text:
What is a concussion?
When I was a kid and someone got a concussion, I seem to remember people telling me that it was when your brain impacts the side of your skull, accelerating fast enough to do so despite the cerebrospinal fluid buffer.
But wikipedia doesn't mention this explicitly. Is this just one possible cause for concussions? Is it possible to generalize about them? How much don't we know?

Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.
Since it's connected to the head trauma by definition, there is in principium no other cause of it.
The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:

the acceleration of brain causes increase of pressure
the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)

These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:

Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.

The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and

Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.

Microinjury is also linked to triggering of cell death pathways in brain cells.
The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.
Sources:

Overview study
Robbins and Cotran pathologic basis of disease

Does "concussion" imply "brain impacted the side of the skull"?

The brain doesn't have to impact the skull. Acceleration itself and the rise of pressure it causes if big enough can according to the article cause enough stress for some of these changes to occur.
Morover the impact is always hindered by the cerebro-spinal fluid, but the thing that matters is how much of the energy is absorbed by the fluid and how much by brain tissue. If impact is small, much of the energy is absorbed by the fluid and little damage is done to the neural tissue. If it's big, proportionally less is absorbed by the fluid and the rest can cause the damage to the brain.

The CDC has a nice webpage about concussions and traumatic brain injury, as does the Mayo Clinic. The brain and head move rapidly back and forth due to impact or sudden acceleration or deceleration, in spite of the cerebral spinal fluid bathing the brain cavity. This causes chemical changes in the brain and/or damage to brain cells, affecting brain function.
Symptoms are not always instantaneous; sometimes it can take hours or days for symptoms to arise. There are multiple diagnostic tools that exist, including graded symptom checklists, the Standardized Assessment of Concussion, neuropsychological assessments, and the Balance Error Scoring System. These are summarized in this American Academy of Neurology (AAN) article from 2013.

"...sometimes it can take hours or days for symptoms to arise." I think that is true of some symptoms perhaps, but all people diagnosed with a concussion show one of a number of symptoms immediately after impact. I've never, ever heard of a concussion diagnosed without any symptomatology - even relatively minor, such as dizziness or cognitive impairment - post impact, and as an ED doc, I've assessed many, many head injuries. Diagnosis may be delayed because people think the symptoms are minor.

Also, just checked your references, which do not support your statement. The closest it comes is in the Neurology article, which states "...many of whom do not obtain immediate medical attention."

The note about symptoms taking time to arise might be referring to symptoms caused by bleeding in the brain, which could be caused by trauma but is separate from concussion.


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Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage?
From first principles, it seems surprising that a blow to the head would cause unconsciousness rather than just impaired function.
I've heard a lot of analogies to computers -- "Your brain has to reboot." But computers reboot when there is an error because they are explicitly designed to do so, in order to recover and prevent further damage.
So, did we evolve the capacity to get knocked out for similar reasons -- because it helped us recover or prevent further damage? Or is the capacity to get knocked out just an "accident" or an inevitable consequence of the way our brains are designed, without a good evolutionary explanation?
(I realize the answer might be: "we don't know". In that case, I'd wonder what the prevailing opinions are and what if anything we've ruled out).

peripheral nerves also do this, when touched (eg in surgery) they completely stop working for some time

It is worth noting a blow to the head causes unconsciousness by doing enough damage to the brain to disrupt its function, a knockout is a concussion. This is why knocking someone out is actually very difficult and very risky. The movie knockout is a myth. We did not evolve to be knocked any more than we evolved to go into cardiac arrest.

https://en.wikipedia.org/wiki/Concussion#Mechanism
We did not evolve in order to become knocked out. See the wikipedia link. The "water" in the head is designed to not make us get knocked out that easily. However each dampening system has a limit.

source: Stack Exchange

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Is abiogenesis possible today?
Life on earth started about 3.5 billion years ago. I would assume abiogenesis happened because the conditions were right.
Would the current earth conditions allow for new abiogenesis and completely independent (in terms of phylogeny, not ecology)?

What do you mean by "new life"? Yes, single cell organisms reproduce to form new organisms. And yes, evolution still operates to create new traits, and ultimately a new kind of organism.

"However, the conditions are still right, if not much better, for new unicellular life to form and thrive"... this is completely incorrect. "Is new life still being created?"... this is a question based on a wrong premise.

@GerardoFurtado Can you explain why the statements are incorrect?

I think what @GerardoFurtado was trying to imply is, different organisms need different environments to thrive. As a result, because conditions on Earth are right, say for a human being like yourself, it might not be right for certain other organisms.

@AMD I drastically edited your post to try to improve its clarity. Feel free to roll back if you don't like it.

Highly related (eventually even duplicates): Why did abiogenesis only happen once? and How did the first self replicating organism come into existence?. You should also look at wikipedia > abiogenesis.

@ImtiazRaqib That's not what I said at all. There is no condition today for any abiogenesis to occur.

Theories of abiogenesis invoke a process that starts with inorganic molecules, proceeds through simple organic molecules and macromolecules, and culminates in replicators and cells. Even if there are places on the planet today that favour this process, the emerging organic molecules and macromolecules would have to escape 'predation' by existing organisms. I think this makes contemporary abiogenesis even less likely.

I agree with @AlanBoyd. So much of Earths materials interact with already existent organic life that the generation of "new life" would be extremely unlikely/improbable to the point of complete impossibility. Perhaps we could observe abiogenesis in a completely sterile environment over large expanses of time, but that seems practically impossible as well.

I will argue that yes, it is POSSIBLE. It is possible on earth like on other planets. Given enough time, matter, and energy, "something" that resembles life will emerge. The problem I see, however, is that life has already conquered our planet, so any "new living thing" will have to compete with other long-time adapted living organisms, in practice, no chance of survival. The right conditions you refer to are the ones that allowed "life as we know it" to emerge. Given other conditions (other chemicals, other energy forms, etc), something completely different will emerge.
Of course, without final proves, this is still speculation.
Some speculative links:
http://speculativeevolution.wikia.com/wiki/Alternative_biochemistry
http://www.dailygalaxy.com/my_weblog/2015/05/alien-life-habitats-nasa-brainstorms-alternatives-to-water.html
http://www.nature.com/news/2009/090513/full/news.2009.471.html

Why is this down-voted? I think the answer summarises fairly well what has been suggested in the comments. Maybe a bit to little detail and under-referenced - but still fair enough for a speculative topic like this. +1

I'd just like to add to this response that should abiogenesis be possible at all, and I think like many that it's quite likely, then under whatever differences in conditions between the original event(s) here on earth, certainly mankind is ready to "assist" nature with state-of-the art equipment. The fact that we can manufacture diamonds at fractions of the time required by natural processes attests to how our technology practices expedite natural processes.

Unlikely
Th early earth lacked oxygen which is very harsh on organic chemistry and lacked living things gobbling up all the organic molecules. precursor molecules form all the time on earth but living things gobble them very quickly. Both of those things makes abiogenesis basically impossible on the current earth. Abiogenesis is all but impossible when you have complex evolved life competing for the same resources, fortunately the early earth lacked that.

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What is this yellow-pink flower?
Found in Pennsylvania, Philadelphia County
This is intentionally planted, not sure if it is indigenous to this region. Thank you for your expertise!

It resembles Lantana Camara, from the family of Verbenaceae that is native to American tropics according to Wikipedia.
They come in variety of different colors, and the one you have photographed is the Pink Caprice.

Image Source: Cindy Dyer's Blog

Glad I could help :)


text:
Did Smilodon become extinct because they were too specialized carnivorous?
Specialized in two senses,

Teeth were too big. I.e. too specialized to hunt.
Only hunted large herbivores

Have you done any effort on your part, like going through peer-reviewed articles?

Smilodons were specialized on hunting large herbivores. The decline of Smilodons comes with the decline of these large herbivores. The large herbivores were indeed progressively replaced by faster and more agile herbivores such as deers. The extinction of these large herbivores is at least partially caused by humans. It is possible also that humans may have been in competition over territory and not only food source. As the Smilodons got extinct, smaller species of feline slowly evolved.
Just have a look at wikipedia > Smilodon#Extinction for more info


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How the electrons from electrode play a role in stimulating the neuron?
I am trying to understand how a neuron fires action potential after being stimulated via electrode (extracellular stimulation). GHK equation gives the membrane potential,which is -70 mV when neuron is at rest. When the membrane potential increases to -55 mV, it fires AP. But then an electrode gives electrons, which do not appear in the equation. Then how the electrons from electrode play a role in stimulating the neuron? Also,   is there a way to calculate how many electrons or how much current would be required to stimulate a  neuron?

You might be interested in this.


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Inheritance of mitochondria
Imagine an isolated population in which each adult female has a distinct mitochondrial genome. In each generation, every adult female has two children (with a 50% chance of being male or female). After each generation, we will assume that all the adults die out, and all the children become adults.
After four generations, what is the expected percentage of mitochondria from the original population of females that will still exist in the population’s children? Express your answer as a decimal between 0 and 1, rounded to three decimal places.
Note: after one generation, there will be 100% of the mitochondria from the original population present in the population’s children since male children receive the mitochondria from their mothers (but do not pass them on to their own children.)

Welcome to Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. Also, the question has nothing to do with bioinformatics (unlike suggested by your tag).

I don't really get the question. Is it asking what fraction of the unique mitochondrial copies will remain after 3 generations. If it the case, it is impossible to answer without knowing the population size. I guess the question is weirdly formulated and it actually ask whether the allele frequency for this specific mitochondrial haplotype (that is 1 after the first reproductive event) will vary in the successive generations (and I suppose we assume, no mutation and no migration) but that sounds like a too simple  and too unrelated to the special inheritance type of mitochondria

@Remi.b no, AFAICS the answer is independent of population size, and is equivalent to the asking "what is the probability that a female from the initial population has a daughter who has a daughter who has a daughter?" (which, aside from that realization, has nothing to do with bio at all).

@adjan I removed my comment as it contained a math mistake. I tried to write an answer but realized the math are even a little more complex than I first thought (so I have deleted my wrong answer). I think the wording make the question more complex than it seems. What kind a course is it? Also, You are still suppose to show your effort at answering the question

@Remi.b I'm not the OP though

Oops sorry! Wrong name!

This is a question that is not as straightforward as it may seem.
One could make arguments, some better than others perhaps, for several different answers. The way it is worded, one could defend answers from 0.000 and 1.000 and many of the intermediate numbers as well.

After four generations, what is the expected percentage of mitochondria from the original population of females that will still exist in the population’s children?

0.000; the original women died; THEIR mitochondria died as well. None of the original mitochondria still exist.
That may seem, and it largely is, a matter of semantics, but in some ways, it is true without word games.  Every time the mitochondria split, the copies are not EXACTLY the same.  The changes may be so minute they are not always detectable with the current technology, but that does not mean they do not exist.
Some changes occur to the underlying genome; they are rare and may not be readily observed, but that does not mean they do not exist as well. When one of these changes occur, all subsequent mitochondria will have the new genome assuming, of course, that the genome is viable.
If the change will not allow the cell to function properly, this will undoubtedly affect whether the child, as a whole organism, is able to survive.  Depending on the severity of the malfunction that results from the new genome, it may make it more difficult, perhaps impossible, for the offspring to thrive, to mate, and to produce their own offspring which can accomplish the same.
It is also likely that some of these genetic mutations will result in change that is too minute to have an effect on the mitochondria or how it functions. By the same token, it is likely that eventually there will be a mutation in the mitochondrial genome that will have a marked effect on cell function. The change may even improve the overall function of the organism to an extent that will enable the offspring to thrive, to mate, and to produce their own offspring at a greater rate than organisms that do not have this change. Needless to say, the 'improved offspring' will pass on their 'improved genome' to the lucky offspring that will be more likely to thrive and pass it on to the next ..... etc.
There are many factors influencing how well the new genome is going to spread. The population in this particular question was somewhat isolated; this will encourage the genomic change to spread through the general population more quickly. The rate of the spread, however, is affected by many variables.
So in a world with no mutations or any other factors that can result in changed mitochondrial DNA, it would be 1.000 as every offspring gets its mothers, who got it from hers, who got it from hers, so the four types, on an isolated island, would remain four types.
However, in reality, changes do happen. An error(s) in transcription would be one of the most common, but certainly not the only, process that could result in any DNA being changed in a heritable manner.
There is an average rate of mutations. In fact, one can look at the mitochondrial DNA of two individuals and calculate how long ago the genomes were essentially the same. In other words, one could look at a mitochondrial genome from some ancient fossil and tell how many generations it likely took for it to evolve in to the genome of a particular modern individual.  However, as these changes start as mistakes, it can take several generations for a change that is adaptive and will spread to occur.
The only way humans can observe these changes are in animals with very short life spans, such as fruit flies.
There would be very little change likely in only four generations; therefore, unless you had a very large sample size, any prediction would have little more than a theoretical chance to be correct.

Please cite your source.

I think there is an error in the following piece of reasoning: "So in a world with no mutations or any other factors that can result in changed mitochondrial DNA, it would be 1.000 as every offspring gets its mothers, who got it from hers, who got it from hers, so the four types, on an isolated island, would remain four types."
There could be female that have 2 male offspring and others that have 2 female offspring. This phenomenon, called "drift" will cause some genotypes to increase their frequency, and others to decrease theirs, even in absence of selection.


text:
Temperature threshold of a cell
While human body as a whole will find a increase in temperature by 2 C fatal, what about individual cells? If temperature of a cell or tissue is maintained at higher temperature via external mechanism , say a sophisticated heating rod, how much temperature rise it can take before dieing? Say, endothelial cells lining blood vessels. Or,any other cell.

different cells and tissues have different tolerances, so you will have to be more specific.

A core body temperature of 39°C is far from fatal, so you are starting from an incorrect assumption.

Talking about cells in general, the main problem about higher temperatures is the denaturation of proteins (when proteins lose their structure and then they don't work anymore), and every organism has a specific range of temperatures in which its proteins have evolved to work in that determined range.
The most common example of bacteria living at high temperatures is Thermus aquaticus (or others) which proteins are widely used in laboratories for their peculiarity to be able to work at more than 70 °C (e.g. polymerase chain reaction).
In humans the mean temperature is 37 °C, and it's not unusual during severe fevers to get it rising to 39-40 °C (so the assumption that over 39 °C occurs death is incorrect). Of course you can reach higher temperatures but reaching 43-44 °C leads to multi-organ damages. You can find out more in this review.
Another thing to take in consideration is that cells must contain water in liquid phase, so over the 100 °C limit (at atmospheric pressure, so the limit can increase alongside pressure) it's kind of impossible to find living cells.

The highest I found is 122 °C (http://www.pnas.org/content/105/31/10949) but you have to consider the high pressure that keeps water a liquid and not a gas.

I think the question was about the temperature tolerance of human cells, not extreme thermophile bacteria, so this seems to be veering off topic ...

Reading the question and the comment wrote by John I thought it was clearer to take them as example, anyway the thermophile-related sentences can be easily deleted.


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What kind of microorganism is this?
It moves like a worm pretty much. I found it in a pretty big pond with brackish water. The water temperature was around 10 celsius.

Here's a video of it moving

Could you add some more details? Where you found it, what kind of environment it lives in, size, etc?

Now  I cannot really tell the name of it without knowing more of its properties and characteristic features, e.g. size. (I am afraid I am not very good with faces, especially of microorganism :D)
But I am 90% sure it might be an
Oligochaete

Please do not post guesses as answers and always provide references to your claims. I recommended deletion for your post as it does not fulfill standards for good answers. Please feel free to edit accordingly to avoid deletion or - after possible deletion - give a new, well-researched and comprehensive answer. Thanks!

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

@AlexDeLarge ok


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Watering plants with soaked forest soil
I am thinking of mixing forest soil with water and water plants with that.
I was hoping that nutrients from soil would get released into the water, so in effect, fertilize the soil.
I am not sure if this works, since I am not aware in what chemicals P, K, Ca, Mg is "stored" in forest soil. If it is oxides that it should dissolve rapidly.
So, overall, is it beneficial to the plant to water them with water in which forest soil was dispersed?
Plant in question are tomatoes, peppers.

So basically you are trying to make your own liquid fertilizer. You might want to search DIY liquid fertilizer, compost sources are common. A small amount of soil is not going to contain much in the way of nutrients. I also recommend reading up on fertilizing practices and nutrient requirements of the plants in question as fertilizer burn is a real thing and if you are seeking multiple sources of fertilizer you can over do it.

forest soil can be very acidic indeed, its good  for alkaline/clay soils. pond/river silt and dung is much favored. typically place fist of dung beside plant roots to feed them, else mix in 1/4-1/3rd mammal dung depending on its strength/check multiple forest soil pots with tomatoes to see best dose results after 2-3 warm weeks.

I'm voting to close this question as off-topic because it is a better fit for Gardening.SE

You are thinking about something like "compost tea".
http://www.homecompostingmadeeasy.com/composttea.html
The problem is that a random piece of forest soil may or may not be rich in nutrients.  If that soil has water soluble nutrients in it, wouldn't the rain have already rinsed them out?
If you make tea out of compost, there has been no chance for rain to rinse out nutrients because the decomposed stuff has been in your compost bin.
Last piece: if you are making tea out of forest soil or compost, when you are done you will have a soaked clump of wet soil or compost.  What are you going to do with it?  Probably throw it on the ground somewhere.  It might make more sense and be much less messy to skip the tea step, put the forest soil or compost on the ground next to your plants, and then water them.


text:
what is this mushroom and how to grow this mushroom?
What is this mushroom?

And how to grow this?

If I knew how to grow this particular mushroom, I would start a side business doing exactly that. They are very marketable.

Please add the location the picture is from

i find this in my village forest  in india himanchal pardesh kinnaur purbani

SEARCH "MOREL CULTIVATION", it is difficult, technical, requires good rainwater / special water and good microclimate, and it's low production quantities. some people cultivate morels. experienced pickers can find many of them in certain places. its interesting. the best thing is to put them in blender with other ingredients and throw all the spores everywhere shadey rainy and well drained. i found this vid for example https://youtu.be/lTFugHA2WaI?t=310

Regarding how to grow it, try https://gardening.stackexchange.com

This is an Ascomycota from the genus Morchella, called morel:

Morels are edible: despite the Wikipedia page I linked above saying that Morchella has hydrazine, according to Ammirati, Traquair and Horgen (1986):

There is no evidence that Morchella species contain gyromitrin* or related compounds.

* A hydrazine compound.
Source: Ammirati, J., Traquair, J. and Horgen, P. (1986). Poisonous mushrooms of the northern United States and Canada. 1st ed. Minneapolis: University of Minnesota Press.
PS: Your second question ("how to grow this?"), however, seems to be off topic here at Bio SE.


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Is a part of the spinal cord from the mesoderm?
The caudalmost part of the neural tube is formed by the caudal eminence. Isn't this mesodermal? So does it mean that, a part of the spinal cord is mesodermal in origin?
Does it have any significance apart from being something just academic?

@JM97 zara ye bhi pls :)

The caudalmost part of the neural tube is formed by the caudal eminence. Isn't this mesodermal?

No,the neural tube is not mesodermal at caudal end.
According to Gray's Anatomy:

At the time of caudal neuropore closure, the caudal midline cells are generically termed the caudal eminence (O’Rahilly and Müller 2004). A specific population of mesenchymal cells, the caudoneural hinge or junction, shares the same molecular markers as the primitive node. These cells aggregate at the midline and undergo mesenchymal/ epithelial transformation, producing a cellular cylinder that is contiguous with the caudal end of the neural tube. Further elongation of the caudal neural tube involves cavitation of the neural cylinder.

So, the cells in the caudal eminence form a solid cylinder(medullary cord) which is made hollow by elongation of neural tube. Therefore, mesodermal cells of caudal eminence are not forming the caudal end of neural tube.
Let's see the process of neural tube elongation from the citation given in the Gray's textbook:

Abbreviation used can be seen here
Schematic diagram can be seen here


text:
How do baby birds get fed when they are only a day or two old?
The eggs belonging to the robin on my porch hatched. The baby birds are very tiny, just lumps. They are not opening their mouth and cannot even seem to lift their heads. How do they get fed when they are so helpless?

The hatchling's neck muscles are stronger than you think, because hatching from the egg requires strong neck muscles. Newly hatched songbirds and others do indeed open their mouths after they have had sufficient rest following hatching, though you don't seem to have witnessed this. They have little neck control and their heads wobble initially, but feeding is so important that they are born with this ability.

Songbirds and most seabirds have altricial young, meaning that the newly hatched birds are blind, featherless, and helpless. Immediately after hatching, altricial birds can do little more than open their mouths to beg for food. They remain in the nest where the parents can feed and protect them while they continue to develop. For the first week of life, most altricial birds cannot control their own body temperature and must be constantly brooded (kept warm) by their parents.

This makes sense, as most altrical birds only spend about two to three weeks before flying off to start their own separate lives.
Newly hatched poultry chicks (precocial birds, which also include ducks and sea birds) can live for 48 hours on the last of the egg yolk that they take in just before the strenuous work of hatching out of the egg.

Incubation periods are longer for precocial birds than altricial birds, allowing for increased embryonic development in the egg, and therefore they have relatively advanced motor and sensory functions at hatching.

Feeding poultry is actually not necessary during that time. The chicks are strong enough to stand, drink, and peck for food soon after birth, but it's not necessary for life. What they cannot do is regulate their body temperatures well.
Nesting Cycle


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Prokaryote or just a small worm
In the following photos can be seen a thread-like (almost like longkou vermicelli) things. At first I was convinced that it was cyanobacteria, however a classmate said it look more like a little worm, and other person said it look like it was probably nothing (nor prokaryote nor worm). I can't find a way to settle what it is, how can I know?

Zoom 40x
This is from another sample

EDIT:
Could the first one be lyngbya? I found this website and the second to last picture kind of looks like what it is in my picture:
And also could my second picture depict nostoc bacteria?

The first picture shows something different than the two following picture, doesn't it? Did it move? What is the zoom? You might want to review a little bit your knowledge about the diversity of eukaryotes (incl. unicellular eukaryotes).

If it doesnt have a mouth and anus and organs it's not a worm.

@Remi.b I added that the zoom is 40x. It didn't move, at least not enough for being noticeable. I agree that I need to study about the diversity of single celled organisms, but why do you say eukaryotes? is that a hint? I thought it had to be a procaryote since it sort of look like a very long bacillus. Also, I was convinced it was cyanobacteria, but now I doubt it

What was the source of these creatures?

@Tytoalba Pond water... very dirty pond water

@AnaGalois Because you talk about worms! A worm is a eukaryote. You uploaded twice the same picture. The first picture was maybe the most interesting you might want to make sure to upload it as well.

@Remi.b Right!!! I'm sorry. Yes  I'll upload it again, however it is from a different sample

This would be a suggestion rather than a precise answer.
Your sample being pond water a highly probable candidate of the first two photographs would be Euglena sp., though the red eyespot is not visible.
They are freshwater Excavates   and according to Washington State Lake Protection Association a common pollution-tolerant genus in Washington water bodies.

Another picture reference: A website

I think Euglena is a good guess for one of the things in the picture, but I don't think that's what OP meant by "like longkou vermicelli"

:P I missed that.

Thank you. I also added another picture I found on the web, perhaps those two are related?


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Retrieve the associated annotation from Uniprot
I have a dataset that I extracted using Cytoscape and STRINGAPI
Hoz can I retreive the annotation of that network from uniprot  as it has more than 1k proteins . and doing it manually is not possible

Do you want anything specific from the annotation?

not really but it should contain the name the associated id , function maybe ...

You can upload your list of accession numbers to the batch retrieval service for the UniProt Konwledgebase, http://www.uniprot.org/uploadlists
A video tutorial for this service is available at https://www.youtube.com/watch?v=kLdgjqWoMZc
Once you have retrieved your proteins, you can click on "Columns" to customize your output and add columns, e.g. for function annotation. See also http://www.uniprot.org/help/customize or http://insideuniprot.blogspot.ch/2015_03_01_archive.html
Results can then be downloaded in tab-separated format.
If you have any additional questions, please don't hesitate to contact the UniProt helpdesk.


text:
Trying to make a homogeneous phantom
I am making a T1 weighted phantom for an MRI project. It consists of distilled boiling water, 7g/L agar, 10g/L NaCl and 1g/L CuS04. As the phantom cools it will get a jelly like texture. What I would like is for the phantom to be as homogeneous as reasonably possible when it solidifies. What do you think is the best way to do so?
I was thinking of having the mixture on a vibrating plate, or maybe a centrifuge or even just inverting the mixture at regular intervals. Any ideas would be greatly appreciated.

I don't know what a weighted phantom T1 is but having used soft agar I do know that 0.7% agar is extremely sloppy, sort of semi-solid. If it is present as a thin  layer on top of a standard 1.5% agar plate and you jerk the plate then the top layer will deform. This is with microbiology-grade agar, maybe less pure versions behave differently?

Hi Alan, that's from a recipe I saw before. But I've looked at other recipes and they say 2.3% which seems a lot more realistic! Thanks for confirming my suspicion!


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R Stringdb bioconductor
I 'm using STRINGdb package from biconductor to manipulate String database of ppi
I'm newbie and I don't find the documentation of the package useful for me .
I wanna extract the associated network of cancer fo example ,
I tried to used this function s <- string_db$get_term_proteins(terms_id,string_ids =NULL , enableIEA =TRUE )
and I don't know  what that terms_id attribute stand for .
second , is there a simpler way to get the full network using R interface  given in the url as an example
https://string-db.org/cgi/network.pl?taskId=2hQuabKoXe02

The terms_id is meant to be a vector of GO or KEGG IDs that annotate to the proteins of interest. As it's described, the method get_term_protein:

Returns the proteins annotated to belong to a given term.

My substantiation in part comes from the vignettes for STRINGdb that use terms in a separate set of functions like so:
>head(enrichmentGO, n=7)
term_id proteins hits pvalue pvalue_fdr
1 GO:0048545 383 15 2.337593e-07 0.000368020
2 GO:0006952 1286 28 3.806997e-07 0.000368020
3 GO:0002252 405 15 4.756829e-07 0.000368020
4 GO:0010466 234 11 1.767763e-06 0.001025745
5 GO:0045861 330 12 8.407161e-06 0.003765892
6 GO:0010951 228 10 9.735179e-06 0.003765892
7 GO:0002443 141 8 1.224368e-05 0.003839606
term_description
1 response to steroid hormone
2 defense response
3 immune effector process
4 negative regulation of peptidase activity
5 negative regulation of proteolysis
6 negative regulation of endopeptidase activity
7 leukocyte mediated immunity
>head(enrichmentKEGG, n=7)
term_id proteins hits pvalue pvalue_fdr
1 04115 66 6 9.969204e-08 1.475442e-05
2 04610 68 5 3.577966e-06 2.647695e-04
3 05168 174 5 3.254067e-04 1.605340e-02
4 01100 1161 12 5.277721e-04 1.952757e-02
5 04380 123 4 8.399948e-04 2.486385e-02
6 00590 61 3 1.197959e-03 2.638087e-02
7 05161 139 4 1.322517e-03 2.638087e-02
term_description
1 p53 signaling pathway
2 Complement and coagulation cascades
3 Herpes simplex infection
4 Metabolic pathways
5 Osteoclast differentiation
6 Arachidonic acid metabolism
7 Hepatitis B

And so usage would follow, for example, I want proteins that associate with cell growth, I can use c("GO:0016049") as my terms_id to retrieve that list.
library(STRINGdb) #load package

string_db <- STRINGdb$new(version="10", species=9606, score_threshold=0, input_directory="") #set environment, 9606=human

string_db$get_term_proteins(c("GO:0016049")) #use new environment variable to query the database, 0016049 refers to cell cycle just as an example.

Output (annotation column w/ text descriptions removed for brevity):
               STRING_id    term_id preferred_name protein_size
1   9606.ENSP00000002829 GO:0016049         SEMA3F          785
2   9606.ENSP00000211998 GO:0016049            VCL         1134
3   9606.ENSP00000212355 GO:0016049         TGFBR3          851
4   9606.ENSP00000216037 GO:0016049           XBP1          261
5   9606.ENSP00000216911 GO:0016049          AURKA          403
6   9606.ENSP00000221930 GO:0016049          TGFB1          390
7   9606.ENSP00000225792 GO:0016049           DDX5          614
8   9606.ENSP00000230732 GO:0016049         POU4F3          338
9   9606.ENSP00000238682 GO:0016049          TGFB3          412
10  9606.ENSP00000239462 GO:0016049            TNN         1299
11  9606.ENSP00000245479 GO:0016049           SOX9          509
12  9606.ENSP00000255448 GO:0016049          DCLK1          729
13  9606.ENSP00000256951 GO:0016049           EMP1          157
14  9606.ENSP00000258106 GO:0016049           EMX1          290
15  9606.ENSP00000258743 GO:0016049            IL6          212
16  9606.ENSP00000261023 GO:0016049          ITGAV         1048
17  9606.ENSP00000261918 GO:0016049         SEMA7A          666
18  9606.ENSP00000262017 GO:0016049          ITGB3          788
19  9606.ENSP00000263713 GO:0016049        EPB41L5          733
20  9606.ENSP00000263980 GO:0016049         SLC9A1          815
21  9606.ENSP00000264057 GO:0016049           DGKD         1214
22  9606.ENSP00000264279 GO:0016049          NOP58          529
23  9606.ENSP00000265136 GO:0016049           COBL         1261
24  9606.ENSP00000265362 GO:0016049         SEMA3A          771
25  9606.ENSP00000265371 GO:0016049           NRP1          923
26  9606.ENSP00000266058 GO:0016049          SLIT1         1534
27  9606.ENSP00000268182 GO:0016049         IQGAP1         1657
28  9606.ENSP00000270221 GO:0016049           EMP3          163
29  9606.ENSP00000272134 GO:0016049         LEFTY1          366
30  9606.ENSP00000276416 GO:0016049           BIN3          253
31  9606.ENSP00000278671 GO:0016049        LAMTOR1          161
32  9606.ENSP00000281321 GO:0016049         POU4F2          409
33  9606.ENSP00000283027 GO:0016049          NUBP1          320
34  9606.ENSP00000284981 GO:0016049            APP          770
35  9606.ENSP00000296388 GO:0016049         LEPRE1          736
36  9606.ENSP00000296755 GO:0016049          MAP1B         2468
37  9606.ENSP00000296875 GO:0016049           GDF9          454
38  9606.ENSP00000301067 GO:0016049           MLL2         5537
39  9606.ENSP00000303351 GO:0016049          ITGB1          798
40  9606.ENSP00000305133 GO:0016049          SOCS5          536
41  9606.ENSP00000306157 GO:0016049           IL7R          459
42  9606.ENSP00000306662 GO:0016049         ADRA1B          520
43  9606.ENSP00000307156 GO:0016049          LAMB2         1798
44  9606.ENSP00000307272 GO:0016049          RPTOR         1335
45  9606.ENSP00000316357 GO:0016049          USP9X         2570
46  9606.ENSP00000316543 GO:0016049          RAPH1         1250
47  9606.ENSP00000317257 GO:0016049          CPNE1          542
48  9606.ENSP00000322957 GO:0016049           PAK7          719
49  9606.ENSP00000324549 GO:0016049         CYFIP1         1253
50  9606.ENSP00000324560 GO:0016049           ULK1         1050
51  9606.ENSP00000324856 GO:0016049          STK11          433
52  9606.ENSP00000329623 GO:0016049           BCL2          239
53  9606.ENSP00000330382 GO:0016049          PDGFB          241
54  9606.ENSP00000332643 GO:0016049            NDN          321
55  9606.ENSP00000333982 GO:0016049          NDEL1          345
56  9606.ENSP00000334458 GO:0016049          GATA4          442
57  9606.ENSP00000335246 GO:0016049         ENTPD5          428
58  9606.ENSP00000337146 GO:0016049          ENOX2          610
59  9606.ENSP00000337332 GO:0016049          SIRT6          355
60  9606.ENSP00000337697 GO:0016049            DCX          441
61  9606.ENSP00000339740 GO:0016049         CAMK2D          499
62  9606.ENSP00000340820 GO:0016049           MAPT          776
63  9606.ENSP00000341940 GO:0016049           CAV3          151
64  9606.ENSP00000347906 GO:0016049          PRMT2          433
65  9606.ENSP00000348769 GO:0016049          ARIH2          493
66  9606.ENSP00000351049 GO:0016049           PAK4          591
67  9606.ENSP00000351591 GO:0016049          NLGN3          848
68  9606.ENSP00000351905 GO:0016049         TGFBR2          592
69  9606.ENSP00000353362 GO:0016049        CACNA1A         2506
70  9606.ENSP00000353582 GO:0016049           NRP2          931
71  9606.ENSP00000354558 GO:0016049           MTOR         2549
72  9606.ENSP00000354829 GO:0016049          SGMS1          413
73  9606.ENSP00000354877 GO:0016049           ULK2         1036
74  9606.ENSP00000355627 GO:0016049            AGT          485
75  9606.ENSP00000355785 GO:0016049         LEFTY2          366
76  9606.ENSP00000355896 GO:0016049          TGFB2          442
77  9606.ENSP00000357288 GO:0016049        LAMTOR2          125
78  9606.ENSP00000357470 GO:0016049           IL6R          468
79  9606.ENSP00000357494 GO:0016049           ROS1         2347
80  9606.ENSP00000359095 GO:0016049          PRMT6          375
81  9606.ENSP00000359729 GO:0016049         SLC9A6          701
82  9606.ENSP00000360973 GO:0016049          AGTR2          363
83  9606.ENSP00000360988 GO:0016049          LUZP4          313
84  9606.ENSP00000361423 GO:0016049           ABL1         1149
85  9606.ENSP00000362092 GO:0016049          RRAGC          399
86  9606.ENSP00000362717 GO:0016049           LHX2          406
87  9606.ENSP00000363822 GO:0016049             AR          920
88  9606.ENSP00000365663 GO:0016049           NPPA          151
89  9606.ENSP00000366396 GO:0016049           XRN2          950
90  9606.ENSP00000367123 GO:0016049         SLC3A2          631
91  9606.ENSP00000367830 GO:0016049          PRKCZ          592
92  9606.ENSP00000368030 GO:0016049         ATAD3A          634
93  9606.ENSP00000368169 GO:0016049           DVL1          670
94  9606.ENSP00000368683 GO:0016049           EDN1          212
95  9606.ENSP00000369014 GO:0016049           NDNF          568
96  9606.ENSP00000369816 GO:0016049           SHBG          402
97  9606.ENSP00000369960 GO:0016049         ADRA1A          475
98  9606.ENSP00000370330 GO:0016049        ERBB2IP         1371
99  9606.ENSP00000376800 GO:0016049           MTPN          118
100 9606.ENSP00000377823 GO:0016049          NDRG4          391
101 9606.ENSP00000377947 GO:0016049           RARG          454
102 9606.ENSP00000378306 GO:0016049         PPP3CB          525
103 9606.ENSP00000379003 GO:0016049          NUPR1          100
104 9606.ENSP00000385610 GO:0016049          MEX3C          659
105 9606.ENSP00000395359 GO:0016049          CADM1          442
106 9606.ENSP00000411672 GO:0016049       ATP6V0E2          213
107 9606.ENSP00000414303 GO:0016049           BDNF          329
108 9606.ENSP00000419782 GO:0016049           CDK5          292
109 9606.ENSP00000422591 GO:0016049          SLIT2         1529
110 9606.ENSP00000427941 GO:0016049       ATP6V0E1           81
111 9606.ENSP00000430333 GO:0016049          SLIT3         1523
112 9606.ENSP00000465742 GO:0016049        RASGRP4          673

so If I want to retreive the protein protein interactions I use the same function , or should I use get_proteins() or get_interactions() function ? apperently the function get_term_proteins() isnt the right one for my needs

So let me first figure out, what data are you starting with? Do you have a list of genes already that you're just trying to figure out their interaction network? In that case you can try the get_link() method to get a nice output directly from the STRINGdb site.

I don't have an interaction network in mind yet , actually I'm looking for a 3k 2k network , I'm thinking of cancer for now . Do you know any genes (proteins ) where I can get this volume of data ?                                           ps : you mean get_interactions() method?


text:
What tree is this?
Can you please help me to identify this mystery tree. I have been trying to identify it for four years (Leafsnap app didn't help). Here are a few things about the tree.

All the leaf veins are parallel. They remind me of a dogwood tree, but it's not a dogwood tree.
The leaves are very small, about 3 cm in length, 2 cm wide.
Here is a ripped leaf.
The leaves grow together from a joint point.
Here is another picture:
There are some flowers, but they don't look like flowers. They look like tiny green buds. They smell like honey (or this is just my imagination), but no petals ever show up. The flowers are extremely tiny, all grow from a joint point.
After blossoming (if you can call it this way) there are no berries or fruit. All the seeds mysteriously disappear.
The bark is black.
The tree is not tall. It equals an apple tree in size.
It is growing in Eastern Europe, but it was planted by someone. It is not a native plant and there are no plants like this around.
It's deciduous. The leaves are gentle and soft, not like apple or pear tree leaves. The leaves are not shiny.

I am attaching pictures of leaves and flowers. If you need a picture of a tree trunk, let me know, I can take some as well.

Where is it from?

Right now it is growing in Eastern Europe, it was definitely planted by someone, but the tree is definitely not native species. It's the only tree like that I have ever seen my whole entire life.

Okay, I will take one soon and post here.

It's deciduous, of course.  The leaves are very soft and gentle.

I added a picture of a ripped leaf. It is a zigzag clean break, no stringy strands.

It looks like a Purging Buckthorn (Rhamnus cathartica) - Native to Europe and North Asia. It is the food-plant of the Brimstone butterfly.

See Woodland Trust
If it is isolated from others perhaps it is rarely pollinated and never produces berries.

From http://www.sussex-butterflies.org.uk/conservation/allotments/
It is unusual to see such a large specimen but here is a photo taken in Oct 2016 at Kingley Vale National Nature Reserve in West Sussex, UK. The vale has many Purging Buckthorn of a mature age and size as shown in middle of the photo with people to give some scale. Well worth a visit if you ever get a chance, it is one of Europe's most impressive yew forests.

https://en.wikipedia.org/wiki/Kingley_Vale_National_Nature_Reserve
See also http://www.hainaultforest.co.uk/5Purging%20buckthorn.htm

I too suspected this species but its leaf size is larger than OP's leaf  (if 3cm is not an average lower limit). Size

Maybe it is undergoing senescence and its leaf size is naturally diminishing?

If this is Rhamnus cathartica, it must be one of the biggest ones I have ever seen. I only know it as a small shrub, up to 5 meter max. Can't it be another Rhamnus species?

Added a photo of Kingley Vale where there are many large Purging Buckthorn 'trees'. Of course, yes it could be something else.

First and foremost I want to thank you for trying to identify this tree. I believe you are on the right track and it is most definitely some buckthorn. The only two things that puzzle me are: 1. the leaves are very tiny. Like 2x3 are the biggest leaves out of the bunch.

I never saw it fully bloom. Like those little green buds stay there for a week and then they mysteriously disappear. The buckthorn in your picture has flowers. Could my be male? Also, my tree looks like an actual tree where buckthorn is more like a shrub.  Wiki says buckthorn is spiny. "My" tree does not have any thorns. Thank you for your guess. It's nice to know that somebody actually can identify this tree. You are amazing.

@treehugger Buckthorns can lack spines.

Then most likely it's a buckthorn, just a very old one.


text:
If your body can slow down your metabolism, why doesn't it do that all the time?
I've read that in cases such as in anorexia or a lack of food, the body slows down the metabolism to preserve the little food it does get. If it can do this, though, why doesn't it keep your metabolism slowed, preserving energy? Are there effects to slowing down your metabolism?
Edit: I read it in various realistic fiction books about anorexia, which claimed to have accurate medical information. One was Wintergirls, by Laurie Halse Anderson, where the girl with anorexia says she has a slow metabolism, and her doctor mother says something to the effect of "your body's slowed down your metabolism because it thinks you're in a famine."

Low metabolis-> Low ATP. ATP is needed for activity so more activity-> Need of more ATP. Since we didn't need to be very slow like a sloth , therefore our metabolism is not less always.

If I have time to answer I will... but the short answer is that when your body "slows down" metabolism in times of starvation or famine, that also halts growth and reproductive functions as well. Maximal growth and reproduction require an individual with sufficient energy stores.


text:
Mealworm beetles in my attic
I'm having a problem which has been troubling me for the second straight summer. Since 2014 I'm living in my parents attic. I had a very small bedroom and since I had my first girlfriend at that time I wanted a bigger bed. The first two years nothing seemed to be wrong. But last year around June when I came home and wanted to sleep I saw all these little insects on my bed. Pretty weird ofcourse, but since my room was a mess(food,clothes,etc.) I thought it was just because of my bad habits. Since then every day when the temperature was 25 degrees celcius or higher these insects appeared. They came from under my bed, they were in closets, they literally came from everywhere. Not during daytime, but around 10/11 am. Since our attic has this crawling space all around it in which we store stuff we almost never use I thought they had a nest there. But when I crawled through it I couldn't find anything. After some research I found out that this creature could be a mealworm beetle. I bought some insect spray and it all around the baseboard off my attic. I also sprayed some other places where they could be hiding. This worked for a day or two before they came again. The problem is that I never have established where they came from. So they just kept on coming until around September.
All of this kept me from sleeping a couple of hours every week, not to mention the graveyard off all these little creatures(I think I killed around 100 of them by directally spraying insect spray on them or other methods). Ofcourse I also found alot of them the morning after killed by the spray.
A couple of minutes ago I found the first one of this year. It was pretty high on a wall(Around two meters) and I killed it by spraying the insect spray on it. It fell down and after a couple of minutes it gave up. I will also include a picture of the dead insect. Some other interesting things about these creatures were that they actually made sound when walking around and falling down. Also when I tried to flat one it made a bit of a crunching sound and it was pretty hard too.
I live in the Netherlands in a remote village.
Can someone confirm me these are in fact mealworm beetles and what is the best way to make sure my attic is not filled with them this summer again. I have a cleaned up room now with no food leftovers but alot of cables everywhere


text:
Found Skull(?) in Ontario Canada, help identifying please
skull?...now maybe thinking its a bird pelvis?...(I don't know thats why I'm here!)on the beach in Northern Ontario Canada, have been wondering what it is. Any ideas? As you can see it is very small, fits in the palm of my friends hand.
Thanks so much!
Kimberley,

An old post about Id-ing the same bone,Synsacrum .

Yes, this is a synsacrum, a part of a bird's pelvis. I would say it's from a cormorant, as I have found this comparison of different synsacra online (third from left):
No idea about the exact species, though.

Image source:
https://hiveminer.com/Tags/cormorant,skeleton

but is the OP's specimen large enough to belong to a cormorant? Please research a little more and update your answer with the expected dimensions/size of a cormorant's synsacrum if possible. Thanks!

@theforestecologist how does that help? It might be too small for an adult cormorant (even thought theres a wide range of cormorant sizes among the species), but who says it could not be a juvenile?


text:
Please help Identify these algae
Found this algae in a small stony stream that feeds a medium sized river. I can not identify either of the filamentous algae in this photo

A photo would help...

@GerardoFurtado sorry, just uploaded

Please add a location and the relative length /width. (and add a scale/let us know the magnification) . Thanks.

@theforestecologist, I do not know the relative size, but that is 40x magnification. I apologize all i have access to is my high school science lab

@theforestecologist This sample was from green algae growing on large granite rocks in a stream feeding the Dan river in North Carolina

@northcarolinaalgae you could mention that in the question.


text:
Are mutations accumulating far faster than selected out?
I just want to see the mutation accumulation rate in human populations. Versus the rate at which mutations are selected out. Just wanted to check if the genome is deteriorating

Welcome to Biology.SE
Is the rate at which new mutations occurring higher than the rate at which alleles fix today in humans?
Human populations are exploding! Genetic diversity within a population is a function of the effective size of its population. As the population expansion in human is extremely recent, we ought to expect that our genetic diversity is much lower than what would be expected from our population size and structure. Therefore, yes, genetic diversity is currently increasing, or in other words, more mutations appear than there are alleles that fixed.
Is the genome deteriorating?
I am not sure what you mean by "the genome is deteriorating" but the answer to "Is the genome deteriorating?" is likely no!
Actually, larger populations tend to suffer from less drift load and as such our mean fitness would rather be increasing. However, given the population size, I doubt that would make such an important difference.
On the other hand, medicine is greatly affecting our environment and is reducing the strength of purifying selection. As a consequence, modern populations would eventually be less fit than our ancestors if placed in the environment experienced by our ancestor (that is an environment with little to no medicine). But this will not be true in our current environment.
Prerequisite to understand the answer
This answer felt quite introductory but it actually contains all the following concepts:

Allele
Allele fixation
Genetic drift
Effective population size
Population structure
Drift load
Purifying selection
Genetic diversity (typically defined as the expected heterozygosity)
Effective population size
Environment (and even niche construction)

If any of the above concept is unclear to you (and I very much suspect that at least the term "drift load" will be new to you), then you might want to start with an intro course to evolutionary biology and population genetics.

Yes it is of course deteriorating, as can be proven with simple math, see for example Lynch (2009) or this later paper by Lynch (2016).
Thus, although there is considerable uncertainty in the preceding numbers, it is difficult to escape the conclusion that the per-generation reduction in fitness due to recurrent mutation is at least 1% in humans and quite possibly as high as 5%. Although such a mutational buildup would be unnoticeable on a generation timescale, over the course of a couple of centuries (approximately six generations), the consequences are likely to become serious, particularly if human activities cause an increase in the mutation rate itself (by increasing levels of environmental mutagens). A doubling in the mutation rate would imply a 2% to 10% decline in fitness per generation, and by extension, a 12% to 60% decline in 200 years.

So, this means about 6000 years after the world was created we'll be unfit to do anything? ;)

@JollyJoker I am not sure what you are referring to when you talk about the creation of the world but if you refer to either the big bang or the agglomeration of matter that ended making earth what it is, then there was no life 6000 yet years after that event. There was therefore no "we" whatever "we" may refer to in your comment.

@Remi.b Just jokingly referring to young Earth creationism

@JollyJoker Fair enough. I should have known given your user name!


text:
In the event of an abrasion, do mast cells cause vasodilation or vascular constriction?
Or both? I am unsure as to what mast cells will do in the event of a wound either on the epidermis or the epithelial. I know they secrete factors that mediate vascular constriction / dilation, but I can't find information anywhere as to what they do in the area where the wound is located.
Based off my current understanding, this is what I think happens:
Wound. Mast cells release mediators that cause constriction around the area of the wound, but dilation further upstream to increase the delivery of essential leukocytes (white blood cells), plasma and red blood cells.
Any help is greatly appreciated!


text:
Why don't we feel hungry after waking up?
Yesterday, I was fasting (drinking only water until I had dinner at 9 pm). After dinner, I went back to my lab (I am a Master's student) and worked till 1:30 AM. By 1 o' clock, I was feeling quite hungry, probably because I hadn't eaten anything all day and only had a light meal for dinner. However, I didn't eat anything then and just slept. Today morning I wake up (around 9 AM) and I don't feel hungry! I could surely eat something if I wanted, but I am not feeling the acute hunger that I was feeling last night!
More generally, what could be the reason for the behavior that a human experiences acute hunger, but after sleeping for an extended period of time, he/she may no longer have the hunger. Since a passage of time has passed, one would expect the hunger to increase, which would have certainly happened if the person had not slept. Is it the case that sleeping somehow affects the overall hunger/glucose demands of the body?
I suspect that it is possible that the body's food needs could be majorly affected by the circadian clock, but I wanted an explanation to contrast the situation when one is not hungry and when one is very hungry before sleep. How can the difference between both the situations be easily trumped by the circadian rhythm's effect? (if it is the explanation!)

Do u think its normal to feel hungry when we wake up?

@JM97, no its not. but the interesting question then is, that it means that the hunger situation of the body before sleeping seems to have no bearing on the hunger situation post sleeping. This I feel would warrant an explanation

@another'Homosapien', I have edited the question to make it more specific and non-personal (and interesting, i think!). Could you have a look?

@JM97, I have tried to do now. Feel free to edit to improve it

Yeah, rewording seems to have made it better. I have voted to reopen this (in fact, I voted to close as I thought I would have chance to retract my vote by the time you edit it, but this was too fast :P). And, I can answer this as soon as the question opens again :)

My suggestion is to perform this ritual repeatedly and record your hunger levels several times. This might give you a better picture, and might help us make a clearer analysis

I will try to keep the answer as simple as possible, but feel free to point out if I make this too simple.
Well, you are not alone with this observation. This is quite a common, but rather complex, phenomenon which controls our apetite and causes us to not feel hungry after waking up.
The feeling of being hungry is under constant regulation by two antagonistic (having opposite effects) hormones:

leptin, released from adipose tissue, decreases our apetite and suppresses our hunger
ghrelin, released from stomach, does just the opoosite i.e. increases our hunger.

And guess what, these hormones are controlled through the circadian cycle. When you sleep, your body produces more leptin and stops the production of ghrelin. Why? The answer is quite obvious: because you're sleeping. While sleeping, your metabolism is lowered because your body needs to repair the damaged cells and tissues. To control metabolism, we need to control our apetite, and to control our apetite, we need to suppress our hunger. So...? When you wake up, you still have a hangover of this effect. In other words, it takes some time to change the secretion rates of leptin and ghrelin and the resulting effects.
Lets get into some analytical details now. According to Sharma et al, 2010, metabolic rate and brain temperature are lowered during non-REM sleep to deal with the damages that may have occured during time of wakefulness. In their study, the subjects were deprived of sleep for 2 nights (4 hours per night) and then allowed to sleep for next 2 nights (10 hours per night). The result? Leptin levels decreased by 18% and ghrelin levels increased by 28%. The subjects also craved for more carbs. Also, craving for salty foods increased by 45%. Overall hunger increased by 23% due to reduction in leptin levels. They also showed that people who sleep less than 5 hours have increased Body Mass Index (BMI). All this points to the fact that sleep does cause reduction in apetite and hunger. In short, don't think of missing your breakfast.
References:

Sharma, Sunil; Kavuru, Mani (2 August 2010). "Sleep and Metabolism: Overview". International Journal of Endocrinology. 2010: 1–12. doi:10.1155/2010/270832.
Wikipedia contributors. "Sleep and metabolism." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 8 Feb. 2017. Web. 26 May. 2017.

so if you're hungry and you can't eat, just sleep! BTW, you can't suppress hunger by sleep for long, right?

Yeah, when the body really needs energy, it will cause you to wake up. Also, IMO normal sleep duration is not enough to deplete body's food reserves. "If you're hungry and you can't eat..." I must say I didn't get that :/

i meant that if you are hungry and have nothing to eat, you can just sleep as it would reduce the hunger. is this right?

Seems you used (kinda) improper words here. I'd say if you are hungry and have nothing to eat, you can just sleep as it would 'delay' your hunger for some time. ;)

yes, fair enough

of course! just want to give it a couple days before accepting, for obvious reasons


text:
Is human genome editing more complicated than mice genome editing?
A lot of genome editing trials are being done on mice and rats, but I often read that the step from mice- to human genome editing is complicated. What are precisely? I guess it has something to do with human's more advanced immune system, but I would like to have a better general understanding of this.


text:
How many molecules NADH are produced in the Krebs Cycle?
I don't know which source i'm going to follow.
Some say its 3 molecules NADH per cycle → 2 cycles × (3 NADH) = 6 NADH
Some say its 4 molecules NADH per cycle instead?

This question is not off topic for the reason you chose. OP is clearly asking: "there are two different information out there, which one is correct?" The main point in this question is: is respiration divided in 3 or 4 phases? That is, dehydrogenation of pyruvate is part of Krebs cycle or not? That being the case, the question is clearly valid and useful, as you can see by the number of upvotes.

This is slightly depending on which reaction you want to include into the cycle. I count four:

One when Pyruvate is converted to Acetyl-CoA,
one when Isocitrate is converted to α-Ketoglutarate,
one for the reaction of α-Ketoglutarate to Succinyl-CoA and
finally one for the reaction of Malate to Oxaloacetate.

If you see the reaction of Pyruvate as happening outside of the cycle, it's only the later three.
See this image (from here) for an overview:

The alpha-ketoglutaric dehydrogenation to form Co~A.The NADH energy is released.Therefore 6 molecules of NADH is produced
You can see the above picture to understand better.

This question already has a good answer, upvoted by the community. Even so you decided to write an answer which not only is poorly worded and confusing but it is also wrong.


text:
Name and Behaviour of Arthropods near a Cactus
Background Story
I have a small, old cactus on my sunny, south-facing window sill in southern Germany. Since a few years, small black dots gathered around its pot. At first, I thought the dots were dust or sand and wiped them away. But the dots appeared again and again, so I had a closer look at them and saw that they were tiny insects or arachnids, probably lice or mites. We just call them arthropods from now on.
More information
The following picture shows my cactus with some of the arthropods around the pot. Click here for higher resolution.

Here are some close-ups.

The arthropods seem rather dead. They do not move and most of them lie on their back. However, they are not dead. Once they are picked up and set on a paper towel they start to move. If they get on their legs (with a little help) they walk around, which can also been observed by the naked eye.
I inspected some individuals using a detached camera objective as a magnifying glass. The arthropods are brown, shiny, somewhat translucent, and have 8 legs. I could recognize a small head without a neck (like most bugs have) but couldn't recognize a mouth or eyes – probably because of the size.
I couldn't take a picture, but tried to draw what I saw:

Later I got hold of a cheap microscope and took a few videos. The video quality is miserable. In reality, the arthropods are not that dark, see my drawing and the photographs.
Here's on individual laying on its back, flipping over, and walking away.

Here's another individual walking.

The Strange Part
As said, the arthropods keep on re-appearing around the plant pot. But in all those years, I never saw any of them on the pot, inside the pot, or on the cactus. I also have other cacti right next to the "infected" cactus, but their pots were never surrounded by the arthropods.

Question
What are these arthropods, where do they live, and why do they leave their habitat?
My Theory
I suspect the arthropods to live inside the dead and cracked part of the cactus. They could walk on the spikes of the cactus and jump from the ends of the spikes to the ground. If they land on their backs, they cannot get up and stop moving after some time.
I don't think that the arthropods live inside the soil. Two reasons for that:

The arthropods could have drowned often. From time to time I put too much water in the pot, such that all soil is fully covered by water, often for more than 8 hours (yes I know that can't be good for a cactus *cough*).
In order to get to the window sill, the arthropods would have to walk quite a while. Over time, I should have seen at least some of the arthropods on their way to the outside world.

There are some kind of ticks according to 8 legs and lack of segmentation.  And they can live in the soil despite the drowning and damage the cactus roots.

It's hard to tell from these photos (you'll need a macro lens for good shots), but they seem indeed to look like mites (Acari).
There are mites that feed on rotting cacti, Bonomoia opuntiae for example. There is a film here about this cactus mite.

Thank you for your answer! It's very interesting to see that new species are still discovered today. I don't think that the mites from the video are of the same species as the mites from my cactus. The mites from the video have long legs that are evenly spaced along the body. The mites from my cactus are darker and have not so long legs that are attached near the head.
I am sorry that I cannot provide better images.

The mites in the video are probably not the same species, but your cactus neither. Maybe each cactus species has its own specific mites? I don't know if a real entomologist is present on this site.

In the last weeks I haven't found any of the mites. It seems like they are gone since I moved the cactus from the window sill to a shadier place.

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


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Whitening of hair at old age
Human beings have evolved from their ancestors to their modern forms adapting many changes in structure and I would assume that every change has a significance.
So, what is the cause of our hair turning white at old age? Was it meant for frightening away predators at old age when our body is weak? Or what is it actually?

Not everything what changes has a significance. It can also be neutral - as for whitening hairs. Hairs grey and eventually whiten due to the loss of pigment, nothing else.

It would be incorrect to assume that

every change has a significance

from an evolutionary point of view. In many cases, the changes could be happening at an age where it does not affect it's selection, since it's past the reproductive age. This could certainly be true for greying of hair.
If you want to understand from the point of view of an evolutionary theory, there are at least two possible explanations. One is the Mutation Accumulation (MA) theory. It says that mutations causing late life deleterious effects can build up in the genome more than diseases that cause early life deleterious effects. This is for the simple reason that cases of the latter would be eliminated as they will usually affect in the reproductive period, but chances of a 60 year old grey-haired man to have offsprings is low. In essence, if a trait reduces survival in the post-reproduction period (which is the case here), then the effect of selection is weak for it. So, since grey hair arrive so late, they might not really be selected out.
Another is the Antagonistic Pleiotropy theory. Pleiotropy means a single gene having more than effect. So it says that if a gene improves fitness early on, but causes an undesired effect later in life, it will be selected for in the population. This is simply because the later deleterious effect does not affect the advantage the gene provides at the stage were reproduction happens. So, it is possible that the gene responsible for grey hair may also be making you more fit.
So, in summary, there seems to be no direct advantage of having grey hair. It could be the result of Mutation Accumulation, or the antagonistic pleitropy effects of the responsible gene.
You can read more about it in this and this answer.


text:
Determine the chances of blood group type and rhesus factor of unknown parent?
First of all, I'm not a biologist so my jargon might not exactly be common on this site. I'm a programmer and as a hobby project I try to make an algorithm that does two things:

Determine the possible blood group and rhesus factor of a child based on the blood groups and rhesus factors of both parents.
Determine the possible blood group and rhesus factor of an "unknown parent" based on the blood group and rhesus factors of the child and the known parent.

I found two great examples online, the "Child Blood Type Calculator" and the "Parent Blood Type Calculator" calculator on endmemo.com.
The first calculator shows some percentages of the chances. But the second calculator does only show a static answer when it comes to the blood group type and rhesus factor. According to the calculator that indicates that the rhesus factor of the "unknown parent" can only be negative when both the child and the known parent have a negative rhesus factor too.
In case the known parent and child have both RH+ the calculator shows that the unknown parent must have had RH+ as well. But isn't the statistical chance  6.25% that the unknown parent still have had RH- instead?
Secondly, how can I calculate the likelihood/chance that the unknown parent has a certain rhesus factor or blood group type? Now the calculator shows 'A/B/O' and 'RH+' when the child has 'O+' and the known parent has 'O+' but what are the chances the unknown parent has A, B or O or RH- anyway?
Side-note: I'm not related to endmemo.com.

I see you know PHP, thus I believe you're gonna easily understand my answer explaining the problem with that site, if statements are pretty standard in most languages I'm aware of.

Simple explanation: that "Blood Type Calculator" is wrong.
Inspecting the source code of that page we can find the if statement that chooses the outcome for the unknown parent, regarding the Rh factor. And it has a problem. Whoever knows JavaScript will understand the problem, but even people that don't know programming languages can follow this, it's not complicated. Let me explain it.
When you choose the Rh blood type in the dropdown menu, the Rh+ blood is associated to the value p and the Rh- blood is associated to the value n. Those are just strings, the programmer can chose any value he/she wants, that's not important, as you know. The variables that hold those values are msel2 for the known parent and csel2 for the child.
Now comes the if statement:
var frh = "+";
if (csel2 == "n" && msel2 == "n") frh = "-";

Let's break it down:
The default value that will be printed on the result, called frh, is + (positive), as you can see before the if statement. As already said, msel holds the value for the known parent, and csel holds the value for the child.
In the if statement, only if the user chooses the known parent type as Rh- (msel2 == "n") AND the child as Rh- as well (csel2 == "n"), the value of frh will be changed to - (the double && represents the AND). Any other combination will not change frh, which will remain +.
And that's plain wrong!
There is no need for me to explain you the genetics of Rh factor, there are plenty of resources online and answers here at Bio SE as well, but here is a summary:
Given that Rh+ individuals can be either DD or Dd, it's easy to show that the unknown parent can be Rh- in case that the known parent and the child have both Rh+:
(Known parent)     (Unknown parent)
    D_ --------------- dd
              |
              |
             Dd
           (Child)

The lesson to learn here: don't trust everything you find online.
Correct algorithm:
For your second task ("Determine the possible blood group and rhesus factor of an "unknown parent" based on the blood group and rhesus factors of the child and the known parent."), let's see all possible cases:

Known parent Rh+ and child Rh+: the unknown parent can be either Rh+ or Rh-.
Known parent Rh+ and child Rh-: the unknown parent can be either Rh+ or Rh-.
Known parent Rh- and child Rh-: the unknown parent can be either Rh+ or Rh-.
Known parent Rh- and child Rh+: the unknown parent has to be Rh+.

As you can see, in only one case the unknown parent cannot be either Rh+ or Rh-. That being said, this is a possible solution:
var frh = "+/-";
if (csel2 == "p" && msel2 == "n") frh = "+";

What this snippet does is this:
It assigns the default value for the unknown parent (frh) as +/- (meaning that he/she can be Rh+ or Rh-, we can't know) for all possible combinations. However, if the mother is Rh- AND the child is Rh+, that value is changed for + (because, in that situation, the unknown parent has to be Rh+).

Thanks a lot, you confirmed my thoughts on the wrong "calculator". The ABO group algorithm works like a charm already. But the one thing that I'm stuck with is the chances of Rh+ / Rh-. I get your "Correct algorithm" but does that mean it's always a 50/50 chance? I'd like to use percentages, just like the ABO group calculator in my example. I'm not sure if it's possible with the rhesus factor. Can it be more accurately determined in some cases? (For example: not 50/50 but 80/20)?

Nope, saying "+/-" doesn't mean 50/50, it means only that the unknown parent cannot be determined: he/she can be either + or -. To have a better estimation of the probabilities one has to know the frequencies of the alleles in the population, which is certainly out of the scope of such "calculator".

so with child/known parent being +/+, +/- or -/- the chances of the unknown parent having either + or - are (because it's unknown, statistically 50%) in the three cases? Or can is be more "confident" in a certain combination? Cause a 50/50% estimation seems quite useless. The only useful thing to "predict" is the -/+ relation. 2. Is the outcome -/+ relation always 100% + or can (as a rare exception) the outcome be - anyhow?

I'll say the same thing I just said in the previous comment: it's not a 50/50 estimation. And it is not useless, as you said: eliminating some genotypes is very important in genetics.

Ok, so not 50/50 but chances cannot be determined? I would expect that based on the known parent and child, at least some kind of "confidence" percentage could be estimated.

No, it cannot be determined, unless you have all the allele frequencies in that population (as I said in my first comment) and assume some conditions, like random mating between the individuals for instance. Again, totally out of the scope of such calculator. If you want, you can post a new question like this: "How to determine the chances of the father being Rh+ or Rh- when the mother is Rh+ and the child is Rh-?", and see what people will answer.


text:
Can exercise strengthen tendons and ligaments?
Is is possible to strengthen tendons using exercise to prevent injury, for example preventing shoulder dislocation?

I don't have the background to give a definitive answer, but it would make sense if especially tendons and maybe ligaments grow stronger through exercise... otherwise the risk of tendon damage should increase sharply as a function of muscle strength. I recall having heard/read somewhere that abusers of steroids have increased risk of tendon damage due to a too fast gain of muscle strength. Maybe someone can elaborate with a better answer.

yes..It takes approximately 10 weeks of regular resistance exercise to strengthen your tendons, and it takes longer for them to thicken. You can expect up to 20 percent increase in strength and thickness of your ligaments and tendons with regular training.

Can you add some sources for your information? Unreferenced answers are frowned upon here.


text:
How can my sister have dark brown eyes, while my parents have blue eyes?
Both my father and mother have blue eyes, just like me. But my sister has dark brown eyes, contrary to what I've read about the dominance of brown eye genes and recessive blue eye genes. What happened (apart from the possibility that my mother dated a brown eyed guy from which she was born, which for sure didn't happen because we both look like our father and mother; though you never know with those Italians...) that gave her those dark eyes?

A related 5 year old post.

you can visit this page it's fully explained how blue eyed parents can have brown eyed children by just - carrying the gene -http://genetics.thetech.org/how-blue-eyed-parents-can-have-brown-eyed-children

Another post.

And what would be the answer? I can't infer it from what is written there. Besides the question is about a man with blue eyes and a woman with brown eyes.

@descheleschilder The answer is that the simple "blue eyes are recessive brown eyes are dominant" explanation is wrong, because that infers that there is a single gene involved in eye color. That is not true.


text:
Biogrid interaction protein network
I need a ppi network for cancer or Alzheimer .
I'm using BioGrid , In the search field I can specify the gene id only ,
I want to know how can I make an interaction network for one of the disease ? the only condition is the network ought to be huge , 3k 2k proteins .
I had used IntAct , String but none seem to give me what I'm looking for
If not could anyone give me a direct download link of such network


text:
What is operating temperature of the human brain?
I've heard several times that human brain can die in temperatures over 40 °C, or under 10 °C, as an engineer I'm curious.
In what temperature region can brain properly work?
And just an underlying question what is a TDP (thermal design power) of human brain?

What did your research tell you, and how/why did it confuse you?

@anongoodnurse Most articles on this differ, and I wasn't able to find any that would have sufficient sample size (more than 1) or would be peer reviewed. Also I'm not very good at searching for medical papers, there is a chance I've missed something that would be good.


text:
Why does closing one eye in bright light allow me to open the other?
I often find it physically painful to open my eyes past a squint after stepping out into the full summer sun. However, if I close one eye entirely, I can keep the other open without pain. This seems odd. Naively, one would assume the pain results from too much light entering the eye and doing some sort of damage to the interior, but if this were true, closing one eye would have no effect on the other. Does the fact that it does imply the discomfort is actually related to (e.g.) the sum-total of information reaching the optic chiasma?

Not an answer but an addition to your question. Might help to achieve better results. As far as I can remember I have always closed my left eye in bright light. I am right eye dominant. This is in Indiana which is not extraordinarily high in UV light. I went to Guam recently and I found I could not open either eye without extreme discomfort. Guam is notably high in the UV spectrum. Sunglasses were a must at all times. I am Caucasian with blue eyes. In the latitude of Indiana I have not had extreme discomfort as in Guam but have had to close my left eye more than enough. As a Biologist, I hope

I do not think that there's any scientific reasons why, but it is like a reflex. Your brain knows we do not enjoy bright light in the morning, especially when the eyes weren't open for a long mather of time. It is why peeking slowly to give time to your iris to get adapted to the strong light. Some people open one eye at the time, some people opens both of them and blinks repeatedly.

I thought of this same question today. Wish there was an answer!

A couple of factors play into this. First, you're halving the number of nociceptors that are signaling the brain. Second, there is a psychosomatic effect. Your brain continuously combines the visual data from both eyes to form one image. With one eye closed, your brain combines the brightness of both inputs to form an image that is roughly half as bright as reality. As a result, your brain not only ignores a portion of the nociceptor signals from the open eye, but it also doesn't assume the presence of pain like it normally would.
I've no publicly accessible sources to cite, as this is something I learned in my EMT class. Someone actually asked your same question in class

This happens to me as well. Complete guess (and probably somewhat of a poor answer) but I think it has something to do with focusing problems (similar to an extreme astigmatism) jerking the eye muscles around.
Closing 1 eye removes the need for a coordinated focus, eliminating the problem.

your right eye is dominant making it a reflex to close the other which in this case is your right eye which is the "Weaker" one

Just A guess Sorry :(

If you could add some references, and expound, that would be good :)


text:
Where to download gene list of human genome?
I am looking for a place where I can download a full gene list of human genome. Either by HGNC symbol or ensemble ID as long as it is usable on the consensusPathdatabase. Up until this point I have only found fasta files which include a bit too much information and unfortunately not in the format I would like. I am not in the biology field myself so if I am asking for something unreasonable call me out on it!
Reason for this is I am trying to stress test an application that uses the output tabular forms from the gene set analysis tool on consensusPathbase. The stress test on the entire human genome seemed to be the best option as a bigger data set than that will probably not occur.
Thanks in advance

The database you are looking for is ensembl [Yates (2016)].
Go here and chose  Customise your download. There you can select a dataset (e.g. genes and then specify human genes - currently uses build GRCh38; you can also go the same way here to do the same for hg19/GRCh37).
After chosing your dataset, you can click on Attributes to specify what to include in your download (HGNC symbols, IDs, regions, GO terms, and a ton of other stuff), click on Filters to apply filters to your choices (only genes from a chromosome, region, and a ton of other stuff).
Then click Results and download your selection in a format of choice.
(Hint: click Count first and use it as a a sanity check to see if the number of selected genes fits your expectation.)

This is exactly what I was looking for. Thank you very much for the help!


text:
What industry regulations protect the privacy of DNA results in the US? (UK, or EU wanted as well)
I am writing computer software that allows users to learn more about their own DNA and (optionally) allow some of that data to be used for research purposes.
I'm very concerned about a future/theoretical situation in which an insurance company uses that DNA data to disqualify someone on the basis of pre-existing conditions.
Question

What privacy regulations exist that would assure users that there is no insurance risk in a collecting information about one's own DNA? (Primarily interested in the USA, but UK and EU would be valuable)
Outside of legal regulations, what should users look for when shopping among providers? (for quality, scope of services provided, etc)

There might be different regulations in different parts of the world. Maybe you want to specify a country/area.

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

That might be a question for Law.SE. I am voting to close for the same reason than canadianer

While the subject is biology based, ethics and laws are not... so I am voting for closure as well.


text:
How does blue, yellow and orange coloured light affect photosynthesis?
I've been conducting an experiment with different colored light and photosynthesis, and so far my hypothesis states that red light will grow the plant, green will slow or kill it, and white will grow it as normal.
I'm wondering what would happen with blue, yellow, and orange.
Thanks.

You know what they say, do the experiment and find out. Just remember to include controls.

Your thought process should revolve around optimal spectrum for photosynthesis, since whether that happens sufficiently will determine the health of your plant. Just poking around, I found this document.
What light will be usable for photosynthesis depends on which version of light absorbing protein is being used to capture energy from photons.
This diagram would indicate that pure yellow would be pretty ineffective for any pigment. Blue is fine, as is darker orange/red for chlorophyll A and B.
Keep in mind that a lightbulb, unless a very special one, will still have lots of other spectrum bleed.  It won't be a pure single color (even though it may look like a single color to your eye).

Another source from Khan Academy.


text:
Which organs can be donated after clinical death?
The information I found about organ donation does not address clinical death. For example:

The process of donation takes place only after physicians declare a
  person brain dead [...] cessation of brain function [...] is
  irreversible. However, the vital organs (heart, lungs, liver,
  pancreas, intestine and kidneys) can be kept viable for a few days, if supported by artificial mechanical means (i.e. a ventilator).
  (source)

However:

Blood circulation can be stopped in the entire body below the heart
  for at least 30 minutes, with injury to the spinal cord being a
  limiting factor. Detached limbs may be successfully reattached after 6
  hours of no blood circulation at warm temperatures. Bone, tendon, and
  skin can survive as long as 8 to 12 hours. (source)

Assuming the organs were not damaged by the cause of death itself, are there any organs that can be transplanted after clinical death?

It depends on why the patient died, and how long they were dead before the opportunity arises to harvest the organs. If you want to modify the question to narrow the scope, it is answerable. Death from a head injury on the highway or in the home - without any other significant injuries - provides the maximum potential for organ donation, with time being a critical component.

@anongoodnurse I'm actually interested in an answer covering the parameters you mentioned, assuming the organs were not damaged by the cause of death itself.

As the question stands, I think it might be too broad.


text:
Stringdb using R Bioconductor package
I need to retreive a large dataset from String-db.
I 'm newbie in R so even with the documentation , I could not get the dataset fron String
How do I do to retreive a network from String 2k to 3k proteins
what are the functions  to use for such matter  ?

I think this question belongs to [SO]

String uses REST API, although the link to the help page for that results in a blank page instead (contact the authors!). In general, I would use the API. Alternatively, just download the database locally, they have a quite neat collection ready to be downloaded

If I donwload it locally  , I can retreive 200k proteins ? and download the network I need right ?

Correct. Check the download page, they have different "packets" download the one you are interested in.

Okay I'm downloading the first packet in the interaction data section  for homosapien. What I don't get is that how am I going to use it ?  how would I know the proteins or the specific network for cacaner ?

It has 11353057 interaction , I have no Idea how to get only cancer network ?

You need to have list of protein you are interested in. There is no shuch a thing like a "cancer network" you may find different databases online, like the COSMIC, that lists genes found to be linked with cancer. You can start there. But this goes beyond your question.

Now I have alist of proteins of interest how do I proceed ? Is there any tool I can use to gget the 200k I need

If don't know how to start then please take time to study and try out. This forum is not meant to ask other people to do your job. One thing is if you have a particular question,  but you are asking to solve a rather complex bio information problem without knowing the basics. Now you have a database and a list of proteins of interest. Write down what is that you want to know about them and use the database to answer your questions. If you don't know how to do that than step back and start studying how to query a database with R.

Well thank you for clarifications, Actually I did and I used R to retreive neighbors , which got me 5827 mapping identifier, with 3916 interaction. yet I need more like 200k  mapping identifier to work with . and I have no clue how to proceed as the resources are so limited down there

Try ask on https://www.biostars.org It's specific for bioinformatics.


text:
Difference in callus formation during healing of bones of different origin
My study material from pathology states that during fracture healing after hemorrhage and coagulum formation the mesenchymal progenital cells from periostium that are closer to the fracture differentiate into chondrocytes and form hyaline cartilage, while the ones that are farther differentiate into osteoblast.
Result is production of hyaline cartilage in which enchondrial ossification and subsequent remodeling into lamelar bone occurs.
My question is: Does this enchondrial ossification also occur in bones in which Intramembranous ossification normally occur during development? (e.g. clavicle and some skull bones.)
NOTE:
in this stackexchange post and Wikipedia article on this topic, only chondrocytes are noted.


text:
How does a cell know what function it has within an organism?
Given that all cells in a multicellular organism contain the same DNA (ignoring random mutations during mitosis), how does any given cell know what purpose it is supposed to have within an organism.
For example, how does a cell know to become a muscle cell, a neuron or a liver cell?

As this is a very shallow question, I've voted to close. Search the topic "epigenetic regulation", and you will find your answer. If anything specific about this topic confuses you, please open a new question and we will be happy to help.

Your question is basically answered in a full semester course in Developmental Biology. It is far to broad for this forum. Suffice it to say it has to do with chemokine gradients and signaling producing differential translation in the cells of a developing multicellular organism.

The answer to this question can be split into two parts: cell differentiation from stem cells and simple mitosis. Also, the answer I am providing mainly only applies to species that sexually reproduce.
During the primary stages of growth, immediately following the fertilisation of the female gamete, the zygote begins to divide. Most of these initial cells will not be specialised, they will be stem cells and these have the potential to asymmeterically divide. When they do this, each of the daughter cells will have a specific specialisation path to follow. Which path they will follow, muscular, neural etc. is determined by transcription proteins.
Once the stem cells have produced the correct daughter cells, the general structure of the organism will begin to take form. Once this happens and the cells have followed their development paths until they hit their final specialisation, mitosis takes over. This means that a muscle cell will divide, causing the organism to grow. A muscle cell, will only ever divide into a muscle cell, the same goes for all specialised cells. This is how an organism grows and maintains itself.
However, some stem cells do remain after the organism has matured. For instance, a mature neuron is unable to undergo mitosis, so stem cells are needed to allow for the production of new neurons to replace those that die, to take one example.
You can find out more here.

But how is specific path recognized ? Arent the stem cell equiped with the same transcription proteins and DNA ? I assume for each type of cells there are different genes, how they will evolve, but the stem cell must be told which genes are to be translated.

@Marvin Cell fate is controlled by intercellular signalling. A lot is not well characterized. See this answer: https://biology.stackexchange.com/a/24022/6307

But yet, the signalling toggles the dna demethylation and histone modification, which changes genes promotors. So two same stem cells with different fate dont have same intracrine hormones at the begining ?


text:
What is this bird of prey?
I recently took a picture of this bird flying around Geneva, Switzerland:

In the beginning, and because it was bright and the subject was against the light, I though it was simply another Buteo buteo as there are many around here. Now by tweaking the brightness and contrast a bit in Lightroom, I can be 99% sure that it is not a Buteo buteo and my mind goes more to a Pernis apivorus, which is another bird of prey present in the region in summertime (May-Sep).
Can anyone tell me if I am correct and what field marks can be deduced from my picture to be sure that it is the right bird?

You can also tell that is an adult male, you can tell it from the very spaced bars on the tail and wings. Beautiful light individual.

Nice photo - Yes, I would agree with you the bands on the tail and the wings suggest that it is a Honey Buzzard Pernis apivorus
http://www.birdwatch.co.uk/categories/articleitem.asp?item=995
http://www.gobirding.eu/Photos/HoneyBuzzard.php

Photo by Dominic Mitchell http://www.birdingetc.com


text:
Picture of spider for identification
Would like to get spiders identified . Specimens can be sent for detailed examination if required .

Spider seen on floor inside house - at Phoenix USA

White off color spider on twigs and flowers of oleander tree with white flower in backyard of house at phoenix USA  - seen dropping off on disturbance and camoflouging with. White flowers. Picture can be magnified spider sitting on green stalk  below brownish dried flowers.

It is advisable to post one question(here specimen) a post.

The first is a male Theridiid, probably Parasteatoda tepidariorum (see below)

https://bugguide.net/node/view/1320395/bgimage.
The second is one of the "flower spiders" in the Misumena/Misumenops/Misumenoides/etc. group of Crab Spiders.  It would take a better photo to get closer than that, since this is a young female and isn't showing the color marks that make it easier to ID.  There's a hint of patterning on the abdomen, but it isn't clear enough to ring any bells with me.  In a comment below, I'll include a link to the Bug Guide page for these spiders so you can look at it - the relatively useful marks for field observation are the greenish bands (if any) on the sides of the cephalothorax, the 'mask' (if any) over the eyes, and the pattern (if any) on the abdomen.  Also, the reddish 'racing stripes' on the sides of the abdomen of fully adult females can be helpful in working out which spider it is.  I suspect that for most of us, most of the time, "Flower Spider" is going to be good enough.

Here's the link.  I'm not inclined to favor any particular species, offhand, without a better look at the abdominal pattern that appears to exist.  https://bugguide.net/node/view/1957/tree  My best guess is that it's likely to be somewhere between Mecaphesa (unlikely) and Misumessus.

The trouble with these (and many other) spiders is that it usually takes a good look with a dissecting microscope to get a confident ID.  You could send it to someone for such a check, but I'm no longer current with active spider folks, and I can't suggest anyone offhand.  What you could do is to do a search on "thomisidae" "research" or "taxonomy" and see what pops up.  Check recent papers for the authors' names, and write off to one or more to see if they would help.  Good luck!

White one: Flower crab spider white, They can be all white or have purple or even pretty red stripes along the sides, kinda cool.

Thanks.  Kinda cool  .  Further I would like to know its scientific name . Else if someone can suggest the contact to send the specimen to know it's scientific name .