text:
How does carcinoma enter into blood or lymphatic vessels？
When carcinoma begins to metastasize, it enters into blood vessel or lymphatic vessel to migrate to the site of metastasis. In that case, although I think breaking down the basement membrane is necessary for epithelium such as carcinoma to enter into them, I can't find out the reports.
Are the basement membrane actually broken down in the first step of metastasis？What are the molecular mechanisms in which carcinoma enters into blood or lymphatic vessels？

You can read about epithelial to mesenchymal transition. It is one of the processes that usually precedes metastasis of carcinomas.

Thanks for answering my question, I have already known that the EMT system is one of ways of metastasis. However what i want to know is whether carcinoma actually breaks down the basement membrane when it stats to metastasize. Do you know some reports showing histochemically the broken down basement membrane？

@ironKUMA The linked Wikipedia article has many citations to the primary literature, I would suggest starting there. You should also perform some appropriately-worded Google Scholar and PubMed searches for more information.


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What technique biologists use in order to determine the function of organs?
How the biologists were able to determine the functions of body organs? Using a specific example organ for an answer would be ideal.

Do you mean historically how were the functions determined or in present day how are they studied? You question is quite broad at the moment.

I mean how biologists collected data which we are provided about functions of organs? Like they determined structure of cell by observing it under the microscope but observing how it works seem difficult out of body because after cell is taken out of body it will no more be able to perform functions.

Yes I mean historically how were the functions determined

Are you asking for the entire history of an organ, the definition of an organ, or a reference that shows some tissue being described as an organ/organ-like structure?

I want to know that how scientists determined function of organ for example it is said that hypothalamus of brain is responsible for controlling blood pressure, homeostasis, body temperature, hunger , thirst etc but how did they know this?

A very common way of getting information on the function of an organ, part of an organ (such as a region of the brain) or a protein is to look at the outcome (symptoms or phenotype) in cases where it is not functional. E.g., a lot has been understood about brain function for speech production by studying aphasia in stroke patients (see wikipedia) and linking the symptoms with the brain region that is damaged.
This is still the way we mostly study living cells or organisms: mutants defective for such or such protein, or in which external disruption (such as ablation) is used and the resulting phenotype or symptoms are studied.
This is indeed very different from what can be done for research in physics e.g., where reduced systems with simpler functions can be studied. The approach in biology is much closer to reverse engineering, where a given system has to be studied as a whole but a rational approach on some subpart allows to build an understanding of that subpart.

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How much does the Vitamin D3 concentration of the blood of a human change over the course of a day?
Are there studies that measured how much the blood concentration of Vitamin D3 changes over the course of a day? If so, how strongly does it change? Does it change in predictable patterns?

Did you check on Pubmed?

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Concept and analysis of Pedigree
Pedigree analysis is a process of establishing a virtually correct inheritance pattern of a genetic condition in a proband's family. I call it virtually correct because in many a cases we assume the genotype of a parent to be something by weighing the genotypes of the offsprings.
Now in a given problem like in this one where the trait follows autosomal dominant inheritance pattern I have problem deciding the genotype of I-3.

My opinion:
The genotype of II-6 is AA'. (Obtained from a calculation which I have decided to not to mention as it will make it lengthy and complicated)
(here A=Normal allele on autosome and A'=Mutant allele on autosome)
II-6 receives allele A from mother I-4 (who is obviously AA) and allele A' from father I-3. Now the genotype of the father could be either AA' or A'A'.Since the probability of having a AA' female child becomes 100% if we assume the genotype of the father to be A'A' so the genotype of the father I-3 is A'A'.
But one of my instructor says that it cannot have a genotype A'A' because it is fatal and I am not convinced with his reasoning.
In Huntington's disease presence of one HTT gene is enough to cause death of the person. It is a dominant lethal allele. While in achondroplasia, an autosomal dominant disorder the mutant allele when present in two copies is fatal.It is a recessive lethal allele. A heterozygous person survives with symptoms of Achondroplasia.
So death is not always caused by two copies of a mutant gene of a dominant autosomal trait. It may be caused by only one copy of gene as in Huntington's disease or may not be caused at all(I've no proof of this. Its my assumption).
So in a pedigree where nothing has been mentioned about the lethality of the genes concerned we shouldn't assume them being recessive lethals. This is all I think. Am I correct?
Finally: Should the genotype of I-3 be A'A'?

I-3 can be either A'A' or AA'. In Huntington's disease or Achondroplasia, the father could still survive to adulthood and reproduce. If the father had a chromosomal disorder such as Kallman's syndrome, he would be unable to reproduce. However, this is not a simple mutation, and it is not heritable. You should ask your instructor to clearly define the problem.

Could you cite an authentic reference to your answer ?
I have been reading about lethal alleles from wikipedia:
https://en.wikipedia.org/wiki/Lethal_allele#Types_of_lethal_alleles


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Why do Proteins store energy when the body already contains Carbohydrates and Lipids?
We already know that lipids are a source of long term energy and carbohydrates are much faster energy releasing sources. So why do we need specific proteins within the body to store energy?
Are proteins some sort of much quicker sources of energy?
I really can't understand.
Thanks for answering.

Which protein energy-stores are you referring to? Could you add sources to your claim?

Well I was referring to plant seeds and eggs which have proteins which act as energy sources.

Proteins aren't used to store energy but to build structures. They can be burnt if needed though.

Any molecule (and atoms also), contains some-amount of energy (unstability, or ability to do some work), within its structure.

I think user @Mithoron should write their comment as an answer.


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How many sensory neurons are in the human body?
While I understand that there is a wide disparity of precision when it comes to specifying what constitutes "sensory neurons/receptors", I'm trying to find an authoritative source to provide at least a rough order of magnitude estimate on the number of receptors in the human peripheral nervous system (including skin, tongue, eyes, ears; but also mechanoreceptors and proprioceptors as well). The only sources I have found so far (here and here) only provide hints at the answer. I have found estimates as high as 15 billion, and as low as 3,000,000, but none of these guesses cite authoritative sources.
As I'm sure you can tell, I am not a student of anatomy (my interests lie in cognitive science and artificial neural networks), so forgive me if my question is too imprecise.  But to put it simplistically: what I want to know is, roughly how many externally-produced sensory signals (channels) does the human brain have the capacity to process? Again, I am not looking for a precise answer, but I'm hoping to at least reduce the uncertainty to less than four orders of magnitude.

CONTEXT: My purpose in this investigation is to try to quantify the magnitude of the computational capability of the brain with regard to processing external signals. If one were to imagine an "artificial nervous system" (as distinct from an artificial neural network), how many input sensors would it be able to simultaneously process if it were on par with a human brain?

UPDATE: I recognize from the comments the inherent ambiguity of my question, so let me attempt to clarify. Assuming that the number of incoming signals to the brain at any one time is limited by the number of neural connections between the brain stem and the spinal column*, can someone provide an indication of what that number might be.
* (if that assumption is overly simplistic, feel free to enlighten me)

nerve endings are often used to denote free nerve endings that convey pain sensations. Are you after how many receptors there are, as in photoreceptors, mechanoreceptors, olfactory receptors etc etc? Do you want internal sensations too (balance, proprioceptors etc etc)? You might want to define specifically what you are after (which senses, which cells etc.)

@Christiaan - From your description, "Receptors" is what I am really after. I will edit my post accordingly. Thank you.

The problem here is that,  eg, the number of photoreceptors in the retina exceeds by far the number of retinal ganglion cells that make up the optic nerve. Your concluding sentence, therefore, is unfortunate,  as it combines sensors and the brain. It's just quite complicated. If you are after sensors and sensors only, or otherwise,  please specify.

I'm afraid,  actually, that the order of variance you found may be quite acceptable, given the hazy definitions set.

And the 3M is an underestimate I guess. It's likely higher than that, given there are as much as 1M ganglion cells in each retina alone.

@Christiaan - thank you for pushing me to clarify my question. I have attempted to do so yet again in my post. I understand that the physiological complexity of this system might prevent any clear-cut answers. But for the purpose of this question, I'm not interested in how many cells there may be at the extremities of the nervous system, but specifically how many signals can be delivered to the brain at any one moment. If "receptors" is a reasonable proxy to that question, great. But, as I suggest in my UPDATE, perhaps "number of neurons in the spinal column" might be more appropriate.

Not all senses go through the spinal cord - most notably the auditory, visual and gustatory senses all head straight to the brain stem or even the brain. Again, it's not all that simple :) +1 for your continuing effort in improving this challenging yet relevant question.

@Christiaan - again, I really appreciate your help. I think the problem is my ignorance regarding the appropriate terminology. Would it be possible to continue this discussion in chat?

Let us continue this discussion in chat.

I'm voting to close this question because the original question is poorly scoped, but the edits that the original poster made to save the question changed entirely the meaning of the question.

(note: I would strongly recommend OP repost with the new question, if OP is still around)

This is a really interesting question.  However, I'm going to try to address the context and update sections of your post rather then attempt to quantify all afferent signals in the nervous system.  This is because quantifying those signals would be an exceedingly difficult task.  It's not only logistically difficult to measure on an individual level, but to say anything definitive regarding the entire species would be superfluous.  The number of signals at any one time is constantly in flux, as not every sensory receptor generates an action potential at the same time.  Even in instances where similar or "competing" receptor types are simultaneously stimulated, those transmissions will be modulated and/or pathways suppressed.  A good example can be found in this editorial article[1] on pain, where inducing painful stimuli can alleviate an itch sensation.  I reference this to illustrate that sensory signals are not entering the brain unchecked. In the most simple of terms, they are heavily regulated.
Based on the context on your question, it seems what you really want to know is what is the maximum threshold.  In an artificial nervous system, how many signals could we pump into it before it becomes inefficient or overwhelmed?  However, what makes the nervous system unique is that it's a living system that adapts to stimuli.  When there's more signals then it can handle or process, it regulates them.  You can read more about the process and its importance in this article on sensory gating[2].  For this reason, a healthy brain that isn't being artificially stimulated shouldn't become overwhelmed.  In fact, this process makes it far more efficient then any super computer.  A fun example of this was the six chess games between Kasporov and Deep Blue in 1996.  Think of the sheer number of moves Deep Blue could calculate compared to Kasporov: hundreds of millions of moves per second.  It lost that match.  Computational capability isn't conditional on the number of inputs the system can receive, it's how that information is processed, utilized, and applied once it's in the system.
I know I didn't answer your question in regards to a hard number, but hopefully it helped give a different perspective.  Please let me know if you'd like anything further clarified.
[1]: Focus on pain.  Nature Neuroscience 17, 145 (2014). doi.org/10.1038/nn.3644
[2]: Sensory gating, inhibition control and gamma oscillations in the human somatosensory cortex.  Scientific Reports 6, Article number: 20437 (2016). doi.org/10.1038/srep20437

Estimates of the number of sensory cells range from a low in the first decade of millions to as many as double digit billions. The number of neurons going to the brain is not an indicator of how many signals are in the body. Think of it like one would the internet. Billions of people are connected, but they all go to nodes from individual devices to local data centers, to a relatively few major cables to which everyone is connected.
The way this happens on the web is that every individual user has an IP address, and even though the signals pass through cables that carry millions of messages only those directed to that IP address will be received on that device.
This all happens on a digital basis, but the human neural system is analog, which gives a much broader range of possible addresses and data combined than can pass in a digital signal. So what you are asking is far more complex than your question. You need a thorough understanding of analog information transfer as well as the digital domain from which I believe you are operating.

I like how your answer is set up; however, please do add some references.

The difference in your analogy is that digital trunks can handle millions of simultaneous messages, because each message contains its own "mailing address", so to speak (in the packet header). That analogy breaks down in the neural system because there, every message must have a dedicated point-to-point channel to travel on. (I.e., the nervous system contains no routers.)

I disagree on some level with both Richard and @kmote and agree on some level... On one hand, axonal communication isn't truly analog, it's more of a hybrid between digital and analog, with binary signals. There are of course some analog sensory responses, but these are eventually converted to a (mostly) binary signal. And while there are no "routers" there can be information in spike patterns, both spatial and temporal, such that the number of unique messages to be conveyed is not equal to the number of fibers, just like a network cable.

I agree with @BryanKrause. Also, this analogy with computer network can be very misleading.


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Sugars which are Carbohydrates and vice-versa?
Is it right that are all sugars are carbohydrates but not all carbohydrates are sugars?
If so, which carbohydrates are sugars and which aren't and why all sugars are carbohydrates?
If I had to answer I'd say there are carbohydrates of three kinds: sugars, starch, fiber and from which we can deduce that "not all carbohydrates are sugars".

there's also glucose and fructose i think...

Sugar is a common name for the scientific word carbohydrate. Carbohydrate are of four types basically on the basis of the number of units: Monosaccharide(1unit of sugar molecule), Disaccharide (2 units) Oligosaccharide (3-10 sugar units) and Polysaccharide(more than 10 units of sugar molecule).

@SanjuktaGhosh: Does that mean all carbohydrates are sugars?

@cpx I won't say that. I'd say sugar is another name for carbohydrate.

You need to make a distinction between polymers and monomers (or dimers).
Typically, sugars are monomers like glucose, maltose, or fructose. Sucrose (table sugar) is a dimer. These are all carbohydrates (made up of carbon, oxygen, and hydrogen).
Polymers of these sugars are also carbohydrates. For example, starch, glycogen, and cellulose.
Cellulose, which you called fibre, tends to be structural, and is only found in plants (think celery, or wood, or paper). Starch, is also synthesized by plants, and could be used for energy storage (as I recall). In animals, monomeric glucose is stored as glycogen in skeletal muscle, where it becomes available as energy for short bursts of energy.

Doesn't answer the question.

I'd edit your last sentence to stop after the first mention of the word glycogen. It is stored in liver and brain as well as muscle, and you must surely regret writing "energy for short bursts of energy".

The statement in your question is correct. All sugars are carbohydrates but not all carbohydrates are sugars.
In fact, sugars are by definition carbohydrates. Wikipedia defines sugars as :

Sugar is the generalized name for sweet, short-chain, soluble carbohydrates, many of which are used in food. They are composed of carbon, hydrogen, and oxygen

Not all carbohydrates are sugars. In addition to those you have named, there exist chemicals such as inositol, chitin, and various biologically important carboxylic acids.

Although one might naïvely imagine that the term carbohydrate is used for a molecule containing carbon, hydrogen and oxygen, this is not the case as, if so, it would include compounds like fatty acids. According to the Wikipedia entry it is more restricted, although still somewhat imprecise:

A carbohydrate is a biological molecule consisting of carbon (C), hydrogen (H) and oxygen (O) atoms, usually with a hydrogen–oxygen atom ratio of 2:1 (as in water); in other words, with the empirical formula Cm(H2O)n (where m could be different from n). Some exceptions exist; for example, deoxyribose, a sugar component of DNA has the empirical formula C5H10O4. Carbohydrates are technically hydrates of carbon; structurally it is more accurate to view them as polyhydroxy aldehydes and ketones.

By this definition all sugars are carbohydrates if one accepts the authoratitive definition of a sugar by Ron on SE Chemistry:

Simple sugars have the molecular formula Cn(H2O)n, where n is at least 3. They also have to be capable of forming an aldehyde or ketone carbonyl group.

He uses the qualifier of being able to form an aldehyde or ketone to exclude certain carbohydrates such as inositol from being classified as sugars:

…compounds in the inositol family [that] fit the molecular formula requirement, but are not considered to be sugars because they are incapable of forming a carbonyl.

So, yes, all sugars are carbohydrates, but not all carbohydrates are sugars. (Which, despite the unsatisfactory nature of the definitions, is what is generally accepted.)
Disclaimer
This answer describes the terminology used in biological sciences. Because it exists one has to work with it, but one should realize that it is not chemically exact, as illustrated by the following.
Chemists (and biochemists) refer to reducing sugars — and hence by implication there must be non-reducing sugars. The disaccharide sucrose — which is what most of us think of as sugar — is a non-reducing sugar. But the reducing property is a feature of the aldehyde or ketone group, which by Ron’s definition (which I emphasize is that accepted by biologists) would exclude sucrose from being a sugar! Clearly there is a conflict here.
The Wikipedia entry for Reducing Sugars includes the following:

A reducing sugar is any sugar that is capable of acting as a reducing agent because it has a free aldehyde group or a free ketone group. All monosaccharides are reducing sugars, along with some disaccharides, oligosaccharides, and polysaccharides.

and

Disaccharides are formed from two monosaccharides and can be classified as either reducing or nonreducing. Nonreducing disaccharides like sucrose and trehalose have glycosidic bonds between their anomeric carbons and thus cannot convert to an open-chain form with an aldehyde group; they are stuck in the cyclic form. Reducing disaccharides like lactose and maltose have only one of their two anomeric carbons involved in the glycosidic bond, meaning that they can convert to an open-chain form with an aldehyde group.

The way out of the dilemma available to chemists (but not to dieticians) would seem to be not to talk about sugars and carbohydrates at all, but refer to specific chemical types: monosaccharides, disaccharides etc. and their derivatives; and for other dietary/storage molecules refer to fatty acids, triglycerides etc.

Interesting, I had not heard of the aldehyde/ketone thing before, but it makes sense --- all sugars I know of are classified as either aldose (aldehyde forming) or ketose (ketone forming). Some refer to inositol (and sorbitol, mannitol, xylitol ... ) as sugar alcohols, as they form only alcohol (hydroxyl) gruops. Perhaps this distinction is important in that aldehyde and ketone groups permit certain reaction mechanisms?

@Roland I'm no expert (my chemistry degree was years ago, and I never 'practiced') but on thinking about the question was uncertain about the situation and googled a bit. However it all seems to be a bit of a 'fudge' as the term 'reducing sugar' suddenly welled up in my memory from the distant past. I'll add a footnote to my answer, but in brief the reducing sugars are the ones that are the aldehydes or ketones, so there must be non-reducing sugars, which then violate the definition. I think the get-out is to say that chemists would talk about monosaccharides and (in this case) disaccharides.

Sugar is a very casual term used for monosaccharides and oligosaccharides, which normally tastes sweet.
The polysaccharides (starch, cellulose etc) usually does not considered as sugar since they are normally tasteless.
Monosaccharide, Oligosaccharide and Polysaccharide, all three make the chemical-class carbohydrate. So Polysaccharide is the group of carbohydrate that is not sugar.


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Can growth rate be used as an indicator of fitness in fish populations?
I would like to calculate selection gradients in order to gain insight into the strength and type of selection influencing my study population.
(see here for review. http://jgking.web.unc.edu/files/2012/06/Kingsolveretal.AmNat_.Mar2001.pdf )
(see here for what I would like too do in the end. http://onlinelibrary.wiley.com/doi/10.1111/evo.12077/epdf).
For this I need an indication of fitness.
My question is this:

Does it make sense to use growth rates (in mm. per year or other) as a "proxy" for fitness?

Thanks in advance for your time

Welcome to Biology.SE!
Possible confusion
When talking about growth rate as a proxy for fitness, most authors think of population growth rate (whether in terms of the Malthusian parameter or the net reproductive rate). Such methods are typically used for unicellular that have very short generation time. You seem to be referring to the individual growth rate.
Possible proxies for fitness
There are a number of different proxies for fitness one can use.

growth rate
Some phenotypic trait correlated with fitness such as:

seed production
body size
etc..

Competitive abilities
Experimental evolution

How to chose a proxy
The proxy you want to use depends:

The accuracy you need
The organism you are working with
The a priori knowledge on the biology of the organism of interest.

For example, if you have little knowledge of what phenotypic trait could be correlated with fitness and if the organism of interest have a very short generation time, then growth rate might be good (and accurate) proxy to use indeed.
Ressource
You should probably read some papers that have used a method of potential interest before doing it yourself.
At page 1232 of Kawecki and Ebert 2002, there are a few paragraphs reviewing the different proxies and their usage. They cite key papers you might want to have a look at.
Proxy for fitness in fishes
I know little about fish biology in general but I doubt there is such thing as a generalization of whether "individual growth rate" is a good proxy or not. As you don't specify what species of fish you are working on, I don't think it is possible to answer this question accurately.
You should look at previous work done on the species (or related species) you are working on in order to figure out what would be a good proxy.
Issue in your post

I think it is clear from above that you should indicate what species you are working on.
The paper you link should come with more explanation. You say a paper is a review but a review about what?
You cannot say "I would like to do something like them" and link a paper. You should describe with you own word what you are trying to achieve.

Excellent and thanks for your time :) .... I did not want go into to much detail of the study and so I omitted some info. The species I am studying is small benthic (dwarf) Arctic charr and I am aware that individual growth rate in fish populations in particular can vary greatly among individuals and that in some instances these differences in growth rate do not translate directly into differences in individual fitnes. That is to say, fish with variable growth rates can have very similar fitness.


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What kinds of light attract moths best?
On average, do we know what kind of lights attract moths best?
LED, filament bulb, candle...?
And what about colour? Does that matter?

Interesting question. However I've commonly seen they're attracted towards bright, high-power lights of large sizes. Probably they're not enough attracted towards small-sized lights such as small decoration light.

Multiple studies have found moths along with most other insects to be significantly more attracted to lamps that emit smaller wavelengths such as ultraviolet (UV). Some species of moth appear to be more attracted to shorter wavelengths than others. The visibility of the light to the moth, the distance between the moth and light, and the brightness of the light are also contributing factors in whether the moth will be attracted to light.
Why Moths are Obsessed with Lamps | Nat Geo Wild

Langevelde et al. found that actinic lamps with a mean weighted wavelength of 382 nm (lamp type a) were the most attractive to moths in both abundance and species richness when compared to other lamps that emitted longer wavelengths. The lamp types used along with the data they collected are displayed below:

References & Further Reading
Hsiao, H. (1972). The attraction of moths (Trichoplusia ni) to infrared radiation. Journal of Insect Physiology, 18(9), 1705-1714. doi:10.1016/0022-1910(72)90100-x
Google Scholar | Crossref
Owens, A. C., & Lewis, S. M. (2018). The impact of artificial light at night on nocturnal insects: A review and synthesis. Ecology and Evolution, 8(22), 11337-11358. doi:10.1002/ece3.4557
PubMed | Google Scholar | Crossref
Somers-Yeates, R., Hodgson, D., McGregor, P. K., Spalding, A., & Ffrench-Constant, R. H. (2013). Shedding light on moths: shorter wavelengths attract noctuids more than geometrids. Biology Letters, 9(4), 20130376-20130376. doi:10.1098/rsbl.2013.0376
PubMed | Google Scholar | Crossref
Truxa, C., & Fiedler, K. (2012). Attraction to light - from how far do moths (Lepidoptera) return to weak artificial sources of light? European Journal of Entomology, 109(1), 77-84. doi:10.14411/eje.2012.010
Google Scholar | Crossref
Van Langevelde, F., Ettema, J. A., Donners, M., WallisDeVries, M. F., & Groenendijk, D. (2011). Effect of spectral composition of artificial light on the attraction of moths. Biological Conservation, 144(9), 2274-2281. doi:10.1016/j.biocon.2011.06.004
Google Scholar | crossref

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Requirement of energy for metabolic processes
Sorry if this is too elementary, but can someone explain why the following reaction can occur without a net influx of energy from some other process?

$C_6H_{12}O_6 + 6O_2 \to 6 CO_2+6H_2O$

And why does this one need an influx of energy?

$6CO_2+6H_2O\to C_6H_{12}O_6+6O_2$

Wait is the second one hydrolysis?

Changed "influx" to "requirement" in your title, as we don't really use that word in metabolism  in the sense you describe. The energy is generally provided by the use of ATP in reactions, which is hardly coming from the outside, as influx implies. Left it in the question body, but change makes a better title for indexing etc. Hope that's OK with you.

I’m not quite sure which of two questions you are asking here, but as this is basic to understanding metabolism, I think an answer to both questions will be of most general utility, even if you personally already understand the answer to the first.
[1] The Gibbs Free Energy Change in a chemical reaction determines whether it will proceed spontaneously

If a reaction involves a negative change in Gibbs Free Energy (ΔG), it
  will proceed spontaneously; if not, an input of energy is needed to drive it.

The breakdown of glucose to carbon dioxide and water has a large –ve ΔG and therefore does not require input of energy — the reverse reaction has an equivalent +ve ΔG and therefore requires an input of energy to drive it.
This basic aspect of chemical reactions emerges from the laws of thermodynamics, and is explained in detail in section 1.3.3 of Berg et al., available on-line.
[2] Reactions that break bonds tend to involve negative changes in free energy
Why does the oxidation of glucose have a –ve ΔG, and its synthesis a positive –ve ΔG? This is because glucose oxidation involves breaking covalent bonds, and its synthesis making covalent bonds.
To understand the thermodynamic contribution of bond energies, the account in section 2.4 of Lodish et al. (available on-line) is recommended. In brief, ΔG = ΔH – TΔS, where H is enthalpy and S is entropy. The bond energies contribute to ΔH, and there is also generally in increase in entropy when two moieties become one, as mentioned in the answer by @MangoPrincess.
Footnotes

Not all chemical or biochemical reactions involve net formation or breakage of bonds — for example molecular rearrangements. In these cases more sophisticated chemical considerations are needed to understand the experimentally determined changes in free energy.
The importance in discussing biochemical reactions in terms of Gibbs Free Energy changes is that an energetically favourable reaction can be coupled to an energetically unfavourable one to drive the latter, and it is the quantitation of the ΔG that allow one to predict or understand this. It is also important as ΔG can be quantitatively linked to oxidation–reduction potentials.

Is my second equation an example of hydrolysis? and the first one a dehydration reaction? Studying them more closely, that is what it seems like.

@Anonymous 1. Each equation is just a representation of the overall balance of constituents of glucose. You cannot consider them as a reaction as they are the balance of many reactions. 2. The overall reactions are oxidation of glucose and reduction of carbon dioxide — not hydrolysis and dehydration. 3. The equations omit the oxidising and reducing agents NAD+/NADH and FAD/FADH2 — not to mention ATP and ADP — so are incomplete. 4. I‘ll look at the individual reactions in another comment as I’m running out of characters.

@Anonymous 4 cont. You can see tables which classify the inidividual reactions of glycolysis and the TCA cycle (for the oxidation of glucose) in Berg et al. Table 16.3 and Table 17.2. The reactions that break C–C bonds are not hydrolyses but an aldol cleavage and decarboxylation/oxidations. Hydrolysis breaks a bond by adding water, for example the peptide bond ~CO–NH~ becomes ~COOH + ~NH2. Other examples are hydrolysis of phosphodiester and glycosidic bonds.

The first reaction is catabolism. It does require some energy input in the beginning ("energy investment" of glycolysis) but ultimately leads to net energy release through "energy payoff" of glycolysis, citric acid cycle, and finally electron transport chain and oxidative phosphorylation.
The final result is oxidation of glucose, and reduction of oxygen.. At various points, electrons transfer to NAD+ and FAD. Then, the reduced forms of these 2 electron carriers (NADH & FADH2) go to the electron transport chain, where electrons transfer to oxygen at the end (reduction of oxygen). Meanwhile, protons were pumped into the intermembrane space to create the proton gradient that drives ATP synthesis.
The second reaction is anabolism. The Calvin Cycle requires energy from ATP and NADPH to create the necessary bonds to build up sugars.
In terms of bioenergetics, degradation of a molecule is exergonic. This is favorable if you think about the second law of thermodynamics: there is more entropy when there are multiple, separate sub-units, while there is more order when one molecule made up of those sub-units. Synthesis of a molecule is endergonic (requiring energy). It IS favorable in the sense that we get sugar to eat and burn in the future.
In summary:

Breaking down a molecule = catabolism = release energy from chemical bonds
Building up a molecule = anabolism = absorb energy to FORM chemical bonds (think of the resources needed to construct a new building)

Note my answer leaves out specific details about the processes, but I hope this is basic enough to answer your question!
Source: Lehninger Principles of Biology, David Nelson & Michael Cox

Welcome to Biology.SE. Please add some references that give both evidence for your claims and input for further reading. With these basic processes, Wikipedia articles should suffice.

But if I didn't recognize those processes as glycolysis and the citric acid cycle, how would I know? I'm searching for a more generalized way of figuring out my question.

Oxygen has a high electronegativity, in other terms it really likes electrons.

In this scale neon has the highest electronegativity of all elements,
  followed by fluorine, helium, and oxygen.

https://en.wikipedia.org/wiki/Electronegativity#Allen_electronegativity

These are redox reactions. In the first reaction carbon was oxidized 0 -> +4 and oxygen was reduced 0 -> -2. In the second reaction the reverse happens. Nomen est omen oxygen is an oxidizing agent, so it does not like the reactions where it will be oxidized, since by oxidation it loses electrons. And it likes electrons. Really.
Forcing somebody to do something they don't want, always requires energy, and oxygen is not an exception. ;-)
Just to mention there is always an activation energy regardless of the exothermicity of the reaction. Remember; sugar doesn't burn spontaneously at room temperature... These are multi step reactions and enzymes lower the activation energy of each step, that's why you don't need to invest much by the first reaction. Ofc. a similar reaction can happen by burning sugar, but in that reaction the activation energy is much higher, and it is coming from the heat of the gas flame.

It's a bit misleading to say "these are redox reactions". The equations representing the overall process are, but they represent a whole series of reactions, only some of which are redox reactions. And the principle of whether a reaction requires energy is applicable regardless of whether the reaction is redox. The point about activation energy is important, but one needs to stress that in metabolism the reactions proceed at room temperature etc. because of the enzyme lowering the activation energy (or raising the ground state).

@David I did not want to be perfectly accurate with this answer. Ofc. I could have described it in more detail, but I don't think that would be necessary. If you feel the need you can always edit it, but please try to keep the same length and simplicity.


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Clonality of tumour cells
Does all cancer cells come from a single clone of cells or are there evidences of polyclonal cancer cells too?

Both. There exist homogeneous and heterogeneous tumors. Just depends on the type, its site and cell type of origin, and other factors.

Most tumors are probably not strictly clonal; all cancer cells in a tumor seldom have the exact same set of mutations. Tumors tend to be subclonal, with all cancer cells having a single common ancestor but with later evolution resulting in some mutations shared among all cancer cells but others restricted to sub-populations of cancer cells. This fact and its implications for therapy were noted 40 years ago by Nowell (Science 194:23-28, 1976), and verified by much recent work as reviewed for example by McGranahan and Swanton (Cancer Cell 27:15-26, 2015).
A tumor might need to have a billion ($10^9$) or so cancer cells to be clinically detectable. Thus many years and many cell divisions have passed since the time that a single cell developed the set of mutations originally needed to produce the invasive tumor. With a probability of some uncorrected mutation at each cell division, particularly in cancer cells that often have defects in DNA replication and repair and in chromosome separation, it is essentially impossible for all of the billion cancer cells in the tumor to have identical sets of mutations. See, for example, the work of Bozic et al (eLife 2: e000747,2013). So although there is a clonal origin of the tumor, the tumor is typically a collection of related but genetically distinct populations best considered to be subclones.
Differences among subclones present a major barrier to traditional cytotoxic therapies, to more modern targeted therapies, and to the immunotherapies that presently receive so much attention. Even if most of the tumor is sensitive and responds, a subclone whose mutations somehow provide resistance to the therapy will be able to repopulate the tumor thereafter. Bozic and Nowak (PNAS 111:15964-8, 2014) estimated that a clinically detectable tumor may have 10 or more subclones resistant to any targeted therapy, due to mutations accumulated during the subclinical growth of the tumor.
As examples from immunotherapy for cancer, McGranahan et al recently showed (Science 351:1463-1469, 2016) that responses to immune checkpoint inhibition in melanoma and non-small cell lung cancer were best in patients with clonal rather than subclonal tumor neoantigens for the immune system to attack. Zaretzky et al (New Engl J Med 2016, epub ahead of print) identified subclonal mutations in interferon-receptor signaling and antigen presentation in some patients, mutations enriched in the recurrent tumors following immune checkpoint inhibition and thus likely accounting for relapse following that therapy.
It is possible in principle for a single physical tumor to have multiple cells of origin. Tumors often develop from a region of tissue that has been subject to field cancerization, where carcinogenic challenges have produced many cells with mutations that lead to dysregulated but not invasive behavior. This can lead to multiple independent cancers arising from the same general location, as individual cells later develop the full complement of mutations needed for an invasive tumor. In principle, such multiple cancers might coalesce into a single tumor mass so that the tumor is polyclonal, but I'm not aware of any well documented cases. So it seems that tumors are seldom truly polyclonal with multiple independent cells of origin.

Can you provide some peer-reviewed citations for your claims in the first 3 paragraphs?

@MattDMo I've reorganized a bit and provided some references. Many more available in the McGranahan and Swanton review.

Looks much better. +1


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Principle of 16 S rRNA technique for bacteria identification
Why do we isolate DNA not RNA in 16 S rRNA technique for bacteria identification?

Please ask only one question at a time. Your other questions have already been answered here and across the web. Please do your own research before asking.

There are several reasons some of which are fairly obvious:

The most obvious reason is that PCR only works with DNA, because it uses DNA-dependent DNA-polymerase. One can argue that you can use an RNA-dependent RNA-polymerase, but it has several drawbacks, mainly the cost and synthesis accuracy (Lauring et al., 2013, Nature). Since RNA-polymerase itself has higher error rates than DNA-polymerase (Berg et al., Biochemestry 5th edition, 2002) RNA transcripts might already have some variation from the original gene and using a low-fidelity polymerase in PCR will only lead to exponential error accumulation, which reduces identification resolution.
RNA is less stable in aqueous solutions due to the additional -OH group at the 2' position in the ribose, hence RNA extraction and storage is more complicated and expensive in most cases.
In community studies DNA and RNA have different biological implications, hence metagenomics and metatranscriptomics are different fields.

There are several issues with this answer. (Point 1) RNA sequencing is cheap, easy, and very accurate nowadays. cDNA conversion of RNA, also known as reverse-transcriptase RCR, has been common for quite some time now, with highly accurate RTases being used from many different suppliers. A study from 1988 about HIV is not very current evidence of your thesis, especially in the incredibly rapidly-changing world of mol bio. (Point 2) RNA-Seq instruments are provided by a number of companies, and they all work (initially) with RNA. It is also possible through a variety of methods (...)

(...) to get quite good results using nanopore sequencing nowadays. (Point 3) the second part of the sentence is just wrong. Take a sample, throw it in RNeasy, and store it in the freezer indefinitely. Buy a cheap (depending on your budget) Qiagen spin column, purify the RNA at your convenience, aliquot, and store indefinitely at -20 or -80. Cheap and easy. I'm not sure what the point of Point 4 is.

@MattDMo thanks for your feedback. 1. I removed the revertase-related statement, though I've found no papers comparing error rates of high fidelity DNA-polymerases and high fidelity revertases (it would be great to get one from you); 2. I've been unaware there are machines, except for nanopore, that directly sequence RNA; as for nanopore, although huge improvements have been made, I haven't seen any reports with accuracy > 0.9 (which is laughable when we speak about identification). 3. I've used that kit myself, that's why I wrote that RNA extraction is more complicated and expensive...

... As with RNA-sequencing, I haven't written that it is impossible or something, I've only said that it is more expensive and complicated than DNA-sequencing. And when you only need to identify something, you go for the cheaper and simpler solution, given equal precision; 4. in community studies RNA-seq is commonly used to distinguish active and dormant microorganisms (though it is a complicated theoretical issue), while DNA-sequencing is used to assess structure and composition at the highest possible resolution; DNA-seq usually uncovers more diversity.


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Where do I find standard tissue and cell names?
I am developing specialized database on some desease microarray experiments. The initial data is retreived from NCBI and ArrayExpress databases. The problem is that sample attributes sometimes specify similar or same things but in different manners: as cell and tissue names, desease names, age, ethnicity of donor, ect. Where do I find conventions for naming experiment sample attributes?

I doubt there are many. There are some conventions regarding naming cell types corresponding to what surface and internal markers are expressed (or not), but to my knowledge those are in early stages. In papers, authors generally define their own naming conventions, which may or may not match up to others. The problem is there's a lot of argument about how to name things, with each lab or institution having their own preferences. As a simple example, tuberculosis is also known as Koch or Koch's Disease. You'll probably need to pull from a lot of individual databases, and just use synonyms.

Also there can be conventions without controlled vocabulary ( http://www.ncbi.nlm.nih.gov/geo/info/MIAME.html )

It turns out that ArrayExpress itself uses various ontologies (dictionaries structured as trees) available at Ontology Lookup Service when it processes users' search queries. Experimental Factor Ontology is the precisely one I was searching for.
Medical Subject Headings (MeSH) dictionary turned out to be handy as well.


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Stem cell and organ growing genitals
I've been reading a lot about stem cell research and the work on growing artificial organs.
I assume, with sufficient advance in the technology, there is no theoretical reason it would not be possible to grow genital organs (gonads, uterus) in particular?
So my question is: is there any theoretical reason you could not use this process to grow the genital organs of the opposite sex of a stem cell donor?
So then, would an ovary grown from male stem cells potentially ovulate Y-gamete eggs?

No one knows if a uterus is capable of producing so-called "Y-eggs", because in persons affected by sex chromosome abnormalities (XXX and more, XXY, X, XYY, etc.), the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gene SRY and other male developmental and fertility factors. In contrast, people with only X chromosomes (regardless of the number) are generally female-appearing, with at least some development of the associated organs and structures.
A second question is whether a male-derived stem cell could be coaxed, hormonally and otherwise, to become a uterus in the first place. An X is already present, so all the purely genetic (though not necessarily epigenetic) instructions are there, but, as far as I know, the question of whether a Y would interfere with the development process has not been answered in humans.

For some reason I'm having a difficult time finding information on persons with only a Y chromosome. Going back to my undergraduate days (boy, was that a long time ago), I seem to recall that they're likely non-viable, but I can't find anything now to back that up.

From what you say, it sounds like it would be even more of a stretch to create testicles from a woman's stem cells.

@StephenPosey correct, as women lack the necessary Y chromosome.

"the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gen" : Did you consider chimerism arising from "vanishing twin syndrome" & the like, the guest cell lines arising from this most often take their cues from their host organism, so a male vanished twins cells can persist in a female sibling but should in no way result in a male phenotype

^ further, were the larger portion of one of these colonies of cells from a male sibling to be in the ovaries of a female host there is absolutely no reason to suppose that (having "gone native" & taking all of their cues from the host body on what they're supposed to become & do) they wouldn't produce perfectly normal egg cells, half of which could be expected to carry a Y chromosome.

^ though as the ovaries are internal the chances of any loose cells sloughed off from a twin in the womb being absorbed into the area slated to become the ovaries seems slim at best, the other way around though, a sample of a female twins cells colonizing the external location of a male sibling in the womb where the gonads are slated to form, doesn't seem that unlikely.


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Summary statistic that can distinguish between migration from pop2 to pop1 vs. pop1 to pop2
Given two sister populations that diverged some time ago, say pop2 migrates to pop1 and breeds there, giving offspring with sequence segments similar to those from pop1 but not in pop2. There are stats to find how similar two populations are; for instane, mean dxy takes the average of number of pairwise sequence differences between the two sister populations. Say if there is no migration, mean dxy at a locus of length 10000 is 100. Then with migration, say mean dxy at that locus is 300. Detecting a dxy that's unlikely under the null hypothesis of no migration indicates migration and interbreeding occurred.
I've been thinking for a while on if there are summary statistics which can distinguish between migration from pop2 to pop1 vs. migration from pop1 to pop2 (assuming only one of these events occurs). Do such statistics exist? Without loss of generality assume pop2 members migrate to pop1. Then pop1 will have members that are more similar to pop2 compared to if no migration occurred, but pop2 will be as if no migration occurred.
If we run simulations of a population w/ no migration, we can expect to see some value of pi and # of segregating sites. These measurements may be different in pop1 when pop2 migrates into pop1; some members of pop1 will have SNPs that pop2 do not have, and thus there would be more genetic variation (higher pi and ss) in pop1 compared to its expected pi and ss under no migration. So dxy can say that there's some similarity between pop1 and pop2 that's not expected under null hypothesis, and then pi or ss can say which of the two has a higher genetic variation than expected. Can some statistic that depends on dxy and pi distinguish between migration from pop1 to pop2 vs migration from pop2 to pop1?

Yes, migrants affect patterns of genetic diveristy
Immigrants yield to higher effective population size and therefore higher genetic diversity. They will also affect the site frequency spectrum and I would expect that if the migrants are numerous enough, they would yield to positive Tajima's D.
Therefore, unidirectional migration will definitely yield to differences in patterns of genetic variance among populations (that can be measured by any summary statistic of the site frequency spectrum).
Existing methods for detecting directional selection
I have never had to do such inference so I am not able to do a good review of the existing technics.
You should probably read Slatkin and Maddison 1998 and more importantly Beerli and Felsenstein 2001. Beerli and Felsenstein 2001 has been cited 1,341 times and you should probably quickly see whether some of these papers suggest more recent methods. John Novembre has some very interesting work on how to estimate migration rate between any two populations (e.g. Novembre and Stephens 2008). He might have done something of interest to your problem.
You can always use Approximate Bayesian Computation (ABC;see for example Jeffrey Jensen's work for example of inferences with ABC in population genetics) to figure out what pattern of migration is most likely. With a simple enough model, a good ABC algorithm is not that long (with good computing ressources). The question then is what statistic(s) to use for the rejection algorithm. Again for that, you should have a look at the existing literature to come up with a set of potentially useful statistics.


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Does capillary blood pressure have any effect on how much oxygen or nutrient gets distributed to tissues?
From what I have read regarding blood pressure and blood flow, I've come to the conclusion that, apart from the osmolarity of blood, the only determinant of how much oxygen/nutrients the tissues get per unit time, is blood flow.
Does blood pressure (not systemic, but within a theoretical capillary) have absolutely no effect on this, and if so, why? Intuitively, it seems to me that if the force by blood on the walls of a capillary increases, that would imply a higher number of molecules touching endothelial cells, and thus a higher likelihood of molecule transport per unit time.
Or is it perhaps that they both have positive effects on oxygenation/nutrient transport; but blood flow's effect greatly excels that of blood pressure?


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Does ChEMBL have a specific definition for what they mean with "Max phase for indication"?
ChEMBL lists various properties at pages for substances. I would like to copy some of the data that resides under "Max phase for indication" over to Wikidata. For that it would be good to know the exact definition that ChEMBL uses for "Max phase for indication". Unfortunately I can't find it on their website. Is a definition available somewhere?

@Gerhard OK, I see your point. I'll retract my close vote.

This refers to the phase a compound has "achieved" in a clinical trial.
Phases are typically ordered from 1 to 4
(although phases 1-3 are most talked about, as they are needed to bring a drug to market):

Phase 1: Testing of drug on healthy volunteers for dose-ranging
Phase 2: Initial testing of drug on patients to assess efficacy and
  safety
Phase 3: Testing of drug on patients to assess efficacy, effectiveness
  and safety (larger test group)
Finally, there is Phase 4 (referred to in your example), which is
  after a drug has been approved (by e.g. the FDA or the EMEA): here,
  the effects of a drug while used on the general patient population are
  monitored.

See also https://en.wikipedia.org/wiki/Phases_of_clinical_research
Your example has been approved (i.e. it can be brought to market, or might already be available), while others might still be in ongoing clinical trials. Others might have been "killed" earlier due to e.g. toxicity or side effects. Or have not even entered clinical trials (which would be the majority of compounds).
https://en.wikipedia.org/wiki/Phases_of_clinical_research

This answer partly tells me what I already know and partly is wrong and doesn't answer the question. The "max phase" is "4 (Approved)" but that's not what's written in the "Max phase for indication" line. My example scores differently for different illnesses for the "Max phase for indication". More importantly the Wikipedia article doesn't tell me whether ChEMBL only counts FDA or EMA registered trials or whether it counts trials more broadly.

@Christian: I'd suggest emailing EBI's helpdesk in this case, as they will be the only ones who can give you a definite answer.

@Christian This post got a community bump so I'll weigh in with my understanding: Gerhard's answer seems to be right on, and I don't see anything besides numbers 1-4 in the column you are talking about. Indeed, this is different for different indications: in your example, Risperidone has been in phase 4 trials for anorexia, but only in a phase 2 trial for cocaine dependence.


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Is it possible to identify a particular gene sequence from next gen sequencing techniques (especially RNA-seq )?
I have to check the expression of a gene in a fish whose sequence is not known in the fish in question. Sequence is known in an another fish (zebrafish) but the gene has 10 isoforms. The genome of fish in question is not sequenced, however RNA-seq data is available. I have no knowledge of RNA seq data analysis. Is it possible to know the sequence of gene of interest from this RNA-seq information?

Okay, so you have RNASeq, but no reference genome for your fish?  Just transcript sequence from zebrafish?  Are you just trying to see if this gene is expressed, or you need to a more global view to compare it to?
If you just want to see if the gene is expressed, easy thing to do is to make a reference just made up of zebrafish transcripts, align to that.  If there are too many differences between your fish and zebrafish, that won't work.
In which case, the next thing you could try is de novo assembly of your RNAseq data, then use blast to compare the zebrafish trasncripts to your assembled transcripts.  Blast will make alignments where a short read aligner might not.

Yes, it is possible, if the gene was expressed in the cells where the RNA was harvested from.
With RNA seq basically you sequence the RNA of some cells, usually it is mRNA that you sequence, that means that the sequence you are looking for is not an plain copy of the DNA gene sequence you have. Mainly because it results from splicing and other post-transcription processing.
However, if you know the DNA sequence of the gene and you have RNA seq data (and if that particular gene was expressed in the cells the RNA is coming from), you can spot the exons of the gene in the data. If the gene is expressed in zebrafish you can find on ENSEMBL all the information about the transcripts of that gene and look for those in your RNA seq data (using BLAST for example) to confirm the presence of the expressed gene.


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Do all fungi dislike acidic environments?
I know that some fungi prefer mildly alkaline environments and dislike acidic environments. Is that true of all fungi, or do some fungi prefer acidic environments? If so, are such acidic fungi rare exceptions or is it common for there to be acid-loving fungi?

Many fungi prefer acidic environment. Such as most skin-disease causing fungi prefer acidic environment. (However this does not mean they'll be cured at alkaline environment)

To add to @AlwaysConfused's comment, the skin has naturally an acidic pH at around 5.5 http://skincarerx.com/article-ph

Fungi that grow in acidic media are well known, here just one reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC518635/pdf/jbacter00651-0183.pdf
About their spread, they are less common in mild environments (like you hands, or your garden soil) but of course in acidic environments, they will be predominant.


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How can one identify an organism from its dissymmetry ratio?
If I am given the dissymmetry ratio of an organism ((A+T)/(G+C) is a constant), how can I identify the source of the DNA and classify the organism?

What information have you found so far on your own?

@kmm uhh absolutely nothing scratches head

The point is that we need to better understand you motivation for trying to do this. What do you know, what do you need to know, etc. Take a look at the  tour to see how the site works: http://biology.stackexchange.com/tour Without more information, your question will likely be closed as either too broad or without sufficient information.

You cannot. That information is too little for identification.

It depends what lineage (bacteria, virus, eukaryotes) you are interested in and what level of accuracy you are hoping to reach.
We know the (A+T)/(G+C) ratio for a handful of eukaryotes only. So if you were thinking about eukaryotes, there is no need to look much further. You cannot match a (A+T)/(G+C) ratio to a species because we don't know the (A+T)/(G+C) for the vast majority of species.

You could compare the (A+T)/(G+C) to those of higher orders; see "applications in systematics" on https://en.wikipedia.org/wiki/GC-content
( While the (A+T)/(G+C) ratio doesn't provide enough resolution to identify the species, OP didn't ask for identification of species.)


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Find Mutations Frequencies by Cancer Type
Is there somewhere that has mutation frequencies by cancer type? So if I were looking at CML, AML, or even more generally at something like leukemia. Is there some database that would contain mutation frequencies? So that I could find that in leukemia 50% of cancers contained a T100G mutation.
I have looked through COSMIC but haven't had much luck.

What exactly are you looking for? There is a paper which looked at the mutation frequencies of different cancers, I can look it up in my database if you want.

@Chris If that much info is in a paper that would certainly work. I figure this sort of thing would be in a hosted database though.

Try http://dcc.icgc.org

There is one paper called "Mutational heterogeneity in cancer and the search for new cancer-associated genes" from the "The cancer genome atlas" which should be interesting for you. This project aims to map the mutations occurring in different cancers, one of the results is this figure (from reference 1):

The project itself has numerous data on the different cancers available on the project website, which can be found in reference 2.
References:

Mutational heterogeneity in cancer and the search for new
cancer-associated genes
The cancer genome atlas project website

Thanks I actually remember this paper, I have it in my ref manager as well. I'll go back and look at it and check those sites to see if I can find what I need.


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How does gold chloride stain neuromuscular junctions?
Gold chloride is used in muscle biopsies to stain the NMJ. What is the substrate that it binds to?


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Do animals only breathe through one nostril at a time like humans?
Humans breathe through one nostril at a time.
Do non-human animals also do so, or do they breathe through both nostrils at once? Has any actual study been conducted on this topic?

From the explanation given here (which you should definitely have a look at if you haven't yet), there is really no reason to expect that it would be any different in other mammals or at least primate. However, I doubt we will find a study that investigates this question though as it is extremely specific and I would guess of little interest to most people! My best guess that probably all mammals do that! By the way, there is a Ted talk on how dog smell

Humans do breath one nostril at a time...generally. Those who practice Yoga tend to train themselves to control the side of the nose through which they breath.

Suggested edits: correct spelling "breathe" in title; change "animals" to "non-human animals" in title and question (humans are animals too!)

The post linked by @Remi.b says

The nasal cycle is a natural ultradian cycle (see here and here. Not only is it present in humans, the nasal cycle has been observed in rats, rabbits, domestic pigs, cats and dogs (see references in Eccles 1996).

Proceeding to Eccles 1996 (p. 372):

The nasal cycle is not only limited to the human nose, as it has been found in the rat and rabbit [31], the domestic pig [32, 33], the cat
  [34] and the dog [35], and appears to be a universal phenomenon at least in all mammals and possibly other animals.
  ...

Bojsen-Moller F, Fahrenkrug J. Nasal swell bodies and
  cyclic changes in the air passages of the rat and rabbit
  nose. Anat 1971; 110: 25–37.
Eccles R. The domestic pig as an experimental animal
  for studies on the nasal cycle. Acta Otolaryngol (Stockh)
  1978; 85: 431–436.
Campbell WM, Kern EB. The nasal cycle in swine.
  Rhinology 1981; 19: 127–148.
Bamford OS, Eccles R. The central reciprocal control
  of nasal vasomotor oscillations. Pflügers Arch 1982;
  394: 139–143.
Webber RL, Jeffcoat MK, Harman JT, Ruttimann UE.
  Demonstration of the nasal cycle in the beagle dog. J
  Comput Assist Tomogr 1987; 11: 869–871.

A Pubmed search for '"nasal cycle" animal' gets a total of 18 hits, including refs 32 and 35 above, as well as

Spontaneous nasal oscillations in dog. A mucosal expression of the respiration-related activities of cervical sympathetic nerve. Asakura K, Hoki K, Kataura A, Kasaba T, Aoki M. Acta Otolaryngol. 1987 Nov-Dec;104(5-6):533-8.
Proceedings: Studies on the nasal cycle in the immobilized pig. Eccles R, Maynard RL. J Physiol. 1975 May;247(1):1P.

A bit more digging forward & backward through citations finds the article on cats (also by Eccles):

R. Eccles & R. L. Lee (1981) Nasal Vasomotor Oscillations in the Cat
  Associated with the Respiratory Rhythm, Acta Oto-Laryngologica, 92:1-6, 357-361, DOI: 10.3109/00016488109133272

You might find more if you poke around (Google scholar/Pubmed, look at citations backward & forward, try search terms like "'nasal cycle' bird" or "'nasal cycle' reptile"), but at this point I doubt that anyone's bothered to check this in non-mammalian animals ...

Good answer (+1). Citing the post I cite, you proved wrong my assumption that we would not find a reference on the subject.

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


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Pichia pastoris and ornithine
Can Pichia pastoris (species of yeast used for recombinant protein) produce the non-protein amino acid Ornithine? Or does it express ornithine at all?

is the pichia pastoris genome available from some sequence database? you could search for ornithine synthetic genes

yes, i can look for the pichia pastoris genome sequence on NCBI. do you suggest that i compare the genome sequence of pichia and ornithine and see if there is a match between them ?

Yes, it contains arginase. Thise enzyme converts arginine to ornithine and is probably part of the urea cycle.
You might notice the arginase is listed as coming from Komagataella phaffii GS115, but this is just another (new?) name for Pichia.


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How fast can our skin recuperate from sunlight?
Imagine that you get burned in the sun after half an hour. But a quarter and another quarter is also a half hour. So if you go into the sun 15 minutes and after one hour another 15 minutes do you get equally burned? Or what in case you pause half an hour etc. Is there a kind of schedule for recuperation times/pauses?

It depends a lot on skin type. Pale skin has higher sensitivity to sunlight and is burnt relatively more easily than dark skin.


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What is the half-life of dNTPs at 95 °C?
I'm looking for the half-life of dNTPs, either as a whole or broken into individual bases, at 95 °C (or similar). A titration would be great if that exists. I can provide more specifics if need be, but broadly the idea would be 'able to polymerize' vs. 'unable'.

Interesting question. FWIW, I was able to get strong bands on a 6 hour long PCR reaction with Pfu polymerase, so it is unlikely that dNTP stability would be a very big concern under most circumstances.

@MarchHo Thanks for the insight. To confirm, when you say 6 hour long PCR, that is the total length of the program, and not a total time of 6 hours at 95C (or 98C perhaps with Pfu)?

The total time was 6 hours long, most of which was extension at 72C. I would say the time taken at 98C was roughly 25 minutes (30s per cycle)

I think almost every molecular biologist must have wondered about this (as we always assume that (d)NTPs are unstable) but there seems to be no study that checks the stability of (d)NTPs at different temperatures. The closest I could find is this article which says that 40% of ATP survives after 1h at 95⁰C (10mM in distilled water). Mg²⁺ would increase the stability and stability of dATP may probably be higher.

Instead of searching for the stability of dNTPs, consider the stability of their constituent parts.
Caveat: ignoring the bonds between the different parts of dNTPs likely misrepresents the stability of the intact molecule, given that the covalent bonds between the nucleobase, sugar, and phosphate pieces each have their own relative stabilities. See my related Chemistry.SE post: Do the phosphoester and glycosidic bonds of dNTPs increase thermal stability?

Hydrolysis of Purines and Pyrimidines

In The stability of the RNA bases: implications for the origin of life,1 there is an Arrhenius plot showing the rate of decomposition of the most common nucleobases (A,T,C,G,U) at pH 7 in 50 mM phosphate buffer.  According to ThermoFisher, the pH of PCR buffer is between 8 and 9.5, though the authors of the paper linked above observe that the pH rate profile for the decomposition of purines (A,G) is relatively flat between pH 5 - 10.
At 95° C, the least stable nucleobase has a half life of 10-1 years, or about 1 month.

Fig. 2. Arrhenius plot for the decomposition of A, U, G, C, and
T, pH 7. ∆, data from Garret and Tsau (10). Equations are as follows:
log k(A) = -5902/T + 8.15; log k(U) = -7649/T + 11.76; log k(G) = -6330/T + 9.40; log k(C) = -5620/T + 8.69; log k(T) = -7709/T + 11.24. [red lines added for emphasis]

Decomposition of Pentose Sugars

The same research group investigated the stability of the sugar moieties of nucleic acids in Rates of decomposition of ribose and other sugars: implications
for chemical evolution.2  The analysis is slightly obscured by the use of deuterated water, though the authors observe that the rate of decomposition of ribose in H2O at 100° C and pH 7.0 is identical to that in D2O at 100° C and pD 7.4.
At 100° C and pD 7.4, ribose, the sugar component of RNA, has a half life of less than 2 hours.  Interestingly, the authors note that 2-deoxyribose, the sugar component of DNA, decomposes 2.6 times slower than ribose with a half life just shy of 4 hours.

Fig. 1. Rates of ribose decomposition as a function of pD.
The curves were fitted by assuming a functional form k = k0/(1 +
[H+]/Ka), where Ka and k0 are adjusted constants. [red lines added for emphasis]

Hydrolysis of Triphosphate

Getting to the heart of your question, i.e. at what point are dNTPs no longer "polymerizable", the stability of the triphosphate is vital, as the hydrolysis of the two distal phosphates and the creation of a phosphodiester bond with the remaining proximal phosphate is the rate-limiting step in DNA polymerization.
An older publication, The Hydrolysis of γ-Phenylpropyl Di- and Triphosphates,3 investigates the hydrolysis of nucleotide analogs at 95° C, over a pH range of 0.3 to 10.  For the ATP analog, the rate of spontaneous hydrolysis to ADP is very low, 17.5 × 10−5 s−1 at pH ~5.  Assuming first order kinetics, the half life of the triphosphate form is ~4000 seconds, or a little more than an hour at 95° C.  In a buffered solution closer to a neutral pH, we can expect triphosphate to be even more stable.

Table 5. A Comparison of the Rates of Hydrolysis of γ-Phenylpropyl Di- and Triphosphates and ADP and ATP at 95°

A worked example
A PCR with one 2-minute initial melting and 20 cycles with 15-second melt steps will expose dNTPs to 420 seconds at 95° C.  Considering only the hydrolysis of triphosphate, which is the least stable component of the 3-component dNTP molecule outlined above, the equation for exponential decay can be used to calculate the proportion of unincorporated dNTPs that are still "polymerizable" at the end of cycling, using the rate constant provided in Miller and Westheimer.3
$N_{\text{final}} = N_{\text{initial}} × e^{-kt}$
$N_{\text{final}} = e^{(-17.5 × 10^{-5} s^{-1})(420 s)} = 0.929$
For some perspective, a 50 μL PCR with 0.2 mM dNTPs contains enough raw materials to create 1.51 × 1013 copies of a 200 bp dsDNA amplicon, ignoring the contribution of primers to the amplicon body, and assuming perfect fidelity of the polymerase and primers in excess.  A 20-cycle PCR with 106 molecules of template will yield 1.05 × 1012 amplicons, assuming perfect duplication at each cycle, meaning dNTPs are supplied in more than 10-fold excess and heat decomposition is unlikely to have an effect on PCR fidelity in this system.

References

Levy M, Miller SL. The stability of the RNA bases: implications for the origin of life. Proc Natl Acad Sci USA. 1998 Jul 7;95(14):7933-8.
Larralde R, Robertson MP, Miller SL. Rates of decomposition of ribose and other sugars: implications for chemical evolution. Proc Natl Acad Sci USA. 1995 Aug 29;92(18):8158-60.
Miller DL, Westheimer FH. Hydrolysis of Gamma-Phenylpropyl Di- and Triphosphates. Science. 1965 Apr 30;148(3670):667.


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How does air pass through when we breathe through the mouth?
When you sleep with your mouth open, does air pass through the nasal cavities? If not, how will you describe the air that enters the mouth?

Welcome to Biology.SE. I am not sure what you mean by [..] how will you describe the air that enters the mouth? Are you looking for a specific adjective to describe this air? I wrote a short answer, let me know if this was the kind of answer you were looking for.

The oral cavity and the nasal cavity merge into the trachea which yield to the lungs. As a consequence one can breath in and out through the nose or the mouth.

When you breathe, air follows the path of least resistance. Since the mouth (to pharynx to trachea) has a larger diameter than the nostrils, most of the air will pass through the mouth (unless obstructed by the tongue, etc.)
However, some will enter the nose and proceed towards the lungs by virtue of decreased air pressure in the nasal cavity while inhaling.


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How is phenol antiseptic?
What makes phenol an antiseptic, is it because of its acidity which may increase the proton concentration at cell membrane? I am unable to figure out the exact mechanism.

The main reason for phenol being antiseptic is it's effect on proteins which it denaturates. It also causes leakage of cellular membranes. See the paper in reference 1 for some details and a load of references. They say in the section on phenol:

Phenolic-type antimicrobial agents have long been used for their
  antiseptic, disinfectant, or preservative properties, depending on the
  compound. It has been known for many years (215) that, although they
  have often been referred to as “general protoplasmic poisons,” they
  have membrane-active properties which also contribute to their overall
  activity (120) (Table (Table22).
Phenol induces progressive leakage of intracellular constituents,
  including the release of K+, the first index of membrane damage (273),
  and of radioactivity from 14C-labeled E. coli (242, 265). Pulvertaft
  and Lumb (386) demonstrated that low concentrations of phenols
  (0.032%, 320 μg/ml) and other (nonphenolic) agents lysed rapidly
  growing cultures of E. coli, staphylococci, and streptococci and
  concluded that autolytic enzymes were not involved.

Reference:

Antiseptics and Disinfectants: Activity, Action, and Resistance


text:
Myoblasts Formation
Myoblasts arise from mesenchymal stem cells (MSCs), and are precursors to myocytes. In muscles, in the basement membrane, there are also present satellite cells which can divide to generate muscle fibres, to repair injury to muscle. Are satellite cells intermediates in the lineage from MSCs to myocytes?
Is the lineage then MSC > Satellite cells (a committed stem cell or progenitor) > myoblast (precursor) > myocyte?
If not, then what are the progenitors for myocytes, and how do satellite cells fit in this lineage?

Read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4073943/


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How do I identify the different stages of meiosis under microscope?
This is a question I'm troubled with as my exams are knocking at the door. I need help so I decided to post this here.
Here's what I know and understand about meiotic stages:
Specimen: Grasshopper (Gesonula punctifrons) testis whose 2n= 23
Note: The character in bold and italics is the identifying feature of the concerned stage.
Prophase:
Leptotene

The uncondensed chromosomes are visible as a cloud of thin threads.
Each chromosome consist of two chromatids which are not visible.
The single darkly stained X chromosome is found at the periphery of the nucleus.
Late in this stage the chromosomes attach themselves by telomeres to the inner membrane of the nuclear envelope forming a bouquet.
Nuceolus and nuclear membrane are present.(not visible under compound
microscope)

Zygotene

The uncondensed chromosomes are visible as a cloud of threads.
Homologous chromosomes undergo synapsis  forming bivalent.
The single darkly stained X chromosome is present slightly off the periphery of the nucleus.
Nucleolus and nuclear membrane are present.(not visible)

Pachytene

The chromosomes show some degree of condensation.
The sister chromatids separate to form tetrad a structure with four chromatids.
Crossing over between non sister chromatids of homologous chromosomes occur leading to formation of X shaped chiasmata.
Nucleolus and nuclear membrane are present.(not visible)

Diplotene

The chromosomes are thick and darkly stained.
The chromosomes are wooly in appearance.
The paired chromosomes separate from each other except for the chiasmata.
Nucleolus and nuclear membrane begin to diappear.(can't be detected)

Diakinesis

The chromosomes are thick and darkly stained.
Terminalisation of chiasmata initiates.
The bivalents appear rod, diamond or oval shaped.
The nucleus and nuclear membrane disappear completely.

Metaphase-I

The chromosomes are thick and darkly stained.
Presence of twelve chromosomal elements (11 tetrad + X chromosome).
The chromosomes are aligned at the equitorial plate.
Terminalisation of chiasmata completes.

Anaphase-I

Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are T or V shaped.
Each chromosome is in dyad state.
The centromere is undivided.

Metaphase-II

There is 11-12 dyads present.
The chromosomes are thick and darkly stained.
The dyads are arranged in circle or flower like fashion.
The chromosomes are rod like

Anaphase-II

The sister chromatids of a dyad separate due to splitting of centromere.
Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are rod like

Here's an image which has nearly all the stages except telophase.Can someone label the stages?

Here's what I feel about them:

Finally am I correct? How do I identify them correctly? Could you site some authentic references?

ID characteristics that can help you recognize diplotene  better:
diplotene :
the only difference between this phase and Diakinesis is that The centrosomes reach the poles.
you can see the photos of diplotene and diakinesis here :
http://www1.biologie.uni-hamburg.de/b-online/e09/meiosea.htm

(a) polyploid nutri-tive cells with many heteropicnotic chromatin bodies; (b) leptotene-zygotene; (c) pachytene; (d) diffuse stage; (e) di-plotene; (f) diakinesis; (g) metaphase I; (h, i) anaphase I; (j) telophase I;. (k) metaphase II; (l) anaphase II; (m) telophase II; (n) round spermatids; (o) elongating spermatids; (p) head of sper-matozoas. Big arrows indicate sex chromosomes, small arrows point to nucleoli and arrowheads indicate m-chromosomes
You can see all the phases clear and perfectly separated here :
http://biology.about.com/od/meiosis/ss/meiosisstep.htm#step1
by the way , try to adjust microscope as best as you can & don't put much  oil immersion .

long answer for this Question ?! there is no other thing to explain .
Sanjukta Ghosh asks how to identify different phases of meiosis under microscope and I provided a link that show all 10 phases perfectly clear . I could upload every single photo by my self on the answer if you are asking for it   . why should I put some additional content and confuse the questioner ?

The images you have linked are not light microscopic views. They are far too clear for light microscope. Besides it lacks the substages of prophase I. I was also looking for an answer that specifies the key identifying characters. It will be helpful if you could improve the answer. Moreover I have attached an unedited image of meiotic stages. Could you label the stages there and explain how you are identifying them.

They are light microscopic view of course the background is white for better contrast they've been coloring very good and adjust very well . that's how it's gonna be in the exams as far as I've seen . but don worry I will improve the answer by specifying the key id characters . but you should know it's a tricky skill some times no one can say what the phase is as it is really unclear  ... these cases are not gonna be on the exams or so .


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How does aspirin "thin" blood?
As we all know, aspirin doesn't actually thin the blood, as it has been explained to me, it makes it "slippery". Slippery blood doesn't stick to itself hence this helps prevent internal blood clots (or allows blood to pass more easily around an existing clot). I also understand that having your blood too "slippery" can lead to the body attempting to counteract that and making it too "sticky".
Anyhow, my question regarding that is this, how does aspirin work? How does it make the blood "slippery"? (If there is a more medically correct term for "slippery" and "sticky", I'm all ears).
P.S. I paid the Mayo Clinic's website a visit before coming here, the information about aspirin's mechanism wasn't particularly helpful to me.

Aspirin doesn't make blood slippery (like lubricant's might allow machinery to work.) Blood clots require thrombocytes (aka platelets) and blood proteins to form. Too many platelets and clotting is more likely; not enough (or inactivation of some of the platelets) and clots don't form as easily. Anything that activates platelets (as described below) can result in a clot. Aspirin inhibits that.

Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.

Aspirin  inhibits COX in the endothelium which is required for prostacyclin (PGI2) production. PGI2 is an anti aggregant and vasodilator  . Aspirin also inhibits thromboxaneA2 ( TXA2) production in the platelets. TXA2 is a platelets aggregant and vasoconstrictor hence antagonist of PGI2.
So aspirin decrease both PGI2 and TXA2 production but endothelium cells  can reproduce new COX inside them hence can quickly come over the inhibition of aspirin while platelets can't reproduce new COX so once they are inhibited then they can come over this inhibition only when new platelets are produced in the bone marrow so it takes too much time .
So what aspirin does it that it shifts the PGI2-TXA2 equilibria towards PGI2 so reduce platelets aggregation. Hemostasis , Harper 31st edition.
https://www.webofpharma.com/2021/02/harpers-illustrated-biochemistry-31st.html?m=1

Can you add sources to this answer as well to allow others to background read on your material?

Yupp now I added my resource: hemostasis chapter  form Harper 31st edition

Please do not upload book pages. This is a copyright violation and not tolerable.

Ohhk ,,I apologise

Thanks for all your efforts ro improve your post. Kudos. Can you please add a weblink to the book you cite?

https://www.webofpharma.com/2021/02/harpers-illustrated-biochemistry-31st.html?m=1


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Anatomical Angle Made by the Fingers of an Extended Palm
Does the angle made by the fingers (excluding the thumb) of an extended palm (as shown in the figure below) have a name (such as the Lovibond or Cobb angle, for instance) ?

I have already checked Modeling the Constraints of Human Hand Motion, published by the Beckman Institute for Advanced Science and Technology at the University of Illinois at Urbana-Champaign, but it failed to provide any answers. (Perhaps there aren't any ?) Any input would be deeply appreciated.

I searched through a few documents such as Biesecker et al. (2009) but could not find anything so far. I would guess there aren't any terms for that. Did you make the figure or did you find it somewhere? Where is it from? Knowing your interest for this term might eventually be helpful. [english.se] could also be a good place to ask this question.

@Remi.b: The question originated in my own mind, as an unintended byproduct of various measurements performed on my own body, in an attempt to understand the ancient and medieval measuring systems, such as those still employed by the Anglo-Saxon world today.


text:
Why can myopic eyes focus on nearby objects, but not on distant ones?
In myopic eyes, far away objects get blurry. I understand that myopia means that the focus of the lenses concentrates light at a point in front of the retina, thus by the point the light rays reach my retina they've already spread apart so they aren't coalescing on the same point as they ought to.
My question is, why is it that this deficiency only apparently manifests itself when things are far away?  Why is it that the focusing of light in front of the retina doesn't cause the same blurry vision up-close as it does far-away?

There are four common refractive errors, namely nearsightedness (myopia), farsightedness (hyperopia), astigmatism (Fig. 1) and presbyopia.

Fig. 1. Refractive errors. source: Excimer Ophthalmologic Clinic
myopia (nearsightedness): The eye ball is too long, or the cornea too steep, causing light to focus in front of the retina and making distant objects appear blurry.
hyperopia (farsightedness): The eye is too short, or the cornea too flat, causing light to focus behind the retina and making near objects appear blurry.
Astigmatism: is caused by an irregular cornea or lens, causing images both near and far to be distorted or blurry.
Presbyopia: a common age-related problem that is caused when the natural lens in the eye loses its elasticity, making it difficult to focus on near objects (hyperopia).
Focusing of the retinal image is mainly regulated through the process of accommodation (Fig. 2). Accommodation is mediated mainly by changes in the shape of the lens. A more globular lens results in a larger refraction of the light to focus on near objects. A flat lens refracts light less and is suited for focusing in the distance.
The lens is held in place by the suspensory ligaments. The ligaments in turn are attached to the ciliary muscle (Fig. 2). When the ciliary muscle contracts, it shortens. This effectively moves it closer to the lens and so any tension in the suspensory ligaments is released as the ligaments go slack.  Slack ligaments mean the lens adopts a more globular shape.
When the ciliary muscle relaxes, this changes its position to increase the tension in the suspensory ligaments. Taut suspensory ligaments (caused by the relaxed muscle) will pull the lens into a long thin shape.

Fig. 2. Accommodation. source: PMG Biology
In the case of myopia, objects in the far distance are blurry. Objects far away tend to send near-parallel light rays onto the lens and the lens needs to be maximally flat and hence the ciliary muscles should be maximally relaxed. If in this case the image is still in front of the retina, the lens cannot relax any further and hence the image is blurry. Because there is enough dynamic range for the ciliary muscles to contract, there is not any problem with objects close by, because the lens is perfectly capable of assuming a concave (fat) shape.

It took me about three read-throughs to understand, but great answer.  The sentence, "If in this case the image is still in front of the retina, the lens cannot relax any further and hence the image is blurry." really drove it home.


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Is it possible for any impurities to get through the apple peel?
My parents always told me not to eat from the apple trees near the  road, because some kind of bad toxic dirt might get through.
This sounds to be physically possible but not really probable in my view. In the time apples grow on the tree they never rot. The rotting procces starts as the apple falls down and damages - the wound will quickly change its colour and it begins to decay - from this I assume the peel is almost perfect defense against bacteria & toxic penetration.
I think the only danger may come from the dust microparticles spread by the cars - which can be easily washed by water or wiped off with a piece of cloth. Am I right? What about other types of fruit?

Have you considered the possibility that the stuff might get dissolved by water and taken up by the tree by the roots?

Hmm... Why the irony?

FWIW, apples can and do rot on the tree, for instance if they're pecked by birds, or have been infested with codling moths.

it's waxy so it's a very good barrier, and the truth is that apple peel contains more good stuff that most of the inside of the apple. You can consider the peel to be the same as a leaf, perhaps a lot more resistant and waxy, so you can search for real science in a lot of research about leaves content of roadside pollutants, for example: https://www.ncbi.nlm.nih.gov/pubmed/17294646

The answer I got from Jan Kolář of Charles University:
The spores of fungi or bacteria in apples don't just emerge from nothing, they have to get into it from the surroundings. I often see apples, which rot while still hanging on the tree, the hole needed for the infection of the apple is usually made by a worm. The problem of the apples near roads isn't that they would rot. Indeed, plants can absorb all kinds of harmful substances from soil, water or air, including heavy metals, chlorinated organic compounds or organic compounds from the exhaust gases of cars. How much and which substances, that usually depends on the type of plant (specifically on where it stores most of the substances).
It's not enough to wash an apple because the impurities are absorbed in the fruit itself as well. And on the surface of the peel, there are waxes and other unsolutabe substances which can absorb toxic aromatic carbohydrates from the exhaust gases, and can't be simply washed off.
The greatest risc near the roads used to be contamination with lead because petrol used to contain it. Many of the plants can recieve the lead and hoard it up in some organs. Now, when the lead petrols are forbidden, the biggest risc pose the fumes from the diesel engines. So I'd rather not eat fruit near the roads (especially near the busy ones).


text:
Is this a bedbug or a book lice or what?
So basically i found this thing in my home. It's super small so I had to zoom it for you. Whiteish/yellowish colour. We had bedbug problem back in our dorms and I'm worried I somehow managed to transfer them home but I don't know if it's a bedbug nymph or a book lice or what kind of insect, so I'd really appreciate someone's opinion on this.
Edit: It's really small, like. really small. my mother wouldn't even see it and thought me crazy. Just zoom made it look bigger. I'd say 1.5mm maximum at the very best. Moves kinda quickly and I thought it jumped two times when i was trying to capturing but maybe it was just me doing it to it. Living in Europe, Slovakia specifically.

Only except its extra long antannae this bug seems to be Cimex sp.

Welcome to Biology.SE. How small is it? Where do you live? (You can edit those info directly in your post with the 'edit' button).

Heya. I edited it so maybe that could add some input. I know how an adult bedbug looks like but this one baffles me cause of it's size, that's why I even thought it could be nymph stage

This is not a bed bug, but some sort of book louse (order Psocoptera). Bed bugs have a more compact body shape, even in the early stages:
 (from http://www.bedbuginspectiongroup.com/facts/)
Compare this with a book louse, and I think it is much closer to your specimen:

(from https://commons.wikimedia.org/wiki/File%3ABook_louse_01.JPG)
Also, here is a page comparing them: http://bedbugger.com/2008/03/04/book-lice/
Hope you stay bed bug free!

Thanks a lot man! I shall calm myself down now. I'm moving tomorrow and I don't wanna infest everything where I go, my personality does the job good enough, who needs bed bugs with that. Thanks once again


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What happens when the congenitally blind brain receives visual input?
If a congenital blind person gets eye sight (either hypothetically, or in the near future due to advancements in technology), will their brain be able to handle that information, or will it become overloaded?

Short answer
Congenitally blind people can regain visual function at a later age.  However, the longer they were blind for, the lesser their visual function will be and the longer it takes for them to rehabilitate. Immediately after receiving first eye sight, the visual experience of congenitally blind people is not comparable to that of normally sighted people. They may need months of rehabilitation training to make sense of their newly acquired sight, especially when they were blind for many years.
Background
There are various treatments for blindness to date. Since you mention technology in the question, visual prosthetics come to mind. Visual prosthetics already exist, and there are at the time of this writing two retinal implant systems commercially available; the Argus II and the alpha-IMS (Stronks et al., 2014). Retinal implants are used to provide a crude form of vision to those with severe retinal degenerations, such as end-stage retinitis pigmentosa. However, visual prosthesis technology is still in its infancy and at the time of this writing, only people that lost their vision later in life are implanted. So there is as yet no data available on your question whether congenitally blinded people can benefit from it.
However, from a related technology, cochlear prostheses, we know that the earlier a congenitally deaf person is implanted, the better the result is. Early-implanted folks can learn to understand speech, and develop speech relatively normally. Nowadays infants as young as 3 months receive cochlear implants. Early implantation is critical, because the brain is plastic. When the auditory cortex is not used due to sensory deprivation, it will quickly be taken over by other cortical areas. Once this cortical recruitment progresses for too long, a person can never gain functional hearing at the level reached by early-implanted people (Teoh et al., 2012).
Very likely the same holds for visual prosthetics. A congenitally blind person should be implanted as soon as possible after birth. This, because it is known that cross-modal plasticity results in the visual cortex being recruited for tactile and auditory processing. As with the auditory system, once this restructuring progresses long enough, my educated guess is that a person will never be able to develop functional vision comparable to an early implanted subject. And this is the reason why at present, only the acquired blind receive retinal implants.
For example, a case report of a subject who was blind for over 50 years regained his eye sight after corneal surgery. Although the subject did develop visual function after the surgery, visual performance remained greatly compromised. This was particularly evident when the tasks targeted finer levels of perceptual processing Siki et al., 2013).
Important clues are being obtained in the "Project Prakash", an ambitious project to provide opthalmological support to the people in poor, rural parts of India. Routine cataract surgeries have been performed in people with cataracts, including in people with congenitally present cataracts, where the lenses in the eyes were opaque from birth. Older kids, like teenagers, that were blind from birth typically show non-functional vision after the bandages are removed after surgery. It is thought that these first moments for the newly sighted are blurry, incoherent, and saturated by brightness, akin to swirls of colors that do not make sense as shapes or faces or any kind of object. However, after months of rehabilitation, they do develop functional vision. The lower-level markers of visual function never reach normal values. Specifically, they continue to suffer from poor visual acuity - the gold standard to assess visual function. Nonetheless, some higher-order aspects of vision do seem to be improving. Within a week to a few months after surgery, the children can match felt objects to their visual counterparts (source: The New Yorker, August 28, 2014).
References
- Siki et al., Iperception (2013); 4(8): 498–507.
- Stronks et al., Expert Rev Med Devices (2014); 11(1):23-30
- Teoh et al., Laryngoscope (2004); 114(9): 1536–40


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Is there a maximum limit of connections between a pair of neurons?
As neurons fire and work together, their connections strengthen. I was wondering if there was a limit on how connected neurons can be. If these neurons were constantly connecting then surely there would be an overload of connections at some point?

There's several ways neuronal connections can strengthen: growing the spine, increasing the amount of vesicles that carry neurotransmitters at the synapse, sensitizing and increasing the amount of receptors and yes creating more spines and synapses also.
Roughly, neurons can make tens of thousands of connections to multiple neurons the size of each spine is estimated to be between 0.01 µm3 to 0.8 µm3.
You are correct in saying that as life happens the connection would tend to grow to max and not encode anything anymore, however the brain seems to re-normalize all of its connections during sleep through special membrane channels.
Check out:
https://en.wikipedia.org/wiki/Neuron (especially the connectivity part)
https://en.wikipedia.org/wiki/Long-term_potentiation
https://en.wikipedia.org/wiki/Long-term_depression
https://en.wikipedia.org/wiki/Ion_channel


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Why don't onion root tips show mitotic stages?
It was back in the winter that we did the Onion root tip experiment in college. We were able to see wonderful stages but now in this monsoon-autumn transition the root tips hardly show any mitotic stage. Why is it so?