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No. of genes in chromosomes. phenotype
Why do cells need all the genes of all the 22 pairs (excluding the 2 X- or Y-chromosomes) of autosomes in every somatic cell, when each and every cell which is specialised for its function does not manifest all the phenotypes that are encoded by the genes present? Aren't the genes other than those whose phenotypes (& hence some chromosomes) are expressed by that cell, redundant?

Somatic cells require genes on all chromosomes, regardless of their specific phenotype.

This may have to do with the fact that the cells require 'housekeeping genes', which are typically constitutive genes that are expressed in all cells of an organism under normal and patho-physiological conditions. Housekeeping and other essential genes are distributed uniformly across different chromosomes thereby making any chromosome indispensable.
"Housekeeping genes are genes that are required for the maintenance of basal cellular functions that are essential for the existence of a cell, regardless of its specific role in the tissue or organism. Thus, they are expected to be expressed in all cells of an organism under normal conditions, irrespective of tissue type, developmental stage, cell cycle state, or external signal."
http://www.cell.com/trends/genetics/pdf/S0168-9525(13)00089-9.pdf
Intriguingly, chromosome X lacks housekeeping genes. A recent study suggested a possible explanation for this, as follows: "In the end, we have found the answer to be quite simple. Whereas most chromosomes operate in pairs, meaning there are two copies of each gene in every cell, in contrast, we only have one active copy of the X chromosome. This means it is not sustainable for highly active genes to be on the X chromosome. Housekeeping genes tend also to be highly active – they just couldn't survive on the X.”
http://www.bath.ac.uk/news/2016/01/12/x-chromosome/
Gene expression is regulated through transcriptional and translational regulation of genes to generate tissue-specific mRNA. Moreover, through alternative splicing a gene can code for multiple types of proteins. Alternative pre-mRNA splicing is widely used by (higher) eukaryotes to generate different protein isoforms in specific cell or tissue types. This means that the same gene can have different gene products in different cell types.
"Alternative splicing is a mechanism for generating a versatile repertoire of functionally different proteins within individual cells. The significance of alternative splicing is clearly evident in highly specialized cells such as neurons. For example, all of the main neurotransmitter receptors contain subunits that are alternatively spliced, which influences their localization, as well as their ligand-binding, signal-transducing and electro-physiological properties."
http://www.nature.com/nrn/journal/v2/n1/full/nrn0101_043a.html
http://nar.oxfordjournals.org/content/30/17/3754.short
http://genomebiology.biomedcentral.com/articles/10.1186/gb-2004-5-10-r74
Protein-coding sequences account for only a very small fraction of the genome (approximately 1.5%), and the rest is associated with non-coding RNA molecules, regulatory DNA sequences, LINEs, SINEs, introns, and sequences for which as yet no function has been determined. Furthermore, gene expression is controlled by regulatory elements that can be located far away along the same chromosome or in some cases even on other chromosomes. Genes and these regulatory elements physically associate with each other resulting in complex genome-wide networks of chromosomal interactions.
https://en.wikipedia.org/wiki/Human_genome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653627/
The genome is very intricate and consists of elements that interact with each other to regulate gene expression and to carry out various functions. Loss of any of these elements may affect other elements and disrupt cellular homoeostasis, resulting in cellular dysfunction, death or cancer.
I hope this somewhat answers your question.

Perhaps you can add a note that the housekeeping and other essential genes are distributed uniformly across different chromosomes thereby making any chromosome indispensable.


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Is it possible to remove one strand of double stranded DNA in vivo?
Assume we do have a double stranded DNA sequence in human cells, say
...ATCGATATCGATATTGCAGAGCATAGCTATAA...
...TAGCTATAGCTATAAGCTCTCGTATCGATATT...

Now I want to cleave one strand, such that I do have
...ATC..........................TAA...
...TAGCTATAGCTATAAGCTCTCGTATCGATATT...

The distance is not so important to me, so it can be 20 bp I remove or 1000s. Hence, if I need some PAM or so and it is not nearby the target deletion site, I will simply move in 5' resp. 3' direction until I find it and cleave there, as long it is ensured that I have the target site single stranded then.
I would be very grateful I you could help me here!

I don't understand what your question is - why are you trying to remove a single strand in vivo? What is PAM in this context? Please [edit] your question to add additional explanations and details.

Both TALEN and ZFN gene editing technologies use a pair of single-strand endonucleases that ultimately lead to a double strand break. Cas9 in CRISPR-Cas technology, however, cuts both the DNA strands (there are some Cas enzymes in certain bacterial species that cut only a single strand [ref]).

Image courtesy: http://www.xenbase.org/other/static/CRISPr.jsp

So, if you use a single unit of the pair, you can cut one strand of the DNA. You can use another nuclease to impart a cut at another site in the same strand. This will still not lead to the removal of the DNA sequence between the two cut sites. There is no available technology that can do this in-vivo. Possibly (a wild guess), you can use a modified oligonucleotide (or even an IVT synthesized RNA) that can bind to this stretch of sequence and break its interaction with the other DNA strand. In any case, a stretch of ssDNA would not be stable and be repaired quickly by polymerase.

Many thanks for your reply. Another thing that would be sufficient for my project would be that on a specific site the DNA gets unwinded in vivo (perhaps by some CAS enzyme like dCas9, though others might be better suited here). Then one of the strands might be "hidden" by the machinery, but the other one should be accessible to toy around with it. Is such a thing possible?

@tobias Possibilities are infinite but we should go with the one that is simplest in principle and is easy to implement.

Sure :). What would you suggest for it?

@tobias I don't think such a protein has been engineered yet. That would be a research project in itself and you would have to do many experimental try-outs. So, I cannot suggest much regarding that- you would have to try it. What I said in the answer (the guess) would be the first thing that I would try because it is easy.

Many thanks for your reply. Regarding the second question, where I try to have a large strand of ssDNA, could I fuse dCAS9 to a helicase, such that the dCAS9 bind in sequence-specific manner to the dsDNA, opens the DNA and the helicase opens it for, say several tens of bps. Is that realistic?

@tobias Sounds good but as I said, it may be a research project in itself. Sometimes even the most perfect designs on paper may not work out in the lab (happened to me three times). There is always some risk with designing a new tool. It may or may not work. If you wish, then you can try. Moreover, even the design step would involve a lot of thinking (how to fuse the proteins, how will the domains interact etc).

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Ribosomal Turing Machines, DNA/RNA computation
I'm a computer science guy, recently crossing over to do some research in computational biology on RNA secondary structure prediction. While looking through the materials I got a crazy idea, what if you could design a synthetic ribosome that acts as a Turing Machine on strings of RNA? (you could do similar things with DNA enzymes)
The immediate applications could be stuff like correcting mutations in RNA to cure genetic diseases, which is a relatively simple computation:

Check if a string is bad.
If so, fix bad letter.

Another could be "shredding" DNA/RNA of viruses:

Check if a string is a virus.
If so, shred it.

I'm not sure the status of the literature on this is, or synthetic biology's ability to create something like that. Do you think it is a good idea to pursue this idea or not?
I realize this is a soft question. Perhaps a better one would be, is this possible?

There are some papers on simple computations using nucleic acids, if nobody answers I'll look them up later. As for your examples, nature already does some of them (see RNA interference). And for correcting genetic diseases, the hard part is actually correcting the sequence in all cells in your body, not the detection itself.

Where would the 'table' of the machine be? In other words how would the 'bad string' be recognised?

@AlanBoyd An immediate thought would be to keep a copy of the bad string, say a mutated RNA strand, in the machine. Combine it with an enzyme bound to it with 2 functions, check if the letter it's currently bound to matches the current input letter, and slide right. That could do the check step. For the replace step you could do the same backwards and then splice the correct protein in. For a general Turing Machine, you could keep a string of the current state in RNA, keep the rules in another string, and slide along it to find the rule and execute it.

I'm no expert at this but I don't think you need a Turing machine to achieve this, at least for DNA, since in conventional sense (not including carcinogenic factors such as UV) the most probable stage in which a DNA mutation can happen is during DNA replication so DNA polymerase (http://en.wikipedia.org/wiki/DNA_polymerase) engages in proofread to ensure accurate DNA replication, and then the DNA can get back into being heterochromatic (eventually). This will be more difficult for RNA as they are single stranded although they do fold onto themselves.

Also there many many strands of RNA that are produced through alternative splicing, VDJ recombination and RAG imprecise rearrangements for antibody production, which can give rise to infinite possible RNA productions. So how would you know what is "good" and what is "bad" in terms of RNA and its production. Half the time we don't even know what they do and what their roles are and the only reason we call something as a "bad" or "faulty" RNA is because it is having a negative effect not because we understand the precise role of the sequence, which means a theoretical table would be useless.

So in short, a turing style protein machinery is neither possible (due to almost infinite potential number of RNA produced) not feasible (since the number of proteins that would have to check each RNA sequence would in turn have to be almost infinite). And none of these takes into account SNPs i.e. individual variations, which ban produce proteins with different sequence but identical structure/function, since obviously any lethal variations would be selected against but thats a whole different argument.

In answer to first part, isn't this exactly what mismatch repair genes do? They scan for errors, I'm not fully confident with my understanding of Turing machines to give you a definitive answer, but I'm fairly sure this is the case.

@Bez could you change your comments into an answer? It's a decent answer worth saving before this question gets closed

@ChrisStronks done! :)

I'm no expert at this but I don't think you need a Turing machine to achieve this, at least for DNA, since in conventional sense (not including carcinogenic factors such as UV) the most probable stage in which a DNA mutation can happen is during DNA replication so DNA polymerase engages in proofread to ensure accurate DNA replication, and then the DNA can get back into being heterochromatic (eventually). This will be more difficult for RNA as they are single stranded although they do fold onto themselves.
Also there many many strands of RNA that are produced through alternative splicing, VDJ recombination and RAG imprecise rearrangements for antibody production, which can give rise to infinite possible RNA productions. So how would you know what is "good" and what is "bad" in terms of RNA and its production. Half the time we don't even know what they do and what their roles are and the only reason we call something as a "bad" or "faulty" RNA is because it is having a negative effect not because we understand the precise role of the sequence, which means a theoretical table would be useless.
So in short, a turing style protein machinery is neither possible (due to almost infinite potential number of RNA produced) nor feasible (since the number of proteins that would have to check each RNA sequence would in turn have to be almost infinite). And none of these takes into account SNPs i.e. individual variations, which can produce proteins with different sequence but identical structure/function, since obviously any lethal variations would be selected against but thats a whole different argument.

It should be possible to create Wang tiles using DNA or RNA. Different colored edges could be represented by different sequences selected to bind to each other selectively (DNA and RNA are very good at this!). Wang tiles can be used to implement a 1D cellular automaton, which can implement a Turing machine -- it will keep a record of its complete history as a big wobbly mat. Wang tiles are collections of square tiles in which each edge has a certain color, adjacent edges having matching colors. They can produce infinitely extendable patterns that can't be periodic (similar to Penrose tiles).

@PaulHarrison - Welcome to SE Biology. I really feel, like the original post over four years ago, you are on the wrong list. One reason there was only one answer to the original question is that few biologists know what a Turing machine is, and most of those who do feel it has no relevance with biology. I have even less idea what Wang tiles are. However if you feel that you have a useful point to make you can post your own question on SE and then answer it. I would suggest that you do that on SE Bioinformatics, though, as you are more likely to get a response there.

@PaulHarrison - I don't see how your post targets the question in any way. It's more of a comment to the other answer I think. As David says, I indeed know what a Turing machine is but the tiles are over the top of my head too. I'm converting the answer to a comment of the other answer for now. Feel free to modify it to make it a more specific answer to this site in a biological context. Don't forget to include sources to your material.

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Metabolism of different saccharides
Learning about carbohydrates, I wonder what the differences there are in terms of metabolism, and overall health between the different types of saccharides. In other words, does the body use polysaccharides, such as starches the same, or similar to how it would use a disaccharide like table sugar, sucrose?
It piqued my interest because people seem to put sugars and other types of carbohydrates into totally different categories, and one is seen as "healthy", the other "unhealthy".

Sucrose is made of glucose and fructose, both of which can enter glycolysis. Starch is made form glucose; if it can be digested, it can thus also enter glycolysis. Is that what you're getting at?

If you can digest (break down) the polysaccharides to useable monosaccharides, then they can be incorporated into glycolysis (or some other metabolic pathway!). The metabolic pathways around glycolysis are complex, but here is a representation of some of them:
As you can see in, in the top right corner, sucrose/starch, but also other sugars like nucleosides, can enter the overall simple sugar metabolic pathways. How and what exactly happens to the complex sugars will depend on how they are broken down (if they can be broken down at all) and they will have their own more or less complex metabolic pathways associated with that.

authors: Наталья Рюмина


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Why are hens so different from other birds?
Hens lay many eggs during their lifetime (at least, I don't know of one which can lay more eggs) and they can't fly. Compared to other domestic animals it seems to me they are the least capable of defending themselves or escape if it comes to be left alone in open wild. What is their evolutionary story?

Hens can fly, animals that are kept for farming purposes have their wings clipped

Domestic organisms are bred to serve specific purposes for humans. Sheep are bred to produce wool; Cows are bred to provide meat and milk for human consumption; dogs are bred for service and companionship. Since domestic animal do need to survive in the wild in order to reproduce (ignoring feral animals, which is an interesting topic by itself), most of the other aspects of that animal relevant to its survival tend to be minimized.
So one could just as easily point out that there is no other animal that produces as much wool as a sheep, and yet producing copious amounts of wool isn't particularly useful to the animal itself (i.e. other than the fact that humans will tend to select good wool producers for breeding). So sheep are not particularly good at surviving in the wild, and yet they are incredibly successful as a species and are widely distributed, thanks to humans.
In short, domestic hens evolved to produce many eggs in their lifetime because over the past millennia since humans have started keeping them as livestock, humans tended to preferentially breed those individuals which produced more eggs and to eat those individuals which did not. Chickens tended to be kept in pens and guarded by humans or other animals, so the ability to defend themselves or flee from danger was not important to their survival, and in fact, those that did attack their handlers or escape were probably less likely to be bred.
This process is known as selective breeding or artificial selection.


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Strange Cordeyceps-looking Mushroom in Australia
In the past few weeks, after the rain started up I noticed these mushrooms around my local area. I'd never seen them previously out of the 20 years I've lived here (a town in Queensland, Australia).
Sometimes they have a net-like section, and they sometimes have 10+ flies around a mushroom cluster.
What are these mushrooms? Are they common in Australia?

Given the gumtree leaves this had to be down under :) I haven't seen them anywhere her in the ACT. Too dry, perhaps :)

You found a member of the stinkhorn family, The Phallales (in the family Phallacea), probably a Veiled Lady (Phallus indusiatus) or a Phallus multicolor (they have other names as well.) They are common in Asia, Africa, the Americas, and Australia. Don't eat them; they're attractive to dogs (lovely aroma!) and there have been dog deaths.

These fungi produce a spore slime which has an intense smell of rotting meat or sewage, which is why flies are attracted to them.
They are commonly found in rotted woody material.

The link also says " An edible mushroom featured as an ingredient in Chinese haute cuisine, it is used in stir-frys and chicken soups. The mushroom, grown commercially and commonly sold in Asian markets, is rich in protein, carbohydrates, and dietary fiber. The mushroom also contains various bioactive compounds, and has antioxidant and antimicrobial properties. Phallus indusiatus has a recorded history of use in Chinese medicine extending back to the 7th century AD, and features in Nigerian folklore."

@Jay - Yes, I saw that. The Japanese eat pufferfish, too. That doesn't mean it's not poisonous. That isn't the only site I checked. The reason I gave that caution is that there have been dog deaths. It might, on the other hand, be more toxic in dogs than humans.

According to the Wikipedia page that you took this image off, the image shows a P. multicolor instead.


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What is a positive epitope fragment
What is a positive epitope fragment? I found one paper on the subject:

COBEpro: a novel system for predicting continuous B-cell epitopes by
Michael J. Sweredoski and Pierre Baldi

The group tries to predict possible epitope sequences for the generation of antibodies. This includes also non-linear epitopes where not all amino acids of the epitope are line up behind each other, but come in close contact due to a 3D-structure. To train their algorithm, they use data, where the boundaries of the epitopes and the non-epitopes are known and clearly mapped.
The "Dataset and Preparation" section in this paper contains the following:

In this article, we used several different datasets to train and
  benchmark COBEpro. These datasets were derived from several different
  previously published sources: BciPep (Saha et al., 2005), Pellequer
  (Pellequer et al., 1993) and HIV (Korber et al., 2003). The BciPep
  datasets consist of epitope/non-epitope sequence fragments. The
  Pellequer and HIV datasets consist of whole antigen proteins annotated
  with precise epitope boundaries.

The "positive epitope fragments" are known and verified ("positive") epitopes from these datasets in the training database. The fragment refers to restriction of length to 20 amino acids which they choose to apply. Shorter epitopes got amino acids added so they get 20 aa long, longer got truncated.

so basically what this means is that epitope fragments which has been verified as epitopes are called positive epitopes??

For this paper: Yes. I haven't seen this term anywhere else, though.


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

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

Please indicate where this is located.

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

It appears to me to be a Night Blooming Cereus:

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

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

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


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Does anyone know what kind of caterpillar this is?
I was out hiking, and was walking along the side of a road, and saw this little guy on some gravel. Hes a light blue/grey color, hairy, spotted with red,and looks like he has horns and a tail. I've been trying to search for what species it is. If anyone knows, please share!

(Click to view full image)

Nice picture! Where and when did you take the photograph?

In colorado springs, Cheynne mountain, and just a few days ago!

Looks similar to a Rusty Tussock Moth (Orgyia antiqua) caterpillar, but you might want to check the bugguide page for the species, or submit your photo there for a second opinion.

Thank you so much! I looked the moth up and there was a youtube video of one. Thats definitely my little guy. once again, thanks!


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Does Dorsal Raphe Nuclei firing pattern change in response to voluntary breathing?
I'm reading this paper, which discusses how Serotonin may be involved in motor functions of mammals: 5-HT and motor control: a hypothesis .
The paper includes the following diagram of the Dorsal Raphe Nuclei (DRN) firing pattern in a walking cat, and cat on a tredmill. Each step is associated with a distinct firing pattern. I'm wandering if the DRN firing pattern, in humans, changes in a similar way in response to voluntary breathing?

After searching wikipedia, I found a line that says:

REM sleep is turned on by acetylcholine secretion and is inhibited by
  neurons that secrete serotonin. (Psysiology of sleep stages)

I'm interested in dreaming, and at times have practiced entering dreams consciously, from the waking state after laying in bed for a long time. One of the obstacles to entring a dream was seizing control of breathing and starting to breathe voluntarily. This prevented me from entering dreams on a number of occasions, and appears to support the idea that voluntary breathing would affect the DRN. But I'm looking for a more scientifically-validated answer.
Thank you for your input!


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AlphaFold: How do they determine the 100% accuracy threshold?
From what I read, it seems the current situation is like this: latest cutting-edge lab techniques get to an accuracy of around 90%. For example, they put a protein under an electron microscope or something, and from the images obtained they achieve a precision of 90%. Now Deepmind features an AI that has demonstrated in contests that it can also virtually fold proteins to 90% accuracy. Therefore, the problem is kind of solved.
Please correct me if my interpretation is wrong. But if it's correct, then a big question remains: how the hell can they know if a configuration is 100% true? Even the best technology can only reach 90%, so where do they get that 100% for comparison?

Just a guess - they could have created a synthetic protein where they know the exact sequence and used it as a reference?

Can you tell a bit more on the source which claims 90% precision of the laboratory methods of structural determination?

It seems I've made a mistake there. Lab results were actually set out as the 100 threshold, and Alphafold was compared against it. Because even lab techniques can have errors, they consider 90+ scores are about as good as 100.

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Is there any reason to use an upright microscope over an inverted microscope?
I've never actually owned an inverted microscope, but it seems it has only advantages compared to an upright microscope: taller, heavier samples; no crashing the objective into the glass slide; easier to operate, etc.
Why then do people still use regular, upright microscopes? Is there a disadvantage I'm missing?

Cost?  A quick search shows inverted microscopes costing several thousand dollars, while a decent upright can be had for a few hundred.

@jamesqf Yup, seems obvious now... Should I delete the question?

There might be other reasons - I'm certainly not an expert!

For metallurgical microscopes there is little difference. I would say individuals chose on the basis of  quality ( image ,light, and mechanical). We nominally had about a dozen , mostly different , from Leitz to Unitron. Some console types like Richert (?) were only used for special jobs as they tended to be less convenient My boss loved old B & L where you physically removed the objectives - no turret.

As already mentioned in the comments, cost is one of the primary reasons when you're looking at simple light microscopes. Inverted scopes have more complex optics, along with the convenience factor of being able to examine larger samples, generally having a more stable frame, etc. All this leads to higher cost.
An advantage I can think of for smaller upright scopes is the ability to use them as a dissecting scope, where the sample is opaque and you need to see it from above. Another advantage is this:

Many fluorescence microscopes are upright, as there is a significant amount of extra equipment that needs to be mounted in addition to the eyepiece, including lasers, stage motors, and cameras and other detectors. This can take up a lot of room, and for convenience's sake it's often easiest to mount it up top where it is accessible.

Doesn't the extra equipment usually have to be built in, though, or at least have ports & fittings on the microscope to allow it to be added?  Which would raise the cost.

@jamesqf correct, which is why I clarified that the cost argument really only applies for simple "magnification-only" light microscopes. Once you start getting into very high magnification, fluorescence, live sample chambers, etc., cost starts to skyrocket.

Because inverted microscopes use a long working distance condenser (which allows them to fit plates, flasks, roller bottles, etc) - the resolution in transmitted light is inherently limited.  An upright microscope with a standard condenser will deliver much better results at higher magnification when you are imaging slides.
Consider your resolution in transmitted light a function of objective resolution AND condenser resolution.  If you have a high resolution objective but a low resolution condenser then you are inherently limited by the condenser regardless of how good of an objective lens you have.
A typical condenser on an upright microscope has a working distance of 1mm and a numerical aperture of 0.9/1.25.  So the condenser is right on top of your sample delivering the light needed by higher resolution objectives to perform.  A typical condenser on an inverted microscope has a working distance of 72mm and numerical aperture of 0.30 (of course there are alternate choices, this is just the most common).  So on the inverted the microscope the condenser that delivers light into your objective lens is 72mm away and has limited NA/resolving power.  This is just fine for the lower mag and long working distance objectives used for tissue culture because the LD objectives already have limited numerical aperture/resolving power.  But if you were imaging slides with standard working distance objectives which have higher apertures (especially if you are using oil immersion objectives i.e. 100x or 63x) - the condenser on an inverted microscope doesn't cut it and you need an upright microscope.

This looks like a great informative answer, but it would be helped by citing sources.


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Why aren't native predators in Australia able to handle the mice problem?
Australia is currently dealing with a mouse infestation problem, but Australia is awash with different types of predators that presumably eat lots of mice like animals.  Snakes in particular are well suited to kill mice, especially in close quarters. Snakes can fit in places most other predators can't due to their size. Additionally large invertebrates (like huntsman spiders) should also be able to take on some of the mouse load.
And it would be one thing if this was the first time the population ever boomed like this, but mice population booms have apparently have happened since Australia has existed. So why aren't we seeing large spikes in those predators when mice populations boom like this?

it takes time for the predatory population to respond - mice can breed in as little as 6 weeks (42 days), snakes take 45-70 days from laying to hatching, don't know how long from hatching to breeding...

Well for one thing we hunted many of the native predators to extinction. For another why haven't predators wiped out mice on other continents, because predators rarely wipe out their prey.

@bob1 yes but this has happened before, and I've seen no mention of increasing predator populations.

No doubt people have killed most mouse eating snakes in populated areas where mice find food easily. I see the same thing here in east TX; Copperheads ( mice eaters ) were common when I moved here 25 years ago. More people moved in and killed every snake they could . Now these same people are the ones who whine the most about the increase in mice and rats.  I have encountered many copperheads , they were about the most docile type snake I know .

a) you've got most of Australia's predators in your list: spiders and snakes.  Snakes aren't that populous and spiders don't have a huge appetite: 1 mouse per week would be overfeeding.  Dingoes don't eat 'em coz that's a cat's job.  We have no native cats, no rodent eating mammals like stoats, ferrets etc.  Basically it's up to eagles & goannas.  and b), Australia has existed for over 65,000 years.  Rodent plagues have been around for 200.

The mice aren't invading Australia, they are invading the wheat producing zones, where the tractors are leveling the land and putting on pesticides. The local frog, amphibian and snake populations downstream of the farmer's fields is strongly affected by the farmland, and so are the birds of prey, if they weather the pesticide use, they have to hide in dense trees, hollow logs, caves, and old barns, which are very lacking in Australian farmland.
If the government enforced laws for field edge habitats for local ecology, then there would be less mice.
Have a look at the map of wheat producing areas.
Rodent Outbreaks: Ecology and Impacts pages 225-238
PDF Google book
The map of mice infestations:

From pestsmart.org.au, though no longer available.

and a map of Australian climate:

wikimedia

Very nice answer and awesome images! Makes me wonder how a cold desert can be so directly adjacent to a hot desert, but perhaps it's just a matter of definition.

@Sixtyfive: See https://en.wikipedia.org/wiki/Desert_climate. A few different definitions are in use, but in all cases there's a temperature cutoff directly from "cold desert" to "hot desert". There are no in-between types. (And the names shouldn't be taken too literally. The Gobi Desert is a "cold desert" climate, but at the height of summer, temperatures there regularly rise above 100 °F or 40 °C.)

@sixtyfive The barrier of the warm vs cold desert is defined where the annual temperature average is higher and lower than 18'C, Koppen was a botanist, he devised regions based on vegetation types, the mix of temperature and rain where the same plant-types can grow. The temperature map is very different: https://www.researchgate.net/profile/Ferne-Edwards/publication/232319271/figure/fig1/AS:203062393217069@1425425255862/Average-annual-temperatures-in-Australia-showing-states-territories-and-their-capital.png Vs rainfall maps http://www.bom.gov.au/climate/how/newproducts/images/annrain2.jpg

Central Australia at Uluru and the cold desert regions can both sometimes be freezing on the thermometer for three/four months of the year, averaging 5'C at night. I think it's the summer that is hotter by about 10'C, i.e .30 vs 40'C.


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What species is this mammal?
I saw a mammal that looked like a large squirrel. I haven't seen anything quite like it. Can you help me identify it?

Squirrel-like, "hunched over" posture.
It was too large to be an eastern squirrel—approximately 2.5 feet, from nose to tail.
It had a fluffy tail like an eastern squirrel, not short and rat-like like a ferret.
Black face with white nose, body was chestnut-brown.
I saw this on the ground, not in a tree.
I saw it in a pine forest in east-central Alabama.
At one point, it sat up on its hind legs.

It sounds pretty much like a fox squirrel (or better: as masked face fox squirrel which are found in Alabama).
They look like this (taken from this website):

There seems to be quite some variation in terms of fur color, some animals are more greyish:

Taken from here, this website also contains some additional information.


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Are there beneficial genetic mutations identified by consumer DNA genotyping?
I'm looking at services like 23andme, and see that they identify a wide variety of genetic-based risks, like predisposition to diseases, hair loss, cancer, etc.
Are there a more "positive" DNA analysis outcomes out there? Like increased strength, cheerfulness(resistance to depression), etc?

First of all, I think it is, to a large extent, the way you perceive it. Instead of cancer-causing allele and hair-loss allele, you can think of them as cancer-protection and great-hair alleles. If you don't have disease alleles, that means that in some sense you have "life-extending" genes! Sounds much better, doesn't it?
Second of all, most funding for research is directed at disease so it is not surprising that most of the scientific knowledge is regarding this type of genetic variation.

Lactase persistence is a recent mutation which enables the people who have it to drink and digest milk as adults, while the default state has people unable to digest milk after childhood.
There is also a loci for muscle performance. People either have fast-twitch or slow-twitch preference, which affects your sprinting vs long-distance ability. Which one is "better"? It depends!


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Why are omega-3 fatty acids so easily oxidized when they're incorporated in cellular membranes?
Apparently, this has led to results with clinical significance, as we can see at http://extremelongevity.net/2011/10/03/daily-fish-oil-consumption-may-reduce-lifespan/...

The researchers fed a special genetic variety of mice diets that
  either included 5% daily fish oil + 5% safflower oil or instead 10%
  daily safflower oil. The mice used were SAMP8 mutants that were bred
  to have accelerated aging and shortened lifespans. These mice are
  often used in longevity experiments because their average lifespans
  are only typically one year. They were fed these diets from 12 weeks
  of age on. The researchers hypothesized since fish oil is so easily
  oxidized it may lead to greater oxidative stress within cells and thus
  actually accelerate aging, a process believed in part due to
  accumulative damage from oxidative stress. Safflower oil is an omega-6
  fatty acid and is not readily oxidized – it could have beneficial
  effects without causing oxidative stress.

Let's not debate the clinical significance here - but I do wonder - why are omega-3 fatty acids so easily oxidized as compared to omega-6 fatty acids?

I think the explanation for this description of fish oils as "easily oxidised" can be found in the Introduction to the actual paper (Nutrition 27 (2011) 334–337) that is cited in the article linked to in the question.

Fish oil contains high levels of eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3), which are omega-3 polyunsaturated fatty acids. EPA, DHA, and fish oil have been shown to have protective effects against coronary heart disease, thrombosis, inflammatory processes, carcinomatosis, and metabolic syndrome. Therefore, fish oils and components of the oils are marketed as health supplements. However, the effects of omega-3 polyunsaturated fatty acids on aging and lifespan are unclear compared with those of omega-6 polyunsaturated fatty acids contained in safflower oil and soybean oil. EPA and DHA are oxidized easily compared with linoleic acid (18:2 omega-6) and oleic acid (18:1 omega-9) in vitro .

In other words, the fish oil omega-3 fatty acids EPA and DHA have, respectively, 5 and 6 double bonds, whereas the omega-6 fatty acids in safflower oil, linoleic acid and oleic acid have, respectively, just 2 and 1 double bonds. So the fatty acids in fish oil are more prone to oxidation simply because they have so many more double bonds.
Incidentally, as you can see from the two structures below, both of the omega-3 fatty acids, EPA and DHA, also have an omega-6 double bond.
EPA:

DHA:


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Why are beta-galactosidase proteins overexpressed in senescent cells?
Wikipedia explains that it's a hypothetical hydrolase enzyme that catalyzes the hydrolysis of β-galactosides into monosaccharides only in senescent cells.
I'm just wondering - what causes it to be overexpressed in senescent cells - to the point that it often becomes a biomarker of senescence? And what exactly happens to the particular cell when you catalyze the hydrolysis of more β-galactosides (like lactose) into monosaccharides?

Looking at the articles referenced in the Wikipedia article, there's probably no direct physiological link between senescence and beta-galactosides. Lee et al (2006) and others before them have shown that the "hypothetical" protein is just regular lysosomal beta-galactosidase, which is present in higher concentrations in aging and stressed cells because the number of lysosomes increase under those conditions. There's a collection of references in the Discussion section of the Lee paper that delves deeper into the aging-lysosome connection.
I'm well out of my depth by this point, but if I were going to take a wild guess I'd suggest that lysosomal upregulation could be part of a stress response involving autophagy (i.e. the cell breaking down and recycling intracellular materials to meet critical demands), though I don't know the specific connection to aging. As far as beta-galactosides go: if you have any hanging around, you get to eat them, is all, I bet. I bet the references in Lee would tell you if I'm on track or not.


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How does the body repair extracellular damage caused by glucose?
So we know that glucose is an aldehyde that can cause cell damage to the lysine and arginine residues on proteins through the Maillard Reaction (among other damaging reactions that glucose participates in). Since everyone needs glucose to survive, though - I'm wondering - how does the body repair damage to its proteins+blood vessels that are caused by all this glucose? I'm especially interested in the blood vessels, as the damage to blood vessels is common in diabetics.

Is the fructose-glucose mixture found in most beverages and many processed food even more damaging than just glucose?

The Wikipedia article on "Advanced Glycation Endproducts" (or AGE) is quite nice and in this case especially the section on "Clearance", which also contains a few references.
In short the AGE which are inside of cells are taken up by the lysosome and then broken down until AGE-amino acids are left. These are secreted into the blood stream and excreted with the urine. Bigger extracellular AGE which cannot pass through the cell membrane are taken up by special receptors first and then processed, here macrophages and Kupffer cells are included. An involvement of the liver is also discussed.
The following articles are also interesting:

Advanced glycation end-products: a review
The biology of the receptor for advanced glycation end products and
its ligands
Pathogenic effects of advanced glycosylation: biochemical, biologic,
and clinical implications for diabetes and aging.


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If inhibiting S6 kinase decreases protein translation, then could inhibiting S6 kinase could possibly slow down long-term potentiation in neurons?
From http://en.wikipedia.org/wiki/P70S6_kinase...

Phosphorylation of S6 induces protein synthesis at the ribosome.
P70S6 kinase is in a signaling pathway that includes mTOR (the
  mammalian target of rapamycin). mTOR can be activated in distinct
  ways, thereby activating p70S6K. For example, branched chain amino
  acids such as leucine are sufficient to activate mTOR, resulting in an
  increase in p70S6K phosphorylation (and thereby activating it). mTOR
  is also in a pathway downstream of the kinase Akt. Akt is typically
  activated upon stimulation of a cell with a growth factor (such as
  IGF-1). Akt then activates mTOR (by inhibiting the Tsc complex),
  leading to p70S6K activation.

We also found a paper showing that downregulation of S6 kinase also results in a decrease in protein translation in yeast (but I'm waiting for Matt Kaeberlein to email me the slides from yesterday).

Could you please summarize the potential link between S6kinase and neurons? Your question seems to rely entirely on an abstract and lacks context.

S6 kinase is involved in protein translation.
Long-term potentiation relies on protein creation. So fewer proteins are made with reduced S6 kinase levels, which could imply slower rates of memory formation through LTP

I can't rule it out, but it sounds a lot like trying to tune a piano with sledgehammer.
Neuronal LTP depends on protein translation, but so does absolutely everything else in the cell. Inhibiting protein synthesis at the ribosome will block the formation of all proteins, not just the ones responsible for LTP. Unless there's a link I don't know about between LTP and total levels of protein translation, you're really going to want to look into inhibiting the production of proteins specifically responsible for LTP and not protein synthesis in general.


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Are humans the only animal that requires "clean water"?
I've seen a number of animals - dogs, cats, squirrels, ducks and geese, etc drink from puddles, some of them were muddy, others had green flora growing under water. Same goes for lakes and rivers. A human would not drink that. Do animals experience gastrointestinal discomfort or can they die from drinking water like that?
At the same time I hear about the problem of "clean water" in 3rd world countries and how diarrhea is the #1 killer of children under 5.
Are humans the only animals that require a certain purity of their drinking water? Why is it that a dog can drink from a puddle, but a human is likely to get sick from doing the same? Do baby animals get sick from drinking "dirty" water?

I wouldn't say that a human is "likely" to get sick by drinking from a puddle, I'd say "at some risk". It isn't desperately dangerous, although don't take that as a recommendation. There are many infections you can get from water (bacterial, viral, amoebal, and I presume fungal). You don't want to risk them, but probably won't actually encounter them in that puddle in your garden you see your dog drinking from. If the water is stagnant then the list of things in it that might hurt you is longer than if it's flowing. If you can avoid the mud, and anything that's been standing long enough to grow algae, fresh rainwater is a pretty good bet as these things go.
The same is true of other species, but the risk per drink is lower, since they drink it more and develop resistance to more of the things on the list. Humans are no different. For example some areas tend to have Hepatitis A in the tap water. The local population is immune after they've been infected once, and most childhood infections cause no symptoms, so it's not a problem for the locals. But to an unvaccinated visitor, the water's not safe. Hep A normally won't kill you, but is still well worth avoiding since it will make you sick for several weeks.
So basically, humans drink clean water because we can, not because we absolutely need to.
The lifespan of humans living "in the wild" (that is, populations prior to or independent of human agriculture) is pretty well agreed to be rather less than that of typical modern lifestyles. Water-borne disease is only one of many things responsible for that. The expected lifespan of a person used to purified water and so on, dropped into "the wild", is even lower again.
The "clean-water" problem in developing countries is primarily one of high population, relative to what the same area could possibly support in the absence of agriculture and other technology. The biggest risk of water-borne disease comes from contamination by human waste (although there are other sources, for example rats can contaminate water with Weil's disease). A small group of humans living in a large area doesn't have to worry about human contamination, they just drink upstream of where they defecate. This strategy doesn't help much once the population is dense enough that someone else is doing the same thing 20 metres away from you.
And of course, human agriculture also supports a much higher rat population than would otherwise be present (they're omnivores too, so they'll eat pretty much any food humans do). I suspect most human disease can be blamed on agriculture one way or another: if not on the animals then on the close-quarters living. If the population of humans was closer to what it was in the palaeolithic (a few thousand or tens of thousands of people in Europe), and was used to drinking from natural sources, then the water would be mostly (not entirely) safe.
So it's not so much that humans need perfectly clean water, it's that humans have figured out how to live in populations so large that we tend to make all the nearby water particularly dirty. Other species aren't completely unaffected by this, but they are less affected because our waste is specifically contaminating the water with diseases that affect us.

Dense population sounds plausible.

@Steve, Btw, 1) for the local population, why does "childhood infections cause no symptoms" yet "it will make you [visitors] sick for several weeks"? Also, 2) regarding your last sentence, why is our waste contaminating the water with diseases that affect us, yet " contaminating the water with diseases that them" doesn't happen for other animals?

@Pacerier: (1) I don't know the mechanisms, but there are several diseases which are less severe if contracted in childhood. I would guess that a visitor who happens to be a young child similarly would most likely suffer no symptoms from Hep A, but don't take my word for that! (2) Other animals do ruin water for their own use to some extent, but their populations tend to be limited by other things first. Humans have developed technologies to work around many limits on our population density, to the point where we gained the opportunity to make fouling the water a limiting factor.

Just to add to the above: faeco-oral/waterborne transmission is a classic example of a density-dependent transmission pathway - increased population density results in more frequent transmission, so modern population densities are certainly a key factor.

Animals do sometimes experience health problems from microbiologically polluted water. But they drink it, because they probably don't have as many options to choose from as humans have. Additionally, wilderness is very harsh, sick animals get eaten by predators quickly, so the short term evolutionary selection pressure in wilderness works very strongly in favor of good immunities in animals. So yes, I would expect animals would be a little less sensitive than humans, but still susceptible to illnesses. When I searched for examples about dogs I found:

"Giardia and Cryptosporidium [...] can cause inflammation of the intestinal tract and diarrhea when in gested by dogs (or people) even in small numbers. Most dogs with healthy immune systems are able to recover from this infection but severe diarrhea may, in some cases, lead to dehydration and significant illness. Puppies and older dogs with other underlying health issues may be more severely affected. Leptospirosis is a less common [...] illness transmitted by bacteria. [It] may lead to fever, lethargy, vomiting, kidney failure, liver failure, and even death in some untreated individuals."

Another webpage talks about wildlife water-borne illnesses. Giardiasis, leptospirosis and tularemia affect animals as well as humans.

Also, I guess civilization would have its effects on the human immune system (both positive and negative).
The more exposed you are to microbiological pathogens, the better the chance of developing a more robust immune system.
In a very civilized (or rather a very clean) environment, humans would not be exposed much to external pathogens and hence would not have developed immunity to many of the diseases caused by those pathogens.
In comparison, people who live in "less clean" environments (take some of the 3rd world countries for example), would be exposed to a higher level of pathogens and would naturally develop immunity to more diseases.
There's a Reddit discussion on this.
The same applies to humans vs animals I guess. Animals don't usually live in artificially clean environments and hence develop a better immunity.

Scientific sources for this guess would be great. The reddit-link is great.


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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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Does sleep in humans re-structure based on the expected sleep time?
I've read about anecdotal evidence that human brain has a fairly good internal clock that can be used to judge the amount of time that has passed. I'm wandering if there are any mechanisms in the human brain by which the brain can make adjustments to biological processes, based on the expectation of getting so many hours of sleep in the upcoming night. In this case, an alarm clock is not used.
For example, a person typically sleeps for 8 hours a night. On one day, that person realizes that he/she will sleep for only 5 hours that night, has there been any studies that demonstrate that the person's sleep would be "different" from the regular sleep? Will the person's sleep on that night be just a "cut short" version of regular sleep, or will the sleep be restructured to accomodate sleep time restriction?
For example a person's normal sleep cycle is 90 minutes long, so in 8 hours there would be about 5 complete cycles. Would there be any observable adjustments to the sleep cycle length or the amount of deep/REM sleep within the cycle, if a person expects to sleep only 5-6 hours or 10+ hours?
Thank you for your input!

From my personal experience, I can tell you one thing for sure: If, before going to sleep, I know that I have to wake up early or sleep less, and I think about this positively and say something like "ok, buddy, this time you've got just 4 hours to sleep. we need to get as much rest as possible. prioritize sleep over all other for these 4 hours. and don't get surprised being awoken after 4 hours of sleep. so make your cycles well fit this period to get as much rest as possible." - and play with these thoughts and anticipations, you know, it works. Maybe its more about auto-training, but still..

I haven't heard of studies like the one you're proposing, but you can test this hypothesis on yourself with this app.
Knowing you need to sleep less than your usual amount will probably affect the quantity and quality of your sleep, but not because of an "internal clock". Most likely, whatever you need to wake up early for will cause you some anxiety, which will affect both sleep duration and quality.

you are suggesting my own app... :)

:D It's a nice one.


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Under what circumstances will a human neuron divide?
I read somewhere that a mature neuron loses its ability to divide, except for very specific situations. I was unable to find the description of those situations. What are they?
(I'm sorry I'm not saying where I read that, but I simply can't find it.)

I was under the impression that neurons do not divide - will have a look around later, but will be interested to see other answers too!

Mature, differentiated neurons do not divide (undergo mitosis), but apparently there is a small population of self-renewing neural stem cells in adults that can produce new neurons. Neurogenesis predominantly occurs in the subventricular and subgranular zones of the brain.
Peripheral nerves can regenerate along its axon as long as the endoneurial tube and the Schwann cells are intact. Here's a picture of a neuron regenerating.

As was pointed out by @jello differentiated neurons do not divide, instead new neurons are recruited into existing networks from undifferentiated cells. This process is called neurogenesis. A high level summary of adult neurogenesis:

Neural progenitor cells differentiate into new neurons that have zero (or very few) synaptic connections, but are sensitive to the local chemistry.
(Optional) Sometimes (such as in adult neurogenesis in the olfactory bulb) these immature neurons-to-be are produced far away from where they are needed and follow standard pathways to migrate to the correct brain region
The immature neuron extends dendrites towards upstream neurons and starts to develop an axon
The immature neuron extends axon towards downstream neurons, and
The neuron matures and becomes indistinguishable from the network it joined.

For more information, consider the question: How are newly created neurons recruited into existing networks?


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Is the Common Cold an Immune Overreaction?
It's my understanding that the majority of symptoms associated with the common cold (runny nose, inflamed sinus, slight fever) are essentially the result of the immune system's response.
I've never heard of someone dying of the common cold (unlike influenza), even in immune compromised people. As such, what damage would the cold virus inflict if there was no immune response? Would it be catastrophic?

Related

Generally, you need some immune response. For the particularly bad immunodeficiencies, even something as seemingly benign as a rhinovirus will extend beyond it's preferred niche in the nose, infect the lower respiratory tract and cause death. Perhaps if I get some time I'll write an answer about this.

Can someone die of the common cold?
No.
The common cold is a clinical syndrome restricted to upper respiratory tract involvement. By clinical syndrome, I mean it is the constellation of symptoms (rather than the consequence of a specific pathogen). As you mention, these symptoms are the result of the immune response, rather than tissue damage or compromised function as a direct effect of a pathogen or its toxin (e.g., the watery diarrhea in cholera).
As defined (see, e.g., Cecil Medicine Ch. 369), this clinical syndrome cannot lead to death.

The common cold is an upper respiratory syndrome of rhinorrhea and nasal obstruction, frequently accompanied by sore throat, sneezing, and cough.

Can the viruses that cause the common cold cause death?
Yes. Many viruses that cause the common cold also cause other clinical syndromes that can cause death. This occurs when viral replication moves to the lower respiratory tract. As an example, influenza viruses are responsible for 25 - 30% of common colds (see Bennett, Principles and Practice of Infectious Disease, Ch.58). When it moves beyond the upper respiratory tract, influenza is responsible for substantial mortality. Other virus families that are responsible for both a common cold syndrome and lower respiratory tract syndrome in immunocompetent individuals (e.g., bronchiolitis, pneumonia) include parainfluenza virus, metapneumovirus, adenovirus, and (rarely) coronavirus. Rhinovirus, responsible for 40-50% of common cold cases, is uniquely unsuited to lower respiratory tract involvement, because of its preference for the cooler environment of the nasal mucosa, replicating best at 33 C (Murray Medical Microbiology, Ch 56). However, in individuals with Severe Combined Immunodeficiency (SCID), lower respiratory tract involvement does occur. There are a number of case series reporting death due to lower respiratory rhinovirus. This is an example.
Can the common cold lead to serious illnesses other than lower respiratory tract involvement?
Yes. Other morbidity can occur as a result of the immune response that produces the common cold syndrome. Rhinorrhea and congestion can progress to a viral rhinosinusitis, a separate syndrome with its own complications, or a secondary bacterial infection, which can lead to bacterial sinus involvement and/or bacterial lower respiratory tract infection. Otitis media is another common complication, especially in children, and has its own potential complications. Asthma (and, generally speaking, most lung diseases) can also be exacerbated by what would otherwise be a simple common cold and predisposes to lower respiratory tract involvement. Asthma does deserve special mention, because rhinovirus associated exacerbations can be fatal, but this is a consequence of asthma rather than a common cold syndrome. Further discussion of these syndromes are beyond the scope of the question, but are discussed briefly in the chapters referenced above.

I don't think coronavirus is that rare as a cause for LRTI. "Coronavirus Causes Lower Respiratory Tract Infections Less Frequently Than RSV in Hospitalized Norwegian Children" shows that coronavirus (in particular, HCoV-OC43 and HCoV-NL63) was in 44% of the LRTI patients in the sample (of coronavirus or RSV), RSV was in 71%, and 15% had both. So RSV is more common, but not overwhelmingly so.

@Charles look at the methods section. Those are nasopharyngeal samples, upper respiratory tract samples. Members of the coronavirus family are not typically isolated from lower respiratory tract samples. It occurs in some specific important syndromes, e.g., SARS, but the common viral families responsible for both upper and lower respiratory tract syndromes are influenza, parainfluenza, metapnuemovirus, and adenovirus. Rhinovirus are even less likely to be isolated from the lower respiratory, but, again, it does occur, especially in severely immunocompromised children.

@Charles Generally, be skeptical of any study that says: "look, i isolated this very common virus from the site where it typically lives. It must be responsible for this particular thing". Rhinovirus and coronavirus are also quite commonly isolated from the nasopharynx of healthy individuals.

Yes, the samples are collected from the upper respiratory tract, and every patient has an URTI. That's the context we're working in here: colds, which are URTIs. But some URTIs progress to LRTIs, and I gave the numbers for LRTIs. The numbers of URTIs are larger and have a higher fraction of HCoVs.

@Charles as discussed,URI predisposes to LRI, but if rhinovirus or coronavirus cause the URI, it's typically a secondary infection by some other virus or bacteria that causes the LRI. Isolating a very common virus from the upper respiratory tract is not useful for determining the cause of a lower respiratory tract infection.

You think that you'd have a URTI progress to a LRTI without leaving any virions in the nasopharynx? I mean, the study authors clearly disagree with you, given the causatives (e.g., "Nevertheless, it should not be forgotten that HCoV-OC43 or HCoV-NL63 may also cause severe lower respiratory tract infections.") throughout the paper and in other cited papers.

Let us continue this discussion in chat.

The common cold is not the result of a single virus. Over 200 viruses can cause a cold, so specific symptoms could vary depending on the virus in question. However, in the absence of an immune response, the virus is may destroy bodily tissues as it completes its life cycle of infecting a cell, using the host cell machinery to replicate its genome, and causing the cell burst open and release the next generation of viruses. This destructive effect could lead to catastrophic symptoms. Especially since the infection is in your respiratory tract, severe tissue destruction could be fatal. It should be noted, though, that the infection generally subsides in a week even with a compromised adaptive immune system (like in HIV/AIDS). This is probably why you've never heard of people dying from the common cold, since it is likely that if their immune system is that compromised as to make such a thing possible, the cold would be the least of their problems.
Sources: https://www.cdc.gov/antibiotic-use/community/for-patients/common-illnesses/colds.html
The most common virus that causes the cold is the rhinovirus, which undergoes the lytic cycle: https://en.wikipedia.org/wiki/Lytic_cycle
clarification: as kindly pointed out by De Novo (thank you!), Rhinovirus itself does not lead to tissue destruction in respiratory epithelia. The Rhinovirus was mentioned simply as an example of the lytic cycle of viral replication, which results in the destruction (lysis) of infected cells and could result in tissue destruction.

So would it be fair to say that because a lesser immune response would suffice for many common colds, e.g. those caused by Rhinovirus, the symptoms are often "unnecessarily" strong? So the immune system essentially says "better safe than sorry"?


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Why can't Turner Syndrome occur in males?
In Turner Syndrome, one X chromosome is missing, meaning that the resulting egg or sperm has 22 chromosomes (without pair) and the 23rd chromosome is missing.  If this develops in an egg, and a normal sperm carrying a Y chromosome fertilizes that egg, then due to presence of a Y chromosome, can a male with Turner Syndrome develop?

Can you clarify what you're asking.  What is the chromosomal makeup of this proposed individual?

Because it is not viable to not have any X chromosome (non-peer reviewed reference).
The X chromosome is much bigger than the Y chromosome and carry a lot of essential genes (see here). A zygote just does not appear to be viable without X chromosome.

Why the tag markup for X and Y?

@arboviral clarity, I assume.

Tag mark removed. I did that in the past already. I suppose, it once was handy to not confound chromosome names with variables, with locus names or allele names.

I can't get it into my head and can't imagine it properly .Firstly ,if there is an egg containing 22 chromosomes with one chromosome missing and that is an x chromosome but an egg contributes only one x to zygote and other x or y comes from father  So,Can't that female contribute its other x chromosome to zygote as it has two x chromosomes?

@RabikJohn After production of the egg, there is no way for the female organism to "do" something about the chromosomes. If the egg or sperm was incorrectly built, the zygote develops as far as it can. And in case of no X chromosome that is not very far. Maybe you can read more about egg and sperm production processes to fully understand.

I think it maybe like that, egg has one missing chromosome which is an x one and if that egg is fertilized by a y chromosome carrying sperm, then there would be no further development of male because as remi has mentioned that without x chromosome  further development cannot takes place so essentially it would be a female with only one x chromosome and no male with turner syndrome develops


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Must RNA and DNA be the way it is?
We're carbon-based based life form with (mostly) iron-based oxygen transportation for apparently good reasons.
Is the same true for why life on Earth developed using nucleotides, amino acids, RNA and DNA: "the chemistry" just works easiest that way?
For example, are A, C, G, U the RNA bases for some "good chemistry reason", or would any C-N ring work?  I'm dubious about that, since dinitrophenol is also a C-N ring, and it's highly toxic.

Unclear what you're asking. Are there other imaginable configurations? sure. RNA could be made of 4 different bases that aren't A, C, G, U, or maybe 5. DNA could never have been used in genomes I suppose. I can come up with lots of superficially plausible ways for life to happen. But the only way to really know for sure is to "replay the tape of life" and see what happens next time, or go look at other planets where life has developed. Alternate proposed configurations (e.g. arsenic instead of phosphorus in DNA) have generally been debunked.

@MaximilianPress "arsenic instead of phosphorus in DNA) have generally been debunked" is the kind of thing I'm looking for.  As for "imaginable configurations"... we can imagine a lot of stuff that doesn't really work.  To clarify: are A, C, G, U the RNA bases for some "good chemistry reason", or would any C-N ring work?  (I'll edit the question to add that.

Yes, exactly. There are many superficially plausible (not merely imaginable) biochemical configurations for life. See the field of exobiology/astrobiology, and alternative biochemistries. Trivially, there exist synthetic nucleotides. Ultimately, the only test is that of empiricism: you have to go find / build biology that uses these systems to know whether it works, and that has only been successful for rather minor variations.

@MaximilianPress your link to alternative biochemistries is the exact same as what I mentioned in my question.

If you've read that page then I'm not sure why you're asking the question, honestly. It didn't occur to me to look at it when it seemed to be a reference for us being carbon-based life, which was not really under dispute.


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How strong of an electric field is dangerous to adult humans?
Given that "a potential difference is introduced over the membrane, the associated electric field induces a conformational strong in the potassium channel" is required for our muscles to move, how powerful of an electric field is required to cause our muscles (including the heart) to fire irregularly?  How much stronger would it have to be to kill someone?
https://biology.stackexchange.com/a/53330/7973
https://en.wikipedia.org/wiki/Voltage-gated_ion_channel
(No, I'm not an "electrosensitive" afraid of cellphones or high-tension wires.)
Thanks

You can find out about that from google... Electric fields are not large or small. They are powerful or weak, they vary in voltage, wattage etc. A high voltage signal can be like a bullet, small and very light and penetrating anything. A low voltage signal can be like a train going very slowly, able to heat metal red but having trouble going through it.

@com.prehensible what exactly would I Google?

It's a fascinating topic, and there's a mass of research on it: google: minimal electric current to cause death, first page is: https://hypertextbook.com/facts/2000/JackHsu.shtml ... change to "minimal electric current to cause death nerves" have info on nerve physiology: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763825/ ... "conduction electric through body" with specific topics, cardiac arrest, nerves... Pacemakers are designed to last a long time, a 10 gram battery can supply enough energy to change the rythm of the heart for 20 years.

Research published by WSU Professor Emeritus of Biochemistry and Basic Medical Sciences, Dr. Martin Pall, bears directly on your question about potassium channels.
https://www.researchgate.net/project/microwave-frequency-radiation-acts-via-voltage-gated-calcium-channel-activation
He has concluded that weak EMFs cause cascading health impacts that derive from false electrical signaling of voltage-gated ion channels, and that these impacts include heart disease and the dreaded social bugbear elctrosensitivity (microwave disease).


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Does this "fleeing spiders leaving fields of webs" phenomenon have a name?
I have recently seen images of big areas covered in spider webs:

After flood in Australia

http://news.nationalgeographic.com/news/2012/03/pictures/120307-spiderwebs-australia-floods-wagga-wagga-world-science/#/spider-webs-australia-floods-bush_49725_600x450.jpg
http://www.dailymail.co.uk/news/article-2111390/Australia-floods-Spiders-cover-fields-cobwebs-flee-rising-water.html
http://www.hoax-slayer.com/spider-fields-australian-floods.shtml
http://www.theatlantic.com/infocus/2012/03/spiders-flee-australian-flood/100265/
http://io9.com/5891091/massive-spiderwebs-engulf-australian-town-as-arachnids-escape-floods

I would like to read about this on wikipedia. So I am looking for a name of this phenomenon. Do you know how it is called?

I doubt it will be called anything specific. It's just spiders fleeing a flood like any other animal.

It's called ballooning! To flee a flood, spiders will cast webs into the air to be airlifted to higher ground. They'll also trail web behind themself as an 'anchor' point. When thousands of spiders balloon during a flood, you get these amazing/haunting looking landscapes.

https://en.wikipedia.org/wiki/Ballooning_(spider) - interesting!


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Do prokaryotic chromosomes have centromeres?
I found this here.

Eukaryotic chromosomes are always linear. ... In contrast, prokaryotic chromosomes are either completely devoid of centromeres or carry the so-called “plasmid centromeres” which are not essential (with a few exceptions, such as Caulobacter) (57,–60).

What does it mean by prokaryotic chromosomes carry "plasmid centromers"?
Their chromosomes carry the centromeres of plasmids? Do they have centromeres or not?

Did you look up what plasmid centromeres are? What did the references say?

No, prokaryotes do not have centromeres.  They do, however, generally have a somewhat analogous structure used during cell division to partition the replicated chromosomes and plasmids between the two daughter cells. The analogous place on the chromosome or plasmid is the parS element, a DNA sequence on the chromosome or plasmid which is part of the parABS system.  This system, consisting of two proteins (parA and parB) along with parS, forms a mechanism to segregate the copies of a chromosome or plasmid for the daughter cells.
parS is usually called a "centromere-like" site, but is sometimes referred to as a "plasmid centromere”, which is why the quote uses the phrase so-called “plasmid centromeres”.

Do they have a centromere-like protein that links a pair of sister chromatids?


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Do birds have pharynx like mammals?
I saw this in Wikipedia:

Birds do have a larynx, but unlike in mammals, it does not vocalize.

And this pdf in Google.
It claims that birds do have a pharnyx.
Do birds have a structure called pharnyx? (Mention the ref. please)

Pharynx and larynx are not the same.

@kmm I said that they are?

Yes, birds do have a pharynx.

Birds can breathe through the mouth or the nostrils (nares). Air entering these openings (during inspiration) passes through the pharynx & then into the trachea (or windpipe). {1}

The larynx can't produce sound -- it's only there for breathing and eating. Instead, birds' sounds are produced at the bottom of the trachea, just above where the trachea branches into the lungs. This juncture, made of cartilage, is the syrinx.

The syrinx is the vocal organ of birds. Located at the base of a bird's trachea, it produces sounds without the vocal folds of mammals. The sound is produced by vibrations of some or all of the membrana tympaniformis (the walls of the syrinx) and the pessulus, caused by air flowing through the syrinx. This sets up a self-oscillating system that modulates the airflow creating the sound.   {2}

Since birds have both a syrinx and a larynx, it's unclear exactly when the syrinx took over sound production duty for the larynx.
{1}-http://people.eku.edu/ritchisong/birdrespiration.html#:~:text=Birds%20can%20breathe%20through%20the,as%20long%20as%20the%20neck.
{2}-https://en.wikipedia.org/wiki/Syrinx_(bird_anatomy)


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Why do humans hear better between 2kHz and 5kHz?
I've recently seen the following image:

Source: https://commons.wikimedia.org/wiki/File:Hoerflaeche.svg
Translation (from German):

The upper boundary (Schmerzgrenze) is where it starts to hurt
"Musikwahrnehmbarkeit" is where you can hear music
"Sprachwahrnehmbarkeit" is where you can recognize speech
"Hörschwelle" is absolute threshold of hearing (ATH)

While the ATH seems to be relatively smooth, there is a noticeable "gap" between 2kHz and 5kHz. Does anybody know why this is the case?
Some possible explanations I've heard are:

Evolution: Hearing a baby cry
Evolution: Hearing leafs rustling
Coincidence: There is no good reason for that.

The image is from wikipedia commons and has no references. It might be wrong. Do you know similar graphs? Do you eventually have this kind of information for other animals?

The main reason is this is the area where harmonics in human speech are most prominent.

Acoustically, we hear better in the 2-5 kHz range because our auditory canal resonates in that range (specifically, around 3 kHz). Our ear looks something like this (U Miami):

The auditory canal is part of the outer ear, which amplifies sound so that it can be converted into electrochemical signals by the middle and inner ear. We hear better in the 2-5 kHz range because the resonant frequency of the auditory canal is in that range.
The mechanical question of "how does this work" is usually easier to answer than the "why did this evolve?" question. Since reproductive fitness is the driving force of evolution, hearing babies crying (between 1-5 kHz) is the best guess I can come up with.

Do you think the resonant frequency could be different without severely influencing other properties how we hear / what we hear? Is this different for other animals with similar ears?

Changing the resonant frequency wouldn't change what we hear but would change the threshold at which we hear different things. I don't actually know about other animals, perhaps ask another question if you want more information?

This doesn't really answer OP's question, it only gives the mechanics behind it, and almost puts effect before cause. The reason the auditory canal is tuned to that frequency range is because our voices' harmonics are most prominent in that range.

You may never see this, but I also had this question - I think this may be a fun take.
The 2-5kHz range is associated with the third and fourth formants of the human voice, and these formants are used primarily in singing.1 After reading some discussion about possible evolutionary reasons that humans sing - It seems that sexual selection could have played a role2,driving improvements in perception of that frequency range.
Also, as mentioned earlier in this thread - the ear's resonant frequency is most sensitive around 3khz, which correlates nicely to the f3, f4 frequency range.

"... our auditory canal resonates in that range (specifically, around 3 kHz)." - Luigi

Finally, I'll link a neat video 3 in which a primatologist explains a phenomena in which female gorillas sing to emanate comfort/safety. Could possibly have a related function in humans.
p.s. please excuse the 3rd source :)
1^ Frequency range of human singing formants f3,f4
2^ A thread discussing the evolution of singing
3^ Gorillas singing analysis

This is exactly why, except that it's not just for singing. Human speech itself has a lot of energy in these bands.  We're most sensitive in this region because it helps us to hear each other speak better. A lot of voice CODECS specifically oversample this region as a result.

@stix on the other hand, why didn’t the human speech/voice cord evolve to be in a different frequency band?

@kal The average human trachea is around 11cm. The wavelength of 3 kHz is around 11 cm. That band is the resonant frequency of the average human vocal tract. It's due to the size our bodies evolved to be.

@stix thanks for verifying/clarifying :)


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How exactly are petri dishes used (e.g. in medicine)?
I know that petri dishes with a growth medium are used to grow micro organisms. I guess this works as follows:

The petri dish has to be kept sterile. To make it easier, I guess one could cool it.
The microorganisms are somehow put on the petri dish.
The petri dish is put in an incubator (e.g. 37 °C if one wants to simulate the human body).
After some time (how long?) one can look at the colonies.

Does one only look at them with the naked eye or is there a way to make more detailed studies?
For example, when I have an illness, can the doctor (for some illnesses) simply use this petri dish / naked eye technique to confirm a hypothesis what kind of illness I have?

What exactly is your question? Please read http://biology.stackexchange.com/help/dont-ask Petri dish with appropriate medium can be used to count number of cells in liquid culture. You spread 100uL of liquid and after incubation count colonies. Each colony comes from exactly 1 cell if you dilute liquid culture enough.

My answer to this question, http://biology.stackexchange.com/questions/40750/how-sterile-is-working-next-to-a-bunsen-burner/40755#40755 , may give you an idea of the steps that might be taken to prevent contamination when working with plates, though in a diagnostics setting, it is unlikely that the plates will have an antibiotic on them. Also in a modern clinical laboratory, there would be other methods used, but the basic principles of asepsis are still the same, keep your work area clean and do your best to prevent any airflow onto the surface of an uncovered plate.

Also a trained technician or clinical scientist will recognize the morphology of the bacterial colonies that grow on the plate and whether or not they grew where the plates were streaked or on an unstreaked area. Contamination will pretty much cover the plate where as sample will only grow where the plate was streaked.

I think this is too broad, there are various uses depending on the objective which is probably an extremely long answer, if you have a question about how to test for specific diseases using petri dish methods that would be better. Petri dishes are just a piece of very broad use lab equipment.

I think the petri dishes you are referring to are also called agar plates. Agar is a 'growth medium' for microorganisms. It provides the nutrients that the microorganisms need to survive. It can also contain main other 'things', such as antibiotics or pH color change indicators. There are many types of agar, for example, tryptic soy agar is used to grow E. coli. I think the oven you are referring to is called an incubator. Incubators provide the atmosphere, particularly temperature, needed for the organisms to grow. There are many types of incubators. Some microorganisms actually cannot grow in oxygen rich environments, and some only grow at specific temperatures. These organisms must be incubated under their preferred conditions in order for them to grow.
And yes, a lot can be learned from simply looking at the agar with the organisms on it. What exactly can be learned depends on the growth medium (agar or other medium).
To summarize, petri-dishes are just the plastic dishes that contain growth medium. And incubators are usually refrigerator looking things that provide the proper temperature for the organisms to grow. The goal is generally to mimic the natural environment of the organism, but as I stated, scientists often add many other things to the environment for experimental and diagnostic purposes.
Here is a list of common agars used in bacteriology http://learn.chm.msu.edu/vibl/content/differential/

Oh, as for the time, this depends on the organism. Some grow very fast, E. coli replicates about every 20min under 'log growth' conditions, and some grow very slow, like Mycobacerium tuberculosis. The rate at which the organism replicates is highly dependent on the environment in which the organism is living. Some bacteria only grow at very high temperatures, like Thermus aquaticus, which was isolated from a hot spring in Yellowstone National park.

Also, cooling a petri dish will not sterilize it. In  fact, low temperatures are often used to preserve bacteria. To sterilize a petri dish, one must autoclave the petri dish. An autoclave is like a big steaming pressure cooker.

I did not think that cooling a petri dish will sterilize it. I was talking about keeping the petri dish sterile. My thought was that when you produce a petri dish, it will probably get "contaminated" by just being surrounded by bacteria. Or that "sterile" probably only means that there are very few bacteria on the plate.

Why is it called 'log growth' condition when the number of bacteria grows exponentially (with respect to time)?

Well, log base 10 is 10 to the power of some number. Example 64 = 2^6 so log base 2 of 64 is equal to 6. It just implies exponentiation.

Sorry, didnt mean to say you thought cool = sterile.In case you were thinking of experimenting yourself, and you do want to keep your petri dishes sterile, you should keep the lid on them and probably keep them in the plastic sleeve they are shipped in until you are ready to use them, and avoid exposing them to the air, because there are microbes floating around in the air that can contaminate your dish. But I guess you were just asking out of curiosity. At any rate, perhaps it supplements the answer.

Hopefully Im not talking too much, but to answer the question of sterility, sterile by definition means no organisms. Sanitary is often used to describe what you were saying - very few organisms.


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What is the name if this glittery fly seen in Pittsburgh?
I have photographed the following fly which is iridescent green in Pittsburgh, PA.
I guess it was about 0.5-1.5cm long.
Can you help me to identify it?

And here it is: https://commons.wikimedia.org/wiki/File:Lucilia-sericata.jpg

Gorgeous photo!

Thank you for making your photo available as Creative Commons. I use many CC-licensed photo in my classes. Perhaps I will one day use yours.

@moose Iridescent is probably the word you are looking for.

It's a blowfly. They sometimes ruin my compost heaps (the larvae).

This is the most annoying fly from all the commonly found flies!

Looks like a green bottle fly.
https://en.wikipedia.org/wiki/Green_bottle_fly
Might be a Common Green bottle fly.
https://en.wikipedia.org/wiki/Common_green_bottle_fly


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How do legs of tiny insects/spiders like mosquito/Opiliones work?
I think I understand how legs of humans work. We have bones to which muscles are attached. Muscles can only contract / relax. By the combination of many different muscles we can make complex movements:

Image source: https://commons.wikimedia.org/wiki/File:1015_Types_of_Contraction_new.jpg
However, I have no idea how this works for insects / spiders. On the one hand, I'm not sure where the muscles should be attached to due to the exoskeleton. On the other hand, I have difficulties imagining that the same system works for legs which are this tiny:

Image source: https://commons.wikimedia.org/wiki/File:Spider-IMG_1630.jpg

@AlwaysConfused Yes, thank you. I fixed the spelling.

Well the subject of how insects move their limbs is a bit more complicated than suggested by Kasper.
Insects do have flexors and extensors muscles to move their legs. But there are other options too.
Spider legs work by hydraulic fluid. The spider has flexor.. but extension is done by pumping hemolymph into the leg.
Also it has been discovered that certain movements of insect legs is due to the chitin skeleton flexing and join structure. ie energy is stored in the chitin, and the structure of the joint cause the legs to return to the rest position.
https://www.sciencedaily.com/releases/2013/07/130718130524.htm

Arthropods use basically the same system to operate their legs. Yes their legs are tiny, but so are their muscles.(Is it so hard to imagine everything is downscaled? Their digestive system is also much smaller, but they don't need to eat the same amount as we do either...)
In general it's just a kind of smaller-sized mechanism that is based on the same principles: use a muscle to create tension over a joint, and so move the appendages. The big difference is off course that in mammals the muscles work against an internal skeleton, and in arthropods the muscles attach to the inner surface of an external skeleton.

I try to save daddy-long-legs spiders that can't climb out of my bathtub. I do so by grabbing one of their legs. Sometimes the legs detaches. If I squeeze the end of the leg that was attached to the body of the spider, the leg extends. How does this work?


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How does a smoker's pleasure work?
I smoke. For some reason, I've always had this idea that the pleasure of smoking works more or less like this: from the lungs, the nicotine reaches the blood, with which it travels to the brain, and there it does some difficult chemical stuff to make me feel all good. But that's also never made sense to me. I mean, the gratification is instant. I don't even inhale very deeply, and, momentarily, I feel the feeling for which I do the thing. I don't know how fast the blood travels -- I only know it varies -- but it seems impossible for it to travel this fast. Or is it?
Could you explain to me, a non-biologist, how it works?

May be you just like the smoke smell, like those who like barbeque and smoked products. In many people the smell of smoke increases appetite and the like.

@Anixx I don't think so because I still need to inhale a substantial amount of the smoke to feel the gratification. When I said that I don't inhale "deeply" I meant that I don't hold the smoke in my lungs for any extended period of time and I don't inhale as much as I could without starting to cough. The smell of cigarette smoke rather makes me crave an inhalation than gratifies me.

20-30 seconds is all it takes to reach the brain, then levels continue to increase with a peak at around 15 minutes and normal levels by about 2 hours (hence the craving). Smoking increases your heart rate directly and also indirectly through reducing the oxygen levels in your blood so your body compensates by increasing heart rate as well as makes each beat stronger, so it pumps more blood with each beat. Nicotine itself is really soluble, it goes straight through the lungs (alveoli) because the lungs get an incredible amount of blood (which they need to do their job) so massive surface for the nicotine to go through so enough nicotine gets into the blood and concentrations are really rapidly high enough for you to feel the nicotine. Carrying on from that, the blood rapidly gets back to the heart and around the body with the brain being practically a direct connection away. Consider the classic cyanide capsule death seen often on TV. The reason people seem to lose consciousness within 30 seconds is because they inhale the cyanide.
Nicotine replacement therapy used to stop smoking uses similar mechanisms to give the same speedy delivery of satisfaction without the massive risks of smoking, stopping cravings and really improving one's quality of life.

I agree with all of this, but would add that any instant gratification could be psychological - if you know what's coming you can presumably experience relief.

Yes, Alan is absolutely correct. Particularly in nicotine, which activates the dopamine system which is responsible for habits. Psychological reasons are frequently the most important barrier to stopping. Smoking and other drugs like heroin becomes a thrilling ritual.


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Can you tell the sex of a white willow when it's not flowering?
Can you tell whether a salix alba tree will produce male flowers or female flowers by looking at it, touching it or generally using your unaided senses? If not, is there any way to do that without specialized equipment or lots of expertise?

Neat question. I wonder if there are any common trends / rules of thumb that hold true across many taxa for sexing dioecious plants?

DNA sequencing?

@shigeta If you know of a way of sequencing DNA by looking at trees, please post an answer. But do make sure that after applying your method I can actually tell what the flowers will be. I've never sequenced any DNA.

Not answering your question as written, but you can always try looking around the base of the tree to find fallen fruits/flowers from earlier in the year.

I wonder how many different senses people have tried to use. E.g., could the wood smell different? Could they sound different when you knock on them? Could the wood taste different when you lick it?

did you check for signs of old seed pods underneath the tree?

I remember overhearing a botanist some 10 years ago, that he cannot tell male poplar from female when they are not flowering or producing seeds. Poplars and willows are related, so it is a weak indication for you, you will likely not find any visible features in willow neither. But it is an old information, too.    (Are you interested in DNA sequencing evidence or not ? I can look it up for you, but it seems your statement in comment question was ironical.)
EDIT: have just found an article which says: "In Salix viminalis, the sex of plants cannot be confirmed until the first time they flower." At that time, 1997, there were no DNA markers for plant sex determination, but it is apparent, they did not know how to differentiate the sex of this willow just from morphology. This example is even closer to Salix alba than poplar. I find it even more likely now, that you will not find the morphological features.
I took the suggestion of Oreotrephes. This is what to look for under the tree - fruit and seeds:
.
Source.
( C. Alström-Rapaport, M. Lascoux, U. Gullberg. Sex determination and sex ratio in the dioecious shrub Salix viminalis L. Theoretical and Applied Genetics 1997, Volume 94, Issue 3-4, pp 493-497).

Thanks for your answer, Barbara. Well, I'm generally interested in knowledge, and it might be useful for somebody, so there's no harm in posting that, and I'd be glad to learn. I just asked the question because I wanted to know if I could impress people by telling them, "Look, this is a lady willow," with as much wisdom about my looks as I could summon.

Thanks for the edit too. This seems to answer my question completely. I will wait a bit with accepting, but I find it unlikely that a better answer could show up. :)

Data from year 2012: still unable to morphologically discriminate individuals before the reproduction age, plus no reliable DNA- based method, genetic basis for sex poorly understood. Source. The best is a DNA method, which predicts that Salix viminalis is a female with only 96 % accuracy.


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on/off behavior of neural networks
What causes a group of disembodied neurons in a dish to fire after a silence? If there are no neurons providing a stimulus for more firing (as in a dish of disembodied rat neurons), then why don't they simply cease firing after the synchronized burst completes?

Are we talking of tissue slices or dissociated cell cultures?

The similar phenomena (spontaneous brain activity in rats after ~ 20 seconds of silence following decapitation) is studied in Zandt B-J, ten Haken B, van Dijk JG, van Putten MJAM. 2011. Neural dynamics during anoxia and the “wave of death” and is explained as a result of membrane depolarization. I don't know whether such reasoning could be applied to cell cultures though.

@aland: it mainly depends on the neuronal type. Not all neuron display bursting behaviour, and not all are synchronised. Certain (e.g. SCN) can be kept in vitro for days and continue with their "bursting life" with no problem. I am quite busy right now, when I have time I will try and give an answer.

There are a number of different wiring scenarios that could lead to this type of behavior, even in a dissociated neuronal cell culture.  The two major cases are neurons that are truly isolated from each other, and collections of neurons that connect together.  Since your question refers to firing and synchronized bursts, I'll restrict my discussion to the generation of spontaneous action potentials - but keep in mind that not all synaptic communication requires an action potential (the vast majority of internal connections within the retina, for example)
In the case of ensembles neurons in vitro, spontaneous activity is fairly typical.  One simple way to get this activity is for a subset of cells in the network to be inherently spontaneously active.  In the case of single, isolated neurons, this kind of individual cell spontaneous activity could also result in a single neuron firing spikes in a periodic fashion.  So for example purposes, let's explore how a single cell could produce this kind of activity.
Since action potentials are triggered by a sufficiently strong depolarization, we need to identify potential membrane polarizing sources.  When dealing with single cells, the major controllers of cell membrane voltage potential are the voltage gated ion channels.  When open these channels can cause, depending on their type and cellular/extracellular conditions, either a depolarization or hyperpolarization in the cell.  And, most interestingly, whether they are open or not depends on the cell membrane's polarization state.
That makes voltage gated channels excellent at feedback:

a depolarizing channel that is depolarization gated will further activate itself once activated, leading to yet more activation.  This is a positive feedback cycle.
a hyperpolarizing channel that is depolarization gated will, upon depolarization of the cell open and serve to hyperpolarize the cell until the initial depolarization has been removed.  In this way it would serve as a negative feedback source.

Physiologists have thoroughly characterized many of these cells, and they have many more states beyond an "open" and "closed", such as different levels of "inactivated".  But we don't need to know about those to answer your question.
The last piece we do need is brownian motion which is the movement of particles due to their bombardment by other particles.  This motion can with some frequency cause voltage gated channels to spontaneously open or close, which introduces noise into the system.
As you can imagine, if you have a positive feedback channel that is gated spontaneously, it will make it briefly more likely for other depolarization gated channels to be activated.  Positive feedback can quickly lead to a rapid depolarization of the cell, which could be observed as a burst of spikes.  If you include a set of slower reacting depolarization gated hyperpolarizing channels, then it's easy to construct a scenario where the cell would depolarize spontaneously with no apparent input, then have a quiescent period where a prolonged hyperpolarization makes it less likely to fire spontaneously.
Voila, bursting in an isolated neuron.  Place a set of those neurons in a network and you can get generate a lot of spontaneous activity.

Great response, and I'm sorry it took so long to get back to you! After a month or so of reading and coding, I've finally got a respectable Hodgin-Huxley network simulation running. I'll definitely look into coding up some noise inspired by brownian motion. Thanks!