I still prefer the good old[tm] Labnotebook. No dependencies on (proprietary) software or a computer. I generate quite some digital data (blots, sequencing etc.) this is stored on the servers of my university. We looked into this in our lab, but discarded the idea pretty fast. Most solutions are either expensive and/or proprietary. Then a lot of these programs are not bought, but rented for a monthly or yearly fee, so once you are in you basically will not get out there anymore. Or it takes a lot of work.
I found one free (for up to three projects), this is Labguru.
There is an article about this on Bitesizebio, which has a few interesting comments. And there is another blog entry about this worth reading.
One of the problems with ELN is a legal one, since a labbook is a legal document providing evidence a what has been done and the results of it. They can be very important when it comes to patent legal battles.


Q. “What do they mean?”
A. Two different things

“…share 99.7% of their DNA” is fairly straightforward.

This means that if you compare, base for base, the total DNA sequences of a group of Neanderthals with a group of humans — doing appropriate statistics — you will find, on average, 99.7% identity.

“1–4% of the DNA of living non-African humans…likely come from Neanderthals” is more nuanced.

This is because that 1–4% (generally thought nearer 2%) that is thought to come from Neanderthals could still be 99.7% identical to the human DNA it is thought to have replaced.
How can that be?
First let us assume that there are no genes unique to either humans or Neanderthals. (This may not be true, but the assumption emphasizes that we are considering the same genes.) Now suppose that after the divergence of Neanderthals and humans from their common ancestor the Neanderthals acquired a mutation that produced a new haplotype for a particular gene that spread to all Neanderthals. The percentage difference in DNA would be small, but the haplotype and hence the gene counts as Neanderthal. If it enters the European human population by interbreeding after emergence from Africa, then that gene is regarded to have come from Neanderthals. So the idea is that this is true for approx. 2% of non-African genes, even though the originating Neanderthal DNA may be 99%+ similar in sequence. Likewise, differences are observed between Africans and non-Africans in these gene haplotypes, even though the DNA sequence otherwise is very similar.
I have not discussed the evidence for this 2% gene haplotype difference here as I recently covered it in an answer to another question, specifically on that topic. (Hence my somewhat late interest in this question when it re-emerged.)


What is the name of this small black insect?

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

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


observed luminescence in a piece of plaice

It's probably bacteria.

Here's a pdf describing the phenomenon, along with an in-depth history of the reported occurrence, which should tell you everything you might want to know.

  These seafood products exhibited luminescence due to the presence of certain bacteria that are capable of emitting light.  Luminescence by bacteria is due to a chemical reaction catalyzed by luciferase, a protein similar to that found in fireflies... Most of these species require salt except for the two nonmarine luminescent bacteria.

There is some link to potential pathogenicity, so I'd recommend not eating it.  That document also requests that you contact the researcher, so why not?  Here is a potentially-relevant paper but 1. is very old, 2. is in Russian, and 3. I have no access to it.  And this supposedly tells you how to isolate them.


What are the survival limitations of alcohol?

I commented above that it will depend heavily on at what pace you drink your rum, but in short, no, no you cannot.  If you do it quickly, you'll die of alcohol poisoning, and if you drink it slowly, you'll probably die of dehydration[1].

io9 summed up some research a few years ago, the majority of which is largely bunk.  One study (ncbi, free pdf) however, from 1996, claimed to find that:

  These results suggest that alcohol has a negligible diuretic effect
  when consumed in dilute solution after a moderate level of
  hypohydration induced by exercise in the heat. There appears to be no
  difference in recovery from dehydration whether the rehydration
  beverage is alcohol free or contains up to 2% alcohol, but drinks
  containing 4% alcohol tend to delay the recovery process.

So stick to (American) beer.

Sidenote: In Belgium, they divide their (truly excellent) beer into two categories: special, which are stronger and often bottled, and thirst-quenching, which have a lower alcohol content and are often had with lunch.

[1]: Citation: Personal experience and the story of Johnny Tarr.


Survival of E. coli on agar plate at -20 degree C without glycerol stock

Over time I suspect that ice crystals will form in the colonies from defrost cycles in the freezer and the moisture in the agar.  This will cause rupture of the bacteria membranes and over time may destroy the bulk of the bacteria cells.  The plates will also desiccate over time as well from the defrosting cycles of the freezer.  You may be able to leave them in the freezer for a while but I can't foresee them surviving indefinitely.

If the strains are really important I recommend just sucking it up and spending the small amount of time necessary to make the glycerol stock.  Glycerol is used in bacteria stocks as a cryoprotectant to prevent the crystallization of the stock.


What is the length of gene when calculating TPM (transcripts per million)

Assume we have

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 10 & 15 & 30 \\ B\: (5kb) & 25 & 25 & 70 \\C\: (2kb) & 6 & 10 & 17 \\D\: (8kb) & 1 & 1 & 3 \end{bmatrix} \: \:$$

To transform this into TPM format, we need to normalize for gene length, and then normalize for gene depth, in that order.

Normalizing for gene length..

Step(s) To Perform: Divide each replicate count by the length of its respective gene.

For $Gene A$, it has a length of $2kb$ (kilobases), with replicate counts $10, 15,$ and $30$. Performing this operation on the entire table,

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{10}{2} & \frac{15}{2} & \frac{30}{2} \\ B\: (5kb) & \frac{25}{5} & \frac{25}{5} & \frac{70}{5} \\C\: (2kb) & \frac{6}{2} & \frac{10}{2} & \frac{17}{2} \\D\: (8kb) & \frac{1}{8} & \frac{1}{8} & \frac{3}{8} \end{bmatrix} \: \:$$

yields

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 5 & 7.5 & 15 \\ B\: (5kb) & 5 & 5 & 35 \\C\: (2kb) & 3 & 5 & 8.5 \\D\: (8kb) & .125 & .125 & .375 \end{bmatrix} \: \:$$

Normalizing for gene depth..

Step(s) To Perform: 1) Sum all counts within each replicate column; 2) Divide each column sum by the desired depth (this yields scaling factors); 3) Divide each replicate count within a column by its respective scaling factor.

$Rep1$

Sum: $5 + 5 + 3 + .125 = 13.125$
Scaling Factor:  $\frac{13.125}{1,000,000} = 1.325 \times 10^{-5}$

$Rep2$

Sum: $7.5 + 5 + 5 + .125 = 17.625$
Scaling Factor: $\frac{17.625}{1,000,000} = 1.7625 \times 10^{-5}$

$Rep3$

Sum: $15 + 35 + 8.5 + .375 = 58.875$
Scaling Factor: $\frac{13.125}{1,000,000} = 5.8875 \times 10^{-5}$

Applying these values to the table,

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{7.5}{1.7625 \times 10^{-5}} & \frac{15}{5.8875 \times 10^{-5}} \\ B\: (5kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{35}{5.8875 \times 10^{-5}} \\C\: (2kb) & \frac{3}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{8.5}{5.8875 \times 10^{-5}} \\ D\: (8kb) & \frac{.125}{1.325 \times 10^{-5}} & \frac{.125}{1.7625 \times 10^{-5}} & \frac{.375}{5.8875 \times 10^{-5}} \end{bmatrix} \: \: $$

yields

$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 377358.49 & 425531.91 & 254777.07 \\ B\: (5kb) & 377358.49 & 283687.94 & 594479.83 \\C\: (2kb) & 226415.09 & 283687.94 & 144373.67 \\ D\: (8kb) & 9433.96 & 7092.20 & 6369.43 \end{bmatrix} \: \:$$

The dataset is now TPM formatted, which offers an easier analysis of read proportions throughout the sample.


Protein half-lives range from less than 30 min (e.g., oxidoreductases) to more than 200 hr (e.g., some nucleic-acid binding proteins) and up to, at least, 2000 hr [Rahman & Sadygov, 2017, PLoS One 12(7): e0180428].

More ubiquitination sites, shorter half-life; more/larger intrinsically disordered regions, shorter half-life; more tightly coupled with the cell cycle, shorter half-life.

Note: Not all eukaryotic proteins are degraded via the ubiquitin-proteasome proteolytic pathway.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0180428


I consulted with Prof. Henk Mienis, the curator of the Israeli Mollusca Collection, and the valid name is Cornu aspersum. The Israeli subspecies is Cornu aspersum megalostomum.


Extracellular acid base homeostasis in human physiology is maintained primarily by the bicarbonate buffer, as regulated by both the kidneys and the lungs (and to a certain extent, the intracellular phosphate buffer). Outside of illness or injury, (arterial) blood pH is kept between 7.35 and 7.45. There is an excellent review of acid base homeostasis in Pubmed central that covers these points. Be aware before diving in, though, acid base homeostasis is one of the most complicated topics in human physiology.

As discussed in the reference above, a healthy pair of kidneys can usually compensate for a dietary acid or alkaline load. In these cases, what changes is not your blood, but your urine. There, is, though, some evidence that high blood pressure, diabetes, and possibly poor bone health may be associated with a chronic dietary acid load. Though an alkaline diet is being investigated as a treatment for chronic kidney disease, it is not currently approved for the prevention or treatment of any disease in the US.


From 46 human chromosomes, is each one from a single parent?

Yes, each single chromosome came from one parent.  However, it is not true that each chromosome came from one grandparent.  Due to crossing over in meiosis, the copy of Chr 1 that you got from your father is partially from his father, and partially from his mother.  And the same for all the rest of your chromosomes.  You will not pass on a whole chromosome as you inherited it onto your children, crossing over will happen in your gametes, so that your kid will get whole chromosomes that are part from your mother, and part from your father.  The sex chromosomes are exceptions, because in men, they can't do crossing over, since men have a mismatched pair.  (At least in biologically "normal" men.)


Where does the inverse seconds unit come from in the association constant?

First order association reaction:

$$\ce{A + B <=>[k_f][k_r] AB}$$

Rate of association (units: concentration per time) = $k_f\times[A]\times[B]$
 Since [A] and [B] are concentrations and LHS is conc. per time the units of $k_f$ has to be such that it gives conc per time when multiplied by conc2 ([A] ×[B])  Which is conc-1 × time-1

Rate of dissociation (conc. per time) = $k_r\times[AB]$
 Therefore units of $k_r$ would be time-1.

Dissociation constant is actually $\dfrac{k_r}{k_f}$; Its units therefore would be conc.


The number of nipples (breasts) a species has?

The number of mammary glands a species has is related to litter size. The relationship generally follows the "one-half rule," which states that the average litter size is equal to half the number of mammaries. The number of mammaries also tends to put an upper limit on litter size. It's not necessarily a hard limit, but survival tends to drop noticeably when number of offspring being nursed exceeds number of mammaries.

The number of mammaries is almost always even, but a notable exception is the Virginia possum, which has thirteen.

Gilbert, A.N. 1986. Mammary number and litter size in Rodentia: The "one-half rule". Proc. Natl. Acad. Sci. USA. Vol. 83, pp. 4828-4830.


What are the biochemical interactions between human body and Polyethylene?

PE is not bothered by acids and there is no way humans have a pathway for it, except that for choking or being obstipated. But neither do bacteria or fungi make a dent in the molecule. That's why it's not degraded and collects in the oceans.


Do animals get Post Traumatic Stress Disorder after escaping from a life threatening situation out in the wild?

Peter Levine speaks to this in his book, "Waking the Tiger:  Healing Trauma".  Most animals in the wild which experience a trauma through natural species interactions will go through a sequence of recovery stages.

First, when the trauma or death is considered inevitable, the animal will "faint", losing sensory awareness and consciousness. If the trauma or death is averted, the animal will then partially waken out of that faint, and "shake off" the trauma.

This "shaking off" looks remarkably like an epileptic fit, but when the movements are analyzed, they are a muscle-twitch repeat of the sequence of movements that animal took from the time it realized its hazard to the time it fainted. It is this same muscle-twitch capacity which allows human athletes to practice their skills both mentally and physically, without moving from one spot.

Once the "shaking off" is complete, the animal is able to rise and continue its life activities without any longer-term impacts such as PTSD.

Neurologist Dr. Robert Scaer has an explanation for this lack of PTSD.  Lasting trauma is only taken on when the "victim" experiences repeated episodes of the same kind of helplessness and hopelessness.  We humans are very good at giving ourselves and other species repeated episodes of helplessness and hopelessness, and animals which interact with us often pay a price in PTSD.


Troubleshooting SDS-PAGE of trypsin-treated BSA

I'm going to treat this as a partial homework question but provide some guidance as to how you can potentially address your question and have solid theory to back it up. Chymotrypsin preferentially cleaves peptide amide bonds where the carboxyl side of the amide bond (the P1 position) is a large hydrophobic amino acid (tyrosine, tryptophan, and phenylalanine). So one solution which is often used by experimental biologists (such as myself) performing mass spectrometry (MS) is to put their protein sequence (in this case BSA) in an algorithm such as PeptideCutter (from ExPASy), which performs a theoretical digest of the protein sequence having chosen the desired enzyme or combination of enzymes) and see what peptide fragments are expected to be produced and work out their length/molecular weight and compare that to your experimental data.

Having had an initial look, I noticed that your protein marker/ladder is missing, which is quite important in figuring out the peptide sizes produced! Also what is 1-8 lanes? are they different concentration of enzymes? if so then it looks ok to me since the higher the enzyme concentration from left to right, the higher the amount of digest products you have. If the peptide sizes obtained are not the ones expected then perhaps increase or decrease the digestion time since you could have a problem due to either incomplete digest or unspecific digestion, depending. I guess since BSA MW is ~ 66kDa your gel concentration is appropriate since you have a problem with the 15% gel as the products are too small and too abundant to resolve.


What kind of beetle is this (2cm long, brown, "V-shaped" body)?

Honestly, that looks like a stink bug, family Pentatomidae.

You can see some slightly different coloured ones here on Insects of Scotland

Here is a photo of the one that I used to see in the States (From Master Gardening):


What is the outcome of a human population starting with only 2 individuals?

Indeed natural selection decrease variability and therefore decrease information and mutation recreate this information. You can think of a bunch of pens of different colors. If you select
for the red pens you will decrease the variability in pen colors as the other colors will slowly disappear. If you allow for mutation to occur you will recreate blue and black and purple and yellow pens to occur again in your population of pens.

Is it an accurate statement that less variability means less total information?

Yes, less variability means less information. Information is a concept that increases as predictability decreases. If no variability exist, you can predict at 100% what allele a given individual is carrying. You may want to have a look to shannon's theory of information here on Khan academy. Note: this has not much to do with biology but it has to the mathematical definition has to do with mathematics, probability and computer science.

Are there any known mechanisms besides mutation that replenish the variability in alleles?

No, there is nothing else than mutations that creates new alleles. "Mutation" means any kind of structural change of DNA. So by definition any change in the DNA is due to mutations, therefore only mutations creates new alleles. Note: that some people may use the word mutation in a more narrow sense including some kind of DNA change such as indels but excluding chromosome rearrangement for example. I used here the word mutation in the broad sense.

Segregation and Recombination

Two other concepts may interest you though: Segregation (See Mendelian inheritance) and recombination(also called crossing over).

For example if 2 individuals $AB$ (Allele $A$ on one chromosome and allele $B$ on the other chromosome) reproduce they can create the individuals $AA$, $AB$ or $BB$ thanks to segregation.

Two Genes set on chromosomes and if two genes are on the same chromosome, one might think that these two genes cannot segregate independently one from the other, they are linked! For example imagine an individual has the alleles $A_1$ and $B_1$ on two loci of one chromsome and alleles $A_2$ and $B_2$ on the two same loci but of the homologous chromosome. If this individual transmit the allele $A_2$ it must necessarily transmit the allele $B_2$ and can't transmit $B_1$ if recombination does not occur. But recombination does occur and allows for partially independent segregation of these two genes.

You will find more information about these two concepts on wikipedia. I don't want to go too much into details but in short these processes can in some conditions increase the phenotypic variance but in any case these phenomenon do not create new alleles. New alleles are created by mutations only.

Can 2 individuals carry as much genetic information than today's world population?

No! As a very simple argument, two individuals can only have 4 different alleles. But we know several loci (sing: locus, position on a chromosome) where there exist more than 4 different alleles. Therefore, mutations must have happened at some time.

And only to enjoy some further arguments: if these two individuals had together 4 alleles at all loci, it would be extraordinary unlikely that their variation would have remained in today's population. Let's imagine two heterozygote (=who has two different alleles on their two chromosomes for a given locus) individuals are $AB$ and $CD$ that have two offsprings. The probability that their 4 alleles are present in the two offsprings is $1/4$. I don't when Adam and Eve were supposed to exist but it very sound like their variability would have not been maintained through times. This random process which diminish variability is called genetic drift. To be a bit more accurate, in a population that do not change in size, the expected loss of alleles due to genetic drift at each generation $1/2N$, where $N$ is the population size. So the bigger is the population size, the lower is the loss of alleles due to genetic drift. In the above example $N=2$ and therefore the expected loss is $1/4$.

I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents?

Yes, as said above, one individual can only have two alleles at a given loci and can therefore not transmit more than two different alleles.

Without a population to start with, wouldn't the lineage eventually turn into clones of each other[..]?

Yes, because in absence of mutations (and in absence of different special types of selection such as overdominance) the variability is slowly lost due to the randomness of segregation. This process is called genetic drift.


Why high quality DNA should be between 10 and 20 kb?

The website specifically talks about DNA samples intended for sequencing. The DNA in these samples was/is/will be extracted from cells and this extraction procedure leads to fragmentation (breaking into chunks). Since the expected average chunk length will greatly depend on the extraction process, I guess its reasonable to assume that 10-20kb can be expected from the most common protocols.

Much larger or much smaller fragments will also cause problems with the sequencing. (This is again method dependent, but generally true with varying fragments sizes that can be sequenced with the different available methods)


Mitochondria variability per tissue in humans?

BioNumbers is a great site to answer this kind of question.

This search produced a link to this paper , which has measurements for mitochondria per cell for multiple species and cell type.


Cat's tail movement as an indicative of tension

According to Desmond Morris in Catwatching: The Essential Guide to Cat Behaviour, a cat wags its tail when...

  The cat is in a state of conflict. It wants to do two things at once, but each impulse blocks the other. (emphasis mine)

Then, some pages after that, Morris talks about what he called the dilemma of the suburban cat hunting a bird on a lawn:

  To start with, the open, manicured lawn robs the cat of all its natural cover, exposing its whole body to view. This is doubly damaging to its chances. It makes it almost impossible for the cat to creep near enough for its typical, close-quarters pounce without being seen. This puts it into an acute conflict between wanting to stay immobile and crouched, on the one hand, and wanting to rush forward and attack, on the other. The conflict starts its tail wagging furiously, and the same lack of cover that created the conflict then cruelly exposes the vigorous tail movements to the frightened gaze of the intended prey. (emphases mine)

That being said, your observations are probably of urban cats in this kind of conflict, in a situation where a successful attack is almost impossible. It's the conflict that makes the cat wag its tail and, as you can see, this behaviour doesn't help the cat at all.

A feral cat in the wild, in a effective attack, will not wag its tail.


Late control mechanisms of blood pressure (arterial) level?

Capillary fluid shift mechanisms

If the pressure of the blood is high, there is high hydrostatic pressure. Simply put, this means fluid exits the capillaries at the arterial side due to this pressure, and less fluid returns at the venous side. With less fluid in the circulation, blood pressure falls.

Stress-relaxation of the vasculature

Imagine the arteries are like springs. The more you pull them the stronger the recoil force. However if you stretch them too much for too long, they stay stretched.

Renin-Angiotensin-Aldosterone system

When the blood pressure is high, there is less release of renin from the kidneys. This means less angiotensin II production. Angiotensin acts to increase blood pressure by increasing vasoconstriction and increasing retention of fluid and salt (via aldosterone). With less RAA system activation, the blood pressure drops.


Cucumber contains a compound called trans-2-nonenal (reference 1 and reference 2) that repels insects. This particular compound (reference) has can also be used in insecticide foams for repelling ants (reference)


Lambda red recombination without electroporation

Since Lambda red recombination is a rare event you want to have to have a good transformation efficiency, thus electroporation would be your best choice. Also since the expression of the recombination system usually needs growing bacteria at 42º you will probably inhibit the expression of the recombination machinery with the chemical method.


What would EEG recordings reveal if their resolution was better?

The temporal resolution of EEG is already considered to be very good. The problem is spatial resolution. Even the loss of very high frequency activity, like individual spikes, is really a problem of spatial rather than temporal resolution: the spiking cells are too far away, so it is only possible to detect them if they are very synchronized (in which case they still show up as lower frequency signals).

Because EEG recordings are so far from the sources they are recording from, and because even structures deep in the brain can contribute to surface potentials,the signals end up as complex averages over a large space. There is an entire field called EEG source modeling that tries to use signal processing methods to improve this spatial resolution.

However, you don't really have to ask this as a hypothetical question, since we already have methods that have better resolution than EEG. Electrocorticograms (ECoG) are the most similar, and most applicable to human studies. ECoG arrays are very similar to EEG, but they are placed directly on the dura, under the skull. They increase spatial resolution because they cut down distances dramatically by not having to record through the skull.

As you mention in your question, local field potentials (LFP) get even closer to where the measured currents are occurring, by recording from within the brain itself. The spatial resolution of LFPs themselves can also be improved by recording from multiple electrodes and computing a current source density. This also helps mitigate the effects of volume conduction.

fMRI is a completely separate issue. Often, EEG and fMRI results can act in conjunction, using EEG to determine time and fMRI to determine space (note that although there are limits to the spatial resolution of fMRI, for a human subject it is dramatically more spatially precise than EEG, especially for any structures not at the very surface of the brain, including any of the sulci of neocortex). fMRI spatial resolution can be improved by using stronger magnets, but eventually there are technological (and expense) limitations, but as you say the temporal resolution is fixed, and even the spatial resolution has some practical limitations.

To generally answer your title question: if the spatial resolution of EEG is improved (practically, this means either source modeling or using ECoG or LFP), one is better able to identify the brain structures that are producing the signals observed in the EEG, and able to be more confident that the signals observed are "real" rather than an artifact of filtering over space. For example, a higher-frequency traveling wave could appear as a lower-frequency signal on an EEG, or a localized, high-intensity event could appear like a generalized, low-intensity event; higher spatial resolution would allow you to distinguish between the two in both cases.


What is the function of spongin in sea sponges?

If you have ever used a natural bath sponge, you know that the structure of a sponge's spongin skeleton is great for absorbing water and squeezing that water back out.  The sponge's skeleton contains millions of tiny holes, all connected in a massive network of internal tunnels, through which the sponge takes in food and eliminates waste.  It feeds by use of cells that wave tiny cilia to push water into the sponge.  Nutrients are absorbed by the animal and spent water and waste are expelled by the help of similar cells, spinning their flagella to force the water out of the sponge.  A third class of cells, comprising a basic immune system, move around the organism engulfing microbes potentially dangerous to the animal.

This unique system is facilitated by the structure of the spongin skeleton.  The skeleton needs to be strong enough to retain this complicated microstructure, while also having enough give and flexibility that its network of delicate tunnels don't buckle under the force of water pressure, deep currents, or fish and other matter bumping against it.  Notice that, when you squeeze the water out of a sponge, it snaps back into place, the tunnels still open for business.  Given that these tunnels are how the sponge eats, this is very important.  To build a complex tunnel system with millions of tiny little tubes running through it out of something hard and brittle would make it very easy for tunnels to collapse, cracks to form, and other damage to be sustained.  Some sponges, as you mention, have hard, brittle "spicules" in addition to the spongin, but these sponges tend to live in deeper regions and need extra strength to deal with the pressure.


Can genes that activate transcription factors also called be called transcription factors?

Yes.  For an example, see this list of targets of NF-kB (a transcription factor).  Many other transcription factors are included there.  As for a TF that does nothing except activate another, single TF?  I don't know that those exist - TFs tend to modulate multiple genes.


Does the term 'protein expression' refer to the production of proteins only or also their regulation?

There are no formal definitions accepted in science for ambiguous
phrases such “protein expression”.

If you wish to know what a particular author who uses such a shorthand phrase means you need to examine the context. If you wish to write scientific reports that are comprehensible to others you must express yourself precisely, defining any shorthand phrases that are necessary to avoid clumsiness.
In the context of the question, all that “protein expression” means to me is “expression of protein” — the synthesis of the protein from some entity that has the potential to do so. It a fundamental level that would be a gene or mRNA that encodes a protein (or proteins — that too is unclear), in which case this might be less ambiguously expressed as, for example:
“…expression of protein from gene X inthe plasmid construct Y…”
“…expression of proteins from mRNA in vitro…”
(I would generally retain the preposition. Be kind to it, poor little thing!)
To indicate that one was interested in the potential of tissues to synthesize proteins, then (with all due respect NCI, who are probably simplifying for the layman) one would need to write something like:
“…expression of protein in liver cells (after prolonged starvation etc.)…”
Under no circumstances would I imagine the term “expression” to imply or include “regulation” or “post-translational modification”. To illustrate why, consider the following example of a perfectly valid use in this sentence:
“A problem with expression of mammalian proteins in bacteria is that the required post-translational modification does not occur.”
If I wished to indicate I was also writing about regulation I would say so specifically:
“The expression of haemoglobin in reticulocytes and its regulation”
(and expect others to do so too.)
The fact that, as a professional molecular biologist, I disagree with @MattDMo, who is likewise a professional scientist, only demonstrates that the term is ambiguous. We would both like the context.


Basic text/notes on DNA structure (for non-biologists)

this is a special topic, I'm assuming you have looked over the basic Watson and Crick stuff.

Maybe closer to your interests DNA does tangle and needs constant maintenance of the amount of winding to keep it properly ordered.

I would look at topoisomerases and DNA origami to start with.

Topoisomerases are a class of enzymes that help DNA pack up and wind up into the compact forms of the chromosome when its wound into solenoids in chromatin and unwind into the looser forms when it is loose.

DNA origami is a field of study which uses DNA as a self assembling template for making three dimensional structures.

Maybe this helps?  let me know if we can narrow the specifics of your interests.


The number of recombination events (chiasmata) varies dramatically from species to species.
It is also unlikely that this number has any universal relationship to selection, though for specific cases it has been shown that selection can change recombination frequency.
For some more information about the processes controlling this in present-day species and the inferred mechanisms driving among-species variation in recombination frequency, you might see this paper.


If life began at sea, why organisms are less salty than the sea?

Many biological processes require regulation of the salts (or more precisely ions) in fluid compartments of an organism. These processes include muscle contraction, filtration of the blood by the kidneys, and so on. Without these processes, a fish would certainly be dead. So it's not necessarily that regulating ions aids evolution or metabolism, nor that the sea changed salinity - the reason is that many biological processes required for an organism's survival wouldn't work without proper regulation of ions.

One such important process is active transport. In essence, by creating gradients of ions across a cell membrane, you can let the flow of ions into the cell drive other processes. This is a bit like how the flow of water through a water wheel can drive other machines.

I've never come across any reference to a cell with an ion concentration of its intracellular fluid greater than that of the ocean, though I'd slightly doubt that to exist since it would disrupt active transport. I'd also doubt that you could discern the ion concentrations of any fossilized cell since ions need to be dissolved, but how would you see this in a fossil?

I'm not sure whether I've completely answered your question, so let me know if something's still unclear.


Ligaments at the posterior superior iliac spine

It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more. What is the name of these "dimple of venus ligaments" and what is their purpose?

First, re: what a ligament is, you're correct in your understanding that ligaments generally bind bones to bones (vs. tendons), but the term is used more broadly as connective tissue that binds things together, holds them in place, is a remnant of a fetal structure, or a mesenteric fold. Your wikipedia link acknowledges this. Some examples are:

Round ligament of the liver: a remnant of fetal structure
Broad ligament of the uterus: a mesenteric fold
Median arcuate ligament: this one actually binds two muscles together
Sternopericardial ligament: binds the pericardium to the sternum

The unnamed short ligaments Kumar describes (and wikipedia, quora, and stack exchange have repeated), are probably unnamed because they are difficult to isolate and study, and they are not clinically relevant. They may even be theoretical. There are no studies on them indexed in medline, and they aren't discussed in any anatomy text I've read. Dimples are generally thought to be caused by fibrous connections between the skin and muscle, bone, or other deep tissue. If you ever cut into the back of a cadaver or surgical patient, you'll see that there are a great number of unnamed fibrous connections to the skin. It's not unreasonable for Kumar to invoke them as the cause for these dimples.


Comparing the amount of domestic animals and wild animals?

And how to estimate the amount approximately?

You cannot. Most of the earth is water, and fauna diversity is highest in water. We are still tagging and tracking the movement and reproduction cycles of animals, and that is a never ending task. I say we cannot reach an accurate approximation because of how these projects work. They are targeted towards the monitoring of specific species. Next, different countries have different approaches towards conservation of the same species, and above all this many countries choose not to report numbers. The example which comes to mind is the Red panda. As many animals come inside the radar of active conservation efforts, even more remain outside it.

In fact, some time ago I read a compelling article about why the WWF should change their logo to a Red panda (or known as the lesser panda) rather than the giant panda, the argument being that awareness about the giant panda is very high while red pandas are still misunderstood as pandas. Unfortunately I cannot find that article now, but you can visit the red panda network to find out more.

  Which has the greater amount on Earth?

Second, what do you consider as a wild animal? are insects included? are gutter rats included? Is the infestation of wild boars near the now defunct Fukushima plant included? If yes then they outnumber domesticated animals by a long shot. I would dare to say that cities are habitats more for members belonging to Animalia but not belonging to Homo.


Can exposure to blood make pathogens resistant to the immune system?

You have got the concept of vaccination a bit wrong. Pathogens have to evolve to acquire resistance to immune system (or antibiotics). Technically, the white blood cells also evolve to acquire resistance against pathogens if they don't have a strong innate immunity. Development of immunity after vaccination is also not instantaneous. The pathogen population has to "grow" in the blood for at least a few generations to become resistant. A drop of blood would probably not give the pathogen enough time to evolve. Moreover, your white blood cells will die quickly outside the body unless they are cultured in a controlled environment. Therefore, the selection pressure to evolve would also not be there.


How many nucleotides are there in the LMO1?

1274bp

http://www.ncbi.nlm.nih.gov/nuccore/NM_002315.1

If you need to know gene size and are confused w search results, search for gene name + "cDNA"


After we have eaten... the maximum blood supply is transferred towards the digestive system so that digestion is done, and therefore the brain to does not get adequate blood supply. Am I right about this?

This is a very, very common myth, but it is a myth. Because blood flow and oxygen delivery to the brain is critical for survival, cerebral circulation is one of the most tightly regulated systems in the body. Blood is not shunted from the brain to the gut for digestion.

  In a normal physiological state, total blood flow to the brain is remarkably constant due in part to the prominent contribution of large arteries to vascular resistance.

Eating, sleeping, walking, etc. are all normal physiological states. If we had blood shunted away from our brains after eating, we'd literally collapse after every meal.

  In normotensive adults, cerebral blood flow is maintained at ~50 mL per 100 g of brain tissue per minute, provided CPP is in the range of ~60 to 160 mmHg.

As eating alone doesn't normally cause our blood pressure to rise or fall, cerebral perfusion is constant regardless of what is or isn't in our digestive systems.

Blood flow to the gastrointestinal system (or GI tract) is also regulated, but the flow varies widely:

  Estimates of blood flow (in ml /min × 100 g) to the quiescent gastrointestinal tract of dogs and cats range from 15 to 100 for the stomach, 35–120 for the small intestine, and 10–74 for the colon. Somewhat lower values for resting blood flow to the stomach, small intestine, and colon have been reported for man.

So, the basic answer is that, yes, blood flow to the gastrointestinal tract varies, but blood is not shunted from the brain in favor of the GI tract.

So why do we get sleepy after a meal?

Sleepiness after a meal is caused by the level of peptides in your brain called orexins (aka hypocretins).

In 1998, two groups of researchers simultaneously discovered 2 small neuropeptide hormones that regulate, among other things, wakefulness and feeding behavior.

One group discovered them while searching for molecules that could bind to "orphan" receptors, that is, a brain receptor with an unknown "binding" molecule (called a ligand). They found that the prohormone prepro-orexin was found in a very small area of the hypothalamus which had been implicated in the regulation of feeding behavior and energy homeostasis; this suggested the possibility that the neuropeptides might be involved in the regulation of food intake. When administered into free-feeding rats' brains, one of these peptides (orexin A/hypocretin 1) stimulated food consumption in a dose-dependent manner (with attention to light and dark periods, i.e. the circadian rhythm), with a lower dose increasing rat feeding about 2-fold, and the higher dose inducing a 3+-fold increase in feeding compared to rats injected with a solution without the peptide (the other stimulated feeding to a lesser degree). The effect persisted for 4 hours. Furthermore, fasting rats produced more than twice as much orexins as rats feeding freely. For this reason, the molecules were names "orexins", after the Greek word orexis, which means "appetite". They speculated that the orexin-secreting neurons might somehow be modulated by glucose.

At the same time, another group of researchers using a completely different approach found that the same group of hypothalamic neurons were stimulated by a peptide hormone similar in composition to the gut hormone secretin. They identified the same prohormone and its two peptides, naming them hypocretins for "hypothalamus" and "secretin". They found that at least one of the peptides had a neuroexcitatory activity in specific areas of the brain (they mapped effects in the hypothalamic neurons, the posterior hypothalamus, the septal nuclei in the basal forebrain, the preoptic area, the paraventricular nucleus of the thalamus, the central gray, the locus coeruleus, the colliculi, the laterodorsal tegmental nucleus, and the nucleus of the solitary tract) suggesting that the peptides acted within the central nervous system as homeostatic regulators with a role in nutritional homeostasis.

Scientists have not decided on whether to call them orexins or hypocretins yet, so both are used. They are found in all vertebrates.

Mammalian orexin A sequences thus far identified (human, rat, mouse, pig, dog, sheep, and cow) are all identical, whereas the sequences of orexin B show some differences among species. From Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System, Natsuko Tsujino and Takeshi Sakurai

In 1999, a group of scientists found that narcolepsy (a sleep disorder characterized by extreme daytime sleepiness) was caused by a lack of a hypocretin/orexin receptor 2 gene in certain dogs, therefore establishing that they play a very important part in the regulation of wakefulness.*

Since then, an enormous body of work has shown that orexins/hypocretins (O/H from here on in) are involved in the regulation of a wide range of behaviors, including wakefulness and vigilance (needed to find food), systems that regulate emotion and reward (including drug-seeking behavior when stressed and eating for pleasure - "consumption beyond homeostatic needs" - leading to obesity), and more.

What does eating have to do with sleepiness?

Several studies report that the firing rates of O/H neurons are influenced by serum glucose, triglycerides and amino acids.

In English: You are awake (O/H is being secreted by O/H neurons in your hypothalamus). You eat. Your serum glucose rises. The elevated glucose causes depolarization of inhibitory neurons that hyperpolarize O/H neurons decreasing the amount of O/H. released. Result: wakefulness decreases.

Control of Cerebral Blood Flow
The Gastrointestinal Circulation.
Comparing these two papers - the first and second references - is a wonderful example of the completely different methods used by scientists to investigate unknowns and up with the same basic conclusion.
Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior, Cell 92 (4): 573–85
The hypocretins: Hypothalamus-specific peptides with neuroexcitatory activity Proc. Natl. Acad. Sci. U.S.A. 95 (1): 322–7
The Sleep Disorder Canine Narcolepsy Is Caused by a Mutation in the Hypocretin (Orexin) Receptor 2 Gene
The role of orexin in motivated behaviours A Nature Neuroscience Review
The role of orexin-A in food motivation, reward-based feeding behavior and food-induced neuronal activation in rats
*Human narcolepsy - caused by a destruction of O/H neurons - also is associated with metabolic abnormalities, including increased frequency of non-insulin-dependent diabetes mellitus and increased body mass index.
Hypothalamic Orexin Neurons Regulate Arousal According to Energy Balance in Mice
Orexin/Hypocretin: A Neuropeptide at the Interface of Sleep, Energy Homeostasis, and Reward System


What is the purpose of two cell divisions in meiosis?

For developing a 2N cell, we need a N cell from each parent. In any division(meiosos or meitosis), chromosomes are doubled at first. In firs meiosis a 2N cell in divided into two N cells and as you know these N chromosomes are doubled( 2N chromatids). In second meiosis a N cell is divided into two N cells but this time chromosomes are not doubled(in fact N chromatid cells)
1.Firs division in meiosis is needed because we need N cells to combine, if they are 2N the result of recombination is a 4N cell.
2.Maybe your question is: why a 2N cell is not directly divided into two N cells without doubling? the reason is same in mitosis and meiosos, it is because of a stage of division as you know it is called anaphase in which a kind of protein, connects centromer to centriol, this stage is needed because we need one chromatid of each chromosome in each cells so if this part is not done there is no guarantee to have all N chromosomes in both cells and in fact a kind of distribution is made.
( I hope that I could understand you, well.)


Crossing white eyed Drosophila with sepia eye

I posted this on Reddit as well, so credit to km1116 for working this out. Here is his response which follows my original logic (though I'm not sure if he is right):

  female x male:

  w x se

  F1: wild-type females and white males

  F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males, 1/4
  white-eyed females, 3/16 wild-type females, 1/16 sepia females

  se x w

  F1: all wild-type offspring

  F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males; 3/8
  wild-type females, 1/8 sepia females

  wt x dp (either direction)

  F1: all wild-type

  F2: 3/4 wild-type, 1/4 dumpy

My rationale for his answer is the genotype of the cross looks like this:

XwYNN with XWXW nn , where "W" is normal eyes, "w" is white", N is Wildtype and n is sepia.


Why haven't land animals evolved beyond urination?

It is probably true that toilets and other resting-ish area are always a great place to think about biology, I agree $\ddot \smile$.

Why do we urinate?

In short, urine contains the waste from our blood while defecation is just the stuff that we haven't digested. Kidneys are the organs responsible for draining wastes (mostly nitrogen-containing, or nitrogenous, wastes) from our blood.

Trade-off: energy cost vs. water loss

You're correct that the loss of water through urination is a considerable cost for an organism (especially those living in dry environments). But the amount of water used to excrete nitrogenous wastes is negatively correlated with the energy it costs to perform this excretion. In other words, there is a trade-off between water and energy loss during nitrogen excretion. Also, the question of toxicity is important.

Three ways to excrete nitrogenous wastes

Animals basically have three choices to excrete nitrogenous wastes:

Uric acid (excreted by uricotelic organisms)

Solid (crystal) with low water solubility
Low toxicity
Little water is needed
Lots of energy is needed

Ammonia (excreted by aminotelic organisms)

Highly soluble in water
High toxicity
Lots of water is needed to dilute it because of the toxicity
Not much energy is needed

Urea (excreted by ureotelic organisms)

Solid but highly soluble in water
"medium" amount of water is needed
"medium" toxicity
"medium" amount of energy is needed

What method is most beneficial for a given individual?

The amount of energy and the availability of water are very important aspects to understand whether a species is ureotelic, aminotelic or uricotelic. Another developmental constraint must be considered too. For example, birds are uricotelic (uric acid) probably because during the development of the embryo the wastes cannot be excreted outside the egg and therefore, excreting uric acid allows to greatly decrease the toxicity of the embryo's environment. In short, we must consider

Water availability
energy loss
developmental constraints

Note: This domain is not at all my field of study and I have no reference, typically for what concerns the toxicity, water amount and energy amount. One should not take my words for granted!


I take it that the question is about the mis-shapenness of the apple, that the stick we see in the dip is the core. The morphology (shape) of fruits such as apple and pear are very sensitive to how well the fruit was pollinated. As we know there can be a variable number of seeds in an apple, but the important fact determining shape is that there should be viable seed develop in each of the five seed pockets resulting in balanced development of the fruit. If the pollination is poor and only a few embryo seeds are fertilized, then the development of the surrounding flesh will favour the pockets that contain viable seed, resulting in possibly mis-shapen fruit. Once you have wondered enough and decide to eat, cut open carefully and on the small side you should see that the seeds are either too few, non-existent or failed to develop.


How does the number of chromosomes evolve through generations?

A mutation is a general term referring to any alteration of a nucleotidic sequence. It includes small mutations like indels (insertion or deletion of a single nucleotide) and substitutions, or bigger mutations such as e.g. chromosome fusions, whole chromosome duplications, Robertsonian translocation, whole genome duplications and gene deletions. Some of these bigger mutations can affect the number of chromosomes (and ploidy number).

Such of these mutations can typically be caused by the non-disjunction of homologous chromosomes during meiosis.

Most of these mutations are deleterious but some aren't and might eventually fix (fixation = reach a frequency of 1.0) in the population.

A very common example of such mutations in humans is the mutation that is causing the Down syndrome.


Method for preparation of LB agar plates with Ag+?

You add the silver after autoclaving. Just make sure that you make your stock concentration of silver in sterile water to avoid unwanted contamination. Do it in liquid form; it is easier to dilute from a stock.


Source of information

See the post The best free and most up to date phylogenetic tree on the internet? for info about how to find such information.

Generally speaking, you might be interested in an intro to phylogenetics such as the one provided in this answer for example.

Where are dinosaurs in the tree of life?

Dinosaurs fall within the Reptiliomorpha clade. Please note that Reptiliomorpha does not quite correspond to what we today call reptiles. Please see the post If dinosaurs could have feathers, would they still be reptiles?

Reptiliomorpha is the sister clade to Amphibia (from here) which contain all living amphibians.

If you look within the Amniota, you will find all of the following

Here, you see that turtles and mammals are an off-shoot of Diapsida. So dinosaurs are not mammals and there are not closely related to turtles. Now if you click on Diapsida you will find ...

the Archosauromorpha which contains all crocodiles, birds and dinosaurs. You can keep going to find Therapoda which contains many dinosaurs and birds. You can keep going like this for yourself and discover the entire tree of life!

Reacting to your sentences

  What did dinosaurs evolve from?

When asking this question, please do not forget that no species evolved from an extant species. If this is unclear to you, you should have a look at this post.

  Was it the reptiles that evolved from amphibians?

Well... the term reptile is a mess because it does not represent a monophyletic group (see this post). If you do not understand the term monophyletic, then you should have a look at this answer.

  Amphibians evolved from fish...

Well... sure. However, fish is also not monophyletic so it is misleading. Also, I am afraid when you say "Amphibians evolved from fish" that you are thinking of modern extant fish which would be wrong.

  reptiles from amphibians...

Nope, this is wrong. Reptiles and amphibians are sister(-ish) clades.

  dinosaurs from reptiles (?)...

This is more or less true although again, do not think of modern reptiles and also, reptiles is a mess because it is not a monophyletic group. But Dinosaurs are Reptilia

  and birds from dinosaurs.

Yes, this is pretty much true.

Note generally though that it is misleading to say "birds evolved from dinosaurs", "humans evolved from apes" and "mammals evolved from vertebrates". It is more correct to say "birds are dinosaurs", "humans are apes" and "mammals are vertebrates". I would be even better to use the latin names to avoid confusion with misuse of these words in the popular culture.


One of the simplest measures of photosynthesis is just measuring how much your plants grow (i.e., weigh them). Of course this technique is imperfect because of other influences on growth, the amount of time you have to wait to get a measurable change, and ideally you would want to use the dry mass of your plants to avoid water content differences, but you have opted to exclude the methods that get around those problems.


Deduce length order of 4 decapeptides based on the Ramachandran plot

When φ = ψ = 180° the peptide is in the fully extended conformation i.e. it is the 'longest' it can be.

If it isn't possible to deduce a length order based on this information then I guess you will have to do some geometry to calculate the sums of the distances between the α C atoms using the known values for all of the bond angles - sounds laborious to me!

This site tabulates values of φ/ψ for typical structures (helix, sheet, turn) so it may be possible to decide if some of peptides are adopting these.


Is there any biological reason for humans to rest after x days of work?

I think your main assumption is not true -- we do not really rest on weekends.

I do not know many people who only rest on weekends. Usually this is the time for socializing, doing home-related work, physical activity (sports, hiking), spending time with your kids, all of which is often almost the opposite of a rest.


Is the salt obtained from meat (as the primary diet) nutritionally sufficient?

Hunter-gatherers rarely if ever added salt to their foods, and studies of salt-free Yanomamo Indians have shown these indigenous people to maintain low blood pressures that do not increase with aging (Oliver et al, 1975).

--The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. European Journal of Clinical Nutrition (2002) 56, Suppl 1, S42–S52 (PDF link)

(The Yanomamo Indians were/are hunter-gatherers, but that doesn't necessarily mean their diet was mainly meat - plants and fruits are important components. However, meat is likely to be higher in salt than plants, so this just supports the general principle.)


What is this insect flying in my Los Angeles bathroom?

Looks like the common clothes moth (Tineola bisselliella). And, yes, the larvae (caterpillars) are likely the source of the holes in your shirts. You can purchase traps online or from hardware stores, or you can go the pesticide route if necessary (e.g., Delta Dust is available from online retailers).
See this site for further info, or search the web for more info on this species. https://en.wikipedia.org/wiki/Tineola_bisselliella


In Drosophila, Toll receptors are used during embryonic development as well as innate immunity. See The Drosophila Toll Signaling Pathway by Valance, et. al.

Toll-like Receptors are pattern recognition receptors found in organisms other than Drosophila that recognize common motifs found on pathogens.

Toll receptors were first discovered in Drosophila and orthologous receptors were then found in many other organisms, not only Human. Both will transduce signaling and will lead to transcription of genes.


What are the effects of oxygen toxicity in human blood?

This is from a Wikipedia article:

Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness.
Oxygen toxicity - Wikipedia
https://en.wikipedia.org/wiki/Oxygen_toxicity

It says there's hemolysis of red blood cells - i.e., they lyse = break open.


Term of the type xxx-troph for a compound not used by an organism

Perhaps you're looking for the word mixotroph?

A mixotroph is an organism that can use a mix of different sources of energy and carbon.

In other words, as stated by Schoonhoven (2010):

The capability of one organism to be autotrophic and heterotrophic at the
same time.


Does bioluminescence occur in humans too?

From the article you linked:

  virtually all living organisms emit extremely weak light, spontaneously without external photoexcitation. This biophoton emission is categorized in different phenomena of light emission from bioluminescence, and is believed to be a by-product of biochemical reactions in which excited molecules are produced from bioenergetic processes that involves active oxygen species

They reference these two works. The first is a 1988 review from Popp et al. (1988):

Biophoton emission - Experientia 44:543–600. (sorry, I cannot find the link to a full text...)

Fritz-Albert Popp is the biophysicist who first developed the biophoton theory.

The second work they reference is by the same first author:

In vivo imaging of spontaneous ultraweak photon emission from a rat's brain correlated with cerebral energy metabolism and oxidative stress. - Kobayashi M, et al.

Finally, a search in Pubmed reveals various other articles by different authors studying different species.


Differences between synaptic connections

Neurons are all about specialized structures having specialized roles. You've given a good justification for dendrites---an efficient way to fit lots of connections in a small space. A pyramidal neuron in cortex, for instance, will have tens of thousands of synapses. If you only had axosomatic connections, the soma would have to be enormous to fit all of them (and this would cause lots of other issues).

Dendritic structure also allows the cell more efficient electrical properties (see cable theory) and to process inputs independently. In fact, different parts of the dendrite are now thought of as independent computational compartments. For instance, the cell might want to selectively strengthen a single synapse or all the synapses on one dendritic branch. By physically isolating those synapses in small dendritic structures, it is easier to make those targeted changes without unwanted "crosstalk" on other synapses or cell activities. What's more, incoming connections from different areas often segregate into regions of the dendrite (e.g. in CA1 hippocampal pyramidal neurons, cortical connections to the most distant part of the dendrite, internal hippocampal connections to the part of the dendrite closer to the soma).

When a cell has a large dendrite (some neurons have no dendrites), its useful to think of axodendritic synapses as the normal inputs that contribute to fine-grained computation, and axosomatic and axoaxonic synapses as more global gates. These latter types take advantage of their location to short circuit the "normal" computation in the dendrites. An inhibitory axosomatic synapse, for example, will reduce the effect of all dendritic inputs when activated.


Why is polyploidy lethal for some organisms while for others is not?

Great question, and one about which there has historically been a lot of speculation, and there is currently a lot of misinformation. I will first address the two answers given by other users, which are both incorrect but have been historically suggested by scientists. Then I will try to explain the current understanding (which is not simple or complete). My answer is derived directly from the literature, and in particular from Mable (2004), which in turn is part of the 2004 special issue of the Biological Journal of the Linnean Society tackling the subject.

The 'sex' answer...

In 1925 HJ Muller addressed this question in a famous paper, "Why polyploidy is rarer in animals than in plants" (Muller, 1925). Muller briefly described the phenomenon that polyploidy was frequently observed in plants, but rarely in animals. The explanation, he said, was simple (and is approximate to that described in Matthew Piziak's answer):

  animals usually have two sexes which are differentiated by means of a process involving the diploid mechanism of segregation and combination whereas plants-at least the higher plants-are usually hermaphroditic.

Muller then elaborated with three explanations of the mechanism:

He assumed that triploidy was usually the intermediate step in chromosome duplication. This would cause problems, because if most animals' sex was determined by the ratios of chromosomes (as in Drosophila), triploidy would lead to sterility.
In the rare cases when a tetraploid was accidentally created, it would have to breed with diploids, and this would result in a (presumably sterile) triploid.
If, by chance, two tetraploids were to arise and mate, they would be at a disadvantage because, he said, they would be randomly allocated sex chromosomes and this would lead to a higher proportion of non-viable offspring, and thus the polyploid line would be outcompeted by the diploid.

Unfortunately, whilst the first two points are valid facts about polyploids, the third point is incorrect. A major flaw with Muller's explanation is that it only applies to animals with chromosomal ratio-based sex determination, which we have since discovered is actually relatively few animals. In 1925 there was comparatively little systematic study of life, so we really didn't know what proportion of plant or animal taxa showed polyploidy. Muller's answer doesn't explain why most animals, e.g. those with Y-dominant sex determination, exhibit relatively little polyploidy. Another line of evidence disproving Muller's answer is that, in fact, polyploidy is very common among dioecious plants (those with separate male and female plants; e.g. Westergaard, 1958), while Muller's theory predicts that prevalence in this group should be as low as in animals.

The 'complexity' answer...

Another answer with some historical clout is the one given by Daniel Standage in his answer, and has been given by various scientists over the years (e.g. Stebbins, 1950). This answer states that animals are more complex than plants, so complex that their molecular machinery is much more finely balanced and is disturbed by having multiple genome copies.

This answer has been soundly rejected (e.g. by Orr, 1990) on the basis of two key facts. Firstly, whilst polyploidy is unusual in animals, it does occur. Various animals with hermaphroditic or parthenogenetic modes of reproduction frequently show polyploidy. There are also examples of Mammalian polyploidy (e.g. Gallardo et al., 2004). In addition, polyploidy can be artificially induced in a wide range of animal species, with no deleterious effects (in fact it often causes something akin to hybrid vigour; Jackson, 1976).

It's also worth noting here that since the 1960s Susumo Ohno (e.g. Ohno et al. 1968; Ohno 1970; Ohno 1999) has been proposing that vertebrate evolution involved multiple whole-genome duplication events (in addition to smaller duplications). There is now significant evidence to support this idea, reviewed in Furlong & Holland (2004). If true, it further highlights that animals being more complex (itself a large, and in my view false, assumption) does not preclude polyploidy.

The modern synthesis...

And so to the present day. As reviewed in Mable (2004), it is now thought that:

Polyploidy is an important evolutionary mechanism which was and is probably responsible for a great deal of biological diversity.
Polyploidy arises easily in both animals and plants, but reproductive strategies might prevent it from propagating in certain circumstances, rather than any reduction in fitness resulting from the genome duplication.
Polyploidy may be more prevalent in animals than previously expected, and the imbalance in data arises from the fact that cytogenetics (i.e. chromosome counting) of large populations of wild specimens is a very common practise in botany, and very uncommon in zoology.

In addition, there are now several new suspected factors involved in ploidy which are currently being investigated:

Polyploidy is more common in species from high latitudes (temperate climates) and high altitudes (Soltis & Soltis, 1999). Polyploidy frequently occurs by the production of unreduced gametes (through meiotic non-disjunction), and it has been shown that unreduced gametes are produced with higher frequency in response to environmental fluctuations. This predicts that polyploidy should be more likely to occur in the first place in fluctuating environments (which are more common at higher latitudes and altitudes).
Triploid individuals, the most likely initial result of a genome duplication event, in animals and plants often die before reaching sexual maturity, or have low fertility. However, if triploid individuals do reproduce, there is a chance of even-ploid (fertile) individuals resulting. This probability is increased if the species produces large numbers of both male and female gametes, or has some mechanism of bypassing the triploid individual stage. This may largely explain why many species with 'alternative' sexual modes (apomictic, automictic, unisexual, or gynogenetic) show polyploidy, as they can keep replicating tetraploids, thus increasing the chance that eventually a sexual encounter with another tetraploid will create a new polyploid line. In this way, non-sexual species may be a crucial evolutionary intermediate in generating sexual polyploid species. Species with external fertilisation are more likely to establish polyploid lines - a greater proportion of gametes are involved in fertilisation events and therefore two tetraploid gametes are more likely to meet.
Finally, polyploidy is more likely to occur in species with assortative mixing. That is, when a tetraploid gamete is formed, if the genome duplication somehow affects the individual so as to make it more likely that it will be fertilised by another tetraploid, then it is more likely that a polyploid line will be established. Thus it may be partly down to evolutionary chance as to how easily a species' reproductive traits are affected. For example in plants, tetraploids often have larger flowers or other organs, and thus are preferentially attractive to pollinators. In frogs, genome duplication leads to changes in the vocal apparatus which can lead to immediate reproductive isolation of polyploids.

References

Furlong, R.F. & Holland, P.W.H. (2004) Polyploidy in vertebrate ancestry: Ohno and beyond. Biological Journal of the Linnean Society. 82 (4), 425–430.
Gallardo, M.H., Kausel, G., Jiménez, A., Bacquet, C., González, C., Figueroa, J., Köhler, N. & Ojeda, R. (2004) Whole-genome duplications in South American desert rodents (Octodontidae). Biological Journal of the Linnean Society. 82 (4), 443–451.
Jackson, R.C. (1976) Evolution and Systematic Significance of Polyploidy. Annual Review of Ecology and Systematics. 7209–234.
Mable, B.K. (2004) ‘Why polyploidy is rarer in animals than in plants’: myths and mechanisms. Biological Journal of the Linnean Society. 82 (4), 453–466.
Muller, H.J. (1925) Why Polyploidy is Rarer in Animals Than in Plants. The American Naturalist. 59 (663), 346–353.
Ohno, S. (1970) Evolution by gene duplication.
Ohno, S. (1999) Gene duplication and the uniqueness of vertebrate genomes circa 1970–1999. Seminars in Cell & Developmental Biology. 10 (5), 517–522.
Ohno, S., Wolf, U. & Atkin, N.B. (1968) EVOLUTION FROM FISH TO MAMMALS BY GENE DUPLICATION. Hereditas. 59 (1), 169–187.
Orr, H.A. (1990) ‘Why Polyploidy is Rarer in Animals Than in Plants’ Revisited. The American Naturalist. 136 (6), 759–770.
Soltis, D.E. & Soltis, P.S. (1999) Polyploidy: recurrent formation and genome evolution. Trends in Ecology & Evolution. 14 (9), 348–352.
Stebbins, C.L. (1950) Variation and evolution in plants.
Westergaard, M. (1958) The Mechanism of Sex Determination in Dioecious Flowering Plants. In: Advances in Genetics. Academic Press. pp. 217–281.

(I'll come back and add links to the references later)


Is there a web tool for species identification?

I'm going to go out on a limb and say NO. I'm a professional biologist developing a natural history website, and I've never encountered such a thing.


Embalming solutions for cadaver study differ from institution to institution (and are reportedly somewhat different from embalming for funerals, but I'm not sure of those details). Typically embalming solutions for cadavers meant to be stored indefinitely consist mostly of water with lesser but roughly equal amounts alcohol (usually methanol), gylcerin, phenol, and a smaller percentage of formalin/formaldehyde to prevent mold.

A document from Albert Einstein College of Medicine lists:

Methanol: 11.1%
Glycerin: 11.1%
Phenol: 9.3%
Formaldehyde: 1.9%

If you want to know what your institution uses, you should just ask, and they should be willing and able to tell you.


Osmosis is the diffusion of water.  Pinocytosis is the endocytosis of liquid/water.


How to convert a genus name to a noun or adjective

I think that it boils down to taking a Latin name and removing the case ending to get an acceptable English adjective. Given that it might be a purely linguistic situation, it's possible another SE site would be better (English language?), but this topic is definitely relevant to biologists, as they're probably the ones who run into it most frequently.
We can look at IAPT article 60.10 and it suggests a systematic way to do this, albeit for an unrelated reason. I don't see that they directly address the anglicized Latin adjective form:

A noun or adjective in a non-final position appears as a compounding form generally obtained by
(a) removing the case ending of the genitive singular (Latin ‑ae, ‑i, ‑us, ‑is; transcribed Greek ‑ou, ‑os, ‑es, ‑as, ‑ous and its equivalent ‑eos) and
(b) before a consonant, adding a connecting vowel (‑i- for Latin elements, ‑o- for Greek elements).

I think that we want to apply step (A) but not step (B) here, as their goal is the formation of compound names, and step A alone will get us -id, which is an anglicized adjectival ending (-idus --> -id).
Taking your examples:

Cambaridae --> remove Latin genitive suffix -ae --> cambarid.
Procambarus --> make Latin noun into the adjective procambaridus --> remove suffix -us --> procambarid.

Unfortunately, it looks like there are a ton of possible Latin adjectival endings- the -id examples seem pretty straightforward because you can get an English adjectival ending directly, but other taxonomic names don't resolve so neatly. For example, if I want to use "Lachnospiraceae" as an adjective, I could imagine the following (applying only step A above doesn't seem to work well: "lachnospirace"):

lachnospiraceid
lachnospiraceal
lachnospiraceous

and I don't really know how to pick among them!
I have left a comment on a blog post from Stephen Heard on a related subject (comment above), perhaps he'll see fit to weigh in here.


Possibility and feasibility of producing designed antibodies with bacteria

I'll preface this by saying that I'm talking about antibodies of mammalian/human origin, consisting of two identical heavy and two identical light chains disulfide-bonded into the classic antibody structure:

It is possible to produce antibody-like molecules known as single-chain antibodies, including single-chain variable fragments (scFv) in bacteria and viruses, where it is also known as phage display. These hosts can also produce a modified Fab fragment that is engineered as a single polypeptide chain, and multiple other single-chain antibody-like molecules as shown below. In the past, this has primarily been done in E. coli, as they are a common tool used in protein expression, and have many advantages as an experimental system in general. However, single-chain antibody production in E. coli is hampered by the fact that these exogenous proteins tend to form inclusion bodies instead of being secreted into the medium, where they can be collected and purified much more easily, without the need for lysing the host cells. The paper you linked to describes a method for producing scFvs in the Gram-positive bacterium Bacillus megaterium, which is becoming more common for the production of recombinant proteins.

So, it is possible to produce antibody-like molecules in bacteria. However, unlike insulin, full-length antibodies are made up of multiple polypeptide chains, and are both glycosylated and disulfide-bonded. While there is evidence that bacteria can accomplish both of these biochemical tasks, the processes seem to require additional chaperone, trafficking, and regulatory proteins that bacteria do not possess, and as far as I know scientists have so far not been successful in producing full "proper" antibody molecules in prokaryotes.

However, there are many mammalian/human expression systems for producing fully functional recombinant antibodies in very high yield, and a number of FDA-approved monoclonal antibody drugs are now on the market, with many more in various stages of development and clinical trials.


There's a 2003 paper published in the Journal of Korean Medical Science describing a case of a 'homunculus' within a teratoma: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055135/

It contained some hair, brain tissues, cranial and other bones, but no internal organs.


If you look on a very basic plasmid map, you usually see three different features: An origin of replication (often abbreviated ori or origin) which is necessary for the replication of the plasmid, a resistance gene (not necessary but useful to select for) and and multi cloning site (abbreviated MCS) which contains a number of unique restriction enzyme recognition sites, see the figure (from here):

In molecular biology plasmids are used to overexpress proteins in bacteria (or other cells) which are of any interest. To do this, you bring in the coding information for this gene into the plasmid using the MCS. Here you can cut the plasmid controlled (only open the ring on one site) and insert DNA of interest. An empty plasmid in this context means that it can readily used for cloning purposes as it does not contain any foreign DNA.


Resource plant anatomy/lifecycle vocabulary

specifically development-focused

An Introduction to Plant Structure and Development by Beck looks comprehensive and has been well-reviewed. It has both photos and diagrams, and sections certainly deal specifically with growth/lifecycle. It's available to preview or purchase as an ebook on Google Play.

more general plant anatomy vocabulary resources

In print, Plant Identification Terminology: an illustrated glossary by Harris and Harris is a fairly standard reference, and I've found it very useful both for looking up terms and for just flipping through.

Online, but with fewer diagrams, you could try the Glossary page on the Angiosperm Phylogeny Website.

This might sound silly, but if you're looking for more of a course on the fundamentals rather than a dictionary of the specifics, the Botany Coloring Book is actually a great, seriously useful work.


RNA and proteins are not electrical systems, but the idea of translating a signal between incompatible systems can be applied here.

Proteins are made through a process called Translation, where instructions stored in a piece of mRNA are used by the Ribosome to make protein.

tRNAs adapt the mRNA nucleotide sequence into a protein's peptide sequence by acting as an intermediary. A tRNA is charged by attaching an amino acid to one end, it then binds the ribosome mRNA complex at the position defined by a codon. A codon is a sequence of 3 nucleotides that codes for an amino acid.

You could think of the tRNA being like a SD Card to USB adaptor to get information from one device to another.


How do scientists know what part of DNA does what?

This is a tough question (scientifically)! Generally speaking, it's impossible to look at a DNA sequence and predict what function it might have. It's easier to go backwards: identify a function/trait of interest, figure out what proteins are necessary for that function, and then deduce the sequence.

I'll describe one strategy to go from protein to gene, and name some techniques which you can read up on if you want to learn more.

To find the amino acid sequence of a protein, you can chop it up using proteolytic enzymes. This gives you fragments of varying lengths, since the enzymes will cut semi-randomly at different sites in the protein. Run these fragments on chromatographic paper. You can deduce the amino acid sequence from the pattern, because larger fragments will move slower. This is the same idea behind Sanger sequencing (aka chain termination sequencing) of DNA, and was invented by the same guy.

If you know what the amino acid sequence is, you now know the mRNA sequence, since protein is translated from mRNA. However, in eukaryotes, you don't know the DNA sequence, since we have introns - i.e. bits of the sequence which get cut out between transcription and translation. We need a way to get from mRNA (protein precursor) to DNA (gene).

To do this, purify mRNA from a cell and generate a library of complementary DNA (cDNA) using reverse transcriptase. Then, sequence the cDNA library to generate expressed sequence tags (ESTs), which are subsets of the full cDNA sequence. Because the ESTs are subsets of the sequence instead of the full transcript, it's possible to "CTRL+F" the organism's genome and find the gene which contains the EST.

Scientists have been doing this for decades, so nowadays you can search a gene/protein database and instantly know which sequence is responsible for, say, a specific channel protein.

To go in the other direction from gene to protein to function/trait, you have to do a fair bit of legwork as well. In very, very simplistic terms, you "cut" some DNA, put it into a package, and deliver the package to your favorite organism. As you said, it's a bit more complicated than that. :)

For complex, polygenic traits, it's harder to (1) identify the genes responsible and (2) successfully engineer an organism to have all of those new genes. You're unlikely to see a human with tiger legs any time soon. It's much easier to give an organism a few genes that confer very specific traits. Look at this list of genetic modifications to crops and click on one of the traits; usually only 1-3 genes have been introduced.


No obviously inactivating variants are found in this gene, which provides at least negative data (humans generally seem to have at least somewhat functional ACE2). Exome sequencing across >200K humans has found a series of variants, mostly low-frequency, in the population.
Some of these variants may affect gene function, but it is not clear how, and none of them are obviously complete loss of function variants (e.g. nonsense mutations).
A more complete analysis of the data, including e.g. CNVs, might be necessary to fully address this question.


Herbivorous plants that consume falling leaves

Many plants do this, with varying degrees of specialization - for some it is perhaps incidental, others have evolved this strategy to gain nutrients (often water as well). You are probably thinking of bromeliads, a diverse group of plants in which many species have specialized leaves that form cups at the base to collect water and litter. These structures, a type of phytotelmata, have similarities to some carnivorous plant traps.

These tank bromeliads are able to efficiently absorb nutrients from animal or plant matter which falls into the tank:

  Considerable absorbed nitrogen is mobilized in the rosette center. Tested bromeliads appear to be well equipped to utilize minerals and organic nitrogen originating from tank-impounded plant and animal debris as nutrients.

This litter catching habit occurs in other lithophytic and epiphytic plants, i.e. those which don't grow in soil, because it allows them to capture nutrients when growing on rocks or trees. Examples include the staghorns/elkhorns and basket ferns:

  They form a characteristic 'basket' that collect litter and organic debris, hence the common name. The collected debris decompose into humus, providing the plants with nutrients it would otherwise not have received from being suspended above the ground.


What is the difference between a polysaccharide and a macromolecule?

A macromolecule is a class of biomolecules that are made of monomers. These include polysaccharides (i.e. sugars) polypeptides (i.e. proteins) nucleic acids (like DNA and RNA) and lipids (fats ans phospholipids).

A polysaccharide is one type of macromolecule made up of monosaccharides like glucose and fructose. An example of a polysaccharide is starch or cellulose.


What is this grainy surface on my two-week-old sourdough starter?

Naturally, when you create dough you expect it to rise in size the following few days. That's just a chemical reaction that allows air to enter the dough body and traps it in tiny bubbles. My theory is that if the dough is not as high as expected that the air has escaped it because of the extra time you left it.

The pattern is not unusual and is the result of the deflation I'm talking about.

It's probably still safe to eat, but the bread won't be as good(eat at your own risk)


Unfortunately the term "wave" is ambiguous in neuroscience. What you are referring to, alpha waves, only means that neuronal activity tends to oscillate at about 10Hz. Neural oscillations are a widespread phenomena occurring in all brain areas. But it doesn't necessarily mean these waves travels. There are examples of traveling waves, whose speed can vary a lot (from $10^{-1}$ to $10^{-5}\ m.s^{-1}$ depending on the studies). Oscillations across brain areas tends to be synchronized during a task (so one could argue, infinite speed), and within area activity tends to hold a specific phase relationship which varies spatially (as if a wave was "frozen", in which case its speed would be 0). Traveling waves and neural synchrony/coherence might be different phenomena implementing different functions. It is still unclear what brain oscillations are for, or even if they have any purpose at all. Below are some reviews on these topics.

Ermentrout, G.B. and Kleinfeld, D. (2001) Traveling electrical waves in cortex: insights from phase dynamics and speculation on a computational role. Neuron 29, 33–44

Sato, T. K., Nauhaus, I., & Carandini, M. (2012). Traveling waves in visual cortex. Neuron, 75(2), 218-229.

Engel, A. K., Fries, P., & Singer, W. (2001). Dynamic predictions: oscillations and synchrony in top–down processing. Nature Reviews Neuroscience, 2(10), 704-716.

Fries, P. (2005). A mechanism for cognitive dynamics: neuronal communication through neuronal coherence. Trends in cognitive sciences, 9(10), 474-480.


Dilute DNA plasmids with distilled water

Buffer EB is simply 10mM Tris buffer, ph 8.5. I think you are worried about the ions present in your electroporation. There are two things to consider:

What is the concentration of your DNA and how much do you need for the electroporation?
In which final volume is the electroporation taking place?

In my experience, usually you add a very small amount of DNA (a few microliters) to 100, 250 or 400µl (depending on the cuvettes used) final volume. Here a tiny amount of Tris does not interfere or cause a short circuit.


Extract protein sequences from a GBK(GenBank) file without scripting

My colleagues and I have recently published a toolbox of command-line utilities that are modeled after GNU Textutils (e.g. grep, cut, tr, uniq) called FAST: Fast Analysis of Sequences  (cite).

To install FAST you can use:

perl -MCPAN -e 'install FAST'

Or install the current development version from github. The FAST install comes with a cookbook, sample dataset and all utilities have man pages. The cookbook is also available on the github wiki.

To convert the features annotated in a genbank file to fastA sequences you can use gbfcut. Below are examples of using gbfcut:

To convert all annotated features of a genbank file to fastA format:

gbfcut genbank-file

Output only tRNA features:

gbfcut -k tRNA genbank-file

Output all feature sequences with a "note" qualifier containing "telomere":

gbfcut -q note=telomere genebank-file


Calculating sample concentration factor (opposite of dilution)

Your original sample is more dilute than the sample you counted. The concentration is less and therefore you should divide your counted concentration by 10 to get the concentration in the original sample.


Datasets of aligned nucleotide sequences

You can find 46-way multiz alignment from UCSC genome browser, it is down on comparative genomics part and labelled as "cons 46-way", which is a genome alignment of 46 vertebrate species. You can use data on their genome browser on the site, or get download information here.

If you are interested in pair-wise alignments, I don't know of any pair-wise alignment database, but in fact you don't need one. You can search for nucleotide sequences from NCBI nucleotide database and align them using BLAST on their website. BLAST is maybe the most common tool for pair-wise alignments and also for database alignment searches, where a single query sequence is searched for matches throughout a database of sequences. If you want to do a large number of alignments, you can download BLAST to your computer to do them faster.


Did the hyoid bone of Australipetichus afarensis have a hyoid bulla?

Short answer:

Yes.

Longer but still short answer:

H. heidelbergensis and H. neanderthalensis have a modern human-like hyoid bone. A. afarensis has a hyoid bulla similar to modern chimpanzees.

The hyoid bone is thought by some to be important in human evolution because of its position in the throat and the possibility that morphological changes in the hyoid were important for the development of speech. However, this view is not without controversy, and it is probably not sufficient to use hyoid bone morphology as a definitive marker for development of speech similar to modern humans, though it may be suggestive.

Some quotes from two references on the morphology of the hyoid of A. afarensis:

Alemseged, et al. 2006:

  [the hyoid of A. afarensis] "...is
  most similar to that of juvenile African apes, and unlike that of
  modern humans11,12. The exposed greater horn is slender, and the
  body is expanded anteriorly, forming a bulla that is deep relative to its
  breadth and height..."

Steele, et al. 2013:

  "...the Dikika juvenile australopith hyoid is deep for its height (Figure 9) and width and is morphologically chimpanzee-like. This similarity applies both when comparing only subadults from the three extant species (Figure 9A), and when comparing across all observed age classes (Figure 9B..."

References:

Alemseged, Z., Spoor, F., Kimbel, W. H., Bobe, R., Geraads, D., Reed, D., & Wynn, J. G. (2006). A juvenile early hominin skeleton from Dikika, Ethiopia. Nature, 443(7109), 296-301.

Steele, J., Clegg, M., & Martelli, S. (2013). Comparative morphology of the hominin and african ape hyoid bone, a possible marker of the evolution of speech. Human biology, 85(5), 639-672.


Why does enteral carbohydrate yield higher energy than parenteral?

Parenteral carbohydrate is usually dextrose which is actually D-Glucose monohydrate. Monohydrate implies coupling with a water molecule, such that 1 gram contains a lower relative component of glucose, resulting in a lower kcal yield.


Why do mammals produce more carbon dioxide than insects?

As you said, endothermic animals such as mammmals or birds consume more energy and therefore expelmore CO2 not only because of a higher betabolic rate or to keep warm, but also because they are more active. Even taking all that into account you are missing the biggest difference between them: size. The consumption of energy is not directly related to the size, in fact, the energy requirements drop exponentially with the reduction of size. The same phenomenon explains why they are far stronger, fall-resisting...


If the brain has no pain receptors, how come you can get a headache?

Brain, indeed, cannot feel pain, as it lacks pain receptors (nociceptors). However, what you feel when you have a headache is not your brain hurting -- there are plenty of other areas in your head and neck that do have nociceptors which can perceive pain, and they literally cause the headaches.

In especially, many types of headaches are generally thought to have a neurovascular background, and the responsible pain receptors are associated with blood vessels. However, the pathophysiology of migraines and headaches is still poorly understood.


Do conservation oriented genetic database exist?

First, it isn't entirely clear to me why you would want such a database.  Essentially all sequences are available in one (typically all) of the big databases.

For example if I search the NCBI database for "extinct" I get this.  There will be many more sequences for species that are "only" endangered.

Second, having a genome sequence isn't sufficient for "de-extinction" of a species.  The reasons for this are beyond the scope of this question, but can be explored starting from this section of the wikipedia article.

You will likely also find this discussion to be of interest.


A few possible explanations are named in the Wikipedia article you link:

  Regarding spontaneous or natural monozygotic twinning, a recent theory
  posits that monozygotic twins are formed after a blastocyst
  essentially collapses, splitting the progenitor cells (those that
  contain the body's fundamental genetic material) in half, leaving the
  same genetic material divided in two on opposite sides of the embryo.
  Eventually, two separate fetuses develop. Spontaneous division of
  the zygote into two embryos is not considered to be a hereditary
  trait, but rather a spontaneous or random event.

  Monozygotic twins may also be created artificially by embryo
  splitting. It can be used as an expansion of IVF to increase the
  number of available embryos for embryo transfer.

Interesting references for this are:

"The epidemiology of multiple births"
Twinning.
On the possible cause of monozygotic twinning: lessons from the
9-banded armadillo and from assisted reproduction.
Monozygotic twinning associated with assisted reproductive
technologies: a review.
Developmental biology: Two by two (on overview article conatining a
lot of other references)


Additive genetic variance components from LMER in R

From what I understood of your code and what you are asking I am guessing that you do the following:

Generating a virtual set of 40 individuals (lines) of which you have 200 measurements (repetitions). You say that they are full siblings, so they share both parents. Then you use the lmer function (which I am not familiar with) to give you the total variance, within-group variance and between-group variance, ($V_{T}, V_W, V_B$ respectively). What you call $V_L$ would be the $V_W$.

We know that $V_P=V_A+V_D+V_E$

In full siblings we also know that $V(A,A')=\frac{1}2V_A+\frac{1}4V_D$ where $A$ is the additive value and $D$ is the dominance value because they share a quarter of their gene combinations.

If you are treating with full siblings the $V_W$ should be then the $V_E$ and the $V_B$ would be the $\frac{1}2V_A+\frac{1}4V_D$ as you are seeing the variance between siblings.

So no, you are not calculating correctly the $V_A$ because you are missing your $V_D$ on your counting. The code itself looks fine for what I understood, but maybe you should take that to corssvalidated with the R tag


Identify the fluff that I have found in tea

It's kind of hard to tell from the picture, but maybe it's a variety of Milkweed seed-pod that got into the tea?


Does DNA influence death (e.g. by cell aging)

Perhaps the best type of study to examine the role of genes (DNA) in human aging are twin studies.  They have either: the same DNA (monozygotic, one egg, "identical" twins (MZ) ) or similar DNA (dizygotic twins, two eggs (DZ) ) and are perhaps exposed the same, or different environments.   I won't repeat the information in the link, above, but studies of this type guide that our DNA is not an absolute roadmap of our future.

DNA damage can be caused by exposure to excessive radiation, viruses, chemicals and just 'random events'.  Cells and tissues can also be damaged by oxidative damage - literally oxygen and related molecules that are produced within the body and can react with components of cells (e.g DNA, proteins and the lipid cell membrane).   The accumulation of these oxidized products in and around the cell disrupts tissue function and leads to many of the symptoms of aging, a process called sensescence.

We obviously cannot avoid having oxygen around us.  In the same way, our cells need the sugar glucose as a source of energy. Glucose can spontaneously react with proteins and lipids to form advanced glycation endproducts (AGEs).
 AGEs are pro-inflammatory.  In diabetes, where blood glucose levels may remain at higher than normal for extended periods, the formation of AGEs can lead to nerve and kidney damage.   The chemical reaction that is occurring is the same as when you toast a piece of bread or fry a steak.  So paradoxically, two of the ingredients essential for life - oxygen and glucose - are slowly but surely disrupting our body's function over the course of decades.   Although the body can replace some of these damaged proteins, they accumulate over time, as evidenced by the increasing lack of elasticity of older skin as collagen proteins are cross-linked.

Regular exercise, good diet and friendships all add to mental and physical health, quality of life and longevity.  So, to live a long time, don't stress, have ONE slice of cake and make new friends who will exercise with you.


Is it possible to kill parasitic worms by intoxicating oneself?

In summary, there is no convincing evidence to say that alcohol intoxication helps to treat or prevent parasites in humans.

1) The evidence from in vivo human studies does not support the idea that alcohol consumption helps in treating parasites.

Alcoholism and Strongyloides stercoralis: Daily Ethanol Ingestion Has a Positive Correlation with the Frequency of Strongyloides Larvae in the Stools (PLoS, 2010):

  The frequency of Strongyloides was significantly higher in alcoholic
  patients than in control group (overall prevalence in alcoholic 20.5%
  versus 4.4% in control group; p = 0.001).

2) Even a strong alcohol beverage gets diluted when it reaches the intestine.

Ethanol concentrations in the human gastrointestinal tract after intake of alcoholic beverages (European Journal of Pharmaceutical Sciences, 2016):

  In a cross-over study, five fasting volunteers were asked to drink two
  standard consumptions of commercially available alcoholic beverages,
  including beer (Stella Artois®, 500 mL, 5.2% ethanol), wine (Blanc du
  Blanc®, 200 mL, 11% ethanol) and whisky (Gallantry Whisky®, 80 mL, 40%
  ethanol).

  The median gastric ethanol Cmax (min–max) for the beer, wine and
  whisky conditions amounts to 4.1% (3.1–4.1), 4.1% (2.6–7.3) and 11.4%
  (6.3–21.1), respectively...Median duodenal ethanol Cmax (min–max) for
  beer, wine and whisky are 1.97% (0.89–4.3), 2.39% (2.02–5.63) and
  5.94% (3.55–17.71), respectively.

So, the maximal ethanol concentration in the duodenum after drinking 80 mL of whisky was 17.7%. Most of ethanol is absorbed in the first part of the small intestine (Scandinavian Journal of Gastroenterology), so it does not reach the more distant parts and does not likely kill the parasites there.

3) Even strong intoxication is associated with low blood alcohol concentration.

In strong intoxication, your blood alcohol concentration would be only 0.2-0.3%. In one study (Table 1), the 50% lethal concentration (LC50) of ethanol, which killed 50% of the bloodstream forms of the parasites Trypanosoma brucei, was 10.6%.

4) Alcohol intoxication and brain dehydration

Alcohol intoxication or hangover are not automatically associated with dehydration. Anyway, even in severe dehydration, you still have a lot of water in your body, including the brain, so the parasites living there do not necessarily get dehydrated as a result of your dehydration.

In general, dehydration increases the risk of infections, because it dries mucous membranes, for example in the urinary tract (BMJ Open Quality, 2019).