text:
Signaling between Organelles
I'm confused about how organelles communicate with each other. I understand signaling between cells and the whole transcription and translation of DNA process. However, how does a motor protein know the destination of its package? How does a lysosome know when to break down a worn out organelle? How does the cell distribute ATP to the organelles where it's needed (how does it figure out where the ATP is needed?)?

There's no single common mechanism for intracellular communication, and some of the mechanisms (and some parts of some of the mechanisms) are known in much greater detail than other. For each of the processes you mention, we at least know that they proceed via very different mechanisms.
ATP distribution, for example, proceeds mostly by simple diffusion. ATP is a small molecule and is able to diffuse fast enough that it can move from one end of a cell to another in about ~20 ms on average [1].
Our picture of how ATP actually gets taken up by the various organelles is much murkier. For the case of the endoplasmic reticulum (ER), there is evidence that ATP is brought in via an ATP/ADP antiporter [2]. Transporting ATP via an ATP/ADP antiporter would have the effect of keeping the ratio of ATP/ADP stable in both the cytosol and the ER. It is reasonable to assume that similar mechanisms control ATP transport across other organelle membranes, but you'd have to dig into the literature to find out details.
References
1: Diffusion coefficients of ATP and creatine phosphate in isolated muscle: pulsed gradient 31P NMR of small biological samples
2: Transport and transporters in the endoplasmic reticulum

Thanks, but can you tell me more about how motor proteins know where they need to go and lysosomes knowing when an organelle needs to be degraded?


text:
If you measure the O.D. of cells at one wavelength, is it possible to find its equivalent O.D. at another wavelength?
For example, I measured the optical density (O.D.) of some cells at wavelength 550 nm but I should have used 600 nm. Is there a way of converting my O.D. to its equivalent in another wavelength?

It would be better if you explain what's OD?

It would be useful if you could tell us what you were using your measurements of optical density for?

O.D. can mean 30 different things, many of them being related to science and to optics (see here)! I'll assume you mean absorbance (for Optical Density I'd guess) or light scattering as @canadianer said
Each substance has its own absorption spectrum and reflectance spectrum. Knowing only the absorption is a given wavelength does not tell much about the absorption at another wavelength (at least not without some other a priori knowledge about the substance studied).
So, the answer is 'no'.

Your answer is essentially correct except that OD600 readings of cell cultures are a measure primarily of light scattering, not absorbance.

As already said by Remi.b, there is no way you can directly convert the O.D.550 to an O.D.600.
However, in case you already made numerous experiments using O.D.550, you may not have to do them all over again. You can try to draw a calibration curve of O.D.600 as a function of O.D.550:

take a cell culture (of the same cells you used for your experiments) and prepare several dilutions of it, so that their respective O.D.550 range from 0.1 to 1.
then, measure O.D.600 for each one of these dilutions.
then, draw O.D.600 as a function of O.D.550.

If, and only if, the points form a straight line, you can apply a linear regression to your data. You can then use this linear regression to convert your O.D.550 values to O.D.600 values. However, as pointed out be Jack Aidley in comment, it can be expected that the relationship is not linear. Provided that the curve is smooth enough, you can still calibrate to a curve.
Be careful:

this kind of conversion is totally empirical and will only apply to cell cultures of the same species in the same conditions.
this conversion only applies for values within the measured range of O.Ds.

Depending on what kind of experiment you were doing, it can be better to try this, and even replicate step one and two, or it can be better to start your experiments from scratch... Only you can tell

600 is traditionally used because it gives a more linear relationship between OD and cell count. I would expect that this would give a curve rather than a linear relationship; however, providing the curve is smooth and the conversions occurs within the measured range I do not thing calibrating to a curve is a problem

@JackAidley Thank you for the feedback. I've edited my answer accordingly.

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text:
How does a cell regulate what leaves its vacuole?
Suppose a plant cell wants to take something out of its central vacuole. Some specific substance. Well if the vacuole is a bit of a soup of water and other dissolved substances, how does the cell get some specific substance out? Without letting any of the water/solution into the vesicle that's budding off? Or do they just let the solution right in?
Clarification: Since a vacuole is full of water and other dissolved substances, wouldn't that solution get into a budding vesicle? How is this prevented? Is it prevented?
When the cell is creating a vesicle, it starts pinching off part of the membrane, correct? My question is how the solution in the vacuole stays out of the vesicle, if it does at all.

could u pls clarify this part:Without letting any of the water/solution into the vesicle that's budding off? perhaps any research done on your part...that would be helpful.

Generally the vesicle budding off will contain the fluid from the organelle it comes from, plus it's cargo. The vesicle can then be modified, e.g. pH changed once it is separated from the original organelle.

@alpha When I wrote my answer I was not sure about your question... now, after the second edit (which you wrote after accepting my answer), I'm even less sure! What "vesicle" are you referring to? What do you mean by "how the solution in the vacuole stays out of the vesicle"?

Sorry! I'm confusing myself too. So, I was told that a vacuole will form a vesicle (like the Golgi apparatus) when it's transporting substances out of it. I want to know how specific substances are transported out, without any water or other liquid in the vacuole getting into the vesicle. But I was also unsure whether or not the cell cares if this liquid gets in the vesicle in the first place. Does that help at all? Sorry again! Thank you!

There is vesicular transport involved, but not to transport substances out of the vacuole. Have a look here: Plant vacuole morphology and vacuolar trafficking.

Your question is not entirely clear, even after the edit. However, I believe it's worth mentioning that the vacuole, just like any other membranar organelle1, is surrounded by a biomembrane.
Such biomembranes have transport proteins, which can be channels, carriers or pumps, and those transport proteins can determine which substances will get in/out of the vacuole, either down the electrochemical gradient (channels and carriers) or independent2 of it (pumps).
Here is a diagram showing the membrane of the vacuole with some transport proteins:

Therefore, since the cell can open or close a give gate or activate/deactivate a given pump (just like the transport proteins in the plasma membrane), that helps to explain how the cell decides what gets in or goes out the vacuolar lumen.
1: Unfortunately, there is not a consensus around the definition of organelle. The definition I use states that all organelles have a surrounding membrane (therefore, a ribosome is not an organelle), which renders the expression membranar organelle pleonastic.
2: It's very common reading that pumps will transport the substance against the electrochemical gradient. That's not correct. They will transport the substance independent of the gradient, that is, they can pump a substance against the gradient or down the gradient.

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Why fingers in human fists get folded in absence of neural stimuli?
Background:
I noticed that the fingers in our fist tend to get folded in absence of neural stimuli. The same thing happens in case of our hands and legs.
Question:

What is the mechanism behind this phenomenon?
Is there any positive or negative outcome of this phenomenon?

https://www.reddit.com/r/explainlikeimfive/comments/2yupq3/eli5_why_do_our_fingers_naturally_curl_when_our/

I would assume that as a result of the lengths of the tendons and the arrangements of the various flexor + extensor muscles, the slightly folded positions (curved) fingers, hands, legs, etc. are the "default" positions, in which both antagonistic muscles are in their relaxed state (thus without neural stimulation)
The evolutionary benefit of the slightly curved fingers, hands, legs, etc. may have been more relevant in our primate ancestors than it is today


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Names of different cyclins
Different types of cell cyclins are designated as a to y
Why are some letters like m, n, p, q.. etc. skipped?

Source: https://en.wikipedia.org/wiki/Cyclin

Biological nomenclature can be impenetrable. Almost certainly, at some point in history, there were cyclins designated with these letters. Researchers would have discovered apparently novel cyclins which were subsequently determined to be part of an existing family and renamed. For example, this paper reports the discovery of:

a new cyclin, cyclin M, which appears to be most closely related to cyclin L. Its biological function is unknown, but it is related to cyclins that regulate transcription.

It is now called cyclin L2.
I hope this answer satisfies you to some extent. I doubt anyone is going to sift through the literature and try and determine why all cyclins are are named as they are; that is certainly a losing proposition. The naming of genes/proteins is rather trivial and doesn't generally follow any specific set of rules. Outside of curiosity, the knowledge of cyclin naming doesn't have much, if any, practical relevance.

Before directly answering your question, it's first worth mentioning that: within the table you provided, each cyclin protein is actually being referenced to by using the name of the gene that codes for it. That being said, in order to explain why the naming is the way it is, we need to consider the naming system for genes!

The institution that regulates gene naming is the HUGO Gene Nomenclature Committee, and within the HGNC website, they have a page that outlines the gene naming guidelines.
By considering the gene naming guideline page, and the cyclin-coding gene family, we can immediately say that the first three letters represent the CCN family, which stand for: Connective tissue growth factor, Cystein rich protein, and Nephroblastoma overexpressed gene. (source)
From there, the remaining letters in each acroynm represent the subfamily that the gene belongs to. These subfamilies are defined by a domain within the protein, and are abbreviated based on how that domain is named. For example, when considering CCNF, the F stands for "F-Box", which is a protein structural motif that, in this specific case, mediates protein-protein interactions.

So, to now answer your question as to why the letters are skipped: there is no specific reason (sorry to say it)! It really just comes down to who/when/how the protein motifs were discovered/named, and the fact that a single person/institution didn't discover them all, and that sometimes (quite often) biological naming isn't fixed after the fact to be so perfect.
A (somewhat) similiar situation of this can be seen with how vitamins are named.. they were originally named using the (English) alphabet, in a sequential manner upon discovery, but then it was decided to stop this convention (I'm not sure why), and upon doing so went go back and declassified some vitamins because they no longer conformed to newer standards, which broke the (nice) sequential naming that was originally in place. So, it truely is a purely historical reason, and has no meaning beyond that.
And lastly, just to be inclusive, the number(s) at the end of each acronym are used to uniquely identify the multiple members within each family.


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Why does frost increase soil fertility?
I was reading this paper: https://link.springer.com/article/10.1023/A:1011398431524, which makes claims based on the the idea that frost can increase soil fertility. How/Why will frost increase the fertility of the soil? I was always under the assumption that frost was bad for soil and plants in general.

I found this article on why frost increase soil fertility - specifically nutrient density in the soil.  101 years old!
The Occurrence of Bacteria in Frozen Soil
E. C. Harder  Botanical Gazette  Vol. 61, No. 6 (Jun., 1916), pp. 507-517
https://www.jstor.org/stable/2469064?seq=3#fndtn-page_scan_tab_contents
Relevant text pasted below.  In short: it is bacterial action and nitrogen fixation which contributes to soil fertility.  Freezing increases bacterial population and these metabolic activites.  The theory is that freezing kills bacterial predators on higher trophic levels (protozoans) but the bacteria live and thrive in the absence of predators.

An analogous hypothesis proposed by RUSSEL3 for increases in the number of bacteria after partial sterilization by heat, frost, or other means is that by such partial sterilization the protozoa are killed, thus permitting the unhindered development of bacteria which under normal conditions is held in check by protozoa.
BROWN and SMITH (loc. cit.) in their investigations dealt mainly with the physiological activities of bacteria under conditions of low temperature and frost, although they also made some determinations of the number of bacteria in frozen soil. Their principal conclusions regarding the ammonifying, nitrifying, denitrifying, and nitrogen fixing powers of frozen soils are as follows: (1) that "frozen soils possess a much greater ammonifying power than unfrozen soils"; (2) that "during the fall season, the ammonifying power of the soil increases until the temperature of the soil almost reaches zero, when a decrease occurs, and this is followed by a gradual increase and the ammonifying power of the soil reaches a maximum at the end of the frozen period"; (3) that "the nitrifying power of frozen soils is weak and shows no tendency to increase with extension of the frozen period"; (4) that "frozen soils possess a decided denitrifying power which seems to diminish with the continuance of the frozen period"; (5) that "during the fall season, the denitrifying power of the soil increases until the soil freezes, after which a decrease occurs"; (6) that "frozen soils possess a nitrogen fixing power which increases with the continuance of the frozen period, being independent of moderate changes in the moisture conditions, but restricted by large decreases in moisture"; and (7) that "in the fall, the nitrogen fixing power of the soil increases until the soil becomes frozen, which in almost ceases, after which a smaller nitrogen fixing power is established."

hmm how interesting, I never would of thought of that

It is interesting, and I was glad your question provoked me to read up.

@Willk  - Probably better to use newer references. A lot changes in 101 years. (Also, a lot stays the same, so...)

From the introduction (bottom of page 167 and top of page 168) of the paper you linked (Masters and McMillan 2001)

We use newly available worldwide climate data to quantify the prevalence of seasonal frosts, hypothesizing that what the tropics have in common is an absence of winter frost, "the great executioner of nature" (Kamarck, 1976, p.17). A hard frost that kills exposed organisms in nature could have a major influence on the productivity of human investment in agriculture and health, by reducing competition from pests, pathogens and parasites.

But what does that have to do with the soil?

Frost kills pathogens in the soil, making the soil more fertile for crops (it is their hypothesis). Is it unclear?

then why are there no plants in the north pole?

I am not making any claim myself. It is their hypothesis. You're going to have to read the paper to learn more about whether they found support for their hypothesis. Note that your north pole argument is extremely poor because 1) there is no land in the north pole, only ice (unlike in antartica) 2) there is no seasonal frost int he north pole (they are specifically talking about seasonal frost).

oh␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣

A lack of plant pathogens is great but that is not the same thing as increased soil fertility.  Fertility and pathogens are completely different things.

@Will sure but it is really not the point to discuss whether their hypothesis is true or not. The question was about understanding in which way could the hypothesis make any sense. If you would like to investigate more about their finding, just have a look at the paper.

@Remi.b - Yeah, I don't see this as answering the question directly either.

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Mathematics for genetics
What types of mathematics are useful for studying genetics? Of course, statistics is, and I'm guessing set theory and group theory, but anything else? What about ordinary and partial differential equations?

Calculus is used pretty extensively in population biology. This can often overlap with genetics (modelling change in allele frequency over time for instance).

Genetics is a very wide field of knowledge and many different areas of mathematics are being applied to genetics. Here is a probably not exhaustive list of the fields of mathematics that I have encountered in genetics (you will note that the elements of the list are not mutually exclusive)

diffusion equations
differential equations
markov processes
birth-death process
probability theory (a lot of it)
Bayesian probabilities
statistics
Math related to MCMC processes as well as HMC processes
Many fields of theoretical computer science are being applied and I guess theoretical computer science is a field of mathematics.
Graph theory
numerical integration
Analysis of dynamic systems

You say

set theory

Yes of course

group theory

Probably not so much or maybe I jsut don't really know what it is

ordinary and partial differential equations

I think pretty much any field of science applying mathematics will use differential equations.

But of course, not all geneticists are good mathematicians. Each geneticist specialize in a particular subfield. Some of them do a lot of mathematical modelling, others don't do any. Statistics and everything related to data science will always be useful though.

Your answer is very intersting, however I'd find it even greater with a short explanation of how each  area is used for genetics. For example, it is not obvious to me how diffusion equations are applied to genetics.

From my understanding, it depends a lot on the sub-field you're in.
Data science, statistics and machine learning follow a different paradigm than calculus. Whereas data driven approaches to problem solving are generally concerned with developing predictive models of the underlying system, differential equation based approaches describe a mechanistic model.
These 'top down' and 'bottom up' approaches both have their benefits and drawbacks. On the data science side, it is very difficult to get a low-level understanding of the system. An oversimplification would be:
"The cell is a black box, so let's figure out the output for a given input to get a better understanding of what's going on inside."
On the calculus side, although mechanistic descriptions are a mathematical formalism of what's going on inside the system (and thus imply a complete understanding of the system - in theory), there is still so much that is unknown about most biological systems you'd care to model. This kind of modelling (from the discussions I've had) will be important in the future, when more is known about these biological systems, but for now it is constrained to small sub-systems. A good analogy might be:
"It's hard to figure out how an engine works when we don't know what half of the parts do."
Of course, there are many projects that bridge the gap between the above two methodologies.
So, to answer your question, statistics, computer science, machine learning, linear algebra, calculus, graph theory, set theory, optimization and combinatorics are all useful.


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Do pigeons have the smallest legs-to-body ratio of any bird?
Proportional to their size, do pigeons have the smallest legs of any bird?

What measure do you want to use for size? There are likely different answers depending.

Here's data on body mass and limb length for 163 species of birds (including pigeon):

The information you really want is the ratio of the two. The shortest legs per mass are not quite all flightless birds:
                             Common Name   Hind   Mass Leg_per_kg
1                                Ostrich 1256.7 94.210   13.33935
2                           King Penguin  326.2 13.650   23.89744
3                                    Emu 1036.1 40.670   25.47578
4                           Whooper Swan  405.0 10.675   37.93911
5                       Macaroni Penguin  197.7  4.819   41.02511

whereas the longest legs per mass are:
159            Yellow-Bellied Flycatcher   51.3  0.011 4663.63636
160                   Common Treecreeper   41.8  0.008 5225.00000
161                 Whiskered Flycatcher   51.2  0.008 6400.00000
162        Southern Beardless Tyrannulet   47.5  0.007 6785.71429
163            Ruby-Throated Hummingbird   21.8  0.003 7266.66667

The pigeon falls somewhere near the middle:
106                        Scaled Pigeon  108.7  0.260  418.07692

Swifts are actually down near the bottom:
153                        Chimney Swift   49.9  0.023 2169.56522

While they do have tiny legs, they are actually quite long for their body mass.
Of course if you chose a different measure of size, then these relative numbers would be all different.

Length per kg in my opinion is a really really bad measure. In general, body length increases with the cube of mass. This measure just tells you the biggest bird. Pretty obvious if you look at the leg length of on ostrich - those are long legs, almost half the height of the bird, even when including a very long neck. That doesn't seem to be at all what OP was asking for.

Technically it's exactly what the OP asked for ("proportional to their size ...") but I agree it's probably not what they actually wanted to know. I upvoted for the interesting chart, but was tempted to downvote again because there's no reference. Where do the data come from?

@iayork I collected the data from the Museum of Comparative Zoology (Cambridge, MA).

@BryanKrause Agreed, which is why I said that if you picked a different measure of size, you would get different results. I can think of good reasons not to pick any of the other obvious possibilities: wing length (penguins, ratites), trunk length (penguins, loons), mean vertebral length (swans, geese, herons, etc.), synsacrum breadth (Anseriformes). So given the tradeoffs of picking any proxy for size, mass is as good or as bad as any other, as long as you interpret the results in that context.

That achievement probably belongs to the Swifts, specifically known for their short legs. Their name Apodidae derives from the word for "footless" in Greek.

"absolute shortest legs: virtually non-existent in swifts (Apodidae)"


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Protein phosphorylation in the cytoplasm. Typical time scale?
Is there a typical protein phosphorylation rate in the cell cytoplasm under physiological conditions, or at least an upper-bound?
Suppose a protein $A$ is being phosphorylated into $A^*$ with the first order reaction
$A \to ^k A^*$
where $k$ is the reaction rate ($k$ unit is $\rm time^{-1}$).
In reality a phosphorylation reaction involves multiple agents (protein, enzyme, ATP) and multiple reactions, therefore cannot be accurately mapped onto a first order reaction. However this makes sense if we are only interested in the order of magnitude of $k$. According to this first order reaction the evolution of the $A$ concentration is given by
$$
\frac{d A}{dt}=-k A
$$
and therefore $1/k$ is the time scale at which $A$ vary.
So my question can also be formulated as: suppose that at a given time a cytoplasmic protein $A$ starts to be phosphorylated into $A^*$. What is the typical time scale at which the concentrations of $A$ and $A^*$ reach their equilibrium values?
From few things I read it looks like it is of the order of seconds or minutes or hours, and 1 second seems to be an upper bound. Any references?

Phosphorylation is not a first order reaction, it always Protein + ATP -(enzyme)-> Protein-P + ADP  (in rare cases a different Phosphate carrier might be used as well). While the concentration of ATP is somewhat kept stable, you shouldn't/can't assume it doesn't matter.
Otherwise I'm not sure, the Brenda database might have some numbers for Kinases, but getting 'average' or upper/lower bounds might be tricky

Sure it is not a first order reaction, but to some extend you can always look how fast the concentration of the unphosphorylated protein (A) changes with time and get the coefficient $k$ which will be your "effective first order rate", that will be function of ATP, enzymes, etc. That is just to get roughly an order of magnitude.

@Nicolai I just edited the question, I hope it makes more sense in this way.

yeah, I think with the edits it's much clearer why you would assume a first order reaction in this case. Did you take a look at the Brenda database for some kinases (phosphorylation enzymes) and possible reaction values? I'd also assume that depending on the kinase (not so much the target), the order of magnitude for k might be very different.


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Does Batesian mimicry rely on constant reinforcement?
If the species being mimicked, the monarch butterfly, for instance, were to become extinct, would the species mimicking it loose all of the benefit gained by their Batesian mimicry immediately?
I realize that the Monarch may be a poor example as it is a Müllerian mimic with the Viceroy butterfly, however their ranges do not overlap everywhere. Would the extinction of the monarch reduce the ranges of Batesian mimics to that of the Viceroy?


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Do we see protocells forming in nature today?
I understand that the current theory of chemical evolution (aka origin-of-life, abiogenesis) involves lipid-based protocells that enclosed RNA and perhaps some other compounds as a first steps to life.
I'm wondering if we see them forming today in nature, and if not, why not?
Are there successful experiments creating them in the lab?  If so, what are the required conditions?

we don't think so, some parts are easy. liposomes form all the time, and can be created in lab quite easily. They quite readily encapsulate any material present when they form, including DNA. So once you have the right stuff (likely RNA) it is very easy to enclose it in a lipid bilayer.
RNA has been formed from scratch in a lab it is even easier than we thought it would be. It may form in nature today but is unlikely , the current atmosphere is very oxygen rich and bacteria are not just willing to eat RNA but also basically all the chemical building blocks as well so it is difficult to build up a concentration of the precursors in nature today.
Worse evidence of it forming today would be ridiculously difficult to demonstrate because there is a constant contamination of biologically produced RNA from decaying organisms. There is basically no place on earth today with liquid water that does not have life in it.
Here and here is a review of our current models for the origin of life, Be warned the first link is a file.There are many steps involved to get a cell but it all starts with the first molecule capable of making copies of itself.
Forming self catalysis strands in a lab would be the best evidence but has one major problems, Money. Earth had an ocean sized laboratory and millions of years to stumble one of the strands with one of the right codes through random chance (remember a self-replicating code only has to happen once) which likely could only be duplicated by doing millions or even billions of identical laboratory experiments.
Finally while the Urey-miller experiment was historically important it is by no means the best nor most modern experiment you can find much more information about the variety of experiments at this question.

The file link doesn't work for me - seems it's a local link.

My bad, there that should fix it, if not here is a different link https://www.scribd.com/document/166508345/entropy-12-01733-v2

sorry - still having problems.. could you put up as a google doc or dropbox?

did you try the scribd.com link? I don't personally have the document.

In present environment  the conditions are not favourable for the new type molecules /coacervates or microspheres formation because the present atmosphere is oxidizing in nature, presence of oxygen inhibits primary molecules formation.
The early conditions were of reducing nature it has enormous lightning, high temperature, decaying radioactive compounds. Moreover, there were no organisms to feed on newly created molecules in water bodies
.
The first organisms formed on earth were Chemoheterotrophs i.e they feed on others for food and they cannot make their own food from sunlight.
The first major toxic was Oxygen in gaseous form, earlier it is present in combined form or as metallic oxides in the water bodies as H2O.
Now in atmosphere O2(in gaseous form) and tiny microorganism present oxidizes the the basic elements like C, NH3 to other forms like CO2.
However, experiments by Miller and Oparin in-vitro conditions shows the formations of primary cells having amino acids, purines, pyrimidines - The basic requirements.
Miller and Urey proved the Chemical Evolution theory in their experiments showing the formation of many amino acids, sugars, nitrogen bases.  Oparin stated that mixing large protein with a polysaccharide leads to formation of coacervates; same experiment was also done by Sydney Fox.

Welcome on SE.Biology. In order to improve your answer, please add some references and links

Thanks for the answer - but I don't understand. Wouldn't the protocells be forming underwater?  You're talking about oxygen in the water?  Why would other organism eliminate all trace? - eg, even for bacteria that eat other bacteria, some of the original survive - they don't eat them all.

some of the original survive - they don't eat them all. It's not the bacteria. The abiotic factors themselves inhibit development of protocells.

@PrittBalagopal - I was referring to the statement "Moreover, there were no organisms to feed on newly created molecules in water bodies".  Which I assume means "even if they could form, they would get eaten..".  But I would still expect that we could control the factors and build them in the laboratory which would have neither problem.

But I would still expect that we could control the factors and build them in the laboratory which would have neither problem. Of course, if you have the perfect environment, you can have anything. But life doesn't evolve in perfect environments. Besides the title of the question is "Do we see protocells forming in nature today?"

@Yehosef The first organisms formed on earth were Chemoheterotrophs i.e they feed on others for food and they cannot make their own food from sunlight.
The first major toxic was Oxygen in gaseous form, earlier it is present in combined form or as metallic oxides in the water bodies as H2O.
Now in atmosphere O2(in gaseous form) and tiny microorganism present oxidizes the the basic elements like C, NH3 to other forms like CO2.
However, experiments by Miller and Oparin in-vitro conditions shows the formations of primary cells having amino acids, purines, pyrimidines - The basic requirements.

@PrittBalagopal - The question was about in nature today - but I added the question about success in the lab in the details.  "Of course, if you have the perfect environment, you can have anything."  Do you have references where they have done these experiments and found these results?  I would expect that if it could happen in natural under non-ideal conditions, it would be able to achieve in ideal conditions.

@AbdulKhan - thanks for the explanation - do you have references of where they formed "primary cells" in-vitro?  I had never heard of such an accomplishment.

@Yehosef Miller and Urey proved the Chemical Evolution theory in their experiments showing the formation of many amino acids, sugars, nitrogen bases.  Oparin stated that mixing large protein with a polysaccharide leads to formation of coacervates; same experiment was also done by Sydney Fox.  For references you may have to search the google.

The Miller/Urey experiments are a long way from "proving the Chemical Evolution theory" - they basically showed how amino acids formed which a step but far away from proving the theory.  The closest I've found is this article: https://www.nature.com/articles/ncomms9352 - but it requires a delicate balance of external conditions to stimulate "reproduction".  I'm not sure what natural selection is going in their experiment.

There are some examples of lab-made protocells although they cannot reproduce and they die because of dilution of their components after a while.
In nature we haven't seen any, most probably because 1) nobody is looking for it and 2) even if they form they have to compete with all the other life-form, that are already optimized for that particular environment, leaving no chance of long-term survival.

Basically the closest we've come to a living organism from scratch is an autocatylitic RNA set. Look it up.
But we haven't actually made any self contained life yet, although this video is VERY interesting.
Life can't form anymore. We have oxygen, which like Abdul said, smashes delicate primordial molecules. Also, we have an ozone layer, which stops the UV rays from hitting the earth, which as demonstrated in variants of the miller Urey experiment, were probably instrumental in the formation of life.

don't tell them to look it up, provide a source


text:
What are the differences between a liposome and simple cell membrane
I'm learning about chemical evolution and the transition from RNA to protocells to cells.  I understand that the protocells have a phospholipid structure called a liposome.
I recently saw a video showing CG animations of the workings of a cell and it seemed that the cell wall was much more complex than what it seems a liposome is.
I'm looking for information about the differences between a liposome and a basic cell wall (not sure of the difference for different types of cells -
 but I guess for prokaryote since that would have been first.)

By looking on wikipedia I found:
About liposome

A liposome is a spherical vesicle having at least one lipid bilayer. The liposome can be used as a vehicle for administration of nutrients and pharmaceutical drugs. Liposomes can be prepared by disrupting biological membranes (such as by sonication).
Liposomes are most often composed of phospholipids, especially
  phosphatidylcholine, but may also include other lipids, such as egg
  phosphatidylethanolamine, so long as they are compatible with lipid
  bilayer structure. A liposome design may employ surface ligands for
  attaching to unhealthy tissue.

About cell membrane

The cell membrane (also known as the plasma membrane or cytoplasmic
  membrane) is a biological membrane that separates the interior of all
  cells from the outside environment.The cell membrane is selectively
  permeable to ions and organic molecules and controls the movement of
  substances in and out of cells. The basic function of the cell
  membrane is to protect the cell from its surroundings.
It consists of the lipid bilayer with embedded proteins. Cell
  membranes are involved in a variety of cellular processes such as cell
  adhesion, ion conductivity and cell signalling and serve as the
  attachment surface for several extracellular structures, including the
  cell wall, glycocalyx, and intracellular cytoskeleton. Cell membranes
  can be artificially reassembled.

So the major difference seems to be the presence of "embedded proteins" inside the cell membrane.


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How dirty are bugs? And is it okay if they touch food?
Sometimes I see people throw out an entire drink or bowl of food because a small bug was in it. Are they justified in doing this? Is there enough bacteria on common species of bugs (like ants, flies, beetles, dragonflies, caterpillars, moths, etc) to warrant any kind of health concern for a larger amount of food than what the bug was in contact with, or at all?

Most people don't care about hygiene. It's mainly the "eww" factor. However common houseflies often sit on fecal matter, so that's an issue though.

You actually eat a lot of insects without even knowing it:
https://blogs.scientificamerican.com/but-not-simpler/i-hate-to-break-it-to-you-but-you-already-eat-bugs/

Well, first of all you should consider that insects and generally animals don't have so much hygiene, like us humans. Some of them, let's say the ants, yes some kind of hygiene is present, but not in the human degree. In fact, most insects are responsible for the most dangerous deseases in the world such as malaria , yellow fiver, sleeping sickness (espacially found in Africa because of the tsetse fly) and many kinds of encephalitis. This article claims that most of insects are carriers of deadly deseases. Also, about the second part of your question, you mentioned " If it is okay for bugs to touch food"... Well the answer is ofcourse no, because you don't know:
1. what the insect was touching before it "lands" to your food
2. If it has dropped any fecesto your food
3. And last but not least if the insect layed any kind of eggs to your food.
4. Some insects carry fungi that if a human being consumes them he might have serious problems, because some fungi are responsible for poisoning or infection.
The third one that I mentioned is responsible for the most cases of Tapeworm infection. This means that the eggs and larvae pass straight to your digestive system and create the infection. To sum up, unknown factors (like bugs) must not touch our food, because there is a chance of infection. To help you here's a wikipedia list that shows the most easily transmitted diseases to humans fron insects: List of diseases caused by insects.

A lot of the carried disease you mention depend on insect bites, not food contamination.

If bugs are really that bad, how come so many people eat them raw or nearly raw without getting negative side effects?

@DaneJoe Each human has different hygiene rules....

@The_Mad_Fish No matter who you are, if you just eat a slice of raw chicken that's been sitting out for a day, you will get sick. This is not dependent on some cultural preference, there is at absolute statistical answer at least for individual species of bugs.

This answer is misleading; the mosquito is the most deadly insect by numbers on the planet, and it doesn't result from landing (or pooping) on your food.


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Bioenergetics of bioconversions: is there a surplus of energy?
By bioconversion, I mean a microbial process during which resting cells are used in order to convert a substrate to a desired product, whithout cell growth. For example, in this paper, they used Lactobacillus reuteri to convert glycerol to 3-hydroxypropionaldehyde, while L. reuteri can't grow on glycerol. Basically, during bioconversions, cells produce energy for their metabolism, but do not grow.
The energy thus yielded by cells is supposed to ensure their energetical maintenance cost. I was wondering what happens to cells if the energy gain is superior to maintenance needs? Is there some kind of homeostatic regulation of the ATP/ADP ratio? If not, what could be the consequences of too much ATP?

I am not sure about this pathway that u have mentioned but if u see metabolic regulations of pathways like glycolysis for example or krebs cycle their enzymes are feedback regulated with ATP/ADP ratios.


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Body's response to second dengue attack
I have read in wikipedia that the first dengue virus infection is cleared by the body very easily. The second infection, however, is dangerous. How does body fight second infection, or does it has any tool to fight it given earlier antibody will be ineffective?

From the Wiki page for Dengue fever, I believe the text you're referring to is:

... those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk.

Notice that the text says, "...infected with other serotypes of dengue fever ...". That being said, your focus should be on the effects of reoccurring infections brought about by different forms of dengue fever.

In 2011, the School of Public Health at University of Berekeley published a study that addressed this very situation. According to the article:

In two clinical studies of dengue in Managua, Nicaragua, we observed an abrupt increase in disease severity across several epidemic seasons of dengue virus serotype 2 (DENV-2) transmission. Waning DENV-1 immunity appeared to increase the risk of severe disease in subsequent DENV-2 infections after a period of cross-protection. The increase in severity coincided with replacement of the Asian/American DENV-2 NI-1 clade with a new virus clade, NI-2B.

And to quote lead author Molly OhAinle, which I believe answers your question:

With the second infection, the antibodies sort of recognize the new type of viruses, but not well enough to clear them from the system ...  Instead of neutralizing the viruses, the antibodies bind to them in a way that actually helps them invade the immune system’s other cells and spread.

So, given that the immune system represents all behaviors within our body that defend against foreign bodies considered to be a threat, if the immune system itself is helping the virus, then no, there is no other line of defense against  the infection (excluding treatment intervention).

Lastly, here's an image from that publication, showing the seasonal patterns of dengue fever with respect to the various serotypes:

For finer details, you can access (and download) the publication for free; you just need to create an account on this site.

that is my question  "Instead of neutralizing the viruses, the antibodies bind to them in a way that actually helps them invade the immune system’s other cells and spread."  does organism scummub to it as it will not be attacked by immune


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Is it hydrogen atoms or electrons that are passed along an electron transport chain?
I am so confused because my book says it is electrons which are passed along the electron transport chain but all we are considering is hydrogen ions (H+) and hydride ions (H-). Can someone clear that up for me ?

ELECTRON transport chain. Hard to answer the other parts without more context from the book/class...

@Zhe  never mind it is electrons in the form of hydride ions. I found out from chem.libretexts.org

As explained on the Wikipedia page of the electron transport chain:

An electron transport chain (ETC) is a series of complexes that transfer electrons from electron donors to electron acceptors via redox (both reduction and oxidation occurring simultaneously) reactions, and couples this electron transfer with the transfer of protons (H+ ions) across a membrane.

Electron are thus transfered from the electron donor (NADH, H$^+$ produced by the TCA) to the electron acceptor (O$_2$) through the successive enzymatic complexes of the electron transport chain.
Complexes I, III and IV are proton (H$^+$) pumps: they use the energy gained thank to the electron transport in order to translocate protons across the membrane.


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what is allelic sequence variation?
When DNA polymorphism occurs mutations can take place.  If these mutations occur in the germ cell and do not destroy its capability to reproduce, it is said that the mutation might move on to the next generation. My book says it might lead to allele sequence variation. But what does it mean?

You should take a look at this question; and specifically, my answer, as it explains the relationship between mutation and variation, and will help you better understand what your book is talking about. https://biology.stackexchange.com/questions/43159/what-is-the-definition-of-a-mutation/64288#64288

Can you please give a direct quote? I am pretty sure your textbook did not say exactly what you said!

When DNA polymorphism occurs mutations can take place.

In genetics, polymorphism just refer to the existence of genetic variation among individuals in a population (often referring to a specific locus).
Mutations is the ultimate source of polymorphism. It is not polymorphism that allow mutations to occur.

If these mutations occur in the germ cell and do not destroy its capability to reproduce, it is said it might move on to the next generation.

Indeed!

My book says it might lead to allele sequence variation.

'allele sequence variation' is just some kind of another generic term for polymorphism. For this expression to make sense to you, you should start by looking up the definition of allele


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What happens to deep sea creatures if they reach the surface?
Since deep sea creatures are adapted to incredibly high pressures, I would assume they would not be able to survive in the low pressure environment of the surface.  What exactly happens physiologically to a deep sea fish if it reaches the surface?  Would cell walls rupture?

What if you opened a door in a spaceship without a spacesuit? and wiki > Space Exposure are related.

It varies depending which creature is considered. The faster they are made to lower the pressure and raise the temperature, the worse the effects are. Some animals have a liver, which can help to counteract toxic effects at lower pressures, and some fish at 2000m have an air bladder, so they explode if they are hauled up.
Deep sea fish sometimes arrive at the surface with their inner organs popped out of their mouth.

They have different lipid types than us, because lipids are packed together differently at high pressures, and lowering the pressure on their lipids can make them malfunction.
Chemicals can act differently at high and low pressures, so a chemical that can be inert at a low pressure, can produce a different reaction at high pressure, producing gas, precipitating into component chemistries. Urea can be toxic at high pressures and fine at low pressures.
Proteins fold and change shape under pressure, so deep sea animals can use different proteins that may chainge their shape and function at lower pressure.
Dolphins can get the bends if they are scared back to the surface by deep sea exploration industries, too fast for their bodies to adapt.
here are some info sources:
http://www.deepseanews.com/2016/03/under-pressure/
https://www.quora.com/Do-deep-sea-animals-experience-decompression-sickness-if-brought-to-the-surface


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Why do type 1 diabetics experience hypoglycemia?
I know that type 1 diabetics do not produce enough (possibly none) insulin since beta cells of pancreas are damaged and as far as I know glucagon is produced by alpha cells (which are healthy in diabetic body, I suppose). So, my question is that since glucagon is released when the blood glucose is low, why do the diabetics experience hypoglycemia? Shouldn't the glucagon be released and increase the blood sugar?

Note that in Role of Alpha Cells in Diabetes1, the following is stated:

Glucagon responses to hypoglycemia have been known to be blunted in
  type 1 diabetes of long duration, and this may be a result of a loss
  of alpha- and beta-cell communication secondary to insulin deficiency.

Rudy W Bilous. Role of Alpha Cells in Diabetes - Medscape - Apr 11, 2003.

Have you attempted to solve this on your own? Can you show us what you found?

@anongoodnurse What I found is that it may be a result of a loss of alpha- and beta-cell communication secondary to insulin deficiency.

Key to this question is that untreated, type 1 diabetics would never have hypoglycemia.  It is insulin treatment that causes the hypoglycemia.  Insulin brings sugar down and without insulin (as the case with type 1 diabetics) sugar just goes up.    Exogenous insulin will bring sugar down in anyone, diabetic or no.  Since Type 1 diabetics use insulin all the time, there is more chance for an accident (hypoglycemia).
Also, some Type 1 diabetics might not compensate against hypoglycemia or correctly perceive that they are hypoglycemic.  Reasons for this are laid out in the following article:
From Hypoglycemia in Type 1 Diabetes

Three major defects in this homeostatic response contribute to the
  high frequency of hypoglycemia in type 1 diabetes.

The article summarizes what those are - basically a blunting of normal reactions to hypoglycemia stemming from the disease itself.  It then summarizes:

Thus, the glucose counterregulatory defense against hypoglycemia in
  individuals with diabetes becomes impaired at almost every level and
  rendered even more defective through intensive insulin therapy


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Differential Gene Expression
I have a matrix two gene expression datasets, one from 10 normal individuals and ten from diseased individuals, which are normalised log fold change values--, i.e., already processed.
My question is: how do I obtain a list of differentially expressed genes?
That is the up and down expressed genes. I was thinking of getting means for each group and then sorting the average fold change values would work, but I am not sure...
Thanks.

Note that there is also a bioinformatics stackexchange site: https://bioinformatics.stackexchange.com/

It hard to figure out what sort of data you have. qPCR? Let me give you an example with tools involved on how I get differential genes for RNAseq data, that is whole transcriptom and for mouse that transcriptom that's about 23000 genes.

Step 1. Map raw reads to the reference genome.
Step 2. Count number of reads within the feature. Feature can be several things, but lets just take protein coding feature (feature == gene).
Step 3. Do differential expressions analysis

From step 2 you get a matrix of counts.
      sampleA_rep1 sampleA_rep2 sampleB_rep1 sampleB_rep2
gene1      2             5        20             23
gene2      10            12       50             50
gene3      20            23       4              6
..
geneN

The packages that I use are limma and/or edgeR. You can find them on bioconductor Both packages take raw counts and give you topTable of DEG, default is top 100 genes.
I recommend reading edgeR or limma manuals, there come with great explanations as well as examples. Also A scaling normalization method for differential expression analysis of RNA-seq data is original paper that explains TMM normalisation (mention a bit more in depth below)
Two things; one you need to filter genes with low counts, convert to cpm() counts per million before filtering as this takes library size (depth of sequencing) into consideration. two calcNormFactors() will do TMM
The hardest thing (I understand) in RNAseq is to get total RNA output for each sample. Because a treatment will effect the number of transcripts expressed in that sample, increasing or decreasing amount of transcript, which give you unbalanced counts. You won't know just by looking at raw counts if geneA has less counts because it's been down regulated OR because that sample after treatment has more transcripts present in the cell and geneA simply has less coverage, due to other transcripts also getting reads now. I can't really explain that too technically because I don't understand this myself, but TMM normalisation takes care of this and  gives you an estimate of degree of variability.
I know that I'm not giving that much info on actual differential testing, which was your question. edgeR has exactTest() which is Exact Tests for Differences between Two Groups of Negative-Binomial Counts , which might help you, but you might have normalise your counts differently as mentioned above. The general idea (I understand) is you need to fit a model (lmFit()) and then do the test eBayes()
Other

Degust this is very nice tool that uses limma and edgeR in the backend, but simplifies a lot of things as well as gives you nice interface to work with your data. You upload raw counts! in the format shown above
DESeq one of the other rather popular R packages that can also do differential gene testing

There is software for this, but if you want a very primitive way to analyze it, do a t-test (which is basically looking at both the difference in means and the STDEV of each group)

At least suggest reliable software. 2) This primitive suggestion is actually a very bad idea, it ignores many of the crucial features of this type of data including compositional problems (which actually make this entire field of differential expression a bad idea generally), the overdispersion and count nature of the data.


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Do all human cells have all the same organelles?
I know that not all human cells have nuclei (erythrocytes eject theirs before they are fully matured), but do all human cells have all the other organelles? The two I'm particularly concerned with are the Golgi apparatus and lysosomes.

sperm often lack certain organelles, so are you including germ cells.

The presence of an organelle in a cell is strongly connected with its main function. For example in red blood cells, to have maximum space for haemoglobin and hence oxygen storage, many of the organelles are not present such as nucleus, golgi complex, lysosomes, etc. Another example can be of liver cells or muscle cells having a very high amount of mitochondria and ribosomes for high ATP production and protein synthesis. Similarly, each cell is designed in the most efficient way that aligns with its main function.
The answer to your question is no. Not all cells have golgi complex or lysosomes.
One thing that is important here is that the presence of golgi complex is linked with the presence of lysosomes. If there are no golgi complexes, lysosomes are also not present there.
Hope it helps.

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

I believe that yes.
Here is more to read about:
https://bscb.org/learning-resources/softcell-e-learning/golgi-apparatus/
"is found in all plant and animal cells"
and explanation why so
https://sciencing.com/would-did-not-golgi-bodies-8657737.html
I am no expert in this but I was looking for it as well, I believe it is right.

This is wrong. Erythrocytes and thrombocytes do not have golgi complexes. OP asked if all human cells have all the other organelles, so he is including those blood cells that lack nuclei. Anyway even then, I would not be surprised if some cells don't have a golgi complex some of the time.


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If an insect becomes upside down, do they have mechanisms to turn themselves right side up?
This question is mainly applicable to beetle's and cockroaches. If I flip them so their legs point upward, they usually squirm around and wiggle trying to come back upright. Sometimes they succeed, and turn right side up again; sometimes they don't. Do insects have any built in mechanisms to unflip themselves.
I was unable to find any sources, but I believe they should, since insects climb stuff, and they may land inverted if they fall, so a mechanism might've been evolved to unflip themselves.

Why don't you consider their attempts to come back upright as a mechanism to do so? If they are having difficulty, it might be because artificial surfaces provide an environment they have not experienced over evolutionary time: that is, very flat surfaces, with no debris around for traction.

Why don't you consider their attempts to come back upright as a mechanism to do so? I could attempt to fly, although I'd die if I tried, since I have no mechanisms (wings, hollow bones) to fly.

Pinging @BryanKrause

@Pritt Air is not the natural fluid for us to fly, you would fly if you change the fluid to water( that is swimming). Hope u understand the analogy.

You seem to have skipped the second half of my statement. I think your question is a bit like putting a human on glare ice, perfectly smooth, and asking them to try to run. Then, when they slip and fall, you ask "Do mammals have mechanisms to keep themselves from falling while running?"

But @BryanKrause insects getting flipped isn't an artificial phenomenon is it? It could happen as an insect climbs a wall and slips down. It could happen anywhere on Earth's landmass.

I'm suggesting that the beetles and cockroaches you see are probably only struggling because you have them on a very flat surface. In natural environments there are almost always going to be other things around to grab on to.

@BryanKrause I'm led to this sort of thinking. Human civilizations (with flat floors) has been here for centuries. Insects have been regularly invading human settlements due to the great abundance of food there. Given that insects have short lifespans, haven't they evolved mechanisms to unflip themselves? (P.S. I believe cockroaches are more commonly found in human settlements rather than in the wild, correct me if I'm wrong.

https://biology.stackexchange.com/questions/3278/why-do-cockroaches-flip-over-when-they-die The answer to this question suggests healthy cockroaches flip back no problem.

Thank you @BryanKrause . Would you care to write all you told as an answer so that I can accept and upvote it? It would also mark this question as resolved.

Well, many insects have developed ways to right themselves when they get turned over.
One of the more interesting families are the Elateridae, or click beetles: so named because they press their prosternum and mesosternum against each other which causes pressure. That pressure is eventually released causing a "clicking" sound and springing the insect upward (or away from predators).

You can see an additional video of a click beetle doing so here.


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Properly changing the time scale of a parameter in a growth model
I have a two-population model, where one of the populations is a bacterial culture with its growth described as a logistic growth, with a reported growth rate of $2 \log\hbox{bacteria hour}^{-1}$ and a death rate of $1.5 \log\hbox{bacteria hour}^{-1}$ and a carrying capacity of  $7 \log\hbox{bacteria}$. However, my model studies the interaction between bacteria and fungi in a time scale of days, but if I try to directly rescale these parameters, I get a growth rate of $48 \log\hbox{bacteria day}^{-1}$ and a death rate of $36 \log\hbox{bacteria day}^{-1}$, which is absurd, given the carrying capacity of bacteria.
Is there a standard method for properly rescaling these parameters for bacterial growth, without having to change the model? What alternatives do I have?

These values are not absurd: it's just a different unit, it does not change the reality of th phenomenon.
The fact that your population can grow by a $48$ or $36~\mathrm{log}$ factor in one day, while the carrying capacity is $10^7$ bacteria, only means that the growth happens in less than one day (once the latency phase is over). Many bacterial population can grow in less than one day, it is not shocking.
In my opinion, it is not absurd to use the growth rates in $\mathrm{log}~ \textrm{bacteria} \cdot \textrm{day}^{-1}$. There is not need to rescale values if you just want to convert hours into days.

My issue is that when performing simulations day-by-day the model is doing huge jumps each day, which the carrying capacity is unable to sustain. Would in that case perform jumps hour by hour be better?

It appears to me that a day-by-day study is not in line with the time scale at which bacterial growth occurs. Bacterial growth is generally studied hour-by-hour, or even min-by-min


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Law of Segregation (Genetics)
What if the two factors/different factors of a character did not segregate during gametogenesis and blended together?

Welcome to iology.SE. What do you call a "factor of a character"? If you have a hard time to explain what you have in mind, you may want to try with a (eventually made-up) example.

When you say "did not segregate", you are thinking of a single event of reproduction where the two loci have not been separated by a recombination event or are you thinking about a case where two loci are perfectly linked?

According to the law of segregation:- Pair of contrasting factors or genes for a given character, never blend but segregate during gametogenesis. My question is what if the opposite of the above said law happened

The factors that segregate according segregation law are the two alleles of any gene (https://en.wikipedia.org/wiki/Mendelian_inheritance). The only way to avoid that two alleles segregate at meiosis is to have them inherited in the same gamete, as shown in the picture below . Thus, if the two alleles would not segregate you will double you number of alleles (and chromosomes) at each generation. The effect on any given allele would depend on the level of dominance (dominant, recessive, additive), but that would be the least, since at each meiosis the offspring would have twice the number of chromosomes compared to the parents.

Not all genes are bi-allelic unlike implicitly suggested in your first sentence. 2. The law of segregation does not only apply to genes but to any loci 3. Your diagram shows a case of selfing with whole genome duplicate which may be a little confusing.

if the two alleles would not segregate you will double you number of alleles this is simply wrong. You misunderstand the definition of segregation (at least as used in the Law of Segregation). 5. Your comment on dominance is misleading as well.


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What kind of larva is this?
It has a body which is divided into three parts:

The head, which is small, with a black, needle-like structure on the tip which I think is the mouth.
The upper body, which has a pure white color that is softer than the lower body.
The lower body, which is hard, has some blacks spots on the rear end with a yellow spot on the very tip and, compared to the upper part, has a clouded clear white color.

It moves very strongly when touched, but not that much.
My classmate found this when he opened a leaf from a small plant, thinking that it was a butterfly pupa because it was covered with a silk like cover but very thin to be compared to a butterfly cocoon.
Larva pictured here:

What about adding location?

That's going to be a moth. You can identify the wings forming, and which end will be the abdomen. You're upside down; the little black needle part is the eliminating end of the moth pupa. The head is at the end with multiple dots. When it is far enough along, you'll be able to make out everything: eyes, antennae, etc. They often encase themselves in silk (think silk moths caterpillars).

Location, and the plant it was found on may help.

+1 for the efforts in description. I agree with @anongoodnurse that you got the orientation wrong, though. What you see on the photo is the ventral face, with the head to the right. You can also guess the legs forming on the right part.


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Are we capable to generate sounds of animals to the point that they mistakenly recognize it as members of their species?
From Animal language (Wikipedia), there are many evidences that we can communicate with animals, at least to baboons and dolphins. There is a case that fish moving away when hearing a record of whale sounds, however no examples mentions about the sound we actually make to communicate with them. We can even dog whistle, but this doesn't mean the dogs thinks that there is another dog. In my opinion, the answer is yes, since once we can capture the sound with spectrograms we can ultimately generate it. Is there any research on this?

Consider the long history of using various calls and audible lures in hunting.

I used to work on a ranch and could imitate calves well enough that their mother's would come running over.

@jamesqf can we make all the sound of the animal?

@Ooker: Who is "we"?  Personally, I can't even make all the sounds that other humans make, like the trilled 'rrr' sound in Finnish, or the click (often represented by '!') in some African languages.  And I certainly can't sing soprano :-)

@jamesqf well, but if you learn phonetics and spend ten years to learn opera, maybe you can? "We" means people.

@Ooker: That's what I was trying to say.  Not all people can make the same range of sounds.  Sometimes it's physical, as with the difference between a baritone and a soprano, or why two people with the same vocal range can be good and bad singers.  Sometimes it's a matter of needing to learn phonemes like 'rrr' or '!' at a particular point of childhood development.  So it's not surprising that some people can duplicate some, but not all, vocalizations of animals.

The most clear and indisputable case of a human being generating a sound (using his own voice) that was mistakenly recognised by an animal as a sound made by a member of its own species is the case of Konrad Lorenz and the imprinting on birds.

Lorenz needs no introduction. However, in the case you don't know him, he is the father of modern ethology, together with Niko Tinbergen.
Among several other things, Lorenz studied and explained imprinting, specifically filial imprinting. According the Wikipedia link above:

Lorenz demonstrated how incubator-hatched geese would imprint on the first suitable moving stimulus they saw within what he called a "critical period" between 13–16 hours shortly after hatching. For example, the goslings would imprint on Lorenz himself (to be more specific, on his wading boots), and he is often depicted being followed by a gaggle of geese who had imprinted on him.

For imprinting in an object (the mother), some species depend on movement that object makes, some depend on the sound it makes and some depend on a mix of movement and sound. From Brittanica:

Lorenz demonstrated the phenomenon by appearing before newly hatched mallard ducklings and imitating a mother duck's quacking sounds, upon which the young birds regarded him as their mother and followed him accordingly. (emphasis mine)

During his life, Lorenz had several bird children, making several different youglings imprinting on him. As you can see in pictures like this one below, those animals will follow Lorenz (for the rest of their lives) as if Lorenz were their mother.

The funny thing is that, during some time after his early publications (but way before his Nobel Prize in 1973), some people had problems accepting Lorenz's discoveries, because they could not reproduce them.
It turned out that Lorenz was very effective in imprinting a lot of different bird species because of his uncanny ability of mimicking that bird species' sound, be it a goose, a chicken or a duck.
Of course, raising so many children has its problems:

He's an interesting man. Anyway, isn't that imprinting happens when the younglings see  the first big object? Also, do you know other examples on well developed animals?

@Ooker No, for most of bird species imprinting depends on the sound the "mother" makes, replying to the baby's call. Also, have in mind that, for the visual ones, they will not imprint in the first thing they see, but in something that's moving a certain way in a certain critical period.

I see. Do you know any other methods that they use? Smelling for example. And do you know any success on mimicking mature birds?

The problem regarding mimicking mature birds is that you cannot actually tell if they think that the sound comes from another member of their species. For instance, I like to imitate magpies, and they not only reply but sometimes approach me, showing curiosity. However, as they can clearly see me, it's very unlike that they think I'm a member of their species.

I think the Chinese room example works well here. Can we make a sound to a matured bird when being outside of the bird's eyes, so that it will react to the sound as if it comes from an unseen bird?


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Can the same target gene be regulated differently by the same transcription factor under different conditions?
I'm very new in biology and doing more computational analysis. I'm confused with the type of interactions between Transcription Factors (TF) and target genes.
Is it possible that the same transcription factor interacts differently with the same target gene under different conditions?
e.g., TF1 up-regulates Gene1 under condition 1 while TF1 down-regulates the same gene Gene1 under condition 2
Does the above example take place in biological systems?
I can only think of different TF complexes which are regulating the gene Gene1 under different conditions with different effect. However, it would be great to know if, in case TF1 does not participate in any TF complexes to regulate Gene1 under certain conditions, it is then possible that "TF1" regulates Gene1 differently under different conditions?

It also depends what you take as "normal expression". Even if you have only an ON and an OFF state for a single interaction, the system can display "upregulation" and "downregulation" of target genes if expression is normally somewhere between completely ON and OFF.

Short answer - yes but probably somewhat rarely.
Transcription factors aren't necessarily limited to being either repressors or activators. In practice they mostly do one a lot more than the other - e.g. if they have an 'activation' domain then they will mostly activate, but they can still do the opposite, directly or indirectly.
A single TF will often regulate different genes in different directions. This can be due to indirect effects - our activator activates a repressor which then switches off a gene. It can however also happen through direct means - for instance a factor might bind a repressing or activating domain at different locations, or displace different factors.
Most of this variation is probably specific to the target gene, so factors are probably more specific in their effect on a given gene. However, since our factors action depends on other genes,and different genes will be active in different conditions, there's no reason a factor couldn't do different things under different conditions while at the same location - perhaps one condition activates a repressor that binds with it, or a stronger activator that it competes with.
It's a matter of ongoing research, but I would expect this kind of thing to be the exception rather than the rule. In general complex interactions between TFs at a given location seem to be rarer than more or less additive effects.


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What does the end of DNA look like?

EcoR I ........ 5'-GAATCC-3'
  BamH I ....... 5'-GGATCC-3'
  Hind III........ 5'-AAGCTT-3'
The enzyme BamHI recognizes a palindromic sequence and leaves one strand longer than the other. A piece of DNA is cleaved by BahM I. What does the end of the DNA look like?
A. ...GATCC-3'
       ...C-5'
B. ...C-3'
       ...GATCC-5'
C. ...G-3'
  ...C-5'
D. ...G-3'
  ...CCTAG-5'
E. ...CTAGG-3'
  ...GATCC-5'"

I understood that one strand should be longer than the other, that's why I eliminated the "C" and "E" answer choices.
Then, I thought the answer choice is the "A" one. The first strand is similar to that in the data in the task, while the second is palindromic to it.
But this answer choice is incorrect. Then, I chose the "B" one. I thought: if we are given the sequence 5'-GGATCC-3', then the sequence 3'-GGATCC-5' is palindromic to it. (In this case, we have different letters near each number. That probably means they are vise versa versions of one another.)
It turned out the correct answer choice is the "D" one. I found such an explanation:

The end of the DNA cleaved by BamH I is complementary to the
  recognition site sequence shown in the table. One strand must also be
  longer than the other. The sequence CCTAG-5' is complementary to
  GATCC-3'.

But I can't understand this explanation... Please tell me what I do wrong..

Here is a quick drawing of how BamHI cuts the DNA:

As you can see, after cutting, the two ends are actually the same (always read sequences from 5' to 3').


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Can a protein go outside of nucleus after go inside with nuclear localization signal (NLS)
To make a protein (for example Cas9, GFP...) able to enter the nucleus, we need to add a NLS tag for it. So will it able to go outside the nucleus after get inside ?

It seems that I need to add a NES (nuclear export signal) if I would like to make it able to export the nucleus : https://en.wikipedia.org/wiki/Nuclear_export_signal  .


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Range of dry matter yield per kg CO2 of different plant species
The photosynthetic equation tells us that for every sugar molecule produced 6 molecules of carbon dioxide are used.
I'm interested in how much organic matter is produced by a certain quantity of CO2. Obviously there are differences between plant species so I'm basically looking for a list of plant (categories), which tells how much CO2 does produce how much dry matter.

A plant contains about 50% of it's mass absorbed from the air, from CO2 which it converts with 45% efficiency. 40-45% CO2 fixation/respiration seems to be optimal for all plants, it's the balance of how much their cells need aerobic respiration day and night, compared to photosynthesis. That 50% absorbed from the air is fixed with H2O which provides most of the other 50%, and the rest is ashes.
According to this research:
The CO2 captured by plants is the result of the differences between
atmospheric CO2 absorbed during the process of photosynthesis and the CO2
released by the atmosphere during respiration. This difference is converted into
biomass and tends to fluctuate between 45 and 50% of the plant’s dry weight.
(the research states dry weight C measurements, they don't seem to measure CO2 absorption directly)
So it's better to search for "photosynthesis respiration ratio" to find research that measures the efficiency of the CO2 absorption:
the ratio of respiration and photosynthesis (R : P) was relatively constant, 0·40–0·45, and independent of temperature. This was consistent with earlier work by Ryle et al. (1976) [...] Some mechanistic understanding of the constancy of R : P was provided by Atkin et al. (2005), who found that respiration and photosynthesis in most examined plant species acclimated similarly after temperature change. More recently, Atkin et al. (2007) confirmed homeostasis of R : P, in Plantago spp., but this was not maintained when plants were subjected to higher temperatures than usually experienced in their habitats. Differences between photosynthetic and respiratory acclimation to temperature have been reported by Campbell et al. (2007) and Hartley et al. (2006). Cheng et al. (2000) found that the R : P of sunflower was also insensitive to changes in atmospheric CO2 concentration. Overall, the research confirms Monteith's (1981) assessment that the ratio may vary over short time periods but is constant over periods of weeks and longer.
That document has lots of research references and technical words and concepts to follow up.
It's good also to see google images for R P ratio graphs and tests.
https://www.researchgate.net/publication/263676467/figure/fig1/AS:278855131648023@1443495652845/Figure-3-Bottom-curve-simulated-10-d-running-average-leaf-respirationphotosynthesis.png
The conversion ratio is visible here, day is white, respiration is black.
https://www.researchgate.net/profile/James_Bunce/publication/43291524/figure/fig1/AS:273738792960009@1442275822297/Figure-4-The-ratio-of-average-night-time-respiration-rate-R-to-average-day-time.png


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Tropical Plant Identification
After searching extensively I have been unable to find a name for this plant. It was found growing in the Eden Project Tropical biome in the UK. The flowers were approximately 7-8 cm across.
Any help greatly appreciated!

Beautiful photo. I'm looking forward to an answer.

Leaf shape often helps identifying plants. Do you remember how the leaves looked like, or do you have photos where they appear?

They seem to closely resemble the shape of the "Golden Chalice Vine" (Solandara Maxima). Although they are a more yellow color and their leaves fold outward rather than inward, it is entirely possible that the flowers you found were still in the process of fully blooming.
I also found a it growing in the Eden Project Biome you mentioned, here is the link to the plant page on their website: http://www.edenproject.com/learn/for-everyone/plant-profiles/golden-chalice-vine
And for some more pictures and information: https://toptropicals.com/catalog/uid/SOLANDRA_GRANDIFLORA.htm
Hope this is the plant!

The Solandra you show doesn't seem to have the thick part on the "leaves" (wich are technically petals and / or sepals) we see on the photo taken by the OP.

Hi Bli, unfortunately I do not have a photo of the leaves. It was a spur of the moment shot due to its location (being on the side of some busy stairs). On future trips I must remember to photograph leaves as well as the flowers of those plant I am not familiar with. Although I can see a similarity with the Solandra maxima that Johnny linked me to, I do agree with you in that the thick bands of green on the petals to seem to be absent in any photos I can find of it online. Thanks very much for taking the time to help me identify this, much appreciated.

Hi Johnny, thanks so much for going to the trouble that you have in helping me identify this plant. I certainly think we are on the right track with Solandra though as I remember the flowers were somewhat smaller than those described in any online site and the thick green bands I witnessed on the photo I posted also seem to be absent. Can I ask whereabouts in the dome you saw it growing? I found this one on the right side of the stairs going down from the viewing platform. If I was still in that part of the country I would go back to get more detail - leaves, growth habit etc. Thanks again!

Sorry, what I meant to say was that I found on the Eden Project Website :P. Apologies. I agree that the flowers are larger than what you described seeing, which is why I thought it might not have been fully formed yet, but I'm no botanist so I can't say much about it, but glad I could help!

After continuing to search I have located the name of this plant. It is Ipomoea alba or 'Tropical white morning glory'.
On locating the area of the Biome on a map where I had found it, I could conclude it grew in tropical and sub-tropical areas of South America and north of there. This narrowed down the search somewhat.
Thanks again to all involved for helping to identify!

Apparently similar to "moon vine" an ipomoea of the US that opens in the evening.


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does small different between 16s ribosomal DNA leads to diffrence into protein products?
I have bacterium isolate after BLAST of its 16S  the different between its and the similar seq. on NCBI was 4 nucleotides my question is, does it lead to difference between whole genome seq. or I will obtain the same seq. consequently. does this also leads to  the same protein products from them.

The 16s ribosomal DNA does not code for any protein, it codes for the 16s ribosmal RNA, which is part of the (small subunit of the) ribosome.
The differences will most likely not affect the ribosome much, but to be sure you'd have to check the exact position of the mutations in a reference structure and see if they are at important positions (i.e. binding of the Shine-Dalgarno sequence)


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Why do we see better on stretching our eyelids to the side?
I've often noticed that on stretching my eyes to the side I see a lot better. On searching, I read that this happens because the cornea reshapes itself (due to the ciliary muscles). But is that all, or is there a more accurate biological explanation for this?

It is indeed because you're distorting the cornea. I don't think the ciliary muscles are involved (source?) Also, it depends on your vision. Some people with perfect vision will see less perfectly.

You might get pinhole effects in some circumstances, but for me this technique just makes my vision much much worse (and certainly wouldn't be the best way to introduce a pinhole).

@BryanKrause - Although changing the transmission of lightwaves is altered in both pulling the eyelid and looking through a pinhole, the mechanisms are very different. Pulling your eyelid is akin to squinting in the effect it has on the cornea. Pinholes limit the area over which lightwaves can reach the retina.

@anongoodnurse Squinting does both; a quick look around the interwebs suggests the pinhole effect predominates, though I didn't look for actual peer reviewed publications.

@BryanKrause - You're right! "So basically, squinting allows us to see better in two ways: by changing the shape of our eye and letting in a limited amount of light that is more easily focused." TIL. (And I didn't look on Scholar either. But two science pages stated this. Good enough for me for comments. :))


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The death of Earthworm
In rainy season when children sprinkle salt on earthworm ,it dies.But salt is not dangerous.We use it daily.Then why earthworm dies?

Welcome to Biology.SE! What research have you done before asking it here?

"salt is not dangerous" - Citation needed.

We use salt daily and ofcourse children don't take it off from mines just to sprinkle it on earthworms.I'm talking of table salt.Any more citation?

Ever heard of what happens when you drink salt water? Alle Dinge sind Gift, und nichts ist ohne Gift, allein die Dosis macht dass ein Ding kein Gift ist: the dose makes the poison.

Re "salt is not dangerous", you might consider why low-salt diets are recommented for people with high blood pressure or some kinds of heart disease, or why rubbing salt into wounds has become a common saying.

Well it is dangerous but it is not poisonous.

@Sara Asfar: Salt certainly is poisonous, it's just that it takes a fairly large amount to kill you.  Per Google, the LD50 of sodium chloride is about 3000 mg/kg, so eating about half a pound would likely be fatal.  Note that it's fairly common for things to be harmless or even necessary for health in small quantities, but harmful or fatal in larger amounts.

It's because on the earth worm skin's special mucous. Acording to this article: Why do earthworms die when salt is sprinkled on them? the mucous makes moist to the worm's skin, which is  vital for their survival. Moreover, the worms don't have a respiratory organs, like lungs, gills, etc. This means that Carbon Dioxide and other characterized as "dump" gases can not be exchanged with the Oxygen. But worms breath through their skin, with the help of these special mucous that are developed on its skin. If their skin dries out the result will be death, because the gas exchange will not last without the mucous help. Similarly, the circulatory system won't function, because its main role is to trade gasses with the cells via red blood cells.
What about salinity?
Salinity is a very important factor for the earthworms health, because high salinity destroy their valunable and sensitive skin and kills the mucous that in fact help the worm to "breathe". Low salt concentrations are very beneficial for the worm, because not only their mortarity level is increaced, there are size changes to the worm's body (noticeable bigger size).
Here are and some photos of a worm that its enviroment has low salinity and high salinity:
High salinity:

Low-to-medium salinity

Source: Why do earthworms die when salt is sprinkled on them?.

When quoting an article, the quotes should be clearly marked, otherwise it's considered a form of plagiarism.

Either it is plagiarism or not but it really gave me answer to my question.Why the people like you seem to proof read other's post just for criticizing them or down vote them@anongoodnurse

@SaraAsfar plagiarism is quite a serious problem. It's not just about getting your answer, the answerer should write a proper answer for this whole community, acknowledging all its conventions and restrictions.

@OP - plagiarism is considered serious malpractice. Please convert your answer into your own words, or explicitly mention where the citations were obtained from at the appropriate places in your answer.

@AliceD Okay I am making it community wiki.

@The_Mad_Fish and why would that make things better?

@AliceD Please check my new anwer that it is based on the article and doesn't show any plagiarism. Thanks.

Also, edits are welcome :)


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Which colourful insect is this?
I found it on my plant this morning while watering it. Location: Hyderabad, Telangana, India. Any ideas?

Nice find! That most definitely is a Poekilocerus pictus, also known as a "Painted Grasshopper".


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How to determine the height/bits in a sequence logo?
I am trying to create a sequence logo, and I am completely confused by how to determine the height/bits for each column. So, for example I understand how to create the flat sequence logo: (add up all the letters, the letters should represent their ratio for that position) but not the normal sequence logo:.
I have been reading this paper "WebLogo: A Sequence Logo Generator" again and again and I can't figure out how to determine the bits/height for each given position.

Can you provide a link to the paper you're referring to? I believe I've found it myself, however, there is no mentioning of normalizing data.

It's http://weblogo.berkeley.edu/Crooks-2004-GR-WebLogo.pdf

Wikipedia has a page on sequence logo which discusses the calculation briefly.
The "bits" here are related to those used in Shannon entropy. This is an information-theoretic equivalent to the Boltzmann entropy from thermodynamics. This is a measure of how "disordered" the position is, or more precisely how specific the distribution is.
The general formula for the total entropy (expressed based on probabilities/fractions) is
$$ S = -k \sum_i p_i \cdot log( p_i ) $$
where $i$ ranges across all the various states (e.g. each nucleotide).
The difference between Shannon entropy and Boltzmann entropy (aside from the contexts where it's used) is the value of the constant (one for Shannon, Boltzmann's constant for Boltzmann entropy) and which logarithm used (the natural logarithm for Boltzmann entropy, and typically base-2 for Shannon entropy.) As it uses base-2 logarithms, the Shannon entropy is typically measured in units named "bits".
The wrinkle is that the entropy of a distribution isn't really what you want to display in a sequence logo. Instead, you want something that gets larger (not zero) when the sequence becomes more defined. As such, the values displayed are not the entropy itself, but the "entropy loss" from a completely random (maximal entropy) distribution.
That's how you get the total number of bits at a position (the total height). The height of the individual letters comes by taking the total height and multiplying it by the probability of each state. This might not have rigid theoretical justification (you can't attribute the entropy loss to individual nucleotides like that), but it fulfills the display purposes of making the more prevalent nucleotide identities larger in display size.

For example, if you have a position with 70% G and 30% C, then you have
$$ (4 \cdot -0.25 \cdot log_2(0.25)) - (-0.7 \cdot log_2( 0.7 ) + -0.3 \cdot log_2( 0.3 )) = 1.12$$ bits of total height. G gets a height of $1.12 *0.7 = 0.78$ bits, whereas C gets $1.12 *0.3 = 0.34$ bits.

I don't understand the example: what is (4⋅−0.25⋅log2(0.25)) ? I would replace this part with 2 since it is log2(4)−S @R.M.

@Manuela (4⋅−0.25⋅log2(0.25)) is the entropy of a random sequence: 4 possibilities, each with a probability of 0.25.

ok perfect thank you !


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Human can't digest cellulose.....but the length of small intestine is approximately same in humans and herbivores
My question is why herbivores are able to digest cellulose and why can't we??

Depends on what you mean by "digest". Herbivores aren't able to digest grass on their own, they keep bacteria in their guts to do that. Grass-eating herbivores also tend to have long digestive cycles and some have several stomach chambers.
In short, cellulose is a pain to digest.


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Does our heart have to work harder in hot or cold weather?
In hot weather our perspiration is higher and often old people get tired faster when it is hot. But is there a relation between hot weather (sweating) and our heart if so what makes it have to work harder?
And does our heart have to work less (compared to hot) in cold weather where capillaries and vessels constrict, making it harder for the heart to pump blood.

If body temperature is higher, then yes, the heart will work harder to cool the body by pumping blood more quickly (to spread the heat more evenly). Likewise, the converse can be said about cooler body temperatures and the heart not pumping as hard as to retain heat. This is true, under the assumption that body temperature is dependent on environmental temperature. I think you will have a difficult time finding studies on this that do not involve rigorous physical activity as the reason for increased body temp, as most of them do, of which wouldn't provide the most relevent data, IMO.


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What happens to the human ear as it naturally goes deaf?
I was always told that when the human ear goes deaf to a specific sound (auditory frequency), then that sound is heard one last time, and upon fading away, will never be able to be heard again.
Is this in fact true? If so, why do we hear that sound (which seems to happen randomly and is somewhat loud for a split second) just before the ear becomes deaf to it?
Ultimately speaking, what exactly happens as the human ear naturally goes deaf?

Do you have any source for your claim ? maybe you are interested in tinnitus.

@JM97 No, I don't have any sources for that claim.. it's just something that I've heard over the years. My main curiosity though  is with natural hearing loss,  not the sharp sound. The mentioning of a sharp sound is irrelevant if in fact that's not what happens as the ear naturally goes deaf.

I don't think you will hear the frequency "one last time", before it fades away. More likely you will slowly lose your range of hearing from high to low frequency.
Hair cells in the cochlea are arranged in a spiral on the basilar membrane, with high frequency cells at the apex. For some reason, high frequency cells are more sensitive to damage, either by loud noises, drugs (including certain antibiotics that cause deafness), or old age. By adulthood, humans have already lost a significant portion of their high-frequency hearing (children hear up to 22kHz, adults 16-18kHz from memory).
Significant hearing loss can also be caused by the loss of outer hair cells, which act as a cochlea amplifier, or loss of the type I spiral ganglion neurons that connect the hair cells to the brain. But typically age-related hearing loss is normally caused by the death of Inner Hair Cells.

+1, I believe this to be generally correct, but find there are cases which could lead to hearing frequencies "one last time" as a component of acute tinnitus.

True, I assumed "naturally goes deaf" was referring to age-related hearing loss. +1 for your more detailed answer.

Hearing loss is caused by different things, but your probably thinking of age-related hearing loss.
When people go deaf, it is be because "hair cells" in the ear break.
This breakage results from overly loud frequencies, or just random damage to cells over a lifetime.
If your last remaining hair cell that is tuned to a certain frequency after all the other ones have died gets killed somehow, it will depolarize and send an action potential to your brain telling it to hear that sound.
But that would be a very faint sound, since only one or a couple hair cells die off.
But in reality, it usually isn't that you hear a sound for the last time before going deaf, you have a faulty premise hear!
it's NOT like the ubiquitous "seeing the light" that happens when your heart stops.

Just to note, sensory hair cells do not have action potentials (at least not after a short developmental period pre-hearing), they release glutamate that stimulates depolarisation and action potentials in the afferent fibres of the cochlear nerve (type I Spiral Ganglion Neurons).

I guess you're right!

NIDCD has a wonderful description of hearing, and how it's lost here.
Sorry I'm late on this, meant to have it up for your bounty, but ended up with a busy weekend.  The short answer to your question is no, you don't normally hear or notice anything as you lose your hearing.
However, what you’re describing can occasionally occur in noise-induced hearing loss by acoustic trauma, which is not all that common (though not rare).  Though it isn't normally tightly banded around lost frequencies, just a general "ringing" that contains some of the damaged/lost frequencies.

Hearing In Depth:
First, let's cover how hearing actually works, and then we'll see how it can break down.  I'm going to stick with Air Conduction hearing for the sake of simplicity.  To get everyone on the same page visually, here's a good open source diagram of the ear:

Generally, I think most people can understand that sound waves are captured and deflected by the "ear" (pinna and auricle) and then transverses ear canal (external acoustic meatus) where they finally hit the eardrum (tympanic membrane).  The ear drum marks the division between the external ear to the middle ear.
The eardrum vibrates, not entirely unlike a drum, with the sound waves causing the little bones in your ear (ossicles) to vibrate.  The signal is amplified and passed on to one of the best named body parts, the bony labyrinth (via the oval window).  At this point the fluid (perilymph) in the inner ear moves about in different currents depending on the mix of wavelengths at the time (which can be described in detail, but is beyond the scope of this answer).
The main tissue that actually detects the movement of the fluid is the organ of Corti (you might think don't you mean cochlea, but note that this is the portion of the cochlea that actually process the movement of the perilymph).  Hair cells react to waves in the perilymph differently depending on their placement and the wave itself. As the hair cells go up and down with the wave, the stereocilia on their surface get bent up/crushed/deflected against tectorail membrane.  The hair cells with bent stereocilia then open up ion channels (though they don't have an actual action potential), which leads to action potentials in the nerve cells of the spiral ganglion.
Those nerves send signals to the inferior colliculi where the signal is "bundled and filtered," and finally sent to the primary auditory cortex where the brain will finally process the signal as auditory information.  I realize there are plenty of intermediate structures I didn't mention, but I believe this gives an overview appropriate for the question.

Hearing Loss:
Viewed simply, hearing loss occurs when any part of the complicated system above has a problem.  The most common kind of hearing loss is sensorineural (SNHL), which is most commonly induced by noise (NIHL), but could also be do to degradation from aging, etc.
To get to a ringing effect, we need to consider the physiology of acoustic trauma. Often the energy wave is great enough that much of the proper Air Conduction pathway is skipped.  Either way, the hair cells get slammed against either of the surrounding membranes.  As you can imagine, under normal volumes the stereocilia become deflected (bent down), and then return upright as the sound wave passes.  However, in acoustic trauma you hit the cells hard enough that it tears the cell membrane and lets ions leak en mass onto the nerve cells (1).  If the damage is bad enough, or frequent enough, this will lead to an interesting effect called excitotoxicity (a cell stimulated to death).  This in turn will be perceived, at least at the moment, as "ringing" in the frequencies covered by the neurons.  In general, the damage tends to be broad enough that it isn't held to one particular wavelength or tone, and that the nerves become overwhelmed so a clear signal can't be distinguished (ibid).
Now your body will try to repair this, which will lead to swelling, repair mechanisms, and eventually scar tissue.  This in of itself can interfere with proper hearing.  If you're lucky, you'll be able to recover some of the hearing at the damaged frequencies, if not then you've lost the hearing in that range, and the last thing you heard there was ringing.


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Are there any known examples of animals with air-conditioner type cooling?
Sweating is often poor at cooling, particularly on humans and animals with a lot of hair or fur because it collects on clothes and other coverings, trapping heat in while promoting the growth of potentially pathogenic bacteria. Additionally, sweating leaks out important electrolytes and water.
With that in mind, are there any known examples of animals that mimic an air conditioner's heat pump? In particular, consider a special channel where blood (or even better: a specialized cooling fluid) is pressurized (almost similar to inflammation) and pumped through a fin, then depressurized on the way out.