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Does anyone use bootstrapping to report mass gain during experiment?
When performing an experiment to report gain of body mass in an experiment, do any of you know of a paper whose authors have used a bootstrap to improve their confidence intervals?
I have a n = 10 per group for a total of 6 groups, measuring whole body mass on a weekly basis in small animal models of a disease. Experimental design is essentially treatment by the use of a drug, over a period of ten weeks, and analysis of the final gain of body weight
(essentially think of a google search term as bootstrap, body mass, mouse)

Can you add more details? For example number of samples, metric measured, basic statistical estimates (mean/variance) and the experimental design. For your question, as it is now, searching bootstrap+body mass in google scholar would do.

@WYSIWYG I am not able to find a study that has explicitly used a bootstrap for body mass in the context I am seeking (see updated post).. am I missing the obvious here?

You should clarify why you want to use bootstrapping - what statistical tests you performed and what was the primary observation (which you say, has low significance). Is it 6 groups each for treated and control plus 10 individuals in a group? Anyways see this.

@WYSIWYG bootstrapping enables us to understand the true range of confidence intervals (and subsequently increase the accuracy) much more, than the usual way obtained by means and variances.

Also have a look at this paper. Basically what I wanted to ask was, whether you need bootstrapping. Is there some variation between groups?

@WYSIWYG the thing is, my mice are at their maximal body weight, and hence body weight gain is minimal, and since there is variation in each individual mouse is slightly masked by the std. error. It is significantly different by t tests, however an ANOVA followed by multiple comparison corrections masks the effect completely (1 test group ~ 5 control groups). So, I was recommended to go down the CI route (rather than a p value route) and I know from my stats lessons that bootstrap and CI's usually go hand in hand... does this make sense?


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Will bark-beetles infest the Methow Valley?
What is the Methow Valley (esp. Winthrop, WA) area's susceptibility to bark beetles?  Did the 2014 Carlton Complex wildfires increase the vulnerability due to the large numbers of dead, dying, and stressed pine and fir species in the area.  Are there ways I can reduce the vulnerability of my property, which is already in open, park-like stands?

I had trouble finding any academic or governmental references for rates of spread of Scolytids (bark beetles) in your region, but the answer to this would require speculation (i.e. prediction). Many factors, including the 'health' of the trees surrounding your home, and the connectivity of your trees to invaded areas, would aid in bark predicting whether these beetles will eventually make their way onto your property.
If your property is large, consider cost-share programs for management/prevention in your area.
See the bottom of this .gov webpage for more references. Good luck.

source: Stack Exchange

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Merge several .ab1 sequence files into a single FASTA file?
I have several .ab1 files generated from Chromas. I want to merge all of them into a single FASTA sequence file. How can I do this in an automated way?
Note that I don't have Chromas installed (the files were generated by someone else). I am using linux, so open-source, command line tools are preferred.

In general you should use a base calling algorithm to generate the sequences from the chromatogram and not directly convert it to fasta (Courtesy: Sven [SEQanswers] ). As mentioned in the link, phred and TraceTuner are popular base calling software that can generate a fasta output.
The software mentioned by The Nightman can be used for converting .ab1 to fasta. You can also try this BioPython module called abifpy. You can easily read each .ab1 file, using a python script, and write the sequences in fasta format as a single file.
Combining multiple fasta is quite trivial. You can use cat as mentioned by others.

DNA Baser has a batch abi to fasta converter here. After files have been converted to .fa files, they can be concatenated together in UNIX/MAC using cat *fa > output.fa

Typical possibilities that come to mind are programs available in EMBOSS and Staden. However the question of how to access the sequence data stored in .ab1 files has been asked on Biostars a number of times, so I suggest having a look at the various answers there for options that are suitable for your environment and use case, see Biostars search "ab1".

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Approximately how long do bacteria live for?
I would like to know how many days or years do the bacteria live approximately.

I think this depends on species and particular conditions. E.G. An amp resistant strain of bacteria would be fine if you grew it on an amp plate and a non amp resistant one would die. Plus how much room does it have?

room? What you mean?

The amount of space they have to grow.

a human body you mean?

Um, no. I mean where is it growing and how much space does it have to grow - I.e. is it a huge area or are they confined to a Petrie dish? - also, how much food do they have? Are they arobic or anaerobic?

Sure arobic and what about a huge area 1-6 meteres

@Orphee Are you trying to ask how long pathogenic bacteria live for in the human body? Because that's a completely different question

Yes, I mean how long bacteria (pathogenic) live in the human body (aproximatly).

They're effectively immortal, albeit in a Phoenix-rising-from-the-ashes sort of way.
In general, a bacterial cell will divide as soon as it's biochemically able to do so, leaving behind two daughter cells. Neither daughter cell is actually the same as the mother cell, so in one sense the mother cell will have "died". On the other hand, the daughter cells are genetically identical to the mother cell and all of the physical material present in each of the daughter cells at the moment right after they split came from the mother cell.

It should be noted, however, that cell viability relies on a number of different factors.

I love how you describe them as immortals. :-)

related: https://biology.stackexchange.com/questions/21111/do-bacteria-die-of-old-age


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Will a 0.2g/mL sugar concentration cause vomiting in humans?
This infographic claims that the sugar content in a can of Coca Cola would cause vomiting if not for the phosphoric acid.

In The First 10 minutes: 10 teaspoons of sugar hit your system. (100% of your recommended daily intake.) You don’t immediately vomit from the overwhelming sweetness because phosphoric acid cuts the flavor allowing you to keep it down.

Now this question came up on skeptics.SE and the remaining question is whether (flavourless) water with sugar would cause vomiting. Very specifically we're talking about 200ml of final concentration and 39 grams of sugar. I would try it out myself, but per the rules of skeptics.SE I am not allowed to do this so I am posting it as a question here.

No, we've had a 2M (360 g/ 1000 ml = .36 g/mL) glucose in water solution for a lab in Molecular Genetics and nobody threw up, even if it was unpleasant to drink. In 200 mL of water my solution would contain 72 g of sugar. I'd put his in an answer but I have no other evidence but personal experience and we only had a mouthwash cup full but it was of multiple different concentrations of the sugar water.

By sugar, you mean sucrose, right?

@WYSIWYG Well, very technically speaking you will find 'high fructose corn syrup' in traditional Coca Cola apparently.

Why in heaven's name would phosphoric acid prevent vomiting if this claim were true? Infographics are about as accurate an memes.

Sugar (be it sucrose, glucose, fructose or honey) does not have emetic properties in any concentration, unless there is a personal (and highly individual) psychological adverse reaction to sweet substances.

Sugar is not a local gastric irritant (like dishwashing detergent, or syrup of ipecac, copper sulphate, zinc sulphate; yellow mercuric sulphate, ammonium carbonate, powdered mustard and other local gastric irritants.) Some non-irritating substances (e.g. cod liver oil) may induce emesis because of a repugnant smell, taste, or texture. Few people find the taste of sugar repugnant. Gastric distension to the point of emesis does not occur with 12 or 16 oz. of fluid.
Psychological causes of vomiting include aversions (e.g. some people vomit when they see someone else vomit.) That would involve a cerebral cortex mechanism.
No sugar of any concentration is listed here as an emetic. If it were true, we would have a much less significant incidence of obesity.


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Big cat in heat for months?
In this documentary about a lioness and a leopard the leopard is in heat for months.
https://www.youtube.com/watch?v=MGqmylkOuKw
Usually a big cat would be in heat for 5 days and then not in heat for 27 more days. Doesn't matter if it is a lion, tiger, cheetah, jaguar, or leopard, they have a very similar estrus cycle.
Why then is this leopard in heat for months until she finally becomes pregnant? The lioness is only in heat for 2 days because after 48 hours she becomes pregnant. In fact the lioness has 2 litters in the same period of time as the leopard has 1 litter.


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Calculation of final magnification when using a CCD camera
I'm trying to empirically calculate the approx final magnification (mag) of digital images rendered through our confocal microscope. Using a micrometer and the microscopy equipment I have, the following is known:
Objective mag = 63x
Ocular mag =10x
Diameter of field of view when viewing specimen through occular = 320µm
Diameter of field of view when live viewing specimen on the screen = 100µm
What is the final mag of the rendered image on the screen?
This is not a homework question. The manufacturers specification for the degree of magnification that the camera and confocal  (and obviously there is some) provide is unknown.

what is the pixel size? what is sensor size? how many real-life microns fit in one micron of pixels is your magnification

@aaaaaa  live view on the screen is 920 W X 1200 H. No idea the size of the sensor unfortunately.

What is the camera model?

Usually the software that comes with the camera has the option of adding a scale bar. For all compound microscopes the final magnification = eyepiece magnification × objective magnification. The camera itself doesn't have any lens (AFAIK) and the image is not further magnified. However there are some settings that ensure that the digital image preserves all the optical information: the pixel size must be smaller than the inverse of 2.3-times the cut-off frequency [source].

@WYSIWYG if the image on the screen as compared to what your seeing through the occular is mag by a factor of 3,2, then the mag is different correct?

Assuming that the FOV that is captured by the CCD on the screen is 100µm wide as determined by the micrometer, and you are viewing the 920 pixel wide image on a standard 96 ppi monitor, the zoom would be approximately 2434 times.
$$\frac{920p}{96p/in}/100µm \approx 2434$$
Additionally, you should ensure that the minimum resolution on the micrometer is at least twice as large as each pixel on your microscope CCD.
The reason that the pixel size must be at least 2 times smaller than the minimum resolution present in the image is due to the Nyquist-Shannon sampling theorem.
This being said, all microscopes (and arguably all measurement devices) should be calibrated against a standard. This paper explains the usage of a standard to calibrate confocal microscopes.

A similar technique used to calibrate normal optical microscopes using a stage micrometer standard can be used if you do not possess such a standard. First calibrate the normal microscope, then image an identical sample using both microscopes in order to obtain the size of the field of view.

This is great info but doesn't answer ?, I already did this. The fov is above.

@rhill45 Sorry for initially misreading. Added my interpretation of the digital zoom.


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Why do people die?
what is the reason people die naturally even though they have no known disease?
I see people become physically weak at times they get old and die eventually in case they are not attacked by any known disease.
My question is what reasons leads human to death?

What Does it Mean to "Die of Old Age"

the question, called senescence is kind of an open one in evolutionary biology.  There are some organisms which appear not to die - dividing amoeba and perhaps the microorganisms called hydrae.

Because people aren't supposed to live forever. We evolve trough generations.


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What is this butterfly?
The following guys (about an inch long) were seen in the Willamette Valley of Oregon in summer.  When one would fly by a resting one, they'd get into a high-speed little "dogfight".  What genus might they be (or species, if you know).  Are they in the "skipper" group of butterflies?

That last picture reminds me of an Underwing Moth. But the clubbed antenna don't match.

Yes, it's a skipper. But I don't know the species.

Yes, it is a skipper (family Hesperiidae) and very similar to European species in Ochlodes, and my guess is that it belongs to one of the North American species in this genus. For instance, it is very similar to Ochlodes sylvanoides (also called Woodland Skipper), which is common in the western parts of the US. However, I'm not familiar with North American butterflies, and there might be closely related similar species that I'm ignoring.
Images of Ochlodes sylvanoides from http://butterfliesofamerica.com/t/Ochlodes_sylvanoides_a.htm:

More pictures can also be seen at Bugguide.net

This led me to open my copy of Robert Michael Pyle's The Butterflies of Cascadia (Seattle Audubon Society, 2002); the species of the question IS Ochlodes sylvanoides, which Pyle illustrates on Plate 4 (page 81), and discusses in full (with further pictures) on pages 99-101; the range map provided on page 99 is a solid mass of blue (which means the species is found throughout the region Pyle covers).

A late addition to my comment above: Pyle also illustrates Ochlodes sylvanoides on Plate 3 (page 77), and covers two additional species of the genus; the range maps given for both of the latter have no blue in Oregon's Willamette Valley.


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What happens when a genome is shorter than the other?
Say there were 2 creatures of the same species. Creature 1 has a longer genome than creature 2, it may be just a few base pairs, but what would happen when the genes were crossed to create creature 3 (via Sexual Reproduction)? Do the genes know where to match up or are there genes that end up being corrupted during this process?
Thanks in advance

there wont be a third species when you cross two organims of the same species with one which has a mutation in some areas of its genome. All of us have some mutation or the other and our genomes are never identical. So when humans have kids, you can expect some mutations in the child but never another species. Unless you are talking about evolution over millions of years or a case where there is crossbreeding between species like a horse and a donkey

@TheLastWord a second or third species was never mentioned. OP talks about Creatures 1, 2, and 3, but they are all the same species. The question seems pretty clear to me - What happens when homologous sequences of DNA have short insertions or deletions on one chromosome but not the other?

What type of "matching up" and possible "corruption" (during recombination?) are you referring to? Mitosis in creature 3, meiosis in creature 3 or normal gene expression during the life of creature 3?


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Have webs woven by LSD-intoxicated spiders ever been studied for their efficiency in fly catching?
I ask, because I have a different interpretation of the experiments performed on web-weaving spiders. The famous Robert Pirsig maintains that LSD is somehow helpful to web-weaving spiders, because it makes their web more straight. Pirsig seems to imply, as I remember, that the spider is somehow more attentive to its web while on LSD.
However, I maintain that it isn't the case and that it is actually the reverse.  The spider is much less attentive, for it needs chaos in its web to catch the fly!

Could you add a reference or link to his work?

Why do you think a chaotic web would be more effective?

I thought the titled question itself was related to Pirsig's claim, however upon further thought they are not related, and thus an answer to the titled question wouldn't disprove Pirsig's interpretation of the experiment.
However the quote does exist and is on p. 36 of Lila:  Inquiry into morals!

It also depends on how you measure efficiency. Of course the spider must expend fewer calories than it takes in from prey, but there is an implicit movement cost as well, in terms of N spiders caught moving around by, say, birds. There's also variety in species - some orb-weavers repair their webs, others construct new ones regularly. Clearly, we need to give more spiders more LSD.

In my flawed thought experiment I was thinking the fly could somehow sense the web, however, that is not the case in most circumstances.

Short answer
A low dose of LSD has been shown to lead to larger, more regular webs. This obsessive perfection of the web comes with an increased effort and likely an increased required building time. Whether LSD-affected webs are more effective or not has not been assessed as far as I am aware. Personally I think that, if anything, larger webs are more efficient for their purpose, regardless of their enhanced regularity.
Background
I traced down the experiments with d-lysergic acid dietheylamide (LSD-25) and web-building spiders to the experiments of [Peter Witt]*1 performed in the 1950's and 60's.
The original article of Witt (1951), dealing with the effects of LSD on the web building behavior of spiders (Zygiellax nohta) is not accessible to me. He reiterates on the data in a review (Witt, 1971). In this review he discusses the effect of a low dose of LSD on web building (Fig. 1).

Fig. 1. Web of an untreated spider (Araneus diadematus) (left) and a web of a spider (Zygiellax nohta) treated with a low dose of LSD-25. Source: Witt, 1971
Witt concludes that low dosages of LSD increase the regularity of the webs. Spiders which had received less than 0.05 pg LSD-25 built larger webs, with fewer oversized angles and significantly more regular central angles. The spiral was unusually regularly spaced. He did not investigate the effectiveness of these webs (Witt, 1971). However, I reckon that because of the larger size they may be more effective.
Witt notes that the normal web is far from a perfect geometric structure and that one can think of a web as a compromise between regularity, which serves to cover a wide area with a trap of a certain mesh size, and a quick construction. For example, Araneus diadematus makes a new web every morning before sunrise. It requires quite some labor producing and the webs are, arguably, structures of precision and beauty (Fig. 1). The webs take between 20 and 30 minutes to build. (Witt, 1971).
The balance between regularity and quick construction of the web is what may be distorted after relatively low doses of LSD (Witt, 1971). The spider seems to put too much and almost compulsory effort in making the perfect web, and likely without too much benefit in efficiency (The Guardian, 1971). But again, the author has not addressed this hypothesis directly.
Note that higher dosages of LSD (>0.05 pg) result in smaller and more irregular webs. The Guardian (1971) reproduced some figures on this (Fig. 2), showing an example of a grossly distorted and inefficient web.

Fig. 2. Web before and after a high dose of LSD. Source: The Guardian (1971)
References
- Witt, Experientia (1951); 7(8): 310-1
- Witt, Behav Sci (1971); 16(1): 98-113
Note
*Robert Pirsig is an American writer and philosopher who has not devoted his time to spiders as far as I know.

Although he didn't perform the experiment, his interpretation of it appears on p 40 of "Lila:  An Inquiry into Morals".

I might also add, he is a trained biochemist, and a living, breathing guy.


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Possible calculations with temperature, humidity, images and VIS spectrum of a plant in an Integrating sphere
I am currently working on a project which involves growing some plants in a integrating sphere made of foam. I have added temperature, humidity and soil moisture sensors as well as a Spectrometer (350 - 800nm) and a webcam which takes images of the plant every 30 minutes.
I thought of calculating the LAI (Leaf area index) from the webcam images.
Does anyone have any other suggestions/ideas on what I could calculate with the given data from these sensors?

Are you designing an analysis around the data or have you gathered data to do an analysis? In other words, do you have a goal with this experimental set up?

Both. I have already gathered some data from a previous set up, but only with the spectrometer and webcam. The main goal is to observe water stress in different plants.  I curious what else i could calculate and predict once i have the data from the new set up.

Thanks for elaborating. Perhaps you could add this background to the question proper. Regardless, +1, thanks and welcome to Biology!

With the images you could, perhaps, assess growth rate of the plant which can be plotted against spectral content of light to investigate effects of light quality on growth. Using moist and water and temperature the same can be done. Multivariate analysis can help to implement all the values, while ANCOVA may may help to correct for covariance.
A detailed experimental set up may help to answer this question. Not specifically the hardware, but how the effect of water stress is measured. E.g., are multiple plants tested under different watering conditions? In that case all the other measures (temperature, light) are probably used to check whether everything is constant across all specimens except water availability. This may limit the usefulness of analysis of these additional measures. I think the other parameters (light, water, temperature) may be not so interesting other than covariates for water stress as they are either not controlled or deliberately kept constant. Moreover, probably their effects on plants are pretty obvious too.


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What is the name of this flower?
A flower has grown on a leaf in our garden. What is the name of this flower? Give some description.

This searchable image database may have the flower you are looking for.
http://plants.usda.gov/gallery.html

Please indicate where this is located.

Great picture of what looks like a cactus; cf "White Torch Cactus". However, it would be helpful to have a picture of the leaf, and to know where and when this was flowering.

It appears to me to be a Night Blooming Cereus:

We had one in our greenhouse in Botany. It rarely bloomed, and the bloom was wilted by mid-morning.

Night-blooming cereus is the common name referring to a large number of flowering ceroid cacti that bloom at night. The flowers are short lived, and some of these species, such as Selenicereus grandiflorus, bloom only once a year, for a single night. Wikipedia

Dave's garden lists it as "Dutchman's Pipe Cactus, Night blooming Cereus"
Epiphyllum oxypetalum.


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Are mitochondria dead?
In the video "What is Life? Is Death Real?", the subject of mitochondria is raised at 2:58. At 3:12, the narrator says "[mitochondria] are not alive any more: they are dead."
What currents of thought lead to this affirmation?
When I search for mitochondria are dead on Google, I get many links about the role of mitochondria in cell death, but I don't see anywhere that the assertion in this video is discussed.

idea probably is that mitochondria can't survive outside the host cell.

@aaaaaa: That seems a strange qualification, since most (probably all) organisms can't survive outside the environment they're adapted to.  Humans, for instance, die pretty quick if you don't provide them with oxygen and keep them between roughly -50°-50°C.

See this related post

@jamesqf SolarLunix made a great point, please consider accepting it

also, i find all question like "what is life"useless in our fight against death and disease.

Does it really matter why some Youtuber decided they are alive or not? Clearly an argument can be made for them being alive (have DNA, replicate, process chemicals) and not being alive (cannot survive very long outside cells, not very complex) and it comes down to an arbitrary distinction. It's an irrelevant concern, nothing about your (or anyone's) life would change if the Czar of Science decreed one way or another.

http://arxiv.org/abs/1207.4803 "...determining which phase (non-life or life) a given system is in requires dynamical information and therefore can only be inferred by identifying causal architecture."

related: Can you consider a human as alive, or is it the cells on the body that are alive?

You should restate the argument given in the video in your question (to make it more self-contained), and highlight what parts you find unclear. At the moment, I think the question is unclear, and answers will mostly depend on how you define the terms alive, dead, and life (you haven't included working definitions of these concepts in your question).

SolarLunix posted an excellent answer detailing the criteria for being classified as "alive", and showed that by those criteria, mitochondria could be considered as "dead".
However, I would argue that the narrator's statement in your video does not make any sense. The currently-accepted theory of the evolution of mitochondria (and possibly other organelles) from free-living prokaryotes is called symbiogenesis and postulates that the mitochondrial progenitors began living symbiotically with the precursors to eukaryotes some 1.5 billion years ago. Life originated on Earth about 3.5 billion years ago, so eukaryotic cells (carrying mitochondria) have been around for a little less than half of that time.
In that incredibly large span of time (if you counted 1 number per second, you'd reach 1.5 billion in about 47.5 years), what used to be an independent organism (we assume) has become an organelle - an integral part of the eukaryotic cell. It absolutely could not survive outside the cell on its own, and relies on signals from the cell (mainly, the cell's energy needs as detected by "sensor" proteins to key molecules like glucose and ATP) to reproduce.
Therefore, it is most appropriate to think of mitochondria simply as another organelle, just like the endoplasmic reticulum, lysosomes, or the nucleus. It doesn't make sense to think of those other structures as "alive" or "dead", just as it doesn't make sense to think of mitochondria in the same way. Yes, they used to be independent, but are no longer; instead they are a well-integrated part of the whole cell.

My thoughts exactly. Though here's an interesting observation: individual human cells are alive, but individual human organs are not. Both are constituent parts of the human organism, and individual cells are even strongly dependent on the rest of the body. Our individual cells have evolved from their ancient independent forms into the super-symbiotic system of the modern body. They form structures (organs) which are not alive, but those structures combine to form something that is alive. The longer I stare at this strange system, the less inclined I am to care about the definition of life.

So, long story short, they are no more "dead" as a part of a cell, than, let's say, liver as a part of human body? Do I get your meaning right?

@Mołot correct. We don't think of the liver, or spleen, or lungs as "alive" or "dead", and it doesn't make sense to think of organelles in that regard as well.

Short answer: According to the definition of life, yes, Mitochondria are "dead".

To be considered alive an organism must meet the following criteria:

organized structure performing a specific function
an ability to sustain existence, e.g. by nourishment
an ability to respond to stimuli or to its environment
capable of adapting
an ability to germinate or reproduce

Are Mitochondria organised?
Yes, they have a structure that allows them to metabolise energy brought to it by the cell.
Can Mitochondria sustain their own existence?
No, many of the genes that mitochondria need to function are no longer in the mitochondria. They need the host cell to provide much of what they need for them.
Note that I am pointing to the Mitochondria's genetics. They used to be included in the Mitochondria itself and have been moved into the cell host DNA. This is why I consider them to be "dead" because they are no longer their own organism, they are an organelle that helps the cell stay alive.
We can stop here since this disqualifies Mitochondria from being considered alive. However, for completion, I will continue.
Can Mitochondria respond to stimuli?
Yes, in order for it to divide it receives signalling from the cell. I would consider this a response to its environment.
Can Mitochondria reproduce?
Yes, their reproduction is much like a bacteria reproduces - through a process called fission.

Conclusion: Since Mitochondria cannot sustain existence, alone (thanks to no longer holding their full genome) they are dead.

This question seems like a (meaningless) exercise in semantics. By this logic, then my skin and heart are "dead", since they can't sustain their own existence.

The issue I am having is that it seems like you have gone from "Not alive" to "Is dead". Are all things that are not alive dead?  Eg the sun is not alive, but I would not call it dead. A spoon is not alive, but also not dead  (Also Cthulu :-P).
I feel like to be dead you means be "not alive" and also "previously was alive."
(whether previously alive refers to individuals or not I am not so sure.)

-1. By your logic, parasites such as tapeworms (which can't survive outside their hosts) are dead.

@Oxinabox Btw.. I can argue that sun is alive :P.. It is self sustaining and perhaps will some day die.. It is organized and can adapt to stimuli (at the celestial level of course). Earth is alive too that way.. SolarLunix: Actually every living organism is living only with respect to its environment. Heterotrophs are dependent on autotrophs (but we cannot call them dead, can we)

I do think that "sustain their own existence" is a remarkably high bar, of which I am unaware of any member of any species attaining.  Humans, for instance, do not survive long in the cold vacuum of space without anything sustaining them.  Most every biology text I am aware of recognizes that we live in a network, not in isolation.

Just move one comma in your conclusion: "since mitochondria cannot sustain existence, alone they are dead". Inside cells, on the other hand, party on. Anyway, I think you're using a definition of "a living organism" or "a form of life" (and even then one has to be generous as regards independence, as others have noted). It doesn't imply a definition of "dead" that is or sensibly can be applied to parts of living organisms.

@Sparhawk but unlike Mitochondria, your skin and heart have the genetics to survive on their own.

@MarchHo but unlike Mitochondria, tapeworms have their full genetics and their offspring can move into a different host. Mitochondria are stuck in the same host lineage from generation 1 to generation infinity.

@SolarLunix That argument is not consistent with the points in your answer.

@Sparhawk I specifically pointed out the genetics as to why they are not able to survive on their own. I made it clearer since the point wasn't obvious. I can edit again if you still think I wasn't clear enough on that point.

@CortAmmon it does seem like a remarkably high bar, but I was t looking at putting them in another place so much as I was looking at them in relation to what they used to be. Because all of their genetics are no longer located within them anymore I don't consider them an organism, just an organelle.

@SteveJessop done, thanks. You made a good point.

@Oxinabox
I think that when talking about biology, you're either dead or alive. anything in between if caused by our lack of understanding. The sun cannot be analysed in the same manner as a plant (if you pick the sun then i would pick any random rock. Is it alive?)
Why isn't the sun alive if it fits all the given criteria except reproduction  - which, if we wanna be picky about it, then mules are dead.
So, the way i see it, the first distinction to be made is whether we are talking inanimate or not.

@SolarLunix If one wishes to look at "what they were" to develop a subjective position on whether they are alive, that is fine.  I just find it important to note that any argument which claims to have declare the livingness or deadness of something to be "case closed" runs into trouble with definitions.  The line between them is not as crisp as we may wish.  For example, instead of "sustains existence," Wikipedia has "metabolism," which a mitochondria clearly has.

The sustain its own existance part is too vague to make sense. Everything requires an ecosystem to sustain it: we can't sustain ourselves without food! Many vitamins, amino acids,  etc. Cannot be made by the human body because we lack genes for that; so are we not-alive like the mitochondrea?

@Sparhawk skin and heart cannot survive on their own. The component cells need things that are made by others. And it's not just a matter of being switched off, as no cell in the human body can make vitamin C, as the gene for that has been moved out to the "host" ecosystem at large.  Out genetics are no longer located within our cells, in exactly the same manner  as SolarLinux points out for mitochondrea.

@JDługosz : "Our genetics are no longer located within our cells..." that is subtle and frightening!

I would like to expand a bit on SolarLunix's post, because the logic used in the conclusion would also mean that endosymbionts, such as https://en.wikipedia.org/wiki/Buchnera_(bacterium), who cannot survive outside their host are also "dead".
I think many of us disagree with that notion, so instead I would say that it's the fact that so many of their genes have been relocated to the nucleus that makes them organelles and thus substructures of the eukaryotic cell and thus "dead".
Ultimately though, I think it's more a matter of semantics, since you could argue that they represent an advanced stage of endosymbiosis.

Agreed. And if we're moved just a few miles (straight up or down) from our environment, we survive just as poorly as various endosymbionts.

That's what I was saying that everyone seems to have missed....

@user2338816 or a few thousand north or south

What a brilliant question for promoting a discussion.  Mitochondria definitely reproduce, they maintain a better energy flow than any other part of the cell, and they maintain a very low entropy state by exploiting that energy flow.  It may not be a textbook answer but being alive really is about decreasing your local entropy by exploiting a flow of energy.  I suspect that mitochondria have ceased to change under the pressures of natural selection, but so what - they have been practically perfect for a billion years.

Jeremy England's hypothesis that life arises naturally as a way to capture energy and dissipate it as heat: https://www.quantamagazine.org/20140122-a-new-physics-theory-of-life/


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Why do crabs spit?
Last year I photographed this juvenile Sally Lightfoot Crab (Grapsus grapsus) 'spitting' (click for larger view):

I thought I'd look up more information on this behavior, but couldn't find any explanation regarding its actual function. I can imagine a few potential functions this could serve:

Secreting excess salt—just as Marine Iguanas sneeze.
A means of evaporative cooling—like the mosquito's behavior described here.
An attempt to eject irritants from the crab's mouthparts.
Possibly a means of self-defense.
Any combination of the above or something I hadn't even considered.

Has there been any research regarding the biological function of this behavior? On a side note, I'm curious about how widespread this behavior is—is it only this species or is it nearly all land crabs?

No idea but excellent photograph.

Watching some videos of them it seems like it could have a number of uses, possibly even as a fitness indicator to mates. Smelling your partner's sneeze - so romantic.

Breathing during digging

And if all that wasn’t enough responsibility for these claws, they also are used for digging. While most digging crabs use their back legs to burrow backwards into the sand, the shame-faced crab uses the claws like little bulldozers, excavating the sand forward so the crab sinks downward until it is completely covered by the sediment.
Burrowing underground is fine and all, but how does it then breathe? Again, it’s the claws that solve this problem as well. When beneath the sand, the crab regularly shoots a stream of water from its mouth (when you remove one from the water it spits for a few seconds, creating a little fountain that can be up to half a foot long. The crabs themselves are only about two inches thick.) The stream of water ricocheted off the inside of the claws, shooting upward and moving the overlaying sand grains, briefly allowing the crab to take a breath.

Expelling salt water

SALLY LIGHTFOOT CRAB
Born much darker (almost black) in color as to avoid predation,
Sally Lightfoot crab grows gains more vermillion, as it grows
larger. Nimble-footed and photogenic,these crabs make for
excellent models --though they may be a bit shy for close-ups,
scurrying away sideways, up slopes and even upside down.
Occasionally you may see a crab “spitting” from near its eye.
Actually,the stream of liquid you notice is the Sally Lightfoot
crabs way of expelling salt water that seeps into its exoskeleton.

Although neither source sites a reference, they support the hypotheses of secreting excess salt and ejecting irritants (sort of). Thanks for the response.

@p.s.w.g I know, I'll try to also find a reference later. And you are welcome :)


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Protein that exit from the cell - as marker
Searching for some protein, that I could use as extracellular marker for mammalian cells. I need to insert mRNA to cell, and to detect the protein outside the cell (not on membrane) if the mRNA successfully enter and been translated. (not GFP, I need protein that exit from the cell in big numbers)
Thank you.

You might want to check secretome analyses like http://www.nature.com/nbt/journal/v30/n10/full/nbt.2356.html

I don't know of any that are exported by all cells, e.g. both neurons and . All blood proteins, e.g. serum albumin are exported but by specific cells.

You can always express GFP or your favorite protein in a secretory vector like pSecTag or pSecTag2 from Invitrogen/Life/ThermoFisher/SuperUltraBioMegaMart. There are probably others, but those were the first ones I came across. They contain the mouse Igκ signal sequence for efficient secretion (so the website says, I've never used it).
I don't know the details of your experiment, but are you sure you want to use a secreted protein as a transfection marker? Remember, it's possible that only a small fraction of your cell population will take up the vector (or mRNA, if that's what you're using, but there are issues with that), but you will see secreted protein regardless of the number of cells that take it up.

Thank you! Looks good. It's ok, I just need to know if some cells get the vector, doesn't meter how many of them.

SEAP, secreted alkaline phosphatase, and vectors engineered to express fusions to this reporter gene may be well-suited to solve your problem.


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Why are lions the only social cats?
We know that almost all cats are solitary.
How did the Lions (Panthera leo) end up social animals? Do we have an explanatory evolutionary path describing how the Lions became social while the rest of the felines remained solitary?
I'm not asking what general rules apply to evolution, but, rather - what evolutionary path has led to this specific outcome.
I know a bit of evolutionary game theory. No need to reiterate the obvious. I'm asking if we know the mechanism or the evolutionary pressure in this particular case.

Evolution does not have a reason. It just happens. So any question on "why such or such a thing happened", tends to be purely philosophical. You can edit your question to make it precise and non-phiosophical. For e.g. you can ask if socialization increases the survival probability of lions in the environment that they live in i.e. the savannas.

possible duplicate of If a trait would be advantageous to an organism, why hasn't it evolved?

Simple answer - it was probably beneficial to them but not other species. This is a duplicate in my opinion http://biology.stackexchange.com/questions/35532/if-a-trait-would-be-advantageous-to-an-organism-why-hasnt-it-evolved

I think http://biology.stackexchange.com/questions/35532/if-a-trait-would-be-advantageous-to-an-organism-why-hasnt-it-evolved is the reverse. That is the sort of question targeting "why haven't all predators evolved poison-slash-high speed running capability-slash-guns-slash-more nonsensical stuff?" This question seems well researched (I have a cat and, oh my, is she solitary!) and seems to make sense. For example, investigations on fossils tends to include the interpretation of geographical grouping (did they form herds?) etc. I vote to leave open. I'm not an evolutionary expert, though.

Could you elaborate more on your claim that "We know that almost all cats are solitary"?

I'm not entirely sure, but the impression I got from reading about felines was the they are mostly solitary. Although there is ample evidence that house cats can socialize: http://katzen-verstehen.at/wp-content/uploads/2013/04/social-organization-of-the-cat.pdf, I don't recall seeing material on social organization in other felines other than lions.

I guess it has to do with the failure of dogs and wolves to be able to take down large prey animals in Africa, so that left the door open for felines like lions and hyenas to collaborate and hunt for big prey animals.

@mousomer It is also very difficult to ascertain what kind of pressure would have selected a socializing trait in lions. This also tends to be speculative. I guess most grassland animals are social, even cheetahs.

Well, between @WYSIWYG and Count Ibis, now we do have a glimpse of a direction. Grassland animals form larger herds, so there is a niche for socialized predators. More questions: why are cats unsocial outside Africa? (possible answer: Homo Sapiens?). What is the mechanism forcing large herds on Grasslands? (large, open space)

Yeah, to me it seems like the perfect excuse we "scientific evolved sapiens" tend to make to masque the obvious  which is: "we-don't-know, we-can-make-a-stupid-guess-and-call-it-educated-and-if-its-made-by-some-renowned-author/scientist-it-will-be-professed-as-truth".

This is not a direct answer to your question, but I want to point out that your basic premise is partially incorrect. Other felines also form social groups. For instance, male cheetahs form coalitions (also see Cheetah outreach at http://www.cheetah.co.za/c_info.html), often for life, which generally makes them more successful in defending territories. Female feral cats also form social groups in some environments (see e.g. Natoli et al, 2007), where females sometimes co-rear kittens. There is even evidence that tigers share kills with related or unrelated individuals (see Wikipedia: Tiger for examples), and tiger home ranges can overlap in complex ways. On the other hand, lions (both males and females) are sometimes solitary, and this partially interacts with their living environment.
My point is mainly that sociality (in general or in felines in particular) is not either/or for a particular species, and other felines also show social behaviours and sometimes form groups (so sociality should be viewed as a sliding scale). Granted, lions are definitely the feline with the strongest social behaviors, and they form the largest social groups. It is therefore interesting to think about why that is the case, and what group dynamics and tradeoffs that determine the social behaviours of lions.

I think it's actually a direct answer: there is no explanation to find for a non-existent fact.

@biozic I definitely think that the Q should be rephrased and stated in less either/or terms. However, to look at the evolution of sociality in relatives of lions, as well as the costs/benefits of social behaviour in lions would still be interesting. To ask for the specific evolutionary path and its reasons is asking a lot though.

I agree with some comments that have been made on the validity of the wording used by OP. However there is a legitimate thrust to the question. What could drive Lion sociality?
Females are the base unit of lion social groups. Males are generally the nomadic sex. Male lions will try to take over a group of females by killing the current cubs and mating with the females. By having groups of females they can drive off males that are not related to their offspring.
Males are equally rewarded for banding together to defend females and to subdue larger groups of females or other bands of males. Lion packs are therefore formed by these antagonistic interaction between male and female lions. More research is needed!
http://www.sciencedirect.com/science/article/pii/000334729580157X

In brittle environments we often find very large range lands(grasslands, savanna etc) that are inhabited by mixed mega herds of numerous, large, grazing herbivores. It takes pack hunters to successfully predate upon these herds. Note that all the apex predators in the more densely forested biomes of non brittle environments are solitary hunters(Tiger, Jaguar, Bear etc). Remember that various sub species of Panthers leo once roamed from Africa, across Eurasia and into North America. There are many extinct Panthera species too.


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How do animals end up in remote areas?
I was thinking specifically about random marshy water holes on farmers fields. It seems that you can visit just about any one of these and you will find frogs if you look hard enough.
They usually don't seem to be connected to each other. If it were any other land animal I would figure they walk from one spot to another, but in the case of frogs, I don't imagine their range is very vast. But often these marshy spots can be separated by fairly large distances to a frog.
So this brings me to my question: how do each of these spots end up with frogs in them?  I don't imagine a frog is going to go hopping over a hill to get to a marsh on the other side, is it?

The same with fish - how on Earth do they find their way to isolated lakes?! ! I love this question. +1

I have read that hurricanes can carry animals up into them and displace them. https://en.wikipedia.org/wiki/Rain_of_animals#Frogs_and_toads

First, i would look at statistics:
just because (hypothesis) you visit 1000 watering holes /marshes a year and they have frogs in them it doesn't mean that its a common occurrence; Second, i think froglings (yeah, i know :D ) hatch whenever there is rain, grow, mate and deposit new eggs that survive droughts. Now, these can be relocated by earth movements and birds and wind (i don't think frog rains could help with this level of dispersal).
Basically, they don't end up in remote areas; They were already there in some form.

I think you should narrow down the question (question title) to frogs (if you are mostly interested in those), or a group of organisms with similar biologies. "Animals" is too unspecific, and answers will differ widely between organism groups (e.g. birds, rats, frogs, dragonflies, fish etc), so the question is "Too broad".

You should clarify how great is the distance between two nearest habitats for a certain organism. Frogs can move about in some range. Sometimes their eggs or tadpoles can get washed away with runoff water to land up in distant places.

You would understand it much better when you consider the fact that your question encompasses a geographical aspect more than a biological one, the biological aspect being the creation of a new habitat. Migration/dispersal of offsprings from their parents depends much more geographical aspects such as lay of the land or climate. These links may be of some interest. http://goo.gl/JL1vp3 , http://goo.gl/agcr0d , http://goo.gl/6vb6yp

@Koustav, yes it seems to make more sense being dependant on droughts and floods rather than by glaciation as suggested by MattDMo. Your comment would be better as an answer.

If you are a creation believing person, then the universal flood clearly gives the answer you are seeking about fishes @AliceD

@OneFace - I'm not and if I were, it still does not explain why fishes inhabit new puddles formed after the universal flood :)

This question pertains to organism dispersal, which is a very active field of study with relation to it's impact on conservation efforts. Much of what I will say below has been covered in this wiki.
Definition: From the Wiki

Technically, dispersal is defined as any movement that has the
  potential to lead to gene flow.

It can be broadly classified into two categories:

Density dependent dispersal
Density independent dispersal

The question of frogs and fishes both refer to Density independent dispersal, while an example of density independent dispersal can be the competition for habitat space between big cats and humans (this is a WWF pdf)
From the wiki:

Density-independent dispersal
Organisms have evolved adaptations for dispersal that take advantage
  of various forms of kinetic energy occurring naturally in the
  environment. This is referred to as density independent or passive
  dispersal and operates on many groups of organisms (some
  invertebrates, fish, insects and sessile organisms such as plants)
  that depend on animal vectors, wind, gravity or current for dispersal.
Density-dependent dispersal
Density dependent or active dispersal for many animals largely depends
  on factors such as local population size, resource competition,
  habitat quality, and habitat size.

Currently, some studies suggest the same.
This study in particular studied the movement and habitat occupancy patterns within ephemeral and permanent water bodies in response to flooding. They found that during flooding these frogs moved out to flooded ephemeral water bodies and later on moved back again to the permanent ones.
Other suggested readings for those highly interested in the subject may include this (a phd thesis) and this (a project report)

I don't imagine a frog is going to go hopping over a hill to get to a marsh on the other side, is it?

Why not? In wet weather, the conditions would be just fine for an enterprising amphibian to go exploring, perhaps driven by predators or lack of available resources, not to mention Ro Siv's comment about wind-borne dispersal of animals. Birds of prey may also pick up small animals, fly away with them, then drop them for whatever reason.
You are also neglecting the fact that these organisms have existed for millions of years, and the landscape has changed tremendously in that time, with glacial periods interspersed with interglacials every 20-50,000 years or so. As glaciers melt, large lakes form, and as those dried the organisms were dispersed across the land into smaller bodies of water. Streams and rivers form, transporting aquatic life forms, and may dry out and form isolated ponds, or they may be blocked for any number of reasons (mudslides, earthquakes, volcanic eruptions, beaver dams, fallen trees, etc.). As erosion and landscape remodeling occur, all traces of the original body of water may be erased, except for the wide distribution of similar organisms.

Yes, but marshes have come and gone on an almost yearly basis (or over several years, maybe a decade or so). We're not talking eons here.

@Octopus marshy areas tend to remain marshy areas over the short term (decades to centuries) unless acted upon by an outside force, such as the rerouting of a water supply or human activity. I'm not sure what you mean by coming and going on an almost yearly basis - could you give some examples? Also, as I mentioned in my answer, during prolonged wet weather (maybe over a week or more), frogs and other amphibians could travel relatively long distances with ease. I'm not terribly close to wetlands, yet I often find frogs in my yard during/after a long rain that are no longer there when it's dry.


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What would be the impact of depositing limestone in the oceans (to reverse acidification) on ocean life forms and biodiversity?
This question asked: What is the evidence it is feasible to reverse ocean acidification by adding large quantities of a base (bicarb soda)?
The result was:

Danny Harvey of the University of Toronto has already looked into this. His solution is to deposit 4 Gt/yr of limestone into the oceans. To put this in perspective, global coal production in 2013 was nearly double this at 7.823 Gt and it is more than global iron ore production in 2014 of 3.22 Gt.

The respondent then posed the question: What impact would such a huge annual deposition of limestone have of ocean life forms and biodiversity?
My question is: What would be the impact of depositing limestone in the oceans (to reverse acidification) on ocean life forms and biodiversity?

Harvey recommended 40 µm powdered limestone, delivered to certain points and depths in the oceans. The amount of fossil fuels consumed to mine, powder, transport, and precisely deliver the limestone each year would necessitate a much larger quantity of limestone to offset it, increasing fuel use even more, requiring more limestone, and on and on, not to mention the amount of machinery, trains, trucks, and ships that would need to be produced to even put this operation into effect. This idea is completely unfeasible, so I'm voting to close this as opinion-based.

From What types of questions should I avoid asking?: avoid asking subjective questions where (…) you are asking an open-ended, hypothetical question: "What if ______ happened?"

To simplify, acidification of oceans is due to excess anthropogenic carbon dioxide CO2:

H2O + CO2 → H2CO3 → H+ + HCO3-

Seawater is naturally saturated with another base, carbonate ion (CO32-) that acts like an "antacid" to neutralize the H+, forming more bicarbonate.

CO32- + H+ → HCO3-

You want to alkalinize the ocean by dumping CaCO3. That sounds pretty good, and not only would it add more buffer (and decrease acidification) but it would also help the sea creatures which use dissolved Ca2+ and CO32- to make shells of calcium carbonate CaCO3. (The other effect of excess CO2 is the leaching of CaCO3 from shells and corals or other marine organisms:

CaCO3 + H+ → HCO3- + Ca2+

The limestone mined today is used for gravel, in concrete, road surfacing, foundation support beneath weight-bearing structures, the boulder faces of earthen dams, Portland cement (N.B. the burning of limestone in the cement-making process liberates CO2 gas), Aglime (pulverized limestone) and quicklime (process liberates CO2 gas) which are both soil stabilizers, hydrated lime used to filter potable water supplies and to treat solid and liquid waste and in processing petroleum. These are only the major uses of limestone.
The average annual limestone production in Missouri (the largest deposit of limestone in the world) is about 89 million short tons/year. The cement industry alone is a MAJOR producer of CO2. Producing a ton of cement requires 4.7 million BTU of energy (some of which will release CO2), equivalent to about 400 pounds of coal, and generates nearly a ton of CO2.
So, in addition to the CO2 produced by the use of limestone in everyday life, you want to mine it and dump it into the sea. Unfortunately, even finely ground limestone (remember all that CO2 it takes to mine and crush it) is poorly soluble in water (pH 7.0). It does increase with acid, but still is very slow. Also, it sinks. The worst acidification of the ocean is in surface waters.

Some estimates suggest that close to 100 million tons of limestone are mined globally each year. (It's probably much more than that; see Missouri alone.) You want to mine, crush (to between 40µm - 10µm!!), and deliver an additional 4 Gt/yr of limestone, even though in the paper you cite, that amount per year would not help:

Extraordinary additional measures (adding 4 Gt limestone/yr to the ocean for > 200 years) provides a modest additional benefit (additional to cutting CO2 emissions.)

Why? What difference would knowing the effect on biodiversity be when just procuring, processing and delivering the stuff would generate more CO2 than it could possibly buffer, and would have a minimal effect anyway?


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What is the top speed of muscle contraction?
Currently I am looking into what muscles groups are most used during a football kick. I have a hypothesis that the quadriceps are not as used as most people think because the momentum the swing creates makes the knee extend to fast for the quadriceps to contract.
To prove this I need to know the speed the knee extends during a football kick and the time it takes for the quadriceps to contract. I know how fast the knee extends through my own research.
Does anyone have any information on the speed of muscle contraction?
Quadriceps contraction time would be optimal, but any information relevant would be very helpful

Your question is a good one. The velocity of muscle contraction depends on the:

Initial length of the muscle
The Load on the muscle

Source: Medical Physiology : a cellular and molecular approach by Walter F. Boron, Emile L. Boulpaep - 2nd ed. Page 248

From the above picture we can see that:

The velocity of muscle contraction is not constant. Initially it is zero and then it accelerates to reach a peak
The maximum velocity of muscle contraction is constant at any different initial muscle length
The lower the load the steeper the rise of velocity

So the velocity of muscle contraction should be calculated on a case by case basis.
What can be calculated
What can be calculated is the displacement and frequency of actin myosin cross-bridging.
Under microscopically isotonic conditions, the quantal displacement of a single cross-bridge is ~11 nm.
The frequency of actin-myosin cross-bridging depends on atleast:

ATP concentration
Temperature

At an ATP concentration of 1 µM the frequency is 3.8 ± 0.4 M-1s-1
At 170C the mean time for single displacement was 15±20 ms. While at 250C the mean was 6.4±3.6 ms.

Source: Characterization of Single Actin-Myosin Interactions by Jeffrey T. Finer, Amit D. Mehta and James A. Spudich.
Biophysical Journal, Volume 68, April 1995, p.291s-297s

Concerning your actual question regarding the quadriceps velocity and the velocity of the swing, you should keep the following in mind while calculating:

Quadriceps acts over a second order lever: The Knee is the fulcrum, the effort is put over the tibial tuberosity where the quadriceps is inserted and the load is the foot and whatever it hits/lifts...
The contraction of the quadriceps is calculated as linear velocity while the kicking action is circular - so what you actually observe is the angular velocity. So appropriate angular velocity to linear velocity conversion should be made.

All the best!


text:
Can HIV mutate to become airborne?
HIV has a very high mutation rate due to its inability to correct errors in DNA replication and it is very adaptable to its environment. Hence I wonder whether is it possible for it to mutate such that it becomes an airborne virus and what mutations was needed for it to occur. After all other viruses such as influenza have done so before. Furthermore from the virus point of view, doing so will allow it to be more successful evolutionary speaking since that would allow the virus to infect more people and hence reproduce itself more quickly. And what will be the consequence if it happens?

Quick answer: likely not. HIV is extremely vulnerable outside the body, which is why fluid-to-fluid transmission is required. A huge number of mutations, all in the same virion, would be required to give it the resistance to molecular oxygen, sunlight, dehydration, temperature changes, etc. to become airborne. Also, your statement it is very adaptable to its environment is not quite correct. It is adaptable to escaping immune surveillance, but not to other environments. In fact, many (if not most) of HIV's mutations render it incapable of completing its life cycle in one form or another.

"...other viruses such as influenza have done so before." Are you saying that there was a time when the influenza virus was not transmissible through the air? When was that? As far as I know (I'm not a virologist), the virus doesn't fly through the air with the greatest of ease unless someone sneezes or coughs it out on a droplet.

See this post. It is exactly about what MattDMo is saying. I am afraid this question is quite opinion-based.

I think questions like these can offer some value if you approach them as Fermi problems. MattDMo seems to have correctly identified the barriers the virus would have to overcome, and we can roughly gauge the chances of all of those changes occurring in sequence. Which, without putting too much thought into it, I'd say somewhere around "when pigs fly."


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What are the evidence that all life today descended from a common ancestor (LUCA), and which organisms (if any) challenge the concept?
If I understand correctly, the concept of the LUCA (last universal common ancestor) is based on the hypothesis that archaea and bacteria share common ancestry.
In the realm of mathematics, the same discoveries have often been made more than once, in different places. Sometimes (like with calculus) these independent discoveries were made almost simultaneously. Sometimes the discoveries appear to  be totally unrelated (Hipparchus affirmative compound propositions before 100 BC, and David Hough's work on inserting parentheses in 1944).
If "life" started on Earth in some kind of primordial soup, it is conceivable that it started not once but many times, in different places and at different times.
How strong is the evidence that bacteria and archaea do not represent quite separate discoveries of "life", which (because of the nature of the chemical substances that they use) happen to share a number of features, such as DNA?

Multicellular, or metazoan, life may have evolved more than once, because sponges (Porifera) have a life-cycle and body plan unlike any other plants or animals (although this notion my be outdated).  Check out the evolution of the aminoacyl-tRNA synthetases. Some authors have argued that the fact that there are two discrete families, and that each family can charge tRNAs for the major classes of amino acids as evidence that this capacity, to prepare a limiting substrate for protein synthesis evolved at least twice.

It is quite likely (but impossible to study) that the first stages of life originated more than once. However, the evidence that all currently existing life originated from the same population is very strong.
On the most basic level, many of the basic building blocks of life, RNA, DNA, amino acids are chiral, which means they come in multiple forms, but for the basic processes in nature, always the same one is chosen. For example, the DNA double-helix is almost always right-handed in nature,
see also here. If there were multiple origins of archaea and bacteria, we would expect some to pick another form, if not other molecules. In addition, many crucial proteins such as DNA- and RNA- polymerases are very similar between all species, the probability that they would have originated independently is simply minuscule.

Isn't the right-handed nature of DNA the result of energy requirements ? Wouldn't any new life form tend to adopt the configuration that requires lower energy levels? Is there no evidence of genetic transfer between archaea and bacteria that could account for the sharing of proteins? Might not the choice of molecules have been dictated by what was available in the original "soup"?

(energy) you could build left-handed DNA with the same energy levels as right-handed DNA using L-Ribose (since the sugar is also chiral). 2. there is likely genetic transfer, but at this point you might want to think which parts of an organism you would consider ancestral, 3. at least for amino acids, the version not occuring in proteins is used for other things.

The universal nature of the genetic code strongly supports the hypothesis that unicellular life evolved once on  the planet (or that the organisms that used this genetic code won out).

If life did originate multiple times, it'd be quite a coincidence if it ended up with the same specific amino acids, nucleotides, sugars, genetic code and on top of that also the same chirality (for basic processes).

The genetic code of the tree of life is actively studied. So far, all the living beings have conformed to LUCA model. They are all RNA and DNA dependent, and no other life forms are known. All the RNA and DNA life forms share a tree like inheritance pattern with more simple organisms.
Sometimes there is doubt about wether mushrooms are more closely related to animals or plants.
Sometimes it is debated wether Prions are life forms or not. They are proteins that can reproduce by tricking human cells to making them and then transmit themselves, but they have not developed into anything else than a protein.
Some Virii have a special relationship with DNA, in that they just hyjack and eat DNA using RNA tricks, but their code is basically a lego block of other DNA they have hyjacked, they have fascinating evolution mechanism.
Here is the Tree Of Life, for the moment all genetic testing has found a tree structure shared by common acenstors, in all organsims, hence a LUCA:

here you can see it in detail, so far 50 000 species are on there, from the same philae and DNA -tested, and soon they will have more species, like 200k or something.
huge pdf poster:
http://www.timetree.org/public/data/poster/timetree24x32.pdf


text:
What leads to the different types of navels?
Obviously, there are "innies" and "outies" in the human belly button world.  Both are the result of a knot tied in the umbilical cord just after birth.
But why do some belly buttons become outies while others become innies?  Is it related to how the doctor ties the knot, or is it related to how the knot heals?

In my opinion, this question doesn't belong here.  Biologists, and biology itself, are not responsible for belly buttons.  Doctors are.  Thus, the question belongs where I asked it - on the Health.SE.  However, I will be indebted to anyone who can answer the question, wherever it happens to be.

After childbirth, the umbilical cord is either tied (similar to a tourniquet - the cord itself is not tied into a knot) or clamped to cut off the blood supply. It is then cut distal to the clamp/tie, separating the child from the rest of the cord and the attached placenta. The remaining cells die and dessicate, and the stump eventually falls off, forming the umbilicus or belly button. The default result, barring any issues, is an "innie". However, an "outie" may form if the child was born with a tiny umbilical hernia, or there was a small unnoticed infection at the base of the umbilical cord. Either of these could lead to the formation granulation tissue, described colloquially as an "outie". People can also have combination navels, with the indentation of an "innie" but a small amount of protruding granulation tissue inside.


text:
dAT joining: please define
I came across a reference to dAT joining in my reading of Genentech by Sally Hughes. The technique is described in passing as a technique for joining DNA fragments used around the late sixties to early seventies (likely prior and after, too, of course).
A quick query into earlier visits of the topic on the exchange returned no relevant results, but the results may have been have been obscured by the copious references to the neurologic "DAT" term (dopamine transporter).
Please provide a quick explanation to this concept/technique if you're familiar.

In the context of this book, dAT joining is a method used in molecular cloning to join two DNA molecules. Basically, terminal transferase is used to add polyA or polyT to the 3' ends of each DNA molecule. This creates cohesive ends which can anneal and then be ligated together, giving a covalently closed circular DNA molecule.

Image from: Jackson DA, Symons RH, Berg P. 1972. Biochemical Method for Inserting New Genetic Information into DNA of Simian Virus 40: Circular SV40 DNA Molecules Containing Lambda Phage Genes and the Galactose Operon of Escherichia coli. Proc Nat Acad Sci USA 69(10):2904-2909.
See also: Lobban PE, Kaiser AD. 1973. Enzymatic end-to-end joining of DNA molecules. J Mol Bio 78(3):453-460.

dAT joining can also refer to an assay of DNA ligase activity. Linear dAT oligomers are incubated with the ligase, which can circularize them and make them resistant to exonuclease digestion. This resistance to digestion correlates with DNA ligase activity.
Modrich P, Lehman IR. 1970. Enzymatic Joining of Polynucleotides. J Biol Chem 245(14):3626-3631.


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Evolution of protein and protein efficiency
Suppose we have a bacterial protein that performs a function and let's say we can measure the efficiency of the protein. Let's say we have two species, species A and B, both of which have this protein. One of these species, species A, is close to the common ancestor of A and B, in terms of evolutionary distance, while B is farther although for both cases, it took two speciation events to end up with species A and species B.
Let's say for both for species A and species B, we measure the protein efficiency in different environments. The species A protein has the efficiency highest in an environment most similar to its own and the same is true for the species B protein. But let's say we have two situations:

When species A protein has best efficency, it has a lower efficiency compared to species B best efficiency
Species B protein best efficiency is lower than the species A best efficiency

In these two cases, what conclusions can we make in particular about the evolution of the protein itself? Can we show that the protein evolved to a degree to suit the different environment of species B compared to species A?

A few details

One of these species, species A, is close to the common ancestor of A and B, in terms of evolutionary distance, while B is farther although for both cases, it took two speciation events to end up with species A and species B.

I have two issues here.

I don't understand why this information matter for your question.
There are several metrics of evolutionary distance. In terms of time to common ancestor and therefore, in terms of number of neutral substitutions (it is ok if you don't understand why I talk about neutral substitutions) species A and species B are at exactly the same "evolutionary distance" to any of their common ancestor. However, you may want to talk about evolutionary distance in terms of "By how many standard deviations of a quantitative trait did the mean trait value shifted since the common ancestor (in haldanes unit by definition)", then one species might be more closely related to the ancestor indeed. But in such case, you need to talk about the quantitative trait resulting from protein changes and not directly at the discrete, non-ordinal (nominal) nature of proteins.

And a third general issue I have

As I understand the question, I don't think the question is specific to proteins at all. The question seem rather to relate to "environment specific adaptation in comparative genomics and reaction norms" and would be completely legitimate to look at that at the level of a protein or of a quantitative traits.

To answer your question
You are interested in the measure of fitness as a function of both environment and the protein under consideration. The relationship between the fitness (and other quantitative traits) and the envrionment is referred to as the reaction norm.

Here the graph display the quantitative trait (could be fitness) in the Y axis and environment in the X axis (as it is usually represented).There are two lines, for two different genotypes (the two different proteins in your case).

Can we show that the protein evolved to a degree to suit the different environment of species B compared to species A?

Well, looking at the graphs it looks like indeed one protein has been under selection in one environment while the other has been under selection under the other environment. Testing this is just a matter of statistics. Basically, to test for this, you run a linear model with the quantiative trait (eventually fitness) as the response variable and the environment, the genotype and their interaction as explainatory variables. If the interaction term is significant (and if the directionality of the interaction is the one you would expect, that is genotypes are more fit in the environment where they live and if each genotype outcompete the other in at least one environment), then the genotypes are locally adapted.
EDIT

what counts as significant?

You can chose the level of significance that you wish (0.05 for example). If this is unclear, you'll probably want to learn more about stats before.

can you provide an example of when this method you have described was used the literature to show the evolution of a protein?

If you want example from the literature you can just type Genotype by Environment Interaction on google scholar and will get tons of hits. Here is a paper discussing this methodology specifically and here is a (old) book on the subject. I am not sure why you're still talking about proteins. Most often those studies are done at the level of the gene (or directly on the phenotypic trait). But you can find the gene and get the protein sequence from it or even play around to visualize it with various biophysics softwares.

could you explain the stastics further, and give an example? other thstn that, great answer!

Sure. Can you point to what exactly is unclear/incomplete? If it is the very end (what follows "To test for this"), then you'll probably read a bit by yourself on wikipedia (linear regression, interaction) and eventually ask questions on stats.SE.

When you mean the interaction terms are signficiant, what counts as significant? Also, can you provide an example of when this method you have described was used the literature to show the evolution of a protein?

Please see the Edit section in my answer

In these two cases, what conclusions can we make in particular about
  the evolution of the protein itself?

It's not clear to me that it is right to make any evolutionary conclusions based on function alone.  DNA sequence would be a FAR better way to estimate evolutionary relatedness.


text:
Photosynthetic efficiency and light harvesting efficiency
Is there some sort of measure of the light harvesting efficiency (possibly like transfer time) that is directly related to the photosynthetic efficiency in some sort of equation? Also, how important is light harvesting efficiency to photosynthetic efficiency?


text:
When did mouth pipetting stop becoming a way to handle liquids in a lab?
Almost all modern lab protocols have an addendum prohibiting pipetting by mouth, instead mandating that a Gilson pipette, a rubber pipette ball, or a serological Pipet-Aid be used.
However, it was clear that some time in the previous century, prior to the invention of the aforementioned tools, many labs did in fact use mouth pipetting to transfer liquids, some of which were highly hazardous. An example can be seen here (from this IO9 article, which dates the photo to the year 1943):

When did pipetting by mouth stop being recommended in labs?

I have done that! And that was 1990s

I stopped mouth pipetting in the '60s.

Although the use of pipettes in the early chemistry laboratories undoubtedly led to accidental aspiration of undesirable toxic and poisonous substances, the first recorded laboratory infection due to mouth pipetting occurred in 1893, the case of a physician who accidentally sucked a culture of typhoid bacilli into his mouth...
It Was Dangerous, Hence was removed... Even though, it is removed, we often see the use of this in some countries..

Late to the party, but apparently "Mouth pipetting" is a thing for single-cell sequencing: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554467/
In the micromanipulation, single cells are usually aspirated into a glass capillary (typically 30 μm in diameter9) by applying a gentle negative pressure which can be provided by a manual/automated micropipettor (called micro-pipetting) or even a researcher’s mouth (called mouth-pipetting). It relies much on personal skills because the key process of single-cell aspiration should be carefully completed under microscopic field.

Mouth pipetting, while almost unheard of in modern laboratories in developed countries, is still very much a current protocol in many parts of the world.
For example, this paper analyses the proportion of clinical labs in Pakistan and found evidence of poor biosafety practices (emphasis mine):

Results: A total of 1,647 (92.4%) males and 135 (7.6%) females
  participated in the study, with over half (59.7%) having more than
  five years of work experience. Results showed that 28.4% of the
  laboratory technicians from Punjab, 35.7% from Sindh, 32% from
  Balochistan and 38.4% from Khyber Pakhtoon Khawa (KPK) did not use any
  personal protective equipment. Almost 46% of the respondents (34.2%
  from Punjab, 61.9% from Sindh, 25.2% from Balochistan and 85% from
  KPK) said they reused syringes either occasionally or regularly.
  Furthermore, 30.7% of the respondents said they discard used syringes
  directly into municipal dustbins. The majority (66.7%) claimed there
  are no separate bins for sharps, so they throw these in municipal
  dustbins. Mouth pipetting was reported by 28.3% technicians.

Additionally, a Google Scholar search for papers published in the past 5 years involving mouth pipetting turned up 670 hits out of 284000 total hits, a proportion of 0.23%. This is further evidence that this dangerous technique has not been fully eradicated from labs.


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Lack of A/B-antigen equivalent to Rhesus disease
Rhesus disease occurs when an Rh- mother is exposed to Rh antigens (often due to blood contact with an Rh+ child during delivery) and mounts an immune response which eventually results in the production of IgG Rh antibodies. In subsequent pregnancies, these antibodies cross the placenta. When the foetus is Rh+, these antibodies can bind to the corresponding antigens on the foetal erythrocytes and cause haemolysis, which can result in anaemia or even, in serious cases, stillbirth.
Given all of this, why does the same principle not apply to A and B antibodies? In other words, what is special about Rhesus antigens or antibodies that does not apply to other erythrocytic antigens or their corresponding antibodies?
I'm specifically wondering about Rhesus disease and its effects on the foetus, and why similar effects do not occur on the foetus in the case of an ABO type mismatch between mother and foetus.

It does happen. That's why you need to know a patient's blood type before giving a transfusion - AB is the universal acceptor, and O is the universal donor.

This question is specifically about the effect on the foetus in pregnancy, not normal blood agglutination. Sorry for the confusion; I'll edit the question to clarify.

So it turns out it can occur. It's called Hemolytic Disease of the Newborn (ABO), and according to the article (the relevant citations are a book and some journals to which I do not have access), it is very rare, and severe cases are even more rare. Apparently anti-A and anti-B antibodies are typically of the IgM isotype, which cannot cross the placental barrier. However, occasionally IgG is produced, which can cross.
This is what causes the hemolysis in the fetus - if the mother is type O, and the baby is either A or B, the mother is exposed to unknown antigen and produces antibodies. If they happen to class-switch to IgG, they can cross the placenta and, if in large enough quantities, cause the opsonization and lysis of red blood cells.

It occurs much less commonly for a reason. Many/most people who produce natural antibodies against the A and B antigens they do not possess. (Type Os against both A/B, As against B, etc). These antibodies are typically IgM produced by a specialized class of B cell (B-1 B cells) independent of a T-cell response. The coating of fetal RBCs with these IgM antibodies in the maternal blood stream facilitates their removal while dampening the generation of a T cell response against these antigens. B-1 B cells may also be resistant to IgG class switching.

One more point is that the ABO antibodies are cold antibodies. They react when the temperature is less than the body temperature generally.

@OneFace do you have citations for that? I honestly don't believe a word of it. Why would the human body make antibodies that bind optimally below 37°C? It's not doing Western blots...

http://www.webmd.com/a-to-z-guides/cold-agglutinins MattDMo, it is good practice to check if something is wrong before accusing!


text:
Gene and Protein isoform
What is the relationship between term "Gene isoform" and "Protein isoform"?
Say a gene can make 3 isoforms, will it produce only (maximum) 3 isoform protein?

where are you seeing these terms - context will help answers

The term isoform has become a little ambiguous over the years (see http://blogs.cornell.edu/collinslab/2012/05/30/protein-isoform/)... still some things are consistent:

In some genetics literature 'isoform' has been used in the place of allele when talking about the allele states at a locus for a gene
Typically a gene isoform is equivalent an alternate transcript. The gene isoforms are the set of mRNAs that can be produced by a gene.
Protein isoform commonly refers to the set of proteins produced by a gene, this can include variations produced by alternative splicing and post-translational modification. Note that in some contexts the set of products from closely related gene duplications can also be included.

Note that databases will typically have a specific definition in mind for their use of isoform in their annotation, check their documentation for details (e.g. in UniProt see What is the canonical sequence? Are all isoforms described in one entry?)


text:
What is the strand specificity of a reference genome?
It's a simple question but I've come across many people who have this question, is the reference genome Positive of Negative strand? Indeed, I've had heated arguments over the same issue.
So here's to putting all those questions to rest.
Is the reference genome a positive or a negative strand? And why so.

Koustav. Thanks for your effort; it is quite commendable. IMO Q/A such as this which are intended to serve as a reference can be made a community wiki. It makes posts easily editable without much rep requirement; flipside is that you don't get reputation points. It is just a suggestion and it is up to you whether you want to do that or not.

Done! I didn't notice that option before!

@WYSIWYG — why is this question a community wiki? It is imprecise and based on a false assumption, as my answer makes clear.

@David The post sounded like a popular question for which an authoritative answer can be provided and therefore I proposed CW. BTW, the assumption is not entirely incorrect.

First of all, the reference genome strand specificity is referred to as sense (positive strand) or antisense (negative strand). Now let's consider to sequencing data or FASTQ files. When we align reads, a resulting SAM or BAM file has a column specifying strand information, we usually see a + or - strand.
For more background on the strand names here's a somewhat incorrect note from the wiki article under sense (molecular biology)

The strand names actually depend on which direction you are writing
  the sequence that contains the information for proteins (the "sense"
  information), not on which strand is on the top or bottom (that is
  arbitrary). The only real biological information that is important for
  labeling strands is the location of the 5' phosphate group and the 3'
  hydroxyl group because these ends determine the direction of
  transcription and translation. A sequence 5' CGCTAT 3' is equivalent
  to a sequence written 3' TATCGC 5' as long as the 5' and 3' ends are
  noted. If the ends are not labeled, convention is to assume that the
  sequence is written in the 5' to 3' direction. Watson strand refers to
  5' to 3' top strand (5' → 3'), whereas Crick strand refers to 5' to 3'
  bottom strand (3' ← 5').[4] Both Watson and Crick strands can be
  either sense or antisense strands depending on the gene whose
  sequences are displayed in the genome sequence database. For example,
  YEL021W, an alias of URA3 gene used in NCBI database, defines that
  this gene is located on the 21st open reading frame (ORF) from the
  centromere of the left arm (L) of Yeast (Y) chromosome number V (E),
  and that the expression coding strand is Watson strand (W). YKL074C
  defines the 74th ORF to the left of the centromere of chromosome XI
  and denotes coding strand from the Crick strand (C). Another confusing
  term referring to "Plus" and "Minus" strand is also widely used.
  Whatever the strand is a sense (positive) or antisense (negative), the
  default query sequence in NCBI BLAST alignment is "Plus" strand.

Although it is correct when it says

Watson = Sense = Plus Strands
Crick = Antisense = Negative Strands

A satisfactory answer/convention is provided/suggested in this PMC article covering the terminology of the Watson and Crick strands
Below are some interesting excerpts from the publication:

The earliest reference that we could find to the "Watson strand" and
  the "Crick strand" is somewhat tongue-in-cheek and comes from a pair
  of papers in 1967 by Wacław Szybalski and colleagues. They
  bound the two DNA strands of phage λ to the synthetic polynucleotide,
  poly(IG), which has an affinity to cytosine-rich regions. They then
  separated the two strands by density, which turned out to be
  determined by the amount of bound poly(IG). In a cesium-chloride
  density gradient, the strand with more bound poly(IG) was denser and
  heavier than its complement. Because the "dense" strand was
  cytosine-rich, Szybalski and colleagues called it the "C strand."
  Logically, thus, the complementary strand, which was guanine rich,
  should have been the "G strand." Instead, it was christened the "W
  strand."

So the authors note that the Strands started on their terminology journey with their roles reversed with the Crick strand specifying the heavy strand (with IG) and the Watson strand specifying the lighter one.
They also note that the present day terminology of the WC model is non-arbitratrily based on the current horizontal drawing convention where one strand is placed on top and the other at the bottom.
They also suggested a typical convention which is followed today. If it was due to their suggestion is a different matter altogether, but beyond the scope of this question.

Given the amount of effort already spent on standardizing such
  databases, and their influence on other disciplines, we feel that the
  genomic definition of Watson and Crick strands has the most mass
  behind it. Specifically, we find that the unambiguous usage of the
  Saccharomyces Genome Database to be the most useful. Under the first
  part of our proposal, the centromere is a reference point that divides
  a chromosome into two arms of unequal length. The chromosome is
  oriented so that shorter arm is on the left and the longer arm on the
  right. Furthermore, the top strand has its 5'-end at the left
  (short-arm) telomere and its 3'-end at the right (long-arm) telomere.
  This strand is the Watson strand. Similarly, the bottom strand has its
  5'-end at the right telomere and its 3' at the left telomere and is
  the Crick strand. We further propose that "top", "forward", and "plus"
  be used as synonyms for the Watson strand and "bottom", "reverse", and
  "minus" for the Crick strand.

and later on...

If it is ultimately impossible to distinguish Watson and Crick strands
  using biological properties, then we propose that Watson should refer
  to the stand arbitrarily used as a reference in a database (i.e. the
  "plus" stand) and the Crick strand should refer to its complement

But let's come back to sequencing data or FASTQ files. When we align reads, a resulting SAM or BAM file has a column specifying strand information, we usually see a + or - strand.
Which suggests that the product originated from either the Watson (positive) or the Crick (negative) strands. For example, a read is actually the reverse complement of the product, but since you do a PCR step during you library preparation, that particular bit of information is lost and therefore the downstream analysis protocols tend to consider the entire loci any single product aligns to.
The difference between strand specific sequencing and non-strand specific sequencing are covered here.

The present state of this answer seems to confound terminology appropriate for gene-relative purposes with that appropriate for chromosome-relative purposes. Gene-relative uses Sense/Antisense (or Coding/Template), while chromosome-relative uses Forward/Reverse (or Plus/Minus).  A Forward strand will have both Sense and Antisense sequences on it.  See Bio_X2Y's answer here for an accurate and concise description.

I'm sorry I'd go further than @mgkrebbs and say both question and this answer are nonsense. I am not familar with Community wikis, but this should definitely not be some standard reference. I have written an answer explaining why.

The + and - is a bioinformatics classification. The reference sequence is by default the + and all the genes in the opposite orientation are annotated as -.
For linear eykaryotic chromosomes, the reference genome sequence is in the orientation of the chromosome (based on older cytogenetic assignment; usually the short arm is 5').
For prokaryotes, I guess the origin of replication is the beginning of the reference genome (Eisen et al, 2000).

I would replace "bioinformatics classification" by "data file designation". GenBank files and the like are human-readable, so they have strictly nothing to do with informatics, and I don't think there is any classification involved.

Answer
There is no such thing as a positive or negative strand for a genome (reference or otherwise), for the simple reason that the genomes of almost all organisms contain genes in both orientations, and hence each strand contains genes the sequence of which are in the sense and the anti-sense direction with respect to the mRNA.
The exception is single-stranded RNA viruses, where a single strand may act as the mRNA. This is where the ‘+’ and ‘–’ nomenclature is mainly used — to distinguish which strand is used in the virus genome.
I have previously addressed this topic in my answers to related questions about sequence direction in databases and reading frames.
Further Clarification: Where do reference genomes begin and on which strand?
To find the answer to this question you should look at the documentation in the database for the particular genome of interest. However, as far as I am aware, the following is generally true. (Others may be able to improve on this.)

In bacterial and plasmid genomes the sequence usually starts from the (single) origin of replication, proceeding in the direction in which replication occurs, written to the right of the origin. The strand represented in the database is the one starting with a 5′ end on the left at this origin.
In eukaryotic genomes that have been well studied there is a recognizable cytochemical assymetry of the chromosomes (in terms of banding of heterochromatin and, in some cases, ‘arms’) and there is a convention to designate one end ‘left’ and one ‘right’.  In the reference genomes the sequence starts from the conventially viewed left of the chromosome, presenting the DNA sequence of the strand that has the 5′ end. I provide an example of how Genbank indicates the ‘reverse’ directionality of genes using the term ‘complement’, below.
In single-stranded RNA viruses — where the ‘+’ and ‘–’ nomenclature is used — the sequence is of the ‘+’, starting at the 5′ end.

     gene            complement(11566..11952)
                     /locus_tag="YAL065C"
     CDS             complement(11566..11952)
                     /locus_tag="YAL065C"
                     /note="Yal065cp"
                     /codon_start=1
                     /inference="non-experimental evidence, no additional
                     details recorded"
                     /product="Putative protein of unknown function; has
                     homology to FLO1; possible pseudogene"
                     /protein_id="NP_009335.1"
                     /db_xref="SGD:S000001817"
                     /db_xref="GI:6319252"
                     /db_xref="GeneID:851232"
                     /translation="MNSATSETTTNTGAAETTTSTGAAETKTVVTSSISRFNHAETQT
                     ASATDVIGHSSSVVSVSETGNTKSLITSGLSTMSQQPRSTPASSIIGSSTASLEISTY
                     VGIANGLLTNNGISVFISTVLLAIVW"
     gene            12047..12427
                     /locus_tag="YAL064W-B"
                     /db_xref="GeneID:851233"
     CDS             12047..12427
                     /locus_tag="YAL064W-B"
                     /note="Yal064w-bp"
                     /codon_start=1
                     /inference="non-experimental evidence, no additional
                     details recorded"
                     /product="Fungal-specific protein of unknown function"
                     /protein_id="NP_009336.1"
                     /db_xref="SGD:S000002141"
                     /db_xref="GI:6319253"
                     /db_xref="GeneID:851233"
                     /translation="MAGEAVSEHTPDSQEVTVTSVVCCLDSVVEIGHHVVYSVVTPLI
                     VAVLIDTMAGEAVLEHTSDSQEEIVTTVVCSVVPLVCFVVSVVCFVISVVEIGHHVVY
                     SVVAPLTVTVAVETIAEEMDSVHT"
[Example of part of Genbank file (NC_001133) showing how directionality of two genes with opposite orientations is indicated using term ‘complement’.]
Postscript: Bioinformatics programs
As @WYSIWYG indicates in his answer, certain bioinformatics programs that produce tables of genes indicate their direction using ‘+’ or ‘–’ to indicate ‘left-to-right’ or ‘right-to-left’ respectively.

There is however a natural direction depending on the direction of replication.

@JackAidley — Direction of replication? This may hold for bacteria, but not for eukaryotes. But, although it wasn't strictly the question and the poster is long gone I'veadded something about where the "reference genomes" start from.

@WYSIWYG — I see your point that  + and – are used in the data files but the poster's question "Is the reference genome a positive?" clearly indicates that this is not what he meant, otherwise the answer is the trivial '+'. And the terms + strand and – strand were used in molecular virology before nucleic acid sequencing was invented, so although I have written programs to read GenBank files and am familiar with this designation, I never heard them refered to as + strand. The other answer also assumes that the poster is talking about "sense" strands, although he goes off on a tangent rather.

"...never heard them refered to as + strand..." I allegedly just have seen "minus" used by a data sheet (shown here on Stackexchange; I might be able to refer to) As  the minust strand is the template used in engeneering, data banks refer to minus-, not the "coding strand"/plus-strand?


text:
Is household ammonia okay for plants?
My father-in-law claims that since plants need nitrogen to produce proteins, and since ammonia is NH3, that Ammonia should be fine for the plants, since it's just nitrogen and water and hydrogen, according to him. We were cleaning a rusty chain and a bunch of spilled into our garden. I'm talking about household ammonia.
Is that true?
I'm thoroughly convinced he is an utter idiot but then again he could be right since he does say he minored in Chemistry in his college days.

Before this gets kicked over to biology.SE, I would like to point out that the OP's initial assessment of his father-in-law is correct (I would also like to hear about the logic behind cleaning a rusty chain with ammonia, but that's another story, I suspect). Ammonia is part of the food cycle for plants, but not directly: It has to be converted into nitrate and ammonium for uptake and use. See, for example, this Wikipedia entry on the nitrogen cycle.

Plants need nitrogen in a form which they can take up. This is either ammonium ions or nitrate.

Okay, he's not wrong, technically speaking. Practically speaking never ever fertilize your plants with ammonia.
The ammonia you spilled will be converted into nitrates eventually, so it's not like you spilled lead into your garden. On the other hand the populations of nitrifying bacteria take a fairly long time to adapt to a bounty like "a bunch" of household ammonia (their idea of a banquet beyond their wildest dreams is 2-4 ppm ammonia) but they will eventually eat it all.
(Fishkeepers should know about the nitrogen cycle, because you have to set up a complete yet tiny version of the real thing, which takes at least a week to establish)
So your plants will be fine... next year. This year they might have a little bit of trouble considering ammonia is a base and can burn plants directly or indirectly. Don't fertilize your plants with ammonia. They will probably die.