How do infectious bacteria determine when their numbers are high enough to attack a host?

I think the current answer to this for bacterial infections is quorum sensing.  Quorum sensing is a signalling pathway in bacteria which senses a molecule that the bacteria themselves secrete.  When the concentration of the quorum signal reaches a certain level, the bacteria interpret this as their population density reaching some threshhold.

Bacteria are always around - even infectious Staph, as described in the other answer, the bacteria are always being cleared out by the immune system, but when they find the right place where they can get critical mass, they dig in, form a biofilm and secrete toxins, which can help them divide more successfully.

This is a description of the process from a paper on Staph infection, a common bacterial infection in humans.

  S. epidermidis is considered part of the of the normal human microbial flora, while S. aureus is usually regarded as a transient member. Colonization by either species usually does not lead to adverse events. However, when these organisms or their extracellular products are allowed to breach the epithelial layer, serious disease can result (1). S. aureus has many cell surface virulence factors (such as protein A and clumping factor) and secreted exotoxins and enzymes that allow strains to cause a myriad of infections. These diseases range from relatively benign furuncles and subcutaneous abscesses to scalded skin syndrome, sepsis, necrotizing pneumonia, and toxic shock syndrome (TSS). While no single cell surface virulence factor has been shown to be uniquely required for mucous membrane attachment, once colonization occurs, numerous secreted exotoxins, including the pyrogenic toxin superantigens and exfoliative toxins, definitively cause serious human disease. Other secreted exotoxins, such as the four hemolysins (α, β, δ, and γ) and Panton-Valentine leukocidin have also been suggested to contribute to significant illnesses. S. epidermidis does not possess the array of extracellular toxins that S. aureus does, and its primary virulence factor is considered to be its ability to form biofilms.

  To improve their ability to cause this variety of human disease and to occupy numerous niches within the host, staphylococci have developed quorum-sensing systems that enable cell-to-cell communication and regulation of numerous colonization and virulence factors.

Viruses are typically simpler - as @MattDMo describes. They seem to rely on finding an environment where they can infect more cells at such a rate greater than the immune system can clear them out.  For influenza, this is more of a 'shock and awe' offense where they infect and multiply quickly, trying to outpace the immune system.  Another virus like HIV will actually multiply so slowly that the immune system can't find the host cells, allowing HIV to slowly spread over the host cell population.

Here's a bonus topic... When they were looking a cholera in the 1990s they found that V cholerae bacteria actually take up phage with toxins in them that convert benign bacteria to virulent ones (that cause dysenteric cholera).  They do this by conveying both the pili that attach to human cells and the toxin that causes the violent G.I. reaction of dysentery.  I think this is not unusual for bacterial diseases.  (the reference is Science 272, 1910-14 BTW).

This has lead to a suspicion that bacteria might be even adapting to infectious phenotypes through genomic changes.  This study had sequenced the genome of C difficile from 486 patients and found that relatively few of them really were capable of patient to patient infection:

  The results of the study indicated that, although transmission between patients is likely to occur, it actually happens at relatively low frequency. In particular, concerns that healthcare teams were spreading infection between different hospitals seem to be misplaced. One exception to this general finding is that there were a large number of cases of infection from one particular strain that does appear to have been due to patient-to-patient transmission, emphasising the epidemic nature of this lineage. Notably, this strain has declined in UK hospitals in the last five years.


How can I use this data to make a function?

I will not go too deep into the details but here some information to facilitate your understanding of these ubiquitous statistics in biology.

The F, $r^2$ and p-value are all equivalent statistics to measures the goodness-of-fit of a model against the data.

The F is the ratio of the $unexplained~variance~/~explained~variance$. I let you look out what the variance is. The F (originating from a F-test) allows, using the proper F-distribution cumulative density function (cdf) for the number of observation you have, to compute a p-value.

The p-value gives you the probability of obtaining the observed fit with your model (here a linear one) by random chance only. For example in your case a p-value=0.01 means that you have a 1% chance to observe this correlation just by chance. Usually the p-value threshold used to claim statistical significance is 0.05 (i.e. 5% chances to observe that fitting by random chance). In linear regression, the lowest the p-value the closest the distance (called variance) of the observed data point to the line.

The $r^2$ is the coefficient of determination (or the square of the correlation coefficient). This measure is very interesting as it give you an estimate of the "proportion of the data" explained by your model. For example a $r^2$=1 means that 100% of the variance of the data is explained by your model, in other terms your model perfectly fits the data. A $r^2$=0 in the other hand means that your model does not at all explain the data (no fits between your model and the data).

The $r^2$ and the p-value can be computed for any type of fitting, like trying to fit an exponential curve instead of a linear one. What you usually look for when modeling data is the highest $r^2$ possible. As all of this statistics are linked a higher $r^2$ means a lower p-value for an identical number of observations.


Where I studied, every undergrad read Campbell Biology. You can start it as a non-specialist but you will not be one at the end..


What are the buoyancy control mechanisms of Chambered nautilus?

The various species of nautilus use a combination of active transport of salts and passive diffusion of water for buoyancy (Denton and Gilpin-Brown 1966, Ward 1979, Greenwald et al. 1980). The chambers are filled with seawater. Salts from the seawater in the chambers is removed by a structure called the siphuncular epithelium. This process makes the chambered water hypotonic, meaning it has lower solute concentration relative to the animal. The hypotonic water then diffuses from the chambers into the blood, creating air pockets in the chambers. Greenwald and Ward (2010) have a recent summary of what is known about nautilus buoyancy, if you want to know more.

The diffusion of water in  is not a rapid process. The maximum ascent and descent rate of Nautilus from depths appears to be about 3.0 m m$^1$ (Dunstan et al. 2011).  This does not seem like an efficient process or rate of depth change for an underwater robot.

Literature Cited

Denton, E.J. and J.B. Gilpin-Brown. 1966. On the buoyancy of the peraly nautilus. Journal of the Marine Biological Association of the United Kingdown 3: 726-759.

Dunstan, A.J., et al. 2011. Vertical distribution and migration patterns of Nautilus pompilius. PLoS ONE 6: e16311. doi:10.1371/journal.pone.0016311

Greenwald, L., et al. 1980. Cameral liquid transport and buoyancy control in the chambered nautilus (Nautilus macromphalus). Nature 286 55-56.

Greenwald, L. and P.D. Ward. 2010. Buoyancy in NAutilus. Topics in Geobiology 6: 547-560.

Ward, P.D. 1979. Cameral liquid in Nautilus and ammontites. Paleobiology 5: 40-49.


The breeder's equation as you wrote it:

$$R = h^2S$$

The heritability that is the ratio of additive genetic variance over the total phenotypic variance is called the heritability in the narrow sense and is noted $h_N^2 = \frac{V_a}{V_P}$, where $V_A$ and $V_P$ are the additive genetic and phenotypic variance respectively. In contrast the heritability that consider the total genetic variance is called the heritability in the broad sense and is noted $h_B^2 = \frac{V_G}{V_P} = \frac{V_A + V_D}{V_P}$, where $V_G$ is the total genetic variance and is equal the sum of the additive genetic variance $V_A$ and the genetic dominance variance $V_D$. We can rewrite the breeder's equation using the standard notation for the heritability in the narrow sense:

$$R = h_N^2S$$

The so-called response to selection $R$ is the mean deviation of the trait in the next generation. In other words, $R$ is the difference between the mean trait of the parents and the mean trait of the offspring, So to answer your question, yes, the breeder's equation gives the value of the mean trait in the following generation. It does not give any information about the frequency and number of alleles though.

$S$ is the the mean trait of the individuals which reproduce weighted by their reproductive success minus the mean trait of the parents. In other words, it is

$$S=\frac{1}{\bar w}\sum_{i=1}^{\text{nb inds}}m_iw_i - \bar m$$

, where $m_i$ is the trait measurement and $w_i$ is the fitness of this individual, $\bar m$ is the mean trait of the parents and $\bar w$ is the mean fitness.

The mean trait of the parent generation does not appear in the breeder's equation but only their mean trait weighted by their reproductive success. In the standard case of truncated selection (common in artificial selection programs) all $w_i$ are equal and $S$ becomes the mean trait of the individuals that we allow to reproduce in the parent population. And it is exactly the same thing for the multivariate case except that the variance-covariance matrix should be taken into account.


Is it a coincidence that the sensory systems for smell, vision, taste, and hearing are all near each other in the head?

No it's not a coincidence that eyes, nose, mouth, and ears are all near each other in the head. As you note the layout is inherited from an ancestor, that's your answer.

A study of vertebrate head sensory systems shows that the

  The olfactory, vestibular auditory, and lateral line sensory organs displayed a strong link with the urochordate-vertebrate ancestor.

So this paper highlights that these structures go back earlier than the animals in your list. The development of vertebrates is very complicated so major departures from this developmental program which are successful are going to be rare events. This is reflected by blind cave dwelling animals that have vestigial non-functional eyes. The lack of selection pressure means the eyes don't work but they are still there because building an eye is part of a deep developmental programme. The image below shows (in orange) the key drivers of differentiation for various cell types. It makes it obvious that the program that produces olfaction also produces vision (otic) so modifications to the developmental program will have wide-ranging effects.

The theories that you've listed are interesting and there is work going into developing new senses. Udo Wachter wore a belt that vibrated to north 24/7, "north" became part of his dreams, he always knew where home was, and he mourned the loss of the the sense. So proximity to the brain is not a critical factor for the senses.


Adenosine monophosphate activated protein kinase or AMPK is not a single protein, but is a trimeric enzyme composed of $\alpha$, $\beta$, and $\gamma$ subunits. There are 2 alpha genes, 2 beta genes, and 3 gamma genes, each coding for closely-related but not identical isoforms. In addition, like most protein kinases (and many other proteins), it is regulated by the phosphorylation and dephosphorylation of some of its residues, most notably Thr172, but at numerous other locations as well.
A "pan-AMPK" antibody will bind all of the AMPK isoforms independently of phosphorylation or other post-translational modification (PTM) state. There are also isoform-specific total AMPK antibodies that just bind the $\alpha2$ subunit, or all 3 $\gamma$ subunits, for example. Finally, there are phospho-specific antibodies to various residues that only bind when the protein is phosphorylated at that site.
Both the pan and isoform-specific antibodies are known as "total" antibodies, as they bind independently of PTMs and will show the total amounts of their target(s) on a Western blot, for example.

Source:
I used to be a Product Scientist for a company that makes antibodies, PTM-specific and total, to AMPK and many other targets.


The ampicillin plate is selecting for bacteria transformed with the plasmid, either the original or recombinant, whereas the tetracycline plate is selecting only for bacteria transformed with the original plasmid. Since you are only interested in the recombinant plasmid, you need to do some form of replica plating and compare the two plates to infer which colonies contain the recombinant plasmid (those which grow on ampicillin but not on tetracycline).


Can disease resistance from vaccination be inherited?

Not usually. I say usually because there's a fairly new (~15 years old) branch of genetics known as epigentics which has been shown to allow for inheritance of acquired traits. So it's possible that if the way in which a vaccine worked was altering your epigenome or genome, that it could be passed down to your children. However, that's just a hypothetical since none of the vaccines that I know of currently work in that way, but maybe something in the future will.

As of now, vaccines generally give you immunity by introducing some portion of the virus you're vaccinating against and "sensitizing" your immune system against it. This could be the viral envelope, it could be viral DNA/RNA, could be a viral protein, etc. However, in all of these cases, your immune cells are carrying out a fairly complex process in which they make antibodies with an almost random pattern constantly, and when one is produced that binds to this virus, it tells the B cell that produced that antibody to start making more. In this way, it "confirms" that this B cell is onto something.

Having said that, the B cells themselves are not passed on from parent to child, so a child would not be permanently immune to a virus even if the parent was. BUT, some antibodies can be passed from mother to child through the umbilical cord. These antibodies have a finite life and since they're not cells, they don't replicate and device. So the child would be immune to whatever a given antibody works against as long as that antibody remains in their system (usually on the order of weeks to months). Once the antibody is degraded, they no longer have any immunity, just as their parents did not have immunity before being vaccinated.


Why is this oxoglutarate dehydrogenase and not oxoglutarate decarboxylase?

I'm new to citric acid cycle and I'm judging this question based on my previous knowledge of biochemistry and organic chemistry.
I've looked into several protein databases and shockingly it seems oxoglutarate dehydrogenase is the correct name for it.( See :Uniprot , PDB 1 , PDB 2 )
Although the nomenclature of biological enzymes sometimes does not sound right to me , I believe this naming is appropriate for this molecule. First take a look at these definitions:
(Definitions from Oxford Languages / Google)

Dehydrogenase :  an enzyme
that catalyses the removal of hydrogen atoms from a particular
molecule, particularly in the electron transport chain reactions of
cell respiration in conjunction with the coenzymes NAD and FAD.

(Wikipedia)

Dehydrogenase (also called DH or DHase in the literature) is an enzyme
belonging to the group of oxidoreductases that oxidizes a substrate by
reducing an electron acceptor, usually NAD+/NADP+ or a flavin coenzyme
such as FAD or FMN.

(Wikipedia)

Decarboxylation is a chemical reaction that removes a carboxyl group
and releases carbon dioxide (CO2). Usually, decarboxylation refers to
a reaction of carboxylic acids, removing a carbon atom from a carbon
chain

Here is why the usage of "decarboxylase" in the name of the enzyme is incorrect :
Recall amylase (Amylase-Wiki) . That enzyme consumes amylose as substrate and produces maltose out of it. It sounds weird if one calls it "Demaltase" just because it gives out maltose. Instead, in this case , consumption of amylose plays a more important role in digestion.
According to above definitions , the "goal" here is simply the movement of H+ and the electron to FAD (to generate FADH2) and then to NAD+ (To generate NADH), Not the removal of CO2. That is just a by-product resulting from the mechanism. see :Reaction
Here's why the usage of "dehydrogenase" in the name of the enzyme  is correct :
Take a look at this  .
The whole process involves the movement of one proton from thiamindiphosphate and one from CoA-SH and also 2 electrons from two S-H bonds (I've traced the Hydrogens for you. Trace the electrons yourself ! :) )
Recall the concepts of carbonyl functional group from organic chemistry. One way to perform any reactions on carbonyls is to use an acidic catalysis which is most of the times H+ resulted from H2SO4 or HCl.Take a look at this. Also see Morrison-boyd organic chemistry or Vollhardt's This H+ Activates the carbonyl functional group , allowing it to participate in nucleophilic substitution more easily. The addition of H+ to Carbonyl oxygen is reversible and thus it is important to optimize this equilibrium. The indicated enzyme operates on this equilibruim to gain the maximum yeild. Plus it may induce TPP to lose a H+ . These two processes (the removal of H+ from TPP and the addition of H+ to oxogultarate ) can not be done with the help of the enzyme , hence the name Dehydrogenase for the enzyme.


It is a artificial fishing lure.specifically a soft worm T-tail, there are hundreds of variations.


How to measure the biomass of hydroponic plants in netpot/rockwool DWC system?

If you did enough replications in your experiment, you could harvest one or more plants and measure fresh weight, and then gently oven dry for about 48 hours at like 160 degrees F and then take a dry weight as a measure of biomass. I don't know a non-destructive way to do it. A lesser alternative would be to measure plant height and number of leaves, though this would be less accurate. There are devices that measure leaf area, and I know a simple, low-tech way to measure leaf area.


How to get a list of kinases that phosphorylated a particular protein?

I use PhosphoSitePlus too. I use it in combination with ELM as it finds linear motifs and generally gives a good generic candidate.

The literature if not. Checking all close homologues sometimes pays off.

Checking protein protein iteraction databases such as StringDB or IntAct may help too, but that gets very iffy —XL-MS (a smoking gun) is rare and does not pick up low concentration enzymes like kinases.

(A note: this question ought to have been asked in bioinformatics SO)


How compelling is the hypothesis that dinosaurs were killed by toxic plants?

Things in the paper that strike me as suspicious
Associating toxic plant defenses with the Cretaceous

Although there continues to be uncertainty about precisely when plants
first evolved toxic defenses, this period of angiosperm proliferation
would seem to be a strong candidate case. (pg 50)

Against this Gleadow and Moller (2014) discuss Cyanogenic glycosides (CNglcs), a class of organic compounds that can kill overgrazing herbivores from cyanide poisoning,

CNglcs are unusually widespread in the plant kingdom. They are found
in the oldest of terrestrial plants (the ferns) and in gymnosperms and
angiosperms.

Similarly, poisonous terpanoids are found in the Ginkgo; Proanthocyanidins, of which oak or wine tannins are a member, is found also in maritime pines; etc. There doesn't appear to be a strong link between angiosperms and chemical defenses against herbivory in plants.
Claiming that the angiosperm proliferations and extinction of dinosaurs are linked in time

The relative co-occurrence of angiosperm proliferation and the
disappearance of the dinosaurs has not gone completely unnoticed.(pg 50)

The diversification of angiosperms occurred starting about 112 MYa for the Monocots, and 100 MYa for the Eudicots, according to De Bodt, et all (2005). From Figure 1 of that linked paper, we can see that both branches of the Angiosperms were approaching their modern diversity by 90 MYa; a time still 25 million years before the extinction of the dinosaurs. 25 million years ago, our nearest ancestor hadn't diverged from the line that would lead to Old World Monkeys, and was probably arboreal. Evolution can do a lot in such a time. Calling these two events linked in time is suspicious, at best.
Using crocodilians as a test case for taste aversion

Since crocodilians are descendent from the same creatures that gave
rise to dinosaurs, this creates the opportunity to evaluate the
tenability of the proposition that dinosaurs went extinct due to an
inherent inability to learn to avoid eating toxic plants.

Reptilian cladistics are far from settled, but I would suggest that crocodilians diverged from dinosaurs by at least the early Triassic. They are almost certainly more divergent from all dinosaurs than birds. Here is what the authors have to say about birds.

However, in contrast to caimans, birds are in fact capable of forming
learned food aversions. (pg 51)

That seems to really undermine the argument here.


Complementarity Determining Regions (CDRs)

The paratope is the part of an antibody that binds the epitope on the antigen. The CDRs (heavy chain CDRs shown below) are part of the structure of the variable domain, and contain the hypervariable regions that bind to the epitope.

From Wikimedia

The actual paratope is within the hypervariable regions, which are within the CDRs - the paratope is not necessarily made up of the entire CDR region, and in fact may only be composed of amino acids contained within one or two of the three CDRs on each antibody chain (heavy and light).

If you're in the market for a good introductory immunology text, I highly recommend Janeway's Immunobiology. An earlier version is also available on the NCBI Bookshelf.


Why is DNA polymerase added at the end of PCR reaction?

True, the template is double stranded, but the primers could begin amplifying themselves, and any other stray DNA. You don't want any nonspecific amplification in the early stages that could compete with the target fragment. Also, even though Taq polymerase is a very hardy enzyme, it is standard practice to treat enzymes with special care, on ice so they don't degrade (although I have forgotten them on the bench overnight, and they survived that).


So if you're interested in the detailed anatomy of the glans penis, I recommend this as a nice article to go to after you've checked general references.  Opening two sentences are worth quoting here:

  The human glans penis is covered by stratified squamous epithelium and
  a dense layer of connective tissue equivalent to the dermis of typical
  skin. Rete ridges of the epidermis are irregular and vary in height
  depending on location, age, and presence or absence of a foreskin. The
  papillary layer of the dermis blends into and is continuous with the
  deep connective tissue forming the tunica albuginea of the corpus
  spongiosum of the glans penis.

And as pointed out in The Last Word's answer, foreskin covers the penis if you look at humans in an evolutionary scale of time.  The exception being an erection, which should lead to foreskin retraction (at least at some level).

So the question then becomes if the squamous epithelium and connective tissue are more prone to infection than the dermis. First, it's worth pointing out that the epidermis is not equally protective across the body. Think about the skin on your face vs. the bottom of your foot, or vs. a baby's.

I think comparing the glans penis directly to the surrounding tissue -- the prepuce (foreskin), fossa navicularis, and urethra -- makes the most sense. To make a plumbing analogy, is it the pipe (urethra), the fitting (glans penis), hole (fossa navicularis), or insulation (prepuce) that is most prone to infection?

Well, first we need to look at our pathogen, "what's doing the infecting?" For HIV, probably the urethra, but if you're interested in bacterial infection, the best things to look into are balanitis and balanoposthitis.  That would be the inflammation of the glans or glans & prepuce. Here is a good review on infectious causes.

Unfortunately, there is going to a strong sampling bias due to circumcision rates.  Also most studies are not going to be asking the the specific question we are trying to answer here. And it would be hard to prove that infection occurred during the erection, not immediately before or after.

I have found little evidence of bacterial infection of the prepuce but not the glans penis.  I do know of cases of the reverse however, which may indicate that the glans has a greater infection rate.

However, I think it's worth pointing out the difference is not likely to be drastic, and that the surface of glans has many similarities to skin.  For example, it has an epidermis and dermis. It stretches quite well, and I think dryness will be an issue far before porosity.


Why not replace the human genome with it's decoy genome version?

To clarify, when you say "decoy genome" you hopefully mean the decoy genome and the reference genome together; the decoy genome itself is not a complete reference, but a collection of contigs assembled from reads that didn't map to the current reference genome, but are known to be human sequence.

The decoy genome certainly seems to be a useful supplementary data set for speeding up read mapping to the human genome but it cannot be better than the reference because it is not comparable to the reference.


Why can I raise my left eyebrow independently from the other but not the right?

The muscle responsible for being able to raise both eyebrows is one and the same (m. occipitofrontalis). You can not raise one eyebrow because the whole muscle is connected to both eyes. It is possible that one side is not connected or less connected but that's usually not the case and such a person would not be able to raise both eyebrows at will.

What happens in almost all people is that they are not raising one eyebrow, but instead keeping one eyebrow down and raising both at the same time thus giving the impression of only raising one. There are various muscles that are able to lower the eyebrows.

So if one person is "not able" to raise one eyebrow, it actually means that they are not able to keep the other side down.


The issue is based on your perception of what an individual ought to be. The concept of individual is actually often hard to apply in biology and therefore is the concept of ageing. In other words, the wish to categorize is a rather human tendency but it may fail to make objective representation of biodiversity. The book The Major Transitions in Evolution Revisited makes a very good job to explain the difficulties to deal with the concept of individual in biology.

You seem to be happy to consider an offspring be a different individual if you can still perceive the parent individual. In bacteria, both resulting cells could be considered as offspring and therefore new individuals. Note however, that asymmetrical division bring some more blur into these categorizations.

Note also that single cell bacteria do age. See the wikipedia article on bacterial ageing. You might also want to have a look at the wikipedia article on biological immortality as well as the posts Why is the Hydra Biologically Immortal? and Do crocodiles age?.


I really need some help with a plant identification

That's an Apocynaceae, from the species Strophanthus speciosus. Its common name here in Australia is corkscrew flower or poison rope.

It's not native to Australia, though: it's native to Africa.

You can easily identify it by the flower:

Flowers of Strophanthus speciosus in the Royal Botanic Gardens Victoria, Melbourne (source of the image)


Why are the human knees and elbows bent in an opposite direction

I am no expert on comparative anatomy, but I will give this a shot. Please edit if you know more about this subject!

The configuration of opposing elbow and knee joints is a feature we humans share with large group of mammals. For example, below is an image of a shrew skeleton.

Opposing joints are course a major feature of mammalian anatomy, and there are many studies on its functions and advantages. Among other things, this configuration allows for characteristic gaits of mammals such as the gallop of a horse, and it allows mammals to rest with legs protected under their body. See this page for some basic information.

Neil Shubin's book Your Inner Fish on human evolution also discusses the opposing joints arrangement, noting that this is a "key feature that gives us the capacity to walk, one we share with other mammals". A preview of the book is here.

A quick literature search turns up many technical articles on this subject, such as this review series. I'm afraid the details are beyond me (again, experts please edit), but I think it's fair to say that there is plenty of evidence for advantages of this joint arrangement in mammals.


What happens to an ant colony when the queen dies?

Not really my field, but I can point to this review which discusses a couple of different ways in which ants organize their communities:
Heinze. 2008. The demise of the standard ant (Hymenoptera: Formicidae)

I know that in some species there can be several queens per colony (so more robust to queen deaths). In many species, workers can start laying eggs if the queen dies, but these will develop as males (since they are unfertilized). However, in some species (e.g. Platythyrea punctata) the workers can reproduce by parthenogenesis which can stabilize the colony to some extent after the queen dies.


Can human organs be transplanted indefinitely?

First of all, it will be practically impossible to make an estimation of how long a transplanted organ will live and how many times it could be transplanted. However, it is relatively safe to say that it will not live forever.

To be able to receive an organ transplantation, the HLA MHC-complexes of donor and receiver need to be matched very carefully, to limit the host-vs-graft reaction. This limits the number of possible donor-receiver patient pars drastically. So to be able to do a "row transplantation" (one receiver to the next and so on), they need to have matching MHC-complexes.

Otherwise the immune system of the receiver turns against the transplanted organ and will eventually destroy it. To avoid this reaction, transplantation patients also receive drugs, which severely suppress their immune system, thus making other infections potentially dangerous. This reaction will still take place, since you cannot shut down the immune system of the receiver completely (for obvious reasons), though it happens at a much slower rate. Transplanted organs will only live for a certain time (see estimates from a number of transplantations below) and it is possible that people need to receive transplants twice in their life.

For this reason, no doctor will put their patient at risk by giving them an organ which might have a reduced lifetime. The risk of the operation itself is also substantial.  Additionally, the original receiver needs to be dead to do this, as he would otherise need another organ in exchange.

What we can do is to take the average number of a lot of transplantations together and calculate some average life-years for a transplant. According to table 2 in this paper ("The Life-Years Saved by a Deceased Organ Donor") the "average benefit by type of transplant (life-years)" is:

Kidney: 7.2 years
Liver: 16.9 years
Lung: 2.1 years
Heart: 14.5 years
Kidney-Pancreas: 12.9 years

These numbers are not definite, since the life style of the donor and the receiver as well as infections of the transplated patient (who has a severely suppressed immune system – this is critical) also play an important role in determining the lifetime of the organ.


Not really no.  Most blood transfusions we think about are red blood cells or platelets, which don't have the immune function you're asking for.  That's a good thing.  Usually, if there are white blood cells in the transfused blood, the host's immune system will recognize them as foreign and destroy them.  Remember, your cells all look like foreign invaders to my cells; blood transfusions of red blood cells are carefully matched to limit negative reactions.  There is also a process called transfusion-associated graft versus host disease in which the donor white blood cells will attack the host cells; this mainly occurs in immune-compromised individuals, but GvHD is definitely something to avoid.  Blood transfusions are usually filtered and irradiated to remove, among other things, white blood cells.

That being said, people are beginning to use white blood cells as treatment.  A new therapy being studied heavily for all sorts of diseases, from cancer to HIV, is to take the hosts own white blood cells and grow them up in the lab to select for the strongest and most effective cells.  The researchers then wipe out the individual's immune system and give them a dose of their own, super-powered white blood cells, hoping that works.

Sometimes it kind of does.  They've also been trying a new system, similar to what you propose, using bone marrow.  They had a huge success with an HIV-positive individual now referred to as "the Berlin patient."  They gave him a marrow transfusion which would produce HIV-immune white blood cells and replaced his immune system.  He was and is effectively cured of HIV/AIDS.


Light signals in the courtship and mating

Many Ostracods (esp. the Cyprididae) use bioluminescence to attract mates. The Bermuda fireworm (a polychete worm) also uses bioluminescence to attract mates.

If you have not yet, you should definitely have a look at wikipedia > Bioluminescence


why didn't natives of south america evolve darker skin?

Could not fit in a comment....

Northern Africans and Indonesians have pretty much the same skin color (to my first impression). Sub-Saharan African (that you don't talk about) are darker. And Northern Africa in not an equatorial region (not more than Los Angeles) as it is right under the tropic of cancer.

Also I am a little confused about who you call "we" and who call "they". I think that by "we", you mean any non-sub-Saharan African human but I am not sure. If this is the case just naming sounds more appropriate that to make a big category that you call "we" to exclude some ethnic groups :)

I think that when you are talking about Brazilians (and other people in South America living close to the equator such as Ecuadorians), you are mostly talking about people from Spanish and Portuguese descent. So let's talk about the great migrations

The Indonesians arrived in their lands about 70,000 years ago. The indigenous South-Americans arrived in South America about 10,000 years ago. The Spanish and Portuguese arrived in South America about 500 years ago.

I think you might want to read a bit more about the geography of those big migrations.


How can antibodies in rapid antibody tests be kept at room temperature without denaturing?

Antibodies have no problem with room temperature. Naturally, antibodies expect to survive for many days or weeks at body temperature, which is much higher than room temperature (at least, mine is).

-20°C is recommended for very long-term storage (many months or years) of antibodies, but they are typically very stable proteins and don't denature very readily at all. Storing them at room temperature can be done for a long time -- certainly weeks, in my experience, with the only real concern being the possibility of bacterial or fungal growth if the antibodies aren't sterile.


No, the L axis in the HSL color space does not really correspond to lightness as perceived by the human eye, except in the very crudest sense that, for given values of the H and S components, increasing L produces an increase in the perceived lightness.

The L component of the standard HSL color space is simply calculated as the average of the lowest and the highest RGB component of the color (in whichever RGB color space in being used): $$L = \frac{\min(R, G, B) + \max(R,G,B)}2$$

This definition alone should make it obvious that the L value cannot correspond to perceived lightness, since it completely ignores the middle one of the three RGB channels.  Thus, the color (R=0, G=0, B=1), i.e. pure $\color{#0000ff}{\rm blue}$, has exactly the same L value (0.5) as the color (R=0, G=1, B=1), i.e. $\color{#00ffff}{\rm cyan}$, yet it's obvious at a glance that the latter color is visually much brighter.

Indeed, the HSL color space doesn't even try to match the perceptual lightness of the colors; rather, the definition of the L channel is chosen because it has the convenient feature that it maps black to L=0, white to L=1, and all the six maximally saturated pure RGB colors (red, yellow, green, cyan, blue and magenta), despite their wide perceptual lightness differences, to L=0.5.

A much better approximation to the perceived lightness of a color is the luma Y', which is defined as a weighted average of the RGB channels.  The precise weights depend on the definition and the RGB color space used, but a common choice (from ITU-R Rec. 709) is: $$Y' = 0.2126\, R + 0.7152\, G + 0.0722\, B$$

The weighs are chosen to account for the different perceived lightness of the different RGB primary colors.  A striking feature is the that the green component alone accounts for over 70% of the luma, nearly ten times as much as the blue component.  Yet a visual comparison of $\color{#0000ff}{\rm 100\%\ blue}$ with $\color{#00ff00}{\rm 100\%\ green}$ does clearly confirm that this choice of weights is justified: the pure green appears much brighter than the blue, and almost as bright as the cyan (which is their sum) above.

However, the definition of the luma still ignores the non-linearity of both the standard RGB color spaces (such as sRGB) and the human eye.  While these two effects partly cancel out each other, allowing luma to be used as a reasonable approximation of perceptual lightness, for truly accurate results they need to be accounted for.  This involves several steps:

Convert the RGB color into a linear color space.  For sRGB, the following formula may be used: $R_L = f(R), G_L = f(G), B_L = f(B)$, where: $$f(C) = \begin{cases}C / 12.92 & \text{if } 0 \le C \le 0.04045 \\ ((C + 0.055) / 1.055)^{2.4} & \text{if }  0.04045 < C \le 1 \end{cases}$$ (Here, $R$, $G$ and $B$ are the sRGB component values, and $R_L$, $G_L$ and $B_L$ the linear ones, both scaled to the range from 0.0 to 1.0.)  Alternatively, a very close approximation to the formula above is given by simple gamma-expansion with $\gamma = 2.2$: $f(C) = C^{2.2}$.
Calculate the relative luminance as a weighted average of the linear RGB component values: $$Y = 0.2126\, R_L + 0.7152\, G_L + 0.0722\, B_L$$ (The weights are exactly the same as for the luma formula above, because that's where they come from; the luma calculation just blindly applies them to the gamma-compressed RGB values.)
Convert the relative luminance value into an approximation of the percieved lightness, using something like the CIELAB formula: $\ell^* = 1.16\, g(Y) - 0.16$, where: $$g(Y) = \begin{cases} \tfrac13 \left(\tfrac{29}{6}\right)^2 Y + \tfrac{4}{29} & \text{if } 0 \le Y \le \left(\tfrac{6}{29}\right)^3\\ Y^{1/3} & \text{otherwise} \end{cases}$$ (Note: In the CIELAB standard, the $L^*$ value ranges from 0 to 100, but for the sake of consistency, in the formula above I chose to define $\ell^* = L^* / 100$, so that its range is also from 0 to 1.)


How do I determine this logistic growth model formula?

The growth of the yeast can be studied with a Logistic model (i.e. differential equation) as follows:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
This is an ordinary differential equation that tells you how the population of yeast is changing with time (in fact is telling you how the concentration of Yeast $X$ changes with time).
The two parameters in the equation are the specific growth rate $\mu$ and $X_{max}$ the carrying capacity following the Verlhust model.
We could also write the equation following your notation:
$$
\frac{dN}{dt}=r N \left(1 - \frac{N}{K} \right)
$$
where $r (\mu)$ is the specific growth rate, $K (X_{max})$ is the carrying capacity, and $N$ is the number of elements in the population.
Note that this is a dynamic model that you need to solve (i.e. integrate the differential equation) to be able to compare with your experimental data. This model tells you how any population of this time behaves not only your Yeast in the mentioned experiment.
The solution of this model is the following Logistic equation:
$$
N(t) = \frac{K}{1+\frac{K-N_0}{N_0}e^{-rt}}
$$
Where $N_0$ is the initial number of Yeast cells.
If you fit this equation (i.e. with least-squares) you get the following values for your experiment (with their 95% confidence intervals):
K =       603.6  (594.3, 612.9)
N0 =      2.108  (1.179, 3.036)
r =      0.6729  (0.6196, 0.7262)
And the following curve.

$r$ is the growth rate (in $hr^{-1}$) that is related with the doubling time by the following formula:
$$
t_d = \frac{ln 2}{r} = 1.0301 hr
$$
Check also this answer about growth models


What is this red orange insect with black dots found in Japan?

I was able to find it in an insect lexicon. It is all in Japanese, but the description fits the image. The insect is in fact a カミキリ、a ホシべ二カミキリto be exact. And the binomial name is Eupromus ruber

Here is also some more information https://www.insects.jp/kon-kamihosibeni.htm
And a Wiki page in english https://en.m.wikipedia.org/wiki/Eupromus_ruber


Would my hands sweat this much if I wasn't wearing gloves?

Hand sweating has been fairly well-studied, both because sweating from the hands is one of the main mechanisms of heat dissipation at higher temperatures and because there is a significant effect on palmar sweating by the autonomic nervous system (the main cause of hyperhydrosis of the palms).

Disregarding autonomic effects (stress response), the single most important determinant of hand and foot blood flow is the thermal status of the body core. Heat dissipation is more marked in the hands than feet, and remains so as temperature increases.

Studies have been done of palmar sweating in extremes of temperatures, palmar sweating changes with aging (decreases), palmar sweating in disease, etc. But what has not been studied is the effect of localized heat on sweating of the palms, which would be of interest to you if sweating was a result of the insulating capacity of the gloves.

What is known about palmar sweating is that it is an ongoing and important process in both genders, at all temperatures, and at all ages. The most reasonable assumption then, given the limits of the literature, is that your hands sweat continuously and steadily at a given temperature, and it is highly likely that you are noticing it when wearing gloves only because the vapor barrier caused by the gloves prohibits evaporation.

The roles of hands and feet in temperature regulation in hot and cold environments
OBSERVATIONS ON THE ACTIVITY OF SWEAT GLANDS WITH SPECIAL REFERENCE TO THE INFLUENCE OF AGEING
Why do I get sweaty palms?


Where do the four ADPs come from in the second stage of glycolysis?

I think I understand your question, and stumbled upon it because i was wondering the same thing while studying for my Microbio test. I know its a year late, but someday someone else might need this info...so here it is.

To put it simply: there is a second pair of phosphates added to the two 3-carbon molecules cleaved from the preparatory stage before the 4 ATP are finally formed. These get added by an enzyme while reducing the NAD+ molecules.

In depth: The first pair of phosphates the cell uses to synthesize ATP come from the initial 2 ATP invested during the prep stage, but an additional 2 phosphates are added when the cell oxidizes the two Glyceraldehyde, 3 Phosphate (G3P) molecules to form NADH. In this step, two electrons are taken away from the G3Ps and an available inorganic phosphate is added to the "1" position, forming "1,3 Biphosphoglyceric Acid " (1,3BPG). Afterwards, the molecules each have 2 phosphates for a total of 4 phosphates available to get oxidized and used to synthesize 4 ATPs.

This step, (the addition of an inorganic phosphate as an intermediary step) is SO overlooked by regular textbooks that its not even funny. mine doesnt even list the enzyme; I had to look it up.
but yeah, that's the source of the additional phosphates available for forming the 4 ATP molecules of glycolysis, and possibly why you didnt see it from the diagram in your textbook (you're not alone!).

Hope that helps!

Sources, as of 4/18/17:

https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/glycolysis/a/glycolysis
https://en.wikipedia.org/wiki/1,3-Bisphosphoglyceric_acid


Study case of the inheritance system of Oenothera

I would recommend looking at this paper, and in particular the section "A SHORT INTRODUCTION TO OENOTHERA GENETICS":

The genetics of Oenothera is a genetics of entire haploid genomes (Renner complexes), which inherit as single units and are entitled with names such as hjohansen, Galbicans, or Gflavens (for terminology, see materials and methods). All loci of a Renner complex are in linkage disequilibrium.

Figure 1 from that paper shows what that looks like in meiosis, in terms of its impact on chromosome pairing- basically chromosome pairing forms rings of chromosomes linked by translocations.

Figure 1.
Additionally, it appears that plastid inheritance is biparental to some extent. These also contain pollen-lethal factors related to autosomes, such that cytonuclear incompatibilities kill pollen recombinants between a Renner complex and plastids (eggs are unaffected, Figure 2, 3):

Consequently, the F1 generation is identical to the parental generation without segregation of traits, since chromosomes separate as a set without intermixing.

The set of plastids ("plastome") will then break down in the F2 such that assortment can happen.

Selfing of appropriate flowers ensures that only plastome I is inherited to the next generation. However, in F2 the nuclear genome splits into the progenies CC-I and AC-I...

Since the ring of 14 chromosomes should inhibit free segregation of individual chromosomes and practically homologous recombination between haploid genomes in the hybrid AC, the coding potential of the A and C genomes is not mixed and a seemingly unchanged, homozygous CC genotype, now associated with plastome I, occurs in F2.

Figure 2.

Figure 3.
So it's rather complex. Hopefully that sheds some light on it, but it's understandable if it's still confusing!


intravenous (IV) in the tail vein of an anaesthetized mouse

Cleaning the tail with ethanol is of some help and also, as you said, warming the tail. We sometimes put one of those flexible lamps (such as this) to heat up only the tail.

When anesthesized (ketamine/xylazine or isoflurane) we keep our mice on a heated pad anyways.

Cannulation in the tail does not sound like a good idea to me, especially if you are going to have the animal wake up afterwards. If you're going to cannulate then go for the jugular, but be aware that doing it on a mouse requires quite a bit of experience and it's definitely way longer than a tail injection.

It really depends on your experiment


Why are large amounts of DNA required for analysis?

Firstly, A DNA sample obtained from a cell or whatever is never going to contain just the DNA sequence you want but will instead contain the entire genomic DNA, plasmids, RNA sequences and whatnot. By using PCR you can selectively multiply the amount of desired DNA sequence while the undesired sequences do not get copied. Keep the PCR going long enough and the amount of undesirable DNA versus the desired DNA sequence is going to become negligible. At that point you can do whatever experiment you want with your DNA sample and be reasonably sure that whatever result you get is caused entirely by your DNA sequence of interest.

Secondly, even if you could isolate a single DNA molecule what would you do with it? You couldn't determine its length by gel electrophoresis as a single DNA molecule wouldn't make a visible band and building it into a plasmid will most likely fail as you only get 1 chance. You probably wouldn't even be able to tell you had a DNA molecule as machines in your everyday lab aren't sensitive enough to detect a single DNA molecule.

Thirdly, having a large quantity of DNA allows you to perform different experiments from the same sample. Most DNA analysis methods I know of are destructive in that the DNA used cannot be reused for another experiment, so a large enough quantity of DNA to perform all planned experiments without having to obtain a new sample (and introduce all kinds of potential problems) is useful.

So, in summary, PCR allows us to filter the desired DNA sequence from a sample, perform meaningful analysis on this sequence and lets us use one sample for multiple experiments. There might be even more advantages to PCR that I have missed but these the ones that sprung to mind.


The dominance variance on a single locus

It looks like I could solve the question. My understanding is as follows.

Let $(X_1,Y_1)$, $(X_2,Y_2)$ (corresponds to $i,j$ and $k,l$ in the question) be the genotypes of two individuals
 at some location. We assume that neither individual
 is in-bred. In this case define,
 \begin{align*}
  \Delta_7&= \text{Pr}(\text{Both alleles $\{X_1,Y_1\}$ and $\{X_2, Y_2\}$ are IBD}),\\
  \Delta_8&= \text{Pr}(\text{Exactly one allele pair of the four pairs is  IBD}),\\
  \Delta_9&= \text{Pr}(\text{ No IBD between the two individuals}).
 \end{align*}
 $\Delta_7$, $\Delta_8$ and $\Delta_9$ are calculated from the pedigrees.
 For example, for non-twin siblings, $\Delta_7 = \frac{1}{4}$, $\Delta_8=\frac{1}{2}$,
 $\Delta_9 =\frac{1}{4}$.

We note that the IBD coefficient (also called kinship coefficient) $\Theta$ is
 \begin{align*}
  \Theta = \frac{1}{2} \Delta_7 + \frac{1}{4} \Delta_8.
 \end{align*}
 Also the fraternity coefficient, $\Delta =\Delta_7$.
Thus we have that the covariance between the genotypic
 value of two individuals is given by
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \Delta_7 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] + \\
  &\Delta_8 \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] + \Delta_9  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}].
 \end{align*}

Further note that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{both IBD}] &= \mathbb{E}[G^2(X_1,Y_1)],\\
  &= \sigma_A^2 +\sigma_D^2.
 \end{align*}

\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{no IBD}] &= \mathbb{E}[G(X_1,Y_1)] \mathbb{E}[G(X_2,Y_2)],\\
  &=0.
 \end{align*}

\begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)| \text{one IBD}] &= \mathbb{E}[(\alpha(X)+\alpha(Y_1)+\delta(X,Y_1))(\alpha(X)+\alpha(Y_2)+\delta(X,Y_2))],\\
  &=\mathbb{E}[\alpha^2(X)] + 2 \mathbb{E}(\alpha(X) \delta(X,Y_1)) + \mathbb{E} [\delta(X,Y_1)\delta(X,Y_2)],\\
  &= \frac{1}{2} \sigma_A^2 + 2 \mathbb{E} [ \alpha(X) \mathbb{E}[\delta(X,Y_1) | X] ] +  \mathbb{E} [\mathbb{E}[\delta(X,Y_1)|X]\mathbb{E}[\delta(X,Y_2)|X]],\\
  &= \frac{1}{2} \sigma_A^2.
 \end{align*}

Thus we have that,
 \begin{align*}
  \mathbb{E}[G(X_1,Y_1)G(X_2,Y_2)] =& \left(\frac{1}{2}\Delta_7 + \frac{1}{4}\Delta_8\right) 2 \sigma_A^2 + \Delta_7 \sigma_D^2,\\
  &= 2\Theta \sigma_A^2 + \Delta \sigma_D^2,
 \end{align*}
 which is as claimed.


Don't understand how multiple replication bubbles work

You mistake replication direction with polymerase synthesis direction. Indeed, the polymerase synthesizes new strands 5' -> 3' but if the replication of each strand was continuous, there would be  no such structure as a replication bubble whatsoever. Take a good look at the drawings:

The thing is the direction of replication is consistent with the direction of leading strand synthesis, so the bubbles will "spread" outwards. Lagging strand is synthesized in the form of fragments 5' -> 3'. If you look closely fragments that are closest to the center of the replication bubble are synthesized first, then polymerase detaches and works on the next fragment which is actually closer to the 3' end of the lagging strand.
Here's an article on Wikipedia about those fragments: https://en.wikipedia.org/wiki/Okazaki_fragments

Hope this makes things clear.

Cheers and happy learning,

Krzysztof


From the interleukin wikipedia page for IL6 :

  number of other cytokines may be grouped with IL6 on the basis of sequence    similarity.[21][22][23] These include granulocyte colony-stimulating factor (GCSF) and myelomonocytic growth factor (MGF)

from the Leukemia inhibitory factor wikipedia page:

  LIF derives its name from its ability to induce the terminal
  differentiation of myeloid leukemic cells, thus preventing their
  continued growth.

From this we can suggest that LIF is grouped with the IL6 because of its action on myeloid leukemic cells and specifically on their growth (MGF).


What determines whether a reaction using ATP produces ADP or AMP?

Summary
It is the nature of the biochemical reaction that determines whether a reaction of ATP involves hydrolysis of the β- or γ- phosphoanhydride bond. If a part of the ATP molecule is incorporated into one of the products, the choice of bond to be cleaved emerges from the chemistry of the reaction. If the hydrolysis (with a negative free energy change, ΔG) is being coupled to a reaction with a positive ΔG, hydrolysis of single (γ-) phosphoanhydride bond usually suffices, with the production of ADP and Pi. If the free-energy of hydrolysis of the phosphoanhydride bond is being ‘transferred’ to another molecule in order to ‘activate’ it for a specialized group-transfer role (often in the synthesis of macromolecules) two bonds are often broken: the first (β-) transfers the free energy with the production of pyrophosphate, whereas the second (now in the pyrophosphate) is hydrolysed non-productively (free energy lost as heat) to ensure that the overall reaction is irreversible.
Energy considerations in reactions involving ATP
I have discussed some of this at greater length in an answer to another question, however it is important to clarify this at the outset. In considering biological reactions, it is usual to adopt a thermodynamic approach in which the thermodynamical (Gibbs) Free Energy change (ΔG) of the reaction is considered. This is because, to quote from Berg et al.:

A reaction can occur spontaneously only if ΔG is negative.
A system is at equilibrium and no net change can take place if ΔG is zero.
A reaction cannot occur spontaneously if ΔG is positive. An input of
free energy is required to drive such a reaction.

The literature provides values of the standard free energy changes, ΔGo, for reactions, i.e. the values obtained under conditions in which the concentration of all reactants and products are set at the same concentration. The actual free energy change, ΔG, depends on the concentration of reactants and products (mass action effects).
The hydrolysis of the β- and γ- phosphoanhydride bonds of ATP both have a high negative values of ΔGo of ca. –45 and –30 kJ per mol, respectively†.
Use of ATP to drive unfavourable reactions
In many cases the hydrolysis of ATP is coupled to an energetically unfavourable reaction (one with a +ve ΔGo) so that the coupled reaction has overall negative free energy change and hence the energetically favourable reaction can take place:
A → B                    ΔG =  20 kJ/mol (unfavourable)
ATP → ADP + Pi           ΔG = –30 kJ/mol (favourable)
A + ATP → B + ADP + Pi   ΔG = –10 kJ/mol (favourable)

In this hypothetical example, 20 kJ/mol of the free energy of hydrolysis of ATP is used to convert A to B, the other 10 kJ/mol is lost as heat, but makes the reaction essentially irreversible. The energy of hydrolysis of only a single phosphoanhydride bond is sufficient for this, and is achieved by the hydrolysis of the γ bond with the production of ADP. (Hydrolysis of the β bond would ‘loose’ the second bond in pyrophosphate, where its hydrolysis cannot be used productively.) An example is the conversion of pyruvate to oxaloacetate in gluconeogenesis, in which energy is required to form a carbon–carbon bond:
CH3COCOO– + HCO3– + ATP → COO–CH2COCOO– + ADP + Pi
Incorporation of ATP into products
In some cases there is not only hydrolysis of a phosphoanhydride bond, but a chemical component of ATP is incorporated into one of the products. In this case the actual chemical reaction determines which bond is hydrolysed.
In the first type of reaction a phosphate group is incorporated into the product, in which case this will obviously be the γ-phosphate and ADP will be generated. A simple example of this is the hexokinase reaction:
Glucose + ATP  → Glucose 6-P + ADP
The reaction is essentially irreversible as the energy of the hexose phosphate bond is much less than that of the phosphoanhydride bond.
In the second type of reaction the AMP component of ATP (or similar molecules) is incorporated into one of the products, so that the other product must be pyrophosphate. The obvious example is the RNA polymerase reaction, which for our purposes can be represented as:
------ribose-3′OH + ATP → ------ribose--3′O-PO2-O-5′-Adenosine + PPi
ATP and ‘activation’ reactions: rationale for pyrophosphate
In certain reactions of ATP the energy of a  phosphoanhydride bond is being used to created a bond of similar free energy of hydrolysis, which can itself be used subsequently to activate other reactions. In this case the reaction may involve little of no free energy change, so that it would appear to be easily reversible. In many such cases the β phosphoanhydride bond is cleaved, generating pyrophosphate. The rationale for this is that the pyrophosphate is then converted to phosphate in a reaction catalysed by pyrophosphatases, which has a high negative DG and is hence essentially irreversible because the free energy of hydrolysis of the phosphoanhydride bond in pyrophosphate is lost as heat.
A + ATP → B + AMP + PPi     ΔG = 0 kJ/mol (reversible)
PPi → 2 Pi                  ΔG = –33 kJ/mol (irreversible)

The examples often given to explain this are the nucleic acid polymerase reactions, but, although this applies also to them, the nature of their reaction necessitates the generation of pyrophosphate. To some extent this is the case with most other activation reactions, but it may be clearer to consider one in which the component of ATP is incorporated as a temporary intermediate, rather than as a component of the end product. Such a reaction is amino acid activation for protein synthesis:
amino acid + ATP → aminoacyl-AMP + PPi
aminoacyl-AMP + tRNA → aminoacyl-tRNA + AMP
The ‘activation’ is the formation of bond with a high free energy of hydrolysis in the aminoacyl-AMP from the β phosphoanhydride bond. This is then used to drive the reaction forming a bond between the amino acid and the tRNA. The generation of pyrophosphate ensures the effective irreversibility of this key step in protein biosynthesis.
†Possible role of differences of free energy of hydrolysis
The fact that the standard free energy of hydrolysis of the β phosphoanhydride bond is greater than that of the γ phosphoanhydride bond may also be relevant in some cases, as @user1136 has argued in his answer to this question.


What distinguishes "coding" from "noncoding" DNA?

You are correct in thinking that any sequence of bases corresponds, via the genetic code, to a sequence of amino acids. However not all stretches of DNA are actually transcribed into mRNA for translation into proteins. For this to happen the stretch of DNA requires (DNA-encoded) elements to promote and regulate the transcription and translation processes, and this, very broadly, is what defines a gene: a segment of DNA which has the required components to direct the synthesis of a protein (or in some cases an RNA that will not be translated into a protein). The segments of DNA that correspond to mRNA for proteins and to other RNA molecules are referred to as coding sequences.

Now, I've omitted lots of details here: some genes encode RNA molecules, such as ribosomal RNAs, which are not translated into proteins; eukaryotic genes include stretches of sequence (called introns) that are spliced out of the transcript before the mRNA>protein step. The original definition (if there ever was a definition) of "junk" DNA included these introns, as well as regions of DNA lying outside the coding sequences. We now know that there is useful information stored in much of this DNA, even though it doesn't code for anything directly via the genetic code.


This neotropical leafhopper belongs to the subfamily Coelidiinae. According to this publication though, there are 25 genera & over 75 different species, and so, I'm having a difficult time narrowing it down from there (my current best guess would be genus Jikradia).

If I'm not mistaken, this insect is displaying an alarming signal by spreading its wings like that.. it must have felt threatened by you when you were taking the picture (assuming that it wasn't already like that when you approached it).

For more information on this subfamily, I strongly suggest that you explore the text of the previously linked publication, as it contains great information regarding the various tribes of subfamily Coelidiinae, including distribution, origin, host plants, a bit of history, and so forth.


Yes. All proteins actually begin to get synthesized on cytoplasmic ribosomes but if they are going to be used for extracellular purposes, they are tagged and whole ribosome is taken to ER where protein synthesis is completed. The proteins are exocytosed with help of Golgi body, the post office tagging and packaging organelle (the Golgi body packages these proteins into the vesicles that fuse with the plasma membrane).

Examples of this process are: the pancreas secreting insulin for blood sugar control, digestive enzymes for digestion, the immune system telling the body there's a bacterium we must fight it and calls more immune cells (cytokines). Most proteins of course stay in the cell, and are necessary to make the cell or carry out metabolism or DNA transcription.


Does the DNA stick to surfaces we touch?

Yes, we leave DNA on everything we come in contact with. Even simply standing, we shed skin cells and hair (although only the follicle has DNA) etc. DNA may also be transferred from clothes to clothes.

You might be interested to read this article :) http://www.forensicsciencesimplified.org/dna/how.html


Have there been any positive public health effects due to UV lights?

There have been some studies regarding the use of intensive UV light installations in surgical wards or other settings as a anti-microbial tool. Generally speaking, these are part of a general interest in non-cleaning based anti-microbials in hospitals, such as UV light, O3-based machines, and copper/silver coated surfaces.

The answer to your question will depend on what you consider "lasting" and "significant". They're a relatively new technology, and haven't had a huge penetration into the market yet, so the only evidence you're likely to find is hospital-sized non-randomized trials.

So basically, the answer to your question, as I read it, is "No, but..."

There hasn't been an opportunity for these technologies to show any sort of lasting, significant reduction in hospital acquired infections. But there is some promise that these types of technologies, and those like them, may help reduce the burden of infections when they're used appropriately. The current state of research is figuring out just how workable they are, how to best use them, and what they can and cannot be expected to do. That kind of evaluation is actually what I'm doing as part of my dissertation work, though my focus is on the general concept, rather than a specific device.


Why is maintaining a circadian rhythm important?

In theory, having a circadian rhythm should help anticipating daily environmental changes (light, temperature etc.) so that the metabolic performance is maximized.

In practice, mice chronically exposed to environmental light-dark cycles with a period length dramatically shorter or longer than that of their circadian clock are prone to become obese. Moreover, animals kept under short cycles die earlier than mice kept under normal or extended cycles. So, chronic circadian disturbance by a shortened light-dark cycle increases mortality (at least in mice). In humans, shift workers are likely the population that is more susceptible to circadian cycle derangements.

Ref: Park et al., Neurobiol Aging. 2011


Questions on mid-2019 Covid-19 Spread in Spain

To judge about this assay, it is important to see how they worked. They used different sets of primers to analyze for SARS-CoV-2. Namely targets IP2 und IP4 from Institute Pasteur in Paris (see reference 1) and to validate results also primers targeting the "E" sequence (reference 2) and two against the nucleoproteins N1 and N2 (reference 3).
Then they tested frozen samples taken between January 2018 and December 19. Of those, only the sample from March 2019 come back positive for 2 out of 5 primer pairs, none of the samples before and after tested positive, despite mentioning that samples where already positive as early as January 2020 again.
If you look at the published amplification curve you see a very late Ct value for the sample (I would eyeball it somewhere between 39 and 40), which is basically in the area of non-specific amplification. Running the PCR another 10 cycles until 50 is highly unusual in my experience.

Conclusion: I see this result as a PCR artefact and I doubt, this will be published (at least I hope it will not). The reasons for it are:

only two of five sets of primers is positive. Since these are highly specific, I would expect all five of them positive.
the Ct value is very high, around the usual endpoint of qPCR. If you let PCR run long enough, it will eventually amplify something. The also show no melting curve to prove the have a good PCR product.
it is highly unlikely that the virus appears in March 2018 in the wastewater of Barcelona and then disappears again without leaving any trace. This is clearly not the experience we have been making throughout 2020.

References:

Protocol:Real-time RT-PCRassays forthe detection
ofSARS-CoV-2InstitutPasteur, Paris
Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR
CDC 2019-Novel Coronavirus (2019-nCoV) Real-Time RT-PCR Diagnostic
Panel


Start studying mathematical biology from basics

There is one book that will perfectly suits your needs:

A biologist's guide to Mathematical Modeling in Ecology and Evolution, by Sally Otto

It is a very good book that is very easy to understand and in the meantime goes pretty far (It ends with the use of diffusion equation in Evolutionary Biology). I highly recommend it.

It covers:

How to create a model
Function approximation
Find general solution with $n$ variables for discrete and continuous model
Stability analysis
Find equilibrium
Analyzing cyclic behavior
Gives very good introduction in linear algebra and probability theory
Class structured population
Stochastic modeling (birth-death processes and diffusion approximations)
Transformations
All examples are from the field of ecology and evolution and the author derives many of the most important equations in ecology and evolution.

Online ressources

Also I think that Khan Academy is a very good and easy source of information for improving your math skills but it takes quite a bit of time to go through all these lectures.

For a good and complete introduction to probability theory, I'd recommend this MIT Opencourseware but again, it takes time to go through all these videos.

For further recommendations in population genetics, you should have a look to this post.

If you are interested in theoretical biology, you may also want to learn about programming (if you don't already know much about it). $R$ is used for data analysis purposes, $Mathematica$ or $Matlab$ for deal with mathematical modeling and $Python$, $Java$ or $C++$ for individual-based simulations.

Note: A bit less than 2 years ago, I had the same interests than you and had to face the same issues than you.


Mostly it is because of the scalp and a decrease in the hair follicles ability to maintain production of sturdy hair (keratin along with melanin for hair color). In some cases, it is also genetic such as in Male Pattern Boldness.

Hair thickness changes with age. Hair is made of many protein strands and a single hair lasts between 2-7 years on your head. The hair then falls out and is replaced with a new one. How much hair you have on your body and head is also determined by your genes. With age, the rate of hair growth also slows down. Source

I would say however that the major impact-factor ought to be testosterone production especially in the case of MPB. More specifically DHT (Dihydrotestosterone) which is a derivative of testosterone. The amount of DHT is higher in balding scalp than non-balding ones.

In addition, it has been shown that the number of DHT receptors on the hair follicles also increases in balding scalps. Also, blocking the conversion of testosterone to DHT delays progression of hair loss and onset of MPB. That is why DHT is usually held responsible for miniaturization of hair follicles leading to hair loss, and this can happen at any age based on the DHT amount, but usually happens as we get older. Source

Testosterone is mainly found in man, but women certainly do produce it, even though it is present in minuscule amounts. Under normal conditions, women have a very small fraction of the level of testosterone that men have. However, even a low level of it can be converted to DHT and trigger hair loss in women. Source


How difficult is it to make a shRNA/miRNA/siRNA to silence/knockdown NaV1.7 voltage gated sodium channels in humans?

The major hurdle for novel treatments to make it into humans is the assessment of its merits and added value over existing, proven treatments. And more importantly, the safety for humans has to be validated to a sufficient extent. The notorious from bench to bedside (Goldblatt & Lee, 2010) bottle neck. To answer your questions:

Technically, going from animals to humans may be a small step. Just increase the dose according to body weight. However, ethically it is a giant step. In fundamental research, lab animals are typically investigated only for the positive effects (e.g., amelioration of symptoms). In preclinical research, the animals have to be tested on side effects. Systemic injections, and even localized administration of potentially harmful virus vectors carries considerable risk. What if it returns to an infectious state? What are the side effects? Further, while animals can be treated systemically via iv injections, humans don't like needles. The FDA will put every possible danger and every possible discomfort to the patient into the spotlight.
Getting grants is hard. Going from bench to bedside is even harder, as the FDA, institutional review boards and the scientific community at large will scrutinize the plans.
To undertake clinical trials with humans is a team effort involving medical professionals, review boards, patients or healthy volunteers, an independent monitoring committee and so forth. It's not something you'll be doing in a few months. It can take years or decades to bring novel treatments to patients. It doesn't take one grant - it takes many, and development costs easily run into the tens of millions.

Reference
- Goldblatt & Lee, Am J Transl Res (2010); 2(1): 1–18


What causes the pain when a bone fracture is healing?

At the initial phases of the healing the broken ends are mobile (and this is time when it can be set and put into a cast).

At later stages soft callus than hard callus forms and now any movement will pull on the broken ends and stimulate the nerve endings: it hurts.

This also has the effect that the nearby muscles will spasm in an attempt to immobilize the bone. Another source of the pain can be that these muscles become tired and start to hurt as well.

The pain will continue until the two broken ends are completely welded together so there is no longer any movement that would stimulate those nerves.


Can pheromones in perfume be formulated to cause agitation?

Insects generate and respond to pheromones. But despite what sci-fi TV might have told you, there is no evidence that humans make or respond to pheromones like that.  Humans don't have that good sense of smell, for one thing.

The fact that you know it's a Playboy brand of perfume is affecting you?  That's obviously not chemical, is psychological.

Also, historically, perfume was used just as much to mask unpleasant odors as it was to attract anyone.  When men go through puberty, their sweat changes odor.  That's not to attract other men.

If this perfume is affecting you emotionally it's psychological, not chemical.


These terms are quite similar and, for many, confusing:

Chromatin
Chromosome
Chromatid

But they are not synonyms. According to Molecular Cell Biology, Lodish, 4th ed:

  Chromatin: Complex of DNA, histones, and nonhistone proteins from which eukaryotic chromosomes are formed.

Which brings us to:

  Chromosome: In eukaryotes, the structural unit of the genetic material consisting of a single, linear double-stranded DNA molecule and associated proteins.

So, you can think of chromatin as the building material of chromosomes.

But chromatid has a very different definition:

  Chromatid: One copy of a duplicated chromosome, formed during the S phase of the cell cycle, that is still joined at the centromere to the other copy; also called sister chromatid.

So, one should not use the term chromatid as synonym of chromosome. Chromatid is the name of each copy of the chromosome after the S (synthesis) phase. According to that terminology, there is no chromatid before the duplication.

I have to confess that I personally don't follow that terminology: I like to say to my students that, before S phase, each chromosome has 1 chromatid and, after the S phase, each chromosome has 2 chromatids. Even this not being the most correct terminology, it has some advantages: it makes the student understand that the number of chromosomes doesn't double after the S phase.

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman


Does male or female DNA contain more information?

Define "information" — females have more base pairs and more individual genes because X's are larger than Y's, but males have a large number of unique loci and thus unique genes, because they have an X and Y chromosome.


Do primate RGCs have overlapping receptive fields?

Short answer
Associated ON- and OFF-center retinal ganglion cells can show 100% overlap in their receptive field.

Background
When looking at the elementary neurophysiology of the retina, we can see that a single cone generally synapses onto two bipolars. Because photoreceptor cells hyperpolarize when illuminated, glutamate release from their synapse is inhibited. In turn, OFF-center bipolar cells are hyperpolarized and ON-center bipolars are depolarized. The OFF-center bipolar synapses onto an OFF-center retinal ganglion cell (RGC), while the ON-center synapses onto an ON-center RGC (Fig. 1).

 Retinal circuitry linking cones to bipolar cells (left panel) and bipolar cells to retinal ganglion cells (right panel). source: Washington University.

Then to your question - the basic circuitry shows that the ON- and OFF-center RGCs receive their input from a single cone and hence have 100% overlapping field. In the foveal region, bipolars link 1:1 on cones, as in Fig. 1, so in this example case, they show 100% overlap.

Note that there are an estimated 30 types of retinal ganglion cells, about half of them being not even described yet, as per a 2015 review article (Sanes & Masland, 2015). Hence, this answer is anywhere from exhaustive, but it does show there can be substantial overlap between RGCs.

Reference
- Sanes & Masland, Ann Rev Neurosci (2015); 38: 221-46


How can you improve solubility of colloidally dispersed substances?

In my case, three-four rounds of sonication greatly helps in having smaller and more homogeneous hydrophobic particles dispersed in water.


Short answer
Sensory neurons are invariably considered to be located in the periphery. Interneurons and motor neurons are part of the CNS.

Background
There are various classifications possible to categorize neurons.

One classification is the one you mention (Furness, 2000), which is a broad classification based on where the neuron projects to. It divides all neurons in:

Sensory neurons (feed information to the central nervous system (CNS));
Interneurons (are stimulated by sensory neurons and/or other interneurons);
Motor neurons (feed information from the CNS to the periphery).

Sensory neurons are invariably considered to be part of the peripheral nervous system. Their cell bodies are located in the periphery. Their projections may feed directly into the brain. For example, olfactory sensory neurons directly project onto the olfactory bulb in the brain.

Motor neurons include the motor neurons controlling muscles. Their cell bodies are located in the spinal cord, which is the CNS, but not the brain. Here the terminology becomes confusing, as this functional classification uses overlapping terminology with the projectional classification. That's why I, personally, prefer to talk about efferent fibers (away from CNS) and afferent fibers (to the CNS). Especially because motor neuron implies something motoric. In case of neurons driving glandular secretion this is counter intuitive. Efferent and afferent fibers are essentially the same names for motor neurons and sensory neurons. One way or another, motor neurons controlling muscles have their cell bodies in the spinal cord and hence are part of the CNS.

Interneurons are invariably located only within the CNS. Interneuron is also a confusing term, because often they are implicitly considered to be inhibitory. Often they are, but they don't have to be. In the classification scheme discussed, most CNS neurons can indeed be classified as interneurons. For example in the neocortex, 70–80% of the neurons are excitatory pyramidal cells, while the remaining 20–30% are inhibitory interneurons (Markram, 2004). The spinal cord also contains interneurons.

In all, most interneurons are located in the CNS, but not all CNS neurons are interneurons, because motor neurons are part of the CNS too. I agree with 243's answer that the classification scheme is most appropriate for the relatively simple neuronal circuitry characteristic of the spinal cord.

References
- Furness, J Autonom Nervous Syst (2000); 81: 87–96
- Markram, Nature Rev Neurosci (2004); 5: 793-807


how do I find the number of bp in chromosome 3 by knowing number of bp in chromosome 1?

You cannot.  BP numbers vary between the chromosomes.  Chromosomes are numbered by size, so you can always say that 2 is smaller than 1; however, there is no function to determine the exact size of one chromosome based on the exact size of another.


Is it possible to establish a newer animal model completely based on Bioinformatics studies?

It is naïve to think that the extent of protein similarity is sufficient to determine what is the best animal model for a human disease. The physiology of the animal and the question of compensatory genes are all factors that contribute.

Indeed, if the protein is functionally similar, it may be irrelevant if it has diverged in other regions. And, of course, there are ethical and cost considerations — the animals closest to humans are the apes!

I suggest you search for literature on the subject. It’s not my field, but Googling brought up this paper discussing models for kidney disease, and no doubt you could find much more yourself.


I believe this plant may be Rotala rotundifolia

Quoting from Wikipedia,

  It is a common weed in rice paddies and wet places in India, China, Taiwan, Thailand, Laos, and Vietnam, and has been introduced to the United States.

This makes sense, as Bangladesh is located near both India and China.

  The emerse form has rounded leaves, the submerse leaves are narrow lanceolate. It is very variable dependent on light and environmental conditions. Under strong light, the leaves can become almost wine red. It has pale pink flowers.


Why is thymine not incorporated into mRNA?

Nice question! But sadly, it comes under the category of questions about which we don't know everything yet. We don't yet know how RNA Polymerase differentiates between uracil and thymine while adding nucleotides to growing mRNA chain (at least, I was unable to find research papers online), most probably because it has proved difficult to know the exact mechanism of RNA synthesis which RNA polymerase undergoes. But we do know what factors it could use to do so. For general introduction, these factors are:

mRNA chains contain NTPs instead of dNTPs. Now, TTP is very (very) rarely found in cells. So, RNA Polymerase can look for 2'-OH in nucleotide for adding base (pay attention that RNA polymerase is not known to have proofreading mechanisms, but there is growing evidence that RNA polymerase can correct a faulty base pair matching, see Thomas et al). RNA polymerases are known to be able to distinguish between NTPs and dNTPs (Svetlov et al), although the precise mechanisms in multi-subunit RNA polymerase remain elusive. Yet, this property certainly plays a role (refer to EDIT 1 for details about this).
UTP and dTTP have another basic structural difference: of a methyl group. This difference is crucial for differentiating the two, especially for DNA repair machinery. It is so because cytosine can spontaneously convert to uracil (by deamination). So, there has to be something for repair enzymes to look for while repairing mutated cytosine, and a methyl group saves thymine from repair. See the following image for comparison:

source

Just for information, we know the flip side i.e. how DNA polymerases prevent dUTP from adding in DNA chains, because dUTP is much more common than TTP. Simply saying, they don't. Mutations can (and do) occur, leading to faulty addition of dUTP in DNA. But, this is where repair machinery helps. Cells contain an enzyme, uracil DNA glycosylase, which replaces uracil by thymine in DNA (Longo et al). So, until we find the exact mechanism for RNA polymerase, you can assume that it uses much similar mechanism for proofreading (along with the first one of course).

EDIT 1: I will add some details about the mechanism of base pair matching by RNA polymerase as just leaving the point at yet, this property certainly plays a role makes the answer misleading to some people. But, because putting the whole mechanism here would make the answer too long and also out-of-scope (keeping in mind you asked 'why', not 'how'), I'll try to keep this part as small as possible. Giving a diagram for better understanding:

Pay attention at the Tyr639 and His784 (sugar discriminators), this is how the RNA polymerase distinguishes NTP from dNTP. It has also been shown that removing Tyr639 will convert the RNA polymerase to DNA polymerase(!), though removing His784 would just decrease its activity, suggesting its role to be minor w.r.t. Tyr639. For more information, have a look at this page from Brooklyn college website.

EDIT 2: In another answer, the answerer says RNA synthesis requires rNTPs instead of dNTPS as precursors, but does not explain why it is so (which is indeed an important part). So I'll add that part in my answer. It can be explained by following points:

The sugar discriminators of RNA polymerase (describe above) do not allow dNTPs to add to the growing chain. Thus dNTPs cannot act as substrates for RNA synthesis.
The enzyme for synthesis of thymine (dTTP) is thymidylate synthase, which requires dUMP as substrate. Thus, it is not possible to create rTTP instead of dTTP.
Conversion of uracil to thymine requires energy, meaning uracil is energetically less expensive than thymine. This also directly explains (partly) why mRNA doesn't incorporate thymine into the chain.
Degradation of mRNA requires an enzyme ribonuclease which cannot degrade dNTPs. Also, in the mechanism of degradation of mRNA, 2' -OH plays a role. This can be explained by diagram below:

As is visible, 2' -OH is an important part for RNA degradation. Thus, it wouldn't be possible to degrade mRNA in this way if it contained dNTPs.

References:

Matthew J Thomas, Angelina A Platas, Diane K Hawley, Transcriptional Fidelity and Proofreading by RNA Polymerase II, Cell, Volume 93, Issue 4, 15 May 1998, Pages 627-637, ISSN 0092-8674, http://dx.doi.org/10.1016/S0092-8674(00)81191-5.
Svetlov V. Vassylyev D.G. Artsimovitch I. Discrimination against deoxyribonucleotide substrates by bacterial RNA polymerase J. Biol. Chem.  2004 279 3808738090
Mary C. Longo, Mark S. Berninger, James L. Hartley, Use of uracil DNA glycosylase to control carry-over contamination in polymerase chain reactions, Gene, Volume 93, Issue 1, 1 September 1990, Pages 125-128, ISSN 0378-1119, http://dx.doi.org/10.1016/0378-1119(90)90145-H.
Dziuda, D.M. (2010). Data Mining for Genomics and Proteomics: Analysis of Gene and Protein Expression Data. Wiley
Roberts, Gordon C. K. et al. “THE MECHANISM OF ACTION OF RIBONUCLEASE.” Proceedings of the National Academy of Sciences of the United States of America 62.4 (1969): 1151–1158.


What species of Cerapoda lived during the Jurassic?

Here is a cladogram from "The phylogeny of the ornithischian dinosaurs", Butler, Upchurch, & Norman, Journal of Systematic Palaeontology (2008):

Of these, :

Ferganocephale (Pachycephalosauridae)
Chaoyangsaurus
Camptosaurus (Ankylopollexia)
Uteodon (Ankylopollexia)
Callovosaurus (Dryosauridae)
Dryosaurus (Dryosauridae)
Dysalotosaurus (Dryosauridae)

lived during the Jurassic.

The synopsis explains well why this classification is subject to adjustment, and why you may have seen contradictory models in your research:

  SYNOPSIS Ornithischia is a familiar and diverse clade of dinosaurs whose global phylogeny has
  remained largely unaltered since early cladistic analyses in the mid 1980s. Current understanding of
  ornithischian evolution is hampered by a paucity of explicitly numerical phylogenetic analyses that
  consider the entire clade. As a result, it is difficult to assess the robustness of current phylogenetic
  hypotheses for Ornithischia and the effect that the addition of new taxa or characters is likely to have
  on the overall topology of the clade.

  The new phylogenetic analysis presented here incorporates a range of new basal taxa and characters
  in an attempt to rigorously test global ornithischian phylogeny. Parsimony analysis is carried out
  with 46 taxa and 221 characters. Although the strict component consensus tree shows poor resolution
  in a number of areas, application of reduced consensus methods provides a well-resolved picture
  of ornithischian interrelationships. Surprisingly, Heterodontosauridae is placed as the most basal
  group of all well-known ornithischians, phylogenetically distant from a stem-defined Ornithopoda,
  creating a topology that is more congruent with the known ornithischian stratigraphical record. There
  is no evidence for a monophyletic ‘Fabrosauridae’, and Lesothosaurus (the best-known ‘fabrosaur’)
  occupies an unusual position as the most basal member of Thyreophora. Other relationships within
  Thyreophora remain largely stable. The primitive thyreophoran Scelidosaurus is the sister taxon of
  Eurypoda (stegosaurs and ankylosaurs), rather than a basal ankylosaur as implied by some previous
  studies.

  The taxonomic content of Ornithopoda differs significantly from previous analyses and basal
  relationships within the clade are weakly supported, requiring further investigation. ‘Hypsilophodontidae’
  is paraphyletic, with some taxa (Agilisaurus, Hexinlusaurus, Othnielia) placed outside
  of Ornithopoda as non-cerapodans. Ceratopsia and Pachycephalosauria are monophyletic and are
  united as Marginocephalia; however, the stability of these clades is reduced by a number of poorly
  preserved basal taxa.

  This analysis reaffirms much of the currently accepted ornithischian topology. Nevertheless, instability
  in the position and content of several clades (notably Heterodontosauridae and Ornithopoda)
  indicates that considerable future work on ornithischian phylogeny is required and causes problems
  for several current phylogenetic definitions.


Why can action potentials not be initiated at dendrites?

The exact site of action potential generation is debated, as is the underlying physiological mechanism (Colbert & Johnsten, 1996). It is generally agreed upon that the initiation site is beyond the soma, at the axon hillock, or even further in the initial segment of the axon.

The reason for the distal axonal initiation site of action potentials is, according to the classical view, that the density of Na+ channels is not high enough in the soma, while the density in the axon initial segment is substantially higher and sufficient. However, it has also been proposed that the threshold of action potential generation is lower at the initial segment (Kole et al., 2008).

Regarding your questions in the comments:

So can't action potentials be initiated at dendrites and soma with the help of VGCCs?
Answer: No. Channel density is too low;
What are the channels required for AP?
Answer: Basically Na+ and K+ channels;
How is it that action potentials are initiated at axon hillock, although the input is at dendrites? Why can't enough depolarization happen at dendrites and soma?
Answer: Either due to a low density of Na+ channels, and/or a higher action potential threshold (e.g., due to the presence of K+ channels in the soma counteraction depolarization);
As a corollary,if enough depolarization cannot occur at dendrites and soma,how then is it propagated to the axon, which is further down anatomically , in the neuron?
Answer: If the EPSP reaches a region with sufficient Na+ channels, depolarization becomes sufficient to activate a critical amount of Na+ channels that causes a sufficient increase in the membrane potential to sustain a full-blown action potential. Along the way, leaky K+ channels decrease the depolarization so a critical amount of channels is necessary, otherwise the EPSP dies out.
What about backpropagating APs from axon hillock to dendrites ? How is that possible?
Answer: the soma and dendritic region are believed to represent too big an electrical load to ensure action potential propagation in both the orthodromic and the antidromic direction. This impedance mismatch can be overcome for an action potential propagating from the axon back into the somato-dendritic region when the initial segment and axon hillock provide additional current. This can be achieved with a high density of sodium channels in that region (Lüscher & Larkum, 1998).

References
- Colbert & Johnsten, J Neurosci (1996), 16(21): 6676–86
- Kole et al., Nature Neurosci (2008); 11: 178-86
- Lüscher & Larkum, J Neurophysiol (1998); 80(2): 715-29


It's probably mostly fungal contamination if you did not sterilize and left the container open. This video on how to isolate bacteria better may help: https://www.jove.com/video/3064/aseptic-laboratory-techniques-plating-methods

Good luck!


Homeopathy is placebo, but isn't placebo good?

The point of a double-blind trial is that treatments are compared to placebo effect. Therefore, conventional treatments that "pass" double-blind trials are better than placebo.  If homeopathy is equal to placebo, that means that homeopathy is worse than conventional treatment.  Therefore, people who treat with homeopathy are giving worse than standard care.


No, the human body cannot utilize externally applied electricity.  Applying electricity to the body will either have no effect, if the amount is small, or will disrupt normal functions of the body or cause injury if the amount is larger.

An overview of the effects of electricity (for doctors) can be found in "Conduction of Electrical Current to and Through the Human Body: A Review".


How does a spider's legs not get caught in silk when wrapping prey?

There are two parts to this answer.
Spider Legs
First, I would like to mention that spiders avoid sticking to their webs by more means than just non-sticky anchor strands to walk on.  To help keep the glue from sticking to their legs, an oily substance apparently covers spider legs.  Furthermore, the same study found that:

In addition, Eberhard and Briceno also noted that the spider’s gait seemed specially designed, such that it “reduced the area of contact between the sticky droplets and the setae [spiny leg hairs].” This, combined with the fact that the thread touched many (rather than only a few) branching hairs, made it very unlikely that any glue would slide all the way down the hairs to make contact with the main part of the leg – which would have made permanent adherence more likely.

Spider Wrapping Silk Fiber is Different
The main reason spiders do not get stuck to their silk when wrapping prey is because wrapping silks are different from silks used to make webbing.  There there are seven known types of silk that spiders can produce.  Aciniform, or wrapping silks are the strongest silk from a spider and specifically designed for wrapping.  This silk is typically dry, and does not contain the high amounts of N-acetylgalactosamine which give the distinctive quality of being sticky.   For a very detailed study on wrapping silk architecture, please see this recent study from 2015.


What is the most genetically simple organism except viruses?

Mycoplasma genitalium was one of the first full bacterium genomes sequenced and since its a symbiotic organism that lives on the moist and warm genital skin surface it doesn't need as many genes as many bacteria.  It has a 582 kbp genome sequence with only 521 genes.

But that is so 1995.

The 159 kbp genome of Candidatus carsonella was published in 2006. It is thought to only contain 182 genes.  Its an endosymbiont of some sap eating insects.

But the current record holder, published this year, is Nasuia deltocephalinicola, discovered survey of insect endosymbionts, has only 112 kbp in its genome. Smaller than some viruses.  It's thought to contain 137 protein coding genes with 29 tRNA genes, so its not a lot smaller than Carsonella in terms of gene count.

There's no reason to expect that this is the minimal viable genome by any means.  I'm sure this response will need revision in a year or two.

M. genitalium has become the model system for minimal genome work.  Many of these other bacteria might be difficult to culture, molecular biology lab techniques might have to be developed, so hopping onto newly discovered bacteria isn't always the best idea from a standpoint of producing science.  It does suggest that M gentalium doesn't need all of its genes!  A possible cause for these extra genes might be a more complex immune response in human beings where its found.  It might also be because of the symbiotic requirements of insects is simpler.


What color was the most recent common ancestor of all swans?

According to the known phylogeny of Anserinae in this paper,

Cygnus atratus (the black swan) is most closely related to Cygnus melanocoryphus (the black-necked swan). All of the other swans in the genus Cygnus are white, or close to white.

Therefore, it is reasonable to assume via maximum parsimony and maximum likelihood that the two genera evolved their blackness from a white ancestor, and not that all of the swans independently turned white from a black ancestor.


What is this bizarre in-growth in this red bell pepper?

This is very likely to be parthenocarpy, which is an “internal proliferation” and varies from an irregular fruit to an almost carbon copy of the larger pepper. What is known is that it shows up in seed lines through natural selection and is unaffected by weather, pests, or other external conditions. Please see page 27 of this document.


What is the distinction between chemokines, cytokines, interferons and interleukins?

Cytokines is the general class of molecules to which chemokines, interferons, interleukins and others belong. Biologists dispute whether something is a hormone or a cytokine, but generally the consensus goes with if it's to do with immunology it's a cytokine or if the resting concentration is in the picomolar range, but that's a very rough distinction.

Chemokines are molecules that drive cellular chemotaxis. That means they make cells move towards a desired place. Generally chemokines refer to immune cells and there's loads and loads of them.

Interleukins are anything which are messenger molecules between immune cells (inter- means between and -leukins means leukocytes/white blood cells). They're typically denoted by IL + number. However the interferon and tumour necrosis families come under interleukins too in most people's opinion. The interferons are a special group that typically inhibit viruses by making cells non-permissible to viral replication. They also do a few other things like activate macrophages or promote Th1 response, which both also interfere with viruses but there is bacterial overlap. The TNF family is a bit weirder as some are interleukin-like but others aren't as much. TNF-alpha (the classic one) is involved in macrophage maturation. However not all interleukins are strictly between white blood cells, as IL1 acts on the hypothalamus among other leukocytes.

See the problem is everything is a bit grey because most cytokines (if not all) have more than one role and there's never consensus in the world of immunology when it comes to cytokines because more and more keeps getting discovered.