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What is difference between "Syngonium" & "Pothos"?
They both look the same to me, but they are different from each other.
Please help me in figure out the difference in both of these species.

Probably their genome, for one. Can you please provide more information? Syngonium and Pothos are not full "identifiers" of a species. They actually look more like Genera to me, potentially from the same family.

Pothos is a common name for Epipremnum aureum, which, like the genus Syngonium, is in the monocot family Araceae.
From Wikipedia:

E. aureum is an evergreen vine growing to 400 m (1,312 ft) tall, with stems up to 4 cm (2 in) in diameter, climbing by means of aerial roots which adhere to surfaces. The leaves are alternate, heart-shaped, entire on juvenile plants, but irregularly pinnatifid on mature plants, up to 100 cm (39 in) long and 45 cm (18 in) broad; juvenile leaves are much smaller, typically under 20 cm (8 in) long. The flowers are produced in a spathe up to 23 cm (9 in) long. This plant produces trailing stems when it climbs up trees and these take root when they reach the ground and grow along it. The leaves on these trailing stems grow up to 10 cm (4 in) long and are the ones normally seen on this plant when it is cultivated as a potted plant.

 Source: Wikipedia
Syngonium species, on the other hand, can have broader stems, stems that lose their chlorophyll, and different leaf shapes, to anme a few descriptions. From Wikipedia:

juvenile leaves, whole ovate or elliptical; mature bisector leaves up to 11-secant and fan-shaped

Wikipedia also mentions some unique traits of this group of plants:

The climbing stalks have elongated internodes and are elastic to some extent, however, after bending the stem's skin often breaks and peels off, turning brown or yellowish. The stem in section shows a distinct layer of the plant directly under the skin of the stem. The border between the colenchyma and stem stem is poorly scratched. In the parenchyma, starch grains are randomly distributed. The tissue of the stem also contains idioblasts with calcium oxalate crystals and drusen. The stem also contains secretory cells, containing tannins and milk juice, which solidifies in the air.


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What is R.ornitholytica? Is it a misspelling of R.ornithinolytica or a different species?
I'm trying to find out which of these is correct, or whether they are different organisms:
Raoultella ornithinolytica
Raoultella ornitholytica

I have come across both spellings in various articles, papers, etc.  They seem to be used interchangeably, but I'm not sure if they are the same thing, if one is a misspelling of the other, if they are equally acceptable spellings or if they are separate organisms.

I can't really be sure, but NCBI Genbank only "knows" Raoultella ornithinolytica, the variant ornitholytica does not exist there. So I would guess they are not separate organisms.

Thanks. Although this shows two results, I can't find them in the linked documents: https://www.ncbi.nlm.nih.gov/pubmedhealth/?term=%22Raoultella%20ornitholytica%22. I can't find any actual hits in any of the other databases there.

Probably someone misspelled the keywords for some articles including "ornitholytica". Nobody ever proofreads the keywords I guess.

source: Stack Exchange

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

sort: votes


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What moth is this?

Location: Rural area near the Western Ghats, Kerala, South India.
Date: Sometime in December, 2016
Climatic Conditions: Humid, frequent rains.
Brief Description:
Couldn't have been bigger than an inch. Took the picture at night. Has characteristic orange stripes across wings and dorsal thorax. A pair of black dots present on either wing; one pair located on the distal region of the wings and another (less conspicuous) pair located on the proximal region of the wings (laterally over thorax). No immediate/visible response when I shone a flashlight at it (eventually moved the torch up to the antennae, still no reaction).

That is a red striped tiger moth. An initial search hasn't found a picture I'm sure is redistributable, so I've linked a Google image search instead.
The number of spots on the wing seem variable. The pictures show examples with four and six spots as well as two spots.
Later:
As discussed on the Physics Stack Exchange chat, this is probably Cyana perornata.

-1'd because biology deals with scientific names; which are based on documented  specimen. The same common/colloquial name can indicate more than 1 things. You would rather put it as a comment. Early acceptance of an incomplete answer hinders the question reach the experts' hand.

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


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Moth that resembles a leaf. What species is this?

Location: Urban area near the Western Ghats, Kerala, South India
Date: Sometime in September, 2016
Climatic Conditions: Humid, frequent rains.
Brief description:
Head isn't prominent from the dorsal view. Wings outstretched even when at rest. Antennae largely concealed under the fore wings. Also it...um...does a pretty good impression of a leaf.

It resembles Pelagodes antiquadraria, which belongs to the moth genus Pelagodes in the family Geometridae.

Image Source: FlickRiver

Not a Moth, it's a Geometrid emerald butterfly.
http://www.fnanaturesearch.org/images/stories/ns/marked/M/7002.jpg

But that picture looks quite different from the one above, especially the white lines and maybe the "feathery" edges of the wings.

Although it belongs to the family of Geometrid, its belongs to a moth genus


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What is the name of this plant with Fig-like leaves & mulberry look like fruits?
Location: Napa, California
Size: It's 20' tall now.


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Where does oxygen come from in winters?
Since plants shed their leaves and don't perform photosynthesis during winters, where does oxygen come from?

1-There is a lot of oxygen. Certainly enough to last the winter. 2- Equatorial rainforests don't lose their leaves as the seasons are less severe. 3- The Taiga forest in Russia and the Boreal forest of Canada have evergreens which also do not lose their leaves.

4 - Generally "winter" is not "winter" at the same time everywhere on the world.

Oceans are the largest producer of oxygen

As others have pointed out, it's not winter everywhere at the same time, and there's a lot more oxygen than would be used up in one winter.  However, if you look up "Keeling Curve", you can see the annual variation in CO2 (and hence O2, inversely) due to winter in the northern hemisphere.  It seems to be on the order of 6 ppm.

These all look like answers to the question.


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Is the transcription starting site located before or after the promoter?
It's maybe a stupid question, but I really want to know the answer.
The definition of Promoter (From Wikipedia):

In genetics, a promoter is a region of DNA that initiates transcription of a particular gene. Promoters are located near the transcription start sites of genes

And the definition of the transcription start site (From Wikiversity):

The transcription start site "is the location where transcription starts at the 5'-end of a gene sequence.

I also Found this image (The source):

I'm asking this question because as far as I know, the RNA Polymerase binds to the TSS, and a friend of mine told me that's it binds to the Promoter.
PS : I'm interested in bacteria.

You might be interested in this.

From what I remember the promoter is not necessarily transcribed and not necessarily close to the Gene being transcribed, but somehow brings RNA pol to the right place, i.e. the TSS... I'm not sure it's a hard and fast rule though.

Note that that image is wrong: the gene includes both of the untranslated regions. You can also consider the regulatory regions as part of the gene, some do, but I have never heard of a definition of "gene" that limited itself to only the coding parts of a transcript.

You will find the answer to this question in any standard text book of Biochemistry, Molecular Biology or Molecular Genetics. There are several on-line at NCBI bookshelf, and these are generally far better than Wikipedia. I quote from section 28.1 of Berg et. al., dealing with transcription:

Transcription starts at promoters on the DNA template. Promoters are sequences of DNA that direct the RNA polymerase to the proper initiation site for transcription.

This is then followed by a description of prokaryotic promotor sequences and the consensus TATA box.

A striking pattern is evident when the sequences of many prokaryotic promoters are compared. Two common motifs are present on the 5′ (upstream) side of the start site. They are known as the -10 sequence and the -35 sequence because they are centered at about 10 and 35 nucleotides upstream of the start site.

The methodology by which this was established is described, from which it becomes evident that another way of regarding the promotor is the site on the DNA at which the RNA polymerase binds.
From the embolded part of the quotation above (my emphasis), the promotor is clearly before (5′) of the start site. This is summarized in another small graphic:

Sorry if this is an east question to answer but, what designates a specific part of the DNA to be the “transcription start site”?

Just in addition to David's answer, there are examples of internal promoters (those which have elements 3' of the transcription start site). As an example, internal promoter elements of tRNA genes direct binding of and transcription by eukaryotic RNAP III:
White RJ. 2011. Transcription by RNA polymerase III: more complex than we thought. Nature Rev Genet 12:459-463.

Many class I retrotransposons also contain internal promoters which allows them to be transposed along with the other elements:

LINE - internal RNAP II promoter
SINE - internal RNAP III promoter


text:
What digitally encoded smell formats exist?
Is there a defacto format for storing and transmitting smell digitally? Where can I obtain samples of such smell encodings? What reference dataset exists against which I can compare my smell sample to determine it might be the scent of an 'orange' or other scent?
There seems to be a lot of mostly theoretical material about how smell can be analysed, but little if any actual digital samples or reference data for conducting concrete experiments on that data.

hilarious tomd (for a 5 year old), only serious replies would be appreciated


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Finding protein motifs by running sequence analysis in protein BLAST
I've run the following sequence (bottom of page) in NCBI protein BLAST and its been identified as Zn-dependent alcohol dehydrogenase. Next I want to see what protein motifs are in this protein. Where in the programme is it possible to see the motifs?
Thanks in advance!
Sequence:
MDRNRLAIVFPIFARCISAADFSTDLYLSEIYQQKVVTMKAAVITKDHTIDVKDTKLRPLNYGEALLEIE
YCGVCHTDLHVKNGDFGDETGRISGHEGIGIVKQDGEGVTSLNAGDRASVAWFFKGCGHCEYCVSGNETL
CRNVENAGYTVDGAIAEECIVVAEYSVRVPDGLDPAVASRITCAGVTTYKAVKVSQLQPGQWLAIYGYGR
FRQSSPSICQDMYFNAKDEQLAYYAKELGGADMVINPKNEAAKIIQEKLGGAHATVVTAVAKSAFNSAVE
AIRAGGRVVVVVAVGLPPPEKMDLSIPPRLVLVGIEVLGSLVGTREKEAFQFAAEGKVKPKVTKRKVEEI
NQIFDEMEHGKFTGRMILPTHHIWIVIGWQSFSLYSQDVSQPQIFRLTSISPRYINKRSPKQPSLLKIIR
STKTPNYALITGKRFWKSNIAGYVIPISMKTGISAMKPAEFQGMKVVSSSRTGKGLLLMPVTAPVLHGSS
KAAAIANIVSAGMKRFAATLKMPVIRLTALQKNASSSPNTRSACQMVLILRLPAGSLARVPPIKQRFLSY
SPDNGWPSMATGGLGNLALRYAKTCISTPKMNSSHTTPKSWAAQIWSSIRKTKLPKSFRKSSGEHTRRWR
LLPNPPLTRLLRLSARVAVLLLLSPLVCLLLKKWIAFLLVWCLSVSKSVPWSERGKRRPSSLQPKVRSSR
KLPSVKSKKSTKSLTKWNMVNSQAVYYQPITYGSSAGNRFPYIRKMYLSRRFFDPLSLRDISTKGSHHES
SRHYRSYDRRERHQITPSELRGSASGNRILRGMSYRSPCEKRGFRRNRQNFRARYRYRQAGRGRGYFSEC
RPRQCCMVLQRLRPLRILCQRENALPQRKCRLYGRRYSRRMHRRRRILGPRARWSSCGCQQDHLRGCNHL
SSKGFSATARTMAGHLWLRAVAIPFDMETPRHVFQRQRTARILRQRVGRRRYGHQSEKRSCQNHSGKARG
STRDGGDGCCQIRLLGCGYPRGWPCCCCCRRWSASSKNGFEHSSSFGACRYRSPRFLGRNAGKGGLPVCS
RRGQAESYQASRRNQPNLRNGTWIHRPYDITNPSHILYVMGWYHTACEFTMFHFVKDLVDFFDFTLGNFR
LDLTFGCKLEGLLFPRSDQGTDFDTDKHQTRRNAQIHFFRRRQTNGDNNNNTATRADSLNSRVKGGFGNS
RHHRRVCSPELFLNDFGSFVFRIDDHICAAQLFGVVCELFIFGVEIHVLAYRRARLPKPPVAIDGQPLSG
LLRNLYCFIGGYTRASDPAGNRRIKTIWHADRVFGDDDAFFCYSAVNRITGIFNVAAKRFIPADTIFAMA
AAFEEPCNTGAVTGIQRSNPFPVLLDDTYTFMPNSAGFIAEIPVFHMEIGMTYPAIFDFQKRFPVIQRAF
GVFHVDRMIFSNDGCFHGDYLLLIYLGEIEVSRKICGDTSCEYRENDCQPITIHYMWVGNIIRPVNLPCS
ISSKIWLISSTLRLVTFGLTLPSAANWKASFSRVPTKEPRTSIPTSTKRGGMLKSIFSGGGRPTATTTTT
RPPARIASTAELKADLATAVTTVACAPPSFSMILAASFFGLMTISAPPNSLAYASCSSLALKYMSWHIEG
LDCLNRPPMASHCPGCSETFTALVVTPAQVILLATAGSRPSGTRTEYSATTMHSSAIAPSTVPAFSTLRQ
SVSFPLTQYSQWPQPLKNHATLARSPAFREVTPSPSCLTIPIPSCPEILPVSSPKSPFFTWRSVHTPQYS
ISRSASPFRGRNLVSFTSIVSLVMTAAFMVTTFCYISERRSVEKSAAEIHLANIGKTIASRLRSICDGLV
ISYGLIYHVPFRQRFGFLRLYAWLSAPYLRLQTGRPPFPAFRPRNLGLRYRQAPNEEECSNPFFQEEADQ
RRQQQQHGHPRGPQQPSRRIWQQPSPPSRVLPRAFPEFWQLRFSDPYLRRPTLWRSMRAVHLWRNTCLGI
SKGIATARSHRWPAIVRAVAEKPLLLYRWLHPRKSCWQPQDQDHLARGPSIRRRRCILLLRRQPYNRHFQ
RCGKAFHSRHNIRNGRSLRTMQHWRGHRHSEKPLPRPARYLYLHALKFCRFHRRNPRFSHGDRYDIPRNI
RFPEALPRNSEGVIWCLSRRSYDLRLLSWLPFVDISRRDRGQSKNLRLRYILRIGKRLPADYDP

MOTIF search
First of all this is not possbile in BLAST (at least nog direclty).
There are a lot of tools to search for motifs in your sequence. I think a good way to start is to use MOTIF search. This searches for motifs in your sequence based on infomration in: Pfam, NCBI-CDD, PROSTIE PATTERN and PROSITE PROFILE (you can select which of these you want to use). Further you can also use INTERPRO (which also searches through serveral database, note that INTERPO searching can take a while but will give a nice graphical view). If you want to find new motifs you can use MEME (as suggest by @mxwsn). However to do this you have to find (or have) a set of sequences which resemble your seqence to find motifs. Because off course the algorithm is not able to find motifs in one sequence because it needs to compare a set of sequences to find some frequently occuring motifs, which could be of your interest.
So to summarize you can use MOTIF search (or INTERPRO etc...) to find motifs in your sequence which are already known. Or gather a set of sequences and find new motifs in them using MEME or a similair tool.

However, how did you conclude that your sequence is a Zn-dependent alcohol dehydrogenase? Because BLASTing the sequence you provided will give matches with this enzyme but only covering ~17%. Nonetheless a good way to find information about your sequence is indeed to find motifs and compare the sequence with HMM's or PSSM's of known proteins.
For example MOTIF search will give these results:
PROSITE:
    Zinc-containing alcohol dehydrogenases signature.
PFAM:
    Zinc-binding dehydrogenase
    Alcohol dehydrogenase GroES-like domain
AND A LOT MORE>>>

Searching PFAM will give you this:

Notice that the second domain (Zinc-binding dehydrogenase) is not completely present, more information can be seen in the detail overview:

I would advice to also take a look at how important these "missing" residu's are (e.g. using a MSA and look at conservation). Because your sequence could contain these domains but that does not necessarily mean that this IS A Zn-dependent alcohol dehydrogenase. It could be non-functional for example.

To find de novo motifs present in your protein sequences, you should use MEME or some other motif-finding tool instead of BLAST.

MEME discovers novel, ungapped motifs (recurring, fixed-length
  patterns) in your sequences.


text:
Was Myxomatosis Man Made?
I can't seem to find any conclusive information about the origin of Myxomatosis. According to Wikipedia

It was first observed in Uruguay in laboratory rabbits in the late 19th century. It was introduced into Australia in 1950 in an attempt to control the rabbit population.

However I find this passage unclear.
Was this a naturally occurring disease that we then used as a means of population control, or did we have a hand in its creation?

It was identified as a disease in 1896.  How do you think people were able to "create" viruses in 1896?

@layork That would depend what you mean by "create". As far as I'm aware, a virus present in rats doesn't mean that it is necessarily transferable to rabbits without modification.

Do you suggest that myxoma virus was first found in rats? @Pedr

Myxomatosis has natural origins in the wild rabbits of South America. In 1942 Aragao showed that wild Brazilian rabbits has acquired (not innate) immunity to the myxoma virus from a previous infection.


text:
Why are synthetic Auxins capable of killing dicots such as weeds at high concentration but do not cause damage to monocots?
I read that synthetic auxins like 2,4-D and 2,4,5-T can be used as herbicides against dicots but they don't affect monocots. Can someone explain how they damage dicots and not damage monocots

A similar, if not identical, question was answered in 2015.


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Nose breathing and swimming
If you're standing and holding your nose closed, it becomes quickly uncomfortable; although you can breath fully through your mouth, it still feels like your lacking air since you're naturally trying to breath through your nose and you can feel the restriction.
On the other side, when swimming with a nose plug, you can have your nose totally shut down, breath only through the mouth and somehow you do not have the feeling of nose obstruction blocking your air intake.
Why is this?

Hi Thomas, could you include some kind of citation for the uncomfortable feeling you describe when plugging your nose. Ive never noticed/heard of this phenomenon. Could it have to do with humidity? If you're standing and breathing through your mouth it likely gets dry quickly where if you're breathing through your mouth at a pool, the humidity keeps it from drying out.

I explained the feeling more clearly, where it's a restriction that matters standing on land and one we totally ignore when swimming.

The holding your nose shut is uncomfortable because you are not holding any air in your nose, as for the nose plugs I think you should just blow out your nose while jumping in, it works for me.

@Thomas, a source for this feeling would still be nice, I have never experienced it, not unless you are talking about the throat drying out.

the best example I can give you is to stand, hold your nose shut. you can breath, but someone it is not very comfortable, you can feel that something is altered. My orl told me a while back that the nose has a sense of air velocity which is used by the brain, but I don't have any data to know if this is the case.

One possible answer for your question could have to do with the level of exercise the subject is doing.
While the nasal passage is the main route for breathing, it provides cleaner air and allows for more even and slow respiration rates, a greater volume of air can pass through the mouth LaComb.
There is no discomfort in mouth breathing during exercise because mouth breathing can deliver greater amounts of oxygen and release greater amounts of CO2; it is the preferred method of breathing for increased activity.
Secondly, discomfort in oral breathing stems from a perception of breathlessness due to stimulation of receptors in the oral mucosa. When patients were required to breath orally with humidified air, no instances of breathlessness were reported (Source).
Based on these two studies, when exercising oral-breathing is required to deliver adequate amounts of O2. Therefore, nasal-breathing is not required and an obstruction of the nasal passage is not percieved. When exercising in a pool, discomfort of oral-breathing is diminished due to the humidity of the surrounding air. When not exercising, and breathing orally in low humidity air, discomfort is felt due to the stimulation of receptors in the oral mucosa.

The study you quote seems to conclude that around 60 L/min of air (for males) people switch from nasal to oral breathing. It is possible that, while exercising, that threshold is reached and nasal breathing doesn't matter anymore. I'll wait for a bit more feedback to see if this is the case.

"Mouth breathing at rest could be uncomfortable because the oxygen delivery is greater than needed and more importantly too much CO2 is expelled." This is just a guess, and an inaccurate one. Breathing is regulated by blood CO2 and O2 concentrations, not the other way around, so mouth breathing will not cause 'too much O2' or too little CO2 unless it is intentionally too deep/frequent (hyperventilation). The reason it's disliked is that we are accustomed (correctly so) to having a moist oral mucosa, and mouth breathing causes mucosal dryness. In the water/shower, this doesn't happen.

Just do it for an hour. No cheating, no drinking, no candy, etc. If you do, and you still need a reference to believe that it causes discomfort, let me know.

I've removed conjecture and provided reference to an additional study which hopefully provides a more comprehensive answer to your question


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Can someone explain what exactly each score of the BLOSUM62 matrix means?
The descriptions that I've found say it's the log odds ratio (observed/expected) where expected is the assumption that there is no correlation between amino acids.
I'm slightly confused as to what this means? Do we have a database of sequences and if there are 10 A's out of 1000 amino acids is it's expected simply 10/1000 * sequence length for all sequences?
What is the observed? Is the observed different for every sequence so there is a different BLOSUM matrix for each sequence? And can someone explain how this table represents 62% of "kept identity"?
Sorry if these questions seem nonsensical or vague, I'm not of a biology background.

From your bio you appear to have an interest in computing science and mathematics. I am not sure that the answer to this question is mathematically complex (although it is outside my sphere) but it appears quite extensive and may not be suitable for anyone who understands it to present here. For that reason I give you a link to an account I found on line. If someone wants to present an introduction in an answer fine. Likewise if you are still not clear how the blocks are selected (that's the easy part) say. http://www.cs.columbia.edu/4761/assignments/assignment1/reference1.pdf

@David Thanks! This is pretty much exactly what I was looking for. Quick question on expected freq though. Is each sequence given its own BLOSUM scoring matrix and the expected freq is generated for different profiles of proteins?

I have voted to mark this as a duplicate and have modied the overlapping question and my own answer to it to take into account the specific concerns of the Poster her. I think that this is the best way of deal with this. Anyone who wishes to add or extend an answer to the previous question is, of course, free to do so.


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Spruce growing high up in a maple trunk: Can a partially rotted trunk completely sustain another tree?
I've come across a spruce tree that is growing 15ft up in the crotch of a sugar maple tree:

According to Google StreetView, the spruce has been there since before 2007 (over 10 years ago!).
I've seen other trees growing out of rotted stumps or in trunks near ground level before, but I've always just assumed that the roots of those trees reached down to soil -- in one way or another -- to get the nutrients they need for survival.
But with the subject tree, it's so high up that I would assume that that the roots do not have access to any soil. It's my guess that the spruce is getting all of its nutrients from decomposed wood in some rotten portion of the trunk.
I didn't know biology worked like this. I wouldn't have guessed that a live, partially decomposed trunk could contain 100% of the nutrients that a tree needs to survive for 10+ years. I know soil is made, in part, from decomposed wood, but it's my understanding that there are a lot more ingredients too.
Can the decomposed wood in a partially rotted trunk completely sustain a tree?

keep in mind the biggest nutrient it needs is water, which the tree will catch enough of as long as the spruce stays small, as it grows however this will cease to be true.

Is the maple rotting? It would be interesting if the spruce was parasitizing it somehow.

@canadianer I don't know for sure that the trunk of the maple is rotting. It's just a best guess, since the spruce needs to get food from somewhere, right? I'd probably get arrested if I drove up with a ladder, propped it up against this person's boulevard tree, and started rummaging around. Wish I could though!

@canadianer Since your name is canadianer, you might be interested that this tree is in the GTA.

Yes you'll need a flashlight and a diversion… ;)

Note  This answer makes the presumption that the crotch in the maple's trunk is indeed a breach through its bark, and does reach the inner woody tissues.

The heartwood of most trees consists of the dead connective tissues, xylem, which surrounded the cells that once formed the living layer of phloem under the protective bark.  That connective tissue itself mostly cellulose, and is a polymeric chain of glucose i.e. sugar molecules bonded and linked in such a way as to make them indigestible to most lifeforms.
Certain bacteria and fungi, among others, are able to do so, and they are among the first responders in the decomposition scene.  When these microbes, often present in the gut of various insects, are able to break down the woody fibers into forms that permit their re-use by other plants, the detritus is comprised mostly of carbohydrates, alcohols, carbonic acid, and water.  Phosphates and various other trace elements which were present in the cells of the woody tissues are released also.
Later, visiting birds and mosses will further augment the ecosystem, adding nitrates and various salts — potassium, sodium, chlorides, and the like.
Another thing that needs to be considered is the drainage.  Where does the excess water go?  Pressure on the capillaries inside the xylem of the maple should be able to channel some water downwards, but not much will exit through the roots.  I've never heard of such a thing.  The hole in the maple will widen and exacerbate, deepening the rotted area, but it will be acidic and somewhat saline due to the lack of drainage.
Can it completely sustain another tree?  As the ecosystem flourishes, probably; unless the new tree has special requirements for the pH or salinity of its soil which are not maintained by the rotten wood, then it should be able to gain enough nutrition in the form of nitrates, phosphates, and water, but not all of that will come from the other tree directly.
The branches of a tree will only grow so large as can be sustained by their root system, of course.  The limited space in which this little sapling has taken root will result in the less than maximal form that you see in the photographs.
So, in conclusion, that spruce will probably not thrive by any means, but it will manage to survive.  Spruces do favor more acidic soils — lower pH — than many other trees, so it has that going in its favor.
That much is obvious, I suppose:  ten years, and it no larger than a four–year shrub.
There is a problem if all this occurs inside a tree which has not fallen, however.  Usually, the outer bark of a tree protects it from such decompositional actions, because the inner woody tissues of most trees do not contain adequate chemicals to deter insects and fungi from chomping or ‘mycelizing’ their way through the heartwood.
Eventually, the maple will either need to be cut down or will be weakened enough that it will collapse.

Thorough and interesting answer. But please add some references to support your claims. Thanks.

Well, holes in rotting trees are not only going to contain rotten tree matter (aka compost :p), but they will also slowly gather fallen leaves, dead insects, dirt, dust and other debris. Even minuscule layers of these substances will essentially form a pile of "soil" with nutrients and minerals needed by the tree.

In fact, spruce trees are capable of growing on relatively thin soils and often grow with very shallow root systems[Source].
B/c so little of these substances can exist there, however, the tree will never grow large and will likely not live nearly as long as it's species' mean lifespan. But sometimes nature does funny things.

So it's not unheard of for plant to survive in these conditions.
Plants that grow (harmlessly) on other plants are called Epiphytes, and they derive moisture and nutrients from the air, rain and debris accumulating around them.

Though epiphytes are much more common and diverse in the tropics, common epiphytes that those of us living in less tropical places might recognize include mosses and lichens (and to some degree ferns).

It is true that many tropical epiphytes have modified biologies/anatomies to capture and mineralize nutrients from air and rain water (Yoon Lee,
 n.d.), but some epiphytic species do develop roots to take advantage of soil/debris/decomposed materials that have accumulated. (Cardelus & Mack, 2010)

Yoon Lee compared these accumulations of "arboreal soil" to terrestrial soil and found there were no significant differences in all primary nutrients between epiphytic and terrestrial soils, but that pH between the two soils differed significantly.

Citations:

Cardelús, C. L., & Mack, M. C. (2010). The nutrient status of epiphytes and their host trees along an elevational gradient in Costa Rica. Plant Ecology, 207(1), 25-37.
Lee, Yoon. n.d. Nutrient contentand biota of epiphytic and terrestrial soils in a tropical forest in Moorea, French Polynesia. unpublished. UC Berkeley.

In the Hoh Rainforest in Olympic National park, there are many "nurse trees" and "nurse logs"; the latter are trees that have fallen and now act as a nutrient source for smaller trees growing on them.

Some of the larger trees' roots find their way into the soil, which facilitates their growth, but some smaller trees do not.

...but it's my understanding that there are a lot more ingredients too.

I would not say 'a lot', but rather 'some', mostly water. The log provides most of the nutrients the new tree needs, the rest being supplied by rain, fungi, mosses, leaf litter, etc.

I think you should be more detailed with regards to the nutrients:  Fungi can't, so far as I know, obtain elemental nutrition except from their substrate; some mosses can, via symbiotic bacteria, fix nitrogen from the air; rain may contain in dissolved state whatever compounds were present in the raincloud where it formed — sulfur, nitrogen, halogens, et al.

@can-ned_food - I intended to say that these (fungi, mosses, leaf litter, etc.) can break down the tree and free as well as provide nutrients. If you're looking for halogens in my answer, you'll need to supply an answer of your own. I'm definitely not a botanist.


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Why do my peptide samples turn yellow and red?
The protocols for (brain) tissue digestion I am trying out are: lysis (buffer containing 0.1% SDC or SDS in 100mM TEAB + phosphatase inhibitor which is sort of yellow), reduction with TCEP, alkylation with iodoacetamide, digestion with trypsin, and acidification with trifluoroacetic acid (TFA) to deactivate trypsin. After that I usually dry the sample and do a C18 clean-up.
For some reason my samples become yellow after the addition  of TFA (and this was also the case with lysis buffers with SDS or SDC so I don't think it is detergent related). As this happened to a colleague who didn't use the phosphatase inhibitor, I don't think it's related to it either. When I do the C18 clean-up this yellow goes to the eluate (elutes with peptides). Would anyone know why this yellow colour occurs? The most disturbing thing for me is that it does not always happen to every sample, as you can see in the photo 0.1%SDC is clear.
Moreover, for the last digestion, I decided to try out Rapigest (0.1% in 50mM TEAB). When I added the TFA for acidification step, the sample was still clear, but after a while drying it in SpeedVac, when I checked up on it, it had a bloody red pellet-like oddity as you can see in the photo. I left it in the SpeedVac to dry out completely, and when I checked it again, the red colour disappeared and it was clear-whitish again. Would anyone know why this happens and if it interferes with subsequent steps such as C18 clean-up or LC-MS identification? So far, I have asked my colleagues, but they have never seen it before and are calling it magic.

Is your preparation of TFA fresh and protected from light?

Do you mean is it kept protected from light after it is diluted and added to the sample? Because TFA usually comes in dark bottles, but then when we dilute it to 0.5 or 5% it is kept in light in transparent ones. Once a dilution is prepared, it is used for a long time (couple of months) in our laboratory. Does this usually cause problems?

After a few months or if the solution begins to take on a yellow hue I'd discard it. TFA on its own is light sensitive, however, and personally I'd try to store it out of direct light. It could also be a reaction breaking down the TFA, but im not sure. In the rapigest tube I'm 100% not sure. I actually saw a protocol somewhere though, if your solution turns yellow you can add some 1% v/v TFA to make it clear again. I'll keep looking into it.

The TFA solution I used was still clear. However, when this happened I made a fresh one, so I will let you know if it happens again. Thank you I will try that next time.

@E.T., Rapigest is an acid-cleavavble detergent which precipitates after cleavage, because of which it can be removed before LC-MS analysis. After digestion, TFA would acidify it and you should keep the sample at 37 ºC for 30 min to cleave all Rapigest that then would precipitate and should be removed by centrifugation.

Also, after lysis and before reduction/alkylation/digestion, do you remove insoluble cellular debris by centrifugation? I would always denature a protein sample before starting  reduction/alkylation/digestion procedure, by 2% SDS or 8 M urea or TCA precipitation.


text:
Why a brain's hemisphere controls the opposite side of the body?
As a physics student with very little understanding of biology, in a course about physics foundations diagnostic techniques I have come up with this question. I don't even know if it does make sense or not; in the latter case, please excuse me.
As far as I know, in the human brain the right hemisphere controls the motion of the left side of the body, while the left hemisphere controls the right side. Moreover, the part related to sight is on the back of the brain.
To me, it seems that there is a sort of opposition between the part of the body considered and the area of the brain that have to control it. Is this statement right? Only for human beings or also for animals? Are there any exception to this sort of pattern (if there is anyone)? Is there a logical reason to the fact that we show this characteristic and it couldn't be different from how it is?

See the linked answer, but a tl;dr is that this organization is very very old, as old as bilateral symmetry. In my opinion the best explanations are developmental ones, and the lack of any particular evolutionary pressure to untangle the connectivity. For most movements an organism makes, both sides of the body are involved. Even a reaching motion with one arm requires activation of postural muscles in the other flank to prevent you from tipping over, for example.

As far as exceptions, on the sensory side olfaction doesn't cross, probably for anatomical reasons (the olfactory bulbs are part of the brain and reach out almost to the nostrils), for vision the crossing is not by eye but by visual field: your left visual field from both eyes goes to the right side of the brain; also, since the image is flipped onto the retina, that means the left side of the retina stays on the left, and vice versa. Lastly, the cerebellum does same-side control: information to the cerebellum from the rest of the brain has to cross over before entering the cerebellum.

Another exception is hearing, the cochlear nerve enters the brainstem on the ipsilateral side and only downstream processing neurons cross the midline (and some descending projections from the cortex I believe).

"How" is easy to answer (signals from the right side of the body cross the midline and end up in the left cerebral hemisphere; answered well in a previous question). This pattern of wiring appears to have existed since bilateral symmetry first evolved.
"Why" is not a well-defined question; the possible evolutionary advantage gained by having cross-wiring is unclear.
To answer your explicit question: there is no "opposition" in any meaningful sense between the location of a sensory nerve on the body and the location at which the information is processed in the brain. There are a raft of visual areas in the neocortex, spanning from the back but extending forward. The areas that control eye movement are much more frontal ("frontal eye fields"). Before arriving in the neocortex, signals from the eyes pass through the dLGN, a nucleus in the thalamus which is a subcortical structure closer to the middle of the brain than the rear. This flow of visual information is similar across many (most? all?) mammals.


text:
Specificity in MAPK/ERK pathway and PC12 Cells
Background
PC12 Cell stimulation leads to distinct outcomes upon stimulation with either EGF or NGF (epidermal and nerve growth factors). The outputs are transmitted through the MAPK/ERK signaling pathway; stimulation with EGF causes transient activation of the ERK, via a negative feedback loop, leading to cell proliferation whereas stimulation with NGF leads to sustained activation of ERK, via a positive feedback loop, leading to differentiation.
Question
How does the signaling pathway know which kind of feedback loop to initiate at the ERK level from upstream stimulation by EGF or NGF?
Helpful Image to explain question
To reiterate: I want to figure out how EGF binding at the membrane level triggers negative feedback downstream, and NGF binding triggers positive feedback?
A link to the image is (http://www.nature.com/nrm/journal/v12/n2/fig_tab/nrm3048_F4.html)


text:
Why do birds sing?
Some birds sing. But why do they do it?
Does singing gives them any biological advancement? Like in mating, communication etc. Or they do it for enjoyment like humans? ( Might be possible!)
Edit: I have seen most birds which live close to human habitation sing; I really don't know if wild birds sing like these birds. And another good thing is that they do it usually at dawn and dusk. So, it can be a kind of signalling. I think when dawn arrives, they do it for signalling others to go for searching food, materials to make nest with etc. At dusk, they do it for signalling everyone for returning home. Maybe it's kind of an hour-bell.
It's my guess. I don't know for sure!

@canadianer What did you edit?  I don't understand.

I was trying to improve the grammar. It's still a little off.

Maybe you'd be interested in why humans sing...

According to this paper:

Song Function and the Evolution of Female Preferences: Why Birds Sing, Why Brains Matter
by Stephen Nowicki and W. A. Searcy

A birds song can have two main functions.

Male bird's song is used as a mating call to attract Females. Females in turn prefer birds who can sing longer and have complex songs. The quality of a birds song is an indicator of their good genes. A bird infected with parasites is considered to have a considerably low quality song.

It is also used by Male birds to mark their territory. If a male bird hears another birds song it would start singing or increase the rate of its singing. Also in another study linked in that paper refers to a study where birds with punctured lungs who were unable to sing and had a hard time maintaining their territory.

And also a bird's song should not be confused with it's call. A bird's call is mostly used to alarm other birds of the flock of danger, communication and locating members of the flock. A call is less complex and more noisy.

But I also hear birds 'singing' (honestly, it sounds like shouting) at dusk. And if you have read the other answer, I think you know you're only talking about the dawn songs. But what about the dusk 'songs'?

@Mockingbird added another paragraph to address this

Some birds do sing at dusk (European example: Blackbird, every evening). Why should singing at dusk have a different reason?

There's actually info for that on the web:
https://www.google.fr/search?q=Why+do+birds+sing%3F&oq=Why+do+birds+sing%3F&aqs=chrome..69i57j69i60&sourceid=chrome&ie=UTF-8
quotes from easy to find web pages:
songbirds make up almost half of the world’s 10,000 bird species including warblers, thrushes, and sparrows.
Bird song is a very specialised form of bird call that, unlike all the quacks, honks and tweets we hear throughout the year, serves one function only – to ensure the breeding success of the singer, to indicate clearly that the singer is healthy and fit and ready to breed.
It's largely a boy thing, designed so that other females of the same species are attracted and males of the same species are repelled.
Bird song is most highly developed in a group of birds called passeriformes. Don't worry, we are surrounded by them, wrens, robins, blackbirds, song thrushes are all passeriformes. Some tropical birds are know to duet, with the female singing too.
Females need to know this if they are to choose the right partner. Then, the song has to say something about the health of the singer. A long, loud song for instance indicates a certain amount of stamina, a bird in good condition.
Similarly with repertoire. It appears that in some species, a wide variety of sounds in a song is especially attractive to the ladies. Many species even mimic other birds' songs just to increase their repertoire, and it's not unknown for other sounds, such as cats' calls, to be included as well.
As bird song is part of the breeding cycle, most birds sing in the breeding season. This means that birds will start singing in late January and stop singing in July.
They are prompted to start singing, it appears, by increasing daylight (more light sets their little hormones racing and in response, they sing).
They stop singing when they start moulting, usually July time, as the last thing you want to do when your feathers start falling out and you are not quite as quick off your perch is to advertise your presence to predators.
Some birds, of course, sing in winter, robin being the best known, but this is linked to defending feeding territories rather than breeding. Interestingly, in winter, female robins sing as well as males.
Just as there is a seasonal cycle to bird song there is also a daily cycle, with the most intense period being at first light, the so called 'dawn chorus'. Why sing so intensely at dawn though?
First of all, male birds may die overnight if they have not been able to feed well during the previous day.
So, first light is a time when when birds can announce their survival, and this advertises something of their feeding abilities to potential mates - and of course, it's important that females know if males can find food or not, especially when they will be relying on this after their chicks have hatched.
Also, a side product is that birds looking for territories can hear where the spaces are and move in.
Secondly, many females lay eggs at first light and immediately after this are at their most fertile. This is a time when males need to fend off other potential suitors, and as we now know, song is a key way they do this.
Hence the dawn chorus.

Are these all quotes? You should make that clearer and add citations.

They are excerpts yes, i read through 1-2 pages and chose the best information to edit from the BBC page and a couple of other pages titled "why do birds sing" ... i would love to spend more time on it, but considering that typing "why do birds sing" brings up 15 ornithologist zoologist pages titled "why do birds sing", i figured it was best to not take time over it beyond answering briefly and in great depth using resources that are 2 seconds of search away. searching google for 2 seconds is the minimum research necessary for a Stack question. wouldn t you say so?

I doubt that the original authors you plagiarized would care about any of that.

Are you having a problem? you should make that clearer and add adult behavioural credentials. Because i doubt that the comments you insinuated would make anyone care...  It's the BBC, a wildlife conservation and information broadcasting governement organization that i pay and that have never cared about anything like that, just like NYC museum archives. it's the BBC.

I thought I was quite clear: give proper attribution to your sources.

i thought i told you i don't like stentorians... i was tired last night my reply is from 12ocklock. the attribution got erased when i edited the question, as you may recall the original reply had attribution. i dont know where it went. erase the answer i don't have time for stentors.


text:
What is the name of this small black insect?
Location: South India
Size: 1-2 cm

Did you see it recently?  Time of year would be useful.  More useful would be the habitat in where you saw it:  woodland?  Swamp?  Metropolitan?

Metropolitan, 2017, Night Time, Its on my front door, may be it is new invented species found by me, may be who knows.

+0. Your photo isn't of such good quality. Try to use the best camera you have available — preferably an SLR camera — and forcing the flash setting to "on". It might help to boost your camera's ISO setting.

Was there a strong pungent, stinking smell along with the insect (that could be perceived from more than 1 meters distance)? Also mention the size.

Precise identification of insects requires use of microscopic lens and an immobile specimen.
I have neither of those here; also, my reference material is focused on North American species.  Nevertheless, with what I have available to me, it is most likely a member of order Hemiptera, family Alydidae:

Alydidae are mostly active during the day, so your specimen was probably resting and saw a nearby artificial source of light.  They use their piercing mouth-parts to suck the juices out of herbaceous seeds.  Unless yours was discovered in a heavily urbanized area, I would venture that this one feeds off nearby grasses and trees.


text:
Medical term for "holding urine for a long time"
Sometimes I get/feel pain in my stomach because of holding urine for long time. Is there any medical terminology describing: "holding urine for a long time", or pain associated with this activity?

Holding in feces for a long time is called "stool withholding". I don't know if there's an equivalent term for urine. In future, consider posting such questions to http://health.stackexchange.com instead. Why do you hold your urine in? Are you a schoolteacher or a bus driver? It's not the wisest move to hold your urine in for a long time; it carries risks.

A swollen organ may be described as distended if the swelling is symptomatic of a medical disfunction.
The purpose of most bladders is to collect and retain a fluid; if that fluid needs to be discharged periodically, and is not able to do so, then there is usually pain as a result of the distension.
Inability to urinate is known as ischuria or urinary retention, and could be the result of obstruction to the urethra, could be a failure of the bladder to fully contract during urination, or could many other possible causes.


text:
Why did my isolation streak of an unknown organism on Mannitol Salt Agar turn yellow where there was no growth and magenta where there was growth?
I repeated a culture twice in an entry level microbiology class for our final lab project of culturing a provided unknown organism.  One of the required tests on our dichotomous key was to culture a gram positive cocci in mannitol salt agar.  After repeating the experiment twice as instructed, and doing an isolation streak as instructed, the part of the agar with no growth was acidic while the part of the agar with growth was neutral or slightly basic.  Both cultures were incubated for around 48 hours, and the first one then refrigerated for another 48 hours while the second one was examined directly after incubation. My professor told me to disregard the results and treat it as a negative in my report, but I'm perplexed as to how this result came about.

Yeah it seems kind of impossible on first thought. The sterile plates are red, yes? Do you know what result is expected with your organism?

So she's not allowed to tell me the expected result, but I'd imagine since she told me to treat it as negative the expected result was supposed to be negative.  And yes they were certainly red when sterile.

I just realized I forgot to mention something that now seems important.  I also did a simple dextrose test that came out as orange with phenol red in it when it was expected to come out as red.  Could these issues be caused by a error in the preparation of the indicator?  It makes me wish I could incubate a sterile plate and see what happens.

In my experience, many TAs are not that thoughtful. Are you able to monitor the growth at more time points over the two days? If the plates were red to begin with, the only explanation I can think of right now is that the organism fermented mannitol and produced acid, turning the entire plate yellow. Once the mannitol was exhausted, it started metabolizing peptones which produces base and reverts the colour of the agar surrounding the growth to red.

I was going to say that, if the plate was yellow to begin with, someone might have used the wrong indicator when they were preparing the plates (eg methyl red instead of phenol red).

The orange colour you see is intermediate between red and yellow. It's likely that the pH was near the transition point (pKa)  of the indicator.

The exhausting of the mannitol and utilization of peptones was my first thought and why I was going to mark my first result as positive but the prof redirected me. My knowledge of the creation of the medium is limited however and I was wondering if there might be a simple chemical answer. Sadly I can't check at different intervals or run any other tests so I think I'm just going to write an excessive lab report and leave it in the direction the professor sent me. Thank you for your help thinking about it, though.

I can't think of a chemical explanation unless someone left an uncapped bottle of hydrochloric acid in the incubator. The plates are pretty simple.


text:
Why should benzalkonium chloride (an antifungal agent) be used during your laundry machine's "rinse" cycle, not its "wash" cycle?
I'll first provide lots of background information. My actual question is at the very end.
Background
The spread of athlete's foot
Athlete's foot is a fungal infection which is mildly contagious. The infection can be spread by skin particles left on towels. (Source.)
If one person in a family has a fungal infection (e.g. athlete's foot or jock itch), their laundry may also contain fungi. I suspect that towels and laundry machines might make it easier for these fungi to spread: e.g. from the patient's feet to their groin. See, for example, here.
Water at 140 °F
You can kill fungi using water at 140 °F (60 °C). Unfortunately, your water heater probably doesn't produce such hot water, because such hot water is dangerous and can kill unsuspecting individuals. (Sources.) Still, you can make such hot water in other ways. (Source.)
Antifungal rinses
Another option is to use a suitable antifungal rinse.
The most common cause of athlete's foot is T. rubrum. (Source.)
T. rubrum is a dermatophyte-type fungus. Dermatophytes spread through spores. These spores can sometimes live for up to 20 months. (Source.)
Canesten Laundry Hygiene Rinse is 7% benzalkonium chloride. (Source.) A competing product is Bluo Laundry Sanitiser, which is also 7% benzalkonium chloride. (Source.) These products are sold in Australia but not in North America. (How safe are they? I dunno; I'm not a toxicologist.)
The Canesten rinse label makes an impressive claim: "eliminates ... fungi from your washing". Still, it looks like these rinses' fungistatic effects are stronger than their fungicidal effects. In reality, they're not perfect at killing T. rubrum, but they're still better than nothing. An Australian lab found that, in 20 minutes, these types of rinses reduced T. rubrum by between 90% and 99%. (Source.)
(Each rinse is marketed as both antifungal and antibacterial, though there's limited evidence that people can catch bacterial infections from clothing. I'm not convinced that their antibacterial effects are really necessary.)
Use during the rinse cycle, not the wash cycle
Each manufacturer says that its benzalkonium chloride rinse should be added during your washing machine's final rinse cycle, not its initial wash cycle.
You can do this using your clothes washer's fabric-softener dispenser, if present. On a top-loader, this is usually a cup-like device on top of the machine's central agitator post. (Source.) Or you can buy a softener dispenser ball, though they're not always 100% reliable. Or you can add the rinse manually at the correct moment.
A sample washer program
Washing machines can vary. Here's a description of the normal program of certain inexpensive top-loading Whirlpool agitator-type washing machines:

Fill - agitate: 16 minutes.
Drain: 2 minutes.
Spin: 2 minutes.
Rinse, fill, & agitate: 4 minutes.
Drain: 2 minutes.
Spray & spin: 2 minutes.
Spin only: 4 minutes.

Total: 32 minutes.
(Based on: wiring diagram W10118358, rev. A.)
The wash cycle is longer than the rinse cycle.
My question
To summarize the above background information: Canesten laundry rinse (7% benzalkonium chloride) has both antifungal and antibacterial effects.
And so I wonder: Why does the manufacturer recommend that it be used during your laundry machine's rinse cycle instead of its (longer) wash cycle?
Any answers or guesses are welcome.

I think your question has been answered below (with the caveat that you should stop the washer in the rinse cycle to allow more time to disinfect.) But please note that a contaminated towel usually means an unwashed one. I strongly suggest you do not use benzalkonium chloride in the wash. Tines pedis is not highly infectious in the home. It is rather much more related to your individual susceptibility to the fungus. People live together for decades without ever passing it on to members in close quarters. The potential to harm the environment far outweighs the benefits here.

I've since done some more research.  Indeed, it turns out that an expert body doesn't recommend to use benzalkonium chloride to kill fungi in the wash.  Instead, it recommends the use of a washing powder containing activated oxygen bleach, as well as various other techniques.  See this post for more details.

The label of the veterinary product Fung-A-Way, which is Benzalkonium Chloride 0.15%, states that "Efficiency is neutralized by soap or detergent residues."
The website http://www.mpbio.com has the following under its description for Benzalkonium Chloride:
"Incompatible with anionic detergents, such as soap, and with nitrates."

Benzalkonium chloride is what's known as a quaternary ammonium cation, or quat. These are disinfectants commonly used in medical settings, for example. The mechanism of action is thought to be due to the long alkyl chains, causing membrane leakage (ref1, ref2).
Like any disinfectant, however, two things are required for effective disinfection: The appropriate concentration, and the minimum required contact time. The following report goes over the importance of contact time but also makes a significant discovery: many disinfectants dry before their required contact time while failing to marginally kill anything except bleach.
The required contact time for quats happens to be 10 minutes. So on a hard non-porous surface youd spray it wet, come back in ~5 minutes and spray it wet again to ensure disinfection. The reason you would want to introduce a quat on the final rinse is because if you immediately wash it off or wash it off within minutes, your disinfectant is most likely to do nothing.
Edit: You said laundry but when I think washer in the US, I think dishes, which made no sense anyways.

My question describes a sample laundry-machine program. It looks like the "wash" cycle is about 15 minutes long. Wouldn't this be enough time for the disinfectant to kill enough fungi?

A) Find a top-loader agitator laundry machine. Use your thumb (or a scrap of cardboard) to defeat the lid switch. (Also watch the drain hose, if the machine drains into a sink.) You'll quickly learn that the wash cycle does not provide a constant clean water flow. The machine fills itself, agitates for 15 minutes, then drains itself to prepare for the rinse cycle. B) OK; good to know. On second thought, I'm thinking I'll indeed avoid the chemical.

Interesting! I redacted that last comment because I obviously know nothing about my own appliances. So some extra thoughts: I don't know how the quat reacts with your clothes over time, if it'll ruin them, or if the detergent may block the mechanism of action. The manufacturer might be able to tell you if you call them.

This is actually very informative. Maybe OP should rinse the suspect items, then leave them to soak in benzalkonium chloride and only then add them to the wash. Environmentally cleaner soaking options are soda, vinegar or boiling water.

Most disinfectants are rendered ineffective or much less effective in the presence of organic materials. Washing your clothes prior to adding Canesten in the rinse allows removal of organic matter and therefore more effective action.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!

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


text:
identification of purposeful (engineered) genetic changes vs. random mutations
Okay, first - I'm not a proponent of intelligent design. I do not think it's a valid scientific theory (it has no mechanism of change/design). Second, I could be wildly off on what I think I know, in which case, my apologies for the question.
My question is, I know that scientists manipulate the genes of organisms (both animals and crops we use as food). I think this could be considered legitimate intelligent design (right? I'm talking as opposed to looking at an organism and saying that this couldn't have evolved naturally, therefore it was intelligently designed).
So, mankind has modified organisms - outside of knowing we did this, can we tell they were intelligently created? If so, how? Can we tell when a genome has been altered?
Also, if I'm totally off base, please correct me.

to be fair we have engineered segments of their DNA, not the entire thing.

"To create" (to me) implies more than "to alter", which is what gene-splicing does. But that is just semantics. Can we tell if they were purposefully altered by man? I doubt it. Maybe if a particular, trademarked nonsense sequence was inserted into the genome as well, yes. But I doubt that is done (yet). These tactics have a way of backfiring on one. Animal husbandry is not the creation of an animal, but merely selecting for characteristics. Semantics matter here.

Honestly I thought about rephrasing just because of what you suggest - all we've done is alter genomes, but I wasn't 100%. I'm open to your question as well: Can we tell if a genome was purposely altered?
Should I edit my OP?

Yeah, I answered that in my comment. I highly doubt it, but I didn't post that because I never post an answer I'm unsure of, and I didn't want to slog through a bunch of scientific literature to find out if I am correct. If you want to edit, feel free. I changed the title because left as it was, few peple would click on it.

I did want to say that I have in mind what my friend (a CSI) has said in the past, that there is almost always evidence when a murder is committed; I grant that altering genes is not a murder, but I was thinking that the general principle might apply towards anything that mankind has messed around with. I'm probably wrong here, but that's where my head is at.

You are correct. Where man has been, there is usually evidence left behind. If man has been mucking about in a genome, maybe there is evidence, but if there is, I don't know about it. :)

One should be able to tell this from comparison of the sequence with that of the original organism in GenBank etc. The differences in an engineered organism will generally be extensive and of such a kind that a specialist in the field will be able to identify their origin and deduce that they did not arise naturally.
However there is no general and guaranteed method. If I were to engineer a single base change, there would be no way to distinguish that from a natural mutation. The only thing is that if the mutation were beneficial then it would probably have occurred naturally and I wouldn’t have needed to engineer it.

It has to be on a case by case basis. If I see a mouse or a fruitfly expressing jellyfish green fluorescent protein I know it cannot have acquired it by vertical transfer. That's why I deliberately mentioned a specialist or expert. The answer may not be the neat one the OP hoped for, but it's the way it is. It's like asking how an art expert can tell a genuine Picasso from a forgery.

Depends on the type of alteration.
If we are talking insertion/alteration/deletion of whole genes, we can easily discover the changes by genome sequencing and comparison.
If we are talking a single point mutation somewhere in the genome, it is harder to detect the change as such mutations can occur naturally (roughly 20-30 such mutations occur per human generation).

The number is higher. The 1000 genomes project estimates it around 20-30 de novo mutation per generation, see.


text:
What is the best alignment definition for the Multiple Sequence Alignment (MSA) problem?
For simplicity, suppose that I am penalising mismatches and gaps with -1 and adding a score +100 for each match.
Does the optimum alignment of the three DNA sequences
AAATTT
AAAGGG
GGGAAC
equal to:
AAATTT---
AAAGGG---
---GGGAAC
with the total score S =  294 + 294 - 6 = 586? In this case I sum the alignment score for each of the three pairs.
Or does it equal to:
---AAATTT
---AAAGGG
GGGAAC---
with the score 200 - 7 = 193? In this case I am rewarding only the matches that occured across all three sequences at the same time.
Which of the two scores are the common Multiple Sequence Alignment algorithms trying to optimise for? Or if both are valid, then which optimal alignment (i.e. with respect to which definition) is preferred if realistic reward/penalise values were used?

Please do some reading on a topic before posting a question. This one is based on simplistic and false assumptions. A look at the WIkipedia page on MSA (https://en.wikipedia.org/wiki/Multiple_sequence_alignment) would make you aware of what a complex topic it is.

Further would you please avoid or define abbreviations in the titles of questions. This helps people searching for a topic and those who may be interested in it but are not familiar with the jargon. I am altering the title to include the full name. Please do not revert it.

A common scoring method is "sum of pairs", which is essentially the sum of scores of all pairwise alignments. The wiki page has mentioned this. You can find more discussions in Durbin's book biological sequence analysis, section 6.2.

In your case both answers are equally valid.
The scoring matrix, for example DNAFULL (http://rosalind.info/glossary/dnafull/) usually contains various penalties for wrong alignments.
Also the introduce gap score should NEVER be set at 0 as it will cause the aligned sequences to be filled with artificial gaps!
The only thing the algoritms try to optimise towards is the score, therefore you need sane values for calculating the score and those you propose does not result in usefull alignments.

The scoring matrix you mention is used (to the extent that people actually use it) for pairwise alignment. At least for Clustal, a dynamic position-specific scoring system is used as successive sequences are added. Therefore the question does not relate to actual MSA — at the most is is only a weekend newspaper puzzle.

The DNAFULL matrix can be used instead of the PAM or BLOSUM matrices for multiple alignments. The fact that it is mainly used for PAIRwise alignment doesn't exclude it from being used for MSA.

Jeppe Nielsen is right: MSA programs do use pair-wise scoring matrices. David is talking about progressive alignment, which is a heuristic to do MSA as finding the optimal solution is NP-hard.


text:
What is this feather like bug with no legs?
Seen on leaf in North Texas, USA in April 2017. Critter will attach itself to any object put next to it.

Could it be a feather? What made you think it's an animal?

Can you see any features that appear animal in nature? Eg. Head, eyes, antennae, mouthparts. Could you describe them if yes?

It is a specialized feather called "down" (like in down pillows, etc.)

Down feathers have a rachis that is shorter than their longest barb. They are completely plumulaceous and have a fluffy appearance, which results from filamentous, noninterlocking barbules.

Anatomy, Clinical Presentation, and Diagnostic Approach to Feather-Picking Pet Birds

Great diagram presentation

This indeed simply looks like a feather.

 Source: Pattaya Daze
Many predators, particularly hawks and other birds of prey, will typically pull these whimsical down feathers off of their prey before eating.

 Source: Kruger Sightings

 Source: Tom Strong Reviews

Wow wonderful gif animation.


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What is full form of r and K in r-selection species and K-selection species?
What is full form/ meaning of 'r' and 'K' in r-selection species and K-selection species? Does this 'r' means "Random" and the 'K' means "constant"?

This is from Wikipedia (with no other references): "In the etymology of the Verhulst equation, r comes from rate while K comes from carrying capacity. In German, the word for capacity is Kapazität and K stands for the "Kapazitätsgrenze" (capacity limit)." I haven't been able to find the first paper defining them, which is apparently from the early 19th century.

If anyone can find this paper, the answer may be inside: Verhulst. 1838. notice sur la loi que la poulation pursuit dans son accroissement

I'm not sure exactly what you mean by full form. The wikipedia article you cited defines r and k selection and also describes which each variable means in the Verhulst equation. Could you clarify exactly what you're confused about?

Not the real answer but a good mental handle -
r is rabbits' strategy, K is Kangaroos'.

@gill-gabel we were taught to remember it as r = "rapid" and K = "Kautious" :)

This article discusses the origin of the terms. They come directly from the equation used to describe population dynamics. As Canadianer mentioned the Wiki also covers it quite well.
"r" stands for "rate" {growth rate}, r strategists have a high r value and a low K value. They grow fast but most die.
"K" stands for Kapazitätsgrenzen which is german for capacity limit, now called carrying capacity, K strategists have a low r and a high K. They grow slow but more survive.

@Canadianer Thanks for catching that I meant to reverse the terms and then forgot to go back and do it when I started trying to get an equation to import.

That should be Kapazitätsgrenze. "Grenze" is the German word for limit/border.

Correctly answers my question, and accepted using green tick mark.

If you are looking for a way to understand and remember these letters, because I too found these terms confusing initially, then I use the following.
r-strategy = focus is on Reproduction Rate as much as possible - then all the other traits, grow fast, die young, etc, tend to follow.
K-strategy = focus is on the Kapacity (Germanised spelling) of the environment, i.e. do not exceed the carrying capacity of the local environment for your species.

The question is about the origin of these terms. Your answer doesn't seem to address that.

Upvoted since it may indicate possible etymology but op wasnt finding mnemonic rather op was misleaded where somehow a mnemonic was misinterpreted as a techinical. definition.

WYSIWYG: The questioner was asking about the etymology, but I think not out of interest in linguistics, but out of a need to (1) understand and (2) remember these terms. When the letter cannot be related to a word (in a language you know), this becomes difficult in both respects. So my response answers the implied need. In any case, my response also contains some etymology. Obviously, making the word Kapacity tells you that this letter comes from the German for Capacity. And R standing for Reproduction Rate surely tells you that that is the etymology/source of the user of that letter?


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Function of Co-enzymes
Is the function of a co-enzyme to make a reaction run quicker? If catalysts speed up reactions, and enzymes are catalysts, and co-enzymes make enzymes work better, does that mean the co-enzymes just make reactions quicker?

Where coenzymes are used, they are generally required for catalysis.

What research have you done to answer this question for yourself? Have you googled for "coenzyme"? This site expects posters to demonstrate that they have put in some effort themselves.

@David I think the biggest problem with the question is that it is unclear. We need to know what enzyme/co-enzyme OP is asking about before google even enters the fray. Either way, I think the question needs to be developed further.


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Identification of a purple flower

What is this purple flower? Picture taken from a garden in India.

It closely looks like Tibouchina urvilleana* or any other Tibouchina species. You can have a look here.

[Source:Wikimedia common]

Tibouchina urvilleana is a species of flowering plant in the family Melastomataceae, native to Brazil. Growing to 3–6 m (10–20 ft) tall by 2–3 m (7–10 ft) wide, it is a sprawling evergreen shrub with longitudinally veined, dark green hairy leaves. Clusters of brilliant purple flowers up to 10 cm (4 in) in diameter, with black stamens, are borne throughout summer and autumn.[Source]

*Credits to @RHA for suggesting the right species.

Thnx. It looks like that


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What do spiders do all day?
I found a question about ants sleeping - Do ants or other insects sleep, and if so why?, but I don't think it really answers my question.
For the question, I'm mostly referring to web-making spiders, say orb webs.

So a spider set up shop inside my house late last year. It built a web high up in the corner and started catching moths and stuff. I know it's been there and it's the same spider because I've watched it grow.
But when the spider isn't catching something, eating or building a web - what is it doing? Just waiting for web vibration?
I imagine if it was outside it would be hiding or trying not to be prey. I also imagine it might be looking for a mate. What I can't figure out is what this spider does all day.
Why would it build a web where no other spiders are and then stay there for months doing nothing?

It is meditating. But the one outside my back door is plotting just when and how to scare me to death by jumping on my head. I can tell by looking deeply into the largest of its four pairs of eyes. Where is @Roland when we need them?

Why don't you think it could be hiding or trying not to be prey indoors? I doubt the spider is quite aware of the barriers your house provides to entry of certain predators, or that it has chosen a place that is less likely to be frequented by its conspecifics. I think what you are describing: building a web and waiting, is essentially the activity of "hunting" for a spider.

@BryanKrause - Indeed, house spiders are just that: house spiders.

@anongoodnurse I thought house spiders didn't have a long enough lifespan for the amount of time it has been here.

They can live about two years if they have food. And they can survive on really tiny things, like drain flies.


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What is this small black spider found in NY?
I found this small, black, spider with a yellow mark at the top of its abdomen, crawling on my desk in my office (located in the Lower Hudson valley in NY). I have never seen a spider like this before.

What is this spider, and is it native to NY, or is it an invasive species?

It is hard to see in the picture, but did the spider have 3 distinctive yellow marks in its abdomen. If so, it could be a jumping spider.

I did some searching on line, and see it looks like phidippus audax, but it didn't seem to do any jumping.

Jumping spiders are the largest family of spiders on Earth; now that you've seen one, I'm pretty sure you'll notice them around. And they almost all look like this, but with different coloring, sizing, and back leg modifications. And, yes, they can and do jump when they need to, though it's more like a hop. A scary hop, when they are trying to scare you off. They make me jump.

If one of the answers below have answered your query, consider accepting it by clicking the green checkmark, giving you and the other user some reputation points. This aids in closing the question as solved. There is no obligation to do it either.

It resembles a juvenile Phidippus audax, of the family Salticidae.

Image Source: SpiderZule
According to Wikipedia >>

They are typically black with a pattern of spots and stripes on their
  abdomen and legs. Often these spots are orange-tinted in juveniles,
  turning white as the spider matures.

Phidippus audax is a common jumping spider in North America and definitely not an invasive species.

Are the number of spots on the abdomen variable? I am sure the one in my picture had only one, not three like the one in the image you provided.

@lzam There are varying patterns for the distinctive markings, ranging from strokes to spots. Most commonly observed are a collection of 3 spots with one of them being bigger than the rest of them. I cannot be sure, but maybe the number and type of spots change during maturation - this guess can be made because the color of their  spots does change on maturation. Again, I could be wrong.

It is the Bold jumper, Phidippus audax. The “Bold Jumper” is one of the largest and  common species of jumping spider in North America. The spider is mostly black with a white, orange, or red triangular patch in the center of its abdomen.


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What is linkage strength?
Background

If linkage strength between any two gene loci is 70%,
  what would be the amount of crossing over between
  these loci?
(a) 15% (b)30% (c) 70% (d) none of
  these.

My approach at understanding the concept
I didn't find much about linkage strength from any authentic source.
I can think of two things :

The strength of a linkage would be greater if the spatial separation between two genes is less and the lesser if the separation is more. This is semantic. But,
how can it be represented in percentage? What does this 100 mean in this 70%? The separation between two genes can be more than 100 map units.

Question:
What does linkage strength mean? How is it related to amount of crossing over (number of recombinants)?
N.B. I would appreciate answers citing some authentic sources.

https://www.nature.com/scitable/definition/linkage-51

With the above source answer is b) as the two gene loci are inherited together in 70% of the cases (which is the linkage strength). In cases were the distance is large the linkage strength depends on the ploidy level of the organism. Eg. 100% if haploid, 50% if diploid, 33% if triploid and 25% if tetraploid. In other words the linkage strength can only reduce to the lowest level possible, if the process is entirely random.


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Genetic pros or consequences of children born to parents of mixed nationalities?
I've gleaned a potentially flawed impression over time that a more diverse gene pool should, in theory, result in healthier progeny. Something about dominant genes promoted over recessive genes..
As a result of the above, I always assumed I should favor a mate from another region if I want to have children, thus hopefully ensuring the children have a diverse mix of DNA bits to assemble out of.
I'm an American male (almost 38), and by a curious chance I find myself dating a Russian female (almost 29) who is in a US PhD program. We've been together a little over a year, and we've discussed marriage/children. So far so good.
However there's an observational wrinkle.. She sometimes associates with a local group of Russians and I tag along. Not long ago at a gathering with several young families, of which I think many are mixed-national (Russian and American), I was discouraged to observe what I thought was a disproportionate number of children with various disorders. If memory serves, there were 2 or 3 autistic and one down syndrome child out of about 11 or 12 kids of the same age.
[It might be worth noting that this is a church group. Church might provide a kind of social safe-haven that allows these families, particularly the children, to socialize with fewer concerns. As such it might make sense to see them in greater numbers.]
Anyway, suddenly I'm doubting my prevailing assumption about genetic diversity and wondering if there is a correlation between autism and the children of parents of mixed nationalities.
In this article, I read:

In the studies conducted in Nordic countries, a statistically
  significant 58% increased risk of autism was observed among the
  offspring of mothers born abroad.

So I find myself vexed. Is there a propensity for genetic challenges in children born to parents of mixed nationalities?
(FWIW I realize our ages dip into another risk factor, but I'm specifically asking about regional genetics.)

Related: Does it make sense to classify all humans in a single species?

Did you read the rest of that article? The authors suggest many alternative possibilities for the effects they observe:

Several hypotheses have been postulated, including the idea that fathers with social disability potentially due to a genetic mechanism associated with autism may be less able to find a spouse from their own country and may therefore find a wife from a foreign country with whom to have children91. More likely, Gillberg et al.91 suggested that women born in another country may not be immunized against the common infectious agents in the country in which she gives birth and may therefore be more susceptible to relatively innocuous infections which may increase the risk for autism. Other possible explanations include a potential role of maternal stress due to the demands of residing in a new country, particularly with limited social support, or stress resulting from the experience of emigrating, perhaps due to economic or social factors. These hypotheses do not explain the relationship with maternal place of birth seen in a cohort study of children born in California between 1989-199416, which showed a 40% decreased risk of autism among the children of women born in Mexico as compared to California. The association between maternal immigration and autism risk requires further examination in other areas of the world to examine whether the relationship can truly be generalized.
  Gardener et al., 2009

(emphasis mine)
In addition to these factors, note that p-value for that trend was only .06, and although there are a lot of problems with basing conclusions on fairly arbitrary p-values, a p-value of .06 suggests that differences of the magnitudes observed would often occur by chance. I'd say it's an area of open study, but it is quite a leap to jump to a conclusion that mixed nationalities result in higher incidences of things like autism from 1) the observation of a very small cohort of 12 children and 2) this other study which suggests many alternative possibilities for what is a small and possibly insignificant effect.
There are two main benefits for populations to avoid becoming inbred. The first is that there may be many deleterious alleles with low-incidence across a whole population, but you have a very high likelihood of producing a homozygous recessive offspring with a close relative. The second is overall maintenance of genetic diversity across a population, which could be important if suddenly exposed to a new disease, for example.
However, it is also possible for outbreeding depression to occur, which is a reduction in fitness after mating genetically distant individuals. However, outbreeding depression usually occurs either when fitness of some variable is low at intermediate values: for example, high fitness for small or large animals, but not for medium-sized animals, perhaps due to slightly different niches within the same species. Outbreeding depression can also occur when there is sufficient genetic separation between two individuals such that their whole protein milieu has evolved on a different background, such that alleles that cause no problems in either population alone are incompatible with alleles in the other population.
This previous answer here on Biology.SE talks about the lack of evidence for outbreeding depression in humans and a bit about why. Briefly, there is simply not the type of disparity in fitness conditions or sufficient genetic variability within humans for either of those situations to occur.

The site has apparently queued my upvote, but you got me--I skimmed the article and missed those alternate theories. However, would it not be true that statistic (58% increase) describes the mere condition that the mother was an immigrant...and the correlation does not regard why, which the alt theories then consider? Maybe it can be immunization and/or maybe it can be stress...or even something else, but the fact is, being a female immigrant was still the common denominator...no?

@user31840 That's my understanding - the point, though, is that being a female immigrant is likely to be correlated with all of those other factors, and based on our understanding of not only the unlikelihood of outbreeding causing autism (for the reasons I state later) as well as the poor relationship between autism and purely genetic causes, those are much better explanations than outbreeding, especially because, like the other answer I linked notes, there isn't really any evidence for outbreeding depression in humans in any circumstance.

Given a couple of centuries of European immigration to the US (and presumably a good deal of intermingling of European peoples in previous millenia), could mating between a (mosty caucasian) American and a Russian really be consideed outbreeding?

@jamesqf Yes I'd agree that intermingling and immigration means there are very few groups of humans that are truly isolated from each other over an appreciable number of generations, although I don't think there is a specific definition for outbreeding, or inbreeding for that matter, it's all relative.

@Bryan Krause: I think you possibly could find such groups, depending on how much isolation is enough.  Say Japanese and the !Kung people of southern Africa, or Inuit and Australian aborigines.  But any two populations of mostly European descent, no.

@jamesqf Exactly why I said "very few" groups - those are all fairly special cases. However there are also some groups of European descent that are slightly isolated from other Europeans, including some Amish communities or Ashkenazi. The other point I was making is that inbreeding and outbreeding don't have specific definitions, it's all relative.


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Can any one help id this bug or at least tell me if it could be biting my kids
We live on the gold coast in australia. We started looking into what these bugs were after my son became covered in severe bites. Hes always reacted a little bit to bites but this was intense.  The initial bite looked somewhat like a raised welt which he has scratched at but now over a week later hes saying they are still itchy and even with bandaging and covering the areas hes still getting more bites.  I have attached a photo of the bugs that are around at the moment but also some of the bites. we get alot of mosquitos and midgies (sand flies) but hes never reacted to those bites like this. We have recently had a flood in the area so everything is still wet. Its change of season so its cooling down.  Any help would be amazing in helping treat our son but also hopefully prevent further issues

Questions seeking medical advice are not allowed here. You should rewrite your question so that it just about identifying the insect.

it looks like a biting midge to me.

It is certainly a Diptera. How big is it? Biting midges are usually very small, 1-3mm, this one looks bigger.


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Why aren't nucleic acids on Nutrition labels?
All the other macromolecules are listed on the Nutrition labels and nucleic acids do have some caloric value, why aren't they on the nutrition facts?

Please remember to provide reasons for a down vote so the OP can make appropriate edits to this and future questions.

nucleic acids are in nearly all foods, with the only exception being certain condiments. that alone could be the reason no one bothers labeling them.

They're probably counted as carbohydrates. Ribose and deoxyribose are carbohydrates after all.

Despite the question being interesting, I am voting to close. I am voting to close because it is clearly a public policy / food security question and not a biology question.

This FAO report can tell you all about food analysis and why things are and aren't on the label: http://www.fao.org/docrep/006/y5022e/y5022e03.htm#TopOfPage

First, not all nitrogen in foods is found in proteins: it is also contained in variable quantities of other compounds, such as free amino acids, nucleotides, creatine and choline, where it is referred to as non-protein nitrogen (NPN). Only a small part of NPN is available for the synthesis of (non-essential) amino acids.

The DNA in food would contribute to the nitrogen content. Then (using a food-specific "Jones" factor) total nitrogen content is converted to protein content. So in a way it's already there.
Listing DNA separately would require extra testing, and also the difference in daily use would be negligible. There's not that much DNA in food anyway and, like protein, DNA can be converted into new protein and energy. The Jones factor already accounts for this.


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A suggested ancestor of cyanobacteria consumed manganese. Why not magnesium?
Joseph Kirchvink and others have suggested a theory that a precursor to cyanobacteria consumed manganese (I believe in the form of Mn2+ dissolved in water). Why wouldn't dissolved Mg2+ work equally as well? It was more abundant and is the central ion of the porphyrin ring in chlorophyll.

There is no conclusive proof of why those organisms chose Mn over Mg (for obvious reasons). I'll just give an opinion on how Mn could be beneficial over Mg.
Even in the photosynthetic organisms present today, $Mn^{2+}$ is the ion used for oxidation of water while $Mg^{2+}$ is used to just get electrons by input of photons (from Kirschvink, 2015, if you're talking about this). When electron is removed from $Mg^{2+}$ (from 3s orbital), the formed $Mg^{3+}$ quickly oxidizes $Mn$ in the oxygen evolving complex (see this answer for more details). This suggests that $Mg^{3+}$ is much more unstable than $Mn^{3+}$, maybe too unstable for enzymes to use it to catalytically oxidize water.
Another point could be energy requirement. The third ionization enthalpy of magnesium ($ Mg^{2+} \rightarrow Mg^{3+} + e^-$) is 7732.7 kJ/mol. On the other hand, the third ionization enthalpy of manganese ($Mn^{2+} \rightarrow Mn^{3+} + e^-$) is only 3248 kJ/mol (which is still higher than other elements nearby it in periodic table, but thats another point). Now, though this energy is available today via sunlight for magnesium, it was most probably too large an energy input (keeping in mind the environmental conditions, like low sunlight due to excess sulfur dioxide in atmosphere, Kirschvink, 2015). Thus, manganese may have proved to be more beneficial than magnesium. As time passed, slowly there would have been enough energy available to oxidize magnesium, so it (sort of) took over manganese in the race.
Again, this is just a speculation. The real reason can remain elusive for a long time (until very strong, conclusive evidences are found).


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What species of snail is this?
I found it in Washington state, in a city south of Seattle. I found it next to a bush after it rained on someone's driveway. Here are two pictures of it:
( originally posted in instagram )

If anyone can identify this species, kudos to you.

where is the location?

@TheLastWord It's in the question…

If the answer below have answered your query, consider accepting it by clicking the green checkmark, giving you and the other user some reputation points. This aids in closing the question as solved. There is no obligation to do it either.

It resembles Cepaea nemoralis, or commonly called Grove Snail, belonging to the family Helicidae.

Image Source: WikiMedia Commons
According to Wikipedia, these snails were introduced to North America from Europe. These fascinating creatures occur in diverse forms of shell color as well, as shown below.

Image Source: Metodologie di Programmazione
Here I have found a very detailed shell and body markers for Cepaea nemoralis.

Image Source: ResearchGate


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What drives max heart rate on beta blockers?
In a healthy human being, the increase in heart rate from rest to around 100 to 110 beats per minute at low intensity exercise is due to withdrawal of the parasympathetic nervous system's influence. If exercise intensity increases beyond that point, the matching increases in heart rate above 100 to 110 beats per minute are due to sympathetic nervous system influence.
There is a transition range around 100 to 110 beats per minute where the intrinsic rate of the heart beat is determined by the body's metabolic activity.
However, when a person takes a beta blocker, the sympathetic influence on the heart rate is attenuated, so that the person's max heart rate is lowered to around 110 beats per minute.
What is driving the heart rate at high intensity exercise in patients who take beta blockers?  Is the heart rate around 110 beats per minute in patients on beta blockers driven primarily by the metabolic influences in the blood? What other factors are influencing heart rate around 110 beats per minute in patients who take beta blockers?


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Explain a gene network to a first year undergrad
I have an adjacency matrix with list of genes connected to each other which signifies the gene network. How do you get this information that one gene is connected to other in the first place. Is it that you do a microarray analysis and find genes that are upregulated and downregulated and assume that all the genes that are upregulated, regulate each other. Kindly explain.
P.S The microarray example is what I assumed. Doesn't mean that it should be the way that a gene network is deduced. My network is an undirected one.

As for unsupervised networks, you could start by explain some rudimentary network inference methods. Here is a good review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956069/.

There is no single answer, because networks (or graphs, as they are called in discrete mathematics) are flexible tools that can be used to model all sorts of relationships between genes, transcripts, proteins, or other entities in biology. (And networks are useful models in many other disciplines too, like sociology.) Depending on the type of network you're considering, there are various experimental methods for determining connections. I give only a couple of examples below. For general information on networks as abstract models, look into graph theory.
Gene regulatory networks
A gene regulatory network is a directed graph where one gene (A) regulates another (B). In this case, the connections between genes are directional and can be represented by arrows A $\rightarrow$ B. Depending on exactly how you define "regulation", a connection A $\rightarrow$ B can mean different things, for example:

Gene A encodes a transcription factor that binds to gene B. In this case, evidence for A $\rightarrow$ B comes from assays of proteins binding to DNA, such as chromatin immunoprecipitation (ChIP). Large collections of such data are available in databases like Transfac.
Expression of gene A causes regulation of gene B, by any mechanism (possibly indirectly). In this case, data for an interaction can come from experiments where gene A is induced (forcibly expressed) or suppressed/deleted and the resulting changes in other genes are measured, for example by microarrays or RNA sequencing. A famous early example of this is the "Rosetta" data set on yeast deletion mutants.

Inference of gene regulatory networks is a large and complicated topic that I cannot cover here. It depends on many factors, such as how you model the time dimension (do you have steady state or transient data), and how you parameterize the network to model expression data quantitatively. The review suggested by @CMosychuk looks like a good place to start.
Coexpression networks
This type of network represents coexpression between genes (or more accurately, between mRNAs or proteins). This is typically a representation of pairwise correlations between genes across some set of conditions, so the data source can be any collection of mRNA or protein level expression data. (Here is one example.) Because correlations are symmetric, connections in this type of network have no direction, and can be represented simply as a link A$-$B (not an arrow). Partial correlations are sometimes used to filter out indirect associations, but still these networks contain no causality information, and should not be confused with the directed type.
Protein-protein interaction networks
These are undirected network models where a link A$-$B means that two proteins interact physically. Data supporting such connections come from various biochemical assays for protein interaction, such as the two-hybrid assay or immunoprecipitation. There are large databases collecting protein-protein interaction data that can be used to build these network models, for example BioGRID.
There are many other types of networks, but this is already a long answer :) As you can see, it's important to be clear on what type of network you are working with. Often the data you have available will determine what network model is suitable --- for example, if you have only a collection of unrelated transcriptome profiles and no causality information, a coexpression network might be the best model.


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Maximum biologically possible age for a human being?
Today, most of people die because of some kind of illness that we do not yet have a cure for. However, if that was not the case, how long can human body possibly live for? Is there a theoretical maximum at which our brain will simply refuse to function due to age alone, or can we remain conscious forever if we could simply swap our brains into new bodies without any risk?

technically we mostly die becasue the body systems start failing as we age this makes us susceptible to disease. Its kinda like AIDS, if you have it it is an infection that will kill you but really AIDS is the reason you got the infection in the first place. Technically the infection killed you but ultimately it was having AIDS that did it.

@John - Body systems failing is directly fatal disease. Does kidney failure predispose you to other causes of death? What about congestive heart failure, or straight up myocardial infarction? The only common examples of killer infectious diseases in the elderly I can think of are UTI's and pneumonia.   Can you be more precise perhaps?

Yes sorry that is a bit confusing the way I worded it. My point was that if we have a cure for all illnesses then you have a cure for aging. The current theory of senescence "detrimental aging" is that it is a product of our own genes not be proof test by evolution for how they interact much beyond our reproductive age combined with them not producing structures that last forever. It is difficult to cure age related illness  becasue they are a product of a "healthy" body acting as it naturally would. If you can "cure" this then you can make people live as long as you want.

Even in perfect environmental conditions we would age. Living is associated with a myriad of deleterious processes, both random and deterministic, which are caused by imperfectness, exhibit cumulative properties, and represent the indirect effects of biological functions at all levels, from simple molecules to systems. Here is a good read on this topic https://www.ncbi.nlm.nih.gov/pubmed/27060562
Even if nothing else was wrong (which is not the case) the accumulation of intracellular and extracellular junk which our systems are unable to dispose of (lipofuscin, amyloid beta, etc) would eventually kill us. https://en.wikipedia.org/wiki/Senile_plaques
As for the maximum age - nobody we know of made it past 125 years yet. https://en.wikipedia.org/wiki/List_of_the_verified_oldest_people


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What would happen if all magnesium was removed from a person's body?
Magnesium is essential to bodily functions. It enables ATP from which most energy is produced in cells. It regulates over 300 biochemical reactions in the body. It is important to the transfer of nutrients through cell walls. It stabilizes the structure of DNA and RNA.
What would happen to a person if some alien micro-organism totally depleted his/her body of magnesium? How quickly would they die? (Yes, there may be a sci-fi story being written here.)

well oxidative phosphorylation and glycolysis would both stop for a start, it is essential for several of the enzymes involved.