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Cold adaptation in proteins, at sequence & structural level
When looking for cold adaptation in unicellular eukaryotes there is not much work found. Most of the time general sequence comparative sequence analysis between marine mesophile & psychrophile also does not give clear results. If I am planning to study at structural level (homology modeling) will I get answers? What type of parameters can I look to study? Which proteins are expected to provide cold adaptation apart from ice binding or antifreeze proteins because IBP & AFP cant be found by sequence comparison. Is it possible to give some ideas regarding this?
Thanks

There are research groups working on this exact question; understanding cold adaptation in enzymes. You can read about this in several articles such as 'Computation of enzyme cold adaptation', or 'Molecular Structural Basis for the Cold Adaptedness of the Psychrophilic β-Glucosidase BglU in Micrococcus antarcticus', or 'Specific amino acids responsible for the cold adaptedness of Micrococcus antarcticus β-glucosidase BglU'
On a general level there are several sructural characteristics that are typically found. They are usually far more flexible (i.e. less salt-bridges and other such stabilising bonds). The flexibility come from having fewer strong bond between and within the polypeptide chain, and even containing disordered regions. The flexibility also means that they are usually far less stable, and more difficult to work with. They are industrially interesting, as developing enzymes that can work at low temperatures can reduce the cost of running reactions. This is essentially a step towards a greener-industry. There are also speculations about various ratios and abundance of the amino acid types, and where they are located.  You would have to read articles on specific proteins to investigate this.
From a practical view-point, cold adapted enzymes are usually isolated from arctic microorganisms and characterised in the lab - in order to determine their temperature tolerance. The structure of such enzymes are then solved (after lots of work) and form the basis for understanding cold-adaptation.
To answer the question more specifically, no its not realistic to know if something is coldadapted directly by looking at the protein sequence (on its own), this has to be determined experimentally in the lab. However, if the protein is from a cold adapted organism (typically arctic bacteria) there is reasons to assume it is cold adapted before you test it in the lab. You can also apply som bioinformatics (e.g. blast search) to determine if its related to cold adapted proteins.  Also, If that specific type of protein that you are looking at, is well studies, you could also try to make homology models and see if its structurally similar to cold-adapted relatives or if it is more structurally similar to its mesophilic or even thermophilic counterparts. This is however very speculative, and i would not put too much weight on theoretically assumed adaptations - you should at minimum know that the protein of interest is from a cold adapted organisms, to even begin to look (computationally) on why and how it could be cold adapted.


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Most well studied termite species or a species that I could use to compare termite genes for functional annotation
I am working with termites and I have a set of genes that I would like to compare with a species similar to termites so that I could elucidate its function. I am looking for a species that is similar to what Drosophila Melanogaster is to bees where to elucidate the functions of bee genes, it is compared to genes in D. melanogaster. Or how most worm genes is compared to genes in C. elegans. Similarly, if there is a well studied termite species, I could work with that.
The ultimate goal is to create a gene network with termite genes, hopefully on STRING.

Apparently, the most closely related insect to termites is cockroaches. Interesting article I found on the subject. However, that still didn't help because cockroach genes are not included in the STRING database.

source: Stack Exchange

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

sort: votes


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What are these tiny, almost transparent, dots in my vision?
Sometimes when I stare at a very bright thing such as the sky I see little dots. It's actually more of a circle with a little dot inside it. They are half-transparent and they move around a lot. When I first see them they tend to appear in a group out of nowhere. I have seen one that is gray and almost black. What is this?

You are probably seeing floaters.

Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent. At a young age, the vitreous is transparent, but as one ages, imperfections gradually develop

You might as well be seeing Scheerer's phenomenon

The blue field entoptic phenomenon or Scheerer's phenomenon [..] is the appearance of tiny bright dots (nicknamed blue-sky sprites) moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky.

Please have a look at the wikipedia article for more information.
I only now realize that your question is a duplicate of Seeing strange things in light

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


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Does boiling or frying fish make Omega3 be denatured?
I read some articles about omega-3, and I found there are two different opinions about how sensitive omega-3 is to heat. one is Applying heat to omega-3 make omega-3 become trans-isomer which is very bad for the body. and the other is Applying heat to omega-3 doesn't make omega-3 become any bad compound. I want to know which is true. I think maybe Applying heat to omega-3 make trans-fatty acid, but I want to know exact temperature. and what about boilling or frying fish? Wiil applying heat to fish make trans-fatty acid too?


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What type of bug cocoon is this?
My question is about these cocoon like things that are all over my house and fence in Florida (USA).

FL being Florida? Or Flanders? Why do Americans always assume... Ah, forget it.

@RHA It does not matter, these moths would be the same everywhere. And if you really want to know the answer to your question, it is because America is huge, and surrounded by only 2 other countries. Most Americans live a great distance from the border of these two countries. It is equally arrogant to assume that Americans are uniquely insensitive. People are the same, regardless of where they live, and are shaped by the circumstances that surround them (like geography)

It does matter, one should always be clear about location. See https://biology.meta.stackexchange.com/questions/3452/are-there-any-guideline-about-species-identification-questions

Related: https://biology.stackexchange.com/q/51252/16866

That is a bagworm. Order Lepidoptera, family Psychidae. You can read about them here https://en.wikipedia.org/wiki/Bagworm_moth


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Is protein folding symmetric with respect to reversing the sequence order?
Suppose that I have two proteins, protein A and protein B, and suppose that the sequence of amino acids of protein B is exactly the reverse of the sequence of protein A.
For example (these are made-up proteins):
protein A = [G,A,L,G,M,F,R]
protein B = [R,F,M,G,L,A,G]

Will the 3D structure of protein B be somehow identical, or perhaps the mirror image, of the 3D structure of protein A?

Think about where the N and C terminals are with respect to "R" for example.

@AdamRadekMartinez — Correct usage is terminus (end) and termini (ends). Terminal is an adjective in this respect (even though in English it may be used as a noun in specific contexts e.g. Railway Terminal.

I suggest that you are in a little less hurry to accept answers that cite references to something other than the situation in your question. The wa SE works is that when people answer others can vote and comment on that answer to help you decide what is correct.

@David Thanks for the advice. If you happen to have more info regarding my question, or an alternative answer, I'm still interested and listening.

related: www.reddit.com/r/askscience/comments/34npph/if_you_reversed_a_proteins_primary_sequence_would/

No! Although there is a relationship, the protein would not fold properly since the C and N terminals are reversed consider the following:
H(NH)-A-C(=O)(NH)-B-C(=O)(NH)-C-C(=O)(NH)-D-C(=O)(NH)-E-(C=O)OH
as appose to :
HO(C=O)-A-(NH)(C=O)-B-(NH)(C=O)-C-(NH)(C=O)-D-(NH)(C=O)-E-(NH)H
These are completely different molecules!
http://www.ncbi.nlm.nih.gov/pubmed/1604320 http://www.pnas.org/content/95/13/7287.long http://www.pnas.org/content/111/32/11679

Although the two are different molecules, and you may well be correct, the two references you quote are not for reverse sequence proteins but for proteins of the same sequence built with D-, rather than L-amino acids.


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Around what time did dark skin disappear from Europe?
As Europeans gradually became lighter skinned, there would have been people that still had dark skin. Around what time period did Europeans become completely light skinned?

This should be relevant: How europeans evolved white skin) (http://www.sciencemag.org/news/ 2015).


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does the amount of blood circulate in a body is same before and after amputation?
if a person loose his hand in an accident do the blood flows through his body is equal to the volume of blood before accident? how human body manage with that blood which is deserved by the missed body part? if human body have such a mechanism. does it effect other body parts? or is there any change in the proportion of blood flows through different arteries?

The kidney regulates the amount of blood being produced and removed from/recycled in the body. Even if somehow the body lost no blood when it lost the limb, the kidneys would remove the excess blood as it filters.
I think the misconception in asking this question is that the body knows how much blood to produce for the body. Yet, that isn’t the case, it just regulates the amount based on different signals it gets from the blood.
More info: https://www.ncbi.nlm.nih.gov/m/pubmed/17630596/

Still doubt remaining. does it affect the volume of blood received by other body parts?

If you are talking about due to the arteries being severed, the blood vessels remodel themselves to make sure the body still gets enough blood. If you aren’t talking about it, the kidneys remove the excess blood until the other parts of the body receive the same amount.

okay. do you have any reference papers associated with these kind of remodeling of  arteries. if so please share the link

@DJoseph I guess I don’t specifically have an article on amputation, but here is just a general one about wound healing https://www.sciencedirect.com/science/article/pii/S0022202X15528571 and using general knowledge that it amputees do regain circulation.


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What repairs faster when injured: white matter or grey matter?
This was the exact wording of a test question given by my biology teacher and she said that white matter would repair faster, because there is a myelin sheath to protect the cells.
Do you agree with this answer? Could you give me a more detailed, real life (not school, but real neuroscience, real data) explanation?

I disagree with the close votes based on homework - this is not the type of question that close reason is intended for.

Short answer
As @BryanKrause indicates, neither answer really makes sense.
Background
This is basically per the answer of @BryanKrause. Myelin is the stuff that forms the main characteristic component of white matter. White matter being

[the tissue] found in the deeper [in] the brain (subcortical). It contains nerve fibers (axons), which are extensions of nerve cells (neurons). Many of these nerve fibers are surrounded by a type of sheath or covering called myelin. Myelin gives the white matter its color. It also protects the nerve fibers from injury. Also, it improves the speed and transmission of electrical nerve signals

I think what the question aimed to target was your understanding what a myelin sheath is for (and, hence, what it is not intended for). Quoting from (Morell & Quarles, 1999):

What

[A] greatly extended and modified plasma membrane wrapped around the
  nerve axon in a spiral fashion. [It] originates from and are a part of
  the Schwann cells in the peripheral nervous system (PNS) and the
  oligodendroglial cells in the central nervous system (CNS)

What for

Each myelin-generating cell furnishes myelin for only one segment of any given axon. The periodic interruptions where short portions of the axon are left uncovered by myelin are the nodes of Ranvier, and they are critical to the functioning of myelin.

How

In myelinated axons, the excitable axonal membrane is exposed to the extracellular space only at the nodes of Ranvier; this is the location of sodium channels. When the membrane at the node is excited, the local circuit generated cannot flow through the high-resistance sheath and, therefore, flows out through and depolarizes the membrane at the next node, which might be 1 mm or farther away []. The low capacitance of the sheath means that little energy is required to depolarize the remaining membrane between the nodes, which results in local circuit spreading at an increased speed. Active excitation of the axonal membrane jumps from node to node; this form of impulse propagation is called saltatory conduction (Latin saltare, “to jump”). Such movement of the wave of depolarization is much more rapid than in unmyelinated fibers. Furthermore, because only the nodes of Ranvier are excited during conduction in myelinated fibers, Na+ flux into the nerve is much less than in unmyelinated fibers, where the entire membrane is involved.

What not
Although the myelin sheath is formed by a glial cell type, and although glial cells do structurally and metabollically support neurons, I would not say that this means myelinated tissue heals faster. Instead, myelin is more about the functional role of white matter, namely efficient, fast and reliable long-distance transfer of information across distant brain regions.

Reference
- Morell & Quarles. The Myelin Sheath. In: Siegel et al (eds); Basic Neurochemistry. 6th ed. Philadelphia: Lippincott-Raven (1999)

Your biology teacher's question is unfortunately poorly formulated and the justification is even worse, not just biologically but also logically. For the logical error, consider this statement: Knights wearing chain mail heal faster because they are protected by their armor. This makes no sense. Perhaps if you allow that the initial damage is less, but even that makes little sense.
It doesn't really make much sense to talk about healing speed of white matter and grey matter because you are talking about two different things. White matter is mostly axons and their myelin sheets, whereas grey matter consists of cell bodies and neuropil. Grey matter damage implies cellular death. White matter damage implies loss of connectivity. Grey matter damage can also lead to white matter degradation (i.e., the cells that sent projections are now dead). White matter damage can also lead to grey matter degradation due to loss of connectivity.
However, it is true that different types of brain injury could differentially impact white versus gray matter, but going into all the different causes of brain injury is too broad of a topic for a single question at stack exchange.
Furthermore, repair of CNS tissue is just as much about compensation rather than repair per se. Repair processes are important for limiting damage, cleaning out dead tissue, and restoring some types of connectivity, but recovery from a major injury is just as much about brain plasticity and effectively relearning how to function after an insult.

I'd like to upvote here, but w/o references I'm hesitant to do so. I'll spare you the banner though ;-) Thanks for your efforts here, I voted to leave open (too). If you like a question, it can also help to upvote it (I did)

Yeah, I agree with your statement, the test question was definitely not a well formulated question, extremely unclear for everybody.

@AliceD Yeah, I didn't put much effort into my answer but also didn't want to leave it unanswered - although I don't love the question itself I also don't want to leave someone hanging who is currently being instructed by someone uninformed. I'm not sure your answer really gets to the question although it does have good information about the distinction between white and gray matter and you are also probably closer to what the instructor was aiming for.

And a lot of times myelin is lost after injury.


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Creating ideal conditions for life
Suppose some scientists built a large vat, sterilised it and filled it with distilled water. Then they start dissolving compounds into the water such as amino acids or what ever they deem conducive to life. They can also control temperature, radiation and other environmental factors.
They periodically capture a sample of the water and examine the results.
Would they be able to inadvertently create self replicating molecules and the precursors to life?
Would this kind of experiment be worth attempting?

There are groups attempting this. Check out this (paywalled) paper from 2010 that tries to see if life could form from such a primordial soup on a simulation of Titan. Plenty of others too!

Suppose some scientists built a large vat, sterilised it and filled it with distilled water. Then they start dissolving compounds into the water such as amino acids or what ever they deem conducive to life. They can also control temperature, radiation and other environmental factors.

Your direct question is whether this experiment would be worth attempting, and as other answers have said, it has been attempted many times.
I'll address the question implied in the title "Creating ideal conditions for life".
You talk of dissolving compounds into water and controlling temperature, radiation "and other environmental factors"; I assume you mean this to imply all the possible variables are being manipulated, but that is not the case. "Being in a large vat" is also an environmental factor, and there is good reason to think that large vats don't provide ideal conditions to develop life at all.
If that sounds silly, consider all the chemical reactions that could be happening in your vat. Chemical reactions are typically reversible: molecules A and B can meet and interact and form molecules C and D, and molecules C and D can in turn meet and interact and form molecules A and B. In a large vat, nothing is preventing all those molecules from meeting and interacting with each other; this leads to an equilibrium, depending on the rates of both reactions, and you'll end up with a stable quantity of A, B, C and D.
Now imagine instead you have two vats, with a system between them that transfers molecule C from vat 1 to vat 2. Now molecules A and B continue meeting and forming molecules C and D, but as that happens C gets transferred from vat 1 to 2, so you get a buildup of molecule D in vat 1 while A and B gradually run out because they keep forming C and D but not being reformed in turn, while in vat 2 you have a surplus of molecule C, so any molecule D that is formed from the interaction of A and B is likely to meet a C to re-form A and B, meaning you'll end up with more molecules A, B and C and very little D.
In other words, you got very different results from the case where everything was in a single vat. The macroscopic and microscopic environment your molecules are reacting in is a variable you cannot ignore.
As for large vats not being conducive to developing life, this 2010 article by Nick Lane, John Allen and William Martin summarizes those issues with the "large vat" experiments, and the "primordial soup" hypothesis in general:
https://onlinelibrary.wiley.com/doi/abs/10.1002/bies.200900131
(full article downloadable here: http://nick-lane.net/publications/luca-make-living-chemiosmosis-origin-life/)

Setting aside the absence of geochemical evidence that a primordial soup ever existed, there are grave difficulties with the soup theory. To give a single example, polymerisation into RNA requires both energy and high concentrations of ribonucleotides. There is no obvious source of energy in a primordial soup. Ionizing UV radiation inherently destroys as much as it creates. If UV was the primordial source of energy, why does no life today synthesise ATP from UV radiation? Worse, every time an RNA molecule replicates itself, the nucleotide concentration falls, unless nucleotides are replenished at an equal rate. UV radiation is an unlikely energy source for rapid polymerisation and replication, and an unpromising initiator of natural selection.
The reason that nucleotides and other organic molecules are reluctant to react further in a soup is that they are at thermodynamic equilibrium. They have already reacted, and the homogeneous soup has no internal free energy that would allow them to react further. Life is not just about replication; it is also a coupling of chemical reactions – exergonic ones that release energy and endergonic ones that utilise it, preventing the dissipation of energy as heat.

That article was in 2010, and those people have been investigating the hypothesis that life began in hydrothermal vents under specific thermodynamic conditions since; Nick Lane recently published the book The Vital Question on the subject, that I highly recommend to anyone interested in how life might have begun.
Their hypothesis for how life formed also implies very different kinds of experiments to try and reproduce it. Putting chemicals in a large vat is one thing, trying to recreate the conditions of a hydrothermal vent is another.
Here is a video of Nick Lane presenting their research; at 30:15 he briefly talks about where they're at experimentally, with a picture of their setup.
https://www.youtube.com/watch?v=PhPrirmk8F4
ETA: Stealing John's comment here:
Creating ideal conditions for life
The experiments described in the article that yielded RNA are also more complex than just dumping molecules in a vat, and the cycles of heating and evaporation described are the kind of energy input and mechanisms to force disequilibrium that can make it thermodynamically possible for those molecules to form. This highlights another variable that can matter, which is variations in the environment over time as well as over space.

That question was asked in 1953 by a classic experiment by Miller and his mentor Urey. You can find it on Wikipedia under "Miller_Urey_experiment"
Basically they zapped basic molecular building blocks to life with electricity and more complex molecules (amino acids) formed.
The experiment, with updates is nicely discussed here.
The experiment showed that the molecules required for life could be formed spontaneously on Earth from lightning. You would need amino acids, but also bipolar lipids, which can spontaneously form compartments. However, attempting to create life this way would not be worth attempting for two reasons, relating to time and scale. First (time), life has evolved only one time on Earth over 4 billion years. Second the scale of the entire Earth over billions of years is a pretty big experimental "test tube". It happened once in all this time, over all that space. A small side-issue; the fact that the codon table is optimized (and pretty universal, with only small differences), such that common amino acids have more ways to make them (more codons), and codons close to stop codons are for rare amino acids. This indicates that some early life experimented with alternative suboptimal codes that didn't make it.

Earlier description in Goethe’s Faust: “Es wird ein Mensch gemacht”. Publication lacks experimental details though.

A much more modern and updated version of the experiment can be found here, https://www.wired.com/2009/05/ribonucleotides/ got all the way to RNA. After all codons are meaningless without nucleic acids.


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Why do we feel numbness and an electric sensation in our legs after standing for too long?
We have all felt that numbness while standing immobile for a while.It gets difficult to walk.It can also happen if we are just putting some pressure on our legs
Why does this happen?
I'd like to know what specifically happens in the muscular tissue(if that's the origin of this sensation) for us to feel like this

Not all of us have felt that.  Is it in your calves or thighs or both?  Is it any different from the numbness and tingling when a leg or arm "falls asleep" from sitting or lying on it too long?

Its in my calf. Apparently it occurs due to pressing of sciatic nerve but still I'd like to know a tad bit more if you know

This relates more to nerves than muscles. Each nerve has a small artery supplying it with nutrients and oxygen. A good example is the sciatic nerve, which is the largest nerve in the human body and requires a relatively large artery to supply it with blood:
http://article.sciencepublishinggroup.com/html/10.11648.j.ijcda.20150103.14.html
When we sit in a particular way that causes pressure over that nerve, or stand for a long while in a way that stretches the nerve, we effectively reduce or block its blood supply. This may result in temporary loss of signal leading to numbness, weakness or even temporary paralysis. If the pressure on the nerve is prolonged beyond a certain point, there will be irreversible necrosis of the nerve causing permanent nerve damage. An example of this is when a drunk person sleeps on the floor with pressure on the outside of the knee over the "Peroneal Nerve", causing "Peroneal Nerve Palsy" or "Zenker Paralysis".
https://en.wikipedia.org/wiki/Zenker%27s_paralysis
As for the electric sensation we might feel as a result of nerve damage, the answer is more interesting:
The transmission of signal in the nerves requires variable amounts of energy depending on the type of nerve fibre. Nerve fibres are mainly divided into "Myelinated" and "Demyelinated" ones, with further subdivisions. To put it simply, myelinated nerves have a coating of myeline formed by specialist cells called Schwann cells. Myeline allows the nerve fibre to act as a super conductor to transmit signal faster, but needs more energy to do so compared with demyelinated fibres, which are thiner, slower and more energy efficient.
One of the functions of the super-conducting large fibres is to modulate the pain signal. The damage or loss of these fibres results in "neuropathic pain", which is felt as sharp electric shocks or pins and needles along with many other reported descriptions. This is thought to be the result of the small pain fibres working uncontrolled, leading to the perception of pain without an actual painful stimulus. The super conductors "Myelinated Fibres" are much more vulnerable to injury due to reduced oxygen, while the smaller fibres, some of which conduct pain, are more resilient. This is why we might feel neuropathic pain as a result of reduction in signal rather than due to a painful stimulation. A good example is what happens in an auto-immune disease called Guillain-Barre Syndrome, where the immune cells attack and destroy Schwann cells, leading to significant neuropathic pains as a result of the loss of signal in the corresponding nerve:
https://en.wikipedia.org/wiki/Guillain–Barré_syndrome
Another common example is first degree burns, where the pain continues for a few days following a minor burn due to selective damage of the highly sensitive myelinated fibres leaving the non-myelinated ones intact. Pain improves gradually as the Schwann cells regenerate, improving the signal speed.

Next to the fine answer from MattDee, I just wish to add that the 'pins and needles feeling' is called paresthesia.
Paresthesia can be caused by a variety of mechanisms and can be reversible or permanent, the latter usually due to nerve, spinal cord, or brain damage.
While the nerve is squeezed as in your prolonged standing example, so are the arteries that feed blood to the nerve. The nerve can't work for long without a steady supply of oxygen and glucose. This causes a limb to “fall asleep.” When the pressure is relieved is removed, the nerve cells start to be active again, and this is the uncomfortable pins-and-needles sensation, as the nervous system tends to become hyperactive as nerves regain normal function. This irritability is caused by spontaneous neural firing in the affected area (source: University of Rochester Medical Center).


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MIT's Programming Language for Cells
I have read a lot about the programming language, Cello, that MIT created to program DNA; however, I cannot seem to find any sources online that shows you how to program with Cello. Are there any good sources out there with regard to this topic?
Thanks

Since this isn’t necessarily on topic I won’t make this a full answer, but I think this is what you are looking for: https://github.com/CIDARLAB/cello/blob/master/README.md

I’m not sure that this is on topic, as you really could have found this information yourself.

You don’t quote a source for your info about this, which doesn’t help you or anyone interested in this topic. Here is a Nature News article.
If you click on the link in that article you get to the Cello site. You need to choose a name and password to gain entrance, but are not asked for any personal information. All they will have is the IP number of your computer.

The info on this site will not mean much to anyone not involved in synthetic biology.


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What is this cloud of red pond creatures?
Today I came across a pond in the Netherlands where I noticed a cloud, for lack of a better word, of small red creatures swirling around near the surface of the water, as can be seen in this video:
https://youtu.be/ZQMox-bbJ9s
And here is a picture:

The surface was unfortunately quite reflective, but the motion is visible. The creatures were too small for me to see any structure to them with the naked eye. Some tadpoles can be seen in the video, which are much larger. They would swim straight through the cloud now and then, so perhaps the tadpoles consider the red stuff food. The entire cloud consisted of various dense clusters connected with less dense or thinner parts, as can be seen to some extent in the video, and its total size was perhaps 2 meters or so.
What was I looking at?

Can you kindly add some pics/screen-shots here too as: 1-) Not everyone can check a video link 2-) External links are prone to modifications or even deleting. Thanks!

Where were these pictures taken? Also,the video is too short.Try to get a longer one next time.

You don't say where this was, but my first suspicion would be some sort of algae bloom.

@JeffreyBarber it was in the Netherlands, I added it to the question. Are algae generally mobile?


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What does it mean for sodium and water reabsorption to be "coupled" in the nephron?
If sodium is transported across the tubule membrane down the concentration gradient established via the $Na^+$/$K^+$ exchanger via symport with glucose and antiport with hydrogen, and water is transported via aquaporins...how is this coupled? They don't have the same transporter. This seems like they are independent.
Is this related to concentration gradients (more $Na^+$ in epithelial cells --> water wants to follow osmotically)? If so, why is $Na^+$ controlling whether water is reabsorbed or secreted, and not some other ion?


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Is it possible to get a XYY genotype by the first meiotic non-disjunction?
I have read that the cause of XYY-Syndrome is a non-disjuction in the secondary non-disjunction in the meiosis. I was woundering if it is possible to get the XYY-Syndrom by the first meiotic non-disjunction? I would assume yes, since you would get XX and YY Gametes.


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How can you design a drug to modify apoptosis to treat a disease such as cancer?
How can you design a drug to modify apoptosis to treat a disease such as cancer? Im in highschool so can someone please explain in simple terms. Thankyou.

The new cancer drugs are custom designed antibodies that have a cell-killing agent attached to them. These antibodies specifically attach to the cancer cells, and kill them. Other methods, like traditional chemotherapy target cells that are actively dividing, like hair in addition to cancer. Cancer cells are defined by uncontrolled cell division. But traditional chemotherapy, in simple terms, stresses the body to near death, differentially killing actively dividing cells. The new targeted methods are much less toxic.


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What bird is this seen trekking in Nepal during descent on Manaslu circuit?

What bird is this seen trekking in Nepal during descent on Manaslu circuit?

You found an Alpine accentor (Prunella collaris). It's a bird of mountain areas in the Paleartic.
Here is a picture for comparison:

The only similar bird in the area is the Altai accentor (Prunella himalayana), but you can tell it apart because your bird does not have streaked flanks and the more uniform grey head (in your picture it is clearly visible the supercilium)


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Heat shock vs electroporation
I've been transforming E. coli via heat shock in order to insert oligonucleotides (around 50 nt); however, none of my experiments have given positive results so far. I begin to question the efficiency of chemical transformation, especially for short DNA fragments. Is there such a notable difference between chemical and electro transformation?
EDIT: I'm checking for CRISPR array expansion, so my oligos have a protospacer length and structure. I'm using BL21(DE3) cells which have an IPTG-inducible T7 that I'm first transforming with a Cas1-Cas2 plasmid. Then, I induce the cells in order to express those proteins, make them competent, and transform then once again but with the oligos and an eGFP plasmid (for some sort of selection). To check for positive results, I'm amplifying the leader-repeat junction of the CRISPR array and compare its length (via electrophoresis) with a usual array that has no integrands.

How do you do your chemical transformation? Do you make the cells yourself? Do you have a positive control?

Yes, I make the cells competent myself. I do have a plasmid control for antibiotic selection which, on the other hand, is successfully transformed.

In an allusion to Damir's answer below, how are you testing positive results? A plasmid with an antibiotic resistance gene is easy to test for. But 50 nucleotide oligos won't carry a useful reporter gene.

When transforming, I insert around 30 times more oligonucleotides (as mol) than plasmid, assuming that if the plasmid has entered the cell, the probability that some oligos have also entered is higher. Indeed, that's still pretty much luck, but testing hundreds of colonies and getting 0 results makes me believe that something's wrong. By the way, I'm checking for CRISPR array expansion, so for testing positive results, I'm comparing the amplicon length (which is the leader-repeat junction) via electrophoresis and after that, I'll be doing some digestions to confirm the presence of my oligos.

How do you detect a potenially positive transfection? Short fragments might have proper teriary structures which may make them behave differently than you would expect. Also, noncircular DNA and RNA is targeted much faster for degradation in most cells if the right head or tail signals are missing.
To your question: pulsed electroporation with well prepared bacteria (state, buffer,...) is usually 5-100 x more efficient than chemically competent bacteria.

See my anser above. Regarding oligo degradation (by endonucleases for example), I should mention that before transforming, I induce the expression of the necessary proteins for the CRISR adaptation stage.


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Exhaustion of skeletal muscle and ligaments
I read somewhere that while doing lifting back should be straight(means normal curve), so that erectors muscle in back do the work but it gets tired easily. Hence we form curve on our back like when we sit on chair our back curves and this curve put stress on ligaments of spine which is harmful.
 Since ligaments dont get tired we feel curved back as easier. Does ligament have any mechanism ti get tired like lactic acid in muscles?


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Are some polyketides enzymes?
I am currently reading a "book" (rather an article) called "Protein Modelling & Molecular Docking: Modeller, Autodock".
The abstract starts with the following sentence :

Polyketides are a large family of complex enzymes synthesized by
  polyketide synthases.

Before reading this article, I knew nothing about polyketides. I looked it up online, and I saw that they were secondary metabolites, which adds up with the rest of the article. However, I could not find any mention of some polyketides being enzymes, hence my question:
Are some polyketides enzymes or is this a simple mistake in the article ?

It's a typo. Now let's close the question.

You are correct.  Polyketide synthases (PKS) are the enzymes that synthesize polyketides.  PKS are derived from fatty acid synthases via evolution.  Polyketides are of great interest becaus many are of important medical use.


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Is there any standard of notation for ecological diagrams?
General Question
Is there any convention of how to express different types of relations (e.g., eats, turns into, is beneficial to) and agents (e.g., species, nutrient) in an ecological diagram? I know that inhibitory relationships are indicated by barred arrows, but I failed to find anything going beyond this.
Example
Suppose, I want to express that Species A excretes Nutrient X, which in turn is metabolised by Species B. Naïvely, I would sketch this as follows:

However, this it not necessarily clear:

I here arbitrarily used squares and circles to distinguish species and nutrients.
If you do not know this, you could not immediately distinguish them.
(Of course, I may just use specific examples like tree instead of A, but then for my theoretical cases, a tree is too concrete.)
The arrows mean different things.
The left arrow means excretes, the right arrow means is metabolised by.
Moreover, the arrows could be mistaken for something like turns into or a general is beneficial to.

How would I denote the above relation unambiguously in a diagram?


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Mystery bug photographed in Brasil

Shot in Brasil.  Anybody know what it is called!!?

Hazarding a guess here: you've got a true bug that's about to take flight. Given that event, I don't think the evidence at hand is enough to go deeper.

From this photo (beautiful shot, btw!) you can see that it must be a true bug - admittedly, the diagnostic characteristics are hard to spot, but I will try to walk you there.
Most apparently, we see an insect (six legs) with sucking mouthparts. Admittedly, the rostrum is hidden behind the bucculae (for an explanation of the bucculae compare this graphics here and here).
But besides the bucculae, the absence of chewing/biting mouthparts is apparent.
We further see long, segmented antenna, sclerotized forewings, a considerable pronotum and a dorso-ventrally flattened abdomen.
From the entirety of these characteristics, we can conclude it must be a true bug.

True bugs are divided into seven infraorders, of which three are (semi)aquatic (Gerromorpha, Leptopodomorpha and Nepomorpha), one comprises only miniature species (Dipsocoromorpha) and one comprises only ground-dwelling, cryptic species (Enicocephalomorpha).
The two remaing infraorders are ideally distinguished by microscopic dissection (compare the detailed Wikipedia articles in German for Cimicomorpha and Pentatomomorpha), but from experience, I think it must be a Pentatomomorpha.
With this knowledge, I run an inverse Google search on the photo - caution: this is not best practice in species identification - what to my surprise already correctly identified the specimen as a true bug.
Among the images (whereof several were arbitrary red-colored insects) was an image of Sphictyrtus chrysis on iNaturalist, that looks very similar to the photographed specimen. Besides the habitus, this would be the:

black forewings
black pronotum with red margins
black antenna with a club-shaped last segment
black legs
red head with black eyes
dorsal segments red with black margins with a thin, white line

According to GBIF, S. chrysis seems to be common in eastern South America, including Brazil.
There is the possibility that similar species (maybe even from the same genus Sphictyrtus) exist in Brazil, but this is the best I could infer from this photo as someone unfamiliar with the South American true bug fauna.


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What is this mushroom that only grows next to my tomato seedlings?
So far something like ten out of fifty seedlings (20%) have had this mushroom grow right next to a tomato seedling and nowhere else in the planters.
The black gooey caps are between a peppercorn and a small pea in size. They only seem to grow at night and collapse within a couple of hours after
I have removed the glass jar cover in the morning. The jars are used to keep out the slugs at night. What type of mushroom is this and is this a symbiotic relationship?

(Answering my own question from three FB remarks a friend of mine received):                                                                                ...this is a pin mold fruiting body...
...deliquesced Coprinoid...
...genus Coprinopsis...


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What are some good biological tests you can do to yourself?
I would like to do things like study my own blood and DNA. What kind of things can one do at the present time that are fairly simple. Or require minimal equipment like a microscope?
Are there some genetic diseases or predispositions that one can do self tests?
I mean there are a few tests I know of that are very simple, like measure your own heartbeat or eyesight. But these are a bit too easy.

what is your final goal? if you want to self-diagnose, i doubt this website is a good place. If you have concerns about your health, you should consult medical doctor or other health professional. Maybe check https://health.stackexchange.com/

no my health is fine. Just have intellectual curiosity to study one of the most advanced systems in existence. (me!)

One category of tests that are relatively safe to perform on yourself - are reflex tests. Some of them are actually very fun to test, say Babinski reflex.
No body fluids are used; however, I would still qualify those as "biological" enough.


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Why would a bumblebee regularly hover over a arborvitae hedge?
I have observed bumblebees hover over an a abrborvitae (Thuja occidentalis) hedge. A bumblebee will hover in a in one spot over the hedge for about 5-7 seconds, zip to another spot, hover for about 5-7 seconds, then another spot, then another. The bees will never land on the hedge. At any one time during anyone day, there will be only one bee hovering over the hedge. This behavior will go on like this all day.
Why do the bees do this?

The behavior sounds more like a hoverfly than a bumblebee.

It's not a hover fly,they don't fool me. I've walked right up to it and it didn't move. I considered that it might be guarding something,I've seen them guarding an especialy fragant viburnum. This bush was covered in bumble bees. I had to crawl backward to get out of there or one would have stung me.

Perhaps it is a solitary bee that has a mud nest on the Thuya tree, or another variety that has a burrow.

Could you perhaps make a picture of the bee? BTW: Bumblebees rarely sting.

I can't get a picture of it in september,that's for sure.

Could actually be a male carpenter bee. They hover around like that waiting for females to pass by. If it is a male carpenter bee dont worry about it, they arent equipped with a stinger.

I'll check to see what it is,but why would a male carpenter bee do this? Can you include some kind of reference for this? Maybe a link?

Today I hit the arborvitae In my yard, in which at least 5 or six HUGE bumblebees fell to the ground. After my initial shock, I hit each of the arborvitae along my fence and a dozen more fell out.
I believe these Bumbles have nested in my trees, which  may explain the hovering behavior; they are either scouting out a place to rest or visiting their young, not entirely sure. Hope this helps


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Can two proteins have equal primary structure but different secondary structure?
I've been reading lately about primary (which I understand completely) and secondary (which I do not understand that well since I'm not very good at chemistry) structure of proteins. My question is: Can two proteins have equal primary structure but different secondary structure?

By equal I assume you mean identical.
Yes, in fact several known proteins have different folding patterns for the same primary structure as part of their function. but most proteins can take on more than one folding pattern, in fact specialized proteins called chaperones exist to encourage (force) a particular folding pattern in some other proteins, especially ones that are essential or in which the other foldings can be dangerous.
The easy way to understand the difference is the primary structure is the amino acid sequence and the secondary is the first stage in how the protein folds (the other being the tertiary). the primary creates the secondary (and tertiary) but there is usually more than one stable folding.
this video contains a further breakdown of the different levels of structure.


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Can humans derive any nutrition from eating the bones of animals?
Bones contain many nutrients like Calcium and phosphorus.
And I'd take a guess that some kind of bones like bones of a chicken(hollow) aren't dense enough to be much of a  problem during digestion.
So,is there any benefit in eating for example say chicken bones?

Just the actual bone, or the marrow as well?

The actual bone.I know we derive nutrition by eating the marrow.


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Spoiled 1% milk
A friend of mine gave me a jug of 1% milk and when I got home to put it in my fridge I noticed that it was already out of date so I set it on the counter next to our trash can and at the time we didn't have a vehicle to holler trash off so it's not on my counter for about 3 days and all of a sudden one night me and my boyfriend are sitting there in a room and the milk just starts projectile shooting out of a hole that it made in the side of the jugs not out of the lid just spraying everywhere all over the kitchen and I want to know why it for 1 started spraying spoiled milk as if it was pressurized and for 2 how did it make its own hole in the plastic jug???

Interesting story, well told. It was pressurized. When the microorganisms fermented the milk, they give off carbon dioxide, which builds up and creates pressure. This is why beer is carbonated. They did not however make the hole in the milk container directly. It was likely a weak spot that burst from the pressure.


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If evolution is true, how do all organisms have varying amount of chromosomes?
I thought genetic mutation changes genes and therefore evolution happens, but it doesn't explain how  chromosomes are created/removed if the first organism had a set amount and now all the organisms have different numbers of chromosomes. How does this happen?

Your understanding of evolution is over-simplified.  There are chemicals (colchicine is a common one) which can cause the number of chromosomes in a cell to double.  This is regularly used in e.g. plant breeding, as multiploidy often makes larger & stronger plants.  Do a search on "inducing tetraploidy in plants" if you're interested.  Other copying errors can affect single chromosomes &c.

Number of chromosomes. Amount of DNA.

Are you asking about hte origin of chromosomes or how they change?Bacterial chromosomes are very different than eukaryotic chromosomes so which are you talking about?

A mutation is a general term referring to any alteration of a nucleotidic sequence. It includes small mutations like indels (insertion or deletion of a single nucleotide) and substitutions, or bigger mutations such as e.g. chromosome fusions, whole chromosome duplications, whole genome duplications and gene deletions. So yes, some mutations do change the number of chromosomes (and ploidy number).
If you are interested in a very short and very introductory course to evolutionary biology, consider having a look at Understanding Evolution by UC Berkeley


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Mint twisted like a spiral
My friend has a mint plant with a spiral-shaped stem, and the leaves are positioned like this:

Why could such deformation happen? Other mint plants, growing in the same pot, are normal.


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Is it true reduction in sensitivity to dopamine due to over stimulation from addicting behaviors can be permanent, if yes how come?
I've read somewhat conflicting things.
General concept is this:
Addiction -> Over product of dopamine -> Reduction/Desensitization of dopamine receptors -> problems
And if you let go of addiction you go through period of withdrawl that can last from 90 days to a year.
BUT forever for some people... Why?


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How does one go from a couple of DNA sequences to a distance-matrix?
For a project we need to explain the subject of UPGMA.
We think we understand thee method itself but I fail to see how you go from a number of DNA-sequences to the distance matrix.
I understand that the lower the number, the more related two species but on what scale is this number and how to interpret the exact meaning of this number.
For example if the number between A and B is 17 what does that mean?


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What snake is this one?
I'm wondering what kind of snake is the one in the attached photo. It looks like Vipera aspis but It seemed a bit too big (lenght of about 1 meter).

This photo was taken near Como, in the north of Italy, in the woods of Parco Spina Verde.

Did the snake have dark V on his head?

I'm afraid I can't tell.. the snake quickly run away and I didn't have enough time to look closely the details on his body

So i think you really cant expect much more then my answer. Unfortunatly because i want to know true name..

I think it could be Vipera aspis, but that leght what did you descripe is really rare. Anyway it can be Smooth Snake(https://en.wikipedia.org/wiki/Smooth_snake) too. But you know personaly i cant do more from this point of view. The smooth snake is much more common and longer so there is a bigger possibility.

In my opinion a very nicely patterned individual of the recently newly described Barred grass snake. Used to be part of Natrix natrix. Non venomous, not dangerous.


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Do hornets remember and recognize a human? Do they have any (kind of) memory?
hornetology
So it happens that a hornet (vespa crabro) flew inside my house today and now is being held in a plastic container (I made some holes to let it breathe). But it also happens not just this once, but twice and I guess it's not over (we live by a small forest, probably it builds its own nest there). I wonder if hornets may have some memory - can it  remember and later recognize a human?
And if I take it to another place of the town I live in and let it go there will 'he' come back, 'cause it will remember where 'he' lived before?
Thanks for any advice, I just don't want to simply kill it... 'him'.

As far as I know, many vespids have very good orientation, which is used to find food. If they find something with sugar like ripe fallen apples, they will start by scouting and mapping the area, and then they can fly back to base and to the food area again. so, they recognize their home and food places very well. to disorient them, I 'd figure you can test it out... mark him and take him a mile away, i think it would be enough, 10 would more probably be ok.

There is strong evidence that wasps can recognize color patterns of other wasps. Whether that extends to humans I don't think is known but given some remarkable work on bee learning, I would not be surprised. https://www.youtube.com/watch?v=rx7lEBE-wJE

Most studies show that a hornet will give off a hormone that tells others in its hive that you or someone else is target and threat to the colony as a whole. They also are able to remember their surroundings near the hive or nest fairly well.

The aforementioned studies should be linked in the answer.

@G.Shepherd, do you have articles on this? I tried to google it but without success :(


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Why slow worm lost ability to walk in evolution/ecology perpective?
Can  lost of legs for slow worm be considered as Batesian mimicry?

I just want to be sure why does it lost its  legs.

Your first link is broken

For what reason does losing its legs could be an anti-predator adaptation? Can you please explain your thoughts?

i am sorry but i dont know how to fix this. But anyway i hope this is clear what i am askingfor.

He is looks like a viper commune, most common poisonous snake in middle europe so i thought that can be possible connection.

You can use the edit button to fix it. If you are uneasy with the formatting you can see how I fixed it. Can you please explain your thoughts for why being legless in slowworm could be an anti-predator adaptation?

I thought it is because slow worm looks like a snake and snakes are usually danger with their venom, so part of the slow worm population whose looked more like snake had advantage. In the end the the subtype of slow worm spread in whole species. But  I am quite confused with the part of the lost legs, because it is logicaly much more disadvantage in live (possible trade-off to look like snake?).

Oh you mean Batesian mimicry then, isn't it? You should edit that!

@L.Diago Your last comment suggests that a loss of legs is generally a disadvantage. That is hardly the case, since a loss of legs has evolved independently with Squamata multiple times (>20 it seems). With your assuption, you could just as well argue that all snakes should have legs. So the premise of the question is probably incorrect, and mimicry is not likely to be the explanation (at least from what I've seen).

I actually quite dont see a any diffrence between Batesian mimicry and muller actually (even dont know about batesian). I didnt know that lost of legs was multiple times, but i thought thet slow worm is diffrent case because it is actually lizard. That why i thought this  case is adaptation after the snakes lost legs (secondary). Anyway i got your point with my premise.

@L.Diago Batesian~= harmless species mimicing dangerous species (eg hoverflies vs wasp) ; müllerian~= several distasteful/poisonous species having warning patterns that resemble eachother.


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Can anyone identify this tall vine that has volunteered in our back yard?
What is this 5-foot tall vine in Kentucky? It volunteered in our back yard.

The species with the dark triangular leaves is also a vine - I reckon you are aiming at the plant with the lighter rounded leaves in the middle of the image? If yes, it's a bummer the leaves in close-up are out of focus.

@AliceD the dark triangular one is hedera helix.

Or are you aiming for the heart-shaped one on the top left? Perhaps you could provide a close-up image of a leaf and add an arrow in the existing figure to point out the species in question?

@AliceD: I'm sure they mean the plant most featured in the photo (having palmate leaf veining or patterning).  The leaves towards the bottom of the image are largely in focus.

@mgkrebbs — Is that generally used in the US or is it regional? Never heard it when I lived in Chicago and it is not British usage.

The term "volunteer" is used a lot here in Indiana USA, as in "It came up volunteer" to refer to a plant that just appeared.

@David https://en.wikipedia.org/wiki/Volunteer_(botany) - I admit myself I have never heard it as a verb in this context (though the wiki page does make reference to the verb form), but rather as an adjective or noun.

I believe it is in the genus Dioscorea which is a wild yam.  There are several species native to the Eastern US.  A common species is Dioscorea villosa but you will have to look up details and compare to your specimen.


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Is this claim about equine anatomy true?
While bumping through obscure corners of the Internet, I encountered the following image posted somewhere.

The horse anus is a marvel of evolutionary biology.
Like most mammals, rhythmic contractions of the bowels move the feces up to the end of the gut to be expelled.
What sets the horse anus apart is the bafflingly complex autonomic contractive motion of 4 muscular rings which function like sphinctoral guillotine. As the feces is squeezed out, the rings expand and the
  outermost ring is retracted into an interior skinfold resembling the human foreskin, leaving an interstital tissue fold to open air.
The two inner rings then contract, and push apart, severing the horse feces cleanly, allowing to drop free as the outer ring folds back through the interstital flap, creating a intrinsic wiping motion with the fourth ring as it contracts back into the horses rectum.
This advanced biological mechanism is so effective that many industrial companies have copied Nature's design for self-cleaning viscus liquid dispensers housed within complex machinery.

Quite interesting, but anyone who saw one, recognizes an imageboard post - probably the infamous 4chan, where each page bears the warning: "The stories and information posted here are artistic works of fiction and falsehood. Only a fool would take anything posted here as fact." Accordingly, I'm skeptical. So, a verification please?

Can you please quote them by posting their text as text and not as image. It is hard to read from this image. Also, images are not searcheable and poses trouble to visually impaired people. Also, if the text makes a number of claims, then which one exactly are you willing to question in this post?


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What is(are) the mechanism(s) that stop cells from fusing in vivo?
I just learned about the phenomenon of 'cell fusion' in which two diploid somatic cells can combine into some aneuploid cell in vitro and proceed to proliferate in culture. Apparently this can even happen interspecifically. My question is, what stops cells that grow naturally in the body from fusing all the time and creating abnormal cells?
Or, does this happen somewhat often and produce potentially cancerous cells, which are then destroyed by the body's normal regulatory mechanisms (I guess it could slip these as well and turn into a problem).
Could this be why we normally have many benign growths over the course of an animal's lifetime?
Any related reading would be super appreciated, thanks!

Maybe an easiest question is why and how do such a cell-fusion occurs?

@Untitpoi afaik it happens spontaneously among in vitro co-cultures, and that using some fusogen (like polyethylene glycol) 'speeds up' the process by disrupting the cell membrane. I'll investigate further, thanks!

@Untitpoi So I've looked into that a tiny bit more and you are totally asking the right question, thanks so much!

Interesting question, it would be strengthened by linking to a paper.

If as a result of the suggestion @Untitpoi made you have answered your question, it would be useful if you could include it in an answer here. This is quite permissible and good practice in such cases.

@David haha it does kinda sound like cheating, doesn't it? I'll compose an answer within 48h!


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How does the stomach differentiate between liquids and solids to initiate churning?
Or maybe it doesn't at all. Can the stomach tell the difference between liquids and solids and change its churning process accordingly despite that it has no nerves? Because liquids don't need to be churned, so I figure there's a chance animals, or at least humans, evolved in such a way that the stomach wouldn't waste the energy trying to do it.

"...despite that it has no nerves" Why do you think that?

Because there are very very very very very very few cases where people generally "feel" anything they have eaten in their stomach in any way, shape or form. Of course, it still has neurons that transmit signals for motility and secretion.

So, simply because you believe that, you state it as a fact? To use your words, there are very very very very very very many cases where people generally "feel"stuffed they have eaten a Thanksgiving meal. Your stomach isn't 'wired' to feel like your fingers. But it has plenty of a variety of afferent neurons.

I don't need to believe anything, it's a commonly held fact that there are no "nerves" in the stomach. The "feeling" from turkey has nothing to do with any nerves in the stomach, it's commonly known that not only does meat take a lot of energy to digest, but tryptophan also contributes to sleepiness.

It's also a commonly known fact among scientists that most people don't know much of anything about human anatomy and physiology. You are living proof. I didn't say anything about sleepiness, and if you want real "facts", look up orexin/hypocretin. Also see this for afferent nerves of the stomach.  You should quit while you're only behind to an acceptable degree. Keep showing off your "commonly held facts" and you'll only come out more behind.

Also, just ask yourself: if your stomach has no (afferent) nerves, why  do ulcers hurt? Why do antacids (like Mylanta) help?

Subjective opinions aren't commonly known among scientists because opinions such as yours aren't science. Humans don't have somatic receptors like nociceptors in the stomach. You have the legal right to pretend whatever you want, but your article doesn't disprove that, viscera only encompass the area around organs, they are not the organs themselves, and viscera are sensitive to things like stretching and inflammation, that's why ulcers hurt.

How about you ask yourself why you're so desperate to feel superior to other people? What shortcomings have you made of your own life that lead to be that desperate? At this point it's obvious you're just a troll.

@VaneVoe Please watch your tone. As I already said in your other question, writing answer is voluntary. With this kind of behaviour you will not attract anybody to spend time writing an answer.

@Chris Actual experts have expertise for the benefit of society. If these self-proclaimed stackexchange "experts" are so childish as to impede the assistance of potentially hundreds of viewers over their own childish, arbitrary whims, then they were never experts in the first place and their words were never worth regarding. Remember that it is your site that brags about experts answering questions Chris, so I expect to see questions answered if no one is lying about the presence of experts. Otherwise, the site should reevaluate its false-advertising campaign.

@VaneVoe Nope, you are wrong. We don't have to - we can.

@Chris Other than the fact that it literally says "expert communities" on the stack home site, you only don't have to if and only if the site is fraudulent, if there aren't actual experts here. Otherwise, if there are, then the question will be answered. You can say there are experts all you want, but the more the question goes unanswered, the more and more evidence there is that you too are a fraud.

@VaneVoe One last time: Your attitude is one of the problems. EOD

It's clear that I am teaching you some science (you read an abstract and learned some things) but not enough, e.g. you state, "...viscera only encompass the area around organs, they are not the organs themselves..." however, the actual definition follows: vis·cer·aˈ, visərə/ noun: the internal organs in the main cavities of the body, especially those in the abdomen, e.g., the intestines. (emphasis mine) I'm done here too.

You're not trying to teach anything because you're too busy trying to pat yourself on the back. Neither somatic nor visceral pain are perceived within the organs, only in the areas around. When people have heart attacks, does their heart hurt? Nope, that's why people report "chest" pain and not "heart" pain. Your arrogance defeated you before you even arrived, you were already done.

Confirmed: there are no experts here, or such a simple question would have been answered, which means stackexchange is false-advertising when it claims experts reside here.

Tbh I'd like this question to be answered but I can see now no one would even bother.Man,why fight over stuff? I daresay youre the one in wrong when you said it had no nerves but anyways this is a really good question. How does the stomach differentiate between liquid and solid food?And what bout semi solid food?

No one is fighting over anything, if you choose to argue instead of answering, then you can only inevitably be the problem you complain about. Clearly stackexchange only cares about having self-absorbed excuses to pat itself on the back rather than contributing to humanity which is not the mark of an expert. Stackexchange has had every opportunity to prove me wrong and yet has failed to do so. The fact that such a simple question is still unanswered despite that an actual credible graduate has already answered it proves me right.


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Can you identify this mystery bur?
I found this strange bur on a stray cat in my neighborhood.  I've never seen anything like it, and Google reverse image search thinks it's an earring.  Found in in northern California, just south of Clearlake.  (38.90 N, 122.60 W)
The spike structure is almost exactly one inch long.

A friend has informed me this is from the redstem Filaree, and there are some cool time-lapse videos on Youtube of their spinning behavior when they are exposed to water, which is thought to help them burrow into the soil.  (I'm just glad it didn't get a chance to burrow into the kitty!)

Well done, and fascinating! +1


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Significance of Nissl bodies
What is the significance of Nissl bodies? How are Nissl bodies different from any other RER seen in any other cell of the body?

Hi there, I think this is a homework question. Please add a refference and try to solve it on you own first. Otherwise you may not get answer.

https://en.wikipedia.org/wiki/Nissl_body this might be a good start.

I am going to try answer this question.
The origine of this name came from article writen by Franz Niessl (18660-1919) and published in 1894. HE found this substance after he visualized it by nissl stainning method invented by him.
This basophilic substance was just only find in dendrites of neurons, not axones. It is composed by RNA polyribosomes.
Basicly i am tring to tell you that Niessle body is just older name from old ages of histology.
Niessel body is not diffrent with others rought endoplasmatic reticulum(RER). It same pourpose as normal RER.


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Is hydrothorax considered as edema?
In _Robbins Basic Pathology 9th ed., edema is defined as

[E]dema is an accumulation of interstitial fluid within tissues. Extravascular fluid can also
  collect in body cavities such as the pleural cavity (hydrothorax), the pericardial cavity (hydropericardium), or the peritoneal cavity (hydroperitoneum, or ascites).

Though hydrothorax is mentioned here in relation to edema, it is not mentioned explicitly whether it is actually a subtype of edema or not. I also looked into multiple sources for edema definition; “accumulation of fluid in the interstitum”; interstitium refers to the tiny spaces between cells which is not the case for hydrothorax since pleural cavity is not interstitium (right?). So is hydrothorax considered as a subtype of edema?

Welcome. You might wish to consider asking this over at Health.SE. It's best practice not to double-post across the SE network. I'm happy to migrate it for you.


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Can E. coli make pyruvate from acetate?
What pathway would E. coli use to make pyruvate from acetate? I have found several papers that refer to a possible mechanism that could move acetate to pyruvate via a three-step process:
Step 1: Acetate Kinase (EC 2.7.2.1)
Step 2: Phosphate acetyltransferase (EC 2.3.1.8)
Step 3: Ferredoxin oxidoreductase (EC 1.2.7.1)
Is this the pathway that would be used in an E. coli system?

This is definitely not homework. I am asking because the pathway is not listed on MetCyc. No one has answered yet because it is a hard question and acetate-pyruvate flux pathways are beyond most biochem classes. Anyway, I assume it could be done in three steps for most prokaryotes and impossible for eukaryotes.

But what provoked your question? And why pyruvate particularly? It's too late at this side of the Atlantic, but I would reckon a few more than three steps. Also remember plants are eukaryotes. Perhaps tomorrow.

OK. Your mention of MetCyc convinces me, so I have taken the opportunity to provide a detailed explanation of the glyoxylate shunt. The reason you didn't find anything iin MetCyc is that acetate to pyruvate (or even PEP) is not regarded as a single "pathway" per se. This is also the case for other conversions that may utilize certain reactions of the TCA cycle itself.

I have just added a section regarding the suggestion you made in response for my request that you show you have searched for the answer yourself. Fine, I have withdrawn my close vote and deleted my comment about homework. Having looked at your bio I am still puzzled as to why you are interested in E. coli converting acetate to pyruvate. Is it anything to do with the 'metabolomics' tag, which seems inappropriate. Are you trying to explain metabolomics experiments that show increase in pyruvate, for example? Knowing the context would help us to help you.

Summary
Several pathways/metabolic reactions are required for bacteria to convert acetate to pyruvate — or more pertinently to the gluconeogenic pathway — but the key is the glyoxylate cycle or shunt. The sequence of reactions is:

2 acetate → 2 acetyl CoA (acetyl CoA synthetase)
1 acetyl CoA + oxaloacetate → citrate → isocitrate (entry to Krebs TCA cycle)
isocitrate → glyoxylate + succinate (glyoxylate shunt)
succinate → oxaloacetate (Krebs TCA cycle)
1 acetyl CoA + glyoxylate → malate (glyoxylate shunt)
malate → oxaloacetate (Krebs TCA cycle)

Thus, the two molecules of acetate replenish the original molecule of oxaloacetate used for one of them to enter the tricarboxylic acid (TCA) cycle, with — in addition — a second molecule of oxaloacetate. This is available for:

oxaloacetate → phosphoenolpyruvate (PEP carboxykinase of gluconeogenesis)

The phosphoenolpyruvate (PEP) could, in principle, be converted to pyruvate:

phosphoenolpyruvate → pyruvate (pyruvate kinase of glycolysis)

Although this sequence of reactions would normally be used to generate glucose etc via gluconeogenesis.
The link betweeen the TCA cycle and glucose metabolism
In addition to oxidizing acetyl CoA, the Krebs tricarboxylic acid cycle (TCA cycle) can act as source of certain metabolic intermediates for other pathways. As shown below, oxaloacetate (OAA) can be converted to phosophoenol pyruvate (PEP), in a reaction that is part of the gluconeogenic conversion of pyruvate to PEP.

Although certain bacteria can convert acetate into acetyl CoA in a reaction catalysed by acetyl CoA synthetase the TCA cycle per se does not perform a net conversion acetyl CoA to OAA, because a molecule of OAA is needed for acetylCoA to enter the TCA cycle and must be regenerated. The TCA cycle, in effect, oxidizes acetyl CoA to carbon dioxide. The TCA cycle, per se, can only convert to OAA and PEP those intermediates that enter the cycle directly after the acetyl CoA stage.
The glyoxylate shunt
The foregoing explains why most animals cannot convert fat to glucose. (Acetyl CoA cannot be converted to pyruvate by pyruvate dehydrogenase is this reaction is effectively irreversible.) However plant and certain bacteria (including Escherichia coli) can overcome this limitation by means of the glyoxylate shunt. A text available online that explains this is Berg et al., in a section entitled ‘The Glyoxylate Cycle Enables Plants and Bacteria to Grow on Acetate’. To help clarify this I have prepared my own diagram, below.

This involves the conversion:
oxaloacetate + 2 acetyl CoA → 2 oxaloacetate

i.e. the net conversion of
2 acetyl CoA → oxaloacetate

The glyoxylate shunt reactions are imposed on the TCA cycle with a pink overlay. One molecule of acetyl CoA condenses with OAA to enter the TCA cycle in the normal manner. However the isocitrate formed from citrate, instead of being decarboxylated, is converted to glyoxylate and succinate. The succinate — a dicarboxylic acid — regenerates the original molecule of OAA used to allow acetyl CoA to enter the TCA cycle.
What of the glycoxylate produced in the isocitrate lyase reaction? It reacts with a second molecule of acetyl CoA to produce the dicarboxylic acid malate in a reaction catalysed by malate synthase, the second unique enzyme of the shunt. This TCA cycle intermediate is converted to OAA. This second OAA is a net gain from the metabolism and can be converted to PEP, as indicated in the first diagram.
The poster asks about production of pyruvate from acetate. This is technically possible through the pyruvate kinase reaction. However I do not quite see the point of this. I would normally expect PEP to be channeled allong the gluconeogenic pathway towards glucose.
Coda: Pyruvate:ferredoxin oxidoreductase
The poster suggests a series of reactions to convert acetate to pyruvate, the final one being that catalysed by pyruvate:ferredoxin oxidoreductase. Although the pyruvate:ferredoxin oxidoreductase (EC 1.2.7.1) reaction is reversible, it generally functions to oxidize pyruvate to acetyl CoA. It is used as an alternative to pyruvate dehydrogenase by bacteria under anaerobic conditions (as it does not require NAD+), and this is regarded as its role in E. coli, and to an even greater extent in obligate anaerobes such as Clostridium.
The reverse reaction suggested by the poster, involving the synthesis of pyruvate from acetyl CoA, is restricted to autotrophs


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Can you extract specific data from EEG
First of all, sorry if this is the wrong place to ask this question, please redirect me if it is so.
I have a project in mind involving and EEG, which is the following :
Using a "consumer-grade" EEG (see this one, for example) I would like to be able to control a binary system with my mind (for example, turning a led on and off). From what I've seen until now, this seems to be possible since the headset is able to detect eye blinks, for example. It also gives access to two variables "focus" and "relaxation", which you can learn to control somewhat accurately (accurately enough for a binary system, at least).
Now here's my problem. While the methods that I described above do work, they would also continuously activate even when I don't want them to. Everytime I blink, my led would turn on, even though my intention wasn't to turn the led on. Everytime the "focus" level goes over 50/100, the led would turn on, even though I'm just focusing on my physics problem.
Having said that, I was wondering if it is possible to pick up more subtle and "controlled" information on the EEG. One thing I was thinking about is, if I think and visualise the color red, maybe that could cause a signal that can be picked up ?(Of course the led would activate when I look at something red, but that's still an improvement) Or even looking at the led I want to turn on, would that have any discernable effect on the EEG ? My guess is that those "thoughts" are way to subtle to be picked up by an EEG, which is just an average of the brain activity, but I'm not an expert on the subject !
So I guess my question is : what are the "kind" of thoughts that I can somewhat reliably see on the EEG data ? For example, I know I can reliably pick up a eye-blink. Are there any thoughts that are not related to muscle movement that can also be reliably read on a EEG ?

I'm sorry, although this is an interesting question there is way more to this than you are probably realizing. Like, this is the sort of thing people write entire theses on. You really just need to read scientific papers about this sort of thing, there's no quick fix for EEG processing from the perspective of biology. It's an interesting question but I am voting to close as too broad.

If there are papers discussing this, that would be great if you could suggest some ! If you want I could change my question to be less broad : what I really am interested in is if I can control a binary system with my mind, so I really need to know if it is possible to detect a binary signature of something in my mind, that isn't related to any muscle movement.
I do understand your point of view though, and if it gets closed, so be it !

https://scholar.google.com/scholar?hl=en&q=brain+machine+interface

You can add "EEG" or "binary" to limit to EEG studies of binary detection.

It is certainly feasible if your device is decent enough (not sure about the model you linked to). You either need to select a frequency range or a component of the event related potential. According to the first paper I linked to, you could imagine making a movement towards the target. Just don't expect 100% accuracy.

Short answer
The key word in EEG-driven mind control is brain-computer interface (BCI). In contrast, eye blinks can simply be detected with an eye tracker.
Background
As far as I know, EEG-driven computer control (The force is strong in you) is based on recording the EEG while thinking of certain actions, or simply doing them. As you likely understand by now, thinking of moving your arm activates much of the same brain circuitry as actually making the move, up until the pre-motor cortex. The motor cortex itself stays silent (otherwise you would actually make the move (Griggs, 2013).
So EEG correlates of motor activity can be translated into digitized electrical brain activity. In turn, these brain waves can be put to use from playing pong by mind force, to state-of-the-art applications like driving artificial (bionic) limbs for the lame. By using artificial neural networks / deep learning techniques / and multiple EEG electrodes, the combined activity can be registered of many brain regions and certain signatures may pop out and be trained for a computer to learn them. In tun, that can be used to, say, play a computer game.
For a commercial alternative, delivered with an SDK, check out (Pogue, 2012):

Emotiv's EPOC

References
- Griggs, New Scientist, January 2013
- Pogue, Sci Am, December 2012)


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Spectogram of mimicry vs original
Suppose the mimicry of a voice is very accurate. Will it  have similar spectogram as the original voice?


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Advanced books about molecular biology and genetics
I'm finishing my third year of biochemistry and doing gene therapy practicals during the summer. I'd like to buy a book that describes flow of genetic information (transcription, translation, replication, splicing...) and its mechanisms in depth (such as transcription factors, regulation, etc). The closest thing I currently own is Lehninger's Principles of Biochemistry, but most of it deals with metabolism. I've also got to know about Molecular Biology of the Gene, but I'm not sure if it's what I'm looking for. I'm not interested in books about heredity or population genetics.

The classic, "The molecular biology of the cell" https://en.wikipedia.org/wiki/Molecular_Biology_of_the_Cell_(textbook)With answers

As the title implies, Molecular Biology of the Gene deals with the molecular biology, e.g. what you're looking for. There are no population genetics in that textbook. In the vein of gene therapy I also like to recommend immunology texts, since CAR-T has become an approved gene therapy modality.

Molecular Biology of the Cell is a great text book, and an older edition is available for free on NCBI bookshelf. However, the book covers a broader range of topics than perhaps you're interested in and may not go into the same depth as others (though I haven't actually done a side-by-side comparison).
Watson, who along with Crick developed the central dogma of molecular biology, literally wrote the book on this subject: Molecular Biology of the Gene. It sounds exactly like the text book you’re looking for, and was one of my favourites as an undergrad. You can check out the contents of the book yourself to make sure it's what you want.

Note for NCBI version of Molecular Biology of the Cell: By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

@GuyCoder Yes it’s a bit cumbersome, but you can get into whole chapters just by searching for their title.

The classic, "The molecular biology of the cell" https://en.wikipedia.org/wiki/Molecular_Biology_of_the_Cell_(textbook) helped me a great deal...30 years ago. It has been continually updated and is the best source I know. However, books take years to write, and are therefore always years behind. With answers to every imaginable question on the internet, why limit yourself to books?

Well, it's not about "restricting" myself to anything, but I consider that books can be helpful and are more manageable. There are lots of good websites, especially certain "Review" articles at NCBI, but sometimes it's so much that you don't even know where to begin.


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What is this plant with distinctive leaves?
Location: Vienna, Austria
Leaf size: two big thumbnails
Plant height: large thumb

I assumed it might have come from the seeds of some fruit I ate.  I consulted these websites:
https://www.baumkunde.de/baumbestimmung/
http://www.blattbestimmung.de/blattform-herzfoermig
but found nothing. Perhaps it is neither shrub nor tree.
Edit:
This is how it looks now, ten days later:

Seedlings are often tricky to determine, but I think this may be the common weed Chenopodium album (from the family Amaranthaceae). This is common across Europe, and the leaf shape, growth pattern and the silverly underside seen on the top leaf in your picture fits well.
Here are pictures of a seeding and a larger plant:

(from flickr.com)

(from https://plants.ces.ncsu.edu)

I totally agree on Chenopodium, however, members of this group are extremly hard to distuingish, so maybe you should just settle with the family?

@blabbath Where you write "settle with the family", are you referring to the actual family (Amaranthaceae) or the genus (Chenopodium). In general, I agree though, which is also why I phased it as "may be". It could well be another species in the genus, even though C. album is most common in many parts of Europe.

The genus of course, my fault. But I can live with your answer as it is =)


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Why do live crabs in a bucket prevent each other from escaping?
It has been observed that crabs in a bucket will stop others from easily escaping. This observation has lead to the English language colloquialism crabs in a bucket. Has this phenomena been studied? What are some animal psychology explanations of this?

you might want to either explain the behavior in more detail or cite a source showing it actually occurs, otherwise this is likely to be closed as unclear.

Yeah human beings have always been randomly ascribing human psychology to animal/plant behaviors, which simply makes no scientific sense. Don't think one should treat such interpretations too seriously. They're more of a means to reflect on human beings themselves.

There should be a dictum somewhere that states, "Never ascribe to psychology what is caused by instinct."
By that I mean, the captured crab has a survival instinct. It's not going anywhere on the bottom of the bucket; it needs (I don't even know if I would say, "It wants") to get out. Out means "up", since "sideways" doesn't get them out, which doesn't prevent them from trying that as well (as shown by scuttling around the bottom repeatedly.)
The sides of the bucket are slick; there's nothing to grab onto. So if one crab climbs atop another, suddenly there's something "above" (a shadow? An outcropping? Another crab?) to grab onto to hoist itself up the side. So the crab instinctually grabs onto something above it. Unfortunately for the higher crab, there's nothing for it to hold onto above it, so he falls back into the bucket.
If only they would work together, a few of them might make it out. If they were chivalrous, the females and the young ("women and children") would go first.
I don't really know crab psychology, nor do I know any crustacean psychologists. All kidding aside, however, there have been some attempts to study stress in crustaceans. Science Daily published an article about stress in declawed crabs. What you and I think of as "stress" may be different than how the author thinks of it, but from the article, it's pretty clear that Dr. Elwood means psychological stress. However, there is no evidence to support that; the increased mortality of declawed crabs is more likely to be due to physiological stress (as in the second cited paper.) He has been called out on this by fellow biologists.
Crabs are invertebrates. If you want to learn about invertebrate psychology, the octopus is your animal.
Declawing Crabs May Lead To Their Death
Assessing Stress and Predicting Mortality in Economically Significant Crustaceans


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is having more copies of gene better then having it less? if it's why is it ?
I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.
so I wonder if it's better to have more copies of the gene then having 2

I think you're reading that information wrong. They are referring to a single gene, not genes in general.

Here is one news article about the research. They are talking about p53 tumour suppressor. Rather interesting.

I also posted the equivalent article from Nature with Remi's answer @canadianer

It depends on the gene. Multiple copies of one gene in humans can result in Huntington's Disease, while multiple copies of TP53 in elephants is beneficial. Mostly, though, it's either benign or not a good thing. NB: Not a lot known about Copy Number Variations, but one article states: "Some CNVs have no apparent influence on phenotype, while as many as 40 others have been definitively linked with disease."

I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.

Where did you read that? Please always include your sources.
What you're saying is unclear but I suppose you are referring to ploidy variation among species and not to CNV (Copy Number Variation) for specific genes. It is also possible that you mistake alleles for genes but it is impossible to tell where your misunderstanding is without reading from your source. I will assume you talked about ploidy variation.
Elephants are diploids, just like humans. So, the claim appears flat wrong.

so I wonder if it's better to have more copies of the gene then having 2

There is no general rule. Because having a single working copy is often enough, high ploidy can be a pretty good defense against loss of function mutations but that's only valid for some time just after a recent polyplodization event as the relaxation of selection pressures against such mutations will lead these deleterious mutations to higher frequencies (at mutation - drift - selection equilibrium).
Note that doubling or halving the number of gene copies often yield to issues in dosage of mRNA and protein expressed. Related to that you might to read about dosage compensation

OP is almost certainly referring to https://www.nature.com/news/how-elephants-avoid-cancer-1.18534

(not sure where the downvote came from by the way, was not from me or related to my comment, I was just providing additional information)

Down vote solved :) I think it is good answer, and who down voted it is fool actually.

I think the OP is referring to CNV.


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How to get phased haplotype from vcf file?
Although I'm reading all days and nights, still confused in this area. I have hundreds of BAM files (from whole-genome sequencing of a given human population). I was wondering how I can obtain phased haplotype from raw vcf file? I read also about GATK, but didn't find a clear answer to my question. Please kindly tell me if this tool is suitable for this goal?
Would you please introduce me some practical guides and pipelines that explain such an analysis step-by-step?
Thank you for your help

What format are you hoping to end up with? Note that your question would be a better fit on bioinformatics.SE.

Thanks. vcf file format. Sorry, what's bioinformatics.SE, is the bioinformatic forum?

See bioinformatics.stackExchange for your future questions of the kind.

You should be able reformat BAM files to VCF files with PGDSpider.
I find using specific softwares for this type data formatting tends to be error prone and not practical when having a large number of files to reformat, so I personally like to simply read about the format standard and write the code to reformat myself but that's very much a matter of personal preference.

Thank you for your response and forum. However, variant calling from bam file is a long story, beyond just file conversion.

You can use either HapCut2, WhatsHap or my package.

There are multilple packages to achieve this. I have personally used bcftools (SAMtools). Here is a non exhaustive list:

SAMtools (bcftools);
VarScan2;
FreeBayes;
Platypus;
Deep variant


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What kind of a fly is this?
I have a couple of new pictures of insects which I am really curious about. This is one of them. I found this fly near my cottage in Prague, Czech Republic.

It is fluffy with very long proboscis (almost half of an inch in length).

That is in the family Bombyliidae. https://en.wikipedia.org/wiki/Bombyliidae

This is indeed a fly from the genus Bombylius. However, I think this is not the common B. major, but Bombylius discolor.
The reason is that your specimen clearly has small dots on its wings. These dots are characteristic of Bombylius discolor, B. major lacks these dots. Furthermore, B. major has a black part at the front of its wings, that is very distinct. In discolor, this black part is less pronounced or even hardly visible.
Picture from the Dutch Wikipedia:

https://nl.m.wikipedia.org/wiki/Gevlekte_wolzwever

Thank you for your answer. I am so happy that i finally get the right ID of this nice creature and this still amaze me how much i have to learn in ID of bugs.  :)

I found out that this is on of the most common specious from this family in whole Euroupe called Bombylius major. From wikipedia article (same with picture):

The adult is 14 to 18 millimetres (0.55 to 0.71 in) in length, squat and very hairy, with a wingspan of around 24 mm (0.94 in). It has dark patches on the anterior half of the wings and long hairy legs that dangle while in flight. The very long proboscis is used to feed on the nectar of many species of flower, especially primroses. While its wings continue to beat its front legs grip the flower and its long rigid beak is inserted to collect the nectar.[2] Despite its fearsome appearance, the beak is quite harmless.[2]
Bearing a mimetic resemblance to bees their body is stout and furry, with the top of the thorax being black and shiny and the pile either brown, yellow, or white. They have long spindly legs as well as a long rigid proboscis found in the front of the head. Their boldly patterned wings have a distinct dividing border through the horizontal middle between the dark and clear portions. Their antennae are typically very short and pointed. In the field they will be seen hovering and darting above bare ground or flowers, in an up-and-down movement, accompanied by a high-pitched buzz.


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What kind of insect is it?
I found it hanging on the wall at night. It was approximately an inch long. Near my dormitory there is a lot of birch trees. The photo was taken in Prague, Czech Republic.

It is a moth in the family Noctuidae. I don't know the species.

This is the heart and dart moth (Agrotis exclamationis). Its name refers to the special black spots, which have shape of dart and heart.

This moth is one of the most common in the Paleoarctic ecozone. It has a wingspan of 35-44 mm. The larva of this moth is brown above and grey below. It is capable of feeding itself on a variety of plants.


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How many species can have the same scientific name?
For my science homework, a question came up asking how many species can have the same scientific name. I'm pretty sure that each species has a different scientific name, but just to be sure...

It is actually possible for two species to have the same genus and species names. The two-part name (binomial) is unique only within a kingdom, so organisms in different kingdoms can have the same genus and species names. For instance, Orestias elegans is the scientific name of both a plant and a fish.

The scientific name (better known as latin name or binomial name) of a species is unique to this species. No two species can have the same latin name. Also, a single species cannot have two different latin names. But of course, mistakes happen and we don't seem to bother too much about them (esp. when the two species are very unrelated; see What instances are there in which two species share the same binomial name? (thanks @fileunderwater and @HRA).
Of course, the above is true as long as there is agreement in the limits of the definition of a species. In absence of such general agreement, there can be some issues. Consider for example, Homo neanderthalis who is often called Homo sapiens neanderthalis. See the post How could humans have interbred with Neanderthals if we're a different species? for more information about the definition and delimitations of species.
Have a look at wikipedia > Binomial nomenclature for more information.

I thought so too. However, the link provided by @fileunderwater proves that there are examples of a species name not being unique. #looking dazed and confused#

This is not to try and replace Remi.b's great answer, but just to supplement it for any later visitors: biological nomenclature is controlled by international codes which regulate how and what species can be named.
For example, the ICN (International Code of Nomenclature for algae, fungi, and plants) governs the naming of species and groups within those taxonomic groups, while the ICZN (International Code of Zoological Nomenclature) governs naming of animal species.
One piece of trivia about the two: tautonyms, or tautonymous names, are species names where the genus and species epithet are the same, for example Rattus rattus (black rat) or Vulpes vulpes (red fox). These are allowed under the ICZN, but are explicitly prohibited in the current edition of the ICN (the Melbourne Code published in 2011).


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Might new bones evolve from soft tissue?
I wonder how bones evolve where there are none. (This is the question, read the sub-questions as examples :) )
Lets take an elephant as an example. If it was adaptive for the elephant, could bones somehow evolve in their soft-tissue trunks? If so, what tissue would they develop from?
Perhaps the sheet of cartilage in their ears are more likely to somehow calcify and become a new bone?
And would then several connected bones and joints evolve from the new bone tissue?
Is it very rare for new bones to evolve from scratch? Or, do today's bones entirely trace back to the set that evolved in early tetrapods?

I remember being curious about how bones were made and I eventually found out that bones develop from cartilage, so bones develop from cartilage. Is this what you were looking for?

New bones do form occasionally so it is not impossible, Ornithischian dinosaurs are defined by a evolution of a new bone (predentary). There are many pieces of cartilage in the body that become ossified in some animals and not others, the kneecap is a great example since a bony kneecap has evolved and been lost many times independently, it is just a matter of ossifying existing tissue. The trunk however is more difficult since it does not have any suitable cartilage.
Cartilage however is not necessary to form bone, but it is the most common way to get it. Endochondral ossification forms bone from cartilage and is responsible for the majority of the bones in the body. Intramembranous ossification forms bones in other connective tissue, the bones of the skull and dermal bones are examples of this process. Dermal bone has evolved separately many times but tends to form in the skin.
Given enough time  and the right selective pressures it is certainly possible for bones to evolve in the trunk but it is not going to happen quickly.


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Northern Europe tree identification
I've seen it in Nordic countries (Sweden, Latvia). It's a tree that reaches maybe 5 or more meters high and its flowers have a beautiful scent.

Looks like maybe a kind of dogwood, anyone?

Not a dogwood, they have 4 large petals.  I would put in the genus Prunus from the general appearance of the flowers and leaves (https://en.wikipedia.org/wiki/Prunus).  Could be any of a large number of domesticates, maybe the list is shorter that far north.

It's the common Prunus padus, which flowers with its strong scent now in many parts of Sweden (including my yard). At least if you are referring to the common species found in the wild (there are planted domesticated varieties as well). It is common across many parts of Europe though, and not only the Nordic countries, and can be found in Asia as well.