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What is the name of the bug that emerging from a wood chip like cocoon?
We found it on the wall of a home at West Palm Beach Florida. Is this a kind of infestation or a sick tree near the house fall on the wall?

That is a bagworm moth, in the family Psychidae. https://en.wikipedia.org/wiki/Bagworm_moth


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The extinction of the passenger pigeon
During the time when the passenger pigeon was hunted down to only captives in the zoo, how could the zoo not maintain a small population and keep the species alive? Why did the population slowly die out? I thought a bird can successfully raise multiple young, given the near perfect conditions in captivity in which the people there are trying to keep them alive?
Just a question I ramdomly thought of, so answers would be appreciated!
Edit: this is not a duplicate. Birds can have multiple young. That will increase the population success rate.

Too small of a population to maintain I believe.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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Can mitochondria become cancerous?
Given that mitochondria have their own DNA and can replicate independently, can they ever become cancerous? For example, could a mutation in their DNA cause them to rapidly replicate, ultimately killing the cell it's in?

Interesting question.
As a prelude, I should probably mention that single celled organisms cannot get cancer as we understand and define it. Mitochondria are not, of course, single celled organisms, they are organelles, but this interesting question involves treating them as if they were autonomous. We'll come back to that later. First, single-celled organisms and cancer...
Of all the hallmarks of cancer, unregulated replication is probably the most fundamental, but all the same, cancer is necessarily a disease of multicellular organisms with differentiated tissues. Bacteria do not get cancer. Protozoa do not get cancer. Yeast do not get cancer. I'm spending too much space on my prelude here, but let's pretend like this isn't an issue and just address unregulated replication. Incidentally, the review I linked is an updated version of the classic review of cancer biology. If you're interested in cancer biology, I highly recommend reading it, and perhaps the original 2000 review.
Ok, now to the question. Let's put aside the problem of a single organelle or single celled organism getting cancer, and consider whether mitochondria can develop mutations in their DNA that cause them to replicate in an unregulated fashion.
Yes, mitochondria do have their own DNA, but they are not fully autonomous.  They do "replicate independently", but what is meant by this is that mitochondria replication (via fission) is a process that occurs independent from the replication (via mitosis) of its enclosing cell. The process is regulated by proteins encoded in the nuclear genome (not the mitochondrial genome)
Both fission and fusion are regulated by dynamin related proteins, which you can read about in this, fairly dense review. The mitochondrial genome encodes very few genes, 14 at last count, and while problems with those genes and proteins are implicated in a few diseases, uncontrolled replication is not one of them.

Hmm, thanks for the detailed response. However, that brings me to ask: if the nuclear DNA regulates mitochondrial replication, then if that  DNA is damaged or mutated, could that result in uncontrolled replication of the mitochondria?

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Why is Cacao a stimulant?
As I write this I've just eaten a fair amount of cacao (not cocoa) powder and it's given me quite a buzz. I've googled the effects and the Internet seems to think it's somehow psychoactive although it's hard to find a reliable source for the details.
Some sites describe the ceremonial preparation of cacao but I'm wondering if someone here knows the actual science behind the effects of cacao.
Can you please help me understand the underlying processes better?

I'm voting to close this question as off-topic because it is not about biology as defined here.

@BryanKrause Seems on topic to me. Is there a known systematic mechanism explaining active compounds in Cacao? TLDR: yes, flavonoids.

@James OP is asking about how to prepare cacao to maximize those effects, not about the biology.

@BryanKrause Good point, I removed that from the question. Hopefully, that should stave off further close votes. OP feel free to roll back if that's your real question.

Cacao and products made from cacao contain a number of bioactive compounds. As far as the subjective sensation of a "buzz", there are three related alkaloids present in cacao that may account for this effect. Theobromine is present in the highest concentration, but is probably less potent of a stimulant. It's not well researched. Theophylline has a number of effects, and is well studied. It has CNS stimulant effects, with a similar mechanism of action to caffeine, as a competitive antagonist at adenosine receptors. Caffeine is also present in cacao. The stimulant effects of caffeine are known generally, but if you'd like to read more about the pharmacology this is a good review.

There are probably over a hundred compounds in cacao that might possibly have effects on humans. I don't want to speculate on the ones that are not known.  One that is known is theobromine.
I have seen a claim that cacao does not actually have caffeine, but I haven't checked it. Cacao might not have theophylline either. The link did not work for me.
no caffeine in cacao
Here is a picture of the structure of adenosine.
.
Here is a picture of the structure of theobromine.
.
Theobromine is kind of similar to a part of adenosine. Adenosine causes your heartbeat to slow etc. There are four known receptors for adenosine which cause different cells to do different things. It's complicated.
what adenosine does
So it's plausible that theobromine might interfere with adenosine attaching to those receptors, and might cause the result you'd get with less adenosine in your bloodstream.
Salsolinol is kind of similar to dopamine. It is created in the human brain and some gets excreted. It might possibly have some use itself and not be a waste product of something that matters. Here's one link from 2006 speculating about that.
salsolinol
The link I gave which appears to show serotonin up to 5% by weight is probably extremely misleading. Other sources have that in micrograms per gram. Serotonin in food is emetic -- you shit it out fast. Likely serotonin in cacao doesn't give you a lot of serotonin in your bloodstream. But it could be worth a better lit search.
serotonin effects


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How does the bear mother ensure her cubs don't escape during hibernation?
I have some questions relating to bears- more specifically, the brown bears we have in Scandinavia.
When they go into hibernation, do they fall asleep as we know falling asleep? If a bear mother brings her cubs into the den, how can she keep track of them? How can she make sure they don't wake up, leave the den and get lost in the snow?

Are you aware that brown bear cubs are born during hibernation? Or are you thinking about subsequent years when they remain with their mother?

Yes Bryan Krause - I'm thinking of the next year, when they go to sleep in the den together.

She probably can't, but a bear that wanders out of the den away from it's mother probably won't be doing much reproduction.  Infant wanderlust will be strongly selected against.

Can you afd sources to back up your answer? It looks like a comment.


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Confused about plant phyla
My kids and I are doing a fun project collecting pictures of life in parks and national parks around us. We are trying to classify what we find down to genus and species.
However, I'm confused about what the plant phyla are. With animals, it is pretty clear (e.g. arthropods, chordates), but I don't understand what they are for plants. I see informal groupings and divisions, but not what phyla.

So I may cite from Wikipedia:

The term phylum was coined in 1866 by Ernst Haeckel from the Greek phylon (φῦλον, "race, stock"), related to phyle (φυλή, "tribe, clan").[4] In plant taxonomy, August W. Eichler (1883) classified plants into five groups named divisions, a term that remains in use today for groups of plants, algae and fungi.[1][5] The definitions of zoological phyla have changed from their origins in the six Linnaean classes and the four embranchements of Georges Cuvier.[6]
Informally, phyla can be thought of as groupings of organisms based on general specialization of body plan.[7] At its most basic, a phylum can be defined in two ways: as a group of organisms with a certain degree of morphological or developmental similarity (the phenetic definition), or a group of organisms with a certain degree of evolutionary relatedness (the phylogenetic definition).[8] Attempting to define a level of the Linnean hierarchy without referring to (evolutionary) relatedness is unsatisfactory, but a phenetic definition is useful when addressing questions of a morphological nature—such as how successful different body plans were.

I recommend reading the full article... It is really well-written

Phyta means plant... The different 'phytae' mark different levels in the taxonomy...
Example:
Streptophyta from the Greek strepto, for twisted, i.e., the morphology of the sperm of some members and phyta (plant), a group including land plants and some algae
Embryophyta - land plants
Tracheophyta - vascular plants (from Ancient Greek τραχεῖα (trakheîa, “windpipe”) + -ophyta)
To answer your question... Phyta is a part of many plant taxonomy levels... It is not one type of plant but it marks the membership of a group to the kingdom of plants.

What I was really wanting to know was what the plant phylums (or phyla) are. My confused brain thought phyta = phyla. So your answer was perfect--it was just that I was asking the wrong question and didn't realize it. I've updated my question to ask what I was really asking.


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Can the natural loss of memory be modeled with a continuous function?
Disclaimer: I have little to no background in biology, so this question is based on anecdotal evidence. I've tried to spell out all of my suppositions, but please let me know if I'm making any leaps I'm not explaining.
Some Context/My biology assumptions
There are some things I can recall very clearly and quickly, other things that are maybe a little fuzzy and take me a second to remember and others still that will feel "on the tip of my tongue" for minutes before I can recall them. And then there are things that I don't remember at all or that I know I knew but can't recall.
To me it seems there's a range of how "clear" or easy a memory is to recall. This clarity and "recallability" seem to decrease over time (assuming I don't use the memory) and it seems there's some minimum clarity/"recallability" that is required for me to recall a memory. Can the clarity and "recallability" of my memories be modeled with a continuous function? And if so...
A (maybe false) Conclusion
According to the Intermediate Value Theorem,

if a continuous function, f, with an interval, [a, b], as its domain, takes values f(a) and f(b) at each end of the interval, then it also takes any value between f(a) and f(b) at some point within the interval."

So if we can model the clarity and "recallability" as continuous functions, and I can perfectly quickly recall a memory at one point and not recall it at all at another, then there should exist times with every flavor in between.
If this is true, would it be true to say that there existed a moment when my clarity/"recallibility" of a memory was high enough for me to recall it should I have chosen to and there is another moment when it wasn't (where these moments are some small distance apart)? Or is my understanding of memory incomplete to where this is all horribly wrong?
To put it in other words, how small can the time be between when you are able to recall something and when you no longer can? And following my logic, could this time be seconds or moments?


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What are the obstacles to modifying an algae to secrete fuel?
I've been reading a bit about algae fuel. It sounds like people did some work and then decided it was too difficult. This link mentions Exxon's work:
https://en.wikipedia.org/wiki/Algae_fuel#Commercial_Viability
And this next link shows the ex-CEO of Exxon talking about how they wanted an algae genetically modified to secrete oil, so they didn't have to kill and harvest it. He then says they encountered a low-level problem with the basic science, but doesn't elaborate.
https://youtu.be/vGv0R3zJ3cc?t=4m26s
Anyone know what that problem was?

If I remember correctly, Solazyme was founded to produce algal biofuel. It turned out that was not cost-effective, so they pivoted to nutraceuticals and the like — which did not save them. Sapphire Energy tried to produce algal biofuel in the Southern Californian desert, in open tanks. They also went bankrupt. If you grow the algae in transparent plastic containers, it's expensive. If you grow the algae in open tanks, your precious algae will be competing with all sorts of microorganisms that happen to find their way into those open tanks.


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I found these in my bathroom and WC
Are they somehow dangerous? What are they and how can I get rid of them?

These are silver fish (Lepisma saccharina) and harmless. Wikipedia says (image taken from the article):

Silverfish are nocturnal insects typically 13–25 mm (0.5–1.0 in)
  long. Their abdomens taper at the end, giving them a fish-like
  appearance. The newly hatched are whitish, but develop a greyish
  hue and metallic shine as they get older. They have two long cerci
  and one terminal filament at the tips of their abdomens; the filament
  projects directly off of the end of their body, between the left and
  right cerci. They also have two small compound eyes, despite other
  members of Zygentoma being completely eyeless, such as the family
  Nicoletiidae.
Like other species in Apterygota, silverfish are completely
  wingless. They have long antennae, and move in a wiggling motion
  that resembles the movement of a fish. This, coupled with their
  appearance and silvery scales, inspires their common name. Silverfish
  typically live for two to eight years. Silverfish are agile runners
  and can outrun most of their predators (including wandering spiders
  and centipedes). However, such running is possible only on horizontal
  surfaces, as they lack any additional appendages, and therefore are
  not fast enough to climb walls at the same speed.[citation needed]
  They also avoid light.

disgusting. They look like cockroaches with their antennas.....


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does being battered build muscle?
My crude understanding of how people normally go about building muscle is something like this following 2 step process:
1) a person can lift weights (for example), which tears muscle and stimulates the nervous system.
2) They can then eat protein and get sleep, which build the muscle back up stronger than it was before, as the nervous system tells the body that more muscle is needed to handle the type of stimulation its been getting.
Now to my question: exotic training techniques like EMS exist which do the same in principle as lifting weights.  What about something as simple as the muscles taking a beating (as in kickboxing)?  If a muscle is battered in a systematic way, will it be built up stronger as per the muscle building process?  If so, what type of muscle would this be (Fast twitch/slow)?  Would it transfer well to overall strength?


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What is the reason behind studying seroprevalence of a disease?
Scientific literature on viral disease, specifically ones like Zika and Dengue, contains seroprevalence data. What is the reason behind understanding seroprevalence?

Seroprevalence tests people for the presence of a disease based on serologic methods. Often you do ELISA (or related methods) to test for pathogen specific antibodies.
This gives you information on how common a disease is, especially when it might infect people without them showing symptoms. It also can help detecting cross-protection when the seroprevalence is lower than expected. This is something shown in micronesia, where the seroprevalence was much lower than expected (from: Zika Virus Seroprevalence, French Polynesia, 2014–2015)

Our findings show that <50% of the population of French Polynesia had
  detectable Zika virus IgG. This seroprevalence rate is much lower than
  the 86% attack rate estimated by Kucharski et al. (14) using a model
  that assumed the French Polynesia population was 100% susceptible to
  Zika virus infection. However, in a setting where DENVs are highly
  prevalent (8), the possibility of cross-protecting immunity preventing
  infection from Zika virus (12,13) cannot be excluded. The attack rate
  and the asymptomatic:symptomatic ratio in French Polynesia were also
  lower than those described for the 2007 outbreak on Yap Island (73%
  and 4:1, respectively) (4); this finding supports the perception that
  the drivers of Zika virus transmission vary depending on geographic
  context. For other flaviviruses, such as DENV, previous model-based
  studies showed that the herd immunity threshold required to block
  viral transmission is ≈50%–85% (15). Thus, if Zika virus has the same
  epidemiologic characteristics as DENV, the seroprevalence rate of 49%
  would not be sufficient to prevent another outbreak.

It can also help to make predictions about the spreading of a disease. With a high seroprevalence epidemic spreading is unlikely, while this is pretty much different with a low prevalence. This is something which was observed in Brazil when Zika occured there first.


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Is this tall, white tree in central Australia a kind of Eucalyptus?
This is near Alice Springs NT, Australia, about -24°S latitude, 550m. Area is arid but it's in a maintained park.
I don't know the exact size, but the photo is hand-held from the ground and clearly the tree is quite tall.
I only have this one photo to work with (it's not mine). I've added some cropped sections of the same original image below for easier viewing.
It reminded me of the tree I saw in the linked video below, which is likely a Eucalyptus considering the koala context.
I don't need an exact species, just confirmation of my genus hunch.
Oh! No koalas were seen in the tree eating leaves at the time, which would have made a "differential diagnosis" easer.

From Koala Bears and Eucalyptus - Periodic Table of Videos at about 02:10 (Sir Poliakoff reminds us a few times in the video (himself as well) that koalas are not "bears"!)

Yes it is a Eucalyptus tree.That's known as a Ghost Gum. (All Eucalyptus' are referred to as Gum Trees) .

Thanks! I can certainly see how it got that name. I also see that Ghost Gum refers to a group of closely related species. Do you also think that this is probably Corymbia aparrerinja?

This tree is ilwempe (Corymbia aparrerinja) or  Ghost Gum. It is endemic to Central Australia where you saw it, and depicted in the paintings of local aboriginal people.
https://en.wikipedia.org/wiki/Corymbia_aparrerinja
Before the 1990's all trees of this form were in the genus Eucalyptus (and usually called gum trees), since then many have been put into the genuses Corymbia and Angophora

Wow, thank you for the new, updated information!

This is Eucalyptus apodophylla, the so called whitebark.
Further information can be found here

I'm not convinced about this ID: Alice Springs is well outside the known distribution of E. apodophylla. See Atlas of Living Australia http://bie.ala.org.au/species/http://id.biodiversity.org.au/node/apni/5194695

The tree stands in a maintained park and not in the wild...

@JulPal that's right, and is a good reminder why adding as much information as possible to a species ID question is important. Next task would be to estimate the age of the tree and the age of the park ;-)

@uhoh have you read the first sentence of the OP? I cite: This is near Alice Springs NT, Australia, about -24°S latitude, 550m. Area is arid but it's in a maintained park.

@JulPal I don't understand; I am the OP, and I wrote that sentence. My point in the comment is that we (or at least I) don't know when the tree started growing there and when this plot first became a maintained park, so we don't know if the tree first grew there by itself and then later a park was built, or if the land was first cultivated and watered, and the tree was then planted there. However, if you are more familliar with Alice Springs, perhaps you can address that specifically?


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What does $g_0$ mean for a centrifuge?
I'm about to make some Graphene Oxide and in the paper for Tour's Method it uses a centrifuge to isolate the solution. However it requires $319g_0$. What does this mean, and will a centrifuge with 3300rpm suffice?
https://www.researchgate.net/publication/234084399_Graphene_oxide_for_effective_radionuclide_removal

$g_0$ is the standard gravity.
You can look up the rpm-equivalent using a nomogram or calculate it yourself.
On some centrifuges you can switch between both. Some vendors provide conversion tables in their centrifuge's manual.


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Why are there few tetrapod dinosaur carnivores?
Today, most big carnivores are quadrupeds. Bears, Tigers, wolves.
During the Jurassic and the Cretaceous, carnivores were mostly bipedal, dinosaurs mostly from the Therapod family.
Why was bipedalism previously a very efficient predator mode for dinosaurs, when evolution could have made some quadruped familes, at least for the 10-400 kilo carnivores? For the Paleogene, there were briefly terror birds, and since then all the major carnivore families have been quadrupeds, and mammals have not evolved dinosaur convergeant evolution towards Therapod body formats. Why not?

A lot of bipedal birds eat fish and many eat rodents and other things.

birds are not parralel evolution of therapods. why is there no parrallel evolution of therapods in the paleogene, and no parellel evolution of wolves, tigers and fast quadrupeds in the cretaceous-jurassic?

This is actually a really good question.  Several large groups of dinosaurs (theropods, most famously) were bipedal, and highly successful at it; while today, very few mammals are bipedal.  What was it about dinosaurs that made bipedalism a successful solution, while mammals typically prefer quadrupedalism?
There were two important differences between the immediate ancestors of dinosaurs and of mammals that made bipedalism more likely in the former, and both are related to lizard tails.
The classic lizard shape puts the center of gravity relatively far back: They have smallish heads, their front limbs don't have much musculature, and they tend to have long, heavy tails. So as soon as they start to accelerate -- which moves the center of gravity further back -- they automatically rear up, like a race-car starting up. In fact, as modern lizards run faster and faster, it's not unusual for them to raise up and basically become temporarily bipedal.  For example, around the 45-second mark in this YouTube video. For a detailed analysis see Why go bipedal? Locomotion and morphology in Australian agamid lizards.
So as a consequence of basic lizard anatomy, they're prone to become bipedal when they accelerate. This could work out relatively well for lizards, because dinosaur ancestors started off with bigger, more powerful tail muscles that could be coopted into muscles for hind limbs.

Bipedalism, when combined with a caudofemoralis musculature, has cursorial advantages because the caudofemoralis provides a greater source of propulsion to the hindlimbs than is generally available to the forelimbs. That cursorial advantage explains the relative abundance of cursorial facultative bipeds and obligate bipeds among fossil diapsids and the relative scarcity of either among mammals. Having lost their caudofemoralis in the Permian, perhaps in the context of adapting to a fossorial lifestyle, the mammalian line has been disinclined towards bipedalism, but, having never lost the caudofemoralis of their ancestors, cursorial avemetatarsalians (bird-line archosaurs) were naturally inclined towards bipedalism.

--The functional origin of dinosaur bipedalism: Cumulative evidence from bipedally inclined reptiles and disinclined mammals
Another argument that has been made is that bipedalism freed up the forelimbs for other uses, but that last reference pooh-poohs that notion in favor of the better transportation concept - though of course they're not mutually exclusive, early dinosaurs could have mainly gone bipedal for transport but have had some impetus from forelimb use that became less important in later species.

Most of the dinosaur predators were derived from a common ancestor. The body plan was efficient, and the theropod predators speciated widely (including birds). But statistically, the number of therapod predators are not independent observations, but linked to each other through ancestry. Similarly, most mammalian predators (Carnivora) are linked to a common ancestor. Both forms worked, but there is not evolutionary pressure to evolve toward a particular form; only pressure to favor successful accidents. So it is an interesting question, but it could be that the predator niche was filled by bipeds in dinosaurs and quadrapeds in mammals.

Because most dinosaurs evolved from bipedal ancestors. Your evolutionary baggage has a huge impact on what adaptations you can develop. Usually organisms only change their form of locomotion drastically when there is very unusual circumstances or a strong and more importantly consistent pressure. The ancestral form for dinosaurs is bipedal, this is lost in several groups but the earliest forms in each group is bipedal. Bipedal is the default. The groups that did go quadrupedal also developed many specializations for herbivory, like chewing teeth, herbivory requires some specialization including a much larger gut so becoming quadrupedal can be an advantage, although even among the herbivores many stay bipedal or hybrid bipedal unless they are very front heavy.  If you are already bipedal there are not many advantages to becoming quadrupedal.
You can look at a large version of illustration here.

Mammals on the other hand have lost several key adaptation that make evolving bipedalism difficult, Mostly the drastic reduction of the tail which shifts mass and muscle forward, but also a weaker ankle and hip structure. The lumbar region of the spine is also a serious weakness for a biped. Most of these features are either holdovers form mammals long evolutionary history as tiny insectivores, during which we lost many features, or in the case of our lumbar region due to our breathing mechanism so they cannot be easily changed either.


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Where can I find resources of the biological processes occurring after death of a mammal at various temperatures?
Using google I usually end with results in cell death. I found some layman articles, but that does not help.
My main interest is the brain part.

I believe William Bass has written on this, probably in the Journal of Forensic Sciences, but no specific articles come to mind. I'd start by looking for his articles, then probably with a variety of search terms using a filter for that journal. It's not open access, so you'll need to use a library or institution that has a subscription.


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What is (roughly) the net charge of the DNA in an average human cell?
I was wondering about what general range for the net charge of DNA in human cells is in Coulombs.  I imagine that kind of thing would be hard to measure but could be approximately calculated/estimated.  Could you approximate it by taking the average number of base pairs in the human genome and multiplying it by the charge of a phosphate group?  Would you have to multiply by two as well because there are two phosphate groups attached to each base pair?

That reasoning seems to work for Harvard's bionumbers database. They use a charge of -2 per base pair, and then estimate the linear charge density as 2e / 0.34 nm, where 0.34 nm is the length of a base pair. There are approximately 3.08 billion base pairs in the human genome, so you could run the same calculation: $2e \cdot 3.08 \cdot 10^9 = 9.86 \cdot 10^{-10} C$.


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What makes the electrical charge inside the neuron more positive at the end of action potential and returns it to resting potential?
When a neuron's stimulated by something, electric potential difference changes immediately and inside of the neuron, becomes more potentially positive than the outside of it.
I've read that sodium-pottasiom pump returns membrane potential back to its resting potential at the end of action potential's process.
How sodium-pottasiom pump returns membrane potential back to its resting potential and makes inside of the neuron more potentially possitive when three sodium ions are transported to the out of the cell and just two potassiom ions are transported back into the cell?
I mean, in this condition, it is expected that inside of the cell is gonna be more potentially negative, not more positive.
(Sodium-pottasiom pump ➡ puts 3 Na+ outside - brings 2 K+ inside ➡ 1 negative charge inside...!??)

The issue is the permeability of the membrane to Potassium and how membrane potential is created in the first place. The resting membrane potential of the neuron is very close to the equilibrium potential of Potassium. Large fixed anions (proteins) in the cytosol are represented in the image below by [An-]:

If Potassium and cytosolic proteins were the only thing inside the cell and the outside were water (ignoring osmotic effects), then in Figure 1 there is an outward K+ concentration gradient.
In Figure 2, we allow the membrane to become permeable to Potassium (as it is in the cell). The Potassium begins to leave [green arrow], but as it does, it begins to create a charge separation that sets up a negative voltage in the cell that pulls the Potassium cation back in [red arrow].
In Figure 3, we see that enough K+ has left the cell to the point that the membrane potential has grown negative enough that the rates of K+ leaving and entering are equal, so no net change in K+ concentration occurs. This is the definition of chemical equilibrium, and so we call this voltage the equilibrium potential of this single-ion system (~-80mV for biologic concentrations of K+).

We could do a similar experiment with Na+ starting high outside in Figure 1, with the arrows reversed, and the equilibrium potential of the Sodium-only system would be ~+60mV.
So, if a real cell has both K+ and Na+ concentration gradients in opposite directions, why don't they just cancel each other out? Why is the resting membrane potential negative, and in fact, much closer to the equilibrium potential for Potassium alone? The answer is: permeability. Imagine if you had Figure 1 again, with [K+] high inside, and [Na+] high outside, as it is in the cell, but in Figure 2 you ONLY made the membrane permeable to K+. Would the Na+ gradient change at all? No, because there would be no pathway for it to move. Thus, if ALL the permeability is for K+, then K+ has all the influence on the membrane potential. If both are equally permeable, it would be their average (-10 mV, or about neutral).
However, the permeability for K+ AT REST is about 20 times the permeability for Na+, so we'd expect the cell's resting potential to be 1/20th of the 140mV "distance" between the equilibrium potentials for K+-only and Na+-only systems, or: -80mV + 1/20(140mV) = -73mV. The fact that it's not exactly -73mV is explained by the existence of a small amount of Cl- and other ion permeability. But, in essence, Potassium determines the resting potential, with a little offset due to sodium permeability.
Now that you understand that, understanding the action potential graph should be easy:

Rising Phase: major increase in Na+ permeability, voltage rises almost to the equilibrium potential of Sodium.
Falling Phase/Undershoot: Na+ permeability shuts down, major increase in K+ permeability, voltage drops back down to equilibrium potential of K+.
Restoration: K+ permeability drops back to normal (not completely shut down), and the Na+/K+ pump just restores the concentration gradients that allow the resting potential in the first place.

So, really, your initial confusion about the electrical work done by the Na+/K+ pump existed because you didn't take it in context with the permeability. Yes, the pump by itself makes the voltage more negative, but some of the potassium it stuffs back into the cell immediately turns around and leaks right back out until it's 95% of the way to its own equilibrium point again, as determined by the membrane permeability.

So do you mean that after action potential some K+ channels are actually open and they allow K+ ions to come inside the neuron, and it is, therefore, returned to resting potential, and the neuron becomes more potentially positive in a way that it neutralizes the activity of Na+/K+ pump?

Yes, sort of. Remember: Without a concentration gradient in the first place, there would never be an electrical gradient. There are two transport proteins which are always on/open, and their actions combined make the resting membrane potential: the Na+/K+ ATPase and ungated K+channels. They perform their function even throughout the duration of the AP. [1/2 - trimmed for length, see next comment]

Neurons and striated muscle have other K+ channels that only open when the voltage gets to about ~0mV, near the end of the rising phase of the AP, and are thus voltage-gated. Their closure is what causes the change in slope during the overshoot phase. Like any other chemical process, the membrane potential then returns asymptotically to what the steady state is when all the voltage-gated channels are closed.[2/2]

But all in all I cannot find out this sentence I've read in lots of books: "Sodium-pottasiom pump returns membrane potential back to its resting potential at the end of action potential's process." It is K+ channels  that does this action NOT Sodium-pottasiom pump, I suppose!

No. As I said in the above comment, It is BOTH the Na/K pump and the non-gated K+ channels that create the steady state (resting) membrane potential. Think of the AP as a disturbance, like a wave in a calm pond. Gravity is what made the water flat before the wave, and gravity will return it to the calm flat state. Gravity didn't stop pulling down on the water's surface while the disturbance occurred. Similarly, the Na/K pump creates the flat line in the above graph, keep trying to create it while the EPSP and voltage-gated disturbance happens, and they are responsible for re-flattening it.

What do we exactly call those special K+ channels?

The "always-on" channels aren't the special ones. They are ubiquitous in the body. The voltage-gated ones are the special ones. They only exists in excitable cells. For a better list of potassium channel types, check Wikipedia

The undershoot or afterhyperpolarization arises due to the increased K+ conductance at the end of the action potential. This is because K+ channels where open during depolarization and it takes some time to close again. Also Na+ channels are inactivated and getting out of this inactivated state also takes time.
So why the potential rises again after this undershoot?
This is because K+ channels start closing and thus the membrane permeability for K+ decreases. This makes the membrane potential increase, until it gets back to the resting potential.
The role of the pump is to maintain the ionic gradients of the neuron helping to maintain this resting potential.


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Getting Started with ELISAs
I'm interested in designing an ELISA to detect the presence of Aflatoxin B1, but I'm having a hard time finding information about designing an enzyme and some sort of guidance on how ELISA protocols are designed, and generally where I can get more information. I'm in Grade 9 and am extremely unexperienced to a lot of the terms I'm coming across, but I'm very interested and would be grateful if anyone has a book or a website I can visit to get started or give me some sort of direction.
Thanks,
Joshua


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Why do neutrophils need to die after pathogen phagocytosis?
From referenced article below, neutrophils need to be removed because its granule contents and oxygen metabolites (used for killing phagocytosed pathogen) are harmful to the surrounding tissue. Thus, the process used for this is that neutrophils undergo apoptosis, then are phagocytosed by macrophages.
However, I do not see why neutrophils need to first die to be phagocytosed by macrophages. Do macrophages not phagocytose living cells?
Source: http://www.sciencebrainwaves.com/the-immune-cell-the-neutrophil-the-good-the-bad-or-the-ugly/

Once the pathogens have been dealt with, and to completely resolve inflammation, neutrophils need to be cleared from the tissue... For removal, neutrophils firstly need to die.

Macrophages can certainly phagocytose living cells, as you can read in Sompayrac's "How the Immune System Works", Chapter 1 and 2, but they do need an "eat me" signal of some kind in order to do it. For a bacterium that might be lipopolysaccharide and mannose. For endogenous cells, there is a balance of "eat me" and "don't eat me" signals. Apoptosis, in addition to neatly packaging up potentially toxic intracellular components, involves downregulating the don't eat me signals and upregulating the eat me signals. Macrophages can phagocytose live cells that seem to have some sort of problem (for example, tumor cells), but they are much more efficient at phagocytosing apoptotic cells.
As far as why the neutrophil has to die, in addition to making them more efficient targets for phagocytosis, they die pretty quickly anyway. There is some debate about the exact length of their life span, but from the time they're released by the bone marrow, the average circulating life span is probably less than 24 hours, regardless of whether they exit the blood stream as part of an inflammatory process or not. The exact function of this short lifespan is the source of some speculation, but we do know that, after being recruited in the inflammatory response, apoptotic neutrophils help suppress that inflammation, playing an important role in regulating the processes that sent them out into the tissue in the first place.
Sompayrac's book is a good overview, but if you want to read the gory details this is a good review.


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What kind of red/green/black, spiny caterpillar is this?
It's red and lime green with black on its back and a few white spots as well. Found in Tulsa, Oklahoma (USA).

Looks like a greenish variant of Hemileuca maia – the Buck Moth, which according to here does occur in Oklahoma. This source also suggests that touching the caterpillar (or its relatives) is a bad idea...

 Source: statebystategardening


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Carbon sink and carbon storage
Articles commonly state examples of carbon sinks are plants, soils, and oceans (e.g., link). My understanding is that carbon sinks must directly take up carbon from the atmosphere. Therefore, other organisms such as herbivores and carnivores are not considered carbon sinks (I understand their roles as carbon sources) although they store much carbon. Is this interpretation true?
If so, what is the main mechanism that soils (independent of plants) directly absorb carbon from the atmosphere? It looks as if most articles simply say that soils contain much carbon from plant organic matters, which is a carbon store rather than a carbon sink.

According to Wikipedia:

A carbon sink is a natural or artificial reservoir that accumulates and stores some carbon-containing chemical compound for an indefinite period.

The key point here is the "indefinite period" part. For example, although my body stores some kg of carbon, I can't qualify as a carbon sink because most of it is likely to be released again in some decades.
On the other hand, soils store large amounts of carbon, and as the soils keep developing that amount tends to grow, making them an effective carbon sink. The mechanism consists mostly on accumulating organic matter, as you say, but as long the amount of that organic matter keeps growing, soil works as a carbon sink.


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Would an h1 Full Agonist Prevent Sleep
According to Wikipedia the h1 receptors stop firing to effectively manage sleep.  Assuming I understand how blocking and non blocking receptors work would a full agonist on the h1 receptors effectively prevent sleep instead of create it.

The histaminergic neurons of the tuberomammillary nucleus become active during the 'wake' cycle, firing at approximately 2 Hz; during slow wave sleep, this firing rate drops to approximately 0.5 Hz. Finally, during REM sleep, histaminergic neurons stop firing altogether. It has been reported that histaminergic neurons have the most wake-selective firing pattern of all known neuronal types.


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Question about vitamin b6 product and cycling
Can the b6-product of a vitamin b6 reaction such as transaminase be recycled back to active vitamin b6 in man, and if so by means of what reaction?


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What do these novel splicing sites mean?
I'm sure that the anwser is obvious for some of you but I just endend my internship where we found novel splice junctions (junctionseq; RNAseq data) (see the attached file) and I have some difficulties with splice junctions.
I understand that reads can map in the junction of 2 exons (which can be linked to quality assesment) and that comparing 2 conditions, we can find groups of exons more "associated" but I dont understand :

How a novel junction can be discovered in a previous junction (sub1), or behind the last exon of a gene (sub2) and thus, what can be the consequence(s)

I think you should explain the graphs a bit more. junctionseq is not a standard method (I have never heard of it before) and showing the read counts of junctions and exons side by side like this (not even indicating the size or type of each elements) is - at least to me - almost confusing. So I can't properly interpret this data for now (without reading up on the details of the methods used, but that's too much work right now)

Can you please explain the diagrams as @Nicolai said?

A splice junction is formed from a pre-mRNA (or primary transcript) whenever an intron is removed, or spliced out.  Two segments of RNA that used to be separated in the pre-mRNA are now ligated to each other, forming a junction of two exons.
RNA-Seq reads that span such a splice junction site would not align very well to the genomic sequence, however if you create a file of all the potential simulated splice junctions there may be some RNA-Seq reads that now align perfectly.
The distinction between what constitutes an intron, and what constitutes an exon is purely empirical.  While it is true that the spliceosomal complex preferentially recognizes and binds to properly juxtaposed splice donor and splice acceptor sites, a variety of different processed, mature, transcripts can result from a single primary transcript.  This differential parsing of the cis-acting sequences at the boundaries of potential introns and exons is called alternative splicing.


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Which extant species has the largest horns?
Among the bovids (cattle, antelope and all member of the Bovidae family): which species has the largest and longest horns? Please answer when including and excluding domesticated livestock and cattle.
I know that the Addax has about 85-110 cm long horns and they seem pretty long, but not as robust as a bull's horns.
Wikipedia writes that Greater Kudu has 120 cm long horns with a record of 187 cm (this figure, however, has a "citation needed" warning).
The extinct bovid Pelorovis had 1 meter horn cores and covered with keratin their length is estimated at 200 cm.
I saw in photos several (live) specimen of specially breaded cattle that had exceptionally big horns but I could not measure them.
For comparison, the longest Triceratops (an horned dinosaur) horns I know of are "Yoshi's Trike" 115 cm long horn cores with estimated total length of 130-150 cm when covered in keratin. However, the horns of Triceratops were thicker and more robust than any extant bovid's horns.

Why do you want to know something like this?

General interest. I am interested in numbers, records and records breakers.

Seems to me more Guinness Book of Records than biology, then, but who am I to judge.


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Identifying a shrub with unusual "many shoots" growth behavior
While recently hiking in the southern mountains of New Hampshire, we came across a plant, and some of them were exhibiting what we interpreted to be a disease, or least unusual growth. On some of the nodes, there were a large number of extra stalks:

On each plant, the number and locations of these things varied, and not all of them had it. And we first assumed it was some ivy, or parasite, or separate plant, but it seemed pretty clear to us that it was coming right from the same branch.
We soon saw there were dead versions of this plant, and all of them had this "extra shoot" variation:

So we reasoned that no matter what this thing was -- natural variation or some kind of disease -- it was killing the plants.
Google image search was no help. It possibly identified the plant as a "viburnum", but was unable to help with the growth.
Anyone know what plant this is, or what this growth behavior is the result of?

Given the location and the harsh weather there, one possibility is that this is a kind of scrubby growth pattern in which the harsh weather kills a portion of the plant and then fresh shoots emerge the next spring.  If you found these in more exposed locations that would be consistent with this idea.

They not in exposed locations - quite the contrary, generally around the trail, underneath a canopy. But something to look up at least!

Based on the poorly-detailed pictures, I'd say it doesn't look like a Viburnum species to me sinply because Viburnums are oppositely arranged. If leaves are somewhat toothed (again, I can't tell), I'd say the leaves remind me of a cherry...

Possibly an example of a "Witch's Broom."

Witch's Broom is a deformity in plants (typically woody species) which typically causes dense patches of stems/shoots to grow from a single point on the plant. The name comes from the broom-like appearance of the stems.1
Witch's broom may be caused by many different types of organisms, including fungi, oomycetes, insects, mistletoe, dwarf mistletoes, mites, nematodes, phytoplasmas, or viruses.2

Sources:
1. Wikipedia
2. Book of the British Countryside. Pub. London : Drive Publications, (1973). p. 519
 Image1. Gardeningknowhow.com
Image2. Iowa state University

Oh awesome, this has got to be it. The Arnold Arboretum (in Boston), has a page which lists common species in my area to be afflicted by this - although it does not seem to include something like what we saw. I'm going to investigate a few more days, but this seems like the likely answer


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can one be infected with Naegleria fowleri by taking Steam?
will Naegleria fowleri be present in the steam molecules.
Many people take steam from hot water to get relief from sinus.
I read somewhere that Naegleria fowleri gets killed over 70 C. So steam will also kill it?

N. fowleri infection can occur after nasal and sinus irrigation, swimming and other exposures to contaminated water. The infectious agent in this case is the trophozoite, not the cyst. Boiling water contaminated with this amoebae kills it, preventing infection. Though it does thrive in warm water (37 C), it doesn't survive in steam (100 C).
Despommier's Parasitic Diseases Ch. 14 discusses N. fowleri in some detail. It's also covered in Murray Medical Microbiology Ch. 82, and Cecil medicine Ch. 360. There's also useful study in The Laryngoscope on the viability of various pathogens in contaminated water after sterilization methods.

To see how these data compare with those obtained in the semiquantitative tests, the ex- posure times for a 99.9% cyst destruction were extrapolated from the survival curves in Fig. 2 and came out as 65, 26, 17, and 3 min at 55, 57, 60, and 65C, respectively.. 3 minutes in 65 degree water might be more severe than 100 degree steam. Note that if the habitat of the bacteria surpasses 65 degrees, the sinus area also is hotter than 65 degrees for 3 minutes.

Ah, this does consider the cyst though, not the trophozoite. My point about inserting boiling hot water/heating your ear up to 65 degree remains valid though.


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Basic questions about human genome project
The "human genome" was sequenced by the Human Genome Project around 2000.  But I don't understand what was done and what its significance is.  Questions:

Wasn't a single person's genome sequenced?  I.e. we have the 3.3 billion base pairs for some individual, right?  So how does that pertain to me since I undoubtedly have different alleles than that person.
Isn't most of our DNA so-called "junk DNA?"  Did the human genome project distinguish the portions that code for proteins from this junk area?
What determines a "gene"?  How do we know where one gene begins and ends, especially given that a gene can comprise up to 2 million base pairs?
Suppose I have the 3.3 billion base pairs for some individual.  What can I do with that information?  Don't I need to know much much more in order to make any use of those data?

We welcome new contributors to SE Biology, but expect them to check out what questions are appropriate on this site, even if they have used other SE sites. This section of the help should make it clear that posters are expected to ask specific questions and show evidence of having researched them themselves before posting. Yours is a set of four basic questions, for which you show no evidence of having consulted the obvious source. I have therefore voted to close.

Okay, a quick answer since I don't have time to go into all the details:
1) As correctly mentioned in the comments already the human genome project had multiple DNA donors, however up 70% of the final genome assembly was from a single person. In order to gt a deeper understanding of the genomic variance in the human population we now have the 1000 genomes project.
2) The fact a such a large portion of the human genome is not gene-coding (the term junk-DNA is not really correct/misleading since quite a bit of it does have unknown or regulatory functions) was not really known before the completion of the human genome project - only after we knew the full genome sequence this became obvious.
3) Genes can either be detected experimentally by doing transcriptome sequencing and comparing the recovered RNA sequences to the genome. This tells us which parts of the genome are in fact transcribed (and includes more than just protein coding genes). It's also possible to find genes just by analysing the genome sequence and looking for open reading frames (in exons), transcription start sites and other known elements. However, this method is only good for finding protein coding genes, other genes (i.e. miRNA or lincRNA) will most likely not be found.
4) Yes, the full genome sequence of an individual alone doesn't tell you anything. In order to get interpretable / useful information out of it you need to compare it with other database sources, such as the SNP-database.

The answer to 1. is wrong: The HGP sequenced a small number of individuals from european descent. Without doing so, they wouldn't have been able to find differences between different allels in the individuals. Celera on the other hand sequenced mostly the DNA of Craig Venter.

@Chris — "The answer to 1…". Quite. The poster has four questions. That is what needs addressing in my opinion. When the answer is a book chapter, people here will provide "quick answers" of limited utility.

@Chris Yep, I didn't check the sources there properly. I edit my answer.


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Any examples of a group of micro-organism that continuously spans two or more species classifications?
Are there any examples of a group of micro-organisms where two different, established species are designated and these two groups meet all aspects of the definition of species (perhaps can not reproduce with each other?), but it turns out that there is a continuous distribution of occurences of this group such that they can reproduce "locally" with nearby members?
I lack the sophistication in biology to know the best possible words to use here so some guidance is welcome, and since the concept of species classification has been around much longer than genome sequencing and analysis, the topic itself draws on concepts from several different centuries.
So I've draw a simple diagram with a 1-D simplified "spectrum" of genetic difference, whereas of course it would likely be multi-dimensional.

I think the biggest problem for this question is that most microorganisms only reproduce asexually (by copying themselves). At that point the definition of where one species ends and the next begins has to be done one either observable characteristics or on a sequence basis. At least for sequence based species classification a 'spectrum' is possible, but then the classical species definition doesn't make sense anymore.

@Nicolai It seems that I've seen too many Gary Larson cartoons; yes of course most do reproduce asexually. I wonder how to proceed — do you think the question is answerable as-is in some way, or should I modify the question? If you can expand on your comment a bit as an answer, that might be enough, especially if you touch on species classification in microorganisms. Or, I could just ask "how was species classification done for microorganisms before DNA sequencing?" separately.

For those who learned about biology sans Larson: (e.g. 1, 2, 3, 4)

@uhoh classification of bacterial species before DNA sequencing relied on morphological, physiological, and ecological characteristics.


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Why do crocodiles have a high concentration of lactic acid in their blood?
Crocodilians have high concentration of lactic acid in their blood. This is the cause that prevents them from prolonged intense activity, since prolonged intense activity causes the muscles to secrete more and more lactic acids, up to the stage where the lactic acid level become lethal - even for the crocodile.
So the shortcomings of high level of lactic acid are clear, it restricts activity and endangers the croc to death.
So why in the first place crocodiles have high level of lactic acid? What is the advantage of this?

Remember that not every evolved trait is advantageous. Some can be maladaptive, brought about by selection for another adaptive trait.

Do you have a reference showing that lactic acid is normally high in the blood of crocodilians? Or is it simply that they can tolerate higher levels of lactic acid? The two are quite different circumstances.

https://en.wikipedia.org/wiki/Lactic_acidosis#Reptiles Reptiles, which rely primarily on anaerobic energy metabolism (glycolysis) for intense movements, can be particularly susceptible to lactic acidosis. In particular, during the capture of large crocodiles, the animals' use of their glycolytic muscles often alter the blood's pH to a point where they are unable to respond to stimuli or move.[19] Cases are recorded in which particularly large crocodiles which put up extreme resistance to capture later died of the resulting pH imbalance.[20]
some reptiles can sleep underwater anaerobically.

As far as I can tell from a brief literature search, the explanation for the high concentration of lactic acid in the blood of crocadilians is two-fold:

The lactic acid is generated from the anaerobic muscular activity involved in capturing their prey.

In a gloss from Science Daily a journalist writes:

Concealed below the water's surface, crocodilians stealthily approach animals that have come to drink, spring upon their prey, and drag them into the water and drown them. This powerful burst of activity generates an extraordinary amount of lactic acid in their muscles…

It is maintained at a relatively high concentration in blood so it can be used to acidify the stomach for the digestion of its meal.

I am less sure about this. Certainly the crocodile needs to acidify the stomach, and the scientific article glossed by the Science Daily shows how the lungs are bypassed to allow carbon dioxide to reach the stomach:

During this period of digestion crocodilians divert blood through a special vessel that bypasses the lung, named the left aorta… …when crocodilians are digesting a meal, they chose to shunt and direct CO2-rich blood straight to the stomach where glands make use of the CO2 to form gastric acid and bicarbonate. Consequently this shunt enables crocodilians to secrete gastric acid at a rate that is approximately 10 times the highest rates measured in mammals.

My supposition is that lactic acid also contributes to the acidity, but I may be wrong on this point. If anyone has information about this, I shall be happy to add it to my answer.


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What characteristics do living organisms (like humans or plants) have that viruses don't?
I am not too sure if viruses are considered living organisms.
I learned that living organism:
-Change their size
-Reproduce
-Heal themselves
-Need energy (by eating)
-React to the environment
-Have a lifespan
-Made of at least 1 cell (some exceptions)
Which features that are listed are not in viruses?
If I need to be more clear, please tell me as I'm not very good at explaining.

@DeNovo Hm the answers to those questions are very helpful. I just would like to know which of the characteristics I've posted are the same characteristics in viruses.

Linving organisms have intricate metabolic pathways that viruses donot have viruses stay in equilibrium till they infect host meaning that they they donot exachange matter and energy with surronding when they are outside the body but is a property shown by humans and living organisms.

Hi Udaya, welcome to BIO.SE! In general, we ask/require that answers provide support (typically through reputable sources + images) for their claims. In this way, we can better ensure more accurate responses. Please update your answer with more details and some reputable sources to avoid having your question closed. Thanks!


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Tree of Life in Text Format
Wondering if there is a tree of life in Text format for open data sharing.

Perhaps not though the tree of life website, but the Open Tree of Life exists to fulfil this need. You can export newicks of nodes which you are interested in.

I don't see how to export, would help if you wouldn't mind explaining.

@LancePollard if you look to the bar on the right hand side you should see a heading called "Download subtree as newick string". For large trees this will take you to the repository, but for smaller subtrees there should be an immediate tool.

Note that such a huge tree will be difficult for most treeviewers; Dendroscope is probably a good bet

The NCBI taxonomy database contains an (as far as I know most complete/up-to-date) database with information about all classified species.
I haven't tested it, but I would guess that its accessible through the E-utilities tools, which will usually allow you to query and download information in xml or raw-text format.
Additionally the whole data the taxonomy database is built on is available on the NCBI ftp-server, they also include readme files so you can figure out how the data is formatted.


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Regarding plant stress
I have to plan a bioinformatic study on a plant. Microarray data is available for various stress treatments (drought, cold, osmotic and flood stress) on root and shoot tissues. I am a bit confused as to which tissue is more important for the perception of stress and its direct effect. I want to start with one of them as of now, since the study will get too complicated with so many stress conditions and tissues. I am not from a botany field and look for some thoughts. Sorry if my question sounds silly.Thanks a lot.

All of them are too multifaceted for such a simple breakdown, imo. Drought stress, for example, can be detected at the root which generates ABA for signalling into the shoot, but can also be mediated by changes in air vapour pressure which provides a signal directly to the leaf.

I know this is not what you want to hear back, but I think you should go with all the samples/replicates at once. Only this way you will have the highest possible statistical power to claim the results that (hopefully) you'll have in the end.
When it comes to microarrays and RNASeq, also, it is important to remember that these are mostly whole-transcriptome techniques, therefore the way they are thought to be used is more like "sequence all > analyze all > fish for specifics" than the opposite.
I would use all of them, feed them to a proper pipeline (there are many, not my duty to suggest you one) and see what has a good score/p-value. If you had something in mind before doing the microarrays you probably would have assessed only a subset of the genes, and not the whole transcriptome. So go for both tissues and see what pops out!


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Is α-keratin a fully functional protein?
Is α-keratin before it coils with another polypeptide, makes chains, and build intermediate filaments a fully functional protein?
I mean, is the single monomer of α-keratin a protein or does it have to become a dimer to become a protein?

This question appears to be answered in the wikipedia article on α-keratin ...

What we call as protein is the final quaternary structure. Whether it is translated from a single gene or from multiple genes (as in haemoglobin), always the structure with all bonds and interactions taken into account. Similarly here the alpha- Keratin forms Disulfide bonds to form a functional protein.


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Abrupt movements of birds and reptiles vs. smooth movements of mammals
How can it be explained (in evolutionary and/or neuronal terms), that the  spontaneous movements of birds and reptiles are seemingly "abrupt" and not so "smooth": Their spontaneous movements seem to start abruptly and end abruptly (while the spontaneous movements of mammals tend to be smoother: starting more slowly, ending more slowly)?

One line of (speculative) reasoning might go like this: Making smooth (= not abrupt) movements is "evolutionary better" (for the muscles and tendons - they don't wear out so fast). But it takes more computational power (= neurons) to perform smooth movements.

My experience with birds and mammals doesn't agree with the dichotomy you present. Can you provide objective data showing the movement patterns you suggest?

No, it's just a subjective impression (which might be backed by data of relative velocities and acceleration).

Exactly. My subjective impression doesn't match yours, so we each have n = 1. How can this question be answered?

Why do you say n = 1? We both have observed hundreds of birds, reptiles and mammals during our life time. (Only the level of exactness (= time resolution) could have been better.)

Rats make rather abrupt movements too. I would expect the difference you observe in movement speed is caused by size more than it is caused by being a bird vs a mammal. But why size would matter?
An increase in the linear dimension $x$ lead to an increase in the cross-section of muscles $x^2$ and an increase in the volume (and hence mass) of $x^3$. The strength of muscles is affected by their cross section $x^2$. Hence as animal grow bigger, the ratio $\frac{x^2}{x^3} = \frac{1}{x}$ becomes smaller and so does their ability to create large acceleration of their body parts. Their movement become smoother and less abrupt.
You might want to have a look at this highly related post too.


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What is a chromosome?
I read the wikipedia article and am confused if a chromosome is the pair of two chromotoids or if each chromatoid is considered a chromosome.
I've heard someone say we have 23 pairs of chromosomes for a total of 46 chromosomes.
I am trying to be precise with my words here.
Even more confusing they always seem to pick this certain state of the chromosoes lifepsan to describe them.
The point at which it replicates to create a pair.
Why not just describe the chromosome before it replicates for simplicity sake.
Would it be correct to say that before the chromosome divides, there are simply 23 of them?

Possible duplicate of Chromosome and chromatid numbers during cell cycle phases

Welcome to Biology.SE! Please let us know if the post I suggested as possible duplicate answered your question(s). If it does not, please let us know why

Possible duplicate of Does common X-like picture represent one doubled chromosome or two homologous chromosomes?

Would it be correct to say that before the chromosome divides, there are simply 23 of them?

No, in a normal, non-dividing cell of the human body there are 46 chromosomes in the cell's nucleus. The 46 chromosomes are separate, but are often considered as 23 pairs of chromosomes.  The two chromosomes of a pair are called homologous chromosomes because they contain very similar, but not quite identical, information.  One member of each pair comes from the mother and one from the father.
Each of these non-dividing chromosomes effectively consists of a single chromatid, but because there is only one, indistinguishable from the chromosome as a whole, it is not talked about.

Why not just describe the chromosome before it replicates for simplicity sake.

It is often described in that form (as one very long molecule of double-helix DNA).  However, a chromosome is also very commonly illustrated in the mid-replication form where it has two chromatids and takes an X-like shape.  One  reason for this is that chromosomes can be seen in a light microscope only in this mid-replication form, and that is the form in which they
were first observed and first shown to be the basis of heredity (long before they were known to be composed of DNA).

Firstly, it's important to understand that this is indeed a very common point of confusion. Tip: don't be thrown off by the color coding, because there are different things you can color-code for. I think what I show below is the minimum picture necessary to understand the difference between a chromosome, pairs of chromosomes, chromatids, and sister chromatids.
Humans have 23 pairs of chromosomes. One originally from the mother, one originally from the father. Chromosomes can be homologous as a single chromatid, or as a paid of chromatids. Let's assume we are looking at chromosome 1 below. It's important to understand that chromosome 1 is BOTH in purple AND in green. We can have a single chromatid chromosome, we can have a pair of single chromatids, and we can also have a pair of chromosomes where each is a pair of chromatids:

As you can see above, we can have 4 chromatids of chromosome 1, or even two copies of two pairs of chromosome 1 (that would be 4 chromosomes; not pictured). I'll explain further.
Crucially, the replication process depends on whether it is mitosis (two diploid daughter cells from one diploid mother cell) or meiosis (four haploid daughter cells from one diploid mother cell) we are talking about. Remember, almost all cells arise from mitosis, except the sex cells, which arise from meiosis.

Best to draw it out and just take a moment to look at it, and compare it side-by-side for a while. It's not that complicated when you start with the knowledge that the imaginary cell below has 3 CHROMOSOMES, OR 3 PAIRS OF CHROMOSOMES (just as we have 23 pairs of chromosomes):

Remember, in this image, 2n=6 (diploid) which means that n=3 (haploid).
In humans, 2n=46, n=23. In other words, we have 23 chromosomes that we keep in pairs (46). To make a mitotic cell division, we have to duplicate what we have (92). Then each daughter takes half of those, and so now each daughter cell is still diploid (46).

In meiosis, it's slightly different. You start with 92 chromatids, of pairs of 23 chromosomes, and first divide them into daughter cells (46 chromatids, but only 23 chromosomes!). In a second division, you remain with 23 chromosomes but all 4 daughter cells have a single chromatid each! Like so:

And then we have fertilization: when sex cells combine their genetic material, the mom chromatid 1 (in egg) and the dad chromatid 1 (in sperm) pair up to create a new chromosome, chromosome 1. n+n=2n! We've made a diploid baby!
Congratulations.


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How much of a DNA difference is between Chicken of the Woods, and Hen of the Woods?
I've noticed that when a COW is touching the ground it turns a gray color, but when on a log/tree it's bright orange. Is there a correlation between the DNA, and where it grows?

I do not understand your question. What is changing color? The grass? The grass is going bright orange when you put a a tree log on it and grey when a cow step on it? Do you mean a change of color that takes a season to happen or is instantaneous? You ask Is there a correlation between the DNA, and where it grows? DNA of what? Are you talking about cows and trees, here? Is this question related to the claims about colors you made above? The title is talking about Chicken and hen but those are absent from your post!

Sorry, title is talking about "chicken of the woods" and "Hen of the woods" (not chicken and hen). And COW is a priori short hand for Chicken of the Woods. So, I suspect you talk about the color of the mushroom. Is your question "Are there genetic predisposition to growing low or high on a tree for a chicken of the woods?" or maybe "Are hen of the woods more likely to grow at low height on trees than chicken of the woods?"?

Yes, I'm asking essentially if the COW is just a hen growing on the side of a tree or not.

I will assume from your comment that your question is

Is a chicken of the woods just a hen of the woods growing on the side of a tree?

, which is very similar to me to

Is a chicken of the woods and a hen of the woods the same species?

No, they are not the same species. Chicken of the woods is the common name of a number of species of the genus Laetiporus. Hen of the woods is the common name of the species Grifola frondosa. In fact, Grifola and Laetiporus don't even belong to the same family but only to the same order (order Polyporales).
According to the wikipedia links posted above, Grifola frondosa is indeed usually found at the base of the tree while Laetiporus is generally found in the wound of trees (mainly oak trees).


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What’s this bug? Sign of an infestation? Found crawling up the side of my washing machine. [WA]
Just spotted this bug on the side of my washing machine after putting some dirty clothes in the hamper and transferring a damp load to the dryer. I’m hoping it came in from outside somehow, and isn’t some type of vermin (I live in an apartment and I’m probably the cleanest resident in the building. I’m also paranoid about household pests.) It’s very small, photographed against a damp paper towel. Please tell me this is not a baby roach?

Rob Dunn's lab at NCSU does all kinds of neat projects looking at the diversity of organisms living in people's homes. Possible household organisms includes over 1000 possible insects, and often times more than 100 invertebrates living in single home -- and cleanliness has nothing to do with it! (source: Michelle Trautwein).

Don't worry, it is definitely not a roach. It is a true bug, Hemiptera. Not a household pest.

Can you say a few words how you know this? What sorts of features allow you to characterize it as Hemiptera? Mostly for those of us (me) who know nothing about insect phylogenetics.


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How loud a sound would need to be to wake someone up?
I have been researching about this and it looks like the term would be auditory arousal threshold. Imagine you fall asleep while listening to music with earbuds. Out of a sudden, the device starts playing really loud music (let´s say 40 dB higher compared to what you were listening). This sound would be quite loud that it would damage your ears.
My question is, is there any study showing which would be the minimum dB level of a sound that would make you wake up (and, well, remove the earbuds)?
I would assume this would depend on the frequency of the signals as well. But, what about the age of the person?

I don't think this is generally answerable with a single value for all people. The answer would vary from "not very loud" for light sleepers to "impossibly loud" for those who are completely deaf.

Yes, I understand what you mean. But I was expecting something like an offset that would be a general norm for most people. Let´s say: Subject A has no hearing loss and we could say they would wake with a 90 dB sound. Subject B has a hearing loss of 20 dB and therefore they would need 110 dB to wake up in the majority of cases. Let´s assume hearing loss is flat and the sound is white noise for simplicity. I have also read that the brain can adapt as well and if they are accustomed to white noise during the day, it might not wake them up.

Can we say no more damage can be caused to the ear when the threshold is exceeded an damage has been already caused? Let´s say a person with no hearing loss, according to OSHA, would not get their ears damaged if they do not listen to 90 dBA for more than 8 hours. If this limit has already been exceeded and the subject has hearing loss, can we say instead of 90 dB, they can be exposed to 90 dB + Offset for 8 hours now?

No general answer would make sense, as kmm points out. It's too dependent on the conditions and the individual: it will even vary for an individual from day to day. This is one reason alarms often have volume controls... Loud noise is not safe for people simply because they have hearing loss, if anything it's putting them more at risk for more profound hearing loss.

Ok, not even something similar to what I suggest in my first comment? I have been researching but could not find anything like this and wanted to give it a last try here. My background is EE and not medical... I can understand that someone that is completely deaf would not detect air pressure change as their hair cells could be nonexistent or maybe the nerves may be ruined. But, what if the brain gets a volume change (after the signal gets into the brain) of 20 dB, would this be enough for it to wake up?

It's not just about hearing loss. Your threshold for wake up is going to depend on how tired you are, the nature of the sound, what stage of sleep you are in, other personal differences, etc etc. From an engineering perspective, you need to consider the risks of failure: you will want a different level of sound if wake-up is very necessary (i.e., fire alarm) versus if it's okay to miss some % of the time.

@Bryan Krause: Yes.  I can be woken up by stealthy movements in my supposed-to-be-empty house, yet in my younger days slept through any number of raucous parties in neighboring apartments.

@BryanKrause, Yes, I am actually trying to look for a dB level which would guarantee that any person would wake up to (except deaf people, for sure). Imaging you have BT earbuds that play an alarm that the rate of failure must be 0%. The question would be how loud the sound needs to be and of course the type of sound. In other words, how high that threshold could reach considering all the circumstances known

@the_moon Yeah, sorry I don't feel like that's something answerable here, it's not relevant to biology, just your engineering project.

Well, it is the biology of the human ears and the auditory system. I thought that my question would be useful and interesting here. Of course, it has value to me now but it might have value to others as well.

Humans are not standardized components, which is what makes human factors engineering so hard. 80 percent of children between the ages of 2 and 13 did not wake up from a standard issue alarm.

A conventional wisdom is that a sleeping mother can hear her child crying on the other end of the house, but not a cannon firing next to her ;) So it is not just sound intensity that matters.


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What advantage does the pseudostratified epithelial structure type provide over squamous, cuboidal, and columnar?
I'm currently and have had difficulty receiving an answer about the role the pseudostratified columnar structure provides.
I understand that that the following have their respective advantages:

Cuboidal: Very tight cell junction
Columnar: Increased Surface Area relative to volume
Squamous: Allows easy passage for materials across

In the tissue we observed from a trachea, the ciliated pseudostratified columnar was responsible for the movement of material across its surface, however it seemed that the cilia provided that, not the structure.
Why not have ciliated columnar tissue? What does pseudostratified bring to the table?

Incidentally, your description of the advantage of columnar should probably be further explained. Columnar cells actually increase VOLUME of the cell relative to (apical) surface area. This is why secretory epithelial structures are usually columnar. And cuboidal cells do not necessarily have tighter cell junctions than other epithelial cells. That's a function of the actual junctions, not the shape of the cell. As far as the best barriers, those are actually stratified squamous epithelial tissues.

Why not have ciliated columnar tissue?

The respiratory epithelium in the trachea is columnar. The three classifications you bring up in your question: cuboidal, columnar, and squamous, describe the shape of individual cells. The trachea, as you saw in your trachea sample, has columnar epithelial cells (when healthy). The cells are longer along the axis perpendicular to the basement membrane than they are along the axis parallel to it.
You can also classify epithelium according to the number of cell layers between the basement membrane and the free surface of the epithelium. The two possible classifications here are simple (one cell layer) and stratified (more than one cell layer).
The classification pseudostratified means it looks like it's stratified, but it is actually simple. As with any other histological classification, this classification describes structure rather than function. The epithelium in the trachea is simple columnar because all the cells touch the basement membrane, but without knowing that (just by looking at a cross section) it would appear to be stratified because the nuclei of all the different cells do not line up. That is why it is called pseudostratified. The difficulty in distinguishing pseudostratified and stratified from an ordinary cross section of a trachea may be difficult to appreciate without an image. It is not obvious that there is only one cell layer above the basement membrane here, but there is:

As with other simple columnar epithelial tissues, the trachea is specialized for both secretion and barrier formation.
You could speculate on the possible strengths and weaknesses of the pseudostratified structure, but it just happens to be the case that a certain cell population that has nuclei that are closer to the basement membrane (here labeled BC), and a certain cell population has nuclei that are further from the basement membrane (here labeled CC). Those cells with the lower lying nuclei are sometimes called basal cells, and are not terminally differentiated. They provide a reserve for cell replacement in response to normal loss of cells and/or pathophysiological processes like infection and inflammation.
Now, other simple cuboidal epithelial structures, e.g., in the intestine, do not have a pseudostratified structure. If you look at a healthy section of large intestine, the nuclei of the epithelium clearly line up, and it's not hard to see that the structure is a simple epithelium. For those unfamiliar, the epithelium here is only the outer layer. The seemingly disorganized mass of cells deep to the epithelial basement membrane are connective tissue (labeled CT). Look for a thin pink line in each of these slides to help orient yourself to the epithelial tissue. That's the basement membrane.

This simple cuboidal epithelium is also renewed in response to normal loss of cells and pathophysiological processes like infection and inflammation, but doesn't have a pseudostratified structure. This means, clearly, you don't need a pseudostratified structure in order to renew an epithelial surface. So I would caution you not to expect structure and function to be so neatly tied together in histology. It's a descriptive science. You can learn and understand what these structures do, but it's not necessarily a good idea to try to shoehorn the structures into logical rules. The usual answer to "why" in histology, is "because that's what it looks like".
You can read the details in Ross Histology, Chs. 5 (for general classifications and the general concept of pseudostratified epithelium), 19 (for respiratory epithelium and the details on pseudostratified epithelium), and 17 (if you want to compare the respiratory structures to the epithelial structures in the GI tract). Images are from Ross Ch. 5.

I am not sure , but I think I read somewhere that the cells having their nuclei towards the base function as stem cells , i.e they function in replacing the tall cells ( cells with apical nuclei)

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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Lipids that are not found in human body
I know that human body contains FA some of which are essential and the other is not depending on the ability of the body to synthesize them in a sufficient amount, but I need a reference of the lipids types that are found at animals, plants, insects, microorganisms,....etc but not in the human body.


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On which chromosomes were the traits studied by Mendel?
In his experiment with peas, Mendel mainly studied two traits : yellow/green colours and round/wrinkly shapes.  I've heard that the pea genome is very large and its sequencing is a challenge. However, is there any information about the chromosoms involved in the traits on which Mendel worked ?

The yellow/green color of seeds is on chromosome 1, but the color for for the pods is on chromosome 5. The smooth/wrinkly seed shape is on chromosome 7; however for the pods a similar contrast is governed by chromosome 4. The pea has 14 chromosomes (diploid).

What you mentioned however are not all of the pea genes Mendel studies. He actually studied 7 genes (see table above) but only 4 chromosomes host all of the genes he studied. Mendel was lucky that two combinations don't usually show linkage because of the large distance between them (on the chromosome 1 and 4 respectively). There was one linkage which he should have detected though between plant height and the shape of the pods (both close enough on chromosome 4); apparently Mendel never published anything on that combination though. I don't know whether it was because it befuddled him or he just didn't study it.
Referernce: Blixt, S. Why didn't Gregor Mendel find linkage? Nature 256, 206 (1975). doi:doi:10.1038/256206a0


text:
Efficacy of sonic kangaroo deterrents
Bender (2003) tested the efficacy of sonic kangaroo deterrents. Their device is static (and apparently ineffective).
Has there been any rigorous testing of the whistle-like 'kangaroo deterrent' devices fitted to the front of vehicles?


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Boletus or Xerocomellus?
I have been trying to identify a mushroom I collected in the nearby forest, and while I think I have it identified, it seems to have a couple of names and I am confused about which grouping is correct.
According to one site, the mushroom is Boletus Chrysenteron :http://www.mycokey.org/result.shtml?genSpec=Species&ID=213&showList=DropDown&random=11837
According to Wikipedia it is Xerocomellus Chrysenteron (picture on right) https://en.wikipedia.org/wiki/Xerocomellus
But the info suggests that this Xerocomellus group is relatively new and belongs to the family Bolataceae.
Are these two different mushrooms (Xerocomellus Chrysenteron and Boletus Chrysenteron)? Or is it that the mushroom is now in a new group?

As you will see in the Species section of the Wikipedia Xerocomellus genus page you linked, Xerocomellus chrysenteron has a basionym (original name) of Boletus chrysenteron.  The Xerocomellus genus was first described in 2008.  The Wikipedia page for the X. chrysenteron species similarly gives three synonyms for X. chrysenteron in the box at the top; among them is Boletus chrysenteron Bull. (1789).  Thus the two names are referring to the same mushroom species.
One should note that Wikipedia says about this species:

Macroscopic observation of Xerocomellus chrysenteron is not sufficient
  to determine this species with certainty, as many intermediate forms
  occur between it and other taxa

It appears from this that correct identification of a mushroom as being X. chrysenteron is not a trivial task.


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Tight Junctions in Cell Types
I took a quiz today on cell structure basics, which included cell junction types. I disagree with the "correct answer" according to the teacher.
Here is the question:
Which cell type would have the most tight junctions?

a) Pancrease cells
b) Ovarian cells
c) Epithelial cells (in the intestine)
d) Muscle cells (skeletal)

According to my teacher, muscle cells is the correct answer.
I argued that the answer should be epithelial cells, as muscles cells (according to the text) primarily use desmosomes for cell-to-cell adhesion, while epithelial cells rely on tight junctions primarily.
I searched it up quickly on Google, and from what I have found, epithelial cells is the correct answer.
Is my teacher incorrect?

Tight junctions are very specifically a structure found in epithelial cells, so your teacher is incorrect. Tight junctions are what allow epithelial cells to form a selective barrier between compartments. Fibroblasts can be induced to form tight junctions under certain experimental conditions, but I'm not aware of any case where a skeletal muscle cell expresses a tight junction. Regardless, it would not be normal physiology.
You can read more about tight junctions here, in the online Albert's Molecular Biology of the Cell. This figure from that Chapter illustrates the barrier function.

If you want to get into more of the details re: what we know about the various proteins involved in creating and regulating tight junctions, this is a good review.
One small correction to your reasoning, though, I wouldn't say the primary purpose of tight junctions is cell-to-cell adhesion, per se, it's selective permeability. These junctions may help the cells to hold together, but the tissues can resist shear stress in knock-out models. A knockout model without a necessary tight junction protein, however, will not maintain selective permeability.


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Can oral baking soda effect tumor cells in mice
Could anyone explain me please, how exactly (according to research article in Cell journal) adding the baking soda in drinking water can influence the acidity of tumor cells? What about homeostasis and ph buffer systems?
In this article in Cell, discussed in this news source, in addition to a number of experiments with cell lines, a live mouse model with xenograft tumors was used to show the effect of oral bicarbonate on tumor acidification, and support the in vitro results re: the effect of tumor associated acidification on the circadian clock.
How is it possible that oral bicarbonate could make tumors in these mice less acidic? Wouldn't the physiological buffer system prevent any changes to the pH in tissues?

its Ludwig Institute for Cancer Research, they like baking soda stuff)
full name of article is "Acid Suspends the Circadian Clock in Hypoxia through Inhibition of mTOR"

Welcome to SE Biology. This is a question and answer site that is self-contained. The questions should be complete and comprehensible without reference to external sourses. Your question refers to an article in a journal, and its title presuposes a knowledge of some previous controversy with which you are engaged. I appreciate your feelings, but this is not the forum on which to express them.

@David I read the post script as context for why the OP was asking, possibly defending against a potential accusation that this is a personal medical question. The question itself seems to be on topic, since it's about the impact of oral bicarbonate on acid base homeostasis. Maybe it would be helpful to edit out that paragraph...?

It would really help if you had links to the exact studies you are talking about.  Links to articles talking about the studies are not what's needed.    The 2018 Cell paper is not about mice getting drinking water, but cell lines.  So what paper are you talking about that has mice drinking water?

@swbarnes2 it uses both cell lines and a live mouse model (with SCID mice). Look at figure 7K: Immunohistochemical pS6 staining of HCT116 xenograft tumors hosted by mice drinking tap water or 200 mM sodium bicarbonate ad libitum throughout tumor hosting (up to 3 weeks).

Okay, they do mention that, but they got the samples from another lab?  A link to the original paper there would say much more about the "drinking water changes the tumor" angle than this one.  And on an unrelated note, the use of FPKM in the RNA-seq is painful.  It's been deprecated for years.

@swbarnes2 the effect is well established and has been used in this mouse model for nearly 20 years. See my answer :)

OP, I've edited your question to try to make it the biology question more obvious (as well as its relationship to the study that prompted it. If you don't agree with the edit, feel free to roll it back!

@swbarnes2 I'd say that the "oral bicarbonate increases sensitivity to rapamycin" angle here is NOT what got this article a spot in Cell. It's the mechanism for the abolishment of the circadian clock. Baking soda cleans cancer is a more compelling (and misleading) news bite, though.

@DeNovo — Then I suggest you edit the post radically to fit your interpretation of the question. At the moment the question is unacceptable in my opinion. If you don't, then I have no qualms about doing it for you.

@David and OP I made one more edit, which I believe makes clear the question and keeps it clearly on topic. OP, if you don't like this (or any edit) feel free to roll back.

@DeNovo — That's fine. Makes your excellent answer worthwhile.

What can oral baking soda do?
If your question is (which I don't think it is):

Does baking soda cure cancer?

The answer is that there is no support for that statement.
If your question is:

Can oral bicarbonate alter the pH of tumors in a mouse model?

The answer is yes.
This effect has been observed in this mouse model and replicated many times
This is an effect that has a been used for a while, and was first demonstrated in this 1999 article in the British Journal of Cancer.  The addition of bicarbonate increases the buffering capacity in the live animal model, preventing the acidification of the tumor. It does not increase the pH of other tissues.
How does this work?
The idea here is not that adding a base increases blood or tissue pH directly, but it increases the amount of a physiologic buffer in a situation where that buffer has been depleted or is insufficient, allowing a better response to a pathologic excess of acid. Your question suggests you believe that an oral acid or base load will not change the pH of body tissues. This is true in normal physiology because there is a robust system of buffers. The primary extracellular buffer actually is bicarbonate. However, in diseased states, the buffer may become depleted or be insufficient. Oral (as well as intravenous) bicarbonate therapy is used in humans in several disease states, including certain forms of metabolic acidosis (Cecil Medicine, Ch 63, 120) and kidney disease (Ch 124, 128, 132). What is happening in these cases, and in the mouse model, is not a change in pH from the normal set point, but an increase in buffering capacity that allows the pH to return to the normal set point.
I would caution, though, that just because oral treatment is used in certain specific forms of acid base pathology, however, does not mean that there is support for the various forms of quackery that use arguments about flushing acids from your body, or using alkaline water as a general health tonic. It does address the question about whether it is very strange that orally administered buffer would impact a tissue with excess acid. It's not (strange).
The effect of changing the pH in the tumor microenvironment
The effect in the study behind the article you referenced, as well as others, is an increased sensitivity to cancer chemotherapy in otherwise resistant tumors. This is not horribly surprising, and doesn't mean by any stretch that baking soda cures cancer or that, e.g., an acidic diet causes cancer.  Other studies, including this one (also in this very particular mouse model), show decreased invasion and metastases, also presumably because of the increased buffering capacity (and decreased acidifcation of the tumor and tumor microenvironments), so there may be other possible effects.
There has been a good deal of interest since 1999 in human studies adding bicarbonate to other treatments, but none have been published that I'm aware of, though I haven't checked the clinical trial registry.
EDIT:
On checking the clinical trial registry, on first glance it looks like some safety and tolerability studies have been completed, but it would take a fair amount to do a full analysis of what has been done and what hasn't. Maybe someone else wants to do it and include it in an answer? I'm fairly certain I would have seen and remembered an article showing that bicarbonate cures cancer in humans, though, so I don't think that's on the list :)

I added some edits here to be clear that baking soda is not a miracle cure. An unsuccessful google news search looking for news reports of the 1999 study reminded me that there is an entire subsection of quackery built around faulty reasoning about acid-base balance.

Although i'm a girl, i'm not so stupid to read tabloids or believe in quasi-science. The problem was i had no answer for people who believe in soda miracle, because they literally put this article to my face, with a spoon of soda. My question was not about "cure cancer by soda", it was about mechanism of influencing of baking soda taking peroral to tumor's acidity, i just couldnt understand how it works on the biochemical level. Thank you for the answer, i will read articles deliberately.

Hi @DariaMorozov. I didn't mean to imply you believed in the quackery. That seemed clear from the way you phrased your question. I just wanted to make sure my answer wouldn't be misinterpreted by others as evidence for a baking soda cure.


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Example Clade Names in PhyloCode
After looking through the PhyloCode, the only thing I found that looked like an example was in Article 9, Chapter 4:

A node-based definition may be abbreviated "<A&B" or "<A&B&C&D [etc.]".
A branch-based definition may be abbreviated ">A~Z" or ">A~Z∨Y∨X [etc.]".
An apomorphy-based definition may be abbreviated ">M(A)".

Then from the following lines, I assume that that is actually how the names would appear in print:

The system of abbreviations used here adopts the following conventions: > = "the most inclusive clade containing"; < = "the least inclusive clade containing"; & = "and";  ∨ = "or"; ~ = "but not"; A, B, C, etc. = species or specimens used as internal specifiers; Z, Y, X, etc. = species or specimens used as external specifiers; M = an apomorphy; () = "of" or "synapomorphic with that in"; >∇ = "the most inclusive crown clade containing"; <∇ = "the least inclusive crown clade containing". The inverted triangle meaning "crown clade" resembles the representation of a crown clade on a phylogenetic tree diagram.

I'm wondering if one could clarify what an actual real-world Clade name would be using the PhyloCode. Maybe just a few examples or even just one. For example, there is this fern Equisetidae, a subclass of Polypodiopsida. Altogether it has this set of names:
Kingdom     Plantae
Subkingdom  Embryophyta
(unranked)  Tracheophyta
(unranked)  euphyllophytes
Class       Polypodiopsida
Subclass    Equisetidae

I am wondering how you would rewrite this using the PhyloCode. If it's too complicated or requires a bunch of additional work to initialize a basic set of codes or something, then that would be good to know too. But from the documents I've seen, it seems to suggest one can translate existing Linnaean classification terms to the PhyloCode somehow. My attempt at it without having gone thoroughly through the whole document is this:
A = Plantae
B = Embryophyta
C = Tracheophyta
D = euphyllophytes
E = Polypodiopsida
F = Equisetidae

So the full name of it would be something like A>B>C>D>E>F. Or maybe it's more like this:
A = Plantae
A>B = Embryophyta
A>B>C = Tracheophyta
A>B>C>D = euphyllophytes
A>B>C>D>E = Polypodiopsida
A>B>C>D>E>F = Equisetidae

Looking for some help on better understanding how to translate existing Linnaean terms/species to PhyloCode. Wondering if you are actually renaming things like Tracheophyta, which has a descriptive Latin name, to A>B>C, which is a non-descriptive identifier. Thank you.


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What is the number density of fungal spores per unit of volume of air?
Fungal spores are present all over in the air around us. I understand that they generally range in size from about one to one-hundred microns.
What is the number density of fungal spores in air on a volume basis? I imagine this will vary based on location, season, and indoor vs. outdoor. An ideal answer would account for all of this in the ranges but I'm broadly interested in indoor air conditions around the world.
If measurements of a single spore density are too difficult, I would find the density of CFUs to be acceptable (assuming that those are multiple spores) but would appreciate being directed to information on how many spores typically make up one CFU. Similarly, a mass density of spores would be acceptable as well if experimental methods make that easier. At the simplest level, I'm just curious how much fungal spore material is in the indoor air around us.

Bamba et al. (2014) Case study of airborne fungi according to air temperature and relative humidity in houses with semi-basements adjacent to a forested hillside. Biocontrol Sci. 19: 1-9.

This is neither the first nor the last report of this kind. Search PubMed database using this query:
"air"[Title/Abstract] and "fungi"[Title/Abstract] and "spore"[Title/abstract]

This is very helpful. Thank you. I see that CFUs really seem to be the standard on this as you can more easily count cultures than individual spores. Any guidance on mass or number of spores per CFU?

Assuming (1) the sample is properly diluted and (2) each spore germinates: 1 spore ~ 1 CFU.