Chromosome related problems. 1.) How many versions (alleles) of a gene can we carry if every chromosome is in pair?

2) What happens during the gamete formation (meiosis) ? Do the gene pairs stay together?

3) What happens then to the paternal and maternal sets of genes that we inherited ?

My attempts

1) I think that it could be any number, but confused with 2 as an answer.

2) Gene pairs must refer to homologous chromosome pairs which remain together in meiosis-I and get separated in meiosis-II. So in net process, it get separated.

3) It is used for producing proteins essential for body functioning by the process of transcription and translation. These genes with some changes (due to crossover) will also be transferred to second generation.

How many versions (alleles) of a gene can we carry if every chromosome is in pair?

The phrasing "if every chromosome is in pair" sounds a little bit funny. But it probably mean "or a diploid individual".

If an individual is diploid, then it has two copies of any given locus. If the term is new to you, a locus is a position in the genome (it may correspond to a gene or not). With two copies an individual can carry maximum two different copies, that is two alleles. The answer is two.

  What happens during the gamete formation (meiosis) ? Do the gene pairs stay together?

You nailed it!

  What happens then to the paternal and maternal sets of genes that we inherited ?

This is a slightly vague question IMO but I would suppose the main point that is being expected is a description of segregation and recombination (cross-over). You answer was good but I would suggest.

"The maternally and paternally inherited haplotype will recombine (cross-over) during meiosis so that a gamete resulting from meiosis will contain a single haplotype which is a 'mixture' of the maternally inherited and paternally inherited haplotypes."


Abbreviations for molecules: What are CheW, CheA, CheY? I've encountered the abbreviations such as "CheW" and "CheA" for certain organic molecules.  For example:

  Proteins associating with the Tar complex include the autophosphorylating protein kinase CheA, the transducing protein CheW, the methylating enzyme CheR
  and perhaps the protein phosphatase CheZ.  (Morton-Firth et al. 1999, p. 1060; available here)

What does "Che" stand for?  What do the capital letters at the ends of the abbreviations mean?

Let me know if this would be a better question for chemistry.SE.

Here is the paper that first defined them:

Armstrong JB, Adler J. 1969. Complementation of nonchemotactic mutants of Escherichia coli. Genetics 61:61-66.

Che is an abbreviation of chemotaxis. In this paper, complementation studies revealed three different loci that, when mutated, result in defective chemotaxis. These were termed CheA, CheB and CheC. Originally they were thought to be genes, but the following paper refined the definitions when the CheA locus was found to contain CheA and CheW genes while the CheB locus contains CheB, CheX, CheY and CheZ genes:

Silverman M, Simon M. 1977. Identification of polypeptides necessary for chemotaxis in Escherichia coli. J Bacteriol 130:1317-1325.

I'm not going to search for the discovery of every Che gene, but hopefully you have an idea of where the letters come from.


Why did the yeast rise? Here are the notes I made for an experiment I was doing (I didn't put it here as it is too long)

(please ignore the numbers at the end of the pdf file)

The graph looks like this:

As you see on the graph, the numbers are the same as the ones below

1. The effect running out of glucose has on the yeast growth
Our yeast increased in number by dividing rapidly. They use glucose to respire and release energy. They need energy to grow.

2. Why the yeast starts to grow again
The yeast  starts to decrease in volume when they ran out of glucose.

3. Describing patterns in graphs
The yeast breaks down the starch to glucose

The problem is, why did the yeast rise at the end, I forgot?

Thanks in advance

First, the glucose is reduced by anaerobic fermentation to ethanol and carbon dioxide. The yeast uses the produced energy for a fast growth and division (1). As soon as all glucose is consumed the metabolism of the yeast changes from anerobic fermentation to aerobic respiration (oxygen is required). This is called diauxic shift. During this time the yeast stops growing (2). After this shift the yeast further reduces the ethanol to carbon dioxide and water. The generated energy is used for the second growth phase (3).
Hope this answers your question.
Best
Vanessa


Are the cells (structures) of deep sea fish different? And can they survive in shallow water? In the deep oceans the pressure is enormous. But still there are fish living. But are the cells of them different from fish who just live at the surface of waters?

For example, are the cells smaller because of the pressure? And if so, does that influence the inner metabolism? If not, how do they succeed in maintaining their size?

Cells consist mainly of water and the compressibility of water is very low. Wikipedia states:

  The low compressibility of water means that even in the deep oceans at 4 km depth, where pressures are 40 MPa, there is only a 1.8% decrease in volume.

This means that the pressure alone does not affect the size of the cells much. However, the pressure affects the cells and the metabolism of organism living in extreme depths in other ways:

Under pressure, the folding and unfolding kinetics of proteins can change drastically. Which means, that the protein structures may need adaptation to great pressures.
Under pressure the fluidity of the cell membrane lipids changes, requiring adaptations in membrane lipid composition.

In conclusion, I would say that the pressure in the deep sea does not directly affect the size of cells but rather their metabolism.

Edit: I just saw the second part in the heading of your question ("and can they survive in shallow water?"). Again, I'll quote Wikipedia:

  The extreme difference in pressure between the sea floor and the surface makes the creature's survival on the surface near impossible;

The reason for this is that pressure works thermodynamically in many ways similar to temperature: As explained above, changing the pressure significantly alters reaction kinetics and phase transitions. Thus, the whole metabolism has to adapt to increased pressure (similarly to the adaptation to increased temperature).

However, at least some deep sea creatures seem to be able to adapt to surface pressure if the transition is not too abrupt (from the same wikipedia article as above):

  A marine biologist, Jeffery Drazen, has explored a solution, a pressurized fish trap. This captures a deep-water creature, and adjusts its internal pressure slowly to surface level as the creature is brought to the surface, in the hope that the creature can adjust.


SPINAL CORD: Do the axons from white matter synapse with the cell bodies in grey matter? After wading through a sea of information, I understand the main differences between the white matter and grey matter of the spinal cord.

I know that white matter contains myelinated axons in the ascending and descending nerve tracts from the brain to the spinal cord. I know that grey matter contains somata which contribute to sensory and motor functions from and to the peripheral nerve fibers.

With the differences in mind, I am confused about the relationship between the two.

The main question being: What signaling, if any, takes place between the myelinated axons of white matter and the somata of grey matter? More pointedly, do the myelinated axons from the nerve tracts in white matter ever synapse with dendrites from somata in grey matter?

My guess is yes, that this is a key aspect in how the brain and the spinal cord communicate. But I haven’t yet found any definitive source that addresses this question directly.

Here is a great diagram (from here) that outlines all of the different white matter tracts running up (blue) and down (red) the cord.

The portion in the center, as you have found in your research, is the gray matter.  In there are the different interneurons (cells that exist in the network to integrate information from descending controls and do further processing on it) and all of the different motor neurons.  The corticospinal tract descends to the appropriate level (for example, a neuron in charge of moving your arm, to keep it simple, will have a cell body in the brain, and descend to the thoracic level), enters into the gray matter and either synapse on an interneuron or directly onto a motor neuron).
The sensory neurons are a slightly different animal.  Some (pseudo-unipolar cells) have what are basically two "legs", one that runs out into the periphery, which will take the signal from something like a Pacinian corpuscle in the skin, propagates a signal to the cell body, which is outside of the spinal cord in the dorsal root (see below), and the other "leg" runs all the way up the dorsal column into the medulla of the brainstem.

from here
So that should give you some idea of the two major tracts.  To see some of the finer detail, you can look into the different layers (laminae) that the gray matter is composed of, so that you can trace the connections all the way in.


Does the term "Biophysics" have two different meanings? 1.
Some sources (including  the current Tag-info at biology SE)  state; biophysics is the adoption of techniques / methodologies from physics to study biological systems.

The use of methods from the physical sciences to aid in the study of biological systems…

Bio-SE- Tag biophysics.

Biophysics or biological physics is an interdisciplinary science that applies the approaches and methods of physics to study biological systems…

Wikipedia (permalink).

Biophysics — the branch of biology that applies the methods of physics to the study of biological structures and processes…

Dictionary.com

2.
According to other sources, biophysics is the subject concerned with how the laws or phenomena of physics work in living systems.

“The subject of biophysics are the physical principles underlying all process of living systems.”

Google Book: Biophysics, An introduction, By Ronald Glaser (permalink).

Biophysics is a bridge between biology and physics. ... Biophysics looks for principles that describe patterns. If the principles are powerful, they make detailed predictions that can be tested. ---

Biophysical society

These two, although apparently quite similar (and I agree, have overlapping areas) basically indicate completely different things.
The first group of definitions refer to techniques and methodologies; such as “how does an electron microscope work?”, or “what could be the best strategy to separate membrane-lipids?”, or “how could you identify cells with the expression of certain RNA”; etc.
The second group refers to the physical principles applicable to living systems. Such as “why do phospholipids form a bilayer?” or “how do brain waves reach the scalp?” or “how does a humming bird move its wings when it hovers in a stationary manner?” or “what are the mechanisms working in the path of transport through phloem?”.
Now my question is: Is there a dual and different meaning, or use of the term ‘biophysics’?

Short answer
Biophysics encompasses the study of biological systems in physical terms and the methods involved to achieve that goal.

Background
I'll approach this question first from the area of research I'm actively involved in at the time of this writing -

Psychophysics is

  [...] the scientific study of the relationship between stimuli
  (specified in physical terms) and the sensations and perceptions
  evoked by these stimuli. The term psychophysics is used to denote both
  the substantive study of stimulus-response relationships and the
  methodologies used for this study.

source: (RIT)

In short this would translate as

  The study of the sensation and perception of physical stimuli and the methods involved to accomplish this.

To illustrate I will cite the titles of two well-read articles in this area highlighting the dual use (study & methods):

Issues in psychophysical measurement
Spatial hearing: the psychophysics of human sound localization

And to illustrate a compelling example that merges both uses in one:

Psychophysics: Method and theory

Now to  your question; I've done electrophysiology which might, arguably, be considered biophysics, but I'm less comfortable in the arena of biophysics. But given my reasoning above, you can safely replace Psycho with Bio and say that Biophysics is

  The study of biological systems in physical terms and the methods involved to accomplish this.

For example, the University of Wisconsin describes it as:

  [B]iophysics combines state-of-the-art physical measurements with computational models to understand the detailed physical mechanisms underlying the behavior of complex biological systems.


What is the use of eye banks, if eyeball transplants do not exist at present? Corneas are donated and transplanted, but not the eyeball.

I don't understand. What is the purpose of donating a cornea without an eyeball to a blind person?

You are asking two questions that you think are connected but are actually not.

  Question 1 - What is the use of eye banks?

Answer: It's to store corneas for transplant for people with cornea damage.

  Question 2 - What use is cornea transplant to a completely blind person?

Answer: It depends. If the blindness is due to clouded cornea (several diseases cause this) then replacing the cornea will reverse the blindness. If the blindness has other causes then cornea transplant is of no use to the person.


How would a different solar day affect evolution? Has anyone theorized how evolution would be affected by a different length of solar day, what were the conclusions?

The thought came from thinking about life on other planets/moons, but I'm initially thinking about it from the frame of "How would life on earth and humans specifically have evolved (or if they would have) if a day were 12 hours or 48 hours?

I imagine the actual effects on evolution and lifestyle would be extensive.

Note: this question How would the human body adjust to sleep times if we were to live in a place with different day lengths? is slightly related, but just to clarify I'm intersted in effect on evolution, not adaptation if an indivdual moved between planets.

It depends on how different. Day length affects more than just how long the periods of light and dark are. Let's assume a very slow rotation, and a very long day, maybe 1 month light, 1 month dark. The light side would get much warmer while the dark side would get much cooler. At the border between light and dark sides, you'd expect to see powerful storms as the hot moist expanding air moved into the cooler side and had to lose moisture. Any life on a planet like this would have to adapt to surviving in both hotter and cooler temperatures. We can take this to an even worse extreme and look at a planet like uranus. Uranus's axis is tilted at 97.7 degrees, so even though it rotates, the day/night cycle is controlled by it's rotation around the sun. If the earth were tilted like this, then we would 6 months of light followed by 6 months of darkness. Life would either have to keep moving to stay in the moving temperate twilight zones or adapt to hibernate.

If we assumed a shorter day/night cycle, I think the changes would be less significant. Lets say we had a 4 hour day. ( There has to be a speed where things get thrown off the planet, but I don't think 4 hours per day is fast enough ) A 4 hour day would have 2 hours of light with 2 hours of dark. My guess is that circadian rhythms would be less important. Temperature changes from light to dark would be less significant than currently.

It's an interesting thing to think about because the Earth's day is slowly getting longer as the moon exerts a tidal force on our planet, slowing our rotation and escaping further into space, but this change is so slow I doubt it will ever become a problem for humans.


Why so fewer birds in the yard come late summer and early autumn? We've enjoyed watching birds in our yard this past summer. We're in a suburb, fairly forested, inland northeastern USA hardiness zone 5. As we scaled up the amount of diversity and net primary production around the house, and added a bird feeder, we notice an uptick in various kinds of wildlife. However, we're surprised to see a stark decline in the amount of birds starting around late summer/early autumn.

What could cause the sudden decline in birds in late summer? Is there a migratory trend starting up around this time; it seems early to me for birds to be flying south?

The birds in question include a family of cardinals, occasional blue jay, downy and hairy woodpeckers mid-summer (some are still around), many various sparrows, yellow finches, chickadees, et al.

We continue to fill the bird feeder as usual. We haven't changed anything about our yard routine. We have a rescued feral cat which goes outside and hunts despite our efforts to stop it, and it has killed many mice and a few chipmunks mid-summer, so perhaps the birds have become wary of him and the dead bodies of small mammals left in forested edges around the yard.

One possible cause is Cooper Hawks. We are in east TX and put out a lot of seed ; we had more birds. Fewer in recent months due to the Cooper Hawk(s). Our yard is a buffet for them ,I hear them often, see them occasionally ;they will perch in the under story.  And we hear birds hit the windows as they panic from the hawk ; it happens 0 to 4 times a day. The hawk has developed a technique of diving and after the small birds when they knock themselves out on the windows , the hawk walks on the patio to pick one up. I have been going out after a bird strike and picking up stunned birds and put them in a shoebox for 30 minutes. They usually recover, had a cardinal yesterday. If you are home during the day , listen for window strikes and watch for sudden flights of all the birds. The Sharpshin Hawk is also here but not a problem.......... And there is a degree of randomness to migrations: Some years we get many Goldfinches, Pine Siskins, Robins, and some years a few or none. And birds like Cedar Waxwings are notorious for their unpredictable movements.


What are the limitations to current nucleotide sequencing technologies? Using the Illumina platform, it is cheap and (relatively) easy to sequence huge amounts of DNA or RNA. There are various other platforms out there (Roche/454, SOLiD, PacBio, Ion Torrent) each with their own distinct advantages, but Illumina seems to be pretty popular for many applications, despite its limitations.

Ideally, we would like a sequencing technology that produces long, error-free reads with high throughput. However, at this point it seems we have to make a choice: throughput or length (and quality). PacBio seems promising, but the last I heard they have still been unable to deliver on their claims.

What are the molecular and biochemical limitations to our current sequencing technologies? Why don't we already have long, error-free reads with high throughput?

It seems like you answered your own question,the signal from a few molecules running through an enzyme or a polymerase tend to fall out of synch after a few hundred bases.  If an enzyme for sequencing was more rigorously in time step that could help for instance.  The machines read traces in four channels with nice bumps for each base.  See this article for a nice example. You can see that if there are too many of the same base consecutively it gets hard to tell how many bases there are there.  Over time all four traces will start to smear out and you cant tell Adam from Thelma if you take my meaning.

But there are other bottlenecks.

The sequencers currently put out such a high volume of data that the analysis of the meaning of the output data can't be analyzed fast enough.  This follows the trend in biotech over the past 12 years or so - more sequence data, micro array data, more mutation data, more genomes than people who can actually use it to understand the biology.  There is a bit of an analysis bottleneck now.

So some of these sequencers have greater read lengths, which can make it easier to assemble a sequence.  These sequencers generally cost more.  For instance if you have a library to sequence a little fungal or algal genome - you will get the answer back in a day or less now.  In the form of 1 Tb of reads maybe 50 to 200 bp long.  It might take quite a bit of time to put that together into a novel genome sequence, still more to find the genes, build the gene networks from a template of pathways etc.  Just imagine a thousand sequencers pumping out day and night and you get the picture  I'm trying to paint here.

About cost.  Ion Torrent and the new oxford nanopore sequencers are really cheap - \$50k to perhaps \$900 for Oxford Nanopore's USB sequencer.  Most other systems cost hundreds of thousands of dollars.  Ion torrent and Nanopore have more disposables - you throw away a chip or even the entire sequencer - at a cost of hundreds of dollars a sample.


What are some examples of undirected weighted networks in ecology? I'm a math major with a current interest towards network theory. A network can be considered as a collection of nodes, and edges between these nodes signifying some relation between them. The most ubiquitous example would be a social network like Facebook with nodes representing people, and an edge connecting two nodes if they're friends.

A network is called directed if the edges have a direction. This means that if there's an edge directed from A to B, it's not the same as an edge from B to A. An example of this would be a food web network, where the nodes represent species and an edge from species A to B means that A eats B. Obviously, this does not necessarily mean that there's an edge from B to A (rarely does the prey eat the predator).

A network is called undirected if it is not directed, i.e. none of the edges have any direction; if there's an edge from A to B, it necessarily means that there's an edge from B to A.

Now, one can assign weights (numerical values) to the edges in a network to signify the relative importance of edges. In the Facebook example above, this can be considered akin to assigning values to edges which indicate the strength of friendship/distance between the residences of friends, etc.

I wish to study ecological networks to see if I can make interesting inferences from my study of weighted networks.

So can you give me some examples of undirected, weighted ecological networks?

Epidemiology, the spreading of diseases, is probably one of the most famous applications of network theory in biology, going all the way back to John Snow.

A more relevant example would maybe be something like graph models of habitat mosaics. Populations are often both spread out over landscapes and clumped together in smaller pockets of suitable habitats. While fragmented, these populations still have a certain amount of contact, resulting in gene flow and the creation of what is often called a meta-population. These things can happen on a vast range of scales, from your back yard to whole continents, but by modeling them like graphs they can all be studied comparatively and tested for resilience agains disturbances, habitat loss etc.

You mention social networks, but there is no reason why you can't study the same in animal populations. Say one individual learns something useful, maybe the location and route to a rich feeding ground. That information can then be shared with other individuals, either by show-and-tell, or maybe by some kind of abstract communication. The information spreads in familiar exponential fashion until everyone knows, then any one of those individuals can relay or be "eaves dropped" on by a neighbouring population, it doesn't even have to be the same species in some cases, and the information flows again. As with the habitat mosaics the benefit of these models is that very different systems can be compared and tested on an equal footing, anything from fish, to birds, mammals, even some social insects, lend themselves well to this.


Species identification - greenish blue ocean worm (nudibranch?) in Perhentian Islands, Malaysia We found this on a beach at the Perhentian Islands, Malaysia in March, 2016 and cannot identify it.  It's some sort of worm-type creature with many legs and bluish back about 15cm long.  The legs undulated along the body as it swam.

back:

belly side:

It's hard to identify from the photos provided, but I think it is Chloeia flava (a species of polycaete worm, within the phylum Annelida), also known in English as the "Golden Fireworm".
The size is roughly similar to what you describe (they are typically about 7-10 cm long). The individual you observed looks like it lives in sandy bottom environments (not a typical environment for a nudibranch), and this worm does also. It is commonly found all across the warmer Indo-Pacific as well, and looks like the individual observed in your photo.

If it is not this species, I think it is another species of the same family, Amphinomidae.


Do dolphins really sleep? I have always wondered, if dolphins sleep with one eye opened, do they really sleep at all?
According to this article dolphins indeed shut down their brains.

I already googled it. No help from wikipedia or other articles and publications found.

I'd say that unihemispheric sleep and adaptations like it really are sleep - the brain activity on one side of the brain gives a characteristic sleep pattern.  It certainly must satisfy the needs of an aquatic mammal like a dolphin or a whale since they have to be partially conscious to breathe by surfacing regularly.

It does seem to affect the brain physiology, but is there a reason you would not call it sleep?


How much electrical energy is required for intracellular stimulation of a neuron? How much electrical energy is required for intracellular stimulation (firing) of a human neuron? Electrical energy is measured in joules, and equal to voltage multiplied by current. If you don't know energy,  you may specify voltage applied and current. Just for example, to capture heart, a pacemaker must discharge 0.1 microjoule of electrical energy.

There might be more parameters involved like pulse width,  phase etc.  Energy combines all the parameters in one single value. In case you don't know energy level,  please specify the defining parameters as well.

I think this question is somewhat ill-posed, but I'll try to answer it:

None.

All you have to do is to short the inside of the cell to the outside/ground. Of course in reality this means expending some energy somewhere, but at that point it's an engineering problem, not one of biology, and it has nothing to do with the neuron itself.

Action potential firing is a completely passive process. The only part that requires energy (besides protein synthesis) is for the sodium-potassium ATPase that maintains sodium and potassium gradients.


Query for gene upregulation in cBioPortal there! Could anyone help me with some biostatistical problems using cBioPortal.

We are looking for cell lines with upregulation of certain genes on cBioPortal. My supervisor is teaching me to use this website because I have no prior experience. She is using EXP >= 0.5 to define upregulation. Although I am of no bioinformatics background, my opinion is that 0.5SD away from the average is not strong enough to define an upregulation. I think it better to use EXP >= 2 or 1.5. I have discussed this with my supervisor but she insists using EXP >= 0.5.

Does anyone have any experience with this issue since I am still not convinced by what I was told. Thanks a lot!

Well, I have worked with expression patterns. Unfortunately there is no clear cut or magical numbers for cutoffs . I agree with you that 0.5 is not stringent. However, to explore data usually one can parse it using lower cutoffs and later on you can rise the bar to see what happens.


What are the methods for infering genetic interactions? Is there a classification of methods for inferring genetic interactions? I mean some work published, utilizes genetical genomics data.  Is this possible with expression data alone? And how about perturbation screens? I guess they all need information about mutants/genetic variations?

BioGRID is an interaction database, and they catalogue interactions by (among other things) the class of experiment that discovered them. See http://wiki.thebiogrid.org/doku.php/experimental_systems#genetic_interactions

Other than that, you should look at recent reviews and publications, but you will easily get lost unless you figure out some important particulars, like:

What species? Yeast, worm, human, cell line?
What sort of interaction? Synthetic lethality? Complicated, fancy epistasis?
How much? Genome-wide? 2-3 genes?


What is intracellular retention? On the wiki page for proto-cadherins, they write, "The cytoplasmic domain also mediates intracellular retention, a property which distinguishes the clustered protocadherins from the related classical cadherins." citing the following source.
Unfortunately, I was unable to find much anything to go off. Anyone know off-hand what this terminology is referencing?

Based on this line from the paper you linked, it seems like they are using intracellular retention to refer to proto-cadherins being taken up in to the cell via endocytosis.

It is possible that the effects of deleting the intracellular domain might be a result of loss of an organelle retention signal located in the cytoplasmic domain of the protein and/or a decrease in endocytosis of the protein accumulated in the membrane.

This paper also refers to intracellular retention of cadherins in the context of endocytosis of proto-cadherins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216661/
Based on this information, the quote from the Wikipedia page ("The cytoplasmic domain also mediates intracellular retention, a property which distinguishes the clustered protocadherins from the related classical cadherins.") seems to be saying that the cytoplasmic domain regulates proto-cadherins on the cell membrane being taken back up into the cell via endocytosis, hence retaining them intracellularly.


Cell proliferation limit and senescence of embryonic stem cells and fibroblasts I am trying to understand the importance of proliferation limits and cell senescence. In particular, I would like to compare the proliferation limit of Embryonic Stem cells (ES) and fibroblasts (which would be trans-differentiated) and describe how this difference plays a role when thinking about engineering organs, for example a heart transplant.

How do ES cells and fibroblasts compare with regards to the Hayflick limit?

Telomeres (caps on the ends of chromosomes that are gradually shortened during each cell division) determine the maximum number of times a cell can divide, known as the 'Hayflick limit'. Cells that are able to express telomerase, an enzyme capable of extending the telomeres, can divide indefinitely.

There are various types of stem cell in a body which replenish the 'pool' of cells in the tissue once they reach the end of their useful lifespan. Each stem cell expresses telomerase to lengthen the telomeres after a round of cell division. The inhibition of telomerase in somatic (normal) cells is a major 'challenge' for cancerous cells - in order to achieve uninhibited proliferation, they must express telomerase. Thus, there are many molecular similarities between stem cells and cancerous cells (well, with regards to telomerase, anyway!) [ref].

Fibroblasts are somatic cells - they are the 'normal' cells that make up the vast majority of organsisms. The only cells not known as somatic are gametes/germ cells and stem cells. They thus do not express telomerase, and have a replicative lifespan, also known as a Hayflick limit.

With regard to your question about engineering organs, there are many resident stem cells in tissues (and thus organs) that 'top-up' the somatic cells when required. As organisms age, this pool of stem cells becomes depleted [ref]. Artificially engineering an organ such as the heart (I assume this is what you mean) would be inherently difficult, as many vascular cells are not replaced, but can last a whole lifetime - this is also true for many neuronal cells. So replicative lifespan is not necessarily related to lifespan!


How to refer to person-derived and place-derived species names Are there words that categorize latin specific epithets by how they're derived? Specifically, I was wondering if there exist adjectives to refer to:

Person-derived species names as in Nothura darwini (these could be "eponymic" or "eponymous" perhaps, but that seems grammatically wrong )

Place-derived species names as in Amolops hongkongensis (would these be "toponmyous", or maybe "loconymous"?)

According to A Source-Book of Biological Names and Terms by Jaeger, the appropriate terms are the simple, obvious ones:

"Geographical" for place-derived names and

"Personal" for person-derived names.


Do nucleosomes ever completely unwrap during transcription? In eukaryotic transcription will the nucleosomes ever completely unwind the DNA and the histone complex disassemble? If an operon is more 160 base pairs it seems it must.

Yes, nucleosomes are completely unwound. Histone chaperones such as FACT (for H2A/H2B) and ASF1, CAF-1, HIRA, Nucleophosmin etc (for H3/H4), associate with RNA Pol II and handle the displaced nucleosomes. As you surmised, the histone octamer complex is disassembled, into the H3/H4 tetramer and two H2A/H2B dimers. Right behind the elongating Pol II, the chaperones reassemble nucleosomes. During the process of reassembly, it has been shown that "new" H2A/H2B dimers (and possibly H3/H4 tetramers too) can get incorporated into an "old" histone octamer. Finally, nucleosome remodelling complexes such as SWI/SNF re-space the nucleosomes.

This is a decent review of the process (by one of the discoverers of the FACT complex, incidentally): "New chaps in the histone chaperone arena". Campos & Reinberg. Genes & Development (2010): 24: 1334-1338

This is a comprehensive review of histone chaperones and nucleosome dynamics during various DNA-dependent processes (such as transcription, replication and repair). There is an entire section on their role in gene transcription, which is the main thrust of this question: "Histone Chaperones: Assisting Histone Traffic and Nucleosome Dynamics". Gurard-Levin, Z.A., Quivy, J., and Almouzni, G. Annual Review of Biochemistry (2014): 83: 487-517

And finally, a good overview on histone dynamics and chromatin structure during transcription: "Histone exchange, chromatin structure and the regulation of transcription". Venkatesh & Workman. Nature Reviews Mol. Cell. Biol. (2015): 16:178–189

I should add that an inability to disassemble nucleosomes (or displace any other factor bound very tightly to DNA) can actually pause an elongating Pol II complex.


How chameleons change color? Well, I was watching a video about chameleons and I saw that their cells can change color. Can someone explain me how is this possible?

When it comes to displaying color, most organisms use chromatophores. Chromatophores are pigment-containing and light-reflecting cells, or groups of cells. Chromatophores reflect the color that they look like.

Chameleons also use chromatophores. The outermost layer of the chameleon’s skin is transparent. Beneath this layer are the chromatophores. The deepest layer contains melanophores, which are filled with melanin. Above that layer are cells called iridophores, which have a blue pigment that reflects blue and white light. Layered on top of those cells are the xanthophores and erythrophores, which contain yellow and red pigments, respectively.

For a chameleon to change color, it must expand or contract certain chromatophores depending on the signal of the nervous system. The expanded chromatophores block the contracted ones and the color of the expanded chromatophores determine the color of the chameleon. For example, to make the chameleon green, the iridophores and xanthophores must expand, and melanophores and and erythrophores contract.

Reference

WIRED - How Chameleons Change Colors

More to read
This Nature article provides a detail description and explanation of how this occurs - Photonic crystals cause active colour change in chameleons


What is this flower? I was in Germany recently, and I saw again a flower that I'd only ever encountered before at Meijer Gardens. It's interesting to me because I'd never seen a flower with color variation in only the 'interior' petals. Try as I might, however, I can't seem to find it anywhere! Can anyone tell me what this is? I'd like to be able to learn more about it.

It's Verbena hybrida Voss (See here; the page is in French though).

It belongs to verbena genus in the family Verbenaceae. It's about 10 to 50 centimeters tall with a squarish stem and opposite leaves.The flowers are small with five petals, and borne in dense spikes on the top. Verbena hybrida Voss is always used as ornamental plant. They are drought-sensitive, tolerating full to partial sun, and enjoy well-drained, average soils. It's always plant in warm and dry and sunny environment. About why a flower with two colors in one petal, it's because there are always two kinds of pigment in the petals. The pigments in different temperature and different acid alkaline environment present  different colors. When the flower is open, the acid-base property changed will lead to petals present different colors (K. Yoshida et al., 2009).


Does contracting Rubella give one some kind of immunity to Measles and vice versa? Both these diseases- Measles and Rubella, have very similar symptoms, have similar complications and are often confused for one another. And both the diseases have a common MMR vaccine. So, are the culprit viruses also related, so that contracting one can give one at least partial immunity to the other as well?

The similarity in symptoms is striking. Both the diseases may start with cold and fever. Both give one rashes, that start from face, and spread to rest of the body. Both have similar complications associated with them like brain infection. In the end, both can cause miscarriage, preterm birth, or stillbirth, as well as a variety of birth defects in pregnant women.

I know from this source that lab tests exist which can tell whether a person has immunity to one of the MMR diseases (Measles, mumps and rubella) and not the other, implying that there is a possibility of immunity to one and not the other. But since the vaccines like MMR only ensure immunity for 99% people who get the shot, my question is- does there exist partial immunity (in some people and not others, or in less severe attack and not otherwise) to Rubella if one has contracted Measles before and vice versa?

Short answer: No, there is no cross immunity between these two diseases. Having the same symptoms doesn't mean that diseases are related.

Both have in common that they are caused by viruses, but similarities end here. Rubella is caused by the rubella virus, which is the only member of the genus Rubivirus and belongs to the family of Togaviridae and are encapsulated positive strand RNA viruses.

Measles on the other hand are caused by the measles virus, which belong to the genus Morbillivirus within the family Paramyxoviridae and are negative stranded enveloped RNA viruses.

Historically speaking, the measles vaccine was available first in 1963, with mumps following in 1967 and rubella in 1969. All three are attenuated live vaccines which have been combined into a single vaccine in 1971. The sequence of this developments also shows that there is no cross immunity. You wouldn't develop another vaccine, when the disease is already covered by another. Drug development is a very expensive business.


DNA of identical twins I read an article which says that identical twins have 100% similarity between their DNA, but they have different fingerprints. Does that mean the DNA is different in the fingers? What body features can be used to exactly identify the identical twins?

DNA is not the only thing in biology that determines a phenotype (observable trait, e.g. fingerprint). Far from it.

Traits can be affected by the environment (a very good example, temperature-dependent sex determination), stochastic (random) phenomena - these are know to occur in transcription ("reading DNA") or the decay of mRNA (messenger molecules which instruct protein building) - and by epigenetic phenomena. The degree to which DNA is actively read, or silenced, does not wholly depend on the DNA. In fact, this depends on the exact state of the cell or nucleus. Roughly speaking, cells in your brain (e.g. neurons) and the cells that line your lungs have identical DNA, but they are shaped, look, behave and react differently to the outside world. This is due to epigenetics, think of it as the life history of the cell.

Here's an analogy: reading the exactly same book can have different effects on people. The book is the DNA, its information unchanging, but the person and their exact status are the complicated world of the environment and the cell that is using its DNA for some purposes. PS. Terrible analogy but it may help.

By no means is my list exhaustive. Hope you can see how that identical twins with identical DNA can have a different shade of skin color (tanning!), different fingerprints (subtle and complex differences during digit development), or a different sense of fashion (psychology, cognition, what have you).


What does a hornet nest foundress feed on? After wintering, hornet queens will build a new nest from scratch. Once the new workers have hatched, they will fly out and collect carbohydrates to feed themselves and the queen and will also hunt for protein to feed the larvae.

I’m interested in knowing how food collection for both larvae and queen are taking place before the role is taken over by the workers (as none have hatched yet).

Does the queen collect both carbohydrates and protein?
Does the queen leave the nest to collect food when there’s already larvae (as opposed to having stored enough food before starting to breed)?
How long (in terms of weeks) after the queen started building a new nest until she can fully rely on her workers for food supply?

While I assume the answers to the first two questions to be ‘yes’, I have failed to find a source confirming this. My questions primarily refer to the Vespa Velutina (invasive in Europe), but I’m also interested to hear about differences in other wasps/hornets present in Europe.

I used the below articles to get the information.
1. the queen does collect both carbohydrates (nectar mostly) and protein (often bee flight muscles).

Only found one case study of one nest for this, so not sure. The queen did leave the nest during the period when it would be expected to have larvae. The articles I read did not mention food storage in the nest.
Same case study, the queen left the nest probably for longer than four weeks.

The developmental period was about 4I-42 days (egg 6 days, larva about 15 days, pupa about 20-21 days.
 from "Taxonomy, distribution and nesting biology of the Vespa bicolor group" (Hym., Vespinae) (1994) by Michael E Archer. found at https://www.academia.edu/4236740/Taxonomy_distribution_and_nesting_biology_of_the_Vespa_bicolor_group_Hym._Vespinae_1994_

This review article has a good overview. "Vespa velutina: a new invasive predator of honeybees in Europe" by Karine Monceau, Olivier Bonnard, and Denis Thiery.  DOI 10.1007/s10340-013-0537-3. accessed at https://www.doc-developpement-durable.org/file/Elevages/apiculture/maladies&parasites/Vespa%20velutina_frelon%20asiatique/Vespa%20velutina%20a%20new%20invasive%20predator%20of%20honeybees%20in%20Europe.pdf

A case study of a captured nest (one queen, four workers) found that the queen stayed inside the nest permanently after 27 more days.

From "Observations on the colony activity of the Asian hornet Vespa velutina
Lepeletier 1836 (Hymenoptera: Vespidae: Vespinae) in France" Article in Annales- Societe Entomologique de France · January 2009 DOI: 10.1080/00379271.2009.10697595 downloaded from ResearchGate

There are also other articles that may have the answer, but in languages that I could not read.


In DNA replication, are there phosphodiester bonds in the primer ? between the RNA nucleotides before being replaced When hydrogen bonds happen between the RNA nucleotide bases and the DNA bases , do phosphodiester bonds form between the RNA nucleotides in the primer ?
No source I read is clear about this, are their bonds between the RNA nucleotides ?

A primer is by definition a short single strand of nucleic acid (i.e. a series of nucleotides linked together by phosphodiester bonds). See also this wikipedia article.


Is a lion a bony fish? If you ask Wikidata "Does the species lion (Q140) have a parent taxon line up to the Osteichthyes (Q27207, bony fishes)?", it answers yes:

SELECT ?item1
 WHERE {
  wd:Q140 wdt:P171* ?item1.
  ?item1 wdt:P171 wd:Q27207.
 }

Here's a direct link.

Now, I assume that this must be wrong at some level (I'm no biologist, so please correct me if I'm wrong), so I tried to find the error.

This query displays that path more explicitly, starting with mammals:

Mammals (Q7377) have Tetrapoda (Q19159) as a parent taxon.
Tetrapoda (Q19159) have Tetrapodomorph (Q1209254) as a parent taxon.
Tetrapodomorph (Q1209254) have Rhipidistia (Q150598) as a parent taxon.
Rhipidistia (Q150598) have Sarcopterygii (Q160830) as a parent taxon.
Sarcopterygii (Q160830) have Osteichthyes (Q27207) as a parent taxon.

The third point seems strange, because Rhipidistia are described as a taxon of fish, which would mean that all mammals are fish.

Maybe this comes from the fact that tetrapods (and therefore mammals) evolved from Sarcopterygii 390 million years ago, as described here.

Is "having evolved from" considered a parent taxon in biology? If not, which of the five statements above is wrong?

The path is correct. The safest reading is to say that the lion shares a set of characteristics with the lungfish. You can also say that lion and carps are bony vertebrates (Euteleostomes).

In evolutionary taxonomy, each taxon does not need to consist of a single ancestral node and all its descendants: it allows for groups to be excluded from their parent taxa (in other words, not "being part of" but, as you said, "having evolved from"). Thus, lungfishes are closer to the lions than they are from, e.g., sharks or trout. In other words (even if this is too simplistic to say so), their "common ancestor" is more "recent".

In the Linnaean taxonomic system, all fishes were in the same class. This corresponds to our "everyday life" classification of fishes but not to the most recents findings about the "common ancestors".

To make things clearer, you need to understand the concept of paraphyly. The bony fishes group is paraphyletic with respect to the tetrapoda. In other words, it consists of the group's last common ancestor and all descendants of that ancestor excluding the tetrapoda. "Bony fish" is therefore not a clade, but "Osteichthyes/Euteleostomes" is a clade (= a monophyletic group of the bony vertebrate with a common ancestor that looked like our "modern" fishes).


What kind of object is this? I'm unsure whether to call it a fruit or a vegetable. I found it on the road in a neighborhood and decided to pick it up before a car squashed it. (Thus, my initial guess was a squash.)

Should be a Papaya, thus a fruit, an outline of your geographical location would be helpful to determine it.


What is this viny plant in the UK? I am in Northumberland, UK. This is growing in my veggie plot and cannot find out what plant it is....looks like a triffid!! It is one stem growing out of the ground and has many stems growing on the side of the main one which lie along the soil with no roots appearing.

I placed a couple of pea pods beside the brick to show the size. Hope someone can help. Thank you.

Alan is right to call this a Cichorium. It is  Cichorium endivia, Endive. It is a tropical plant that is widely cultivated for its edible leaves. However, when it flowers the leaves die, so you don't recognize the plant as Endive. The dying leaves can be seen on the picture below, from the Dutch wikipedia page.

https://nl.m.wikipedia.org/wiki/Andijvie


What is the definition of "dry weight" and "dry cell weight"? As I understand it, the dry weight of something is its weight minus the weight of its water content. Is this the definition? What about dry cell weight?

According to my Henderson's Dictionary of Biological Terms, dry weight is

  The weight or mass of organic matter or soil after removal of water by heating to constant weight.

So yes, your definition is correct and it is also applicable to cells. The dry weight of cells is the weight left when their water content has been removed by heating.


Why is lead dangerous? Lead is known to be bad for your health for a long time, but I can't find a explanation why is it so.

In school they teach that heavy metals are poisonous, and they are trapped inside our bodies. I can just assume that the liver can't process those elements. But I still don't understand why this happens.

And finally why is lead different from, let's say, gold that is also a very dense metal, but is safe.

Lead acts as a poison in a variety ways relative to what tissue it is exposed to. For example, lead is able to pass through the blood-brain barrier where it can act act as Calcium homolog to interfere with neurotransmitter release. In the blood, Lead inhibits porphobilogen synthase, an enzyme required for heme synthesis.

Lead's toxicity mechanisms include:

Its ability bind sulfhydryl groups, common to many enzymes
Its ability displace metals in enzyme complexes
Its ability to act as a Calcium homolog

Lead's valence electron configuration is $\require{mhchem} \ce{[Xe] 4f^14 5d^10 6s^2 6p^2}$; which means it has two electrons in its valence shell. This pair of valence electrons contribute's to Lead's ability to act as a Calcium analog and to Lead's tendency to form compounds in which it has an oxidation state of +2. Many such compounds dissolve in lightly acidic solutions. This has created lead exposure hazards when acidic tap water was pumped through lead pipes and when fruit juices have been served from ceramic vessels with lead-containing glazes.

Lead Poisoning

Lead


What is the difference between ferritin and hemoglobin? I have been reading that ferritin is the store of iron but hemoglobin is actually the amount of this in blood.

Does hemoglobin get sourced from ferritin? Is it possible for a person to be low on ferritin but normal on hemoglobin? Will he feel any symptoms of anaemia, if so?

Does hemoglobin get sourced from ferritin?

Yes, of course it is. Ferritin is the superior Group.

  Is it possible for a person to be low on ferritin but normal on
  hemoglobin?

Yes, since these things don't have something in common.

  Will he feel any symptoms of anaemia, if so?
  Why should he?? No, he won't get any crazy feelings from this.


A question about gag reflex If left glossopharyngeal nerve and right vagus nerve are intact, but there is a lesion at left vagus nerve, would stimulating the left side of pharynx elicit a gag reflex?

The sensory and motor components are  required (GP and vagus respectively). Similar to the corneal reflex and cranial nerve 5 and 7, if a lesion exists in either the sensory or motor component there will be a defect. In your case, there is no motor innervation on the left due to the lack of the vagus nerve so there is no vagus nerve response.


Mitochodria's Role For Neuron Regrowth Recently an interesting study has reported.  Zhou et al., 2016. J. Cell Biol. http://dx.doi.org/10...3/jcb.201605101

According to this study, enhancing anterograde axon transport of mitochondria is essential for regeneration of injured axons.

Neurons need a large amount of energy provided by ATP to extend their axons when they are injured. Mitochondria transported to axons produces
ATP which is necessary for that.

This study shows that in mature neurons, the motility of mitochondria is reduced and the reduced mitochondrial motility might
be the cause of the deficit in regrowth capacity of mature neurons. Moreover, this study found that enhancing mitochondria transport enables mature neurons to recover their regrowth capacity.

It is said that mature neurons typically arrest their cell cycle and fail to proliferate and regrow. However, considering the fact that
only enhancing mitochondria transport enables mature neuron to recover their regrowth capacity, I can't help but doubt the commonly accepted theory.

Do mature neurons actually not arrest their cell cycle？

What do you think of this finding ？

Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.


Are all antibodies against a common antigen identical? I understand that when some antigen (e.g., virus, bacteria, etc.) is recognized in the body, antibodies specific to this antigen are produced that, in turn, bind to the antigen and effectively neutralize them as a potential threat to the organism.
Are all the antibodies that are produced against a specific antigen necessarily identical?  Either within a single organism (e.g., a single person), or between different organisms (e.g., between different people, different species, etc.)?  If two people get sick with the same disease, develop antibodies, and recover, are these antibodies the same?  If a human and some other animal get sick with the same disease, will the antibodies each develop match?
Key to the operation of the antibodies is their specific recognition/binding of the antigen.  I assume that the structure and composition of the antibody is tuned to bind to specific exposed moieties on the antigen.  I can imagine that there are many different potential binding sites on the antigen to target and many possible combinations of ways to recognize those sites by the antibodies.  I would think that it would be a remarkable coincidence (highly unlikely) if separate organisms both, independently, happened to develop the same “molecular strategy” for recognizing a particular antigen.  This outcome seems to be implied in this question,
How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?

Alright, there are two major questions:
(a) Are all the antibodies that are produced against a specific antigen necessarily identical?
Not in most cases. Antigens can either be monovalent or polyvalent, meaning that they can either have one epitope or various different epitopes (an epitope is the site of the antigen that binds to a T-cell receptor or a B-cell receptor). Most antigens are polyvalent, which implies that a single antigen may interact with several different T and B cell lineages. Each B cell lineage is only able to produce and export one type of antibody. Because the antigen will interact with different lineages, it will promote the production of different types of antibodies. These multiple antibodies produced against one antigen are called polyclonal antibodies, since they arise from multiple clonal lineages. When the antigen only has one kind of epitope, it will induce the production of only one type of antibody, which are called monoclonal antibodies, because they arise from only one clonal lineage.
(b) Do the antibodies produced against a certain antigen differ between members of the same species or between species?
Yes, in both cases. There is an important genetic variability surrounding immunoglobulins and T cell receptors.
Reference: Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


Experiments on abiogenesis in laboratories Has any scientist created an organism in a laboratory using the primitive kind of Earth's environment, like the one used by Miller, etc.?

I read that protobionts (coacervates and microspheres) have been created in the lab by Alexander Oparin and Sidney Fox respectively. I also read that these were not 100 percent living.

Now the question you have is really very interesting and deep but the short answer is we still don't know enough to be able to decide

1.Precisely when an assembly of molecules and their interactions becomes a living organism and

2.We have no idea what the "alternatives" of what we know today as life are, so we can't be really sure what kinds of "other possible life forms" can be generated both in the laboratory and in the outer space on some distant planets.

In order to tackle the first question in the last decade or 2 new science has emerged-the field of synthetic biology whose goal is to "recreate" life in the laboratory from materials generally not considered to be alive-like cell membranes and DNA alone out of the cell but they are also trying to upgrade our current technology for manipulating the DNA of living organisms to the point where we can literally create new species in the laboratory. Here are some very good publications by the most renowned expert in the field of synthetic biology Craig Venter-here and here . These are seminal works for synthetic biology but if you want to know more you can search entire journals dedicated only to synthetic biology-here,here and here. There are actually hundreds of articles pertaining exactly to the answer of the question you are posing-what are the experiments we have done in the laboratory to recreate life in controlled conditions and how much we can "model" it to our own desires. Even if you only skim the abstracts of the articles in these journals you will be able to see how far we are in the de novo genesis of life and what we can do with our newest technologies to mimic the process by which the first cells arose. You would also find good work showing the prospects for manipulating current living cells to "synthesize" what scientists would consider new "man-made" species of bacteria. Although we aren't quite there yet the prospects are exciting at the least and really mind blowing at best. The discipline (I call it discipline because it isn't "just" a science but a combination of recombinant DNA technology, advances in the chemistry of large biomolecules, cutting edge genomics and proteomics, novel methods for computational modeling of metabolism and genomics and many more disciplines combined into one direction) is just in its "infancy" but even only what we can do now is enough to open the door for an entire new array of biotechnologies to come. However, I personally advise you to begin with the 2 papers of Craig Venter I already showed you and also this one and then go to these journals.

I would also recommend you seeing the reviews of Pier Luigi Luisi on the attempts of constructing self-replicating vesicles in the laboratory-here,here and here. He in my opinion is the man who has got the closest to actually achieving in the laboratory the synthesis of systems close enough to the living cell-self-replicating lipid vesicles. I think if we are ever to recreate life in the laboratory this is the closest shot we have. You might also be interested in this paper here and this here who pertain to the same field-the use of lipid vesicles as a simple way to recreate the origins of life and to build living cells in the laboratory.

Lately, there is also one brand new interesting paper from this year on the issue of creating molecules and systems of molecules capable of evolving themselves into more complex ones here.

Now on the second question-how to recognize what kinds of forms of life can exists in the universe, there is also a fast growing new science-the science of astrobiology whose goal is to devise a broader perspective on what life is. can be and how it can arise in the wide context of the cosmos. not only in the particular context it occurred here on Earth. There are 2 good journals pertaining to this field here and here which can give you very good perspective as to what the field is about and how it can shed more light both on what life generally is in the universe and how can we recreate it on Earth. I would also recommend you to read the articles Life as we don't know it, Defining life,How rare is complex life in the Milky way? and The potential of detecting "Life as we don't know it" by fractal complexity analysis. Those papers should be nice "introduction" to the world of astrobiology and if you follow through browsing the journals I just showed you can get a pretty good idea where we are today in the quest to answer your question.

You might also want to consider learning more about the origins of life. It also is a field directly related to the question you posted. Nice review on the topic is here and you can also check out this article and this article here. Then, you may want to check out the journal dedicated specially to investigation on the origins of life-Origins of life and evolution of biospheres and watch this online lecture on the subject.

Another issue pertaining to the question is the definition of life and how difficult it is to be formulated. If you become familiar with the issue you will understand why it's so difficult to tackle the problem of how to synthesize life, where it is throughout the universe and how it originated here on Earth. I recommend you these 2 seminal works on the definition of life here and here. But I would also recommend you to read this,this and this article to get a deeper look at the problems we face even defining life today. If we can't even agree on what life is how do you expect to be able to understand how it originated or how to create it?

Another direction you could also look at is our attempt to model and describe what we can call life at all levels it can appear-the field of artificial life. You can learn more about it in the journal Artificial life which deals with our attempts at modelling complexity in abstract systems close to the dynamics of the living ones. Yet another attempt at understanding the dynamics of the living is the interesting field of biosemiotics about which you can read short overview or get more accustomed into in its journal here. I think this list is more than enough to cover all the major directions your interests can take you on.

But to get "the bigger picture" of the question here you need to do much more than that and to follow virtually every publication pertaining to the definition, origin, synthesis and location of life throughout space and time and this can be daunting task, believe me, I do it every day since years! But despite the enormous quantity of papers and articles I go through there are always newer and newer things to discover and no matter how many hours I dedicate to this task and how much it fulfils me there are still gaps in my knowledge and am learning new things about different perspectives on the BIG question-What is life? all the time!

So, to give you an advice derived from personal experience-the question you tackle is really very interesting and fundamental one but even if it consumes all your time and efforts you would still not be able to follow everything which can be pertained to it, so my advice is to take only 1 or 2 approaches used in either of the fields I just described you and concentrate only on their keywords to follow the advances of the people behind them. Take something from synthetic biology, something from the origin of life field or something from astrobiology and visit the journals I just showed you from time to time to search with these keywords and see what is new. Then you would have good enough idea how close we are to synthesizing life in the laboratory and knowing more about its nature and origins. This is my long answer and the best advice I can give you.

Hope it helps :)


Genetics problem-Height of a plant An inbred strain of plants has a mean height of 24cm. A second strain of the same species also has a mean height of 24cm. When these plants are crossed the F1 are also 24cm in height.However, when the F1 are crossed the F2 plants show a wide range of heights, the greatest number are similar to P1 and F1 but apprx. 4 out of 1000 are only 12cm tall and 4 of 1000 are 40cm tall. What fraction of the F2 plants will be apprx. 28cm in height ?

a)3/4

b)9/16

c)56/256

d)none

The answer given is c).

From the source that Amory cites :

  You know that the number of offspring is shown by Pascal's triangle,
  right?

  For two alleles you have 1 : 2 : 1

  For three alleles 1 : 3 : 3 : 1

  For four 1 : 4 : 6 : 4 : 1 etc.

  So, if 4 in 1000 are 12 and 36 cm
  tall, that means that every in 250 plants is tall like that. And on
  which level of Pascal's triangle you have sum of 250? For two alleles:
  1 + 2 + 1 = 4 For threee: 1 + 3 + 3 + 1 = 8 For four: 1 + 4 + 6 + 4 +
  1 = 16 etc. until 1 : 8 : 28 : 56 : 70 : 56 : 28 : 8 : 1 Here you see
  that you have 9 options of height. The difference is 36 cm - 12 cm =
  24 cm. 24 cm /9 = 3 cm, so 1 plant will 12 cm, 8 plants will be 15 cm,
  28 plants will be 18 cm, 56 plants will be 21 cm, 70 plants will be 24
  cm (i.e. "the majority of F2 are like P1 and F1") and 56 plants will
  be 27 cm tall out of 250 plants. Thus C is the closest.


Did any dinosaur molt? Like snakes or lizards, did any dinosaur molt ?

if yes, have we any proof of it ?

Richard Prum (the author of Evolution of feathers) says that ornithology is mostly a science about dinosaurs. He insists that dinosaurs were very close to birds, part of them had feathers and these feathered dinosaurs "shed (molt) them as birds of our days do".

Thus, we can conclude that dinosaurs probably possessed at least one molting-like mechanism, while others are the subjects for consecutive investigations.

sources
Moulting tail feathers in a juvenile oviraptorisaur. Nature, 2010.


Effect of extracellular molecules on membrane potential I am reading about the effect of extracellular potassium and chloride on the membrane potential, and now a question has come to my mind about what would happen if we added some molecules that have no charge to the extracellular? (consider that only K+ and Cl− can cross the membrane.)

I think that membrane potential and volume does not change, but I'm not sure about that.

The absolute answer would depend on a lot of factors, but the basics of it would be that - Yes, the volume does change and Yes, it would have an affect on the membrane potential.

By adding mass to any liquid solution, you are changing the volume. Plain and simple. Liquids are not compressible, and the only way to maintain volume while adding mass would be to increase the density of the liquid. [Edit] I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell

The membrane potential would change, but how much depends on a lot of factors. It would most likely change due to the movement of ionic solvents down their concentration gradients. Osmosis would move water out of the cell and into the extracellular environment, and ultimately reduce the membrane potential as more water outside the cell would essentially decrease the molarity of the solution. The cell would have to pump more ions out in order to regain the membrane potential.

The exception might be if you added so many hydrophobic molecules outside the cell that you basically saturate the environment, which could prevent exchange of all charged or partially charged atoms and molecules.


How can I normalize mRNA samples for sequencing? Is there an easy, inexpensive, not too labor intensive way to normalise mRNA samples so that even though one loses information of gene expression levels, each of the transcripts in the transcriptome is equally represented in the sample for sequencing? This is to say, one has a uniform distribution of transcripts, so that the lowly-expressed transcripts still have a good chance of being sequenced.

I have seen a few papers mentioning protocols for mRNA normalization, but I can't tell if any of them are practical in real life wet lab situations.

I found the link to a commercial product by Evrogen here:
http://www.evrogen.com/technologies/normalization.shtml

They claim their method is compatible with nextgen sequencing platforms:

  cDNA normalization using duplex-specific nuclease (DSN) is a highly
  efficient approach that can be applied for normalization of
  full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
  2005). The resulting cDNA contains equalized abundance of different
  transcripts and can be used for construction of cDNA libraries and for
  direct sequencing, including high-throughput sequencing on the next
  generation sequencing platforms (Roche/454, ABI/SOLiD or
  Illumina/Solexa).

And the most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503


How can dehydrogenation steps in some biochemical pathways produce ATP? Dehydrogenation reaction of alkanes is inherently endothermic as one removes two thermodynamically more stable C-H bonds and replaces it with one less stable C=C. Although the product is conjugated with the carbonyl group, this stabilization should be negligible, shouldn't it?
How comes then according to the scheme below, the result of this reaction are two high-potential electrons capable of forming ATP from ADP? Is the reaction concerted with some other not shown here? Or is the enzyme regenerated afterwards with some input of energy?

You have to consider the full redox reaction to determine if the reaction is favourable or not. It's not correct to think of enoyl-CoA alone as "higher energy" than acyl-CoA, because of the free energy difference $\Delta G$ of the half-reaction:

acyl-CoA  $\leftrightarrow$  enoyl-CoA + 2 $e^-$

cannot be determined without knowing what the electron acceptor is. You might be thinking of the enoyl group as "higher energy" because it is reactive towards H$_2$ (as in hydrogenation reactions), but that's not the relevant redox couple here.

In this case, we should consider the energetics of the entire process of electron transport, as shown in your diagram. Since the intermediates (FAD, ETF, quinones) all cancel out, the overall reaction without ATP synthesis is:

acyl-CoA + 1/2 O$_2$  $\leftrightarrow$  enoyl-CoA + H$_2$O

This reaction is highly favourable, with a $\Delta G$ of about -150 kJ/mol, because O$_2$ is a very good electron acceptor. (See this site for free energy calculations.) This is more than enough to drive ATP synthesis (about 45 kJ/mol).


Why do Great White Sharks not survive in captivity? Keeping any large marine predator in captivity is a challenge. While it has been done with both mammals and some sharks, it has never been successful with Great White Sharks. The longest a Great White Shark has survived in captivity is something like 4 – 5 weeks, if I am not mistaken.

I have heard this can be because they are used to swimming such great distances in the wild. However, both Killer Whales and Dolphins also swim great distances per day in the wild and are known to survive (sometimes even breed) in captivity.

So why is it that Great White Sharks are so hard to keep in captivity?

I am aware that most large predators kept in captivity live less long than in the wild, with some the exceptions (crocs just chill). It just seems extreme to me that Great White Sharks die within such a short period of time.

Most of the reasons why Great Whites are hard to keep in captivity are actually quite practical in nature:

Great White Sharks are expensive to keep because they eat a lot of food; their tanks need continuous re-stocking;
They refuse to be fed by humans, leading them to die of starvation. They do not seem to accept dead small fish for food;
The correct saline balance seems very important and difficult to maintain;
Logistics are difficult; they have to be safely captured in the wild, transported to a tank and that all the while keeping them in appropriate living water;
Due to their size and aggressive nature, great whites are hard to handle;
As you said already in your post; they are open water fish and cannot be confined. Sharks can swim hundreds of kilometers within a matter of days. This exercise and freedom may be essential to their well-being. A small 4-feet 'Great' White was kept alive for 6 months in a 1-million gallon tank. And even that was hardly enough;
They seem to get depressed in captivity. Great White Sharks that are kept within tanks have been known to head butt their noses into the glass walls and lose their appetites. It has also been noted that they get increasingly aggressive in their depressed state.

Sources
- IFL Sciece
- Science Alert
- Shark Bookings


What is this black shelled insect found in Western Arkansas? This bug was running around my driveway last night. It was very fast and wouldn't hold still - this is about the clearest shot that I got of it. As far as I could tell, there were no legs behind that 3rd segment - it was just dragging those.

I've never seen this, or anything like this in Arkansas. What is it?

Looks like the larvae of a carrion or burrowing beetle (i.e. some beetle species of the family Silphidae). Not sure on the species yet.

Wikipedia provides a good introduction to this family of insects.

Here's a picture:

And another:
Silphidae larvae

Did you see (or more likely smell) any dead carcasses around your property?


How does exercising/starved muscle import glucose (released by liver)? Adrenaline releases glucose from the liver during sport or if starved. This glucose goes to the blood through GLUT2 transporter. But how does it get transported into the muscle cells? GLUT4 is the glucose transporter into muscles, but it is activated (translocation to plasma membrane) by insulin, but when exercising/starved, there is no insulin. So is the glucose transported through some other transporter?

GLUT4 is the major glucose transporter in muscle even in exercise. However, during exercise, it is translocated to the cell surface by contraction-triggered, insulin-independent mechanisms, such as AMP-activated protein kinase (AMPK) activation.

For more, you could read this review.

Note:

'No insulin' is too strong a phrase; exercise and fasting are associated with low but detectable insulin levels. The reference range for fasting insulin in healthy individuals is $<174 \ \text{pmol L}^{-1}$ (contrast this with levels upto $1917 \ \text{pmol L}^{-1}$ one hour after glucose ingestion). Exercise studies have shown levels around $60-80 \ \text{pmol L}^{-1}$.


Can protein structure be determined by X-Ray Diffraction in a single image? I'm reading about the use of x-ray crystallography to determine protein structure. According to my book, data is collected at 30-360 angles (dependent on the symmetry of the protein). An illustration is given with concentric rings labelled with distances - the further out the points are, the higher the resolution.

Is the image a composite (where the angle of the point point from the centre is equivalent to the angle of the reading) or is a separate image taken at each angle? Are there any other reasons why more images would be required?

Thanks.

You cannot solve a structure with a single frame, even with perfect diffraction.

The reason you need images over a large swath of angles is because the diffraction pattern is also in three dimensions, in the so-called "reciprocal space".  At minimum, a 180° rotation of the crystal is needed to sweep the entire reciprocal space sphere with the plane of detection, though symmetry in the crystal structure can reduce this further (some of my proteins only required 90°, I think hexagonal unit cells with 6-fold symmetry can live with 30°).  Because crystals are real things (read: non-ideal, doubly so for protein crystals), the sweep is extended to gain some redundancy.


Does Blood Loss Shorten Telomeres? If blood loss necessitates immediate cell division to replace lost cells, does the increase in cell division correlate to shortening of telomeres? Does it further cause the Hayflick Limit to be reached sooner? Does blood loss accelerate apoptosis?

Nope, nope, and nope.  A cursory glance over any page on hematopoesis will reveal that blood cells are replenished from HSC, hematopoetic stem cells, which are self-renewing stem cells.  Telomerase is activated in stem cells.


How to analyse an ECG? I have a project about extracting features from a homemade ECG. I need the PQRST points from the signal of the heart beat. The ECG I'm using has 3 electrodes that attach to the chest.

The problem is I don't know where I should define the PQRST points because the result does not look much like an ECG. I want to try to create a program later that can find those points.

Here are the raw ECG traces data taken from 3 subjects that were alcohol-intoxicated (0.2 to 0.3 promille):

I'm guessing the red and orange points here. And I'm pretty sure the green points are accurate located:

Green points is easy to locate but the orange is a little harder and the red ones are really hard to pin point out. Those points can be used to define the length of different complexes, intervals and segments of PQRST.

Which points is safe to extract? Where exactly are those points located in the graph?

Is the data too inaccurate for finding abnormalities?

Is there any other useful feature, beside heart rate, I can extract from my graph?

First bump is called P point, middle is QRS wave (as in Q-down, R-up, S-down), and last bump is T. Every feature is representation of electrical activity in certain region of heart. E.g. P bump is contraction of atrium. See more here. Bumps are P/QRS/T.

The reason why you see so many different recordings is that it was taken with many-lead ECG. Heart has very distinct shape, its atrium is on top of ventricle, it is a bit tilted to the right, etc. Your recording is a projection of electrical activity vector onto vector that connects two leads used for given recording. Pick two other electrodes and you will have different picture just because axis of projection changed.

via NIH

It seems to me that recording you show are from different pairs of electrodes, but it shouldn't matter. As you can see, different pairs of electrodes will "pick up" some processes better that the other.

Now, because ECG is electrical activity recording, heart rate is least useful information to extract from it. Measuring pulse will be less of a hassle and as accurate. But what you can do is estimate biophysicals properties of given heart. For example, distance between P and QRS (PR interval) complexes is time that it takes for heart to contract ventricle after atrial contraction. Any abnormalities will cause lengthening of PR or other change. Lengthening of PR interval often indicates 1st degree AV block (AV node is not conducting as usual).

There is bunch of information out there on ECG and abnormalities, you can find useful this page from U Utah with examples of many severe conduction abnormalities.


Artificial Propagation and it's relation to asexual reproduction I know that asexual reproduction is also called vegetative reproduction. However I do not understand it's relation to artificial propagation. Is it a technique used for asexual reproduction (the method by which plants reproduce asexually) or is artificial propagation another name for asexual reproduction.

Am I right when I say artificial propagation techniques provide the means for plants to reproduce asexually?

Also, is my understanding of asexual reproduction and artificial propagation correct:

In asexual reproduction, a parent plant produces offspring that are genetically identical to it and to each other. Asexual reproduction produces clones as the offspring and the parent are clones of one another. Asexual reproduction can be an advantage when environmental conditions are stable and an organism is well-adapted to its environment. The genetically identical off spring will also be adapted to that environment. Asexual reproduction is carried out by the different artificial propagation techniques. Artificial propagation is the cloning of a plant from a portion of its roots, stems, or leaves. In asexual reproduction in plants, also called vegetative propagation, new individuals are grown from a portion of the roots, stems, or leaves of the existing plant. Artificial propagation involves using plants’ natural ability to reproduce vegetative. This process enables farmers and gardeners to select the parent plants for specific traits.

Artificial propagation is (generally) human-directed, while asexual/vegetative reproduction is a natural process. Take a look at the wikipedia article on vegetative reproduction for more information on how and why artificial propagation is sometimes preferred to vegetative reproduction.


Does cell culturing contribute to dangerous antibiotic resistance to the same degree as livestock? According to the CDC, antibiotic resistance is one of the biggest public health challenges of our time. The largest incubator for antibiotic resistance is the factory farming of animals where livestock are administered large antibiotic doses often and kept in infection-prone conditions.
Another area where antibiotic use is common is in cell culturing for biological research and engineering. To what degree is this use of antibiotics contribute to the public health challenge today, and moving forward as the biotechnology sector grows?
I am curious both about the impact for yeast cell culturing, and also for the culturing of meats as a future food source. I wonder how the problem differs from the antibiotic resistance problem in the livestock industry, and how this might affect the outlook of a future filled with synthetic biologic products and lab-grown meat.
I see two differences off the bat between livestock farming and cell culturing:

animals have much more powerful immune systems than cultures
culture contamination can be much more readily monitored and responded to by operators

Antibiotics are used in very different ways in cell culture and in livestock farming.
As you note, in farming, antibiotics are used to manage infection in unsanitary conditions and also to increase animal growth. Farming is essentially an inherently non-sterile environment and so there's not really any good way to keep microbes from spreading and interchanging, potentially carrying antibiotics resistance with them.
In cell cultures, on the other hand, one is typically working with a largely sterile environment, and it has to be maintained that way in order for the cell culture to work. They are far, far more delicate than farm animals---but they also can be entirely enclosed in a sealed vessel. Getting a significant contaminant into such an environment is not a "treat the sick animal" situation but a "sterilize and purge the bad batch" situation. Antibiotics are indeed often used as part of this defense, but the potential modes of infection are very different than with animals, which rules out many classes of pathogen simply because they are adapted for respiratory or gastrointestinal transmission, and a cell culture does not have these things.
Moreover, for most current industrial cell cultures, if the product is not the cells themselves, everything alive including pathogens will generally get killed off during later stages of the process (e.g., pasteurization of wine and beer).
If the cells themselves are the target of mass-scale culturing, e.g., cultured meat, however, then there will indeed be opportunities for antibiotic resistant pathogens to be developed and spread, particularly as increasing scale of operation
offers more opportunities for sloppy operations and regulatory evasion by low-cost operators.
Bottom line: antibiotic resistance is generally far less of a concern with cell culture than with livestock, but may still be at least somewhat of an issue.


How do we know that dinosaurs were related to lizards and/or birds? Do we clearly know what the living closest relative of the dinosaurs are? And connected to the first question, in scientific manner how do we know these relationship between extinct species and living ones?

In general the answer is always the same: you construct a phylogenetic tree. In order to locate different species on this tree in relation to each other, you use various features to compare which species are more similar to each other than others.

The best way of doing this is by comparing their DNA sequence, especially orthologous genes (i.e. genes common to the species compared).

Unfortunately, genetic sequences usually aren’t available for extinct species. You can still compare homologous features though. For instance, the class of mammals are all characterised by the possession of mammary glands. Similarly, all vertebrates have a vertebral column and all aves are feathered, warm-blooded, egg-laying vertebrates.

The collection of many such features from fossile records allows the creation of more or less detailed phylogenies. The Wikipedia explanation mentions several transitional fossil forms which trace the evolution from dinosaurs to modern birds via several intermediates. All of the inferences are based on anatomical resemblance.

This may sound weak evidence but in fact anatomical homology has proved to be sufficiently accurate in constructing other phylogenies, where we have been able to verify the correctness using genome comparison data. So while there is much uncertainty about the precise branching point of birds from dinosaurs (or maybe archosaurs), there is near-certainty that the common ancestor of birds and dinosaurs was, in fact, an archosaur.


Is Parthenogenesis known as Sexual reproduction or Asexual reproduction? I have seen that in some books refer to Parthenogenesis as sexual and in others as asexual.
The ones that say it's a form of sexual reproduction,they focus on the fact that meios has happened in the process and also,we are using a sexual reproduction system in that animal to produce the offspring.
The ones saying it is a from of asexual reproduction focus on the fact that although meios is involved,we only have one parent in the reproduction process and we cannot have any new alleles in the offspring than the ones the parent has.(unless we have mutation)

so how can we conclude in the end?which is it ?

and also,what is the evolutionary explanation for this phenomenon(parthenogenesis)?

Only a matter of definition

It is only a matter of definition. When it comes to sex, there is such a diversity of mating system that it is very hard to make a good definition that won't be challenged by limit cases.

Sexual reproduction can typically be defined based on the presence of meiosis (but again this will lead to limit-cases), on the need for two distinct parents + meiosis, or on the need for two distinct parents which have different gender (anisogamy) + meiosis.

Diversity of reproductive systems

At the end of the day, what one wish to call sexual reproduction does not matter too much as long as the definition is being made clear especially when dealing with potentially limit-cases.

If I remember correctly the intro book to evolutionary biolgy called Evolution by Futuyma makes a good overview of the diversity of reproductive system. Having a vague understanding of this diversity will help you undermine your hope of finding a clearly defined definition for sexual reproduction.

Applying the definition of wikipedia to parthenogenesis

Here is the definition from wikipedia

  Sexual reproduction is a form of reproduction where two morphologically distinct types of specialized reproductive cells called gametes fuse together, involving a female's large ovum (or egg) and a male's smaller sperm

Using this definition and applying it to the specific case of parthenogenesis, one would conclude that parthenogenesis is not a form of sexual reproduction (despite the presence of meiosis). Note by the way the even within the term parthenogenesis, there is quite a bit of diversity (see the wikipedia entry for parthenogenesis).

  what is the evolutionary explanation for this phenomenon(parthenogenesis)?

I will ignore this question because

A post should always be limited to a single question
This question is very broad
There is not a single answer to this question given the diversity of types of parthenogenesis.

For a start on the subject, you might want to have a look at Jaenike and Selander, 1979 for example.


What are these white spots on a dracena I have a Dracaena Marginata which started to have some white spots. They turn out to be some kind of "mold"

which can be removed when swapping the leaf and then leaves some discolored spots

They usually appear when the leafs get yellow (because of it, or because I have forgotten to water for too long) and seem to be more present at the base of the leaf.

What is this?

And more importantly: is it a problem for the plant? (minor issue, though it is a gift from my children) or for me? (major issue, and death sentence for the plant)

These are plant pathogens commonly known as scale insect (Coccoidea). Among the genera mentioned to infect Dracaena marginata here and here the most likely candidate is Pinnaspis.

They are close relatives of aphids and psyllids (and more distantly -- also to true bugs). Cochineal is probably the most famous representative of the superfamily. Scale insects suck host's sap and can be quite dangerous to the plant. Adult females are immobile and the spreading is performed by nymphs and (when present) males.

As far as I know they are harmless to humans. When digested (products of) at least cochineal can cause allergic reaction in some persons.


Bird identification- Crane What species of crane is this?

Today afternoon, I found this crane among a group of white cranes that were moving around a herd of buffaloes. I live in West Bengal, India if it matters.

Is it an eastern cattle egret,Bubulcus ibis coromandus in breeding plumage?

Yes, this is a cattle egret displaying its breeding plumage.

The cattle egret (Bubulcus ibis) is a cosmopolitan species of heron (family Ardeidae) found in the tropics, subtropics and warm temperate zones.

Specifically, this is the eastern subspecies, B. ibis coromandus.

 B. ibis coromandus [source: Wikimedia Commons]

 B. ibis ibis © Larry Thompson, 2007-2015

The cattle egret is the only member of the monotypic genus Bubulcus, although some authorities regard two of its subspecies as full species, the western cattle egret and the eastern cattle egret.

The eastern subspecies B. ibis coromandus, described by Pieter Boddaert in 1783, breeds in Asia and Australasia, and the western subspecies (B. ibis ibis) occupies the rest of the species range, including the Americas.
The eastern subspecies (B. ibis coromandus) differs from the nominate subspecies in breeding plumage in that the buff color on its head extends to the cheeks and throat, and the plumes are more golden in color.

B. ibis usually feeds in seasonally inundated grasslands, pastures, farmlands, wetlands and rice paddies. Their name comes from their tendency to often accompany cattle or other large mammals in these areas, where they catch insects attracted to and small vertebrates disturbed by these animals.

Originally native to parts of Asia, Africa and Europe, B. ibis has undergone a rapid expansion in its distribution and successfully colonized much of the rest of the world in the last century.

 [Source: Discover Life]

Major Source: Wikipedia


How much energy does a lion contain? I was looking into the following problem:

Obviously, the solution lies in how much energy either can output per unit of time.
The total energy output of the sun is $3.8×10^{26} \frac{J}{s}$.
The number of lions alone pales in comparison ($10^{12}$).

However, I'm now trying to figure out how many lions it would take to have an output equal to the sun, but I seem to be having a hard time finding good data.

What's the peak energy output of a lion per second (or where/how can I find such information)?

Wow, as an astrophysicist who has just logged into biology SE for the first time, I didn't think I'd have a question I could immediately answer.

You are correct about the Sun's output, so what about the lion.

If the lion is in its usual passive state, i.e. lying around as shown in your picture, then you would not go far wrong in treating them as black body radiators (well this will give you an upper limit, though the emissivity of human skin is quite high, so it should be a reasonable approximation.). To estimate a power I need a lion's temperature and its surface area.

According to this site the body temperature of a lion is 311.33 Kelvin.

I found a calculator that used the DuBois formula for surface area (for humans) and put in 440 pounds and 7 feet 10 for the weight and "height" of a (male, adult) lion - this returned a surface area of $3.6\ m^2$ (about twice a, male human, so sounds roughly ok).

Now using the Stefan-Boltzmann formula $P = \sigma A T^4$, I get the power output of a "black body" lion to be about 2 kW.

Thus $10^{12}$ lions have a power output of $2\times 10^{15}\ W$, which is 11 orders of magnitude less than the Sun.

But now take the question at its most basic. Compared to the Sun, the lion is a pretty effective power generation unit. The Sun only generates $2\times 10^{-4}\ W/kg$, whereas a lion-based power source weighs in with a massive $10\ W/kg$!

EDIT: Note that the calculation just assumes the Lion can produce this kind of power output whatever environment it is in. In practice a Lion absorbs a large fraction of this power from its surroundings and its internal metabolism does not need (and probably cannot) supply 2kW. Thus the 2kW should be reduced to some extent, though I'm not sure a simplistic $T^4 - T_{\rm env}^{4}$ calculation can be correct, unless one of you biologists tells me that a Lion's metabolism shuts down once the ambient (African) temperature approaches 311K (I guess in a human a lot of it goes in evaporating sweat?) Whatever, the order of magnitude of the answer is unchanged.


What is Biradial Symmetry? I am trying to visualize biradial symmetry. I have read the section in the Wiki entry on Symmetry in Biology but it is quite brief and there is no example to illustrate it. I haven’t been able to find one anywhere else on the internet.

In biradial symmetry, in addition to antero-posterior axis there are also two other axes or planes of symmetry at right angles to it and each other such as the sagittal or median verticular-longitudinal and transverse or cross axes. Such animals have two pairs of symmetrical slides i.e there are two planes of symmetry.

You can visualize it as a combination of radial and bilateral symmetry. The body has similarity on either side of a central axis but slight differences in sections next to each other if divided across any plane.

E.g.ctenophores.

for more info

In this image you can see that there are two planes of symmetry, one passing along the oral-aboral axis and the long axis of the mouth. The other passing along the oral-aboral axis and short axis of the mouth. The antimeres on either side of one plane are slightly different from the antimeres on either side of the plane (Imagine in 3D). The comb plates give it radial symmetry and mesogleal layer (jelly-like) give it bilateral symmetry.

If you are interested in the evolutionary aspect, then read this.


How can I use this data to make a function? I'm currently in high school biology (final year) and am currently working on an assignment. I need to create some sort of interactive model, so I've decided to make a simulation-type program.

I've looked a bunch at lots of papers and journals and I was wondering how I could take the data and make a function out of it.

Here is one example (Pleasants & Oberhauser, 2012):

In particular, I want to know how to make sense of the values F_1,11; r^2; and P. I am finding a lot of these values in the papers I'm looking at so it would be awesome if one of you guys could point me in the right direction.

Thanks!

I will not go too deep into the details but here some information to facilitate your understanding of these ubiquitous statistics in biology.

The F, $r^2$ and p-value are all equivalent statistics to measures the goodness-of-fit of a model against the data.

The F is the ratio of the $unexplained~variance~/~explained~variance$. I let you look out what the variance is. The F (originating from a F-test) allows, using the proper F-distribution cumulative density function (cdf) for the number of observation you have, to compute a p-value.

The p-value gives you the probability of obtaining the observed fit with your model (here a linear one) by random chance only. For example in your case a p-value=0.01 means that you have a 1% chance to observe this correlation just by chance. Usually the p-value threshold used to claim statistical significance is 0.05 (i.e. 5% chances to observe that fitting by random chance). In linear regression, the lowest the p-value the closest the distance (called variance) of the observed data point to the line.

The $r^2$ is the coefficient of determination (or the square of the correlation coefficient). This measure is very interesting as it give you an estimate of the "proportion of the data" explained by your model. For example a $r^2$=1 means that 100% of the variance of the data is explained by your model, in other terms your model perfectly fits the data. A $r^2$=0 in the other hand means that your model does not at all explain the data (no fits between your model and the data).

The $r^2$ and the p-value can be computed for any type of fitting, like trying to fit an exponential curve instead of a linear one. What you usually look for when modeling data is the highest $r^2$ possible. As all of this statistics are linked a higher $r^2$ means a lower p-value for an identical number of observations.