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Tool use by animals: research history
I was under impression that data about quite a lot different species using different tools is a fairly modern phenomenon, i.e., all of the research is fairly recent.
Around 50 years ago it was widely believed, by scientists too, that it was only apes that are able to use tools. I was recently told that it's basically nonsense and scientists have been studying different tool-using animals since the beginning of the 20th century or earlier.
Where could I get more info on research done in this area? I'd be especially thankful for those done in USSR, since it used to be my country and my knowledge on everything was basically limited by the Iron Curtain. However, I am also interested in research done worldwide as well.

Best tip I can give you is buying a textbook or popular science book about ethology. That should give you an overview about research done in the past decades. Konrad Lorenz was a pioneer of ethology, so a book should summarize his work, e.g. this one
For more current stuff look up some journals in this field:

Animal Behaviour
Journal of Comparative Psychology

Animals having a small brain compared to mammals but nevertheless showing very intelligent and reflective behaviour like this rook are currently interesting research objects. This kind of research is not really tricky or expensive as you see, it just has to be done by a student :) But behaviorism as the leading paradigm in the middle of the 20th century has probably made a lot of more fruitful research approaches impossible.


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How are memories stored in the brain?
I've been thinking about this for a while and I can't figure out how a memory can be stored in the brain.
I understand that important memories are favourably retained, such as a near death experience, the birth of your child or your wedding day. But I cannot comprehend how this can be stored biologically in the brain.

Firstly, I'd like to emphasize that the understanding of memories and learning as we know it is still in its very early stages. In fact, the mechanisms behind short-term memory are still under intense debate.
As for long-term memory, it is essentially caused by chemical changes in synapses between neurons in the brain. When you sense stimuli from your environment, action potentials follow a specific trail of afferent neurons towards the central nervous system, which then sends a message back through efferent neurons to initiate a response. The high frequency of these action potentials from the same stimuli of whichever sense allows for the strengthening of specific connections between neurons, which is called long-term potentiation. This phenomenon is one of the major components of synaptic plasticity, which also applies to the weakening of synaptic connections between neurons due to lack of transmission, as well as the change in the number of connections the neurons are receiving and making. Synaptic plasticity is also influenced by the change in quantities of neurotransmitters being expulsed into the synaptic cleft, and how cells react to these neurotransmitters, which is highly regulated by calcium levels. Ultimately, synaptic plasticity in accordance with learning is referred to as Hebbian theory.
We are still not exactly sure where memories are stored within the brain, but we do know that the hippocampus does play a big part. It definitely aids in the storing and structuring of memories in the form of these millions of synaptic changes. Finally, memory consolidation occurring in others regions of the brain over longer periods of time is likely, but still debated by some.

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Is there sufficient evidence that human cells are not intelligent?
Being structurally composed of one or more cells, which are the basic units of life.
Yet within a cell, there seems to be the same behaviors that define life:

Regulation of the internal environment to maintain a constant state;
Organization: Don't most cells have organs?
Metabolism.
Growth ~ not sure about this one.
Adaption ~ Think this is accurate, but I'm not well versed in cellular biology at all.
Response to stimuli. Cells interact with external whatnots.
Reproduction - Cells do this, at least many of them.

Most of what lead me to this question came from chapter 5 of Spontaneous Healing by Andrew Weil, M.D.. I'll type the parts relevant to the discussion below - in case he's wrong and I'm basing my thoughts on wrong information. bold sections indicate my interjection

DNA takes the same form in all organisms, from human beings to viruses - an enormous molecule with a double-helix structure made up of two chains of sugar molecules, with "rungs" linking the two chains. The rungs form between complementary pairs of nitrogen-containing subunits 'nucelotides', whose specific sequences differentiate the DNA of one organism from that of another. Only four different nucelotides occur in DNA; they are the "letters" of a genetic code spelling out "words" of information that direct the construction and operation of all forms of life. The so-called Central Dogma of modern molecular biology states that DNA replicates itself in order to pass its genetic information on from one cell to another and from one generation to the next reproduction; DNA also transcribes its information into another macromelecule, RNA, that can travel out of the cell  nucleus; RNA, in turn, transslates this information into the manufacture of specific proteins that determine the structure and function of organisms. regulation? These three processes - the replication, transcription, and translation of genetic information - are the most basic processes of life. They are also amazingly intricate and risky, because there are so many points at which things can go wrong.

Snipped for relevance.

Therefore, sophisticated mechanisms have evolved for the repair of this molecule in order to assure nearly error-free transmission of genetic information from one generation to the next, even in the simplest forms of life. organization, regulation, reproduction - evidence of response to stimuli?
All of the mechanics of replication, transcription, and translation are directed by a special class of proteins called enzymes. A great deal of the genetic code specifies the manufacture of enzyme molecules, which, in turn, oversee the chemical reactions that develop the genetic code into biological reality. evidence of intelligence?

much snipping.

In practical terms, they (enzymes) function as ingenious machines that alter the substrate molecules: cutting them apart, putting them back together, snipping particular pieces off them, adding others back, all with astonishing precision and speed.

more snippage

Therefore, polymerase I actually proofreads its own work, editing mistakes as it directs the synthesis of new copies of DNA.

He goes on to talk about plasma membranes, which seem to be how cells interact with the "outside" world..

Is there a question somewhere in here?

Is there "sufficient" evidence that human beings are intelligent?

Hi!  You need to edit your question to make it more obvious as to what you actually want answered, then please flag it for reopening :)

something you would need to clarify is your definition of intelligence

You seem to be asking if single mammalian cells are capable of intelligence. Yet, in your introduction, you mention that within a cell there are these seven characteristics that are fundamental in defining life. Then, you target more of your supporting quotations and interjections toward the definition of life. Of course cells are alive. You are alive, and so are the bacteria on your skin. Your title question is:

Is there sufficient evidence that human cells are not intelligent?

You have strayed from your question in your line of reasoning. Let's get back to answering the title question.
Is there sufficient evidence that human cells are not intelligent? The definition of "intelligence" is controversial, but let's look at Wikipedia:

Intelligence has been defined in many different ways including, but not limited to, abstract thought, understanding, self-awareness, communication, reasoning, learning, having emotional knowledge, retaining, planning, and problem solving.

Human (or any mammalian, fungal or bacterial) cells are able to communicate, and solve problems, but most likely lack abstract thought, understanding, self-awareness, reasoning,  and emotion. Retaining and planning are somewhat more difficult.  Cells are able to retain information about a state of "being" and transmit that to progeny, a recent phenomenon known as epigenetics. Does this qualify as retaining and planning? I don't know. Cells also change based on environmental pressures through stochastic processes (a process known as evolution). Does this qualify as learning? Probably not, since the changes are usually pre-existing. The human equivalent would be finding out that you can swim by falling into water and not drowning. Did the person "learn" how to swim, or did they already possess an aptitude for it?

but most likely lack abstract thought, understanding, self-awareness, reasoning, and emotion...
I'll give you abstract thought, but what are the grounds against self-awareness vs. proofreading?

Proofreading is an entirely mechanical/chemical process. When a nucleotide is inserted into a double stranded DNA molecule, it pairs with the complementary nucleotide by hydrogen bonding. Complementary nucleotides also possess a space-filling quality such that an incorrect pair produces a "bump" or "dip" in the helix. All proofreading does is look for this type of physical inconsistency. Hardly self-awareness.

Why is the nucleotide inserted? How does it look? Why does it look?

@user1432 I couldn't parse that. It's inserted to replicate DNA. Proofreading looks for this physical inconsistency in a variety of complicated mechanisms. And the "why" is simply to reduce the error rate in DNA.

Intelligence in evolution and in the field of AI is often defined as the ability to apply previous or existing abilities to successfully solve entirely novel problems that were not present or trained for in the first place. Intelligence is always adaptive. For instance, I've never ever in my life performed the addition of 10 plus 10.1234 but I'm intelligent insofar as I understand the operation well enough to be able to apply it to new numbers. I know the answer is 20.1234. A proofreading enzyme is very inflexible in its catalysis and does only one thing, regardless of context.

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Are there any intersections between the biochemical pathways of uracil biosynthesis (or metabolism) and methionine degradation in eukaryotes?
Is there any way in which uracil biosynthesis or metabolism could help cell in degradation of toxic levels of methionine?

Uracil degradation doesnt produce aspartate, but beta alanin

No, I don't think there are any intersections, and I can't see how uracil metabolism would have any influence upon methionine degradation.
Methionine degradation is shown in Figure 1 below. The end product is succinyl CoA which is fed into the TCA cycle. The only obvious by-product is cysteine which doesn't have any connection with uracil biosynthesis.
Uracil biosynthesis (as UMP) is shown in Figure 2: it is built from CO2 and NH3. Uracil degradation produces CO2 NH3 and aspartate.
There are certainly no shared intermediates in these pathways, and I can't come up with any convincing indirect connections either.
Figure 1. Methionine degradation

Figure 2. Uracil biosynthesis

Theoretically, produced CO2 would buffer (minor) acidity from sulfate but that's both minor.


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Can the sleep/wake cycle be influenced by non-visible spectrum electro-magnetic radiation?
I've been reading a few papers on Melanopsin and Suprachiasmatic Nucleus (SCN), and see that the sleep/wake transition is influenced and entrained by visible light, particularly in the blue spectrum that is registered by special cones in the eye and is transmitted to the SCN.
I've seen a fleeting hypothesis/mention in two of these articles, that electromagnetic radiation may also play a part in the sleep/wake transition and melatonin release, on top of the blue light. It was some time after I read those articles that it dawned on me to ask this question, and I'm unable to find the exact lines where the mention was made.
Has there been any modern studies on the connection between electro-magnetic radiation (non-visible spectrum) and the human's circadian rhythm entrainment?
Can humans be affected or feel the influence of electro magnetic radiation at all?
If there is a connection, what is the name of a process/organ/gland by which humans can be affected with electromagnetic radiation?
Thank you for your clarification!

Maybe this question can be better answered (or is already) at skeptics


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Can we make any judgements about sleep or readiness to sleep from a heart rate metric and/or pulse oxymetry?
I'm looking at inexpensive and un-intrusive ways to quantify the state of human body/mind . One of these is Actigraphy, which is a study of human motion over time. This can be done with an iPhone mounted on a wrist. There are algorithms that correlate actigraphy measurements to sleep and allow to calculate sleep onset latency, sleep efficiency, etc. I'm looking for additional metrics that may be added to actigraphy.
Recently, there has been a new iPhone app called "heart rate" which uses a camera to shine light through a finger, capture a series of images of the finger and count the heart rate based on the blood flowing in and out of a finger, changing the color of camera images. This is similar to pulse-oximetry derived heart rate, and maybe the technology would evolve sufficiently to give information about the blood oxygen content as well.
As a sleep researcher, I'm wandering if there are any known algorithms or studies that relate heart rate (as beats per minute) and/or pulse oximetry to sleep or human's ability to fall asleep?
It appears to me that with a device like an iPhone measuring pulse at the same time of the day, it should be possible to create a history of heart rate, while accounting for the diurnal variation of heart rate. I'm wandering if there's anything biologically or medically relevant that can be glimpsed from such history of heart rate metric.

This is not an answer, but you may find it interesting. A friend of mine was doing his thesis on the development of a kind of hat that could detect when its wearer was about to fall asleep (the idea was to stop people from falling asleep at the wheel). This worked by detecting changes in the electrical output of the brain. It needed electrodes attached to the scalp but nothing more invasive than that. I have lost touch with the friend in question so I cannot give you more details, but it may be worth looking into.


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Do humans sneeze or cough in their sleep?
As far as I know, I've never seen anyone sneeze or cough while they're sleeping. Google wasn't very helpful either; a lot of contradicting claims.
So the questions remains: do humans sneeze or cough in their sleep? (a few other things I've never seen with sleeping people are yawning and vomiting) If they don't, why?

Babies may sneeze, cough and vomit while asleep, but it is not common even when they are ill. No reference, this is just my personal experience. I would think it's a matter of control over body muscles, babies have limited control (my kids would very often burp or sneeze and pass gas at the same time), but as they grow they learn to keep certain muscles in a certain state while asleep.

I've heard people sneezing and coughing in bed a lot. I can't be certain they were really asleep that moment though. They might have been woken up for just a minute by the discomfort that then caused the cough or sneeze.

Sneezing does not occur during REM sleep, due to REM atonia.(1)
The coughing reflex is  also suppressed during sleep, but coughing may still occur occasionally during sleep. (2).

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Why is membrane potential not zero at equilibrium?
For the squid giant axon, the membrane potential computed by the Goldman equation is -60mV. And the Nernst potentials are (the differences between the K+ and the Na+'s Nernst potential and the membrane potential let the mechanism work):
  K+ = -74mV
  Na+ = 55mV
  Cl- = -60mV

I am wondering if the membrane potential is 0mV, whether the K+ and Na+ Nernst potentials still cause the mechanism to work, so can 0mV be a reasonable value? (That is, I think the value of potential is not important at all as long as the mechanism works well, is this true?)

You have to consider that there are plenty of voltage-sensitive channels that will open at 0mV so, no, you will not be likely to have an equilibrium at 0mV with the "classic" amount and type of channels on the membrane.

Not only are you battling the electronic potential, you're also battling chemical potentials. I'll let a cellular physiologist handle the answer.

Rephrased a little, why do neurons need to have nonzero resting potential, given that most of the driving force is in chemical gradients? See this answer: http://biology.stackexchange.com/questions/8811/why-do-neurons-have-a-negative-resting-potential

The value of the membrane potential does not affect the location of the resting potential.  The membrane potential affects only the fraction of channels that are open, thus allowing net current to change, which allows for the depolarization and repolarization of the membrane (the action potential).  During the action potential, the resting potential does not change.
The value of the resting potential is governed only by the distribution of ions (how many are on one side of the membrane vs. how many are on the other).  This is relatively constant even as ions cross the membrane for the action potential; it is really not a very large fraction of ions moving at all compared to the reservoir they are in, so the reversal potentials are preserved over time.


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circulating microRNAs are functional?
In plasma and other body fluids, miRNAs can be found. They not only originate from dying cells but also from active secretion and are usually 'packed' into vesicles/lipo-proteic structures (i.e. exosomes) protecting them from the action of ribonucleases. Thus, miRNAs in plasma are very stable, offering diagnostic opportunities.
My question is whether they may also have a functional role. Exosome transfer between cells has been demonstrated, so it is likely that miRNAs can be secreted by one source cell and reach a target cell, similarly to how hormones works. However, this has not been quantitatively assessed. Is the concentration of miRNAs in plasma known? Is it sufficient to hypothesize functional regulation of gene expression in target cells?

See papers by D Bianchi for reports of miR levels in blood of pregnant humans, both of maternal and fetal origin.
A review by Steer and Subramanian offers a number of examples pertaining to your question.
Lastly, Vickers, Palmisano, et al. (2011) show that some miRs are present in the HDL-cholesterol particle and that those levels differ between normal and familial hypercholesterolemia human subjects.


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Can a person die instantaneously from internal damage to the brain?
Given the human heart is autonomous, can a person die instantly from internal damage to the head/brain? I would expect the heart to continue to pulse until it ran out of energy ...
My contention is whether brain-injury can cause death, albeit Memming raised a deeper question - What is the biological definition of death?

What do you mean by instantaneously? What do you mean by die? If one looses consciousness irreversibly in 10 ms, would you consider to be instantaneous?

Indeed, I would.

I did not downvote, but this question is not clear.  It sounds like there are two questions, a rather difficult philosophical question about the meaning of death in unspecified cases where it is difficult to tell if someone is dead and another question as to whether one can die quickly (again not sure how quickly) from brain injury, which seems a little to simple.  I mean why wouldn't someone die instantly of a brain injury?  What's the trick are you talking about nanoseconds?

Please consider this only as a starting point (although a lengthy one), and a race against an acute onset of  tl:dr ...
A person cannot die instantaneously from internal brain damage (under everyday circumstances). The reason is the non-centralized architecture of the brain and that consciousness is a global phenomenon which underlie the activity of many brain structures.
These brain structures are themselves comprised of a cellular hierarchy, with each cell being self-sufficient for at least a time regime in the order of minutes. As such the brain underlies to some extend the study of networks and robustness thereof. The brain also maintains a scale-free organization . Actual Scale free networks in nature are known to be robust.
Instantaneous in this context means a consciously discernible difference in time, which is on the order of tens of milliseconds (See: Inspection time, mental chronometry).
Also I narrow the medical cause of death down to a intracerebral haemorrhage, systemic shock or hypoxia. I definitely leave out all (rare) CNS-immunological phenomena (e.g. explosive brain death, Immune reconstitution inflammatory syndrome related,... )
But, effects that can mimmick instantaneous brain death are very plausible.
Notably, this question can be answered despite there being no rigorous consensus model of consciousness.

Consider the following just as pointers, but not as qualified, thoroughly sourced information, - contrary to a paper or review ( I will gladly include your resources, or turn this post into a community wiki if demand to do so exists):
**** Consciousness**:
The brain weighs only 2% of the human body mass, yet consumes 20% of the total energy at rest. Crucially the brain can deplete oxygen at a great rate, which is proportional to the brain activity in various regions, giving rise to indirect measurements of brain topology and images like these:

"Visualization of a DTI measurement of a human brain"-2006,
author: Thomas Schultz, DOR: 25/09/2012

Humans have different states of consciousness which show different overall patterns of brain activity. As such the result a scientist would witness through an high-resolution fMRI/PET scanner in a stroking-individual would differ during sleep, sleep/wake transition or various levels of awareness during the days. Stroking and the effects on the brain is studied quite extensively with rats(See: rat, fMRI, stroke).
Moreover the brain activity, fine-anatomy and orchestration of brain utilization differs from individual to individual. In short the brain is what neurologists call "plastic" Neuroplasticity is the change of entire brain structures, and the brain itself from experience and physical stress/trauma (on the brain).
We are biologial enetities which have evolved to be in-sync with the planetary rotation and solar energy influx. As such brain activity changes during the day, in accordance with our circadian rythm or biorhythm, and if it weren't for artificial lightning brain activity would change over the seasons as well.
Connecting all the dots: Describing brain death in a seconds-regime comes down to which areas in an individual brain consume the most oxygen and "shut down" first, and which processes steer brain activity till organic shutdown.
Since Stackexchange has a strong programmatic background, to put it in a somewhat programmatic analogy:
The output of a memory dump and its analytic result depend on the hardware, the software and the state of the application. Unfortunately the software is spread across processors, has multiple threads and applies a genetic algorithm with dynamic recompilation.
Death Definitions:
The notion of instant death is a cultural meme (which one can witness in child's play) and is further propagated in the media.  Additionally "death" is a highly political matter...
"Death" has numerous legal definitions (throughout various cultures) medical definitions and biological definitions depending on the context. Legal definitions depends on the culturally dependent legal corpus, medical definitions on the state of (pragmatic) technologies. The medical definition of human death is influenced by the legal definition. The legal definition in turn is influenced by politics.
The biological definition of death depends on the context and a threshold thereof, which in turn describes the level and and of hierarchical systems or one large system comprised out of systems such as organs. An organ is the collection of units in one structural one to serve a common purpose.
Finally to answer more accurately, a person cannot (under everyday circumstances) shutdown brain activity within the time-interval of one reaction time-unit or 'cycle', but may transition between discernible states of global brain-activity. Such states may only be measurable with functional Imaging techniques and classifiable using computer algorithms.

Interesting answer but please don't use random code formatting as it's not really suitable

I've replaced all instances with more appropriate highlighting, however I'm not sure they're all necessary so you might want to remove some of the emphasis.


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In which way would the yeast cell cope with the excess amount of methionine in the growth media?
I guess that when there is surplus of methionine in the cell it is incorporated in the TCA cycle as a succinyl CoA, with cysteine as a by-product. But now the cell has the surplus of cysteine. What does it do with it? How does it remove excess sulphur from the cell? Would that process somehow influence NAD+/NADH balance?

Is there any evidence that methionine is toxic to yeast?

I know there are some strains of yeast that are unable to form colonies on the medium that has high concentration of methionine in it. I have reformulated the question.

In humans, cysteine first fills the glutathione pool (which itself is a reservoir for cysteine, apart from reduction equivalents and biotransformation). Excess cysteine can go three ways,

oxidation to sulfoalanine and further hypotaurine and taurine, via still unknown enzyme(s)
degradation to lanthionine and toxic H2S
degradation to serine and toxic H2S

Since cystathionine gamma lyase which (its L-cysteine desulfhydrase activity) catalyses 2 and 3 has homologues in yeast, my guess is that H2S is produced there too. Further oxidation of H2S happens through an ancient mitochondrial pathway which is highly conserved as well, yielding sulfite and sulfate. Sulfate then makes for a bit acidic environment but else is non-toxic.
I have linked to reactome.org entries where you can find references. Filling up the yeast's glutathione pool (if it happens) would move the NAD+/NADH balance to the NADH side, i.e., fill up reduction equivalents, too.

Thanks for pointing me to reactome.org. Wasn't aware of it :)


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What elements are a possible basis for life?
I've been told that life on earth is carbon-based, Then I got curious about one thing: What are the possible bases for life and under which circumstances could lifr based on other elements exist?
If the existence of a silicon-based life is possible and if it is, under what temperature, pressure, etc?

The general consensus is that carbon is unique in its ability to form stable chains, to bond to a variety of other 'useful' atoms (e.g. N,O), and to form stable double bonds, all of which are central to life. There is some useful speculation at http://en.wikipedia.org/wiki/Silicon_based_life#Silicon_biochemistry

This is more of a chemistry than a biology question. You are basically asking what other element has similar bonding capabilities as carbon and could be used to form the chemical backbone of complex macromolecules. Maybe you should try your luck at Chemistry.SE

I've found also a book on astrobiology, but still don't know if it's gonna be useful.

OK, I'll bite...

One thing that hasn't be mentioned and should is that there is no consensus on how to define what life exactly is. Basically, all known life form is carbon-base, so say you would find some other "life-form" that is not carbon-based, how would you even tell if it is alive?

@Bitwise But isn't there a consensus on what is it?

@GustavoBandeira the consensus is that what is "similar" to what we define as alive is also alive (of course you have to agree what "similar" means). The problem is what happens when you consider something which is a bit different than what we know... This is a well-known problem. For example check Wikipedia or any other place.

For the time being, I think the best bet is to regard things as life if they look like life as we know it on Earth. It is dreadfully anthropocentric but at least its a starter until  we really understand what separated living from non-living.

This is an interesting question, particularly considered in the context that Cairns-Smith (1985) even suggested that clays (silicates in solution) may have had some sort of early selection acting on them due to their surface chemistries.
However, there are a number of major problems with Silicon. Some are chemical and some are astrophysical in nature. For example:

Silicon has a lower electronegativity than carbon and a longer bond length. Silicon can polymerize, but many conformations (such as rings) are highly reactive or unstable.
Silicon lacks chirality. Since biochemical reactions are very specific this may present a fundamental problem for alien biochemistries.
We don't see silicon macromolecules in nature. Large carbon molecules are seen in space such a polycyclic aromatic hydrocarbon rings. The largest silicon molecule seen in space is a chain of SiC_3 (and maybe SiC_4).
On reacting with oxygen (which it does readily) silicon likes to form solids like sand.
Silicon is much less common than Carbon in the Universe. The Solar abundance of silicon is 1/10 that of carbon, and supernova yields suggest that the silicon abundance may be as low as 1/100 that of carbon during nucleosynthesis in low/intermediate mass stars.

To form complex silicon molecules we would probably need to keep it in an oxygen-free environment and somehow maintain it in solution. One possibility would be to hold it at high pressure and temperature such as in the interiors of planets (think deep hot biosphere theory) but this presents another host of problems for conceivable biochmistries and is very speculative.
Apponi, A.J., McCarthy, M.C., Gottlieb, C.A., & Thaddeus, P. 1999, Journal of Chemical Physics, 111, 3911
Cairns-Smith, A. G. (1985) Seven Clues to the Origin of Life  Cambridge University Press, New York, ISBN 0-521-27522-9.
Woosley, S.E., & Weaver, T.A. 1995, Astrophysical Journal Supplement, 101, 181

It's an interesting question. However I suspect we'll be finding lots of weird carbon-based slime rather than anything silicon based. However,  it's a big Universe out there!

I was thinking about another environmental condition where it could happen, but I have no idea if such a thing would be possible.


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Why do I smell flowers after sneezing?
Often when I sneeze, I smell flowers for a few seconds afterwards.
I've done some searching on the internet, and apparently it's something that is at least not entirely uncommon, although the exact smell description seems to differ. It's sometimes also referred to as a 'honey sneeze'.
Just to be clear, there are no flowers anywhere in sight when I sneeze.
Biology has never been a field of study of mine, but the scientist in me finds it fascinating. I've yet to come across any real explanation for this phenomenon, only guesses.
Does anyone know what causes this, or can you at least give a somewhat likely explanation?
Edit:
When I sneeze through my mouth, I do not get the same smell sensation.

it might just be the sneeze might be pushing air around the nasal cavity, putting the flower pollen and other molecules into contact with more olfactory sensors.

I get the same sensation and the same floral scent. I am an ecologist and can only relate it to smelling like the yellow oil seed rape plant. It's very weird!

Every time I sneeze really hard, it smells like beeswax rather than flowers.  Not sure what the cause is, either.

I have experienced this weird floral smell too.  I can also confirm that other people generate this smell after sneezing.  Someone sneezed next to me and then I smelled it.  When my husbands allergies kick up and he sneezes all day the whole house smells like that weird floral smell when you walk in the door.

I knew an italian at school who liked to stick straws from grass up his nose to intentionally sneeze. He would say "it's great man, when you sneeze your body releases opiates for a moment so I get high for free"

This will be a hypothetical answer for the moment, so take it with a grain of salt until I can find sources or someone else does:
My best (educated) guess would be that the smell is there all the time, and when you sneeze you reset what's currently being "ignored" (in that you are not aware of it, though it is being sensed) by your brain momentarily. The source of the smell may be up in the air - it could be cologne/perfume, fabric softener residue on your clothes, what you ate for breakfast and are currently digesting, the bar of soap in the kitchen, etc. - but I haven't heard of "scent illusions" before.
One very quirky way of possibly testing that out is to remove yourself from your regular environment, sniff some ground coffee beans for half a minute, and then re-enter your home or smell your clothes to see if any of the scents match up with what you do smell when you sneeze.
My apologies that this isn't a thoroughly-sourced answer, but hopefully it acts as a good starting point.

My observations agree with this. We're unconsciously filtering out a lot of, even olfactory information.

I have my doubts.. the smell is quite pronounced, and always the same. Even when I haven't been near a flower for a week.

It doesn't have to be a flower, it could be anything that has a floral scent. Fabric softener, deodorant, cologne, soap, lotion, hair products (shampoo, conditioner, gel), aftershave... We filter out a lot of scents. If you don't believe it's something you're encountering in your daily life, then it might be a product of your own system - maybe a compound in your nasal mucous that encounters the receptors when you sneeze. Haven't heard of that happening, but it's not my best area.

Another starting point (apologies if this has more considerations than a 'thoroughly-sourced answer') ...
A sneeze is a violent, temporarily mechanically stressful event. See How much force is generated by a sneeze?
(Temporary) mechanical stress on the brain can have many effects.
One point you should consider for your Testing Hypothesis: If you sneeze through your mouth, do you still have this effect?
I would also suggest looking into the interplay of short mechanical stress, serotonin, and the olfactory system...

I rarely sneeze through my mouth, but I'll try to pay attention next time :)

I forgot to update earlier, but when I sneeze through my mouth, I do not seem to get the smell.

You may have some liquid in your nose after sneeze. This liquid can contain microbial flora, which can have a smell, which is interpreted by you as of flowers. Check your health with a doctor to be on the safe side.


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Can female Drosophila melanogaster lay eggs without males?
Can female Drosophila melanogaster lay egg without males?
I maintain our lab stock but find a line that seems to have all females (or all males). The flies have been in the vial for two weeks, but I don't see any eggs hatching or become larva.

wow - so just like chickens... i wonder how this is an evolutionary avantage for the females?

Yes, I regularly have to collect female virgins (12500 of them in the last week). They will lay eggs especially when there is extra yeast available. It is actually a good way to check virginity (in case a fly hatched early and was already mature, or a male made it through sorting etc.) - put some extra yeast grains in the vial when you collect them, leave them for a few days and then check for larvae, if they are not virgins there will be eggs and larvae, if they are virgins there will only be eggs!

Very old females (such as those in vials that have not been flipped for a long time) will often lay unfertilized eggs in the absence of males.
This happens to me occasionally when I am collecting virgins and then forget about them for a while.

I find even young females do this, but do you add extra yeast to the vial? perhaps this stimulates mine to produce more eggs (see Ashburner, Sullivan and Hawley) more rapidly.

Usually this happens to me when I'm collecting virgins, so there's often no yeast; this probably explains our discrepancy.

cool, there is definitely research suggesting yeast increases egg production. and as useful way to check virginity whilst getting them really fired up ready to mate!


text:
Why did mammals evolve to have two testes?
What makes mammals tend to evolve to have two testes?

My guess would be symmetry and redundancy. :-)

I guess the same could be asked of ovaries

And, you could probably ask the same about: ears, eyes, nipples, etc.

Two eyes and ears is to do with stereo receptivity, having two sensors of the same type in different places helps to gather much more information about distance and position (triangulation) of the source. One cool example of this is the hammerhead shark. It's believed that it has smell sensory organs in either end of its head. The further apart they are the better the sharks are at finding prey. It is also why predators have the eyes on the front of their head - so they work in tandem.
http://news.bbc.co.uk/earth/hi/earth_news/newsid_8376000/8376740.stm

Mammals inherited them, testes are paired way back in fish.

EvoDevo is not my field, but I will try to give you some pointers.
Mammals as vertebrates, start out as fertilized oocytes, transform into a rapidly dividing lump of cells with eventual polarity through numerous gradients of numerous chemical messengers, and form a neural tube.
The forming body is ever more segmented through the use of gradients and thresholds (see french flag model) and (dorsoventral) axial symmetry is maintained throughout development, and as such two testes represent the default development.
Therefore, it may be more interesting to ask for singular organs which require more information, and thus maintenance throughout evolution of this information. But when considering the energy requirements, the need for synchronization, the need for a separate blood supply and thus the introduction of additional faults, it is easy to see why we only have one heart.

Wikipedia; author: Zephyris, title: "The first few weeks of embryogenesis in humans", DOR: 25/09/2012
See:

Inversion
Evolutionary developmental biology

I hope this helps as a starting point.

I might further speculate that the female reproductive system has strong axial symmetry and the testes are probably following the conservative development pattern of the female reproductive system.


text:
How can chromatin state be measured?
I have some RNA-Seq data and I'd like to align it to the physical genome and see which sections of chromatin are geometrically open and being transcribed.  The data are already sequence-aligned, and every Google search I do for tools that might help ends up sending me down a rabbit hole.  What computational tools have helped you?

Starting out with RNA data is great, since you already have fully spliced entities, despite  being in a different dynamic regime.
As the chromatin landscape itself is dynamic and High throughput data exploration has only begun in the last decade, consider the following tools and results with care...
You may find the following tools helpful:

Archalign , Publication (didn't work well during my day of trials)
Ensembl chromatin-state map data (See the database layout, Regulatory Build, and the lincRNA
genes in the web-interface of the Ensembl databases)
HaploReg, Publication (the most recent)


text:
What is the difference between an antibiotic and an antibacterial?
Concerning medicine, what are the differences between antibiotics and antibacterials?

An antibacterial is any compound that will kill or at least slow down the growth of strictly bacteria, a domain of prokaryotes.
An antibiotic is often used synonymously, but denotes a compound that kills or slows down the growth of any cellular pathogen, prokaryotic or eukaryotic. So, certain antibiotics can kill bacteria, fungi and parasites but antibiotics have no effect on viruses and prions.

Just to add to your answer: bacteriostatic agents slow down the growth of bacteria, whereas bactericidal agents kill it.

Waksman defined antibiotics as being produced by other living organisms. http://www.acs.org/content/acs/en/education/whatischemistry/landmarks/selmanwaksman.html

Can resistance form from anti bacteria from people using soaps etc to clean bathrooms or kitchens. I only ever hear resistance being due to poor use of anti biotics not anti bacteria?

The word antibiotic refers to metabolic products (chemical compounds)
 of one microorganism that has detrimental or inhibitory effect to another microorganism. These are kind of chemotherapeutic agents used for treatment of infectious disease or disease caused by proliferation of malignant cells.Although some are prepared synthetically but most of them are prepared by microbial synthesis for commercial purpose. The treatment of one antibiotic differs from another by its mode of action. Antibiotics also can have broad spectrum and narrow spectrum of action and it is also possible that out one antibiotic is more active than other antibiotic against a particular pathogen and the effect is more impressive. Antibiotics can be antibacterial ( only and only against bacteria, either inhibition, destruction or suppression of bacteria. E.g. Bacitracin), same way some antibiotics are antifungal like Nystatin and some may show antitumor activity anthramycin. Antibiotics sometimes also have non-medical use like growth stimulants in poultry and live-stock feeds.
Whereas Antibacterial agents are those agents which "specifically" show their action against bacteria. (broader spectrum of action than antibiotic) They can act bacteriocidal (agents which kill or destroy bacteria) or bacteriostatic (agents which hinder the normal growth and reproduction of bacteria without killing them). Antibacterial agents can be  metabolic compounds of microbes (antibiotics), they can be physical agents like radiations, heat (at particular temp that can kill only bacteria) or antibacterial agents can also be chemical by nature like alcohols,halogens (Iodine, chlorine, chlorine compounds).
So we can say that antibiotics can be antibacterial agents but all antibacterial agents need not be antibiotic.

Could you add references?

http://amrls.cvm.msu.edu/pharmacology/pharmacology and chapter 24, Antibiotic and other Chemotherapeutic agents from the Microbiology book  by author Michael J. Pelczar, JR.

Antibiotics are a broader range of antimicrobial compounds which can act on fungi, bacteria, and other compounds. Although antibacterials come under antibiotics, antibacterials can kill only bacteria.
Penicillin was the first discovered by Alexander Fleming antibiotic and antibacterial.
There are certian classes of compounds which are bacteriostatic, which will not allow bacteria to grow (Ampcillin kills dividing cells) in number.

Could you clarify the middle sentence ("Penicillin was..."), it's ambiguous and I wasn't sure what to make of it.

Penicillin was discovered by a Scottish scientist and Nobel laureate Alexander Fleming in 1928. Later Selman Abraham Waksman discovered another antibiotic named Streptomycin.

Yes, thank you, I meant it's confusing whether it was the first discovered by him or the first discovered.  I don't believe it was the latter.


text:
Do Viruses produce a biomagnetic field?
From wikipedia:
Biomagnetism is the phenomenon of magnetic fields produced by living organisms.
The present scientific definition took form in the 1970s, when an increasing number of researchers began to measure the magnetic fields produced by the human body. The first valid measurement was actually made in 1963,[1] but the field began to expand only after a low-noise technique was developed in 1970.[2] Today the community of biomagnetic researchers does not have a formal organization, but international conferences are held every two years, with about 600 attendees. Most conference activity centers around the MEG (magnetoencephalogram), the measurement of the magnetic field of the brain.
Do viruses produce such a field?

viruses are not bio, but they can be magnetic. Just ask any virologist... ;)

possible duplicate of Do viruses have a magnetic field?

Hi user1432.  You've got the right idea in trying to improve your questions to get answers, however please use the edit link to do so rather than creating a new question.

Noted. Thanks. I'll try to delete the closed one when I have more time.

Viruses are bio.  Something does not need to be alive to be biological.  For chemistry all that is required is that it contains carbon.  Would you consider a random strand of DNA not biological?

Interesting related article suggesting perhaps biologists are over-estimating biomagnetism.

Please excuse the phrasing, which is not scientifically rigorous. The post only serves as a starting point.
Any electric current (the net movement of electrons) induces an magnetic field, and any magnetic field in turn induces an electric field. Indeed, each other is just one side of the same coin. The first to join these two into what is known as electromagnetism was JC Maxwell in his four fundamental equations.
Biomagnetism results from the flow of electricity within special functional tissues, located in organisms. (Some organisms have pure electrical junctions rather than 'interconnects' which rely on chemical messengers as vertebrae do. See this classical paper, and Evolution of nervous systems )
Certain heavy atoms have asymptotic magnetic field effects (a thankful property for many  NMR structural biologists).
As such, even if a metalloprotein with such heavy metal-atoms were to move inside the virus, driven for instance by a chemical oscillator (which would eventually come to a standstill), the effect would really have to be theoretically predicted first, and then empirically measured, rather than coincidentally just discovered (like say Penicillin). That is because it is very expensive to do science at such small scales, and the required hardware and human resources are in competition with projects that promise greater outlooks.
Further Questions:
My answer would be another question:
What sense would it make for a terrestrial virus to potentially benefit from producing an electric current inside, to motivate theoretical scientists to look into such a matter?
Or, what virus features would account for the sufficient flow of electricity to be considered a mechanism ( - as the magnetism at these scales is just the 'side effect') ?
Considerations:
( During the life-cycle of a typical virus, the virus does produce a magnetic effect, as the information-carrier molecule is charged, and the production of a new virus requires the net transport of charged molecules. Note, that by convention viruses are not living entities. )
Afaik, the field of biomagnetism only really took off due to the invention and commercialization of the SQUID.
This is just a starting point, motivated by the challenged notion of viruses. Virologists have a much better and up-to date grasp on the matter.
Killing a virus:
On a less serious side-note, one way to kill any virus is to put it on a Magnetar.
I hope this helps as a starting point...

What sense would it make for a terrestrial virus to potentially benefit from producing an electric current inside, to motivate theoretical scientists to look into such a matter?

First - let's leave off the motivations of theoretical scientists to theoretical scientists.
My core notion is to find evidence that running your biomagnetic fields at certain frequencies and amplitudes through emotional regulation naturally functions as shield.
In furtherance of "Darwinism", if viri tune themselves to the biomag attractor for suitable hosts - we can up the sales of mind-heart meditations.

Every atom produces a magnetic field, so the formally correct answer would be "yes" (assuming that viruses belong to the tree of life, which is disputed -- otherwise, one would not use the prefix 'bio').
However, biomagnetism as a science (and not pseudoscience) is concerned with more measurable effects. The biomagnetism of a virus will be negligible compared to all the surrounding cells, and hardly measurable.

Given that viruses are using the same building blocks as the rest of the known organisms (RNA/DNA), claiming that they do not belong to the tree of life sounds odd.  Of course they do (as in, they share a common ancestor). Is this really a notable position?

I think you're probably right, but is there any study to support "The biomagnetism of a virus will be negligible compared to all the surrounding cells, and hardly measurable."?

Many living things have significant magnetic fields.  they are mostly the result of bacteria who assemble a tiny cluster of magentite within their cell bodies.  These tiny iron magnets are sensitive enough to respond to earth's magnetic field, which seems to be the best known function of the magnetic particle.
Symbiotic magentobacteria are one of the mechanisms of migratory bird's uncanny ability to find their way along their magnetic route.
I don't believe a virus has ever been a magnetic particle discovered in a virus, though you never say never in biology, esp with microlife.
There are other means by which electrical and magnetic fields may be sensed by living things, but the individual magnetic fields of typical atoms in biological samples are too weak to sense without a big-ass magnet.  I don't know of any verified theory that gives any validity to this being important except maybe metal atoms inside proteins whos electromagnetic fields help guide ions and electrons along specific paths in the cell.  These are very local phenomena - spanning only 100 nm or so.

My markedly unverified theory is that we should be able to alter our own magnetic fields to improve resistance to viruses, similar to the manner in which the earth's EM field shields us from solar excretions.

From what I can see, this is hard theory to support.  Its hard to verify a theory when the magnetic fields cannot be measured.  the magnitudes of field you seem to be pointing at wouldn't stop something as large as a viral particle.  The fields are weak partly because non metals can't make magnets in the sense that we typically see them.  Look up ferromagnetism for more details on this.

Apart from that, what kind of magnetic field would you need to influence a virus? Not influencing your own cells at the same time?

it would be hard to influence a virus with a magnetic field - if this were obvious how to do this it would certainly be tried.  you might want to study MRI and how it differentiates between different kinds of tissues.  this might be a good direction, but it is still a bit of a long road to making something work.

@shigeta RNA and DNA can be partially aligned in a magnetic field in an NMR spectrometer due to their elongated shape. You could likely do the same with viruses, as long as they aren't globular. But that still wouldn't do more than slightly change their preferred orientation in solution.

@MadScientist Good point.  It seems like MRI/NMR might be able to pick up DNA, though the signal is really weak compared to that of water. Like you say, it seems unlikely you could use this as a handle to differentiate viruses from other cells in a mixture like a living thing.

@shigeta Viruses consist mainly of nucleic acids and proteins, just like cells. Without isotope labelling or very high levels of overexpression you have no chance of distinguishing specific components of such a mixture.

To be fair MRI can differentiate between some bizzare things. for instance tumor cells vs non tumor cells and metabolic processes, without using isotopic labeling.   Though I think we both agree; the density has to be within the resolving capabilities of NMR and its doubtful that most viral loads are enough to be seen much less manipulated.


text:
Can DNA act as a translation substrate?
I get conflicting answers.  One would think if it was true, it would be rather seminal and widely known.
There are papers from Khorana[1], Holland[2], and Bretscher[3] (late 60s) that suggest that it is quite easy in the presence of antibiotics like neomycin.
But more recent papers like this one[4] still openly ask the question, and that the only thing we know is that the initial ribosome binding step is similar between RNA and DNA.
I can't reconcile these papers.

Morgan AR, Wells RD, Khorana HG. 1967. Studies on polynucleotides. LXXIV. Direct translation in vitro of single-stranded DNA-like polymers with repeating nucleotide sequences in the presence of neomycin B. Journal of Molecular Biology, 26(3):477-497, doi:1016.10/0022-2836(67)90316-6.
McCarthy BJ, Holland JJ. 1965. Denatured DNA as a direct template for in vitro protein synthesis. Proceedings of the National Academy of Sciences USA, 54(3):880-886.
Bretscher MS. 1969. Ribosome Initiation and the Mode of Action of Neomycin in the Direct Translation of Single-Stranded fd DNA. Cold Spring Harbor Symposia on Quantitative Biology, 34:653-651, doi:10.1101/SQB.1969.034.01.075.
Damiana L, Marty-Detravesa C, Winterhalterc M, Fourniera D, Paquereaua L. 2009. Single-strand DNA translation initiation step analyzed by Isothermal Titration Calorimetry. Biochemical and Biophysical Research Communications, 385(3): 296-301, doi:10.1016/j.bbrc.2009.05.044.

But the first sentence of the abstract of the 2009 paper says that it is (still) an open question and refers to discrepancies: Is single-strand DNA translatable? Since the 60s, the question still remains whether or not DNA could be directly translated into protein. Some discrepancies in the results were reported about functional translation of single-strand DNA but all results converged on a similar behavior of RNA and ssDNA in the initiation step. This paper looked only at initiation and binding, no protein product was detected AFAICT. I think this is what they are referring to in terms of ef

As far as I can tell from the paper you linked to (Damiana et al) it is possible but inefficient:

Naturally, we tried to translate ssDNA, but as previously described
  elsewhere, direct DNA translation was not really efficient in absence
  of antibiotics such as neomycin [5] and [6]. It seemed that the
  elongation phase was the limiting step in the direct translation of
  single-stranded DNA. Whether direct participation of DNA in protein
  synthesis could play any role in vivo must be excluded, although such
  a role could be attractive for modelling the evolution of the earliest
  forms of life.

Yet Damiana et al. still say:
"Is single-strand DNA translatable?"
"With these experiments, our purpose was not to test whether or not ssDNA could be used as a translational template in cells but..."
By "not really efficient", they mean they could not detect their intended peptide product, which seems more like "no, it doesn't work".
"All previous work had tested if ssDNA allowed direct translation, but results obtained were not really convincing and the possibility that only some steps could be restrictive was not checked."


text:
Use of amino-acid sequences versus use of nucleotide sequences in phylogenetic analysis
Reading a  paper about gene evolution, I see that they do phylogenetic analysis for bacteria using protein sequences. They take the method from another paper.
I can suspect that amino-acid sequences are more stable than nucleotide sequences, to the presence of synonymous substitutions.... but, is this stability required between closely related species? doesn't it make the analysis less powerful? does it make it more reliable? In other words, what's the advantage of using amino-acid sequences versus using nucleotide sequences for phylogenetic analysis?

This is a good answer to a similar question. http://www.quora.com/What-are-the-advantages-disadvantages-of-using-Protein-Alignment-vs-DNA-Alignment/answer/Alex-Siegel

In general, many sequence alignment programs can use multiple substitution models, distinguishing between nucleotides, amino acids, and codons. A protein sequence has functional information that is not directly visible in the nucleotide sequence.
The papers you link deal with horizontal gene transfer, where a gene is passed to more distant  organism. Different species have different codon usage biases, i.e. the translation efficiency is different for different codons. On one hand, this means that HGT is more likely to occur between species of similar codon usage. On the other hand, "codon usage of horizontally transferred genes approaches the host usage over time." Thus, on the nucleotide level, the phylogenetic signal will get lost due to the evolutionary pressure on translation efficiency, while on the protein level, there will be more conservation.

Due to the fact that several codons can code a same amino-acid, the amino-acid sequence is usually more conserved than the nucleotide sequence.
For small scale studies, the higher variability of nucleotide data brings useful characters to establish relationships between closely related organisms that might not be differentiated at the amino-acid level.
With long evolutionary distance, the nucleotide signal tends to become erased by multiple substitutions at a same site. A more annoying feature is that genomes tend to have a preferred nucleotide composition. A site undergoing substitutions will have an increased probability to display of the preferred nucleotide, particularly if the substitution has no effect at the amino-acid level (synonymous substitution). This mainly affects third codon positions, because, as you can see in the genetic code, this is where most codon families vary. It may happen that distant species share a same composition preference. The sites free to vary will then tend to display the same nucleotide in both species as the number of substitution increases. This can induce phylogeny reconstruction errors, especially if the models of nucleotide evolution are not sophisticated enough.
The larger the evolutionary scale, the higher the chance that such misleading features will appear in the nucleotide data. This makes amino-acid more suited to large scale studies. But ultimately, one could hope that using better models will enable to use the signal present in the nucleotide data to its fullest without being too much mislead. Using amino-acid data amounts to discarding some of the information present.
It should be noted that some methods use codon evolution models instead of nucleotide or amino-acid models: all the signal is kept, but it is possible to incorporate the knowledge that some codons are more likely to transform into one another, due to synonymy.


text:
How can an albatross stay airborne for months?

Albatrosses, of the biological family Diomedeidae, are large seabirds allied to the procellariids, storm-petrels and diving-petrels in the order Procellariiformes. They range widely in the Southern Ocean and the North Pacific.

  Short tailed Albatross , Source: Wikipedia, DOR 16/09/2012

I read that albatrosses can stay airborne for up to a decade and that they can cycle brain activity between hemispheres. How do they do this feat, and how did they evolve this ability?
Possible points to consider:
immune system, predation, cycling solar output, weather, seasons...

Could you give a reference as to where you read this?  It's interesting!

@RoryM I heard about it in the great IMAX movie Legends of Flight (2010). Subsequently, I felt compelled to at least verify this online. Indeed, very interesting!

Albatrosses drink seawater; without this ability they could not be sea-bound for long periods of time. Regarding sleeping in the flight, I find this article convincing http://www.onlinemathlearning.com/animalfacts-albatross.html

I'm not really inside the field but few weeks ago I noticed a Plos One article that was dealing with this. Indeed albatross can fly for thousands of miles and this is possible at no mechanical cost, because they use a dynamic way of flight that takes the energy from wind (dynamic soaring) (ref-1). Their muscle-skeletal system further evolved so that no energy is required to keep open the wing.
In addition, when foraging, they minimize diving and landing activities because they follow Killer Whales, so that food is always in proximity. (ref-2) Very smart birds.
ref-1 Sachs et al., Plos One 2012
ref-2 Sakamato et al., Plos One 2009 both references are open access.

That article on dynamic soaring is fantastic.


text:
What are some of the immediate challenges to break through before finding a cure for mad cow disease?
What are the immediate challenges to break through in seeking a cure for mad cow disease?
I know that mad cow disease has no treatment as of yet.

The main problem is that Mad Cow disease is not caused by a "normal" pathogen but by a prion, a protein.
Traditionally, disease causing agents can be classified into viruses, bacteria, fungi, and parasites. Bacteria, fungi and parasites are all living organisms, alive in the traditional sense. It is, therefore, possible to design drugs that kill them.
Viruses are trickier, while not really alive in the traditional sense, they still have to make copies of their genetic material (DNA, or RNA in the case of many viruses) in order to cause infection. Therefore, drugs like ganciclovir that stop the formation of viral DNA can be an effective treatment.
Prion based diseases such as Mad Cow disease, Creutzfeldt–Jakob disease and Kuru, are not caused by a classical infectious agent but by a simple protein, a prion. Prions are misfolded versions of proteins already present in the host's body. When a prion interacts with the host protein, it causes this protein to adopt the same, misfolded, state as the prion. Protein function depends directly on the protein's structure, the way it is folded in three dimensional space. Therefore, the misfolded protein can no longer carry out its physiological role and disease symptoms occur.
Now, since the prion is just a protein, one single molecule, there is no essential life process that we can disrupt. We have to attack them using chemical agents that target the prion while not affecting the healthy, correctly folded, host protein. This is very hard to do.
The blood-brain barrier mentioned by Larry_Parnell is another problem. Briefly, the BBB, is a kind of fence that only allows certain of the various items circulating in the blood stream to enter the organism's brain. This is a wonderful defensive feature but it makes it much harder to design drugs that can enter the brain and target pathogens found there.


text:
Why are antibiotics prescribed with a viral infection like a cold?
I've heard both ways; people going to the doctor for a cold and then getting a prescription for antibiotics and those that go to the doctor and told they have ride it out because it's a viral infection.  Do antibiotics really help in true cases of a viral cold?

I have been told that in some cases patients will refuse to leave without some kind of prescription and rather unethically some doctors go along with it for a quiet life.

No, they don't. I'll return to this question if I have time with a full answer, but the largest reason people receive antibiotics if they have a viral infection is because they expect the doctor to give them antibiotics and will pester the physician about it. Sometimes the "prescriptions" are placebos to simply give the patients something, but physicians are well aware that antibiotics rarely do anything for viral infections.

And a recent german govt report states 50 per cent of AB prescriptions are inadequate.

@MCM Better cite sources for that since I know doctors who do prescribe antibiotics for the reason outlined in Bitwise’s answer. Can’t say I’m a fan of this wasteful use of antibiotics but there you go.

@KonradRudolph - So do I. I didn't say it was the only reason, nor practiced by all Doctors. But the reason I stated was the most common while I volunteered in my local E.D.

Isn't it the case that sometimes, the symptoms of a viral cold are hard to distinguish from a bacterial infection, so instead of playing playing guess the pathogen the doctor just hedges and treats for both?

Ultra-resistant bacteria are a real concern even to WHO. But anyway doctors keep on prescribing antibiotics as if it was tap water...

In general antibiotics don't help with viruses. However, sometimes a bacterial infection may follow a cold virus, so there might be some scenarios in which antibiotics would be needed. However in many cases it could be due to people demanding antibiotics from their doctor.
You can read more here (CDC site): http://www.cdc.gov/Features/getsmart/

You only forgot to comment on the third cause of deaths in the USA.

Antibiotics kill bacteria, not virus! So it's just plain wrong. If a bacterial infection appears after the cold, then the antibiotics should be prescribed because of the bacterial infection, not because of the cold. There is a serious concern about misuse of antibiotics promoting hyper-resistant bacteria through natural selection, but doctors keep ignoring alerts from WHO and prescribing antibiotics without even knowing the bacterial strain. It's absurd that a doctor should prescribe an antibiotic just because "the patient needs to get some medicine to be happy". In this case he/she should prescribe a placebo, not a real antibiotic (and there's still the point that killing most bacteria in our body destroy one of our defensive lines against pathogens). Confirming this point, according to American Medical Association, medical error is the third death cause in USA. So in many cases, yes, it might just be a medical error.

Now for those that think this is not an answer, explain me why?

"7000 deaths/year from medication errors in hospitals"

You're general sentiment is correct. However, it does not address the reality of how doctors end up prescribing the antibiotics in any case. The main reasons come down to: viral and bacterial infections may look similar in early stages and so it is prophylactic; patients can be "demanding" and get a prescription before leaving the office; and some doctors may use poor judgement. Prescribing a placebo is unethical when the potential for harm can be real (what if a patient is immunocompromised?). Lastly, the 7000 deaths/year is not specific to antibiotics and is an irrelevant statistic to cite.

WHO alerts about misuse of antibiotics are not irrelevant. If a doctor don't know if an infection is viral or bacterial, how can a medicine be prescripted? And medical error as a "third cause of death" is irrelevant, in your opinion, really?

"Well you said "medication errors in hospitals" which is ambiguous. To which classes of medications does that statistic refer? It's not at all clear it applies to antibiotics. And it applied to hospital prescriptions. It's fair to say most people get antibiotic prescriptions from family/general physicians and thus outside of a hospital setting. Lastly, antibiotics are generally not a fatal medication, so how would a death occur? Perhaps the patient was severely allergic and had a reaction, or, perhaps they received a totally different drug than the antibiotic they were meant to, then died.

Man, IF doctors make SO MANY mistakes, then of course ONE OF THE REASONS they prescribe antibiotics for cold is "MISTAKE". Or is it almost impossible for you?

You're missing the point, and clearly you have some agenda to make. I agreed that doctors can mis-prescribe, or even err on the side of caution to prescribe, antibiotics. It takes a long time to assess whether common infections are bacterial or viral because they have to wait for strains to grow or viruses to be immunoassayed. You seem to be taking a lot of "facts" completely out of context. For instance, 7000 deaths/year, where? The USA? So that is 0.002% of the population, or several of orders of magnitude smaller consider the number of hospital visits.

Have you READ the link I gave? "In any case, 225 000 deaths per year constitutes the third leading cause of death in the United States, after deaths from heart disease and cancer."

Please read the FAQ section on civility and keep comments on track.

Doctors are like the saints of today. Nobody can say they are there for the money, and not for the health. Even worse, we cannot even suggest they commit lots of mistakes. You can even point to solid statistics: not even this will allow you to tell many doctors are mercenaries. It would be laughable, if it wasn't tragic!


text:
Why do carrots spoil so fast?
The carrots we buy from a supermarkets spoil very fast, albeit giving many consumers a false sense of preservability due to their structural rigidity. The answer extends to many other vegetables many of us eat:

 Larsinio (2006)- wikimedia, public domain, DOR 27/09/2012
The question is, why do well aerated carrots spoil in the matter of days, at room temperature?
Things to consider: a tuberous rhizome with rough and segmented skin / oxygen levels / levels of aeration / relatively high sugar content / differences in immediate microbiome / lack of possible synergies which the earth provides...the majority of antibiotics is extracted from soil microorganisms {1},{2}....

Remember that tubers are designed for a relatively anaerobic environment. My guess is that what you are seeing is related to that. Oxidation perhaps? Aerobic bacteria gone wild?

I think carrot keeps long time in refrigerator. Why store it at room temp when optimal storing condition is refrigerator ?

@Andrei Initially I wanted to explain that in the post as well and include storage conditions. But I consider it best to just ask one question at a time. Regardless, did you have consistently success w. long-term fridge storage?

can you reference your declaration that carrots spoil fast please since I also think that it depends on a lot of factors like where it was grown, the kind of fertilizers used etc

Strange question...Carrots usually (>95% of the time) last for 1+ months for me in the fridge. I'd hardly say that's a quick rate of spoiling

First we will take a look at the lines of resistance of a carrot. There are three

The skin - The first line of resistance is the outer membrane or skin of the carrot and chemical compounds that are normally present
  there. Two antifungal polyacetylenes, falcarinol and falcarindiol, and
  an isocoumarin, 6-methoxymellein, are present in small amounts in a
  normal carrot and present the first barrier in undamaged carrots.
Post Harvest - If during harvest or post harvest handling this barrier is broken, the surface is punctured, scraped or sliced,
  microorganisms may begin to grow. The carrot at this point begins a
  wound healing process by accumulating suberin, a complex
  polysaccharide, at the wound site. Along with suberin, lignin is also
  accumulated. Suberisation is complete within 48 hours after wounding,
  and lignification is complete within 168 hours of wounding..
Phytoalexin barrier - The last and most important line of resistance is the phytoalexin barrier. Phytoalexins are chemicals
  produced by plants that impart disease resistance in response to
  mechanical injury, physiological stimuli or infection. Scopoletin, a
  coumarin,and para-hydroxy benzoic acid, a phenol, are apparently early
  arrivals on the scene but later disappear (reference).

There are three enemies of carrot storage: wilt, re-growth and rot.
Some reasons for carrots rotting faster:
Many fruits and vegetables start to produce ethylene gas when they start to ripen. Some foods are extremely sensitive to ethylene gas which makes them rot faster (reference). I am guessing that you keep different vegetables close together. Maybe if you stored carrots separately, it might make them last a bit longer.

Major post-harvest losses in carrots are due to Sclerotinia rot,
  Botrytis rot, Bacterial soft rot (Erwinia) and Sour rot (Geotrichum).
  Of these, Sclerotinia rot is the most prevalent.The Sclerotinia fungus
  infects the carrot roots in the field through the crown. During
  storage, the Sclerotinia fungus produces a white, cottony mycelium
  which covers the roots. Infected roots are usually soft and watery (reference).

There would definitely be more reasons but I am guessing that these are the major contributors to it rotting faster.


text:
Why do neurons have only one axon?
I have just learnt about neurons. I wonder why neurons have only one axon. Can they transmit nerve impulses faster and more rapidly when they have more axons? Does having more axons help in coordination?
Could anyone tell me why neurons have only one axon?

"Technically", not always true...
http://www.psyweb.com/Physiological/Neurons/NImages/Unipolar.gif

are you considering multiple axons that transmits a single (synchronized) action potential? Or multiple action potentials generated at separate axon hillock?

i saw from a website that mentioned that "each neuron has only one axon" but i didn't understand why.

http://www.csuchico.edu/~pmccaffrey/syllabi/CMSD%20320/362unit12.html paragraph 7

Perhaps it's to do with the timing and energy of the ion flow in the Neuron, because the cell hasn't got the flexibility to efficiently manage two axon timing and energy potential with as much precision and power as two cells with one axon. After all, with millions of neurons to coalesce into systems, flexibility is there, added flexibility would be redundant and efficiency of the individual building blocks is necessary.

Neurons generally have one axon, because of the way it sums potentials from its dendrites. Right at the axon hillock (the little area where the axon protrudes from the soma), all the potentials are summed together. Now, you have to consider that what is actually summed here is dependent on the shape of the neuron, potentials lose amplitude as they travel towards the axon hillock. If there were multiple axons protruding from different sites, they would send out different signals and compromise the computational integrity of the neuron.
Instead of having multiple axons, a neuron simply branches its axon with axon collaterals. This way, all post synaptic sites are receiving virtually the same message.

I think during the early evolution of nervous systems it was very important to have long axon cells. For example a worm has 3 giant axons which are almost the same length than the worm itself. So there was selection pressure on the length of the axon. The neuron requires a lot of energy to send signals to other neurons. Neurons use energy on nanowatt scale, average human cells use energy on picowatt scale... By long axons it requires less energy to send the message through a single axon than send it through multiple axons. That's the same why we use limited amount of undersea internet cables - currently about 200. If there is more data than a single cable can handle, only then lay we a parallel cable. So a possible answer is evolution of worm nervous systems combined with energy consumption optimization.
Another answer can be that neurons would be never capable to build multiple action potentials parallel. Maybe they cannot consume enough energy to hold charges separated by multiple axons. I don't intend to look for the details of that. It is technically possible to have neurons with multiple axons, so you can grow things like that, but it is not clear if their axons can work parallel or not, and if they don't work parallel does they interfere the communication of each other.
About single axon neural networks there are existing mathematical models. Until there is no mathematical model how a neural network with multiple axons would work, or there is no evidence of it is not possible to build such a thing, you cannot say for sure that it is because of the mathematics of neural networks.
So I have this 3 theories. I think you can find more about this topic by googling a lot, and making new experiments. For me it was enough. :-)


text:
Does mixing alcoholic drinks really make you more drunk?
There is plenty of anecdotal evidence ("beer after wine and you'll feel fine, wine after beer will make you feel queer") that mixing alcoholic drink types leads to a stronger effect, but I can't find any true studies.
In fact the only studies I found are looking at mixing energy drinks and alcohol (mixing with energy drinks increases motivation for more alcohol (in college students) [1]), and discussed mixing caffeinated beverages with alcoholic ones [2].
Are there any studies specifically looking at mixing alcoholic drinks? They would have to compare people drinking the same amount of alcohol, but some people mixing, others drinking the same thing. Maybe even a cross-over study design? Same people do both, one after the other? The only way to get an unclouded answer!
I am also interested in the follow-up why question: Why does mixing some drinks make you more drunk? Presumably it is something in wine (for example) that interacts badly with something in beer at the chemical level (the metabolites maybe)?

Marczinski CA, et al, (2012). Mixing an Energy Drink with an Alcoholic Beverage Increases Motivation for More Alcohol in College Students. Alcohol Clin Exp Res, epub. doi: 10.1111/j.1530-0277.2012.01868.x
Touyz LZ, (2011). Mixing drinks and concocting troubles. Curr Oncology, 18(6):262-3. PubMed; FullText.

There are some very general answers to your question.

Definitely, there is a lot of magical thinking. We as humans are very prone to anecdotical evidence and extrapolations from incomplete data, even more so when we are drunk.
As an interesting "proof" is the fact that the German counterpart of the saying "beer after wine and you'll feel fine, wine after beer will make you feel queer" is "Wein nach Bier, gönn' ich Dir, Bier nach Wein, lass es sein" -- which means the exactly opposite of the English saying (beer after wine is bad, wine after beer is fine).

Many kinds of alcohol contain unwelcome additional substances, for example fusel alcohols. Definitely, "mixing" broadens the range of these additions.

Mixing can lead to a misperception about the actual amount of alcohol that was taken in. Many people who would not drink a vodka and drive have no problem driving after a half a liter of beer (which contains same amount of alcohol two shots of vodka).

That is very interesting about the saying in different languages! Many thanks.

Mixing of alcohol and energy drinks can be detrimental to ones health as both alcohol and the caffeine in energy drinks are both stimulants which can cause adverse effects on the heart especially if one has a natural sensitivity to caffeine.  One also has to be careful as both caffeine and alcohol are diuretics which when combined can cause even greater risk of dehydration.  And some studies suggest that taurine, which while naturally occurring (and even quite necessary in the developmental stages of humans) may cause adverse affects on kidneys and combine that with two diuretics all tied together...it could cause serious potential for health risks.  At least in some individuals. [ 1 ] [ 2 ]
I conducted a non-scientific experiment one night when friends were discussing the merits of 'alcohol before liquor' and vice versa where I decided to mix a pint of beer and three shots of Bacardi 151 in stein and consumed it as I would a straight beer.  Personally I felt no ill effects but I also had a hell of a tolerance for alcohol.  I agree that mixing alcohols can 'confuse' someone regarding just how much alcohol they have consumed and should be watched carefully.  Although vigilance is often not one of the virtues displayed by people who consume such drinks.

Kristen Kirkpatrick M.S., R.D., L.D. - http://www.doctoroz.com/blog/kristin-kirkpatrick-ms-rd-ld/energy-drinks-demystified
Time Magazine Online - http://time.com/3677044/alcohol-energy-drinks/

Welcome to Biology and thanks fore your answer. We appreciate scientifically sound answers and the first paragraph needs sources to back it up in my opinion. The second part is anecdotal and is better of as a comment.

Thanks, but you have not actually provided an answer for the question asked: "Does mixing alcoholic drinks really make you more drunk?"

"both alcohol and the caffeine in energy drinks are both stimulants" - alcohol is a depressant, is it not?


text:
Are there any multi-cellular organisms out there that do not sleep?
Looking around I see animals - ants, bees, birds, lizards, roaches all the way up to humans appear during a part of the day and not other parts. I would guess there is a sleep/recovery cycle involved.
Is there any multi-cellular organism with a nervous system, on record, that works without sleep/rest?

Well, you may want to re-state your question. There are numerous multi-cellular organisms without a nervous system. So you could say that they never sleep: sponges, plants, mushrooms.
This paper on the evolution of sleep concludes:

A phylogenetic evaluation of sleep demonstrates that all
  mammals, birds, and reptiles engage in sleep, and evidence
  for sleep in amphibians, ﬁshes, and invertebrates is strong if
  not certain.

So it seems that once you have a nervous system, you also have some rest periods. However, it may not be clear if the rest periods are dictated by the lifestyle (e.g. nocturnal foraging) or by a requirement to "recharge" the nervous system.

That paper does not exist there. Do you have another link or just title/author

Google is your friend :) John A. Lesku, Niels C. Rattenborg, and Charles J. Amlaner. "The Evolution of Sleep: A Phylogenetic Approach" Sleep: A Comprehensive Handbook. Ed. Teofilo L. Lee-Chiong. Hoboken, NJ: J. Wiley and Sons, 2006. 49-61.

Thanks. I can't find an accessible copy though.


text:
How are babies born without a brain?
In the United States, anencephaly occurs in about 1 out of every 10,000 births. There are several forms of this condition, wherein the forebrain is absent. The forebrain is host to most of the higher functional areas in the mammalian brain. In the most extreme case of anencephaly, the so called holo-form, only the brain stem remains.
In MacLean's model of the brain, the term brain stem is used interchangeably with the term reptilian brain, to designate the most primitive parts of the central nervous system. Many are taught this model.

An anencephalic newborn (warning: graphic content)
  ("An anencephalic newborn", wikimedia, author: Almazi, license: public domain, DOR 27/09/2012)

From my layman's perspective I can't help but notice a reptilian likeness of the anencephalic newborn. Whilst it goes without saying that correlation doesn't equal causation, I would like to know what is known so far about the cause of this condition to yield this particular morphology (as seen in the picture)?
Perhaps someone (eventually) has even some evodevo insight to share as well?

http://www.youtube.com/watch?NR=1&feature=endscreen&v=WMlVNFpzKNI

the autonomous portions of the brain that control breathing and other physiological functions are lower in the brain.  If the newborn is viable it just have just enough lower and back brain function to survive at least in utero.  If a fetus expires in utero it does not go to full term as you probably know.

I think more should be discussion about induction factors, differentiation and transforming factors in the answers. Current answers do not answer this explicitly.

Know your databases! This is just the query fit for OMIM.
http://omim.org/entry/206500

Anencephaly is considered an extreme form of neural tube defect
  (182940), which has been associated with variation in several genes.
  The entity described here is believed to show autosomal recessive
  inheritance.

The genes are those associated with neural tube effects, i.e., VANGL1, T, CCL1, and FUZ. See also folate-sensitive neural tube defects.
http://omim.org/entry/182940
The folate evidence was so convincing that the US/Canada in the 1990s introduced folate supplementation in all bread, flour, and cereal products. Today, US/Canada have a lower incidence of NTD (neural tube defects) than Europe, where folate supplementation is completely left to one's choice (and if women actually care they take it too late).

good catch! I find the formation of the eyesockets striking. I am puzzled whether this is within the range of developmental plasticity as the result from different biomechanical forces due to craniosynostosis (premature skull fusion) OR if mutant genes (and/or pleiotrophies) are involved. OMIM unfortunately shows a practical lack of animal models. On a  sidenote, the related spina bifida is known to interfere with the "eye" (opthalmic) devleopment....

From what I've read and I know from my Biology classes, during the formation of the embryo a whole bunch of things may go wrong. In these cases, during the neurula stage, in which the brain is supposed to begin its development, something goes wrong while the neural tube is forming.
The causes? Some people argue that a lack of folic acid may lead to defective brain development. Studies seems to show that most factors don't affect the formation of the neural tube, which include age of the mother, occupation, and exposure to chemicals.


text:
What causes the characteristic 'gleam' in the eye of a living being?
The title is pretty much what I seek to know.
Unless the other person is play-acting, one can often make out the eye of a living person has a shine-of-life to it; a cadaver does not. Similarly the gleam appears brighter when a person is feverish, or excited otherwise ... or has some infection in the eye itself.
What causes this gleam? Is it merely nervous electricity at work that disappears when the system is shutdown/crashed?

I think this is good question. The mysterious part is that sexy, energetic people seem to have special "gleam", while those lacking enegy do not have. Is it hormonal-related ? I am pretty sure nobody did research on this.

@Andrei, can you back that up with evidence? I've never ever heard that before...

Not being an opthalmologist, if one happens along and gives a better/correct answer, listen to them.
Otherwise, let's take a moment to look at the eye:

What is not pictured here is the saline-like solution that keeps the conjuctiva moist. If we include the lubrication in all of the surfaces which interact with light, our list would look like this:

Lubrication
Conjuctiva
Cornea
Anterior aqueous humour
Iris
Posterior aqueous humour
Lens
Vitreous humour
Retina
Fovea

Out of that list, the Iris, Retina, and Fovea are designed to absorb light; not reflect it. The Vitreous humour merely serves as a medium for light to pass through and probably would not reflect light on its own. The same is true of both aqueous humours - they do not modify the light so much as serve the eye structurally.
That leaves us with the Lubrication, Conjuctiva, Cornea, and Lens - surfaces which also interact with light, but act to some extent to reflect or modify it as well. The Cornea is what's actually operated on when a person undergoes corrective surgery; a pattern is etched into the Cornea which redirects light similar to the person's previous prescription and giving them better vision.
Now, because you mention the difference between an excited person and presumably someone at their normal state, it's worth to note (when dealing specifically with the eye) a very common side-effect of psycho-active drugs and emotional states (particularly fear and interest/curiosity) is the change in pupil size when lighting conditions don't change:

The reflection is different depending on the size of the pupil, and I would venture to guess the pupil size difference between someone who's excited or manic (whose system is flooded with endorphins) and the person at normality is part of what you define as 'gleam.'
The other situation you draw a difference between is a dead person vs. a living person. Before rigor mortis sets in, the relaxed state of the ciliary body is to stress the suspensory ligaments - resulting in pupil dilation. In addition, and I think this is the most important distinction: dead people don't blink. The act of blinking spreads the lubrication on the surface of the conjuctiva, and can be mimicked with tear-drops for people with dry eyes. Because the lubrication acts as another surface to reflect light (similar to having a thin layer of water on a surface), the dead person's eyes will have less of a "gleam" than a living person's.
So, to sum up: The "gleam" in a person's eye is probably due to hydration and/or pupil dilation. Pupils will dilate at lower light levels, under the influence of certain drugs, or when showing interest. Hydration is constant, except when the lubrication is not produced in the quantities necessary or when the person is unable to blink ('dead' in your example).

Also worth noting that circulation stops at death, causing changes to the appearance of the eye over time.  See e.g. http://www.defrostingcoldcases.com/guest-post-post-mortem-ocular-changes-are-not-conclusive-post-mortem-interval-evidence/


text:
Is there life on other planets and if so how frequent?
Some shed tears of joy as the news about the successful landing of the Mars Rover Curiosity came in. Then the most comprehensive 3D map of our observable universe was published. 2012 is literally an astronomical year.
As an layman I would like to know about scientists current understanding about the frequency models that life forms on other planets?
See also:

Drake equation

Although we are getting very encouraging signs, there is no indisputable evidence that life has been found other than earthly life.  I think Europa is probably more exciting than Mars, where giant reservoirs of water have been found and the temperatures are imaginably hospitable.  Too bad its so far away!

Giant reservoirs of water have not been found on Europa, although it is hypothesized that there may be a subsurface water ocean due to the way that the surface ice has deformed. However, I do agree that Europa is an exciting target. Enceladus also, which has been seen to have cryovolcanos spurting out water-ice. I suspect Mars is too dry and cold. We'll see.

It’s interesting to note that at least among leading astronomers there seems to be no question about this at all: the existence of extraterrestrial life is simply assumed. The only question is about when we find it, not whether (see e.g. some New Scientist issue from earlier this year).

@Konrad Rudolph Astrophysicist Max Tegmark believes that we are alone. Alone as in any other life being beyond the horizon of the visable universe (he's big on multiverses). It is a valid standpoint since we never have observed extraterrestrial life and we don't understand how life originates. He certainly seems to be in the minority, though.

Wrong forum. Try for astronomy.stackexchange.com. We can't even attempt to answer the bio half yet.

OK, so we know a couple of things about life in the universe. Note, however, that this is not really an answer and is also not very biological in nature.
So, we don't know how life began on the Earth. However, do know that:

The probability of life evolving on a planet in the universe is non-zero (since we exist) and,
So far, we have not found evidence for life elsewhere in the universe.

So this leaves us with two main possibilities:

Life is rare in the universe.
Life is common in the universe but for some reason we do not detect it.

This latter possibility is basically a restatement of the Fermi Paradox which says

"The universe is very big and there should be lots of alien life out
  there. Where is everybody?"

In the case that life is common, we can speculate extensively on why we have not detected  it so far. For example:

We haven't been looking long enough (SETI has been running for only a few decades)
We haven't been looking hard enough (the budget of SETI etc. is not large)
We haven't been looking in the right way. We are currently looking mainly in the radio regime, maybe aliens broadcast in X (where X is part of the E/M spectrum or something else entirely, e.g. gravity waves, tachyons)
Life is common, but intelligent life is rare (this would be my guess)
Life is common and intelligent, and doesn't want to answer (why? ask a xenopsychologist)

OK, so these are just some examples of "solutions" to the Fermi Paradox. There are many more which are much more exotic. My personal favourite of these is that we live in a simulated universe and the coders have not included additional alien life in the simulation. It would explain some strange "coincidences" about fundamental physical constants, but what simulation, no matter how good, would ever come up with cauliflower cheese for example?
However, until we actually detect life on another planet we will still be in the dark. The next generation of telescopes will be able to do this for nearby exoplanets if life is present on them and has affected the biosphere in a detectable way.
Edit - You mention "frequency models", but all we can currently say is that the probability of life on other planets is not zero - due to our existence - as I mentioned at the start
Some references:

A joint analysis of the Drake equation and the Fermi paradox, 2012, arXiv, Prantzos, N.
The Fermi Paradox, Self-Replicating Probes, and the Interstellar Transportation Bandwidth, 2011, arXiv, Wiley, K.B.
Interstellar colonization - A new parameter for the Drake equation, 1980, Icarus, vol. 41, 193, Walters, C., Hoover, R. A., Kotra, R. K.

"the probability of life on other planets is not zero" We can't even say that. The anthropic principle, you know. We cannot count ourselves as an observation, because our existance is necessary for making any observation. Our existance is perfectly consistent with us being alone. We have zero data.

Poshpaws, good answer.
As I understand we can only "look" into the past, since cosmologically speaking light is really slow. Light also disperses and becomes incoherent with long distances.
"Simple" cellular life seems to be an evolutionary prerequisite, and they are not in the habit of sending out powerful radiotransmissions into space (i.e. weak-point of the SETI Proj.).
There is also no reason why life should have terraformed a planet to the point of being spectroscopically detectable in the albedo.
A lower bound on the number of habitable planets in a galaxy like ours, would be great.

An amusing thing happens. We know that earth is already disappearing as a cosmic radio source. If you substitute 100 years for L in the drake equation, you get expected number of civilizations = 1. That must be us.

According to this, 1.2% of stars have planets that can support life. According to Google, there are 300,000,000,000 stars in the Milky Way. That means 3,600,000 stars can support life. Each of these stars  is estimated to have 1-2 planets that can support life. For the sake of simplicity, I'll use 1.5 to represent this, since it is the average of 1 and 2. 1.5×3,600,000=5,400,000 planets capable of supporting life. Looking around the web, there are wildly different estimates of the odds of life evolving on one of these planets (from 1%-100%), but 100% seems like the most common. This means that, statistically, the odds of extraterrestrial life existing are extremely high.

One thing is whether a planet is in a habitable zone - something we can begin to estimate with exoplanet observations - another is to know the probability of life evolving on the planet. Until we start to see evidence for extraterrestrial life (e.g. biosignatures) this is still a complete guess.

Uhh the number of possibly life-supporting planets per star is << 1 because most stars forming planets end up with hot jupiters.

Can we extend this to ask (excluding our own solar system), how far away we would have to look before we might reasonably expect to find some form of extra-terrestrial life? In other words, combine the likely number of life-supporting planets with the spatial distribution of stars in the galaxy to derive a mean distance between possibly/likely life-bearing star systems.