Why nerve fibre is infatiguable?( is my conjecture correct?)

One can imagine that each action potential causes a small amount of $\ce{Na+}$ goes inside the cell, and a small amount $\ce{K+}$ goes outside the cell, thus weakening the electrochemical gradient of both ions. If each action potential has (approximately) the same flux of $\ce{Na+}$ and $\ce{K+}$ then higher frequency of action potentials means more flux, thus a quicker depletion of the electrochemical gradients. The absolute refractory means there is a maximum firing frequency.

Thus the Sodium-Potassium pump only needs to be able to "recharge"  the maximal possible depletion of ion's gradients. If there was no absolute refractory period then theoretically the action potential frequency could be faster than the Sodium-Potassium pump can keep up. A abnormally fast firing rate in theory could deplete the potassium gradient and sodium gradient thus would result in a fatigued neuron.

Edited to add in reference to the conjecture:
Absolute refractory periods are cause by sodium gate inactivation, thus no matter how much current one adds the sodium gates will not open until sodium inactivation ends. However, over long periods of time (in seconds) and in the absences of a ionic pump, the lack of sodium (and potassium) gradients will cause fatigue.

However, "fatigued" neurons may not act like one expects.


The answer is probably No.

"Long" bones - like the tibia, fibula, femur, humerus, etc. grow at the ends during childhood via a special formation called the Epiphyseal plate (also known as "growth plates"). The plates are composed of a special cartilage that grows, and slowly calcifies as a person reaches adulthood.

When the growth plates completely stop expanding is left to genetics, but generally happens 2 years after puberty finishes - about 16 for women and 18 for men. So after those ages there's little, if any, significant growth - though it can happen in very rare cases.

To date there aren't any exercises you can perform that will elongate bones. It doesn't make physiological sense; stretching puts stress on muscles and tendons - not bones. Weight lifting will compress bones, making them more dense and will make you shorter in the long run.

While there's been some success in getting chondrocytes to grow cartilage in vitro, there has yet to be significant gains in vivo, thus there aren't any medications available that would cause growth.

The only widely practiced way of gaining height after adulthood is with very painful surgery that involves a lot of braces. The bones are systematically broken, held in place, and allowed to heal. The setup looks like this:

While we get closer and closer to being able to control such things every day, for the time being (and I wouldn't count on this changing anytime soon) everybody is stuck with the height they were genetically programmed with.

As an aside: Being tall isn't all it's cracked up to be. At ~197cm I can tell you it is hell finding pants that fit.


This looks a lot like a double-barred finch (Taeniopygia bichenovii). Your note about this being an "owl-like" bird is supported by it's less common name, the "owl finch", so named for the dark ring around the face.

 Source: Wikipedia; Credit: Glen Fergus

If this is in fact the bird you saw, you're right that it's not native to your country (or continent or even hemisphere!). The Taeniopygia genus is in the Estrildidae family, and it only contains two species native to Australia! According to Wikipedia, T. bichenovii is found:

  in dry savannah, tropical (lowland) dry grassland and shrubland habitats in northern and eastern Australia

You can read more at eFinch and The Atlas iof Living Australia.


what do I need to use for protein protein interaction network

If you are asking solely about data structure, the two data formats that you have given are essentially the same. Each row represents a PPI, so in a network a line (edge) will link the proteins (nodes) given in columns one and two. Column three is an edge score, but it can indicate a few things,  confidence in the interaction or strength of the interaction. Your network will for a single central node with 5 nodes linked to it in a wheel shape.

PPI networks may also be represented in Proteomics Standards Initiative Molecular Interaction XML Format. This provides a controlled vocabulary for programmatic access to data.

The choice of data structure, there are many, is yours but simple formats (as above) are often sufficient. It is important to be mindful of the meaning of the network, are the PPIs directional? Do you have estimates of interaction (edge) confidence? Do you have estimates of interaction (edge) strength?

Cytoscape will allow you to visualise a protein-protein interaction network (PPI) such as the two that you have given. The Bioconductor project provides a number of options for the visualisation and analysis of PPI networks in R.

If you want to create or build a PPI network from a single protein or list of proteins then Cytoscape, and possibly plugins such as Genemania, can also do that.

String is also useful for building PPI networks. The developers have focussed on a wide-range of species and their data export options will allow you to see the same network in a variety of data formats.


Why do stars disappear when I look at them?

When there is little light, the color-detecting cone cells are not sensitive enough, and all vision is done by rod cells. Cone cells are concentrated in the center of the eye, whereas rod cells are very rare in the center (image source):

When you focus on the star, the light is projected close to the center of the retina, where it will hit few rod cells. Thus the star appears to vanish.


What is meant by `individuals do not evolve, populations do`?

The statement individuals do not evolve, populations do is rooted in the (classical population genetic) definition of evolution. Here is this definition:

  Evolution is a change of allele frequency through time in a population

Evolution is defined for a population, it is not defined for an individual. And it makes intuitive sense once you get more used to how evolution works. For example, the so-called fundamental principle of natural selection states that at any given time, the rate of increase in the population mean fitness is exactly equal to the variance in fitness.

Indeed, evolution is all about phenotypic and genetic variance (for fitness or other phenotypic traits) and without a population to observe, there is no variance. It is within this framework that people say individuals do not evolve, populations do but you are correct that as populations evolve its constituents (the individuals) changes. The sentence has the advantage to reinforce the concept that evolution happens at the level of the population.


I haven't done this exact experiment. I am just deducing from the known facts about PCR.

The product of PF and PR2 will serve as a template for both 1kb product (P1) and 2kb product (P2).

Lets assume that after 2nd cycle there is 1 copy each of P1 and P2 (Delay of 1 cycle to make a smaller length product. See here).

Lets assume that the primer binding affinity is equal (and for just preliminaries consider that only one primer can bind a template — such as in overlapping binding sites). So half of P2 will bind to PR2 and half to PR1.

Number of copies at nth cycle is:

P2(n) = 1.5 × P2(n-1)

P1(n) = 2 × P1(n-1) + 0.5 × P2(n-2)

However this is not really the scenario; the primers are not competing for the template.
Which means that both primers can bind to the substrate simultaneously.

DNA polymerases (except Klenow) will remove any DNA strand bound to the template, ahead of it. In that case P1 will not form. But when PR2 runs out, the unused PR1 can produce P1.

Now there are additional factors, such as the distance between PR1 and PR2 binding sites. If the distance between the primer binding sites is less than the smaller product then the abovementioned case occurs. If the inter-primer distance is larger than smaller product then both products will form (and just like the competing primers case, P2 will serve as a template for both products). In this case the copy numbers will be:

P2(n) = 2 × P2(n-1)

P1(n) = 2 × P1(n-1) + 1 × P2(n-2)

This means that P1 will dominate.

Other assumptions:

No limiting concentrations of dNTP, primers etc
PCR efficiencies are equal for both primers and is equal to 2 (in non-competing cases)
Primer annealing temperatures are same i.e binding affinities are same.


How many cells should be seeded for passaging?

This answer is relevant in case of cell lines and not so much for primary cultures

When I first started doing cell culture, I used to count the cells before passaging. The idea is to seed enough cells to keep the population viable but not so much that you have to re-passage within 2 days. However as I became good with the technique I stopped counting as I would have a decent estimate of how much to seed. For seeding cells for some experiments (transfection/drug treatment etc) it is crucial to count the cells.

How much to seed depends on what the division time of the cell type is and how much you need after a given duration of time. You have to calculate it accordingly. For example a fully confluent well of a 6-well plate will approximately have 1 million Hela cells (this number would vary for different cell types because of the difference in sizes). Hela cells have division time of ~17h (see this post). If you need ~70-80% confluency after 17h then you should seed ~0.3 million cells.

Likewise, a T-25 flask would have ~3 million cells in full confluency. So, if you need a confluent flask in 3 days you can calculate how much cells to seed.

See this table in Nunc website for number of cells at confluency and optimal seeding density for different culture vessels.

Note that some cells (mostly primary cultures) may need to be seeded at high densities because they may need contact with other cells for survival. So, I cannot give any authoritative answer for primary cultures. Moreover, since it depends on the cell type, all examples cannot be listed here.


Why does it hurt when you take sweets, if you have cavities in your teeth?

The outer shell of a tooth is enamel, which is hard and dense so that not much can penetrate it.  Under that is dentin (or dentine), which is bony but has microscopic channels running through it to the center of the tooth where the pulp and nerve reside.  If the enamel is breached, as with a cavity, crack, or wear, the dentin is exposed to the environment of the mouth.  When sugar comes against the dentin, it draws fluid out of the microscopic channels (because sugar attracts water strongly).  The fluid flow causes pressure changes around the nerve of the tooth, which reports the change to the brain where it registers as pain.  Dentin is highly sensitive not just to sugar, but also to hot, cold, pressure, and other stimuli.  (This sugar response is a short term one; the influence of sugar on bacteria is a longer-term effect in which the acid generated by the bacteria eats away the enamel layer.)


There is a substantial variation in some human traits: hair colour, eye colour, height, weight, skin colour, build etc. etc. HOWEVER there is also considerable variation within other species, to suggest otherwise is naive (though quite common). We often feel like there is more variation within our own species because we are more aware of the subtle differences within our own species (we have evolved to be able to recognise those that are more similar to us). Cows for example also have a lot of variation:

But to answer the question of why traits vary so much generally... There are two principle reasons that demographic patterns might evolve in traits (for example, "Why do Scandinavians tend to have blonde hair?" - [this is just an example, I'm not sure if blonde hair is actually more common in Scandinavia, it could just be a stereotype])

Firstly there is the selectionists view. This is the view that traits tend to evolve for some kind of adaptive reason, therefore most traits (and demographic patterns of variation) exist for some kind of purpose. A selectionist would argue that blonde hair offers some kind of advantage in Scandinavia, over other hair colours, that it doesn't in others. It could be a naturally or sexually selected advantage (perhaps blonde hair is more useful when hunting prey in snow, or there is mate preference for blonde individuals etc.)

In the 1960's though a scientist called Motoo Kimura proposed the neutral theory, a theory that most variation and traits have evolved by neutral processes. For example, scandinavians might be blonde because the humans that colonized Scandinavia were, coincidentally, blondes. Neutralists would argue that the demographic variance we see in humans, and within animal species, is due mainly to random genetic drift.

Here is some more on neutralist vs selectionist, and some on genetic drift. And just to show that other animal species also vary:

Here are some dogs (which have come under a lot of artificial selection specific to generating different physical variants)...

And here are some apes...


Why are mammals the only animals with pinnae / outer ears?

Short answer Mammalian hearing is unique and amazing.

The mammalian ear is unique and highly sensitive with a built in amplification system that means even minute changes in sound can be detected. The bony amplification is also the reason the mammalian (or at least therian) cochlea is huge, every incremental increase yielded markedly more information, it has to get quite large before you hit the point of diminshing returns. This means mammals can get a lot out of even small investments into improving hearing. The vast majority of other groups just would not get any benefit from an external ear. their ears are not sensitive enough to gain anything the faint echoes external ears collect. The one group that would get some benefit (owls), has something functionally similar to an external ear.

The mammalian ear evolved from the repurposing of vestigial jaw bones no other group had (or more correctly they did not become vestigial in other groups). Mammals are the only group with a single bone in the lower jaw. it is a fascinating story and well worth a look. It kinda makes up for how awful mammalian eyes are.


Can a plate with incompletely filled LB agar be used?

It won't be a problem other than that the surface would be uneven. Seal the plate with parafilm when not using to avoid moisture from accumulating inside. When you pour plates then swirl the plate gently so that the molten agar distributes evenly throughout the plate. The agar will be thin though, and you would have to streak gently so as not to cut the agar; you can add 0.5 % of normal agar-agar to make it a little dense.

Or else use  smaller plates (2 inch) if you have them in your lab.


Shigeta's got a point: the ribosome is latched onto the mRNA so those two are intrinsically linked.  You're really asking whether the ribosome comes off first or whether the tRNA does, but it's actually the new polypeptide, which makes sense:

  The stop codon is recognized by a protein, the polypeptide chain release factor (RF), which triggers the hydrolytic release of the nascent polypeptide chain from the P-site-bound peptidyl-tRNA.

This minireview puts forth a model (see below) where, in E. coli at least, the 50S ribosome subunit is then dissociated from the mRNA/30S subunit/tRNA complex, following which the final tRNA is removed.  An in-depth review from a few years later gives more context.


The short answer is yes, other animals can experience dwarfism, including dogs, although it may not be what you are expecting.  Dogs are apparently particularly susceptible but they often are a special case.  We've so heavily bred dogs for whatever traits we desire, so now entire breeds are affected by dwarfism, such as dachshunds and corgis.

The reality is that dwarfism is a mosaic, with many types, and shouldn't be classified under one umbrella.  You're probably mainly thinking of Achondroplasia, which is just one of many causes.  You may also be aware of Hypothyroidism.  Not every case looks like others, so in animals it may not be what you except.  Other animals are susceptible, such as the sheep mentioned in the above articles, and horses, which are also a long-time target of selected breeding.


What organism most efficiently converts a given quantity of mass into heat?

A small hardy warm blooded omnivore that is easily tamed.  I suggest rats.

Small:  You don't want a lot of metabolic effort going into building bone and structure to support structure.
Hardy:  it needs to be survivable with little care.
Warm blooded:  You want to harvest energy from it.
Easily tamed:  The animal shouldn't try to escape its captivity.


Are the changes required to produce genetically manipulated organisms (GMOS) considered to be mutations

What is a mutation?

A mutation is any change to the DNA sequence. From wikipedia

  In biology, a mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

Whether a given alteration to the DNA sequence occurred in nature or in a lab changes nothing to the fact that we call this alteration a mutation.

How common are mutations?

Just so that you realize how common mutations are: In humans, a couple having a baby typically transmit about 40 new mutations to this baby. This mutation rate is not quite the same between women and men (see Kong et al.(2012)).

What is a GMO?

I have never seen the term "forced mutants" before but it sounds like you might have a misrepresentation of what GMOs are and esp. in your misrepresentation, you might think that there is such natural category which are GMOs and other that are non GMOs but the boundaries between the two is more than vague.

Consider for example that the vast majority of our food has been manipulated by humans through artificial selection. Check out the ancestor of modern-day corn (from Genetic Society of America; original source: teosinte.wisc.edu; thanks @John)

This evolutionary change occurred via artificial selection mainly and without using modern genetic tools.


How does the splicing enzyme recognize where to splice the introns?

There are two factors that involve the ability of enzymes to process RNA.
1) Structure see wikipedia
2) Binding affinitya

Let's take a look at the splicing process:

The active 'sites' (GU,A & AG) need to be in spatial proximity (point one), and the enzyme needs to be able to bind there, aka forming hydrogen bonds with the nucleotides, which is mostly the case if:
a) the nucleotides are 'free' as in they are not paired with other nucleotides
b) it is energetically favorable for the enzyme to bind and do its work, which factors like temperature, and of course on the correct nucleotides

If there were some mutations, the splicing might not work.


Which variables are controlled in the mammalian womb to ensure a healthy environment?

It seems you are referring to this recent advance:

http://www.sciencemag.org/news/2017/04/fluid-filled-biobag-allows-premature-lambs-develop-outside-womb
https://www.nature.com/articles/ncomms15112

Involving putting premature lambs (delivered via caesarean) in bags of nutritive fluid and connecting the umbilical cord to an apparatus to oxygenate the blood.

Your question asks which variables are controlled in a mammalian womb, which I think is a misleading way to look at what a womb does and thus what the difficulties are with reproducing it. Namely, it makes it sound like the womb is a container whose purpose is to keep environmental variables (temperature, pressure, etc) at a good value for the development of a fetus. The problem is the womb doesn't just contain the fetus, it feeds it via the placenta. And the placenta is a structure built by fetus during embryogenesis, that connects to the lining of the uterus and enmeshes itself with it so that there is a huge surface of contact between the blood vessels of the mother and the blood vessels of the placenta, so oxygen and nutrients can pass through the mother's blood vessels to the placenta's and from there to the fetus via the umbilical cord. This allows the fetus to get all the nutrients and oxygen it needs to develop.

The "Biobag" these researchers created for these lambs is designed for fetuses who are advanced enough in their development that the main problem they have with surviving outside the womb is that their lungs are immature; the main purpose of this contraption is to allow oxygenation via their umbilical cord while keeping their lungs filled with fluid. And it also seems like they're being fed via that fluid, which suggests they're mature enough to get nutrition via their digestive system.

The paper gives quite a few details of the challenges involved in even that comparatively low level of uterine service. Infection, setting up the cannulas and oxygenating system so that the blood flow is just right and doesn't overtax the fetal heart, making sure there is no clotting, haemorrhage or brain damage...

I imagine the main challenge of making an actual artificial womb that's usable from implantation on would be emulating implantation itself, with artificial endometrial lining that a placenta could naturally develop in and intermingle its blood vessels with and somehow accurately reproducing the flow of blood that's necessary to feed the placenta. If we assume an artificial womb for a fetus that already has an umbilical cord, so we basically need to emulate the placenta's job not the uterus', but can be used earlier than Partrige et al's Biobag, then I imagine all the concerns they had about cannula size and getting the blood flow just right would be a million times harder with tinier, less-mature umbilical cords and fetuses. Not to mention if they need to put nutrients in the blood and not just oxygen.


Why does our hair turn white before we get old?

Human hair color depends mostly on two pigments: eumelanin and pheomelanin. Eumelanin has brown and black variants, whereas pheomelanin is reddish/orange. Cells at the base of hair follicles produce those pigments and white hair is simply lack of those pigments. There may be many reasons why your hair is turning white at a young age:

melanocyte stem cell damage at the base of the follicles
vitamin B12 deficiency
problems with the thyroid
deficiency of catalase as in vitiligo (hydrogen peroxide would then accumulate and impair pigment production)

But most of the cases are purely genetic and you should not be worried if you are certain your B12 levels and thyroid are OK. Here's an article on that topic: https://www.ncbi.nlm.nih.gov/pubmed/23974581

There's also quite a bit of information on white hair on Wikipedia: https://en.wikipedia.org/wiki/Human_hair_color#cite_note-18
(sections Grey and white hair and Aging and achromotrichia)

Cheers!


How should I put a large phylogeny into a scientific paper?

The simplest way of course is to add it to the supplementary materials. However, 220 species are not that many, you should be able to fit that into a page. You have not shown us your tree so it is kind of hard to give specific advice but I am guessing that you have a linear rather than circular tree. If you convert it to a circular tree you should be able to fit it on a single page.

Here are a few random examples of large circular trees I found on the internet:

If you update your question to show us the actual tree I might be able to give you more specific advice. For example, you could split the tree into smaller ones, each showing a specific order or class or whatever resolution you are working on. There are various tricks you can try but they all depend on the details.


Is there any definition of complexity about gene and protein according their function?

Proteins and genes usually are classified in superfamilies and families acording with its inner structure (mainly its domain organization). Domains are parts of the protein with its own 3D structure that usually have their own function and acts more or less in an independent manner.

However, this doesn't talk very much about their complexity. Myoglobin and hemoglobin, for instance, are very related proteins and thus are classified in the same family. However, hemoglobin forms tetramers, while myoglobin is a single molecule. It's not unheard that very close-related proteins may differ in their association with other proteins, polymeration pattern, addition of new domains, etc. Very similar poteins may have very different functions, i.e. catalyzing similar reaction in opposite directions or in very different pathways, or acting in different parts of the cell or the organism.

In biology, it is desirable for any classification to be based in evolutionary criteria, since not only it is a more neutral and unbiased way to classify biological things, but also provide information about the origin and structure of those. You could classify proteins by their structure, number of motifs, number of domains, number of different domains, size, function (in fact, there is a very useful and widely used classification for enzymes), etc; and you could classify the genes according to its number of exons, structure of its promoter/enhancer, policystronic or not, etc. However, this classification will usually prove itself to be inferior to an evolutionary classification.


The move from RNA to DNA and the necessity of reverse transcriptase

Yes, this is true. This flow of information is called the "Central dogma of Molecular Biology". It basically describes the flow of information from DNA to RNA to proteins. Since a virus needs to amplify its genetic information before it can take over the infected cell and make only viral proteins and its genetic information, it has two possible options.

DNA viruses can use the cells replication and transcription machinery to make copies and express proteins. RNA viruses either have to use a reverse transcriptase to make DNA from its RNA genome to go on like the DNA viruses. Or they have to have a special, RNA-dependent (works only on RNA templates) RNA-polymerase (our RNA polymerase are all DNA-dependent and work only on DNA templates) to make more copies of their genome. Our DNA polymerases are dependent on DNA, the same is true for our RNA polymerases. So if the virus is not encoding (and actually bringing a few molecules with it in the virus) of the RT-polymerase or the special RNA-dependent RNA polymerase it will not be able to spread.

Using ribonucleotide reductases would theoretically be possible, but it is not the way nature went. And since a cell contains huge amounts of RNA, I doubt this would be a feasible way, as the enzyme would reduce all RNA. And later on the new viruses also needs new (not reduced RNA) to be packaged into new viruses. This would also be problematic.


Yes, and no :-)

In the meantime many protein structures can be predicted quite accurately - even those for which no reference fold had been known before.

In this case the important buzz word is "big data": co-mutations (of charged amino acids) that can be found when sequencing many independent genomes. (... which indirectly bypasses the emphasis on dynamics for protein folding)

Editorial: 2017, Science: http://www.sciencemag.org/news/2017/01/hundreds-elusive-protein-structures-pinned-down-genome-data

Perspective: Soding et al. , 2017, Science ( http://science.sciencemag.org/content/355/6322/248 )

Research article: Ovchinnikov et al. 2017, Science ( https://www.bakerlab.org/wp-content/uploads/2017/01/ovchinnikov_science_2017.pdf )


Kinases phosphorylate, or add a phosphate group.

Phosphatases remove a phosphate group.

Beyond that, the concepts for regulating them are the same, though the precise factors of course are different.


Both are forms of immunisation.

Inoculation is exactly that. A live organism is introduced in a controlled way, so as to minimise the risk of infection, and is essentially the same process followed by many people in history.  It is inherently risky.

Vaccination is introducing a weakened version of the pathogen, so that the immune response is triggered and the body is prepared to fight the actual pathogen if necessary. This was pioneered by Edward Jenner, wherein he noticed that cowpox (related to smallpox) immunised the milkmaids against smallpox.


What mechanism suppresses melatonin release in humans?

Take a look at this (especially page 938): Coordination of circadian timing in mammals by Steven M. Reppert & David R. Weaver Nature 418, 935-941 (29 August 2002) | doi:10.1038/nature00965

  Sodium-dependent action potentials provide the primary means by which
  the SCN transmit circadian outputs to other brain areas and are
  essential to its role as a pacemaker1.

  Signalling molecules from SCN efferents include neurotransmit- ters
  and secreted factors. An output role for secreted factors comes from
  the results of SCN transplant studies that suggest that the
  alternating activity of SCN-derived ‘inhibitory’ and ‘activating’
  factors drives locomotor activity rhythms (and hence rest/activity and
  sleep/wake cycles) in rodents

There was also a mention of per/cry gene expression.


Can the third sex be categorized as Male or Female?

When dealing with humans, there are only two Biological genders as defined by the presence or absence of the Y-Chromosome. If the Y-Chromosome is not present, or through some process gets totally deactivated, the human will appear and function as a Female.

XX = Female

XY = Male

XXY = Male (Klinefelter's Syndrome)

XYY = Male (Aneuploidy - Normal Functioning Males)

XXX = Female (Aneuploidy - Normal Functioning Females)

X = Female (Turner's Syndrome - Generally infertile, other issues)

Y = Fatal (The Y-Chromosome is drastically smaller than the X-Chromosome, which contains many necessary genes)

XXYY = Male

...

The list goes on, since there have been records of up to XXXXX.

If there is a Y-Chromosome present, the human born will be male.

However, that is not to say that a person cannot psychologically identify as something else. It's also worth noting that the majority of known species are asexual and do not have genders, and that those which do have genders do not always follow the same rules (Fruit Flies, for instance, use the ratio of genes to determine sex).


Why do chain identifiers in PDB have no standard starting chain id type?

Chain IDs are assigned by authors who submit the structure to the wwPDB.
According to the PDB spec:

  Non-blank alphanumerical character is used for chain identifier.

Usually, the chains are assigned uppercase letters.
But since digits and lowercase letters are also allowed, some people will use it.
And a good reason to allow more characters is to accommodate for structures that have more polymer chains than there are letters in English alphabet. With lowercase letters and digits the limit is 62 chains.
Which is still not enough for some structures.
(Many programs can handle two-character chain IDs, but this common extension has not been embraced by the wwPDB.)


Role of Intermediate Filaments in cell - cell signalling

There are desmosomes and gap junctions (cell-cell-contact), and hemidesmosomes (cell-basal membrane-contact) which enable a stable united cell structure. I'm not so aware with this topic, but I found some papers which may help you :)

Intermediate filament in cell architecture

Desmosomes and hemidesmosomes

Review on gap junctions

Blood-testis barrier and different cell-cell-contact structures


So the general sequencing analysis pipeline is to generate a bunch of read sequences, figure out how they match to a reference genome and align them, then call any differences between the reference genome and the sequencing reads. The following image, from the Broad Institute's Interactive Genome Viewer, may help you visualize what is happening here. As you can see in the image, the human reference DNA is found at the top of the window, and the sequence of bases for the current selection, at the very bottom of the window. Then each of the gray bars that you see below that is an individual sequencing read that matches to that particular location along the human DNA.

When you use a variant caller like Freebayes, it will list out information about locations along the reference genome that had differences in your actual sequences. For instance, as you bring up, DP or read depth. Looking back at the IGV image, you can see a location that had a lot of 'G' showing in the sequence reads, where the reference DNA has 'A'. Variant callers will pick up on this and list it as a possible variant. They will also tell you the read depth at that location which is the total number of sequence reads overlapping that position. In this case there are 21 gray bars (sequence reads) overlapping at that position, meaning that DP=21.

Even though it is not listed in the VCF example to which you refer, variant callers can also give other data like AO, which is times that a variant was observed, and RO which is the number of times the reference base was observed. This information allows you to decide whether or not an identified variant was a sequencing error, or a real variant.

For instance if DP=1, AO=1, RO=0, that means there was only a single read at that location and it was not what is listed in the reference genome. Because the depth is so low, and the error rate of a next-gen sequencer is somewhere between 0.5-5%, you cannot say that this is a mutation or just a sequencing error. However, as DP increases, you gain more confidence in whatever was called. So if DP=10, AO=10, RO=0 you can be quite confident that the reason you read an alternate base at a given location, it is not just a sequencing error because you read this location 10 times and every time you saw the same variant.

Let me know if I can clarify further.


Does electricity cause damage on a cellular level?

Regarding the moss or lichen on the third rail on British train lines: there is no current passing through the moss/lichen as they are not completing a circuit. They are just sitting on one connector. If another connector passed over them, completing the circuit across them, then a current might pass across them for a very short time. But I doubt they grow on the top of the rail (which is the contact part in the UK system) as that is constantly being polished smooth by the contacts from trains sliding across it.

Regarding cell damage: Apart from fibrillation in animals, and burns caused by Joule heating, electricity does cause cellular damage.

At low frequencies (<10kHz), electricity disrupts cell membranes and makes them much more permeable (we actually harness this when we use electroporation to transform bacteria). All organisms rely on electrochemical potential differences across membranes for their metabolism (Berry, 2002). The exact effect is dependent on the previous electrical state of the cells, for example the electrical potential difference across the membrane, and on the surface area to volume ratio of the cell (greater volume relative to surface area leads to more disruption). In any case, extreme electroporation can cause solutes to flow in or out of a cell, and generally disrupt the balance of solute concentrations and cause organelles and other bodies to move out of a cell. When the electrical stimulation stops, the contents are then fixed in a disrupted state. The cell then has to expend enormous amounts of ATP using ion channels and transport proteins in an attempt to reinstate the necessary chemiosmotic potentials, and in doing so exhausts the entire ATP supply and goes into biochemical arrest (no metabolism occurs), which is when a cell is dead. Dead cells break apart because there are is no maintenance occuring.

At higher frequencies (10-100kHz) proteins become permanently denatured. Many proteins carry charges which give them an overall polarity. When placed in an electric field, the proteins reorient themselves and will undergo conformational change to achieve the optimum dipole moment in the direction of the field. Ion channels and pumps are particularly sensitive to these disruptions (since their charges are crucial to their function).

Rather than provide lots of references, there is one excellent review from which I drew all this information, and which you should read for more of the physical detail (Lee et al., 2000).

References:

Berry, S. (2002) The Chemical Basis of Membrane Bioenergetics. Journal of Molecular Evolution. [Online] 54 (5), 595–613. Available from: doi:10.1007/s00239-001-0056-3 [Accessed: 9 February 2012].
Lee, R.C., Zhang, D. & Hannig, J. (2000) Biophysical injury mechanisms in electrical shock trauma. Annual Review of Biomedical Engineering. [Online] 2 (1), 477–509. Available from: doi:10.1146/annurev.bioeng.2.1.477 [Accessed: 9 February 2012].


Please provide more information: fold-change relative to what?

If you did what I think you did (single control gene that you calculated fold change to of your gene of interest) I'd say this is the wrong approach. What you need is a set of genes which have similar expression levels across all your samples (controls and cases) to be able to compare your gene of interest to some common baseline. Selection of such genes should be the first step in the project, and it might be a good idea to use one of the established approaches - I recommend Jo Vandensompele's GeNorm (link to the paper) method. It goes like this: from a panel of potential control genes you select two or three that are most stably expressed across your experimental conditions, and then use these two-three control genes along with your gene of interest in a qRT-PCR. You then normalize the signal from your gene to a mean of the control genes.

It has been repeatedly shown that using a single control gene, even a so-called 'housekeeping gene' is misleading, because those genes do change their expression levels in some conditions. Also, using several control genes protects you against potential problems due to unequal amplification efficiency in different samples/groups. However, if you have multiple gene of interest, they all must have comparable amplification efficiency.


Nonpancreatic digestion of tryglicerides

There are two possibilities concerning the further metabolism of MCTs: the glycerides are absorbed and immediately transported through the portal vein to the liver whereupon they are oxidised to release energy.
Alternatively, dependent on the size of the MCT, ranging from hexanoic acid tails to dodecanoic acid tails, it may undergo the standard catalysis by pancreative lipase to form monoglycerides, diglycerides and free fatty acids.

More information regarding the physiological effects of middle-chain fatty acids may be available from: https://academic.oup.com/jn/article/132/3/329/4687297


Does the number of base pairs between the end of one gene and the start of the next gene have to be a multiple of 3?

There absolutely is not a rule saying that all genes on a strand should be in the same frame.

Your program is looking for ORFs (open reading frames) and it should identify all of them, in every frame.  If you were being very thorough, you should generate the reverse complement of your sequence, and search that for ORFs too.  But I guess if you were given this sequence, presuambly the professor gave you the sequence in the desired orientation.


Can ampicillin resistant bacteria survive penicillin plate?

Short answer: Your assumption is wrong and bacteria, which are resistant to penicillin are are also resistant to ampicillin.

Long answer: There are different classes of antibiotics, which have different mechanisms of action. Penicillin (and also ampicillin) belong to the class of beta-lactam antibiotics which are an irreversible inhibitor of the bacterial transpeptidase, which is needed for the proper formation of the bacterial cell wall.

There is a number of different natural occuring penicillins as well as some which have been generated by modifications of the general structure. The general chemical formula for these is shown below (from the Wikipedia article), the different penicillins differ only in the "-R"-group shown in the molecule (in the upper left):

If you now compare Penicillin G (which occurs naturally and is still used) and ampicillin side-by-side, you will see the the difference is not very big, basically only one amino group:

Penicillin G on the left, Ampicillin on the right.

The difference of this one amino group makes ampicillin more polar and allows it to penetrate the cell wall of some gram negative bacteria (the main action goes against gram positive bacteria).


This definitely possible. Due to the microscopic scale of bacteria and viruses, even very light forces(like those from pulling a tissue out of the box) will lead to those bacteria and/or viruses being tossed to the rest of the box.

However, a large portion of the infectious viruses in humans will struggle to survive on the dry, low nutrient substrate of the tissues and box for extended periods of time(especially given high absorbance), albeit the above comment show many that can(depending on the surface).

To answer why there is no better design, I think the simplest explanation is monetary incentive. There is little incentive to create something better both due to R&D cost and inevitable increase in product price, as well as a steep consumer education cost to let customers know, why this is better. However, if you have a good solution in mind that does not raise product cost beyond a few cents per unit, you should a decent shot(if you patent) to license it to the big players.


Why don't the heads of phospholipid bilayers repel hydrophobic molecules?

Your question is rooted in a misundertsanding of the hydrophobic effect. Hydrophillic and hydrophobic molecules do not repel but, rather, attract one another through van der Waals interactions. The tendency of hydrophobic molecules to aggregate in aqueous solution (ie the hydrophobic effect) is, instead of some repulsive force, actually driven entropically. I don’t think I will go into this in detail since it has been explained well in many places. That said, it is also explained very poorly in many places (which I suspect you have encountered). I recommend this website to learn about it and other intermolecular interactions.

Once you have a firm grasp on that, consider that in order for a hydrophobic molecule to reach a plasma membrane, it must already be solvated by water. The transfer of a hydrophobe from one hydrophillic environment (water) to another (head groups of the phospholipids in the plasma membrane) should be energetically negligible. The limiting step for passive diffusion across a membrane is transfer from the hydrophillic environment of the phospholipid head groups to the hydrophobic environment of their tails. In fact, the rate of diffusion across a plasma membrane increases with hydrophobicity.


What are genome wide functional linkages?

Genome wide functional linkages refers to protein in a biochemical or signalling pathway. Inferences of functional interactions can be obtained from methods such as coexpression data from microarray analysis. Since experimental detection of genome-wide protein–protein interactions is costly and time-consuming a computational scope for essentially predictive genome-wide protein–protein interactions is created  [1], which is what the above paper is referring to. As obvious from the abstract of the paper, there are many ways of obtaining the linkages, which are often inferred by the Rosetta Stone, Phylogenetic Profile, Operon and Conserved Gene Neighbor computational methods [2].

Algorithms that identify genome-wide interactions between proteins mainly focus on coregulation of interacting proteins. These methods assume that the genes that are coregulated often occur close to each other on the genomes and show conserved gene order. Thus the genes, which are part of an operon, could be functionally linked.


Do egg laying animals experience a pregnancy?

In oviparous animals the egg retention phase in the uterus is brief. After fertilization eggshell mineralization is triggered but it seems the initial triggers of the pathway is not understood. The uterine fluid is rich in calcium and bicarbonates and calcium carbonate, in the form of calcite, precipitates around the egg. Shell mineralization is quite a rapid process and there are some specific proteins involved in this pathway. Have a look at these:

http://www.ncbi.nlm.nih.gov/pubmed/22201802

http://hera.ugr.es/doi/15773115

In ovo-viviparous animals the egg is retained in the uterus for a longer time and embryo is quite developed when the egg is laid (happens in boas). You can call it a sort of "pregnancy".

However progesterone pathway exists in birds and is involved in oocyte maturation

Oxytocin pathways also exist in birds, acting through oxytocin homolog Mesotocin, and perhaps they cause development of maternal care as they do in mammals.

This article talks about effects of oxytocin on birds but not exactly about its role in maternal care.

However i believe that the shell size and mineralization time shouldn't differ much between unfertilized and fertilized eggs in oviparous animals.


Can your immune system's cells destroy you? (Critical thinking and Fictional sense)

This is a very interesting question. As others have alluded to, the body generally recognises self and non-self. However, as with any biology it's not that simple. Even leaving aside autoimmune disorders, the body doesn't always attack non-self and doesn't always leave self alone. Think of a pregnancy - the foetus is non-self, and yet the body doesn't reject it. The same can be said for a whole host of molecules that enter the body, such as food or things breathed in (e.g. pollen).  For this reason, Charles Janeway put forward the infectious non-self theory. This postulated that the body had a degree of leniency towards non-self, and would only attack if the macrophages became activated. This is done through recognition of Pathogen Associated Molecular Patterns, or PAMPs, binding to Pattern Recognition Receptors, PRRs. These PRRs are receptors present on immune cell surfaces, though most relevantly on macrophage surfaces, and when they bind to PAMPs it sends a message to the cell that it's likely in contact with a pathogen (or at least there is likely a pathogen in the area somewhere). This causes activation, and starts an immune response.

However, it's also too simplistic to suggest that the immune system always leaves self alone, and in fact one of the key jobs of macrophages is to clean up self cells that are damaged, and undergoing apoptosis - programmed cell death. (You can read more on macrophages here and more on apoptosis/other methods of cell death here). Therefore Polly Matzinger put forward what is known as the "Danger Model". This basically speculates that in order for an immune response to occur, the body has to recognise certian molecules that are evolutionarily associated with danger. PAMPs would indeed count, but there could also be endogenous molecules such as HSPs - proteins produced when a cell is under duress through heat, pH, cold, irradiation, viral infection etc. This tells the immune cell that detects it that the body is in danger, and allows activation and mobilisation of an immune response.

So the question here is, would the body respond to a miniature version of yourself? That would depend on a number of factors:

Where in the body would you go? If you were to stay in the digestive tract, so get swallowed and 'passed through' the body, I would say it's very unlikely you would be attacked. The body has a high tolerance for places such as the gut, because it's constantly exposed to external and non-self molecules. If it were in the blood stream, it's more likely because you're more likely to come across immune cells.
How is this 'shrinkage' achieved? Growth comes in two ways, through increase in cell size and increase in cell number. Which of these are you reducing? Are the cells the same size, but there are many fewer of them (unlikely, especially given that the opening question specifies to bacterium size, which are many times smaller than human cells already) or do you have the same number of cells but each cell is shrunk to a much smaller size (given that the entire body is the size of a bacterium, each cell would have to be many times smaller than a bacterium). If the cells were the same size, or even a bacterium-sized each, then an immune response is much more likely. If the whole organism is the size of a bacterium, the cells are going to be far too small to elicit an immune response.
Are you causing danger signals? As mentioned above, if no danger signals are present then it's unlikely an immune response will be launched regardless of anything else. Provided you're not killing or injuring cells, the body will pretty much ignore you.

I would say you wouldn't be attacked if you shrunk down as far as you've suggested. Everything would be too small for the body to recognise. However, if you didn't shrink down nearly as far, so your cells remained a size the body could recognise, and then started blundering about causing all manner of danger signals around you, the body may pick up some of your antigen and launch a response against you. On the other hand, the body is likely to have become tolerant to your antigens so even if this was the case, a full immune response is unlikely.


What level of cellular radiation is harmful for humans?

Addition to the previous answer

First you need to understand how radiation causes cellular damage.

EM waves like γ-rays, X-rays and high-energy UV (in certain molecules even visible light) can knock out the electrons from the atom and create an ion and free radicals by breaking chemical bonds. This term — ionizing radiation is not used for low energy UV and visible light because these waves can only ionize a few types of molecules and are not ionizing in general. Moreover X-rays and γ-rays can dislodge even inner electrons which UV and visible light cannot (High energy γ-rays can also lead to the nuclear reaction of pair production). These ions that are formed are reactive and can attack other molecules (DNA/proteins etc) around them. DNA absorbs UV and this can cause DNA lesions such as dimerization of adjacent pyrimidines (via a cyclobutane bridge). Both reactive ions and pyrimidine dimers can cause cancer; the former is most frequent in melanomas which happen because of solar UV. Since UV cannot penetrate very deep, they affect mostly the skin (See here).

IR, with energy lower than visible light does not have sufficient energy to cause electronic transitions. But it can cause vibrational transitions such as bond stretching and bending. Microwaves have even lower energy and can only cause molecular rotation. Both IR and microwaves because of their property to make molecules move, generate heat.

Continuous usage of mobile phones can cause discomfort but only because of their heating effect. They can by no means cause cancer and even though mobile phone radiation is classified as a potential carcinogen (IARC Group 2B) perhaps because of the pressing allegations of certain factions, they do not have sufficient energy to cause DNA damage.

If you ask me if mobile phone radiation can be harmful to human health, then I would say yes, they can be potentially harmful with prolonged usage but in no way as harmful as to be causing cancer. I would say that it is as harmful as wine :P


What is the name of this tiny creature? It looks like a tiny piece of moving cotton?

From your image, it looks like it might be a woolly aphid. I just did a bit of cursory research, and it looks like they're often described as floating pieces of fluff, that seem to wander instead of directly heading somewhere. The fluff on their back is actually wax produced as a defense mechanism from predators and the like. I hope this is what you were looking for!


Just the presence of actin filaments does not mean a cellular structure that contains it would be dynamic. Moreover there are different types of actin filaments (filopodia, lamellipodia etc) and they have different dynamics.

Microvilli closely resemble filopodia; both these structures also share some regulatory and structural proteins (other than actin). However, there are some differences which makes filopodia highly dynamic in comparison to microvilli (Sebé-Pedrós et al., 2013; Sauvanet et al., 2016).

Microvilli, though not as dynamic as filopodia, are not static structures. They can grow and retract and there are regulatory mechanisms that govern these processes (Sauvanet et al., 2016).

  REGULATION AND DYNAMICS OF MICROVILLI AND MICROVILLAR COMPONENTS

  Microvilli on cultured cells are dynamic structures with three phases
  in their life cycle: (a) the generation of microvilli growing at 5
  nm/s, (b) a steady state of ∼5 min, and (c) a retraction phase with a
  rate of 1.2 nm/s (Gorelik et al. 2003). This leads to an average life
  cycle of 12.1 ± 5.6 min. The turnover of microvillar proteins has been
  recognized for a long time (Stidwill et al. 1984). The F-actin core in
  the microvilli of Caco-2 cells at steady state treadmills, with a rate
  of monomer addition at the barbed end of approximately 1.5–3.0
  s−1 (Loomis et al. 2003, Tyska & Mooseker 2002),
  corresponding to approximately 0.2 μm/min. The protocadherin
  intermicrovillar link stabilizes microvilli of intestinal epithelial
  cells, resulting in a prolonged steady state (Crawley et al. 2014).
  The actin filaments in the core of stereocilia treadmill more slowly,
  at 0.002–0.04 subunits s−1 (Rzadzinska et al. 2004) or
  hardly at all (Zhang et al. 2012).


Is the occurrence of a particular enzyme in a given subcellular location a random phenomenon?

There are various methods for targetting proteins to subcellular organelles or membrane locations. In general they depend on ‘tagging’ or ‘signal’ sequences in the proteins. Such tags or signals are recognized by specialized proteins that are able to conduct the protein through the membrane barrier to the particular location.

The individual processes for different target locations vary, so I do not think it appropriate to provide details here. You can read a summary of them in this Wikipedia article. For more extensive treatment you can look at the relevant chapters in Lodish et al.  or in Alberts et al. on-line (old edition).

(Please consider donating to Wikipedia, if you use it.)


How many palindromic sequences in human genome?

The human genome contains approximately 1.25*10^7 palindromes longer than 6 bp (that is 8 bp or longer). Some interesting facts are also known about their distribution.

  We found that 24 palindrome-abundant intervals are mostly located on G-bands, which condense early, replicate late, and are relatively A+T rich. In general, palindromes are overrepresented in introns but underrepresented in exons. Upstream region has enriched palindrome distribution, where palindromes can serve as transcription factor binding sites. We created a Human DNA Palindrome Database (HPALDB) which is accessible at http://vhp.ntu.edu.sg/hpaldb . It contains 12,556,994 entries covering all palindromes in the human genome longer than 6 bp.

And no, the number of shorter ones (shorter than 8 bp) isn't mentioned in the paper because they are considered unimportant, biologically.


How does sequence independent single primer amplification work?

This process is called sequence-independent single primer amplification (or in short SISPA). Its used to amplify unknown sequences for amplification, for example in unknown viruses.
The primers used for this process contain random sequences which should bind to the DNA to be amplified and also known sequences, which can be used a adapters. In the first rounds of PCR only the random primers give rise to specific products, which are amplified exponentially in the later rounds of PCR since the primers fit perfectly then. This is described in detail in this publication:"Random priming PCR strategy to amplify and clone trace amounts of DNA"
Another interesting paper describing the method is:"Sequence-independent, single-primer amplification (SISPA) of complex DNA populations."


Does Alzheimer affect more than day-to-day memory?

Oh, yes, though short-term memory loss is often an early sign.

"For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease."  from https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet.  Warning: grim.

Whatever your brain does, Altzheimer's eventually undoes.  For more details:  http://www.alzheimers.net/stages-of-alzheimers-disease/


Fish replace their teeth over time as needed. Thus, they don't maintain the sharpness of individual tooth, they just replace it. This is a passive process not a conscious process.

Source: Barton, M., & Bond, C. E. (2007). Bond's biology of fishes. Thomson.Pg. 414-415.


Brain + ethanol experiment suggestions needed

The main problem with what you are asking is that you want to show effects on vigilance and memory in vitro. That is just not possible: if you want vigilance and memory you need a live animal, there is no way around it.

Next point: you have an audience of non scientists, so you can lose them very quickly if you start speaking about NMDA, LTP or similar things without a clear explanation, so start with that: get a nice review (Pubmed is a good start, as always), and give a simple theoretical explanation of one of the mechanisms involved. It is then important to clearly explain the experiment you will perform, and what you are expecting to see in case there is an effect.

Unfortunately the best way to see effects on NMDA receptors would be electrophysiology. This is not trivial and, if you have never done it, I would not suggest going that way. However, if you have access to an electrophysiology setup you will most likely have access to someone who uses it, and that could make the experiment for you.

I am not an expert on this topic, but a quick research on Pubmed seems to indicate that alcohol can, for instance, reduce LTP in hippocampal neuron.
Maybe what you could do is having someone patch hippocampal neurons and show how an LTP protocol is used. You don't necessary have to show them the whole thing (I doubt anyone in a right state of mind would bare to stay until the whole experiment is performed in control condition first, and alcohol later...).

Also, the results of these experiments are often non obvious to analyse, so you should have some data prepared and analysed earlier and quickly show how analysis is performed, before showing the final results.

Calcium imaging experiments could also be used and would probably give results that are easier to understand for a laymen audience.

See for instance Fig. 1 or Fig. 5 of this paper (just the first one I found, there surely are other):
Ethanol alters calcium signaling in axonal growth cones.


Why does the funnel-mantle locking apparatus exist, and how / why does it work?

Argonauts and other octopuses have a muscular mantle which is the outside of much of the body other than the arms.  A cavity is formed by the mantle in which the gills are located.  Water is pulled into the cavity through valve-like flaps and expelled through the tubular funnel (also called siphon or hyponom).  Here is a video of the flaps and funnel as an octopus breathes.

A typical octopus most often moves slowly by crawling across the sea floor.  They have a faster mode of locomotion, though, which is to quickly contract their mantle to force water out the funnel at high velocity.  This jet of water forces the body of the animal in the opposite direction. Here's a drawing of an argonaut moving with this mechanism:

(Here's a video of an octopus using its jet.)

As this jet propulsion is often used for escape, it is important for efficient movement that jet be directed so that the rounded mantle leads the movement and the arms trail.  Since the funnel is flexible, there is a need for a way to keep the funnel aimed away from the mantle.  The funnel–mantle locking apparatus exists for this reason.  A protrusion on the mantle fits into a slot on the funnel and while the animal is propelling itself holds the funnel in place.


The left auricle is a decompression chamber when atrial blood pressure is high (in systole or in some pathological conditions) [1, 2]. Some research claims it also plays a role in cardiac regeneration because it contains cardiac progenitor cells [3].

Probably the right auricle has less important function; also there are fewer studies about it.

References:

Al-Saady NM, Obel OA, Camm AJ. Left atrial appendage: structure, function, and role in thromboembolism. Heart. 1999 Nov;82(5):547-54. PubMed PMID: 10525506.
Bansal M, Kasliwal RR. Echocardiography for left atrial appendage structure and function. Indian Heart J. 2012 Jul 27;64(5):469-75. doi: 10.1016/j.ihj.2012.07.020. PubMed PMID: 23102384.
Leinonen JV, Emanuelov AK, Platt Y, Helman Y, Feinberg Y, Lotan C, Beeri R. Left atrial appendages from adult hearts contain a reservoir of diverse cardiac progenitor cells. PLoS ONE. 2013 Mar 12;8(3):e59228. doi: 10.1371/journal.pone.0059228. PubMed PMID: 23555001.


The fur coats of polar bears are in fact clear tubes - not white fur as is often believed. It is their skin that is black, to absorb the most warmth from the sun (and the clear tubes allow the majority of the light to pass through to the skin).

I recently watched the BBC's Frozen Planet TV series (with David Attenborough), where I heard the above answer. If you haven't already, I recommend watching it.


Are there any trees that prefer to grow on the floor of water bodies but protrude to the air?

Mangrove swamp trees and shrubs immediately spring to mind. There are many species that fall into this category of trees that grow in intertidal and costal locations. They prefer locations where salt and freshwater mix, known as 'brackish water'.

All roots require oxygen and the species that fall into this category have developed roots that protrude above the surface, called pneumatophores.

Photo from http://www.dutchpickle.com/philippines/palawan/sabang-mangrove-forest-palawan.html

Here is an excellent website with more information
http://www.fao.org/docrep/010/ai387e/AI387E06.htm


In Gastrointestinal Tract Location of Escherichia coli O157:H7 in Ruminants (Grauke et al. 2002):

  in the lower GIT digesta, specifically the cecum, colon

It's about O157:H7, but I think the standard act a same.


Multiple RNA Polymerase transcription complexes engaged on the lacZ gene at the same time, staggered along the gene.


Simulating Drug Entry in Protein and binding?

This is a tough topic, have a look at the following references and see, if they can help you:

Structural modelling and dynamics of proteins for insights into drug
interactions.
Ligand entry pathways in the ligand binding domain of PPARγ receptor
Pathway and mechanism of drug binding to G-protein-coupled receptors
Molecular Dynamic Simulation and Inhibitor Prediction of Cysteine
Synthase Structured Model as a Potential Drug Target for
Trichomoniasis


Dye reduction tests (and there seem to be loads of different ones) are simply assays in which a dye becomes decolourised to give you a visual indication of whether a certain process is occuring. Here you can find an example of a dye reduction test with Methylene Blue and Reazurin which indirectly measures the bacterial densities in milk and cream. See this google book for more info.


Phenotypic Variation of cattle - looking for academic sources

Online Mendelian Inheritance in Animals (OMIA) is a database of genes, inherited disorders and traits in more than 135 animal species (other than human and mouse). At the moment, it has about 400 entries for Bos taurus, mostly disease phenotypes. This is probably the only attempt to exhaustively list such phenotypes.


Do animals suffer from "Human" mental disorders?

You will be hard-pressed to find any scientific data on this question. Psychology in humans is already a difficult study, at times failing to demonstrate results with real scientific rigor. When studying animal psychology, you face another substantial barrier - language. Although some primates have been taught to communicate with sign language, the best of them are still far from the level of proficiency of a human. We can measure brain activity and observe behavior, which can lead us to strong suspicions about what is going on in an animal's mind, but very little can actually be proven.

Mostly, all we can do is speculate about such questions. You will find some veterinarians out there who treat pets for mental conditions, but you will find at least as many people calling them quacks as those who believe in the validity of their work. And certainly, they can't prove to you that a treatment has helped an animal. It's subjective.

If we see an animal do something which in a human might reliably be interpreted as a sign of depression, it's possible that this interpretation is appropriate for the animal as well. It's also possible that there is some totally foreign unrelated explanation. The problem we find when trying to scientifically discuss matters which cannot be proven scientifically is that scientists must be careful to state what they know and nothing more. So they might say "We cannot prove that the porpoise is depressed", or "Science cannot prove the existence of a God." This is often misinterpreted as evidence against the finding - that the porpoise is not depressed; that there is no God. This is a fallacy. Rather, we should recognize that we have different ways of exploring questions like these.

I can't prove it to you, but I know that my Beagle had a rich emotional life. I know this because I spent huge amounts of time with him. He was a close friend of mine. I would just as soon question whether my wife has real emotions as my dog. I can't prove that my wife's emotions are real either, but I don't have to. It would be silly to assume that everything she shares with me is some sort of evolutionary programming, and not real emotion. Now, when I extend this to cetaceans, I must admit that I don't have any friends in those circles. So I can only guess.


They do not, at least not normally or noticeably.  MHC I occurs on all nucleated cells, and red blood cells do not have nuclei.  If they did indeed have MHC on them, blood transfusions would be as successful and as tricky as organ donation.  There are reports of MHC detection on red blood cells, but the amount is orders of magnitude smaller than elsewhere, only present for certain MHC alleles, and often transient.


Small, brownish bird with reddish spot around eyes

It's a Chaffinch (Fringilla coelebs). From the first picture you see the
greyish head and orangish chick. From the second picture the typical whitish/greenish
wing bars. From the third pic the bricky belly.


Compare and contrast "Rubisco activity" and "assimilation rate" (is there a difference, and if so, what is it)?

Both are measures of carbon fixation rate.

RuBisCO activity specifically refers to the rate at which the enzyme RuBisCO fixes carbon to RuBP, and is measured by isolating the enzyme from tissue samples and, usually, using radiolabelled CO2 to measure how much carbon is fixed in a set amount of time in controlled conditions and with controlled supply of substrate.

Carbon assimilation rate is generally a whole-plant or whole-leaf variable, measured on a larger scale. It is usually measured by measuring leaf sugar carbon before and after a set period, again using radiolabelling. Conditions may or may not be controlled, and it can be measured in the field (unlike RuBisCO activity).

RuBisCO activity might differ from net fixation in the short term in plants which have an intermediate carbon fixation step, such as in CAM or C4 plants, if the net fixation measurement includes the intermediates - the pool of intermediate carbon-containing molecules have technically been fixed but not by RuBisCO. However, over longer time periods this effect will disappear, as ultimately all CO2 is fixed or re-fixed through RuBisCO.


Does "mind" has any physical reality in biology? Or is it just an assumptive concept?

The mind is an abstraction which arises from physical and chemical processes within the brain.  For a crude analogy, think of the brain as an incredibly complex, self-modifying, multithreaded program.  The mind would then be the abstraction arising from the behavior of the program as it runs.  Consciousness would be the abstraction arising from the behavior of one particular thread in the program: a thread which has access to a limited buffer of its own (that thread's) behavior, and control over limited input and output from the body.  All of the other (unconscious) threads may affect the conscious thread, but the conscious thread has very limited access to information about the behavior of the other threads.

Since the conscious part of the mind has access to information about its own behavior, there is actually some recursive looping going on when it comes to thinking and feeling.  The feeling that this goes in circles somehow (which you seem to be expressing) is a common intuition, and it's almost certainly a correct one.  But the manner in which this occurs is not well-understood, and it's definitely not well-understood within biology at the macro level because the brain is unbelievably complex and plastic.  We really don't have a clue how to begin modeling the brain's processes.  This is one reason artificial intelligence is still extremely crude today (despite what Elon Musk and Bill Gates may try to say).

If you want to read a scientifically-inspired theory of from whence consciousness comes, and of how it arises from the brain, I would recommend the book Godel, Escher, Bach by Douglas Hofstadter.  Douglas does a good job of combining computational theory with biology, music, and art to illustrate a theory of consciousness the reader can grasp even if you don't have a strong background in any of those subjects.


Is every decision we make already "pre-programmed" because of DNA?

"Do we have free will?" It's a big question.
DNA (among other epigenetic factors) code for proteins, so ultimately it determine our cells, which in turn are responsible for our neurology, although how this translates to behavior is variable depending on factors beyond DNA@Remi.b's answer. De facto you're asking about the extent that our brain structure and neural activity determines our conscious stream. This boils down to "Do we have free will?". That question historically was only accessible to philosophers. It is now accessible (but not completely answerable) to biologists, more specifically neuroscientists. It's a great question, but is still open to a lot of subjectivity.
An evolutionary explanation.
Anil Seth, professor of cognitive and computational neuroscience at the Sackler Centre at the University of Sussex, gives a very good answer to the question at 25:44 in this BBC Life Scientific interview.

We are determined to have it in both senses of the word...
Yes, we do have free will because we can behave the way we wish to behave. We cannot decide what to will.

Paraphrasing the guts of the answer: it's very important for the brain to differentiate between internalized experience, and reflex.
Reflex, such as placing your hand on a hot stove, never reach the "conscious stream". These have an obvious correct choice; in this case, removing the hand from a hot stove is clearly the right choice, every time.
Then there is internalized experience. Complex problems have many potential losses and gains. To cope with this, the brain needs to internalize, reflect, and is taking note and making a plan; the sensation of free will. By taking note of that situation within it's context and the plan, we can perhaps change our actions the next time we encounter a similar event so that we can optimize our choices to attempt to cause the least damage to ourselves and/or maximize the benefit.
How is learning achieved.
We have established that there is a need for new memories to form in order to solve complex problems. Long term memories are the result of new physical synaptic connections in the brain. This connection endures whether it’s being used or not.
Psychologists put these into two broad types are two kinds, implicit (akin to reflex; how to read, how to play your favorite song on an instrument etc.) and explicit (the things we are consciously aware of). Explicit memory comes in two forms: episodic and semantic (Tulving, 1972). (i) Episodic memory includes experience. For example, that time you planted some seeds and a potato grew. (ii) Semantic memory is abstract to your own experience. Something more like "Primordial potatoes originated in southern Peru".

To bring this back to the original question "Is every decision we make already pre-programmed because of DNA?" It's long winded. Our choices are built upon the results of our past choices in a given environment. We are able to make these choices, to an extent depending also on other variables, because of the products and machinery encoded in our DNA.
The philosophers answer
If this answer is a bit scary or makes your choices seem futile, you can simply sit around and do nothing instead of doing whatever you normally would do; it's your choice.
See a similar question answered from a different perspective over at Philosophy.SE.


Is it true that cats can drink sea (salted) water?

Since cats are well adapted to dry environments, the question has some plausibility to it.

The book "Mineral Tolerance of Animals" suggests that cats may be able to tolerate slightly more salt in their diet than dogs (1.37 g salt/kg body weight for cats, vs. 0.64 for dogs).  However, these represent concentrations that were shown to be safe, not the maximum they could potentially tolerate. The reference in the book is Yu et al., 1997, and though the actual reference is not available in the Google Books version I believe it must be The minimum sodium requirement of growing kittens defined on the basis of plasma aldosterone concentration, so the goal was to identify minimum rather than maximum levels.

The ocean is about 3.5% salt.  The 1.37 value for cats came from kittens eating a diet that was about 2.5% salt, but another note in the book says that cats can safely eat a diet that is 3.8% salt, though they don't like it. I can't find the original reference ("Berger, 1979") for this claim, but I am pretty sure that this was with ad libitum water so they could flush out extra salt.  If so, cats would not be able to tolerate sea water unless they had another source of water as well.

It's often said that wild cats can get most of their water needs from their prey's blood.  It's also sometimes said (incorrectly) that the salt concentration of blood is like that of seawater; this is not true (blood is more like 1% or less NaCl) but it may be the source of the statement.


What is the relationship between DNA molecules and the chromosomes?

To cite @canadianer, I don't really understand what you're asking but the following may help you.

Genome composition

First of, in the genome of most eukaryote (incl. all plants, fungi and animals), in general, genes constitute only a small part of the genome. Typically, in humans genes occupy 26% of the genome (24.5 for introns and only 1.5 for exons).

What does a genome look like?

Introduction

You say

  Isn't DNA one molecule?

I think this question shows an important misunderstand you have. Note that I will only talk about the nuclei of eukaryotes below.

DNA is a type of molecule, which is constituted of two anti-parallel strands. In the human genome, we have 46 chromosomes, that is 46 independent DNA molecules. Now, these exact numbers vary depending on the moment in the cell cycle you want to consider but this is a story for another time.

A little more advanced

Below is a karyotype of a human allowing you to visualize the chromosomes. The 46 chromosomes we have go by pairs (pair of homologuous chromosomes) and on the image, they are numbered by pairs, the last pair being the sex chromosomes. By the way, can you identify the sex?

Note now that, depending on the moment in the cell cycle you want to consider, each homologuous chromosome may be constituted one 1 or 2 DNA molecule, each of them being called a chromatid. Chromatids are physically attached by the centromere. Two physically attached chromatids are called sister chromatids.

More information

For the moment, I threw some vocabulary at you but it was probably a bit hard to follow. You can get more information at the posts

Chromosome and chromatid numbers during cell cycle phases
The human has 46 double chromosomes or simple chromosomes?

or simply an intro course to genetics such as the following three courses by Khan Academy

Classical and molecular genetics
DNA as the genetic material
Central dogma (DNA to RNA to protein)


Designing primers with restriction sites

Yes.

If you intend to subclone the fragment via classical restriction enzyme cloning you need the overhang.

Different restriction enzymes require different lengths of overhang to allow them to sit fully on the strand and then cleave the sequence.

NEB has a great page detailing how many bases are needed for the enzymes they sell:

https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments

No, it doesnt matter if the overhang appears elsewhere in the DNA, just so long as your restriction sites don't (obviously).

Here are some considerations I use when designing primers for PCR (though not wholly applicable if you're just having it synthesised):

Use the 3+ basepairs present the given number of nucleotides in your restriction site away in the sequence you're PCRing from as your overhang sequence to allow a few more bases to bind. I.e

With the following primer:

Overhang - Restriction Site - Priming sequence

AAA-GGATCC-ATGACATGCAGTAGC     PRIMER

|||        |||||||||||||||

TTT--------TACTGTACGTCATCG     TARGET SEQUENCE
Alternatively, I use those 3 or so basepairs to add or remove GC content and manipulate the Tm if the annealing temperatures of the 2 primers aren't ideally matches


Well, I'm glad you're curious, but you must realise that your question is highly complex. You'd certainly have to refer to a research paper for the exact, factual information. All the same, I can tell you a bit about Dopamine (the pleasure hormone) based on recent reading.

Dopamine creates pleasurable feelings when it is released in areas such as the nucleus accumbens and pre-frontal cortex. This happens when positive, or rewarding actions are undertaken. Dopamine release in the nucleus accumbens is so consistently tied with pleasure that neuroscientists refer to the region as the brain's pleasure centre. However, this is not the ONLY pleasure centre.

Now this is all I know. You should probably check out this page for more, in-depth info: http://wings.buffalo.edu/aru/ARUreport01.htm

It's a long read, but I'm sure you'll find something worth your time.


Why not surgically resect the tumor before CAR-T cell therapy? Won't that be more efficient?

CAR-T cell therapy (Chimeric Antigen Receptor-T cell Therapy) is most effective in treating hematological malignancies. Hematological malignancies (known as blood cancers in common parlance) mean the cancers produced due to over-proliferation of hematopoietic stem cells and the liberation of the immature cells into the circulation . Till now all clinical trials of CAR-T cell therapy has seen more and more success. With the development of second, third and fourth generation (also called TRUCK T cells) CAR-T cells the percentage of remission is increasing. But  almost all these advances are in hematological malignancies.

Clinical trials on solid tumors has shown that the "efficacy is not as remarkable as in the case of hematological malignancies".

The question asked was about resection of the tumor before treating with CAR-T cell therapy. This question is valid only in case of solid tumors (you can't resect blood as it is liquid). As I already said this therapy is only used for blood cancer till now, so there is no question of surgery before the therapy.

I think I could answer your query above. If you want to gain more knowledge, then read below -

The best use of this therapy in blood cancers is after hemato-poietic stem cell transplantation (note that it is not surgical resection)
If you ask, why this therapy was not successful in solid tumors, I would recommend to read the review published in Springer with the title "Hurdles of CAR-T cell-based cancer immunotherapy directed against solid tumors".

Recently however there are new developments that are helping to apply this immunotherapeutic procedure in case of solid tumors also and in that case it is usually given after surgical resection.


If I am not mistaken, the vast majority of mutations happen during DNA replication.

DNA must replicate itself so that cells can replicate itself. The DNA polymerase is one very important protein that replicates DNA. The human genome (to consider this example) is 3.5 billions nucleotides long. Just to realize how long is 3.5 billions letters, let's make a book analogy.

Book analogy

In the Harry Potter series, there are about one million words (ref).
In the LOTR series, there are about one 400 thousands words (ref).
In the Chronicles of Narnia series, there are about 230 thousands words (ref)
In the King James Bible, there are about 788 thousands words (ref)

This sums to about 2.4 millions words. As, in english, there are 5.1 letters on average per word (ref), this lead to a total of about 12.3 millions letters. Imagine you have to rewrite all of these books almost 300 times (12.3 millions * 300 ≈ 3.5 billions)! How many typos would you make?

There are several cell divisions between a zygote and the ovule/spermatozoid produced by this individual but as most mutations happen during meiosis, I will just ignore mitotic mutations. The DNA polymerase makes about one typo every 100 millions nucleotides (Kong et al. 2012; Rahbari et al. 2016)! So really, the DNA polymerase is doing a pretty good job!

What is causing mutations?

Shit happens

I am hoping that form the above analogy, you may have a sense that mutations are just small mistakes. They happen because the replicating machinery is not perfect. Sometimes a molecule comes sideway, does not bind very well and another molecular passing by sticks to the DNA, etc.. Errors happen just like you would be making a lot of typos, rewriting books.

Mutagens

There are of course factors that can affect this mutation rate. Physical, chemical and biological agents increasing the mutation rate are called mutagens and they include radiation decay, ultraviolet radiation, ROS, benzene as well as some viruses and some parasitic bacteria.

Variation along the genome

Note also that the mutation vary along the genome too. Regions with high repeats (e.g. AATAATAATAATAATAATAATAAT) such as microsatellites for example tend to have a much higher mutation rate.

Variation among species and Drake's rule

Mutation rate also vary among species. There is a general tendency that the per nucleotide mutation rate negatively covary with the genome size, a phenomenon called Drake's rule (see for example Bradwell et al. 2013 or one of the early Drake's paper).


Simulating substitution rate of neutral mutations

I don't fully understand how your model works

I don't fully understand how you model your population. Is it a standard $oop$ (object-oriented programming) where you simulate each individual? Or is it a simulation where you already use some mathematical model? You could eventually copy-paste your code. it is probably not very long, right? What language did you use? Do you have only one locus? Do you simulate several positions within these locus? Do you allow for back mutations?

It seems that you allow the population size to change over time and I don't quite understand how your parameter $K$ does limit the growth rate though. You should write down some equations about that. In any case, change in population size will modify the probability of mutation fixation.

Here is probably some important modifications to do on your code

It is a bit hard to comment on your simulations without actually seeing some equations or seeing the code but I really think that you'll need two important modifications in your code.

fix population size $N$.
To simulate reproduction, randomly choose (uniform distribution) individuals (with replacement) from the population. The chosen individuals form the new generation. For example:

In R:

new_pop = sample(old_pop, N, replace=T)

or directly

pop = sample(pop, N, replace=T)

In Python:

from random import randrange
new_pop = []
for i in xrange(N):
    new_pop.append(old_pop[randrange(N)])

When you get your results, don't forget that you're talking about a stochastic process and you may want to run enough simulation or enough independent loci in order to be able to compare with the predictions from mathematical models.


What current evidence supports the use of hydroxycloroquine used as a prophylactic for (corona)-viral infections?

The only double blind randomised clinical trial I am aware of is this one, examining the use of hydroxychloroquine for the treatment of HIV-1-infected patients.  It finds significant reductions in viral load, but not improvement of CD4+ counts.  How much change could be expected in 8 weeks I do not know.  There are in vitro studies, such as this one looking at dengue virus.

In combination with azithromycin it has been examined for the use in COVID-19 (pre-print, not peer reviewed), but without a control group I find it hard to call it a clinical trial, and there are other criticisms of the work.


Difference between mutation and DNA damage

Have you read the DNA repair article on Wikipedia?  The DNA damage and mutation section answers exactly what you're asking:

  DNA damages and mutation are fundamentally different. Damages are physical abnormalities in the DNA... [and] can be recognized by enzymes, and, thus, they can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying.... In contrast to DNA damage, a mutation is a change in the base sequence of the DNA. A mutation cannot be recognized by enzymes once the base change is present in both DNA strands, and, thus, a mutation cannot be repaired.

Here's the entry from the NCBI MeSH Glossary saying the same thing:

  Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION... They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR).

And for mutation:

  Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.


How to detect Single Nucleotide Variants (SNVs)?

Your link doesn't link to the paper, and you seem to be ignoring half of what the image is trying to get across.

The point is that since tumors are heterogenous, you very well might have only 40% of the cells heterozygous for a particular SNV, which means it would only be observable in 20% of the reads.  But if multiple reads with different start sites show the same SNV, it's likely to be real.  If coverage is so low that you only get one read showing a real SNV, you won't be able to distinguish it from noise.


The MIT synthetic chemist Gobind Khorana won the 1968 Nobel Prize in Chemistry for his work which successfully was able to make chains of Ribonucleic acids.  The chemistry was difficult at the time but he won the prize for making specific sequences of RNA bases which were then fed to cells, resulting in specific amino acid chains, which ultimately deciphered the specific base to amino acid correspondence of the genetic code.

Khorana was only one of the chemists who worked on nucelotide synthesis, but the technique overall is simple and since nucleic acid polymers are only unbranched polymers,
any sequence combination is easily obtained.  Each sequential reaction adds one base.  Repeat the reaction as many times as needed.

The chemistry Khorana devised was refined and easily extended to DNA polymers since the linkages are identical, the difference between DNA and RNA is only a single alcohol (-OH) group, which is not directly involved in the bond between the nucleotide bases.

By 1983 when Kary Mullis concieved the idea of PCR, short sequences of DNA and RNA could be synthesized on commercially available machines.  In fact Mullis was responsible for just such a machine at Cetus Pharmaceuticals and had been trying to find a way to increase demand for his services.

The PCR oligos were the easy part of the operation.  To prove the concept, the team at Cetus used a conventional DNA polymerase and add it to the PCR mix after every cycle.  By 1986 the Cetus team had succeeded in performing PCR a heat tolerant DNA polymerase from Thermus aquaticus, a bacterium from a hot spring, which basically made it the technique we still use today.


Identification of a spider from my basement

I think it's a common wolf spider, which closely resemble funnel weavers. It's almost a toss-up. I can't tell from the resolution of your photograph, but funnel weavers have spiny legs whereas the wolf spider has smooth legs and has a bit more of a difference in the comparative size of the abdomen to thorax.

Wolf spider (coloration varies) vs. funnel weaver (in this case, a barn dweller)

Another distinctive feature of the wolf spider are the two especially large eyes (The Tenegra domestica's eye arrangement is different) which gives the wolf spider such great eyesight. If the legs are smooth, and you shine a light on your spider and see two eyes shine back at you (called eyeshine), I think you have your answer.

  Wolf spiders can be found in a wide range of habitats both coastal and inland. These include shrublands, woodland, wet coastal forest, alpine meadows, suburban gardens, and homes.


The term you should look up is sperm competition, there is an introductory wikipedia article about it here, where you can get the basic picture and get some references to explore.

Simply said, males often compete with other males in the reproductive tract of the female, thus a higher number of sperm will lead to a higher chance of fertilizing the female in competition with other males - leading to an arms-race of the number of sperms a male eject into the female.

There is a lot more to it, of course, but I believe this well explains the most fundamental driver of why males generally produce and eject so many sperms.


Cellular respiration in plants is slightly different than in other eukaryotes because the electron transport chain contains an additional enzyme called Alternative Oxidase (AOX). AOX takes some electrons out of the pathway prematurely - basically the energy is used to generate heat instead of ATP.

The exact purpose of AOX in plants is still unclear. Plants will make more AOX in response to cold, wounding, and oxidative stress. We know of at least one plant (skunk cabbage) that exploits this pathway to generate enough heat to melt snow. This link gives a pretty good overview.

(AOX is dear to my heart, since my first 3 years working in a laboratory were spent studying this gene <3)


Violation of the law of energy conservation between photosynthesis and respiration?

The Fallacies in the argument

The question contains two main fallacies (some would say sleights of hand) in the energetic comparison of glucose synthesis from CO2 in the Calvin cycle and glucose oxidation via glycolysis, the tricarboxylic acid cycle and the electron transport chain:

  The descriptions of the two reactions are incomplete — important co-substrates are ignored.
  The formulation of the question seems to assume that the energetics of a biochemical reaction series is reflected solely in the
  interconversion of ATP and ADP, rather than the free energy changes
  that occur in all associated reactions.

Detailed explanation

To make a valid comparison of the thermodynamics of glucose oxidation to CO2 with its synthesis form CO2 we have to consider the single reversible reaction:

 (The ‘6H’ may appear rather odd, but it is accounted for in the reduction of cofactors etc.. We cannot include oxygen in the equation because it is not involved chemically in the synthesis of glucose. Therefore for this treatment the electron transport chain is not included, although it is discussed later.)

The reaction from left to right is associated with a certain decrease in Gibbs free energy (ΔG) and that from right to left in a corresponding increase of the same value. In a non-biological context this might involve the evolution and use of heat energy, but in the cell it involves the chemical energy of bonds between atoms. We therefore have to consider all the chemical reactions to which the reaction above is coupled, i.e. which receive or transfer free energy. The additional reactions and the free energy changes they involve can be found in the chapters on glycolysis, the tricarboxylic acid cycle and the Calvin cycle in Berg et al. and are (omitting water, hydrogen ions and inorganic phosphate):

From which it can be seen that the chemical energy input required for synthesis is greater than that obtained, contrary to what is asserted in the question

What about the ATP?

Yes, the cell oxidizes NADH and FADH2 and uses the free energy change to build an electrochemical gradient, the dissipation of which generates ATP (30 molecules per glucose molecule is the current estimate). However that is separate process, with no counterpart in the Calvin Cycle, where the NADPH is generated from photosynthetic reduction and not from ATP. However, if you perform a naive ‘currency conversion’ at the rate of 3ATP per NAD(P)H and 2ATP per FADH2, the balance is: input for synthesis 54 ATP, output from oxidation 38 ATP, i.e. the same general result as above.

Popularizing science is not easy, and those who make the effort can be excused for equating energy with ATP (often as clip-art lightening flashes). However if you wish to study metabolism you need to think scientifically about chemical thermodynamics and free energy. The fact that the hydrolysis of ATP to ADP is accompanied by a decrease in Gibbs free energy is not particularly chemically remarkable in the context of the free energy changes of other chemical conversions in the cell (including NAD(P) oxido-reductions). What is remarkable is that the cell has evolved enzyme that catalyse reactions in which the free energy change from this conversion is not lost as  heat, but can be used to offset the +ve ΔG of a reaction to which it is coupled. Reactions involving NAD(P)H do the same thing, but they are limited to reductions, and the free energy change is inconveniently large.

Why the accepted answer to this question is a red herring

The accepted answer addresses a different question to that posed. It cites a calculation of the photon energy required for converting carbon dioxide to glucose. This is irrelevant to the thermodynamics of the Calvin Cycle, which can occur in the dark. It is relevant only to the efficiency of the use of photon energy in phosphorylating ADP and reducing NADP+ (incidentally in an open system) — a distinct reaction. The thermodynamics of the reactions the question refers to — glucose / carbon dioxide interconversion processes — do not involve the generation of their co-substrates.


Phenol absorbs at 230 nm, this is the most likely contamination in your case. You should try to avoid pipetting from the phenol phase, or use a phase lock gel to make this easier. I assume you washed it a few times with pure chloroform after the phenol/chloroform mixture, that should help to get rid of the phenol.

I only precipitate my RNA with 1-1.5 volumes of isopropanol after the chloroform/phenol extraction, that should be sufficient for most uses. Just add the isopropanol, keep it at -20°C for 30 minutes and then centrifugate it at 9000 g for 20 minutes, redissolve the pellet in water.


Do local potentials always precede action potential?

I have to admit that I have never thought about if lower potential stimuli can add up. I have done some research though and you are correct. If there is multiple stimuli that don't reach threshold potential it is possible that those sum up. Summation is possible due to stimuli that are directly after another or that are at the same location after another.

-> Spatial summation

-> Temporal summation

Do all stimuli have the same effects?

No - some inhibit a reaction, some provoke one.

How do channels react?
Voltage-gated ion channel contain proteins that react to changes in electrical fields .

At first the sodium channels open up when the stimuli reached treshold potential. That causes the sodium ions to rush into the cell, making it more postive. They start to close before the overshoot.

The potassium channels then start to open and repolarize the membrane.

Single shots doesn't have a huge effect on the membrane.

Na+/K+ ATPase keeps the settings for action potential alive.


What does chromosome CHR_Un, CHR_MT in the ftp site of NCBI mean?

chr_MT: List of variations that map to the mitochondria

chr_Multi.txt.gz: List of variations that map to multiple chromosomes

chr_UN: List of mapped variations that are on unplaced chromosomes

see here for more information.

This is the reference genome for human, as far as I know there is no discrimination for it into male/female.


"Valid" in this case is just emphasizing that the Heterotermes perfidus on this island are a different (real) species, and not just a variation of their closest relatives. You need not get bogged down with how we determine species, or define species. It just means that this taxon (named group) exists as a separate species: a "valid" species, based on differences that some taxonomist deemed important enough to describe and give a name. Others may disagree, and write a paper to synonomize it (sink it into another existing species), but that is part of the messy business of taxonomy.