What are some atypical examples of positive transcriptional cooperativity? Cooperativity in gene expression is an important feature of many regulatory networks. Described using the Hill function, the most common example is a transcription factor (TF) that when bound to its target regulatory site, increases the rate of binding of other transcription factors (usually through TF-TF dimerization).

There are numerous example of TF dimerization-based cooperativity in the literature. However, I am trying to find examples of positive transcriptional cooperativity that involve mechanisms other than TF dimerization. In the dimer model, an unbound TF binds to its cognate promoter (containing multiple enhancers) with a certain affinity. With the first TF bound, another identical TF now has increased affinity for its target - binding to the enhancer and binding (dimerization) to the first TF. The expression profile is sigmoidal (near binary) and represents sharp on/off switching in activity.

Although peer-reviewed articles experimentally or theoretically characterizing alternative mechanisms are preferred, I'm also interested in user hypotheses and discussions that are more speculative. Specifically, I'm interested in positive cooperativity that occurs without feedback from the regulated genes.

One potential mechanism could involve a DNA-binding TF consisting of a transcriptional activator domain and a chromatin remodeling or DNA methylation domain. When the TF binds it not only activates transcription but remodels local chromatin. If the remodeling increases affinity for the next TF, they act cooperatively (and positively). Perhaps something similar to this has already been described.

Positive co-operativity without feedback from the downstream genes:

I guess Polycomb/Trithorax complexes will fit this criterion nicely.

Polycomb group (PcG) represses Hox and other differentiation related genes (such as neurogenin) while Trithorax (TrxG) group promotes their expression. They are not like usual transcription factors that bind to promoters and recruit/exclude RNA-polymerase; they bind at regions called Polycomb Response Elements/Trithorax Response Elements and mediate epigenetic regulation of nearby genes by histone modifications (primarily methylation).

PcG froms two main complexes PRC1 (Polycomb Repressive Complex-1) and PRC2. Different components of the complex have different molecular functions. For e.g SuZ has a Zinc finger domain and can bind to DNA/RNA, Ezh has histone methyltransferase activity etc.

This is an old review but is still quite informative.


Biological terminology: "codes for" vs. "codes a" Maybe this is answered already before, but I cannot find it:

Most authors say/write "a gene codes for a protein", some use "a gene codes a protein". The latter seems to me the grammatically correct use of the verb "code".

What's the reason for saying "code for"? Is it because of RNA processing (e.g. splicing)? What about the coding of single amino acid: "AAA codes Lysin" or "AAA codes for Lysin"?
I would also like to know some history of the use of these (and may be other) terminologies.

Tia Udo

This is an English usage question more than one of biology.  The verb code has two main meanings(1):

(transitive) to put into the symbols of a code
(intransitive) to be a code symbol

The first, which being transitive takes an object, is used for the act (as by a person) of translating a plain message into a corresponding encoded form. This is not the meaning used in "AAG codes for lysine".

The second form does not take an object.  It is not being done to something, but rather is just a state of being.  This form is almost always followed by a prepositional phrase "for noun", as in "INS codes for insulin".

Hence it is not correct English to say things like "INS codes insulin", as the use of "insulin" as an object implies the first meaning, as if one were saying "INS takes an insulin molecule and puts it into an encoded form" (whatever that would mean).

The reader would likely try to interpret "INS codes insulin" with the intended meaning, but the incorrect usage makes it seem equivalent to something like "INS is a DNA sequence insulin."  Leaving out the preposition for may be shorter, but it gives a bumpier ride.

(1): Merriam-Webster.  For more variants see Wiktionary, esp. encode.


why do our eyes not go red in response to body temperature? I know that blood flow increases/decreases in response to temperature change, which is why (lighter-skinned) people go red when they are hot.

I know that the eye contains lots of blood vessels.

Why do our eyes not turn red when we are hot?

Skin turns red when light skinned people flush because it contains few absorbers, so photons diffuse through it long distances. During this time green and blue light is absorbed as photons encounter blood vessels. Red photons are not and so the skin appears redder.

The whites of the eyes are strongly scattering and have relatively few blood vessels, so changes in blood flow has a small effect on color.  The (wavelength-independent) scattering dominates over absorption.

The pupils open up on the approximately 22 mm gap between the cornea and the retina. You don't see changes in color here because the entire retina strongly absorbs all colors of light. The few red photons scattered by blood are very unlikely to be exactly aimed at the pupil. Instead most scatter back into the retina and are absorbed. This is compounded by the scattering anisotropy of blood, which causes most incoming red light to be scattered in the forward direction - directly into the strongly absorbing retina.


Is our genome decaying (see "Genetic Entropy"), and, if so, is this evidence for our genome being "young"? In the book Genetic Entropy & the Mystery of the Genome the author says that the genome cannot be old because the genome is "decaying". Decay is a very subjective term, but in this case he means that the fitness of humans is going down not up. Is it true that our genome is decaying over time, and that the fitness of humans is decreasing? Here is a quote from the book, that might explain his argument:

  Kondrashov, an evolutionist who is an expert on this subject, has advised me that virtually all the human geneticists he knows agree that man is degenerating genetically. The most definitive findings were published in 2010 in the Proceedings of the National Academy of Science by Lynch.4 That paper indicates human fitness is declining at 3–5% per generation.There is really no debate on current human genetic degeneration.

Perhaps this more shines more enlightenment in my question. This idea of human fitness going "down" is my main concern. Essentially, in his book he claims that because we are going "down" (meaning fitness is declining) not "up" (whatever that means) our genome must therefore be young. If I understand the issue correctly, mutations "create new information" by creating different proteins or leading to an abnormal protein products. However, I thought that the force of natural selection should be strong enough to get a rid of those genes that are so and so responsible for our fitness declining.

Sanford, John C., and John R. Baumgardner. Genetic Entropy & the Mystery of the Genome. Waterloo, NY: FMS Publications, 2008. Print.

Feel free to point me to similar questions that may been helpful or are similar to this one.

If I understand the question correctly, you are asking why random mutations (most of the non-silent ones are deleterious) cannot create information and improve the overall fitness of the organism.

This is a common creationist statement, and has been shown to be incorrect in many different ways. The best way this can be shown to be false is by simply applying natural selection.

E. coli has a beneficial mutation rate of $10^{-5}$ per genome-generation (source) and a detrimental mutation rate of $2×10^{-4}$ per genome-generation (source).

Therefore, at first glance, the claim that the "genome is deteriorating" appears plausible. However, natural selection quickly acts on these mutants with deleterious mutations due to their low fitness. Therefore, the deleterious mutations are removed from the gene pool and are replaced with their beneficial counterparts instead.

If we define "information" as beneficial adaptations to the environment, random mutations themselves do not directly create the information. It is the application of natural selection that allows the fitness of the organism to increase despite the presence of random mutations.


Olympic's epidemiological impact on Zika? I've seen a lot of fear mongering, misinformation and overall general panic concerning the zika virus surrounding the Rio Olympics. However, little has been said about the actual epidemiological impact of these Olympics concerning zika.

I would assume that sending hundreds of thousands of people into this 'zika hotspot' and then having them return to their home countries will likely only accelerate the spread of this virus. I understand that Zika has been present in other tropical parts of the world for 50+ years, but the South American strain has had a higher incidence of more dire effects.

My question:

Has anyone actually modeled how these 2016 Olympics will impact (likely accelerate) the spread of this dangerous viral strain throughout the world?

I know the CDC and WHO have people working on this, but I haven't seen any direct reports or evidence of such work. I know it's difficult to create too accurate of a model due to the lack of knowledge about other mosquito species' abilities to become carriers, so I would assume that if a model does exist, it's likely just using Aedes species as the main vector.

Regardless, if anyone knows about epidemiological modeling being done about the Olympic's impact on the spread of zika, please provide some resources.

Though I have not found direct access to a model (which is what I'm really looking for), I have found evidence of such modeling efforts.

The CDC apparently put out a risk-assessment report in mid July discussing the results of such epidemiological modeling (reported by FivethirtyEight, ABC and others).

The report (available here), suggests that the risk of accelerated zika spread due to the 2016 Olympics is low.

They cite two major reasons:

Low mosquito activity due to colder winter weather

and more importantly....

The number of increased visits to the Olympics will make up only a fraction of the number of people that travel to/from zika-affected countries on a regular basis.

  The estimated 350,000 to 500,000 international visitors and athletes
  from 207 countries who are expected to travel to Rio de Janeiro for
  the 2016 Olympic and Paralympic Games represent a tiny fraction --
  0.25 percent -- of total travel to and from Zika-affected countries,   according to the CDC report.

According to CDC director Tom Frieden:

  "Compared with all travel to Zika-endemic areas, the Olympics account
  for about one-tenth of 1 percent of travel from the U.S. and globally
  about one-quarter of 1 percent, so even if Olympics didn’t exist,
  99.75 percent would be the same risk."

I will contact the CDC directly and ask for additional information regarding the model they used for this report. I will update this answer with any additional information I can gather. However, I'm sure others are producing similar models using different criteria, so please feel free to add additional examples or provide direct links to any available models.


Can microorganisms (e.g. bacteria) be damaged or killed by 253,7 nm light? The question arose in a hospital, where I saw these flyers advertising lamps that emit such light. It was claimed that they can clean the air of microorganisms up to an arbitrary degree.

Does anyone know if that is a thing? (If it is, doesn't it also kill the beneficent types of microorganisms?)

Online I found quite a bit on the matter, but only from other distributors of similar installations.

This is UV-C radiation and light of this wavelength (which is emitted by low pressure mecury lamps) can indeed be used for disinfection purposes. The nucleic acids (DNA and RNA) has an absorption maximum for UVC radiation at 265nm, causing DNA/RNA damage. The radiation of the mercury lamps is only a little below, making them still quite effective (see the image from here):

This is used in "Ultraviolett germicidal irradiation" for example in water disinfection systems or also for workplaces. The problem with this irradiation is that it causes severe sunburns (and very fast) and also causes plastic materials to decompose (like leaving them in sunlight but much faster). Since I know the precautions for using such devices at workplaces, I wouldn't consider them safe for home use.

The other problem is that you need a pretty clean area for the radiation to be effective. We have to clean our work benches for doing cell culture work entirely so that no shadows are cast in which the UV radiation wouldn't be working since the area is shielded. Imagine this for your home. Additionally I think the fear for germs at home is massively overrated and that there is not need for theses devices at home.


Is there a difference in how Gas is produced which determines if it becomes a burp or flatulence? I know that some gases are heavier than air and in the case of a gas leak it's best to escape to higher ground, while some gases are lighter than air such as Helium. However unlike Helium I haven't seen a burp burst into flames while I have had the unfortunate pleasure of being present at a party where flatulence was lit on fire.

So I am wondering if there is a difference in how the gas is produced which determines if it's becomes a burp or flatulence.

The gas expelled as a burp originates from the stomach. It is either gas swallowed together with food or gas that was dissolved in the drink. One prominent example for the latter is sparkling water where $\ce{CO2}$ is dissolved in the water at high concentration as carbonic acid ($\ce{H2CO3}$). Because of the acidic environment in the stomach the equilibrium between carbonic acid and $\ce{CO2}$ gas is shifted. Consequently $\ce{CO2}$ accumulates and needs to be expelled as a burp.

The gas expelled as a fart is mainly produced by microorganisms in the intestine and usually contains a lot of methane which makes it flammable.


What is the difference between intials cells and meristems cells? Generally plant tissues:

meristems tissue: meristems cells, apilal meristems, lateral meristems
Non meristem tissue: dermal tissue, vascular tissue, ground tissue

my question:

What is the difference between intials cells  and meristems cells? Are intials cells the same as meristems cells?

Meristems are undifferentiated plant cells. There are two types:

apical mesistem that occurs at tips or branches and roots as well as buds which produces elongation, and
lateral meristem or cambium that produces lateral growth (stem thickening).

As cambium cells divide, cells toward the inside differentiate into xylem (wood) - these cells are 'xylem initials'. Cells toward the outside that eventually differentiate into phloem tissues (inner bark) and are 'phloem initials'.

One could similarly label apical meristem cells that are in the postion and/or process differentiating into leaves or flower organs as x-initials.


What is the biological basis for a human's ability to think clearly and be aware while "fighting/competing"? I'm interested in learning more about the biological systems or hormones or parts of the brain that affect short term (<15 minutes) ability to concentrate attention on the task and be aware of the situation.

I'm particularly interested in humans who are engaged in an activity that can be perceived as threatening: martial arts, competitive video games, sports and other activities which may be considered "fight or flight", but a scenario in which the person has chosen to stay and fight.

To clarify the question further: What is involved in the ability to make decisions based on the competitive situation itself, instead of responding with pre-learned techniques and tactics? In one case, a person may be aware of what his/her opponents are doing, while in other cases the same person may "rush in blindly" and attempt to execute techniques that were learned and worked before, but will not work in the current situation.

What influences this choice of responding versus acting on prior knowledge?

thinking and decision making under stress or pressure is significantly reduced.  its sometimes called the 'fight or flight' condition.

This is a pretty well established phenomenon.  Here's a great radiolab segment on stress response.  Psychologist John Gottman notes how our ability to have a conversation where we can even listen to what someone else has to say is practically nil when we are emotionally saturated (frustrated or upset that is).  Even a mildly stressful conversation with your own spouse can shut down most rational processes.  Gottman can predict couples who overcome this problem which is highly corellated with divorce btw - but most of these couples remove stress in conversations rather than learn to work under pressure as it were.

Jonah Lehrer wrote about how tests to rank quarterbacks in their ability to respond on the gridiron are basically non correlated.  I know there have been criticisms of Lehrer, but this is a good piece and well grounded.  The point is that its hard to tell a-priori whether someone will perform under stress and given different sorts of stress.

In the japanese space program they would screen candidates by making them do highly repetitive tasks like folding 1000 origami cranes.  NASA was just doing interviews with panels of psychologists.  That wasn't infallible.

Such a test would be valuable for fighter pilots, astronauts, maybe presidents too! but it doesn't seem to really exist at this point.

In the end you can winnow out those who break into a sweat in the interview, but to know who is going to really take the beach, I think that the only real answer is to see if they make it through a 'live fire' (or whatever) experience.

Or as Clint Eastwood summed it up: "A man's got to know his limitations."

(apologies to the ladies there - you can know your limitations too).


When does identical twinning happen? What is the window during which division into twins is possible (for instance can it still happen after implantation in the uterus)?
Is one twin the "original" and the other its clone?

In the case of two healthy, viable identical twins, the separation generally occurs at the first division from one zygote to two cells. So they are equal partners in the split, not an original and a clone. During the first several cell divisions in the morula and blastula, there is no significant growth. So these divisions produce smaller and smaller cells. If one of these smaller cells is separated, it is very unlikely to be substantial enough to survive and implant in the uterus.


Do brain cells shrink during REM sleep or a lucid dream? In this BBC news article a study shows that during sleep brain cells shrink to open up the gaps between neurons and allow fluid to wash the brain clean.  But do the cells shrink and undergo the whole procedure during REM sleep and lucid dreaming?

For those who have access, here's the full text.

Having read the paper, I can't give you a good answer.  This study was performed in mice, not humans, and "sleep" was achieved in a few ways.  Mice normally sleep most of the day, so it was easy to get mice sleeping normally.  They also induced "sleep" through anesthesia (incidentally, they saw these same results in anesthetized mice, which I think is quite interesting).  The state of "sleep" was confirmed mainly through the measurement of brain waves, in particular the delta wave.  Delta waves correlate to deep sleep, and that's what they measured.  Panels D and G from figure 1 (below) basically confirm just that - the mice were asleep - and that's all we know so far.  More exciting research to be done!


What is this insect flying in my Los Angeles bathroom? We live in the Los Angeles area. This insect has been very common in our bathrooms recently:

They're about 1/4" long, and can often be found resting on our towels. In the months leading up to December, we've been seeing them more and more.

Do they cause any harm?
Could they be responsible for the holes I've
been finding in my shirts?
Even if they're just a nuisance, how can
we get rid of them?

Looks like the common clothes moth (Tineola bisselliella). And, yes, the larvae (caterpillars) are likely the source of the holes in your shirts. You can purchase traps online or from hardware stores, or you can go the pesticide route if necessary (e.g., Delta Dust is available from online retailers).
See this site for further info, or search the web for more info on this species. https://en.wikipedia.org/wiki/Tineola_bisselliella


Why does the definition of a "gene" require it to have a product? In a textbook, I found the following (emphasis in the original):

  At this point, we can provide a molecular definition of a gene as a sequence of DNA that specifies production of a functional product, be it a polypeptide or a functional RNA molecule.

The concept of a gene predates our knowledge of DNA by several decades.  My understanding of the original meaning of the term "gene" is that it was thought as whatever it was that conferred a heritable trait to individuals, and that could mutate and (in the case sexual species) segregate independently (of other such "genes").

Therefore, I don't see why, for example, a distant enhancer (which does not code for product) would be considered a gene.  After all, it is inherited, and could conceivably exist in various forms ("alleles") in the population.  These various forms could have different effects on the phenotype, and thus be grist for selection, just like any other gene.

Are there example of such "non-product" genes?  If so, how common are they?

TL;DR - It's just a scientific convention. Whether it is good, broad enough etc is another question.

The question is a bit like asking why in mathematics, the set of natural numbers does not contain negative numbers. The reason is simply because it was defined like that as it was considered a useful working definition.

As you noted the definition of a gene has radically changed, from being defined by the oberved phenotype, to a molecular definition agnostic to functional consequences.

Maybe your interpretation of the old definition of a gene (as an inheritable, modifiable piece of genetic information) is correct, but modern nomenclatures tend to focus on what one may call defining "minimal functional categories". You could define a gene as a group of all the sequences that lead to a given phenotype, sure, but for a complex phenotype like "being tall", you would have to include a huge part of the genome in your definition of the gene (growth factors, transcription factors, cellular metabolism, all of it!!). Pretty much anything could be a gene of some kind given a certain context. And if everything is a gene, well, then the definition is too broad and not really useful.

That is why a bottom-up definition is more useful: define the gene as small units that may or may not infuence certain phenotypes, and then define the phenotype as the result of all the genes involved.

Many things that can be inherited and that exist in various forms are the product of distant pieces of DNA, some coding for proteins, others for regulatory RNAs, so the scientific community decided to define the gene as the "minimal functional unit" of genetic information. That does not mean that each gene is unaffected by other factors (just like for example a "cell" is a functional unit but must be considered as a part of a broader context to understand how it works), so genes may interfere with each other, overlap etc.

It's also important to emphasize that the gene is not only the protein/RNA coding sequence, but also includes promoter regions, untranslated ends and many other regulatory elements that can also have inheritable phenotypic consequences. So pretty much anything functional is part a gene; enhancers are a special case, and a recent challenge to this contemporary definition of a gene, because they challenge the previously accepted notion that genes are structurally continuous and therefore spatially well-defined.


Significance of upper-case, lower-case and Ns in UCSC DNA files I have downloaded human chromosome's data from UCSC FTP. Some part is in small alphabets and some is in large alphabets. Does it show the coding and non-coding region?

Here is an example from the file I just downloaded:

gagaatcccttgaacccgggaggcggagcttgctgtgagccgagatcgca
ccactgcactccagcctgggtgacagagccagactccgtctcaaaataaa
taaataaataaataaataaaAAAGAAAAAGGTTAATACAACATTAAAGAA
CAAGAATTAATATAGCtttttttttttttttttttttttgagacctagtc
tcactctgttgcccaggctggagggcagtggcatgatctcagctcactgc
aacctccgcctcccgggttcaggcgattctcctgcctcagcctcccgaat
aggtgggattacaggcgtgcaccaccatgcctactttttgtatttttagt
agagacggggtttcactatgttggccaggctggtgtcgaactcttgacct
caagtgatctgcctgccttggcctcccaaagtgctgggatgacaggtgtg
agccactgcacctggccTAATATAGCTTTAATAGAAAAGGAGCTAATACA
AGCTTAGAATAATAAACTTTATGCAGACTTACTGAAACAAACAGTCAATG
CAACCTTAACCAAACAGGAATTGATAACAGTTTAATAAAAAAGCTAATAC
CACTTGAATAGAATATATCTTACTACAACCTTCATAAGAAAAACAACTAA
TAcactttgggagaccgaggcaggcagatcacgaggtcaggagatcgaga
ccatggtgaaaccccgcctctactaaaaatacaaaaaaattagcctggca

Second strange thing is to see it beginning with sequence like NNNN. Like here it is:

>chrX
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
NNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNNN
ctaaccctaaccctaaccctaaccctaaccctaaccctCTGaaagtggac
ctatcagcaggatgtgggtgggagcagattagagaataaaagcagactgc

So the question is two fold:

What is the difference between upper and lower case in nucleotide fasta sequences?
What are the repeating N characters denoting?

Lowercase letters indicate repeat-masked regions. N's represent gaps.

See:
https://groups.google.com/a/soe.ucsc.edu/d/msg/genome/S4Sx8UdJAwM/tLTpVVzdhFMJ


What is the attacking mechanism of RF on IgG? Rheumatoid Factor (RF) attacks Fc portion of Immunoglobulin G (IgG), I want to know the underlying mechanism at molecular level. Also, what type of bond or attachment is made by RF and Fc portion of IgG?

// I'm a student of mathematical physics and have no detailed knowledge in biology, this question comes in my mind because my sister is suffering from Rheumatoid arthritis. All I want is to understand this disease from physical aspects//

RF factors comprise antibodies that your body makes that exhibit auto-immunity (recognition of self as an antigen). They often recognize and bind to IgG antibodies as illustrated in this picture:

So the answer to your first question is that the underlying mechanism is inappropriate recognition of self from your immune system.

For your second question, I am not an expert in the type of chemical bonds employed by antibody-antigen interactions, so I looked it up briefly. This article was quite informative for that: Antibody/Antigen Complexes.  The majority of binding seems to be hydrogen and ionic binding.

Hope that gets you going in your own searches.


Giardia lamblia cases of infections I am wondering if anyone has seen a data of Giardiasis (Giardia Lamblia) cases  in different countries on the world? I have found for different diseases and also for 'diarrhoea diseases' in general, but I need especially for Giardia Lamblia.

Any suggestion where I can try to look for this data will be useful.

Thank you very much!

If you have or can get access to it, you might try looking in the Incidence and Prevalence database: http://thomsonreuters.com/incidence-and-prevalence-database/

Another possibility is the GIDEON database: http://www.gideononline.com/. It is possible to sign up for a 15-day trial.

For Europe, statistics are available from the WHO CISID at http://data.euro.who.int/cisid/ (select "all infectious diseases", then "Giardiasis").

The WHO does not have any global statistics available on their website, so otherwise you might have to piece together data from individual publications. Some examples:

Thailand, 2005: http://www.ncbi.nlm.nih.gov/pubmed/16438174

Germany, 2006: http://www.ncbi.nlm.nih.gov/pubmed?term=19404678

United States, 2006-2008: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5906a2.htm

Portugal, 2002-2008: http://www.parasitesandvectors.com/content/5/1/22

Quatar, 2008: http://www.parasitesandvectors.com/content/4/1/211

Tajikistan, 2009: http://www.parasitesandvectors.com/content/4/1/195

Ivory Coast, 2009: http://www.parasitesandvectors.com/content/4/1/96

Tanzania, 2011: http://www.parasitesandvectors.com/content/6/1/3

Ghana, 2006-2009: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170632/?report=classic

Canada, 1999/2002: http://www.biomedcentral.com/1471-2334/5/72

Canada, 1990-1998: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC194172/

China, 2012-2013: http://www.biomedcentral.com/1471-2334/14/25

Ethiopia, 2009: http://www.biomedcentral.com/1471-2334/13/419

Kenya, 2010-2011: http://www.biomedcentral.com/1471-2334/13/243


What is the brightest color a light source that only emits blue frequency light can achieve? Let's say there is a luminous light bulb that only emits blue light, and you (or a camera if you prefer) look at it from a close distance. Will the maximum brightness perceived not have any "white" to it? Because there is no white light if it's all blue. Probably the brightest it could be would be solid blue? Therefore, blue photons could produce a range of color of black to solid blue depending on the luminous or amount of photons hitting your eye per second? If that's the case then what happens if you raised the intensity of the bulb to an extreme? Is there a cut off point where even if you add more intensity to the bulb, you still see the same solid blue color?

The color that human vision perceives for a specific frequency of light (prior to saturation of any cones) is derived from the relative responses of different cones.  For example, at about 480nm, the response of S and M cones are roughly equal.  However, the human eye is not able to distinguish pure colors (single wavelengths) from combinations of wavelengths which produce the same response in each of the three cone types.

It is possible that a blue light source could appear white to the human eye, because the cones which inform our perception of color are not strictly monochromatic.  Rather, they have a range of sensitivity across the spectrum, and all cones are at least somewhat sensitive to blue light.  (See this diagram.)
If the blue light is so intense that it saturates all cones, S (blue), M (green), and L (red), then it will be perceived as white light.  However, in order to saturate the low-sensitivity M and L cones, the intensity of the light would be blindingly high.  Prior to this point, but after saturating the S cones, the apparent color of the light would shift toward green before eventually appearing white.  For intensities that are not saturating to any cones, the hue of the color blue will remain constant, while it's value (or lightness) may change.


What is an adjective that describes the property of conferring fitness? I find it wordy to repeat

  trait X is a trait that confers fitness.

I wonder if I can instead write

  trait X is useful.

If not, is there an adjective that describes this property of conferring fitness?

Terms

A trait variant that is associated to a higher fitness than another variant is said to be beneficial or sometimes adaptive. On the other hand, a trait variant that is associated to a lower fitness is said to be deleterious or sometimes maladaptive.

"beneficial / deleterious" vs "adaptive / maladaptive"

The terms are very similar but I would tend to think that there are tendencies of using either "beneficial / deleterious" or "adaptive / maladaptive" depending upon the specific context.

These terms can also be used when talking about genetic variants and not only phenotypic trait variants. In evolutionary genetics, the terms "beneficial / deleterious" are used more often than "adaptive / maladaptive".

Also, in general, the terms "adaptive / maladaptive" are often used in absence of variation for the trait in question in the population while the terms "beneficial / deleterious" are most often used when there is variation in the population.

Note

Note that trait X is a trait that confers fitness does not make much sense as is explained here.


Biostatistics: Pollen dispersal directionality What Information am I looking for?

Think about a tree that is sending pollen all over the place. Because of wind, most pollen grain will go toward one direction. Imagine, we split the 2D area around the tree where pollen grains fall into two half disks of equal size. We chose the disks so that the number of pollen grains falling into one half-disk is minimized and the quantity of pollen falling in the other half-disk is maximized.

The information I need is what proportion of pollen grain falls into each disk? Is it $\frac{0.5}{0.5}$ (in which case the wind would have no effect) or is it something like $\frac{0.8}{0.2}$?

Where to get the information from?

I was reading this paper about pollen dispersal directionality and was trying to extract the info I need.

On pages 4 and 5 they explain their analysis under the section statistical procedure. More specifically, in the first paragraph of the 5th page, they seem to describe the meaning of the parameters that are trying to estimate. One of them is the so-called directionality parameter $\delta$. I don't understand how to interpret this parameter $\delta$.  This parameter is part of a logistic regression I think (although the authors do not characterize it as such) of "mating success" $y$ against variables $d$ ("distance") and $h$ ("height") and an angular variable $a = \cos(\alpha_0 - \alpha)$.  ($\alpha_0$ is the "presumed prevailing direction of effective pollen dispersal," which apparently is not estimated from these data.)  The corresponding parameters of the model are $\beta$, $\gamma$, and $\delta$, respectively, hence

$$\phi_j = \Pr(y_j = 1) = \frac{\exp\left(\beta d_j + \gamma h_j + \delta a_j\right)}{\sum_{k=1}^r \exp\left(\beta d_k + \gamma h_k + \delta a_k\right)}$$

where the index $j$ ranges over all $r$ "male(s) in the neighborhood."

Their Results

Using maximum likelihood, they found that the directionality parameter, $\hat\delta = 0.56$ (SE = $ 0.15$; bottom of page 6).

Question

How can I relate their finding to the information I need (even if it is just a rough approximation)?

I think I have to understand the so-called directionality paramter $\delta$ Can you help me to interpret the meaning of this parameter $\delta$?

Reference:

Burczyk, Adams, & Shimizu, Mating patterns and pollen dispersal in a natural knobcone pine ... stand.  Heredity 77 (1996) pp 251-260.

Not receiving any answer on Biology.SE, I asked the same question here on Mathematics.SE but sadly, the question doesn't receive any attention!

(This isn't an answer, but hopefully it will help get it past the experimental design into just solving the equation.)

Where did you get that α0 was not determined from their data? On p. 10 (256), they state, "The prevailing direction of effective pollen dispersal within neighbourhoods (a0) that gave the best ﬁt of the model was 91 degrees from north (nearly due east)."

The best-fit δ parameter value of 0.56 (which determines the size of the effect of the angle between the male tree and the wind) is also determined by their model (table 1, model 9) based on their sample set.

This math is too much for me to solve, but here is how I would go about getting through the experimental setup to just solving the math equation:

Since you're only looking for the effect of wind/directionality, you would set the tree height and distance between trees to be equal. So βd and γh would remain constant and cancel out when you solve for a.

Then you want to determine what angles would give you the highest and lowest pollen counts. Set a0 to wind direction and aj to the angle between a0 and the half disk. The highest pollen count would happen at aj = a0. The lowest pollen counts would happen at aj = (a0-180) or (a0-π or whatever unit of angle is appropriate. Stupid trig.).

With those settings, it should be possible to determine the values of ϕ where aj = a0 and where aj = a0-180.

Then you can get the proportion of pollen grain falls into each disk by finding the ratio of ϕj(a0-180) / ϕj(a0).

Assumptions:
1) There's a linear correlation between ϕ, "the mating success (i.e. fertility) of each outcross male in the neighbourhood" and the distribution of pollen grain dispersal.

2) That a0 ("The prevailing direction of effective pollen dispersal within neighbourhoods") is entirely due to wind. Here I could see terrain being a factor, which would make the effect of wind xδ, such that x<1. If this were the case, the calculated ratio of high pollen / low pollen would be higher than actual.


Can the extinct Chinese Paddlefish be revived? I learned that a rare and unique giant Chinese Paddlefish recently became extinct. I'm wondering if samples of DNA were collected by scientists to allow reviving of the specie in the future.
My quick Google check only revealed one paper that studied DNA of the fish 15 years ago - so there is a possibility that some DNA information exist out there. But is it enough to restore the species?
I'm interested in learning about any organisations or projects that would systematically collect genetic material of all endangered species. Is there a way to ask them about this specific fish?

Informally speaking, there is no real/good way to bring back extinct species. Especially sexually reproducing species; you'd need to revive a male and a female at the very least, and these are markedly different genomes due to unique sex chromosomes.
Some 'bad ways' exist though; in principle, if you found a perfectly preserved nucleus (the organelle that holds genomic DNA of most eukaryotes), it may be possible to insert this nucleus into a sibling or sister species (e.g. wooly mammoth nuclei into denucleated elephant zygotes). This would be the cloning approach. However, you then run into practical issues. You have to guarantee that this embryo will implant itself, which itself is not always the case. The nucleus and chromosomes must also be intact enough (which may not be the case after storing them, e.g. in ice, which may require thawing which often damages cellular structures) to create a rather healthy, fertile organism that will breed at a sufficient rate to restore a stable population. These and many more complications will reduce your chance of rescuing an extinct species to near-zero. Even then, one could argue that it is an incomplete de-extinction because you've only substituted the genomic DNA, and not other parts of the genome (e.g. chloroplast or mitochondrial genomes) which are part-and-parcel of the genetic signature that makes a species a species.
Alternatively, you can create hybrids where fragments of DNA from extinct species are brought into the genomes of similar existing species, by molecular methods such as recombination using CRISPR/Cas9. Here though you are only creating hybrids, not reviving extinct lineages. The extent to which you could do this is also limited and you would have to increasingly troubleshoot why a hybridization didn't work the more host genome you replaced with the extinct species' genome. Transgenesis using individual genes (say, transfering an enzyme into a new organism) is quite plug-and-play, but replacing entire chromosomes would be near impossible to pull off, not least because you would have little insight into why things aren't working - only that they aren't.


What metabolically happens when an egg fuses with the nucleus of a somatic cell In stem cell biology, it is recognized that embryonic stem cells are transcriptionally inactive for the first 3 days of development. However, during somatic cell nuclear transfer, the nucleus is likely to include various polymerases and RNA both coding and non-coding. Does this affect the success rates of cloning?

Somatic cell nuclear transfer is a method for creating a viable embryo from a somatic cell and egg cell. A somatic nucleus is inserted into an enucleated egg, where the somatic nucleus is reprogrammed by egg cytoplasmic factors to become a zygote (fertilized egg).
This requires the use of eggs in metaphase II of the cell cycle. Somatic cell nuclei must be in interphase (G0/G1). Interphase is the portion of the cell cycle that is not accompanied by observable changes under the microscope.
What determines the success rates of cloning
Oct-4 and other yamanaka factor expression is essential for somatic cell nuclear transfer success (Pay-wall).
Outlined here:

"...we now think that the oocyte cytoplasm might reprogramme the somatic cell nucleus too strongly, or that the somatic cell nucleus is more sensitive to oocyte reprogramming factors than are sperm cell nuclei."

Thus, Reprogramming and cloning success is unlikely to be influenced by somatic nucleus polymerases and RNA.


Typical DNA replication times Just out of curiosity (I am completely strange to biology), as I have been unable to find this info on the internet:
How long does the whole DNA replication process take? (say, the replication of a whole chromosome)
Approximately, how long does the DNA spend in a single helix structure during replication?

I am curious about the time scales of these processes, from the moment the polymerase starts cutting the double helix till the moment there are two double helices perfectly formed (one of them a copy of the other). How long can this take? miliseconds? seconds?

A mammalian cell takes about 8 hours to replicate all of its DNA in its S phase; a yeast cell would take about 40 minutes.
Some other information that you seem to not have quite the right information about:

The DNA polymerase does not unwind/split the DNA—that is the job of DNA helicase. The DNA polymerase cannot bind to the single-stranded DNA until the helicase unwinds the double-stranded DNA ("melts"), or the dsDNA is artificially melted in a test tube via high temperature.

The dsDNA is not fully separated before it is copied. There are tens of thousands of sites—origins of replication—across the genome that unwind and begin replicating every time the cell replicates its genome.

"...DNA replication in most eukaryotic cells occurs only during a specific part of the cell-division cycle, called the DNA synthesis phase or S phase. In a mammalian cell, the S phase typically lasts for about 8 hours; in simpler eukaryotic cells such as yeasts, the S phase can be as short as 40 minutes."
"An average-size human chromosome contains a single linear DNA molecule of about 150 million nucleotide pairs. It would take (0.02 seconds/nucleotide) x (150e6 nucleotides) = 3e6 seconds (about 35 days) to replicate such a DNA molecule from end to end with a single replication fork."
"...Approximately 30,000–50,000 origins of replication are used each time a human cell divides."

–Molecular Biology of the Cell, 6e, Alberts, et al.


What is the difference between these terms: clade, monophyletic group and taxon? Wikipedia definitions for these terms are pretty similar:

http://en.wikipedia.org/wiki/Clade
http://en.wikipedia.org/wiki/Monophyletic_group
http://en.wikipedia.org/wiki/Taxon

They sound like the terms are synonyms. Why there are separate articles for them then?

Is it true that every person is a reptilomorph and an eupelycosaur just like he/she is a mammal?

Bonus question: what is the difference between a cladogram and a phylogenetic tree?

PS Please don't just give definitions and/or quote Wikipedia. Point out the differences, if any. Even better, provide examples that can be considered one but not the other.

A taxon (Plur. taxa) is any (monophyletic or not) group of species. For example the group of yellow flowers is a taxon. The group of primates is a taxon. The taxon of aquatic animals is a taxon.

A clade is a monophyletic taxon or monophyletic group if you prefer. A monophyletic taxon (or a clade) is defined as a taxon that contains only all descendants of a common ancestor and the common ancestor. On the following picture, only the Taxon 1 is a clade.

To cite few examples of clades: Primates, Eukaryotes, Rosacea, Reptilomorpha, Rodentia. (The links yield to tolweb.org. See below for more info about this site)

A cladogram is some kind of reduced evolutionary tree that only shows the branching pattern but the length of the branches does not carry any information. At the opposite on a evolutionary tree the lengths of branches usually indicate the inferred time from the divergence.

I think the best tree you can find online is tolweb.org. You can find here the clade of Reptilomorpha and here the clade of Eupelycosaur. As you can see from these links, the mammals form a clade within the Eupelycosaur which itself is a clade within the Reptilomorpha. So yes, every human being is a Reptiliomorpha/Eupelycosaur/Mammalia. You can have fun going through this evolutionary tree and see what are the common ancestors between human and other mammals, human and turtles, human and jellyfish, human and plants, etc… to cite just a few relationships you might be interested to look at.


Cell line immortalisation biosafety Cell lines are often immortalised by artificial expression of proteins which specifically cause the knockout of important cancer suppression genes or the activation of proto-oncogenes.

  Cellular immortality happens upon impairment of cell-cycle checkpoint
  pathways (p53/p16/pRb), reactivation or up-regulation of telomerase
  enzyme, or upregulation of some oncogenes or oncoproteins leading to a
  higher rate of cell division.

However, this would appear to fall under the purview of Biosafety Level 3 since the protein expression vectors are capable of causing cancer in the researcher when they infect the researcher. Cancer can certainly be considered a serious or lethal disease, and aerosolisation of the vectors, while rare, is not impossible (for example during a spill).

According to the biosafety definitions of Columbia University,

  Agents: serious or lethal diseases transmissible via aerosols, e.g.,
  M. tuberculosis, SARS.  Recombinant DNA activities using genetic
  material from BSL-3 organisms or such organisms as host cells.

Why then, does the CDC classify cell line work, including work with viral production cells, as a BSL-2 activity requiring only BSL-2 containment levels, when the act of immortalising the cells would involve working with viral agents that can cause cancer?

  Cells immortalized with  viral agents such as SV-40, EBV adenovirus or
  HPV, as  well as cells carrying viral genomic material also present
  potential hazards to  laboratory workers. Tumorigenic human cells also
  are potential hazards as a  result of self-inoculation.[...]

  Human and other primate cells should be handled using  BSL-2
  practices and containment. All work should be performed in a BSC,  and
  all  material decontaminated by autoclaving or  disinfection before
  discarding. BSL-2  recommendations for personnel protective equipment
  such as  laboratory  coats, gloves  and eye protection should be
  rigorously followed.

Are the transformation cells (eg the 293T viral cells containing the transformant viruses) considered Level 3 biosafety risk, and if not, why not?

Maybe, cells should be contained under BSL-2 and agents (viral particles etc) under stricter BSL-3? That is, after immortalization you can keep cells under lower security.

  Biosafety Level 2 builds upon BSL-1. BSL-2 is suitable for work involving agents that pose moderate hazards to personnel and the environment.

  Biosafety Level 3 is applicable to clinical, diagnostic, teaching, research, or production facilities where work is performed with indigenous or exotic agents
  that may cause serious or potentially lethal disease through the inhalation route of exposure

  CDC Biosafety in Microbiological and Biomedical Laboratories, Laboratory Biosafety Level Criteria

As of HEK 293 cells, check this out:

  Biosafety level 2 practices and containment facilities for all activities involving HEK-293 cell lines.

  HEK 293 Cell Line Risk Assessment - IBC


Genomic DNA isolation from wheat Can I use dry seed, wheat for example, in place of young leaves for isolation and purification of genomic DNA for PCR amplification?

The goal of my experiment is to validate a novel gene which is either absent or present at a particular chromosome.

Yes sure I tried this and give good result. But you most chose the best protocol and need to be do this manually. I recommend that use CTAB-PVP (which is use 3 buffers EBA EBB SDS %10) extraction method from "Integrated DNA technologies" and if you cant find this I will tell You.


Genetic Recombination and Mutation Can genetic recombination yield mutation depending on the new DNA that is incorporated into the genome? I would say yes because when something foreign comes in, the genome is bound to not function properly.

When you say "new DNA that is incorporated into the genome", it suggests that you misunderstand what genetic recombination. You might to ensure you really understand this concept before going any further.

Mutation rate and recombination rate tend to covary throughout the genome (Lercher and Hurst 2002). So, yes processes leading to recombination events also tend to cause mutational events.


How do membrane proteins find their target locations? The question might be asked for any kind of "bound" proteins, but I'd like to restrict it to membrane proteins.

Assuming membrane proteins (or their main parts) don't (or aren't) build in situ but at some distance of the membrane, I wonder by which mechanisms they travel from their generation site to their final destination inside the membrane (inner or outer).

Proteins that are distributed roughly evenly (or randomly) over the membrane don't pose a big conceptual problem: they could have gone their just by diffusion, possibly from many generation sites, distributed roughly evenly (or randomly) inside the cell.

But what about uneven distributions, where some proteins are more densely and non-randomly packed (significant and functional) at some sites of the membrane than at others, e.g.

receptors at postsynaptic densities
Na+ channels at action potential initiation sites like the axon hillock or the axon initial segment
Na+ channels at nodes of Ranvier?

By which mechanisms (forces, signals or structures) are these proteins led to
 their targets?

Maybe it depends, and there are different mechanisms. These I came up with (by contemplating first principles):

uneven distribution of generation sites inside the cell (due to what?)
uneven distribution of origins of attracting signals inside the membrane (due to what?)
some "self-attracting" forces or signals (leading to accumulation by positive feedback)
microtubules

Which mechanism is — possibly — predominant?

Related questions:

Life cycle of proteins
Pathways of ligand-gated ion channels
Distribution of synapses of CA1 neurons
Distribution of dendritic spike generating ion channels on the dendritic tree
Visual maps of the neuronal membrane
Distribution of sodium–potassium pumps

This is a great question. A comprehensive answer would be beyond the scope of an answer on a forum like this. I will summarize the best I can here, but if you are really interested in this you should look at some of the work by Randy Schekman and Tom Rapoport, who have done a lot of pioneering work in this field and have papers from more than two decades ago on their lab websites. I'll talk about membrane proteins generally, but I'm not sure what the state of the field is for Na+ channels specifically, so I can't comment too much on that particular case. Many of the details of the processes I will mention are still areas of active research, so I will try to stick mainly to what has been well-characterized (to the best of my knowledge).

To restate the problem, proteins are generally synthesized in the lumen of the endoplasmic reticulum, which is an aqueous environment similar to the cytosol in many (but not all) ways. However, membrane proteins, which are not stable in aqueous environments, must:

1) Find a way from the ER lumen into a membrane.
2) Get from the ER into the correct membrane so they may perform their cellular function.

We will start with step 1, but the key to both is a critical but often underappreciated aspect of protein biology called the signal peptide. The signal peptide is simply an N-terminal sequence of amino acids that precedes what we would normally think of as the beginning of a mature protein. It is relatively short, usually only ~30 amino acids in length. It is cleaved off the mature protein by a protease once the protein is folded and in the membrane. Until that time, the signal peptide serves as a molecular marker that indicates where the nascent protein should be heading and how it should be handled. Not surprisingly, there are many different signal peptides that serve multiple functions, and they are not only used for membrane proteins.

So let's say we are in the ER lumen, and have some mRNA coding for a membrane protein that is destined for the plasma membrane. The first amino acids that will emerge from the ribosome is the signal sequence, in this case a specific signal sequence indicating that this is to be a plasma membrane protein. Once the signal sequence emerges from the ribosome, it is recognized by a ribonucleoprotein complex (that is, a complex of RNA and protein) called the signal recognition particle. Once the SRP binds to the signal peptide, translation is halted, and the whole complex moves to the ER membrane, where it forms a complex with another large protein complex called the translocon. I can't go into the intricacies of these complexes and their functions in this answer alone, but the simple description is that the translocon contains an ATPase that can insert the membrane protein into the ER membrane as it is translated, with the correct orientation. The hydrolysis of ATP provides energy to move the emerging polypeptide chain into the hydrophobic membrane, where chaperones help it fold. This process is in part driven by the recognition of hydrophobic transmembrane regions of the proteins by the translocon. It can also move soluble, cytosolic proteins across the membrane through a similar mechanism.

Now that the protein has been translocated, a peptidase will cleave the signal sequence off the protein. From here, sorting signals will take over. Generally, these are simple sequence motifs in the first transmembrane domain that act similarly to a signal sequence, but they are not cleaved. However, sorting signals can be stretches of peptide throughout the protein too, in some cases.

These sequence motifs will be recognized by cell trafficking machinery. Without going into too much detail, the proteins will be gathered into vesicles, and transported to other organelles. Usually, the first stop for proteins is the golgi apparatus, which is typically where many post-translational modifications, such as glycosylation, take place. I am a biochemist and not a cell biologist, so I am not the most qualified to go into the details of subcellular trafficking. Suffice it to say, once the protein is finished being processed in the golgi, it will be trafficked into other organelles, such as the plasma membrane using vesicle transport as before. From my understanding, the protein will be sorted into the proper vesicles based on its sorting signals, as well as other markers (in some cases, certain post-translational modifications on certain proteins can influence its trafficking). The vesicles recognize the proper destination membrane in part by the lipid composition of that membrane. For example, phosphoinositides have extensive influence on membrane trafficking, and many membranes can be differentiated by their phosphoinositide signature.

Anyway, that is a very broad overview of the answer to your question. I'm sorry I can't comment too much on the intricacies of cellular trafficking, I don't quite have the expertise to go through that literature quickly enough to answer your question in a reasonable time frame. I hope this is helpful in pointing you in the right direction, and good luck!


How does a person get AIDS? I am inquisitive to know about how a person contracts AIDS.
Among the common masses it's still the belief that having sex with multiple partners causes the disease but that is not the case when read online that it can come only from persons carrying the virus.

So, if a person (male or female) is carrying the virus (HIV positive) does it mean that he/she is suffering from the disease or the person may be carrying the HIV disease and still be free from AIDS. If so how did this chain reaction of spreading the virus start?

Also is it true that immune systems of some rare people in this world can fight with this disease.

You read right: it can only come from people already infected through:

sexual contact
contact with an infected person's body fluids (blood transfusions), although not all fluids carry HIV (saliva, tears)
from mother to child (pregnancy, breast feeding)

Having unprotected sex with multiple partners statistically increases the risk of stumbling upon someone infected.

A person carrying the HIV virus may not show symptoms of AIDS, because the HIV infection passes through a stage of clinical and symptomatic latency (the asymptomatic HIV or chronic HIV) which can last up 20 years (average of 8 years) when only uncommon symptoms like fever and weight loss show up.

Where it started? It is believed that HIV originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. The virus adapted and became strong, because the virus from primates is typically suppressed by the human immune system within weeks of infection.

HIV is a retrovirus that primarily infects components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.

So it destroys the cells reponsible of its removal from the human body. Hard to believe that there are people whose immune can really destroy the virus. A virus lives inside the cell it parasite, so the immune cells must destroy one the other. Also the virus infects and kills them (the good ones). However, as MattDMo suggested an infected person may take antiretroviral drugs and the disease progression can be slowed down.

Source: Wikipedia - HIV, AIDS


Can a human actually be "frightened to death?" I've been watching some classic horror movies as of late, and a trope I see in many of them is where a person will see the big bad monster and "die of fright." I'm curious, for the average person, could this happen? Or would it require a prior medical condition of some kind?

The people whom this happens to consider themselves average people.

The thought is that catecholamine surge caused by the event triggers some predisposition to cardiac arrhythmia - maybe inherited, maybe due to medicines.  People predisposed to this sort of arrhythmia probably do not know that is the case, and consider themselves to be average people.  It would seem that the victims of this are not average and have some sort of predisposition to that problem.  There is a lot of interest in figuring out who there people are in advance - not in the context of being frightening to death but in the context of SUDEP - sudden death in epilepsy.  Epileptic people sometimes just die, presumably for cardiac reasons, but there is no way of knowing who among this large group is at risk.

In the following abstract the frightening thing is being restrained.  Other circumstances that produce a catecholamine surge can do it too.

https://www.ncbi.nlm.nih.gov/pubmed/25628339

  Med Sci Law. 2016 Apr;56(2):85-90. doi: 10.1177/0025802414568483. Epub
  2015 Jan 26. Sudden cardiac death with stress and restraint: The
  association with sudden adult death syndrome, cardiomyopathy and
  coronary artery disease.

  Krexi L1, Georgiou R2, Krexi D1, Sheppard MN3. Author information
  Abstract OBJECTIVE: The aim of this study was to report on sudden
  cardiac death (SCD) during or immediately after a stressful event in a
  predominately young cohort. METHODS: This study used retrospective
  non-case-controlled analysis. A total of 110 cases of SCD in relation
  to a stressful event such as altercation (45%), physical restraint
  (31%) in police custody (10%), exams/school/job stress (7.27%),
  receiving bad news (4%), or a car accident without injuries (2.73%)
  were retrospectively investigated. The majority of the subjects
  experiencing SCD were male (80.91%). The mean age was 36 ± 16 years
  (range 5-82 years). Twenty-three cases (20.91%) were psychiatric
  patients on antipsychotic medication. RESULTS: Fifty-three per cent of
  cases died with a negative autopsy and a morphologically normal heart,
  indicating sudden adult death which is linked to cardiac
  channelopathies predisposing to stress-induced SCD. Cardiomyopathy was
  found in 16 (14.5%) patients and coronary artery pathology in 19 (17%)
  patients, with atherosclerosis predominating in older patients.
  CONCLUSIONS: This study highlights SCD during psychological stress,
  mostly in young males where the sudden death occurred in the absence
  of structural heart disease. This may reflect the proarrhythmic
  potential of high catecholamines on the structurally normal heart in
  those genetically predisposed because of cardiac channelopathy.
  Structural cardiomyopathies and coronary artery disease also feature
  prominently. Cases of SCD associated with altercation and restraint
  receive mass media attention especially when police/other governmental
  bodies are involved. This study highlights the rare but important risk
  of SCD associated with psychological stress and restraint in
  morphologically normal hearts and the importance of an expert cardiac
  opinion where prolonged criminal investigations and medico-legal
  issues often ensue.


What is the optimal frame size for protein secondary structure prediction methods? The whole question is

  What is the optimal frame size for the second and third generation protein secondary structure prediction methods? Justify your answer.

I remember it has something to do with the average length of alpha-helix. More specifically, 3 on both side of a site. So in total the frame length should be 7. But I can't remember the reason behind the argument.

What do you think?

According to what my professor said in class, 2nd and 3rd generation of protein secondary structure reconstruction relies on statistics data of several consecutive residues.  I guess what he meant by "frame size", is how many adjacent residues we should take into account in the algorithm.

By frame size, do you mean sliding window?

I know that if you want to predict a secondary structure of a transmembrane protein, then your window size should be 20 amino acids (this is the average length of 1 transmembrane alpha helix spanning through the membrane).

I found this paper by Chen, Kurgan, and Ruan[1].

It basically says that the window size depends on what kind of pattern you are looking for, but in general, 19 residues should be optimal.

Also, secondary structure predictors rely on many features like hydrophobicity, missing coordinates in X-ray structures, B-factors, motifs, etc.

Chen K, Kurgan L, Ruan J. 2006. Optimization of the Sliding Window Size for Protein Structure Prediction. CIBCB '06: 2006 IEEE Symposium on Computational Intelligence and Bioinformatics and Computational Biology, pp.1-7, 28-29, doi:10.1109/CIBCB.2006.330959.


Basic question about symbiosis( or about kinds of symbiosis) Is there a type of symbiosis where an organism is harmed and the other is neither harmed nor helped?

If not, do you think there's a term for this sort of relation between two organisms?

I see that there exists some confusion over the meaning of Symbiosis itself [in reference to the comments and answer(s)].

Your question/ query seeking information about "some type of Symbiosis" that harms one organism without affecting the other in any form is very much legitimate.

Amensalism (as responded by Sanjukta) is indeed the answer, but saying that "No. There seems to be no intimate association (symbiosis) that does not benefit any partner" is suggesting that Amensalism is not Symbiosis (which is not true).

Amensalism is one of the types of symbiotic associations only (Symbiosis is nothing but 'Living Together' of two / more organisms - which may or may not benefit/ harm either or both or none of the parties involved in the association).

Point to be taken is that, Symbiotic relation refers to the members of two different species (i.e., two populations) engaging in interaction and the interaction can be of any type (Amensalism is just another Symbiotic association).

Edit:
If one looks into the Etymology of the word, Symbiosis, he/she should be able to decipher the meaning of Symbiosis:

One may support the argument using latest updation of Encyclopedia of Evolutionary Biology (Amensalism=Symbiosis) and the classical example of Walnut tree (which tends to kill or inhibit the growth of shrubs that grow around its roots) may be cited. Their growth is inhibited,  but their niche still remains the same. More importantly, the Honeybee - wasp relationship (a long term one) is best fit for Symbiotic Ammensalism.

So, Mutualism, Commensalism, Amensalism, are all Symbiotic Relations.

References:

Miami College of Arts and Sciences, Department of Biotechnology Lecture Notes

Wiki Link about Biological Interactions


Which kind of drugs get absorbed through epidermis? Some drugs such as nicotine can be administered through skin. I thought the layers of skin are designed to prevent in-flow of any chemical/germs. Not all drugs get absorbed in this fashion. So do drugs like nicotine have any specialities(such as a special chemical group) that fool the sentries of skin? A link to an article/site would be very helpful, or even a book recommendation.

According to a review (Prausnitz2004), marketed drugs with a dermal route of administration tend to fulfil the following criteria :

Small molecular size (< 500 Da)
High lipophilicity
Small required dose (up to ~milligram)

This is a consequence of the structure of the skin (with a lipophilic stratum corneum, and low diffusion speed) and practical concerns (everything else equal, a higher dose would need more surface area).

Beyond "pure" diffusion, there has been much work on improving drug delivery through other means : chemical enhancers (ethanol or DMSO being classical member of this class), medical devices (microneedle patch, ultrasonic device), and other more exotic methods mentionned in the paper.

These criteria are also mentionned in (GoodmanGillman2006, chapter 26), with emphasis on concentration gradient being the driving force behind diffusion across the skin. This chapter also contain a list of commonly used transdermal/dermatological drug, and their use.


Are there two varities of dandelion leaves? This is in India. I noticed a dandelion plant which had the familiar leaves.

Right next to it there was another plant which had similar flowers and white tufts, but the leaves were different.

Is the second plant also dandelion? I'm asking because I was considering feeding the leaves to my budgies, but needed to know if it is a dandelion, to avoid having the birds consume a toxic plant species.

Did a Google search, but all of them show the arrow-style leaves only as dandelion.

Although the leaves are similar, these are both not Dandelions Taraxacum species, because:
1. Dandelions have leaves in a rosette, not distributed along a stem.
2. Dandelions have a stem with a single flower at the end, not multiple flowers.
3. The shape of the closed flower heads after flowering is too pointed.     Dandelions usually have the pappus (white hairs) sticking out a little.

These distinctions can be clearly seen in the picture below:

I am not familiair with the flora of India, but I think these could be Sonchus species. Sonchus is known to have  variable leaves.

For comparative purposes, see how Sonchus looks like


How can flies sense mirrors? I've noted that flies in my house have no problem landing on even perfectly clean mirrors. Why don't they fly straight into them? Can they sense that there is a surface there, even though they can't see it?

It might be pretty straightforward. Common window/mirror glass is opaque to UV, so as far as the fly is concerned mirrors are just translucent surfaces.

This of course leads to the question of why flies can't see window glass. Maybe the large amount of light passing through at visible frequencies makes it look like a tinted fog to the housefly? Maybe they're trying to fly through mirrors too, but land on their feet and just roll with it?


Looking for raw cell videos from a light microscope First off, I'm not looking for online lectures.

I am trying to find creative commons licensed videos of live cells moving around without annotation or anything extra. I would prefer a few minutes of video of tumorous somatic cultures of eukaryotes in vitro and at a few different magnifications but it doesn't really matter. I don't have a microscope or I'd just get some pond water and look at multicellular organisms. The license must be creative commons or public domain, the author must be citable, and the subject organism should be known.

Any ideas where to find such video? Thanks!

The website you want is The Cell: An Image Library. They also have movies. A quick search of 'Homo sapiens tumor' revealed several Creative Commons videos of tumor cells moving around in vitro with attribution and no annotation or anything else. Sometimes the site can be a bit buggy, but it's a pretty awesome resource when it works.


When does BLAST fail to align 2 DNA sequences? This is an assignment that had confused me for a long time.  So I think you guys who study computational biology might be interested. The original question is:

  Find the two most similar DNA sequences of length 20 that Blast using a word length of 5 will fail to align.

BLAST works by finding a perfect match between sequences of a length equal to this "word length" and then enlarging it in a standard way -- yet there will be no alignment without this perfectly matched word.

So in your case, you must look for two 20bp sequences with no common 5bp sub-sequence; for instance:

AAAAAAAAAAAAAAAAAAAA

and

AAAACAAAACAAAACAAAAC


By what mechanism is NADP+ converted to NADPH in Photosystem I? Here is my current understanding:

$\mathrm{NADP^{+}}$ takes 2 electrons from Ferredoxin at the end of the electron transport chain to generate $\mathrm{NADP^{-}}$.  An $\mathrm{H^{+}}$ ion in the stroma binds through the extra electron, generating $\mathrm{NADPH}$.  All of this is facilitated by Ferredoxin-$\mathrm{NADP^{+}}$ reductase.

Sources: https://en.wikipedia.org/wiki/Ferredoxin%E2%80%94NADP(%2B)_reductase

http://www.bio.davidson.edu/Courses/Bio111/NADPH.html

OVERVIEW (verbatim from the article)

  Plastidic ferredoxin−NADP+ reductases (FNRs) accept electrons
  by two sequential one-electron transfer steps from two
  molecules of the one-electron donor ferredoxin to generate
  their fully reduced hydroquinone state, FNRrd, through the
  formation of an intermediate neutral semiquinone form, FNRsq.
  FNRrd then transfers both electrons as a hydride to the
  nicotinamide adenine dinucleotide phosphate (NADP+
  )
  coenzyme in a single step (Figure 1A).1,2

Theoretical Study of the Mechanism of the Hydride Transfer between Ferredoxin–NADP+ Reductase and NADP+: The Role of Tyr303 (Institutional access will be required!)

Basically, FNR is a flavoprotein with a stabilized FAD prosthetic group that can alternate 3 oxidation states with 0, 1 or 2 electrons. NADP+ binds in the FNR active site, and recognition of the AMP group causes a conformational change that brings the nicotinamide portion in proximity with the isoalloxazine group of the FAD. Ferredoxin is a single-electron carrier where two molecules of ferredoxin sequentially donate electrons to the FAD group that produces a hydroquinone FADH2. The actual architecture of the charge transfer complex formed in the active site mediates the formal hydride transfer that produces NADPH*. As far as I can tell, the hydride transfer occurs while the ferredoxin is still bound due to the effect electron transfer to FAD has on the pKa and protonation of a Glu312 that stabilizes NADP+ too much in the absence of ferredoxin (source).

NADPH ends up getting released after the catalytic cycle.

*I'm still trying to find some more detailed information on the catalytic mechanism.


"X" in stock solutions We prepare buffer solutions with concentration in terms of x, for example 50x TAE buffer. How do we come up with x? Is x related to molarity in some sense? And how much can we concentrate the solution. We have 50x TAE but usually 10x TBE buffer, why is it so?

1x is the final working concentration of the solution (it could be anything depending on the type of the solution). Stock solutions are made at a higher concentration; if it is 10 times more concentrated than the working solution then it is 10x.

  Why 50x TAE but 10x TBE?

The salts in TBE precipitate at higher concentrations. In other words, the salts in TBE have lower solubility compared to those of TAE. Therefore stock solutions of TBE are usually 10x or even 5x.


Expected dS/dN ratio for exome I am trying to determine whether or not my sequencing data has more/less non-synonymous mutations than would be expected. My understanding is that there is some fixed ds/dn ratio for the human exome that I can use to calculate this. Is this true? And how might I calculate this?

There isn't a fixed value for the human exome AFAIK, nor would it be a good idea to have a fixed value for the exome because different regions and genes can be under different selective pressures.

The norm is to compute the ds/dn ratio and then test against a null hypothesis of the ratio being 1 to infer if your region is under selection or not. If it is greater than 1 it indicates positive selection and if it is less than 1 purifying selection.

You can find a  decent introductory treatment here.


Coronavirus and temperatures An article on bioRxiv, Evaluation of heating and chemical protocols for inactivating SARS-CoV-2, recommends certain treatments to inactivate SARS-Cov-2 for lab work.
The abstract notes: "Although heating protocol consisting of 92°C-15min was more effective rather than 56°C-30min and 60°C-60min to achieve 6-log reduction, it is not amenable for molecular detection on respiratory specimens because of important decrease of detectable RNA copies in the treated sample vs untreated sample."
Do I understand correctly that 56C/30min is broadly as effective as 60C/60min? Given that 56C from previous research seems to be more effective than 22C, I would have expected 60C to require less time to achieve a similar effect to 56C. Especially with 92C/15min being more effective still, though more disruptive.
I'm curious what the explanation may be why effectivity might drop between 56 and 92C. Or why I may be misunderstanding the temperature/time scales. Please keep it simple. Thank you.

They only tested 3 heat treatment regimens: 56C/30min, 60C/60min, 92C/15min (6 if you consider the "with BSA" and "without BSA", but only 3 combinations of temperature and time). They didn't measure the time required at certain temperatures to get to a certain level of inactivation. It seems they chose some of these particular protocols because they have been recommended in the past for other viruses.
They don't really have sensitive enough data to compare the 56C/30min to the 60C/60min or really enough to do any sort of statistical comparison whatsoever (as far as I can tell they only tested a single sample of each); yes, you can say they were roughly as effective, but it would be a leap to say 56C is the same as 60C.


what is the meaning of VIP-cre::LSL-TOM::SOMGFP(GIN) mice? I am reading the following paper and the researchers use

  "VIP-cre::LSL-TOM::SOM-GFP(GIN)"

mice (page 4) for multi cell patch clamp and

  "VIP-cre::LSL-TOM and SOM-cre::LSL-TOM"

mice injected with AAV1 for two photon calcium imaging.

I have tried to look it up in the web.
I understand, for instance, that AAV1 is an engineered virus, and that CaMKII is a promotor, that TOM is a red fluorescent protein, GCaMPis created from fusion of green fluorescent protein with other peptides etc.

However, I have a dificulty in putting together the pieces and understending the whole meaning of "VIP-cre::LSL-TOM::SOMGFP(GIN)" (and the other mice types memtiond).

For example:

Take a VIP-Cre mouse. Does it mean that every VIP neuron in this mouse contains a Cre sequence in it's DNA?
What about other neurons, can they contain Cre also?
When they inject AAV1 virus to VIP-cre::LSL-TOM mice, does this mean that all neurons get the virus? including the VIP and SOM neurons?
Say I have an "VIP-cre::LSL-TOM::SOM-GFP(GIN)" mouse. I understand that VIP cells will be colored red and SOM cells will be colored green. So, why the VIP cells need the Cre promoter and the SOM cells don't?

I'll be greatfull if you could answer some of these questions, of refer me to a suitable reference. I looked a lot but the references that I find are lab references with technical details and numbers. I didn't find anything specific for this mice types that contains explanations.

Thank you!!

I think I can help explain all but your 3rd question.

A transgenic mouse will typically have the genetic construct in all cells. Unless you get a chimeric animal, which is screened for during the making of the mouse.
VIP::Cre means that the promoter of VIP was used in front of the region of DNA that encodes for Cre recombinase.  Note, the animal still has the endogenous VIP gene that makes VIP. This is an additional construct. The intent of this kind of system is to limit the expression of Cre recombinase to only the cells that would also be expressing VIP.
LSL stands for Lox-Stop-Lox cassette. LSL:TOM is the gene that encodes for tomato red protein with a premature stop in the transcript such that it never makes a correct protein (and no red).
If Cre is expressed in a cell with the LSL-TOM construct, it will recombine the LSL and remove the stop codon, thus enabling the creation of functional tomato red transcript and fluorophore (protein). Again, this construct is in the DNA of ALL cells, but the recombination event (and subsequent expression of function TOM) will only happen in the cells that are also expressing Cre recombinase. And for a VIP::CRE mouse this only happens in VIP expressing cells.

Your questions:

1) Actually every cell in the animal has a VIP::Cre (excepting blood of course or sex cells that got the non transgene allele during meiosis. This is because usually the cre genes are kept at Hets during mouse mating).

2) All neurons (and all cells; see answer 1) will contain the genetic construct VIP::CRE.  The intent is in the VIP::CRE mouse, only cells that would express VIP would express Cre recombinase.  This means that other tissues in the body that express VIP should also fluoresce red in a VIP::CRE/LSL-TOM mouse.  As an aside, all cells that normally make SOM should also be making GFP in the SOM::GFP mouse, but every cell will have the DNA transgene.

3) This question is outside my breadth of knowledge. I've done lots of work with transgenic mice, but other than looking up that that viral construct has something to do with calcium and imaging in neurons, I am not sure.

Per Bryan Krause: "...the expectation is that it will infect most if not all cells, not even just neurons, but it is using the 'synapsin' promotor which is neuron-specific (but would be expressed in both VIP and SOM cells, as well as other neuron types). Presumably the authors are using calcium imaging to detect activity across a whole mixed population but then using tdTomato to identify one subpopulation or the other, depending on which animal is used."

4) For VIP-cre::LSL-TOM::SOM-GFP(GIN).   As written, this would imply the expression of Cre is necessary to activate transcription and encoding of tomato red in VIP expressing cells. But that GFP is already active in SOM expressing cells from day one of development.

Some uses of Cre-Lox systems are illustrated here. This picture from that website demonstrates graphically what is going on with a LSL construct.

Your system has tomato red instead of lacz and is using VIP expressing cells as a targeted system.


What is variation in Speciation I read a lot about speciation. To my knowledge, a species is often defined as a group of individuals that actually or potentially interbreed in nature and produce fertile offspring. Speciation is a lineage-splitting event that produces two or more separate species.

Now, some creationists claim that there is no speciation, rather variation in the same species. As in "fruit fly experiment", I read that two groups of fruit flies don't interbreed after the evolution and speciation takes place. As per the definition of species (biological concept of species), they are supposed to be two separate species (reproductive isolation). Nevertheless, creationist claim they are still fruit flies and there is no speciation. They say that's just a variation in fruit flies, not speciation. I can't understand their claim.

You are asking explanations about a creationist argument. One could provide explanations about some hypothesis that you may found in a science paper but not explanations for a creationist argument just because, by definition, a creationist argument is not supported by any evidence and logical thoughts. However, you may want to link to a creationist website making a specific claim of interest and we may eventually talk about whether the claim is wrong/misleading. It would be very handy to have the claim in quotes rather than an explanation of what the claim is.

You say

  [..] after the evolution and speciation [..]

This piece of sentence sounds weird. You could say after the evolution of something (meaning the appearance of this something through evolutionary processes that are mutations, natural selection, drift and eventually others) but just "after the evolution" sounds as if evolution may not exist during some periods of time.

Talking about speciation in fruit flies, you will likely be interested in reading this post.

UPDATE

In general, when talking about fruit flies we talk about the Tephriditae. Tephriditae is a family of flies which contain about 5000 described species (including the model organism Drosophila melanogaster).

So, there is definitely different species of fruit flies. Of course, within any population (to the exception of populations of exact clones by definition), you have variation. This variation is a key concept in evolutionary biology. If this is unclear to you you may want to learn a bit more about evolutionary biology, including the concept of heritability ($h_N=\frac{V_A}{V_P}$).

Speciation took place in Tephriditae (otherwise we wouldn't have the species we have today) and is still taking place. The post I linked above gives an example of speciation between lineages of Drosophila melanogaster that has been directly observed in the labs.

Your issue seems to likely be a semantic one. As there is variation within a lineage and this variation is associated with groups that are in reproductive isolation, then the two lineages you consider do not belong to the same species anymore. Therefore, there was a speciation event.


How to obtain bacteria samples? Would anyone know how to go about obtaining samples of Salmonella or E. coli for purely educational purposes?

Note: I just want to look at the stuff under a microscope.

To be honest, you really shouldn't be buying such things if you're not prepared to handle them properly.  If you work with a proper lab, you will be inindated with vendors trying to sell you these and many others.

But to answer your question, if you are looking to purchase many such items ATCC is an excellent resource.  Not only will you have to meet regulatory requirements, but you will also have to deal with a great many MTA's depending on what you are trying to get.

In response to edit: Salmonella is actually not normally a serious pathogen to a healthy adult.  It is, however, still a human pathogen and should be handled under BSL2 conditions.  So if you have the funds and time to setup a BSL2 lab at your house, by all means go to town.  And I hope you don't live with any children, the elderly, or otherwise immunocompromised individuals.

In response to further edits:
If you just want to look at things under the scope, then I suggest you get started by making your own homemade culture plates.  If you can get your hands on some Lysogeny Broth (LB), agar, and petri dishes then you can make lb plates like a researcher in a real lab (minus an autoclave but you could use a pressure cooker).  These are items the public could get, but might be harder to come by.

I however will assume that you want to make your own plates from common household ingredients (I used to do this a lot as kid, whatever that says about me).

**

Making your own culture dishes:

**

1) The "plates" themselves.

I recommend getting the smallest Tupperware like
containers your can find that are microwave safe, dishwasher safe, and
really make a good seal (water tight at the least).  They really
don't have to be big, and you will make your life easier if you buy a
bunch to match.
They need to be super clean.  After running them through your
dishwasher at home, put them all in a boiling pot of water until you
are ready to pour in your "media." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.

2) Your "Media" or Broth

I highly recommend using pectin as your gelling agent if you can't
get your hands on some agar.  After that comes plain unflavored
gelatin, but I recommend pectin.  You can get it at almost any
grocery store and my recipe is made assuming that.  You can determine
how much you want to make, just scale up the ratios.  I'm going to
list things as rough volume by volume so you won't need a scale.

i) Make the powder first:

45mL of pectin;
4 bouillon cubes ground as finely as you can (you can get different
types and results depending on if you start with vegetable, beef, or
chicken.  I recommend starting with vegetable.);
125mL of refined white sugar;
Additives (more on this later)

ii) Mix the powder into 500mL of water

Before you mix in the powder, hear the water to 50-75oC (mid low
heat), but not boiling.  Mix the powder in while stirring until
dissolved.

iii) Bring the mixture up to a boil.
Let it boil for about 2 min, stirring all the while.

iv) Cover the pot and let it cool for 4-5 min.

You by no means want it cool down to room temperature, you just want to get it a little below boiling.  If you are at 55oC or bellow it's definitely time move on.

v) Dip/fill your "plates" 1/3 full of media using clean/sterile utensils and seal while hot but not boiling.

You may have noticed this seems an awful lot like canning, and that's because it is.  Again you want to be as clean as possible in this step and of course try not to burn yourself on anything.

vi) Let your media plates set and chill over night in the refrigerator.

You really probably only have to wait a few hours if you are anxious to get going.  You are going to want to store the plates that you are not using in the refrigerator anyway.  Also if you made a bunch of plates, let the cool on a counter before you put them in the fridge so that you don't raise the temp of your fridge too much.

Remember the thing about additives?  You can play around with adding different amounts and different types of salts, vitamins, food, or other items to see how they effect the cultures you get to grow.  All kinds of fun there.  First go round, leave them all out.

Now you have your own home made culture plates!  The above recipe was empirically tested by my childhood, and repeated by my son's.  Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company).  I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.

Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate.  While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.

Leave your plate in a warm wet place, but not in direct sunlight.  Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow.  On top of our dryer is where I leave.

After a day or so you should have colonies you can streak out on a slide and look under a scope.  You will find all kinds of things this way.  If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.

You are actually quite likely to run into E.coli if you sample enough "areas" this way.  Obviously don't eat or huff the stuff that ends up growing.  Maybe you can post some fun pictures of this if you try it.


Identification of a spider I have found this 8mm spider in my home, North London. I've been told it may be a false widow but wanted a second opinion.

Note: The silvery parts in the picture are actually brownish in colour

It does appear to be a young spider, and seems consistent with a young Steatoda of some sort, so "False Widow" sounds OK.

Edit:  I just did a quick Google search and pulled up a useful paper (link below) that pretty clearly indicates that this is almost certainly a young Steatoda nobilis, one of the 'False Widows'.  See the top left - image A

Dugon, M.M., et al. 2017. Occurrence, reproductive rate and identification of the non-native noble false widow spider Steatoda nobilis (Thorell, 1875) in Ireland. In Biology and Environment: Proceedings of the Royal Irish Academy 117(2):77-89


Spider Species Identification Can anyone identify this species of spider and whether or not is is venomous?
Location: South Carolina, USA.

That is a Nephila clavipes, a.k.a, "golden silk spider". According to Wiki, this is the only golden web-orb species that's indigenous to America.

  Can anyone identify this species of spider and whether or not it is venomous?

"..there is little real danger from an encounter with the golden silk spider. The spider will bite only if held or pinched, and the bite itself will produce only localized pain with a slight redness, which quickly goes away. On the whole, the bite is much less severe than a bee string." (source)


Why is cannibalism not an evolutionary stable situation? In the 'the selfish gene' Dawkins writes (page 109):
"The reason lions do not hunt lions is that it would not be an ESS (evolutionary stable situation) for them to do so. A cannibal strategy would be unstable for the same reason as the hawk strategy in the earlier example."

To quickly summarise this: we consider an interaction between two animals where one possibly stands something to gain. Dawkins then defines 'hawk' behaviour as attacking behaviour, whilst 'dove' is described as peaceful and retreating behaviour. He then argues that a population of purely hawk or purely dove is unstable, since in either of the situations the other kind of behaviour is more favourable. As it turns out, the stable situation is 7:5 for hawk:dove.

Turning to cannibalism, we can regard the hawk behaviour as 'engaging in cannibalism' and dove to be the refraining party. Why, then, don't we see similar behaviour when considering cannibalism, i.e. why don't we see a reasonably large amount of lions engaging in cannibalism whilst the others refrain from it? If I am not mistaken we see in fact the situation more closely described by completely dove?
Any insights are appreciated!

Cannibalism is incredibly common in nature. There are more species that eat their own kind than do not. Chimps eat other chimps. Lions eat other lions. Wolves eat other wolves. Prairie dogs go into the burrows of other prairie dogs and eat their babies to get the protein-rich meals needed to produce milk for their own litter. The only animals that don't regularly engage in cannibalism are some birds, and that is more because they physically cannot fit other members of their species down their throat than any moral qualms.
However, cannibalism is typically a bad evolutionary strategy, long term. For several reasons...

in a dioecious species (i.e., one with two sexes), cannibalism means a 50% chance of eating a potential mate and losing the opportunity to pass on your genes
diseases are more likely to transfer between species the more closely related they are. If you are a cannibal you are eating a species with a 99% similarity to you and are more likely to get diseases or parasites. Like kuru/mad cow/chronic wasting disease.
it precludes social behavior and all its benefits. Why engage in mutually profitable behavior when you can just eat those around you? This is thought to be one reason why pack-hunting is rare in some groups of vertebrates like monitor lizards.
on a broad-scale evolutionary perspective, cannibalism means removing members of your own population from the gene pool. It may be good for the individual but it's bad for the species as whole
cannibalism means you are feeding on an animal that is potentially your own size. That's a bad strategy in general. Most cannibalism in nature tends to be adults eating infants or adults scavenging carrion of their own species. By contrast predators are normally larger than their prey, with a few exceptions like pack-hunting wolves and lions.


Downloadable worldwide database of disease statistics? I am looking for a downloadable database of disease statistics. I have emailed the good folks over at HealthMap, but they haven't gotten back to me yet.

As far as I can tell, their data relevant to my project is gathered from the World Health Organisation, ProMED Mail, GeoSentinel, Google News, Moreover, Baidu and SOSO.

I can scrape the data from each of these sites and aggregate it in the same way HealthMap has, but that is a large project in and of itself, and I only have a couple of months for this not-for-profit project.

Do you know of a downloadable worldwide database of disease statistics?

I took a quick peek and HealthMap and their JavaScripts are publicly viewable.  As such, I believe cross site scripting would be quite feasible.  In other words, call their JavaScripts from a page you develop on your server to create a feed of the data you want.

In this way, minimal effort on your part could leverage their data scraping efforts.  If you're adding your own data then you're basically doing a Mashup.

That said, my concern with doing this is potentially violating their copyright.  I would email them saying if their database is not available then you wish to use cross site scripting to access this data for your project, and unless they let you know otherwise by (specific date) you will assume this is acceptable.

I'm not a lawyer, so use this advice at your own risk.  =)


Can plants get cancer? I can't think of any reason why plants wouldn't be able to get cancer, but I've never heard of a plant growing a tumor. I've also never seen a plant with a noticeable abnormal growth. Can plants get cancer?

Yes, plants of all sizes can have cancerous growths.

Agrobacterium tumifaciens, the causative agent of crown gall disease, produces what is called a tumor. See this link for detailed information on these growths. Alternatively, use a plant physiology textbook to look up the above terms. (Here, is where a textbook is better than a single abstract in PubMed.)

I am certain that you have seen such growths on trees, such as this. Other smaller versions can occur on smaller plants - on stems and leaves, for example. The plant builds up tissue around the A. tumifaciens infection in an effort to isolate and contain the infection and its effects.


Reason for aquatic plant roots My question is about why aquatic plants have roots. At first they seem a bit superfluous to me because leaves of the plants could just absorb nutrients directly from the water thereby skipping a need for root function that land plants have to pull nutrients from the soil. I then wonder if nutrient trafficking is the reason for the root system as diffusion may not occur efficiently through thick leaves.

Among terrestrial plants, roots have two major functions - obtaining water (as well as nutrients) and anchoring plants in place. (However, roots may have other important functions as well.) Aquatic plants obviously don't have a problem obtaining water. So roots presumably function primarily as anchors.

There are rootless planktonic plants that float on the surface of water bodies. However, aquatic plants like cattails and water lilies are probably a little more discriminating in their habitat preferences. Imagine a rootless water lily being blown by a hard wind into a patch of water lilies, which block out the sun.


What is the number of cells in a line of a fingerprint? I have been reading a little about the size of cells and was curious as to how small they really were.

I have noticed that on my finger, the outlines of the fingerprint are made up of thin lines. In fact, some of them are so thin that I have difficulty imagining anything thinner I can make out with the naked eye.

I have read that the naked eye has a resolution of 0.1 millimeters = 100 micrometers, whereas eukaryotic cells range in diameter of 10 - 100 micrometers.

Putting this information together, would it be reasonable to conclude that the lines on my fingers have a width ranging from 1 - 10 skin cells? Is there any satisfactory method to verify this without fancy equipment? Is it even true?

P.S.

Are there also more scientific names for these "finger lines" so that I can look it up somewhere? Googling "finger lines" brings up a lot of stuff about palm reading.

I am not sure that this can be accurately estimated because the outer layer of skin is ill-defined in terms of cells and cell boundaries. The outer layer or epidermis is composed of dead cells and dead cell parts that is tough and interconnected by design. Individual cells are not readily discernible.