Separation of smaller DNA fragments and larger fragments without using gel electrophoresis? For an upcoming experiment I would have two kinds of DNA fragments in a sample after a particular reaction step: First there would be fragments of a length of approx. 170 bps and then there would be Fragments of a length of approx. 270 bps or more.

I would like to maintain all fragments with a length of 270 bps or more and throw out all fragments with a length of 170 bps.

Of course, I could run everything on a gel and collect just those bands above 170 bps.
However, I am wondering whether there is something more elegant to reach that aim. For instance, we could use a filter that collects just those fragments with a size of 200 or 250 bps or more and those fragments with a smaller size flow through the filter.
Is such a thing possible and if so, how? Or would you suggest something else?

Many thanks for your support in advance!

One option is to use SPRI beads, like those sold by Ampure (Ampure XP beads) to separate DNA fragments by size. By adjusting the ratio of beads to sample, you can selectively bind fragments of certain lengths by excluding those of other lengths, as seen in the following image:

From this image, you might try using a beads-to-sample ratio of 0.7 to exclude fragments below 200bp, or a ratio between 0.7 and 0.6 to exclude only those fragments below somewhere between 200 and 250bp. The advantage to beads over a gel is the time it takes. Size selection by beads takes only around 10 minutes, versus maybe 30 minutes or more for a gel (including the extraction).

As with any molecular biology procedure, it's important to test it and make sure that it works for you. For instance, it might be a good idea to take aliquots of your samples and compare the lengths and yields that you get from a range of bead concentrations and/or to compare the yields that you get from using gel vs (in this case) beads.


Why are there three stop codons but only one start codon? I was wondering whether there is any specific reason that there are three stop codons but only one start codon in prokaryotic and eukaryotic cytoplasmic mRNAs.

Disclaimer

It is important to realize that it is not possible to answer questions of this sort (the evolution of translation)  in anything other than a speculative manner. Please bear this in mind, especially if you find the speculation below persuasive.

Summary

It is suggested that the redundancy of termination codons is largely similar to that for ‘elongation codons’ decoded at the A-site of the ribosome, although protection against suppressor tRNAs may also be a factor. The consideration here is, therefore, mainly focussed on the question why there is only a single codon for methionine (initiation and elongation), and I suggest this may have been a combination of the late appearance and infrequent usage of methionine, together with the particular requirements for an initiation tRNA at the P-site of the ribosome, where standard wobble is apparently not possible.

Disposing of a Red Herring

Although alternative initiation codons are sometimes used, this usage differs in prokaryotes and eukaryotes, is very limited, and is not seen with the use of methionine in elongation. I would therefore consider this does not invalidate the question, but perhaps rephrase it as:

  “Why does the genetic code have only one codon assigned to methionine,
  the initiation codon, whereas other amino acids and termination have
  generally more than one?”

Time of appearance of and extent of use of Methionine

It is generally thought that genetic code initially encoded a small number of amino acids, and that this number increased over time. Methionine is one of the most complex (and energetically expensive) to synthesize (see Wikipedia entry), so is likely to have appeared late. One can argue that most of the codons would have been ‘taken’ (assigned) by that time. This argument is consistent with the situation for tryptophan, the other amino acid which has only a single codon, and which is also synthetically complex. Furthermore, these are the two least abundant amino acids so on can argue that their number of codons reflects their relative usage.

Admittedly, there need only be one stop codon per protein, but it is possible that the mechanism of termination evolved before that of methionine-specific initiation. (Initiation might originally have been from the 5′-end of the mRNA.) There is also the question of protection against suppressor tRNAs, but I shall delay discussion of this until the end.

The unique features of the initiator tRNA

Elongation involves several dozen amino acyl-tRNAs being recognized by an elongation factor which binds them to the A-site of the ribosome, at which 3′-codon wobble occurs where the redundancy of the genetic code allows and the anticodon of the tRNA has evolved appropriately.

In contrast initiation involves exclusive recognition of a special tRNA by initiation factors but not elongation factors, and subsequent binding at the P-site The tRNA has unique structural features that allows it to be N-formylated — structural features that are retained in eukaryotic initiator tRNA, even though there is no transformylase in eukaryotes. (see this SE Question]

This uniqueness may explain why there is only one tRNA for initiation. However one might ask why there is a not a group of methionine codons (e.g. AUA as well as AUG) recognized by the same initiator tRNA through wobble. The reason for this would seem to be that the P-site does not allow third position wobble (as I explain in the answer to a related question), so the initiation met-tRNA would be codon-specific.

Loose Ends

Although perhaps straying a little from the question, one might still ask why there are not alternative elongation codons for Met — e.g. AUA, which could have been ‘stolen’ from Ile, which already has AUU and AUC. In fact in mammalian mitochondria this codon reassignment has happened, but unfortunately does not help explain things. In mitochondria there is only one tRNAmet for both these codons, consistent with the simplification of tRNAs for the small mammalian mitochondrial genome. Initiation requires the formylation of the methionine.

I will finish by returning to the question of multiple termination codons, which are not really consistent with my suggestion that the extent of redundancy reflects usage. Although termination codons, like elongation codons, are recognized at the A-site they are recognized by protein release factors rather than tRNAs. This means that they will be affected differently by a mutation in a tRNA that alters the anticodon. For an amino acid codon, an altered non-cognate tRNA would only cause some misreading and an altered cognate tRNA might be neutralized by wobble or by duplicate or redundant tRNA genes. AS termination codons are not normally decoded by tRNAs, a suppressor tRNA would cause read-through at all the suppressed codons. The presence of two alternatives means that termination would be likely to occur within about 30 codons 3′ to the original termination codon. Variation in the length of the N- and C-termini of proteins is common among related species, and thus need not be deleterious to the cell.

Related SE Questions

‘Wobble’ in Initiation and Elongation — I have contributed an answer to this.
Why is AUG the Initiation Codon? — I will respond to this presently.
Redundancy of the Genetic Code — I have contributed an answer to this.
Initiator and Elongator tRNAs in Translation — I have contributed an answer to this.


Where exactly is pleasure Question from an outsider: have we been able to pinpoint where exactly the feeling of pleasure comes from?

I know that there are several types of pleasure, I'm talking about the 'liking'. If that involves several separate pleasure centers (which is probably the case), I'm interested in any/all of them.

I am wondering if it is the electrical stimulation part, or maybe the release of some chemicals/hormones (but then, where do they go to produce the feeling?), or maybe a chemical reaction somewhere? How much have we been able to narrow it down? Do we know which part of the chain reaction is actually responsible for the feeling of pleasure?

Is it possible to like without a body, just a "head"? Are there experiment on rats (or people) whose body is completely paralyzed?

Any reference to scientific paper, as well as personal opinions or suggestions as to where I could find this type of information would be greatly appreciated.

Well, I'm glad you're curious, but you must realise that your question is highly complex. You'd certainly have to refer to a research paper for the exact, factual information. All the same, I can tell you a bit about Dopamine (the pleasure hormone) based on recent reading.

Dopamine creates pleasurable feelings when it is released in areas such as the nucleus accumbens and pre-frontal cortex. This happens when positive, or rewarding actions are undertaken. Dopamine release in the nucleus accumbens is so consistently tied with pleasure that neuroscientists refer to the region as the brain's pleasure centre. However, this is not the ONLY pleasure centre.

Now this is all I know. You should probably check out this page for more, in-depth info: http://wings.buffalo.edu/aru/ARUreport01.htm

It's a long read, but I'm sure you'll find something worth your time.


Genetic effects on personality It is said that genes are partly responsible for the choices we make in our life; our genes help to create our environment, and then that environment can influence our personality. So, beside genes, what else is responsible for the other choices? Is there something else at work?

Many genetic studies in this area have found that variation in serotonin receptors associates with differences in a number of personality traits. That one gene, or a very small number, turns up time and time again for something so complex as human personality makes me a bit suspicious.

Other factors at play:
Family dynamics
Culture and cultural norms
Society and societal norms (these could clash with the above two)
Exposures - drugs, toxins, diet, and many others
Traumatic events


Can extinct animals be cloned? Scientists have found mammoth blood, and are planning to clone a mammoth.

How does one go from having its blood to a full blown living mammoth? Is it possible?

Why does it matter if the blood is frozen or not? Suppose one found dinosaur blood, could one clone a dinsosaur (as in say 'Jurassic Park')?

DNA degradation half-lifetime within fossilized/frozen species is ~ 500 years., even when the conditions are perfect for preservation.

Thus, in theory, if we could sequence anything that is less then 13 000 years old (expected length of preserved nucleotide sequences ~30 bp, which is just enough to stitch together two unique regions). If we have several copies of DNA (several cells), we can go a little bit further by sequencing same reads several times. If we assume an average cell is 30 um in diameter, we have ~40 000 cells in a cubic mm of tissue samle. this will allow us to extend the sequencing horizon by another 8000 years. With a cubic sample of intact, perfectly preserved tissue (this is REALLY A LOT and REALLY RARE) we could get an additional 5000 years, limiting our possibility to know the genome, let alone reproduce it to 26-30 000 years.

By using a couple of sequence assembly tricks, such as existence of reference genomes of closely related species, we could either decrease the amount of tissue sames or allow the DNA to get a little bit more degraded. However, even with a cubic centimeter of tissue we won't be able to go beyond 50-100 000 years.

The furthest we have gotten now is a Neanderthal sequence (~30 000 years) and it was already tough. It would be impossible to get a hand on dinasaurus DNA sequence, let alone trying to clone it. Mammoth, Saber-tooth Tiger and Dodo should be ok, provided we can find their remainders.

Now, Once you get the raw DNA sequence, you have to get the epigenetic code right, find a compatible egg of a related spicies (that is quite hard), inject your DNA into it, and hopefully, with lots of ifs you can get your clone and hope it survives. However the part about getting the epigenetic code right and finding a compatible egg is really not easy. Personally, I won't parry on anything that doesn't have close related species still living.

UPDATE: as of June 2013 a genome of a wild horse 700 000 years old have been sequenced, which is the furthers we could get so far.


Ipsilateral vs contralateral side of body I know that the dorsal columns carry ipsilateral information. Is this fact relative to the dorsal column in question?
If I want to talk about the right dorsal column, then the right side of the body would be considered ispilateral. But, if i then go on to talk about the left dorsal column, does this mean that the left side of the body is now considered ipsilateral?

Yes. Ipsilateral and contralateral always have to be relative to something; ipsilateral means "same side" and contralateral means "other side" - you can't really be the same or other side of something unless you have a reference point.


Definitions of robustness and canalization The concepts of robustness and canalization are fashionable today in the biology literature. However, I am not sure of their definitions and I am not sure either that all authors actually use the same definition.

I am therefore asking here for a the definitions of these terms or for a short review of the common definitions of robustness and canalization. How do different authors define these words? I am particularly interested in...

The differences between robustness and canalization (canalization seems to apply more in developmental biology than robustness who seems to be a more general concepts)
At what level do these concepts apply? To populations, to genotypes, to both, ..?
How does the concept of adaptation link to these definitions.
How does the concept of plasticity fits in opposition of the concepts of robustness and canalization?

As canalization is defined in your question (also in wikipedia) it means robustness.

Semantically it is possible to differentiate the two.

Robustness of a system refers to its sensitivity to perturbations. In other words small differences in parameters would not affect the steady state of the system (parameter changes in a physically plausible range would not lead to bifurcations).

By system I mean a set of entities connected to each other in a defined fashion. For example an ecosystem in which different species are connected to each other by interactions of the food chain. At steady state a system configuration (for instance- 10 foxes, 100 rabbits, 10000 grasses, 1000 honeybees etc) remains constant over time (that, however, doesn't mean it is static). Or in case of development a system may be the body defined by a set of certain phenotypes.

Canalization/channelization refers to mechanisms that make the system follow a certain trajectory. So if you see it mathematically canalization keeps the trajectory dictated by a  given set of eigenvectors. In case of development you may call mechanisms such as dosage compensation, functional compensation by isoforms, parallel metabolic flux channels etc as canalizing mechanisms.

So in contemporary usage we can call a system robust (a property of a system) whereas we should address mechanisms that help to preserve trajectories as canalizations. The final aim of canalization is to render robustness to the system but it is not the only mechanism that is responsible for robustness (for e.g. the steady state may just be independent of certain parameters).

Robustness is a property of the system and is dependent on how the different entities of the system are coupled and what their interaction parameters are (rates etc).

You should note that these are parlances that are adopted by different groups in the scientific community and may perhaps mean the same thing- this is merely my attempt to remove redundancy of terms by the means of semantics.

Now, plasticity is a different concept altogether. Plasticity is in a way opposite to robustness. This means that the qualitative nature of the system can change if certain parameters are tweaked. However, the system should still maintain its stability. In a stable system mild perturbations from steady state will result in system going back to that steady state - like a ball in a well. However, a system may inherently allow for multiple steady states (like switches), and depending on certain parameters the system can be in either of the states (but if pushed too far then the system can go to another stable steady state). This is called multistability.

NOTE: some people also use the term plastic to mean "responsive". The above definition may not be exhaustive or the most perfect.


functional hypocholesterolemia due to very high HDL or low LDL? Nutritional and medical recommendations about cholesterol seem to focus exclusively on hypercholesterolemia, and as such, they provide only a maximum desirable level for LDL and a minimum for HDL. I've found a little bit of information about hypocholesterolemia caused by inadequate cholesterol in the body (due to overuse of statins, malnutrition, or other disorders), but not about cholesterol deficits due to lipoprotein levels.

It seems like it should be theoretically possible to have so much HDL or so little LDL activity that organs don't maintain enough cholesterol to function properly, even if cholesterol synthesis is adequate. Obviously this might or might not ever occur in reality. Is there any research that has found an upper bound on desirable HDL in humans, or a lower bound on desirable LDL or LDL:HDL ratio?

Upper bound of HDL doesn't really exist. The greeks are known for their incredibly high levels of HDL and the so called mediterranean diet/genetics combination that causes this is only beneficial to health (supposedly - although never been proven that incredibly high HDL levels are beneficial, they're just not harmful).

As for too low LDL levels/cholesterol levels - that's interesting. Unfortunately it isn't possible because any mutations that caused this would be fatal, cholesterol makes up an essential part of cell membranes etc. That's why our body makes our own. A mutation preventing this would not even manifest.


Conversion and storage of glucose to glycogen Why is excess glucose, synthesized to glycogen, stored only in limited amounts, as compared with lipids/triglycerides that are stored in our body?

Why is mature glycogen arranged (polymerized) in 12 tiers polymer?

Glycogen storage limitation is due to these additional facts also:

Glycogen is a hydrophilic molecule. This means an increase in glycogen concentration will cause a proportionate increase cell weight due to water accumulation. As cells can contain only limited volume the amount of glycogen stores are limited. Lipids are hydrophobic hence can be accumulated without increasing the volume and weight of cell due to water accumulation.
As a source of energy lipids are approximately 2.5 times more efficient than glucose.


Is it possible to identify this microscopic particle? So I was playing amateur scientist with my 11 year old.

This photograph is from rainwater in a bird-feeding bowl in south England, at 300x.

It looks biological, but I have no idea what this is. Is it possible to know, beyond speculation, what this item is?

This is an plain old ice crystal. Welcome to the microscopic world! When water evaporates, high-energy molecules escape, leaving low-energy molecules of water. The droplets cool this way, and they freeze - the dirt or debris in the crystallizing droplets make curious patterns. Here are some in my samples I made last week, for comparison:

How about a close-up?

Here's one I made by accident, this time featuring a fluorescent dye.

Notice how cooling droplets never freeze the same way twice. You'll never find two identical crystallized droplets!

If you want to avoid these, prevent evaporation by putting nail polish or glycerol around and between your coverslip and slide, so that water cannot escape.

OFFTOPIC: You should also encourage your kid to try make some of his/her own crystals. You can use food dyes to make beautifully patterned art. Good moment to teach your kid about nucleation; why water doesn't freeze at 0° C, but rather at temperatures that tend to decrease as the volume of the water decreases and as the water impurity increases. And maybe sneak in a funfact about how the freezing of small water droplets into ice is an important process in cloud formation.


Do our ears or brains gradually adapt to noise pollution? Having lived in various places all over the world for the past 9 years of my life, one thing stood out to me throughout this time, and now in particular. From a quiet place on the countryside in Sweden, I moved to Manchester for my studies. When I first arrived there, I felt the city was very noisy, a feeling which gradually reduced as I presumably got used to the noise levels there. From Manchester I moved over to Saitama in Japan, an enormous city right next to Tokyo with a considerable amount of noise during the day, and buildings that have little to no sound insulation. With the exception of particularly loud noises, I again adapted to the sound levels in the country, which at the time, I felt was no more than a natural response in terms of how much attention we pay to the noise. If I'm distracted by work or other activities, I have little reason to dwell on the sounds of driving cars and talking people.

The thing I couldn't explain purely by the 'paying attention' argument however was when I moved back to the Netherlands, to an apartment with excellent sound insulation. My apartment is located in front of a somewhat larger road, and cars pass by almost consistently. However, when I moved in I could barely hear these cars driving past, something that stood out to me as fairly pleasant. I thought a little bit of ambient music would kill the sound of these vehicles driving past altogether.

Now skip ahead one month, and I can hear the cars almost as if I'm standing next to them, an exaggeration of course, but the sound is much clearer than it was when I moved in. I know that nothing has changed in terms of insulation and I know that no windows are open. Strangely the only thing that appears to have changed is the clarity in which I perceive this noise, as none of the other people whom I've asked seem to share the same opinion (that is, that the noise has grown louder). This made me wonder - does our hearing adapt to noise pollution, and if so, how does it work?

This is a fascinating case of sensory adaptation and neural adaptation. Another example of this would be when you stop smelling something after being exposed to it for long periods of time (as you probably know, this "long period of time" happens to only be a few minutes). A great representation of this happening with the nerves in the skin was done by Georg Meissner:

This image is from https://www.boundless.com/psychology/textbooks/boundless-psychology-textbook/sensation-and-perception-5/sensation-37/sensory-adaptation-160-12695/

When stimulus is applied, these nerves begin rapidly sending messages to the brain in the alarm period. The rate of these signals slowly start to decrease over time in the resistance period until they finally reach exhaustion and stop completely in, of course, the exhaustion period. Keep in mind that the time it takes for all this to happen varies greatly upon what type of cell it is (obviously olfactory cells have a much shorter exhaustion time than, say, hair cells (hearing cells)). After these cells have had a chance to recover (more like recalibrate actually), we can begin to hear/smell/feel/taste again.

I hope this helps.


Why do house geckos take so long to react? This is the Common house gecko found abundantly where I live.

I've been observing this for quite long and I used to ignore it after thinking on it for a short while. Today I decided to write this here on Biology SE.

So in my lawn there's this large wall on which there are usually around 3-4 geckos foraging for their favorite insects in night. Everytime I walk towards them some of them instantly go into their hiding spots (within 1-2 seconds of my arrival) with lightening speed. But most of them initially look cool and not actually bothered by my presence. Not only that -I can even wave at them; go closer towards them and nothing happens. But suddenly after all of my actions they also run towards their hidings as they were daydreaming. (Though not instantly)

Just curious-

Is there any real lag between their signal reception and processing?

Are there some other animals which show such behavioural responses?

(Maybe they are just kidding with me :P)

This is entirely behavioral and is quite widespread.

If they ran away everything something large passed by they would waste a lot of energy, many animals wait first to see if you are just moving through, and thus can be ignored, OR if you are going to hang around and thus are a potential threat (and in the case of camouflaged organisms have a much higher chance of spotting them).

It is seen in many animals gazelle are known for it for instance.  This paper on the behavior in other lizards should help with understanding the evolutionary pressures behind it.


Would humans eventually evolve to fight off fatal diseases if we didn't treat/vaccinate for them? I am definitely pro vaccination, and the question is a bit morbid because people would die, but assuming that we didn't treat or vaccinate people for fatal diseases such as Ebola or the black death, would the surviving people pass along a trait that eventually would lead to near immunity for that disease?

Are there any examples of diseases that humans "contract" but they are immune to? Or any examples of immunity through human evolution?

What about in animals? Are there diseases that have been naturally eradicated?

Sure.

When the Europeans settled the Americas, 90%+ of the native American inhabitants were wiped out due to diseases like smallpox that the Europeans clearly had developed resistance to. Clearly, the surviving native americans had resistance, and the Europeans had gone through some similar event previously in history.

The bubonic plague that was the cause behind the black death wiped out large percentages of populations, but selected for survivors with resistance:

Black Death Left a Mark on Human Genome

Caveats:

Often evolving to fight off disease involves mass death, like with >90% of the native american population dying.
There is always the chance that a future pandemic can come that human biology fails to simply evolve a resistance for and gets wiped out.
The Earth is changing rather quickly. The past is not a guarantee for the future.


Do serotonergic (5-HT2A-mediated) psychedelics elicit stimulant effects? I know that 5-HT2A partial agonism is the key mechanism of action of serotonergic psychedelics but I also know that some research (e.g. the selective (no activity on any other known receptor sites) 5-HT2A inverse agonist/antagonist eplivanserin was being investigated as a sedative) says that central blockade of the 5-HT2A receptors induces sedation which is in opposition to the effect of 5-HT2A partial agonists.

I have a partial answer to my question. I heard from LSD users that they find it regularly causes sleeplessness for the duration of its effects, which is likely due to stimulant/wakefulness-promoting (eurogenic) effects. Albeit just because it is true for one serotonergic psychedelic doesn't necessarily mean it is true for all serotonergic psychedelics. Especially since LSD affects a wide range of serotonin and other receptor subtypes.

I think you'll like this article. It's on monoamine release / reuptake inhibition for a host of different psychedelic and empathogenic drugs.

This wakefulness inducing effect you describe for LSD is widely reported for all common 5-HT2 mediated psychedelics.


Proteins in Milk, Oat , Eggs and Soy I have read that there are proteins in oat which are similar to those in soy, milk and eggs. I know nothing about biochemistry, and I'm struggling to decipher the info i find..
the closest Ive got to an answer is albumin - which i believe to be a group of proteins, all present in the above?
Can you be intolerant to albumin? or a derivative of?

a simpilar version of the question - what is the name of the protein(s) found in milk/oat/eggs and soy, if any?

the reason for my question, my daughter has a milk/egg/oat (protein) intolerance and I'm just interested to find out if its a particular protein (or group of), or if its an intolerance to random things.

Many thanks!

Allergies are often caused by the immune system reacting to a part of a specific protein, therefore it is in fact a specific protein in the food that is causing the allergic reaction to occur.

Milk allergies are caused by casein and whey (Source: Mayo Clinic)

Oat allergies can be caused by avenin (Source: EJCI)

Soy and egg allergies are caused by their respective albumin proteins. Additionally, egg lysozyme can also cause allergy. (Source: Cleveland Clinic, Food Allergy)


Are there natural selection experiments that quantitatively agree with theoretical modeling? Has anyone ever conducted an evolution experiment and quantitatively compared it to theory?  For example, has anyone ever put bacteria in a million petri dishes filled with antibiotics and calculated the number of petri dishes that should develop drug-resistant bacteria, and then compared that calculation with the experiment?

I imagine that both the experiment and theoretical modeling would be very difficult, but maybe someone has been ambitious enough to try it.

I think the closest example to this is Greg Lang's work at Princeton. His work will take a population of yeast and let it grow for 1000 generations. At each generation a sample will be kept allowing sequencing of the population at each generation.
His website is available here: http://www.genomics.princeton.edu/glang/

And some of his work has already been published here: http://www.genomics.princeton.edu/glang/papers.htm


What does "Mutational Variance" mean? Background

The concept of mutational variance can be found in many articles including this one for example. The mutational variance of a trait number $i$ can be found in the M-matrix in position $m_{ii}$ (in the diagonal). Elements of the off-diagonal represent mutation covariance. For example element at position $m_{ij}$ of the M-maitrx is the mutational covariance between traits $i$ and $j$. More info about the M (and G) matrix can be found here.

Question

What does "Mutational Variance" mean? What does it mean for a population to have a high or a low mutational variance?

Does "mutational variance" refers to:

Average effect of new mutations on fitness (mutational effect) (parameter $s$)
Variance in the effect of new mutations on fitness (variance in $s$)
Average effect of new mutations on phenotype
Variance in the effect of new mutations on phenotype
The increase in genetic variance ($V_G$) due to a new mutation
The increase in additive genetic variance ($V_A$) due to a new mutation
Genetic variance in the population at mutation-selection-drift equilibrium.
Is it a concept that is opposed to genetic canalization?
...

In Pigliucci (2004) (repeated in Hansen (2006)) the mutational variance is defined as being the new additive genetic variance entering in the population each generation due to mutations.

In consequence the mutational variance is not define at the level of the mutation in the sense that we do not care about how many mutations yield to this new genetic variance. So none of the suggestions of possible answers in the OP's question is correct.


Is this insect some kind of pest? I live near Paris, France. I would like to know if this small flying insect was some kind of pest or not. More specifically, I want to know if it might be a meal moth or a clothing moth. Here is the little fella :

It's approx 1.5 cm (0.6 in) long

This is Hypena obsitalis, aka the Bloxworth snout, a moth of the family Noctuidae.

Personally I hate the word pest, but this little beauty eats Parietaria und Urtica (Nettle) so I can't think of anyone seeing this as a pest species.


what are the factors that can be used to compute the probability of getting the coronavirus? Our team and I work on a project for the Lauzhack 2020 and to achieve this work, we need to determine some factors that can tell us what is the probability of contracting the coronavirus.  Is there any one who know what are the determining factor to compute the probability of catching the virus ? (for example some research paper about it). For example, we know that if we are old, and if we are in contact regularly with people, we are most likely to catch the disease. We would like to have some basic knowledge about the transmission of the virus. We would need data about the probability of being infected as a function of the time we had been in contact with someone who have the disease. Any help would be appreciated !

I'd refer you to a couple of papers in Lancet, here and here. They, in fact, have a mathematical treatment of this very question, and in the supplementary material they list some parameters that might be useful to you. Good luck!


What is this liriope looking plant? They look like monkey grass, in the midst, a tall, skinny stem with bright orange flowers on top.
One of the plants, although it looks just like the others, has pink, purplish flowers instead of orange.

I would like to know what these are so I can start to take care of them properly.

Your question' better suited to Gardening SE where members can identify plants. As it is, I'm an active member there and the identity of these flowers are straightforward. They're all different cultivars of the daylily (plants in the Hemerocallis genus). If you use Google image search, you'll see photos of various cultivars. Basic structure:

Notice the flowers on a branched (or unbranched) scape (tall stem); leaves arise from the base of the plant. Flowers can be single or double (sometimes more); single flowers (as in your lower left photo) have six petals.

While Asian and Oriental lilies are toxic to pets (even the pollen is toxic to cats if they lick it off their fur), daylilies aren't. They're easy to tell apart as the daylily has long narrow strap-like leaves with flowers on stems with no leaves. Asian and Oriental lily have small leaves continue up the length of the stem like this -

This includes Easter lilies.

Daylilies are named for the reason individual flowers lasts only one day. But each stem has many buds on it that continue to mature over a few weeks so will produce flowers for about a month (as some stems don't have open flowers yet when the first stems start flowering).


Lactobacillus casei and paracasei I am carrying out a study of lactobacilli isolated from different samples.
Genus and species are identified using a sequenced 1000pb long 16S fragment in BLASTn.  I cannot distinguish between L. casei and L. paracasei because they have same score and query coverage when they appear as a hit for a sequence.

I read somewhere (cannot remember where) that L. casei and L. paracasei both should be itnegrated in a single L. casei species and their differences should be considered at strain level.

Should I focus my discussion on this fact? Or are they really different species?

As far as I am concerned L. casei and L. paracasei can be differentiated by the amplification of the 16S rRNA gene of the aforementioned species using PCR - please see the work done by Ward and Timmins (1999). An alignment of the V1 region of the 16S rRNA genes of Lactobacillus casei and Lactobacillus paracasei shows the bases comprising the species-specific PCR primers - screenshot taken from Ward and Timmins (1999):

So, perhaps in your study you have not amplified the correct region of the 16S rRNA gene of L. casei and L. paracasei?

With regards to the classification of these organisms. Just as @skymningen has already mentioned in the comment section, the definition of a bacterial species (not even to mention strains) is somewhat debatable and tricky.

However, here is what Mori et al (1997) suggest:

  The primary structures of the 16S rRNA genes of the type strains of Lactobacillus casei and related taxa were determined by PCR DNA-sequencing methods. The sequences of Lactobacillus casei, Lactobacillus zeae, Lactobacillus paracasei, and Lactobacillus rhamnosus were different. The K nuc values ranged from 0.0040 to 0.0126. On the basis of the K nuc values and the levels of DNA-DNA relatedness among the strains of these species, the L. casei-related taxa should be classified in the following three species: L. zeae, which includes the type strains of L. zeae and L. casei; a species that includes the strains of L. paracasei and L. casei ATCC 334; and L. rhamnosus.


Australian Tree Identification - maybe pine? Can you help identify this species?

(Link to imgur album with all images)

It was growing next to the Yarra River (maybe 10 meters from the bank) in Melbourne. At first I thought it was a type of pine however this page says Australian pines at not actually true pines. It does look much like some of the images of Australian Pine Casuarina equisetifolia

However the Wikipedia page for Casuarina equisetifolia says there are 2 subspecies, equisetifolia and incana. Equisetifolia is only found in Southeast Asia & northern Australia so that rules that one out. Incana is found on the east coast of Australia (eastern Queensland, New South Wales) - could it also be found as far down south as Melbourne?

I've also compared it against all the pines on this site as it specifically shows Australian species.

From there I thought it looks a bit like a Port Jackson Cypress Pine Callitris rhomboidea but the needles look longer and narrower.

I think it also looks a little like a Narrow Leaved Wattle Acacia linearifolia if you ignore the yellow flowers.

I'm carving a spoon out of some of it's wood so would like to know for sure what species it actually is. Any help greatly appreciated.

UPDATE:

I went back to the tree to get some more photos but the whole tree had fallen in the river!

I did get a branch off it however to get a close up of the nodes / internodes but I could not find any seeds or cones.

FINAL UPDATE:

I've tried to get a close up of the apical portion (the top bit right?). My twig sample has started to dry up a bit so this is the best I could get.

ONE MORE UPDATE

Due to my last pictures being rather fuzzy I got out the DSLR and the tripod. These photos are very high res and around 8mb each so may take a while to load...

Native cherry, Cherry ballart or Cypress cherryn belongs to the sandalwood family of plants.

http://en.wikipedia.org/wiki/Exocarpos_cupressiformis


Normal cells and the immune system Normal or healthy cells have a natural ability to avoid being attacked by the immune system.
 So if a cancer cell has all inherited 'strategies' for avoiding the immune system (that are from their earlier pre-cancerous states) does this make them hard to detect or be affected by the immune system.

The development of cancer has various reasons. For example in more than 50% of tumors, p53 is mutated. p53 among other things regulates mitosis and forces the cell to arrest in a specific growth state if other systems detected a mutation in the DNA.

But in your special case we have to look at major histocompatibility complexes (MHCs) and NLRC5. There are two types of MHC, namely MHC class I and class II. MHC II presents mostly bacterial peptides to CD4+ T cells causing a immune response. However, MHC I presents viral peptides and peptides from your own body. These peptides are detected by CD8+ T cells which are cytotoxic T cells initializing apoptosis. Without these own peptides natural killer (NK) cells are activated because of a missing-self signal causing apoptosis, too.

Watson et al. (figure 1, Watson et al., Int.J.Cancer, 2006) showed that patients with high MHC I expression or an absent MHC I expression have a higher survival than patients with low MHC I expression. If patients express high levels of MHC I, the chance that these proteins present cancer peptides is higher than patients expressing low levels of MHC I and therefore cancerous cells get killed by cytotoxic T cells probably more often. Without MHC class I, NK cells will initiate apoptosis and cancerous cells will die, too. Patients with low MHC class I expression won´t present so much peptides to cytotoxic T cells and therefore less cancer peptides are presented. But as they have MHC I, NK cells keep inactive. So the cancer finds an escape mechanism in tricking the immune system.

NLRC5 is the biggest member of the NOD-like receptors (NLRs). Expression of NLRC5 can be enhanced by IFN-gamma which activates the JAK/STAT signaling pathway. STAT 1 enhances the expression of NLRC5 and NLRC5 itself can build an enhanceosome with RFX. This enhanceosome raises the expression of MHC class I! NLRC5 is often mutated for example in colorectal cancer. Research now has to focus on how to enhance NLRC5 and therefore MHC class I expression in different cancer types and out of these results to develop an efficient cancer treatment.

I hope that I could help you. Further literature especially on NLRC5 you can find in following paper.

Kobayashi et al., Nat. Rev. Immunology, 2012

Meissner et al., PNAS, 2010

Neerincx et al. (different paper, just google it ;) )

Staehli et al., J. of Immunology, 2015

Yao et al., Protein&Cell, 2012

Of course there are even more, but I think, these paper show a nice overview about this field.


Dreadnoughtus: Why are new taxa named using Dog Latin? Once upon a time, binomial nomenclature was expected to follow Latin rules: the genus had to be a noun and the species had to be an adjective that agreed with the genus according to Latin rules of adjectival agreement with the noun modified by it. That’s why we have species names like sativus, sativa, and sativum seen again and again, the exact form depending on the genus’s gender.

So if knew a bit of Greek and Latin, you could figure out something about what binomials such as Stegosaurus armatus or Dodecatheon pulchellum might be about.

Enter 2014, and with it such new binomials as the ponderous Dreadnoughtus schrani.  That looks more like Dog Latin than Classical Latin: just tack a few Latinate-looking suffixes to words that cannot be decoded using any known roots from Greek or Latin.

When I first read about it, I honestly thought somebody was making a bad joke. It’s not like the Greeks and Romans never thought of fearing nothing; one might imagine a taxon built out of actual classical roots — perhaps like *Timendumnihil — would have been more universally understandable than the Dog-Latin form Dreadnoughtus we’ve been stuck with.

Is there no requirement that new taxa have classical forms?  Was there ever, and if so, when and why did this change?  Or, if there was not, then why did everybody seem to go along with the scheme for so long?

There is an International Commission on Zoological Nomenclature, to which submissions for new organisms' names is strongly recomended. The discoverer does have some leeway within this system if there is no Latin name that well-describes this species. Your example is one of many.
Chapter 31, for example, clearly states:

31.1.1. A species-group name, if a noun in the genitive case formed from a personal name that is Latin, or from a modern personal name that is or has been latinized, is to be formed in accordance with the rules of Latin grammar.

Examples. Margaret, if latinized to Margarita or Margaretha, gives the genitives margaritae or margarethae; similarly Nicolaus Poda, even though the name of a man, if accepted as a Latin name, gives podae; Victor and Hercules, if accepted as Latin names, give victoris and herculis; the name of Plinius, a Roman, even though anglicized to Pliny, gives plinii; Fabricius and Sartorius, if treated as Latin names, give fabricii and sartorii, but if treated as modern names give fabriciusi and sartoriusi; Cuvier, if latinized to Cuvierius, gives cuvierii.

31.1.2. A species-group name, if a noun in the genitive case (see Article 11.9.1.3) formed directly from a modern personal name, is to be formed by adding to the stem of that name -i if the personal name is that of a man, -orum if of men or of man (men) and woman (women) together, -ae if of a woman, and -arum if of women; the stem of such a name is determined by the action of the original author when forming the genitive.

Example. Under this provision, the species-group names podai from Poda, victori from Victor, and cuvieri from Cuvier are admissible. The names puckridgei and puckridgi may be formed from Puckridge.

Similar rules apply for genus and family names.
Since your example was a new genus and species, it didn't "fit" into previous categories (in the future, if and when similar discoveries are made that shed light on the genus' relation to others, the name can and will be changed accordingly, with or without the authors' approval).

According to the research team that discovered the taxon, the genus name Dreadnoughtus "alludes to the gigantic body size of the (which presumably rendered healthy adult individuals nearly impervious to attack)" and to the two dreadnought battleships of the Argentine Navy, the ARA Rivadavia and ARA Moreno. Thus, the genus name also honors the country (Argentina) in which Dreadnoughtus schrani was discovered. The name of the type species, schrani, was given in recognition of the American entrepreneur Adam Schran for his financial support of the project. - Wikipedia

A "good" or "useful" taxon is commonly taken to be one that reflects evolutionary relationships. Since this one does not, in a few decades, this name may well be gone.


How do you interpret this microbiology/ bacteriology research figure? This is a figure from a research article that I am to do a senior presentation for. It is showing  bacterial replication of an enteric bacteria population. The researchers hypothesize that the number of regions near the replication origin will be the highest point (peak) on the graph and the terminus region will be the lowest point because there are least copies of this region in a dividing species. The determine that the ratio of the peak to the trough will reflect the growth rate of the species. That all being said, I don't understand their use of color. The peak has several different colors that do not seem to match any of the examples on the right. Wondering if anyone can help me decipher this? Thanks!

The short answer is that it looks like the colors are meant to represent different, partial copies of the bacterial genome in the process of being synthesized.

When bacteria replicate, they initiate replication at the origins of their chromosomes.  In fact, these origins can be replicated multiple times before it gets to the "end" of the bacterial chromosome (terminus). Looks like the stacking on the right figure shows this, with the colors just aiding in differentiating the partially replicated chromosomes. The coverage plot on the left shows how this might look based on read coverage from deep sequencing (again the colors just show different, partially replicated, chromosomes).


Bird identification: song two low, two high, five short This morning I heard a bird that had a song which was two low notes, two high notes, and five quick notes in succession. Location is New England.

Is there any way, short of asking an expert, that I can find out what a bird is from a description of its song or call?

Update - Bird Song Uploaded

I have been able to host a sound clip on Vocaroo:

Unknown bird, Massachusetts, forested suburban environment

Best guess is that the bird is a Song Sparrow, Melospiza melodia. Cornell Lab of Ornithology has a good website for basic facts about birds. Here is the account for Song Sparrow. There is a sample of typical song, but there can occasionally be some variety.

The song is kind of complex and the recording you linked to seems to garble or not capture some of the song, but the changes in phrases throughout the duration seem to match as does the pitch of most of the phrases.


What causes skewed ladder bands on an agarose gel? I frequently ran into an issue where the bands of my ladder become skewed. What causes this?

Here's an example: 0.7% agarose gel, 100V, 60 minutes. Same problem occurs with 1%. I loaded 10 ul of a 20 ul PCR reaction.

As you can see, the problem is not smiling per se. The lanes themselves are fairly vertical and straight. Just the bands themselves appear warped. What could cause this issue?

If the ladder is on an edge of the gel, it may be a process of different density as a result of how the gel cooled (or was poured too slowly). I've loaded more DNA loaded in a gel and it doesn't cause this kind of warping for me. It may be the buffer of the ladder is different from that used to make the gel. Your bands don't look particularly sharp, so I would suspect that the running voltage is too high and causing the surface of the gel to heat up and therefore "smearing" the bands. Try running the voltage at 75 V  for a proportionately longer time to see if this solves your problem.


How strong of an electric field is dangerous to adult humans? Given that "a potential difference is introduced over the membrane, the associated electric field induces a conformational strong in the potassium channel" is required for our muscles to move, how powerful of an electric field is required to cause our muscles (including the heart) to fire irregularly?  How much stronger would it have to be to kill someone?

https://biology.stackexchange.com/a/53330/7973

https://en.wikipedia.org/wiki/Voltage-gated_ion_channel

(No, I'm not an "electrosensitive" afraid of cellphones or high-tension wires.)

Thanks

Research published by WSU Professor Emeritus of Biochemistry and Basic Medical Sciences, Dr. Martin Pall, bears directly on your question about potassium channels.

https://www.researchgate.net/project/microwave-frequency-radiation-acts-via-voltage-gated-calcium-channel-activation

He has concluded that weak EMFs cause cascading health impacts that derive from false electrical signaling of voltage-gated ion channels, and that these impacts include heart disease and the dreaded social bugbear elctrosensitivity (microwave disease).


How are different types of cells created from zygote? In the process of mitosis that starts from zygote, how do different cells appear? What happens that some cells become one type and some another?

For example, is there a cell that divides into a blood cell and a skin cell?

I'm not sure about the first developmental stages but, given you already have hundreds of cells with slightly different physiology, the next developmental stages like dev. of neural tube happen through excretion of translation factors and growth factors in several cells. Each of those cells that are in a region where more than one excretion overlaps get a higher dose than the others. This is the signal for the cell to differentiate into another type, by changing its physiology. Such factor excretions are important events, and the genes encoding for the factors are evolutionally highly conserved (so called homeobox proteins).

However, this has nothing to do with mitosis. The newly divided cell does not decide on its own but reacts to a stimulus, like skin cells develop into skin cells because they are on the outside of the cell ball. Excreted factors do the fine tuning.


X chromosome "weight"? According to Wikipedia, the X chromosome has approximately 153 million base pairs, while the Y chromosome has only 60 million base pairs. Thus, the difference is roughly 93 million base pairs.

My question is: Could this "extra" 93 million base pairs in virtually every single female cell of the human body slightly contribute to the "extra" relative weight of the female as a whole, in comparison to a male (of course) with a similar amount of cells? Or would this weight be so small that we can consider it negligible?

Theoretically...

93 million bp/cell x 650 daltons/bp x 10^13 cells/body x 1.66 * 10^-27 kg/dalton = 0.001 kg

So I would say it's not too much of a difference :P

however this ignores the rest of the chromosomal material: histones


What is the evolutionary purpose of the topology of the human ear? What is the evolutionary purpose of the topology of human ears? I understand why the ears may have a funnel-like shape but if the various "hills and valleys" do not amplify incoming sound, what purpose do they have?

Humans do not have the ability to move their outer ear in response to sound. Many animals can do that, and use it to determine the source of the sound waves. Thus, human outer ears are equipped with many "hills and valleys". It does not provide amplification (because the waves can lose their energy bouncing around the ridges), but rather gives the brain more information about the sources' location in space. The brain calculates that location by determining minute differences in the time it takes for the sound to reach sensory cells in the inner ear on both sides. The shape basically attenuates the raw information. That way you get different properties of the sound wave that enters your ear depending on the angle at which it fell on you outer ear.


Are all dinosaur bones radioactive? I watching some TV program some time ago and a guy in it mentioned that when-ever museums display real dinosaur bones (as opposed to a replica) the bones are painted over with a lead paint, because they are radioactive.

The sentence was not qualified (so he did not e.g. say that just some bones found somewhere are radioactive).

So is this true of most or all dinosaur bones, or just some of them? If I ever find a huge dino fossil somewhere, should I be concerned?

While it is true that some fossils can be radioactive, not all of them are. According to the ressources I have found, it depends on the place where these minerals are found and also the other minerals present at this place.

When there are uranium and or potassium rich ores available, the fossils seem to enrich these radioactive isotopes in the calcium matrix of the bone during fossilation. See the reference for some more details on this.

The isotopes which are occurring there are Uranium (U235 and U238), Potassium (K40)) and Rubidium (Rb87), all of them with half lives in the billion years. Carbon does not play a role in these very old fossils (millions of years old), as the half life of the relevant carbon isotope is to short. These elements are also used for radiodating these fossils, see the table below (from here):

Regarding the radioactive safety I think there are some fossils where you should be cautious and carry them around all day long in your pocket. Most of these isotopes release $\alpha$ and $\beta$ radiation, some $\gamma$. While the $\alpha$ radiation is relatively easy to shield, lead can have detrimental effects due to the occurance of retardation radiation of the slowed down particles. In the lab we use thick acrylic glass shields to protect us from $\beta$ radiation.

Additionally I have found some secondary sources for painting the dinosaur bones with lead paint, but no real first hand source from a museum or so. Additionally the rules for radiation safety are pretty strict. If the bones would be so radioactive that a short visit would endanger you (how long are you looking at such pieces, a few minutes at maximum I would say) than they couldn't be shown anyway. Let alone the dangers for the scientists which analyze them. So I would think this is an urban legend.

Reference:

Radioactivity in fossils at the Hagerman Fossil Beds National
Monument


In what does Genetic clustering and Cline sharpness differ? They are  both ways to measure divergence in species but I'm not understanding in what exactly the differ if both use hybrid zones and gene frequencies in the study.

Clustering and Clines are two fundamentally different approaches to target the population structure problems. Because many results in classical population genetics are derived from a panmictic population, it is natural to extend them to multiple panmictic populations with some degree of gene flow in between, such as Wright's Island model and Kimura's Stepping stone model. In these discrete models, we view each subpopulation as a breeding group and hence the clustering algorithm can be used to a large number of individuals to classify them based on which subpopulation they belong to. It is 100% valid if the real population is actually discrete (such as in Galapagos), but not so if the real population is distributed continuously in space. In the latter scenario, cline may be more appropriate to describe the spatial variations of the population.

You can check Montgomery Slatkin and Nick Barton's papers on cline theory back in 1970s and 1980s to get the details, but the general property of a cline is that if divergent selection is the primary cause of the cline, then the cline steepness is proportional to the selection differences, but there is a characteristic spatial scale of variation $\sigma/\sqrt{s}$, below which any spatial structure will likely to be swamped by dispersal ($\sigma$ is the mean dispersal distance of an individual, and $s$ is the selection intensity).So Even if the cline is a step function, which is not realistic at all, the cline will still be of finite steepness. As long as $\sigma$ is not zero, you will not get a clear-cut boundary between the two sides of the population, thus invalidating the assumption of clustering algorithm. However, although clustering is not very rigorous in a continuous population, we can still use it to make qualitative explorations of our genetic data and population structure, in fact many people prefer to use that because they are conceptually clear and easy to manipulate in a computer.


Are the cpli and ctli tests time senstive(i.e. is it needed to test right away in order to get accurate results)? I'm sending the blood samples to a lab and this takes some time until the actual testing.

Some information on the tests.

TLI : http://www.vcahospitals.com/main/pet-health-information/article/animal-health/trypsin-like-immunoreactivity/405

CPLI : https://www.vetstream.com/canis/Content/Lab_test/lab00522

From doing a bit of research, I quote

  The various analytes have different stability in serum. Serum TLI and
  PLI are stable for up to 2 weeks at room temperature. However, serum
  folate shows limited stability at room temperature. Therefore, serum
  samples for folate analysis should be kept at 4ºC for not longer than
  48 hours, but freezing is preferred. Furthermore, folate is light
  sensitive and samples should be stored in the dark or wrapped in foil (reference).

So, it should be fine if the tests are conducted in two weeks.


How does the human ear guess the direction of the source? Suppose a sound is produced behind you. You can easily tell that the sound came from behind.

Our ear lobes face towards the front and hence traps the sound waves which come from the front. Yet, we can detect   that the sound came from behind.

How does the ear/brain manage to identify the sources of sound accurately?

The ear doesn't actually find the source, it's how the sound is perceived across both ears.

A sound coming from the side is the most obvious case where you get blasted on 1 ear and a relative muffled identical sound on the other ear.

A sound coming from the front is balanced across both ears. Same as behind, except that the forward-biased shape of the ears will distort the acoustics, leaving a distinct distortion signature that tells you the sound is coming from behind you. (For reference, modern 3D video game engines mimic this distortion so you can tell when something is happening behind your character or the camera if you are wearing headphones).

Sound from above or below you will have slightly different distortion signatures due to how the shape of the ears is different from above versus below.


Recommended applications for commercial antibodies Commercial suppliers of primary antibodies for given protein targets typically list recommended applications, for which the antibody has presumably been shown to work. I am usually looking to use them for immunofluorescence, and my impression (which admittedly may be based on an unrepresentative sample) is that most antibodies are recommended only for use with Western Blotting.

Why is this? Is WB the most common application? The most general? Is it easier to test for than IF?

And, perhaps more to the point, how seriously should one take these recommendations? If an antibody is not recommended for IF, does that mean that it probably won't work? Or that it may well but no-one's bothered to check? Or that it almost certainly will?

Maybe WB is easier for them to test?

In general, however, my recommendation is to check if they provide refs to paper using those antibodies and look at the images on the paper.

Be careful putting your trust in the supplier's pictures, I have seen obviously photoshopped images on commercial websites.
Also always double-check the referenced papers, as sometimes they don't really use the same product that is sold...

Other than that, in my experience, the recommended application is just that: recommended. The antibody may as well work for other application.
That said, note that there is a rationale for an antibody working for WB and not IHC, for instance: perfusion with fixators such as PFA will change the 3D structure of the target protein and may mask (or reveal) certain epitops, so the antibody may be more or less efficient depending what form of the protein you're dealing with (native, fixed in PFA, fixed in glutaraldehyde, SDS-denaturated etc.)


Anatomy of the ear canal When you insert your finger into your ear, you hit a dead end. You can't insert your finger into the auditory canal. What's this dead end called, the medical term for it?

Short answer
There is no dead end from the entrance of the auditory canal to the tympanic membrane. The diameter and shape of the object inserted rather determine whether it can reach deep enough.

Background
The above statement can be proved by following examples:

ENT doctors use an otoscope on a regular basis to directly examine the tympanic membrane (eardrum), meaning the emitted light entering the meatus from the otoscope, and the reflected light from the tympanic membrane exiting the auditory meatus are following straight paths.

Another practical example is the use of tympanic temperature to quickly measure core temperature. Again, the infrared light emitted by the tympanic membrane has to follow a straight path out of the meatus, otherwise it would be absorbed.

Lastly, see below picture that graphically shows the relative straightness of the meatus. There is some curvature, but certainly no dead end. A dead end, or hooked region with a sharp angle would be disastrous for hearing sensitivity, as it would block the passage of sound waves to the middle ear.

structures of the ear. source: WebMD.

The finger is simply too wide to enter the meatus to the tympanic membrane. In contrast, cotton buds do readily enter the meatus up until the tympanic membrane and ENT doctors sadly see quite a lot of cases where folks turn in with ruptured tympanic membranes due to excessively deep insertions of cotton buds.


How to find ion/water channel related genes We now have a collection of transcripts at hand. We would like to investigate some particular ones, which are ion/water channel related. How to perform this? Could anybody point out how to find the annotated genes those are ion/water channel related? If there are some places particularly for fish, that would be perfect. Thanks.

I think your best bet is to blast your transcripts against the TCDB which has all ion channel templates you can get in the literature. Second best would be to blast against a general protein database like UniProt.


Factors of infection rate I refer to J.H. Jones' Notes on R0.

Preliminaries
The standard SIR model consists of a system of three differential equations
$$ds/dt = -\beta  s  i$$
$$di/dt = \beta s  i - \nu i$$
$$dr/dt = \nu   i$$
for the fractions $s, i, r$ of susceptible, infected, and recovered (removed) individuals, $dt$ = 1 day.
$\beta$ is the infection rate, i.e. the number of individuals an infected indiviual infects per day, $\nu$ is the removal rate, being defined as the reciprocal of the duration of infectiousness $d_i$ (measured in days), i.e. $\nu = 1/d_i$. The reproduction number $R$ is the product of infection rate and duration of infectiousness, i.e.
$$R = \beta \cdot d_i$$
To reduce the growth of spreading of a disease, mitigation measures typically target at the infection rate, at least when a reduction of the duration of infectiousness is not at sight.
To estimate the impact of a mitigation measure on the infection rate, it is worth to consider it as the product of several factors, which may be influenced separately and more specifically.
One common approach is to consider the infection rate as the procuct of

transmissibility per contact $\tau_c$, i.e. the probability of getting infected when being in one contact with an infected person and

mean rate of contact $c$, i.e. the number of single contacts an average individual has per day, i.e.

$$\beta = \tau_c \cdot c$$
Let alone that it is not so easy to define what a contact is, other factorizations are conceivable when considering these candidates:

transmissibility per hour $\tau_h$, i.e. the probability of getting infected when being in contact with an infected person for one hour

mean duration of contact $h_c$ (measured in hours)

Let "being in contact" specifically mean "closer than 1.5 m in the average".
We then have
$$\beta = \tau_h \cdot h_c \cdot c$$
We can group factors:
$$\beta = \tau_c \cdot c$$
with $\tau_c = \tau_h \cdot h_c$, and
$$\beta = \tau_h \cdot h_d$$
with $h_d = h_c \cdot c$ the number of hours per day an individual is in contact with other persons.
Question
I am looking for references where such factorizations of the infection rate are considered, especially in the context of Covid 19.

I have not found texts relevant to your question and related to the spread of SARS-CoV-2.  However, here is a publication that discusses the utility of contact duration data when constructing infection models, in the general case --
Simulation of an SEIR infectious disease model on the dynamic contact network of conference attendees
Methods
At a conference, 405 attendees volunteered to wear RFID tags. Over two days, the time and duration of 28,540 face-to-face interactions between these individuals were recorded, with a temporal resolution of 20 seconds. Note the spatial limits of the RFID data:

RFID devices engage in bidirectional radio communication at multiple power levels, exchanging packets that contain a device-specific identifier. At low power level, packets can only be exchanged between tags within a radius of 1 to 2 meters.

From these data, three networks were constructed:

dynamic network (DYN) -- this network preserves the sequence and duration of contacts between individuals.  Using the language of graph theory, this is a directed network with weighted edges.
So, if individual A comes into contact with individuals B and C, and individual B is infectious, individual A must contact individual B before individual C in order to have a chance of A → C transmission.  Causality constrains the chain of transmission.
heterogenous network (HET) -- this network preserves the duration of contacts between individuals but disregards the sequence of contacts. The graph of this network is weighted but undirected. Adopting the previous example, B can infect C via A regardless of the relative order of the A ↔ B and A ↔ C interactions.  Causality is suspended, and the probability of transmission depends on the number and duration of contacts.
homogenous network (HOM) -- this network inherits the topology of HET, but ignores the duration of contacts.  The graph of this network is unweighted and undirected. Each contact event carries an equal probability of resulting in transmission, so the probability of transmission depends solely on the number of contacts.

To simulate the spread of an infectious disease over realistic time-scales, each network was longitudinally extended using three procedures:

repetition (REP) -- the recorded contacts are repeated with the same duration and order.
random shuffling (RAND-SH) -- the structure of the network is preserved, but the IDs associated with the nodes in the network are shuffled between iterations.
constrained shuffling (CONSTR-SH) -- same as RAND-SH, but the reordering of IDs is constrained to preserve individual social activity (i.e. IDs with many contacts are not assigned to a low-contact node in the network) and repeated contacts.  This procedure rectifies the oversimplifications of REP and RAND-SH by acknowledging that people tend to interact with the same people day-to-day, with occasional contacts with strangers.

The authors applied a SEIR epidemic model (Susceptible, Exposed, Infectious, or Recovered).  For each network-procedure pair, they considered two disease scenarios with different assumed values of mean latency period (σ -1), mean infectious period (ν -1), and transmission rate (β):

very short incubation and infectious periods

σ -1 = 1 day
ν -1 = 2 days
β = 3.10 -4/s

short incubation and infectious periods

σ -1 = 2 days
ν -1 = 4 days
β = 15.10 -5/s

A note from the authors on why these values were chosen:

These sets of parameter values were chosen to maintain the same value of β/ν, which is the biologic factor responsible for the rate of increase of cases during the epidemic outbreak, while changing the global timescales of incubation and infectious periods, and assessing the role played by the social factors embedded in the contact patterns.

Results
Epidemic outbreaks in the three networks across the three data-extension procedures were compared by computing the mean R0, defined by the authors as the mean, over all iterations, of the number of secondary cases from the single initial randomly chosen infectious individual.
Considering the simplified REP procedure, higher values of R0 were observed in the HOM network compared to the HET and DYN networks, for all scenarios.  The authors explain this observation by noting that the probability of rapid extinction of the pathogen was smallest for the HOM network; indeed, this held true independent of procedure.
In terms of the final number of cases (R∞) and the rate of spread, the HET and DYN networks were similar for both disease scenarios.  The peak of the epidemic was reached first in the HOM network, on average, consistent with the reduced probability of extinction.
In the RAND-SH procedure, spread was slower but lasted longer, leading to a larger R∞ for all networks.  In general, greater shuffling of ID tags led to more efficient disease spread, such that R∞(RAND-SH) > R∞(CONSTR-SH) > R∞(REP) for all networks and scenarios.  The interaction of more efficient disease spread in the RAND-SH procedure with increased values of σ -1 and ν -1 in the "short" scenario seems to produce consistently higher R0 values across networks (see Figure 3), though high variance in R0 means the effect of this interaction is not significant.
Conclusions
By comparing the different network types across all procedures and scenarios, it was shown that ignoring the direction and duration of contacts overestimates both the rate at which a disease spreads and the total number of individuals infected.  Additionally, shuffling individual positions in contact networks while preserving network topology increases disease spread when compared to a static model, though this effect is buffered by the "realistic" inclusion of preserved sub-networks of repeated contacts.
While this publication does not directly integrate factors for the duration and rate of contacts into the SEIR model, as suggested by Hans-Peter Stricker, the authors are able to show that mapping such a model to networks in which the direction and duration of contacts are encoded as edge weights leads to different measured outcomes (R0, R∞, time to peak) when compared to topologically identical networks lacking these encodings.


Air bubble in addled egg I'm a complete novice in biology. This is just a question that arose during Saturday night warmup and there is no better place to get answers :)

So, as probably most of you know, if you want to decide whether an egg is rotten/gone bad/addled you just put it in a bowl filled up with cold water and some salt.

If the egg stays on the bottom of the bowl then it is good.
If it floats to the top of the water then it is rotten/addled.

I imagine the egg is floating because there is an air bubble in the rotten egg.

But how would that air bubble get in the egg?

Egg shells look as if they're solid, but in fact they're filled with tiny pores through which air can and does diffuse.

  ...up to the time when internal pipping takes place, when pulmonary ventilation is initiated, about 20 liters (O2 + CO2 + water vapor) have passed through 10,000 pores of an 80 gm egg.

--Pores and gas exchange of avian eggs: a review.

  A typical 60-g chicken egg has about 10,000 pores, each with a functional cross section of 150–200 μm^2; therefore, the total pore area is about 1.5–2 mm^2.

--Gas exchange in avian embryos and hatchlings

You only asked about chicken eggs, but chickens have it pretty easy compared to many other avian species.  For example, ostrich eggs have a much larger volume-to-surface area, meaning that exchange is less effective. One way ostriches may compensate is by incubating eggs at lower temperatures, reducing oxygen requirements; more significantly and related, incubation time is relatively slower for birds with large eggs.   Birds at high altitudes have larger total pore size, adapting to the reduced O2 pressure.

Actually, a more serious problem than oxygen exchange is water exchange.  The egg needs to manage water loss (not too much, not too little), and the more gas exchange the more water loss.  Accordingly, birds adapted to different humidities lay eggs with different gas exchange capacities (changing pore densities for the most part); birds in very arid environments, like gulls in Chile's Atacama Desert, have very low gas and water exchange, to the point where their developing chicks are relatively hypoxic:

--Reduced oxygen diffusion across the shell of Gray gull (Larus modestus) eggs.


Which method of gene amplification for toehold switches? My team and I are from a high school and are planning to carry out some research investigating some toehold switch riboregulators which we have designed in silico. However, we have little experience in wet lab work. We plan to order 3 genes containing an arabinose inducible promoter, a riboswitch, a leuciferase CDS and a terminator. These genes are each ~3kb in length.
We plan to order our genes from IDT, but we're not quite sure which strategy to deploy to amplify these genes before adding them to a cell free extract for characterisation.
The four methods we have narrowed it down to are as follows:

Order the genes in plasmids, linearise, PCR,  ligate, add to cell
free extract for characterisation.
Order genes in plasmids, transform straight into E. coli, culture, mini prep, add to cell free extract for characterisation.
Order genes in plasmids, linearise, PCR, ligate, transform into E. coli, culture, mini prep, add to cell free extract for characterisation.
Order genes as gBlocks (not in plasmids), amplify with PCR, ligate into plasmid backbone, transform, culture, mini prep, add to cell free extract for characterisation.

We'd ideally like to use the method which is most simple as we will not have a lot of time in the lab, and we don't have much experience.
Any advice on choosing between these strategies would be much appreciated!

Option 2 is your simplest and easiest. It should give you unlimited plasmid to work from. Note that ordering pre-made sequences of this size isn't particularly cheap and might take a few weeks to get to your destination.
It may be easier (quicker + cheaper) to find a plasmid with the luciferase CDS and terminator already built in. You could then amplify this with primers incorporating your promoter and riboswitch sequences and some restriction enzyme sites to generate a product that looks like this:
RE1-ara-riboswitch-luciferase-RE2
You can then clone this into a(nother) plasmid cut with RE1 and RE2.
Another option is that if you have a plasmid with a luciferase gene in it already and a multiple cloning site (MCS) you can order complementary primers (note single-stranded DNA, anything less than about 150 bases is fine) containing the araC and riboswitch sequences flanked by two restriction sites, you then anneal the two primers, digest off the ends and ligate. You just have to be careful with making sure that everything is in-frame. I don't know anything about riboswitches though so frame may not matter so much.
As you have limited time I suggest buying chemically competent cells for heat-shock transformation (if you don't have some already); make sure you don't get electro-competent ones, as these will only work with an electroporator.  Also get a commercial mini-prep kit (e.g. Qiagen plasmid mini-prep). These are easy to use and reliable.
I think in option 1 you have something a bit odd going on - why would you digest your plasmid then re-ligate it, when it is already in the form that you are going to use?
I am not quite sure why in options 3 and 4 that you think that these are any different in terms of the end result to option 2.


where can I find microarray images? I have investigated some of the links to known microarray databases, such as arrayTrack, omnibus (NCBI), TCGA. I find that when trying to get microarray images I either get an exotic file format (such as .sdf or .cel) or text base information. Does anybody know of publicly available microarray images (preferable with metadata too) in .svg, .png, .jpg or another well known image file format?

Microarray images (at least for Illumina arrays) will come in .tiff format and are huge compared to the summarized formats (.sdf/.cel). Most places will not archive the raw images (so you won't find them online) and even when you run the microarray, you will often times need to make a special request to output raw images. iirc .jpg images are useless due to compression artifacts.

You can use the proper bioconductor libraries to extract data from the 'exotic' file formats. There are many bioconductor workshops archived online that will go through the steps of microarray analysis.

http://www.bioconductor.org/packages/release/bioc/html/affy.html

http://www.bioconductor.org/packages/release/bioc/html/beadarray.html

http://master.bioconductor.org/help/course-materials/2007/BioC2007/labs/oligo/BioC2007-oligo.pdf


Do cockroaches lay eggs in human flesh when they "bite"? Recently, I discovered a "bite" by a cockroach, and not only is the "bitten" area red and swallowing, and more specifically, it have a big hole in that area, but when I clean it with hydrogen peroxide solution, something is happening, that is, a yellowish/greenish thing comes out from the holes from each infecting area.

Do cockroaches lay eggs in human flesh when they "bite", and much more importantly, would hydroxide solution kill the eggs and parasites inside those of those holes?

No, cockroaches do not lay eggs into human flesh. You most likely received an infection of some sort from the bug, or it wasn't a cockroach.


How do seagulls know it is the 9th inning at a baseball game? Multiple times that I’ve gone to San Francisco Giants games, the seagulls sensed when the game was ending so they could pick up food. https://youtu.be/LPra_ZfwanU

Many animals, particularly some birds, are smarter than we give them credit for. Corvids, for example, are known to not only use tools, but are capable of planning and understanding some cause-and-effect scenarios that require patience.

I know practically nothing about baseball, but if it's like any other human gathering, there are probably a lot of clues that the birds learn:

Noise levels. Big events often culminate in some big fanfare with noise (cheering, music, etc.). If the game changes audibly near the end, you can bet the birds have noticed.
Motion/activity: Any large gathering I've ever gone to often has a small percentage of people leaving early because they want to avoid the crowd or traffic. I'd expect a close-scored game has fewer people leaving, but chances are good that as enough people start getting up to leave, it's another signal the birds can use.
Discarded food: Aside from getting up to leave, toward the end of an event many people will start discarding snacks and drinks. Hopefully in the correct bin, but often just on the ground (humans are messy -- which seagulls love). An increased number of people tossing garbage into bins (and missing or they start overflowing) signals a few gulls that there's scraps to be found.
Temporal.  If these events happen regularly, or even irregularly, the birds associate it with food. People filling a stadium or parking lot, playing music, buying food (birds do have a sense of smell, though not as developed as mammals), etc. The birds over time learn: Increased human activity at this location results in more food some hours later.

Gulls are very gregarious, and notice when just one bird has found a morsel. As soon as a few birds get the first discards, the rest of the flock notices and starts to mobilize; circling and calling.

I would argue that the birds don't really know when a game or event is about to end, but they are adept at reading their environment, even if it's an urban one.

Per @theforestecologist's comment, references are requested. While I do not have a reference for each specific behavior described above, the following list covers avian intelligence generally, learning and problem-solving, and physiological adaptations. Many of the described behaviors are products of associative learning and elaborate communication, traits that gulls exhibit in other activities such as dropping clams from heights.

References:

Ravens parallel great apes in flexible planning for tool-use and bartering
Can Kabadayi, Mathias Osvath
Science; 14 July 2017, Vol. 357, Issue 6347
Ecology and Conservation of Birds in Urban Environments
edited by Enrique Murgui, Marcus Hedblom
Springer Nature; 10 February 2017
Cognitive ornithology: the evolution of avian intelligence
Nathan J. Emery
Philosophical Transactions of the Royal Society of London; 7 Dec 2005, Vol. 361
Bird Sense
Tim Birkhead
Bloomsbury Publishing; 2 Feb 2012
Auditory and visual mechanisms in food-finding behavior of the Herring Gull
Hubert Frings, Mable Frings, Beverly Cox, and Lorraine Peissner
Wilson Bulletin 67; January 1955


How does action potential conduct across a branch in a neuron? As the action potential travel in the dendrite towards the cell body, it will encounter many branches. What happens at the branch? What makes it go to the cell body instead of other dendrite?

Also, as the action potential travel from the axon to its branches, does it go to only one or all terminals? If it goes to only one terminal, how is it decided which terminal it has to go?

Awesome question!  Thanks for asking it and giving me the motivation to look back at the literature to increase my own understanding!

I do want to point out one issue of semantics before starting.  Just to avoid confusion, I'm going to follow the example of some of the well-known experts in this field and distinguish dendritic spikes from action potentials.  The main difference is that a voltage spike in a dendrite or dendritic spine will experience attenuation (essentially a weakening of the spike) as it propagates toward the cell body, and it is distinct from the all-or-none voltage response of an action potential.  It is generally accepted that action potentials are initiated in the axon (hillock) because that is where dendritic and somatic spikes will ultimately sum to fire the all-or-none voltage response.  I just want to clarify what I mean by dendritic spike when I use it during this explanation.

What happens at the branch? So, to answer your first question, you're absolutely correct that when a dendritic spike occurs, that spike will encounter multiple branch points along the dendrite as it proceeds toward the soma.  When a spike propagates to a branch point, the properties of the branches determine what happen to the spike.  One important property is referred to as the geometric ratio (GR).  This property was described Goldstein and Rall in 1974 (manuscript here for review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1334570/) and the gist of the equation is that spike attenuation is dependent upon the diameter of the branch the spike is coming from and the branch the spike is going into.  The concept behind this is called impedance mismatch, but that's complex and I won't get into it.  Just know that spike propagation is favorable from a large to a small branch, but is not favorable from a small branch to a large branch.  If you wish to read more about this concept, I'd recommend the Goldstein and Rall paper referenced earlier and chapter 14 of the textbook "Dendrites" by Spruston, Stuart, and Hausser.

Additionally, the presence of leak or voltage-gated channels in that branch can determine how well the spike will propagate or how much attenuation will occur.  This is an easier concept to grasp because the idea is essentially that more channels open when the spike passes through that branch, the more charge leaks across the membrane and causes attenuation of the spike.

All questions regarding preference of flow To sort of attempt to answer all your other questions at once, nothing really forces the spike toward the soma or a specific axon terminal.  There are dynamic changes in membrane potential that may prevent spike propagation down one branch or action potential propagation in a certain direction (like how action potentials aren't thought of as propagating from the axon to the soma because of the hyperpolarization and long inactivation of sodium channels at the area that just fired, preventing what is called backpropagation at that particular time).

I think a little reading on neuronal cable theory might be of some help with this question too.  This link is to a PDF that gives a pretty brief explanation of this concept https://nanohub.org/resources/20112/download/Lecture1_Passive_Conduction.pdf.  This is a pretty math-heavy field, so beware if math isn't your favorite subject!


Does estrogen increase muscular growth in females? Regarding humans it is said that most psychological effects caused in men by testosterone are caused in women by estrogens. There are many studies on that, particularly regarding temporary shifts of hormone levels: Ovulatory shift hypothesis. Also, there are some studies (and possibly controversial) claiming such differences between individuals.

But this made me think if there are any similar physiological diffences caused by estrogens. It's known that in males testosterone affects muscular growth, which means higher testosterone levels will make it easier to gain muscular weight. So, I ask if higher estrogen levels in females affect muscular growth.

While this question is regarding humans, studies about other primates also can be acceptable.

The article named "Estrogen replacement and skeletal muscle: mechanisms and population health supports this hypothesis, when applied to postmenopausal women:

  Evidence suggests that HT will also help maintain or increase muscle mass, improve postatrophy muscle recovery, and enhance muscle strength in aged females.

This particular passage suggests it might not be exclusive to postmenopausal women:

  One of the reasons for the relatively new interest in estrogenic effects on skeletal muscle was the identification of estrogen receptors (ER) in this tissue.

Passage containing more specific information:

  Although research findings over the past 20 yr have reported conflicting results of HT on muscle mass in postmenopausal women, the preponderance of more recent evidence has “tipped the balance toward a positive and measurable impact of HT” and have highlighted the “proanabolic” effects of HT on skeletal muscle. Several recent studies examining postmenopausal women showed significantly greater muscle mass in women taking HT relative to nonusers.


Which insect is this? I just found what i think is an insect on floor of my balcony. From what i know, it is a Praying mantis. I want to keep it as a pet but for that i want to its exact species.

If it helps:
 Location: Bangalore, India
Temperature : $23^{\circ}$ C

Could someone help me identify it pleas.

I presume it is an Indian bark Mantis , Humbertiella ceylonica.

  This mantis can be kept at between 21 and 28 degrees comfortably and does not need a drop in temperature at night.

References: bugzuk.com and Google


RNeasy Mini Kit low 260/230 ratio -- can I purify this RNA for further use? I used Qiagen's RNeasy Mini Kit to isolate RNA from 5*10^5 C28/I2 (immortalized human chondrocytes). However, my yield is low (~25 ng/ul), but my 260/280 ratio is great (~2.3), and my 260/230 ratio is tragic (~0.06). I have already thrown the spin column away, but I would like to know 1) if I could raise my 260/230 ratio for the 40 ul of RNA I extracted, and 2) if I could precipitate the RNA out of solution so as to make a more concentrated solution.

Please let me know if further details are necessary.

Thanks!

RNAeasy kit will not usually give phenolic contamination. Your poor 260/230 is perhaps because of low yield; check the absolute absorbance values. Low 260/230 (and low yield) also happens because of improper lysis. I would advise that you do the cell lysis using more effective methods. I would not advise another phenol-chloroform or alcohol precipitation step- you will lose your RNA. With what you have now, run a little bit on the gel to see the integrity. Also try heating the dissolved RNA at 65-70deg for 10-15min and measure OD again (use nanodrop or a similar device)


Can some prokaryotic cells be larger than eukaryotic cells? Can the sizes overlap in some bacterial species? My science teacher claims so. My research says the opposite. Can someone confirm?

Prasinophytes are the smallest known eukaryotes. They are around 0.5 µm in diameter.

Thiomargarita namibiensis is the largest known prokaryote. They are around 100-300 µm in diameter.

So, yes some prokaryotes are much larger (up to about 500 times larger) than some eukaryotes.


Question about cell signaling pathways (RTK, Jak-Stat, SMAD, etc) I am in an embryology course right now and we've just started covering cell-cell communication in development. We were talking about the roles of the various cadherins and their discoveries but we got to cell signaling pathways and in reading my textbook I'm finding myself confused by these pathways-- some of those that are mentioned include Notch, Wnt, FGF, TGF-beta, RTK, Jak-Stat, SMAD, integrins, PTHrP, Hedgehog, Discoidin domain receptors 1&2, and the unfolded protein response (UPR).

I know the RTK pathway and I know the SMAD pathway, but the others just seem to be specific ligands that are using these pathways -- is this correct?

@Alexandria Jak/Stat are two families of proteins which mediate signals through phosphotyrosines.

JAK is a tyrosine kinase which binds to cell receptors and STAT is dimerized by JAK action.  JAK specificity seems to be your question.  A specific JAK protein (e.g. JAK1 or JAK2..) may mediate for different receptors in different cells.

There may be hetero- or homo-dimers of JAK, there may be more than one receptor in a cell using the same JAK enzyme, which may result in cross-talk between the two signals.  I think its a pathway dynamic that can vary quite a bit from one cell to another, depending on the receptor and cytokine environment the cell is seeing. JAK action can be modulated by any number of proteins which respond to other pathway signals or the cell state.  The diagram below from a review of heart muscle cell JAK action is not unusual nor is it complete.


Does a gene code for protein molecules or a DNA codes for protein molecules? To my understanding, a gene consists of a unique sequence of nucleotides that codes for a polypeptide or an RNA molecule. In my textbook, it is stated that DNA codes for protein molecules.
So I thought, a gene only code for 1 protein molecule or 1 RNA molecule
However, DNA can code for a number of protein molecules or RNA molecules, as a gene is a stretch of DNA.
Is my understanding correct?

Your understanding is correct in that DNA encodes RNA, and this is a one-to-one relationship generally (although there are exceptions, see link below).  However, a given RNA can encode myriad proteins via translation.  This is because of different translation start sites and splicing of RNA.  You can read about this relationship between DNA/RNA/protein (the 'central dogma' of molecular biology), here:

https://en.wikipedia.org/wiki/Central_dogma_of_molecular_biology

But in the title of the quesiton you also ask about whether a gene or DNA encodes protein.  A gene is comprised of DNA; if someone talks about a gene, this just means a transcribed sequence, i.e. a region of DNA that is made into RNA.  Whether or not this is then translated does not impact its definition as a gene.  If it is transcribed, you could call it a 'protein-coding gene', otherwise you can call it a 'non-coding gene'.


Can viruses be used to extract oil from algae? I read that one hard step in algae oil extraction is to rupture (or fracture) the cell walls to get the contents inside. Some people use chemical methods; some use sonication or mechanical forces.

I wonder why nobody is talking about using viruses to accomplish this task? Viruses destroy the cells and release clones of itself. Some article states that there are plenty of unknown viruses in seawater. I'm sure a major part of it infects algae.

Viruses hijack the hosts translational machinery, forcing the host to downregulate translation of other proteins in favor of viral proteins. Your cells will eventually lyse, but in the meantime they would not be producing the enzymes required to make whatever product it is you're trying to get, likely resulting in low yields that are contaminated with virus.


Is dried grain dead or dormant? Is dried grain considered dead or dormant botanically?

Related to a BH-SE question.

Dried grains are very mostly viable means they are in a dormant state until and unless suitable condition are provided. More dried it will be viable for longer.
In fact there are seeds found in Siberia which are ~32,000 years and still viable.

Courtesy: National Geographic
Source:
US Emergency Supply: Introduction to Seed Viability