What is the exact chemical composition of human body?

That conversation is strange. While different tables exist, the very first elements seem messed up. If the body is 60 (some sources say 70)% water, then oxygen has to be the most abundant element by weight (water - H2O - has a molecular weight of ~18 g/mol, with hydrogen contributing only 2g/mol of that weight).

The usual figures are roughly Oxygen (65%), Carbon (18%), Hydrogen (10%), Nitrogen: (3%), Calcium (1.5%), etc.

However, the writers of Breaking Bad weren't stupid. So, they weren't discussing percentages of the mass of each element, but rather the frequency of that atom in the body. The number of hydrogen atoms does indeed exceed the number of oxygen atoms.

So, by atomic percent, Oxygen is 25.6%, Carbon: 9.5%, Hydrogen: 63%, Nitrogen: 1.3%, Calcium: 0.24%, etc. So yes, the numbers are approximately correct for a normal, average, youthful (more water) 70 kg male.

So here is a table incorporating both percent by weight and percent by abundance. The writers were pretty well informed.


Where are eosinophils and basophils phagocytic?

Also to add to this - lets not forget that these cells can function differently in circulation, compared to when they enter in tissue. They look morphologically different, and often one can see phagocytic vacuoles present in the cytoplasms..meaning they probably do participate in some minor "cleaning up" , but like the above poster mentioned, primarily they release granules into the environment wherever they detect damage, or antibody reactions.


Why is it advised to avoid bubble formation during mixing?

A "bubble" per se would do no harm unless you have cells (without walls like mammalian cells) in the suspension. If you agitate the protein mixture vigourously then it may lead to denaturation of proteins by extensive intermolecular collisions. The "froth" formation is an indication of denaturation as denatured proteins stabilize these foams [1, 2].

References:

Zayas, Joseph F. "Foaming properties of proteins." Functionality of proteins in food. Springer Berlin Heidelberg, 1997. 260-309.
Schmidt, Isabelle, et al. "Foaming properties of protein/pectin electrostatic complexes and foam structure at nanoscale." Journal of colloid and interface science 345.2 (2010): 316-324.


Name this green giant insect hanging on the wall

You simply found Parasanaa donovani, Which is the large bush-cricket found in India and various countries in Southeast Asia.


At small axon diameters (<1 µm), why does myelination not increase neuronal conduction velocity?

Graphs like these are based on a complete cross-sectional area. Myelination adds thickness, so if you want to add myelin outside and keep the same diameter, you have to have a smaller lumen inside the axon.
As you can see in the "unmyelinated" plot versus diameter, smaller fibers have lower conduction velocity. Since the benefits of cross-sectional area are most important at small diameters (because the velocity changes with the squart root of diameter), for small diameter axons you end up losing more from losing internal area than you gain from adding external insulation.
If you keep the internal diameter the same and just add myelin, you will always increase the conduction velocity, but the total diameter including the myelin won't be the same anymore.


Is it possible to dock multiple ligands with the target?

Huameng Li and Chenglong Li have done multiple ligand docking in two (AFAIK) of their works:

Multiple ligand simultaneous docking: Orchestrated dancing of ligands in binding sites of protein
Drug Design Targeting Protein–Protein Interactions (PPIs) Using Multiple Ligand Simultaneous Docking (MLSD).....

The method is called Multiple Ligand Simultaneous Docking (MLSD). I am not at all an expert in this field and you should read the first paper for details on how they implemented this. This algorithm was implemented on AutoDock.


Solving Hardy-Weinberg problems

First of all, you might want to have a look at the post

Solving Hardy-Weinberg problems

and eventually at

Assumptions of Hardy-Weinberg rule

After reading the first post, you should be able to answer your question yourself. I encourage you to try it before reading what follows.

Hardy-Weinberg for sex-linked loci

I will make an example. Let's consider a case where males are XY and females XX (like in mammals for example). Let A and B be two alleles of a bi-allelic present on the X chromosome. The frequency of these two alleles in the entire population are $p$ and $q$. Let's assume the locus is present on the X chromosome. We will assume that the allele frequency do not differ between males and females.

In males, there are two possible genotypes. A and B. Their frequency among males are noted $f_{m,A}$ and f_{m,B} and are

$$f_{m,A} = p$$

$$f_{m,B} = q$$

In females, there are three possible genotypes. AA, AB (or BA) and BB. Their frequency among females are noted $f_{f,AA}$, $f_{f,AB}$ and $f_{f,BB}$ and are

$$f_{f,AA} = p^2$$
$$f_{f,AB} = 2pq$$
$$f_{f,BB} = q^2$$

If the sex ratio (the ratio of the number of males over the number of females) is $r$, then the genotypes frequencies in the overall population are the ones from above multiplied by $r$ and $1-r$ for males and females, respectively.


0.1 M sodium citrate in 10% ethanol and DNA solubility

The sodium ions will bind to and neutralize the (-) charge on the phospho backbone of DNA. This reduces hydrogen bonding sites for water, which then results in less solubility.

Edited for clarity and because I didn't answer the question the first time. Sorry about that.

The extraction of DNA is from the interphase layer, which is a very small fraction of the original sample. The extraction of the interphase layer is then mixed with 100% EtOH (300 ul per 1.0 Trizol used in that sample). This should actually be 60% or more EtOH based on my experience using this method.

That is the precipitation step.

The fact that the wash has only 10% EtOH and 0.1M sodium citrate and that is still sufficient to keep DNA precipitated revolves around 0.1M sodium citrate is usually 0.3M sodium ions (sodium citrate can be mono-, di- or tri-sodium, but unless specified..sodium citrate implies tri-). Remember for the wash, you don't need to do a quick precipitation, you just need to prevent it from solubilizing again.

I am removing my comments that contained the same information.


Longevity and extent of transfection after SARS-COV-2 vaccination with Janssen

Both the AstraZeneca (AZ) and Janssen (J) vaccines against SARS-CoV-2 work by using what is known as a viral vector to generate an immune response. In both cases these vaccines use an Adenovirus as the vector (vector in this case means "carrier").
Adenoviruses are a family of double-stranded DNA viruses, most commonly known for being one of the causes of the illness known as the "common cold". There are about 88 human serotypes (how people's bodies react to the virus, different serotypes may not cross-protect by raising an immune response)  of the virus divided over the seven species: Adenoviruses A-G. Overall there are about 50 species from a wide range of animals. Because of the diversity and the abundance of the "common cold" most people will have some immune response to at least some of the human adenoviruses.
Adenoviruses are good vectors for vaccines and for other therapeutic uses such as oncolytic viral therapy because the genomes are easily modified and can be made replication incompetent very easily. To do this essential replication genes are removed and the viruses are replicated in cells that provide the essential proteins for the virus to complete its life cycle, so that you get a viral particle that no longer contains the full genome. These viruses are also tolerant of additions to the genome so they can be used to produce proteins that are not normally found in an adenovirus.
On the other hand the adenovirus component of these vectors can cause its own immune response, lowering effectiveness of the immune response to subsequent vaccines developed using the same or a similar sero-type virus.
The AZ vaccine is based on a chimpanzee adenovirus. The J vaccine on the other hand is based off serotype 26 (Ad26) of the human adenoviruses. In both cases the adenovirus is rendered replication incompetent by removal of essential replication genes.
For adenoviruses to work as vaccines they need to invade a cell and then insert their DNA into the nucleus (as seen in the diagram from OP), where cellular mechanisms produce lots of mRNA copies of the gene(s) and concomitantly produce proteins from these mRNA. These proteins are then translocated to the surface of the cell (this is a natural process).
However, in the process the viral DNAs and proteins are recognized by the cell as non self and trigger the innate immune system causing antigen presentation and activation of the adaptive immune system. This whole process is a natural response of the body to infection and does not result in "self recognition", so there is no auto-immune response to the cellular proteins.
Both the AZ vaccine and the J vaccine are administered intra-muscularly, which is very typical for vaccines. Intra-muscular injection is a good site for injection because it can tolerate a big volume and has a relatively high blood flow (both compared to sub-cutaneous (sub-skin)). However, once injected the virus doesn't necessarily stay in the muscle, it can travel in the blood and a portion will end up in other locations, particularly the liver and alveoli of the lung (places where there is a big blood supply and lots of small blood vessels). The adenovirus can infect any cell that expresses the cellular receptor called Coxsackievirus and Adenovirus Receptor (CAR) on its surface, which includes immune cells. There's a fairly comprehensive review of all the mechanisms and cell types here, but it is in written for the scientist. Here's a suitable quote about cell types:

The cell types present when vaccine is administered i.m. include myocytes, skeletal muscle cells, fibroblasts and endothelial cells, with APCs such as DCs or macrophages representing a minority when compared with the abundance of murine skeletal muscle cells

How long the viral genome persists depends on the paper, but not many people have looked. The data I could find seem to indicate that most protein expression is lost after about 3 weeks, but it may persist longer. e.g.:

Although Ag expression could no longer be detected 3 wk after immunization, examination of Ag presentation within the draining lymph nodes demonstrated that APCs were loaded with Ag peptide for at least 40 days postimmunization, suggesting that Ag remains available to the system for a prolonged period, although the exact source of this Ag remains to be determined.

However, the genomes seem to persist for a very long time, perhaps as much as a year or more:

By days 30 and 90, vector sequences remained detectable in most animals in these tissues but gradually declined 102 to 103-fold. After 1 year, relative copy numbers in liver and the injected muscles were comparable with those seen on day 90, whereas a further decline was seen in spleens.

Note that both of the quotes above are not about either the Janssen or AZ vaccines, but about adenovirus vaccines in general, and several Ad vectors were tested in both. It is highly likely that the AZ and J vaccines will have similar data.
Edited to add: I don't know why the DNA persists for so long, but it does not integrate into our genome. It seems that most replication deficient adenoviruses lack the E1A gene, which allows induction of the cell cycle and frees up resources for viral replication. However, the genes involved in viral DNA replication are E2A and E2B, so are not included in the deletion.
TLDR: Viral genome can persist for a very long time, but protein expression does not - possibly because the immune system deals with it quickly after a few weeks (effective vaccination...). The vectors can reach and infect many tissues in the body, particularly ones with high blood flow and lots of small blood vessels such as lungs and liver.


Questions on adding a protein to a DNA library

For 1, that is how retroviruses such as HIV work, and of which scientists have utilised to use in gene therapy. It requires a process called reverse transcription.
However, this would only show you the gene the mRNA was from, but no information about its location, or if it is repeated elsewhere.

As for 2, this is to do with the fact that one base cannot code for one amino acid; as there are 20 common amino acids used to make proteins. With 2 bases, you are only getting 16 possible codes from the various base pairs you can create. However, with 3 bases, 64 possible combinations are possible, more than enough to suffice for the 20 needed. This is called the triplet code;
and therefore, there are more possible combinations of the base pairs in DNA than there are amino acids to be made from them. The 'left over' combinations can code for the same amino acids as other combinations, making it the code degenerate. Therefore, it doesn't matter, as the combination is always read in 3s (non-overlapping), and if it codes for a particular amino acid, then that amino acid will be produced at the ribosomes when its corresponding code is read.

I hope this increases your understanding of the topic.

http://www.genetherapynet.com/viral-vector/retroviruses.html (Question 1)
http://www.chemguide.co.uk/organicprops/aminoacids/dna4.html (Question 2)


Species identification - greenish blue ocean worm (nudibranch?) in Perhentian Islands, Malaysia

It's hard to identify from the photos provided, but I think it is Chloeia flava (a species of polycaete worm, within the phylum Annelida), also known in English as the "Golden Fireworm".
The size is roughly similar to what you describe (they are typically about 7-10 cm long). The individual you observed looks like it lives in sandy bottom environments (not a typical environment for a nudibranch), and this worm does also. It is commonly found all across the warmer Indo-Pacific as well, and looks like the individual observed in your photo.

If it is not this species, I think it is another species of the same family, Amphinomidae.


miRNA analysis just using BLAST against mirbase.org

You don't need to use TopHat but it is better to use bowtie instead of BLAST. First of all you need to get rid of the adapter sequences (along with other processing steps prior to alignment).

Now there are two aspects here:

miRNA quantification
miRNA discovery

First one is relatively straightforward whereas the second one requires you to perform additional tests such as prediction of stem loops etc. There are published software that can handle both the aspects (mirDeep, miRScan etc). See this review for details on different miRNA gene finders. I have used miRdeep and it uses bowtie-1 to align.

BLAST would work but you have to set parameters which are suitable for small sequences (increase E-value cutoff, reduce word size etc). Moreover, BLAST does not have a cutoff option for the number of mismatches and the length of alignment (it only has a post alignment filter for percentage identity).

I also personally prefer bowtie because it has something called as n- alignment mode. In this mode the entire read is divided into seed and non-seed regions. You can specify the length of the seed region and the mismatch cutoff. Since for miRNAs the seed region (bases 2-8) is critical for its function, I generally set the seed mismatch cutoff to zero while allowing one or two mismatches in the non-seed region (note that in bowtie the seed always starts at 1).

In general, I would advise that you should go for miRdeep instead of BLAST. However, miRdeep doesn't straight away perform an alignment against the mature sequences. It maps the location of mature sequences in the pre-miRNA sequences (stem loops) and then aligns the reads to the pre-miRNA sequences. If the location of reads has a significant overlap with the mature region (you can adjust the window) then the read is considered as a valid miRNA.


Bacterial cell lysis - what solution to use?

What exactly is the purpose of lysing the cells? The "complicated" solutions, as you say, include a bunch of ingredients. The detergent is largely present to dissolve cell membranes (which are lipid-based) and allow for extraction of proteins or other biochemicals from within the cell (and organelles in eukaryotes). There are also two types of detergents: ionic and anionic. Both detergent types will dissolve membranes, but ionic detergents tend to be harsher of the two by strongly disrupting protein structures.

If protein biochemistry is important, then the next most important ingredients will be specific inhibitors of proteases: enzymes which degrade proteins. There are many of these, but some examples include PMSF, EDTA, aprotinin, etc.

Sometimes it is necessary to buffer the pH of lysis solution to monitor protein complexes, or keep a protein natured, or keep DNA in an optimal pH range. General solutions for lysis buffers include Tris-EDTA (TE), PBS, etc. This choice comes down to whether you want a buffer, and in which pH range you wish to keep your lysis solution. Common buffers like TE and PBS are made up for a pH range of between 7-8. There are other buffers that are used for low pH ranges (pH 4-6), but are usually less common.

Lastly, there are ways to lyse cells without using any kind of lysis buffer. One method is to use sonication, which uses directed pulses of high-frequency sound to lyse cells by mechanically shearing them. Another method is to repeatedly freeze-thaw cells from -80°C to 4°C (usually 3 times is sufficient). Lysis in this manner is accomplished by repeated formation of ice crystals which cut open cells, releasing their contents.

If you have a more specific question, one of us can guide you further, but this provides a general overview of what is involved with cell lysis buffers.


Yes, a full kiwi. The method is rather crude and the yield you get is not so high, because you will not break up all cells and also loose some of the DNA which is bound to the cell debris.

Lab filter paper of course works as well, as would a fine cloth (cheese cloth for example). The receipe is designed to work with stuff that people have usually in their kitchen, which is true for coffee filters, but usually not for laboratory filter paper ;-)


An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor.  Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2.

In your example, X and Y inherit each of their alleles from A2, so their IBD value is 2.  Inbreeding is just an extreme form of descent from a common ancestor; it causes on average greater probability of high IBD values than when comparing less-inbred individuals. See the passage here for more detail.


How can humans hear low frequency sounds using the cochlea which is tiny compared to wavelength?

You are thinking of antennas for EM signals such as the dipole antenna. In this type of antenna, an external field (EM waves) excite the antenna (creating an electric current) which you then measure. There is thus something like a transduction step, which is more efficient if you can use the spatial scale of the wavelength.

In the case of hearing sound waves, the ear does not transduce the mechanical signal into another modality, but is directly modulated by the hair cells.


There is a small issue in this question that is: everybody does not always use the exact same definition of stabilizing selection and disruptive selection. These two concepts are sometimes used to refer to phenotypic traits or to genes. For example stabilizing selection might either mean,

selection for the mean phenotypic trait of the population
or
selection for the wildtype allele, getting rid of all newcoming mutations.

Under simple genetic architecture the two concepts are equal.

Although for this question I don't think we even need to give a clear definitions between these two words, we'll use the phenotypic based definition (the first one above) in order to ease the intuitive understanding of the answer.

Let's say the trait breeders select for is mean quality and for ease again, we'll imagine this trait as being one unique trait that we can map on one axis from low quality to high quality. Here is a representation of that where the x-axis represent meat quality (left = low quality) and the y-axis represents the density of cows in the population which has the associated meat quality.

If breeders performed a stabilizing selection, it means that they would not improve the meat but only prevent the meat to change quality. In order to shift the quality of the meat to the right (to better quality), breeders need to perform directional selection.

I think the only problem that you had for solving this problem was the conceptual issue of considering meat quality just like any phenotypic trait. And if you want to shift a phenotypic trait on one side or another, you have to apply directive selection.


Why does the chance of having a baby with Down's syndrome increase with the age of the mother?

The frequency rises with maternal age due to a peculiarity of meoisis
  in female mammals.  Meiosis is originated in the fetal ovary,
  arresting at metaphase I with the homologous  chromosomes aligned for
  segregation. Cells remain in this state until the time of ovulation,
  often  decades later in humans. The longer cells remain in the
  arrested state, the greater the chance  that there will be a
  nondisjunction event when meiosis resumes.

Source : http://www.madsci.org/posts/archives/2005-07/1121714807.Ge.r.html

I think you have the misconception that egg cells have completed meiosis by the time female is born. This is not true ( as indicated above in the answer). At birth, they are in metaphase I , after puberty, each month some of them divide further but only one survives and get arrested at metaphase II . Only after fertilization is the meiosis complete.


Evolutionary chronology - if any, which species have evolved in the last 100 years

Every single species in existence has "evolved" over the past 100 years. Evolution is a constant process. You are asking whether we can observe evolutionary change in a given species over a short time span, not whether evolution is occurring. I know this sounds like pedantry but it is a very important distinction.

That said, yes, of course we've seen evolution in action in short time spans. The classic example is the various bacterial species that have developed resistance to antibiotics. As very nicely illustrated by Garry Trudeau:

If you want more rigorous evidence than a comic strip, have a look at Wikipedia's page on antibiotic resistance or read Demerec, 1948(1).

Another example is described by Yona et al.(2) who show that subjecting yeast to high temperatures (heat stress) for a few generations causes genetic changes that help the cells deal with the stress. This is, clearly, evolution in action. In fact, they even show that the first response is the duplication of an entire chromosome (think of it as a crude, bludgeon-like solution) which is later suppressed by other, more subtle, compensatory mechanisms which arise to replace it.

Demerec, Milisav, "Origin of bacterial resistance to antibiotics." Journal of bacteriology 56(1), 1948
Yona et al., "Chromosomal duplication is a transient evolutionary solution to stress", PNAS, 109(51), 2012.


Standard Process Identification of New Disease outbreak Causing Pathogen

I was first thinking of voting to close the question because it was too broad, but in reconsideration I think the answer of showing why it is too broad would constitute a proper answer in this case.

First of all, the term disease is one of the most general terms for a problem in medicine.  The only term that could be higher up is "medical condition."  It could be an infectious disease, genetic disease, induced disease (think chemicals, tobacco, etc), or [insert organ here, ie heart] disease (which are not necessarily genetic).  There are attempts to distinguish between "diseases" and "disorders," but the difference is not always clear.  The term "disorder" is growing in usage and scope because it is seen as having fewer negative connotations than disease (think disease of the mind vs. disorder of the mind).

Thus each field has it's own ways of identifying new diseases.  As a general trend new diseases are found now by identifying greater specificity within a previously general disease.  For example, a person could be said to have an "adrenal cancer," but now we would want to know if they have an adrenocortical carcinoma.  In an infectious setting, we could think of all the particular pneumonia being specified out of interstitial lung diseases.

Diseases caused by external agents (pathogens, toxins, etc) can sometimes be more uniquely novel, in that they can change into something unpredicted (new compound or virus made by man for example).  Perhaps you meant to ask if there were standard ways for identifying new viruses or microbes?


Why do marmosets have claws when most primates don't? What is the structure of their hands like?

Since marmosets and tamarins are considered the most primitive primates, we can't assume that evolutionary pressure led to the development of claws. Rather, it's accepted that claws disappeared as primates adapted to an arboreal lifestyle. So the question is really "Why did marmosets not completely lose their claws?"

The clues to the answer lie in their unusually large incisors and disgestive system. The marmoset occupies an evolutionary niche where they rely heavily (20-70% of total diet) on exudates (sap, resin, etc.) from trees. Their claws, and incisors allow them to claw/chew holes in the bark to get at the exudates, while a specially adapted large intestine allows them to digest this food. The advantage of exudates is they are not seasonal, offering the marmoset a relatively stable year-round food supply.

Other primates enjoyed the evolutionary benefits of tool use by losing their claws and gaining opposable thumbs (which marmosets don't have). I've come across no papers that describe a different phlange structure for marmosets and other primates, and there doesn't necessarily need to be one.

Most of this information came from the University of Wisconsin's Primate Research Center:

http://pin.primate.wisc.edu/factsheets/entry/common_marmoset

Edited to add (since I can't comment): One way to deduce how different features evolved is to look at phylogenetic trees. There are many out there, but I pulled this one from J.R. Roede et al. Redox Biology 1 (2013) 387-393.

If you look at this simple tree, you'll see that marmosets diverged from humans on a time frame where it's possible they kept their claws instead of reacquiring this trait (it would be unusual, but not impossible, for this to happen). One thing you can do is dive deeper into the phylogeny, square this up with how primate hands evolved, and see if the split of marmosets from the rest of the primates happened when nails began to evolve.


What is the evolutionary cause for various finger lengths?

When you bend your fingers, they all arrive at the same height. I would tend to think that their lengths differ when you keep them straight because they need to have similar length when you bend them. And I guess that there is some optimal length (when bended) for fingers to grasp things.

It is nothing but a quick hypothesis. But it sounds quite plausible to me.

As @JordiZambrino commented, it is possible also that middle fingers evolved to be longer in reaction for the need for throwing things.


Does the Plasma Membrane have a hydrophilic interior/exterior/contain vesicles?

The plasma membrane is a lipid bilayer. Plasma membrane lipids have a hydrophilic head group and hydrophobic tail groups. Since cells are usually in an aqueous environment (and are filled with aqueous cytoplasm), the hydrophilic head groups is face both the exterior and interior of the cell. Between these head groups facing the interior and exterior, the hydrophobic tail groups of opposing lipids associate with each other to create a hydrophobic core within the membrane.

Vesicles are also made of lipid bilayers. Vesicles can exist within cells or be released by cells.


Understanding the concept of a "Place Field" and the difference between place cells and grid cells

Yes, that's correct. Mostly, place cells fire in different places in different contexts, and they don't necessarily share the same spatial relationship in different contexts (like in your picture, the "yellow" cell comes right before a "cyan" cell; those place fields wouldn't necessarily be adjacent in a different context.

1.1. "Field" is just a term that refers to a region of space. I'd say the Merriam-Webster definition closest is #6:

  a region or space in which a given effect (such as magnetism) exists

1.2 The picture you have is probably a schematic, but what it depicts is a recording from several different cells. Each cell is assigned a color. Every time the cell fires a spike, there is a dot placed at the location in space where the animal was at the time of the spike. You let the animal run through the maze and get a record of lots of these points, and you see that they cluster together into place fields.

2&3 - These questions are getting to be a bit too broad and also you are only supposed to ask one question per submission, so I'll be very brief here. Grid cells are located in an entirely different part of the brain, the entorhinal cortex (part of neocortex), although this part does project to the hippocampus where place cells are found.

Grid cells fire in regular patterns in a spatial field, like in this image:
https://en.wikipedia.org/wiki/Grid_cell#/media/File:Autocorrelation_image.jpg

They also keep their relationship of firing locations relative to each other constant across contexts. You can think of them like a nested coordinate system.

Place cells do not do this. For a given environment, they seem to be somewhat randomly arranged relative to each other. Most likely, what actually happens with place cells is that if you could record from all of them, there would be a unique combination of cells active at any location, and this location could then be associated with other information like "I found food here."

Perhaps you could think about grid cells like a GPS location, but place cells are like a map marker.


Nature Scientific Reports vs. BMC Genomics

This is too long for a comment, so I post it here. And these are my personal views, someone else might handle this different. I would submit the paper to BMC Genomics for some reasons:

The editor offered to transfer the paper, so you get past the
editorial review. This is not guaranteed for Nature Scientific Report
(NSR). You still have to get through the peer review, but this is not
different between both journals.
Honestly: Forget about the difference in the Impact Factor. Both are
medium range impact factor journals closely located together. My most
cited paper is published in such a medium impact journal, today you
find papers by a Medline search, so this doesn't matter anymore
(besides prestige). Additionally a lot of citations will raise the
journals impact factor in the future. I would understand this
argument when you would have to choose between Nature and BMC
Genomics, there is quite a difference.
If your work fits better into BMC Genomics the chance for acceptance
is higher, so I would go there. This is of course always a point of
consideration. The same is true for your CV.

If you have the chance to do the decision for yourself without angering your supervisor too much, I would go for it. Even better would be to convince him.


Use control primers targeting something which for sure gives a product. If you have none, ask your colleagues or take some out of literature. Make sure your product is small enough to be amplified in the time given and check for the correct band with a restriction enzyme.


Can a color-blind person see color with filter glasses?

Short answer
Optical filters can optimize color contrast, but never restore color blindness. Filters remove colors, they can never add something. However, glasses like this can prove helpful for certain sub-populations of people that are partially color blind.

Background
First, the term color blindness is deceptive. It is better to talk about colour vision deficiency (CVD). This, because many people labeled as color blind in fact have all the red, green and blue cones like the normally-sighted. These people have protanomaly (abnormal, but still functional red cone photopigment), or deuteranomaly (abnormal green cone photopigment). These two conditions are mild and don't affect daily life too much (source: NEI / NIH).

The other two most common forms of CVD are protanopia and deuteranopia. Protanopes have no working red cone cells and deuteranopes have no green cones. These conditions are more severe and do affect daily life as color perception is compromised. These conditions can be coined color-blindness, as these folks miss one type of cone altogether (source: NEI / NIH).

The glasses of Enchroma target the first two conditions, namely the anomalies and not protanopia or deuteronopia. The Technology page of Enchroma explains why. Basically, protanomaly and deuteranomaly are characterized by the red and green pigments having a shifted spectral maxima. The end result is the same, namely more overlap between the spectral absorbance curves (shown for deuteranopia in Fig. 1). In normal vision, the overlap is already pretty extensive, meaning that green light activates a large portion of red cones and vice versa. In protanopia or deuteronopia this effect is further increased, resulting in a degraded capability to separate reds and grees. For example, protanopes perceive reds, oranges, and yellows as greener, and colors are not as bright. Deuteranopes perceive yellows and greens as more red and they have difficulty telling violet from blue (source: NEI / NIH).

Fig. 1. Left: normal cone spectral distribution vision, right: cone distribution in Deuteranopes. source: Enchroma

What Enchroma has come up with is actually really clever (!) - they've put a spectral notch filter in place and wedge it in-between the red and green spectral optima, thereby removing the large area of overlap. This reduces brightness, but it will enhance contrast when the glasses are worn (Fig. 2).

Fig. 2. Spectral notch filter to enhance green-red color contrast. source: Enchroma

And yes, above considerations hold for any colored object, including monitor pixels.


List of np-hard problems in biology/bioinformatics

I'm no expert in computational biology but I am very much interested and do some big data analysis using R for my own projects so I will try to provide some information.

This (http://www.ncbi.nlm.nih.gov/books/NBK25461/) is an excellent book talking about all the grand challenges in computational biology and the emerging fields so I definitely recommend looking through at least the list on the page, if you don't want to read the entire book. To me all this points to the fact that we are in the big data era, where we have masses of data but making sense of them all and putting them into prospective and analysing them in a way to show us new insights into problems is difficult.

You might also be interested in BOINC, which runs a few computationally challenging projects through crowd sourcing/grid computing (http://boinc.berkeley.edu/projects.php). In more theoretical aspects, here is a list of unsolved problems (http://en.wikipedia.org/wiki/List_of_unsolved_problems_in_mathematics), solving of which will excel our understanding of many modelling problems, which percolate in biological problems as well although I'm not at all an expert in biological systems modelling.

Hope this helps!


Genetic analysis of one sibling relevant to other

If you are siblings, then, outside the Y chromosome (if you are a man, otherwise, you both only have X chromosomes), the results should be very similar. There might be some slight variations of course but it is unlikely to come out as important.

If you are not siblings (e.g. you might be half-sibling if your mother is hiding an affair; sorry for suggesting this possibility but that's no so unusual), then the results might well be quite different.


This is the heart and dart moth (Agrotis exclamationis). Its name refers to the special black spots, which have shape of dart and heart.

This moth is one of the most common in the Paleoarctic ecozone. It has a wingspan of 35-44 mm. The larva of this moth is brown above and grey below. It is capable of feeding itself on a variety of plants.


Why does pETDuet-1 only have one T7 terminator but two T7 promoters?

I think the presence of a single terminator is related to the high processivity of T7 RNA polymerase.

T7 RNA polymerase will transcribe a circular plasmid repeatedly before dissociating. The T7 terminator after ORF2 ensures that the transcript terminates efficiently.

Based on your schematic, these are the potential mRNA transcripts from that construct:

Transcript from T7 promoter #1

 5'---RBS---ORF1---STOP----RBS---ORF2---STOP---[T7 terminator]---3'

Transcript from T7 promoter #2

 5'---RBS---ORF2---STOP---[T7 terminator]---3'

It is doubtful that this vector will produce precisely equimolar concentrations of each protein product, however, the topology ensures that there is at least some of each protein produced. Of course, this could be tested empirically.

I hope that helps!


Effect of the same caloric intake of different macronutrients on body weight

This is a hard question because you will find sources that claim that calories from protein have less effect on body weight gain when compared to the same amount of calories from carbs or fats. Likewise you will find other sources that state that a calorie is a calorie regardless of its origin and hence consuming 2000 calories of protein would have the same effect on body weight when compared to consuming 1200 of carbs, 500 of fat and 300 of protein for example.

A proposed mechanism for protein calories having less effect on body weight gain is "thermogenesis" or in order words that some of the energy from protein calories is lost when processed by metabolic pathways after consumption, but this is not globally accepted by the scientific community. Here is an article from the International Journal of Obesity that discusses the subject. I would suggest being VERY picky with the references you find on the subject since there is a lot of info floating around in the web in sites without any scientific backbone.

Something that can be assured though is that different calorie proportions origin-wise cause different results for other variables different from weight such as body composition. In addition to this, there are several studies adressing the apparent statistical find that protein rich foods increase satiety and hence facilitate body weight control; however, the latter is not related to calorie intake count but rather to other factors that decrease hunger physiologically or psycologically.


How to predict future generations from heritability

"How would I plug those numbers into the breeders equation?"  You would use those fertility rates in calculating the selection differential (S), which would essentially be a weighted intelligence average of the reproducers minus the population average (reproducers+non-reproducers).  So, if the population starts wih 100 IQ and those with 125 IQ produce 2.1 and those with 75 IQ produce 1.9 and those two groups are equally populated, the weighted intelligence avg of reproducers becomes (125*2.1+75*1.9)/4=101.25.  The selection differential is then 101.25-100=1.25.  Response is 1.25*.5=.625.  IQ moves to 100.625.  In your example, S=10.  That is, (x*2.1+y*1.9)/4-100=10, where x is the avg IQ of the above average group and y is the avg IQ of the below average group, assuming the two groups are equally populated.


Why are goosebumps so ineffective at keeping us warm?

When your brain, the hypothalamic temperature centers in particular, detects that the temperature is too warm or cold, it initiates a number of controls to try and correct this.

Goosebumps appear due to piloerection. This is one of the reactions that occur when the temperature is too low.

This causes hairs to stand on end as a result of contractions in muscles attached to hair follicles called arrector pili.

This particular reflex is not actually important in human beings. However, in animals, this mechanism allows entrapment of a layer of air allowing insulation. This way, the heat loss is greatly reduced.

The other mechanisms are very adept at maintaining temperature in the human body. These include sweating, dilation (vasodilation) and constriction (vasoconstriction) of skin blood vessels and increasing and decreasing the body's heat production.

For example, when it's too hot, dilation of the skin blood vessels can increase heat transfer by up to eight times.

Source: Guyton and Hall. Medical Physiology. 11th ed. Elsevier Saunders.


If the DNA is pure, it should last quite a long time.  If there are enzymes and other biological molecules in there, -80C will work much better.

I think you could keep pure DNA at -20C practically indefinitely.

Purity is the main issue there, also pH stabilized, sealed properly, etc.  That makes all the difference.


I can't say for sure but it looks like a species of the Laetiporus mushrooms. Please refer to its wikipedia page for the full info.

edit: I did not read your question fully and now I see that you reached the same conclusion. Just ignore my answer. As to the second part of your question asking if it could be anything else, that is quite hard to visually determine as there are many look alikes in the mushroom kingdom. Read this for some imposters.


I don't get to say this on very many occasions with questions like this...

Your textbook is wrong.

A typical potassium reversal potential in a cell is ~-90 mV. Hyperpolarization through voltage-gated potassium channels can never go more negative than that reversal potential.

An experimenter with access to the cell through a patch clamp electrode could possibly set the voltage more negative than potassium reversal, in which case indeed, potassium would flow against it's concentration gradient into the cell due to the electrical potential. It is not possible to reach those very negative potentials using potassium channels alone.

For a typical cell, the resting membrane potential is more like -70 mV. This resting potential is due to the "leak conductance", which does include potassium but also includes other ions. The ratio of sodium to potassium permeability is typically around 1:20; potassium dominates but you can't just ignore the other ions. A more accurate replacement statement for your textbook would be:

  The leakage conductances tend to drive the membrane potential from hyperpolarized state to the resting state as the net positive flow of ions is inward.

Even at rest, you will always find a slow potassium leak out of the cell. The reason that the cell is at equilibrium at rest is because this leak out of the cell is perfectly balanced by net positive charge flowing in to the cell; this is mostly sodium but can be other ions like calcium as well (note also that that chloride leaving the cell is also a net positive charge in).

Some of the sodium leak current is through specific sodium leak channels, but co-transporters that use the sodium concentration gradient also contribute.

Ren, D. (2011). Sodium leak channels in neuronal excitability and rhythmic behaviors. Neuron, 72(6), 899-911.


Coronavirus origin could be bat, why this happen while people have been eating bats for centuries?

Bats are reservoirs of many important human pathogens, some are emerging infections (e.g., 2019-NCoV, the coronavirus in the news recently), and some are not (e.g., rabies).

Contact between humans and bats is certainly not a new phenomena, but there is more required for an emerging infection than a reservoir and a new host. There must be some bridge that allows a virus to cross a previously effective species barrier. For SARS, there was an intervening amplifying host, the palm civet.  We've now had long enough to study the molecular biology, so this is now quite well described:

  Once SARS-CoV had jumped from bats to civets, it underwent further mutations in civets. The first K479N mutation allowed SARS-CoV to jump from civets to humans and the second S487T mutation allowed SARS-CoV to transmit from human to human, leading to the severe SARS outbreak in 2002–2003.

It may be useful to understand that, as they are RNA viruses, coronaviridae have a high error rate, increasing the rate of mutation. Additionally, making a species jump may allow for novel recombination.


Why do (almost) all energy carriers contain adenine?

As @canadianer comments, this question is unanswerable, and it verges on being classified as ‘opinion-based’. However, because I do not find the answer from the OP appealing, I’ve set out a few points of my own. Hardly an answer — more a list of alternatives as food for thought.

I can imagine adenine being chosen for one of the following reasons (others are welcome to suggest additions):

Functionally best suited
Was there first
Easiest or cheapest to synthesize originally (which would explain why
it was there first, if this were the case)
Random choice

Let’s look at them in turn.

Adenine functionally best suited

There seems nothing in the function of NAD that suggests the adenine ring could not have been replaced by another of the bases, and we know that the free energy of hydrolysis of the beta–gamma phosphodiester bonds of GTP, CTP and UTP can be utilized in an analogous way to that of ATP, so this doesn’t seem very likely.

However one does wonder if a purine (rather than a pyrimidine) ring conveys some sort of advantage in that the other purine-based triphosphate, GTP, is used so widely in the (ancient and essential) process of protein biosynthesis. Perhaps the greater area of contact of the purine ring favoured interaction with proteins (if you don’t argue that these came later).

Adenine was there first

One might consider that early in the evolution of life the bases (or nucleosides and nucleotides) emerged one at a time, in which case the first might have been used for NAD etc. and stuck. One might also consider whether a two-base world preceded a four-base world. If A and U (but not G and C) were in the first RNA (which may have been single-stranded, so I don’t see that the GC content of contemporary thermophiles is relevant) then it may have been a choice between A and U, which A might have won because U is subject to spontaneous deamination (or for the protein-interaction argument mentioned above).

Adenine as easiest or energetically cheapest to synthesize originally

Clearly, the first base might have been the one favoured by chemistry in relation to its synthesis. Contemporary biosynthesis is unlikely to reflect primeval biosynthesis, but it is amusing to observe that adenosine biosynthesis is the only one that doesn’t involve NAD-dependent oxidation. Of course all the contemporary biosyntheses utilize ribosyl pyrophosphate, which requires ATP in its synthesis from ribose phosphate. (Talk about chicken and egg!)

Random choice that stuck

In the absence of any more sophisticated explanation, then it could just be this. Once a choice was made and enzymes evolved to use NAD etc. the choice of adenine couldn’t be changed (or there was no strong enough functional advantage to doing so).

Postscript: When and how did NAD appear on the scene?

One of the reasons I don’t favour the OP’s answer is because it envisages NAD arising after DNA genomes and as a separate entity. I would suggest that it is likely that RNA preceded DNA and that catalytic RNA was responsible for some of the early oxido-reductions. (The first ones were probably catalysed by iron–sulphur centres, either inorganic or associated with simple proteins.) It seem feasible that the nicotinamide ring was an elaboration of a ribozyme which was ultimately almost completely replaced by protein. The adenosine was retained with the functional nicotinamide because it could interact better with the protein. Gross speculation, and it doesn’t explain why adenine was the chosen base, but an antidote to thinking NAD evolved in the fully grown form we see it today.


Does the genome make sense without knowledge of the ovum?

Nice question! Let's start by talking about different forms of heritability.

What is heritable?

Here is a list of things that can be inherited. Some of them are only ('mainly' would be more correct that 'only') transmitted to the offspring while others can also be transmitted to any individual in the population.

The term epigenetics is used with several meaning. In its narrowest sense it refers only to modifications (typically methylation) on top of the DNA sequence or on top of histones (histones are proteins around which the DNA is wrapped). In its broadest sense, it refers to any element of hererdity that is not caused by the DNA sequence. In the below list, I will avoid using the term epigenetics.

What can be inherited:

DNA (obviously)

Modification of the sequence of DNA

Methylation on DNA

Modification of (typically) methyl group added on nucleobasis

Methylation on histone

Modification of (typically) methyl group added on (typically) the tails of the histones.

Environment (or rather macro-environment)

The term environment can be used with different definitions. Histone modification is generally considered as being the environment of the genome typically. I will however make a (somewhat) arbitrary distinction between this micro-environment and the more intuitive macro-environment
Individuals affect their environment and therefore can shape the environment for their descendents. An obvious example is a beaver dam which last longer the the life of a single beaver. Two key concepts here are niche construction and Ecosystem engineering. You should have a look at the post Does modern theory of evolution include modification of physical environment?

Memetics (See wikipedia > meme)

A meme is any idea or element of culture that can be transmitted. This type of inheritence is particularly important is species that have high cognitive abilites such as humans.

In this kind of discussion, there is often someone who stand up to talk about plasticity, developmental noise and mutational noise to mess things up. I will just consider them as phenotypic trait and will not much attention to them for the moment (even though part of my research is focused on these three concepts).

Consideration of the non-genetic inheritence in the literature

I like that you noticed that "the tag genomes is defined as The
entirety of an organism's hereditary information". Such definitions are common and grounded in an old view of inheritance. As listed above, there are other things than the DNA sequence that is inherited by the offspring. While all biologists know that, it is true that few really acknowledge the existence of these other forms of inheritence in their daily thoughts.

Some authors have argued that these other types of inheritence must not be neglected. Odling-Smee and colleagues wrote a whole book on the subject (Niche Construction: The Neglected Process in Evolution). Some have even argued that we should rename our theory of evolution to the light of the existence of non-genetic inheritence (see Laland et al. 2015). My feeling is the vast majority of biologist recognize the existence of these types of inheritence but do not consider that it is worth a renaming of the theory of evolution (current named modern evolutionary synthesis). Some would not consider this renaming necessary either because they neglect the important of these other forms of inheritence or because they just don't think it is worth renaming our theory even in the recognition of the importance of these other processes.

Viewing the cell as a decoder can be misleading

In your question, you are suggesting to view the cell as a decoder of DNA. IMO, this is misleading. In this discussion, I will exit science and enter in the realm of philosophy (identity).

What is generally considered as the mechanism of decoding DNA is actually part of our geome itself (consider typically the importance of tRNA and rRNA). If uneasy with basic concept of gene expression you might want to have a look at an intro course such as Khan Academy from the section Classical and molecular genetics to the section Gene regulation.

Also, I would argue that all the elements that are being transmitted to the offspring shall be considered as being the offspring. If it turns out (which we actually pretty much know is wrong) that histone modification explains more in the phenotypic variance than genetic variance, it would intuitively be unfair to see histone modification as just being a decoder of the genome. We would rather be tempting to see histone modification as central and the DNA sequence as a side-effect.

Layman literature

You say "This question seems never to be seriously addressed in lay literature". Richard Dawkins book called the extended phenotype, while maybe not directly addressing your question does a good job at playing out with thee concept of environment vs gene separation. You might want to have a look at it.

Note that the laland et al. 2015 cited above is easy to read and would be a good source of information for a layman.


Given ATP synthase's structure, how can 3.33 protons ultimately synthesize one and only one ATP?

I might be taking a bit of a simplistic view on this, but I'm not sure what the confusion is.

The ring of 10 c subunits constitute a motor which uses a proton gradient to drive the rotation of the FoFc synthase.

 (image reference is a nice lecture on ATP synthase).

The motor of c subunits has a 10 fold symmetry.  Each subunit releases a proton as it drives a 36 degree movement of the gamma subunit shaft.  The sixfold symmetry of the ATP FoF1 synthease is completely separate from this, and every 360 degree rotation, three ATPs are generated.  As long as the c motor keeps spinning more ATP is created.

This question is similar to asking why the gear ratios of a bicycle or a car are 3:2 or 5:3.   The symmetry of the synthase and the c subunit are independent except that the torque generated by the c subunit motor needs to be enough to drive the ATP synthase.  If the proton gradient were stronger it could well be 7 protons per full rotation and not 10. Think of the two as gears and you might get the picture?


Why do hummingbirds build nests with live ferns instead of dead materials?

From the article titled "Evidence of mutualistic synzoochory between cryptogams and hummingbirds", the specific advantage for the hummingbird is that it gets good nest building material through the selection of cryptograms. The cryptograms though have its seeds dispersed over large distances by birds which is a process called synzoochory.


How to measure the length of mitochondria from z stack fluorescent microscopy image?

ImageJ is usually the standard software to measure cell characteristics, a little bit of a learning curve but there is a large suite of analysis methods and image adjustments/filters.


confusion in types and kingdom system of classification

In earlier days, biological classification systems were often described as artifical or natural, with natural systems reflecting the 'real' relationships among living beings, and artificial ones allowing classification only for some limited purpose (Gilmour, 1937). Natural systems were supposed to be based on a large number of characters, with a focus on characters 'fundamental' to organisms.  Artifical systems were supposed to be based on fewer, arbitrarily chosen characters.
As an example, consider Linnaeus' works on the classification of plants. Linnaeus' Systema Naturae (1735) classified plants based on floral morphology alone. However, his later work Genera Plantarum (1737) included more characters, such as the morphology of fruits. Linnaeus therefore regarded the latter classification as being more natural. (See the Encyclopedia Britannica entry on Linnaeus for a more detailed discussion of this.)
As for the two-kingdom classification, I couldn't find any sources calling it either artificial or natural.
However, the natural vs artificial dichotomy is not always straightforward. For instance, how do we know which characters are 'fundamental' and will help us develop a natural classification system? To quote Judd et al (2008):
For hundreds of years, botanists tried to develop classifications that were "natural"... Unfortunately, the word natural has no fixed meaning; rather, authors have used it to mean something that agrees with their own ideas about nature or about constructing classifications or systems. Eighteenth-century systematists had ideas about nature that were very different from ours—they were certainly not evolutionary—and their systematic practice and classifications are best interpreted in terms of how they understood nature.

Thus, in modern biology, 'natural classification' and 'artificial classification' are better regarded as historical ideas than as useful descriptors. The focus is now on classification that integrates an understanding of evolutionary relationships, i.e. phylogenetic classification.


Where can I find the data on the geographical distribution of the species of Drosophila within various areas of the world?

Source: pinterest.com
I have been unable to find data on a global scale, for now here's a map on the USA.


Species with reproduction barriers that can both reproduce with a third species

How are such species are defined, and at what point dogs stop being
  dogs anymore?

This is a bit like the is-Pluto-a-planet-discussion. A group of scientists have to come together and hold a big conference.
You have a few principles that you want to adhere to and then it's big groups of people making decisions.


Naive T cells hang out in the lymph node waiting for antigen presenting cells (APCs) like DCs to present processed antigens on their MHC molecules. Naive B cells similarly hang out in the B cell zone and are capable of interacting with other T cells and follicular dendritic cells (FDCs). Antigen that ends up in the lymph ends up traveling to the lymph node, where B cells internalize, process and display them on MHC molecules. This is because B cells are also APCs.

Activated (and differentiated) T cells that were previously activated by DCs can identify some of these B cells clones through the TCR-MHC interaction. The B cells process the antigens like DCs, so the resulting heterogeneity of the processed peptides means a fair chance a T cell will recognize it. The result is that B cells receive an activating signal through the BCR and costimulatory receptors.

Differentiated T cells also secrete different profiles of cytokines. For example, Th1 cells secrete IL-12 and IFN-y whereas Th2 cells secrete IL-4, IL-5 and IL-13. Not exclusively, just predominantly or in greater amounts.

The receptor signaling in conjunction with certain cytokines can induce class switching to the resulting antibody production. This swaps the constant or Fc region of the antibody to a different isoform. So Naive B cells are IgM/IgD, and if the cells is receiving Th2 cytokine stimulation, class swtiching results in IgE antibodies, for example.

For elementary immunology I like to reference Cellular and Molecular Immunology, 8th ED. by Abbas et al., but 9th ED is out so keep that in mind. The field somewhat rapidly evolves.


Why is Benzylpenicillin better in Bacterial Meningitis than Amoxicillin?

Amoxicillin is just penicillin with a hydroxyl group off the ring and an extra amine group..

Their mechanisms of action are the same. Their ability to cross the blood-brain barrier are the same. They can both cause seizures.

Both are used to treat to meningitis. The selection of one over the other would be based on the sensitivity of the infecting organism, and the ability to cross the blood-brain barrier in inflamed meninges.

There are better drugs to treat meningitis.

Penetration of Drugs through the Blood-Cerebrospinal Fluid/Blood-Brain Barrier for Treatment of Central Nervous System Infections


Even when you can live without Histone H1, its a widely distributed protein which you find in basically all living cells (except for some yeasts if I remember correct). This points to the fact that it must be available for quite a while. The same is true for the catalytic subunit of the DNA polymerase. Somatropin is still pretty important (and can be found in a lot of organisms), prolamines are quite specific to certain cereals. I would group it 2-3-1-4.


Open protocol for Ligase Independent Cloning

You can look up Gibson Assembly or Circular Polymerase Extension cloning (CPEC).  For both of these the website for J5 has some good protocols.  Here is the one for CPEC:  http://j5.jbei.org/j5manual/pages/80.html

For CPEC you can look at the 2011 Quan paper: http://www.ncbi.nlm.nih.gov/pubmed/21293463

Hopefully that helps.


Why don't phagocytes eliminate mutualistic foregin organisms residing in our body?

Molecular context is important here. E.coli in your colon is OK with the body, it is taken up by phagocytes as part of normal "surveillance". Your immune system will learn and gain "tolerence" to these mutualistic bacteria as long as they are in the correct environment.

If that same E.coli is a pathogenic strain or finds a way into the blood stream (sepsis), your body will recognize that it does not belong and mount a immune response. There are different classes of antibodies with different properties including where they are predominantly found. For instance IgE is found in mucosa but not in serum.

On top of that there are the 'Danger/Pathogen associated molecular patterns' (DAMPs or PAMPs). Cells can 'sense' general molecular patterns such as LPS, unmethylated CpG DNA, double stranded RNA through a class of molecules called Toll-like receptors (TLRs). Different TLRs are found in different cells or cell surfaces and they are the 'first line' response against inappropriate bacteria or viruses.

Once the TLRs are activated the cells will produce 'Danger Signals' called cytokines which initiates an immune response. In the absence of 'Danger Signals' present in the microenvironment, our immune system won't really begin mounting an immune response but just 'surveys'.

In this 'danger' context, you get robust phagocytic response.

If you'd like to learn more about this Mucosal Immunology is what the topic is called. All in all, the vast majority of our immune system is mucosal, it's just less studied relative to humoral immunity since it's harder to study.


What is the exact definition of mitochondrial depolarization?

The inner mitochondrial membrane is important for ATP synthesis (oxidative phosphorylation) to occur. Electron transport chains are situated on the inner mitochondrial membrane where electrons traverse the chain across proteins - causing protons to traverse into the mitochondrial matrix. Creating an electrochemical proton gradient.
This is a very interesting topic and is best understood with an explanation of the JC-1 Dye.
Explanation
Mitochondrial membrane potential changes - depending on cellular events.
The dye 'JC-1' is able to indicate mitochondrial membrane potential in different cells.

If there is a negative charge inside mitochondria then the monomers express green fluorescence.
If there is a positive charge inside mitochondria then the monomers form J-aggregates and now express red fluorescence.

The ratio between red & green florescence shows the mitochondrial membrane potential.

A low or negative mitochondrial membrane potential will show more green florescence.
A high or positive mitochondrial membrane potential will show more red florescence.

Example
One event that may influence mitochondrial membrane potential is an increase in reactive oxygen species.
Reactive oxygen species are molecules that damage cells but are also important to regulate cellular activities. Some examples are Hydrogen Peroxide or Superoxide.
In this image cells are stained with JC-1. The ratio of the dye is ~1:1 at basal. As the reactive oxygen species hydrogen peroxide is added and time continues, there is more green. Showing:

A low or negative mitochondrial membrane potential in each of the cells.


Are there records of monozygotic twins in which one experiences androgen insensitivity syndrome

This is an important question to geneticists because monozygotic twins are the only ethically acceptable way to research genetically identical humans.

I'm sure the sort of non-symmetrical fission where specific DNA coding for genes are not present or are modified to completely different phenotype in the formation of the twins probably has happened, but it incredibly rare.  In stem cells, asymmetric division has been observed frequently (warning: google doesn't like PlosOne right now).  In development, unless its actively been activated as an asymmetric division, this would be incredibly rare- this would be akin to a birth defect in a single fetus - how many cases of mixed male and female cells in a single baby. I can't even find a reference for such a thing.  Much more common are semi-identical twins, where two different sperm fertilize a single egg which may have split.  Semi-twins are still vanishingly rare - the first report was in 2007).

  Such twins are probably very rare. Their existence and discovery relies on three unusual, and possibly unlinked, events: first, that an egg fertilized by two sperm develops into a viable embryo; second, that this embryo splits to form twins; and third, that the children come to the attention of science.

This might be the case you are thinking of?  In one case reported there was a gender difference.

  Souter and her colleagues investigated the twins' genetic makeup because one was born with ambiguous genitalia. This twin turned out to be a 'true hermaphrodite', with both ovarian and testicular tissue. The other twin is anatomically male.

They weren't monozygotic though.  Just others from the same mother ;)

Monozygotic twins are not completely identical, epigenetic fingerprinting - including DNA methylation and chromatin DNA binding patterns (pnas - paywall) change while the fetus develops and as the child and adult age.  This can cause quite significant differences as the twins age. Epigenetic markers change the dynamics of brain development and can make a difference in the occurance of leukemia.

There are also modifications to the DNA sequences of cells, copy number variations (CNVs) are multiple (sometimes hundreds or thousands of times over) repeats of short (2+ base pairs) DNA sequences.  These also occur as the cells differentiate and divide to form tissues and organs.  Twins show significant differences there too as this is not a deterministic mechanism in development.

I can't find any references to twins showing asymmetric AIS. but the number of variants requiring this makes it sounds like its possible.  If you have a reference post it and I can have a look?

note added: this paper shows that methylation profiles appear identical at least in utero.


Are there any organisms with larva more advanced than adult form?

First let me agree with the commenters that your question doesn't really make sense.  Nonetheless here's an example that you may find interesting. Arachnocampa are insects that spend almost their entire lives as larva. These larva spin silk trap lines which capture and poison prey. They can only live in windless places (wind will mix up the lines) so to lure insects into caves they glow. By contrast their imago forms are short-lived poor fliers which are unable to eat.


Probably a Ponerinae.
(Wikipedia, AntWiki)

It's not the easiest picture to work with, but here's what I did.
Going by the location we have the following distribution of ant species in South Australia (see below, or here).
A critical identification point is the petiole, bumpy segments on the thin part of the back of the ant. Your specimen appears to have none or one.
This excludes Dolichoderinae and Mymicinae, who both have two clearly distinguishable petioles (or rather, a petiole and a post-petiole).
Myrmeciinae have different colours and/or mandibles, leaving the following three likely candidates:

Formicinae
Ectatomminae
Ponerinae

Ponerinae are distinguishable by a constricted gaster, so an impression in the posterior section, which is quite clearly visible in the picture.
(This is technically only an identification to subfamily level, if anybody wants to take a shot at species, feel free)


Did the old world have relatives of plants which were brought after the discovery of Americas?

Three of your examples: potato, tomato, and chilies, are from the genus Solanum. Along with the rest of the Solanaceae family, they are most diverse in the Americas but some species are found worldwide.

Species that would be found originally in the 'old world' from the Solanum genus and Solanaceae family include the black nightshade, bittersweet nightshade, and deadly nightshade. There is also at least one cultivated plant variously known as eggplant, aubergine, or brinjal (Solanum melongena) that is thought to have been domesticated in Asia.

The strawberry genus, Fragaria, also has species world-wide.

Of course, because all life on Earth is related, the answer to the general question "are there relatives of X found in some place" will always be "yes" as long as there is life there, it's only a matter of the extent of relation.


Can RNA be extracted from tissue suspended in formalin?

Formaldehyde forms adducts with RNA and can also make it more susceptible to degradation. It can also cause crosslinks to form between RNA and proteins (or possibly other RNAs). For all these reasons extraction of high quality RNA from formaldehyde fixed samples is very difficult and the yields are low (Howat and Wilson, 2014).

Have a look at this article by Evers et al. (2011) which explores optimal conditions for removal of the formaldehyde adducts. However, this study does not involve actual RNA extraction from fixed tissues, which would be even more difficult.

RNeasy FFPE Kit from Qiagen claims to be specially designed for RNA extraction from formaldehyde fixed samples. The product description says that the lysis buffer contains substances that reverse the modifications formed because of formaldehyde. There is a similar kit from Thermo-Fisher. Russel et al. (2013), report that the RNA yield was similar between fixed (using Qiagen RNeasy FFPE kit) and unfixed samples (using Qiagen RNeasy Plus mini Total RNA extraction kit).

  should I homogenize the tissue before removing the formalin, or after?

Homogenize after removing formalin. Since the tissues are already brittle because of formaldehyde fixation, you need not use harsh homogenization procedures. Pipette gently. You can use proteinase-K and DNAse to remove proteins and DNA respectively (RNeasy kit involves these steps).

For future experiments, you can store the tissues in RNAlater solution (Thermo-Fisher; or similar formulations from other vendors/lab). Store one part of tissue in formaldehyde for IHC/ISH and the other in RNAlater for RNA/DNA extraction.


What is the insight of Frank Starling law of the heart?

This is the short answer from wikipedia :) :

  As the heart fills with more blood than usual, the force of cardiac
  muscular contractions increases.[2] This is a result of an increase in
  the load experienced by each muscle fiber due to the extra blood load
  entering the heart. The stretching of the muscle fibers augments
  cardiac muscle contraction by increasing the calcium sensitivity of
  the myofibrils, [3] causing a greater number of actin-myosin
  cross-bridges to form within the muscle fibers. The force that any
  single cardiac muscle fiber generates is proportional to the initial
  sarcomere length (known as preload), and the stretch on the individual
  fibers is related to the end-diastolic volume of the left and right
  ventricles.

  In the human heart, maximal force is generated with an initial
  sarcomere length of 2.2 micrometers, a length which is rarely exceeded
  in the normal heart. Initial lengths larger or smaller than this
  optimal value will decrease the force the muscle can achieve. For
  larger sarcomere lengths, this is the result of less overlap of the
  thin and thick filaments; for smaller sarcomere lengths, the cause is
  the decreased sensitivity for calcium by the myofilaments.

in one sentence, it is a response to tension.


What is the direction of current flow in myelinated nerve cells?

During an action potential current flows across the neuronal membrane. Basically, during depolarization, Na+ goes into the cell, during repolarization K+ goes out. This process for a myelinated axon is shown in Fig. 1.

Action potentials in myelinated neurons jump from node to node, a process called saltatory nerve conduction. These nodes, called nodes of Ranvier, lack myelin and contain Na+ and K+ channels. Outside these nodes there is insulating myelin wrapped around the axon and the axonal membrane lacks Na+ and K+ channels there.

What happens during an action potential at a node is the following: Na+ rushes in at the node. Because of the insulating myelin in the next axonal segment leading up to the next node in line, Na+ can run through the axon to the next node without much signal loss. This passive spread of depolarizing current is much faster than repeatedly generate a new action potential along the length of the axon.

To answer your questions now:

  Question: Is it correct to say electric current flows through the extracellular space or cytosol of a nerve during impulse conduction?

Answer: Yes... and no. No, because electric current and notably Na+ and K+ flow perpendicular to the axonal membrane during action potentials. Yes, because the Na+ ions do move through passive current spread through the axon to the next node.

  Question: How exactly does the current flow in myelineated nerve fibers?

Answer: Your professor was spot on. During depolarization, ions (notably Na+ in this case) are carried from the extracellular space through Na+ channels in the node of Ranvier to the intracellular space. From there it spreads through passive diffusion to then next node.

Fig. 1. Action potential generation in myelinated axons. source: Purves et al.(2001)

Reference
- Purves et al. (ed). Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


downloading a reference genome for alignment

Since you are using Bowtie, you want the indexed genome, see if that's not available here, instead of downloading the fasta and indexing it yourself.

http://support.illumina.com/sequencing/sequencing_software/igenome.ilmn


What is "beto carotene" and how can it turn lakes pink?

The "beto" is a typing mistake. Beta is an organic chemistry label referring to a beta-ring of 6 carbons that exists at either end of a carotenoid polymer C40-Hx.

It is localized in the chloroplast. The plants don't really have a mechanism to release pigments, they can re-metabolize chlorophyll. The volvocalean algea Dunaliella salina is used to harvest beta-carotene in Karratha, Western Australia, from salt lakes. The can have 12% beta-carotene as dry-matter content, the highest of any known source.  The squares are probably salt.

the algea afterwards:

There are over 1,100 known carotenoids of which at least 700 have been identified in plants. They include carotene and xanthophylls, and carotene include beta-carotene. The plants and algea use it to protect themselves from intense sunlight and UV's. It is an anti-oxidant.

Pink doesn't actually exist as a color. It is imagined when green and blue light is sensed by the eye, while red is at a maximum. In the lakes, we know there is 80% red and 20% green pigment in the algea. All that is required would be 20% blue to percieve pink. I don't know where the blue color comes from, the sky/water.
Orange is complex for the eye, and so is pink, because we can only see red green and blue.


The Entomological Society of America has dedicated page called Entomology Resources for Teachers, which might answer many of your questions. It compiles curated links to resources, universities,

Here are a couple of other entomological links/resources that I have saved from before:

Bugguide.net
Pictures, simple keys and taxonomical info. Also has a forum.
The Entomological Foundation: Education
Links, project ideas etc.
Kerbtier.de
Webpage on beetles found in Germny, but relevant for many European countries. Also has general pages on e.g. beetle morphology and a glossary that might be useful.


DNA decomposition isn't a phenomenon that is too common.
In nearly all cases, DNA is broken apart to the accidental contamination with nucleases. Long-term storage of DNA in the -20 is also suggested in order to significantly lower the rates of these nuclease enzymes.

Additionally, DNA only truly fragments at very high temperatures (>90-100 degrees Celsius) due to the nature of the covalent chemical bonds that form DNA. Nearly any organic molecule will degrade at very high temperatures, and some will degrade at lower temperatures due to unstable structures or heat-labile bonds.

Of course DNA will deanneal at somewhat-high temperatures due to its double standedness , but allows for reannealing to the initial molecule once the temperature is brought down.

One additional reason for potential DNA degradation is DNA shearing, which will occurs when you tear up your DNA physically due to exposure to rigorous shaking, resuspending or other "violent" techniques.


The FAM symbols are defined in the HUGO Gene Nomenclature Committee guidelines.

The FAM symbol is an anonymous and temporary identifier that is given to groups of poorly characterised genes which share more than 40% amino acid sequence identity (see Section 4.1).

There are two human genes/proteins in the sequence similarity 166 group; FAM166A and FAM166B. These have some sequence similarity (more than 40%) but  function of this similar sequence is currently unknown. Once further characterisation has been performed for any FAM group they will likely receive more meaningful names.


Are the genes for transcriptional factors close to their targets in the genome?

Is the gene coding for the transcriptional factor always present next
  to (or close to) the transcription unit?

Not necessarily. You can find several counter-examples. Even for prokaryotes this is not necessarily true. The genes regulated by a common factor are called regulons and though the target genes need not be proximal to the regulator, it has been observed for E. coli and B. subtilis that operons within a regulon are clustered in the genome (Zhang et al, 2012). In the same study, the authors note that small regulons have the regulator proximal to them (See the figure below).


It looks like a "Spider lily" from the Hymenocallis genus.

Here is a picture of Hymenocallis caribaea from wikipedia for comparison:

There are however ~65 species in the genus (according to wikipedia), and I cannot say exactly what species you have.


This question has been asked before: Is there an advantage to linear chromosomes?

Firstly, I should state that the generalisation that ALL prokaryotes have circular genomes is incorrect. A growing number of prokaryotes have been discovered which have linear chromosomes, such as Borrelia burgdorferi ,which causes Lyme disease, members of the Streptomyces family and Agrobacterium tumafaciens, which has both a circular and a linear chromosome.

Anyway, on to the question being asked:

Generally, my feeling is that large circular chromosomes would have much greater supercoiling and related torsional problems, making it difficult to unwind them for transcription, replication or repair. This limitation on physical size limits the amount of genetic information that can be carried in a single chromosome, thereby limiting complexity of the organism.

You could increase the number of circular chromosomes to compensate for their lack of size, but again, you end up having a physical limitation (size of the nucleus or size of the cell for anuclear organisms) on how many chromosomes you can pack into the cell.

Linear chromosomes are just a more efficient shape when it comes to larger sizes.

=====================

Here are a few good references to dig further, if you're interested:

A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10802162
Why do we have linear chromosomes? A matter of Adam and Eve. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10422538 -- Proposes that meiosis was the driver for linear chromosomes.


What is the minimum functional biological light sensor?

The minimum biological light sensor is just an existing signaling molecule that, by chance, also has some change in its activity due to light.  There are several ways this could happen.

One extremely simple example would be based on a G-protein coupled receptor (GPCR).  GPCRs are a family of related signal transduction proteins (the largest family) that sit on the surface of a cell's membrane.   Each one is sensitive to a molecule or small group of related molecules.  When exposed to the molecule it is sensitive to, the GPCR sets of a series of chemical cascades that trigger some activity in the cell.  For example, it can serve as a signal for the cell to move towards the place where the chemical was detected, or move away.

Now, imagine that, just by chance, the molecule the GPCR is sensitive to has some sensitivity to light, in that when exposed to light the molecule either has a larger or smaller chance (even slightly) of binding to the GPCR.  This is not improbable, a ton of biological molecules have this characteristic, in fact many have substantial responses to light even though they are not involved in light-sensing pathways.  A good example is called "photoisomerization", where the same molecule can have more than one shape, and switches between two shapes when exposed to light.

This would be a biological light sensor.  Not necessarily a very sensitive one, but once you have such a basic light sensor, natural selection would take over and lead to stronger and stronger effects.

In fact, this is pretty much how our eyes work today.  It uses a GPCR whose target is a molecule that changes its shape when exposed to light, which makes it no longer able to bind to the receptor, shutting of the signaling cascade.  What is more, this molecule is not only used in sensing light, it is a precursor to a molecule needed for gene transcription and signaling.

In fact, you can splice light-sensitive GPCRs from bacteria (which are different than those in animals) into non-light-sensitive animal cells, and those molecules will automatically integrate with existing GPCR signaling cascades, rendering the cell light sensitive.


Why do humans sneeze out mucus if it's a good thing?

Indeed, mucus is essential for in this case protecting the respiratory pathways, which includes the nasal cavity and the pharynx, against different threats, such as microbes. Sneezing, which is initiated by virtue of the activation of mechanoreceptors in the upper parts of the respiratory system, leads to a buildup of intrathoracic pressure, due to the contraction of expiratory muscles against a closed glottis. The pressure gradient, when the glottis opens, will then lead to the rapid flux of air from the lungs, through the respiratory tract and out through the mouth and the nose, whereas mucus containing the initial irritant will follow, merely due to the forces at play.

Note that the epithelia in the resp. tract normally transport the mucus containing everything from microbes which have been breathed in, and different particles, to the oropharynx, so as to allow you to swallow and take it to the GI tract instead.

For further reading, I recommend Boron Boulpaeps Medical Physiology chapter 32 on the "Control of Ventilation" (2012).


Why are some human injections intraperitoneal?

IP injections are used for a variety of reasons:

The peritoneum provides a large surface area for absorption of drug (compared with intramuscular (IM) or subcutaneous); can thus inject a larger fluid volume.

Easier to inject that intravenous.

For some chemotherapy, such as ovarian cancer, IP injection is used to attempt to localize the drug near the tumor (it's through a catheter, rather than with a syringe and needle).  Essentially the goal is to provide chemotherapy to the abdominal region where cancer has spread rather than systemically.

 It is commonly done in animals, such as mice, because it is difficult to find a vein in small creatures.

https://en.wikipedia.org/wiki/Intraperitoneal_injection
http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-treating-chemotherapy
http://www.ncbi.nlm.nih.gov/pubmed/20156151 courtesy of @AMR
http://cpharm.vetmed.vt.edu/VM8314/Administration.htm


What factors may lead to a difference in whole-cell potency compared to cell-free potency?

You are correct in saying that whole-cell potency and in vitro/cell-free potency often differ by quite a bit. There are actually a lot of factors that can contribute to this, but I'll try to give a couple illustrative examples, for increased and decreased potency (when moving from cell-free to a whole-cell assay).

When moving from cell-free to whole cell assays, decreased potency is the more common outcome. As you mention, a big reason is just that you get a lot more things the drug can bind to, so you tend to have less drug effectively engaging the target. However, there are other factors at play as well. Ultimately, the main reason that one sees decreased potency in the whole-cell format is that one is often asking for something fundamentally different than what was asked for in the cell-free assay.

For example, let's say you do some CRISPR of RNAi screen in cancer cells, and you find that if you shut down gene X, the cells die. You look it up, and gene X codes for an enzyme.

So you think, "Great! I'll design an inhibitor for the enzyme, and then kill the cancer cells with that!"

In order to screen for inhibitors and test their effect on this enzyme, you set up an in vitro with purified enzyme, substrate, and some way of measuring the generation of product. You screen, find compounds, and optimize your lead. You eventually end up with a compound that has an IC50 of 1 nM in this assay. Then you decide it is time to move into cells. You treat the cancer cells with the compound, and you notice that your IC50 for cell death is 100 nM - 100x what it was in the original assay. The reason is that you are asking much more of your compound.

In the first assay, the compound had to bind to the enzyme, which may have been the only protein in solution, and inhibit it. You were directly measuring enzyme activity. In the second assay, the compound had to diffuse through the cell membrane or find some other means of getting into the cytosol, where the target protein resides. Then, despite the complex milieu in the cell, it had to bind that specific protein and inhibit it. But inhibiting the protein isn't enough. It has to inhibit the protein enough to kill the cell. Maybe the cells die when the enzyme activity is 50%, in which case you would expect your IC50 values to be fairly close between assays. But maybe it doesn't. You may need 70 or 80% inhibition before the cells start to actually die. Plus, the cells may not go down without a fight. Maybe they up-regulate expression of drug-efflux pumps, which are ATP-powered proteins that literally pump small molecules out of the cell. This reduces the effective concentration of drug you are giving the cells. There are also many other adaptations that the cells may undergo to improve survival, which are beyond the scope of this answer. So what you are demanding from your compound in the whole-cell assay may actually be much more than in the cell-free system.

The other effect - seeing increased potency in whole-cell vs cell-free conditions is much less common. Without seeing the exact study you are referring to, it is difficult to comment. However, one thing to remember about BACE1 is that it is part of a huge complex that is embedded in the cell membrane. Reconstituting this complex in vitro is non-trivial, and it may be that the complex is not functioning the same as in the cell depending on how the reconstitution was performed. For example, maybe BACE1 binds better to the drug only when a binding partner is present that stabilizes a conformation suitable for inhibitor binding. It could also be that the inhibitor is actually targeting another protein in the complex that is not present in the cell-free system.

Anyway, I apologize if this was a bit long, but I hope this answered your question and shed a bit of light on the complexities of assay development and drug development.


DNA-cellulose chromatography is used to purify proteins that bind DNA (Potuzak and Dean 1978, Abdullah et al., 1985).

The idea behind it is quite simple: you attach DNA to a cellulose matrix and keep conditions so that the DNA does not dissociate from the cellulose. This stationary phase is then used as a bait for DNA-binding proteins from the mobile phase. The purified DNA-binding proteins can subsequently be dissociated from the column with high salt concentrations.

The method was (as far as I know) first described by Litnam (1968) who used it to extract a DNA polymerase from Micrococcus luteus.


What is the relationship between snails/slugs and clams/mussels?

The Tree of Life web Mollusc page  shows that gastropods (snails/slugs/etc.) and bivalves (clams/mussels) are two of the major groups within Mollusca:

You can click through to get more detail on the individual groups (but there isn't much more information about the defining characters, date of divergence, etc.). At the very least, these technical names for the taxa (and of the Conchifera, their parent taxon) should help you search for more information, e.g. a Google scholar search on "bivalvia gastropoda divergence", which gets to Investigation of molluscan phylogeny using large-subunit and small-subunit nuclear rRNA sequences ("scaphopods are more closely related to gastropods and cephalopods than to bivalves") or Phylogenetic relationships of annelids, molluscs, and arthropods evidenced from molecules and morphology. (You do have to be careful in reading the phylogenetic literature, as it's rapidly evolving; the latter paper is from 1996 and may well be superseded.)


Is this a counter-example to Darwin's theory of evolution?

Darwin cited the giraffe as an outstanding example of natural selection. Supposedly, as a result of extended droughts, the supply of green leaves could be obtained only at the top of the trees, and therefore the shorter necked giraffe died off.

The term outstanding is funny in its usage here but otherwise this text is quite right so far.

  However, there is no evidence whatever in the fossil record or elsewhere that giraffes with short necks have ever existed.

Actually there is. See this popular science article suggested by @James.

  And what would have happened to young giraffes with relatively short necks?

The answer in the text above. It rightly says the shorter necked giraffe died off.

  Darwin failed to realize that body characteristics in offsprings are determined and programmed by DNA factors of the Genes or the Genetic material of the parents [..]

This is an awfully phrased sentence making it very clear that the author has no idea about genetics.

  not by the stretching of the neck or any other bodily exercise

Sure. The concept that individuals stretch their necks, necks become longer and this characteristic is passed on to the offspring is wrong indeed. This is known as Lamarckism. It is funny because the above text describe natural selection and it then says that it is wrong by making a straw man, misrepresenting natural selection as a Lamarckist process.

  What is the current status of "theory of evolution of species" ?

You should have a look at the post Is evolution a fact?.

You should also have a look at an intro course to evolution. There are several online and free introductory ressource of information on evolutionary biology. Understanding Evolutionby UC Berkeley is probably one of the best. It is very short, very introductory and will already teach you a lot.


What textbook is this? An ATP synthase is not a hydrolase, since it does not use water to break a chemical bond (at least not in its primary function). However, it couples proton translocation with ATP synthesis. Therefore it is a translocase.
See the following passage from qmul.ac.uk what category 7 is and why e.g. ATPase is classified as translocase rather than as hydrolase. (It is a hydrolase as well, but it's not its primary function.)

Translocases (EC 7): A new EC Class
Six enzyme classes have been recognized since the first Enzyme
classification and nomenclature list was first approved by the
International Union of Biochemistry in 1961. These were based on the
type of reaction catalysed: Oxidoreductases (EC 1), Transferases (EC
2), Hydrolases (EC 3), Lyases (EC 4), Isomerases (EC 5) and Ligases
(EC 6). However, it has become apparent that none of these could
describe the important group of enzymes that catalyse the movement of
ions or molecules across membranes or their separation within
membranes. Several of these involve the hydrolysis of ATP and had been
previously classified as ATPases (EC 3.6.3.-), although the hydrolytic
reaction is not their primary function.


Can stress echocardiography show coronary blood flow difference before and after exercise?

No, echocardiography is not sensitive enough to do so. For tracing coronary arteries directly flow angiography is the choice.


Both. You should note that activation in this case involves recruitment of RNA polymerase to drive transcription, and that this process is irrelevant to DNA replication. B in the figure shows amino acid contacts (from CAP) with specific nucleotides in the DNA duplex.

DNA binding by CAP: structure of the CAP-DNA complex.

(A) Structure of CAP in complex with its consensus DNA site (PDB 1RUN) [14], showing primary- and secondary-kink sites. CAP is in cyan; DNA and cAMP bound to CAP are in red. The crystallization DNA fragment contained a single-phosphate gap between positions 9 and 10 of each DNA half-site (Fig 1b).

(B) Summary of CAP-DNA interactions. Shaded boxes indicate positions at which CAP exhibits strong sequence preferences [11,15,16,17]. The black circle, black rectangles, and black diamonds indicate, respectively, the two fold-symmetry axis, the primary-kink sites; and the secondary-kink sites. The black vertical lines indicate the positions of single-phosphate gaps present in the crystallization DNA fragment. The cyan ovals and cyan circles indicate, respectively, amino acid-base contacts and amino acid-phosphate contacts.

Figure from:
Catherine L. Lawson, et al. 2004. Catabolite activator protein (CAP): DNA binding and transcription activation. Curr. Opin. Struct. Biol. 14:10.


In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to?

As I understand it from skimming the Cell paper and that by Bobay and Ochman, 2018, which it cites, the concern is the validity of the established method of defining viral species. Quoting from this latter paper:

  Members of a biological species are defined by their ability to exchange genetic material…

The problem would appear to be that ssDNA and RNA viruses evolve rapidly (rampant is probably meant to convey this idea), but most importantly, not just by acquiring point mutations or deletions, but by horizontal gene transfer from other viruses (and from bacteria).

The net result of this is that such viruses are made up of segments from different sources, some evolved by conventional mutation and others ‘hijacked wholesale’ (my own hyperbole) from other organisms. Another way of putting this is that their genome is a mosaic of genes from different organisms. An example of this is in the diagram below, taken from a paper by Juhala et al. entitled “Genomic Sequences of Bacteriophages HK97 and HK022: Pervasive Genetic Mosaicism in the Lambdoid Bacteriophages”.

For anyone unfamiliar with the word ‘mosaic’ (or its applicability in relation to genomes) I reproduce below a Roman mosaic from Pompeii. The idea is that what appears as an integrated organism is composed of disparate pieces with distinct boundaries.

(The protagonists in the mosaic are about to exchange blows, rather than genes. There are also mosaics at Pompeii depicting the latter type of exchange, but these are a little too ‘rampant’ to present here.)

The implications of ‘mosaicism’ for defining viral species is — I imagine — that viruses which could be regarded as distinct species from examining the sequences of the majority of their genes might still be able to exchange genetic material by crossing-over at genes they have acquired by horizontal transfer.

Oh, and what about paradigm? It would clearly be unfair of me to suggest that this is a fancy word that the authors have used to sound important. The Oxford Dictionary online defines it as:

  A typical example or pattern of something; a pattern or model.

I think that the authors mean that the viruses provide a good example of horizontal gene transfer.