Why does black and yellow indicate danger? It is a well-known fact that combination of black and yellow indicates danger or poisonousness.

In western society it seems obvious this comes from bees and wasps, but it seems like many tropical frogs use yellow and black. Black and yellow also indicates toxicity in some fish species and the order of the colors seems to communicate whether we see a harmless milk snake or a venomous coral snake.

So which came first: the fear of black and yellow or the color of bees? Are there any studies about the color combinations effect on human brain? Is it learned or congenital?

First of all, great question! What you describe here is known as aposematism. Aposematism is the adapation of warning signals against the predator. This word is used for any sound, coloring, and odor used as a warning signal. Of course, for this question the focus is color.
Honest indications
Animal coloration is usually an honest indication of their noxiousness. The brighter they are, the more noxious and toxic they are (http://rspb.royalsocietypublishing.org/content/276/1658/871). In the linked article, there are many references one this positive correlation of toxicity of prey to predator and the brightness of the coloration. In the article they use mathematical models to support the mathemstical evidence. But one thing is for sure: bright colors do mean the prey is armed with defenses, whether the correlation is positive or not.
Why then is it black and yellow?
The conspicuousness of the coloration is very important because it is important to see from a far away distance. The reason colors like yellow and black are used is because (http://rspb.royalsocietypublishing.org/content/279/1728/417):

— They provide high contrast against the background (e.g. red/yellow against green foliage), which promotes detection.
— They are resistant to shadows (which are rich in blue-UV), and to changes in illumination (e.g. black should not change during day, whereas white could become ‘pink’ at sunset and sunrise). Therefore, they provide a reliable signal under varied habitats and light conditions.
— Yellow/red and black has both high chromatic and luminance contrast.
— Such colours may allow distance-dependent camouflage if yellow/red and black ‘blend’ to an average colour that matches the background at a distance when predator vision is no longer sufficient to discriminate individual marking components.
— Such colours are distinctive from profitable species.

What about the combination of black and yellow?
In the same article, they mention that:

Many warningly coloured prey have markings comprising repeated pattern elements. Such arrangements in signal structure may increase redundancy in the signal but improve the likelihood that the strategic component will be detected by the receiver. In addition, repeated elements may be rare in many natural environments, thus increasing conspicuousness of the prey animal. Simple pattern components (such as stripes and spots) may facilitate detection and also speed up avoidance learning if they are easier to memorize.

The research seem to show that the patterns, such as the stripes, lead to increased avoidance, but it is not sure whether or not it is due to the stripes itself or due to the constrast of the black and yellow.
I hope I have answered your question and if you have any questions, feel free to ask in the comments.


Are the byproducts of mammalian digestion simply depleted versions of the food or liquid consumed? When mammals consume food and digest it or drink fluids that are then filtered by their kidneys, are the waste products generated simply depleted versions of what they consumed?

Are there other byproducts of metabolism and filtration contained in that waste that are generated by the body and are not directly a part of the food or liquid that was consumed that are excreted?

The answer really depends on what aspect of the urine and feces one is considering.

On the atomic level, no, urine and feces are composed entirely of atoms taken from our environment. As one would expect, as there is no "Humanium" on the periodic table. In fact, all the atoms in urine and feces were originally created by stars.

On the molecular level, yes. The body produces molecules that we do not ingest, or that we ingest in minute quantities, such as urea and bile.

On the cellular level, yes. The body produces, for instance, red blood cells even if the person eats a vegan diet with no blood intake. The proteins that make up the cells are created by breaking down ingested proteins into their constituent amino acids, which are then used to construct new proteins.

Also at the cellular level are the huge amount of bacterial cells that we support. Estimates of the number of bacterial cells in our body range from ten to 100 times the number of our own cells. The bacterial component in feces is massive - up to 1/3 of feces by weight are bacteria. Urine, being produced from the blood by the kidneys, is relatively sterile.


Tumour resistance: single-cell or population effect? Drug resistance can arise through a number of mechanisms. For instance, EGFR mutation when treating with EGFR inhibitors, or compensatory activation of alternative survival pathways. But does it occur at the level of a single cell, or would it be a population effect? In other words, would cells exposed to e.g. targeted kinase inhibitors slowly compensate with other pathways (and that would happen in every such cell) or would there be a sub-population of cells that is sensitive to inhibitors and another subpopulation inherently resistant and predisposed towards amplifying other pathways.

There certainly can be co-operation or competition among cancer cells within a tumor that can provide some types of population-based influences on cancer-cell survival. Present evidence, however, suggests that resistance to therapy is almost always due to resistant sub-populations of cancer cells within the tumor. In many cases, such as after treatment with EGFR inhibitors, the resistance mutations have been identified. Sometimes these mutations are in such a small fraction of the cancer cells that they can't be detected in the original tumor before treatment, but in most cases they probably were already present before therapy, caused by the mutations that are inevitable during tumor growth. This review on intra-tumor heterogeneity is a good place to start learning about this topic.


What is the role of hippo signalling in oral squamous cells What role do hippo signalling have on squamous cells in oral health & diseases

Mutations in the Hippo signalling pathway cause unusual organ growth in flies.  After a good deal of intensive research, its been shown that Hippo genes are responsible for suppressing organ growth in development, increasing cell death and slowing proliferation.

Given this role, its not surprising that Hippo genes are also important in cancer.  I'm not an expert in cancer, but a quick search turned up an association of cancer with the Yki (YAP in mammals) transcription activator, an oncogene from the Hippo Pathway.  YAP suppression has been linked to cancerous growth.  And its also been shown that YAP is amplified in oral squamous cell carcinoma cells.  This last is circumstantial but consistent with what we know about YAP.


How is energy acquired from ATP? How is energy acquired from ATP (i.e. What is the energy-releasing equation involving ATP plus water)?

I Would be grateful for the answer.

The basic reaction is ATP + H2O --> ADP + Pi + energy

It is the common hydrolysis of ATP, in which the nucleophilic oxygen of water attacks the electrophilic central phosphorus of the last phosphate group, resulting on its separation from the rest of the molecule (which becomes ADP).

In this image: LINK you can see more clearly the steps of the reaction. Keep in mind that the arrow 3 should be pointing to the P and not the O.

To know more about the energy and thermodynamics check this page: http://www.life.illinois.edu/crofts/bioph354/atp_hydrolysis.html

The trick here is the cells being able to utilize that freed energy to their benefit, instead of letting it disperse. This can be done, for example, by adding a phosphate group to a protein, altering its shape and consequentially its function, or by the nucleophilic attack of the first or second phosphate in the ATP molecule of a susceptible electrophilic centre, starting a reaction that could otherwise be energetically unfavourable. If the hydrolysis happens spontaneously in water without coupling it with another reaction, the freed energy will be "wasted" as heat.


Can anyone identify this bird - small flock in ireland? I saw small birds in a flock of about 6 or 8.

Here are details that can be seen on my best photo - The beak looks pointed and also the legs are quite long and the eye has a bar across it.

I have a recording - how do I share it??

With the new image it is still hard, but I think I identified the bird. I think this is a Willow warbler (Phylloscopus trochilus) which is pretty common in Europe.

The drawing from the Royal Bird Protection Society (source here) is pretty similar.

Unfortunately, there are two pretty similar birds living in Ireland which can be confused with the Willow warbler. These are the Chiffchaff and the Wood warbler. Differences are small, the Chiffchaff has dark legs and a smaller eye stripe (both of which the bird in your image has not), while the wood warbler lives in woods and has a more yellow breast (and is also much more rare). The links provide audio files with the songs of each bird, this should help you making a final decision, as they are pretty distinct.


Where are -HCl supplements absorbed in the human digestive system? I see that quite a lot of drugs and dietary supplements sold in the USA have -HCl(hydrochloride) added to their name. For example pyridoxine hydrochloride for Vitamin B6.  I'm interested in knowing where in the digestive system -HCl compounds are absorbed? Is it in the stomach?

It would also help if I get a rough idea of how long it takes for -HCl supplements to be absorbed. Is it an hour or more?

Thank you for your input!

The hydrochloride ions are not what facilitate their absorption into the body. The HCl notation is from organic chemical reactions of a weak base (usually amines are involved here) with HCl to form a salt. The salt is what gets purified as a powder (otherwise the chemical remains in solution and can't be made into a pill/supplement). The bottle may say: "compound-HCl" or "compound HCl" implying that the two are chemically bonded together, but that is incorrect. What actually happens is that the compound is an ionic salt, in the form [compound]H+ Cl-. As far as absorption, that is entirely dependent on the compound(s) being absorbed. Once you swallow them, they dissociate back into the weak acid form and H+,Cl- ions.


Will a 0.2g/mL sugar concentration cause vomiting in humans? This infographic claims that the sugar content in a can of Coca Cola would cause vomiting if not for the phosphoric acid.

  In The First 10 minutes: 10 teaspoons of sugar hit your system. (100% of your recommended daily intake.) You don’t immediately vomit from the overwhelming sweetness because phosphoric acid cuts the flavor allowing you to keep it down.

Now this question came up on skeptics.SE and the remaining question is whether (flavourless) water with sugar would cause vomiting. Very specifically we're talking about 200ml of final concentration and 39 grams of sugar. I would try it out myself, but per the rules of skeptics.SE I am not allowed to do this so I am posting it as a question here.

Sugar (be it sucrose, glucose, fructose or honey) does not have emetic properties in any concentration, unless there is a personal (and highly individual) psychological adverse reaction to sweet substances.

Sugar is not a local gastric irritant (like dishwashing detergent, or syrup of ipecac, copper sulphate, zinc sulphate; yellow mercuric sulphate, ammonium carbonate, powdered mustard and other local gastric irritants.) Some non-irritating substances (e.g. cod liver oil) may induce emesis because of a repugnant smell, taste, or texture. Few people find the taste of sugar repugnant. Gastric distension to the point of emesis does not occur with 12 or 16 oz. of fluid.

Psychological causes of vomiting include aversions (e.g. some people vomit when they see someone else vomit.) That would involve a cerebral cortex mechanism.

No sugar of any concentration is listed here as an emetic. If it were true, we would have a much less significant incidence of obesity.


Help Needed Identifying Corvids I'd appreciate some help identifying these three corvids I photographed in Austria during the Summer:

I know identifying corvids can be difficult and I'm not an ornithologist -- just an amateur bird watcher. After looking through many images of various crow species and their hybrids, I've tentatively identified these as:

Carrion crow (Corvus corone)
Carrion crow × Hooded crow (Corvus corone × Corvus cornix)
Carrion crow × Hooded crow (Corvus corone × Corvus cornix)
I initially believed this to be a Hooded crow (Corvus cornix), but the broken coloration on the wings made me think it might actually be a hybrid as well.

Can someone here either confirm my identification or provide a more informed identification?

1. Carrion crow (Corvus corone)

The plumage of carrion crow is black with a green or purple sheen, much greener than the gloss of the rook. The bill, legs and feet are also black. It can be distinguished from the common raven by its size (48–52 cm or 19 to 20 inches in length as compared to an average of 63 centimetres (25 inches) for ravens) and from the hooded crow by its black plumage

3. Hooded crow (Corvus cornix)

ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.

2. This one is a bit more difficult, but I think it is also a hooded crow or possibly a hybrid  Carrion crow × Hooded crow (Corvus corone × Corvus cornix).

 Hybrid
At first glance, #2 looked somewhat like a Western jackdaw (Corvus monedula) because the grey feathers travel fairly high up on its neck and because the bird appears to be somewhat smaller.

Measuring 34–39 centimetres (13–15 in) in length, the western jackdaw is the second smallest member of the genus Corvus...The cheeks, nape and neck are light grey to greyish-silver, and the underparts are slate-grey. The legs are black, as is the short stout bill.

However, C. monedula has fairly conspicuous grey eyes and its feathers travel up the neck/head almost as far superiorly/anteriorly as the eyes. Neither appear to be the case in your specimen.

All three species are common in Europe.


Why does the gravity of Earth appear in this formula estimating speed? I'm currently reading the wonderful book The Dinosaurs Rediscovered by Michael J. Benton. It contains the formula

$$v = 0.25 * g^{0.5} * SL^{1.67} * h^{-1.17}$$

where $v$ denotes velocity, $SL$ is stride length in $m$, $h$ is hip height in $m$ and $g$ is the gravity of earth. Not being a biologist (in fact not being really familiar with any natural science), I don't quite understand why gravity appears in this formula. I can't imagine this would hold in any meaningful way in circumstances where gravity where different from earth's, so why not simply express the term $0.25 * g^{0.5}$ as $0.78 m^{0.5}/s$, which I assume stems from some fitting of terms to observed speeds given stride length and hip height.

Units
G is going to be different depending on what units you use, the original formula was derived using FEET not meters. As it stands the formula works both with metric and imperial units. With your change this would not be true. Paleontology is often uses both units so a formula that is not unit dependent is preferable.


Recombination fraction( frequency) in Homozygotes I have a question about the recombination frequency I hope you have time to answer.

Background: If we look at homozygous individual A/A B/B which has been formed from the gametes AB and AB, this individual will in turn have the gametes AB, AB, AB, AB. These are the same as the gametes that were used to form the individual.

My question: Is the recombination frequency 0? Or should we consider the A's and B's as different, i.e like A$_1$, A$_2$, B$_1$, B$_2$. Then we get the possible gametes A$_1$B$_1$ (parental), A$_1$B$_2$ (recombinant),A$_2$B$_2$ (par), A$_2$B$_1$ (recomb). We then get that the recombination frequency is 50 percent (which it should be according to the source given at the bottom). Which interpretation is correct?

Definitions used in my question:

"Meiotic recombination is any meiotic process that generates a haploid product with new combinations of the alleles carried by the haploid genotypes that united to form the meiocyte." (Griffiths et. al, Introduction to Genetic Analysis, tenth edition, International Edition, p. 95)

Recombinants: "Recombinants are meiotic output different from meiotic input." (same book).

Recombination fraction: "Recombination fraction (also called recombination frequency) between two loci
is defined as the ratio of the number of recombined gametes to the total number
of gametes produced." (Shizhong Xu, Principles of Statistical Genomics, Springer, Chapter 2, page 11, 2013).

Furthermore: "When genes are unlinked, they have a recombination frequency of 0.5, which means 50 percent of offspring are recombinants and the other 50 percent are parental types." (Source: Boundless. “Genetic Linkage and Distances.” Boundless Biology. Boundless, 21 Jul. 2015. Retrieved 11 Sep. 2015 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/modern-understandings-of-inheritance-13/chromosomal-theory-and-genetic-linkage-97/genetic-linkage-and-distances-427-11654/)

Welcome to Biology.SE

Your question stems from the confusion between measuring a recombination rate and the actual recombination rate.

In the A/A, B/B individuals you describe, recombinations still occur. Those recombination just don't affect linkage disequilibrium between the Aa and the Bb loci as there is no variance at those loci in the individuals you considered. There is therefore, no way to tell whether or a recombination event occurred in a specific case. You need genetic variance at both loci in order to have a linkage disequilibrium which can be affected by recombination. But it is not because you can't measure the recombination rate that recombinations does not occur.


Which sources can I use to study botany and horticulture? I refer with this question to those among you who have a strong background and work in fields like: botanics, horticulture, dendrology, etc.

I would like to start building a solid preparation, both practical and theoretical, in horticulture, with a strong scientific background.

I am a physicist at the moment, but I am trying to lay the basis for a career switch. In September I will attend the RHS courses, but in the meanwhile I would like to start studying something on my own.

Is there any introductory, basic, read that you would suggest? Also, if any of you have in mind a sort of "curriculum" (in terms of subjects, books, etc.) or would like to play with it, this would be of great help! Thanks a lot :)

This book could be a good start: Botany by Mauseth. However if you don't have any knowledge about biology I suggest you to get starting with the basics of cellular biology. A good book could be "The cell" by Cooper, you can find it in electronic version.  There are many books about cellular biology but I recommended this because it is complete and detailed without being too long compared with others.


What is a "pure odorant"? This article about testing for Alzheimer's, via changes in the ability to smell, said:

  She thought of peanut butter because, she said, it is a “pure odorant”
  that is only detected by the olfactory nerve and is easy to access.

I'm not clear on what that means. Assuming a person had their mouth closed, then wouldn't any odor be detected only by the olfactory nerve? Wouldn't a lemon, say, work exactly the same?

I could not find a concrete definition after searching several sources, but after reading a few papers I think the term Pure Odorant refers to its Olfactory Bulb profile. Peanut Butter will stimulate specific Olfactory nerves, and only that set of nerves, whereas impure Odorants may stimulate part of the profile and also other parts of the Bulb depending upon the impurity.

Basically, Peanut Butter has a unique smell that you can't replicate, and thus cannot mistake in either flavor or scent when compared to similar compounds. You may  not even be able to tell it was Peanut Butter at all if not for the scent.

A Lemon would not work the same way, as the major Odorant in a Lemon is Limonene - which is present in all citrus fruits. You would activate the same neuronal pathways for Lemons that you would with Oranges, Limes, and Grapefruits.

That's my best assessment.


How can I obtain a uniform bacterial sample? I'm currently doing a research project wherein I will be testing the antibiotic resistance of a bacterial sample. Due to a risk of contamination during transport, I'm not allowed to request a uniform bacterial sample form a clinical laboratory. So, I have to produce my own sample. Then, I'm planning to identify the morphology of the bacteria to confirm the species or type.
The ideal scenario is obtaining a sample which is entirely one species of bacteria. However, taking a swab, either from somewhere in the lab or from the body will produce a sample with multiple bacterial species. What source of bacteria can provide the most uniform sample, i.e. a sample with a majority of one species of bacteria? Or, is there another way to obtain a uniform sample? Also, note: I will be conducting the experiment in a school laboratory, so I must be able to safely contain the pathogen.
Edit: I have recently updated my project to be specified towards testing on bacteria present in the throat. So, a bacteria present in this area or similar areas would be preferable.

You could inoculate your sample in a selective medium or an enrichment medium to kill off the unwanted species. Of course, you will need to do a literature search to find the optimum medium for the species of your interest.
Another option is to streak plates like so. With successive 'generations' of streaks, the inoculum gets diluted, so that you ultimately get separate colonies. Each colony is founded by a single bacterial cell: by picking up one such colony, you get a pure sample.
For even better results, combine both the methods described above by first growing in a selective medium and then streaking on a solid medium to get individual colonies.


Using formulas to explain why contraction of blood vessels leads to increased blood pressure I know, I know this is probably a question too simple to be asked on a forum like biology stack exchange. Problem is, I looked many places and can't seem to find a more mathematical approach to explain why the contraction of a BV leads to increased blood pressure (BP).
The main formula i'm looking at is Flow = Pressure/Resistance. In addition, Flow = Area x velocity so Area x velocity = Pressure/Resistance. As the BV constricts, the radius, ie. area, decreases, and so the pressure decreases. But clearly, that is not the case.

What am I missing here?

There is an important missing assumption in your statement, I've added it in italics:

  Contraction of blood vessels leads to increased blood pressure if total flow stays constant.

All you need is your first equation:

Flow = Pressure/Resistance

Decreasing the radius increases the resistance. If flow is constant, then pressure has to increase to get the same flow through the smaller vessel.


Is there a term for when a detrimental gene can be positively selected for because of linkage to a very fit gene? Let's say that some piece of DNA would be subject to extreme negative selection if it were independently inherited, but it is very closely linked to an extraordinarily fit gene, and so the complex it belongs to is positively selected for.

Is there a term for this phenomenon?

Genetic hitchhiking / genetic draft

From wikipedia

  Genetic hitchhiking, also called genetic draft or the hitchhiking effect, is when an allele changes frequency not because it itself is under natural selection, but because it is near another gene on the same chromosome that is undergoing a selective sweep.

The term "selective sweep" is used improperly in the wikipedia definition. One should replace the last sentence by [..] but because it is near another allele on the same chromosome that is undergoing positive selection or if we want to reuse the term "sweep", once could say [..] but because it is near another allele on the same chromosome that is sweeping to high frequency

Selective sweep

From wikipedia

  A selective sweep is the reduction or elimination of variation among the nucleotides in neighboring DNA of a mutation as the result of recent and strong positive natural selection.


Which matched normal(s) to use when computing CNAs from exome data with a Read-Depth approach I want to use a Read-Depth algorithm to call copy number alterations (CNAs) from Whole Exome Sequencing data (WES) of a specific tumor.

I have a set of WES tumor samples, some of which also have the matched normal sample. My question is: would be more effective, to call CNAs for each tumor, the whole set of matched normals or, if available, only the corresponding matched normal sample?

I thought that using only the single matched normal could spot only somatic variations, while using the whole set of normals would also add germline variations into account. Is that right?

Which best strategy do you suggest?

For the detection of somatic copy nuber alterations it is best to compare each tumour sample with its matched normal. If you want to call CNVs for all your tumour samples and some don't have matched normals, then pooling together all the normal BAMs to create a reference may be the best way to standardise your calling.


How deep could a human swim with SCUBA apparatus? Using normal SCUBA apparatus and wet suit, how much pressure can the human body withstand? This is assuming that they descend as gradually as necessary for their body to make adjustments. What would be first symptoms that they experience as they descend? And if they descend to the deepest depth that they can reach without immediate permanent harm, how long can they spend at that depth before time related symptoms set in?

As far as I can find the current world record for "scuba" diving is 1,090 ft 4.5 in set in 2014.

The previous record was 1,044 ft set in 2005 so (as with most human endurance & physical achievement records nowadays) we're most likely at the limit of the possible there.

Barring a few more feet (or even just inches) of course.

Howsoever, that's only normal scuba diving equipment

Deep diving using hydrox and trimix has reached depths of 1,644 ft (1977) & 1,752 ft (1988).

So the answer depends on if you're asking about with normal commercial scuba gear using bog standard compressed air or if you want to include breathing mixes etc to help alleviate the bends.


Name of neurons affecting or being affected by a neuron? This question is about terminology:

  By which established and catchy terms are the sets of neurons with
  respect to a given neuron $N$ called which

  directly affect $N$ synaptically
  are directly affected by $N$ synaptically?

These terms came to my mind, but I am not sure which ones are most commonly used:

the presynaptic/postsynaptic neurons of $N$
the afferent/efferent neighbours of $N$
the afferents/efferents of $N$
the incoming/outgoing neurons of $N$
the neurons projecting on/to $N$ vs. the neurons projected on/to by $N$

Or is there no such established term, and anything goes, depending on the context?

At the simplest level, the terms 'pre-synaptic'/'post-synaptic' neurons should cover what you wish to describe.
'Afferent'/'efferent' are usually used to refer to axonal projections, usually between functionally distinct areas, or nerves. However, I wouldn't be too surprised if someone used these terms to refer to synaptically connected populations although I would consider it unusual. Simply, 'connected neurons' is also a term frequently used.

I will now go into a tangent to give you some background that should help you formulate an informed view about the vocabulary being used:

In areas that display a high degree of local connectivity, like the cerebral cortex and the hippocampus, any given neuron is connected with many different neurons. Hebb's theory of cell assemblies posits that a group of highly connected neurons may form over time in order to subsist a specific function. Given the high degree of connectivity, any given neuron will be able to participate in many different assemblies. It is often thought that these assemblies constitute the substrate of engrams, the physiological correlates of memory, at the level of the neuronal network. Hence, the concept of cell assemblies is prominent in our thinking about groups of synaptically connected neurons.

Setting aside the questions of the definition of the engram, recent efforts have claimed to identify engram cells under this or that experimental paradigm, although the connectivity of those cells has not been established. While we know that functionally similar neurons display a higher degree of connectivity and that groups of cells with correlated activity patterns can be formed by artifically-induced synchrony, the direct link between increased connectivity and behaviourally relevance has not been established.

On the other hand, only a handful of studies have directly measured the connectivity between more than two neurons (Song et al., Perin et al.), revealing the intricate properties of neuronal network structure. Depending on the level of description they may refer to distributed cell assemblies, synaptic clusters of neurons, $n$-vertex cliques, and motifs.

All this is to say that as soon as you start considering more than a pair of neurons, it makes little sense to talk about neurons that are exclusively connected with each other. As every neuron is connected to almost all other neurons in its immediate neighbourhood we often focus on the functional implications of their connectivity. Under this light, the concept of cell assemblies is central in modern neuroscience.


Why are ducks more cautious than pigeons? In my city park there are mostly two types of bird:

Mallard ducks
Rock doves (pigeons)

When I feed pigeons, they approach me very closely. Sometimes they peck the food that fell on my feet. If I hold my hand with food in the air some pigeons will land on my hand and eat.

In the same park there are Mallards, who are always very cautious and they try to maintain about 1-1.5 meters distance from me. They also run away when they see some rapid movement of mine.

Why are ducks more cautious? Why are pigeons more careless?

A possible reason is that pigeons in a city live there year around, while urban ducks often migrate, or their populations are refreshed by new "recruits" from wild populations ; so pigeons have more opportunity to adapt to being close to people.  Another possible reason is that pigeons are more agile than ducks on land and are more able to escape if you decide to grab one for dinner.


Antibodies stored in freezer instead of fridge Someone from my lab put the box of antibodies in the freezer instead the fridge.  Can I hope that they will still work?

Most IgGs should be fine when stored in the freezer.

  Freezing at -20 or -80 in small aliquots is the optimal storage
  condition. Ali-quoting minimizes damage due to freezing and thawing,
  as well as contamination introduced by pipetting from a single vial
  multiple times. Aliquots are to be frozen and thawed once, with any
  remainder kept at 4 degrees C.

  Enzyme-conjugated antibodies, should not be frozen at all and should
  instead be kept at 4 degrees C. Freezing and thawing will reduce
  enzymatic activity in addition to affecting the antibody binding
  capacity.

  Antibodies of the IgG3 isotype are unique in their tendency to form
  aggregates upon thawing and should always be stored at 4 degrees C

Personally, I store antibodies I use at -20 (they are in PBS), and they work fine for the first freeze thaw cycle. I have never tried more than one freeze thaw, so cant comment on that.

http://www.abcam.com/ps/pdf/protocols/antibody_storage.pdf


What are mouse LS cells? I have seen the term "mouse LS cell" used in several papers now, but I haven't found an explanation for the origin of these cells (for example, this paper).

What are mouse LS cells? What is their origin (besides coming from mouse!)?

Not an easy question, but I got some references about it.
Mouse LS cells are Fibroblasts growing in suspension culture, the paper in reference 1 has this paragraph in its Materials and Methods section:

This cell line seems to be in culture since the 1940s, as the reference to Sanford, Earle and Likely, 1948 suggests. Digging up this reference (number 2 below) tells a bit more about the isolation:

  The cells of this study were from Earle's strain
  L (6), which originated from normal, subcutaneous,
  connective tissue of an adult C311 strain
  mouse.

Reference 6 in the Sanford et al. paper is:

  EARLE, W. R.: Production of malignancy in vitro.
  IV. The mouse fibroblast cultures and changes
  seen in the living cells. J. Nat. Cancer Inst, 4:
  165-212 (1943).

which gives no further details. It is a methodic paper which analyzes the conditions necessary for cell culture - interesting on a historical point of view, since the techniques where developed at that time. The full PDF is linked in reference 3.

About the name I need to speculate a bit, but since the original cells where named "Strain L", and LS cells where derived from there to grow in suspension, it might translate into Strain L Suspension cells.

References:

The Uptake of Amino Acids by Mouse Cells (Strain LS) During Growth
In Batch Culture and Chemostat Culture: The Influence Of Cell Growth
Rate
The Growth in Vitro of Single Isolated Tissue Cells
Production of Malignancy in Vitro.


What are the differences in ultrastructure of cilia and flagella? Cilia and flagella are aimed for similar perpose, motion. And both of them show the (9+2) microtubule arrangement. They are nearly identical in structure. But to be more specific , where exactly does the little difference lie (except the 5-6 bridge) ?

Perhaps you mean that flagella spin to provide locomotion whereas the cilia tubules themselves beat.  the flagellar motor vs the fixed anchored structure of the cilia...


Anaphase Microtubule Disassembly Centromeres move toward the poles as the microtubules that connect them shorten. This shortening is due to the removal of tubulin subunits from the kinetochore ends of the microtubules.

I'm confused as to how the centromeres can be pulled closer to their respective poles while tubulin subunits are being removed. To me, this is similar to pulling an object by a rope while simultaneously cutting pieces of the rope out. How do the centromeres remain connected to the spindles while tubulin subunits are being removed?

I don't think the microtubules shorten. The disassembly of tubulin (dynamic catastrophe) happens from its + end which in this case is protected by the kinetochore proteins. The separation of chromatids, I guess, happens via a dynein (and in some cases kinesin) mediated movement.

The wikipedia article on kinetochore is quite detailed and you can have a look at it.


Why does Citric Acid occur in Citrus fruits? Why is there so much citric acid in citrus fruits? And how did it evolve i.e. what did it come from? Is it a by-product of the ripening process?  Why have citrus fruit evolved a particularly high amount of citric acid compared to other fruits? Was it due to particular selection pressure for acidic fruits or was there a genetic bottle neck that caused this such as human cultivation?

I've been trying to search for this but google scholar isn't throwing up anything so I'd really appreciate some help.

Actually citric acid is not only available in citrus fruit but also in pretty much any living thing. it is an important intermediate in Krebs cycle, but I guess the main reason that it is available in high concentrations in citrus fruits is because citrate is an inhibitory compound for phosphofructokinase, that means it stops the glycolysis and hence it makes it hard for bacteria to use the fructose available in the fruit body.

Source:
 Stryer, Lubert; Berg, Jeremy; Tymoczko, John (2003). "Section 16.2: The Glycolytic Pathway Is Tightly Controlled". Biochemistry (5. ed., international ed., 3. printing ed.). New York: Freeman. ISBN 978-0716746843.


Why are VAL, MET and ALA substitutions commonly used for protein behaviour and function studies? I have seen that amino acids are commonly replaced with VAL, MET or ALA to study the effects of these specific substitutions.  Why are these specific amino acids used in particular, what are the results of these substitutions expected to show, could substitutions of other amino acids achieve the same results, and what is the source of this technique?

Substituting a single amino acid and checking the effect this has on a protein is a method to determine what this specific amino acid does in the protein. For example, substituting an amino acid that is part of the catalytic core would almost always make the protein non-functional.

Alanine scanning is a technique that methodically replaces amino acids in a protein with alanine. Alanine is probably the most neutral substitution, you essentially remove the amino acid sidechain. Glycine for example would be problematic because it is more flexible and can adopt secondary structurs other amino acids can't.

If you want to find out what a specific amino acid does, you don't want to introduce any other new effects when mutating it. Depending on what exactly you're looking at, substituting other amino acids is certainly possible. Some changes to alanine might be too drastic and you might want to substitute an amino acid that is more similar to the original one. This all depends on what exactly you are looking at.


How does the human liver regrow? I understand that there would have to be a portion of liver present to regrow from, so how much liver would the minimum to be able to regrow?

By what mechanism does regrowth occur?

At least 25% of the original liver seems to be the minimum for regrowth.

The initial regrowth is due to proliferation of hepatocytes: they exit G0 and enter mitosis. The ECM dissolves and is remodeled; the cholangiocytes and SECs also divide.

If you want to read more, you can visit the Google books link above, and the preview lets you read several pages on liver regeneration in rodents.  (If it doesn't work, try changing the URL to your current location: books.google.com is US, books.google.ca is Canada, etc.)


What is the minimum sample size to get reliable results in haplotype and nucleotide estimations? Different software have different methods for estimating diversity and each method will have assumptions about the quantity of
data required to produce a reliable result. I am estimating the haplotype and nucleotide diversity by DnaSP6 program of Sanger sequences. I would like what is the minimum sample size requires to get reliable results.

Thanks in advance.

I'm still a little unclear on what the analysis looks like, but I'm going to assume for the sake of this answer that it's a single locus sequenced across multiple populations, with some number of individuals per population, and that the concern is that some of these populations are represented by only a few individuals. I'm also going to assume that the individuals are diploid, so you in fact have a little more data than it appears.

All the same, this paper indicates that n<5 individuals in a population leads to quite noisy estimates of $\pi$ and $h$ (section "The effect of sample size on haplotype and nucleotide diversities"). This is of course specific to a certain ~500bp region that they collected sequences for. That doesn't mean that you can't compute these metrics, only that they may not be very reliable.

For reference, the early Neanderthal genome papers compute some measures based on only the two copies present in their diploid genomes- of course, they are assisted by a large amount of modern human data for making comparisons. If you have supporting data from other populations, you may still be able to say something about the populations with few individuals. But you will likely have to use measures other than $\pi$ and $h$ to do so.

Some other tools that you might use to "borrow" information from other individuals outside those groups are ordination analyses such as PCA, or clustering tools like STRUCTURE. One way of thinking about how this works is that you can "embed" your populations with few individuals in the population structure of your overall dataset. This allows you to still learn from those populations even if the number of individuals is small. The Neanderthal papers implement versions of this, but with much more elaborate statistical frameworks, for a whole genome rather than just a single gene.

I'm not sure if DnaSP can carry out these analyses, but there are a lot of tools that do similar things, one tutorial here. Of course looking at the DnaSP manual is probably a good idea to see what you can do with your current tool.

Depending on your goals it may also be interesting to compute F-statistics across your populations, this is done by most population genetics tool suites. I used GenePop many years ago to do this, it appears to still work, though I am sure there are better alternatives now.

An important note is that most of these measures are purely descriptive, not inferential. Low sample size makes descriptive statistics noisy, but doesn't invalidate them. Inferential statistics are a bit more dangerous.


What is an effective method for putting on blue rubber butyl stoppers? They look like this.

We have to do a lot of gas sampling and these are really difficult to assemble. I've been scouring the internet for advice but there are none. Do you have experience with these? Have you found a good way to put them on that doesn't destroy hands, hearts, and dreams?

To clarify, the hard part is putting the blue stoppers in the tubes in the first place. Once they go thoroughly in, we can crimp them with our hand crimping tool. Since the time I posted this, I find a (little) better luck using a piece of cloth / putting the cap and the glass vial between a vice. With too much pressure, I actually broke a vial and glass shattered everywhere. The best way to put them in is with a twist, but that usually comes with an expense of bruised hands after extensive use.

Wish I had a camera on me, but they look somewhat like this:

From what I can tell from this machine (https://www.youtube.com/watch?v=TwRtsAG5Oy4), the blue caps are put on the bottles first, then a loose version of the aluminium neck seals are put around the top of the capsule, which is then pressed in the machine to seal the lid hence if you use many gas sampling techniques, it might worth investing in purchasing a similar machine/technology to seal your samples, which would be the most efficient in the long run.

EDIT: as pointed by @user137 there are also hand crimping tools, which you can use, which are considerably cheaper, which as @user137 pointed out, can be found here


If all bacteria in human gut are dead, can they be there again? If someone likes to eat chocolate, she may have gut bacteria which like chocolate according to some articles that I have read.

http://www.theatlantic.com/health/archive/2014/08/your-gut-bacteria-want-you-to-eat-a-cupcake/378702/

If I do not eat chocolate for a long time, would their number be decreased and other (bad) bacteria dominate the gut?

So the question your essentially asking is "Do certain types of bacteria like a specific nutrient, and if so will they dissipate or die off if I do not acquire that nutrient?"

Let's give a specific example for comparison. Lactose intolerance is a prevalent disorder among many people and those who do have the intolerance, if aware, tend to steer clear from lactose containing foods. Some studies have been shown that correlate lactose consumption to amount of lactose-containing bacteria in the gut.

So I would say if your asking if you remove a nutrient from your diet will a particular bacteria suffer i.e die then yes. Although be aware that many bacteria are able to break down a variety of different nutrients, and in the case of a cupcake which is loaded with sugars, and fats, I would say a large majority of gut residing bacteria are able to use that as energy in one form or another.

Here's an article comparing lactose-tolerant, and lactose intolerant individuals, not chocolate, but a good start. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898492/


Does extracted DNA degrade after a certain time period? For direct use as template in PCR runs. Chelex 100 5-10% w/v extraction. Without listing the whole protocol, in the end the supernate is decanted off and then stored at 4°C. I was under the impression that this could be stored and later used almost indefinately but two of four samples extracted several months back failed to produce a product (when it was known they should have).

Assuming no mistakes were made and the reactions were the same, is there a technical reason the template would degrade to an unusable point?

Is there a rule of thumb about how long it can reasonably be expected to last?

My rule of thumb for DNA samples (in TE or water) - if I have plans to use it that week, I store at 4C. If I plan on using it within a month, I store at -20C. If I'm not sure when I will use it, I keep multiple aliquots at -80C. DNA can degrade by acid hydrolysis in water, because of contaminating nucleases in the sample, and by multiple freeze/thaw cycles.


Why do plants create enough energy for the entire ecosystem? In my environmental class, we were recently learning about the $10\%$ law that basically says only $10\%$ of the energy goes from one trophic level to the next.

This got me thinking about why energy flows from one level to the next.  Specifically, why do plants create enough energy for the entire ecosystem?  Wouldn't they do fine without us, and wouldn't that save them the work of creating all that excess energy?

Plants collect energy for themselves via photosynthesis, not for others.
It is used for it's own growth and survival.

It's energy is then redistributed to other organisms when either the plant dies and decomposes or when it is consumed. Many organism cannot collect their energy like plants do, and thus must feed on organisms (like plants) that are able to collect and store energy. This is in many cases detrimental to the plant (it should be intuitive why being eaten might be bad), and many, many plants do have traits to discourage other organisms from eating them (plants with toxins, thorns, etc.).


E coli cotransformation efficiency What is the E coli transformation efficiency for 2 plasmids? Are any studies that have looked at the correlation between number of plasmids transformed and transformation efficiency? Is there a commercial E coli strain that is better at co-transformation?

For example, electroporation with single plasmid yields around 1 × 10^10 cfu/μg. I would like to know what is the limit for co-transformation and whether it can be or has been improved.

There is no problem to transform bacteria with more than one plasmid. The usual methods (either chemical competent cells or electroporation) are working fine, although electroporation might give you better results, as the cells take up more DNA. On the downside you have to make sure that your cells are prepared nicely, otherwise the electroporation cell will produce a short circuit (of course chemically competent cells can be problematic, too).

What you will definitely need are two (or more) different selection markers. The easiest will probably be different antibiotics (something I used in the lab and which works nicely) or other like genes which provide essential substances for the cells. As long as the selection pressure on the cells is held up, both plasmids will stay in the cells, when you take away one of them, the corresponding plasmid will get lost within a few days.

Regarding the efficiency of co-transformations I haven't found any papers. There is however, some data available on factors which influence the effiency of single transformations and I don't see, why these shouldn't be applied for co-transformations as well.

First, there is the size of the plasmid. The bigger the plasmid is, the lower gets the transformation efficiency. The figure from Inoue, 1990 is pretty clear in this point:

So for this reason I would use plasmids as small as possible.

Second, the density at which the growing bacterial culture which is used to prepare the competent cells is harvested has a big influence on the transformation efficiency. Tang and colleagues (1994) found out that growing the cells to a higher density than the classical OD$_{600}$ of 0.6 (which for example Inoue recommends in it paper cited above) is not a very good choice in terms of transformation efficiency. They found an OD$_{600}$ of about 0.94 working much better, see the corresponding figure:

And finally the amount of competing DNA is a big factor. Hanahan, 1983 found out that the transformation efficiency gets lower, the more competing DNA is present:

So I would try to use as little of each DNA to work against this effect.


Do people grow shorter as they age, how common is it, and what triggers it? Is it true that people become gradually shorter as they age?

If it is, is it more common in one gender than the other?

And is it known what triggers this? (Considering that the "shortening" probably does not start immediately after the person stops growing?)

Short answer: Yes, we do shrink with age.

The most important reason is that the cartilage in the joints between our bones gets worn out and thinner, as well as disks between the vertebrae of the spine. This results in a compression of the spine and also to a loss in height. Shrinking bones due to osteoporosis can also play a role, as well as muscular atrophy due to ageing.

According to "The Baltimore Longitudinal Study of Aging" (reference 1) adults start shrinking by the age of 30 by 5-8mm per decade. This is relatively short after you completely stop growing. This process gets faster with increasing age, the study says it goes faster after 70.

Men and women do not shrink equally, men loose around 3cm between 30-70 and a total of 5cm by the age of 80. Women loose about 5cm between 30 and 70 and a total of 4.5cm by the age of 80 (these are average numbers from reference 1). Reference 2 also has a nice summary of this original article.

This effect can be attenuated by regulary excercising as the study listed in reference 3 shows.

References:

Longitudinal Change in Height of Men and Women: Implications for
Interpretation of the Body Mass Index: The Baltimore Longitudinal
Study of Aging
Yes, You Are Getting Shorter
Role of physical activity training in attenuation of height loss
through aging.


What is a typical value of the selection coefficient s? I am trying to gain an understanding of the real world effects of natural selection from the equations, especially comparing it with drift. However I have been unable to find any examples which give an estimated value of the selection coefficient for a population considering a particular trait. Could anyone link me to some studies that give an actual value for a selection coefficient? Thank you in advance!

This is a very fundamental and important question! But first, be cautious not to confound the Fitness effect of segregating alleles with the mutational effects.
Fitness effect of segregating alleles vs mutational effects
One must not confond the distribution of fitness effect of segregating alleles in a population with the distribution of mutational effects. The distribution of mutational effects will always be narrower in comparison to the distribution of fitness effects of segregating alleles as very deleterious mutations won't stay long in the population and very beneficial mutation will sweep to high frequency very quickly so that it is unlikely to see them.
I am assuming you are interested in the distribution of mutational effects. Below are some papers and generalities that will be of interest to you. Some data come from the quantitative genetics literature and some from classical empirical population genetics. I also talk about mutation rate as these two subjects are highly related typically at determining mutation load.
Short answer
A typical deleterious mutation has a mutational effect of $s=0.1$ or $s=0.05$. In theoretical studies, authors often used a constant value of $s$ as being equal to one of these two numbers.
Longer answer
Distribution of mutational effect
Generally speaking distribution of mutational effects (on both the deleterious and the beneficial side) are thought to approximatively follow a gamma distribution with an extra bump of probability density around lethal mutations. shape might take values around 0.5 or 0.05 while the scale parameters might be of the order 0.1 to 0.001, with typically an average around 0.05. See Halligan and Keightley 2009. I have seen (see Nemo's documentation for example) that the dominance coefficent $h$ is modelled as $h=-log(2 Exp[h])/Exp[s]$.
Mutation rate
Concerning the mutation rate, a reasonable approximation is to consider a deleterious mutation rate per diploid genome of 1. This is known as Drake's law (see this post). Drake's law appears to be an underestimate for humans (Keightley 2012), about right for Drosophila, (Haag-Liautard et al. 2007), C. elegans (Denver et al. 2004) and possibly non-human endothermic vertebrates (Baer et al. 2007), and probably an overestimate for many other organisms (Baer et al. 2007, Halligan and Keightley 2009).
Quantitative traits
If you are uneasy with basic quantitative genetics and the below notation, you should have a look at this post.
For quantitative trait, there is evidence that $\frac{Vs}{Vp}≈5$ on average (Kingsolver et al. 2001, Johnson and Barton 2005). If heritability is $\frac{1}{3}$ (as it rarely significantly different from), then $Vs=7.5$. Empirical estimates of the mutational heritability $Vm$ suggests that $\frac{Vm}{Ve} = 0.001$ (Houle et al. 1996)


Why does the apex of the human heart usually point to the left? In the majority of human beings, the apex of the heart (left ventricle) points towards the left side of the body.  Sometimes however (approx. 1/12000 births), a person is born with a condition known as "Dextrocardia", in which the apex of the heart points to the right side of the body instead.

Is there an evolutionary reason as to why the human heart usually points to the left side as opposed to the right side of the body?

(Note:  Please don't answer with, "because there is a notch in the left lung", because I will simply reply with, "is there an evolutionary reason for the apex of the heart AND the cardiac notch being on the left as opposed to the right side of the body").

From a quick look at the paper @ChinmayKanchi links to (Palmer, 2004) it seems that:

  All living vertebrates possess a heart that is conspicuously asymmetrical and normally displaced toward the left (Fishman & Chien, 1997).

So the heart orientation seems to be evolutionary conserved in vertebrates (as are many fundamental traits), and no specific explanation is needed for humans.

This is said with the reservation that human anatomy is not my subject field, and the refered paper also digs deeper into the molecular basis for the orientation/symmetry of organisms. For instance, it also says that:

  Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system.

so the molecular mechanisms governing this seems to differ between species. This could indicate that there is a selective pressure molding species into the same heart orientation. This is pure speculation on my part though.

I also want to mention that evolutionary outcomes doesn't have to have a "reason" (i.e. a selective advantage). Much depends on chance events and evolution can only act on what is present at the moment (i.e. is restricted by earlier evolutionary history).


Does cow urine have medicinal properties? It is a common belief in India that cow urine has medicinal properties.

It is said to be anti-biotic.

It cures diabetes, cancer and many other diseases if not all.

Because this is biology I would like to focus on the anti-biotic property and set aside other claims cos they many be related to medicine and not biology.

Is it anti-biotic?

Does urine not cause infections?

Especially since it is applied the belly of new born babies by orthodox Hinuds.

Interesting question anomdsgf. There are substances present in Bos taurus urine that promote antimicrobial activity. Studies like this and this have shown how the urine can inhibit the growth of certain bacterial strains.

However, with all that said, Bos taurus urine could still contain other harmful bacteria that are not inhibited simply because it was excreted out of a cows urethra and could cause infections. Read more on possible harmful effects here.


How the lungs clear themselves? Looking at my computer's fan I can say that a lot of dust is collected on it not less dust should be collected in the lungs, not to mention some inhaled parts of food.

How the lungs clear themselves from dust, smoke, food particles?

nuhcole is mostly correct.

Airborne particles first pass through the nasal passageways and/or mouth and throat and many are caught, but those that enter the lungs become trapped in mucus.

Your cilia act like a constant escalator, bringing up that mucus from your lungs 24/7.  You reflexively swallow it without even realizing it.  That is why when you are healthy, you might not even notice.

If you are sick (or asthma/allergies), more mucus is produced.  That is when you may notice the increased quantity coming up, and may need to cough to bring more up.

If your cilia are damaged (like in smokers), then mucus does not clear well from the lungs. In this case, people must cough more in order to bring it up.


Why is it that drinking caffeinated tea does not help one to stay awake? I have never felt after drinking tea that I can have the power of being able to work late at night. Neither have I felt that it helps me to be awake while working or keeping eyes opened while I am not in mood for sleeping.

Drinking tea, then, does not helps me to stay awake.

Is it the nature of the tea itself, or does it have to do with how the body processes caffeine?

It could be tolerance if other caffeinated beverages are usually consumed, however it also depends on the type of tea itself, and other properties, such as how long the tea has steeped for.

For example, brewed black tea can have anywhere from 14-61 mg of caffeine, which is a large range and depends on which tea you are drinking specifically.  Whereas if you were drinking green tea that has not been steeped for long, it can have 24-40 mg of caffeine, which at the lower range will probably not help you stay awake.

From MayoClinic.Org:

  The actual caffeine content of the same coffee drink can vary from day to day — even at the same coffee shop — because of various factors, such as roasting and grinding, as well as brewing time. The caffeine content of tea also is affected by how long it's brewed.

Caffeine beverage levels can be found here:

http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/caffeine/art-20049372


What is the technical term for when a clade on a phylogenetic tree does not have an extended branch? (see image) As we see with ZCA2, ECA2 & XCA2 these branches are compressed and do not extend as TCA does. Is there a technical term for this and what usually causes it?

The phenomenon where you have different "evolutionary clocks" of selection is called heterotachy. The branches are therefore heterotachic or simply long branches —long branch attraction is a problem with Bayesian inference for which many arguments have been had, so there is a lot of literature on it.


Why do humans circulate monosaccharides instead of disaccharides as in plants? Plants transport food mostly in the form of disaccharides like sucrose but humans transport them in the form of a monosaccharide -  glucose.

What is the reason behind this ?

One of the reasons could be  -

  humans and many other animals have active circulatory systems,
  there is little need for targeting sugars for specific parts of the
  body. The entire body would rapidly reach equilibrium with the glucose
  level of the bloodstream, and thus there likely never evolved the need
  to target specific organs to receive sugars via disaccharides

Source : This

Other reason could be that disaccharides are harder to transfer inside the cells than monosaccharides.


How do S and L cone cells sense colors like deep blue and red beyond their peak? So I found this diagram of retinal cone cells:

It looks like the S, M, and L cones peak at blue, chartreuse and orange, respectively. If so, how do we see colors past 575 nm and before 445 nm? If the cones really respond to purple, green, and red, (as I previously thought) why do they peak at colors closer to green, as shown in the image?

The answer is actually present in your chart: color perception depends on the ratios of activations of different photoreceptors. For example, as you go "more red" from 575, the responses of the Green photoreceptors are falling off more quickly than the Red ones. The same is true for any colors in between, and on the other end, where 400nm light would activate only the blue receptors, whereas at 445nm there would be some mix of activation of the green.

From the context of Fisher information it is actually interesting that photoreceptors don't actually provide much color discriminability at their peaks.

For example, around 575 nm, the "red" photoreceptors actually don't provide very good color discrimination: the response to 565 or 585 is going to be almost identical, for example. The way you can perceive a difference, though, is that the response from the green photoreceptors will be very different at those two wavelengths (just consult your chart!). In vision, as in all the other senses, the information is really held in the slopes!


Water potential in plants? The concept of water potential in plants tries (and succeeds) to explain various movement and transports in plants. I have learnt that it can be though of being composed of various components like the solute (osmotic) potential, Matric potential, gravitational potential and the pressure potential. I know how to quantitatively determine the osmotic pressure and have worked with the chemical potential of water in solution and pure state. Can someone help me develop an intuitive understanding of all these components quantitatively? I am comfortable with basic thermodynamic treatments of chemical potential and already have an intuition of the osmotic component. Here is the basic definition regarding water potential. (Since this pdf is quite old, I am not sure whether the same definitions operate or rather are used now.)

EDIT:- As an example, we can derive the lowering of chemical potential of pure water on addition of solute and for the ideal case, the lowering turns out to be $RTln(X_a)$ (where $x_a$ is the mole-fraction of solute, $R$ is the gas constant and $T$ the absolute temperature) and this is defined as the osmotic potential or the solute potential. Next, the gravimetric component. We can intuitively understand that the water must flow from higher gravitational potential to lower and hence flow downwards. But I want to understand how can we assign a quantitative basis to our arguments in terms of chemical potential for differenf heights. Same way, how can we ascribe a mathematical (or chemical) basis to all the components of water potential including the turgor pressure and the matric components.

Ok let me try to tackle this one - still could be off - let me know.

The book Chapter from UCDavis that is linked from your wikipedia page is a good reference I think. Overall the term 'water potential' will try to estimate an energy function that describes the behavior of water in a chemo-mechanical sense.

$\Psi_{total} = \Psi_{reference} + \Psi_{solute} + \Psi_{pressure} + \Psi_{gravitational} + \Psi_{humidity} + \Psi_{matrix}$

It looks a lot like a Hamiltonian expression of total energy that tries to see the water as a fluid.  The water potential is not the same as an energy equation for fluid dynamics which tries to understand the motion of a body of liquid and does not typically take into consideration chemical changes like solute in the behavior.

So first we are looking at a set of behaviors that the fluid experiences.  some of them treat the fluid as a body ( pressure, gravitational) others look at the potential for evaporation or diffusion (solute and humidity to some degree).  wetting of surfaces and surface tension (matrix).

The water potential is an equation broken down into a set of measurable or approximately measurable energy terms.  But like a lot of Energy equations, when  you are looking at a biological system, it is more often qualitative than a quantitated entity.  The general observation that surface tension decreases when temperature goes up, or when the solutes have higher concentration is used to make arguments of the mechanism of say physiology

Generally speaking looking at the magnitudes of the various terms you can see how influential they are and then try to focus the hypothesis into a test that can make a distinction about the mechanism with specific measurements.  The actual overall measurement of a water potential or any total energy is almost always intractable.  The difference in energy is what you might be able to measure, but in the case of the water potential, the measurement will usually be an observation, with some uncertainty that water is moving from point A to B and not elsewhere.

Take a look at this paper describing Drought Stress in Arabidopsis.  The water potential is cited as a critical element of drought response - and of course it should be.  But all this work here, with all the proteins acting to change the physiology of the cell, adjust the chemical potential (and therefore the osmotic potential) of the cell membrane, its hard to imagine how measuring a root system at all points would be possible.

  Physical properties of the cell wall play a crucial role in the response of plants to water deficit (Bacon, 1999). Transcriptome analysis of pDr showed the repression of many expansin genes (Bray, 2004), while mild osmotic stress revealed the induction of expansin genes (Skirycz et al., 2010). Cell expansion in response to drought was characterized in the maize (Zea mays) root system as an adaptation to low water potential (Wu and Cosgrove, 2000).


Why are our bodies created to itch when histamine is released by our immune systems? Why do bug bites and cuts itch when scratching them clearly doesn't help us survive? Did our early ancestors need to rely on this itching sensation, or is it just that the receptors for itches just happen to be stimulated by histamine?

Scratching is getting potentially poisonous or at least irritant substances out and removes lodged insects like ticks.

Removing subcutane parasites like scapies mites is not feasible without scratching yourself bloody.

I don't see how "scratching them clearly doesn't help us survive".  Behaviors and skin reactions evolved way before our modern hygiene and parasite cures.


What can we infer from Warburg's Flashing Light experiment? The 'Dark Phase' in photosynthesis as I know is not dependent on darkness, but is just 'Light Independent'. But the Warburg Flashing light experiment, makes me think again. Warburg obtained higher rates of photosynthesis in Chlorella, when he exposed it to rapid alternate periods of light and darkness, instead of illuminating it constantly. But if the so called dark phase is just 'Light Independent', then why did Warburg get higher photosynthesis rate in the setup? I think if continuous illumination was provided ATP and $\ce{NADPH}+ \ce{H+}$ would be present more, and thus should give higher rates of photosynthesis. Can anyone point where I'm mistaken?

according to my understanding, if we compare two situation 1. one hour continuous illumination and other 2. alternating period of light and dark (but the illumination time remain same). the rate of photosynthesis will be more in second case which indicate that even in dark, photosynthesis is taking place (ie. dark reaction)...just my thought...


copper vs aluminum, what's the safest for health? I'm working on a mini project for a milk dispenser machine, using a peltier device to cool the milk down, I have to choose between a copper or aluminum cooling block (see pictures bellow).

But I'm worried about health issues in the long run, (oxidation and stuff), I have no idea what to choose.

What would you guys recommend me ?

Assuming the answer can't be C) Stainless Steel I would go with Aluminum.

The USDA specifically mandates (1) stainless steel 300:

  "Milk contact surfaces shall be made of stainless steel of the 300
  series, equally corrosion-resistant non-toxic metals or heat-resistant
  glass."

Is the copper tinned?  From what I can tell after reading some old sources (2) un-tinned copper will be corroded by milk.  You have the advantage of a cool temperature lowering contamination risk (3), but many states following the FDA specifically removed the allowance of tinned copper (Sec. 22-201).

While the effects of life long dosing of Al are becoming more and more clearly tied to Alzheimer's (4), the effects build up over time.  Copper has a tendency to be more acute (5) and pronounced (6, 7), and further it can tasted in low amounts  and discolor the food (8).  It can be said that water flows through Cu pipes, but soda is put in Al cans.

The research for this has been quite enjoyable, and led to things I didn't even think of.  A alternative cleaning site has even recommended using milk to clean Cu pans.

Again so my final recommendation is to follow USDA guidelines and use stainless steel, but my second choice would be Aluminum.

Citations:

(1) USDA. 2011, July. Milk for Manufacturing Purposes and its Production and Processing.

(2) US DOC. 1917, April. STRUCTURE OF THE COATING ON TINNED SHEET COPPER IN RELATION TO A SPECIFIC CASE OF CORROSION. Technologic Papers OF THE Bureau of Standards.

(3) COMMITTEE ON COPPER IN DRINKING WATER, NATIONAL RESEARCH COUNCIL. Copper in Drinking Water. NATIONAL ACADEMY PRESS. 2000.

(4) Walton, J.R. Aluminum Involvement in the Progression of Alzheimer's Disease. Journal of Alzheimer’s Disease 35 (2013) 7–43. DOI 10.3233/JAD-121909

(5) Reilly C. The dietary significance of adventitious iron, zinc, copper and lead in domestically prepared food. Food Addit Contam. 1985 Jul-Sep;2(3):209-15.

(6) Conor Reilly. Metal Contamination of Food:
Its Significance for Food Quality and Human Health. Pg 50. John Wiley & Sons, Apr 15, 2008

(8) ibid pg. 16

(7) Lee A. Price, et al. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology. 1996, Vol. 28, No. 4 , Pages 316-320 (doi:10.1080/00313029600169264)


Are brown eyes healthier than blue eyes? I have read somewhere brown eyes have more melanin than blue eyes and as melanin protects our body from cancers, I thought that brown eyes are more healthier.

People conflate "Dominant" traits to mean "healthier" which is a huge misconception. The previous answer provided a good example of how what is adaptive in one environment can be Mal-adaptive in another. Many Disorders can be dominant for example Huntingtons disease or achondriplastic dwarfism.


Why does sympathetic activity constrict pulmonary vessels? I don't know understand why sympathetic stimulation constricts pulmonary vessels?
I thought that the sympathetic nervous system activated the body for physical activity. Physical activity would need more oxygen supply. Doesn't constriction of pulmonary vessels reduce the gas exchange?

Short answer
The sympathetic nervous system mediates the fight, flight and fright response. It constricts the arteries and arterioles to increase blood pressure, in turn pushing the blood to the muscles and other organs vital for physical activity.

Background
The sympathetic nervous system functions triggers the fight, fright, flight (FFF) response (Fig. 1). It provides the body with a burst of energy so that it can respond to danger (source: Harvard Medical School).

The FFF response is initiated in the hypothalamus by activating the sympathetic nervous system through the adrenal glands. These glands release epinephrine (adrenaline) into the bloodstream. Epi increases heart rate and blood pressure to push blood to the muscles, heart, and other vital organs. The person also starts to breathe more rapidly and the small airways in the lungs open up. This way, the lungs can take in as much oxygen as possible with each breath. Extra oxygen is sent to the brain, increasing alertness (source: Harvard Medical School).

In blood vessels, as you say, sympathetic activation constricts arteries and arterioles (resistance vessels), which increases vascular resistance and decreases distal blood flow. When this occurs throughout the body, the increased vascular resistance causes arterial pressure to increase (Klabunde, 2012). This enhances the distribution of oxygen already present in the blood.  I don't think the pulmonary circulation responds differently than that in the rest of the body. The stress response is meant to support the evasion of acute dangers. But indeed, chronic exposure to adrenaline may eventually lead to impaired oxygen exchange in the lungs (Krishnamoorthy et al., 2012).

Fig. 1. Fight, flight, fright response. source: Freelap USA

References
-  Klabunde, Cardiovascular Physiology Concepts, 2nd ed. (2012). Lippincott Williams & Wilkins
- Krishnamoorthy et al., Anesthesiology (2012); 117(10): 745-54


Do death rate and birth rate become equal at replacement fertility rate? A population transitions from stage 3 to stage 4 when the fertility rate reaches the population replacement level of 2.1.

My question is that if the population replacement level reached, shouldn't the net growth rate be zero? i.e., birth rate = death rate? But in the figure, in stage 4, birth rate > death rate and there is still a population increase.

How is this so?

The transition to stationary populations is between stage 4 to stage 5 in all exemples of the DT model that I've seen. Not between stage 3 and 4. This is also what is being implied in the figure that you've included. In your link they also write:

  Countries like India in the third phase of demographic transition have fertility rates that have declined significantly from previously high levels but have not reached the population-stabilizing "replacement level" of 2.1 children per woman.

This is not saying that countries reach the replacement level 2.1 at the end of stage 3.

The same stages are also described at the Wikipedia page on DT and at populationeducation.org.

So you are correct; at replacement levels, populations shouldn't increase and the net growth should be zero.


What does it mean for the signals for transcription and translation to be "conserved"? I was reading this article: "Overview of vector design for mammalian gene expression."  for an explanation of why mammalian cell lines are used for expressing cloned genes, and one of the reasons given is that "DNA cloned from higher eukaryotic cells is readily expressed since the signals for transcription, mRNA processing, and translation are conserved in higher eukaryotic systems." What does it mean for the signals to be "conserved," and why does this make mammalian cells a better host than other types of cells?

Follow-up question, in case the answer to that question doesn't make it clear: the article also says the machinery for protein folding and assembly are "conserved" - what does that mean (if not the same thing as in the first question) - and again, why does this make mammalian cells a superior choice of host for expressing cloned genes?

I concur with @Bez but wish to elaborate on the meaning of 'conserved'. It is generally used in the context of evolution. A conserved characteristic or gene or protein means that it has 'survived' a long time without being altered. As @Bez mentions, certain parts of the protein machinery in eukaryotes is very different from prokaryotes, the latter being considered to have arisen much earlier in evolution. For example, some post-transcriptional processes (e.g. splicing and many more differences) only occur in eukaryotes. But there are many similarities as well, such as the basic use of mRNA etc (see book section). The latter are examples of conserved mechanisms.  In the context of your question, it means that when you take eukaryotic DNA to express eukaryotic proteins it doesn't really matter which cell or host organism you take as it will be transcribed and folded correctly. For example, yeast is often used to express DNA from higher organisms as its protein synthesis is much the same across various eukaryotic species. However, expressing eukaryotic DNA in prokaryotes likely ends up in misfolded proteins without proper post-transcriptional modification and should be avoided.

As to your follow-up question: Folding of proteins happens in the endoplasmatic reticulum (ER) in eukaryotes (wiki), a cell organelle absent in prokaryotes as they lack a nucleus and associated organelles. Again, expression of eukaryotic genes in a prokaryotic expression system will end up in mis-folded proteins.

To get back to your overall question - the 'signals': DNA transcription, splicing, protein synthesis, post translational modification and folding are all regulated by signals, such as specific DNA codons to start and stop transcription, RNA codes for splicing and start translation and protein tags that are placed on specific amino acid combinations. These signals are well conserved across eukaryotic species.


How is consciousness linked to the brain? Could the brain be working without consciousness? Does the brain interact with consciousness? Alternately, is it that consciousness can't really control the brain, and you only have the impression that you make the decisions, but your brain does.

If the answer to the last question is yes, it is impossible to know if someone else has a consciousness? Even if he doesn't, he'll say he does, because the brain thinks he does.

We can't be made only from matter. If we would, we'd be a mix of chemicals interacting with each other. What makes us be aware of our feelings, what we think, and our 5 senses?

When and how is consciousnesses created?

This question is difficult to answer and in the end, we'll just have to accept that we don't really know (at least for now). My own understanding is that what we call our consciousness is an emergent phenomenon, arising from the extraordinarily complex network of billions of neurons interacting with each other within the brain. Perhaps the rest of the cells in the body - everything that is interconnected - should also be included. This would mean that we are, indeed, "a mix of chemicals interacting with each other", but in my opinion, that does not make being any less meaningful.

As a side note, although this seems to imply determinism, the future behaviour of complex systems such as our brain, or better yet, the entire universe, is impossible to predict accurately with any computing device. We, as well as the universe, are the best simulators of ourselves.

I think it is really difficult to handle questions like this. To start with, how do you even define "consciousness"? Also, I don't think that such a discussion belongs to philosophy; surely any plausible explanation of conciousness must be rooted within the framework of science.


What fraction of sites are expected to be polymorphic? Question

Consider a very long (eventually infinite) DNA sequence of neutral sites. Consider a panmictic population of constant size $N$ with a per site mutation rate of $\mu$ where all individuals have the exact same fitness.

What is the fraction of sites that we'd expect to be polymorphic in the population (SNPs)?

Motivation behind this question

I am asking this question to verify the results of simulations I run. For example, I run a simulation with $x$ ($x$ will be varying below) neutral sites, with a per-site mutation rate $\mu = 10^{-9}$ and a population size of $N=100$. I run the simulations for 10,000 generations. There is no recombination. When the number of sites:

$x=10^3$ I get 0 SNP
$x=10^4$ I get 1 SNP
$x=10^5$ I get 3 SNPs
$x=10^6$ I get 25 SNPs
$x=10^7$ I get 238 SNPs

Is there a bug in my model or is it what we'd expect given the parameters?

In the human genome, 1 out of 300 sites are polymorphic (SNPs) (ref.). This is a frequency of SNPs that is 100 times greater than what I observe in my simulations. Note however, that the assumption of neutrality and out demographic assumptions would not perfectly hold and this result could pretty far off neutral expectation. My goal is not to reproduce something that look like the human genome but only to reproduce the neutral expectations for the moment.

The fraction of polymorphic sites that exist in a population is dependent on the biology of the organism. For instance, you would expect to find different rates of polymorphism in related plants that have different breeding systems, e.g. in Silene [1]. Past bottlenecks are also expected to decrease polymorphisms [2]. So, the answer to your question would depend on the exact species and population that you are looking at.


Finding steady state concentration given half life and production rate Intracellular molecule B is normally synthesized at a constant rate of 1000 molecules/second. The lifetime B = 200 s.

How do I find the concentration of molecule B when it is at a steady state?

I Tried:

For molecule B. P is concentration of molecule B.

2^-(dt/200) * P + 1000 * dt = P

"2^-(dt/200)" is the half life formula. I multiply it by P to give me current concentration of molecule B. Then I add 1000 * dt to give me the amount of molecule B being produced at an exact moment. Rearranging the variables:

P = (1000 * dt) / (1-2^(-dt/200))

Now I limit dt --> 0 to give me P:

lim t->0 (1000 * dt) / (1-2^(-dt/200)) =

l'hopital's rule: lim t->0 1000/ (0.005 * ln2 * 2^(-dt/200))

Plugging in dt = 0, what I get is a steady state concentration of molecule B = 200000 / ln(2).

However, the correct steady state concentration for molecule B is just 200000.

Suggestions?

tl;dr besides making this a bit harder than necessary, your main problem is that you have confused the lifetime (average time to removal of a molecule), not the half-life (time until half of the molecules are removed, which is $\ln(2)$ times the lifetime ...) Wikipedia has some formulas ...

You can translate the problem into a differential equation (not as scary as it sounds):

$$
\frac{dB}{dt} = \underbrace{1000\vphantom{\frac{1}{200}}}_{\textrm{production}} - \underbrace{\frac{1}{200} B}_{\textrm{removal}}
$$

The only tricky part here is recognizing that if the lifetime is 200 s, a fraction 1/200 of the existing molecules will be removed per second.

Now we have to solve this at equilibrium: $dB/dt =0$. We get
$$
\begin{split}
1000 - \frac{B}{200} & = 0 \\
1000 & = \frac{B}{200} \\
B = 200000
\end{split}
$$

Or you could memorize Little's Law: steady state = arrival (1000/s) $\times$ lifetime (200 s).


How exactly are nucleoli made of NORs? I read that nucleoli are made of DNA, RNA, and nucleolus organizer regions. I don't quite understand how that happens with NORs. Isn't there an envelope delimiting the nucleolus from the rest of the nucleus content? Do NORs from different chromosomes come together? I mean, they are not detaching from the rest of the chromosome and aggregating freely...

No there is no membrane that separates the nucleolus from the rest of the nucleus. The nucleolus is an aggregate of all kinds of molecules involved with ribosome assembly like: precursor and mature rRNA, Small nucleolar RNAs, rRNA-processing enzymes, ribosomal proteins and partly assembled ribosomes (but no fully functional ribosomes)

Aside from all these protein and RNA there are indeed regions of the chromosome called Nucleolus organizer regions (NORs) present in the nucleolus. These NORs are located near the tips of the short p region of chromosome 13, 14, 15, 21, and 22. During interphase these regions decondensate due to proteins like nucleolin and are thus open for transcription. Many of the protein I mentioned are needed to form or present in the aggregation that is the nucleolus.


Does neural oscillation happen at the same frequency in all parts of the brain simultaneously? Does neural oscillation happen at the same rate in all parts of the brain at a given time?

I'm trying to learn and understand about brainwaves, and I know about the various categories of brainwave. Therefore, my question is are all parts of the brain firing off at the same frequency at any given time or are some parts for example operating at a delta frequency and others operating at alpha frequency? Do different types of brainwave occur simultaneously or is always all of the brain operating at one frequency?

Neural oscillations occur on both a cellular level and on a macroscale level, the latter usually referred to as brain waves.

Looking at macroscale brain activity and particularly brain waves is often done via EEG, which has poor resolution and suffers from attenuation. EEG activation is really due to huge numbers of neurons. Hence, it represents a very coarse, averaged view of the current activity. So, even when the EEG shows nice smooth variation, the individual neurons are far from it! Of course, more recently, using other methods (e.g. fMRI) has become more common.

  My question is are all parts of the brain firing off at the same frequency at any given time or are some parts for example operating at a delta frequency and others operating at alpha frequency? Do different types of brainwave occur simultaneously or is always all of the brain operating at one frequency?

No, as I said, most studies look at the cortical areas specifically. But even within the cortex, the brain activity is very complicated, and certainly not subscribing to any one frequency. (In fact, when this hyper-synchronization happens, it is called an epileptic seizure! e.g. see Garcia-Hernandez et al, Understanding synchronization and hyper-synchronization in the the septo-hippocampal system).

In any case, imagine brain activity being measured over time. We then look at the frequency components (e.g. via Fourier analysis). See e.g. Gross, Analytical methods and experimental approaches for electrophysiological studies of brain oscillations for details. Notice these methods usually give the "strength" of the activity across the frequency spectrum. When there are brain waves, we are merely saying that activity is concentrated in a specific frequency band. It is often smeared across the band, and activity usually exists throughout the spectrum.

It also depends on spatial resolution of the frequency analysis. Some studies look at, say, just the Hippocampus. So yes, it is quite possible for some of the brain to operate at one frequency, while others operate at another. Or one could average over the whole cortex. It depends on the study!

So pretty much in all cases, everything is more heterogeneous than you might think.

Some literature to read:

Breakspear, Dynamic Models of Large-Scale Brain Activity
Varela et al, The Brainweb: Phase Synchronization and Large-Scale Integration
Salinas et al, Correlated Neural Activity and the Flow of Neural Information


Pressure change in atria Background:It is said that during the phase of isovolumetric contraction , due to sharp rise in the ventricular pressure, there occurs bulging of AV valves into the atria producing a small but sharp rise in the intra-atrial pressure called c-wave.( in the second cycle of diagram).

Question: I am unable to understand why is then pressure in atria falling after the end of isovolumetric phase, even though the pressure in the ventricles is rising, so this should further bulge the AV valve or atleast( due to action of papillary muscles) have same pressure, So why is pressure falling?

The curve you are talking about is JVPJuglar Venous Pressure Curve.
You are talking avoit x-decent after c pulse.
The downward deflections of x decent is produced by the atrium relaxation and the downward movement tricuspid valve.
This causes decrease in atrial pressure.
A new fascinating question could be why x-decent is greater than y-decent.
Good luck.


How to wash the column during protein purification with GST tag? I have been working with GST tagged proteins for the last 4 years and after loading the cell lysate into the column I was washing it with 20-30 column volumes of PBS and sometimes my proteins were eluted very pure sometimes with a lot of impurities.

A few times I tried washing with NaCl gradient (0-400 mM) but later decided not to do that because it may denature the protein and some of my proteins may not refold.

What do you suggest for washing step?

Note: I don't have any UV detector to see the washouts/flowthroughs/elutions.

The standard when purifying GST with Glutathione agarose beads is to use STE buffer (10 mM Tris-HCl (pH 7-7.5), 150 mM NaCl and 1 mM EDTA) for washes and we have had no problem with this in our lab!


Possible to get Furniture carpet beetle specimen for collection? I was wondering if anyone knows how it'd be possible to get a Anthrenus flavipes (or furniture carpet beetle) specimen for my collection?

I can't find a source anywhere online, only the dermestid beetles used to clean skulls and such. Any help would be appreciated!

Bump

You might try calling up a local exterminator (ideally not a franchise) and asking them to save you a specimen the next time they are called out to deal with such insects. Donate some beer/weed/customer referrals by way of thanks and they'll help you out with future specimen hunts.


How does SDS-PAGE separate based on mass? In SDS-PAGE, electric field and mass-to-charge ratio are approximated to be constant for all proteins. Also, if $F=qE =ma$, then $\frac{m}{q}a=E$.
Thus, all proteins must migrate with a constant acceleration.
So what is the driving force in SDS-PAGE that resolves proteins of different mass? Is it that bigger proteins have a larger size and thus experience larger friction force from the gel sieves? But even if that was true the larger proteins feeling larger resistance forces should be counteracted by their larger migrating force from increased total charge.
Would appreciate if someone could clear up this confusion. Thank you.

You are correct that molecule mobility depends on the mass-to-charge ratio, and this means that different sized molecules with the same $\frac{m}{q}$ will have the same acceleration.  However, the velocity of a molecule moving through a gel matrix depends on the point at which the force exerted by the electric field is in equilibrium with the frictional forces acting on the molecule.  Modeling different sized molecules as spheres of different sizes, we can apply Stokes' Law

$F = 6\pi \mu Rv$

where $\mu$ is viscosity of the matrix (constant), $R$ is the radius of our molecule, and $v$ is the flow velocity.

Rewriting your equation, we see that

$F = qE = ma = 6\pi \mu Rv$

and

$v = \frac {ma}{6\pi \mu R}$

For constant $a$ and $\mu$, we see that velocity varies with the ratio of mass to radius

$v \sim \frac{m}{R}$

For our model spheres, assuming uniform density, radius scales cubically with mass, meaning that $\frac{m}{R}$ decreases as molecule size increases.

($d = \frac{m}{V}$ and $V = \frac{4}{3}\pi R^3$ where $d$ is density and $V$ is volume)

So, larger molecules will reach force equilibrium with the opposing frictional resistance at a lower velocity compared to smaller molecules, thus explaining how different sized molecules with the same $\frac{m}{q}$ will separate on a gel.  One caveat to this explanation is that polypeptides and nucleic acids are poorly modeled by spheres, and that the mass of such molecules scales linearly with length.


What kind of mushroom(?) is this? I found groups of these growing in the Lassen National Forest (Susanville, CA, USA). It looks like some sort of mushroom. I have Googled extensively, but can't seem to find a match.

Found it. It's a Sarcodes or snow plant:
http://en.wikipedia.org/wiki/Sarcodes


Is spiders building webs on plants an example of mutualism or commensalism? In one section of the GED study book I'm looking through to prepare myself for exams, they define parasitism, mutualism, and commensalism, and give examples.

One of the examples they give for mutualism is ants living in an acacia tree. The ants get a home, and they defend the tree.

One of the examples they give for commensalism is a spider building a web on a plant.

Is this actually an example of commensalism? This seems more like mutualism to me. The spider benefits from being able to put its web somewhere, and the plant benefits from protection from bugs (as the spider's web will catch them).

Is this relationship an example of commensalism or mutualism?

You're thinking too broadly and rigidly about these concepts -- both commensalism and mutualism are types of interspecific interactions.

Commensalism is when one species in a given interaction is benefited while the other is neither benefited nor harmed. In a mutualistic interaction, both species benefit from their interaction with each other.

Like any interaction between two organisms, these interactions can vary between individuals. Although some species pairs will consistently undergo the same type of interaction (e.g., shark and prey -- predation), some groups of species may vary in their paired interactions. This variation may result from two different scenarios:

Variation in interaction type between different species within a taxonomic group

E.g., one type of spider catches insects that don't harm the plant -- commensalism -- while another spider species catches insects that would harm the plant -- mutualism. In other words, not all spider-plant interactions are the same, and the interaction type may be dependent on the species involved.

Variation even from the same individual in different circumstances.

E.g., A spider catches an insect that doesn't eat the plant it's growing on (commensalism) but at another time it catches an herbivorous insect that does eat the plant the spider has built its web on (a mutualistic behavior). In this scenario, the interaction type between the same two species (even the same individuals) can vary based on circumstances.

Put differently, commensalism, mutualism, etc. are not behavioral traits, but interactions, and so are dependent on not only the species involved but the circumstances as well.

Note: To further complicate things, each given interaction can be qualified in various ways. For example, from Wiley ELS:

  Positive interactions can be trophic and nontrophic, can act directly or indirectly (mediated by a third species) and can be symmetric (species have equal effects) or asymmetric (species have unequal effects).


Possible? When a pregnant woman suffers an organ damage, fetus would send stem cells to the damage organ to help repair it? I am quite sure that there is this blood-placental barrier between the mother and the baby so that nothing (except a type of antibody) can pass through it.

But I remember reading somewhere that when a pregnant woman suffers an organ damage, fetus would send stem cells to the damage organ to help repair it.

Anything to support that?

Fetal RNA - mRNA and microRNA - has been detected in maternal blood as shown in this report. Here's a second report showing how fetus gives back to repair the maternal myocardium - fetal cells traffic to an injured maternal myocardium and undergo cardiac differentiation.


Are all Autoreceptors Downregulated by their Respective Endogenous Ligands? I know that the 5-HT1A and $\alpha$2 adrenoreceptors receptors serve as autoreceptors for serotonin (5-HT) and norepinephrine respectively and are down-regulated by repeat exposure to their respective ligands, it's believed that this is likely the cause for the therapeutic delay in the actions of antidepressants that target the serotonergic and noradrenergic systems.  My question is this: "Is this the case for all autoreceptors? Are all autoreceptors down-regulated by the actions of their respective ligands?"

Autoreceptors - are receptors of the presynaptic terminal.
α2 adrenoreceptors receptors are down-regulated due to repeated exposure.

Pharmacodynamic tolerance begins when the cellular response to a substance is reduced with repeated use. A common cause of pharmacodynamic tolerance is high concentrations of a substance constantly binding with the receptor, desensitizing it through constant interaction

This is a common occurrence - not just for autoreceptors but receptors in general.
But for your interest here is one for dopamine autoreceptors (Pay-wall).