how does one apply for masters in genetics abroad?

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Why does increased humidity decrease coronavirus "survival"?

I found an answer to this mystery in the literature, but it is a somewhat tentative explanation from a relatively recent (2012) paper by Yang et al. In a nutshell, [respiratory] viruses do worse in small droplets compared to large/unconstrained ones. Even being "totally" dry is apparently somewhat better for them than being trapped in a small droplet. So you get a V (or U)-shaped survival curve as a function of relative humidity.

There appear to be three regimes of IAV [influenza A virus] viability in droplets, defined by humidity: physiological conditions (∼100% RH) with high viability, concentrated conditions (50% to near 100% RH) with lower viability depending on the composition of media, and dry conditions (<50% RH) with high viability. This paradigm could help resolve conflicting findings in the literature on the relationship between IAV viability in aerosols and humidity, and results in human mucus could help explain influenza’s seasonality in different regions.
[...]
After release from the respiratory tract, where RH is ∼100%, a respiratory droplet shrinks by 40–50% in diameter at RH below 90% due to evaporation [16]–[18]. As a result, concentrations of solutes in the droplet increase by up to 15 times, and solutes such as salts (e.g., sodium chloride (NaCl)) that are harmless at physiological levels may become harmful to the virus. For example, avian IAV has been reported to be less stable at salinities greater than 25 g L−1 [19]. Evaporation induces changes to IAV’s microenvironment inside droplets that may affect the virus’ viability, and the toxic effect of solutes may be enhanced at lower RH due to higher concentrations that result from greater loss of water.

Yang et al.'s paper has been positively cited in a couple of subsequent reviews  Lowen and Steel (2014) and Paynter (2014)
So it seems to be a fairly credible explanation as far as influenza is concerned. Paynter's review also discusses similar observations on RSV:

One study examined the effect of humidity on RSV survival in 1 μl droplets of tissue culture medium on polythene at room temperature. Over the first 5 h, RSV survival was highest at the highest humidity, while over the next 67 h, RSV survival was highest at the lowest humidity. The explanation of these findings may lie in the droplet drying time in this study. Droplets exposed to 77% RH were still wet at 18 h (no data were given for drying times at 32% or 52% RH). The relatively high survival at higher humidity over the first 5 h was probably due to the fact that the droplets remained wet in these conditions. The survival over the final 48 h (when all droplets were dry) was progressively reduced with increasing humidity. Consistent with this explanation, only 1% of RSV was lost over the 72 h when stored in liquid culture medium, and in addition, the authors noted that RSV survival was increased with increased droplet size. Similarly, in another study the survival of RSV on countertops was reduced if the virus was in droplets that were dried quickly. These results are consistent with the studies examining influenza survival on surfaces, suggesting that while the virus remains ‘wet’ in droplets, high humidity prolongs its survival, by reducing evaporation.

There might be more recent advances in this area though, especially regarding mechanisms of the "middle regime".


They look very much like Hippoboscidae. https://en.wikipedia.org/wiki/Hippoboscidae
This family are parasites of birds and mammals, but I am not aware that they are vectors of any diseases to humans. So don't worry. One member of the family is a wingless parasite on sheep (Melophagus ovinus)


How to seek for available genetic data relevant to ecology and evolution?

As a bioinformatician, one of my tasks is quite often to get information from databases or find the correct database to compare to. There are several big databases around, but even those are way too many for any single person to know.
There are databases specialising on genetic data, some specialising on taxonomic information, some on ecological information and then there are species specific databases which collect all kinds of data from a given species, genus or clade.

For me the biggest source of generalised information would be the NCBI databases, including GenBank for nucleotide sequence, their Protein database and maybe dbSNP for, well, SNPs. Then there are multiple 16S databases I have used, there is UCSC for the basic data about the human genome, flyBase for Drosophila,... I think the point should be clear. And those are only the ones that just sprang to my mind.

If you don't have a very exact question to answer like "Is there a gene similar to gene x from Drosophila present in any Bacteria?" it can be very hard to both choose the correct database and also find the important information in it efficiently.

Then there is the problem of metadata. I might be able to find sequencing data from the gut microbiome of a human treated with antibiotics quite easily. If I am looking for a specific antibiotic given over a minimal time of seven days to a different healthy humans, preferably including at least one breastfed child and it's mother (which was the one taking the antibiotics, not the child), then it's getting complicated. Here it is generally way easier to scan PubMed for some relevant publications on the matter and find out if they used published datasets or published their own.


Did Carl Linnaeus ever name a species he never saw?

During Linnaeus' lifetime there was two ways to get in contact with exotic specimens other than travelling abroad: by visiting museums and collections or by receiving the specimens at your home/laboratory✻. Natural history museums were not that popular at Linnaeus time but only some time later, in the nineteenth century (the first natural history museum, the Muséum National d'Histoire Naturelle, was created in Paris in 1635).

That leaves us (or even better, Linnaeus) with the second option: receiving the specimens. According to the University of California, Berkeley:

  Linnaeus continued to revise his Systema Naturae, which grew from a slim pamphlet to a multivolume work, as his concepts were modified and as more and more plant and animal specimens were sent to him from every corner of the globe. (emphasis mine)

You could argue that a (dead) llama is a big animal, but one can describe an animal using just its bones, or even just some of its bones. Besides that, it's worth mentioning that Owen received a whole mammoth in UK to study and describe! So, sometimes, size is not a problem.

Answering your second and third questions, a good deal of the animals he described he never actually saw in the wild or alive. Estimating the precise fraction is way more complicated. The same may be said regarding plants, but I guess that the fraction here is smaller: live plants are easier to maintain, seeds are easy to be transported and sown etc. Besides that, botany was Linnaeus' area of expertise. The same link above says...

  Linnaeus was also deeply involved with ways to make the Swedish economy more self-sufficient and less dependent on foreign trade, either by acclimatizing valuable plants to grow in Sweden, or by finding native substitutes. Unfortunately, Linnaeus's attempts to grow cacao, coffee, tea, bananas, rice, and mulberries proved unsuccessful in Sweden's cold climate. His attempts to boost the economy (and to prevent the famines that still struck Sweden at the time) by finding native Swedish plants that could be used as tea, coffee, flour, and fodder were also not generally successful.

... which shows us that he dealt with live exotic plants.

Regarding your fourth question ("did he name species based on other people description but without ever seeing one dead or alive?"), the answer is yes, specially for plants and insects: there are several specimens that Linnaeus described based just on drawings or paintings (which may be considered other people's description), without ever seeing the actual organism. Two examples are Dysdercus andreae (an animal) and Porella (a plant).

PS: Not related to this question or to biology, but this is (unfortunately) quite common in sciences: some of Freud's patients, among them his most famous cases (Anna O., little Hans, etc...), he never actually met or even saw at the distance! He "diagnosed" them using just descriptions and hearsay...

✻ According to RHA comment below, there is a third way: sending people to collect the specimens for you.


By What Mechanism can Felines Reverse Diabetes?

I spent a couple of years working in a diabetes research institute.  And you did hear right.

Cats dogs monkeys all can be susceptible to diabetes, although rats and mice don't seem to have diabetes that behaves the same way as humans - I don't think a mouse has ever been observed to get diabetes without specific gene knockouts.  One could argue that mice simply do not get diabetes the way people do.

There are two causes of type 2 diabetes in the research world.  The first happens because the animal may have a genetic susceptibility and environmental conditions induce the disease (like most people).  The second happens because of mutations in one specific gene or another pretty much cause it to happen when the animal gets to a mature age (google term: mature onset diabetes in the young (MODY)).  MODY genes have not proven to be a great model for type 2 diabetes treatment in most people (about 1% of diabetics have a MODY diabetes though).

Cats and dogs have been animals of interest as models of diabetes because their symptoms are human like and have shorter reproductive cycles.  Some cats (like Burmese) clearly have a greater genetic predisposition to diabetes, but cats who are obese, have high glycemic diets, or who get little or no physical activity are more likely to develop diabetes.

As with humans, the condition leads to the insulin secreting cells of of the pancreas to slowly degrade and if these cells are gone, there is no recovery from type 2 diabetes. All this given its likely that cats get diabetes that is similar to the human condition.

In treating cats its been shown that such diabetes can be reversed.  The most important thing to do - common to all treatments - is to change the cat's diet - restrict calories if the cat is obese and change high glycemic food.  Additionally, insulin or drug treatments that reduce insulin resistance (such as are given to humans) can restart the islet cells that secrete insulin if the animal is lucky and don't always have to be lifetime prescriptions.

The reference I have does not give remission statistics, but it must work a reasonable amount of the time.

But I wouldn't want to leave you with the impression that cats are special.  It turns out that human diabetes type 2 is often reversible.  This reference estimates 80% of the time. This study mostly focuses on the same treatments - change of diet and some fasting, but no exercise regimin as the cats.

There's probably nothing magical about cat diabetes 2... ;)


How do signalling molecules find their receptors at large distances?

Yes, any individual ligand may have the wrong orientation to interact effectively with an individual receptor, but so what?  There are typically thousands of each type of receptor on a single cell1 and there will be many molecules of a given ligand present as well.

For your synapse example, I suggest looking up:

How many neurotransmitter molecules will be present in a synapse
How many receptors will present in a synapse
How many of those receptors need to be bound to get a signal

I think that will help you make sense of this phenomenon and I encourage you to post a detailed answer to your own question!

You might also want to look into molecular dynamics simulations ...

1: Milo, R., & Phillips, R. (2015). Cell biology by the numbers. Garland Science.


Why introduction of an extra copy of a gene related to pigmentation causes RNA interference in Petunia?

The answer is in the slides you provided a link to. The key fact is that Craig & Andy did careful controls to show that it was the presence of dsRNA in both the sense control, and in the anti-sense experimental sample that was responsible for the RNAi-mediated knock-down.  Actually, Ken Kemphues showed this earlier in a Nature paper (the control also knocked down gene expression) but did not pursue the mechanism.

Therefore, I infer that the transgenic gene expression construct introduced into the petunias must also give rise to dsRNA. I am less familiar with the consequences of introducing foreign DNA into a plant cell (e.g., does a single copy become integrated, multiple copies?, is it maintained extrachromosomally?)


First, I must clarify that a nerve is not the same as a neuron. A nerve is a collection of axons (with each axon a part of an individual neuron) in the peripheral nervous system. Thus, when you mention “single long axon such as the sciatic nerve”, this is technically an incorrect phrase as the sciatic nerve is a collection of many long axons. If one of these axons is nonfunctional, this would not severely affect the function of the entire sciatic nerve. However, you are right that if the entire sciatic nerve is severed, then there would be serious consequences downstream.

Second, the primary advantage of conduction velocity is less dependent on length and more dependent on presence and degree of myelination (directly proportional to fiber diameter) and presence of nodes of Ranvier.

With regards to the content of your question, the advantage of length is exactly what one might think--- greater distance. The sciatic nerve is the longest nerve in the body in order for our nervous system to innervate as far as the tip of our toes. Having hundreds of side-by-side series of neurons compared to hundreds of side-by-side axons seems like a far less efficient system in a couple of ways in exactly the two ways you mention: energy and time.

Energy: Having serial neurons would require an increase the number of neurons needed to transmit a message. Having more neurons requires more Na+, K+ and Na/K pumps and individual channels, requiring more energy.

Time: Having serial neurons would also require an increase in the number of synapses between neurons— either electrical or chemical. If the synapses are chemical, then time is increased many-many fold. If the synapses are electrical, then time is slightly increased by 10-fold per synapse compared to chemical synapses, but this would still take more time compared to having a single axon with myelination and nodes of Ranvier which by about 100-fold faster than a single electrical synapse.

In summary, having longer nerves made up of axons rather than serial neurons is beneficial by improving energy and time efficiency, which allows our bodies to effectively innervate structures farther away.

Ref:

Regarding delay of conduction: Chemical v. Electrical/Gap  Ch 10 of Principles of Neuroscience- "Synaptic Integration in the Central Nervous System" (Siegelbaum,
Kandel, Yuste) 5th ed. McGraw-Hill Medical, c2013.
Regarding conduction velocity of myelinated versus nonmyelinated
cells

Regarding the ATPase absolute number increase in serial vs one long axon, I assume this will depend on the number of neurons in series. However, I read this paper, which says that increased length between each node of Ranvier has been physiologically associated with increased conduction velocity. This suggests fewer needed nodes, despite concentrated ATPases at these locations, and thus fewer ATPases. I haven't been able to find studies which compare ATPase concentration in the soma compared to nodes of Ranvier within axons.

Regarding energy use in soma vs axon, mitochondria are not only made in the soma but are concentrated in pre- and post-synaptic membranes (and growth cones). The more of these structures there are (as in serial neurons), the more presumed mitochondria. See mitochondria and neuronal activity.

Finally, my literature search could not find studies which showed longest possible energetically feasible length for myelinated or unmyelinated neurons.


Photosynthesis in oxygen free enviornment

If that "environment" is a closed vessel or bell-jar; certainly the plant would survive in light (when it simultaneously perform respiration and photosynthesis), and in darkness (when it can perform only the respiration) it would survive upto certain time due to the oxygen it accumulated. But should die at prolonged darkness when the plant would finish all the oxygen.

(as suggested by Priestley's classic 1870 experiment * there was enough oxygen to keep a mouse for certain time)

(image link)

However, if we look the effect of various concentration of O2 on photosynthesis rate without altering the CO2 concentration; yes the photosynthesis rate get affected; one known effect is called Warburg effect or Inhibition of photosynthesis by O2.

In this effect, photosynthesis rate only decrease if O2 concentration is increased. And in vice-versa, with O2 concentration decrease, photosynthesis rate only increase. (source: this, this, this and this)

This take place due to mainly 2 causes: 1. O2 work in  competitive way with CO2 for binding with the enzyme RuBisCO, the key enzyme for CO2 fixation in plants. 2. And that induces photorespiration (in C3 plants). (Wikipedia shows reference to here). (However this old paper also tells other hypotheses)

There are 2 type of responses in photosynthesis rate in at different O2 concentration in various plant species.

One group of plants ( known to bel C3 plants, those do not have any any CO2 concentrating mechanism) ), is remarkably affected by O2 concentration; i.e. affected by Warburg effect in true sense.

Another group of plants ( known to be C4 plants, those have a certain type of CO2 concentrating mechanism); does not significantly get affected by O2. I.e. doesn't show the Warburg effect.
(see also : table).

By the way, It seems photosynthesis would increase than normal  if we could make the environment "completely oxygen-free" but other parameters same. (due to elimination of O2inhibition) But I could not find any report about such "completely oxygen-free" conditions; and seemingly it is not possible because while doing photosynthesis; some  of the evolving oxygen molecules will pass through the cytoplasm; some will move in the intercellular space, and few molecules will stay diffused in atmosphere around the plant. We can only decrease the concentration of O2

Also; Warburg effect is completely about photosynthesis rate. It is not about plant's overall health. Removal of O2 increase photosynthesis rate... it does NOT mean the plant would live healthiest in oxygen deprived condition

  Sources:

  Fundamentals of Plant Physiology by Dr. V. K. Jain; revised edition; S. Chand Publications, New Delhi.
  * Biochemistry/ Lubert Stryer/ 4th Edition/ W. H. Freeman and Co.


There is no TSS of a gene. Geneic region will be a union of all the transcripts arising from that locus (including introns).

Sometimes two variants of a gene can have different TSS. You can define a 5' boundary of the geneic region which would be the most 5' TSS amongst all variants. You can also give scores to the TSS based on the expression of the different transcripts.

Nevertheless, I am not sure why you want this.


Yes steroids are a class of lipids which include cholesterol and sex-hormones such as testosterone and estrogen. Only vitamin-D belongs to the class of steroids.

Vitamins A, E and K are isoprenoids. In fact even steroids are synthesized from simple isoprenoids. You can refer to a standard biochemistry book to understand steroid biosynthesis pathway.

There are other classes of lipids too, such as fatty acids, phospholipids, ceramides etc.

Yes all fat-soluble vitamins are lipids. This is the definition of Lipids from the IUPAC goldbook:

  A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

Both fats and fat-soluble vitamins are nutrients but are functionally different. Fats provide energy whereas vitamins perform regulatory activity and are required in little amounts in the diet compared to essential fatty acids.


The main functional reason is we need to be able to grip things with our hands (and feet, which are also hairless), and hair would interfere with that. Physiologically, the epidermis in these parts of the body is very thick and highly keratinized, and when combined with the thick underlaying layer of dermis, this results in skin that does not support the growth and maturation of hair follicles.


Is "TATA signal" synonymous with "TATA box"?

"Box" is an archaic term from long ago. It's little used. "Signal" has now replaced it. "TATA box" and "TATA signal" are synonymous.


Why is LH level much higher than FSH level at ovulation?

It is not the absolute plasma levels that are important, it is about their relative differences during the cycle. The steep rise in FSH during the first days induces follicle stimulation. The LH surge at day 12 induces maturation of the egg and stimulates its release (see wiki page). The fact that LH's absolute plasma levels are higher may theoretically have to do with the fact that more LH is needed to elicit its physiolocal response. However, the differences of their relative levels is way more important from a physiological point of view.


In an ant (or bee) colony, what is the very approximate ratio of new breeders to workers?

So.

This answer is specific to the western honeybee, Apis mellifera, as there are massive amounts of data on them; more, possibly, than any other insect species. There has certainly been more data collected about them than any other hymenopteran.

At around the time of the nuptial flight, there may be as many as 60,000 workers in the hive, though likely number is more like 15,000 - 20,000. There will be either one (virgin) or two (one mated, one virgin) queens (the old queen will stay with the hive, if she is alive). There may be as many as 400 drones from the original colony (though usually the number is less, around 150 is typical; 10 - 50 of them will actually mate with the queen), and an equal number may join in the flight drawn from other colonies, especially in commercial beekeeping operations. Somewhere between 1000 - 6000 workers will take part in the nuptial flight with the virgin queen and the drones.

This means that in honeybees, the nuptial flight contains 1 queen:~5000 workers:~150 drones.

Data is drawn from many years working with bees and beekeepers. Opinions will vary somewhat depending on the beekeeper and the beekeeping methods. These are based, generally, on bees kept for clover and fruit pollination in the western USA.


The exact mechanism is unclear. Here are some possible causes:

rapid collapsing of cavities inside the joint [1];
rapid ligament stretching [1];
breaking of intra-articular adhesions [1];
escaping gases from synovial fluid [2];
movements of joints, tendons and ligaments [2];
mechanic interaction between rough surfaces [2], mostly in pathological situations like arthritis (and it is called crepitus [3]).

There are no known bad effects of joint cracking [1, 4].

  There are no long term sequelae of these noises, and they do not lead to future problems. There is no basis for the admonition to not crack your knuckles because it can lead to arthritis. There are no supplements or exercises to prevent these noises [4].

And no good effects either:

  Knuckle "cracking" has not been shown to be harmful or beneficial. More specifically, knuckle cracking does not cause arthritis [5].

References:

Wikipedia contributors, "Cracking joints," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Cracking_joints&oldid=617403659 (accessed July 22, 2014).
The Library of Congress. Everyday Mysteries. What causes the noise when you crack a joint? Available from http://www.loc.gov/rr/scitech/mysteries/joint.html (accessed 22.07.2014)
Wikipedia contributors, "Crepitus," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Crepitus&oldid=615557134 (accessed July 22, 2014).
Johns Hopkins Sports Medicine Patient Guide to Joint Cracking & Popping. Available from http://www.hopkinsortho.org/joint_cracking.html (accessed 22.07.2014)
WebMD, LLC. Will Joint Cracking Cause Osteoarthritis? Available from http://www.webmd.com/osteoarthritis/guide/joint-cracking-osteoarthritis (accessed 22.07.2014)


Effect of doubling volumes of PCR reagents

The thermal cycler adjusts sample temperature based on the volume of the sample. So if you run samples of different volumes side by side, not all of them will cycle through the optimal temperatures of each step. If you were working with a "hot start" polymerase this is even more critical, as the Taq won't be able to amplify at all unless the sample is heated up to a specific temperature.


Correct color? Yes
Proper antenna shape? Yes
Thorax shape? difficult to assess
Pinched waist? Yes
Heart-shaped head? Yes

Generally speaking, carpenter ants are black/brown in color, have bent antennas, a pinched waist, a round thorax, and a heart-shaped head.

And to address your confusion from seeing winged ants when searching on Google.. winged carpenter ants appear a few years after a nest/colony has been formed, so if you're not seeing any wings, it may be a relatively new colony.

One last thing.. carpenter ants (should) have hair on their abdomen. From your pictures I'm not seeing any hairs.

Conclusion: I'm 90ish% confident that's a carpenter ant.


How would the human body adjust to sleep times if we were to live in a place with different day lengths?

Humans have evolved for 24 hour days and our bodies would not adapt well to this short of sleep/wake cycles (whether or not they were born there, unless they have been there for many generations and have been able to evolve for the new time). Our bodies would still want to spend about the same amount of time sleeping and being awake.

If we tried to adjust our sleep cycles to this planet with 8.5 hour days, we would experience many of the stresses that occur during jet lag (Google Scholar search), which can cause depression. Jet lag is identical to experiencing one day which is shorter or longer than the typical 24 hours.

The sunlight helps set our circadian rhythm, but 8.5 hours would be too fast. I thought I heard for an experiment that used mice that supports this, but I still haven't found the reference yet.

Nbogard referenced the article Plasticity of the Intrinsic Period of the Human Circadian Timing System, which showed that the circadian rhythm in humans can be altered by up to 0.65 hours by the use of lights. This is consistent with what I mentioned that the sunlight helps to set our circadian rhythm.

The best way to adapt would be to use artificial lighting to keep your days about 24 hour days (artificial light during waking hours, heavy curtains during sleeping hours), as mentioned in ThePopMachine's answer.


Short answer
Jelly fish can sting out of the water and even when they are considered to be dead.

Background
I do not have detailed scientific literature available. However, popular sources generally and equivocally warn against touching jelly fish, even on land and even when they appear to be dead. In fact, dead box jelly fish can be as dangerous as live ones (ABC News).

Credible sources
 - National Poison Control Center
 - UK Telegraph
 - ABC News


what's the difference between traditional genetic engineering and and CRISPR?

Bacteria and archaea evolved CRISPR as part of their adaptive immune system to protect themselves from invading viruses and foreign plasmids. The defence system relies on small, non-coding RNA molecules (CRISPR RNAs/guide RNA) that in association with a CRISPR associated (Cas) protein silence foreign sequences by means of cleavage. Twenty nucleotides at the 5’ end of the CRISPR RNA, corresponding to the protospacer region, direct the Cas9 protein to a specific sequence within the DNA using predictable Watson and Crick base pairing between the target DNA and the guide RNA, triggering enzymatic cleavage of the foreign DNA. Essential for cleavage is the presence of a sequence motif immediately downstream of the target region, known as the protospacer-adjacent motif (PAM),the PAM sequence in S. pyogenes (the most widely used system) is NGG. Because a sequence match also exists between the guide RNA and the host’s DNA that encodes it, it is vital that the guide RNA identifies bona fide targets without attacking the host chromosome. Discrimination between the target and host protospacer is achieved by the Cas effector recognition of a PAM sequence that initiates binding and cleavage of the foreign DNA. Changing the DNA target site that is specified by the 20 nucleotides at the 5’ end of the guide RNA redirects the system to target a different DNA sequence, making it a highly versatile and programmable tool. In 2012, the CRISPR system was  programmed to cleave specific DNA sites in vitro and since then, the system has been widely used in many gene modification applications.

CRISPR allow so much more than just substituting nucletodies. Like you say, CRISPR is a much more precise system than restriction enzymes, the guide RNA for CRISPR systems is typically around 20 nucleotides long so it can theoretically be used to target a unique site in the genome (4^20 = 10^12, so only the recognition site is expected to feature once 1 in 10^12 bases, N.B. the human genome is only 3x10^9 base pairs in size).

There are several options using the CRISPR with an active Cas9 protein, the first is to create a gene knockout, which removes the function of a gene. Gene knockouts can be performed by targeting the CRISPR-Cas9 system to the start of the gene and cleaving both strands of the DNA to generate a double stranded break which will be repaired most likely by the cellular repair pathway non homologous end joining (NHEJ). NHEJ results in insertions or deletions and so will most likely result in a frameshift mutation which alters a large amount of the amino acid sequence in the gene or introduces an early stop codon, so the protein produced is non functional. Alternatively a conserved residue (e.g. a catalytically important residue) in the protein can be targeted and mutation of this can remove the catalytic function or recognition domain in an enzyme or protein. NHEJ can also be used to mutate DNA that codes for RNA products. Additionally, the CRISPR system can be targeted to regions outside of the coding sequence such as the promoter or enhancers and silencers/operators (depending on whether prokaryotic or eukaryotic), which can also remove the functionality of the gene.

The CRISPR system can also be introduced to the cell  together with a single-stranded or double-stranded DNA template to make very small and precise changes to the DNA (e.g. single base mutations), or insert DNA sequences up to thousands of bases in length so that entire genes can be incorporated into the target region. This more precise editing method also involves the double stranded break formation by the cas9 protein, but relies on different cellular repair pathways: homology directed repair, the most common form of which is homologous recombination. Importantly, the template DNA must have homologous sequences to the DNA flanking either side of the double stranded break. In the presence of the correct exogenous DNA template, homology directed repair can occur in which the exogenous template DNA is incorporated into the target DNA in exchange for the damaged DNA.

Other use of CRIPSR include using a catalytically inactive cas9 protein (dead Cas9). This system is unable to cleave DNA, but is still able to target specific sites in the DNA. dead Cas9 can be fused to or recruit effector proteins for regulating gene expression at the transcriptional level, as well as guiding enzymes capable of precise base editing without introducing double stranded breaks. The dead cas9 system can be fused to transcription repressor domains such as the Krüppel-associated box (KRAB) or transcriptional acitvators such as VP64 for effective and specific repression or activation of gene expression at sites that don't contain recongion sequences for these effectors. dead Cas9 can also be used to recruit epigenetic modifitying enzymes such as methylases and acetylases to regulate gene expression this way. Additionally, this system can be fused to DNA base editors, which are enzymes created by directed evolution that are capable of causing efficient and specific point mutations in DNA and RNA (this is much more specific and effective than point mutations using homology directed repair), although RNA editing required using cas13.

Gene editing can be used to repair disease causing mutations, introduce new genes with novel functions into organisms' genomes, transiently alter gene expression to treat diseases; create knockout, knockdown and knock in strains for studying the effects of genetic factors on phenotype and even more.

In contrast, restriction enzymes typically have recognition site of 6 nucleotides and so they will cut at many orders of magnitude more sites than CRISPR will (4^6 = 4096, so 1 in 4096 nucleotides are expected to be a cut site for restriction enzymes) so they are not suitable for specific editing of genomes as they will cause non specific fragmentation of genomic DNA, which will kill the organism, so CRISPR is a much better enzyme for editing genomes. Instead, restriction enzymes are used in molecular cloning to generate sticky overhangs (or blunt ends) for the assembly of DNA molecules to generate recombinant DNA.

Although the PAM appears to limit the number of target sites that the CRISPR system can be targeted to (around 1 in every 16), through directed evolution, a Cas9 variant with increased PAM compatibility has been developed. This new Cas9 is capable of recognizing PAM sequences including NG, GAA, and GAT, this makes it  more versatile and greatly expands the number of targets available for site-sensitive genome editing applications.

Whilst CRISPR based gene editing is very exciting, a lot of work is still needed to: increase the specificity of the system as it causes numerous off site mutations, which can be lethal to cells; to increase the effectiveness of delivery of the system in vivo to large organisms such as humans; to reduce the immunogenicity of the system (it can trigger an immune response in humans) so that it is safe to use; as well as increase our understanding of the affect of making specific mutations in humans (e.g. which mutations can treat diseases safely).

References/further reading:

Jinek, M. et al. A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science (80-. ). 337, 816–821 (2012).

Repurposing CRISPR as an RNA-Guided Platform for Sequence-Specific Control of Gene Expression. Cell 152, 1173–1183 (2013).

Liu, X. S. et al. Editing DNA Methylation in the Mammalian Genome. Cell 167, 233–247.e17 (2016).

Zalatan, J. G. et al. Engineering complex synthetic transcriptional programs with CRISPR RNA scaffolds. Cell 160, 339–50 (2015).

Hu, J. H. et al. Evolved Cas9 variants with broad PAM compatibility and high DNA specificity. Nature (2018). doi:10.1038/nature26155

Cox, D. B. T. et al. RNA editing with CRISPR-Cas13. Science (80-. ). 358, 1019–1027 (2017).


Short answer
Neuronal tumors are rare, but they do exist. These cancers develop from neuroblast cells, a population of undifferentiated, dividing precursor cells that will eventually fully differentiate into functional neuronal cells.

Background
Most neuronal cell types have lost their ability to divide, because of their progressed state of differentiation. There are but a few regions in the brains that generate new nerve cells in adulthood, for example in the hippocampus where neuro-regeneration is believed to be involved in memory formation. Because of the rarity of cell division of neuronal cells in adulthood, neural cancers are rare.

The point where neuronal cells actively divide is during development. These cells are basically still stem cells. A prime example here are retinoblastomas. These are tumors in the photosensitive part of the eye, namely the retina. During early development stem cells actively divide to lay down a layered structure in the back of the eye eventually forming the rods and cones and other visual cells. If this division process goes out of control, tumors can develop. Retinoblasomas can now be diagnosed in utero (Paquette et al., 2012).

Tumors with a neuronal origin developing post natally are rare, but do exist. Neuroblastoma being a prime example. This is a rare cancer (prevalence of 1:100,000) most commonly found in children younger than age 5. It affects the sympathetic nervous system, which regulates involuntary bodily functions such as heart rate, blood pressure, breathing, and digestion. Neuroblastoma typically begins in the nerve tissues of the adrenal glands but may also begin in the nerves that are located anywhere along the spinal cord, including the neck, chest, or abdomen. The cancer can metastasize (spread) to other organs.

Note that both examples here are called blastomas, those are tumors caused by malignancies in precursor cells, often called blasts, these cells are dividing cells that will develop into a neuron often after a migration phase. Neuroblasts differentiate from neural stem cells and are committed to the neuronal fate. Hence, although these tumors are from a neuronal origin, they are technically not derived from (fully differentiated) neurons.

Reference
- Paquette et al., AJP Rep (2012); 2(1): 55–62


Could removing non-functional parts of coenzymes improve enzyme function?

The video cited in the question is to be commended and presents a number of points relevant to questions about DNA and RNA posted here previously.

The problem with the question sems to be an incomplete understanding of the role of these coenzymes/cofactors in the function of the enzyme. (The original question implied that acetyl-CoA and vitamin B12 are the enzymes.) In contemporary protein enzymes, these non-protein cofactors are bound to the protein part of the enzyme and complement it in its function. Typically, the protein will have binding sites for the substrates (the reactants) and the coenzyme will provide the sophisticated catalysis or other essential function.

The coenzyme must obviously interact with the protein, and in a way that leaves its catalytic or functional part free to operate. This is what the nucleotide portion of the coenzyme does — in fact it is performing the same role as has been suggested it played in the RNA world, but instead of interacting with an RNA enzyme (ribozyme) by base pairing, it interacts with amino acid side-chains by a variety of weak interactions. An example of this is shown for coenzyme-B12 in the enzyme, methylmalonyl-CoA mutase (my annotations in red and brown).

To quote from the figure legend in the paper: “The lower axial ligand to the cobalt is histidine HisA610, which is in turn bound through AspA608 to LysA604. The pseudo-nucleotide tail is bound in a pocket between the sheet and the C-terminal helix.”

The situation for coenzyme-A (CoA) is slightly different, in that it is involved in the transfer of acetyl and other groups, rather than catalyis per se. However the principle is the same — there is a chemically functional portion and a nucleotide portion that binds it to the protein.

Thus, the nucleotide portion of coenzymes is not redundant and without it they could not bind to the enzyme and enable it to perform its function.


How is the Concept of Simple Diffusion Possible

Simple diffusion is the movement of solutes from an area of high solute concentation to an area of low solute concentration.

Here are a few ways molecules will make it through membrane into cell:

(A) Fuse with the membrane and enter due to like polarities i.e non-polar subtance fuses with non-polar membrane and passes through membrane

(B) Small polar molecules CAN move into cell but at a much slower rate

(C) Through transmembrane integral protein channels such as aquaporins, K+ leak channels, and other channels that DO NOT require energy, and are ALWAYS open

If you want to understand how it was determined which molecules were able to pass through the membrane look for some resources about Overton's Plasmolytic Method.

Alongside that the definition of the partition coefficient will give you some insight on how fast molecules will pass through membrane, if at all.

Good luck on the searching!

@ Ro Siv - Simple diffusion is not facilitated diffusion


How much natural genetic variation is there between bacteria of the same species?

I'm sure the answer will depend on the specific species, but I'm looking for a ballpark figure for bacteria.

Yes indeed it will.  Bacteria are a huge domain of life; you might as well ask for variability between all plants or between all animals.  Bacteria can live in very different environments, and the whole things is made more complex by widespread horizontal transfer.

Still, for bacteria, you can't do much better than E. coli, and boy are they a mess.  Here's a paper from 2010 that blew my mind.  The authors sequenced 61 E. coli genomes and found:

  ...that any given E. coli genome sequenced will have only roughly 20% of its genes part of the E. coli core, and the remaining 80% are not found in all other E. coli genomes.

20% variability within a species.  20%, one species.  E.coli is an extreme example, but still, species is a stupid concept.  Here's a 2006 paper finding that plenty of unique Campylobacter proteins simply aren't in plenty of Campylobacter species.

On a more broad scale, here's an excellent (and free) paper you should look at.  It examines islands of "microdiversity" among various species, finding that some species are easily 50%-75% different.  A simple way to estimate this is too look at gene number for bacterial species, which should make it clear that some of these bugs vary by up to an order of magnitude.

In short: A lot.


It is a silverfish. It is a 'basic lineage' in the insect class. You'll find it here on OneZoom.org.

Silverfish are considered household pests although I don't think they spread disease nor cause much damage (thanks to @WilliamBligh for his comment). They typically live in the canalization (bathroom, kitchen) or anywhere that is wet enough. In a building, they may be hard to get rid of as they can easily move from one apartment to another. You have to keep your place very clean and eventually use toxins such as Permethrin or Deltamethrin.


Is there a statistical analysis test I can perform that will give me a estimate of total population from my own smaller data sets?

I'm assuming you're asking how to estimate population size based on numbers of individuals you capture. Yes, there are many approaches to this. The R library SPECIES-R offers a number of methods of calculating this. They are described in the manuscript SPECIES: An R Package for Species Richness Estimation. Some of the methods described are:

Chao, A. (1984), Nonparametric Estimation of the Number of Classes in a Population, Scandinavian Journal of Statistics, 11, 265-270.
Norris, J. L. I., and Pollock, K. H.(1998), Non-Parametric MLE for Poisson Species Abundance Models Allowing for Heterogeneity Between Species, Environmental and Ecological Statistics, 5, 391-402.
Chao, A., and Bunge, J. (2002), Estimating the Number of Species in a Stochastic Abundance Model, Biometrics, 58, 531-539.

and many more.


Why oxLDL accumulate to form foam cells?

In short, rate of expression of intracellular cholesterol removal proteins like ABCA1 in macrophages and cytokine waterfall molecules in T-lymphocytes beside other anti-inflammatory cytokines has an important role in AS and why oxLDLs accumulate in intima.

When there is high level of oxLDL, rate of removal mechanism must increase to take extra cholesterol out of macrophage and after that to the liver.
And it(increasing the rate of reverse mechanism) could be done by inhibitors or regulators(when natural way could not effort enough excretion). => drugs like TONSHINONE

There is huge amount of information about how regulation of adhesion molecules, costimulatory molecules, antigen presenting molecules and anti-inflammatory or inflammatory molecules could have effect on oxLDL accumulation in macrophages and T-lymphocytes which cause damage induced by hydrogen proxide.

So accumulation of oxLDL molecules in Macrophages has genetic reason and why human being evolved in this way is a question for geneticists but how this happens could be explained by tracing adhesion and signaling molecules.

This is one of the texts about oxLDL accumulation and AS.

Macrophages take in, a large number of oxidized low density lipoproteins (oxLDL) under the intima and then become foam cells, which is one of the early signs of atherosclerotic lesions.

ATP-binding cassette transporter A1 (ABCA1) is an integral membrane protein that transports lipid from the cells to the liver with subsequent lipid excretion by bile at last. This reversal transport inhibits the formation of lipid.

This text shows how regulating cytokine waterfall and pro-inflammatory cytokines could have impact on creation or removal of foam cells.

They experimented that Tanshinone IIA (a molecule extracted from root of Salvia miltiorrhiza) significantly increased expression of ABCA1 in macrophage-derived foam cells, raised the outflow of intracellular cholesterol, and inhibited the formation of oxLDL induced foam cells.

Furthermore, the liver X receptor (LXR) and peroxisome proliferator activated receptor (PPAR) which are members of nuclear receptor superfamily can increase expression of ABCA1 through coupling path. Tan IIA inhibited the formation of foam cells. The mechanism might be that Tan IIA increased expression of PPARa, LXRa, and ABCA1, facilitated reversal cholesterol transport, and ultimately promoted cholesterol efflux.

T-lymphocytes in plaques are mostly CD4+ T-lymphocytes which belong to Th1 subtype. Most of CD4+ T-lymphocytes are active and can induce “cytokine waterfall” as well as secrete proinflammatory cytokines interferon-gamma (IFN-y), IL-12, and other cytokines, eventually leading to inflammation. Experiments showed that Tanshinone significantly inhibited production of Th1-derived IL-12 and IFN-y in a dose-dependent manner. T-lymphocytes play a role in the formation of AS, mainly because of proinflammatory cytokines secreted by T helper type (Th) 1 or Th2. Therefore, Tanshinone can inhibit the formation of AS and stabilize plaques via reducing the secretion of Th1 or Th2. Moreover, T-lymphocytes are activated to express CD40L, and the expression of tissue factor and matrix metalloproteinases (MMPs) is then promoted by interaction between CD40L and CD40.
TanIIA could improve the activity of superoxide dismutase (SOD), decrease the level of malondialdehyde (MDA), and reduce both the expression of CD40 and the activity of MMP-2.

So normally macrophages could excrete cholesterols but problem occurs when your diet contains high level of cholesterol and oxLDL goes high in your blood.

Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 267976, 6 pages
http://dx.doi.org/10.1155/2014/267976


Unfortunately, the answer depends completely on how stringent you are with "Hamilton's rule". If you just mean the equation $r \geq c/b$ then it is important to look at modern usages. In modern usage, all three of the terms $r$, $c$, and $b$ can be arbitrarily complicated. My favorite examples include when $r$ takes into account spatial structure saying that an agent near you is more "related" than a genetically identical agent far from you. Assumptions like that are a must, if you want to look at things that much of modern research is concerned with.

For this "most general" interpretation of Hamilton's rule, only one property is required and this property does not appear on your list: linearity. Note that this is not the same thing as the additivity you describe. Linearity means that your equations for small changes in proportions are linear in fitness: i.e. $\dot{p} = pf(E)$ where $E$ is some description of the environment, and $f$ is a linear function of the variables of interest (I used a continuous or large-population limit here, but similar things hold true for distributions over discrete populations).

Note, that in the above general and super-vague use of Hamilton's rule, the rule itself is not a biological observation but a simple fact of linear algebra. Of course, if you want to get linearity out as a consequence of some biological assumption, then the most common way to do this is by assuming weak selection.

If you put restrictions on what kind of features of the population, interaction, and environment structure $r$, $c$, and $b$ are allowed to incorporate then this will result in biological theories which will be mathematically true under only some of the assumptions you list. The subset of required assumptions will depend on what specific restrictions you place on $r$, $b$, and $c$.

There are no standard assumptions accepted on these parameters, so (unsurprisingly) I can't answer your question further without more specification on your part.


Real-time PCR delay in Cq due to insertion SNP in primer

As @WYSIWYG pointed out, having the indel difference in the 3' end can be informative, but I'm having a harder time finding evidence in the middle of the primer.  Putting the mutation/indel at the 3' end will change the ΔCT.  To do it well, you need wide coverage on your mutation site.

I think that it is possible that there could be a difference with a mismatch in the middle of a primer, but it wouldn't be as obvious as if it were closer to the 3' end.  Unless there was some serious reason why you couldn't put it there (ie Tm below 45 on the reference) that sounds like poor primer design.

I will note I am certainly not a qPCR expert, and I don't think the question has been directly researched (as you surmised).  Again when I've looked for Indels before (was doing some interesting stuff with HLA types...) we used larger primers for the qPCR.

If this doesn't answer your question satisfactory, is there an initial reference you would have us look at?  I imagine things like good quenching and other factors could pull out some significance when comparing two templates (one with indel one without), but again, it's kind of odd to put the mutation in the middle.

Edit to comments:
1: I think the Cq delay is going to depend on things like length, sequence, and mutation.  There may be a grand scheme formula/algorithm to predict the delay, but I don't know of one, and I couldn't find it if it does exist.  Most of the graphs and differences I've seen have been big enough that it convinced me that it was significant.  I don't know if this is like flow where you can sit and argue all day about the biological relevance of 40% to 30% of a particular group.

2: Sorry I didn't have time to come in and give an adequate summery of them.  They are, as you pointed out, tangential to what you're trying to do, but do in fact address the problem through their methods.  I will attempt a better summery as I have time (I've got a grant on I'm trying to get done by Tuesday, so probably after that).  If you have any clarifications to the question to add, please do.

3: This may have grown from the general perception that it was needed, and that I aim for the highest Tm I can generally manage without structure problems being introduced.  I also have the luxury of not needing to worry over the cost of ulta-mers.  It also could have come from history of working in BACs years ago.  Longer primers always increased my success rates when I was knocking out cassettes.


How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon?

As you pointed out sodium as sodium enters the cell depolarizes (becomes more positive). Recall the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge  diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.

So the key is the influx of the sodium ions diffusing down the axon and causing a downstream depolarization of the axon.

I find this website instructive, as well as this picture:

Update:
As the voltage builds up in the soma the charge spills over into the Axon Hillock (an area of high concentration of sodium and potassium gates) If enough sodium ions diffuse into the axon hillock and passes a (somewhat ill defined) voltage threshold then the sodium gates will open and start the action potential. Then the action potential proceeds down the axon as described above

A useful metaphor is the soma, and by extension the Axon Hillock, sums up the synaptic input from the dendrites, and again, if its over the threshold then the sodium gates open, if not, they slowly return to rest.

The synaptic input can be excitatory (cause depolarization) or inhibitory(hyper polarization) depending on the type of receptors and channels in the dendrites, but in general these voltage changes in the dendrite diffuse down into the soma and are eventually reach the axon hillock.


Does the fossil record disprove Evolution?

Fossil records are fossil records. The people who use them to attempt to prove or disprove evolution use them to represent their causes in different ways, gleaning sometimes completely contradictory facts from the same bodies of information, sometimes even the same samples.
It is my personal belief that evolution isn't ever entirely phyletic, I like to imagine that once in a while a pup would be born or an egg would crack open and there'd be a malformed creature in there the likes of which the world has never seen, if only because its deformity has made it more adaptable or stronger to its environment, not the opposite which is usually the case with birth defects. And then yes this prototype would survive and find a mate and have offspring with its varied genes dominating, some same, some different, and begin the phyletic process.

But that's not the answer to your question. Your question isn't really answerable. Fossil records only prove that a creature once lived at that time period, and its bone structure and posture can reveal certain things to any observer, but they dont prove or disprove anything. A great deal of the works you quote speak on the topic with great finality, yet they are decades old.


Meaning of "Antibody is 50% w/w pure of interfering proteins"

Patents are not the best source for reliable information, and obviously are not that readable. In this case they mean that of the purified product (usually that what comes of a protein A column I think), at least 50% of the weight is antibody. Or less (silly patents).

Commercial purification of antibodies (and proteins in general) is usually not that thorough. Most of the times what you'll get is just culture supernatant with cells removed, maybe some ammonium sulfate precipitation fraction or if it's thermostable just the proteins that are left after the production-solution is heated.


Why can hair grow without limit while eyebrow cannot?

Hair actually does have a limit to its growth. All hair cycles between periods where it grows, and when a new stand appears, which pushes the older, long hair out. Hairs that are generally shorter, like eyebrows or arm hairs, have a shorter growth period before a new hair pushes the old one out. The hair on your head actually grows much faster than many other hairs as well, so with the longer cycle and the faster growth, it can grow to be much longer before being replaced.

I remember hearing that for many women (the cycle does vary from individual to individual, which explains why some men can't grow beards while others look like ZZ Top) the growth cycle ends between the waist and butt.

My speculation would be that hair on the head could grow for longer because there are more capillaries in the scalp, which might lead to more nutrients, higher cell turnover (like you see in dandruff), and hence more hair. That's just a guess, mind you.


It might not fully answer your question…

Cost of having a heavy brain

Generally speaking, having a heavy organ is an important cost for flying animals, a medium cost for terrestrial animals and a low cost for marine animals. Loosely speaking, the principle "use it or lose it" does not apply with the same strength in all animals in regards to brain weight. If you create a regression between "intelligence" and "need of being intelligent"(supposing it means something!) in terrestrial mammals and add the dolphin on your graph, you might be surprised that the dolphin does not fit on the regression but it might only be due to the fact that they live in water which is much more dense than air so that it is less costly to carry a big brain. So, yes there might have something to do with "living in the water".

Indexes of intelligence

EQ does not mean intelligence! It is just an index. And we have to understand that people first were happy to think that humans are very smart because they have a big brain but they were terribly confused when they've learned that sperm whales brain weight 8kg! So they tried finding other indexes. EQ is one of them and we're quite happy to use it because it places humans at the first position. But it does not mean that this index is a good representation of intelligence. Some small birds with their tiny brain were shown to be have a spatial memory that is much more efficient that the one of humans for example.

Something else. When looking at these indexes one should not forget that size (or weight) does not equals efficiency. Let's make an analogy with computers. You can have a good software or a good hardware. Big brains are not necessarily very efficient!

Now, it is still true that dolphins are good at performing many tasks that we link to the concept of intelligence. Dolphins have complex social organization that is probably link with their intelligence. I would tend to think (just a guess) that there are many social factors involved into the evolution of their cognitive abilities. Because the social structure changes as cognitive abilities evolves, it seems to me quite hard to know what factors made that clever individuals were more fit than stupid ones at every moment during the evolution of dolphins. But I might overlook the complexity of the problem. And I honestly never learned any article concerning the role or the evolution of cognitive abilities in dolphins.


Can Covid-19 (similarly to HIV) infect T-Cells?

As referenced the publication you shared, other human corona viruses also infect, but do not replicate in T cells, so it's not "Big News" in the sense of being a novel or unexpected finding. This also differs from HIV, which actively replicates in CD4+ T Cells. However, it does seem like CoV-2 patients have reduced T-cells after recovery, and that reduced lymphocyte levels during infection are associated with greater risk of mortality from COVID-19.

It doesn't seem like there's any evidence in the literature for long-term lymphocytopenia in recovered SARS and MERS patients, but it's still too early make any strong conclusions about long-term effects from the current outbreak.


Gel Electrophoresis - loading dye and more

The loading buffer you add to your samples for gel electrophoresis has a few different purposes, but the exact amount does not really matter. The purpose of the loading buffer is

to make the sample heavier so it is easy to get into the pocket and stays there
to visualize how far the gel has run
to denature the sample (only for denaturing gels)

Sample buffers for agarose gels usually use something heavier than water like glycerol or sucrose together with a tiny amount of a dye like bromophenol blue.

So in general there is no issue with using too much dye, but using not enough could lead to the sample being not heavy enough and problematic to pipet, or the sample not being properly denatured. I'd either use 1 ul of the sample buffer (smaller amounts can be annoying to pipett) for your sample, or dilute the sample to 5-10 ul and use the regular amount.


Theoretically, what technique would one use to modify a virus so that it only affected a subset of the population?

Yes, it is possible and probably you won't need many literary artifices to make it work.

Essentially viruses are what is technically called "obligate intracellular parasites".
Parasites because they cannot grow by themselves, they need a host cell from which they "steal" the intracellular machinery to replicate; intracellular because they grow inside cells; and obligate because they cannot reproduce outside their target cell.

Now, each virus has its "favourite cell" to infect. For instance HIV targets a type of lymphocytes (cells of the immune system), other viruses may only target bacteria (these are called bacteriophages) and so on.

How is this specificity achieved? Well, to put it simply, viruses "anchor" to specific proteins (or other molecules) that are sitting on the membrane of their target cells and that allows them to go in. If a cell does not have that specific protein, then the virus cannot infect it.

So, in your story, maybe the target population will have a mutation in their genome that will modify a certain protein. You could then (fictionally) construct a virus that specifically targets cells expressing that protein and you're set!

The virus construction part is just standard molecular biology, really.

A few things to read:
http://en.wikipedia.org/wiki/Genetic_engineering
http://en.wikipedia.org/wiki/Genetically_modified_virus
http://en.wikipedia.org/wiki/Viruses <--this explains a lot


How does the molecular machinery choose where to cut a chromosome for recombination?

In humans and mice anyway ,a lot of it boils down to the recognition of a specific sequence that marks recombination hotspots by PRDM9.
http://www.sciencemag.org/content/327/5967/836

Edit - I'm expanding in response to the comment below...

Meiotic recombination occurs at vastly greater frequencies in some locations in the genome than others and these are called Recombination Hotspots. For example, the figure here, sourced from http://www.sciencemag.org/content/327/5967/876/F1.large.jpg

shows the recombination rate at the hotspot and further away from it for Chimps and Humans.

These hotspots are recognised by the cutting machinery thanks to the binding of PRDM9, a zinc finger protein, to a DNA sequence that it specifically recognises and is present at hotspots. The DNA sequence varies from species to species (as does the sequence and the function of PRDM9) but in humans is a well-characterised motif 13 base pairs long and of the sequence CCNCCNTNNCCNC (where N is any one of the 4 bases in DNA) , and accounts for the activity of nearly 40% of known hotspots.

The first link I posted has evidence to suggest that variation in composition of PRDM9 is a determinant of which hotspots get used. PRDM9, it appears, stimulates the formation of a specific histone modification - H3k4me3 (DNA is wrapped around histones, there are five histones - H1, H2A, H2B, H3, H4, and each of them has a tail that can be chemically modified, and eight of these (2 of H2A, 2 of H2B, 2 of H3 and 2 of H4) form a nucleosome - in this case the fourth lysine residue of the tail of Histone H3 is trimethylated as regulated by PRDM9, and facilitates crossing over and recombination initiation.
Edit Summary


It may be green anoles (Anolis carolinensis). They are harmless I think...


Is it purely the nervous system causing vaginal lubrication (arousal)?

There is a good open access review about the effects of different hormones on sexual arousal. In most instances, the hormone is acting on the brain, which signals the information to gonads and genitals via nerves (i.e., the hypothalamic-pituitary-gonadal axis). However, in a study in which I have participated, we found a more direct and probably ancient signaling pathway where the mouse liver, in response to protein intake, was sending a permissive signal to the uterus for reproduction. Whether this holds true for vagina lubrication was not investigated, but I would be optimistic that mechanisms other than nerve communication could play some roles.


I'm going to take a shot at putting a whole lot of information into a small answer, so let me know what parts need more explanation.  To any others experienced with closure, I am certainly skipping plenty of steps and ideas in attempt to convey the general.

******A general warning that graphic surgical images are used below.******

The Setup:

You asked about "severed" jugular and carotid injuries, so we will focus on neck injuries, with a focus on insults to the R/L common carotid arteries (CCA) and the R/L internal jugular vein (IJV).  To get everyone on the same page visually, we are talking about the large blood vessels in this image:

For the sake of simplicity, we will deal with injuries that are focused directly on these vessels.  In reality, there are so many different and important tissues tightly packed in the neck that there are often many complications and multiple vessels that need to be dealt with near simultaneously.  Further, we will suppose that our patient (pt) is unlucky to have a "severed" vessel in his neck, but lucky enough to have immediate access to ATLS.

Just like you should have learned in your basic neighborhood CPR/aid class, you address the ABC's (MD's add DE): A irway, B reathing, C irculation (D isability, E xposure).  In reality when presented with a pt bleeding from the neck, you will almost always begin by applying pressure at the wound site, while you address the airway.  When I say "applying pressure" I literally mean a nurse or medic putting their fingers up against where it is bleeding and trying to stop it like a hose.

We will assume that a clear airway is established, the pt is breathing normally enough, and under general anaesthesia.  We will also give us the advantage of having the head, and to a little lesser extent body, packed down with ice.  This will give us precious time, and help prevent brain damage.  All else is presumed to be well with the pt, and all we need to do is fix the bleed in his neck.

Identifying the problem:

Now that we have our idealized pt ready to fix, the first thing you have to do is to identify where the bleed is.  Assuming you have serious bleeding, like one would come from a "severed" CCA or IJV that normally means cutting open the wound quickly and in a controlled manner.  Again, the neck is full of tissue you don't want to damage, so a anterior sternocleidomastoid incision is normally called for when you are looking for where the CCA or IJV is damaged.  As opposed to coming from the top the way we would dissect a cadaver (as in the drawing above), the sternocleidomastoid incision will give us a side view into the neck like this:

The point at this stage is to gain control of the bleed.  You don't want to just go digging in where the vessel is bleeding, because you are likely to cause more damage than help (and in this case, loose the pt).  Instead you are going to clamp above and below where the vessel is bleeding.  This will let you suck out the blood and see what's going on.  If you happen to have a large wound in a large vein, there's a chance that a clamp won't give you sufficient control of the bleeding.  In that case you have to also use a catheter to stop the bleeding (in obtaining distil control to be specific).

In our case, this means dissecting the carotid sheath.  This needs to be done very carefully so that you don't damage the vagus nerve.

You may have noticed I kept putting "severed" in quotes.  That's because it matters how the vessels are damaged.  Were they crushed or ground apart? Cut jagged or cleanly? Transverse or longitudinal?  All of these change the exact procedures into how you go forward.  Clearly a vessel that has a small tear is easier to repair than one that has been totally separated with jagged shredding from a crush injury.  Veins and arteries won't retract from the insult in the same way either, so how you find them can be a bit different.  Here is a flow chart that shows the basic decisions:

Put it back together Doc: [warning of graphic images]

You may notice that there are basically two end points for either veins or arteries: repair it or ligate it.  There are many different technical/specific ways either can be done, but those are beyond the scope of this answer.  If the sight of open wounds bothers you, note I am going to start using actual surgical photos below.

When it's possible it's better to repair the vessel.  That means that you can close the artery where it is.  If there is just a small hole, you can suture the hole closed.  With the CCA or IJV it's more likely that you are going to need a patch.  This means that you take another piece of vein or a synthetic replacement, and suture it into the hole.  I always like to tell people surgery is a lot more tailoring than most people realize (not that this is as easy as sewing fabric).  Below is an example of where a patch would be used in the CCA:

First the tear in the artery:

And after the patch has been added:

Suturing and patching can only be used to close the vessels when tension isn't needed to repair the wound.  If the laceration or severing of the vessels are such that it has come mostly (not completely) apart, but you can still get the ends together with NO tension,  end-to-end anastomosis repair can be utilized.  This means that you take the two ends, with branches if there are any at the wound, and suture them back together.

Again here is an example of the opening in the artery (popliteal):

And here it is again after end-to-end anastomosis repair:

Now let's say that you really did get the vessel cut in half.  That's a bit of bad news for you, you're going to have to ligate the vessel.  That means sewing up the end of it to close it down.  You start above the injury in arteries and below in veins, and then you tie at least three loops--many prefer five loops--down on the vein, and make a clean cut leaving at least two loops on the part staying in the body.  Then you do the same thing on the other side of the injury.  I think this is best displayed by a video, unfortunately most of the good ones I know of are not available to the public.

This video certainly not the best technique I've ever seen but it get's the idea across.  I will search for a better video as I have time.

Now if it is possible, a surgeon will try to make a graft deal with the ligation.  The first choice is a interposition graft.  This means taking a larger vein graft and connecting the two ends of the severed vessel.  You do this after making clean ends with the ligations from above.

Here we have the femoral artery prepped for an interposition graft:

And here is interposition graft in place:

In certain cases, this is not possible.  As strange as it sounds, the ligation may just be left in place, depending on where it is.

Is that all?

No, not by a long shot, but that is the basics.  There are many different techniques that can be used, with new and better ones being invented often.  For example instead of suturing, chemical cauterizing of the ligation can be used and is quicker.  That also allows the surgery to be done through a scope.  But the basics remain the same:

Stop the bleeding, gain basic access, get full control of the bleeding, obtain full exposure/access, sew up the problem, put everything back, close up, give fluids, and send them to ICU.  Even after getting everything right in surgery, the recovery can be quite difficult.

Sources and Further Reading

Note: I will try to come back with primary sources, I started from knowing what to do and searched for sources.  Here are two great sources which contain more complete information:

1) Trauma.org  This is a great site for use by actual medical professionals when addressing trauma.  They don't really cover the basics, but they do give wonderful care write ups.  Here is the relevant reference for this answer:

Karim B, 'Peripheral Vascular Trauma' trauma.org 7:3, March 2002. http://www.trauma.org/archive/vascular/PVTmanage.html

2) Acssurgery.com  Even more than Trauma.Org, this site is designed for use by clinicians.  Relevant reference:

Wisner DH, Galante JM, INJURIES TO THE NECK acssurgery.com 7:4, 2010. http://www.acssurgery.com/acssurgery/institutional/getChapterByIDHTML.action?chapId=part07_ch04&type=tab


Heterocyst function in cyanobacteria and its localization

According to wikipedia :

  Heterocysts are specialized, pale-yellow,thick-walled cells with disputed function nitrogen-fixing formed during nitrogen starvation by some filamentous cyanobacteria, such as Nostoc punctiforme...

Thus by definition these are not within the cells, but differentiated cells themselves.

This is a good paper that can give you details on nitrogen fixation in the cyanobacterium Anabaena variabilis.

In general: cyanobacteria are photosynthetic prokaryotes, and many of them are capable of fixing nitrogen (that is the ability to use and incorporate nitrogen from the air as N2 gas). The enzyme called nitrogenase is oxygen sensitive thus either temporal or spatial separation of nitrogen fixing must be done to avoid damage to the enzmye from oxygen produced by photosynthesis.

  In Anabaena spp., aerobic nitrogen fixation is confined to differentiated cells called heterocysts that form in a semiregular pattern in a filament in response to nitrogen starvation. Fixed nitrogen in the heterocysts is transported to vegetative cells in the filament, while vegetative cells supply carbon and reductant to heterocysts

So as you can see spearate cells work together to supply each other with necessary nutrients. It is important to note that when sufficient fixed nitrogen source is available the number of such specialized formations is low due there is no need for extra nitrogen to be fixed

There are plenty of details on heterocysts and nitrogen fixation in the linked article. Also this paper hold details of regulation of nitrogen fixation and also has a thorough image of the process:


Why is there complementary base pairing for DNA?

It's to do with the physical space the base molecules occupy. There are 2 classes of molecules in DNA bases, purines and pyramidines.  One of each always pair together as there will be a total of 3 ring moieties present.

E.g., Adenine (a purine) pairs with Thymine (a pyrimidine).

If you were to pair 2 pyrimidenes together, you would induce a kink in the DNA backbone and destabilise it.

That said, there is no chemical reason 2 purines or 2 pyrimidines can't hydrogen bond, and they do. This causes mismatches and DNA mismatch repair enzymes recognise the torsion it induces in the DNA backbone and they replace the mismatched base in the proofreading process. If the enzymes miss one mispairing, which can happen as it occurrs often (but the enzymes are very effective), then you end up with a mutation.


How can I measure bee and wasp population?

Short Answer

No. You cannot appropriately examine population dynamics using the approach you've described.

You can, however, examine how foraging frequencies vary/correlate with field spraying (though this might take more effort than you're looking for).

 Long Answer

You're not going to be able to properly quantify population levels from casual observance.

Because you would be unable to effectively identify individuals, you would be unable to know if you're seeing different individuals or repeats of previous individuals.
The data are also biased toward those species or individuals that use the habitat features in your particular garden and are biased against those that do not (Parsons & Szewczak, 2009).
Further, you would have no way to identify which hives/nests that individuals are coming from (without watching them leave the nest directly), so you would not know which populations are represented at any given sighting.

Unfortunately, although the question you link to (How best to count bees entering and leaving a hive to measure hive activity?) would allow you to better examine/compare separate populations, those methods likewise suffer from the same shortcomings listed above.

What you can figure out:

Your causal observance can at best be used to quantify foraging frequency in your garden.

In other words, you would just be able to count how many bees visit your garden at any given time and compare those values at different discrete time points. You could compare this to a number of environmental variables to look for trends.

In your case, your approach would look something like the following:

You could count the number of sightings (or landings or feedings) in various random locations throughout your garden.

Each of these locations should be randomly selected, and you would preferably collect numerous random samples from each of various "habitats" (i.e., different locations, different flowers, etc.).
You must return to the same locations each time and spend the same amount of time at each location each sampling period.

You can do simple statistics on these different samples across all sampling periods to examine foraging frequency trends across time.
If you directly measure a number environmental variables (e.g., temp., precipitation, humidity, cloudiness, etc.) you'll be able to rule out variance in your data due to these factors.

Proper background research would be required to determine which variables might be important to measure.

Finally, you could do regression/ANOVA analyses to examine any correlation between nearby field spraying on your foraging activity.

However, there are a ton of variables that could affect the trends you see, so final analyses will likely be weak at best.

Measuring those aforementioned environmental variables will help with this, as will increasing your sampling rate. See Power Analysis

  Power analysis is an important aspect of experimental design. It allows us to determine the sample size required to detect an effect of a given size with a given degree of confidence. Conversely, it allows us to determine the probability of detecting an effect of a given size with a given level of confidence, under sample size constraints. If the probability is unacceptably low, we would be wise to alter or abandon the experiment.

Note: Work by J.E. Eckert (1933) showed that (honey)bees can travel multiple miles from their hive/nest, so unless those fields are mutliple miles away, any pesticides could very well impact the populations visiting your garden.

Another Option:

You could perform Trap Counts to try to approach quantifying populations rather than just quantifying foraging behavior.

This method is used frequently for other insects. However, I found very few reputable sources examining bees/wasps.

One example: Danka & Gary (1987) estimated foraging populations effectively, but they did so by collecting data at the hive entrance.

Though there is an inherent issue with trap studies as well:

As Petrovskii et al (2012) point out:

  Traps are effective at providing relative counts that enable comparisons but are poor at delivering information on the absolute population size.

However, Petrovskii et al (2012) show that a ‘mean-field’ diffusion model is capable of revealing the generic relationship between trap catches and population density.

Their paper is freely available here.

Citations

Danka, R. G., & Gary, N. E. (1987). Estimating foraging populations of honey bees (Hymenoptera: Apidae) from individual colonies. Journal of economic entomology  80(2): 544-547.
Eckert, J. E. (1933). The flight range of the honeybee. Journal of Agricultural Research 47:257-285.
Parsons, Stuart and Joseph M. Szewczak (2009). Detecting, Recording, and Analyzing the Vocalizations of Bats In: Ecological and Behavioral Methods for the Study of Bats. Thomas H. Kunz and Stuart Parsons, ed. The Johns Hopkins University Press, Maryland, 2nd ed., pp. 91-111.
Petrovskii, Sergei, Daniel Bearup, Danish Ali Ahmed, Rod Blackshaw (2012). Estimating insect population density from trap counts. Ecological Complexity 10: 69-82. http://dx.doi.org/10.1016/j.ecocom.2011.10.002.


How distantly related are eusocial insects? Aren't members of a species much more related than 1/4, 1/2, or 3/4?

In evolutionary genetic comparison, you are talking about members within species. They will share almost all genes, because if they didn't they would belong to a different species.

However, within species there exist different versions of the same genes, called 'alleles'. When we say that you are 0.5 related to each of your parents, we mean that statistically, 50% of your alleles should be those which your father has, and 50% of your alleles are those passed down from your mother.

Eusocial insects have different mechanisms. Bee males are produced without fertilisation, meaning that they only have one copy of each bee gene. When the male produces sperm, it only has this one set, so all sperms end up carrying the same set of alleles.

Females on the other hand have the normal double set, with two different versions of each gene. So if you look at one gene, half of the female's egg should have one version and the other half should have the other version. All females of one hive are produced by the same queen and the one male that she mated with. Remember, the male only has one set, so the versions coming from the male are the same in all female offspring.

This means a female's genes are made up of: 50% from the father (these are the same across all females) and 50% from the mother (where half the females have one version and half have the other version). Statistically, this means that looking at one gene, there is a 75% chance that two bees will have the same version of that gene.


What exactly is meant by the expression "differentially expressed"?

Although each cell of your body essentially contains the same DNA and the same genes, cells in different tissues express (turn on) different genes under different conditions. Measuring differential gene expression involves looking at the amount of expression for a gene (or set of genes) in two contrasting scenarios. The contrast could be across different times, different tissues, different conditions, different related species, etc.

When, you say a gene is "differentially expressed", this is very context-specific. The phrase means nothing by itself, and it is only useful in terms of the applicable contrast. For example, the statement "gene A is differentially expressed" is uninformative, while the statement "gene A is differentially expressed in liver and muscle tissue" is descriptive--it tells you that liver tissues and muscle tissues have a significantly different level of gene A products. Often the terms "up-regulated" and "down-regulated" are also used to provide additional detail. In the context of the previous example, the statement "gene A is up-regulated in muscle tissues" tells you that the level of gene A products is higher in muscle tissues than in liver tissues.


Why was disease transfer to the Americas one-way?

In "Guns, Germs, and Steel" Jared Diamond includes quite a bit on this topic. His conclusion is that Europeans, and old world humans in general were much more exposed to their farm animals, often living in the same buildings. This allowed a much greater number of diseases to jump from animal to human, forcing us to development immunity against these pathogens.

The native americans never domesticated as many animals, and weren't exposed to as many pathogens. As a result the foreign pathogens could freely move through their populations.

So why did it only go one way? A lot more Europeans came to American than vice-versa, so there just wasn't as much opportunity for American pathogens to move to Europe. Additionally, the Europeans brought a lot of animals here, including cattle, horses, and pigs. These would have carried pathogens as well, again, very few American animals were taken to Europe.


Statistics on energy consumption breakdown per biological functions across organisms?

This is not a proper answer. Bear with me. I'm in a hurry; will edit the answer to a decent form when I find time.

From the abstract of this paper:

  Of the 80% of oxygen consumption coupled to ATP synthesis,
  approximately 25-30% is used by protein synthesis, 19-28% by the
  Na+-K+-ATPase, 4-8% by the Ca2+-ATPase, 2-8% by the actinomyosin
  ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA
  synthesis and substrate cycling also making significant contributions.

Also check this out.