All UniprotIDs of a cancer pathway I need to download all uniprotIDs of a cancer pathway, say the AKT Signaling. It may be super easy, but I don't know which resource to look at since it is a new field.

How/where do I find these?

I would do this through the Reactome database. Searching for "AKT Signalling" returns, among other things, an entry for PI3K/AKT Signaling in Cancer (Homo sapiens) (REACT_147723). Clicking on that link will take you to the pathway's page, and if you click on "Disease" (under "Locations in the PathwayBrowser"), you will be shown a link to the pathway browser page of that particular pathway.

Once there, click on the "Molecules" tab, select "Proteins" and you will get a list of the proteins involved in the pathway and their UniProt accessions. There, you can click on the "Download" link and retrieve this list:

MoleculeType    Identifier  MoleculeName
Proteins    P31751  UniProt:P31751 AKT2
Proteins    P31749  UniProt:P31749 AKT1
Proteins    Q9Y243  UniProt:Q9Y243 AKT3
Proteins    P16220  UniProt:P16220 CREB1
Proteins    Q12778  UniProt:Q12778 FOXO1
Proteins    P98177  UniProt:P98177-2 FOXO4
Proteins    O43524  UniProt:O43524 FOXO3
Proteins    P98177  UniProt:P98177-1 FOXO4
Proteins    O15530  UniProt:O15530 PDPK1
Proteins    Q92934  UniProt:Q92934 BAD
Proteins    P46527  UniProt:P46527 CDKN1B
Proteins    P38936  UniProt:P38936 CDKN1A
Proteins    Q00987  UniProt:Q00987 MDM2
Proteins    P60484  UniProt:P60484 PTEN
Proteins    Q8WWG1  UniProt:Q8WWG1 NRG4
Proteins    P10721  UniProt:P10721 KIT
Proteins    Q9HCT0  UniProt:Q9HCT0 FGF22
Proteins    P15498  UniProt:P15498 VAV1
Proteins    P05230  UniProt:P05230 FGF1
Proteins    Q15303  UniProt:Q15303-1 ERBB4
Proteins    P08620  UniProt:P08620 FGF4
Proteins    P42338  UniProt:P42338 PIK3CB
Proteins    O14944  UniProt:O14944 EREG
Proteins    O15520  UniProt:O15520 FGF10
Proteins    P21802  UniProt:P21802-3 FGFR2
Proteins    Q13480  UniProt:Q13480 GAB1
Proteins    P55075  UniProt:P55075-1 FGF8
Proteins    O00459  UniProt:O00459 PIK3R2
Proteins    Q9UEF7  UniProt:Q9UEF7-1 KL
Proteins    P09619  UniProt:P09619 PDGFRB
Proteins    Q8WU20  UniProt:Q8WU20 FRS2
Proteins    Q86Z14  UniProt:Q86Z14 KLB
Proteins    O00329  UniProt:O00329 PIK3CD
Proteins    P11487  UniProt:P11487 FGF3
Proteins    Q9GZV9  UniProt:Q9GZV9 FGF23
Proteins    P42336  UniProt:P42336 PIK3CA
Proteins    P42081  UniProt:P42081 CD86
Proteins    P35568  UniProt:P35568 IRS1
Proteins    P04626  UniProt:P04626 ERBB2
Proteins    Q02297  UniProt:Q02297 NRG1
Proteins    P12034  UniProt:P12034-1 FGF5
Proteins    P56975  UniProt:P56975 NRG3
Proteins    Q9NP95  UniProt:Q9NP95 FGF20
Proteins    Q02297  UniProt:Q02297-10 NRG1
Proteins    P22607  UniProt:P22607-2 FGFR3
Proteins    P21802  UniProt:P21802-1 FGFR2
Proteins    Q15303  UniProt:Q15303-2 ERBB4
Proteins    P62993  UniProt:P62993-1 GRB2
Proteins    O60258  UniProt:O60258-1 FGF17
Proteins    P11362  UniProt:P11362-1 FGFR1
Proteins    P15391  UniProt:P15391 CD19
Proteins    Q9Y4H2  UniProt:Q9Y4H2 IRS2
Proteins    Q99075  UniProt:Q99075 HBEGF
Proteins    P21583  UniProt:P21583-1 KITLG
Proteins    P31371  UniProt:P31371 FGF9
Proteins    P27986  UniProt:P27986 PIK3R1
Proteins    P22455  UniProt:P22455 FGFR4
Proteins    P04085  UniProt:P04085-2 PDGFA
Proteins    P06241  UniProt:P06241 FYN
Proteins    P01127  UniProt:P01127 PDGFB
Proteins    P21802  UniProt:P21802-5 FGFR2
Proteins    Q06124  UniProt:Q06124 PTPN11
Proteins    P21781  UniProt:P21781 FGF7
Proteins    O95750  UniProt:O95750 FGF19
Proteins    P21860  UniProt:P21860-1 ERBB3
Proteins    O14511  UniProt:O14511 NRG2
Proteins    P01133  UniProt:P01133 EGF
Proteins    O76093  UniProt:O76093 FGF18
Proteins    P21802  UniProt:P21802-18 FGFR2
Proteins    O43320  UniProt:O43320 FGF16
Proteins    P04085  UniProt:P04085-1 PDGFA
Proteins    P10767  UniProt:P10767 FGF6
Proteins    P06239  UniProt:P06239 LCK
Proteins    Q92569  UniProt:Q92569 PIK3R3
Proteins    Q6PIZ9  UniProt:Q6PIZ9 TRAT1
Proteins    Q9UEF7  UniProt:Q9UEF7-2 KL
Proteins    P35070  UniProt:P35070 BTC
Proteins    P16234  UniProt:P16234 PDGFRA
Proteins    P33681  UniProt:P33681 CD80
Proteins    P22607  UniProt:P22607-1 FGFR3
Proteins    P09038  UniProt:P09038 FGF2
Proteins    P10747  UniProt:P10747 CD28
Proteins    P00533  UniProt:P00533 EGFR
Proteins    P55211  UniProt:P55211 CASP9
Proteins    P22736  UniProt:P22736 NR4A1
Proteins    Q6ZVD8  UniProt:Q6ZVD8 PHLPP2
Proteins    O60346  UniProt:O60346 PHLPP1
Proteins    Q9UKV8  UniProt:Q9UKV8 AGO2
Proteins    Q9HCE1  UniProt:Q9HCE1 MOV10
Proteins    Q9UPQ9  UniProt:Q9UPQ9 TNRC6B
Proteins    Q9HCJ0  UniProt:Q9HCJ0 TNRC6C
Proteins    Q9UL18  UniProt:Q9UL18 AGO1
Proteins    Q8NDV7  UniProt:Q8NDV7 TNRC6A
Proteins    Q9H9G7  UniProt:Q9H9G7 AGO3
Proteins    Q9HCK5  UniProt:Q9HCK5 AGO4
Proteins    Q96RU7  UniProt:Q96RU7 TRIB3
Proteins    Q5T1C6  UniProt:Q5T1C6 THEM4
Proteins    Q96B36  UniProt:Q96B36 AKT1S1
Proteins    P49841  UniProt:P49841 GSK3B
Proteins    P49840  UniProt:P49840 GSK3A
Proteins    O15111  UniProt:O15111 CHUK
Proteins    Q9BPZ7  UniProt:Q9BPZ7 MAPKAP1
Proteins    Q6R327  UniProt:Q6R327 RICTOR
Proteins    Q9BVC4  UniProt:Q9BVC4 MLST8
Proteins    P42345  UniProt:P42345 MTOR
Proteins    Q9UBS0  UniProt:Q9UBS0 RPS6KB2
Proteins    P49815  UniProt:P49815 TSC2


Do RBCs need oxygen? How do our red blood cells (RBCs) get oxygen? Do they even need it? They have no nucleus and no organelles, so I think they don't need it.

Erythrocyte metabolism is unique in that the mature erythrocyte
  contains no mitochondria and therefore no Krebs cycle! Instead the
  energy needs of the RBC are met largely (95%) by anaerobic glycolysis
  in the two pathways: Embden-Meyerhof + Hexose-monophosphate.

+

Virginia University source


How does toluene inhalation damage the brain? We just had a discussion about toluene abuse. It is known, that people inhaling toluene for a long time have significant brain damage, including  decreased intelligence.

I found that toluene is a lipid solvent, and that it can damage the myelin. However, myelin is only present in the white matter, but intelligence is related to the grey matter which does not contain myelin.

Is there any indirect damage, or did we miss some important point in this case? Second, how does toluene get to the brain? Is it able to infiltrate from the nose through the mucous membrane, or is it carried in the blood? I am just curious.

After crossing the blood-brain barrier, toluene, along with other volatile anesthetic agents, had been previously thought to inhibit neuronal transmission by causing a change in membrane or membrane protein conformation. Recent research has shown that interactions with several key brain neurotransmitters, mainly γ-aminobutyric acidA (GABA), to a lessor degree glycine, and possibly dopamine, are responsible for the clinical effects seen. Postmortem studies along with magnetic resonance imaging (MRI) findings have shown diffuse white matter demyelination and gliosis (solvent vapor/toluene leukoencephalopathy), which is postulated to be the end product by which chronic toxicity occurs, although the exact mechanism by which this occurs remains unclear

(McKeown at al. Toluene Toxicity).


Are Nilaparvata nymphs winged? Source: nbair.res.in

I'm wondering if the first individual on the left is a nymph. Even if not do Nilaparvata sp have wings in nymphal stage?

I'd appreciate any authentic source for reference.

The family-level identification I had given I now see was unnecessary; the Wikipedia site for an economically important member of the genus (there called the Brown planthopper) is here: https://en.wikipedia.org/wiki/Brown_planthopper.  The species covered there has long- and short-winged forms; other members of the genus are probably similar.  All of the individuals in the photograph above are adult.  A late-instar nymph will have wing pads (not yet wings) which are fused to the thoracic segment to which they're attached (a life-cycle diagram with drawings of two nymphal instars -- there are probably more -- is found here: http://www.cpsskerala.in/OPC/pages/ricePestbrownplant.jsp [the eighth slide]).
 So nymphs and short-winged adults won't be flying out of danger -- they'll be hopping away.


Explaining the simpson's diversity index In my biology class, we were trying to compare the biodiversity of two site. In doing so, we were instructed to use the Simpson's Diversity index as follows:

$$ \frac{\sum_i n_i (n_i - 1)}{N (N - 1)}$$

Where $n_i$ is the total number of organisms of a particular species; and, $N$ is the total number of organisms of all species.

We were given a method to calculate the index in a class that required almost naught mathematical understanding for the purposes of the experiment. From what I have read, the Index calculates the probability that any 2 randomly selected organisms belong to the same species, and it is thought that the closer the result is to zero, the more diverse the region is.

What I can't understand, is the math behind the index; for example: why is it multiplying n by n-1? And how is this better than dividing the sum of all the organisms by the number of species?

I'm in Pre-Cal, so when explaining, please do so with minimum emphasis on "advanced" math terms.

That's an estimator for Simpson index,
$$ \sum_i p_i^2 $$
where $p_i$ is the probability that $i$-th species is sampled.
This is sum of the probability that two independent samples are from the same species.
There are multiple ways of estimating this quantity from observations $n_i$.

When $n_i$ is small,
$$\hat{p} = \frac{n_i}{N}$$
is unbiased but has high variance, and plugging it in $\hat{p}$ to the definition would also have high variance. (Note that this is equivalent to sampling with replacement.)

If one uses sampling without replacement formula,
$$\hat{p^2} = \frac{n_i}{N} \cdot \frac{n_i-1}{N-1}$$
then, the resulting estimator is
$$ \sum_i  \frac{n_i \cdot (n_i - 1)}{N \cdot (N - 1)}$$

Note that both estimators converge to Simpson index for $N \to \infty$.
But of course, there aren't infinite number of samples, usually.


A better definition of ‘evolution’? Occasionally on this site I’ve noticed the following definition of evolution being given:

  Evolution is a change of allele frequency through time in a population

( For example, from here)

Recently the following (From here):

  The statement "evolution is driven by mutations" is very misleading if not simply wrong. Just have a look at an intro course to evolutionary biology!

  In short, evolution is a change of allele frequency over time.

But mutations are important to evolution, and I feel must be included in the definition.

Here’s why that concerns me:  One group of evolution deniers, and others like them, use comments like these above to try and show a weakness in evolution.
See:
http://creation.com/don-t-fall-for-the-bait-and-switch

With comments like:

  “It is a bit of a trick played by using sloppy language. Evolutionists use adaptation, which is observed, to support evolution, which is an entirely different process. It is an example of bait and switch.”

Also:

  “Next time someone says that evolution is an observed scientific fact make sure you get them to clearly define what they are talking about.
  They will almost certainly be referring to adaptation but want you to believe they have proved evolution.
  Don’t be fooled. Sloppy language leads to sloppy thinking.”

Ok, I hate to give them ‘air-time’ by posting that, but perhaps it will cause us to clarify ourselves better.  Answers like "a change of allele frequency through time" just end up feeding right into this kind of evolution-denial.

SO, here’s my question  Since there’s a lot people here smarter than me:  Can someone please offer up a stronger definition of evolution than just ‘a change in allele frequency over time’?

In researching answers I found this on Berkeley’s site:

  “Biological evolution, simply put, is descent with modification. This definition encompasses small-scale evolution (changes in gene frequency in a population from one generation to the next) and large-scale evolution (the descent of different species from a common ancestor over many generations).”

I like that it goes beyond small-scale (which these others would just call adaptation).  But this doesn't mention natural selection, and mutations; which I feel are important distinctions given the kind of comments these deniers make. Is there a reason Berkeley's definition didn't include those distinctions?

EDIT:  Can someone explain the down-vote?  I followed everything outlined under How to ask a good question

The focus upon definition of term is a rhetorical strategy often employed to confuse the issue, especially by laity when discussing technical matters. Word meaning and use are easily a source of ambiguity, confusion, contradiction and such that the appeal to the dictionary definition is often an appeal to false authority. At the very least it is worth pointing out that aside from etymology and morphology, empirical disputes are not settled by consulting Merriam-Webster.

"Evolution" is a fairly general concept and it can be useful when discussing technicalities to specify "biological evolution".  For example, "water" might mean specifically "H2O" or generally "clear, odorless, tasteless liquid"  or possibly might be used without qualification in distinguishing "potable water" from ocean water, et cetera.

Consider that the definition of term is not so much the pertinent legacy of biological evolution (pace Darwin, Wallace et. alii). The kind of explanation biological evolution uses is it's hallmark. In particular, biological evolution removed teleology (the study of purpose)) from biology.

For example:

A teleological explanation of biology:
1) This plant is photosynthesizing in order to survive.
2) This plants species is surviving.

A biologically evolutionary explanation of species:
1) This plant is photosynthesizing
2) Plant species which photosynthesize have an increased likelihood of survival.

Note that survival is still at play, but the argument is no longer circular. This is not to say that cause has been cited, however, the logical structure of the argument no longer "begs the question"


Where do I purchase this Trypsin? I am currently on the lookout for Trypsin, but I have some trouble finding something that is fairly cheap, ships to Europe and is equivalent to this Trypsin:

http://www.emsdiasum.com/microscopy/products/chemicals/tannic.aspx#22200
Trypsin powder 1:100 from Porcine Pancreas, 25g
Activity >100 NF units/mg
Used for whole cell preparation

I've found Trypsin on Sigma:

http://www.sigmaaldrich.com/catalog/product/sigma/t4799
Trypsin powder from Porcine Pancreas
Activity 1,000-2,000 BAEE units/mg
Suitable for cell culture

However I am not sure how to compare the activity between the two types and ultimately which concentration I should then use in my experiment if I go with the Sigma one (the protocol I am following uses the EMS Trypsin in a 1g:100ml fashion).
Can anyone shed some light on this? Or perhaps show me the way to some affordable Trypsin that can be shipped to Scandinavia?

Cheers!
/Patricia

*The trypsin will be used for diaphonization (see comment)

According to Sigma-Aldrich,

  1 USP Unit = 3.0 BAEE Units
  1 NF Unit = 1.1 USP Units

So 1 NF unit is roughly equal to 3.3 BAEE units. You can then directly compare the two trypsin powders, since they are preparations of the same enzyme.


circular pattern of mold on quince Could someone explain why mold on my quinces grows in well separated circles around a center? To make clear, what I mean I post the picture

Looks like you may have Monilinia fructigena, brown rot, or at something similar (possibly also called brown rot, but from a different species). This pattern isn't special to quince, but to this fungus.
The formation of these rings is called "zonation", and the concentric rings are from areas of growth that are primarily spore-forming versus not.
Hall (1933) gives an extensive description of the different factors necessary for observing this growth pattern, but ultimately the key factor is light. Patterns of light-and-dark conditions while the fungus spreads causes alternating phases of growth, with one phase comprised of more sporulation.
Another source: https://www.cabi.org/isc/datasheet/34747

Byrde, R. J. W., & Willetts, H. J. (2013). The brown rot fungi of fruit: their biology and control. Elsevier.
Hall, M. P. (1933). An analysis of the factors controlling the growth form of certain fungi, with especial reference to Sclerotinia (Monilia) fructigena. Annals of Botany, 47(187), 543-578.


What is the P in LogP? How does this value actually get calculated?
Logarithms are usually written as
log(base 10) of x
So what is the 'P' equivalent of 'base 10'? I know it stands for octanol/water, but what does that actually mean in a computational context?

I've found many explanations of LogP online, but they usually just say the same thing, which is what LogP is used for. How does one actually calculate it?

Sorry if this is a ridiculously simple question. Bridging the gap between chemistry and math is not my strong suit.

It means the following:

$$\log P = \log(P) = \log_{10}(P) = \log_{10} \left(\frac{C_{\mathrm{octanol}}}{C_{\mathrm{water}}} \right) $$

With $C_{\mathrm{octanol}}$ being the concentration of the solute in 1-octanol and $C_{\mathrm{water}}$ the concentration of the solute in water.


How to form biological metallic tissue? There are numerous popular articles claiming that the wasp Apocrypta Westwoodi Grandi features an ovipositor tipped with zinc. You can find such an article here. You can watch an impressive video here. Beyond that, I have found information on the genus to be sparse.

Yet my question is, how metallic tissue can be formed. The popular article claims actual zinc was detected. It seems unlikely to me, these creatures consistently find a source of zinc to feed from, so as to deposit zinc in their tissue. Even so, I don't understand how this zinc can be made to deposit at a specific point. The article clarifies:

  With an x-ray detector and the electron microscope, they discovered the presence of zinc. It was only on the tips of the parasitic fig wasp’s ovipositors. Gundiah said, “We see it very consistently only at the tip and not anywhere else.”

I am no biologist, but, to my feeble understanding the only alternative is that the so called zinc is actually synthesised by the body as a protein normally is. Surely no atomic reactions could take place in the wasp! :-p  Even teeth are mostly Ca5(PO4)3 OH, Calcium is found in plenty of our foods. Phosphorus is present in meats. But zinc? I totally don't understand it!

First and foremost, it looks like the original article is slightly less dramatic:

  Parasitoid ovipositor tips have a higher content of the transition metal zinc compared with the cuticle elsewhere on the ovipositor

So a 'higher concentration' isn't quite the same as 'tipped with'. It looks like they are describing a higher numbers of metal ions, rather than pure metal:

  The presence of transition metals in insect cuticle and mandible is hypothesized to increase material hardness to permit cutting through hard substrates with minimal wear

There are many examples of organisms using inorganic chemistry to make materials. The overall topic is called biomineralization and you even mention teeth - which is hydroxyapatite (not really organic chemistry!).

However, a pure metal like zinc is unusual, I think. There are examples such as the snail that has an iron pyrite 'armor' or even the iron nanocrystals in ferritin.

More spectacular examples include the bacteria that produce gold particles

  As a result, Au
  detoxification is mediated by a combination of efflux, reduction, and
  possibly methylation of Au-complexes, leading to the formation of
  Au(I)-C-compounds and nanoparticulate Au0.

Where Au0 is pure gold. I don't know of any other examples of pure zinc in organisms, but there is a nice review here of zinc biochemistry.

When you say 'synthesise' I assume that you mean 'deposit'.


Intracellular lipid transport I know that lipids are carried around the body in the blood either as micelles or by lipid-binding proteins which allow them to be solved.

Lipids can't always be integrated in a membrane though, the phospholipids used in membranes have to be synthesised somewhere from a precursor which will also by hydrophobic.

Consequently, at some point there will have to be transport of lipids within the cell where the lipids will need to be in solution. How is this facilitated?

Like in the blood, intracellular lipid trafficking is facilitated by vesicular transport and lipid carriers like fatty acid binding proteins. In addition, intracellular membranes are densely packed and they can exchange lipids by collision and transient hemifusion. If you have access to Cell, a good review is from Prinz W. 2010 Lipid Trafficking sans vesicles, Where, Why, How?


When did the most recent common ancestor of all living domestic dogs live? Wikipedia provides a very detailed page on the origins of the domestic dog, but this fact does not seem to be present there. Google searches for terms such as "most recent common ancestor (MRCA) of dogs" didn't reveal any authoritative sources.

From the wikipedia article you linked:

  The origin of the domestic dog (Canis lupus familiaris or Canis familiaris) is not clear. Whole genome sequencing indicates that the dog, the gray wolf, and the extinct Taymyr wolf diverged at around the same time 27,000–40,000 years before present.

They cite Skoglund et al. 2015.

It seems that divergence between the grey wolf and the dog started at Taymyr (northern Russia) about 27,000–40,000 years ago. Therefore, the MRCA of all dogs and grey wolf today would have lived about 27,000–40,000 years ago. Tito et al. 2013 estimated canids fossils found in Europe were 39,000 years old. We currently don't have a better accuracy and we are not able to date the MRCA of all dogs with more accuracy than the MRCA of grey wolves and dogs.


Forgot to vortex antibody before staining Ugh. Did an immunofluorescence experiment last weekend, forgot to vortex both my primary and my secondary antibody solutions.

And my final result looks dimmer than it should be. Is it possible that not vortexing contributed to this?

I guess the question is, is vortexing really necessary? It would come down to the fluid dynamics. How long does it take for a drop of antibody to reach equilibrium in a 1000µL Eppendorf tube? Is it really more than just a few seconds? Is vortexing really necessary?

It depends on how much time elapsed between adding the concentrated antibodies to the diluting solution and adding the diluted antibodies to the slide. If it was just a couple of seconds, then I can abolutely see there being a difference. Even if it was longer - say 30-90 seconds, even - there potentially could be antibody gradients in the solution without vortexing. There are a few reasons why. First, many unconjugated primary antibodies that are not intended just for immunostaining are provided in a glycerol solution, with concentrations ranging from 10% or so up to 50% or more, sometimes in addition to a carrier protein like BSA (I used to work for a well-known antibody company, and theirs are in 50% glycerol with 10 µg - 2 mg BSA per ml, depending on the antibody type). The glycerol prevents the solution from freezing solid at -20°C, eliminating ice crystal formation, protecting the antibody protein from degradation and allowing for longer storage times without loss of activity. As a result, however, the solution takes longer to solubilize in PBS or whatever diluent you're using on its own, with no additional mechanical activity.

On the other hand, even if the primary (or secondary) antibody is simply formulated in PBS, the equal diffusion of the proteins to all parts of the tube can take some time. As an experiment, put 1 ml of PBS in an Eppendorf tube, then add perhaps 10-50 µl of a dark dye, such as methylene blue, bromphenol blue, or Trypan blue. Watch it dissociate into the solution over time against a solid white background like a piece of paper. While none of these have the exact same solubility profile as antibodies, it's good enough to show you what happens over the first 30 seconds or so until you can't distinguish the dye anymore.

So, always vortex, even if it's at a relatively slow speed, for a couple of seconds to ensure everything is evenly distributed.


Is evolution true as Darwin said? I was telling the theory of evolution to my friends. But they asked me for the proof. They said, we are not seeing any such transition species at present. Neither we have such evidence for evolution. What should I do? I saw many proofs like archaeoptaryx, but now it has been proved that it is fully functional bird and others are also not supporting the theory of evolution given by Darwin!

I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.

It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.

1) Do individuals reproduce?

The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.

2) Is there variation among individuals?

Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.

3) Do some individuals die before they get to reproduce?

Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.

4) Do offspring resemble parents?

The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.

5) Does heritable variation lead to differences in reproductive success?

If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.

Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.

Speciation:

It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.

I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).

What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.

In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).

One of the absolute classic examples is an experiment using fruit flies by Diane Dodd.   In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/


Why do I want to urinate when I touch water? I've noticed that whenever I come in contact with running water (especially when I do my dishes), I have a desire to urinate. A quick Google search (link,link) gave me few different hypotheses:

Cold diuresis. Being in contact with cold water reduces temperature on the skin, which then constricts blood vessel to reduce heat loss, thereby increasing blood pressure and prompting the bladder to release excessive fluid.
Afferent innervation. I wasn't able to comprehend all the details of the process, but it seemed like this hypothesis is pertaining to the nervous system than circulatory system, hence different from first hypothesis.
Learnt psychological response. Second article linked above argues that this is a conditioned reaction, where even the sound of tap water triggers the desire to urinate. While it did not mentioned specific details of how this happens, I'm also assuming that this hypothesis is different from aforementioned hypotheses, because this hypothesis sounds more like a psychological response than biological reaction.

Which one of these hypotheses accounts for the desire to urinate when in contact with water? How exactly does it happen? If there is any other reason, feel free to add in the answer.

FIRST PART:
I am writing this answer with an analogy.I have analogised your question to a childhood habit developed by our mothers-when she would want us to urinate all she had to do was to take us to the toilet and make a "siiii" "siii" sound to mimic the sound of running water(more or less)
Since I have analogised in that way I think the third hypothesis (referred in your question)is more apt.
SECOND PART:
What fascinated me more about your  question was your comment-"I'll also be interested to see why the people will learn to have desire to urinate at the sound of tap water. Is there any reason that for that? – Hosea Jul 14 "
Indeed there is because we still have our mirror neurons
[SOURCE]
What I wanted to understand is if mirror neurons contributed to Pavlovian reflexes.The answer was yes
Furthur I could find out from sources that the micturition process has centres in the brain stem which are controlled by higher centres in the brain.One of them was the "medial frontal cortex".
Read the following article:

The Pontine micturition center (PMC, also known as Barrington's nucleus) is a collection of neuronal cell bodies located in the rostral pons in the brainstem involved in the supraspinal regulation of micturition. When activated, the PMC relaxes the urethral sphincter allowing for micturition to occur. The PMC coordinates with other brain centers, including the medialfrontal cortex, insular cortex,hypothalamus and periaqueductal gray(PAG). The PAG acts as a relay station for ascending bladder information from the spinal cord and incoming signals from higher brain areas.[source]

From the outline in the following lines I could conclude that there are mirror neurons in this region which 'may' be involved in the micturition control:

Yoshida et al. [26] recently recorded from neurons in the medial frontal cortex, some of which selectively responded to self or observed actions within a social context
[source]

Although research has confirmed that mirror neurons contribute to Pavlovian reflexes no such pathway has yet been discovered which can directly help us to confirm  and understand its relation to urination urge in contact with water.


Why are the human knees and elbows bent in an opposite direction I can assume that the hands used to be the same as legs. And they got weaken, and changed direction when human started to walk on two?
Also why do the hand palms facing the body and not facing down like the feet?

I am no expert on comparative anatomy, but I will give this a shot. Please edit if you know more about this subject!

The configuration of opposing elbow and knee joints is a feature we humans share with large group of mammals. For example, below is an image of a shrew skeleton.

Opposing joints are course a major feature of mammalian anatomy, and there are many studies on its functions and advantages. Among other things, this configuration allows for characteristic gaits of mammals such as the gallop of a horse, and it allows mammals to rest with legs protected under their body. See this page for some basic information.

Neil Shubin's book Your Inner Fish on human evolution also discusses the opposing joints arrangement, noting that this is a "key feature that gives us the capacity to walk, one we share with other mammals". A preview of the book is here.

A quick literature search turns up many technical articles on this subject, such as this review series. I'm afraid the details are beyond me (again, experts please edit), but I think it's fair to say that there is plenty of evidence for advantages of this joint arrangement in mammals.


Software recommendation for protein in electric field modeling? I'd appreciate a suggestion for software to compare models of two proteins in an alternating electric field. The more detail, or perhaps direction towards an existing and similar paper, the better. Right now I'm particularly interested in comparing rotation of the proteins as a result of the field. The first protein, tubulin (1TUB), will be modeled as a dimer while the second, septin (2QAG), will be modeled as a trimer.

The electric field will consist of a 200Khz field at 1.5V/m with a spatial resolution of 300Ax300Ax300A. I believe that I will only need a temporal resolution of 1.5 milliseconds for 10 solutions(?) per cycle for 3 cycles in the 200Khz field (particularly unsure of this part).

In terms of computational power I have access to two 7870 Radeon GPUs, but am also interested in cloud computing if that's not enough.

MD
Broadly this could be attempted with Molecular Dynamics simulations. As you discovered in your search, one of the most popular softwares is free: GROMACS. This is an atomistic approach to the problem. It also has many electrostatic parameters.
I would point out that generally MD requires careful and robust methods and often an expert lending hand if the results are to be trusted. In order to do MD at the timescales for observing rotating molecules in the field, massive amount of HPC computational time will be required. This is a full blown project to get it to an appropriate level for publication.
This is computationally intensive.
Quick Electrostatics
If a HPC is not available to you then MD may not be an option. If all you want to do is visualise the location of the charge and make qualitative predictions or visualisations, PyMol and ABPS might be a quicker combo. It is also good for quantitative analysis, but obviously is a static model.


What is the minimum length required for a circular DNA ligation? What is the minimum length of a DNA molecule for the ends to come in close enough contact that they can ligate. Assume there are free divalent cations in solution. Does anyone have any idea?

I stumbled across this paper demonstrating it is between 150-200 base pairs.

DNA flexibility studied by covalent closure of short fragments into circles
D Shore, J Langowski, and R L Baldwin
PNAS 1981 78 (8) 4833-4837

http://www.pnas.org/content/78/8/4833.full.pdf


Amount of neurons in the heart Finding numbers for the amount of neurons in the brain is quite easy. Finding them for other human organs is harder. How many neurons are there in the human heart?

In terms of cell bodies? Zero.  There are autonomic projections from the spinal cord (sympathetic) and vagus nerve (parasympathetic) to the sinoatrial node, the atrioventricular node, and at discrete points in the atria and ventricles.


What is meant by 'genes overlapping inherited structural variants'? I am reading a journal paper about genes that are related to autism, and I have come across the following statement:

To assess commonality of biological function among rare risk alleles,
we compared functional knowledge of genes overlapping inherited
structural variants in idiopathic ASD subjects relative to healthy
controls

I am not sure what is meant by 'genes overlapping inherited structural variants'. I searched the definition for structural variants and according to Wikipedia, structural variation refers to the variation in structure of an organism's chromosome, such as deletions, duplications, copy-number variants, insertions, inversions and translocations.
However I am not sure what is meant by genes overlapping the inherited structural variants. Does this mean for structural variants that are common between ASD subjects, there are some common genes that are found in these regions (the inherited structural variants)? Any insights are appreciated.

If I understand correctly, what this paper is looking at is rare copy-number variation in ASD cases relative to controls. So in the context of the paper, the passage you quoted is basically saying we found genes that had copy-number variation between cases and controls, i.e. the cases had a pattern of more/fewer copies of a stretch of the genome that includes a gene than the controls. Then they look at the functions of the genes they found in a gene ontology database to see if they seem like they might relate to ASD.


Can anyone identify this caterpillar / cocoon? This insect is about 0.5 mm in length, so it is very small. It doesn't have legs I don't believe, I am not too good at this but I don't know if it's a worm or more like a cocoon for something.

I do find this alarming because I found this one underneath my bed sheet on the mattress. Now I do recall seeing something similar on the crack of the shaky tile floor, so I can't tell if it's just an apartment pest or it actually lives in mattresses.

Location: Toronto, Canada

It's carpet beetle larvae.
It's a serious pest, right behind the bedbug. The larvae were found on an old mattress.

I found about 4 more afterwards.


What vitamins exist for other animals but not humans? As you probably know, humans are among the minority of animals that require Vitamin C and don't produce it ourselves. For whatever reason (multiple theories exist), we lost the ability. Meanwhile, the vast majority of animals out there that require Vitamin C simply produce it internally, so they have no need for food choices that contain it. Had it not been for the discovery of scurvy as Vitamin C deficiency, we likely wouldn't have ever known that Vitamin C exists at all as a requirement for human health.

Are there known to be cases in other animals of dependence on food containing vitamins that we humans produce ourselves?

The best example I can think of is taurine, which is a non-proteinogenic amino acid.

Taurine is "conditionally essential" for humans1, but essential for cats2,3.

References:

1: Stapleton, P. P., Charles, R. P., Redmond, H. P., & Bouchier-Hayes, D. J. (1997). Taurine and human nutrition. Clinical nutrition, 16(3), 103-108.

2: Knopf, K., Sturman, J. A., Armstrong, M., & Hayes, K. C. (1978). Taurine: an essential nutrient for the cat. The Journal of nutrition, 108(5), 773-778.

3: Markwell, P. J., & Earle, K. E. (1995). Taurine: an essential nutrient for the cat. A brief review of the biochemistry of its requirement and the clinical consequences of deficiency. Nutrition research, 15(1), 53-58.


Is this spider venomous? I found this spider in bathroom. Just wanted to know more about it.

Location : India(South India,Hyderabad)
Temperature : 30°C
Humidity : 74%

Your spider shows an apparently large size, a large round cephalothorax, with smaller and thinner abdomen, very long and sturdy legs, with a long 'foot', and is a general brown color, with some darker markings on the legs.
This is consistent with one of the larger varieties of spider found in the warmer areas of the world, and trading under the name of Huntsman Spider, or Giant Crab Spider.  There are a number of species of these spiders in the family Sparassidae.
As it happens, the most common variety of Huntsman, Heteropoda venatoria, is found pretty commonly in southern India (reference link example included: http://www.southindianspiders.org/south-indian-spiders2.htm ), and I'm quite confident that this is what you have there.  Here is an example, from the US website Bug Guide, of this species:

Like almost all spiders, this spider is venomous, but like almost all spiders, its venom is not particularly troublesome to us humans.  A bite from a spider this big would be moderately painful simply from the large fangs, and the venom doesn't appear to usually add too much to it.  Here's a short but amusing discussion of such bites, from an Australian website: http://sciabc.us/IL2pR

These are sort of the spider equivalent of Geckos - commonly foraging in human homes for the various critters that like to make pest of themselves (cockroaches, mice, etc.) - but they never try to sell us insurance.


Can elephants smell when they have water in their trunks? For humans, humans cannot smell when they have water stuck in their noses. However, I am wondering if elephants can smell scents when they have water in their trunks, as they are designed to hold water.

Yes they can, as the G protein-coupled olfactory receptors detect presence of molecules and no receptors exist that are inhibited by competitive binding of water molecules.
Both you and an elephant can smell (with) water in the nose! Just try it! I am sure you can smell a difference between pure water and water with a tiny drop of perfume in it if you aspirate it though your nose!


What is mitochondrial run length? I am reading the following journal paper and I have come across the following statement:

Overexpression of GSK-3β significantly increases motile mitochondria
in a Tau protein-dependent manner. However, GSK-3β does not alter
mitochondrial velocity or mitochondrial run length.

I understand what mitochondrial velocity is but I am not sure what exactly is meant by mitochondrial run length. Any insights are appreciated.

Run length means how far the mitochondria move, each time they move.
The article this references is:
"GSK3β Is Involved in the Relief of Mitochondria Pausing in a Tau-Dependent Manner".
This article has a figure showing the distances in micrometers, although I have trouble working out interpreting the error bars on the graph to see if the distances ("run length") are really different.


Why aren't plants' roots as diverse as leaves? I have been doing some gardening recently and I suddenly realised that all plants have superficially identical non-woody roots of the same size from gigantic trees to small fruiting plants and vegetables. They are all white, no more than 1 mm across, long and flexible with no distinguishing marks. Only when the root start to become woody do they become different in appearance.

Leaves are very diverse even when they have just started to grow, i.e. before they have reached their full size. I can recognise many different plants from their smallest leaves alone but I wouldn't be able to differentiate plants by looking at their roots. So why aren't roots anywhere near as diverse as leaves?

To answer this type of question, we should start by defining 2 concepts: the functions of the root and the external condition that brought to a specific evolution.
Evolution is a necessary process to all organisms, which evolve to optimize a specific function and to better adapt to the external conditions.

There are 3 main and common functions between all land plant's roots: fix plants to the soil; absorb water and minerals; establish specific relationships with other organisms, principally fungi and bacteria. The external conditions of roots (soil) are quite stable, even though, the different "physical" composition of soil, that is the quantity of sand, clay and rocks, change the physical appearance of size and proportion between the main and the lateral roots.Therefore it is plausible to say that it is not necessary to have a great variety in root's structure; since all roots must carry out same functions, all plant's root underwent a similar evolution.

For the leaves it is a bit different. Leaves must also carry out specific and common functions, as: exchange gas (CO2 and O2); contain photoreceptors to "absorb" light for photosynthesis. However, the external conditions of leaves are shortly and continuously changing and highly different (consider the vary regions of the world, as desert and rainforest) with reference to roots. Therefore each plants underwent evolution depending on these types of external conditions, so as to, of course, optimize their functions but at the same time protect themselves as much as possible. Consider, for example, the intensity of sun's radiation, which, if too strong, can destroy cellular structures, the quantity of CO2 in the air, or the high biodiversity of insects, which can carry diseases, ecc...

Interesting book about evolution is: J.C. Harmon, S. Freeman, "Evolutionary analysis", where it is given an idea of the type of evolution, different species, could undergo.
(hope my english is not too bad)


Why does the right bundle branch not have any terminal filaments in the IVS of the human heart? Dubin's "Rapid Interpretation of EKG's" briefly describes this part of human physiology but doesn't explain the reason behind it.

Is there a specific advantage of the human heart having this characteristic, or is it a flaw/useless trait?

Why is a philosophical question, but you can see, below, the most common anatomic variation, with the ventricular septum receiving terminal branches from the septal fascicle off of the left bundle branch though it can come off the common bundle. The left ventricle is larger, and as might be expected, has a greater portion of the conducting system than the right ventricle.


Pectoralis muscles as push muscles vs pull muscles Pectoralis muscles are the adductors, flexors of arm in addition to medial rotators  of arm. How does this action translate in to acting as helping in push ups or in bench press?
I am having trouble visualizing the primary actions helping in these compound movements.
I also have trouble understanding why this muscle being a powerful adductor does not work in pull up exercise?

The pectoralis major is not just an adductor and medial rotator of the arm. Its clavicular fibres also flex the arm at the glenohumeral joint. This is the action useful in performing push-ups and bench presses.
And yes, its adductor action also plays a role in pull-ups and climbing (along with that of the latissimus dorsi, another adductor).

References and further reading:

https://www.kenhub.com/en/library/anatomy/major-pectoralis-muscle

https://www.kenhub.com/en/library/anatomy/the-shoulder-joint

Romanes GJ. Cunningham's manual of practical anatomy. 15th ed. Vol 1, Upper and lower limbs. Oxford: Oxford University Press; 1986. (ELBS edition, 1989 reprint). 263 p.


What causes pinkish hue to some skins? I know it is caused either by blood vessels beneath skin , or some pigment called "pheomelanin" . But what is it in fact?

The answer lies in hemoglobin, which is responsible for the transportation of oxygen throughout our bodies. It is the protein found in red blood cells, and thus it has a reddish hue to it. When an organism has lightly pigmented skin, the oxygenated hemoglobin causes the pinkish hue that you are describing.


How many hairs per sq. cm. (or inch) do hamsters have on average? How many hairs per square centimeter (or inch) do common pet hamsters (Mesocricetus auratus or Phodopus sungorus) have on average?
I thought this would be easy to find by googling, but the best I've been able to find is this 1986 article, which isn't very clear in answering the question.

According to Paul et al. (2007), shaved fur patches of male Siberian and Syrian hamsters had a mass of about 12 mg/cm2 dorsally and 3 mg/cm2  ventrally.
This search give me the page.

Fig 1 from Paul et al. (2007) compares mass of fur growth across time for 2 groups exposed to differing lengths of daylight (long, LD, and short, SD) to examine winter fur adaptation.

Paul, M.J., George, N.T., Zucker, I. and Butler, M.P., 2007. Photoperiodic and hormonal influences on fur density and regrowth in two hamster species. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 293(6), pp.R2363-R2369.


Alternative protocol for evaluating RNA integrity, using a bleach gel I hate having to run MOPS PFA agarose gels with DEPC and everything just to verify my RNA integrity. I came across an alternative protocol that uses ordinary household bleach in the gel to inhibit RNases and was wondering if anyone here has tried it and what the success was like? Or any helpful insight is welcomed also.

here's a protocol I put together based on what was done in that paper.

For a 50ml gel
IN a RNase-free 250ml Erlenmeyer flask
Mix:
5 mls of 10x TAE that I gave you
42.5mls ultra purified water
0.5g of the agarose I gave you
2.5mls of household bleach (6% sodium hypochlorite, use clorox)

Incubate 5-10 minutes.

Microwave for the minim amount of time on the lowest heat setting that’s needed to completely solubilize the agarose, you don’t want evaporation adjusting your solutions volume
Check your volume with a sterile 50ml serological pipette, if you have lost more than 5% volume I would redo, using less heat.

Add 3µl 10mg/ml ethidium bromide, swirl to mix.
Pour in casting frame, allow to cool, submerge in 1xTAE

Combine 1µg of your total RNA, 2µg RNase free 6x loading dye and q.s to 12µl in RNAse feree water, you can use the water from the qiagen kit for this.
Run at 100V, about 30 min, get  good scanned image of it and use Photoshop to assess the band intensity. The 28S should be twice the brightness  of the 18S in a sample with little to no fragmentation.

I don't think bleach can denature RNA. Bleach is an oxidizing agent and it will damage the RNA. Also, the protocol mentions addition of hypochlorite before heating which I think is illogical because heat will decompose it.

For testing RNA integrity you need not make a denaturing gel. What you can instead do is to heat the RNA with the 2xRNA loading buffer that contains 95% formamide and run it in a normal TBE/TAE agarose gel. Heating with formamide denatures the RNA permanently.

Denaturing gels are only essential for Northern Blots.

You can also run your sample in a bioanalyzer to check for RNA integrity and this is always recommended for RNAseq experiments (even for microarrays but I cannot comment much on that because I have never done it and am not aware of the usual practice).


Is the CDC's reported drop today in COVID-19 cases by date of diagnosis meaningful? I was waiting with bated breath for the CDC update on cases of COVID-19 in the U.S. by date of onset.  To my eyes this looks like absolutely wonderful news - that it means that the exponential growth of the virus has been "flattened" - but I'm still afraid I may be misinterpreting what I see.  It bothers me that the headline for the graph hasn't changed.  But it APPEARS that the number of new cases stopped increasing after 3/3.  Am I missing something?

Top: before noon on 3/16, bottom: after noon on 3/16.  Data from https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html

Note: In today's update (the first in three days) the CDC page shows the number of cases with onset on 3/4 to be 159, and 3/9 is 307.  This doubled in five days rather than every two or three as other numbers would suggest, but given the dramatic changes in this curve, and their overall direction, I think the top answer below has been vindicated.

The information you show is meaningless unless it is also accompanied by the number of tests performed. If the CDC tested 2 people and got two positive results, that doesn't tell us anything at all about the actual rate of infection. And, indeed, the CDC has been testing a shockingly low number of cases:

  ‡ Data during this period are incomplete because of the lag in time between when specimens are accessioned, testing is performed, and results are reported.

(image source)

The last day they give data for, 2020-03-15, includes 0 samples from the CDC and 4 samples from other public health labs. Since only 4 samples are represented in the chart, of course we see a drop in cases, but that's because they are based on only 4 tests. As more tests for those dates and subsequent dates are reported, the numbers will change.

Date Collected  CDC Labs    US Public Health Labs
3/12            75‡         2302‡
3/13            0‡          1511‡
3/14            0‡          165‡
3/15            0‡          4‡

As you can see in the table above (from the same source as the graph), the past few days have seen almost no tests are being included in this analysis either from the CDC or elsewhere, so any drop in cases is completely meaningless.


Where to begin studying Biology in earnest, with preferably free sources? I am a biology enthusiast and would like to study Biology in earnest. I have basic knowledge of biology (high school level) and some extended knowledge of small animals, mainly about mammals as I am naturally interested in them.

So I would like to start studying veterinary and Mammalogy first.
I would prefer free sources for studying since I have little money available.

Before getting into veterinary and mammalogy, you might want to start with the basics. As many people have mentioned, Campbell and Reece is one of the best textbooks to start a foundation in biology. If you live near a public library you might find a 6th or 7th edition to borrow. Amazon has a few 7th editions for cheap as well. Although it is an introductory biology book, it will give you a wonderful tour of cellular and molecular biology that will make it much easier when studying animal physiology (which they also covered in the later chapters to a limited extent).

Free Biology Text Books:

Boundless Biology: Boundless is a company that has many free textbooks for high school level biology to help teachers in have a free online textbook.

I have also found a list of free biology text books here that might be of use.

Free Mammology Textbook:

As part of a National Science Foundation Grant, the Northwest Center for Sustainable Resources created *Introduction to Mammology*. It is a free textbook that was developed for a two-year Wildlife Technology program. It also contains information related to the lab portion of the program, but you can skip those and focus on the material.

Free Online Coursework:

Coursera: A few people have already mentioned Coursera, which is a Massive Open Online Content (MOOC). Here, you can find many courses across a wide range of biology topics (and others!). You can enroll in a course (for free) and many times they come with accompanying free textbooks as well (at least that is what I have experienced).

edX: Another MOOC that was started by Harvard.

Khan Academy: Another great website for explanations of certain aspects of biology. As Tyto alba stated, there are some errors in the videos.


Why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences? Ever since starting to learn about the concept of inclusive fitness during my BSc, I've been bugged by this questions: if inclusive fitness can account for many ‘altruistic’ behaviors, why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences? In other words: when we consider (from a gene-centric perspective) that individuals are temporary vehicles for selfish genes, and if we also consider that the fitness effect of different genes should not be measured in the reproductive success of just single individual, should we not expect to see that genes that promote more broad-scale altrustic behaviour since we share most of our genetic heritage with other individuals?

I understand that my confusion arises from the fact that I fail to sufficiently distinguish between behavioral genes that influence altruism and whose distribution in the population is differentially influenced by different game strategies and genes that have no direct influence on this type of behaviour and are thus not under the same type of selection pressure. However, I cannot seem to manage to produce a clear-cut argument from this distinction.

I'm asking because, when I find myself in the position of having to explain inclusive fitness, I feel a bit awkward when I know in the back of my head that I would not be able to answer this basic question if it comes up.

Relatedness measures a specific type of genetic similarity. In particular, it measures the genetic similarity relative to the rest of the population. When $r>0$, the recipient carries the actor's genes at a higher frequency than the population. When $r=0$ it doesn't mean that the actor and the recipient do not share genes; it only says that the recipient carries the genes of the actor at the same frequency as the population.


Are the arrows in this diagram of ATP synthase correct? I have a question about this image below.
Do you think that the pink arrow is actually going in the right direction?

I would suggest a LTO sequence and not LOT, since it is in the T state that ADP + Pi is converted in ATP.

Yes, the arrows are correct. However, it's not immediately clear what they're trying to show.
ATP synthase
ATP synthase can act as a generator or a motor. Interactions cause rotation of the F0 subunit and the  subunit's axle has a kink in it which deforms the stationary F1 subunits (the axle can turn either way to act as a generator or a motor). Read more at PDB's ATP synthase 101.

What The Asker's Diagram is Trying to Show
The black arrows in the asker's diagram are implying the movement of ADP or ATP (generation) in and out of the catalytic site. The pink line implies the movement of the axle kink and not the transition of ADP+pi->ATP.
Let's focus on the left-hand subunit across the subfigures and it makes more sense (ADP and Pi go in, protein "closes" and ATP is formed, ATP is released). Meanwhile, the "kink" completes a full rotation.


Does A/T, G/C pairing exist in haploid? I'm trying to understanding base pairing. So every linear chromosome is a double stranded double helix. Is this double stranded property the same as saying an organism is diploid? Or do the chromosomes of a haploid eukaryotic organism, like a member of Fungi, each have 2 strands (with the purines always pairing w/ pyrimidines), which would imply that diploids organisms actually have 4 strands?

EDIT: Part of my confusion comes from the fact that in diploid organisms, each parent gives 1 chromosome to the child. If the double stranded property is the same as saying an organism is diploid, does this mean that say if a nucleotide on one chromosome is A, then the nucleotide on the other chromosome in the same loci must be T? Doesn't chromosome mean a paired up strand, not a single strand?

Is this double stranded property the same as saying an organism is
  diploid?

No.  You are a diploid organism because you have two copies of every chromosome.*  You got one from your mother, and one from your father.  All your cells are also diploid, except for your gametes, each of which contains only one copy of every chromosome (due to crossing over, each chromosome is partially from your mother, partially from your father).

Bacteria just have one copy of their genome.  They duplicate it prior to cell division, and each resulting cell has one copy of each chromosome.

*Unless your sex chromosomes are XY, or are anuploidic.


Why even if all requirements for natural selection are met, it may not happen? In the book written by John Endler Natural Selection in the Wild p. 4
it says that even if condition a, b and c are met, evolution by natural selection might occur,

  [...] , but not necessarily, [...]

See last paragraph of the image.
Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press.

I’m wondering in which case it’s possible that everything is in place for natural selection to occur, but is not having any effect.

It seems to me that if every condition of natural selection are met, there will absolutely a change in the phenotypic distribution? Why does the text say evolution is not guaranteed to occur?

Evolution, a change in the trait distribution of a population, occurs by four mechanisms; drift, mutation, migration, and selection. E.g. These mechanisms cause a change in the mean of trait, or variance in a trait etc.. Just to summarise the conditions you gave:

a) Trait $i$ has variation

b) Trait $i$ covaries with fitness ($\omega$)

c) Trait $i$ is heritable from parent to offspring

Genetic drift is the random loss of genetic variance from the population by stochastic processes. Mutation (generally) generates new genetic variation within populations. Migration can lead to loss (emigration) or gain (immigration) of genetic variation from a population, as variants come or go from a population.

Selection is mechanism underlying adaptation. This is what is in condition b of the conditions you gave. We can predict the response to selection using some simple quantitative genetics in the form of the (multivariate) breeders equation.

$\Delta z = G\beta$

Where $\Delta z$ is the response in the trait, $G$ is the genetic (co)variance matrix, and $\beta$ is the selection.

In a simple toy example we could look at a single trait, $i$. We allow $i$ to satisfy all of the above conditions. This means that both $G$ and $\beta$ are non-zero, and therefore, $\Delta z_i$ will also be non-zero. Just putting some random numbers in to the equation to make it clear, if $G = 0.5$ and $\beta = 0.8$ then;

$\Delta z_i = 0.5 \times 0.8 = 0.4$

Mutation, drift, and migration could all oppose or distort the effect of selection. In other words, they can cause the actual and predicted response to be different from one another (i.e. $\Delta z_i \neq 0.4$), and there will not necessarily be a change in the phenotypic distribution.

However, selection is also factor that could cause a difference between the predicted and actual response to selection in trait $i$. This is because genetic correlations can arise among traits, either by linkage (close proximity in the DNA) or pleiotropy (when one gene affects more than one trait). For example, we may see no response at all in $i$ ($\Delta z_i = 0$) when both $G_i$ and $\beta_i$ are non-zero, if selection on a second unmeasured trait, $j$, opposes selection on $i$ ($\beta_i = -\beta_j$), and trait $j$ has equal variance ($G_i = G_j$) and is perfectly covarying with $i$, $cov_{i,j} 1$. Approximately this would be;

$\Delta z_i = (G_i \times \beta_i) +  (G_{i,j} \times \beta_j$)

$\Delta z_i = (0.5 \times 0.8) + (0.5 \times -0.8) = 0$

This is a major issue in the study of evolutionary biology. Genetic correlations can cause severe disparity between the actual and predicted response to selection and univariate methods are insufficient as a result. More studies adopt multivariate methods these days, though these are generally limited to just a handful of traits so its still not perfect. In reality methodological and logistical constraints present a huge obstacle to being able to predict $\Delta z_i$.


NADH vs. NADPH: Where is each one used and why that instead of the other? I know NADH is used in cellular respiration and NADPH is used in photosynthesis. What difference does the phosphate group make that the same one isn't or can't be used for both? Is there a greater reason for this separation or is it just coincidental? Why can't the two be interchanged?

The phosphate group in NADPH doesn't affect the redox abilities of the molecule, it is too far away from the part of the molecule involved in the electron transfer. What the phosphate group does is to allow enzymes to discriminate between NADH and NADPH, which allows the cell to regulate both independently.

The ratio of NAD+ to NADH inside the cell is high, while the ratio of NADP+ to NADPH is kept low. The role of NADPH is mostly anabolic reactions, where NADPH is needed as a reducing agent, the role of NADH is mostly in catabolic reactions, where NAD+ is needed as a oxidizing agent.

You'll find some more information about this in chapter 2 of "Molecular Biology of the Cell by Alberts et al.


Mass Spectrometry Terminology I began reading this paper (http://www.biomedcentral.com/1471-2105/14/56) and had a few questions about mass spectrometry terminology that I couldn't find answers to elsewhere.  Consider the following line:

"The resulting peptide signals in the LC-MS map are referred to as features while the selection of features for fragmentation with MS/MS is called precursor ion selection."

I'm not sure what an LC-MS map is, so I can't properly understand what features or precursor ion selection are: can someone define these terms for me with examples?

LC-MS map they refer to is the projection of two separation method (Liquid Chromatography - Mass Spectroscopy) results into an imaginary plane. It's a conceptual map. From this map, peptide signals referred to as "features" (article uses this term) are selected for the next level of fragmentation and then MS again.

Figure 1 of the article you cite simulates a small fraction of this larger map.


Which modern methods of antibiotic production are there? For my seminar paper in the field of biology, I have to collect modern methods of antibiotic production. The topic is a little overwhelming, but the work should also be quite extensive (approx. 18 pages).
I've already done some research, but most of the results don't help me. I would be very grateful for a few web links and keywords that I could research for in order to break down the topic.
I will visit the university library in the next few days. It would help me a lot if someone could recommend a few good books references.

For Penicillin production try from page 165 of:
Industrial Microbiology: An Introduction
by
Michael J. Waites
Neil L. Morgan
John S. Rockey
Gary Higton
There is also a table in that chapter listing the other antibiotics and which organisms are used to produce the basic form.
I found it very readable.


Designing primers with restriction sites I want to design a forward and reverse primer that include overhangs with restriction sites, with the dna used for restriction enzyme cloning.

If I want to send my dna to a synthesis company should I include the attached overhang with the restriction sites to the dna? Does it matter if the primers have the overhang of the dna within their sequence ?

From the sequence right at the end what bp sequence would be recommended I use for my primers if I want approx. 20-25bp for the primer?

See below for cDNA sequence:

Nde1 cut site: 5' ... CA|TATG ... '3'

Xho1 cut site: 3'...GAGCT|C...5'

cDNA with overhangs that have restriction sites, Ndel1 (5'->3') and Xho1 (3'->5')

5' catatg - ATGGGTTCAAACACTTCCAAAGTGGGTGCTGGTGCAGAAAAACAACAAGTCTATACTCCG
CTAACACAGATCGATTTTTCACAGTCTTTGGTTTCTCAATTGGATTCATCGAAGGAATCA
GACTATGTCACCAAGCAAAATGCAGAAAAGTTCATTGAGAAGAAGGTTTCACAAAGGCTA
TCTAACCTAGAAGTTGAAACGTTAAAGAAGTTTGAAGATACTTTGAACAATTCACTATTA
TCAGACGACGACAAGGATGCCGTTGATGGAATATCATCAAGTTCATTGAATAATCAAATC
GAGTCGTTGAACAAGAAACTAACATTATTTGATCAATTAGAGTTACAAAAGTTGGAGAAA
TATGGGGGTGCCAAAGGTAAATCTGATAAAAAAACCGACAACGGCAGCATTTCTATAAAG
GCAAAATTGACTGAGTGTCTTTTGGCCAATAAGGGCAAGCCATTGAATTGTTACGAAGAG
ATGGAAGAATTCAAGAAGCTCGTTATGGGTTGA - gagctc 3'

Yes.

If you intend to subclone the fragment via classical restriction enzyme cloning you need the overhang.

Different restriction enzymes require different lengths of overhang to allow them to sit fully on the strand and then cleave the sequence.

NEB has a great page detailing how many bases are needed for the enzymes they sell:

https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments

No, it doesnt matter if the overhang appears elsewhere in the DNA, just so long as your restriction sites don't (obviously).

Here are some considerations I use when designing primers for PCR (though not wholly applicable if you're just having it synthesised):

Use the 3+ basepairs present the given number of nucleotides in your restriction site away in the sequence you're PCRing from as your overhang sequence to allow a few more bases to bind. I.e

With the following primer:

Overhang - Restriction Site - Priming sequence

AAA-GGATCC-ATGACATGCAGTAGC     PRIMER

|||        |||||||||||||||

TTT--------TACTGTACGTCATCG     TARGET SEQUENCE
Alternatively, I use those 3 or so basepairs to add or remove GC content and manipulate the Tm if the annealing temperatures of the 2 primers aren't ideally matches


Monochromator in fluorescence microscopy I'd like to ask why are there no fluorescence microscopes that use a monochromator instead of filters?

If there are any, then I should change my question as, which ones use it and why are they so rare?

Zeiss LSM780 uses essentially monochromator to spread all fluorescence across 34 detectors for multi-spectral acquisition. It is used to detect autofluorescence, unmix closely positioned emission spectra (unmix GFP and YFP for example) and to measure precise spectral peaks with ~1nm resolution.

Monochromator is useful when you need to transform frequency domain information into spatial domain. In fluorescence microscopy we usually collect light from wide bands of well-separated GFP-like proteins, so that filters make more sense. We usually don't detect 1-nm wide lines or plot spectra. LSM780 does allow all that, if you need to.

You can use spectral imaging, but for that you will have to either scan for very long time, or spread signal onto array of detectors.


Why is the formation of an enzyme-substrate complex endergonic (induced fit model)? In the section about the induced fit model for enzyme substrate binding, my MCAT textbook claims that "The substrate has induced a change in the shape of the enzyme. This interaction requires energy, and therefore, this part of the reaction is endergonic."

As a chemist, I am a bit confused here because induced fit suggests that some kind of bonding must be happening between the enzyme and substrate (hydrogen, ionic, covalent, etc) that would induce a change in structure of both enzyme and substrate. Any kind of bond formation is STRICTLY enthalpically exothermic, so why is the formation of an enzyme-substrate complex endergonic?

Am I missing an entropic component here? Or is my assumption wrong, regarding how the induced fit chemistry operates?

I would assume that it would TAKE energy to then cleave/break all the bonds that induced structural change and release the catalyzed substrate...

Most reactions require an activation energy to cross an energy barrier (this you may already know) after which the reaction is downhill. Even though enzyme catalysed reactions have a relatively lower activation energy compared to that of an uncatalysed reaction, there is still a transition state that has a higher free energy compared to the products. This transition state corresponds to the enzyme-substrate complex.

              Image Source: https://en.wikibooks.org/wiki/Structural_Biochemistry/Enzyme/Activation_energy

Free energy has enthalpic and entropic components (ΔG=ΔH-TΔS). Even though formation of bonds may reduce the enthalpy, the locking of the substrate and enzyme in a conformation also decreases the entropy. This could lead to overall increase in free energy (See here. For more details you can refer to this book- The Enzymes: Mechanisms of Catalysis by Paul Sigman. ISBN: 0121227200).


What is the smallest scale at which blood vessels, nerves and other structures are deterministic? Super simple question, but I can't find the answer on the Internet (and I'm in a foreign country so the library is not English.) As the title says, what is the smallest scale at which blood vessels, nerves, lymphatic vessels, bronchi, renal structures, etc.. are deterministic (same for most of the population)? For example, I'd imagine capillaries are pretty much random, while (most?) people have an aorta, so where does the pattern break? Is there a scale at which an animal's body is probably similar to their siblings but dissimilar to a complete stranger? Or is it just a statistical distribution thing (the smaller you go the more standard deviation you get)?

Indeed a very good question. I'm afraid it might remain without a proper anatomy-based answer, but my intuition would tend towards agreeing with "the smaller you get, the more deviation you'll find".

Or rather, I would expect the same principle as in conservation of genetic patterns to apply here: the more central a tissue structure is to survival, i.e. the more downstream systems depend on it, the more likely it will grow in conserved patterns.

As an excellent example, the largest blood vessels including the aorta and its first- and second-degree branches are identical in branch number, approximate relative branch size and approximate branching location across probably all living humans (given that babies born with malformations on this scale would probably not survive without drastic surgery). Similarly, the largest-level nerves and nuclei are identical across the species. These are central systems that provide core functionality for survival.

On the other hand, teeth are quite important, but the odd tooth missing or additional doesn't harm terribly as no downstream systems depend on them. Indeed, it isn't uncommon for humans to be missing a permanent tooth and keep their primary (baby) tooth in that spot for decades; similarly, missing 8th teeth or additional 9th teeth also occur.


Why Lungs can't work in water and gills can't work in air? Animals with lungs (such as most terrestrial mammals) cannot breathe if submerged in water, and soon suffocate.
Whereas, fish can variously breathe air (at least for few-hours, as some fish frequently need to get air periodically), including those that are bigger than a human (say sharks).
But why? Do fish require less oxygen than lunged terrestrial-animals, despite being active and variously engaging in activities like predation? (so that uptaking only dissolved oxygen, and probably less surface area of gill than lung-alveoli is enough for them?)

Misleading sentences in your question

  fishes can breathe in water (at least for few-hours)

Fishes can breathe for much longer than a few hours under water as they spend their whole life underwater.

  Animals-with-lungs (such as most terrestrial mammals)

All mammals, whether terrestrial (like a cow) or not (like a dolphin) have lungs. While all mammals have lungs, most fish (but not all) have gills.

Lungs vs Gills

To understand the answer, you need to understand two key organs involved in gathering oxygen from the environment: gills and lungs.

Lungs are organs that allow the transfer of oxygen into the blood when inhaling air, while gills are organs that allow the transfer of oxygen into blood when inhaling water. Lungs don't do their job properly in water and gills don't do their job properly in the air. You should have a look at the following wikipedia entries to further your understanding of these organs:

Lung
Gill

Energy consumption

You say

  does fishes require much-much less-amount of oxygen than lunged terrestrial-animals, though they stay in physical activities including predation?

I am not sure I understand the meaning of this sentence but anyway.

Making generalization about fish metabolic rate can only be misleading as there are an immense diversity of fishes. For example some fishes are endotherm (see here to understand the definition of this term) while some are not and this will vastly affect the metabolic rate.

Although eventually too advanced for the OP, Chabot et al. (2016) is an interesting reading to get an general overview of the Metabolic rate in fishes.


Perspiration after drinking water If we don't drink water for a long period of time(say,10 hours), as during fasting and then when we break our fast by drinking water why is it that our body starts sweating?

During the time when you are not drinking water you still loose some water to sweating and urine. Sweating is (especially in hot climates) an important function of the body to maintain the body temperature in desired range. If this water is not replaced, the body gets dehydrated. This induces a reaction which reduces the activity of the "body thermostat" to tolerate a higher body temperature without excessive sweating to maintain the fluid balance of the body.

When you start drinking again after this the dehydration period, the body starts sweating to regulate the body temperature again, since now the loss of water is not critical anymore for the body. For a detailed discussion (including further references) have a look at this publication:

The effect of water temperature and voluntary drinking on the post
rehydration sweating


How can I re-format my DNA motifs' position weight matrices? I am working with a set of DNA motifs that are predicted as potential regulatory motifs (e.g. transcription factor binding sites).
The motifs belong to several species, and I wanted to cluster these motifs via their Position Weight Matrices (PWMs) (also known as PSSMs) to collapse similar motifs together into groups.

There is a tool called MATLIGN (website here) that does what I need, but their required format for the PWMs are different to what I have, they claim:

  "Matrices must be in the frequency matrix format (only integer numbers
  are acceptable)"

The problem is that my PWM matrices do not have integer numbers but decimals instead. e.g.:

     A        C        G        T
1    0.000000 1.000000 0.000000 0.000000
2    1.000000 0.000000 0.000000 0.000000
3    0.000000 0.000000 1.000000 0.000000
4    0.000000 0.421755 0.000000 0.578245
5    0.289407 0.000000 0.282556 0.428038

In other words, instead of the decimal values I have in my matrix I need to have integer counts. Could anybody suggest what I can do? Would I need to create artificial "pseudo-counts"?

So what you need is basically your data expressed as counts instead of proportions. Even if you do not have the matrix of counts as raw data, these proportions only needs to be multiplied by the total number of binding sites used in the study (e.g. the number of sequences that have been analysed) to get the counts (since proportion = count/total number of binding sites). You should have that information somewhere.

@hello_there_andy: indeed there was this missing piece of information available to me, it came in the form of a variable called nsites which equates to the total number of DNA sites that the PWM was generated from.


How much does a biological experiment to validate a gene function cost? I am computer scientist working on machine learning methods applied to predicting missing Gene Ontology annotations.
In many papers, I wrote that my computational methods are very useful to suggest to the biologists  on which gene functions they should address their research, because my software need less resources (a simple laptop connected to a database) and less time (e.g. with a dataset of all the Homo sapiens Gene Ontology annotations: about 3 hours) than their biological experiments.

Now a reviewer asked me to be more precise. Truly, how much does an in vitro experiment to biologically validate a human Gene Ontology annotation run by biologists cost?

How much money, broadly?

How much time?

Wow that can vary from a couple of months and a few thousand dollars to a lifetime and millions of dollars.  I can give a couple of examples, but this is an extremely broad question.  Wet science is not cheap might be the message here.

Gene Ontology terms are meant to cover all biological roles known for genes.  Terms are added and retire regularly.  They embody thousands of person-years of work to establish the framework of what is going on in cells.  At the same time its a limited vocabulary of gene behavior.  It doesn't represent a complete catalog of all known gene behaviors (e.g. in such detail that it could only be the property of a specific gene) and it is also uneven in the level of its detail of its leaf terms.  Its an ontology that is manually assembled and edited and therefore subjective.

I just did an overview of GO 1.2.  there are 34153 unique GO terms.  That's easily 10s of thousands of separate assays, so picking a group of important ones might be useful. There are also lots of orphan GO terms, where only one gene is currently attached to the term.

For GO annotations, a simple and typical case is a metabolic gene which has a high homology to a known gene and you are only trying to verify that biological role, and you have a functioning biological laboratory.

A breakdown might be:

clone the gene ( \$200 to \$1000 and up): order primers, use PCR to insert the gene into a plasmid or get the gene synthesized if you have to, transform it into bacteria,  ideally sequence it to make sure you have it right.
purify the protein ( \$500 maybe).  Run a check culture to see if the protein is produced, then run a full culture with induction, lyse it and then purify on an affinity chromatography column.  you may need to run a second column to get the protein pure.
do a kinetics study with mass spectroscopic validation of the products (minimally about \$300).  Cost involves reagents - if you have an assay you can use a UV/Vis spectrophotometer this can be simple, if not it can be much more expensive. This part will vary with the enzyme you are looking at.

Hopefully you get all these steps right the first time.  Salaries are not included in this cost.

The more complicated the GO term, the more difficult the work will be - they are not all equal.  If the protein function can't be verified in isolation, but must be in situ (i.e. in the living organism). Then you start to get into time.  What if your gene is involved in protein routing through the golgi apparatus and modulates the function of other proteins for instance?  That's going to require a very specialized and difficult set of experiments that should involve someone with experience in that field.

Finding GO annotations which are not clear from sequence similarity - unknown functions or new genes which reflect previously unestablished GO Terms could cost even more and take a good deal longer.

Still, high throughput studies are being done to find and validate electronic GO annotations.  And with that scale, the cost per experiment will go down.  Take a look at Olga Troyanskaya's research for an example of such an effort.


Conjugate secondary antibody Why is the secondary antibody conjugated to the enzyme in ELISA, instead of the primary antibody? Wouldn't it be easier to conjugate the enzyme to the primary antibody?

Making an antibody-enzyme conjugate isn't trivial. By using a primary/secondary set-up you can use the same well-characterised conjugate in combination with many different primary antibodies (as long as these primaries are all raised in the same species). There is also the possibility of some amplification: for example, if the secondary is an anti-Fab then two secondary Igs will bind to each primary.

Response to OP comment

Most primary antibodies in common use are derived from rabbit or mouse, and most are IgG. So, for example, the secondary antibodies goat anti-rabbit IgG and goat anti-mouse IgG will cover most experiments.


Does terminology for changes in membrane potential refer to additive or multiplicative change? Is the membrane potential just the number of mV, or is it to what extent it differs from 0?

For example: If the mV goes from -40 to -60, can you say that:

The membrane potential decreases, because the number of mV decreases (from -40 to -60)
or
The membrane potential increases, because the difference to 0 increases (from 40 to 60)?

Note to others: this question appears to be about terminology rather than the biophysics behind the membrane potential.

When the terms "increase" and "decrease" are used relative to membrane potential, they refer to additive changes in potential, not to multiplicative change or effects on absolute value. The standard is to relate the potential inside to the potential outside of a cell (so a negative potential means the inside is more negative than the outside; potentials in biology are always relative, just like in physics).

Therefore, a membrane potential decrease means that the value of the potential becomes more negative, and a membrane potential increase means the value of the potential becomes more positive. The changes on the absolute value of the potential depend only on where you start from.

Other terms that are more clear to use are hyperpolarization and depolarization, where hyperpolarization always refers to the membrane potential becoming more negative than rest, and depolarization refers to the membrane potential becoming more positive than rest. Repolarization is also used, particularly in the context of action potentials, to refer to voltage changes in the direction of hyperpolarization when the cell is currently depolarized.


Deciduous trees in tropical rainforest Some books says the dominant plant form in tropical rainforest biome is broad leaved evergreen trees. Other books say it is broad leaved evergreen trees and deciduous trees. What is the most accepted way (or the truth)? Also how do you explain the deciduousness adaptation in tropical rainforest (e.g., when do they shed leaves)?

Deciduous trees are those which shed their leaves once a year at the time of winter season and later grow new leaves, plants those keep their foliage throughout the year are called evergreens. Deciduous trees usually have broad leaves e.g., ash, beech, birch, maple and oak. There is a confusion exists over the dominance of trees in rain forest, but most of the resources suggests broad leaf evergreen trees as the most dominant. But deciduous trees are equally important because the difference may be negligible.

Deciduous trees shed their leaves usually as an adaptation to a cold or dry season. Evergreen trees do lose leaves, but each tree loses its leaves gradually and not all at once. Most tropical rainforest plants are considered to be evergreens, replacing their leaves gradually throughout the year as the leaves age and fall, whereas species growing in seasonally arid climates may be either evergreen or deciduous.Reference

The dominant plants in the tropical rain forest are broadleaf evergreen trees. Unlike evergreens that grow in colder parts of the United States, those of the tropical rain forest have no protection against cold weather or droughts.Reference

Adaptations of Deciduous trees

Broad green leaves capture sunlight needed to make food through photosynthesis.
They cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk, as sunlight and water become scarce, the leaves are unable to continue producing chlorophyll and this produce vibrant colors in the leaves.
In winter, they simply loose their leaves and seal up the places where the leaves attach to the branch. Losing their leaves helps trees to conserve water loss through transpiration.
In spring the trees grows back their leaves and start the cycle once more.

In the spring, deciduous trees begin producing thin, broad, light-weight leaves. This type of leaf structure easily captures the sunlight needed for food production (photosynthesis). The broad leaves are great when temperatures are warm and there is plenty of sunlight. However, when temperatures are cold, the broad leaves expose too much surface area to water loss and tissue damage. To help prevent this damage from occurring, deciduous trees make internal and physical adaptations that are triggered by changes in the climate.
Cooler temperatures and limited sunlight are two climatic conditions that tell the tree to begin adapting. In the Fall, when these conditions occur, the tree cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk. With limited sunlight and water, the leaf is unable to continue producing chlorophyll, the "green" stuff in the leaves, and as the chlorophyll decreases the leaves change color. The beautiful display of brilliant red, yellow, and gold leaves, associated with deciduous forests in the fall, is a result of this process. Most deciduous trees shed their leaves, once the leaves are brown and dry.
Reference


Why do dog's eyes glow green on a photo? Taking my current profile picture as a prominent example:

This photo has been taken with flash. As I gather, this is the same effect that makes a human's eyes glow red on photos, namely the reflection of the flash at the choroid and then passing back through the retina.

The retina is full of bloodvessels and the blood inside them gives the reflected light it's reddish color.

If it's the same effect, why is the color different?

Dogs, cats, and many other mammals have a Tapetum lucidum which reflects light back through the retina to help with night vision. Humans don't have this layer. The tapetum is probably reflecting green light that would have normally been absorbed.


On the genetics behind caste marriages I am in India where it is typically a custom to marry within one's caste. Basically the caste system originated with roots in people's professions - Each of priests, carpenters, troupers, etc had a caste of their own. My question is based on the genetic basis of marriages performed within one's caste.

I know the concept of alleles where there is a dominant allele and a recessive one, like the A and O resp. in blood groups and Rh+ and Rh- in Rhesus factors. Is there a similar genetic information based on our ancestral profession in our chromosomes? Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?
Generally there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

If genetics or biology have any role to play in these fields, I will be happy to know and learn.

Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?

Not everything is coded in the genome, environmental cues play a very important role in shaping who you are. Profession is just one of those things that is not encoded in genes.
Many people do not continue doing the job of their parents, but they do very well in life.
Also note that, aside from the fact that there is no "agriculture" gene, having a recessive allele does not mean you will miss a certain phenotype.
What is true is that someone who has higher education will probably be more keen to have their kids studying. On the contrary, the kids of someone who is a poor farmer and is barely able to provide for his family will probably not have the opportunity of going to school (let alone university) and therefore will continue to work the land. It has nothing to do with genetics.

  Generally there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

Continuing to reproduce in the same group of people will limit diversity in the genome, and create an accumulation of mutations, which is generally a bad thing. That is why it is very common to have particular illnesses in closed communities.

For instance Amish people have an higher incidence of genetic disorders such as Ellis-van Creveld syndrome (a form of dwarfism)

From The Gene for the Ellis–van Creveld Syndrome Is Located on Chromosome 4p16 - Ruiz-Perez et al., Nat. Genetics 2000

  Autosomal recessive transmission of the disorder is supported by
  multiple affected siblings with unaffected parents in families with
  known parental consanguinity. The largest known pedigree segregating
  with EVC is that reported by McKusick and his colleagues in the Old
  Order Amish (McKusick et al., 1964). The prevalence of living persons
  affected with EVC among the Lancaster County Amish was estimated to be
  2 in 1000, whereas the frequency of occurrence among live births was 5
  in 1000. McKusick et al. estimated that the frequency of heterozygous
  carriers in the Old Order Amish is as high as 13% (McKusick et al.,
  1964). All cases of EVC in the Amish at that time were traced to a
  common founding couple, Samuel King and his wife, who immigrated to
  Pennsylvania in 1744.

This is a well known effect, called the founder effect.

As for India, a study on the genetic behind casts has been done a couple of years ago.

Reconstructing Indian Population History - Reich et al., Nature 2010

From the paper:

  Haldane wrote 45 years ago that “if inter-caste marriages in India become common, various… recessive characters will become rarer”. However, it has not been generally appreciated that this applies to groups throughout India, and not only to groups in the south where consanguinity is common. We hypothesize that founder effects are responsible for an even higher burden of recessive diseases in India than consanguinity.
  To test this hypothesis, we used our data to estimate the probability that two alleles from a group share a common ancestor more recently than that group’s divergence from other Indians, and compared this to the probability that an individual’s two alleles share an ancestor in the last few generations due to consanguinity. Nine of the 15 Indian groups for which we could make this assessment had a higher probability of recessive disease due to founder events than to consanguinity, including all the Indo-European speaking groups.
  An additional reason why some diseases are expected to occur at elevated frequencies in India is shared descent from a common Indian ancestral population. An example is a 25 base pair deletion in MYBPC3 that increases heart failure risk by about 7-fold, and occurs at around 4% throughout India but is nearly absent elsewhere.

They conclude that:

  We have documented a high level of population substructure in India, and have shown that the model of mixture between two ancestral populations ASI and ANI provides an excellent description of genetic variation in many Indian groups.
  [...]
  By showing that a large proportion of Indian groups descend from strong founder events, these results highlight the importance of identifying recessive diseases in these groups and mapping causal genes.

It is very important to understand that this results in no way show a genetic basis for the existence of casts, which remain purely social entities. They rather show that an environmental constraint can influence the distribution of genetic traits, due to a restriction in the possibility of mixing genes in the population.