

If that was really your question then you're done.

However, you seem to be preoccupied with a mismatch between the expectations of your own retrieval abilities after a particular "type" of activity and what you can actually remember.

I would be remiss in I didn't say that I agree with WYSIWYG's comment, I'm sure this is not the place for health advise. So with that in mind my 2c:

your expectations can be misaligned, that's always a possibility; your retrieval abilities can be impaired, which means that you learned fine but cannot recover it; or may favorite: you might just be tired! IANTTOAD


microscopic slide cleaning and maintenance we do lot of gram staining and some spore staining. we normally wash our slides with detergent then rinse in D/w, dry it and store it. But on reusing this slide we have to flame it and also clean it with alcohol number of times to make it grease free. also these reused slides have some sort of deposit which does not go with cleaning and evend oes not hamper our staining too.  can anyone please suggest the best simple way to clean microscopic slide and to make it grease free and how to store it.

An old technique to clean used slides is to just toss them in a jar containing equal volumes of distilled water, ethyl alcohol 95% and xylene. Shake from time to time. When needed wipe them dry using a clean, lint free cloth and use.

The techique was at the time (1930's?) in use in the lab of prof. Baudet (Veterinary parasitologist, Utrecht University) and is mentioned in several editions of the "Précis de Microscopie" by Maurice Langeron.

Langeron mentioned that the slides treated that way were "perfectly grease-free".

Another method is to wash the slides, rinse in distilled water and store for some time in a mixture of ethyl alcohol and acetic acid.

When on a tight budget, used Carnoy fixative was (is?) used.

This is a trick that was (is?) in use at some botanical labs in Eastern Europe.

It's mentioned in some of the German literature on microtechnique, if memory serves me right in Braune, Leman and Taubert's "Pflanzenanatomisches Praktikum".


Enzyme Inhibition by alpha-2 macroglobulin Alpha-2 macroglobulin is a plasma protein which acts as an anti-protease. It does so by a "bait mechanism" - the protease cleaves the bait domain, following which a conformational change causes binding of alpha2-macroglobulin with the protease, and consequent irreversible inhibition of the protease.

This seems to be very similar to "suicide inhibition" or "mechanism based inhibition" - when an enzyme catalyses a substrate analog's conversion to an active inhibitor, which subsequently binds strongly to the enzyme to inactivate it.

Is alpha2-macroglobulin's inhibition of proteases a case of suicide inhibition then? If it is, why is not more commonly described as that (I have not come across any description of alpha2-macroglobulin as a suicide inhibitor)?

Lets first see the proper definition of Suicide Inhibition as given by Wikipedia (emphasis mine):

  In biochemistry, suicide inhibition, also known as suicide inactivation or mechanism-based inhibition, is an irreversible form of enzyme inhibition that occurs when an enzyme binds $\alpha$ substrate analogue and forms an irreversible complex with it through a covalent bond during the "normal" catalysis reaction. The inhibitor binds to the active site where it is modified by the enzyme to produce a reactive group that reacts irreversibly to form a stable inhibitor-enzyme complex. This usually uses a prosthetic group or a coenzyme, forming electrophilic alpha and beta unsaturated carbonyl compounds and imines.

Now, lets see how $\alpha$-2-Macroglobulin works, again by Wikipedia (emphasis mine):

  $\alpha$M protease inhibitors inhibit by steric hindrance. The mechanism involves protease cleavage of the bait region, a segment of the $\alpha$M that is particularly susceptible to proteolytic cleavage, which initiates a conformational change such that the $\alpha$M collapses about the protease. In the resulting $\alpha$M-protease complex, the active site of the protease is sterically shielded, thus substantially decreasing access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) the h-cysteinyl-g-glutamyl thiol ester becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain (RBD). RBD exposure allows the $\alpha$M protease complex to bind to clearance receptors and be removed from circulation.

So, clearly, it is not suicide inhibition as:

$\alpha$M protease inhibitor does not form an irreversible complex with the protease, instead it uses steric hindrance to prevent protease from binding any substrate.
this inhibition does not occur during the "normal" catalysis reaction, it is after the protease has catalyzed a reaction that the inhibitor covers it up, more like the consequence of catalysis.
the inhibitor does not bind to protease active site, it covers the active site like a shield.

Putative mechanism of protease entrapment and inhibition by ECAM (Escherichia coli Alpha-2 Macroglobulin)

References:

Suicide Inhibition
$\alpha$-2 Macroglobulin
Structure of protease-cleaved Escherichia coli $\alpha$-2 macroglobulin reveals a putative mechanism of conformational activation for protease entrapment (PDF)


Why do cell membranes have a lipid bilayer instead of a monolayer? Many cells have a cell membrane composed of two layers of lipids. Why is it that they have two layers and not just one?

What purpose do this arrangement serve?

Why use membranes?
Compartmentalising the cell has lots of advantages and purposes. In Koshland's 2002 essay, compartmentalisation was described as one of the seven fundamental pillars of life. Broadly speaking, membranes create different sets of conditions (chemical and biological) inside the cells. This allows more efficient functioning and advanced catabolic and metabolic processing. More complex and adaptable systems were thusly achieved by the evolutionary process.
Why a bi-layer?
There have been several molecular dynamic simulations such as this one carried out to investigate the biophysicochemistry of spontaneous bilayer assembly. There, lipids start in random orientations. The ordered bilayers we know and love spontaneously assemble in under 100ns. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer forms.

On a smaller scale, micelles also form spontaneously, but this doesn't offer the compartmentalization required for biological functions.

It would appear that the conditions for an ordered bilayer are so favorable that they take precedence over any other orientation or combination. One apparent exception is the archael monolayer. Do see @WYSIWYG's answer that refers to the exceptional extremophiles that use a monolayer. Their comment summarises the monolayer succinctly:

They are technically monolayer but resemble bilayer. Like bilayer connected via a covalent bond. These membrane lipids have two hydrophilic heads and a hydrophobic "torso".

Image sources

Image 1: http://www.perkepi.com/cell-membrane/
Image 2: https://en.wikipedia.org/wiki/Lipid_bilayer


What is the probability that there are no substitution between an ancestor and a modern individual? What is the probability that there are no differences if you compare the DNA
of the ancient sample to a single DNA sequence from a modern individual? Assuming the individual was diploid and lived T generations ago.

How would you go about finding this probability? I would assume that drift and maybe selection would change the sequence and the probability of no change over time would be extremely low.

Expected number of substitutions

Let's assume a haploid mutation rate of $\mu$ and a population of constant size $N$. For simplicity, I will assume an absence of selection because otherwise, we would need to talk about what kind of selection you want to talk about.

There are therefore $2 N \mu t$ mutations since this last ancestor. A fraction of $\frac{1}{2N}$ of them drifted to fixation. Therefore, there were $\frac{2 N \mu t}{2N} = \mu t$ mutations fixed.

If we consequence a sequence with a mutation rate of $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome) and $t = 10^5$ generations. Then, there were 10 substitutions (on average).

Of course, the assumption of no selection is likely wrong and violation of this assumption could well drastically affect this estimate. However, you would need to perfectly describe what type of selection pressures (and what selection coefficient and dominance coefficient) you want to consider for more calculations.

Probability of k substitutions

As events of substitutions are independent, the probability that exactly $k$ substitutions happen given the expected number of substitutions ($\mu t$) is given by the Poisson distribution with rate $\mu t$. The probability $P(k | \mu, t)$ of $k$ substitutions had happen in $t$ generations, given the mutation rate $\mu$ is therefore

$$P(k | \mu, t) = \frac{\left(\mu t\right)^k e^{-\left(\mu t\right)} }{k!}$$

Per consequence, the probability of no mutation is obtained by replacing $k$ to zero

$$P(k=0 | \mu, t) = e^{-\left(\mu t\right)}$$

Again, if $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome), then the probability that zero mutation had happen in $t = 10^5$ generations is $e^{-10^{-4} 10^5} ≈ 5\cdot 10^{-5}$


Relationship between DNA strands and mRNA Does the sense strand or antisense strand of DNA code for the polypeptide product? I'm confused because I know the antisense strand is the template for mRNA but it has anti codons so I do not know how this would be the coding strand. Ok so what I was confused about is when you are getting the code for the amino acid you can look at the mRNA strand which is the same as the sense strand except uracil replaces thymine, this is why I thought the sense strand could have coded for the amio acid instead of the anti sense strand.(the question I was looking asked if its the antisense or sense strand)

I would add this as a comment to your question but do not have enough reputation. A simple look at Wikipedia (which is a very good source for general questions like these) would have provided you with an answer. I just did this to see how long it would take if I did not know the answer. It was about 20-30 seconds.

Protein synthesis: Transcription

  In transcription an mRNA chain is generated, with one strand of the DNA double helix in the genome as a template. This strand is called the template strand.

Template strand

  Only one of the two DNA strands serve as a template for transcription. The antisense strand of DNA is read by RNA polymerase from the 3' end to the 5' end during transcription (3' → 5').

If I understand your confusion correctly, you also do not understand how the seemingly "non-coding" strand can be the "coding" one which seems to be a paradox. If this describes your confusion adequately you have to think of the semi-conservative replication of DNA. The "non-coding"/antisense strand is transcribed by the RNA polymerase into its complementary RNA sequence. As this sequence is complementary to the "non-coding" DNA strand, the mRNA sequence is identical (with U replacing T) to the "coding"/sense DNA strand.


DNA Sequencing - Sanger termination method: What effects will more ddNTPs in solution have on the resolution on agarose gel via electrophoresis? Say instead of a small amount of ddNTPs, you add a significant percent of ddNTPs to dNTPs. I was thinking this would reduce the resolution for larger fragments due to more ddNTPs terminating elongation earlier on.

I am doing a project on Sanger Sequencing and was wondering this, thank you. (Any suggestions would be appreciated)

You are correct. The greater the ratio of ddNTPs to dNTPs, the more frequently ddNTPs will terminate the reaction, resulting in shorter mean fragment size. However, Sanger sequencing is not done with agarose gels. The result visualizing a Sanger reaction on agarose, using more ddNTPs would result in a smear closer to the bottom. For actually visualizing the sequences on acrylamide, or with capillaries, increasing the ddNTPs would reduce the resolution of longer fragments. It is a balance you need to optimize.


Do pregnancy and breast feeding increase basal metabolic rate? Since pregnant or breastfeeding women have extra nutritional needs, does that mean they have a higher BMR?

Why I thought the conclusion would be sensible: Since BMR is the energy needed to perform body functions (breathing, respiration, homeostasis, digestion, etc), pregnant woman or breastfeeding women, because of their extra 'activity' (due to the presence of the fetus) will have a higher BMR.

Basal metabolic rate for a particular organism is determined by the amount of calories that the organism needs for basal metabolic processes (i.e. basal energy demands). Since pregnant and breastfeeding women have increased caloric requirements (i.e. increased energy demands), then that means by definition their basal metabolic rate is increased.


Why do some reflex actions involve interneurons, but some don't? According to what I know, the reflex arc of knee jerk reflex doesn't involve interneuron, but other reflex action (e.g. removing your hand when touching hot things) do involve interneurons. Why is that the case?

I did not realize it but the knee jerk reflex is a stretch reflex and thus only involves two neurons (monosynaptic). Many many more reflexes use 3 or more neurons (polysynaptic) so include interneurons.

monosynaptic are common for muscle stretch limiting reflexes, that is why I knew them by their more common name stretch reflexes and did not make the connection. They don't involve interneurons becasue they would offer little benefit, they are self regulating most of the time and only involve a single source and a single destination and will not see much benefit from modification of the signal.

This slideshare on reflexes can provide some detailed information and a place to keep researching from.


Does the body lose energy or gain energy relatively when drinking or eating hot things? Does the body lose or gain energy when drinking or eating hot things compared to more neutral temperature things?

On the one hand,
The body could somehow convert the heat energy into human usable energy,
And on the other hand,
The body heats up and needs to be cooled down, and this way it loses energy.

Gains heat; humans are not particularly well-adapted to make use of heat as an energy source.  In a simple matter, if something you eat is hot when it goes in then the average temperature of the body has increased.  More relevantly (and to get this more on-topic for biology), eating anything will generally increase your body temperature, as in order to digest the food your rate of metabolism will rise.  Metabolism produces a lot of heat, and that's what you feel after eating, especially a big meal.

Something like cold water, however, that doesn't require a whole lot of metabolism, will cool you down.  In fact, even drinking hot water might cool you down.  The paper cited there claims that drinking a hot drink on a hot day will disproportionally increase your sweat response such that you actually cool down.


Depolarization and hyperpolarization in stereocilia of the inner ear It’s a well mentioned fact that when the stereocilia of the cochlear hair cells bend in one direction, the hair cell depolarizes, and when the stereocilia bend in the other direction, the cell hyperpolarizes. When the basilar membrane vibrates, the stereocilia are bent back and forth, creating depolarizations in the hair cells followed by hyperpolarizations. What I’m having trouble understanding is why this is significant. This does not determine the frequency of the sound wave, as that is determined by the location along the basilar membrane that the wave impinges on. I don’t see how this would determine amplitude either, seeing as a greater amplitude would only create more drastic bending of a greater number of hair cells. Can anyone shed some light on this?

There are roughly two modes of pitch coding in the cochlea: place-coding and temporal coding. The place-theory is the most prevalent accepted model of how the cochlea realizes pitch coding (e.g., Zwislocki, 1991). Basically, it is based on a frequency-to-place Fourier transformation on the incoming sound, where each frequency is coded on a different place on the basilar membrane, as described accurately in the question.

However, there is another, much overlooked way of coding pitch, namely temporal coding. Up until about 1 kHz, spiral ganglion cells in the auditory nerve and acoustical brain stem regions (such as the inferior colliculus) have been found to respond in a phase-locked pattern (Du et al., 2011). Electrophysiology in auditory nerve fibers illustrates the phase-locked activity in response to low-frequency sounds (Fig. 1). This phase-locking behavior of neurons in the auditory system is called the frequency-following response (FFR).

fig. 1. FFR in auditory nerve fibers. Upper trace shows the stimulus, middle trace a single fiber, and the lower trace the compound activity of many fibers. The group-response faithfully codes the stimulus waveform. Source: New York University.

However, as you rightfully state in your question - why would inhibition of auditory nerve fibers (ANFs) be helpful? Figure 1 illustrates nicely that the auditory nerve FFR is rectified, i.e. only the upper half is coded, while negative action potential counts obviously don't exist; ANFs fire, or they don't, they don't fire negative action potentials. However, one has to realize that a relatively large proportion of ANFs in healthy ears spontaneously fire, i.e., in the absence of sound the auditory nerve is still remarkably active. Spontaneous firing rates vary from 0 to more than 100 spikes/s (Jackson & Carney, 2005). Hence, suppression of spontaneous activity codes pitch too.

Moreover, as a theoretical and un-referenced side note - the auditory system processes acoustic information on the sub-millisecond level. Left/right sound localization is performed by the auditory system by resolving inter-aural time differences (ITDs). By analyzing the delay at which sound arrives in one ear with respect to the other, the localization in the horizontal plane can be estimated. ITDs do not exceed 0.8 ms, given the speed of sound and the size of the human head. This is well below the time it takes for any action potential to develop(!). Hence, by deploying both phases of the sound, one phase being excitatory, the other inhibitory at the ANF level, no time is lost when a sound wave happens to enter the cochlea with its inhibitory flanking phase first.

References
- Du et al., Neurosci Biobehav Rev (2011)
- Jackson & Carney, JARO (2005); 6: 148–59
- Zwislocki, Acta Otolaryngol (1991); 111(2): 256-62