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

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

Returns the proteins annotated to belong to a given term.

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

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

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

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

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

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

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

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


text:
Can a postsynaptic neuron 'shut itself off?
I am an amateur interested in neuroscience and was curious whether there is a process by which a neuron or group of neurons would close their receptors and stop receiving signals from specific synapses for a temporary period?

I think you might be onto the desentization of neurons. Here's a not very helpful Wiki link and a paper

AFAIK, receptors can not respond to stimuli if 1) they are modified in some way that it no longer binds its ligand, 2) modified in some way that the binding does not induce a change detectable inside the cell, 3) the old ligands are not cleared so any new signals are not noticed...these are the things I can think of right now...

drugs can apparently have this effect of decreasing synaptic sensitivity due to habituation! also see anaesthesia

An example would be the neurons that switch off/switch on based on our sleep cycle. Nerve-signaling chemicals called neurotransmitters control whether we are asleep or awake by acting on different groups of nerve cells, or neurons, in the brain. Neurons in the brainstem, which connects the brain with the spinal cord, produce neurotransmitters such as serotonin and norepinephrine that keep some parts of the brain active while we are awake. Other neurons at the base of the brain begin signaling when we fall asleep. These neurons appear to "switch off" the signals that keep us awake. Research also suggests that a chemical called adenosine builds up in our blood while we are awake and causes drowsiness. This chemical gradually breaks down while we sleep (reference and reference). Here is a study based on switch on/switch off of fear i mice (reference).
There are also artificial ways in which to shut down receptors like our sweet receptors (reference). There have also been studies done on other organisms where one particular study showed the switch on/switch off of olfactory receptors in cockroach antenna (reference).

source: Stack Exchange

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sort: votes


text:
How should I feed and keep an ant queen?
I have captured wandering ant queen. I guess she was just fertilised and was looking for a place to start a hive.
I'd like to create my own ant hive in artificial environment.
I unfortunately only have a small clean chemical bottle (1.5 CM in radius) to keep her in. I was wondering how much space would she need to feel safe.
I'm also not sure what should I feed her. Every morning, I have dropped few sugar crystals in the bottle. She shows much more individuality than an ant, because she has immediately started to collect them. It seems that she ate almost everything. I have also dropped few tiny drops of water in the bottle. Although it's hot and she ate the dry sugar she doesn't seem to drink it at all.
So what does she need? (well, except of natural forest which I don't have in my room)

Why this was downvoted? is it not acceptable question or how it could be improved?

@ruffp Feel free to upvote, like I did (and always do). I agree, the question is entirely on-topic.

First you need to identify your ant, for Czech Ants: http://www.antweb.org/taxonomicPage.do?rank=species&project=czechants&images=true
How should I feed and keep an ant queen?
Home for Pet Ant, Ant Farm:
There are lots of things you can use, for example, a clean transparent glass or plastic jar, or a fish tank of a size which you will decide is best for the ants you're keeping in it. As long as the container provides enough space, and the addition of any air holes small enough to prevent the ants escaping (much easier said than done); and also so you can observe your ants going about their daily activities, then it should be fine! Worker ants like to forage, so your set up needs to allow for the ants to do a spot of hunting for their food.
It is possible to make your own type of "Ant Farm" by using lengths of wood or plastic which have 2 grooves cut into them, like the frame used in double glazing. As long as you can place the frame onto a sturdy base to prevent it from falling over; or you can use plaster and other materials such as aerated concrete blocks, better known as Ytong nests. Two panes of clear glass or plastic can be placed into the grooves and sealed. Use the silicone sealant that is used around baths or sold where you buy glass fish tanks, but do remember to let it set and dry out well, as this will allow any chemicals to disperse harmlessly into the air before you add any ants. Also make sure that you can safely access your ant home, so you can put food in etc. You can also check out this youtube video or Wikihow.

Always try to cover your ants when not observing them to exclude light, as for most of their lives ants live in underground nests or places well away from daylight. This does not mean that they won't tolerate light; but they prefer to be in total darkness if possible, and queens rarely come out from their nests in the wild.
Feed the ANT:
If you are using a  gel-filled ant farms, it  contains all the water and nutrients your ants need for survival. Make sure to keep your kit sealed so the gel does not dry out.

In sand-filled ant farms, you need to add a few drops of water and small bits of food every few days. Ants also love a special treat of water with sugar dissolved in it, but this can’t take the place of fresh water for drinking. You can provide them with a bit of honey at times, and they will probably drink some of that. A small section of meal-worm can help provide her with a protein boost. Again, feeding them until the first workers arrive is not necessary as they do not forage during this period naturally.

Moreover, Interesting Links:
http://askabiologist.asu.edu/collecting-queen-ants
http://ant-farm-stores-review.toptenreviews.com/what-you-need-to-know-about-ant-farms.html
www.tarheelants.com/
Also, try "Ants can be pets" group on Facebook.

Your PDF link is aimed to distinct ant workers, which might look differently than queens. It also only applies on species that live in united states and are considered harmful. You're also generally takling about making the colony - not very much about the queen herself. In an answer on another question, which you have deleted, you claimed she doesn't eat at all...

Sorry, you never gave your geographical region, I have removed that part. As for the last deleted question, I was trying to explain the general scenario. Queen ants doesn't eat after laying eggs as they fend of there flight muscle. It doesn't mean she doesn't eat if given provided to her, she even eat her eggs if she is hungry. There various links says the same thing: www.animals.howstuffworks.com/insects/ant-info3.htm
PS: I don't know why you have me so much. All the answer I gave are mostly liked, if not, I just remove them. I love Biology SO and I am not leaving here.

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text:
Which part of human eyes is getting tired?
It's a thing of common sense that if you read, drive or look at computer screen for too long your eyes will get tired. They burn, itch and try to close all the time.
But I was wondering which part(s) of them need rest so much... Blinking muscles? Lense muscles? Or the eyeball is drying out?

These symptoms have a name: Computer vision syndrome.
Basically our eyes are made to look at longer distances from 1-6 meters without much accommodation. Typically computer screens are located at a much closer distance (30-50cm), which requires constant accommodation by the eye. This leads to high stress on the muscles in the eye which subsequently get tired. Additionally less blinking leads to drier eyes.
One of the common recommendations against this is to regularly focus further located objects to give the eye the chance to relax. This is sometimes called the "20-20-20" rule, every 20 min focus on a 20 feet (about 6 m) far object for 20 seconds. See the article in the Wikipedia and here for more information (and probably also the linked references in the articles).

Was there any success using lenses to make screen appear 6 meters away?

This would be like you sit 6m away from you screen: It would most like be too tiny to read anything.

You could sure make it look 6meters high using proper optics. I heard screens in fighter aircrafts are on the cockpit and appear to be on the sky, so that the pilot does not need to change focus.

Then you need to turn the head quite a lot to read everything. And my guess for the screens in fighter jets is that they are further away than the typical computer screen.

This doesn't answer the question of which muscles are getting tired.

I haven't found any specific information on that. Otherwise I would have added it to the answer.

Wouldn't the muscles that allow the eye to focus be the ones getting tired?


text:
Can ants learn things?
I have an ant nest in a jar. Whenever I want to observe them, I have to remove the cover and therefore put them in light - that scares them. They also can see shadow cast by myself.
I often throw in some food when I'm uncovering the jar.
I was curious if ants will ever remember that I'm not dangerous and that light means food.
If not, are there other things they can learn? Do they teach each other to hunt? Can queen learn things ants can not (queen has shown a lot of individuality compared to ants)?

I was wondering the same with insects in general.

Ants can usually learn patterns, colors and sequences. Species that do not use pheromone trails rely heavily on landmarks for navigation, that is they perform learning walks during which they look backward and circle around the nest to learn what the landscape looks like so they can easily return to the nest after foraging.

Harris, R. A., de Ibarra, N. H., Graham, P., & Collett, T. S. (2005).
  Ant navigation: Priming of visual route memories. Nature, 438(7066),
  302.
Chameron, S., Schatz, B., Pastergue-Ruiz, I., Beugnon, G., & Collett,
  T. S. (1998). The learning of a sequence of visual patterns by the ant
  Cataglyphis cursor. Proceedings of the Royal Society of London. Series
  B: Biological Sciences, 265(1412), 2309-2313.

This is usually the case in large ants that tend to rely less on pheromones and more on visual cues to navigate. Studies commonly focus on species such as Gigantiops destructor or Myrmecia spp.

Macquart, D., Latil, G., & Beugnon, G. (2008). Sensorimotor sequence
  learning in the ant Gigantiops destructor. Animal Behaviour, 75(5),
  1693-1701.
Jayatilaka, P., Murray, T., Narendra, A., & Zeil, J. (2018). The
  choreography of learning walks in the Australian jack jumper ant
  Myrmecia croslandi. Journal of Experimental Biology, 221(20),
  jeb185306.

The type of learning you are referring to may be termed habituation, and habituation has been shown in ants, for example some ants tend to be less aggressive to other colonies that they encounter frequently.

Langen, T. A., Tripet, F., & Nonacs, P. (2000). The red and the black:
  habituation and the dear-enemy phenomenon in two desert Pheidole ants.
  Behavioral Ecology and Sociobiology, 48(4), 285-292.

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text:
How can sodium and potassium from burned organic matter (ashes) reenter the ecosystem?
If you thoroughly burn something you end up with bunch of oxides and hydroxides, as far as I know.
Sodium and potassium hydroxides are plentiful in ashes, which is why lye was created by soaking ashes in water. Lye is not exactly nice to organisms.
So the question is, how can caustic lye ever reenter the ecosystem as potassium. If it cannot, does that mean that nature cannot renew it's potassium content?

Wood ash is commonly used as a fertilizer. It acts this way in natural burning ecosystems also, where the ash from burned plants fertilizes the growth of new plants and those that survive the wildfires.
The primary constituents of wood ash are calcium and potassium salts. Lye is extracted from these salts by extracting them in water; the hydroxide salts are more soluble so the other salts are left in lower concentration than the original ash.
However, when in solution, KOH isn't really a thing anymore: you just have potassium and hydroxide ions floating around separately. Nothing special needs to be done to separate the potassium from the hydroxide ion except dissolving in water. Neutralizing the solution is then just a matter of adding an acid. There are plenty of sources of acid in soil, and rain itself tends to bring acidity. One of the sources of acidity in rain is, in fact, from fires. It is not as strong as the 'acid rain' caused by industrial sources, but there is no magic in fire that causes basic chemicals to be left behind without producing acid ones elsewhere.
The main damaging effects of wood ash are if it is applied in high concentrations where it can directly enter water sources (see for example UGA extension). In this case, it can raise pH enough to be damaging to life. Large quantities from large fires can also raise pH substantially in streams and such (see for example Burton, C. A., Hoefen, T. M., Plumlee, G. S., Baumberger, K. L., Backlin, A. R., Gallegos, E., & Fisher, R. N. (2016). Trace elements in stormflow, ash, and burned soil following the 2009 Station Fire in Southern California. PloS one, 11(5), e0153372.).
Eventually, however, there are enough sources of acid in the environment that there is no way the salts are permanently alkaline from the perspective of the whole environment.

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text:
When you lose weight, how does the mass exit your body?
As a thought experiment, consider the case of Angus Barbiery, who allegedly lost almost 200kg in about a year by not eating at all, save for necessary nutrients provided as supplements.
My question is, where did those 200 kilograms go.
And please, don't suggest that it was "converted to energy". 200 kilograms of mass would be approximately equivalent to 1.8*1016 joules. For comparison, Czech nuclear power-plant Temelín generates approximately  4.3*1016 joules of energy.
So how does the mass exit the body after the glucose is metabolized?

I suggest you consult a text book to find out the chemical products of the metabolism of glucose (or fat). Then blush and withdraw your question.

Closely related/possible duplicate of: Breathing faster to lose more weight

To burn fat it needs to be aerobically.  Cardiovascular exercise is critical...steady state heart rate 65 to 85% of max heart rate using large muscles.  After 10 to 15 minutes, THEN one is burning fat.  So holding onto that rate of exercise for another 30 minutes means major burning of actual body fat calories.  Figure out how much you would be able to lose per day walking for an hour.  Don't be discouraged, you are also changing your body to BURN fat more readily like a race car versus a volvo.  People who are more muscle than fat NEED calories regularly.  Fasting is just stupid and stupider.

Nobody except you is suggesting that the human body is a nuclear reactor, so the strident tone in your question is unfortunate. And what is presented is a calculation, not a thought experiment. (You owe Schrödinger an apology, I think — or at least his cat.)  Energy and matter may be interchangable, but before this was discovered there was a law of conservation of matter based on general everyday experience of how one form of matter is converted into another.

@David I was googling this before asking and a great amount of people have written things like "he converted the fat to energy". The thought experiment goes before the calculation, hence new paragraph.

Possible duplicate of Breathing faster to lose (more) weight?

as CO2 and water
in respiration sugar (or fat) is combined with oxygen to produce energy(ATP and heat), water, and CO2.

fats are converted to Acetyl Co-A just like glucose is, the rest of the metabolic pathway is exactly the same.

Well, you can indulge those who are too lazy to do the required research before asking a question, or you teach them how to find out things for themselves. However I suspect the poster hasn't even the chemistry to understand your first diagram, nevermind the bizarre construct that follows.

Not everyone see the need to mock laymen who are lacking a key piece of information but obviously put some though into their question.

Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. It is not for laymen, although the poster is certainly not a layman, but clearly has an education in physics. Regardless, he should follow the guidelines about posting: "Have you thoroughly searched for an answer before asking your question?". I just suggested that he blush when he realized that metabolism involves chemistry rather than nuclear physics, and a calculation is not a thought experiment.

Let me explain my criticism of your answer.Here is a question about metabolism from a physics student who has forgotten his school biology basics; that glucose is metabolized to carbon dioxide and water. You provide a diagram with terms like "Glycolysis", "Krebs Cycle","Chemiosmosis" — only comprehensible to someone who is already familar with biochemistry. You also use logically inconsistent representations with arrows between an explanation (aa group removed), a compound (urea) and a milieu (urine). Your answer is at the wrong level, and for more detail a link to a text would be far better.

Or was never taught it in the first place, or is lacking a key piece of information, such as that fat are converted into something that can undergo the same process as sugars, which is something few people are ever taught. Additionally a Phd in one subject can be a laymen in another.  Also I did include links.

I think it would be more truthful and interesting to add "and heat and ketones" to your bolded answer of CO2 and water. It's not all just CO2 and water. There are other metabolites excreted in urine as well. It's not a lot every day, but over time, it adds up.


text:
Are turkish hazelnuts edible?
The title of this question is Google suggestion verbatim, when I tried to write it. Yet, I found no answer specifically for Turkish hazelnuts.
Turkish hazelnut is a tree and it's fruit looks different from normal hazelnuts growing on hazelnut shrubs.
One such tree is planted close to my house, so I was wondering if I could eat all the nuts on the ground.

First off all let me say something about this tree.

Turkish hazelnut (Corylus colurna) is a slow growing pyramidal tree approximately around 25 m (82ft) tall, with a stout trunk up to 1.5 m (4 ft 11 in) in diameter. Leaves are deciduous, rounded, 6-15 cm long and 5-13 cm across, softly hairy on both surfaces. Corylus colurna is actually the largest species of hazel. The name Korylos (korys) comes from Greek and means helmet. The tree is dioecious.

Nuts are about 1-2 cm long, surrounded by a thick, softly spiny and bristly involucre (husk) 3cm diameter. The nuts are born in cluster of 3-8 together. The nuts mature in September and are edible, with a taste similar to common hazel (Corylus avellana). The nuts have a very hard shell, approximately 3 mm thick, which it makes them a little hard to open. Nut production is very irregular and occurs every two to three years.

Source
https://en.wikipedia.org/wiki/Corylus_colurna
http://www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?taxonid=277856
https://www.chicagobotanic.org/plantinfo/tree_alternatives/turkish_hazelnut


text:
What happens if the queen ant is removed and taken elsewhere?
Suppose I manually remove the queen ant from a colony, and take it to a completely different place (ant cannot visually travel back to its colony). Will it start a new colony in its new surroundings, similarly to the way in which it did after the nuptial flight? Or will it keep on looking for its old colony?

I didn't find any previous attempts of that artificial test, it depends a lot what kind of new habitat she is placed into. Ants use a lot of chemical queues, that tell them if they are in the right kind of habitat, humidity, rock, wood, to use as a burrow, and queens have an instinct to hide from light. There may be a question of time before the queen ant changes behavior, if she has no colony chemistry to react from, so it may take her 1 hour, 1 day, 3 days to return to solitary behavior. So she would search for her perfect scenario, as similar to a nest as she can find, and start a brood.


text:
Odds to clone a parent
I was asking me something weird, and I thought you might validate or not my theory.
Hypothesis: A brother and a sister have one chance over 78 billions to clone one of their parent if they procreate
Here is my method:
I have 23 chromosomes from my mother, and 23 from my father. My father has 23 * 23 = 529 combinations of chromosomes in his "gametes". If my experience is willing to work, I need to have the exact opposites of my father chromosomes than my sister ones. That means that we can't have any of my father's chromosome in common with my sister. That makes approximately 1/529 * 1/529 = 1/279 841.
Then, if I decide to procreate with my sister, our child needs to have the 46 chromosomes back from my father. So the computation stays the same and I will have 1 chance over 279 841 to make it so.
1/279841 * 1/279841 = 1/7.8*10^10

My question is: Is my theory valid? If not why? If yes, that will make a hell of a story at parties...
Thank you for your scientific answers and have a nice day!

For starters, you're ignoring recombination.

...and mutations

Assumptions
You are ignoring recombination and mutations. If you were to add these things, then this probability would be extremely smaller. In apparence, it would be infinitely smaller. It makes no biological sense to make such assumption but for the sake of the argument, let's assume only segregation happen. We will also assume that the parents are completely unrelated to start with (see @BryanKrause 's comment below).
For on given pair of chromosome
First, for a given chromosome number, both parents must each transmit a different chromosome to each offspring. This happens with probability $\frac{1}{2}$ per parent and therefore $\frac{1}{4}$ for both parents. Then, if the brother transmit the maternally derived chromosome, then the sister must transmit the maternally derived chromosome as well (and vice-versa). This occurs with probability $\frac{1}{2}$. So for a given pair of chromosome the probability to clone the parent pair of chromosomes (assuming no recombination and no mutation) is $\frac{1}{4}\frac{1}{2} = \frac{1}{8}$.
For the whole genome
The probability of this to happen for all 23 pairs of chromosome is $\frac{1}{8}^{23} = 1.69 \cdot 10^{-21}$, that is one chance out of a 1.69 thousands billions billions.
As you ask for the odds, note that for such low probability the odds ratio is pretty much equal to the probability.

Side note: your probabilities would be greatly improved if your parents, grandparents, great grandparents, and so on down the line were also each others' siblings. I wouldn't suggest it. Eventually you'd be down to just mutations, but even clones will have de novo mutations.


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Are there any examples of information compression in nature?
As the title suggests, I am looking for any examples of naturally occurring information compression. Initially, I thought protein synthesis was such a form of compression, creating larger entities (proteins) from a small subset of chemicals (A,C,G,T(U) in DNA) via ribosomal translation. However, I was quickly disillusioned as the amount of information contained in DNA is not increased within proteins after their formation.
So are there any natural processes, whether in animal, plant or otherwise that exhibit information compression?

Can you give some example that, by your criteria, qualifies as information compression? Are seeds, sperms and ova not what you are searching for?

@Jan I think the OP is talking about compression as in typical compression algorithms (like .jpg compression), not just for replicated DNA from germline cells. So something along the lines of a genome consisting of many base pairs being concisely expressed by one of few base pairs, as opposed to a genome within one cell representing the genomes of many cells.

Preliminary Remarks
Many of the posts to this list about biological information (usually equated to DNA) from mathematical and informatics scientists start from what I regard as false premises, especially that the genome is similar to that man-made artefact, the computer. This post does not explicitly make that assumption, but I think it important to address the difference between computer systems and biological systems before considering possible examples of what is requested.
Do biological systems need to compress information?
Although one can argue that not all biological information resides in DNA (or RNA, in the case of organisms with an RNA genome) I suspect the poster was thinking of that, and that is what I shall restrict myself to — i.e. to genetic information. (Other answers may quite validly address other types of information.)
The point, at least historically, of compressing digital information on computers is space limitation. Lossless compression involves re-coding the information in a more compact form. For example, instructions in the PostScript language can substitute ‘d’ for draw, ‘s’ for stroke. Gif or tiff image compression can substitute 20x(256,0,0) for repeating (256,0,0) — a red pixel — twenty times. Such compressed information must generally be decompressed when it is used (e.g. when the gif file is displayed in a web browser).
I find it difficult to think of any compression/decompression of this type in biological systems, and I would point out that genome ‘space’ is generally (but see below) not a limiting consideration in biological systems. One example of this is the fact that many organisms (especially plants) are polyploid — that is they have multiple (apparently unnecessary) copies of the complete genome. Another example is that the genomes of mammals contain at least some DNA that can be regarded as unnecessary. Although there are arguments about ‘junk’ DNA having a function, it is difficult to argue that processed pseudogenes and SINES and LINES are necessary. However genome ‘space’ has not eliminated them.
Where space or size is a problem, there Nature often uses other solutions than compression. For example the genomes of RNA viruses are thought to be restricted in size because of the occurrence of slow non-enzymic alkaline hydrolysis of RNA. Influenza virus, for example, has a genome consisting of several shorter (less vulnerable) RNA segments, which may be considered as a solution to this problem.
However, here are a couple of possible examples, although not with the sort of compression used in computers.
Possible example 1: Antibody Genes
To put it in simple terms, the genome has the potential for expressing millions of different antibodies, but the immune system requires that antibody-producing cells only produce one type. Instead of having millions of antibody-producing genes, only one of which is expressed, there is a much smaller number of segments of the genes, from which each of the two antibody chains are combined in a process called recombination. This is illustrated below for the heavy-chain genes where combination of one of 250 V-regions with one  of 20 D-regions with one of 4 J-regions, giving 20,000 possibilities. The resulting heavy chain can combine with one of 1000 different light chains, giving twenty million possibilities. (The diagram and data are old, but the principle holds. See, e.g. the Wikipedia entry.)

Of course, there is an alternative, and converse, way of thinking about this. Rather than the existence of 500–600 genes being a way to compress 20 million, one can regard the existence of 500–600 being a wasteful way to encode only protein.
Possible Example 2: Alternative splicing of pre-mRNA
This is similar in principle to the first example, although the mechanism is different. Most of the protein-coding genes of higher eukaryotes are built up of two components — exons, which encode sections of the protein product — separated by introns, which do not. Both these components are present in the initial RNA transcript, but the introns are removed from this (spliced out) to produce the mature mRNA, which is translated into protein. An advantage of this arrangement is that there are alternative ways for the splicing to occur, involving removing some of the exons (as well as the introns). This can lead to different protein products, in some cases just two, in others dozens.

So one could regard this similarly as a compression mechanism — or alternatively as an example of wasted space in the genome occupied by the introns.
Possible Example 3: Read-through and frame shift proteins
Certain mature mRNAs have the potential to encode more than one codon by the processes of read-through or frame shift. In brief, a protein of 100 amino acids will have a mRNA with a stop-codon 300 nucleotides after the signal for the start of translation. However in a few cases (and most notably with small bacterial RNA viruses) the structure of the mRNA near the stop codon is such that in a certain percentage of cases a tRNA will misread the stop-codon, resulting in continued translation, producing a longer protein of different function.
Similarly, certain mRNAs have a structure at a certain point that encourages the tRNAs to continue reading in the wrong phase (missing a base or starting a base too early — I forget) so that the continuation of the protein has a completely different amino acid sequence.
There is an old review of this topic in Current Opinion in Cell Biology.
Although this is technically a way of compressing two proteins into one, its rarity makes it difficult to regard its biological rationale as being compression.
&c.
No doubt there are more examples. I had toyed with considering Wobble as a way of saving space for tRNA genes, but have probably written enough.


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HapMap 3 phased haplotype
I need to get HapMap 3 phased haplotype data. Where can I find it?
Actually I need these data for specific populations and a specific gene. What is the easiest way to find data?
I hope I can find an answer. Thank you!

Here is the FTP address. Inside you will find the phase_3 folder. For other questions check this page (the link to the HelpDesk is at the bottom of the page).

Thank you for your quick answer. I used following command for this file tar -jxf hapmap3_r1_b36_fwd.qc.poly.tar.bz2 . But I don't know how can I get haplotype data for ± 1 Mb at LCT gene from this file. Actually I need a data file which include sample ID and alleles to use in R.

That is another question and it is a bioinformatic one, maybe StackOverflow or Biostars are more suitable for that.


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haplotype data for 1000 Genomes
I need to get haplotype data for HapMap or 1000 Genomes for CEU, MKK, TSI, CHB and JPT for ± 1 Mb at LCT gene. I'm quite new in the area. Actually I don't know the meaning of "± 1 Mb". From which sites and how do I get the data? Do I need a program?
As far as I understand, LCT gene is on Chromosome 2. That's why I used following code:
wget -r --reject="index.html*" http://ftp.1000genomes.ebi.ac.uk/vol1/ftp/release/20130502/ALL.chr2.phase3_shapeit2_mvncall_integrated_v5a.20130502.genotypes.vcf.gz
Now I have a vcf file.
I also obtained a vcf file from Data Slicer ( http://grch37.ensembl.org/Homo_sapiens/Tools/DataSlicer ). I chosed populations and wrote 2:135,787,840-135,837,200 for region lookup. What does this file contain? How can I see the file content? What else do I have to do to get haplotypes? I will try to cluster and visualize haplotypes accorgind to populations. If you can guide me, I am very happy.
Thanks!

To obtain population related vcf files I created the respective (CEU, MKK, ...) samples list first using the samples file you can also download the 1000 genome ftp site.
grep CEU integrated_call_samples_v3.20130502.ALL.panel | cut -f1 > CEU.samples.list
Then I installed vcf tools (https://vcftools.github.io/index.html) and used the vcf-subset command.
I got the commands from this faq page:
http://www.internationalgenome.org/faq/how-can-i-get-allele-frequency-my-variant/
I did not compute haplotypes from the files, but I read in another post, that you can do that with PLINK. Have you checked that?


text:
What are these Cocoons/Seeds?
I have found these thingies in my institute at Tiruchchirapalli in India. I have no idea what they are:

Can someone tell me what they are, exactly?

Sorry if the picture isn't clear, the thingy must have been eroded a bit.

@Charles It's about 1 cm across. I took a closeup shot for more accuracy.


text:
Am I entitled to the latlong coordinates of all specimens used in a species revision paper?
If someone publishes a species revision with distribution maps but without publishing all the data used in the paper itself - or in an attached or linked-to  file - are the authors nevertheless required to make all the data necessary to the paper publicly available on request?
I'm assuming they are as this makes sense from an accountability & replicability perspective (and nonsense of the idea of "publication" otherwise?) - but it's not clear to me from searching online.
Thank you!

Unfortunately, there are no general rules for this cases. It depends on the journals rules...

No - you're not entitled to anything. Authors may refuse to share because they want to control future publications arising from their data, either simply to inflate their own publication record or to prevent certain types of anlaysis of their data (see the 'data parasites' fiasco last year for an example of attitudes towards data sharing in some parts of the medical community - this, this, and others).
Alternatively they may simply no longer have the data. Nowadays this is less common, but if you contact an author about a publication from the 1960s it's pretty unlikely that any unpublished data is still in usable form.
Finally, certain aspects of data may not even have been recorded. Before GPS was widely used, accurate lat-longs of collection sites are unlikely to have been measured. As @Kara notes in the comments, it is not uncommon for the collection sites of older samples to be recorded at the country level.
This is why journals are increasingly adopting data-sharing policies (see BES, for example)
However, many authors are happy to share their data, and you lose nothing by asking. Good luck!

Just also wanted to add/re-iterate that in some cases, if the author was referring to old museum material during the revision, accurate lat-long information may be completely unavailable. Some older (1800s) specimens I've worked with in museums have only been labeled "India".

@Kara good point - I'll add it in.


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

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

When DNA polymorphism occurs mutations can take place.

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

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

Indeed!

My book says it might lead to allele sequence variation.

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


text:
What spider is this?
I found this spider in my flat in Berlin, Germany. It looks like a Cheiracanthium, but which species? Mildei? Or is it a different spider?
The body is approx. 8-9mm long and it lost 4 legs when I tried to catch it unfortunately.

I'm not an expert.It seems to be a male Cheiracanthium mildei.

ghost spider,miturgidae ?? Spiders are really a pain to identify


text:
Which analytical techniques could you use to research relationships between 2 proteins?
Two of the proteins I am researching are known to interact. However, I would like to know if they interact with other proteins as well, and possibly form a pathway. Which analytical technique(s) I should use to determine this if I did all in silico analysis already? Any suggestion is welcome.
I am using a nematode C. elegans in my research, and RNAi is not an option, as I have already performed it.

This question is far too broad. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much. The field of protein-protein interactions is quite wide, and there are numerous techniques to consider. This is not the place to list all of them.

There are plenty of methods to use. Here is a overview and background of some common methods as written by ThermoFisher:
https://www.thermofisher.com/se/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/overview-protein-protein-interaction-analysis.html
There is also phage display if you want to find binding partners, which is a very interesting method to narrow down binding partners from an entire interactome. It simple to set up in a lab and you can perform it all in a 96-well plate using ELISA and several rounds of phage selection. And of course there are also e.g. yeast-2-hybrid (Y2H) or co-immunoprecipitation (Co-IP).


text:
Are there endoscopic technologies for blood vessels?
Endoscopic procedures are used to look inside cavities like intestine, esophagus etc. Is it being used to look inside blood vessels?

there are endovascular procedures that we use for looking at vascular anatomy and clots/blockages within blood vessels - these are surgical procedures that are typically performed by Vascular Surgeons, but Cardiologists also do similar procedures for defining the coronary vasculature, and interventional radiologists also perform vasculature procedures as well. https://en.wikipedia.org/wiki/Interventional_radiology#Vascular

Blood is hard to see through, so visualization with a camera isn't used (to my knowledge). However, Intravascular ultrasound can be used, though it is expensive and not all that common. Instead, angiography is usually used, by filling the vessels with a radio-opaque dye
There are also many techniques used to treat vascular conditions, like balloons/stents to open and keep open blocked or partially blocked vessels, or to repair valves. You can read more about Interventional cardiology or minimally invasive procedures.

Another work [1] that might be interesting to look at is the one titled as "Interactive Volume Segmentation with Threshold Field Painting". The work addresses the problem of volume segmentation mainly for blood vessels inside the brain. It is a Human-Computer Interaction (HCI) research, however, the authors used several procedures and devices to work with. Might be interesting to answer your question.
Finally, and most importantly, it might be important to you look [2] at a paper called "3D Reconstruction with Low Resolution, Small Baseline and High Radial Distortion Stereo Images". In this paper, the authors analyze and compare approaches for 3D reconstruction from low-resolution (250 x 250), high radial distortion stereo images, which are acquired with a small baseline.
[1] Takeo Igarashi, Naoyuki Shono, Taichi Kin, and Toki Saito. 2016. Interactive Volume Segmentation with Threshold Field Painting. In Proceedings of the 29th Annual Symposium on User Interface Software and Technology (UIST '16). ACM, New York, NY, USA, 403-413. DOI: https://doi.org/10.1145/2984511.2984537
[2] Tiago Dias, Helder Araujo, and Pedro Miraldo. 2016. 3D Reconstruction with Low Resolution, Small Baseline and High Radial Distortion Stereo Images. In Proceedings of the 10th International Conference on Distributed Smart Camera (ICDSC '16). ACM, New York, NY, USA, 98-103. DOI: https://doi.org/10.1145/2967413.2967435


text:
How many copies of a gene?
I am studying mathematical models of transcription and translation and I am wondering:
In a particular genome, how many copies of a gene coding for one particular protein should one expect? Are they all transcribed at the same rate?
I know humans have two copies of each chromosome, so the answer would be at least 2 in humans. But I wonder if one particular gene coding for a protein we need in abundance might be present in many copies in the genome to increase expression.

Cell cycle
Talking about physical copies of gene, we would indeed have at least 1 copy during the haploid phase, 2 copies during the diploid phase and 4 copies during the mitosis (and during the first phase of the meiosis). Of course, species having mitosis during the haploid phase would have 2 copies of the gene during the mitosis. I am not talking about polyploid species and am not talking about some fungi and other things that have all kind of crazy reproductions system. I am not talking about mtDNA either. Finally, I am not addressing the case of specialized cells that lose part of their genome or the case of tissues that are basically cells who merged together, so that the concept of cell does not even hold any more such as the Syncytiotrophoblast (in the placenta) (see also cell fusion and syncytium).
In short, the variation in the number of copies during the life-cycle is very dependent on the species of interest, the sequence of interest and may also fall under some semantic issue about what is a cell. Note another potential semantic issue result from the question "how similar two genes have to be to still be called copies?".
Mutations and polymorphism
Now, some genes can be found in several copies. When, in a given population the number of copies of a given gene varies from one individual to another, we talk about Copy-Number Variation (CNV). The increase in the number of copies is called gene duplication (or gene amplification or chromosomal duplication when a very big chunk of DNA gets duplicated). The decrease in the number of copies is called gene deletion. There are a diversity of processes that can cause deletions and duplications such as homologous recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.
Evolution of CNV
What mutation is likely to occur first
Gene duplication does not necessarily yield to an increase in the protein concentration (but it can as it is the case for the Pelizaeus–Merzbacher disease for example). If higher expression is selected for, it "feels more likely to me" that the first mutation(s) allowing for this increased expression will affect the regulatory sequences and will not increase the number of gene copies.
Consequences of gene duplications
Gene duplication (if not loss) can yield to subfunctionalization or neofunctionalization. From wikipedia:

Subfunctionalization [is a process] in which pairs of genes that originate from duplication, or paralogs, take on separate functions

...In others words, copies are free to accumulate mutations as long as the other copy is still doing its job

Neofunctionalization, one of the possible outcomes of functional divergence, occurs when one gene copy, or paralog, takes on a totally new function after a gene duplication event

...Basically, one copy gets a totally new function... that can yield to very interesting innovations such as anti-freeze proteins (ref) or snake venom (ref).

Remi.b talked at great length in his answer about copy-number variation and the generation of new genes. However, I don't think he quite answered what I think is a pretty basic question:

How many copies of any particular gene are there in (a human) genome?

The answer to that question is also simple: two - one on the chromosome from the mother, and one from the father. The exception is genes on the X and Y chromosomes, but that's complicated so I'll ignore it :)
Now, that's not to say that there might be several versions of any particular gene, having arisen through such mutational events as Remi.b explained. So, in antiquity, gene ABC123 might have been duplicated, leading to today's genes ABC123a and ABC123b, which may or may not have different functions. But, for ABC123a, there are only two copies per (normal) cell, and the same is true for ABC123b and all the rest.

Are they all transcribed at the same rate?
But I wonder if one particular gene coding for a protein we need in abundance might be present in many copies in the genome to increase expression.

The regulation of gene expression is quite complex. However, the cell (I'm referring to eukaryotes here, I don't know how different prokaryotes and Archaea are) has mechanisms to ensure that the products of so-called housekeeping genes, which are needed in great abundance, are available to the cell. One method is to attract and keep the RNA polymerases (which transcribe the gene into messenger RNA (mRNA), which is the template for translation into a protein - the actual gene product) bound to the gene sequence through a variety of DNA "promoter" and "enhancer" sequences, which other proteins called transcription factors bind to and recruit the polymerase to the gene. These polymerases are kept active for as long as the cell needs the gene's protein product, churning out copy after copy of mRNA. There are many other mechanisms as well, ranging from how the core histone proteins that give chromosomes their shape bind near the gene, to the manner in which the translation machinery (ribosomes) bind to the mRNA and produce multiple protein molecules per mRNA copy. So, even though we may only have two copies of a particularly vital gene, the cell has evolved ways of meeting demand for its product.

Are they all transcribed at the same rate?

No, they are not. This all depends on the number, kind, and placement of transcription factor binding sequences in the DNA surrounding and within a gene, as well as the exact identity of the transcription factor(s) recruited. Some keep the polymerase machinery very tightly bound, ensuring quick and accurate transcription, while others don't bind tightly at all, allowing the polymerase to "fall off" the DNA and/or work more slowly. Each gene is uniquely and exquisitely regulated to be transcribed where, when, and in the quantity needed.


text:
How does kinesthetic work and with what do we sense this?
I know that kinesthetic and proprioception are different things but, in contrast to proprioception, I don't know how kinesthetic works.
A broad explaination as well as very specific(but explained for 17 year olds) would be nice.


text:
What are these curious cetaceans?
At the beginning of the superb documentary film “Un jardin d’Eden sous les mers” (“A garden of Eden under the seas”) [1], we see a group of curious cetaceans. At about 1 min.
What are these cetaceans?
I think that they are odontocetes. But what species are they? This is a mystery.
[1] Documentary film “Un jardin d’Eden sous les mers” (“A garden of Eden under the seas”). It will be rebroadcasted on Arte on 2016‑04‑01 at 7:45 Paris time. You can watch it on-line here.
Thank you.

Adding a screenshot would enhance the change of getting an answer, not many people will go and watch a movie.

I am completely shooting in the dark here, but do you mean the ones between 1:06 - 1:13 minutes in the video? (After Hammerhead and before Baby and Mama white Shark :) )

SPECIES IDENTIFIED: Pseudorca crassidens (False Killer Whale)

Matching image from the internet (used for identification):

Courtsey: UAE Dolphin Project
PS: Images are screenshot from the video Documentary film “Un Jardin d’Eden sous les mers” (“A garden of Eden under the seas”) are completly owned by the owner of the video and "arte HD" channel.
PPS: Anyone reading this, if you haven't already, then please watch the video. Though it is completely in french, the videography is amazing.
References:

Pacific Islands Cetaceans
Other Whales

Yes, I mean these nice cetaceans. I have thought about pseudorcas too, in the meantime. Indeed, these cetaceans are pseudorcas! Thank you for this great answer!


text:
Do High Triglycerides Invalidate Tests for Infections?
Blood donation websites tell you to avoid eating fats a few days before the donation, because when there is a lot of fat in the blood, they can't test for infectious diseases and must discard the blood.
Does that mean that if you have, say, high triglycerides, the result of an infection disease blood test will be invalid? Say you test syphilis, HIV, etc. If at the same time you get a result of high triglycerides, does that mean the results of infectious diseases can't be trusted?

You might want to look at this article about how Lipemia causes interference with some tests.


text:
Can dermatophytes (toenail fungus) survive without oxygen?
I read that fungi in general can switch to alcohol fermentation in the absence of oxygen (https://en.wikipedia.org/wiki/Anaerobic_organism). How about dermatophytes ? (https://en.wikipedia.org/wiki/Dermatophyte aka toenail fungus) I read an interesting comment here http://gizmodo.com/cold-plasma-could-be-used-to-freeze-out-toenail-fungus-1734825446 by bra55orchid that

"Topical infections like nail fungus and warts require access to the
  open air. This is why they don't go systemic. Nail fungus progresses
  as it degrades the nail to allow air to pass through it. Pine sap is
  enough to kill them by sealing them off. Spores may survive in the
  case of fungus, so you must keep them sealed off until the spores are
  pushed out by nail growth."

PS I tried sealing off my nail, but it did not stop the fungus...

Try IPL (laser) treatment for toenail fungus, it's guaranteed to work. All other treatments never remove the entire fungae and they always come back. It will take 3-6 months for the healthy toenail to grow back nice and shiny, the fungae might be dead but the ugly nail growth will take time to be replaced naturally.

Tried laser (not sure if IPL) but it is very painful, as the laser goes deeper than the fungus, so it also hurts healtthy tissue. What worked for me is cutting out the entire affected nail as it no longer attaches to the nail bed.


text:
White water bird with black 'hat'

The white bird in this picture, swimming between the ducks, was seen in Beijing, China, in januari 2017. It was cold: the water seen in the picture is liquid, but not far from this, the water was frozen. We also saw it standing on the ice.
It has an orange beak with what seems to be a small black spot at its end. It also has black as the top of its head. We did not find a similar bird when searching ducks, goose or even swans. What species is this?

Interesting species. I wonder if it is a variant of mallard.

@Sanjukta Ghosh. It is not a species. It is a race/variation/form/etc of the species Mallard (Anas platyrhynchos).

This duck has several features that could put it in a number of variants of domestic duck. It could be a hybird with a magpie duck or ancona duck? Magpie ducks have black caps, similar to the duck in the photo, but also have black backs. Anconas have some black on the face.

@JC11 What breed is the pure white mallard? It is quite frequent.

Possibly a Magpie Duck, but not certain because of the paucity of black elsewhere on the body.

@theforestecologist and JC11 I just want to remark that all the breed that you cite still belong to the species "mallard". Like dalmatian is a bree of the species "dog". I think that at this stage is pointless to assign a specific breed being most likely a mix of different ones (as suggested).

@Sanjukta Ghosh Domestic Mallards can come in a variety of colours including white. I think it we were to pinpoint the origin of the duck in question, it is likely a mix of magpie duck and domestic mallard, but that mix may not be half and half, it could be much more complex. "have fun", The Magpie is not a breed of mallard specifically, it could be an ancestor of an Indian runner which could be a Muscovy. In domestic breeds, the origin species can be many mixtures and complex. I think the best answer for this question is that this is a domestic duck and give possibilities of which type.

It is a domestic form of mallard. They are bigger, often white or mostly white. Try to google image domestic mallard and you will see the phenotypic variety that domestication has created.
Note the irregular and not symmetrical shape of the "hat" and read the description below from the biggest research center on birds of the world.
Extracted from:
http://www.birds.cornell.edu/crows/domducks.htm

(...)lots of white is often involved, including all-white breeds like the popular Pekin Duck (...) Usually these white spots are not symmetrical across both sides, and that asymmetry should tip you off to think domestic influence.

Please support your claim with citations. A claim not supported with references do not make a good answer, even if you are quite certain of it.

@Sanjukta Ghosh. Google image domestic mallard it's more than enough  to prove that is a domestic mallard. There is no wild duck with a pattern of colors remotely similar to the one in the picture.

Google images search is not an authentic reference because it extracts images from different kinds of sources (which include flickr and personal blogs) that may not have the correct information. But the webpage of Cornell Lab of Ornithology you linked is a good reference.


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Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to?
Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to? If not twice as fast, should I breath any amount faster on average than usual when at high altitudes?

Possibly better suited to Health S.E.

Maybe I gave of the wrong impression in my question. This is purely theoretical, and I don't care about the health effects of hyperventilation. I'm interested in the biological basis for hyperventilation and whether hyperventilation occurs due to increased respiration alone, or some combination or respiration and oxygen levels.

Understood. But I think it would have worked on that site as well. I don't believe it will be closed or anything here though. :)

you also breath 2x as much other gases when breathing faster

probably this article (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495772/) will answer some of your questions

By definition, hyperventilation is a state of increased breathing where the exhaled $CO_2$ is greater than what is produced by the body.
Except in artificial condition or in disease process, breathing faster than the autonomously-dictated rate is going to cause hyperventilation. You have a fine-tuned control of respiration that will work out the correct breating rate for you.
Oxygen is actually irrelevant for this phenomenon, first because of the definition of hyperventilation, but also because oxygen is mostly transported through haemoglobin (98+%). This means there is a fixed quantity of oxygen that can be transported by unit volume of blood (and by breath, for a given cardiac output), and the maximum is already reached at normal breathing rate. Breathing faster does not allow for better oxygenation of the blood. (even at an higher altitude)
On the other hand, $CO_2$ is transported by the plasma, dissolved (7%), but also in the form of bicarbonate (93%) through the following equilibrium :
$$ H_2O + CO_2 \rightleftharpoons \underbrace{H_2CO_3}_\text{Carbonic acid}  \rightleftharpoons \underbrace{HCO_3^-}_\text{Bicarbonate} + H^+  $$
In the alveoli, a quantity of $CO_2$  will diffuse to the alveolar air, and be breathed out, the target being eliminating the quantity produced by the body. However, in opposition to oxygen transport, it is possible to overshoot by breathing faster, because removing $CO_2$ drives the equilibrium in direction of $H_2O + CO_2 \leftarrow  HCO_3^- + H^+ $ that is, eliminating additional $CO_2$ through the removal of bicarbonate from the blood.
This is hyperventilation, and leads to hypocapnia, causing that particular sensation of dizzyness. It is also leads to respiratory alkalosis, because, as seen in the reaction equation, this incurs the loss of protons ($H^+$).


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Questions about what a productive cough actually is and where it comes from
When I'm sick with a productive cough, what is the stuff I'm coughing up, is it coming from my lungs, and if so how come it doesn't hurt a lot and trigger a violent cough like if I got even a single drop of water down the wrong hole.


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Quantity of hemoglobin in the cells
According to my book- red blood cells have the ability to concentrate hemoglobin in the cell fluid upto about 34g in each 100 ml of cells.The concentration does not rise above this value because this is the metabolic limit of cell's hemoglobin-forming mechanism.
Furthermore, In normal people,the percentage of hemoglobin is almost always near the maximum In each cell.
The next statement says- the quantity of hemoglobin in each respective cell contains an average of 15g of hemoglobin per 100ml.
So what is the actual concentration of hemoglobin in 100 ml of blood?

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

The reference range for hemoglobin Hb content in whole blood is 13 - 17 g/100ml for adult men, and 12 - 16 g/100ml for adult women.
There are other related metrics : the mean corpuscular hemoglobin concentration MCHC, that is the concentration in a red blood cell (reference range : 31 - 36 g/100mL), and mean corpuscular hemoglobin MCH, which is mass in one cell (reference range : 29 - 35 pg)
So I think that book is refering to different values :  the concentration in the red blood cell itself (MCHC = 34g/100ml), and the resulting concentration in the whole blood (Hb = 15g/100ml).
By the way, there is a value relating Hb and MCHC, the hematocrit Ht, the proportion of volume of whole blood occupied by red blood cells. Reference range 40% - 50% for adult men, 35% - 47% for adult women.


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Can photosyntetic cells be genetically modified to grow at a faster rate?
I hope the question is not silly, but I wonder if a sort of genetically modified plant "cancer" could be used for carbon sequestration. For example, cancer cells like HeLa have been reproduced in tons, and as far as I know their growth rate is very high.

You might be interested in reading about artificial photosynthesis.

Yes! Thanks, I was just reading that. I still think the question is relevant as we are relatively advanced in OGM, and tumors and plants already are there. It seems to me (I'm completely ignorant in biology) that it would be easier than reproduce cheap photosyntesis (i.e. cheaper than planting trees).


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What's the difference between stabilizing selection and balancing selection?
I came across these terms in Darwin's "Origin of Species" and I wasn't sure what the difference is.

Usual meaning
Usually, Stabilizing selection is a concept that applies to a phenotypic trait while balancing selection is a concept that applies to a given locus.
Balancing selection can either be due to negative-frequency dependence selection or due to overdominance (=heterozygous advantage at a single locus).
What Darwin may have meant
Because Darwin didn't know about genes, he was necessarily not using the term balancing selection as I am using it. I can think of several more or less related pattern of selection that might fall withing the definitions for "stabilizing selection" and/or "balancing selection". Maybe he meant "frequency-dependent selection", "positive selection for an intermediate trait", "varying selection through time (temporally heterogenous environment)" and "varying selection through space (spatially heterogenous environment)". Eventually again, that might mean "positively correlated traits that undergo opposite selection pressure (or the opposite)" but that would definitely be surprising.

I think the key distinction here is that stabilizing selection promotes a monomorphic population whereas balancing selection preserves polymorphism.


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In insects, does the Alanine repeat occur on the homeodomain sequence of the abdomen or does it occur on a different sequence?
By "Alanine repeat", I am referring to the suppression of the formation of extra insect legs due to Ubx gene suppression through Distal-less repression.

Some background:

The new work involved misexpression of the Drosophila Ubx protein in the presumptive thorax of transgenic fruitfly embryos. Limb development was suppressed because of repression of Dll. By contrast, the misexpression of onychophoran and crustacean Ubx proteins did not interfere with Dll expression and the formation of thoracic limbs. These results raised the possibility that the Drosophila Ubx protein is functionally distinct from Ubx in onychophorans and crustaceans. One study suggests that Drosophila Ubx has acquired an alanine-rich peptide that mediates the repression of gene transcription; this peptide is lacking in onychophorans. The other study provides evidence that the crustacean Ubx contains an additional peptide that modulates the activity of the alanine-rich peptide, and possibly other repression domains, in crustacean Ubx.

Insect-restricted sequences include four regions N-terminal to the
  homeodomain (I1–I4), a peptide motif (QAQAQK), and an extended run of
  alanine residues C-terminal to the homeodomain
The onychophoran Ubx protein might function as an activator of appendage development. When the onychophorans and arthropods diverged,
  Ubx acquired an alanine-rich repression domain near its carboxy
  terminus. This domain mediates constitutive repression in insects.
  But in crustaceans the addition of the regulatory peptide causes it to
  function in a conditional fashion. As a result, Ubx does not suppress
  limb development in crustaceans. But it eliminates abdominal limbs in
  insects, greatly reducing the overall number of appendages compared
  with crustaceans.

You can read about it here:
Levine, Mike. "Evolutionary biology: how insects lose their limbs." Nature 415.6874 (2002): 848-849.
Galant, Ron, and Sean B. Carroll. "Evolution of a transcriptional repression domain in an insect Hox protein." Nature 415.6874 (2002): 910-913.


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Why is it that heterozygous loci appear as two separate bands during gel electrophoresis while homozygous loci appear as one band?
Is it because heterozygotes have a greater base pair length? (And if they do, why is that?) Or is it because recessive alleles are moving slower than the dominant alleles in the gel?

If a loci is heterozygous there are two different alleles coding for the same Protein. The alleles may differ in their lengths. With a gel electrophoreses you split DNA fragments by their length.
Homozygous -> same alleles -> same length -> one band. | Heterozygous -> different alleles -> different length -> two bands
Is this what your question was about?

Your question is the answer. Hetero = different, thus you have two different bands, representing two versions/alleles of one gene. Homo = equal, thus you only have one version of a gene. These alleles may differ in length and/or restriction sites, resulting in different bands, because electrophoresis is based on molecular weights.

It depends what molecule you are running on the gel and how it was treated beforehand. Are you referring to restriction fragment length polymorphisms of DNA, or another type of assay? You need to understand the method to understand the result!

@WYSIWYG - I think your answer is pretty interesting and I like this question. Could you not convert it into a [short?] answer? My +1 is for you already :) All this closing of questions... sometimes a good answer may actually emphasize the strengths of an apparently weak question! I vote for leaving open.

Okay @ChrisStronks, boss is away today and no work pending. So passing time by digging old unanswered questions :) Will post it as an answer.

@WYSIWYG : sounds good! i just saw that there is already an answer that includes your argument. This may save you some work :)

@WYSIWYG - Nice answer, especially with the resolving power of gels included. +1!

@ChrisStronks Thanks. I had tried to answer some other old questions. Please have a look at them and let me know if anything else is needed. The answered question had gone down by 1% : so all this effort :P

Let us continue this discussion in chat.

A heterozygous locus has two different alleles and therefore it is possible that their DNA sequence lengths are different. However, it is unlikely that they are so different so as to be clearly resolved in a gel electrophoresis. Agarose gels can at best resolve 20bp; polyacrylamide gels can resolve smaller differences but it is only done for small DNA fragments.
I think upto 50bp difference is possible between alleles. But such huge insertions/deletions are rare and the difference between the alleles is usually a point mutation or small insertions/deletions(indels). Big indels are possible when a transgene is inserted specifically in one chromosome; these cases are mostly experimental.
If you consider paralogs as alleles then they can be of different lengths and can be resolved in agarose gels— usually the difference is in the untranslated regions. If you are doing Southern blot and using a probe that can bind to both paralogs then you will end up getting two bands.
Having said that, it is possible to see a difference in gel bands even if there is no size difference. This is possible by a technique called RFLP. In this technique the DNA is digested using a restriction enzyme which basically cuts the DNA at a specific sequence (usually a hexamer). If a point mutation abolishes or creates a restriction site then the fragment length would be different between the alleles. This is detectable on the gel.
A similar technique is AFLP.

the restriction enzyme analyses are an interesting addition for sure

Heterozygous loci have both alleles present at a given time, for example Aa (considering diploid organism), where as homozygous have only one type (AA or aa). Generally, both alleles have different sequence lengths due to deletions, insertions etc. so if any locus is homozygous, it will produce only one length but heterozygous will produce two different lengths. That is why you will only see one band in case of homozygous and two in heterozygous.

Why would AA, Aa, and aa produce different lengths if they each contain two alleles? Shouldn't they each project two different bands on the gel?

Only Aa would produce two bands but AA and aa would produce only one band. Imagine, for example, allele 'A' has length 100bp, allele 'a' has length 95bp. So if an individual is only AA, it will produce two bands, one for each A and A but since both of them are same length, they will overlap and appear as only one band on gel. Similar is the case for 'aa' individual. However, when Aa individual produce two bands they differ in length, so it will produce one band at 100bp and one at 95bp. Hope this helps.


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Are alleles passed down and shuffled randomly to the offspring during meiosis or fertilization?
If it does occur during meiosis, are the alleles switched over from one sister chromatid to the other during the crossing over process in Prophase I?

Crossing over/synapsis in Prophase I of Meiosis I is when alleles are switched over from one non-sister homologous chromatid to another non-sister homologous chromatid. This happens before fertilization ever happens. Meiosis occurs even before birth in females in order to make gametes in the form of oocytes. In contrast, this frequently occurs in men who continue to produce gametes in the form of spermatocytes throughout their lifetime. Fertilization simply refers to the fusion of two gametes-- a spermatocyte and oocyte combining together-- and does not involve meiosis.
Here's a short and straightforward Youtube video about Meiosis.

Crossing over generally involves homologous chromosomes.

Meant to say "non-sister". I'll make the correction. Thanks!


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Are grasshoppers monogamous?
Noticed two grasshoppers jumping together on the porch, and started wondering if they are monogamous? I am aware they have males and females.

Interestingly enough, there are insects that are considered to be monogamous, including cockroaches and other beetles. However, I couldn't find anything on grasshoppers.

which species - there are many grasshoppers, mating system could vary greatly within that.

Male grasshoppers often mate several times with multiple female, and some females will mate again after, and perhaps even before they lay their eggs. So no, they are not monogamous.
Rufous grasshoppers for example have a very special mating cycle, the male will attract other females, possibly more than one with "pursuit sounds". After copulation, he keeps her close to prevent other males from mating with her, and the females enter a defensive mode where they refuse intercourse from other males. After laying eggs however, she enters a "relaxed" mode where she is open to others for mating.
Sources:
jrank
Rufous grasshopper: inaturalist

"some females die after lay eggs. So you could perhaps consider them monogamous" - this doesn't rule out multiple mating by males so is not monogamy


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Would a person live longer, if such a person lived in a planet with lower gravity? (say, Mars)
I was wondering: some companies plan to colonize Mars, many of us know.
But if one were to live on Mars, would this person live longer?
It seems to me that a lower gravity would mean less overall damage to the body cells, so they could last longer: resulting in a longer lifespan.
Or maybe lack of gravity = lack of exercise = lesser lifespan?
I'd like the opinion of some expert in the matter. Thanks.

No, reduction of gravity causes bone decalsification. Also there will be no protection from the sun's radiation in space and on Mars and that has been an issue.

Probably not. There's a thing called Hayflick limit, which is basically a limit of life expectancy caused by a shortening of telomeres with every cell division. And since most of our cells complete cycles more based on time (life cycle of RBC 100 days), and not due to damages to a cell, our telomeres would still shorten at the same rate. Of course the gravity could play a small part once organs have started failing, but there are many other factors that affect how long it takes for everything to completely deteriorate, and wouldn't have a big role. In fact, it could even shorten life expectancy, seeing as how our bodies are currently built to live in our current gravitational field. Without gravity, our muscles could become weak, causing other problems, which is why people at the space stations have frequent dedicated times to workout, to keep their muscles fit.

It sounds reasonable that reducing the physical stress on a body would reduce the wear and tear, and thus increase the owner's lifetime.
However, it's just as reasonable that human bodies are designed to be under stress, and drastically changing the environment will harm the body in subtle and even obvious ways. For instance, some research shows that lung and heart cells won't grow properly if not cyclically stretched.
Until we get some serious long-term research, in space or on a smaller planet, we won't really know.

We don't know is a valid answer, but not without resources to support it, or evidence of effort in not finding anything on the topic.

Is leaving a reasonable question with no answer better than giving the best answer that you have?


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Do herbaceous plants have woody parts?
Do herbaceous plants, especially perennial plants have woody parts, like woody stem?

I'm voting to close this question as off-topic because pasting the Q in google gives wiki as first hit - answer is in second line of wiki article.

By definition, no. An herbaceous plant is defined as a plant that has no woody parts. Herbaceous perennials die down to the roots at the end of the year and then sprout up again at the start of the next growing season, but they do not have woody parts. A plant that is small and herblike but has woody parts may be called a subshrub.

a subshrub :) that's cool

'"Subshrub" is often used interchangeably with "bush".' TIL bush isn't a synonym for shrub!

This isn't entirely true since the OP is asking for woody parts (not only above-ground parts), and perennial herbaceous plants can have "woody" roots (depending on how you define woody). See e.g. herbchronology for age determination of perennial herbs.


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Is thinking with language efficient?
First off, Im not sure, whether to put this into Cognitive Science or Biology. So sorry, if this is the wrong place.
I wondered, whether it is efficent to think with language (of course its efficient for communication). When Im thinking with long words, it takes longer than thinking with short words. Maybe thinking without words would be even faster?
So, do babies, who didnt learn think faster because they dont immediately try to find words for their thoughts to tell someone about them?
In our everyday life, we almost always need to talk to others about our thoughts. This leads to us thinking with these words instead of just thinking and then finding words for it. Its like writing a manuscript just from front to end instead of first brainstorming and collecting ideas.
Main question: Is it possible to think in a two-step process(and would it be more efficient)? First, thinking with emotions(or whatever you want to call it) and then finding words for that to spread your idea?

I'm voting to close this question as off-topic because it belongs to CognitiveScience.SE.

Yes.  And your "Milk tongue" greatly influences your cognitive style.  See Dennett, et al.


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How does botulinum toxin enter the blood stream from the digestive tract?
To my understanding, large polypeptides such as botulinum toxin cannot pass the intestinal lining intact. How, then, can it enter the bloodstream and cause botulism poisoning?

Transcytosis is a process by which large macromolecules are transported across a cell, such as those in the intestinal epithelium. It is used by many toxins and even whole organisms to enter the body. Botulinum toxin also apparently uses this mechanism. I'm not sure how detailed of an answer you want, but the linked to-review is pretty in-depth.

That's interesting +1.

@AliceD "Isn't nature wonderful."


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How can you tell if a protein-coding gene is nuclear or mitochondrial?
New to genes, and have to read literature to find candidate genes for a particular study. I cannot for the life of my understand if all genes are placed into either the "nuclear" or "mitochondrial" category...are there more categories? Some are easy, like cytochrome subunit genes are always written as "mitochondrial" and then rhodopsin are written as nuclear...but other genes like ATPase etc. don't have those descriptions. When I search online further, it still does not clarify, so I am wondering now if there are just more categories to this?

Welcome to SE Biology. It will help people to answer your question if you note what resources you are using to confirm whether you are dealing with a genomic or mitochondrial gene. The databases vary in where they report this information.

I am still very early on in my research, so I am going through journal articles dealing with genes that differ in species found in one habitat vs. another. As of right now my only resource are journal articles. I am not sure what you mean by genomic or mitochondrial gene...i.e. the COI genes were obtained from genomic DNA, so I am not sure how to answer that.

I don't know what you mean by COI genes. I understood your question as a query about the location of genes; genome or mitochondrial genome. If you want to know the likely subcellular location of proteins, your question should ask about proteins and not genes.

http://biology.stackexchange.com/questions/40331/do-eukaryote-cells-contain-dna-that-isnt-part-of-a-chromosome-or-located-in-the
Would this be helpful?

Ahh okay, sorry this is me developing my vocabulary properly. I did mean the location of genes, nuclear or mitochondrial. I meant to use COI as an example where in the literature they always just outright call it mitochondrial. Then I come across something like ATP1 which is just called a membrane protein - so I didn't know if that meant just nuclear membrane or potentially mitochondrial membrane.

@MalharKhushu, I included a link in my answer. Thanks for the link.

I have limited my answer to refer to humans, but the advice generalises to other eukaryotic cells.
In human cells, almost all of the genes that code for proteins are located in the genome, which is located in the nucleus. The mitochondria have their own genetic material, however, the mitochondrial genes only encode for 14 proteins. The answer to this question also notes the existence of extrachromosomal circular DNA. There are also a number of proteins (1192) that are verified to exist but their genomic location is currently unconfirmed.
In your comments you mention ATP1 and note that it is called a membrane protein. The gene is located on chromosome 19 in the nucleus. The protein, that is encoded by the gene, can be found in a variety of places, including the nucleus and also the mitochondrion. The gene for Cytochrome c oxidase subunit 1 (CO1/COX1) is encoded in the mitochondrial genome and it localises to the inner membrane of the mitochondrion.
The links in this answer all point to Uniprot. This is what I use to get an idea of the basic functions of proteins. The database includes information genes but its primary purpose is to describe proteins and their functions. The information is roughly correct, it is not perfect. It includes a many species and links to a number of tools, including the gene ontology which attempts to characterise proteins using a controlled vocabulary.

@DNAngel, I'm glad to hear it. Biologists have created some great online resources. Remember that you have the option to accept answers that have provide a solution to your problem.


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phylogenetic Independent contrasts with unresolved tree
I have a dataset containing morphological and performance measures of species from various groups, including insects, lizards, frogs, spiders etc, and want to analyse the relationship between these measures and the animal's body size  via regression methods, while controlling for common ancestry, similar to what has been done in this work:
Peattie, A. M. & Full, R. J. Phylogenetic analysis of the scaling of wet and dry biological fibrillar adhesives PNAS, 2007, 104, 18595-18600
http://www.pnas.org/content/104/47/18595.abstract
For most of my species, statistically supported branch lengths are lacking, and I was thus wondering what the best way to conduct my analysis would be, and I would be grateful for any hint.

Look also into PGLS. Either way, one thing you could do--it would be ugly--would be to set all branch lengths to 1. Additionally, you could smooth the tree with penalized likelihood, e.g. chronopl() function in ape package in R. Again, this is an ugly solution and look into PGLS (it won't solve the ugly phylogeny part).


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At what saltiness will water simply pass through us?
If water has a low salt content, it hydrates us. When water has too high salt concentration, like sea water, it drains water out of us instead when we drink it. At what salt concentration would water leave us completely unaffected?

given the coment from anongoodnurse here http://biology.stackexchange.com/questions/24058/what-proportion-of-salt-in-water-would-make-it-not-dehydrate-nor-hydrate-someone?rq=1 - the answer is 'there is no such concentration'

@AliceD Thanks for your comment, I didn't come across that question before. However, I don't really agree with the given comment.

As I said before, if you're not dehydrated, you cannot "hydrate" with a perfect imaginary solution. The body will remove the unnecessary salts of anything added. There is no magic "solution". better to disagree with me by posting a better answer; at least then you will understand the physiology behind it.

water leave us completely unaffected Haha!!! this sounds like you are attempting to recycle water without any other recycling material :P

The short answer is that anongoodnurse and moose are correct. The long answer is study physiology. Even when water is isotonic to blood, the composition of it's ionic species differs. Blood contains a wide variety of dissolved proteins, metabolites, and minerals. Na and Cl are major constituents, but are not the only components whose levels are carefully regulated. Your body corrects for the changes in the concentrations of these molecules. Even if you transferred blood which happened to have the same composition, your body also regulates volume and would need to make adjustments for that.

And that's ignoring the key aspect of Moose's answer re:homeostasis. Staying alive requires a lot of energy. Your body is constantly producing/accumulating the waste products of existence. The kidneys, et al are never sitting idle, but always dynamically regulating their output to drive blood composition towards its homeostatic "set points."

"Unaffected" is impossible. If you meant homeostasis, where fluid ingested = fluid excreted, well that happens all the time, and all "output" is not through urine. Sweat, respiration, fluid in feces, etc. are fluid loss. The body constantly needs water. Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested. Under no circumstances would fluid ingested pass through the stomach, small and large intestine, and colon without absorption. Once absorbed from the GI tract to the bloodstream, our kidneys regulate fluid balance. For more reading, reference the renin–angiotensin–aldosterone system.

+1 "Fluid regulation is a highly complex system managed by the body through a variety of osmotic gradients in the body and hormones which is not driven solely on the osmolarity of the fluid ingested."


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Specifics of decussation
Beginner question here:
The definition of decussation I see is the crossing through the midline of a bunch of neurons.  But I was wondering if there was a little more to it than this, because I'm given the impression in readings that this is a somewhat difficult task to perform developmentally, like the body might have to take extra effort to regulate the crossing so that the neurons do not interfere.  So when nerves from both eyes cross, for example, do they pass AROUND each other or do the bundles of nerves all weave through each other?
Thanks in advance.

The optic nerve fibers cross inside the optic chiasm sharing the same shell:

The crossing fibers go ones between others, like on this classical picture -


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How to calculate the Position Weight Matrix score?
Can anyone explain me how to calculate the Position Weight Matrix score?
I know the formula, but I don't understand it. I have a table with the frequences of nucleotides, and a table with the PWM scores:
Frequences of nucleotides:
Position:            1       2        3        4        5

A                    0       0.9      0.1      0.6      0.2
C                    0       0        0.2      0.1      0.2
G                    0       0        0.1      0        0.1
T                    1       0.1      0.6      0.3      0.5

And I have the corresponding PWM scores:
Position:            1       2        3        4         5

A                            1.848   -1.322    1.263    -0.322
C                                    -0.322   -1.322    -0.322
G                                    -1.322             -1.322
T                    1      -1.322    1.263    0.263     1

But, I have no idea how this scores are calculated.
The formula is:

But I don't understand this.
Can anyone explain me step by step how I can calculate this scores?
I especially don't understand how to calculate p(b,i).
Thanks! :)

p(b,i) comes from the frequency of the nucleotide b at position i divided by the number of sequences you have taken for considering the score. This wiki page explains all need to know.


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psychological database with sequenced DNA records
I'm looking for an epigenetic database which includes for each example the psychological history of the persons DNA. Right now I can only find DNA and epigenetic databases. Sadly none of the databases provide "thick data" (qualitative data eg. history of person) to the sequenced DNA.
I want to investigate the effects of psychology on epigenetic and vice versa.

I would be very surprised if such a thing exists. Apart from the privacy issues (OK, you can anonymize the data), there aren't to my knowledge any projects for such large scale sequencing of human samples. The closest I can think of is the 1000 genomes project but I doubt any psychological data will be included.

23andme, for example,  along with SNP data collects information on different traits (including behavioral) from their customers and publishes interesting results from time to time, but their database is not for public usage.

You might want to look at the Danish Data archive:
http://www.sa.dk/content/us/about_us/danish_data_archive
I have never used their data and I don't know what barriers there might be to accessing it, but the impression I got at a talk by Soren Brunak (http://ctbr.hunter.cuny.edu/Brunak), was that this was one of the most complete databases for studying relationships between people's DNA records and other health information that might be available about them.


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Quantitative Comparisons of Phylogenetic trees
I am working on a broad phylogenomic analysis of proteins involved in one particular cellular process.  I have constructed a phylogenetic tree for each protein.  I am now working on comparing those trees in order to extract categories (i. e., allele a of protein a occurs most frequently with allele b of protein b, etc.).  I have attempted to construct a super tree using clann, but the tree is extremely difficult to interpret.  I would therefore like to carryout a quantitative comparison (and subsequent categorisation) of each each tree, but it is unclear to me how to even begin this analysis.  Is there a standardised method for comparison of phylogenetic trees?

I don't know whether it's exactly what you need, but there are formal algorithms for tree comparison.
There are basically two approaches: one utilizing tree lengths (branch score distance) and the other one dealing with topologies only (symmetric-difference metric): details and references can be found in the manual to treedist from the phylip-package, which implements both.
PAUP* has a command under the same name (treedist), which calculates the symmetric-difference metric only. This metric is very intuitive: it describes the total number of partitions (= splits) present only on one of the two trees.