What would life expectancy be in the western world in the absence of Ischemic heart disease? In 2012, the leading cause of death was Ischemic Heart Disease.  In 1st world countries, what is the life expectancy for people who do not die of Ischemic Heart Disease?  I'm interested in the USA, but I'm happy for you to provide information on other 1st world countries if USA data is unavailable.

My motivation for asking the question is a curiosity of how much our life expectancy would increase if IHD was abolished.

This paper from 1991 is intervention-based, so it reports the effects of behavior modification on lifespan in people who turned 35 in 1990.  The authors report the gains for each individual behavior and then say:

  Eliminating coronary heart disease mortality is estimated to extend the average life expectancy of a 35-year-old man by 3.1 years and a 35-year-old woman by 3.3 years

Which they feel is a modest increase but I rather disagree.  This report estimates the that reduction in death due to heart disease of over 50% between 1950 and 1995 gained around 3.5 years, although most of that is probably due to better medical treatments.  This 2004 study used 1998 data from the UK and estimated that:

  The average gain in life expectancy from the elimination of cardiovascular disease risk as a cause of death was 4.0 years for all the 35 year-old men in the sample (n = 24), and 1.8 years for all the 35 year-old women in the sample (n = 32).

Although I would note the low sample size.  I didn't expect to find much, so I was surprised to find these... and with similar results!  One big issue is that a lot of the more recent research has focused on smoking, weight/BMI, and blood pressure reduction, rather than all IHD/CHD/CAD; I found tons of those.  As a side note, simply reducing TV watching to less than two hours a day can lead to a gain of almost 1.5 years.


Can turkeys run around when their head is cut off like chickens do? Chickens may run around after their head is cut off if the head is severed near the base of the skull leaving the brain stem intact and missing the jugular vein.  This usually only lasts for a few minutes, however there is the case of Miracle Mike that survived for 18 months after his head was cut off.  Do turkeys also exhibit this same behavior and if not, what makes this possible in a chicken but not a turkey?

The brain does not control all bodily movements. Some movements are to a great extent controlled by neural networks in the spinal cord. The spine contains a network which is pre-programmed to control the muscles in frequently-used movements such as running or swimming in chickens. This is why a chicken can run away after you chop its head off. Likewise, turtles swim using their a spinal neural network. As long as a signal is received somewhere in this network, the network will activate the swimming movements. Such a system is coined an ‘attractor network’ (source: Science Nordic). A similar system has been shown to occur in a sea slug. I couldn't find similar information in the turkey though. Happy Thanksgiving :)

Note that walking and running in higher animals (mammals) is controlled by the motor cortex higher up in the brain, involving a more complex system including the pyramidal system. Reflexes, however are controlled by quick, short spinal relay circuits in higher animals as well.


fibrinogens and fibrins - are they the same molecule? Some proteins are "activated", like fibrinogens; they are turned into fibrins by thrombins, and then the fibrins can aid in blood clotting.

Are fibrinogens and fibrins the same molecule, just in different states? If so, are all "-ogen" ending proteins and their activated forms the same as well?

If they are different molecules, why do us even bother to convert a protein into anotherto work, instead of simply activating a protein?

You could say they are the same molecule, but a molecule whose function is to change its state and properties very quickly when activated by thrombin.

Fibrinogen is a soluble protein - a complex of six protein chains.
Thrombin is an enzyme called a protease which very specifically cuts the ends off of two of those protein chains.
Once those bits are removed from Fibrinogen, the resulting molecule creates fibers very quickly to form clots.

You could also say that fibrin is a different molecule than fibrin because it really consists of many fibrinogen fragments.


What is the purpose of narwals' tusks? I've heard that narwals can grow their tusks up to 16 ft long. What do they need the tusk for? Hunting?  Comunication?

The evidence shows that the tusk is innervated, and acts as a sensory organ to the outside environment, as well as a mating tool.

Sensory ability in the narwhal tooth organ system


Decision-making in tree limb growth? Sorry if this is a naive question, but it occurred to me as I was walking across campus today; How does a tree decide which limb is allocated the most resources, and thus grows the largest?

My first thought is the first branch to deviate from the base receives the most energy investment, and so on, but I don't have the time (or will) to actually test that. Does it have more to do with efficacy of the limb for photosynthesis? Or is it largely due to chance/unknown variables?

Thanks in advance, I feel this is something I learned back in botany and just forgot completely.

There is Milton’s Law of resource availability and allocation.

It states that branches act as if they were different individuals, and they grow relative to the availability of their own resources.

The cells that grow are called meristems, there are different kinds of meristems, cambium ones that grow the trink, apical meristems that grow at the top,

Apical dominance is phenomenon where one meristem prevents or inhibits the growth of other meristems. As a result, the plant will have one clearly defined main trunk. For example, in trees, the tip of the main trunk bears the dominant meristem. Therefore, the tip of the trunk grows rapidly and is not shadowed by branches.

If the dominant meristem is cut off, one or more branch tips will assume dominance. The branch will start growing faster and the new growth will be vertical.

Over the years, the branch may begin to look more and more like an extension of the main trunk. Often several branches will exhibit this behaviour after the removal of apical meristem, leading to a bushy growth.

The mechanism of apical dominance is based on the plant hormone auxin. It is produced in the apical meristem and transported towards the roots in the cambium.

If apical dominance is complete, it prevents any branches from forming as long as the apical meristem is active. If the dominance is incomplete, side branches will develop.


How are drug metabolism and detection related? If someone is taking treatment for a psychiatric disorder (e.g. diazepine), then would traces of the metabolized drug be detectable in their sweat or saliva?

Any links to resources regarding this, or any help is greatly appreciated!

Short answer: Yes.

Diazepine is a ring-structure that forms the basis for the class of drugs called benzodiazepines. This class includes long acting and short acting agents. If you're actually talking about diazepam, it's one of the long acting agents, which means the half-life of the metabolite in your body (and it's detection) is long.

The National Highway Traffic Safety Administration has good reasons to want to collect samples of various drugs non-invasively, and, indeed, they're headed toward saliva for screening. A neat little item called a Drugwipe can pick up traces of diazepam from not only saliva and sweat, but from surfaces people have touched.*

The real kicker, though, is hair, from any part of your body. Drug use(including diazepam) can be  detected in hair for months after (even single) use, and many employers are now going for hair sample testing to screen for drug use.

*Saliva and Sweat Testing With Drugwipe®.


How do fibers control muscles? My professor says

  Nervus troclearis IV somatomotor fibers supply musculus obliquus superior.

and similarly for nervus oculomotorius III

  Nervus oculomotorius postganglionic fibers supply musculus ciliaris, m. sphincter pupillae.

I understand the verb "supply" as "stimulate" or "allow signal pass from the tract to the muscle that contracts or flexes". However, fibers must have some other functions too. So the verb supply seems to be a general term for these functions.

How do fibers control the muscle?

Read "supply" as "carry action potentials to." When the action potential reaches the junction with the muscle (i.e., the neuromuscular junction), neurotransmitters are released into synapse. A similar membrane depolarization occurs on the muscle cell, ultimately leading to contraction.

Nerves visible to the naked eye are actually bundles of individual axons (hundreds, thousands, or tens of thousands of axons). Nerves have the appearance of branching because the individual axons that travel to muscle fibers don't all go to one muscle.

For example the oculomotor nerve branches:

So what you see as the oculomotor nerve is really a collection of neurons. Some of these carry action potentials to the ciliary muscle and some to the sphincter pupillae. These are the parasympathetic components. There is a completely separate set of neurons (but still contained in the same nerve) that carry signals to the extraocular muscles.

This is really basic material that your professor should have explained to you.


What species is this bird? This bird is a frequent "visitor" at a lake south west of Berlin, GERMANY.

For more pictures here's a link:
https://goo.gl/photos/ADVSZwbDQUpbomCBA

It's a BLACK KITE (Milvus migrans). I bet you took the pics this summer because the great majority of the population is in Africa at the moment.

It is a black kite because:

rather uniform dark brown color
squared tail (it form a shallow v during gliding)
uniform underwing color and lighter head is a shared with marsh harrier but the absence of darker patch around the eye, the dark shoulder and 6 digitated primaries assure us is a black kite.

Here is a picture for reference:


How broad are the conclusions that one can make from a heterologous expression experiment? I am studying whether a neural protein regulates the activity of the protein GSK3. I am using heterologous expression systems where I am overexpressing the neural protein in CHO cells (via transfection) to see if it affects the levels of GSK3 in transfected cells vs controls. I am interested in seeing whether the neural protein regulates the activity of GSK3, and I have found that the levels of GSK3 are higher in the transfected cells vs control. But as I am using CHO cells as a model system, how broad are the conclusions that I can draw from this experiment? For example, will I be able to generalise what I found to neurons, or hypothesise that the same thing that I observed in this experiment occurs in neurons? Any insights are appreciated.

GSK3 is interesting because as a kinase, it is itself regulated by its phosphorylation status (particularly by Akt in neurons). Therefore, more protein does not necessarily mean more activity. For example from E13.5 to E15.5 GSK3 levels do not change but activity steadily increases. Hence if you increase GSK3 levels in neurons, it may not mean that downstream effects would change substantially, so I think although promising the in vivo effects may be hard to deduce from this experiment. If you see similar effects in in vitro neurons, you can be a bit more confident of potentially seeing similar effects with in utero electroporation in vivo


Why not use non-visual self-recognition to test for consciousness in an organism? Background

A well-known test for consciousness in an organism is to observe its ability to recognise itself in a mirror (see wikipedia article: "Mirror test").

Question

Why haven't I come across a "non-visual" mirror test? I.e. one that involves one of the other senses?

For example, how about testing for consciousness in bats by using an "audio mirror", the premise being that perhaps bats may recognise themselves through echolocation?

(image adapted from here)

Reading the page you linked, I found this

  MSR test may be of limited value when applied to species that
  primarily use senses other than vision. For example, dogs mainly use
  olfaction and audition; vision is used only third. It is suggested
  this is why dogs fail the MSR test. (With this in mind, the biologist
  Marc Bekoff developed a scent-based paradigm using dog urine to test
  self-recognition in canines.[19][41] He tested his own dog, but his
  results were inconclusive.[42])

Emphasis mine.

19 Archer, John (1992). Ethology and Human Development. Rowman & Littlefield. ISBN 0-389-20996-1.

41 Stanley Coren. How Dogs Think. ISBN 0-7432-2232-6.

42 http://www.psychologytoday.com/blog/canine-corner/201107/does-my-dog-recognize-himself-in-mirror


Does recombination increase the additive genetic variance for fitness? On this article, first column, eighth line of the introduction:

  By bringing together favourable alleles from different chromosomes, sex and recombination increase the additive genetic variance for fitness [..]

Can you please help me understanding why does recombination increase the additive genetic variance for fitness?

Note: In reaction @mgkrebbs comment, I think that given the subject of this article, when talking about different chromosomes, the authors actually referred exclusively to homologues chromosomes. My question concerns the second part of this sentence anyway: "Why does sex and recombination increase the additive genetic variance for fitness"?

Here is another question on the same article

This is a little tricky.

First of all lets be clear about 'bringing together favorable alleles' (or any alleles) represented by site mutations on 2 chromosomes:

--------A------------------
             X
------------------B--------

If the two dashed lines are two copies of the same chromosome, then a recombination event at X may produce:

--------A---------B--------

Allowing both A and B to be passed along to offspring.

Any given case of recombination might actually harm resulting offspring. But in cases where A and B together are beneficial, over the course of generations you will find AB genotype combinations show up more frequently in the population because of selection and competition.

Firstly each individual variant experiences some selection for fitness and many are lost.  Because of this, recombination will typically put two or more such variants together onto a single chromosome.  Recombination allows for individual mutations of benefit to pool together and collect into a single place.  This multiplies the chance that stronger combinations of mutations will show in the gene pool.  This increases the fitness variance - the most powerful combinations are more beneficial than any single variant alone.  On the other end detrimental combinations will also make some individuals exceptionally weak.

So its not just recombination, but recombination and selection which create favorable combinations of alleles in populations.  The link you give discusses how when selection is not strong, recombination is not so great, but we never seem to lose recombination where these conditions don't hold sway.

By comparison, consider a simple case where recombination does not occur where there is an A genotype and then one waits for B to show up on the same chromosome by random mutation.  That would take perhaps thousands or even millions of generations before such a thing happens at random.  Recombination is a powerful accelerator of evolution.


What is carbon in the soil? I often see the term "carbon in the soil" (example) but I cannot figure out what it is. It's a positive goal too - people want agricultural techniques that do not deplete it.

What form does this carbon exist in and what are the major sources? How does it help plants and other organisms who use the soil?

It refers to organic carbon, i.e. the carbon present in proteins, carbohydrates and other molecules as consequence of the metabolism of living creatures. Carbon rich soil is an indication that microorganisms, insects, and worms are living in the soil. They are the basis for the soil ecosystem and boost the flow of nutrients that ultimately will support plant growth. A soil with low content of organic carbon indicates that it's a harsh environment where living organisms struggle.

Some articles on the matter:

https://en.wikipedia.org/wiki/Soil_microbiology
http://www.nature.com/nature/journal/v501/n7468_supp/full/501S18a.html
http://mbio.asm.org/content/6/2/e02527-14.full


What species of three-tailed flying insect is this? What species of insect is this? Collected in spring in the United Kingdom near a river in an urban area during the late afternoon. They were flying up and down in the air.

Based on this list of mayflies of the UK, your mayfly is from the genus Ephemera.  Of the three species listed at that site for the UK, the closest match is to Ephemera vulgata, and it looks quite close.  The image of E. vulgata below is from Wikipedia here.


How can I download a gene sequence from GenBank (NCBI)? Could you tell me the steps to find and download a gene sequence from GeneBank?

I would appreciate your help.

Go to the NCBI website, fill the search field with relevant information in the upper part of page, select "nucleotide" from the drop-down menu just to the left of the search field and click search. You will get a list of items, by clicking "FASTA" link below any of them will bring you the corresponding sequence.
Depending on your interest, you can choose other databases from that menu, and some of them are interlinked. For example you can do the search by selecting "gene" instead of "nucleotide" and when displaying a selected gene info, you can see the links that lead to nucleotide database for getting the sequence.


Rate of cell division in humans On average, how many cells divide each day in a human being?
How long does a cell wait before dividing itself ?

I have tried to look on the internet but surprisingly the answer is difficult to find..

My first thought was this:

According to Wikipedia (citation provided)

  Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.

For every cell that dies a new one must be born, so there must be at least between 50 and 70 billion cell divisions to replenish these cells in an adult human (no net growth).

But then I remembered erythrocytes. Wikipedia again:

  Adult humans have roughly 2–3 × 1013 (20–30 trillion) red blood cells at any given time, comprising approximately one quarter of the total human body cell number

and...

  these cells live in blood circulation for about 100 to 120 days

So approximately 1% of erythrocytes are destroyed every day and must be replaced. That's 2-3 x 1011 cells formed every day, which dwarfs the cells replenished due to apoptosis (5 - 7 x 109).

  Through this process [erythropoiesis] erythrocytes are continuously produced in the red bone marrow of large bones, at a rate of about 2 million per second in a healthy adult.


How can neuronal signals faithfully be reproduced by scalp electrodes? There is a skull barrier (and possibly other layers too) between the brain and the scalp. I have seen people trying to extract EEG signals from the scalp by connecting electrodes and interface it to other devices. But how do these weak signals pass through these many barriers and reach the scalp electrodes? Also, "scalp cells" will have their own dynamics, right?

I simply don't understand how can we even get a approximate measure of electrical signals inside brain from scalp.

EEG has been recorded beginning in the late 20s, by people who were fairly clueless about electricity. While the strength of the EEG is indeed weak, it is readily observable with even such comparatively primitive technology.

The first thing you should take note of is that EEG measures the aggregate field. It does not see single neurons. It sees the synchronized activity of large neural populations of neurons - tens, hundreds of thousands of neurons at the very least, and probably more on the order of tens and hundreds of millions of neurons. This aggregate activity creates activity on the order of microvolts. This activity is then relayed (via the differential amplifier technique) to a powerful amplifiers. Modern EEG amplifiers have very large input impedances, and are thus able to amplify these weak signals. However, it still only observes mass action of large groups of neurons, not e.g. single action potentials by single cells.

Next, direct EEG analysis is comparatively uninformative for many reasons, including those you mention: that the scalp, the skull, and the other intervening tissue attenuate the signal. Thus, very often, extensive preprocessing is applied, such as averaging over many recordings. However, at least two features are already visible in the waking EEG. The first is the power-law structure of the frequency spectrum (although this is reinforced by the filtering characteristics of the tissue; the tissue filters higher frequencies more than lower ones). The second is the alpha wave, which is a large activity pattern coming mostly from visual areas. However, this is a very coarse feature; it tells us little beyond if the subject has their eyes open and is attentive, or has them closed/is inattentive.

Lastly, it is indeed generally assumed that deep sources (such as subcortical areas) are not picked up by the EEG (but only by e.g. MEG).

A good introduction to the topic is the book Electroencephalography by Niedermeyer and Lopes da Silva.


Identify brain junk - What are all the known intracellular and extracellular substances which build up with age and clog the brain? What are the known junk substances which the body is unable to dispose of and which build up in the brain with age to eventually causes age related problems?

Starting with the most obvious ones:

Amyloid beta - https://en.wikipedia.org/wiki/Amyloid_beta

Lipofuscin - https://en.wikipedia.org/wiki/Lipofuscin

Another example is the paired helical filament of Alzheimer's disease, so-called because neurofibrillary tangles have a ribbon-like structure when viewed under the electron microsocope.

It is now accepted that paired helical filaments consist of a single protein, microtubule-associated protein tau, in a polymerized and hyper-phosphorylated state. (see Lee and co-workers).

This old answer might also be of interest and contains a fuller reference list.

Neurofibrillary tangles are one of the two characteristic lesions of brain first described by Alzheimer, and are intracellular. The other characteristic lesion is the extracellular neuritic plaques caused by the build up of amyloid-beta (as the OP points out), which is itself part of a much larger transmembrane protein (of unknown function), the amyloid precursor protein or APP.


Counting the number of hydrogen bonds of multiple PDB files I've been trying to figure out a systematic way to count the number of hydrogen bonds for multiple PDB files.

DSSP shows me the total number of hydrogen bonds when I make dssp.exe 1A11.pdb, giving me the total number of 24 (am I correct, ok?)

24 96.0   TOTAL NUMBER OF HYDROGEN BONDS OF TYPE O(I)-->H-N(J)  , SAME NUMBER PER 100 RESIDUES

But when I run this command in R:

> require(biod3d)
> x=dssp(read.pdb("1A11"), full=T)

it doesn't look to have the number of hydrogen bonds. It shows this:

> x$hbonds
     BP1 BP2 NH-O.1   E1 O-HN.1   E2 NH-O.2   E3 O-HN.2   E4 ChainBP1 ChainBP2 Chain1 Chain2 Chain3 Chain4
1-A   NA  NA     NA  0.0      5 -2.1     NA  0.0      4 -0.3     <NA>     <NA>   <NA>      A   <NA>      A
2-A   NA  NA      3 -0.2      6 -1.5      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
3-A   NA  NA      4 -0.2      7 -1.8      5 -0.2      2 -0.2     <NA>     <NA>      A      A      A      A
4-A   NA  NA      1 -0.3      8 -1.5      6 -0.2      7 -0.6     <NA>     <NA>      A      A      A      A
5-A   NA  NA      1 -2.1      9 -1.9      6 -0.2     10 -0.2     <NA>     <NA>      A      A      A      A
6-A   NA  NA      2 -1.5     10 -1.3      1 -0.3      5 -0.2     <NA>     <NA>      A      A      A      A
7-A   NA  NA      3 -1.8     11 -1.3      4 -0.6      5 -0.2     <NA>     <NA>      A      A      A      A
8-A   NA  NA      4 -1.5     12 -1.2      3 -0.2      6 -0.2     <NA>     <NA>      A      A      A      A
9-A   NA  NA      5 -1.9     13 -1.1      4 -0.2      7 -0.2     <NA>     <NA>      A      A      A      A
10-A  NA  NA      6 -1.3     14 -2.3      5 -0.2     13 -0.4     <NA>     <NA>      A      A      A      A
11-A  NA  NA      7 -1.3     15 -1.8     12 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
12-A  NA  NA      8 -1.2     16 -1.8     13 -0.2     11 -0.2     <NA>     <NA>      A      A      A      A
13-A  NA  NA      9 -1.1     17 -2.4     10 -0.4     18 -0.5     <NA>     <NA>      A      A      A      A
14-A  NA  NA     10 -2.3     18 -1.6     15 -0.2     13 -0.2     <NA>     <NA>      A      A      A      A
15-A  NA  NA     11 -1.8     19 -1.8     17 -0.2     20 -0.5     <NA>     <NA>      A      A      A      A
16-A  NA  NA     12 -1.8     20 -0.8     17 -0.3     14 -0.2     <NA>     <NA>      A      A      A      A
17-A  NA  NA     13 -2.4     21 -1.9     19 -0.2     16 -0.3     <NA>     <NA>      A      A      A      A
18-A  NA  NA     14 -1.6     22 -2.0     13 -0.5     21 -1.0     <NA>     <NA>      A      A      A      A
19-A  NA  NA     15 -1.8     23 -2.0     20 -0.3     24 -0.3     <NA>     <NA>      A      A      A      A
20-A  NA  NA     16 -0.8     24 -1.5     15 -0.5     19 -0.3     <NA>     <NA>      A      A      A      A
21-A  NA  NA     17 -1.9     25 -1.0     18 -1.0     19 -0.2     <NA>     <NA>      A      A      A      A
22-A  NA  NA     18 -2.0     25 -0.3     23 -0.2     20 -0.2     <NA>     <NA>      A      A      A      A
23-A  NA  NA     19 -2.0     22 -0.2     18 -0.3     21 -0.2     <NA>     <NA>      A      A      A      A
24-A  NA  NA     20 -1.5     23 -0.2     19 -0.3     22 -0.2     <NA>     <NA>      A      A      A      A
25-A  NA  NA     21 -1.0     23 -0.2     22 -0.3     24 -0.2     <NA>     <NA>      A      A      A      A

So, my question: Is the total number of hydrogen bonds hidden somewhere in this output or somewhere else (or doesn't exist)?

If I manage to count the number of hydrogen bonds in a single PDB using Bio3D and R, then I can create a loop and iterate over all remainder PDB files.

Thanks for all!

The number of hydrogen bonds cannot actually be said from software only inferred. But you could try using STRIDE (http://structure.usc.edu/stride/) which takes the file name with a -h flag to output the number of hydrogen bonds. You could then write a small shell script which would pass in each file and store the data you wanted in whatever format you liked.


Why can't we feel pain when the eye lid touches the eye ball? When I press a finger on a closed eye lid it means the eye lid touches eye ball, then I didn't feel any pain.

Now I open my eye lid, then I small touch(not press) the eye ball, it gives me pain, why so?

TL;DR: It's psychological.

Pain is a tricky thing, and it's certainly possible to feel pain when pressing your eyelids against your eyeballs if you press hard enough ("hard enough" in this context is generally quite a lot less hard than is required to cause damage, by the way).

However: Since your eyeballs don't have skin, they also don't have nociception; i.e. they don't have pain receptors in the same way your skin at large does. Eye pains, like headaches, are largely caused by a combination of psychological responses to perceived stimuli and pain responses in associated structures.

Basically, the pain you experience when fingering your eye isn't pain in the same sense as the pain you feel from touching a hot stove or pricking yourself with a needle, it's generated by the brain in response to novel stimulus. Your brain knows what eyelids feel like, and it's okay with them, but once you start introducing fingers into the mix, all sorts of disturbances in salinity and moisture crop up, and your brain freaks out (and rightly so).

The same phenomenon can be seen with regards to swimming in the ocean: If you try to open your eyes under water, you'll find it a painful and disconcerting experience, but if you keep at it and practice holding your eyes open under water, you'll get used to it, and the pain will go away. Similarly, contact lens wearers will soon learn to deal with these stimuli, and be able to handle eye touching.

While I wouldn't advise you to go pawing at your eyeballs, if you for whatever reason have a need to do so, acclimating yourself to the feel of it will make the associated pain go away in short order.


Can anyone identify this object? It was found on the shore of the Ohio River in Kentucky. It is very hard, like bone, and feels hollow but does not rattle.  It is translucent.  I do not think it is skull of a water fowl even though the blunt end appears beak-like. I cannot figure out if it is plant or animal.  It was found in an area where arrowheads were found.
It appears to be hollow. I do not believe it is a shell since there is no margin or growth lines. It appears to be shriveled or desiccated.

This may be, though not sure, one of the supporting bones of the dorsal spine of the black drum,

Pogonias cromis also known as drum or drummer.
It is the only species in the genus Pogonias.
Reference

Freshwater drums are native to Ohio, preferring habitats of deeper pools of rivers and in Lake Erie with clear water and clean bottoms. They spawn from April to late summer.
Reference

Pogonias courbina is distinguished by the following characters: the occurrence of character-
istic thickening of the dorsal spines VII to XI in all specimens larger than 250 mm SL; all pter-
ygiophores in the dorsal-fin laminar, thin; anal-fin pterygiophores slender excluded those of
spines; lateral projections of gas bladder with few finger-like projections; genetic distance
between both species 1%

An important site that helped me to identify this-
https://txmarspecies.tamug.edu/otherdetails.cfm?scinameID=black%20drum%20pterygiophore


Poisonous plants, animals, mushrooms: is this always a kind of defense? I wonder whether developing deadly toxins in the organism's body is always or usually a defensive strategy rather than a by-product.

Developing anything by the body takes energy so generally only useful products are conserved. If some sort of mutation caused an organism to produce some sort of by-product that also happened to be toxic to its predators, then that organism is more favored to survive. No species ever starts producing something with the intention of toxicity in a predator/consumer of said species.

These xenobiotics that the plant/animal produces then can either be selected for because they're useful in whatever pathway they are a by-product of. Or they can be conserved because then this by-product has a defense use, regardless of whether the pathway its part of is necessary. Or both could happen, it could be doubly selected for.


Rigorous definition of the kinship coefficient and proof of a recursion thereof I am reading Section 5.2, Kinship and Inbreeding Coefficients, of Kenneth Lange, Mathematical and Statistical Methods for Genetic Analysis. There the kinship coefficient $\Phi_{i,j}$ is defined for two relatives $i$ and $j$ as the probability that a gene selected randomly from $i$ and a gene selected randomly from the same autosomal locus of j are identical by descent. Then the book states that suppose $k$ and $l$ are the parents of $i$,
$$\Phi_{i,j}=\frac12(\Phi_{k,j}+\Phi_{l,j}) \tag1$$
with some exceptions.

Equation (1) seems intuitive. Yet it is slippery for a proof especially considering the exceptions. The root cause is that the definition of $\Phi_{i,j}$ is vague albeit seemingly plausible. I am seeking a mathematically rigorous definition of $\Phi_{i,j}$ and a proof for Equation (1) together with the condition under which it applies.

The definition as set by Kenneth Lange's book is indeed quite vague and thus unrigorous. It is a probability not conditioned on observing an allele $a$ at a locus of $i$ but conditioned on the following where we focus on one particular locus. It is rigorously defined as follows. Then we will give the correct formulation of the correct recursive equation akin to Equation $(1)$ which is in general wrong.

A graph of lineage contains nodes, which we call persons, of a particular locus. Each node, or person, contains exactly two genes. We draw one and only one directed edge (parental relationship) from a gene of a parent person to the gene of a child person if the latter is inherited from the former.  This is a directed acyclic graph (DAG). Each gene can be connected by no more than $1$ edge directed to (as opposed to away from) it. The two genes in one person cannot be connected by edges. Two persons are said to be connected if there is an edge pointing from a gene of one node to a gene of the other node. Two persons cannot be connected by more than one edge. For a pair of connected persons and their directed edge between them, the edge is equally probable to connect to one gene as the other gene of a person, i.e. the probability is $\frac12$. A pair of genes (persons) are said to be connected if there exists a undirected (simple) path from one gene (person) to the other. Two connected genes are called identical by descent.
In this setting, the DAG with respect to the persons is given and deterministic whilst any directed edge in the DAG assigned to two persons are random with independent probability $\frac12$ with respect to the genes within each person.
For a pair of persons on a lineage DAG that is connected, the probability of one gene equally probably chosen amongst the two genes of one person being connected, or identical by descent, to one gene equally probably chosen amongst the two genes of the other person is the coefficient of kinship.
As an additional assumption, the genes that are connected have to be the same and thus assume the same allele.
Definition: Suppose a lineage DAG is given. Let the kinship coefficient between person labeled $1$ and person labeled $2$ be $\Phi(1,2)$.  Denote the set of parents and children of person $1$ each of which is on an undirected (simple) path between $1$ and $2$ as $S_2(1)$.
Lamma: Denote the set of paths through an ordered persons $p$ in that order as $P(p)$. $\{P((1,i,2))|i\in S_2(1)\}$ partitions $P((1,2))$.
Proposition: $$\Phi(1,2)=\frac12\sum_{i\in S_2(1)}\Phi(i,2).$$
Note: The summation in the Proposition is over $S_2(1)$ rather than the set of all parents and children of person $1$. That fixes the condition under which Equation $(1)$ is valid.
Corollary: $$\Phi(1,2)=\sum_{p\in P((1,2))} \frac1{2^{n(p)}}$$
where $n(p)$ is the number of persons on path $p$. $n(p)=|p|+1$.


Saltwater fish identification Can someone please identify this fish. Someone had asked me to rehome this fish but they were unsure what type of fish it is. Right now I have it in a quarantine tank until I find out what type of fish it is. I know it is some sort of clown but I cannot find the specific type after that. The fish is the one in the foreground of the image being black and white. It is a saltwater fish.

I know it is some sort of clown but I cannot find the specific type after that.

This is a juvenile Plectorhinchus chaetodonoides, which carries the nickname of "Harliquin sweetlips". With respect to the clownfish, they are similar up to the order Perciformes.

  Juveniles are brown with large white blotches and mimic the movement of a poisonous flatworm for defence against predators. They gain more spots and the spots reverse from white to black as they age.


How much variation is there between DNA molecules from the same organism If different but in tact molecules of DNA were extracted from my body, for example hair sample, blood sample, and mouth swab, how much variation would there be between DNA molecules?

The phenomenon is called mosaic single-nucleotide variations (SNVs) in somatic cells and it is an active area of scientific research (e.g., Abyzov et al., 2017, Genome Res. 27: 512-523):

  We estimate that on average a fibroblast cell in children has 1035
  mostly benign mosaic SNVs.

  Similar analyses in adults revealed no significant increase in the
  number of SNVs per cell, suggesting that a major fraction of mosaic
  SNVs in fibroblasts arises during development.


Do fledglings die if they are not fed constantly? There is a bird's nest on my balcony in the wall above the door with birds who breed. They have fledglings who already hatched. (I assume this because I sometimes hear quiet sweet chirping.) I sit on my balcony often for breakfast and sometimes for lunch almost every day. When I do this, the birds stop feeding their fledglings (because they are afraid of me or because it is some natural instinct to not reveal their nest).
A friend of mine (who installed a birdhouse on her balcony) told me that the fledglings die if they are not fed constantly. She told me that she doesn't use her balcony anymore (or at least not longer than 5-10 minutes) because of this.
So my question is: Do fledglings die if they are not fed constantly? How long can they survive without food? (like 30 minutes or so)
I would like to use my balcony because I really enjoy having my meals on it but I also don't want the fledglings to starve.

Depends on the species and their age. All birds have fat reserves that can keep them alive for a relatively long time. It's when fledglings are left for many hours or days that one should start worrying about their survival.
The following link explains more detail on how frequently birds must be fed, even if in your case I suppose you aren't the one feeding them:
https://birdwatchingbuzz.com/how-often-should-you-feed-a-baby-bird/
In my experience some species of birds might become less afraid if you leave food or water stations for them.


Online course on Plant Taxonomy and Physiology After following a course in Permaculture, I realised that if I want to get serious about it, I need to be able to distinguish plants. So I am looking for an online Video course on Plant Taxonomy and Physiology. My understanding is that it is a fairly standard course in basic Botany degrees, and since there are more and more school that put their material online it is quite possible that one of them might have placed this online too. Any suggestion?

Well, I wasn't able to find an online video course. The closest I came was this site, which links to courses that put their material online. Most of these are compilations of the lecture notes. There's also this page from the University of British Columbia, that has a nice little overview of the field of plant taxonomy.

In my experience, botany and plant identification are subjects where one really needs to learn by doing. You really need to grab a plant and take a close look at it while noting why its in the group that its in. A great way to get started might be to join a local gardening club or native plant society. The people in those groups can provide their tips for ID-ing plants.

One of the primary skills you'll want to learn is identifying what family a plant is in. Plant families have (mostly) consistent characters, and learning how to spot the most common families in your area will be a big help.


What's the smallest size a human eye can see? During a biology experiment at school, where we would look at waterweeds under a microscope, my teacher said something about that it's impossible for the human eye to see the cells without a magnifying glass of some sort. So, I saw that as a challenge, and decided to check if I could see the cells. And after holding the leaves really close to my face, I was indeed able to see tiny rectangles.

Since I was curious about it now, I decided to look some more things up. First, I tried to find out the actual size of waterweed cells. Based on this 640x enlarged image, which features cells of 5mm wide and 10 - 15mm long in the picture (which corresponds with of roughly 8µm wide and 15µm long).

I left this in the back of my head for a long time then, but I just looked at my cotton sleeve, and noticed tiny fibers. Not the ones that are woven together, but ones that are standing out from it. So, after looking it up, it turns out that cotton fibers are 10 µm wide.

So, I wondered, what is the smallest size a human eye can actually see? According to a whole bunch of sources all across the internet, it's either 200-400µm, 100µm, or 58-75µm. I also hear 'the width of a human hair' very often, but those can range from 17 to 181µm.

Very nice question!

First of all, the 'smallest size' that a human eye can perceive is called visual acuity, and can be expressed in various ways. It cannot simply be expressed by means of size measures, as objects with a fixed size are perceived as smaller when viewed from a distance (perspective). A familiar example is the train track:

Hence, visual acuity has to be measured as a function of viewing distance, i.e,  in degrees of visual view. Measured in degrees, the visual acuity of the average normally sighted person is 1/60 degree, or 1 minute of arc (1 MAR) (Webvision, chapter "Visual Acuity", by Kalloniatis & Luu).

Using the basic structure of the eye and some trigonometry one can deduce the smallest visible size :

The trigonometric formula becomes: $2d \times tan(\frac{\alpha}{2})$ with d being the viewing distance and alpha ($\alpha$) the visual acuity expressed in radians ($\pi \times \frac{degrees}{180}$) (NDT resource center).

Assuming the closest distance an adult can focus (~100 mm) and an average maximal acuity of 1 MAR, the smallest visible size boils down to 29 microns.

A young child can focus at distances down to ~50 mm, and can have a visual acuity of 0.4 MAR, which yields 6 microns.

Note that 1 MAR encompasses 288 microns on the retina, and some 180 photoreceptors. The optical limitations of the eye (such as diffraction by the lens and light scatter by the neural cells in the retina) limits the resolution of the human eye below the theoretical 'pixel limit' of the eye.

So to sum up, depending on one's age, one should be able to see targets in the order of 6 - 29 microns. The lower bounds of this range are indeed in the range of the waterweed cells and cloth fibers you describe.

PS - the values described are representative under ideal conditions, i.e., under situations of abundant lighting and high contrast.


Does a certain tumor type being invasive mean that it is highly metastatic? Does a certain tumor type being invasive mean that it is highly metastatic?

They are different things, metastasis is not the same as invasion.

Highly invasive cancer means that the tumor spreads beyond the layer of tissue in which it developed and is growing into surrounding, healthy tissues.

Highly metastatic tumors cause secondary malignant growths at a distance from a primary site of cancer.

In order for tumors to become metastatic, they must move and grow beyond their initial location and reach the circulatory system in order to travel to another location. During this phase, depending on the tumor, the malignant growth will acquire the ability to escape (tumors cannot do this at first, because it requires genetic mutations in genes responsible for cell adhesion). There are many other known factors which co-occur in cancer development - it is a rich field of research.

Here is an informative website for you to browse about the medical side of it: http://edcan.org.au/edcan-learning-resources/supporting-resources/biology-of-cancer/defining-cancer/invasion-metastasis


Can cancers caused due to viruses be contagious? Generally, viruses are infectious in nature and there are several cancer-causing viruses that are known (i.e. oncovirus)

My question is:
Are these oncoviruses infectious in nature? If so, what is the way in which they can be transmitted?

(edit:just a background to connect the title and the question (as mentioned by user iayork):While reading my text(which led me to the doubt) I was considering the virus as a causal organism and the disease as cancer(malignant tumour cells).The cancer cells are non-contagious however I wanted to understand if the disease  was.Thus I was interested on the routes of the transmission of the viruses.Also note (which I had already asked user Chris in the comment) "most cancer disease are non contagious but if cancer disease was due to virus if it was contagious or not"

The question title and the question itself ask two slightly (but critically) different questions.

Can cancers caused due to viruses be contagious? NO
Are these oncoviruses infectious in nature? YES

The tumors caused by the viruses are not contagious.  You can't take the tumor and transfer it to a new host and see a new cancer.  The viruses that cause the tumor are contagious, but in many cases by the time the tumor has arisen the viruses are no longer in a contagious form.  A tumor that's caused by HPV doesn't have contagious virus in it (see explanation below), and you can't transplant the tumor into a new host.  There still may be contagious virus present in the patient, but the tumor itself is not contagious.

Explanation HPV causes cancer by having a part (and only a part) of its genome integrated into the host genome, so cancers associated with it inevitably have a defective virus genome. There could theoretically be infectious virus in the neighboring tissues, but the cancer is driven by non-contagious virus. See for example The role of integration in oncogenic progression of HPV-associated cancers for a fairly basic explanation


What are Haplogroups? What exactly does the term Haplogroup or Haplotype means?

How is it claimed that people belonging to the same haplogroups have common ancestors?

I understand haplogroup as the group of people that share the same given haplotype for a region of the genome.
A haplotype is the readout of the DNA sequence for a part of the genome in one of the two copies that diploid organisms have. If you start reading the DNA sequence for a given point in the genome from one of your copies and someone else's copies, it will coincide up until a point where there is a change. It is more probable to have longer identical haplotypes if the two people that are compared are related. The closest the relation, the longer their haplotypes will be identical. What breaks haplotype identity are recombination events that happen in the germinal line in the previous generation, and mutations that happen both in the germinal line and the soma (the rest of your body) along time.


mouse gene translated to human gene I have a list of mouse genes, but all our analysis happens for human genes. Is that possible to translate these mouse genes to human genes? and is there any tool that can help me on this?

I am mostly a computer science guy, I am not sure this is even possible. However, according to someone, this could happen, I don't expect a full conversion though.

Thanks.

I would recommend using Biomart from Ensembl. This is basically a Swiss Army Knife for converting gene names into various IDs, getting corresponding locations on the chromosomes and so on. You can upload a list of gene names and convert them into the corresponding gene IDs of other species and the convert these IDs back to gene names.

If you haven't used Biomart yet, you can either start by going on their help page or by having a look on this tutorial for the conversion of IDs.


Why is protein cyclisation desirable? There are a number of methods to "cyclize" an existing peptide:

Disulphide bond as described in Disulfide Bond Mimetics: Strategies and Challenges by Gori et al.
"Linchpin" based (linker chemistry) as described in Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al.

Why would the "cyclization" of a protein be a desirable goal?

As described in the abstract of Synthetic Cross-linking of Peptides: Molecular Linchpins for Peptide Cyclization by Derda et al., protein cyclization improves:

resistance to proteolytic degradation and conformational stability. The latter property leads to an increase in binding potency and increased bioavailability due to increased permeation through biological membranes.

In simpler terms, a protein that is cyclized is less likely to:

Fold into an unhelpful shape.
Be broken up by an enzyme.

Thus, they are more likely to:

Act as better binders for a given target
Make it across a cell membrane


How is the first Triceratops born? To clarify at first, I have very little knowledge in biology and paleontology so there might be very obvious things I overlook.

According to the evolution theory, there must be a graduate evolution process over millions of years such that the skull and the horns of the Triceratops gradually appear over time. However why there is no fossil record of such "intermediate" form between Triceratops and earlier dinosaurs? I mean there must be some intermediate dinosaurs that has a short skull that almost looks like a small mountain on the neck and very short horns. However based on my internet search I can't find any information that confirms existence of such intermediate dinosaurs.

I just want to know is there any such evidence of graduate evolution among paleontologists or the evolution of dinosaurs is still much based on speculation (without firm evidence)?

Yes, there are many early examples of ceratopsians before Triceratops. The oldest clear member of the lineage is Liaoceratops: "the oldest ceratopsian ever found ... was about the size of a large dog. It had a blunt beak and a dainty neck frill. ... Liaoceratops was a puny forebear of the feisty Triceratops. Size, horns and spectacular frills came later in ceratopsian evolution."  Here's a reconstruction:

Protoceratops is very well known, and is a pretty obvious intermediate between famous ceratopsians like Triceratops and early ones like Liaceratops:

This cladogram shows a number of steps in ceratopsian evolution (right side of the diagram):

Note the steps it describes: Starting with early forms that have a vaguely frill-like structure, we see added: Rostral bone with "horns" that are barely visible; Frill, with jugal "horns"; Enlarged frill and skull; Postorbital horns; Nasal horn.


What is the probablity that SARS-CoV-2 will mutate? In many epidemic/pandemic situations, a lot of time the pathogen in question will mutate. For reference, this is the definition of mutation taken from Wiki:-

  A mutation is an alteration in the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA. Mutations result from errors during DNA replication, mitosis, and meiosis or other types of damage to DNA (such as pyrimidine dimers that may be caused by exposure to radiation or carcinogens), which then may undergo error-prone repair (especially microhomology-mediated end joining) or cause an error during other forms of repair or else may cause an error during replication

So my question is,

1》What is the probablity of SARS-CoV-2 mutating?

2》 How can we predict, in advance the mutation of the virus? (Maybe by studying the environmental factors of a specific place)

3》Lastly (something that makes the biologist cringe) is there any way to prevent mutation? Any way at all to somehow limit the mutations which can be used widely?

  BTW I am not a biologist, only a person among the millions out there, trying to find a way to help prevent the spread of the disease. My aim is to somehow use ML with Covid data to predict mutations (if possible...)

I don't see how you want to prevent mutations - and these don't have to be a bad thing as the mutation of SARS (the original one from 2003) shows, here the mutation (or better the deletion of a part of the viral genome) led to an antenuated pathogenic virus. Since this mutation happened in the early phase of the spreading, it became the major virus. See reference 1.

Mutations are a statistical process which happens all the time, especially for RNA viruse due to errors in the polymerases (see reference 2). So the answer to your first question would be: 100%. It is mutating, which can also be seen in the sequences which have been published so far. The differences are only minimal with a sequence homology between 99.91 and 100% (see reference 3), but this can already lead to changes in the amino acid sequence. You can see this in the screenshot from phylogenetic tree of all sequenced SARS-CoV-2 viruses on [Nextstrain] (see the site for the actual development):

To your question 2: You cannot really predict where mutations happen and which will come through in the long time, as this is a statistical process and the sheer number of viruses around in each infected patient. But there are positions which are more prone to mutations, while mutations at other parts of the sequence will lead to much less fit virus. There is not so much data available yet (remember that this virus is only around since the end of last year), but reference 3 has some data on it (figure 3):

Question 3: I don't see how this should happen, as this involves the polymerases which are involved in replication.

References:

Attenuation of replication by a 29 nucleotide deletion in
SARS-coronavirus acquired during the early stages of human-to-human
transmission
Why are RNA virus mutation rates so damn high?
The establishment of reference sequence for SARS‐CoV‐2 and variation
analysis
On the origin and continuing evolution of SARS-CoV-2


Why doesn't CAS9 cleave the original CRISPR sequence in the bacterial genome? CAS9 is the RNA-guided endonuclease that cleaves DNA as specified by the RNA sequence and is used to target viruses that infect bacteria. So why doesn't this RNA+endonuclease combo also cleave the original CRISPR spacer sequences (which also have the same DNA?). Is it the same reason that the bacterial genome is methylated (and hence protects from restriction enzymes)? Does methylation also make a difference to CAS9 as it does to restriction enzymes?

This actually was a doubt asked to Eric Lander in this lecture.

It is not the methylation status. The crRNA is not only complementary to the spacer sequence within the CRISPR array but also to the repeat sequence flanking that spacer. The additional base pairing of the sgRNA with the repeat prevents a nucleolytic cleavage by Cas9. In addition, the arrays typically do not contain PAM sequences.

Here you will find a nice illustration:


How can we create a living dinosaur using DNA technology? I'm wondering what would we need to do to create a living dinosaur using DNA technology? If it is not possible with current technology, will it ever be feasible?

In the movie Jurassic Park, scientists extract dinosaur DNA from a mosquito which was preserved in amber, and which has sucked blood from a dinosaur. The DNA is incomplete, so the scientists splice it with frog DNA. The DNA is then inserted into a crocodile ova and an embryo is created, and so on.

The Jurrassic park method is dubious. Although dinosaur DNA has been found and isolated, it was too damaged to restore it to its original form using current technology. It's not clear that splicing with frog DNA would work. Let's for the moment forget about how you would get the dinosaur embryo to develop and the eggs to incubate and hatch. I want to know how would we fully sequence the genome of some dinosaur?

It is widely accepted that birds are in fact dinosaurs. Cladistically speaking, no DNA technology is required to create a living dinosaur, as they already exist.

Assuming you want to do the same to a non-avian dinosaur (a paraphyletic group), however, a better idea would be to ask on World Building SE, as there have been little to no scientific research on the topic, and speculative answers are generally considered off topic here.


The phylogenetic definition of the clade Dinosauria Up until two years ago the clade of Dinosauria was defined as all the descendants of the most recent common ancestor of Triceratops and birds. From Wikipedia:

  Under phylogenetic nomenclature, dinosaurs are usually defined as the group consisting of the most recent common ancestor (MRCA) of Triceratops and Neornithes, and all its descendants. It has also been suggested that Dinosauria be defined with respect to the MRCA of Megalosaurus and Iguanodon, because these were two of the three genera cited by Richard Owen when he recognized the Dinosauria.

However, after the resurrection of the clade Ornithoscelida by Baron et al in 2017 (see here), as the clade consisting Ornithschia and Theropoda, the MRCA of Triceratops and birds is defining Ornithoscelida and not the whole Dinosauria, assuming we still define Sauropodomorphs as dinosaurs.

So if dinosaurs include Sauropodomorpha, Herrerasaurs, Ornithoschia and Theropoda,  what is the most updated phylogenetic definition of the clade Dinosauria?

As of right now it is still the same, the evidence for sauropodomorpha being a outgroup is not statistically more reliable, this may change, however this will still not have much impact. There are several ways in which dinosauria is defined.

The most recent common ancestor of Megalosaurus and Iguanodon is also sometimes used since they were the original animals used to define the group.

The last common ancestor of Triceratops horridus, Passer domesticus, Diplodocus carnegii, and all of its descendants is also used just because of Baron's work.

Finally there are several unambiguous synapomorphies used to define the group, including such things as ankle structure. A full list can be found here.

In a group as well known as dinosaurs, a discovery like Baron's (if it holds up) is just going to lead to a change in the definition.


How do chemists calculate the existence of billions of organisms? So the packaging of Bio-Cultures Complex says that it contains a minimum of a billion viable organisms per capsule.

How has such an estimate been drawn?

Have they counted a smaller amount and then multiplied it?

It says a "a billion viable cells". The viable is important because it tells you that they employ a method that determines whether the cells are alive or dead. Most likely they did a simple colony count.

The approach is simple, you take bacteria in suspension, serially dilute them in order to reduce the concentration to numbers that can be counted, and then spread onto a solid media plate (usually containing agar) and leave for 1-3 days (depending on organism) and count the number of colonies produced. You can then multiply up this number by the amount you diluted by to get the number of viable cells present in the original.

A billion is not a lot of bacteria. You can expect 100-1000 billion cells per ml in an overnight culture of these bacteria.

Looking at the product description, it specifically mentions CFUs (colony forming units) so I think we can be pretty sure that this is the approach they are using.

(Note that this is standard microbiological technique rather than something chemists would be doing)


Is there an Exit site (E-site) on the eukaryotic ribosome? One of my professors mentioned something about the e-site (the exit site for the t-RNA) on a eukaryotic ribosome.  There was a student in the class who objected, saying that there is no e-site on eukaryotic ribosomes; it only exists on prokaryotic ribosomes.  I've tried to find some reliable source to figure out who's right, but to date the only thing I've found is an obscure sentence in a wikipedia article, which doesn't look all that official.

Is there indeed an e-site on the eukaryotic ribosome?

Prelude: Thinking about protein synthesis

I remember the time when there were only two sites on the ribosome, and when it became clear there were more, I resented the need to make my lecture notes and my contribution to a venerable text book more complicated. So I am neither a devotee nor an expert on the exit site, but if asked to guess who was right (even if, or especially if, the student was supported by Campbell’s Biology as @CSharp informs us) I would put my money on the ‘professor’. Why? Because protein synthesis and the ribosome are so ancient that although there have been changes in eukaryotic proteins synthesis, something so fundamental as the sites for the fundamental process would not change.

Answer

Yes, Virginia, the eukaryotic ribosome does have an exit site.

The evidence

Although editions of the venerable text book no longer appear and my research no longer impinges on protein biosynthesis, I still collect papers on the subject with my bibliographic software. The latest relevant publication I have is by Khatter et al. from Nature in 2015, entitled Structure of the Human 80S Ribosome.

As not all list members have access to Nature, as a subscriber I have taken the liberty to reproduce a a section from the abstract (my emphasis) and a pertinent illustration:

  Here we report the near-atomic structure of the human ribosome derived
  from high-resolution single-particle cryo-electron microscopy and
  atomic model building. The structure has an average resolution of 3.6A
  ̊, reaching 2.9A ̊ resolution in the most stable regions. It provides
  unprecedented insights into ribosomal RNA entities and amino acid side
  chains, notably of the transfer RNA binding sites and specific
  molecular interactions with the exit site tRNA.

The cryo-EM map and atomic coordinates have been deposited in the EMDB and Protein Data Bank under accession codes EMD-2938 and 4ug0, respectively.

I admit I haven’t researched and rehearsed the evidence, but I think that would be another question.


When giving blood, what is the specific Iron measurement they take? I went to give blood the other day, and they take an "iron" measurement prior to actually drawing the blood. My level was 16.4 -- but what specific type of iron were they measuring?

I've heard of ferritin, transferrin, iron binding cap, total, etc., but when I asked what the upper limit was, she said 19, which didn't really fit within the healthy ranges I can find for the above types.

Thoughts?

Most likely they were measuring the hemoglobin concentration, in units of g/dL (i.e. 101 kg/m3). Assuming by your username you are male, the reference range for [Hb] is approximately 13.8 to 18.0 g/dL (sources vary somewhat), which roughly matches the "19" you were told was the upper bound.

Wikipedia also notes that [Hb] "is typically tested before or after blood donation", making it likely that that was what they measured.

Calling it "iron" isn't strictly correct. The human Hb tetramer's molecular weight is about 65 kDa, yet it contains only 4 iron atoms, so the actual concentration of iron in your blood is actually much less.

Useful resource: Wikipedia's list of reference ranges for blood tests has a very detailed chart of commonly cited reference ranges for many substances, with citations.


Pentaploid genotype frequencies I know that if I am dealing with a diploid case, and I have 3 alleles, then I can have 6 possible genotypes. I am doing this by adding up all the numbers from 1 to 3. $$1+2+3 = 6$$
But if I want to generalize this, say for a pentaploid, how do I effectively compute the number of distinct possible genotypes? (Assuming perfect HW equilibrium)

I want to say this is just a simple problem of combination with replacement, but I'm not sure if the biology allows me to make this statement.

Ploidy number vs number of alleles

You seem to be confounding number of alleles with ploidy numbers. You rightly figured the number of possible genotypes for a diploid individuals when there are 3 possible allelic states.  When you ask for a pentaploid, are you many alleles are you wiling to consider?

Pentaploids are very rare

If I am not mistaken, species with an odd ploidy number are very rare. Tetraploids and hexaploids, while still rare are much more common than pentaploids.

General case

It is indeed a simple math problem. Let's answer to the question in the most general case. If the ploidy number is $P$ and there are $S$ possible alleles, then the number of possible genotypes is

$${P+S-1 \choose S-1} = {P+S-1 \choose P}$$

, where ${\choose }$ refers to the binomial coefficient. For a pentaploid organism, with 3 possible alleles, there are therefore 21 possibilities.

More information

You can have a look at this webpage that offers much more info about the combinatorics of genotypes.


What is the benefit of fever during infections? When people get sick, they often develop a fever. What is the effect of an increased body temperature on viruses and bacteria in the body? Is it beneficial to the infected body? Importantly, often fever-reducing agents like aspirin are prescribed when people are sick. Doesn't this counteract any benefits of fever?

Fever is a trait observed in warm and cold-blooded vertebrates that has been conserved for hundreds of millions of years (Evans, 2015).

Elevated body temperature stimulates the body's immune response against infectious viruses and bacteria. It also makes the body less favorable as a host for replicating viruses and bacteria, which are temperature sensitive (Source: Sci Am).

The innate system is stimulated by increasing the recruitment, activation and bacteriolytic activity of neutrophils. Likewise, natural killer cells' cytotoxic activity is enhanced and their recruitment is increased, including that to tumors. Macrophages and dendritic cells increase their activity in clearing up the mess associated with infection.

Also the adaptive immune response is enhanced by elevated temperatures. For example, the circulation of T cells to the lymph nodes is increased and their proliferation is stimulated.

In fact, taking pain killers that reduce fever have been shown to lead to poorer clearance of pathogens from the body (Evans, 2015). In adults, when body temperature reaches 104 oF (40 oC) it can become dangerous and fever reducing agents like aspirin are recommended (source: eMedicine)

Reference
- Evans, Nat Rev Immunol (2015); 15(6): 335–49


What is the human ear's temporal resolution? What is the smallest sound duration that the human can hear? In other words, what is the lower duration limit for a sound to be translated into electrical signals by the ear?

Suppose the human ear can discern or distinguish between 18 kHz and 20 kHz sounds, this would mean that, if a single wave could  be processed at 20 KHz, the sound duration would be 1 / (20KHz) = 0.00005 second, which would be next to incredible (and probably impossible).

I am particularly interested in the lower duration limit as depending on frequency.

I am expecting something like this (I am not sure)

 Freq   Duration needed to be aware of the sound
 20KHz  0.05S (50 mS)
 10KHz  0.04S (40 mS)
  5KHz  0.03S (30 mS)
2.5KHZ  0.02S (20 mS)

I will provide an answer in 2 parts. The first part is a theoretical approach based on the absolute possible minimum (my original answer). The second part focuses on experiments in the peripheral auditory system (added edited answer).

PART I: Absolute theoretical minimum (original answer)
As you inquire about electrical signals in the auditory human system I have to say that electrophysiological data at such a fundamental level is scarce in humans. That having said, we can start off by looking at auditory clicks, which are generally the shortest possible well-defined auditory stimuli. The shortest auditory click I was able to find, and which was used in a psychophysical context (i.e., audible to a human) was 10 microseconds (Leshowitz, 1971).

Now, (1) assuming 10 microseconds is the lower duration limit of a click (it may well be lower), and (2) assuming this click duration is representative of the lower limit of a tonal burst duration limit (it may well not be), and (3) assuming you indeed wish to know about/use auditory tones and not clicks, and finally (4) assuming we need at least one wavelength of a tone to fit in this window, then we could present a frequency of 100 kHz, or higher. As 20 kHz is the upper frequency limit of the human ear, we would need at least 50 microseconds for one wavelength, i.e., basically what @Dustin concluded, but it does not end here:

Frequency splatter (Fishbach et al., 2001) limits the lower limit of tonal stimuli. To prevent spectral splatter one needs to incorporate rise and fall times (ramps) onto the tonal stimulus. Hence, again assuming you do want tonal stimuli, an onset and offset ramp of one wavelength each would be advisable (at the very least) and hence 3 wavelengths are needed, increasing the duration of a 20 kHz tone to 3 wavelengths, i.e., 150 microseconds (spectral splatter may not be prevented, but at least reduced).

On top of this theoretical approach, it has to be noted that I started off with taking a click as a starting point. A click, being an impulse signal, basically stimulates the entire cochlea (the inner ear), and hence represents the most powerful auditory stimulus. Pure-tone bursts are, as a consequence, weak stimuli as they stimulate a small proportion of the available hair cells. High sound levels may therefore be necessary for short tonal stimuli, in turn degrading the frequency resolution in the cochlea as excitation spreads away from the characteristic frequencies. Mostly, several milliseconds are used as tone bursts.

Moreover, taking 20 khz is kind of an upper limit, and many folks are not even able to hear 16 khz. An upper limit of, say, 12 kHz would be advisable when grownups are used. This means a wavelength of 83 microseconds and for 3 wavelengths (for ramp times) that means 250 microseconds.

If lower frequencies are needed, this number would increase further.

EDIT: PART II. Phsyiological experiments.
As you are also interested in electrical signals, we might take another approach and start looking at experimental (animal) data. The temporal limits of the auditory system are generally assumed to reside in the ribbon synapse that is situated between the inner hair cells and the auditory nerve fiber (Parsons, 2006):

This synapse is considered to be the limiting factor in the temporal characteristics of the auditory system (Khimich, 2005). By analyzing this synapse using very short tone bursts, it was shown that the vesicles of glutamate (the neurotransmitter activating the auditory nerve fibers that lead the signal to the brain) were released as shortly as 2 ms after tone onset. Tone bursts were 8 - 16 kHz, 10 ms plateau, 1 ms
rise/fall (Khimich, 2005). Note the tone burstduration and rise fall times mentioned in answer PART I.

Indeed, when first spike times in auditory nerve fibers were determined, spikes with the shortest latency occurred just under 2 ms (Heil and Irvine, 1997).

SR in the figure means spike rate, showing that higher spike rates are accompanied by shorter latencies. A1 means auditory cortex neurons, which obviously have longer latencies.

Hence, from these experiments I dare say that 2 ms would be sufficient to elicit at least one spike.

Why then leave part I of the answer? The problem is that the experimental data do not show that a spike wouldn't have been generated at shorter stimuli. The data merely show that with an ongoing stimulus the first spike appears at 2 ms. It does not show whether 2 ms of temporal summation is necessary, and that is why I have left part I of my answer in place, as a theoretical lower bound.

As a side note: the spike rates are highly dependent on loudness levels. Lower sound levels result in longer latencies. Specificaly, acceleration of the stereocilia on the inner hair cells in the cochlea is the primary parameter. The faster the cilia move, the faster the spike response.

References
- Heil & Irvine. J Physiol 1997; 78:2438-54
- Fishbach et al. J Neurophysiol 2001; 85:2303-23
- Khimich et al. Nature 2005; 434:889-94
- Leshowitz et al. J Acoust Soc Am 1971; 49, Suppl 2:462-6
- Parsons. Nature 2006; 444:1013-4


How does the mutualism of figs and wasps exactly work? I have just rudimentary knowledge about the mutualism of figs and wasps and would like to know how this works step by step.
Also how do humans use this mutualism? Do they support or hinder it at some points?

Ficus sp. (various sorts of figs); have a close relation with a sort of Wasp's reproduction.

Tiny flowers of Ficus are enclosed inside a hollow, pear-shaped concave  special-type of inflorescence, also called hypanthodium (term commonly used in flower-stage) or Syconus(term commonly used for fruit stage) when flower stage sometimes c ( from outside it looks like a single fruit but it is not).

There is a very narrow entry-hole or orifice at the apical portion of the inflorescence.

Inside the inflorescence, there are  3 types of flowers.
1. Male flowers, 2. Female-flowers, and 3. 'Gall-flowers' those are assigned as female flowers but their 'style' is much shorter.

Male flowers located towards the orifice, whereas female and gall-flowers locates in deeper regions.

Blastophaga, a genus of wasp, brings in required pollen,  also called gall-wasp, lay eggs inside figs.

To do that, they enter inside the fig inflorescence, lay eggs on these dwarf 'gall flowers' using ovipositor.

The eggs develop larvae, which fed on some ovules, and form pupa.  When the pupa-stage develop into mature wasps, the try to crawl-out from the orifice, they brush against the male flowers.

This pollen-laden insect when enter in another fresh fg, it also pollinate that-fig.

Image URL : https://media1.britannica.com/eb-media/17/24017-004-98EF07A1.jpg .

Image Page-Source: https://www.britannica.com/animal/fig-wasp

  Source: College Botany, Vol-1 / Gangulee, Das, Datta; New Central Book Agency.

P.S: I think my answer is NOT satisfactory enough

This question require more scientific details.

Widely known fact is, fig-wasps pollinate figs. But really there is a lack of detailed information like does the mother-insect die inside the fig and only the young insect go-out? or the mother insect come out from fig after laying eggs? if the larvae eat the ovules then isn't it harmful to the fig plant at any extent? How female-figs (in dimorphic members) are pollinated... does the wasp travels from one fig to another? When the young wasp come out from the fig it certainly take some months to reach maturation to lay eggs. Within that period does the pollens sticked in their body , and viable to germinate on stigma? There are many sorts of figs. Does all of them require wasps? Would figs survive without the wasps? --- What the question seeks, is, out of the popular children-book story; the Scientific-details behind figs and wasps. I assume the answer would not broader than reasonable; if someone knows their life-cycles and structures, I think it is possible to give very point-to-point answers within limited space.


Why is the consumer/producer biomass ratio higher in the oceans? According to Bar-on et al. (2018) (see figure 2), the terrestrial consumer/producer biomass ratio is 20/450  while the marine consumer/producer biomass ratio is 5/1 (in Gton of carbon).
Why is the consumer/producer ratio much higher in the oceans?
Is it perhaps because marine animals are more efficient? Or is terrestrial plant biomass underexploited by surface animals?
 Bar-On, Y.M., Phillips, R. and Milo, R., 2018. The biomass distribution on Earth. Proceedings of the National Academy of Sciences, 115(25), pp.6506-6511.

The paper you cited suggests an explanation:

Such inverted biomass distributions can occur when primary producers have a rapid turnover of biomass [on the order of days (34)], while consumer biomass turns over much more slowly [a few years in the case of mesopelagic fish (35)]. Thus, the standing stock of consumers is larger, even though the productivity of producers is necessarily higher. Previous reports have observed inverted biomass pyramids in local marine environments (36, 37). An additional study noted an inverted consumer/producer ratio for the global plankton biomass (16).

To explain/clarify this a bit further: there are two main processes that affect the consumer/producer ratio. One, which you have identified, is efficiency (how much of the biomass is transferred from one trophic level to the next). The other is turnover rate (rate at which biomass leaves a trophic level), which is the reciprocal of the residence time (the average length of time that a unit of biomass spends in a trophic level before transitioning to another trophic level/compartment).
At equilibrium, the biomass in a trophic level is equal to (inflow/turnover rate) or (inflow $\times$ residence time). If consumers at a particular level consume one tonne of biomass per month (assume 100% efficiency for now) and the residence time is 6 months, the standing stock or quantity of biomass at that level will be 6 tonnes. Taking some of the numbers from the paragraph above: suppose the residence time for phytoplankton is 4 days while of consumers is 400 days. If the consumers have a 10% efficiency for taking up phytoplankton biomass, then the consumer biomass will be $(400~\textrm{days}/4~\textrm{days}) \times 10\% = 10$ times higher than the phytoplankton biomass.


Which spider is this? Is it dangerous? So today while clearing the trash out of my room I found this orange spider on an abandoned piece of foam.

 It is carrying a weird ball with it wherever it goes. What is this? And to which genus does this spider belongs?

For a better contrast I placed it on  paper.

EDIT-1

Size: Roughly 1cm in length

Location: Uttar Pradesh, India. Coordinates- https://maps.app.goo.gl/svXoxaH4Z2lK2rFH2

Temperature: 34°C and Humid.

EDIT-2

Adding few more pics

It is clearly a Theridiid (cobweb) spider, but it doesn't look like the Parasteatoda tepidariorum I'm familiar with here in the US.  The egg sac it's holding indicates it's a mature female, and the regular pattern on the abdomen is both distinctive and unlike the variable, blotchy pattern of tepidariorum.  Unfortunately, not being familiar with Eurasian spiders likely to be found in your area, I can't be of much help as to what it might be, beyond limiting it to the Theridiids.
Oh, yes - it's pretty clearly not one of the Widows (Latrodectus spp.), and since those are the only medically significant Theridiids we know, it's not dangerous.


What is structural RNA? In genbank (ftp://ftp.ncbi.nlm.nih.gov/genomes/archive/old_refseq/Fungi/Saccharomyces_cerevisiae_uid128/) there are an archive .frn (nucleotide sequences of structural RNAs in fasta format), and  I want to know the differences between structural RNAs and genes.
Are the nucleotide sequences of structural RNAs a coding region?

My goal is separate the coding region from the non coding region of a given complete genome.

I'm physicist so, I apologize if my question is pretty simple.

To be very brief: A gene is a sequence of DNA or RNA, which is hereditary and has a biological function. In the Saccharomyces cerevisiae genome you posted, every gene is a DNA sequence. The function of most genes is to be transcribed  to messenger RNA (mRNA), which is then translated to a protein. "Coding" DNA refers to DNA which eventually has its sequence translated into protein

Structural RNAs are encoded by genes but not translated to protein, and thus are not coding regions. They are made up of RNA, but function more like proteins. When they enable reactions, like enzymes, they are called Ribozymes. The most well known ones are the Ribosomes, which are an essential part of protein biosynthesis. Others form special structures which help molecules recognize each other. tRNAs are needed for the ribosome to recognize the right amino acids.

As David said, this is very basic molecular biology and gene regulation/expression in eukaryotes can get quite complex. The wikipedia articles provide a good introduction and the Berg biochemistry book he linked is excellent further reading. If you want to know more about yeast genomes, you can check out https://www.yeastgenome.org/. It provides a whole lot of information regarding the amount of coding/noncoding regions and their function. There is also a graphical genome browser, where you can view each region in detail and compare it with your own findings.


Looking for a DNA sequence I am not a biologist. Please pardon me, if my question does not make sense.

I am trying to obtain a DNA sequence for pattern analysis in Matlab. I used to generate random sequence randseq in Matlab. However, I am trying to obtain some real dataset.

Any idea where I can obtain the DNA dataset. I am looking at a dataset having acgt patterns

Thanks

EDIT : Thanks a lot guys, I found it here. : http://www.ncbi.nlm.nih.gov/nucest?term=((human%5BComponent+Accession%5D)+AND+normal+Breast+gene+sequence)+AND+1000%3A10000%5BSequence+Length%5D

There are several nucleotide sequence datbases available. One of the largest is the NCBI GenBank at http://www.ncbi.nlm.nih.gov/genbank/

You may use the search bar at the top to search for nucleotide sequences belonging to a certain organism or gene. For example, searching for "E coli" will give you the full genome sequences for several bacterial species, with a strain of E. coli as the top result. The E. coli genome is about 5 MB large. If you want a single gene sequence, searching for "sonic hedgehog" (without quotes) will return the human hedgehog gene as the top result, which is 1,481 basepairs long.

To get a sequence in raw format, select "FASTA" below the entry. At the page you get sent to  , chose "send" in the upper right corner and under "Choose destination", "file". This will give you a .fasta file, the standard raw sequence format. The first line, starting with ">" will be metadata, while the rest of the file consists of the nucleotide letters only.

Note that in addition to a,t,g and c, you may also find other characters, most often "n". These characters describe ambiguity in the sequence (meaning that the nucleotide at that position could not be determined). For a full description of the FASTA format sequence representation, see http://en.wikipedia.org/wiki/FASTA_format#Sequence_representation


Are non-coding RNAs introns? I am slightly confused as to what part of the genome codes for non-coding RNAs. Is it the introns? This would make sense to me as to why they are not transcribed as the introns are not transcribed. Or is non-coding RNA actually exons which are simply not transcribed? If so, what are the introns actually for? I cannot seem to find a succinct answer to this. Wikipedia, for example, seems rather vague:

  While introns do not encode protein products, they are integral to gene expression regulation. Some introns themselves encode functional RNAs through further processing after splicing to generate noncoding RNA molecules.[18] Alternative splicing is widely used to generate multiple proteins from a single gene. Furthermore, some introns play essential roles in a wide range of gene expression regulatory functions such as non-sense mediated decay[19] and mRNA export.[20]

In either case, does anyone also have any information as to why the ncRNA is not translated? What is the mechanism that prevents it from being translated? My guess is that, for some ncRNAs, it is a matter of them not being able to leave the nucleus as I understand many ncRNAs deal with post-transcriptional gene silencing, although tRNA and rRNA clearly do leave the nucleus...

I would be very grateful for any help about introns/exons/ncRNAs. Thank you :)

While Ankur's answer is correct, it must be noted that not all non-coding RNAs are introns.

An intron must be excised from an mRNA, which therefore means that any non-coding RNA that is not part of an mRNA cannot be an intron.

For example, rRNA and tRNA are all examples of non-coding RNAs that are not introns, since they are not part of mRNA. miRNA may in some instances be produced from introns, but when transcribed separately, they are not introns.

mRNA translation depends on many factors that bind to processed mRNA (a very long process). Other RNA do not undergo this process, and therefore are not reconised by ribosomes and are not translated.


A word that includes plants and fungi, but not animals Hello biologists and biology enthusiasts!
I am working on a project which includes information about plants and fungi. It would be very helpful for me if there a word that means plants-and-fungi, but I'm not sure there is. "Flora" only includes plants, but "biota" includes animals.
Thanks!

Short Answer
There is no such word that I can think of.
 Long Answer
Note: although fungi were once considered to be lumped with plants, such classifications fell out of favor 60+ years ago (or sooner). See here for a summary.
Nomenclature "dead ends"
Using the traditional taxonomic approach (including Woese's familiar 3-domain classification system)  will not provide the collective term you're looking for. Plants, Animals, and Fungi are all of the kingdoms rank in this system; the only higher rank than kingdom in this system is domain (in this case "Eukarya"), which would include all 3 kingdoms.
If we take a cladistics approach instead, we can investigate Phylogenetic nomenclature. This taxonomic approach lacks categorical ranks such as "kingdoms" and instead tends to use hierarchical group names based on nested ancestral synapomorphies. However, using this approach proves to be even less useful for finding the term you're looking for:

Generally ~6 (5-8) informal supergroups (sometimes called "suprakingdoms") have been recognized based on phylogenetic research. Importantly, 2 of these groups (i.e., clades) are the Opisthokonts (which include fungi and animals) and the Archaeplastids (which include plants). Since animals and fungi share a common ancestor more recently than plants, it's not possible to "lump" plants and fungi together without including animals (and a whole host of other organisms).
You can see a recent publication (Burki et al., 2020) discussing an even more recent proposed organization for classifying Eukaryotes that maintains this phylogenetic distinction and separation between animals/fungi and plants.

Comment on the usage of "flora"
FYI, "flora" has broader usage beyond plants. "flora" can also be used for fungi (e.g., search "fungal flora" on Google). In fact, in microbiology, "flora" (or sometimes "microflora") is used to describe microorganisms in/on a system/host, which would include fungi, bacteria, etc. (For example, see gut flora).
I don't think "flora" is what you're looking for. I think referring to "all plants and fungi" as "flora" is not clear and will likely not get across the meaning you intend without further annotation/clarification.
Other thoughts:
I momentarily considered if being sessile would be a possible trait to use for delineating these organisms the way you're trying since by definition animals are not sessile (at least not at all stages of their lifecycle). However, many "protists" are also sessile and therefore such delineation would not be exclusive to plants and fungi. Further, I'm not sure all fungi are in fact sessile (though I can't think of any reason why not).

The phrase "multi-cellular sessile organisms" is probably much more exclusive and encompassing, but probably not 100% perfect. (However, at the point you'd be considering such phrases, I'd just suggest sticking with "plants and fungi" :p).

Perhaps someone else can come up with something, but I couldn't think of any non-outdated ways to accomplish your goal off the top of my head.


RNA polymerase Sigma subunit: transcription factor, coenzyme, or what? Studying prokaryotic transcription, it seems that the α2ββ′ω core enzyme + the sigma (σ) subunit comprise the ‘holoenzyme’ required for prokaryotic transcription. In traditional enzyme nomenclature, this would indicate that the α2ββ′ω is the ‘apoenzyme’ and that the sigma subunit is the cofactor or coenzyme. However, I’ve not been able to find any sources that clarify whether or not the sigma factor is indeed a coenzyme (not cofactor since that has to be non-organic), and if not what it actually is and why. Any clarification would be appreciated.

No.
I don’t think anybody would call the sigma factor of bacterial RNA polymerase — or indeed any other protein — a cofactor or a coenzyme, the subset of cofactors that are organic (the original poster is wrong in his declaration about cofactors, or at least one reputable text book disagrees with him).
I could justify this statement by quoting a definition from the section linked above:

“The catalytic activity of many enzymes depends on the presence of small molecules termed cofactors, although the precise role varies with the cofactor and the enzyme.”

by saying proteins like the sigma factor are not small.
However it is more interesting to me, and more useful to the naive reader, to make some general remarks about definitions in biochemistry and molecular biology.
What are definitions good for?
Definitions of terms are useful for scientific discussion or argument to enable those involved to be sure they are talking about the same thing. They often arise at the stage of a field of science when things are crystallizing after a period of uncertainty or lack of clarity. Even so they may lack precision. Cofactor just means “something else that is needed for certain enzymes to work” — biology is not physics.
Definitions are also useful for students and their teachers. They allow students to try to build a rational picture of a subject that is new to them. They allow teachers to systematize a subject (or lazily set rote-learning type MCQs instead of asking students to explain things).
The student new to the subject might find it helpful to consult glossaries such as those in Molecular Cell Biology, Molecular Biology of the Cell and Pearson’s Biological Glossary.
What are the limits of definitions?
The problem in a fast-growing field like modern molecular biology is that the period of resolution — when old men can form committees to give names to things — seldom lasts. Biology is anarchic, and new things come along that don’t fit into the neat pigeon holes that have been so carefully assembled. Nor do the anarchists or revolutionaries care. They find new things, describe them, and then get on with the next experiment. Why spend one’s time reading yesterday’s newspaper?
But the problem for the student comes when he discovers that everything does not fit into the neat categories he’s been taught, that there is a world beyond lactate dehydrogenase and metal proteases.
Sigma factors — what’s the problem in categorizing them?
The “classic enzymes” studied in early biochemistry catalysed simple chemical reactions between small molecules. However catalysis also occurs in more complex polymerization processes like nucleic acid and protein synthesis, that have the complexity of repetition along a polymeric substrate, and the necessity of having a specific start and stop along that substrate. It turns out to do that, that rather than enzymes such as RNA polymerase being a single catalytic protein they are complexed with other proteins that are necessary for certain of these functions. In the case of proteins like the sigma factor(s), this is complicated by the fact that these accessory proteins do not remain permanently associated with the catalytic protein subunit.
The poster, in his title, asks whether the sigma factor is a transcription factor. The answer to this is yes… and no. And calling it a transcription factor doesn’t really help much. Yes, it is a transcription factor because it is necessary for transcription and different sigma factors can impart a certain specificity to bacterial transcription. No, because the term transcription factor is mainly used for the much more specific proteins in eukaryotes that work in a rather different way.
What to call it? A subunit of the enzyme, is sufficient for Berg et al.. An accessory protein might perhaps add something. But don‘t worry too much about naming it, learn how it works.
Postscript: Other fruitless terminological disputes you may wish to avoid

Why is NAD regarded as a coenzyme and ATP a co-substrate?
Why is it epidermal growth factor, not epidermal growth hormone?
Why is it called vitamin D when it’s actually a hormone?
Should the term, molecule, be applied to double-stranded DNA or the individual chains?
How long must an oligopeptide be before it is called a polypeptide or protein?

No doubt there are others that I have missed that can be found in the list archives.


What can myelination tell you about the evolution of sensory receptors? I am reading Avi Chaudhuri's Fundamentals of Sensory Perception and wondering if the information given about the somatosensory system could tell us anything about the way it evolved.

It seems (at least naively) reasonable to assume that nerves became larger and more myelinated as time went on. The types of somatosensory nerve fibre are (in order from least to most myelinated):

C < A-delta < A-beta < A-alpha

This gives an ordering on receptors of:

warm receptors < cold receptors < nociceptors < tactile mechanoreceptors < proprioceptors

My question is then: was this the order in which these receptors evolved? If not, can myelination still give us useful information about the evolutionary history of the nervous system?

P.S. Meta question: is this question better suited for the Bio or Cog Sci stack exchange? I asked it here since it seemed to be more about evolution than neurons.

Interesting question. I will dissect your question into its assumptions before giving my view on the overall question.

1) ..that nerves became larger.. : Why should there be a general tendency for nerves to increase in size during the course of evolution when there is no need to?

2) ...that nerves became more myelinated...: A general tendency towards more myelination is not the case. Myelination is definitely a trait that has been acquired later in evolution, but "the more the better" does not apply. Imagine an electrical conductor - to insulate it a bit of plastic is enough. Adding more after that doesn't make a substantial difference.

3) ...the order in which these receptors evolved...: myleine sheaths are made up of glial cells that wrap themselves around axons of neurons. Myeline makes neural transduction more efficient and faster. Hence, the amount of myelination tells you something about the efficiency and speed of transduction of the nerve (Hartline (2007)). For example, longer axons tend to be myelinated, short ones not. That, in turn, will have certain evolutionary benefits for the host, as more efficient communications means less energy required, lesser loss of information, and increased processing speeds. The amount of myelin hence tells you something about the importance of efficient communication of that sensory system. However, it does not tell you anything about when this receptor evolved.

Hence, the relation between myelination and receptor evolution is remote at best. In terms of evolution, amounts of myelination may tell you something about the evolutionary pressure placed on faster and more efficient workings of the receptor systems.


What parts of the visual system could be responsible for a fixed, monocular scotoma? Light enters the cornea, crosses the lens, hits the retina. Electric sinal travels from retina through the optic nerve, reaches the chiasma, crosses and makes its way to the visual cortex.

My question is: given a fixed, absolute scotoma in one of the eyes, what parts of the vision could be at fault?

Initially, I believe the cornea/lens couldn't be, otherwise the scotoma wouldn't be absolute and fixed. Moreover, I suspect that, after the chiasma, signals from the same visual position are joined, so, the problem couldn't be after it, otherwise the scotoma would be binocular. As such, am I right to conclude that a fixed monocular scotoma could only be caused by issues on either the retina, or on the optic nerve?

Yes. You're right.

A scotoma only affecting one eye (i.e., one that is not perceived when one eye is closed) is diagnostic of a lesion upstream from the optic chiasm.

See Brust's Practice of Neural Science, Fig. 3-2. The figure demonstrates a full cut, with complete blindness in one eye, but the principle is the same for a scotoma.


Help identify this awesome climbing plant with velcro like stem I got this plant sprouting in my window box this spring. Starting from a single seed, it has grown into an impressive array of branching climbing vines, reaching 6 feet tall. The stem turned red as it matured. The most awesome feature of this plant is that the stem is covered in micro hooks that cling to everything. I've seen it cling to a paint on a metal gutter pipe I can think of these hooks as velcro or gecko feet.

Can someone help me identify this plant?

climbing vine
stem is covered in tiny hooks that are very clingy
grows to 6 feet tall
stem turns to red as it matures
segmented leaves
leaves grow to palm size
new leaves sprout from stem where old leaves were connected
 -

I think this might be Japanese hops. Well, what I have in my yard is Japanese hops.

As I said, it's horrible.
Description and Biology:

Plant: herbaceous annual, twining, shallow-rooted vine that can climb to heights of ten or more feet with the help of rough-textured stems covered with short, sharp, downward pointing prickles that can be very irritating to the skin.

Leaves: leaves are rough-textured, paired, simple, palmate (like a hand) with typically 5-7 lobes; leaf margins are toothed.

Flowers, fruits and seeds: flowering occurs in July and August; male and female flowers are borne on separate plants; male flowers are very small, greenish yellow and occur in branched panicles; female flowers are in pale green, plump, drooping, cone-like structures with overlapping scales that become ‘hops’; hop scales and the seeds are covered with yellow glands; seeds are about 1/8 in. in diameter, roundish with a blunt tip, and light brown with darker specks; seeds mature through September.

Spreads: by seed which begins to germinate in early spring, but new plants may continue to emerge as the season progresses if sunlight and moisture are available; seeds are dispersed by animals (including people), machinery and floodwaters.

Look-alikes: native common hop (Humulus lupulus) looks very much like Japanese hop but it is usually 3-lobed or unlobed; native bur cucumber (Sicyos angulatus) lacks prickles, has tendrils, and the leaves have much less pronounced lobes.

Prevention and Control: Do not purchase, plant or transplant this species.