How does the human stomach handle a mix of digested and undigested food? As I understand it, the stomach digests the bolus into chyme and then passes the latter on to the small intestine. This process takes between 40 minutes and a few hours.

However, what happens when the processing of the bolus is not completely finished and new food arrives in the stomach?

Will the stomach pass on all the food, including the only partially digested "new food" to the small intestine when the time for digesting the first load is up? Or will it keep all of the food until all of it is completely processed? Or does it have some way of allowing only the processed parts to pass on and keeping the unfinished parts behind, like a gate control?

The regulation of emptying of food from the stomach to the duodenum takes place with the help of feedback mechanisms involving the duodenum and stomach.

Nature of the chyme which inhibits stomach emptying by the duodenum:

Excessive acidic chyme.
Chyme contains too much undigested or unprocessed proteins and fats due to which its tonicity and irritability changes.

Regulation by the duodenum:

Nervous regulation:
The enteric nervous system,the vagus and the prevertebral sympathetic ganglia play the key roles in nervous regulation of this feedback mechanism because when food enters the duodenum they provide stimuli that activates them which inturn inhibits pyloric pump.
Hormonal regulation:
Cholecystokinin, secretin and gastric inhibitory peptide inhibits pyloric pump,gastric motility,gastrin effect on stomach emptying respectively.

Thus,when much undigested chyme passes to the duodenum,duodenum regulates if the digestion process should be prolonged or not in the stomach.

Factors promoting emptying of stomach:

Gastric food volume and gastrin hormone promotes emptying by stimulating the enteric nervous system for emptying and enhancing pyloric pump respectively.

Thus, the distinguish between a digested or undigested chyme to be passed to the duodenum or the time for which the food must stay in the stomach for digestion is entirely under the regulation of these factors.

References:

https://www.ncbi.nlm.nih.gov/pubmed/1126597

https://www.ncbi.nlm.nih.gov/pubmed/7943335

https://en.m.wikipedia.org/wiki/Gastrin


What causes drone bees to die? ... when not killed by other members of the hive.

Is it always a consequence of exile (denial of some resource, etc) or does some organ fail regardless of circumstances?

The number of drones in a colony may be hundred-thousand , i.e 15 % of the total population. The drones lack wax glands, pollen collecting-appartus and sting which is present in worker bees which make them completely dependent on the workers, transferring its genes to the next generation is the only contribution of the drone bees. Usually the drones do not mate with the queen of the same hive. The drones that are able to mate with the queen die shortly after mating due to breaking of bulb of endophallus(penis) inside the queen.

The rest, the survivors of the mating flight (mostly drones that could not participate in  mating) are not allowed to reenter the colony. They remain in the vicinity of the hive and eventually starve to death.

In hours of crisis when the colony needs to drop the expenditure of resources(food) the workers eat up larval drones or drive out the matured drones from the colony that eventually die due to the same reason.

Information taken from:

Wikipedia
Bees
The Backyard Beekeeper


Have humans finished evolving? I thought that massive changes among organisms are over long periods of time. This is caused by, to my knowledge:

Evolutionary pressure
Natural/artificial selection
Mutations
Genetic drift

Will mutations be the only factor in human change? Will humans change at all over a long time?

Issue in your introduction

I thought that massive changes among organisms are over long periods of time.

Actually, some evolutionary events can happen on a very short time scale. A single mutation can have a massive impact on the phenotype of an individual (see for example Doebley 2004). If this new phenotype has much higher fitness, then the mutation might spread over the whole population in a matter of weeks (typically if the population is not too large, without barriers to gene flow and more importantly if the generation time is short).

This is caused by, to my knowledge:

Evolutionary pressure

Natural/artificial selection

Non-detrimental mutations

The term evolutionary pressure typically encompass natural and artificial selection, mutations (regardless of their mutational effect, that is regardless of whether they are beneficial or detrimental) and other processes that you don't mention (such as genetic drift for example; you have now edited your post to include drift).
Answer to your questions

Will mutations be the only factor in human change?

By "human change", I will assume you mean "human evolution". The answer is: no, mutations are not the only process that leads to human evolution. All standard evolutionary processes are at play in humans as they are in other species. You might want to have a look at the posts Human Evolution in Modern Times and How is evolution possible in contemporary humans?.

Will humans change at all over a long time?

Yes, humans are currently (and will continue to do so in the future) evolving. Again, you might want to have a look at the linked posts.
Want to know more?
Your questions are quite introductory and show a number of misunderstanding you have about evolution. I would recommend having a quick look at Understanding Evolution by UC Berkeley which is a very introductory course to evolutionary biology that is fast and easy to follow.


Mutation rate in viruses Mutation rate is a phenotypic trait that evolves. The process of evolution of such kind of traits are often referred to as evolvability. I am wondering about the evolution of the mutation rates in viruses. For the purpose of this question, I'll focus only on viruses that do not possess DNA polymerase. Because the replication of the viral DNA is performed by the molecular machinery of the host cell (eukaryote or not) it seems rather impossible to me for a virus to evolve its mutation rate. Is it correct?

Do we have any evidence of adaptive mutation rate in viruses?
Is there a correlation between the mutation rate of the host and the mutation rate of the virus?
Could the virus evolve some structure (or codon bias) of their DNA/RNA in order to adapt their mutation rate?
Is there another mechanism allowing a virus lineage to adapt their mutation rate?

Really interesting question.
I am not sure, if the mutation rate is something "actively done" by the virus. I think its more a byproduct of vast replication after taking over the host cell. Mutations with a negative effect are deleted, those with neutral effects will be there, and those with positive mutations will be selected for. This paper looks interesting in this context: "Viral Mutation Rates". Looking for related publications on the site, I found this two:

Rates of evolutionary change in viruses: patterns and determinants.
A short introduction to the origin and molecular evolution of
viruses.

The whole list is here.

Answering your second question: There is obviously no connection between the mutation rate of the virus and the host. I have found this paper ("Rates of Spontaneous Mutation") which gives some pretty interesting numbers. In short: The rate of mutation for DNA viruses is much higher than for eukaryotic cells and for RNA viruses 2-4 orders of magnitude higher than for DNA viruses.

At least RNA viruses encode for some own polymerases, the reverse transcriptase. Depending on which these have a proof-reading (exonuclease) function they induce more or less errors.


Do hairs in the ear respond to things like shampoo? Shampoo and conditioning products make claims to be the end all be all in hair care. I doubt that they are so advanced "growth formula/anti-breakage/oily treatment". Have any of the claims been shown to be valid? Assuming a positive response do they have application for restoring the hairs used for hearing?

You are mixing up hair cells and hair. Hair cells in the cochlea (wiki) have tiny stereocilia (subcellular organelles) that sense vibrations approaching the atomic scale. These are then translated in hyperpolarizing or depolarizing currents that drive the spiral ganglion cells of the auditory nerve. The 'hairs' on the hair cells will not readily benefit from shampoo I'm afraid. If you should want to test it, the shampoo should be intracochlearly administered in the scala media of the cochlea - so even if shampoo is beneficial it would be hard to utilize it without surgical intervention.


Is tunneling of a proton in our DNA a cause of mutations? Our DNA strands are tight together by hydrogen bonds. Can the proton of Hydrogen tunnel to the other complementary strand, and by this during the replication bind to a different/wrong nucleotide, causing a point mutation?

Keto-enol tautomerism involving proton transfer within a single DNA base can lead to mispairing and mutation during replication.  This is touched on in the previous citation provided by tsttst as well as this section from An Introduction to Genetic Analysis. 7th edition: https://www.ncbi.nlm.nih.gov/books/NBK21897/  I have not found a clear statement of whether the proton transfer is over sufficient distance to constitute "tunneling".


What spider is this? BOLIVIA I was in Cobija in northern Bolivia, and these spiders were hanging around a lamp post. There were over 100 of them.
The picture is not a good one, but I can describe them:

They were black with light blue stripes on their body, and the legs were black and yellow. They formed a big X with their legs.

Anyone know what spiders these are?

The size, shape and leg arrangement as it hangs upside-down in the web, marks this spider as an Argiope, as previously noted.  The big white band on the front of the abdomen suggests A. argentata, but the photo is blurry enough that some of those spiders might be A. trifasciata.  I'd be happy to put it down as Argiope species, in the hope that more, and closer photos of this neat and completely harmless (to humans) spider are forthcoming.

https://bugguide.net/node/view/2033


Need Help Identifying this Critter (Insect?) This creature is hanging out on my kitchen window. I live in Western Maryland, US, near the Potomac River. The creature is about 3 inches long (measured from tip of mandibles to tip of tail). Does anyone know what it is? Is it dangerous? Rare? I've been living here about a year and have never seen one before.

It looks like an adult Dobsonfly (Corydalidae), where the adult males have huge pincher-like jaws. Apparently, the jaws are the result of sexual selection and, even though they look scary, males cannot use them to bite.

I'm only vaguely familiar with the group though, and cannot say what species this is.

(Picture from bugguide.net)


Organs lifespan out of the body What organ can be conserved outside of the body for the longest time and still function when reimplanted?

Depends what you consider an organ. Typically though it's the cells which require the most metabolic activity which have the shortest life span. The kidney is the most of the major internal organs with up to 36 hours with liver coming second at up to 16 hours.


Identification of this fly? So I find these flies every year in my mulch, and I've never seen them anywhere else. The mulch becomes full of their larvae, which I feed to my toad and lizards. There are so many that you can hear them moving. The adults are black, look like a wasp or hornet, and have a curious green patch on the underside of their abdomen, which is a clear patch showing some kind of liquid. The larvae are brown and have a little hair on them.

It's about one inch I think maybe a little less. I hope the quality is good enough, because I used my iPod for the picture and you can't do macro with it. Also, I live in Hillsboro Oregon. I am near a small forest and in the suburbs.

Black soldier fly Hermetia illucens. http://en.wikipedia.org/wiki/Hermetia_illucens

There is a good key to the Dipteran families here. Although it is for British families, it is very thorough.


Is it possible to perfuse chemicals into brain after removal from body? I've read studies where fixatives (eg glutaraldehyde) have been perfused into the brain while it is still inside the skull. I would have thought that this could also be done after the brain is removed, provided all the veins/arteries are connected to a perfusion machine. Is this possible, and are there any major obstacles?

Of course it is possible to perfuse an organ once it has been removed from the body. It is probably unwise to do so with the brain as the delicacy of the structures and high levels of lipids make rapid fixation necessary and difficult. I think the major obstacle is the speed at which the brain could be removed with arteries intact and then perfused as ultrastructural changes occur rapidly once ischemia (oxygen deprivation) begins.


Is the mutation rate in organisms in general consistent over the genome? Coming from computer science with an interest in genetic programming (a process emulating evolution) I'm curious about whether the rate of mutation is homogeneous across the whole genome, or if some parts of the genome differ in the rate of mutation.

For example we could imagine, without going to into details that could invalidate the example, that parts of the genome associated with the immune system could have a relatively higher mutation rate, because this would allow for a quicker adaptation to quickly evolving pathogens.

Is there any empirical support for that different part of a genome of some species have different mutation rates, that would give us empirical support for the possibility that some species under evolution have the ability to adjust (by NS itself or even epigenetics) the mutation rate of specific parts of the genome?

Clarification

I'm only interested in the mutations happening in the scope of the lifetime of a individual organism, I'm not interested in whether the mutations persisted under NS are equally distributed over the genome.

Well, for start, there are "mutational hot spots", regions that are more prone to mutation than others.

As for immune system genes, first of all, lung cells and heart cells and retina cells don't need to mutate those genes, because they don't use them.

But you are right that in immune cells there is a lot of DNA futzing in the sequences for the heavy and light chains, in order to generate diversity in T and B-cell receptors.  Those receptor sequences are built in a mix-and match fashion, like building an outfit from a closet with a few pairs of pants and a few shirts.  Add in some messiness in cutting out the specific sequences, and you have a fair bit of diversity in receptor sequences possible from a single genome.

Later, once a B-cell or T-cell meets a matching antigen, the cell multiplies, and each descendant cell is subject to somatic hypermutation, in the hopes that one of the tweaked sequences will better match the antigen.

But none of that is going to be very evolutionary relevant, since only mutations in gametes or gamete stem cells are passed on to the next generation.


Are there any bacterial lineages which are particularly well adapted to becoming endosymbionts? Is there any particular bacterial lineages which contain a large number of endosymbiotic species and that inhabit a large range of eukaryotic hosts? To me, this would seem to suggest that they are particularly well adapted to becoming endosymbionts.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0027909

  Members of the genus Xenorhabdus are entomopathogenic bacteria that associate with nematodes. The nematode-bacteria pair infects and kills insects, with both partners contributing to insect pathogenesis and the bacteria providing nutrition to the nematode from available insect-derived nutrients. The nematode provides the bacteria with protection from predators, access to nutrients, and a mechanism of dispersal. Members of the bacterial genus Photorhabdus also associate with nematodes to kill insects, and both genera of bacteria provide similar services to their different nematode hosts through unique physiological and metabolic mechanisms.


Is there a database of cell images? We're working on an algorithm for processing images of cells, similar to but much more basic than Cell Profiler, and we are looking for a large database of cell images to test our software. Can anyone point us in the right direction? We found the Cell Image Library immediately, but it seems almost empty.

There is a yearly contest on cell tracking organized by the IEEE International Symposium on Biomedical Imaging, and the associated data sets are freely available.

See for example: http://www.celltrackingchallenge.net/


Is palmitic acid really that dangerous? According to Wikipedia,

"Palmitic acid is the most common saturated fatty acid found in animals, plants and microorganisms. It is also the first fatty acid produced during fatty acid synthesis and is the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to make up 21–30% (molar) of human depot fat, and it is a major, but highly variable, lipid component of human breast milk."
(https://en.wikipedia.org/wiki/Palmitic_acid)

Yet, specifically palmitic acid is also said to be "harmful" (that it increases LDL levels and puts people at risk for heart disease), per the World Health Organization (http://www.freezepage.com/1348239076FHWAJDADVT).

So, I am skeptical --- possibly most ubiquitous saturated fatty acid in nature and a central component of our fatty acid metabolism, is somehow "more" dangerous/unhealthy compared to other saturated (or unsaturated) fatty acids? I'd suspect the opposite should be true -- it seems to me it should be the saturated fatty acid we should be most capable of handling well!

Let's first clarify some concepts. Free fatty acids, including palmitic acid, are not present in animal tissues (or in the diet) to any large extent; they are esterified with glycerol to from triglycerides (fat), which is the storage form. This is a very important distinction, because triglycerides are chemically inert molecules that can be stored in very large amounts in cells without causing problems (adipocytes are pretty much just one big fat droplet), while free fatty acids are dangerous to organisms because they disrupt cell membranes --- fatty acids are basically soap.

When nutrition studies like the WHO report talk about dietary intake of "palmitic acid", they really mean intake of triglycerides that contain a large proportion of esterified palmitic acid as side chains. There is a large body of epidemiological studies indicating that intake of fats rich in palmitic acid correlates with cardiovascular disease and other "metabolic" disorders, although some reports show no significant effect. In clinical trials, replacing saturated with unsaturated fat seems to provide some health benefit; but there also are studies indicating that monounsaturated fat can be worse than saturated fat. So there is some evidence that too much saturated fat is problematic, although the issue is not straightforward.

The causal mechanism is to my knowledge still not clear. You are right that cells are normally perfectly capable of handling palmitic acid; it is a good substrate for beta-oxidation and a common fuel source for human cells. However, in pathological situations, free fatty acids can accumulate in cells and in the blood, probably because of excessive lipolysis. Many studies show that this can cause insulin resistance and trigger inflammatory signals, and even cell death by apoptosis. Some reports show that palmitic acid in particular causes these effects, whereas oleic acid (monounsaturated) does not, but I don't think there's any consensus on why palmitic acid is special.

My own hypothesis (if I may be so bold :) is that palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general. Since fatty acids are clearly dangerous to cells, sensing them is important, and because palmitate is the naturally most abundant fatty acid, it would be the easiest fatty acid to detect. It is known that palmitate is recognized by toll-like receptors, in particular TLR2 and TLR4, and that sensing by these receptors trigger "proinflammatory" signalling. But this alone doesn't prove my "proxy" hypothesis, of course.


Between Cholera and Polio, which disease cannot be controlled by killing the vectors Since Cholera affects only humans, and also doesn't have an insect vector or animal reservoir host. And Polio is a disease of the central nervous system, spread from person to person through infected fecal matter entering the mouth. Then which one of them can be controlled by killing the vector, I'm not completely sure if cholera doesn't have a vector, but if they don't, then I'll like to know if and how polio can be controlled by killing the vector.

Both of these diseases do not have vectors,
Cholera is a foodborne / waterborne disease and Poliomyelitis is spread through fecal-oral or oral-oral contact with an infected person.
They both only infect humans.

Thus, both cannot be controlled through killing any vector.

The best way to prevent Cholera is to avoid potentially contaminated food and water and follow proper sanitation practices.

The best way to prevent polio is through immunisation via vaccines.

For more information:

Cholera

Poliomyelitis


Backcrossing in Hybrid Can anyone help me in understanding how backcrossing helps hybrid to achieve pureline?

I have been looking into the references i possess but couldn't seem to find anything

Back crossing is the process by which a hybrid organism is crossed back (backcrossed) into a pure organism. Let's see an example

Organism 1 is heterozygous for a single gene (e.g. a hybrid), which has alleles that we can call $A$ and $a$. We can write that organism's genotype.

Organism 1 Genotype: $Aa$  (100% chance)

Right now, there is a 0% chance that organism 1's genotype is $AA$.

Goal: increase probability that organism 1's genotype is $AA$

One way to achieve this goal is to cross Organism 1 with another organism, let's call it Organsm 2, that is has a homozygous (e.g pure) genotype of $AA$.

So if Organism 1 is crossed with Organism 2 and produces a new Organism 3 what is its genotype? Well, we're not sure.

Organism 3 Genotype: $AA$  (50% chance)

Organism 3 Genotype: $Aa$  (50% chance)

Now we do the same thing again, to get Organism 4

Organism 4 Genotype: $AA$ (75% chance)

Organism 4 Genotype: $Aa$ (25% chance).

This effect keeps compounding, until there is a very high chance that the final organism has a pure (e.g. $AA$) genotype.


Does it make sense to make my own DNA copy (kind of backup) while I am young? As I understand, when I am getting older DNA becomes more and more damaged in my body.

Does it make sense to make my own DNA copy (kind of backup) while I am young (38 years old or for my kids) in case that in future there will be the technology which will make possible to restore damaged DNA from this copy and make me younger?

Or it does not make sense, because original not damaged DNA always can be found in some places of my body?

If it makes sense, what is the best way to do this DNA backup? Cut a piece of hair or nails or freeze a piece of saliva?

While your DNA gets damaged, not every single cell will have the same damage.  Your consensus DNA sequence will not change.


Can you knockout a gene specifically in the dorsal root ganglion in adult mammals? Since the dorsal root ganglion is so small, would that be easier than the entire body?

It requires two genetic constructs to create a conditional KO organism. One parent with a transgene that expresses a DNA recombinase (such as Cre) after the promoter of a gene that is ONLY expressed in your tissue of interest. The other parent contains a modified gene of interest to be removed in the presence of said DNA recombinase but is fully functional otherwise.

Therefore, the ability to target a Knockout to a specific tissue is dependent on identifying a gene that is only expressed in the tissue of interest.

It is actually easier to create a whole animal KO, but because gene products can have different functions temporally in development and in different tissues, a whole animal KO may be lethal, whereas removing it in a specific tissue may not be and allows study of the effects of said removal.

Thus, if your gene of interest were lethal when removed from whole organism, AND you know of a gene that is only expressed in the DRG, you would have incentive to see if a CKO animal could be made.

A brief search on Cre Lox technology will bring up 1000's of images and articles.
Here is one and a nice illustration:


Can rigor mortis change the anatomical position in which a person died? I've been told as an undergrad in anthropology that the flexed position of the body in which some Neanderthal skeletons were found indicates that they were deliberately buried. Apart from the good preservation of the remains, one of the arguments for deliberate burial was that if the individual had died in this very flexed position during sleep, rigor mortis or post-mortem bloating would have caused the body, if not already buried, to extend (see e.g. Villa's [1989:325] comments to Gargett 1989). Barring sudden death by rockfall and ceiling collapse, this suggests that the body was completely buried before rigor mortis set in, or was deliberately placed in this sleeping position after rigor mortis faded by those that buried it.

But I thought I had heard in a biology course that rigor mortis stiffens the muscles, but does not contract them (see e.g. Faux et al. 2006). If someone died during sleep, could rigor mortis really straighten a highly flexed death position?

Rigor mortis does not cause movement. It causes rigor (Latin for stiffness.)

This is only a comparison, but think of it this way. Superglue doesn't shrink or change the shape of the connection of the two things glued together; it just holds them there with powerful 'stiffness'. So imagine that at death, part of our muscle cells exuded superglue. You would get stiff (the muscle to bone/fascia connections would not change) but you would not move. Immediately after death, some muscles relax; most obviously the eyelids open partially, the mouth, hands, and sphincters relax (you won't have to pry a gold coin from someone's dead hands like in the movies.) But aside from general relaxation, you very closely stay in the position you were in when you die.

Physiologically, this is roughly how muscles work: muscle cells are filled with filaments, actin and myosin (I'm leaving out tropomyosin and  troponin for brevity.) Contraction occurs when the myosin can bind to the actin, break the bond and reform it on the next spot on actin, and repeat, like crawling along the actin. ATP and Calcium ions are necessary for this crawling movement. In death, ATP is quickly depleted (aerobically then anaerobically), whereas Calcium floods the cell, and the bonds within each muscle cell which were formed when death occurred become stable. The muscle does not contract any more; it just stiffens. But since stiffening requires contraction in life, it's called contraction in death.

As a parallel, touch your fist to your shoulder. Without resistance, there is some contraction there. Now keep it there while someone tries to move it; that requires much more forceful contraction, but the position of your arm doesn't change (remember, you're keeping your fist to your shoulder.) All this is thanks to the number and stability of those tiny bonds between actin and myosin. Those tiny bonds develop and stabilize in death. But they don't last forever, hence rigor reverses.

Rigor mortis has been studied extensively for an astonishing number of reasons including forensic studies and how it affects the meat we eat.

I have seen a lot of death; one of my duties was to "pronounce" people dead. Sometimes when someone died during the night in a nursing home, a nurse would wait until morning to call - what difference did it make, anyway? - and I saw bodies in rigor. They were not all drawn up as in a fetal position. The nurses would usually straighten the patients out before rigor set in to make it more dignified and easier to transport the patient. If rigor caused movement, they wouldn't be straightened yet stiff  (rigor is something one needs to document, as is lividity.)

Rigor Mortis


Humans best at long distance running: purely physiological or is it a function also of ability to pace? I have read that although certainly other land animals are much faster over short distances, a human can run down any other animal over time, so that if a human is hunting like a gazelle, etc. eventually the human will catch up. I am wondering if this is purely a physical thing or if humans, knowing how to pace themselves, avoid exhaustion while the gazelle just runs as fast as it can and then collapses -- is it possibly because humans are smarter that they are better long-distance runners? (Now, some birds are able to fly for thousands of miles and I guess also in water we can't compete.)
EDIT: I understand that humans have some physical attributes that contribute to their long-distance abilities but is the ability to understand pacing also part of it?

I would argue that the two factors of physiology and pacing are essentially one in the same. A huge component of pacing for distance runners is breath control. This requires indepndent control over breathing while simultaneously maintaing runnning form, which is simply not an option for most quadrapeds.
This stock photo of two gazelle in sprint illustrates why. With each bound, a gazelle's torso compresses (left) and then expands (right) in sync with it's running motion. That compression forces air from the animal's lungs, syncing the rate of breathing with it's rate of running. Because of this, they cannot control their rate of breathing control without also changing their step rate.

The fact that people can learn from coaches and books to get better at pacing suggests there is a cognitave aspect to it, but it's the physiology of bipedal locomotion that allows for more efficient pacing in the first place. It's not easy to separate the two factors in a scientific (non-speculative) way, since we can't train an animal to do something that it's not physiologically capable of doing.
There are some interesting discussions here about the Iditorod, which I imagine involes some amount of the human driver pacing the sled-dog team.


Can we knock out Caspase-9 *and* avoid breast cancer phenotype in our mouse model? I am trying to design a wet lab experiment with no wet lab experience to name.

Right now, in my dream land, it would be excellent if it were possible to create a Caspase-9 knockout mouse (damage to the Caspase-9 gene is associated with the development of breast cancer), and somehow be able to control the development of the breast cancer phenotype, so I can create a Caspase-9 KO control as well as a non Caspase-9 control group. In total, I would love to have the following control groups:

1. Normal mouse - normal Caspase9 gene, no breast cancer phenotype
2. Caspase9 KO mouse - no breast cancer phenotype
3. Caspase9 KO mouse - breast cancer phenotype

Can anyone help me answer whether or not group 2 above is possible? Can you direct me to any papers, any experiments, where this has been done before, or has been tried below and failed?

Here is a paper that talks about the association of Caspase-9 with breast cancer development: http://breast-cancer-research.com/content/pdf/s13058-014-0443-5.pdf. Caspase-9 is a type 2 member of the Caspase protein family. When I talk of the "Caspase-9 gene", I'm talking about the DNA which codes for these cellular apoptosis susceptibility 9 (Caspase-9) proteins. This isn't my area of expertise, but this is what I currently understand.

The short answer is that it is likely a bad experiment; being that it would be expensive and is not likely to provide useful new information.

The long answer (i.e. why) is identifying an interesting target gene (e.g. caspase-9 in breast cancer) is only the first step, and considerable study of what is already known is required before planning an experiment (especially an expensive one that requires numerous mice).

Caspase-9 is a critical effector of apoptosis through the mitochondrial pathway. Many different signals such as DNA damage, Endoplasmic reticulum stress, etc induce cells to die through this pathway. This is important both in normal development and in preventing cancer. Homozygous deletion of caspase-9 is lethal, the mice will not live to adulthood. (http://www.ncbi.nlm.nih.gov/books/NBK6153/) A conditional knock-out of caspase-9 in breast cancer cells would be needed, not a global deletion.

Furthermore, the given the known functions of caspase-9 this experiment is not likely to provide interesting new information. This pathway is well characterized and known to play an important role in cancer (Resisting cell death; a hallmark of cancer: http://www.cell.com/abstract/S0092-8674(11)00127-9 ) Loss of caspase-9 activity makes cells resistant to apoptotic signals through the mitochondrial pathway(they won't die when they receive these "suicide" signals). This allows mutant cells to survive when they should otherwise die. Cancer cells can also become resistant to this pathway through other means (such as the up regulation of anti-apoptotic Bcl-2 family members.

Many scientists are already studying how to restore normal function of this pathways in various cancers; what do you hope to learn by breaking it that isn't already known (I'm not saying that there couldn't be a good reason, but if you don't have one, you shouldn't do it.)


How animals know which is carnivorous and herbivorous? Deer ran away from tiger or cheetah, but not from giraffe or zebra.
where did deer learn this?

How animals know which is carnivorous and herbivorous?

They probably don't know and probably don't need to. They tend to run away from potential danger and predators in the same evolution environment because those who don't run away will have fewer offsprings that exhibit similar behaviors.

If an animal suddenly sees a predator that his ancestor has never seen before, then it may not run away from it, to its own detriment. Dodo Bird thought humans were harmless.


Was mammal body better suited for some type of the marine environment than the body of fish? When some of the land mammals came back to the oceans, they seem to be successful in the competition with fish at least in some environment even though they seem to have a huge disadvantage in the need of breathing above the water. So how did they succeed in the competition with fish?

By asking So how did they succeed in the competition with fish? you are making the false assumption that they had somehow to succeed at some form of competition. What lead you to this false assumption is I think either of the following two mistakes..

A misunderstanding of the principle of competitive exclusion.
A false assumption about the existing overlap between marine mammals ecological niche and fishes ecological niches

Competitive exclusion

The principle of competitive exclusion states that two species occupying exactly the same ecological niche cannot stably coexist. One must either become extinct or shifts its ecological niche (process that is known as character displacement).

A consequence of the above is that if two species have ecological niches that partially overlap, they can still stably co-exist.

Ecological niche of marine mammals

There are two independent lineages of mammals that evolve marine life (cetacea and sirenia). I don't know which one you have in mind when asking the question and a sensitive complete answer would depend on the lineage of interest. However, in any case, there is such a diversity of ecological niches in fishes that it is hard to really fully address the question.

Marine mammals occupy different ecological niches. There is no question of whether one has an advantage over the other as the species do not compete for the same ressources.

A typically important reason for why marine mammals and most fishes occupy different ecological niches relate to their size differences. Simply put, mammals to be quite big! For example a orca eat fishes (and other things) that had few predators before. There is therefore not much competition involved.

Just to reiterate... in your comment you say so the main advantage was the size?. Size was one of the biggest reason why they would be able to occupy previously unoccupied ecological niches. But it is not an advantage toward competition with fishes as you seem to be thinking as there probably little competition.


bacterial cell wall degradation in humans can human degrade the D-amino acid present in bacterial cell wall, I'm confused about it i have read somewhere that human can do so.If yes than why we need antibiotic to kill bacteria???If it is not so than why??

Humans have at least one enzyme which can break down D-amino acids, the D-amino acid oxidase (DAAO). They are able to break down these amoino acids, interestingly D-serine seems to play a role as a neurotransmitter. For more information have a look at these papers:

Physiological functions of D-amino acid oxidases: from yeast to
humans.
Human D-amino acid oxidase: an update and review.
d-Amino-Acid oxidase and its physiological function

We still need antibiotics, since only a small part of the bacterial cell wall is composed of D-amino acids. The cell wall is made of monomers from N-acetylglucosamine and N-acetylmuramic acid which are crosslinked by small peptides (these are short amino acids chains) to form the peptidoglycane polymer. A part of the amino acids in the crosslinking peptides are D-amino acids. I am not sure if the DAAO is able to attack these peptides in the polymer. Additionally most of the enzyme in the human body is present in liver and kidney, indicating that it breaks down D-amino acids that are transported there by the bloodstream.


Comparing the amount of domestic animals and wild animals? From some material, I read about the ammonia (NH3) emission from animal waste.

I found that the emission from domestic animals are greater than wild animals.

Then, I can't help wondering the amount of wild animals and domestic animals(cow, pig, chicken, etc). Which has the greater amount on Earth? And how to estimate the amount approximately?

And how to estimate the amount approximately?

You cannot. Most of the earth is water, and fauna diversity is highest in water. We are still tagging and tracking the movement and reproduction cycles of animals, and that is a never ending task. I say we cannot reach an accurate approximation because of how these projects work. They are targeted towards the monitoring of specific species. Next, different countries have different approaches towards conservation of the same species, and above all this many countries choose not to report numbers. The example which comes to mind is the Red panda. As many animals come inside the radar of active conservation efforts, even more remain outside it.

In fact, some time ago I read a compelling article about why the WWF should change their logo to a Red panda (or known as the lesser panda) rather than the giant panda, the argument being that awareness about the giant panda is very high while red pandas are still misunderstood as pandas. Unfortunately I cannot find that article now, but you can visit the red panda network to find out more.

  Which has the greater amount on Earth?

Second, what do you consider as a wild animal? are insects included? are gutter rats included? Is the infestation of wild boars near the now defunct Fukushima plant included? If yes then they outnumber domesticated animals by a long shot. I would dare to say that cities are habitats more for members belonging to Animalia but not belonging to Homo.


Do all prokaryotes have ATP synthases and an electron transport chain? I was looking this up and I'm wondering if so far I'm correct about the following:

For the most part eukaryotes do aerobic respiration, which involves glycolysis, the Krebs cycle and oxidative phosphorylation involving ATP synthase and an ETC
Prokaryotes can either do aerobic respiration, anaerobic respiration or fermentation, the first two of which require an ETC and ATP synthases, which would be located in the plasma membrane of the prokaryote

If that is the case, I was wondering if there are prokaryotes that only do fermentation, and if so do they have ATP synthases and an ETC? In other words, are there any organisms without ATP synthases and an ETC (which would force them to survive on fermentation alone, unless there is some other method of energy production in prokaryotes that doesn't use ATP synthases and an ETC that I'm missing)?

Thanks

This is an interesting question (I really mean this — see below), for which a straight answer is remarkably difficult to find on the web. When I googled for it I got pages with statements that obligate anaerobic bacteria still had the electron transport chain (ETC) and ATP synthase as there were different electron acceptors other than oxygen. Yes, we know that things are different in thermal vents and hot springs, but what about gas gangrene? I am not a microbiologist, but I did play with the metabolism of some bacteria for a biochemical bioinformatics lab some years ago, so I can give two instances where anaerobic bacteria appear to lack either the ETC or both the ETC and ATP synthase.

Clostridium perfringens

This is the anaerobic fermenting bacterium that leads to gas gangrene in infected wounds and was a major cause of limb loss and mortality in the First World War. The DNA sequence of Clostridium perfringens has been determined. I quote at length from the paper as it describes the fermentation, but italicise the key statement for those who wish to skip this:

  We could not find any genes coding for tricarboxylic acid (TCA) cycle- or respiratory-chain-related proteins, in contrast to C. acetobutylicum, which has incomplete TCA cycle enzymes. Similar to C. acetobutylicum, we could construct a pathway map for anaerobic fermentation resulting in the production of lactate, alcohol, acetate, and butyrate, all of which have been commonly detected in C. perfringens cultures. In the fermentation pathway, pyruvate is converted into acetyl-CoA by pyruvate-ferredoxin oxidoreductase (CPE2061), producing CO2 gas and reduced ferredoxin. Electrons from the reduced ferredoxin are transferred to protons by hydrogenase (CPE2346), resulting in the formation of hydrogen molecules (H2) that are released from the cell together with CO2.

The related bacterium, Clostridium acetobutylicum, mentioned in the extract, is also an obligate anaerobe. (It ferments a variety of plant mono- and poly-saccharides to acetone, butanol and ethanol — used to produce explosives in the First World War.) Although it has some enzymes of the TCA-cycle, it is unable to use the cycle oxidatively, and, like Clostridium perifringens, lacks the enzymes of the electron transport chain and an ATP synthase.

Ureaplasma urealyticum (Ureaplasma parvum)

This micro-organism is a micoplasma (Mollicute) rather than a bacterium — i.e. it lacks a cell wall. It infects the human urogenital tract. It lacks the components of an electron transport chain but does possess a functional ATP synthase. It generates a hydrogen ion gradient, not by increasing the hydrogen ion concentration within the inter-membrane space by the oxidation of NADH in the ETC, but by reducing the intracellular hydrogen ion concentration by generating ammonia from urea (plentiful in its habitat) in a reaction catalysed by the urease it encodes. The sequence of the organism and references to previous work on its urease activity can be found here.

Evolutionary considerations

The reason I find this question interesting is that anaerobic organisms preceded aerobic organisms, so the question arises whether there are any contemporary anaerobic bacteria that have evolved from these primaeval anaerobes and have never possessed an electron transport system — or are all contemporary anaerobic organisms lacking an ETC derived from organisms with an ETC (aerobic or using some other electron acceptor) and have just lost these functions through non-use (as is most likely in the examples above)? This question must surely have been considered by those in the field.


Will wiping a phone down with isopropyl alcohol daily breed bacteria resistant to disinfectants? The title says it all. If you disinfect something more regularly, aren't you just selecting for bacteria which are most robust to that method of disinfection? I've heard it said about some medications that they "can't cause antibacterial resistance". In particular I've read that this is claimed about topical benzoyl peroxide in the context of skincare. Do these claims have any weight to them?

It is possible to select bacteria in vitro, with some help, to withstand 50 g/L (5% v/v) of isopropanol.   According to this paper, bacteria at hospitals in Peru have a variable but increased resistance to isopropanol.  (That study was preliminary, however)  Since bacteria can produce isopropanol themselves, some degree of resistance is very plausible.  Even so, the fundamental nature of 70% isopropanol's attack on the membrane makes it hard to defeat.  Anything is possible in biology, but the more proper the application of disinfectant in terms of exposure time and concentration, the less plausible the selection of resistant species or strains from the bacterial community will become.


When was the last common ancestor of pig and human? Some religions regard pigs as unclean on the grounds that pig flesh is closest in composition to human flesh. I don't believe this for one instant, but it got me thinking, just how close is pig and human on the evolutionary tree?

Last common ancestor is about 97.5 Million Years Ago.

TimeTree.org Pig vs. Human

That being said, they are close enough to us that they are a vector for influenza viruses that are able to make the jump to human pretty easily.

Also we use their tissue as a homologue for human in forensic research. We also use valves from pig hearts to replace defective human valves.

This Nature News Article reviews some of the work being done with Pig to Human Tissue Transplantation. Though granted the methods they are looking at rely heavily on targeted gene editing.


short-day facultative plant, abrupt change to photo period What happens biologically to a short-day facultative plant that is a few weeks into its short day (flowering) photo period and is suddenly given a 24 hour period of light? Does anything change biologically after one day of long day (vegetative light) or  will it take several days?

If there is any biological change that is of concern what can one do to try and alleviate any negative affects?

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

There is nothing you can do to alleviate the effects of (presumably) gro lights being left on for a 24 hour period. It's not likely to have a particularly dramatic effect on a short day facultative plant, other than to possibly delay flowering - it may mean the plant has to go through an extra period of darkness at nights for a longer time, in other words, the process of flower induction may need to start all over again. Or, as it was just one night, you might get away with it and they'll flower when you expected them to. The biggest interruption in the flowering process of a short day plant is a few minutes light in the middle of a period of darkness over successive nights, but either way, it's not possible to offset that 24 hour period of light in any way. I'm afraid you'll just have to wait and see, but in the meantime, maintain the growing routine with regard to lighting.


How can sodium and potassium from burned organic matter (ashes) reenter the ecosystem? If you thoroughly burn something you end up with bunch of oxides and hydroxides, as far as I know.

Sodium and potassium hydroxides are plentiful in ashes, which is why lye was created by soaking ashes in water. Lye is not exactly nice to organisms.

So the question is, how can caustic lye ever reenter the ecosystem as potassium. If it cannot, does that mean that nature cannot renew it's potassium content?

Wood ash is commonly used as a fertilizer. It acts this way in natural burning ecosystems also, where the ash from burned plants fertilizes the growth of new plants and those that survive the wildfires.

The primary constituents of wood ash are calcium and potassium salts. Lye is extracted from these salts by extracting them in water; the hydroxide salts are more soluble so the other salts are left in lower concentration than the original ash.

However, when in solution, KOH isn't really a thing anymore: you just have potassium and hydroxide ions floating around separately. Nothing special needs to be done to separate the potassium from the hydroxide ion except dissolving in water. Neutralizing the solution is then just a matter of adding an acid. There are plenty of sources of acid in soil, and rain itself tends to bring acidity. One of the sources of acidity in rain is, in fact, from fires. It is not as strong as the 'acid rain' caused by industrial sources, but there is no magic in fire that causes basic chemicals to be left behind without producing acid ones elsewhere.

The main damaging effects of wood ash are if it is applied in high concentrations where it can directly enter water sources (see for example UGA extension). In this case, it can raise pH enough to be damaging to life. Large quantities from large fires can also raise pH substantially in streams and such (see for example Burton, C. A., Hoefen, T. M., Plumlee, G. S., Baumberger, K. L., Backlin, A. R., Gallegos, E., & Fisher, R. N. (2016). Trace elements in stormflow, ash, and burned soil following the 2009 Station Fire in Southern California. PloS one, 11(5), e0153372.).

Eventually, however, there are enough sources of acid in the environment that there is no way the salts are permanently alkaline from the perspective of the whole environment.


How do I create a probe for in situ hybridization? I tried to make the probe several times but it failed again and again. It usually turns out that the probe after hydrolysis is very very short (maybe around 50nt). I did not check the RNA before hydrolysis except last time. However, I saw a band (though very weak) last time, but it still produce very very short probe after hydrolysis.I use Sp6 polymerase to synthesize RNA, and the original length of the DNA is 1.5kb. My expected length after hydrolysis is 500nt.

I'm guessing maybe it's the phenol contamination of the phenol:chloroform extraction step because my 260/280 value is low (around 1.6-1.7), and my 260/230 is also low, which is like 1.6-1.8. Also the peak is not at 260, it's almost at 270.

I dont understand what you mean by hydrolysis in this context.

The way to go about is:

Clone the DNA, that will give rise to the probe, downstream of T7 (or any other) promoter
Linearize this plasmid by digesting at (or ahead of) the 3' of cloning site
Set up an In-vitro Transcription reaction with T7 polymerase (or whatever corresponds to the promoter you used)
Precipitate and purify the RNA (you can use DNAseI to get rid of the DNA).
To check the RNA size: mix ~2$\mu$l of RNA (less or more depending on your yield) with equal volume of 2x RNA loading dye (contains formamide 95%, EDTA, SDS, and the dyes).
Heat at 85⁰C for 5min. Let it cool and run in 1% TAE/TBE-agarose gel (no need to make MOPS-Formaldehyde gel)
dsDNA ladder wont be very accurate but may be used for size estimation (if linear, the mobility of dsDNA and ssDNA/RNA wont be very different. Formamide treatment keeps the RNA linear). Use ssDNA or RNA ladder for better accuracy.

Btw.. the absorbance ratios mentioned are okay.. you don't need an RNA of supreme quality for this application (in fact this suffices for most experiments)


Consumption of NAD+ in glycolysis Out of 10 steps in glycolysis, only one reaction- Glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (PGP), uses NAD+ and thereby producing NADH. Furthermore, this very step is solely responsible for net gain of 2ATP in glycolysis since here phosphorylation occurs without the expenditure of ATP.

Why is NAD+ used only in this step? Is it possible to predict by other information that this is the only step to require NAD+? Is it possible to make this reaction happen without the involvement of NAD(P)+? Is it possible to skip this step and directly produce 3-phosphoglycerate (Lets not worry even if we cannot produce ATP in this process). I am interested in this because, this step necessitates the ferementation for regeneration of NAD+ in anaerobic condition. E. coli produced acetate as a side effect, as expected during anaerobic situations, but also rather unexpectedly during aerobic and high-growth rate situation (acetate-swtich, overflow problem). Production of acetate is unwanted in many industrial applications.

NAD+ is important in this step, since it is co-factor for the glyceraldehyde-3-phosphate dehydrogenase (G3PDH), which acts as a acceptor for the hydrogen atom from the C1 (see below).

If you look at the reaction, the aldehyde from the C1 is oxidized to a carboxylic acid which in a second step is turned into a phosphoester. To do so, a cysteine from the active center of the G3PDH attacks the G3P and forms a hemiacetal. This is oxidized into a thioester, the hydride which is split off in this step is transfered to the NAD+ bound by the G3PDH. In the second step the thioester formed between the enzyme and the G3P is attacked by a molecule of inorganic phosphate to form 1,3-BPG. This step is only made possible by splitting the very energy rich thioester bond. So for this reaction to happen you need both steps, as the formation of an energy rich phosphate ester bond would otherwise not happen. See here for more details.

To go directly from G3P to 3-PG you would need an enzyme which oxidizes the aldehyde group in the G3P. And then you need again an acceptor for the hydrogen which is split off here.


How can frogs tolerate freezing while humans cannot? A wood frog can tolerate the freezing of their blood and other tissues. (wiki, news2), but human beings can not.

Some people plan to freeze their bodies/brains after death, and some of them have done that.

Can wood frogs help us learn how to freeze our brains safely?

Generally frogs are cold blooded animals (more specifically ectothermic or poikilothermic) . Wood frogs can maintain their body temperature by production of cryoprotectants which a human body cannot produce from normal metabolic processes. Such molecules depress the freezing point of tissue and avoid ice formation. Here is a scientific report on the physiology of wood frogs and what helps them survive at freezing temperatures. There are also other mechanisms which cold blooded animals use to survive such conditions.

Now for the human part. Humans are warm blooded (more specifically endothermic). We always try to maintain their body temperature (our normal body temperature is $37^{o}$). That is why we cannot tolerate freezing temperatures, because our physiology does not have a means to avoid cell damage at that temperature. The company which you mentioned uses vitrification methods which uses various artificial cryoprotectants (which wood frog makes naturally).

There is research going on in this direction already. Researchers are using extremophiles and their metabolic products in cosmetics and medicine (like this, this and this).


What are these needle-like plants growing in the ground? I was outside and noticed some strange, needle-like plants growing on the ground. I managed to search for "needlegrass" but couldn't find it.
Here is the photo taken on April 20, 2021 in Long Beach, California; these red circles point at what the strange plants look like:

What you have here is a Filaree/heron's bill/stork's bill (Erodium species). These are widespread in California, being plants of disturbed and unmanaged soils - farms, dunes, roadsides, etc.
Note that I'm not Californian, or even from North America, all I did was google "weed species california" (without the quotes) and hit the first link that looked reputable, then used a small bit of knowledge of plant forms (rosette in this case...) to follow the links inside - and found the species at the link I supplied.


Summary statistic that can distinguish between migration from pop2 to pop1 vs. pop1 to pop2 Given two sister populations that diverged some time ago, say pop2 migrates to pop1 and breeds there, giving offspring with sequence segments similar to those from pop1 but not in pop2. There are stats to find how similar two populations are; for instane, mean dxy takes the average of number of pairwise sequence differences between the two sister populations. Say if there is no migration, mean dxy at a locus of length 10000 is 100. Then with migration, say mean dxy at that locus is 300. Detecting a dxy that's unlikely under the null hypothesis of no migration indicates migration and interbreeding occurred.

I've been thinking for a while on if there are summary statistics which can distinguish between migration from pop2 to pop1 vs. migration from pop1 to pop2 (assuming only one of these events occurs). Do such statistics exist? Without loss of generality assume pop2 members migrate to pop1. Then pop1 will have members that are more similar to pop2 compared to if no migration occurred, but pop2 will be as if no migration occurred.

If we run simulations of a population w/ no migration, we can expect to see some value of pi and # of segregating sites. These measurements may be different in pop1 when pop2 migrates into pop1; some members of pop1 will have SNPs that pop2 do not have, and thus there would be more genetic variation (higher pi and ss) in pop1 compared to its expected pi and ss under no migration. So dxy can say that there's some similarity between pop1 and pop2 that's not expected under null hypothesis, and then pi or ss can say which of the two has a higher genetic variation than expected. Can some statistic that depends on dxy and pi distinguish between migration from pop1 to pop2 vs migration from pop2 to pop1?

Yes, migrants affect patterns of genetic diveristy

Immigrants yield to higher effective population size and therefore higher genetic diversity. They will also affect the site frequency spectrum and I would expect that if the migrants are numerous enough, they would yield to positive Tajima's D.

Therefore, unidirectional migration will definitely yield to differences in patterns of genetic variance among populations (that can be measured by any summary statistic of the site frequency spectrum).

Existing methods for detecting directional selection

I have never had to do such inference so I am not able to do a good review of the existing technics.

You should probably read Slatkin and Maddison 1998 and more importantly Beerli and Felsenstein 2001. Beerli and Felsenstein 2001 has been cited 1,341 times and you should probably quickly see whether some of these papers suggest more recent methods. John Novembre has some very interesting work on how to estimate migration rate between any two populations (e.g. Novembre and Stephens 2008). He might have done something of interest to your problem.

You can always use Approximate Bayesian Computation (ABC;see for example Jeffrey Jensen's work for example of inferences with ABC in population genetics) to figure out what pattern of migration is most likely. With a simple enough model, a good ABC algorithm is not that long (with good computing ressources). The question then is what statistic(s) to use for the rejection algorithm. Again for that, you should have a look at the existing literature to come up with a set of potentially useful statistics.


How long can I store autoclaved disposables and reagents? I want to stock up on autoclaved disposables, such as Eppendorf tubes, pasteur pipettes etc., and some buffers.

If I don't open the container after autoclaving, how long can I store autoclaved materials and consider them still sterile? Does it make a difference if the material is dry or if it is a liquid?

Not really an answer I know, but too long for the comments...

This is still too broad a question.  a well sealed, sterile plastic usually has a use by date, but can probably be used more than a year after you receive it.  But these cases are not usually the issue.

Its sterile medium and chemicals, each of which needs to have their own due date.  LB can be used months after autoclaving, but antibiotics break down chemically in weeks (ampicillin 1000x stocks lose their potency in a month).  Even in the refrigerator Agar plates show colonies after a couple of months and dry out quickly.

So more details would be necessary and the case by case policy is the rule.

added in response to comments

Its really a matter of how well they are sealed. An autoclaved bottle will stay sterile forever, until something gets into the bottle - it depends on how well you have sealed things up and the storage conditions.  For stuff sterilized in lab I would tend to use it within a couple of months. For eppendorfs we'd tend to sterilize a few hundred in a beaker and not worry about them...

Our experiments were working with purified protein were only medium sensitive to bio-contamination; they would be done in a few hours and then sterile filtered again.  If you were purifying RNA for instance you would be much more paranoid I'm sure.

If you start to see contamination I would lower the use date and or improve your protocol.

Plastics that come sterilized and sealed by the manufacturer in 3-5 mil plastic bags have really long use by dates and I've used them for up to a year after we received them.


How many kg of seed can one expect from 230 kg of cotton fiber? So I'm working with data from recent cotton harvest from a seed company. They're more interested in cotton seed than the fiber itself. I'm trying to come up with seed yield numbers for an array of cultivars but the data I was given came in kg of harvested fiber. Excluding any changes between cultivars due to genetics,

Does anyone have an idea of how many kg of cotton seed I can get from a given yield of cotton fiber?

Kind regards,

According to this document (pdf) the rate is around 700 lb seed per 500 lb of fibre.

seed = 1·4 × fibre

230 kg fibre ≅ 320 kg seed

(Strangely, the rate has fallen over time.)


Do we instinctially interpret birdsongs as a sign that there are no predators present? I was outside today thinking how nice it was to hear the birds back from winter when I started thinking about the fact that we like bird song.  It makes us happy in a very basic level, the sort of level that usually implies subtle evolved instincts.  Thus I started wondering, why do humans all over the world naturally love the sound of birds?

The simplest explanation that came to my mind was because birds supposedly will flee or be quite when predators are around.  Thus the presence of birds singing may indirectly mean a lower chance of predation.  In other words it's less that were happy when birds are singing, as that were a little more on edge when they aren't singing.

However, that seems almost too easy an explanation.  Has anyone more intelligent then a random computer geek who's just happy to be away from the computer for a few hours put any more effort into considering this?  What is the generally accepted hypothesis?

Crows and gulls would probably also flee predators but their songs are definitely not really pleasant to listen to! I know it, they woke me up last week-end $\ddot \smile$. The canadian goose or the common starling (see here) are other examples of not really pleasant songs.

Too a selectionist view of evolutionary processes

It is important not to make the mistake to see anything as an adaptation (a result of natural selection only). Evolution is way more than natural selection and it encompasses tons of stochastic processes. This answer has a paragraph on the subject of not thinking of anything as a result of natural selection. This kind of over-consideration of adaptive processes in evolution is a common mistake especially when thinking about how human behaviour evolved.

Evolutionary psychology and evolution of appreciation of bird songs

The field of evolutionary psychology may interest you but note that it is a field that is sometimes still at the limit between psychology, philosophy and biology.

Appreciation of art as a by-product

Appreciation of art (like birds songs) and beauty is a pretty poorly understood subject yet. The first hypotheses came from Darwin and Gould. They pretty much argued that we enjoy sex, grasp facial expressions (kin recognition), have to like logical proof to appreciate learning and acquire language, efficient communication (cooperative hunting), appreciate put oneself into others thoughts (Machiavellian intelligence),  etc... As a result of those selection pressure, we may have evolved, so-called by-products. A by-product is a phenotypic trait that hasn't been directly selected for but that has been  selected via its correlation to some other phenotypic trait that is under positive selection and that is correlated. If this is true, then there would have a correlation between cognitive abilities and art appreciation and therefore a correlation between art appreciation and fitness.

Appreciation of art due to sexual selection

Some have argued that looking at the importance of art appreciation and intelligence in today's mate choice, it is likely that art appreciation may have been reinforced by sexual selection.

Either sexual selection may have reinforced a trait that was correlated to fitness ("evolution of appreciation of art as a by-product" hypothesis).

It is also possible that sexual selection may have selected for art appreciation without art appreciation being correlated with fitness but just because it asks for a big brain and lots of energy (brains consumes lots of energy) and being able to appreciate arts means that the individual has extra-energy to spare and is therefore very fit (handicap principle).


Was Raymond Gosling supervised by Rosalind Franklin? The story of how the structure of DNA was deduced is fairly complicated and controversial, but most parties agree that a key pieces of data was "Photo 51", an X-ray diffraction image of DNA taken by Raymond Gosling in May 1952 (or possibly other similar images taken at the time as part of the same study).
Ray Gosling, who took the photo, was a doctoral student at the time. The Wikipedia page for the photo indicates that he was supervised by Rosalind Franklin, at least for a while:

James Watson was shown the photo by Maurice Wilkins without Rosalind
Franklin's approval or knowledge (although by this time Gosling had
returned to the supervision of Wilkins).

One controversy in the story is that the photo was shown to Watson and Crick without Franklin's knowledge or permission, which should have been sought first as she was his supervisor.
However, this article discussing a 2015 play about the issue (called Photo 51) includes an explanation by Professor Tony North, who was also supervised by Wilkins and shared equipment with Wilkins and Franklin, that:

Wilkins had to know what Gosling was doing, as he rather than Franklin
was his PhD supervisor. Franklin was ineligible for the role because
she did not have a formal university position, but a personal research
fellowship, Professor North said.
“The result is that Maurice had every right to know what Raymond had
been doing and what results he had achieved, so that he had a right to
see photo 51 without seeking Rosalind’s permission,” he said.

A quote from a primary source seems more credible. I also know from experience that other lab members often play a substantial role in training or supervising doctoral students without necessarily having a formal role in their supervision (i.e. being registered as a supervisor).
Was Rosalind Franklin, at any point, formally supervising Raymond Gosling's doctorate?

Well, according to this editorial in Nature:

  Next week marks the 60th anniversary of the publication of the famous Watson and Crick paper — and that of two other papers on DNA that appeared in the same issue. Neither was so high profile, but each was essential to the structure’s discovery. Both were written by scientists at King’s College London: one by Maurice Wilkins and his colleagues Alec Stokes and Herbert Wilson, and the other by Gosling and his PhD supervisor, Rosalind Franklin. (emphasis mine)

There is also a podcast, an interview with Gosling himself (at the age of 86)! The full podcast can be found here: http://www.nature.com/nature/podcast/index-pastcast-2013-04-18.html

Source: Nature 496, 270 (18 April 2013) doi:10.1038/496270a


Why do SRIs help in serotonergic neurotransmission? Serotonin reuptake inhibitors (SRIs) block the action of the serotonin transporter (SERT) which, according to Wikipedia, leads to an increase in serotonergic neurotransmission.

Now this book summarizes serotonergic neurotransmission as follows:

  [The neurotransmitter] binds to specific receptors on the postsynaptic cell, thereby
  generating a postsynaptic electrical signal [...]. The transmitter must then be removed rapidly to
  enable the postsynaptic cell to engage in another cycle of
  neurotransmitter release, binding, and signal generation. [Neurotransmitters are removed by] reuptake into nerve terminals [...].

So my question is the following: If, as stated in the quote, the transmitter must be removed rapidly, shouldn't an increased amount / binding potential of SERT actually be a good thing because if there are more transporters, the process of removing the neurotransmitter is much faster? And consequently, why would blocking the SERTs help in serotonergic neurotransmission? Is it because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell? Or ist there yet another reason?

Excellent question.

Different neurotransmitters operate at different temporal scales (and even the same transmitter can operate at different temporal scales). Examples of the fastest-acting neurotransmitters are glutamate, GABA, and acetylcholine (with the caveat that they can also act more slowly). These neurotransmitters (usually) open ion channels in the postsynaptic cell, and are cleared rapidly after release, which allows for a temporally precise code, with each release event individually important.

Other neurotransmitters are also considered neuromodulators, such as dopamine, serotonin, epinephrine/norepinephrine, and others. While the basic machinery for release is the same, these neuromodulators aren't cleared as fast, bind to g-protein coupled receptors, and their concentrations can build in the synaptic space between neurons when the presynaptic cell fires multiple action potentials in sequence. For these neurotransmitters/neuromodulators, the amount of neurotransmitter sitting around outside the cell acts as a time average of release in the recent past.

SRIs/SSRIs/similar drugs slow down the reuptake process, such that the concentration of serotonin reaches higher levels with the same presynaptic activity.

Although reuptake can also be important to "restock" the presynaptic cell with neurotransmitter for release, there is typically enough precursor around that reuptake is not the only limiting step.

Your suggested reasoning that is closest to the truth is both: "...because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell?" but it isn't that the transmitter "must remain" longer or that reuptake takes place "before" it can bind: it is that if the neurotransmitter remains longer it has a larger integrated effect on the postsynaptic cell.

Lastly, "good thing" is relative - of course increasing SERT activity would help with faster transmission, but faster transmission might not be important/necessary/fit the function of the circuit where serotonergic signalling is involved.


Why are victims of Covid19 being wrapped in plastic? Several articles describe the unique ways Covid-19 patients are being buried.

For example, in this Reuters article about Israel:

  These included decontaminating and hermetically wrapping bodies in
  double layers of polyethylene. For Jewish dead, ritual washing of the
  body would be conducted in one of four special stations in the
  country, the document showed.

And this LA Times article about Iran:

  Nor are they wrapped in traditional white cloth. They are covered in
  hospital plastic, marking them as victims — both young and old — of
  the coronavirus.

People die from viruses all the time but I've never heard of victims being buried in this way. What is unique about Covid-19 ?

The WHO guidelines for VHF victims (Ebola etc.) do say that they should be buried in body bags, and if those are not available, in plastic sheeting.

  If body bags are not available, wrap the body in two
  thickness of cotton cloth and soak with 1:10 bleach
  solution. Then wrap the body in plastic sheeting. Seal the
  wrapping with plastic tape. Spray the body bag as in
  Step 3. Place the body in a coffin if one is available.

Obviously some are treating covid-19 victims with the same amount of caution. I can't tell you at the moment if this is justified or not.


Species-ID: What is this thing attached to my wall (California, USA) I found this thing attached to my wall next to my garden. I live in Simi Valley, California, USA.

At first I thought it was a caterpillar and I left it alone, but after 2 or 3 months I don’t think it is a caterpillar anymore. I touched it today for the first time and it moves. What is it?

This is very likely a chrysalis (or pupa) stage of a lepidopteran.

A similar looking example belongs to the giant swallowtail butterfly (Papilio cresphontes).

 Source: Bill Frank

P. cresphontes is found in southern California [source], so it would not be unreasonable to find it in Simi Valley.


Bolyerine Snakes maxillary bone, split? How is the maxillary bone split in the Bolyerine Snakes described in T.H Frazzetta's "From Hopeful Monsters to Bolyerine Snakes?"

In T. H. Frazzetta, "From Hopeful Monsters to Bolyerine Snakes?" He describes boid snakes on the island of Mauritius as being unique among snakes in that they had a split jaw, connected by a joint. This was said to be an example of how continuous evolution could not be true for all cases, as what is the point of 1/2 of jaw, according to Stephen J Gould.

I dont seem to understand the pictures illustrated in the aritcle though, and how the maxillary bone is split and where it is connected to a joint. I could not find a legible picture of a  Bolyerine Snake described like this, if anyone could help with understanding it with a picture that would be appreciated.

I would provide the pictures, but I am not sure if that counts as plagiarism.

Citation:

Published by: The University of Chicago Press for The American Society of Naturalists,
Available from: http://www.jstor.org/stable/2459073

If you look at Fig. 2 in the paper, the bottom jaw has the split maxillary bone. Do you see how it says "MX" with two lines, instead of "MX" with 1 line on the top skull from Fig. 2? Each of those lines go to part of the split maxilla, with the joint being where it is pinched off (between teeth 5 and 6 on the drawing). There is also a CT image of the skull somewhere online that I've run across a few times (actually saw your question while looking for that image now).

I would also amend your statement a little in that it is not "as what is the point of 1/2 of jaw", it is that you can't have 1/2 of the joint(or split bone) existing. Either the maxilla is 1 piece or it is 2, but you cannot gradually go from 1 bone to 2 (similarly, either the cartilage of the joint exists or it doesn't. There can be a gradual change in how much cartilage there is, but if it's there or not is a binary question).

I hope that helps, off to look for the CT scan!


What enables azacitidine to incorporate into both DNA and RNA? I did a mini-project on the drug azacitidine for my pharmacology class, and I learned that azacitidine has the ability to incorporate into both DNA and RNA. I think this is really unique because a similar drug, decitabine, is exclusively incorporated into DNA. Are there any specific physical/structural characteristics of azacitidine that allow it to affect the structure and function of DNA/RNA? Any help would be greatly appreciated!

If you look at the very beginning of the Wikipedia page, you'll see that azacitidine is an analog of cytidine, the C letter of both DNA and RNA fame. Decitabine is a deoxy derivative, and hence would only be incorporated into deoxyribonucleic acid, or DNA.

Reading further, by structure azacitidine is ribonucleoside derivative, and is preferentially incorporated into RNA. However, it can be metabolized to 5-aza-2′-deoxycytidine-triphosphate and so be incorporated into DNA.


Is once per day the optimal sleep pattern for all mammals? If a typical human body clock is 8 hours sleep, 16 hours awake, interested to know if any mammals have:

a 12 hour body clock (4 hours sleep, 8 hours awake)
a 6 hour body clock (2 hours sleep, 4 hours awake)

And very interested to know if any mammals' sleep patterns are on an "as-needed" basis - i.e. simply sleeping whenever tired, without ever establishing any particular pattern over the days/weeks

So as we know that every mammal needs atleast some amount of sleep or a resting period to perform cognitive functions through out the their day, this however can vary drastically based on the mammal's habits, such as if they are herbivores or carnivores, their place in the food chain (if they are a predator or prey), their habitat, their body size etc.
Starting with humans (to set a point of reference), we ideally need 7-8 hours of sleep in a day. Getting less or more sleep than this ideal can have a lot of different consequences (ranging from feeling tired and foggy to heart conditions and even death). A study performed by a group of researchers to find out the ideal sleep duration in humans showed that just after 14 days the people getting 8 hrs of sleep showed average cognition and a healthy mind, those getting 6 hrs of sleep per day for 14 days showed a similar reaction time to a person with blood alcohol level of 0.1% (which is considered legally drunk in most places), and the group getting 4 hrs of sleep per day for 14 days were tending to fall asleep while performing basic cognitive tasks. This show exactly how important sleep actually is.
Now moving on to some other mammals.
A very commonly discussed example is that of giraffes. Giraffes generally exhibit a cycle of just 2 hrs of sleep per day, and some days they just tend to not sleep at all. A lot of factors contribute to their sleeping habits. Firstly since they are herbivores, and primarily feed on leaves, they need to eat a lot of leaves to get enough energy for their body, having a large body also contributes to this. So, they tend spend about 75% of their day just eating. Other than this since giraffes are prey and a good source of food for lions, they need to stay awake and alert at all times. Sometimes they will take little 10 min long powernaps (this is when they are the most vulnerable, so they don't do it often).
Carnivores however (like lions) sleep a lot more, due to their diets (just like us they feel sleepy after eating) and also since they are minimal risk of being attacked as they are on top of the food chain.
Next lets talk about some sea mammals, they have a hard time trying to snooze because of them being underwater.
Dolphins have very interesting sleep habits as they have to actively come to the surface to breath. Dolphins practice something called "unihemispheric slow-wave sleep", this basically means that they only rest one hemisphere(or side) of their brain at a time(so that they can be awake and asleep at the same time), this is what uni(one) hemispheric(side) means. Slow-wave sleep refers to the deepest phase of sleep, meaning when the one hemisphere is sleeping it is out like a lightbulb. This way dolphins tend to sleep a lot, they have sleep cycle of about 8 hours of sleep a day (resting each hemisphere for 2 hrs at a time). So the dolphins you saw at sea world last year could have been half asleep (literally).
Some birds also practice this uni hemispheric sleep.
I can't think of any animals that sleep "as needed" because activities like sleep and wake are rhythmic and control various hormones and metabolic reactions of the body, this is primarily why we have sleep patterns so that other activities in the body can be done in a habitual manner. This is maintained by our "biological clock", which is the term used to define the natural sleep-wake cycle in animals. The biological clock is regulated by a hormone known as  "melatonin".
So yeah, these were some examples I remembered off the top of my head. I have provided some links to why sleep is important, ideal sleep habits in humans and other mammals and some other stuff for further reading.
Hope this answer helped you understand sleep better.
Sleep: a good investment in health and safety - https://pubmed.ncbi.nlm.nih.gov/19042703/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/
How Animals Sleep - https://www.sleepfoundation.org/animals-and-sleep#:~:text=Giraffes%20need%20less%20sleep%20than,of%2030%20minutes%20per%20day.
Melatonin: what you need to know - https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
This is an animated video series explaining sleep in different animals (highly recommend watching this):
Part 1 - https://www.youtube.com/watch?v=HA1EPRbMMQU
Part 2 - https://www.youtube.com/watch?v=EJzUKsJ-uhA
Part 3 - https://www.youtube.com/watch?v=S4uX2KeEifM
Rare Genetic Mutation Lets Some People Function with Less Sleep (this might also interest you) - https://www.scientificamerican.com/article/genetic-mutation-sleep-less/


Is there such thing as "biological cycles" of activity/performance/etc in mammals? I'm looking for some information about the cycles of increased/decreased activity, mental performance or endurance that are related to a mammal's age and the time of a season.

First of all, I'm not sure what such cycles would be called. I know of circadian rhythm, which is an ~24 hour cycle. The other cycle I've heard about was circa-septan (7 days?). What keywords should I use to search for cycles that may have period of a month to several months?

The second question is - are there are episodes of increased activity/performance over a mammal's lifetime? I can think of two example - mating rituals may involve fighting and hibernation involves almost no movement at all.  Are there additional events that may last more than a month?

The final question is if the age comes into equation of increased/decreased activity. Lets say a younger rat an and older rat are put into the same maze, would their ability to "solve" the maze be related to age?

This question is rather broad. Maybe there are some keywords or a science branch that deals with these questions and I can refine my search?

I appreciate your input!

With regard to episodes of increased activity/performance over a mammal's lifetime, I can add migration to breeding/mating and hibernation or torpor. Birds of course are better known for migration, but some mammals, notably in Africa migrate over an extended time.


Does frequency of eye blinking reveal anything about human biology/nervous system? I'm looking at an output of a single dry sensor EEG headband with the sensor positioned above left eye. As a side effect of it's placement, the device picks up eye blinks, and some eye motion as changes in the amplitude of the raw output waveform. It is clearly visible, and I can probably detect it algorithmically.

My question is - does frequency of eye blinking (not controlled) reveal anything about the state of (autonomous?) nervous system, or processes that take place within the brain? For example, what is the difference between blinking involuntary X times per minute versus Y times per minute for the same individual? Does blinking get suppressed in response to some stimuli, like loud noises, speech, etc?

I appreciate your input!

People avoid looking at what they don't like thinking about.
A feared enemy, an individual whom you have something to hide from..

Avoidance of looking/excessive blinking is a sign of fear.
It's basically a sign that the individual is not having a good time looking at what he is looking.

Sometimes people are lying and then they don't like looking at whom they are lying to... for them it would be nicer to look out the window or something that takes them away from their subject for a bit of time.
I would expect blinking to increase when lying.

Personally I have noticed excessive durational closing of eyes (a second or so), exactly at the moment of stating their lie.
Those are off course people who are honest to themselves but are trying to be dishonest to you. But some people lie to themselves as well and they may be more difficult to detect.


Any examples of animal behavior in response to meteor showers? I just spent two nights observing the Perseids and was wondering whether any animals have been recorded to exhibit unusual behaviour in response to meteor showers.

It is known that some animals change their behavior at night in response to moonlight and artificial illumination (e.g. eagle owls call more frequently at full moon), but I am not aware of any materials indicating behavioral changes in response to short-term lights like those produced by meteor showers or far away lightnings.

Any pointers would be appreciated.

There are a significant number of major meteor showers in the earth's orbit, especially in the Northern Hemisphere. Nocturnal animals have good night vision (obviously) and their acclimation to the dark plus time spent awake at night (if they look up at all) means they see many, many more meteors on average than humans do.

The year's parade starts with the Quadrantid shower.

  January overall has good meteor rates restricted to the last third of the night. Rates to 20/hour can be obtained.

Meteor "showers" (if they can be called that) continue until mid-march, when they drop off to a "very poor" rate of 10/hour or less, continuing this pattern into early June, except for the Lyrids (max: April 22/23) and the Eta Aquariids (max: May 7/8).

  February, March, and April evenings have another notable feature. An unusual number of sporadic fireballs come in this interval, possibly one every few nights.

In the last half of July, we get the Delta Aquariids (July 29/30) and Alpha Capricornids (July 27-28).  Then the Perseids (maximum: August 12/13), rich to our eyes at about 100/hr at their peak, moon and weather permitting.

From September to the first half of December is pretty rich.

  Mid-October to mid-December is a nearly continuous period of heavy meteor activity. The Orionids (max: October 21/22) during the second half of October have a prolonged, plateau maximum for several nights, usually rich. The Taurids (max: October 11 for S. Taurids, November 13/14 for N. Taurids), active for two months, are most numerous in November’s first half, and can be rather variable in strength. This period is the best for a couple of Taurid fireballs each night, if the shower is not too weak. The Leonids of mid-November (max: November 17-19) are quite unpredictable, with rich displays occuring roughly every 33 years.

Finally there's the Geminids of mid-December (max: December 13/14) with "the strongest dependable and observable display" (usually passing 60-70/hour at maximum.)

  Finally, the oft-overlooked Ursids complete the year’s activity, reaching maximum on December 22/23. Nearly half the year’s visual meteor activity is crammed into the two-month interval just described.

What does all this have to do with biology and your question? I'm guessing here that the Perseids, though rich for humans, are probably nothing exciting for animals. The diurnals and crepusculars don't see them at all (they're soundless and certainly not bright enough to wake anyone up). The nocturnals see the (or not, depending on where they're looking) all the time. So a study wouldn't likely detect much, would be challenging to design well, would cost some big bucks, and wouldn't really help humans like studying animal behavior before earthquakes and such.

As a child, I once saw some very funny chicken behavior on my grandmother's farm during a total eclipse of the sun. It was so funny that I remembered it all the years since.

I searched, as I'm sure you did, and the first hit on regular Google was this question. A scholar search brought up possible animal behavioral changes before fireballs.

Major Meteor Showers


What species is this "talking" bird? This YouTube video shows a bird which appears to repeat some sounds (not speech though) after a human. Here're some cropped screenshots from the video:

What species is this bird? Can it actually mimic human speech, or are these sounds in the video its natural sounds?

It is a black-collared starling (Gracupica nigricollis).

According to the title of this other video, which is the same footage uploaded by another user and could be the original one, it has been recorded in Thailand, where the black-collared starling is common.

Also, from the same Wikipedia page:

  In Thailand the collared starling is sometimes kept in captivity and taught to speak.


Is every protein encoded by just one gene? Beadle and Tatum proposed the “one gene, one enzyme” hypothesis in the 1940s, and this was later modified to “one gene, one protein”, i.e. that one gene codes for one protein.

Have any exceptions to this emerged subsequently? Are there single proteins, parts of which are encoded by separate genes?

There are proteins encoded by more than one gene.

It would be a heterodimer protein of quaternary structure. One famous example would be haemaglobin, which is assembled from alpha and beta sub-units.

Also, one gene is capable of coding for multiple proteins!

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

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

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


Is it better to maximize sleep, or align to ~1.5 hr cycles What is better for the body, to sleep 6 hours (4 deep sleep cycles) or to sleep 7 hours, but interrupting the last sleep cycle. I know I feel a lot better with 6, but am curious as to its medical consequences. Does the brain have a chance to repair/clean itself properly with this lesser amount?

Neither
Sleep cycles do not have a set length.

sleep for 7 hours every night and you won't interrupt a sleep cycle. 6 hours may be fine for a person but it is unlikely.

You feel tired when you interrupt a sleep cycle becasue many of the sleep inducing hormones are still present in your system.
http://apsychoserver.psych.arizona.edu/jjbareprints/psyc501a/readings/Carskadon%20Dement%202011.pdf

If you are sleeping different lengths every night (or say sleeping longer on the weekend) that will also make you feel tired. Normally your body adjusts the length of your sleep cycle to how long it predicts you will sleep for, if that is constantly changing however it cannot do this and you often wake up in the middle of a cycle making you feel tired. Sleep the same length of time for ~14 days and you will see your sleep cycle stabilize.

http://journals.sagepub.com/doi/abs/10.1177/1534650103259743

https://www.researchgate.net/profile/Martin_Moore-ede/publication/15765130_Human_Sleep_Its_Duration_and_Organization_Depend_on_its_Circadian_Phase/links/557881b308aeb6d8c01f1715.pdf

http://healthysleep.med.harvard.edu/healthy/science/what/sleep-patterns-rem-nrem


Appropriate Buffer for electerophoresis of DNA & Protein TBE or TAE? Which buffer is best for DNA Electrophoresis and which is best for Protein to be have a sharp bond?

Considering a higher electrical conductivity compared to TAE & TBE and the generation of less heat. If anyone has a particular formulation (add other materials to improve quality) which is obtained as a result of practical experience. I would be grateful if you send me that.

I have had good experience using a lithium boric acid buffer from Faster Better Media. I use it for RNA gels, but it's advertised for DNA gels. I don't think it can do protein, but I've never tried it. I'm not an electrician, but higher conductivity may be the opposite of what you want. The lithium boric acid buffer claims to have less conductivity than a tris based buffer, allowing you turn the voltage up much higher while producing less heat. The higher voltage pushes the DNA down the gel faster, and keeps the bands sharper. My RNA gels take 30 minutes to run, used to take 3 hours. Of course, those slow gels used a MOPS based buffer and formaldehyde to denature the RNA.


Confusion about the brain regions - temporal cortex, hippocampus and and white matter I am a computer scientist working with brain data. I have some data from different brain regions, and the regions are called temporal cortex, parietal cortex, hippocampus and forebrain white matter. I want to show those regions on a brain image in a presentation.

The problem is, when I search the brain images online, I cannot find the regions my data mentions. The regions in the search results are usually called "lobe" rather than "cortex". And when I search for "forebrain white matter", the results are usually about "cerebral white matter". I am totally confused. Here are a few questions:

Are "cortex" and "lobe" the same thing? Or does cortex means gray matter while lobe contains both gray and white matter?
Does hippocampus contain gray and white matter? Or does it reside in the inner side of the temporal lobe, meaning it is in the white matter part of the temporal lobe?
Are "forebrain" and "cerebrum" the same thing?
Why is hippocampus considered part of the temporal lobe although it has the long side of it outside of the temporal lobe?

"Lobe" refers to a section of the cerebral cortex, which is the outer part of the cerebrum. The cerebrum contains several structures, but the one that most people care about is the cerebral cortex, which is the 2-4 mm thick layer on the surface of the cerebrum. The cerebral cortex (or "cortex") is divided into several lobes, e.g. temporal lobe, occipital lobe. So, cortex and lobe are not the same thing, as the lobes subdivisions of the cortex as a whole. (See https://en.wikipedia.org/wiki/Cerebral_cortex)
The hippocampus is a region of the cortex in the temporal lobe. Therefore, it consists of gray matter. However, it is connected to several other structures by white matter (e.g. the fornix), and these structures are related to the hippocampus. (See https://en.wikipedia.org/wiki/Hippocampus#Anatomy)
Forebrain refers to the cerebrum as well as other structures, such as the thalamus and hypothalamus. The forebrain is defined as the telencephalon (which is basically the cerebrum) and the diencephalon (which contains the thalamus and hypothalamus). (See https://en.wikipedia.org/wiki/Forebrain and https://en.wikipedia.org/wiki/Diencephalon)
I don't know what you mean by the temporal cortex having "the long side of it outside the temporal lobe", but the temporal cortex and temporal lobe are basically the same thing.


Evolution of spider webs? Web making seems like a fairly complex behavior built from a pretty strong material.  So how exactly did it evolve? Do we have any clues about what kind of features/behaviors preceded web making and made it possible? Are there any examples of convergent evolution?

I kind of hate using Wikipedia as a reference, but this article offers a general overview of spider evolution...
https://en.wikipedia.org/wiki/Evolution_of_spiders

And this article mentions fungus gnats (and perhaps other species) as examples of convergent evolution...
http://www.mapoflife.org/topics/topic_267_Silk-production-and-use-in-arthropods/

I can't remember with certainty, but I believe some jellyfish (and/or perhaps other marine invertebrates) have sticky tentacles that function somewhat similar to spider webs. In fact, some carnivorous plants have sticky structures that trap prey.


Why are hydathodes called hydathodes and not hydrothodes? I can't seem to find any etymological root for the hyda- in hydathode.  I expected the water-relater structure to be called a hydrothode, but it just isn't!

Dictionaries are your friend.  American heritage says "Greek hudōr, hudat-, water; see wed-1 in the Appendix of Indo-European roots + hodos, way, road."  Merriam-Webster says "International Scientific Vocabulary, from Greek hydat-, hydōr water + hodos road"