text:
How do our eyes detect light at different frequencies?
Here is my confusion: we can see colored light of different wavelengths: form red to violet. To my understanding, these stimuli cause a confirmational change in the photoreceptors in our eyes and results in a STP that eventually leads to an "all or nothing" action potential that sends another signal, again an all or nothing action potential through the optic chiasm to the occipital lobe and we perceive the colors as we see them.
My question is *how does this signaling work? *; How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?
Asked another way, how does variation in a confirmational change at a receptor that results in "all or nothing" signaling lead to specific signals being sent such as colored vision ?
PS: I dont know jack about sensory physiology

Short answer
Action potentials generated to different colors are indeed similar throughout the nervous system and do not encode color as such. Instead, the different color- sensitive cells in the retina are connected to different neurons and these color-specific signals are kept segregated up until the higher visual cortical areas.
Background
Action potentials are indeed pretty similar throughout the nervous system. However, the color-sensitive sensory cells in the retina, called the cones, come in three flavors: red, green and blue. These colors form the RGB system just like in your LED TV and can together make all the available millions of colors. These three cones synapse ultimately onto color-specific secondary sensory neurons (Fig. 1).
Hence, R, G and B cones indeed generate identical action potentials in downstream neurons, the trick is they do so in different retinal ganglion cells, and at different firing rates depending on the intensity of light that particular cone is sensitive to. These different classes of retinal ganglion cells project onto different classes of neurons in the brainstem (lateral geniculate nucleus, or LGN) and ultimately onto different neurons in the higher cortical visual areas in the brain.

Fig. 1. Different classes of cones synapse onto different classes of secondary sensory neurons in the retina. source: Discovery Eye Foundation
The reason why we can differentiate millions of colors can be explained by the Hering model of color vision (Fig. 2). Basically, the different cones converge pairwise onto opponent color-sensitive cells. The red-green opponent system, for example, operates by weighing the amount of red and green in the incoming signal. This weighting results in an analogue system that can code millions of colors along the red-green axis (Fig. 3).

Fig. 2. Hering model of color vision. source: Webvision

Fig. 3. Red-green color axis. source: SO

Beat me to an answer - glad yours came up before I got too far in to mine. You might add something about the nature of communicating via action potentials: that although they are all-or-none, the rate of APs can encode intensity, and a brief mention of how photoreceptors themselves don't have action potentials but rather drive their targets to fire at different rates.

@BryanKrause - thanks. The question is so broad I decided to give a simplified, short answer. However, I do not think rate coding applies to color vision; the message is that the pathways are seggregated spatially (still working on the answer though).

Yeah, I don't think it needs anything but a brief mention, but I disagree that rate coding doesn't apply to color vision. The relative rates of cells affected by different cone types is what gives a broad spectrum of possible colors.

Also related: https://biology.stackexchange.com/questions/52315/photoreceptors-and-light-with-mixed-frequencies?rq=1 though I don't think that question answers this one well, this one goes more toward the basic physiology.

@BryanKrause - I've added the Hering model. How's that?

Added to one of your sentences, feel free to review and revert if you don't like it. Otherwise I think it's great; Fig 3 might not be necessary. Already gave you an upvote so here's an extra 5 Internet Points.

You can also give name of this principle : labelled line principle.

@AliceD Is there any reason for Blue cone not having a connection to Greenness-Redness neural stage? The other two cones are having connection to all neural stages though.

How do our eyes detect light at different frequencies?

Different frequencies are recepted via different photoreceptors i.e. different pigments in cones. Tricolor mechanism being the most famous.
Here, our eyes can detect three different colours Red,  Green and Blue. These are mixed in appropriately for detection of different colours.
For eg: 99:42:0 will give you perception of orange color. Which means 99% Red 42% Green and 0% Blue.

Don't add another low-quality answer on top of an existing post - please write a single answer and edit it instead.

@AliceD Madam, I knew your answer was perfect for question. If you had not written that,  I would have had written same. But, when we look at question, what comes in mind at first glance is Tricolor mechanism. This is the only answer any examiner will write in response to question like How do our eyes detect light at different frequencies?. So, I gave the same, so that anyone who searches for this question on internet, shall find an answer, an answer which OP does not want.

Firstly, you shouldn't write answers which OP doesn't want... You should write answers that target the question. Secondly, I'm a bloke 8-)

How can a minor stimulus, resulting in an "all or nothing" chain of action potentials be converted into something as specific as the vision of color?

Visual phototransduction is the one of answers to your question.
It is a process by which light is converted into electrical signals in the rod cells, cone cellsand photosensitive ganglion cells of the retinaof the eye. This cycle was elucidated by George Wald (1906-1997) for which he received the Nobel Prize in 1967. It is so called "Wald's Visual Cycle" after him.
Overview
The visual cycle is the biological conversion of a photon into an electrical signal in the retina. This process occurs via G-protein coupled receptors called opsins which contain the chromophore 11-cis retinal. 11-cis retinal is covalently linked to the opsin.  When struck by a photon, 11-cis retinal undergoes photoisomerization to all-trans retinal which changes the conformation of the opsin leading to signal transduction cascades which causes closure of cyclic GMP-gated cation channel, and hyperpolarization of the photoreceptor cell.
Signal Transduction
In dark
glutamate is continually being secreted at synapse between photoreceptors and bipolar cells.
In light

1)A light photon interacts with the retinal in a photoreceptor cell.
The retinal undergoes isomerisation, changing from the 11-cis to all-trans configuration.
2) Retinal no longer fits into the opsin binding site.
3)Opsin therefore undergoes a conformational change to metarhodopsin II.Metarhodopsin II is unstable and splits, yielding opsin and all-trans retinal.
4)The opsin activates the regulatory protein transducin.

5) This causes transducin to dissociate from its bound GDP, and bind GTP, then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.
6) The alpha subunit-GTP complex activates phosphodiesterase or PDE.PDE breaks down cGMP to 5'-GMP.
7)This lowers the concentration of cGMP and therefore the sodium channels close.
8) Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.
9)Hyperpolarization of the cell causes voltage-gated calcium channels to close.As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops.
10)A decrease in the amount of glutamate released by the photoreceptors causes depolarization of On center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.
Impulse conduction
As is explained by AliceD above via CN 2 using labelled line principle.

thanks anubhav!! I never knew they worked by hyperpolarization


text:
Why are proteins in the insoluble form when they are in frozen water?
Why would lowering the temperature of water change the intermolecular forces so much that proteins once soluble in water, become insoluble? I know freezing can create a crystal lattice, but I don't see how temperature would connect to the inter-molecular forces of water? If it even does?
EDIT:  So why would a temperature decrease change how a protein interacts with a POLAR solvent

This answer is about cold denaturation of proteins rather than the effect of freezing.
The folded structure of a protein is thermodynamically stable as a result of a small favourable difference between the free energies of the folded and unfolded states. For a small single-domain protein this difference is usually only equivalent to the strength of a small number of hydrogen bonds - folded states are not very stable.
Electrostatic interactions, hydrogen bonds, and van der Waals interactions within the protein, interactions within the solvent, and interactions between the protein and the solvent all have to be considered, together with any entropic effects.
One factor that plays a part is the effect that an exposed non-polar group from the protein can have upon the solvent. Because the water molecules next to such a non-polar group cannot form hydrogen bonds with it they become more ordered or ice-like as they can only hydrogen bond with each other. This is the basis of the hydrophobic effect - as a protein folds and sequesters its non-polar groups in the protein interior then the unfavourable entropy change in the protein (i.e. it has become more ordered) is offset by the increased disorder in the water.
As the temperature falls the water becomes more structured anyway, so an increase in entropy of the water is no longer available to offset the decreased entropy of the folded polypeptide. The thermodynamic balance sheet is altered and the unfolded state is favoured.

If proteins change from being water soluble to water insoluble it means that their three-dimensional structure changed, because this determines how the protein interacts with the water. Most proteins have hydrophilic residues on the outside in their normal structure configuration, which makes the soluble. If this changes and some of the hydrophobic residues come to the protein surface the protein may not be soluble anymore.
The process of the structure changing (sometimes also called 'denaturing') can be caused by a lot of different factors - basically everything that is different from the inside of a cell (for humans: ~37°, salt concentrations, ...). If water freezes then the ice-crystal lattice can force the proteins out of their normal conformation/structure, after thawing the ice they may not get their structure back on their own (this depends on the protein).
To give an answer to your edit: the temperature does not affect the solubility directly, the effect is indirect through a change in structure

I am asking what physical and or chemical properties of the water and or the protein. make a protein go from being soluble to insoluble in a POLAR solvent such as water. Regardless of the temperature of the solution, the solvent remains polar. So why would a temperature decrease change how a protein interacts with a POLAR solvent

@Confusedbyeverything I already explained that: the change in temperature/crystal formation changes the structure of the protein, this in turn changes which residues of the proteins interact with the water/solvent, which changes its solubility

Here is my confusion: how do the changes in the temperature/crystal formation change the structure of the protein and why would this favor the formation of an insoluble form ?       I understand how PH, salts, inter-molecular forces, can effect protein folding. I can even understand how temperature can denature a protein by offering it more energy to undergo different chemical reactions, but what is the underlying concept that explains the change from soluble to insoluble when we decrease the temperature?          PS I am not a chemistry major so thanks in advance

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Measuring the Rate of Photosynthesis
Update: I have just received a grant to pursue this research.  However, I must still perform the preliminary experiment described below before dipping into my very limited funds.  Thank you for any ideas.
What are some accurate methods to measure the rate of photosynthesis that can be performed without access to a professional laboratory?
I am a citizen scientist who is designing a experiment to measure the rate of photosynthesis under different conditions.  Although this idea stems from my interests as an amateur horticulturist, it has grown to into something of real scientific potential.  However, I must conduct this experiment on a low budget without access to a professional laboratory.
Furthermore, I should note that it is almost impossible to quantify photosynthesis by measuring gas emissions in this scenario. The only way to keep the plants in a stable environment with equipment that I can afford is in an open, climate controlled room, (as opposed to a closed testing chamber that could trap gasses).
Any ideas on how to measure the rate of photosynthesis would be greatly appreciated.

One of the simplest measures of photosynthesis is just measuring how much your plants grow (i.e., weigh them). Of course this technique is imperfect because of other influences on growth, the amount of time you have to wait to get a measurable change, and ideally you would want to use the dry mass of your plants to avoid water content differences, but you have opted to exclude the methods that get around those problems.

Thank you for the suggestion.  In fact, when running a similar experiment a few years ago, I quantified my results by taking the mass of each plant.  You raise a good point about taking the dry mass though, a factor which I neglected to consider.  However, I am trying to gather as accurate a data set as possible in order to show definitive correlation between photosynthesis and my variable (if any exists).  That would give me some hope of taking this experiment to a university laboratory for further testing.

Depending on your plant you might be able to mass only a part of the plant, like harvesting one of each of a leaf pair several days apart. You would compare the ratio of the second leaf to the first, in different plants that are your control/test groups. Whether that is feasible would of course depend on the growth pattern of your plant. Also if your hypothesis doesn't depend on a certain plant, you could use a fast-growing model species. Arabidopsis is a favorite in biology labs.

My hypothesis does not depend on a particular plant.  Thank you for the suggestion of Arabidopsis.  Although I will do further research on that species, do you have any other suggestions for fast-growing plants that could be grown indoors from seed with a relatively small footprint (like growing in Jiffy Pot starter trays)?

If you dry the plant and use dry weight, that's how they measure photosynthesis, because all the carbon found in the plant is a balance of respiration at night and over-compensating photosynthesis in the day.
http://ibbiology.wikifoundry.com/page/Explain+how+the+rate+of+photosynthesis+can+be+measured

Thank you for the link.  It raises some interesting points that I will take into account.  Overall, I believe that dry mass will be the most effective method for quantifying growth.  However, I am always open to new suggestions as I design this experiment.

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

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What insect/bug species do these belong to?
I randomly saw what I thought was dust on the counter in my bathroom (NYC Apartment - higher apartment, >10 floors up) this afternoon (June 1st) ... but when I got closer observed that they were little bugs! They were stuck to the counter likely because I had spilled some oil on there and they were unable to get out of there and died on the surface (thankfully). I haven't seen these anywhere else in the apartment or bathroom.
What are these? Are these dangerous or a cause to be concerned? Are there likely more of these elsewhere? Any recommendations for their removal?
[1

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


text:
Have I identified this species correctly? Weird ocean blob
I often comb the beaches in Santa Cruz (central California coast) for weird stuff that washes ashore. The waves have been a lot stronger than usual the last few days, and the today the beach was covered in a thick layer of kelp and other seaweed. There were even two dead seals washed up on the sand. Most intriguing however was this translucent oddity:

Reverse side:

It's about two inches across at its largest. I moved it to a concrete wall to photograph so I could turn it over without coating it in sand, but I found it down much closer to the water. It seems all but certain that it was ripped up from the seabed. I think there's a tiny snail attached to it, visible in the first picture.
Having done some digging, my best guess for the identity
of this species is some kind of ascidian tunicate. The closest comparison I find is this picture of Ciona intestinalis:

due to the orange hue and the distinctive black cord running through it. However it seems much fatter and I didn't notice a siphon on my specimen. Additionally, most images of the species show a much paler color and even more prominent siphon. My specimen might have shriveled from being out of the water though.
So, my guess is Ciona intestinalis. Can anyone confirm or refute?

A coworker of mine was able to identify the specimen as a Lightbulb Tunicate, Clavelina huntsmani. The distinctive "lightbulb filaments" that give the species its name can be clearly seen in the pictures I posted:

So it was indeed an ascidian.


text:
What would bees be doing inside my furniture in the beginning of summer
I have an old chest of drawers in my garden shed. I've been noticing individual bees entering a closed drawer through the keyhole. Recently they've sealed that keyhole with a gray goo that's solidified and seems very hard to the touch at this point. I don't have anything terribly important in there but I'd have to break the goo if I wanted to pry the drawer open. What am I likely to find in there? If I don't disturb them should I be worried about a swarm of angry bees exiting at some point? It's currently the beginning of summer here in Europe.
EDIT:
I photographed 2 bee types that fly around in my garden (though another species might have been around a couple of months ago):

Sounds like they would be building a home or laying eggs. Are they still entering and leaving, or were those solitary bees?

Doesn't sound like honey bees (or other social bees). I'm guessing some sort of mason bee (Osmia) that has layed egg(s) and then covered the entry (that's the "masonry"). If it's not an emergency I'd say you should wait and let them grow up in there, they won't do any harm to you or your stuff.

I only saw solitary bees entering or leaving. It's not an emergency and I'm happy to leave them to grow up in there, the only thing I'd be worried about is if they are easily aggrevated when they mature since kids might disturb them by accident.

don't worry, they are absent parents. they leave food for the larvae and then leave. it's mostly social wasps that need to defend their colony that are aggressive.

As @picapica says, it could well be mason bees (Osmia spp.). Another possibility (but less likely) is carpenter bees, which will actually burrow into the wood. I'm reluctant to give a confident identification from your description without better ID of the actual species, though - if you can get a photo of a dead bee that would be better, or if you can simply describe them it would be a start.

I can't remember exactly what they look like because some time has passed between me noticing bees and then noticing the barricade they've built, but I remember them not seeming very different to the other bees (we have plenty of flowering plants in our garden so bees are very common) and the usual bee here looks like what a beekeeper might keep (I used to know a few).Sorry for the lack of detail but I'm a programmer, not a biologist.. There are also no dead or alive bees around the drawer right now, they are currently in total stealth mode.

@arboviral yes, my guess wasn't meant to be definitive. this question could possibly be considered answered (they are making nests for their young) but getting it down to species will be impossible without more information. keep an eye out for the new generation when they appear!

@picapica Oh yes, I understood. I would agree that mason bees are the most likely culprit, though!

@picapica will keep an eye out for them - I'll take a photo if possible, or of their nest if they escape before I can snap the photos. Any best guesses as to when I can expect them out?

I took photos of the 2 types of bees I can find in the garden now; one of them is very similar to bumblebees which is supposed to be typical of carpenter bees, but mine don't look like the carpenter bee pictures on Wikipedia (mine have hairier butts :P )

Since you have more than one species of bee this might help you.http://bugguide.net/node/view/475348 as should this site which has a dichotomous key for identification. http://www.discoverlife.org/ed/tg/How_to_use_the_discoverlife_guides.html

Thank you, that guide is explicitly made for North America though and I'm from Europe, would that information still apply to Europe in general?

you should add your location to the question. your pictures look like a honey bee and a bumble bee to me, but keep looking!


text:
Did toads evolve from frogs?
I know frogs still exist but that doesn't mean there wasn't ever a frog population that evolved into toads. Did frogs evolve into toads because their available swamp slowly went away and toads could survive better without water? Did frogs and toads evolve independently from similar selection pressure for shape?

I think you're mixed up; tadpoles are the baby form of frogs, not toads.

Oops... That was a translation issue. Sorry about that. I removed my comments.

"Toads", as commonly used, are not a monophyletic grouping - that is, all toads do not descend from a single common ancestor which only produced other toads. Instead, it's a polyphyletic grouping of those frog species which show common morphological characteristics related to a primarily terrestrial lifestyle. As a polyphyletic group, the parsimonious assumption is that various species of toads evolved from frogs on multiple occasions.
There's several possibilities for similar morphological features in the different toad lineages. The first is convergent evolution - similar selection pressure in the shared terrestrial environment selected for novel generation of similar features. Another is that the common ancestor of frogs and toads had morphological aspects that were a blend between frogs and toads, and depending on environment "toad-like" or "frog-like" features become more prominent or recessive - that is, "toad" genes are sitting dormant in the DNA of most frog species, waiting for the right environment to be expressed. In all likelihood the true explanation probably will be a combination of the two.
By the way, most toad species still depend on bodies of water, particularly for breeding. For example, the common toad (Bufo bufo) will go to a pond to lay its eggs, where the young toads will spend time as aquatic tadpoles before they metamorphosize into the adult form. So when thinking about toad evolution, it's probably incorrect to view it strictly as frogs compensating for losing access to water (though that might have happened for some species), but rather toads evolving to take advantage of the opportunities presented by a terrestrial habitat that's coexisting alongside watery environments.

It is more important to understand the entire argument of evolutionary assumption. For instance, we have no solid observational, repeatable or testable evidence that the frog or toad evolved into one or the other.
We are assuming a lot in this instance. Convergent Evolution is totally crazy.
We hinge a lot of belief upon 'possibilities' and unobserved 'data' through computer generation, and uniformity.
The problem is no one considers that the genetic code will not and can not add information to the gene pool (such as teeth to no teeth, hard skin, or wet skin,) some mutations and adaptations can improve a kind of life form but it has its limits in the DNA.
The truth is, we cannot say that frogs and toads evolved into anything because we have not observed this ever.
We have observed species varying among kinds. However, the toad and the frog are different kinds of reptiles just as the lizard differs from the tortoise.
Always go by fact question assumption.

Convergent evolution is amply demonstrated, e.g. ichthyosaurs/swordfish &c/dolphin, pterosaurs/birds/bats.  Nor are toads and frogs reptiles, they are amphibians.

Although I think there is a positive contribution contained within this answer, namely that people should understand where scientific conclusions come from, I think this answer overall misunderstands the tools that are available and is outright misleading in several ways.


text:
Why hasn't life on Earth reached an evolutionary stable strategy?
I heard in some YouTube video that cheetahs only existed 5,000,000 years and according to https://en.wikipedia.org/wiki/Extinction, extinctions are occurring all the time so I assume life on Earth hasn't reached an evolutionary stable strategy. I know some species like ants are in an evolutionary stable strategy and most species are close to their evolutionary stable strategy because the system of the rest of the species is changing so slowly but why hasn't the system of all life on Earth reached an evolutionary stable strategy. Could it be that it's destined to never reach one? That doesn't necessarily mean there isn't one. According to https://en.wikipedia.org/wiki/Evolutionary_game_theory, the side blotched lizard has 3 forms undergoing cyclic evolution so it's destined to never reach an evolutionary stable strategy if the state of the rest of the species on Earth doesn't change. There's another case of cyclic evolution where rabbits outcompete wolves when there are very few rabbits and wolves outcompete rabbits when there are a lot of rabbits? Why are there so many species that have existed for no more than 5,000,000 years instead of the system of all life on Earth being stable with a few species undergoing cyclic evolution? What's causing the current state of all life on Earth to keep on not being evolutionary unstable?

The concept of ESS applies to a population (in a constant environment), not to all of living things on a planet.

Because the environment on earth is not stable on the long run.
Antarctica was on the tropics. However plate tectonics has moved the continent from that location to south pole. And in time the continues will leave the poles and move toward the tropics again.
So a perfectly evolved animal in tropical Antarctica 200 million years ago, would have to continue evolving or it would have gone extinct as Antarctica moved southwards. And the animals living on Antarctica today will have to evolve as the continues continues with its motions.
Also predator-prey relationships... are red queen type relationship. They may appear stable on the outside, but both parties are actually under selection pressure to evolve, to counter the advantages of the other party. They are in an arms races. Pressure to out run the predator. Pressure to outwit the prey. Pressure to better camouflage. Pressure to detect prey from multiple senses (sound, sight smell).
So on the long term, the strategy that a predator uses will change as its prey evolves. And vise versa for the prey.

"are only..." what?


text:
Are baby centipedes poisonous like the adults?
I know that centipedes have an appendage called "poison claw".But I am not sure if the same is there in the baby centipedes and if its functional like that of the adults.
So are baby centipedes poisonous like the adult?


text:
Kidney transplant and adrenal glands
When a kidney is transplanted from a donor to a recepient does the surgery occur keeping the donor's adrenal gland intact over the kidney or is the kidney minus the adrenal gland over it transplanted to the recepient?


text:
Why only mitochondria and plastids?
Why are there only two unique semi-independent organelles? Why are there no others, symbiogenesis seems like it should be a relatively common thing. So do most organelles just lose all their DNA? Or is it something that occurs fairly rarely?

There are. But they are not that universal. See kappa-particle in Paramecium and Wolbachia in insects. Also, there are different origins of plastids (compare red algae and green algae). Some organisms like Rhopallodia gibba even have plastids of multiple origin.

So do most organelles just lose all their DNA? Or is it something that
  occurs fairly rarely?

The organelles of endosymbiotic origin lose their genes gradually. The extent and rate of loss is correlated with the number of organelle the cell harbours. The limited transfer window hypothesis speculates a probable mechanism.


text:
18S rRNA sequence
I have this phenomenon that the human 18S rRNA reverse transcribed with polydT oligos serve as faithful RTPCR normalizers, tested with better known house keepers. I want to know what I'm amplifying exactly, so where can I find the reference sequence for mammalian rRNAs?

If you're looking for reference sequences, RefSeq is a good bet.
http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+AND+srcdb_refseq%5BPROP%5D


text:
Strange fast growing mushroom like entity
I found this in my lounge today.
This room was cleaned less than 48hours ago, with no sign of this growth.
We sweeped and mopped, using the same floor cleaner we always do.
The two images below is of the same corner, but with the growth lifted in one image.
The consistency is like a fungus or mushroom and can probably be removed from the wall as one piece without much effort.
One of the walls close by do suffer from damp on occasion, but we have been in this house for over two years and have not had anything like this appear.
Please help!

How weird. Could it be leaking insulation foam or sealant or something? What makes you think it's fungal?

The way it's spreading looks like dry rot (Serpula lacrymans, Meruliporia incrassata or Fibroporia vaillantii), but the color doesn't look quite right. Did it stay that color or go darker at the center?

It is/was dry rot. The pictures were taken when these "flowers" just appeared, so it hasn't yet opened to show the orange/brown spores.

Builders have been in and ripped it all out, including our 100-year-old floorboards and fireplace :(
It is what it is... Thanks for the assistance though!

@Lizzie or Johan: please write up an answer so that this question can be marked as such. Thanks!

@theforestecologist Done!

This is dry rot. It could be one of several species, including Serpula lacrymans, Meruliporia incrassata and Fibroporia vaillantii. It is a fungus that feeds on and decomposes wood. Despite the name, some moisture is required for growth, so
it makes sense that your wall suffered from damp. The fruiting body will darken at the center as the spores appear.
Example images of dry rot fruiting bodies:

Photo by Seabrooke Leckie

Photo by Dave Brown


text:
Identifying a mushroom (Switzerland)

Does anyone know this type of mushroom? It grew during the last week in large numbers in one of my pots on the balcony, location Zurich, Switzerland. A smaller part of the soil is from the wood in the neighbourhood, so it might have originated from there.
I spent some time researching on the Internet, and think it might be related to the Armillaria family. An expert opinion would be very much appreciated.


text:
What is the name of this green berry tree?
Location: South India
Month: May
Location: Outside, Metropolitan.
Tree with berry fruits (poisonous or not, I don't know):

Its leaves:

@JM97 "Before I die, I will definitely find one or more new unknown species." from the profile - maybe hoping that one day they can post a plant no one can identify?

@AlwaysConfused I am afraid, It is not Carissa carandas, leaf design not matching with my plant.


text:
What is this green micro-organism found living in water?
I study biology in France and experiment on water filtration with plants. I found that some chlorophyll-containing micro-organisms (about 10 micrometers in length) were raised in my basin.

I can't decide if this is a eukaryote (it looks like there are cellular compartments) or a prokaryote (it's very small!). I thought it could also be a cyanobacterium, that combines features of both prokaryotes and eukaryotes. Any ideas what this is?

Have you considered that it might be algae? (I think it is.)

There are many kinds of algae. I couldn't tell you which one yours is.
Algae Under Microscope


text:
Is this a bed bug?
This insect is ~7mm long, it has a dark strip on the body and I found it in Spain. Is it a bed bug?

See this thread for a genuine bed bug; given the less than ideal focus of your photographs I can't do more than guess at what you actually have, beyond "probable Heteroptera nymph" (a bed bug it isn't).

Looks the wrong colour to be a bed bug to me, they've been reddish brown when I've caught them (3 times in the last 5 months in India)...

For me I think it is a nymph of Centrocoris variegatus. But I am not 100% sure beacause the photos are unclear. The facts lead us to that Heteroptera species, and surely it isn't a bed bug. Also here are and some photos of a nymph and of an adult Centrocoris:
Nymph-to-adult:

Adult:

I hope I covered your question! :)


text:
Are there any alternatives to DNA as the hereditary material on Earth?
I wonder are there hereditary materials other than DNA  deoxyribonucleic acid (may be on different planets).
In addition, I learned in my high school that carbon and silicon are similar. Is it possible to have hereditary materials with silicon replacing carbon.
Why and why not?

Welcome to Biology.SE! What research have you done before asking it here? There are alternatives to DNA on this planet too...

Irecommend picking a single question, either ask about alternatives to DNA in carbon based life or about the possibility to silicon based life. The silicon based life question might be better for worldbuilding than here since it is much more hypothetical.

First of, depending on your definition of life (which is a matter of philosophy, not science) you may even accept as living something that has not heritable information passed onto 'offspring'. But let's consider only those hypothetical life forms who would have heritable information.
Of course, it is possible for different life forms to use some other mean of transferring heritable information. In fact, there are life forms based on RNA instead of DNA on earth (see RNA virus) and it is even thought by many that life first evolved using RNA and not DNA (see RNA world hypothesis).
To go further in this discussion you should have a look at wikipedia > Hypothetical types of biochemistry (I got the link from @RoniSaiba 's answer).

Typically virus, are not regarded as lifeforms as they cannot replicate on their own without a host. But your point about RNA as a heritable molecule is correct.

Exobiologists definitely consider viruses as being living things of interest. Physiologist might not consider a virus alive due to absence of metabolism (although see mamavirus and among others). Note also that saying they cannot replicate on their own without a host is not a very good distinction for defining what is living. Parasitoid wasps cannot reproduce without a host either, yet everyone would agree they are alive. But I agree that not everyone would agree viruses are alive. See this post for discussion.

The post has a top answer, which explains my point in detail. Virus rely on the host to provide the basic molecular machinery they need to replicate; ribosomes for protein synthesis and the metabolism of the host to provide the basic building blocks of life, amino acids and nucleotides. Thus without a host, a virus cannot maintain itself and will be destroyed over time.

I suggest a read of this wikipedia article [Hypothetical types of biochemistry].1
From my understanding of bond energies (which are proportional to the stability of a molecule) it seems that Si based compounds are less thermo-stable. Given how planets form from molten states it is more likely that carbon based life evolves first and outcompetes the emerging non carbon lifeforms.


text:
Are fairy rings documented as a growth pattern in ferns?
I planted an Onoclea sensibilis, a single plant, in my garden. After the first season, there was signs that a fairy ring was forming. A few years later it was mostly complete, but then was obscured in the following years by the growth of the next generation ferns on the ring.
I have not seen any documentation in my field guides that sensibilis or any other fern creates a fairy ring.
I would believe that the fairy rings would be rare in the field.
Where would I find documentation on fern fairy rings?

As this was the only result I could find about Onoclea sensibilis fern ring I wanted to add a reference to a wild fern ring I found of the species. This was found in the fall, 2022, in WV during a hike. I do not know the age of the patch of ferns.
This response, I hope, should act as an answer to the question for documentation of a sensibilis fern fairy ring.
As reference and showing ownership of copyright, I originally posted this image on instagram here: https://www.instagram.com/p/CiTl_VvjXq5/


text:
Does vegetable oil allow methane to pass through?
I'm doing an experiment investigating how temperature affects the rate of methanogenesis. I'm using a peat sample that will be kept in a conical flask connected to a gas syringe with a layer of Janus Green B administered (to indicate if aerobic conditions are present) and vegetable oil (to prevent air entry and to allow carbon dioxide to pass through). There are two main concerns I have about my experimental design at the moment. Firstly will methane also pass through the vegetable oil and secondly one of the pathways of methanogenesis (Carbon Dioxide + Hydrogen → Methane + Water) uses Carbon Dioxide as a reactant, so I'm worried that some of the carbon dioxide produced by the decomposition of acetic acid will be used in the other pathway and not arrive at the gas syringe. Does anybody have any suggestions about making my methanogenesis experiment feasible?

Welcome to Biology.SE! This question might be a better fit for chemistry.SE


text:
Bone fracture cause
I had bone fracture twice in the same arm. So I had first bone fracture in right forearm with 45 degree break on two bones, after 3 months of that fracture while I was climbing a slope I fell and I  used my two hands extended to stop kissing ground, I got hairline fracture in upper arm in middle on right arm again. Why left arm did not get fracture while right arm did, was it due to muscle loss I had incurred during first fracture or my bone became weaker in right arm after first fracture?

Its not off topic question is if muscles weakness happens or bone weakness happens after fracture in limb

the issue is the question is still medically liable, rewrite it to be less about your personal event and more about bone weakness due to fracture in general and it should be fine.


text:
Examples of enzymes working in reverse?
I have always been taught that enzymes can catalyze both the forward and reverse reaction, and will increase the reaction rate in both directions. I understand that the thermodynamics of the reaction are not altered by the enzyme, but I have yet to find a good answer / example for an enzyme that actually does this. (E.g. can a nuclease join DNA together if the products are in excess? Can a protease form a peptide bond?) I am having difficulty finding a resource online that actually justifies this claim without just saying "Yes enzymes work both ways."

you are having trouble becasue it is only technically true. In practice becasue of energy profiles, inhibitors, and a few other factors many reactions will never be reversed or cannot be reversed in conditions that the enzyme will survive. This may help http://bip.cnrs-mrs.fr/bip10/stellen.htm

Remember that these chemical reactions have some equilibrium. This can be pushed to to the right side of the reaction by having an excess of educts - then the reaction goes completely in this direction. If it is the other way, the reaction can be reversed...

Enzymes alter the rate of a reaction by lowering activation energy; they have no effect on the reaction equilibrium ($\ce{K_{eq}}$). Since $\ce{K_{eq}=\frac{k_f}{k_r}}$ and $\ce{K_{eq}}$ is constant, an increase in forward rate ($\ce{k_f}$) requires a corresponding increase in the reverse rate ($\ce{k_r}$). Intuitively it may help to think that the same effect an enzyme has on lowering the energy of the transition state in the forward direction should also be present in the reverse direction. Whether or not the reaction actually proceeds in reverse depends on the free energy difference between the reactants and products and their concentrations (among other things). See this answer for a great explanation.
Because their reactions are in equilibrium ($\Delta G\approx0,\ce{K_{eq}\approx1}$), many enzymes in the glycolytic pathway also catalyze the reverse reaction in gluconeogenesis.

[image source]

What about the ATP synthase? https://en.wikipedia.org/wiki/ATP_synthase it uses proton flow to generate ATP but it can also burn ATP to generate proton flow.

Like other enzymes, the activity of F1FO ATP synthase is reversible.
  Large-enough quantities of ATP cause it to create a transmembrane
  proton gradient, this is used by fermenting bacteria that do not have
  an electron transport chain, but rather hydrolyze ATP to make a proton
  gradient, which they use to drive flagella and the transport of
  nutrients into the cell.
In respiring bacteria under physiological conditions, ATP synthase, in
  general, runs in the opposite direction, creating ATP while using the
  proton motive force created by the electron transport chain as a
  source of energy. The overall process of creating energy in this
  fashion is termed oxidative phosphorylation. The same process takes
  place in the mitochondria, where ATP synthase is located in the inner
  mitochondrial membrane and the F1-part projects into mitochondrial
  matrix. The consumption of ATP by ATP-synthase pumps proton cations
  into the matrix.

Examples of enzymes working in reverse?

Except three enzymes of Glycolysis (Hexokinase, PFK-I and Pyruvate kinase) all catalyse reversible reactions.
As these enzymes catalyse the backward reactions too they are part of Gluconeogenesis pathway.
(A comparison between the two pathways)

Beat me to the example!

At first I felt it was a coincidence. :)

I forgot to upvote. This seems like the most salient example.

You mention nucleases and proteases, but if you turn these processes around and think about the actual nucleic acid or protein synthesis reactions an interesting point emerges:

These synthetic processes involve the production of pyrophosphate — not
  orthophosphate — from ATP (etc.).

(In the case of nucleic acid synthesis this should be obvious; in the case of protein synthesis I am refering to the aminoacyl-tRNA synthetase ‘amino acid activation’ reaction which drives peptide bond formation.)
Why pyrophosphate? The answer commonly given is that this is to prevent the reversal of the reaction. The generation of pyrophosphate achieves this because it is rapidly degraded to orthophosophate by pyrophosphatases in the cell. (See discussion of DNA polymerization in Berg et al.)
If this argument is accepted, it paradoxically illustrates the potential reversibility of the synthetic reactions.


text:
Nernst Equation and Membrane Potential
I am a bit confused on how to use the Nernst equation to determine polarization.
I saw in the textbook that if potassium channels were open in a neuron cell, there will be a net diffusion of $\ce{K+}$ out of the cell, making the membrane potential more negative.
However, if you use the Nernst equation
$$V = \rm 62\;mV\times log\left(\frac{[ion]_{outside}}{[ion]_{inside}}\right),$$
it seems that the potential become less negative if there is a net diffusion of $\ce{K+}$ out of the cell.
For example, if we had 6 $\ce{K+}$ ions inside and 2 $\ce{K+}$ outside, and the channel opened, increasing the extracellular $\ce{K+}$ count to 3 and the intracellular to 5. Doesn't this lead to a less negative value?
I am having difficulty where I am going wrong with this. I saw other posts regarding this question, but I do not understand the explanation.
Is there an easier way to understand why this change doesn't correlate with a more negative potential?

Possible duplicate: https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne/57066#57066 (probably should have pointed to this one rather than answering; I can remove my answer if it's agreed this is a duplicate)

Are you just counting up the potassium ions and subtracting them? Don't do that! That's not how it works. Potassium ions don't just exist by themselves, they come paired with negative ions of some sort which dissociate in water. There are lots of other ions of various charges too, we're just ignoring them all because the only ones that matter are the ones that can move.
In your story, a potassium ion has left the cell. A potassium ion has positive charge. When positive charge leaves the cell, what is left behind is more negative, not more positive.
Potassium ions will keep leaving down the potassium concentration gradient because all things tend to move down their concentration gradients. But as positive charge leaves the cell, potassium ions that leave are moving both down their concentration gradient (to lower concentration) and up their electrical gradient (toward positive charge). So, how do you know when those two forces will balance out?
That's what Nernst tells you: the voltage where a given concentration difference will be balanced so no more net flow of that ion occurs. That's what equilibrium means.
If you're thinking that after some ions move, you need to re-calculate the Nernst equation, that's not correct. For one thing, the ion concentrations don't actually change that much: very few ions have to actually move to change the voltage a lot and halt the flow of ions. For another, you can't ignore the ions that have already moved: the voltage they've created is already there and needs to be accounted for.

I think the OP was thinking that the outside of the cell is charged negatively relative to the inside, that's why they are confused.

@DamocleDamoclev Could be. I think it's more likely that they keep recalculating the Nernst potential after ions move, rather than using Nernst to understand when ions stop moving. The linked duplicate explains that not many ions actually move so it's not necessary to recalculate.


text:
Can drugs be administered through penis?
I was reading this paper on routes of drug administration and noticed that it mentioned intravaginal drug administration. It looks like this is a good way to take drugs because there are a lot of blood vessels which means you absorb a lot of the drug and you bypass the first-pass metabolism effect which catabolizes a lot of the drug before it gets to your liver.
I noticed there’s no mention of penile drug administration. Would there be any advantage of taking drugs this way, either by insufflation into the urethra or by injection into the penis? I googled it and it sounds like there are no drugs that are administered this way except for penile injections - similar to Botox, but for your penis, and not used for absorption purposes.

The urethral mucosa is very sensitive (in both males and females) and it would undoubtedly cause significant discomfort - or more - to place and leave medications in it. I can't think of any advantage the urethra would offer when the rectum, which is much less sensitive, is a possibility and a known site (often used for seizures in infants). The paper you linked to is a good one; there are many routes of drug administration available without causing undue pain. Fyi, the first pass effect is metabolism by the liver before the drug reaches arterial circulation.

Just use suppositories.

there's documented case of weirdos administering recreational drugs in every way possible including the penis, so there are surely documented cases of lsd, opiods, and other drugs going that way.


text:
Is this part of a claw to a Dinosaur?
Agitzed claw 1 large and 1 smaller  underneath.  What I found is about 4" long and about 3/4" in diameter which gets smaller towards the tip. Underneath it appears to be another small claw tip about 11/4" long and appears 1/4" in diameter. They look like stone or aeget.

There are  many fossil id forums where specialists often know the latin name of 150 types of ammonites and they know a lot about tdino claws too.

What's the rock matrix - typically fossils are only found in sedimentary rocks...

Where is this from geographically? What formation?

I discovered it in the Pacific Northwest on one of the beaches off vashon

without knowing the rock type or higher quality images it could be coral or crinoid, or a dozen other aquatic animal fossils. dinosaur fossil is very porous so its unlikely.


text:
How to prepare ethanol-preserved insects for imaging using SEM
I have aquatic insect larvae (soft-bodied) currently preserved in 70% ethanol. I would like to image these using a scanning electron microscope (SEM). I am wondering whether I need to/can start at step 0/1 of the prepping process for the SEM or not:
Do I need to take my specimens out of ethanol, fix them using glutaraldehyde & buffer, wash them in the buffer and then return them to ethanol and dehydrate them with increasing ethanol concentrations?
Or is fixing not necessary for my specimens which are already in ethanol, and could I just increase the ethanol concentration stepwise going up directly from the current 70%?
I would appreciate any help!

This doesn’t answer your question, but I have some difficulty imagining that someone would give you access to their SEM without going over the various procedures with you. Have times changed so much since I used one in the 70s? Maybe SEMs are dirt cheap now?

I know what would normally be the required protocol, but I am not sure what to do because my specimens are different. Also the SEM I have access to is not usually used for biological specimens, so there isn't someone I could ask about the specific procedure in my case. If you have an idea I would appreciate the help!

If there’s no one to ask, I suggest you don’t try anything new. If your SEM isn’t set up for biological specimens, you probably don’t have the equipment necessary to prepare a specimen for a vacuum chamber. The specimen must be devoid of anything that might expand in a vacuum, and a special pressure chamber with the proper materials is needed to do that.

E.g. here. We had a small chamber and used liquid CO2 iirc as the final solution, which was then evaporated off in a vacuum chamber, then coated the specimen in gold. If you started with ethanol, I don’t think the final result will be of highest quality.

I will say that the final solution doesn’t need to be CO2. There are alternatives you can search for in google scholar. I found a paper that used 100% ethanol and let it air dry. But none that started with ethanol. Wish I had an answer, sorry. Also sorry for the tone of the first comment; it was uncalled for. You clearly know your way around a SEM.


text:
Hardy-Weinberg Equilibrium help
I am currently working on understanding Hardy-Weinberg Equilibrium problems. I have come upon two examples of a problem in two different Youtube videos which got me confused:
Example 1:
19% of a population shows the dominant phenotype. What is the dominant allele frequency?
The instructor in the video says that we should address 19% as a combination of both dominant homozygous and heterozygous, so:
p^2 + 2pq = 0.19
Example 2:
In a given population of velociraptors that assumes Hardy-Winberg principles, brown skin is homozygous dominant, and gray skin is homozygous recessive. If the percentage of brown-skinned Velociraptors is 64%, what percentage of velociraptors are Heterozygous?
In this case, the instructor says that p^2 = 0.64.
What I don't understand is why in this case p^2 = 0.64 and not 2pq + p^2 = 0.64.
Couldn't the heterozygous velociraptors also have brown skin?
Referred videos:
First: (Minute 17)
https://youtube.com/watch?v=NS3BjKWHK1s
Second: (Minute 5:20)
https://youtube.com/watch?v=IVGEusDdJGk

you might want to try and find the video this is a little confusing without it.

First: (Minute 17) https://www.youtube.com/watch?v=NS3BjKWHK1s Second: (Minute 5:20) https://www.youtube.com/watch?v=IVGEusDdJGk

You are correct and the instructor in the second video should have used p^2 + 2pq = 0.64. The only reason I can think of for leaving out the 2pq term is if the heterozygous individuals do not have brown-skin. This would only happen if the gene controlling skin color displayed codominance (heterozygotes would have patches of brown and grey skin) or incomplete dominance (heterozygotes would be a solid greyish-brown color). In either case you would not need Hardy-Weinberg Equilibrium because you can directly count the number of heterozygotes.

I think what question 2 is trying to imply is that only homozygotes for brown alleles are brown skinned.  But if the heterozygote has a different phenotype from the homozygotes, I don't see how it is correct to call brown "dominant" and grey "recessive".


text:
Left and Right Handedness
Today I found out that the gene for being Left-handed is dominant while Right-handed is recessive. I personally am left handed and so is my father. My mothers father is also left handed and I was wondering whether or not I am homozygous or heterozygous for the left handed gene. Is there any way to determine this without getting genetic testing or by actually having kids? Thanks.
Source: My science teacher

Welcome to SE Biology. Could you edit your question to include a source showing that there is dominance for left/right handedness? It will allow people to more accurately address your question.

Handedness is not determined by a single gene.

I'm afraid your science teacher is wrong. Handedness is a complex trait. It is not determined by a single gene, and can't be described as being dominant or recessive. Handedness does apparently have a genetic component, but many other factors are involved as well. See the Wikipedia article on handedness:

Handedness displays a complex inheritance pattern. For example, if
  both parents of a child are left-handed, there is a 26% chance of that
  child being left-handed. A large study of twins from 25,732
  families by Medland et al. (2006) has indicated that the heritability
  of handedness is roughly 24%.
To date, two theoretical single gene models have been proposed to
  explain the patterns of inheritance of handedness, the first by Marian
  Annett of the University of Leicester and the second by Professor
  Chris McManus of UCL.
However, the growing weight of evidence from linkage and genome-wide
  association studies suggests that genetic variance in handedness
  cannot be explained by a single genetic
  locus. From these studies McManus et
  al. now conclude that handedness is polygenic and estimate that at
  least 40 loci contribute to determining this trait.

What may be confusing is that the preferred hand is often called the dominant hand, but that usage of the work 'dominant' is unconnected to the concept of dominance in genetics.

True. However, assuming a single pair trait, as described, the answer to the question asked would be: Nope, can't tell what pattern someone has on a gene pair with a strict dominant/resessive expression unless the recessive is displayed. You would need to check genetics directly or breed enough to get statistical probability on your side. The latter is less certain and would require considerably more patience. Kids can be quite a headache.


text:
Can a species populated solely by males be saved from extinction?
How, if possible, can a species be saved from extinction if the only surviving population are males that cannot reproduce with each other?

The article does not say it died. I vote to close this question.

It does not say anywhere in the article that the female died.

This question does not apply just to the linked species.

If the "males" can self-reproduce: yes, if not: no.

Than it's too broad and pob

Its more complex, I am going to provide a quick answer.

@AlwaysConfused Consider the fact that a lot of species are critically endangered due to habitat destruction and climate change, populations will dwindle and there is a chance that the population, however small, will only be populated by one gender. Is that not possible?

In 2012 we weren't able to save an species with one male and no females https://en.wikipedia.org/wiki/Lonesome_George .

@Pere Would it be possible for a sole female to save their species?

Well, in 1999 they couldn't but in 2003 they tried again.https://www.nationalgeographic.com/magazine/2013/04/species-revival-bringing-back-extinct-animals/ However, I must admit that neither the failures nor the hope for success were related with the fact that the last individual was a female. I haven't been able to find examples more similar to the question, with several individuals but all of them of the same sex.

The following answer only deals with theorical feasability

Can a species populated solely by males be saved from extinction?

Short answer : No, not with certainty
Nuanced : yes, in some species, it could be possible
It varies in function of how you determinate the sex of your species.
Sex determination is a wide topic, see the appropriate wikipedia page
Some reptilian species are not sexually determined by chromosomes but by temperature. An example is the painted turtle, of which thermal sex determination has been studied by Carrie Lynne Morjan in an article titled Temperature-dependent sex determination and the
evolutionary potential for sex ratio in the painted
turtle, Chrysemys picta
Thermal sex determination allows you to get 2 different sexes from the "same" genome, as temperature will be the driver of the hormonal differentiation.
Cross-species cloning: influence of cytoplasmic factors on development, by Sun and Zhu states that cross species cloning has been successfully made with fishes and mammals.

Nevertheless, cross-species NT has succeeded in cloning some endangered mammals, such as the gaur
In fish, a type of relatively primitive vertebrate, cross-species NT [nuclear transfer] could be achieved in quite a few genetically distant species

It means we are able to use as a mother and egg-layer a different, albeit related, species.
We can, with a massive grain of salt, hypothesize that we could, in a specie solely constituted of sperm producing male, use the oocyte of another specie to clone it, then use the thermal differentiation to make a female out of our clone.
However, I am not aware of any information about how much genome and spermatozoids genetic payload is modified by the sex differentiation. Therefore, it is possible that sex-determined genes cannot produce a sexually naive clone.
For more information, and if you want to research more about it, I recommend you to see the current state-of the art in de-differenciation technics and DNA-demethylation for cloning.
I hope I provided a sufficient answer for you.


text:
Is it possible to synthesize chiral version of an organism (incompatible with our pathogens)?
In theory, it should be possible to synthesize chiral (mirror image) version of some organism: with all molecules replaced with their enantiomers, e.g. L-sugars in place of our D-sugars.
Direct application of such chiral life could be production of enantiomers of proteins in e.g. chiral E. Coli, what might be useful for example as new drugs.
However, the most interesting is that such chiral life would be incompatible with our pathogens, for example allowing to design really sterile ecosystems for harsh environments like Mars. Finally, such chiral human would be immune to most of our diseases.
Nice article: http://wikibin.org/articles/chiral-life-concept.html
The question is if it is technologically possible to synthesize e.g. a chiral version of E. Coli?
Update: Wikipedia https://en.wikipedia.org/wiki/Chiral_life_concept

First off, quick clarification: "chiral" simply means distinct from its mirror image. All current life is chiral, in that it is made up of molecules  which have a "handedness". What you're asking about is life which is made up of molecules of the opposite handedness (which I'll term "mirror chiral").
Such a lifeform is theoretically possible - chemical and biological reactions and reaction rates are entirely the same between the two handednesses - presuming that all participants (substrates, products, catalysts, etc.) are flipped to the opposite chirality. A mirror chiral Jarek would look and function exactly like the normal chirality Jarek, although he would need to eat mirror chiral food instead of normal chirality food.
So what difficulties would you have to synthesize a mirror chiral organism?  The biggest one is the bootstrapping issue. There's a large suite of molecules in the cell which are all needed in order to replicate the cell, or even just maintain it. All of these need to be present in order for the organism to work. The organism can make all these components from scratch, but to do so it already needs to have these components.
Synthetic organisms - that is, organisms with a genome assembled in a computer and synthesized abiologically - have been made. The trick, though, was that the synthetic DNA was then placed into already existing organisms to be replicated and to have its genes expressed. There's no limitation (besides perhaps cost) to synthesizing mirror-chirality DNA - the same machines which synthesize normal chirality DNA can do it if you swap out the reagent bottles. But what do you do with it once you have it? There's no existing mirror-chiral organisms you can place it in to replicate and express the genes.
If one was to make mirror-chiral organisms, you would need to synthesize all of the necessary cellular components in their mirror-image form. So you would need mirror RNA polymerase, mirror ribosomes, mirror t-RNA, mirror ...  If you do things right you can skip most of the cellular components, but you still need a large number of them.
This is not necessarily a pipe dream. Last I knew, the J. Craig Venter Institute, the people who made the first synthetic DNA organism, are actively looking into it. The trick is to trim things down to the bare minimal number of chiral components needed to bootstrap the system. That's (more-or-less) where their current efforts are focused, from what I understand: what's the minimal number of genes needed for a viable cell? Which of these are needed to "bootstrap" a cell from bare DNA?
Personally, I'm pretty confident that a mirror-chiral organism will be created one day. The time frame for this is a little unclear, but there's nothing theoretically limiting it. The biggest issue is our current technical limits in synthesizing sufficient quantities of (non-DNA) biomolecules in a chemical (abiological) fashion. But those are constantly improving, and with additional research into what's needed for bootstrapping a synthetic cell, we'll push down the requirements even further.
Of course, the first mirror-chiral organism will be pretty simple. It's going to be less complex than even E. coli. It will also need to be fed a diet of (expensive) mirror-chiral food (amino acids, sugars), so its use will be limited as well.

I see you agree that it is only a matter of time (20 years?) when first mirror-chiral organisms will be created, maybe just because we can. We need to have in mind that it can also be very dangerous, for example mirror-chiral photosynthesizing cyanobacteria would have nearly no natural enemies - could dominate our planet, disturbing the bottom of our food chains: producing L-sugars instead. This seems a really important possibility we should well understand before it (inevitably?) becomes a reality - why there is no public discussion on this topic?

I have decided to restore the Wikipedia article - please help improving it: https://en.wikipedia.org/wiki/Chiral_life_concept

It is already starting: mirror-image polymerase in 2016 http://www.nature.com/news/mirror-image-enzyme-copies-looking-glass-dna-1.19918


text:
Provisional vaccine for fast spreeding new viruses?
Developing a standard vaccine for coronavirus will take at least a few months - what might be too late:

However, its sequence is already known, and is nearly identical - suggesting a recent single point of origin for human host, e.g.

"The researchers also found that the eight complete 2019-nCoV genomes were more than 99.98 percent identical" https://www.genomeweb.com/genetic-research/coronavirus-genome-sequencing-finds-distinct-genetic-differences-2003-sars-virus

So the question is if/how there could be quickly started production of some provisional vaccine - not perfect but fast to introduce? Also exploiting the fact that these viruses are now nearly identical.
For example synthesizing its outside proteins and putting them on liposomes - would its introduction to blood have a chance to prepare immune system for the real virus?

I think the main issue about developing a new vaccine is not that it it's supposed to be perfect - but that it's safe. You can just quickly put out medicine without rigorously testing for any side effects

Fake virus: e.g. liposome exposing some material of the virus, seems easy to synthesize and safe(?) - definitely safer than the real virus, and preparation of the immune system it could provide(?) might be a matter of life and death (?) Sure, in normal situation there are needed time consuming clinical tests, but the question here is about situation when time is literally translated into deaths, and it is approximately known where the virus will strike?

Perhaps you should address yourself to sites or texts related to clinical virology. People spend their lives working in this area. This site does not exist to solicit the opinions of people whose expertise you know nothing about theories of curing diseases based on no expertise whatever. If you think you are in “A race to save mankind from destruction” you may have been watching too many movies.

I have added the exponential growth plot to remind how serious this situation is, and generally ask if there is some "provisional vaccine" - not perfect, but which could be introduced before it spreads over the world. The comments suggest the answer is 'no', but could anybody elaborate with support of some materials?

Some discussion: https://www.scienceforums.net/topic/121181-provisional-vaccine-for-fast-spreading-new-viruses/

Stack Exchange Biology does not have the remit or expertise to answer questions about coronaviruses relating to the recent 2019-nCoV outbreak. We have compiled a list of what we regard as reputable external sources of such information. Please consult that.


text:
What kind of flower is this?
I was in my garden a few days ago and found the flower shown in the pictures.
Can anybody tell me what this flower is?
Location: Germany / northrhine westfalia
Date: February 2017
Season: Winter

[Edit]:
My neighbour thinks it is a Anemone hupehensis (en.wikipedia.org/wiki/Anemone_hupehensis), could be right.

Probably Gossipum sp.

You mean a cotton plant? This was the first thing I thought about, but I haven;t planted it. Maybe I have to look nearby my garden if there are more them. Thank you.

I'm not sure. It just looked like one.

My neighbour thinks it is a Anemone hupehensis (https://en.wikipedia.org/wiki/Anemone_hupehensis), could be right.

I think it is Anemone hupehensis. We have this species in our garden, and the seeds and dead leaves look very similar to the ones in your picture. The leaves are large,jagged and palmate and they have beautiful flowers in the summer/autumn (I've seen red, pink and white). The fruits/seeds also look very distinctive and cotton-like. The species is originally from Asia/China.
Here is a picture of the fruits/seeds:

(Hard to find good ones, this from Instagram page http://www.ipopam.com/tag/höstanemoner)

Looks very similar to the one I have in my garden.


text:
RNA isolation- role of pH
Why does RNA alone go into the aqueous phase when treated with phenol-chloroform at lower pH? At a neutral or basic pH, both DNA and RNA would escape into the aqueous phase. So how is DNA held back at acidic pH?

Well, because it is more soluble in water than phenol. Are you asking why DNA does not separate into the aqueous phase at acidic pH?

I'm asking why it happens at low pH and not at neutral or basic pH

You should add that to your question or it may be closed.

RNA gets degraded in high pH.

The purpose of acid phenol extraction is to selectively retain RNA in the aqueous phase while DNA partitions to the organic phase or coalesces at the interphase. I have found many people on the internet say that this is due to protonation of DNA phosphates while RNA phosphates remain ionic, thus giving differing solubility. I do not buy this explanation because:

The pKa of the phosphodiester moiety is several orders of magnitude lower than the pH  used in acid phenol extractions, and so should be largely deprotonated.
Given their similar structures, the drastic difference in pKa between RNA and DNA required for it to be preparatively useful, to me, seems implausible.
I found no such claims in scientific literature.

The properties of DNA and RNA that come to mind and which may explain the differential solubility are:

DNA is denatured in acid due to protonation of the nucleobases, which imparts positive charge. This could facilitate aggregation.
DNA is generally longer.
RNA has a 2' hydroxyl group which increase polarity of the molecule.

Somewhat supporting this is a FAQ from ThermoFisher:

Partitioning of the nucleic acids in phenol is pH dependent. At pH 7.0 or higher, both DNA and RNA partition into the aqueous phase. At an acidic pH (below 7.0) DNA is denatured and will move into the organic phase, but the RNA remains in the aqueous phase.

The exact biophysics escape me. I realize this is not an answer but, rather, more of a long comment. I thought it important to address what, in my mind, may be a misconception. Criticisms are welcome.

But isn't RNA more unstable and hence get affected by low pH? What are the ionic interactions that keep them stable?

I understand that RNA is stable in acidic pH and DNA is stable at basic pH. But why is my question.

@user29995 The phosphodiester of both RNA and DNA are susceptible to acid catalyzed hydrolysis under strongly acidic conditions (ie pH < 1). RNA is less stable in basic solutions due to base catalyzed cleavage of the phosphodiester. RNA is more susceptible than DNA because, under basic conditions, the 2'-hydroxyl is deprotonated and the resulting 2'-alkoxide can nucleophilically attack the phosphodiester.

The main reason acid is used in RNA extraction is, as mentioned, to separate it from DNA and not to prevent hydrolysis.


text:
How do cells determine RNA types?
I was reading about the different types of RNA polymerases, and I am confused as to how a cell determines which type of RNA it is transcribing.
According to this nature article:

RNA pol I transcribes ribosomal RNAs (rRNAs), RNA pol II transcribes RNAs that will become messenger RNAs (mRNAs) and also small regulatory RNAs, and RNA pol III transcribes small RNAs such as transfer RNAs (tRNAs)

The system as to how the different types of RNA polymerase are selected makes sense to me, the core promoter's sequence determines the affinity of the polymerase to itself.
But, how does RNA polymerase II determine if the transcript is a regulatory RNA or a messenger RNA? Can someone explain that process to me or point me to where I would find it?
Another question: When RNA polymerases I and III transcribe their RNA, what prevents the cell from processing them the same way as mRNA and sending it off to a ribosome with a poly-a tail?

Well remember that an mRNA, the RNA that is destined for the ribosome, has already been processed by the time it gets there. This is done by the splicing machinery, among other things (capping enzymes, for example). But the splicing machinery isn't smart in itself. Rather, the gene has the elements, just like it does to select the RNA Pol it needs, to direct the sort of modification the RNA needs to obtain. The image below depicts two types of RNA transcribed by RNA Pol II and how the processing elements let the modification machinery know how to handle them:

Source


text:
T-Cell Receptor Receptor-Associated Immune Receptor Activation Motifs (ITAMs) Inconsistency
In reading the information associated with the cytoplasmic machinery of the T-Cell Receptor (TCR), the one tyrosine motif that is consistently mentioned is the receptor-associated immune receptor activation motifs (ITAMs). All sources I can find on the motif says the sequence is YxxL/Ix(6-8)YxxL/I [1]. However, in the CD3ζ chain of the TCR in homo-sapiens, this sequence is not present according to separate protein structure and sequence sources [2,3]. It is only the TCRβ chain that has this sequence motif in it [4]. The importance of the ITAM seems to be it is the binding location of the protein ZAP-70 (which stands for Zeta-chain-associated protein kinase 70), therefore given the name it is canonically associated with just the zeta chain not the TCRβ chain, what is the ITAM truly then?
The sequence seems to be conserved in murine TCR sequences [5], however, many of the articles being written are not specifically talking about murine TCR structures.
Is this an oversight in regard to the lack of clarity in the writing of the papers describing the involvement of ITAMs in TCR signaling or what is the source of the disagreement between the ITAM sequence and what is seen with the protein structure?


text:
What is meant by Gene Expression Level?
I am new to BioInformatics, I want to know what is gene expression level and how it is determined.. Anyone who can answer this silly question.

Are you familiar with the concept of gene expression but not gene expression level or you're not familiar with the concept of gene expression? You might want to have a look at wikipedia > gene expression or at any intro course to molecular genetics.

“Gene expression level” is an imprecise and partially ambiguous term
  that should be avoided.

Many (but not all) genes have the information to produce proteins†, but there is no need for this information to be used at any given time — it depends on the requirements of the organism or cell. For example the DNA of lung cells contains the information to produce the protein chains of haemoglobin, but it is never used in those cells. We can say that “the gene is not expressed”.
So the absence of expression is fairly easy. However, for a protein-coding gene the meaning and quantitation of expression is more difficult. That is because in expressing the information in the gene the DNA is first transcribed into mRNA by RNA polymerase, and then that information that encodes a protein can be translated into protein on the ribosome.
The word level refers to quantification, and is a sloppy substitute for quantity or perhaps rate (quantity produced in unit time) or perhaps relative quantity.
But the main difficulty is whether in quantifying gene expression you measure the quantity of mRNA synthesised under standard conditions or the quantity of protein produced.
If you are a bioinformatician encountering this term, my bet is that it is in relation to the currently (2018) popular RNA-Seq technique, which in fact provides relative measurements of the quantity of RNAs of different types produced under standard conditions. This is generally expressed in units called FPKM — Fragments Per Kilobase of transcript per Million mapped reads. The difference between this technique and the northern blotting mentioned by @Hawkeye, is that the latter is used to detect a single mRNA, whereas RNA-Seq applies to all the mRNAs that are present in a sample.
In the field of proteomics, it is possible that the term is being used in relation to the amount of protein produced, which may be roughly quantified by two-dimensional gel electrophoresis.
†Some genes encode RNAs that do not encode proteins (ribosomal RNAs, transfer RNAs, RNAs involved in splicing and in modification of rRNA, microRNAs etc.). The expression of the genes for these will end with the synthesis of the RNA.


text:
How many cyclic and non-cyclic photo-phosphorylation is required to produce one molecule of glucose?
In non-cyclic photophosphorylation 1 ATP and 2 $NADPH_2$ molecules are produced.
In cyclic photophosphorylation 2 ATP molecules are produced.
For production of one molecule of Glucose 18 ATP and 12 $NADPH_2$ molecules are reqiured.
According to my understanding,6 turns of cyclic and non-cyclic photophosphorylation is required to produce one molecule of glucose.
Because 6 turns of non cyclic photophosphorylation will produce 12  $NADPH_2$ and 6 ATP molecules.
And cyclic photophosphorylation will produce 12 ATP molecules.
Total=12 $NADPH_2$ and 18 ATP.
I think Iam missing something , Please answer me if I am correct or not.

You seem to have mixed up cyclic and noncyclic, as you're first saying that noncyclic produces NADPH (correct) but then that cyclic produces NADPH (wrong). But the overall stoichiometry seems right, assuming the numbers you give at the top.  What is it exactly that you have trouble with?

Yeah!!A mistake while writing but now I have edited.I just want to know if I have said it correct

Well, your conclusion is just plain addition, so not much to say about that. The ATP:NADPH ratio of photorespiration varies though -- since it is a chemoosmotic process, the stoichiometry is not fixed, and it might differ between species, conditions etc. Where did you get your numbers from?

The cyclic and non cyclic part was given in the textbook.but the 6 turns part was a conclusion from myself. So that means there can't be a fixed ratio.

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.
Source: Cyclic, pseudocyclic and noncyclic photophosphorylation: New links in
the chain. John F. Allen. TRENDS in Plant Science Vol.8 No.1 January 2003.
Cyclic photophosporylation, does not occur under normal conditions in higher plants. It is believed to occur only when either light intensity is low (lower frequency so as only PS1 can function) or when carbon fixation is not at par with light irradiance (i.e, too much light).
And hence it is not advisable to come to this generalization "Six Turns of non cyclic photophosphorylation will produce 12 NADPH2 and six ATP molecule"

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.I don't understand what u said . Can u elaborate a little more or provide a link.

Kindly read this: http://jfallen.org/~john/webstar/john/pdf/32775.pdf

I will add the link to the answer

The numbering of 1ATP from noncyclic photophosphorylation and 2ATP from cyclic is little too much to be right. However, the formation of 2NADPH + H+ out of noncyclic photophosphorylation is correct.
Because according to the Chemiosmotic Hypothesis (Mitchell), the number of protons accumulating in the lumen of the granal thylakoid during noncyclic transport of 4e- from P680 towards Ctyb6f complex is 12 (8H+ transferring from stroma by Q-cycle + 4H+ from photolysis of 2H2O at Oxygen-evolving Complex). And at every 5th e- transport, the cyclic electron transport occurs and helps in transporting 2H+(protons) from stroma region towards the lumen of granum. So, a total of 14 H+ accumulates per an O2 release by photolysis of water. These 14H+ find its way to stroma region through CF particle and 3ATP are synthesized.
Therefore, H+/ATP = 4.67, e-/NADPH + H+ = 2, Total ATP release in both photphosphorylation during evolution of an oxygen molecule = 3, total NADPH + H+ during evolution of an oxygen molecule at PS-II = 2
Therefore, ATP/NADPH formation from cyclic photophosrylation at P680 = 7/9 (instead of the expected 3/2) and
ATP alone = 1.29 (instead of 3).

Yes.

One cycle produces 1 ATP and 2 NADPH2.

Cyclic photophosphorylation produces 2ATP in each cycle.

The C3 cycle uses 3ATP and 2NADPH2 in each cycle.

So if if C3 cycle runs one time then both non-cyclic photophosphorylation and cyclic photophosphorylation run 1 time.
For synthesis of one glucose molecule in the C3 cycle, non cyclic photophosphorylation and cyclic photophosphorylation each runs 6 times.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you [edit] it to be clearer (e.g. complete sentences) and include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. In addition, it isn't clear that you've added anything to the other answers. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit or delete your answer accordingly. Thanks!


text:
White blood cell transfusion
Some patient who have low White blood cells need  WBC Transfusion do resist infections.  What is interesting, doesn't transfused WBCs cause temporary autoimmune disease ?   Like recognising patients organs as foreign ?
just like in the organ transplantation.
Regards.

I do not think that the white blood cells received in a whole blood transfusion would be enough to cause a problem, as most WBCs are only raised during an active infection, so would likely be too low to cause problems. The WBCs are likely killed off soon after the transfusion. The problem with organ transplants is that the hosts immune system attack the foreign cells, not the other way around... Also it is funny answering this question as I have a friend named Armin who has a PhD in Immunology... I almost feel like it is a trap.

http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/bloodproductdonationandtransfusion/blood-transfusion-and-donation-types-of-transfusions I don't think they are used much anymore, as there efficacy was questionable, but it does appear they had the ability to produce a fever in the host.

@AMR  Great explanations.  I have found  out, a guy in this link states that "There is also a process called transfusion-associated graft versus host disease in which the donor white blood cells will attack the host cells; this mainly occurs in immune-compromised individuals" http://biology.stackexchange.com/a/10126/17583
Wiki https://en.wikipedia.org/wiki/Transfusion-associated_graft_versus_host_disease


text:
Why Japanese cherry trees blossom so early in spring?
My understanding is that flowers' main benefit are the insects which attracted to the shape/taste of these and facilitate cross pollination. Yet the Japanese cherry trees start (and end) to blossom (in my observation) way before the most of insects become active. What is the evolutionary explanation for such a behavior?

Might be good to read Austen and Weis 2015

Perhaps your assumption about insect activity is wrong?  We're just now getting early spring flowers (crocus, snowdrops, &c), and bees (or something bee-like) are busy pollinating them.

Well in Tokyo now it's just above 10C during the days, and it's half of that in the nights. Yet the local 梅 (ume) trees already have bloomed and now are naked again - the leafs will appear in another 3 weeks I guess. I don't think I could spot any insects so far.


text:
Cells of umbilical cord - mom's or son's?
Let's say we have a mother giving a birth to a son. In a very clear manner the cells of these two individuals are very different, of course. Yet there is an umbilical cord connecting them. Then there should be a clearly defined "border" somewhere on its way where the mother's cells meet the cells of her son, is that so? How is it even possible?! ;)

Cells of umbilical cord - mom's or son's?

Answer: Son's.
The interface you are looking for is in the placenta. https://en.wikipedia.org/wiki/Placenta
Formally the fetal side of the placenta is called the Chorion frondosum, which develops from the outer cells of blastocyst (trophoblast), and the maternal side of the placenta, Decidua basalis, which develops from the maternal uterine tissue.

How is it even possible?

Immune tolerance in pregnancy or gestational/maternal immune tolerance
The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site. For this purpose, it uses several mechanisms

It secretes Neurokinin B containing phosphocholine molecules. This
is the same mechanism used by parasitic nematodes to avoid detection
by the immune system of their host.
Also, there is the presence of small lymphocytic suppressor cells in the
fetus that inhibit maternal cytotoxic T cells by inhibiting the
response to interleukin 2.
The placental trophoblast cells do not express the classical MHC
class I isotypes HLA-A and HLA-B, unlike most other cells in the
body, and this absence is assumed to prevent destruction by maternal
cytotoxic T cells, which otherwise would recognize the fetal HLA-A
and HLA-B molecules as foreign. On the other hand, they do express
the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed
to prevent destruction by maternal NK cells, which otherwise destroy
cells that do not express any MHC class I. However, trophoblast
cells do express the rather typical HLA-C.
It forms a syncytium without any extracellular spaces between cells
in order to limit the exchange of migratory immune cells between the
developing embryo and the body of the mother (something an
epithelium will not do sufficiently, as certain blood cells are
specialized to be able to insert themselves between adjacent
epithelial cells). The fusion of the cells is apparently caused by
viral fusion proteins from endosymbiotic endogenous retrovirus
(ERV). An immunoevasive action was the initial normal behavior of
the viral protein, in order to avail for the virus to spread to
other cells by simply merging them with the infected one. It is
believed that the ancestors of modern viviparous mammals evolved
after an infection by this virus, enabling the fetus to better
resist the immune system of the mother.

Other mechanisms include exposure to immune modulating factors present in seminal fluid from vaginal and oral sex. https://en.wikipedia.org/wiki/Pre-eclampsia#paternal_tolerance

just to add the placenta evolved from the yolk of the ancestral eggs, It makes it a bit easier to see how the structure could evolve.


text:
How to convert skin temperature to core temperature?
As opposed to regular invasive thermometers, there are non-invasive IR thermometers to measure the temperature. For example Thermofocus.
I read in many sources that these IR thermometers only measure the temperature of the object's surface. However, Thermofocus seems to measure the patient's core temperature*.
My question is how to convert someone's skin temperature to their core temperature (Thermofocus does it so I understand that it's possible). I need to use an IR thermometer to measure a patient's skin temperature (say forehead) and predict their core temperature.
*core temperature: I hope this is the correct phrase... I mean the inner temperature as measured with a regular invasive thermometer.

The measurement of core temperature (it is the right term*) is easy using an invasive method. It is also reliable since:

Core temperature is easy to measure and temperatures are relatively
  homogeneous throughout the trunk and head[PMCID: PMC1752199];

However, the measurement of skin temperature is highly dependent on the location of measurement and also ambient temperature, as explained here[DOI: 10.1039/C6EE00456C]:

Also, Xu et. al. concluded in "Relationship between core temperature, skin temperature, and heat flux during exercise in heat" that:

Algorithms for T_c measurement are location-specific and their
  accuracy is dependent, to a large degree, on sensor placement.

They also proposed two relationships for calculation of T_c based on T_s (Core temp. based on surface temp.) which is included in the paper (regarding copyright laws, I'm not allowed to put it here. you have the DOI and can look it up).
*Here is the list of few publications which are using "core temperature" to address the temperature inside the body:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752199/
.../pubmed/23775374
.../pubmed/10655798
Gender Role:
In a study in University of North Texas Source it is concluded that men has different skin temperature, due to different methods of temperature regulation compared to women:

We found gender differences at four different skin temperature locations. These changes might suggest that men retain more metabolic heat in various locations on the back when exercising in a hot, humid environment compared to women.

Also This Work shows that, although the temperature distribution pattern among genders are similar, women have lower skin temperature.
This Masters Thesis from University of South Florida indicates findings in regards to clothing and metabolic conditions role on core temperature, i.e. no statistical difference between T_c of genders. Look at Figure 3 in page 23 for heart rate vs. metabolic rates. In page 24 there is a table for measurements for T_c.

Thank you that's a good finding!
In DOI: 10.1039/C6EE00456C, are the formulas based only on surface temperature?

Yes. They used the surface temperature measurements according to the manuscript.

@AlaaM. I also found more work based on the conversion of surface temperature to core temperature. Updates include citations for those works.

Looks good. I'll check them out. DOI: 10.1039/C6EE00456C is available only by purchase though, am I correct?

It is correct. I'm student I have access through university.

I have the document (DOI: 10.1039/C6EE00456C). At what page is the formula that converts skin to core temperature? Thanks!

Their equation is based on the article by Xu et. al. "Relationship between core temperature, skin temperature, and heat flux during exercise in heat." Here is the summary:
They suggest this: Tc =Ts+HF (d/Lambda) as the steady state condition equation where HF is heat flux (calculated and represented in Table 1 - page 2385) and d and lambda are thickness and conductivity of the tissue.
Lambda value ranges are 0.20–0.70 W/mC (Werner and Buse 1988; Shitzer et al. 1996).
For transient condition, meaning that there is a T variation with time, there are two other equations (Page 2384).

This is not a public document and you shared it as such


text:
Do trap door spiders have 10 legs?
I was reading this National Geographic article, 50 New Spiders Discovered In Australia when I became confused by the two trapdoor spider species photographed. I looked up trapdoor spiders and looking at pictures, they all seem to me to have five pairs of legs. I know spiders have eight legs; can someone tell me what am I missing here?
Ctenizidae:

Euoplus:

Cork lid:

(OK, so I found out that the things next to the mandibles are pedipalps. How are they different from legs on these beasts?)

All spiders have eight legs. The two on front are called Palps

The definition of a leg from Merriam-Webster is

"One of the rather generalized segmental appendages of an arthropod used in walking and crawling"

As Gerardo Furtado has already stated, the front pair of appendages are called palpi and are not used for walking, but for mating and manipulating objects. By this definition, palpi are not legs and therefore trap door spiders have 8 legs, not 10. More information on the rather large pali found on trap door spiders can be found in P.D. Hillyard's The Private Life of Spiders.

Image from Biodiversityexplorer.org.


text:
Why can't we move our toes and some fingers separately?
In our feet, other than the large toe, the other toes cannot be moved separately. If we try to move them, then all the four toes move together. We cannot move each toe by itself.
Same thing occurs in the hands of some of us, where we cannot move the little finger by itself. While folding the little finger, the ring finger before that also has to be folded to some extent, and vice-versa.
An explanation to the problem with the ring finger and the little finger can be found here.
The phalanges make the toes. Are the phalanges of the small toes connected, such that we cannot move them separately?

While I agree there are limitations to the phalanges you mention, I can easily move only my ring finger inwards towards my palm. I think there may be a more definitive way to describe the limitations on motion?

The answer here: https://biology.stackexchange.com/q/60075/107, effectively answers this as well.

Perhaps you should ask this question on the Music site, with special reference to pianists, harpists, and the like.  Or someone like me, who's typing this comment with all 10 fingers. With fingers, it's basically a matter of training.  I expect much the same would be true of toes.  Searching for "toe dexterity" gets over 600K hits, including this: https://themovementfix.com/how-to-improve-your-toe-dexterity/

A relatively new area of the brain's cerebral cortex evolved to enable humans and other primates the necessary small motor skills to pick up small objects and deftly use tools, scientists now say. https://www.youtube.com/watch?v=zyl6eoU-3Rg
Primates can move their ears too, here's a theory of it. Other motor skills that are not often developed are individual eyebrow movement, pectoral flexing, ability to sneeze with your eyes open.
Hand movement is new and developing compared to chimps.
Toe movement is latent and receding.
The human hand is built up onto a squirrel/clawed paw, If you take a while to rotate your forearm and the flexors of the fingers, you will see that it's a mutated simple flexing mitt thing with with a new fine motor dexterity that you use all day, added on top of the vestigial clawing and grasping hand.
https://www.youtube.com/watch?v=vlwAoKpSI7s
This page says:
Signals generated in the primary motor cortex travel down the corticospinal tract  through the spinal white matter to synapse on interneurons and motor neurons in the spinal cords ventral horn. Ventral horn neurons in turn send their axons  out through the ventral roots to innervate individual muscle fibers.
The motor cortex is subject to plasticity and remapping. To know this question is beyond my field of knowledge, someone else can go on from here :) you'd have to learn about the motor cortex, plasticity, vestigial nerves, nerve mappings, it's a fantastically complex topic.
What's interesting is the variety and quantity of different muscular abilities that are inherited by a population, it reflects an optimized level of evolutionary plasticity and specific types of variety of useful traits like muscle and joint proportions to ensure fast and flexible species development.

plenty of humans can move their ears.

Other motor skills that are not often developed are individual eyebrow movement Interestingly, I can do this.


text:
If bortezomib, a cancer drug, inhibits cell proteasomes, wouldn't resulting protein aggregate in normal cells further increase the risk of cancer?
Bortezomib is an anti-cancer drug that inhibits the proteasomes of cancer cells, allowing proteins that stop cell growth to fold and perform their function.
However, wouldn't bortezomib also affect the proteasomes of normal cells? If the proteasomes of normal cells are inhibited, the major factor in the regulation of unfolded and damaged proteins is gone. The resulting protein aggregate would lead to cell damage and diseases such as cancer, Alzheimer's and Parkinson's.
What is stopping bortezomib from affecting normal cells? Does it?

Proteasome inhibitors do affect normal cells to some extent, but the whole point of using them as cancer treatments is that (some) cancer cells are far more sensitive to proteasome inhibitors than are normal cells.  For example, multiple myeloma cells (the first clinical targets of Bortezomib) that overproduce immunoglobulins are dependent on proteasome degradation to eliminate them and are therefore sensitive to Bortezomib.  There are many other aspects of cancer cells that may make them more dependent on proteasome; see for instance
Proteasome inhibitors in cancer therapy: Treatment regimen and peripheral neuropathy as a side effect for some examples.
But of course there are effects on normal cells as well, such as the peripheral neuropathy mentioned in that review.