What are the long term consequences of settling an isolated territory with an extremely limited gene pool?

Minimum number of individuals needed to start a population

But could just one woman be the progenitor of a healthy nation? And,
if not, what is the minimum number of distantly-related individuals
required?

Healthy is a pretty subjective term, and it's perhaps easier to think of things in terms of a minimum viable population, which is more about straight survival than population health. However, Marin & Beluffi (2018) performed some simulations of humans in a multi-generational space exploration scenario, using 'healthy population' as a desired outcome and found:

A initial amount of 25 breeding pairs of settlers drives the mission
towards extinction in 50 +/- 15% of cases if we completely forbid
inbreeding. Under the set of parameters described in this publication,
we find that a minimum crew of 98 people is necessary ensure a 100%
success rate for a 6300-year space travel towards the closest telluric
exoplanet known so far.

So according to this simulation, it seems quite unlikely that a single woman could be the progenitor for some kind of colony. However, as I discuss a bit further down, some human populations went through bottlenecks of ~20 individuals and remained viable. They may have incurred some health costs, but they would be able to propagate the population.
Long term consequences of founder effects
There are several different case studies of modern human populations relating to the founder effect.
Achromatopsia Pingelap
The atoll of Pingelap in the Pacific Ocean is extremely remote, and up until the late 18th century had around 500 inhabitants. Around then, it was hit by a devastating typhoon which reduced the population size to around 20 individuals. In following generations, it was estimated by that 10% of the estimated 3,000 Pinglapese had Achromatopsia (Carr et al 1971), an autosomal recessive form of colour blindness that otherwise has an extremely low frequency of about 0.003% in other populations (Thiadens 2011).
Subsequent studies used homozygosity mapping in order to determine the genetic basis of the high levels of Achromatopsia. Sundin et al (2000) demonstrated that Pingelapese achromats are homozygous for a missense mutation (serine to phenylalanine) in a highly conserved membrane-spanning domain. This is quite solid evidence for the deleterious consequences of the founder effect in modern human populations.
Jewish populations
There is also reasonable evidence of a severe bottleneck in the ancestors of the global Ashkenazi Jew population. Carmi et al (2014) estimated that the total population fell as low as 350 individuals:

The AJ population is much larger and/or experienced a more severe
bottleneck than other founder populations, such as Amish, Hutterites
or Icelanders.

Other studies have suggested that the high incidence of particular diseases found in Ashkenazi Jew populations was the result of genetic drift following the bottleneck, rather than subsequent co-sanguinity (Bray et al 2010):

We identified genomic regions under selection that account for lactose
and alcohol tolerance, and although we found evidence for positive
selection at some AJ-prevalent disease loci, the higher incidence of
the majority of these diseases is likely the result of genetic drift
following a bottleneck

Rapa Nui
Since you asked about Rapa Nui. Gonzalez-Martin et al (2006) have this to say:

The population of Easter Island is one of the most interesting extant
human communities due to its unique demographic history, its geographic
isolation, and the development of an incomparable culture
charac-terized by the towering ‘‘Moais’’ and its enigmatic writing.
Following the colonization of its population by Polynesians from the
Mangarevan Islands in the 5th century AD, the island remained isolated
up until the middle ofthe 20th century. Under these conditions, with
endogamy levels ﬂuctuating between 61.04–96.54% and given such a small
population, a high rate of inbreeding, and consequently, an elevated
level of genetic relationships would be expected. Using data from
church and civil records, we calculated the consanguinity of the
population of Rapa Nui. The results of this analysis do not support
the hypothesis of a high level of consanguinity.

That said, I have heard some unverified rumours that there was a high incidence of having 6 toes on Rapa Nui, but I can't find anything solid to back it up with.
Norfolk Island
One last example. I've taken this text from a nice paper by Macgregor et al (2009):

The population of Norfolk Island, located off the eastern coast of
Australia, possesses an unusual and fascinating history. Most
present-day islanders are related to a small number of the ‘Bounty’
mutineer founders. These founders consisted of Caucasian males and
Polynesian females and led to an admixed present-day population. By
examining a single large pedigree of 5742 individuals, spanning >200
years, we analyzed the influence of admixture and founder effect on
various cardiovascular disease (CVD)-related traits.

Further...

Marker-derived homozygosity was computed and agreed with measures of
inbreeding derived from pedigree information. Founder effect
(inbreeding and marker-derived homozygosity) significantly influenced
height

Non-human species
I think the last part of your answer is referring to the Hoary Bat, which colonised Hawaii from mainland USA. It was originally hypothesised that the population was the result of a single founding event, but this has been disputed by mtDNA markers (Russell et al, 2015):

Our results point to the colonization of Hawai'i by hoary bats on two
occasions by lineages that experienced distinct evolutionary
trajectories

There is some evidence of single-individual founder events occurring, however (Clegg et al 2002);

Here we undertake a genetic analysis of a series of historically
documented, natural colonization events by the silvereye
species-complex (Zosterops lateralis), a group used to illustrate the
process of island colonization in the original founder effect model.
Our results indicate that single founder events do not affect levels
of heterozygosity or allelic diversity, nor do they result in
immediate genetic differentiation between populations

Further..

A Bayesian analysis based on computer simulation allows inferences to
be made on the number of effective founders and indicates that founder
effects are weak because island populations are established from
relatively large flocks.

There is a lot of literature on this in wild populations which might be of interest, e.g. https://link.springer.com/content/pdf/10.1007/s10592-010-0049-0.pdf
References
Thiadens, Alberta. "Genetic etiology and clinical consequences of cone disorders." (2011). APA
Carr, Ronald E., Newton E. Morton, and Irwin M. Siegel. "Achromatopsia in Pingelap islanders: study of a genetic isolate." American journal of ophthalmology 72.4 (1971): 746-756.
Sundin, O.H. et al. Genetic basis of total colourblindness among the Pingelapese Islanders. Nature Genet. 25, 289– 293 (2000).
Carmi, Shai, et al. "Sequencing an Ashkenazi reference panel supports population-targeted personal genomics and illuminates Jewish and European origins." Nature communications 5.1 (2014): 1-9.
Bray, Steven M., et al. "Signatures of founder effects, admixture, and selection in the Ashkenazi Jewish population." Proceedings of the National Academy of Sciences 107.37 (2010): 16222-16227.
APA
Marin, Frédéric, and Camille Beluffi. "Computing the minimal crew for a multi-generational space travel towards Proxima Centauri b." arXiv preprint arXiv:1806.03856 (2018).
Russell, Amy L., et al. "Two tickets to paradise: multiple dispersal events in the founding of hoary bat populations in Hawai'i." PLoS One 10.6 (2015): e0127912.
Clegg, Sonya M., et al. "Genetic consequences of sequential founder events by an island-colonizing bird." Proceedings of the National Academy of Sciences 99.12 (2002): 8127-8132.
Macgregor, Stuart, et al. "Legacy of mutiny on the Bounty: founder effect and admixture on Norfolk Island." European Journal of Human Genetics 18.1 (2010): 67-72.


Can any species be bred selectively/engineered to become as diverse looking as dogs?

Dogs have a genomic structure that allows breeding with high variation in size, shape, coat quality, color and other qualities particular to each breed as well.

Other domesticated animals can be bred for as many qualities, but dogs in particular show a wide level of morphological traits - varying in size from just over a pound to the size of a wolf, from which dogs are derived and genetically are still compatible.  But more interesting than just size or coat color/texture and even their intelligence and personalities, the proportions of their bodies, of their skull length and breadth, are remarkable.

There are over 160 registered breeds of dogs, but this is only a measure of how much time people have put into them.  I think its possible to get nearly anything you want with animals, if you are patient enough - its not clear what is and is not possible with enough genetic manipulating. For instance, horses can be bred over nearly as great a size range for instance (the miniature horse the size of a large dog, the Shire is 3,300 pounds), but it would not be as easy to get both the size and muscularity and shape of a bulldog in a horse.  Breeding a mouse of various colors can be done, and so can interesting behaviors, but body shape seems to be harder: a Weimaraner mouse could take a tremendous amount of time and animals.


How are antibiotic resistant bacterial infections treated?

There are a number of ways to address antibiotic resistance in infectious bacteria. What one gets used depends on exactly what organism we're talking about. But below is a short list of some ways:

Changing the antibiotic being used. Not all antibiotics have the same molecular target within a bacterial cell. Some interfere with the formation of the cell wall, others interfere with protein synthesis, some mess with DNA replication, etc. Similarly, resistance mechanisms don't work equally well on all antibiotics. So often the solution is simply to switch antibiotics. Or, quite often, treating all infections with a combination of drugs that should get around most resistance. This is why you see people getting skittish about things like multi-drug resistant organisms - because it removes this solution.
This isn't as much a treatment as a preventative measure, but increasing antimicrobial stewardship and the appropriate use of antibiotics to prevent widespread resistance from arising in the first place.
The use of non-antibiotic antimicrobials. The most "common" of these is phage therapy - using preparations of bacteriophages that naturally prey on the infecting pathogen to help combat the infection. This was a major "contender" for how we treated antibiotic infections, but has fallen away due to a bad reputation early in its history (due to difficulties purifying phage treatments) and the discovery of antibiotics which were vastly easier to use. But there's still ongoing research, and it may pose a potential to help treat highly resistant infections in the future.


Is H antigen considered as an agglutinogen?

H antigen is a precursor for A and B antigens, and hh (recessive) individuals do not express this antigen. See Bombay blood group. This is an example of epistasis. Since H antigen is present in all A,B,AB and O blood groups, transfusion from any of these to an hh individual will cause a haemolytic reaction. Anti-H antibodies are agglutinins and have been referred to as agglutinins in the scientific literature.

  The fairly strong anti-H agglutinins present in 'Bombay' and
  'para-Bombay' individuals (see 5.5.6) are generally accompanied by anti-A and anti-B, neither of which can be separated from the
  anti-H specific antibodies.

   Schenkel-Brunner, Helmut. Human blood groups: chemical and
  biochemical basis of antigen specificity. Springer Science &
  Business Media, 2000. e-Book ISBN: 978-3-7091-6294-1


Not all pathogens are parasites. Many opportunistic infections can be caused by organisms that are normally commensal or even mutualistic.
For example, this paper describes how multiple bacteria species can be pathogenic as well as mutualistic.

Despite its generally innocuous nature, over the past 20 years S.
epidermidis has emerged as a frequent cause of nosocomial infections.
Several extrinsic factors contribute to the conversion of S.
epidermidis from a member of the resident microflora to an infectious
agent. The bacteria primarily infect compromised patients including
drug abusers, those on immunosuppressive therapy, patients with
acquired immune deficiency syndrome (AIDS), premature neonates and
patients with an indwelling device.
...
Recent studies can be interpreted to suggest that S. epidermidis is a
mutualistic organism, much like the bacteria of the gut. Many strains
of S. epidermidis produce lantibiotics, which are
lanthionine-containing antibacterial peptides, also known as
bacteriocins (Fig. 3). Among the several identified bacteriocins are
epidermin, epilancin K7, epilancin 15X, Pep5 and staphylococcin
1580.37–39 Additional antimicrobial peptides on the surface of the skin have recently been identified as originating from S. epidermidis.
...
The removal of S. epidermidis (i.e. through overuse of topical
antibiotics) may be detrimental to the host for two reasons. Firstly,
removing S. epidermidis eliminates the bacterium’s endogenous
antimicrobial peptides, allowing potentially pathogenic organisms to
colonize the skin more effectively. Secondly, without bacterial
priming of the skin, the host may be less efficient in warding off
infection.


Can defibrillation be done with a car battery?

In general, no.

Car batteries are designed to provide a large amount of amperage, to turn the starter with a high amount of torque via an electric motor.  Generally this is done at 12 or 24 volts.

The current recommendations for a defibrillator requires 200V, and a very small amount of amperage.  This is one of three settings in a standard defib procedure.  The second setting is 300V, and the final is 360V.  The point of defibrillation is not to provide power to the heart, it is to disrupt the heart's built-in electrical (biological) circuitry, such that the heart can go to rest (not beating).

Many cardiac events involve the heart beating in an uncoordinated manner, such that many or all of the muscle fibers in the heart beat in a manner that doesn't provide the squeezing action on the chambers to push the blood forwards.  Defibrillation seeks to correct such an uncoordinated beating by resetting the heart to rest, after which it will hopefully start beating again in a coordinated manner.

In short, attaching a car battery is more likely to cook the heart (if it even gets that deep) because it is providing too much power, and it is unlikely to disrupt the heart's electrical field because it is too low of a voltage.  With this in mind, one could theoretically attach enough electrical transformation equipment to a car battery to use it as a power source for defibrillation.  But there are other issues with such an idea.

Car batteries are not designed for the usage that would mesh well with a defibrillation machine.  Car batteries are designed to be recharged.  Your car battery basically drains pretty heavily upon starting a car, and then the alternator recharges it by harvesting mechanical power from the engine during your trip.  This heavy drain / heavy charge cycling is hard on batteries, and car batteries have been specifically designed to endure in such a scenario.

A defibrillator machine has a different use scenario.  Basically it sits idle for long periods of time, and when it does require charging, it gets electricity from a wall socket, at higher voltage (and generally lower amperage).  This means it tends to charge more slowly, which in general means longer battery life.  Also the battery is built differently, to hold charge better at the expense of not being recharged as quickly.

In short, a car battery is really the wrong tool for the job.


Why are two-winged animals much more common than four-winged?

Note you are talking about two very distinct conditions

In vertebrates, 4 "wings" only evolves once in vertebrates (in early birds) and only one set function as wings the others "wings" are control surfaces for low speed stability, they generate insignificant amounts of lift. for large animals like vertebrates you can't fit two sets of functional wings on the same animal. Large wings need a lot of space to flap and you would need to make the torso longer to give enough room for a second set of flapping wings, which would add a lot of weight and defeat the benefits.

In Insects four wings is the default, the groups with two wings got them by transforming one set of wings into something else useful. Wing covers in beetles ,which protect wings from damage, and Halteres in flies which act as a sort of sensory organ to determine position. Two wings are more common numerically becasue those two groups are extremely successful. Basically if you have two of something but one will also work and evolution can turn the other set into something useful then you have a chance to lose one set of that thing. Two wings are more common numerically becasue those two groups are extremely successful. By turning four wings into two those groups ended up with more abilities than their four winged relatives, becasue they did not just lose the wings they turned them into something else.

In insects wings actually evolved from gill covers, insects could have had six wings, why the first set never evolved would be an interesting question. It may be due how HOX genes are expressed in insect segments.

Source


What do biologists mean when they use the term "biological distance"?

Biological distance is pretty much what you'd guess: how closely related are x and y based on genetic (phenotype or genotype) studies?

There is zero biological distance between identical twins. There is extremely little biological distance between family members (for most intents and purposes, none, no matter where they live). It goes on and on in this manner.

  Biological distance, or degree of genetic relatedness, will be assessed by a comparison of dental nonmetric trait frequencies.1

The phrase has been used in Theoretical Population Biology for decades. Back then, they had phenotypes to measure the degree of biological distance.2 Today, actual genetic determination of kinship is possible.

  Biological distance, or biodistance, is the measure of biological relatedness (or divergence) between and within human groups, living and past, based on human skeletal and dental variation.3

1 Dental Variation of Prehistoric Amerindian Populations
from Eastern Tennessee
2 Kinship, information and biological distance
3 Biological Distance in Bioarchaeology and Human Osteology


Can prawns be classified as fish, or is their position ambiguous?

Introduction to phylogeny

What makes that two species being closely related or not has nothing to do with whether they look a like or whether they live in similar environment. It has to do with their evolutionary history. Evolutionary history used to be inferred from phenotypic traits ('phenotype'≈'how an individual looks like') but today it is most often inferred from genetic data.

First you should have a look at this recent answer to get a short introduction to phylogeny.

Phylogeny of animals

Here is a basic tree of all animals

From wikipedia

  A fish is any member of a group of organisms that consist of all gill-bearing aquatic craniate animals.

Craniates are Chordates, therefore fishes are chordates. You can have a look at the position of chordates on the above graph. Note that all mammals, birds, reptiles and others are also chordates. Note that fishes do not represent a monophyletic group (if you don't understand the term 'monophyletic', then you need to read the linked post above).

A prawn is a crustacean. Crustacean (incl. prawns, shrimp, crabs, ...) and Hexapoda together form a monophyletic group. Crustaceans are arthropods and are therefore much more closely related to insects, molluscs and spiders than to any lineage that we would call fish. Here is a tree of arthropods (and related clades). See the position of arthropods in the above tree. You can also have a look at the position of crustaceans within arthropods below. Please note that the tree is a bit outdated a present crustaceans as being monophyletic which is wrong (according @har-wradim, see comment below).

Your discussion with your friend

There is no doubt about the phylogenetic position of crustaceans as being part of arthropods and therefore not being very closely related to fishes. I think you misunderstood what your friend tried to tell you.

A note on developmental biology

All multicellular animals, undergo a grastrulation during development during whihc a hole is formed called the blastopore. In all deuterostomia (incl. fishes) the blastopore becomes the anus, while in prostomia (sister clade to deuterosomia which includes arthropods), the blastopore becomes the mouth. This a very major difference in how these different clades develop from a single cell (after fertilization) to a multicellular adult.

Online ressources

If you want to have a look at the tree of life, you can find great ressources on this post.


What insect is this? Found this at home, India

That is a parasitic wasp in the family, Ichneumonidae. You can tell by looking for a cell in the forewing that looks like a horse head. The "stinger" is an ovipositor. These wasps lay their eggs in the larvae of other insects


What is the purpose of back-crossing mice for multiple generations?

Depending on the exact goal of the experiment, the researchers may back-cross both to smooth out genetic variation between individuals and to potentially normalize expression of a transgene, although once you get past the chimeric stage gene expression should be fairly stable. In my experience, back-crossing allows you to generate a genetically-altered mouse that differs as little as possible from a (generally well-characterized) parent strain, except at the locus of the genetic manipulation. This way, any differences in phenotype can more easily be explained by the knockout/knockin/transgene/what-have-you, and not by any variations in background genetics.

As an example, C57BL/6 mice, being inbred, have a number of well-known mutations, deficiencies, resistances, etc., and for one reason or another have become one of the most popular and most-characterized mouse strains in biology, so there is a great interest in continuing research using a well-known historical model with so much extant experimental data. These mice are quite different from the 129 strain, which are frequently used to make initial genetically modified strains due to the large number of embryonic stem cell lines available, and other technical reasons which allow for the relatively easy generation of transgenics, etc. However, for various other reasons, 129s aren't used as often in the type of studies that BL/6s are, so it's preferable to create the mutation in a 129, then back-cross it onto a BL/6 background. Both of these strains are quite homogenous from one individual to another (each sibling is practically a twin of the next), but once you start breeding 129s to BL/6s you can generate all sorts of genetic heterogeneity due to random cross-overs and all the other things we like to talk so much about around here when it comes to mutations and meiosis. As anyone who has worked with genetic diseases in humans will readily tell you, it can be extraordinarily difficult to nail down specific genotypes that lead to specific phenotypes when there are so many other confounding factors present. Backcrossing a mutant 5, 10, or even 20 or more generations back onto a reference strain is one of the best ways we have at the moment of controlling for all the genetic variations that are introduced when two inbred "tool" strains are bred together.

And now, cute pictures :)

129 mouse

C57BL/6 mouse

both images from Charles River


That whole thing of being more complex is non-sense, you can't say that for animals and you can't say that for plants either. It all depends on how you look at it. Average number of cells? Size of genome? Size of the proteome? Adaptability to different environments? Mental abilities? You can't place human on the top of any of them (maybe we could argue about if you define it as mental abilities but that doesn't sound right) and you can't place amoeba at the bottom either.

Also, if you look at a phylogenetic tree, an organism is also not more complex by the number of nodes it has behind them (I've seen people thinking this means more evolved and associate that with more complex).


Is it possible to temporarily paralyze someone through the use of electric signals or focused ultrasound?

Yes. Those weapons exist, they are called Electroshock weapon, the most famous of which is the taser.

Tasers spill much ink in the media. You have probably already seen their use (and misuse) in videos.


Bacteriophages and their role in genetic editing?

As explained in the Wikipedia page that you have linked to, transduction is the name given to a particular phenomenon whereby phage can be used to move bacterial DNA between cells.

Depending upon the phage, some aberrant or infrequent process can result in the packaging of host cell DNA into a phage particle during a lytic cycle. The resulting defective phage particle is still infective however, and when it infects a new host cell it injects the bacterial DNA that it is carrying. This DNA can then recombine with the host DNA.

So, for example, if the second host was a lacZ mutant but the parent host was lacZ⁺, then it would be possible to select lacZ⁺ in the second host.

Transduction was an important tool in E. coli genetics. Phage P1 can be used for general transduction, which means that any piece of DNA can be moved. As I said in my comment: anything that can happen will happen.


Is a DNA molecule a single strand of polynucleotide or two of them linked together?

Hmm, I think that the teacher is actually correct and that the previous explanation, although very nicely referring to text book diagrams, is a little misleading.

The issue here is the nature of a hydrogen bond within the DNA structure. Within a chemical context, generally a molecule is a collection of atoms primarily bonded together via covalent bonds. Hydrogen bonds, by their very nature are transient - if they weren't then the double stranded DNA wouldn't be able to opened for reading! So, a strand of DNA, from the 5' end to the 3' end is one molecule. The reverse complement strand to this is another molecule of DNA. This is important as if you were carrying out a PCR reaction (for example), you would use single, stranded DNA as primers - so this would be a molecule of DNA. Also, if we were to use hydrogen bonds as a means of defining a molecular species, then water would only be one molecule - all of those H2O molecules interact via hydrogen bonds with each other!

But what about the double helix structure? Well this is a consequence of the chemical structure of each nucleotide (and the chemical properties of those atoms), aided by the hydrogen bonding to tightly pack the atoms together - it's a form taken by the thermodynamics of the inter-molecular interactions between the two molecules of DNA.

So, a strand of DNA is a molecule. Two strands (two molecules) of DNA give us the natural, stable, helical form.


Does precipitation influence the UV spec reading?

The answer to the question as asked is that yes, any precipitate will affect the value that you are reading in your spectrophotometer. The basis of spectrophotometry is that light passes through a sample, and less light emerges than the amount which entered. The amount of light that has "disappeared" is used to deduce something about the solution in the cuvette. Light can be absorbed by chemical groups (this is the basis for e.g. DNA having an absorbance value) or it can be scattered by particulate material (this is the basis for measuring the cell density of a bacterial culture). If you are trying to make a measurement of the first type (absorbance) and you get a precipitate your reading will be distorted by the light scattering effect.

Precipitates are incompatible with spectrophotometry.

As the comments have noted: if you give more details of your protocol someone may be able to help. Phosphates are, of course, notorious for generating unwanted precipitates.


Why would I see no bands in DNA gel electrophoresis of red blood cells?

It is a trick question. Red Blood Cells (RBC) are anucleated in mammals. You are not going to be able to extract anything about chromosome 1 from RBC.

By the way, if you want to know how they got from 29 alleles to 435 possible combinations (in a diploid), you just have to do 29 + 28 + 27 + ... + 1 = 435.


Where do I find standard tissue and cell names?

It turns out that ArrayExpress itself uses various ontologies (dictionaries structured as trees) available at Ontology Lookup Service when it processes users' search queries. Experimental Factor Ontology is the precisely one I was searching for.

Medical Subject Headings (MeSH) dictionary turned out to be handy as well.


Obviously there is an evolutionary advantage for those animals which has a long snout/muzzle. That is why they are still around.

For carnivores the canine is the most important tooth and it is positioned strategically at the front corners of the jaw. Canines are meant to pierce and is essential for holding on to the prey and preventing from escaping. They are also essential for tearing flesh.

Lower jaw or the mandible is a class 3 lever. The lesser mechanical advantage is compensated by the extremely powerful muscles. Since the muscles are closer to the joint or fulcrum the movement produced by the muscles are amplified at the outer end of the jaw allowing for wider opening of the mouth. Since the canines are sharp and long there is enough force to pierce.

Herbivores like cattle and sheep have no canines (horses do have canines). The longer snout/muzzle may help in grazing as it would help in reaching the ground along with longer necks. The longer snout/muzzle means more space for the premolars and molars which can be more in number or larger fro grinding the food.

Crocodiles which are not mammals also have long snouts.

In short the longer snout/muzzle in different animals developed due to evolutionary advantage based mainly on diet.


Why is angiotensin converting enzyme localized in the lungs

ACE is present on the luminal surface of vascular endothelia throughout the body and is abundantly present in the endothelium-rich lungs.

ACE in the kidney—particularly in the endothelial cells of the afferent and efferent arterioles—
can produce enough ANG II to exert local vascular effects.

Thus, the kidney receives ANG II from two sources:

✓ Systemic ANG II comes from the general circulation and originates largely from the pulmonary region, and

✓ Local ANG II forms from the renal conversion of systemic ANG I.

• In addition, the proximal tubule secretes ANG II into its lumen and thus achieves intraluminal concentrations in excess of
those in the general circulation. ANG II in the circulation has a short half-life (~2 min).


Why are males more likely than females to have autism spectrum disorder?

As the father of two sons with diagnoses of ASD, I think that it is best to think in terms of an extended spectrum which encompasses 'normal' people. We are all somewhere on this spectrum, but there is a threshold zone around where we cross from "normal" to "diagnosable as ASD". Now, if the distribution of spectral position for males is displaced towards the ASD end of the spectrum relative to females (because of some aspect underlying "normal' maleness, such as testosterone levels) then any genetic variation which pushes someone towards the ASD end of the spectrum by some fixed amount will tend to push more males over the threshold than females.


Why should I degas my gel solution for polyacrylamide gels?

The reason for degassing your gels is to remove oxygen. Oxygen in the gel interferes with polymerisation, slowing it down and making it less consistent, so degassing makes it faster and more uniform.

From the EncorBio SDS-PAGE protocol:

  Polymerization is quicker and more uniform if you degas the first three solutions for a few minutes in an Ehrlenmeyer flask on a house vacuum prior to addition of the last three reagents. Molecular oxygen inhibits polymerisation by reacting with the free radical SO4- ions, which is actually the reason why PAGE gels are poured in tubes or between plates and not in open top horizontal apparatuses, as can be done with agarose. Also it's a good idea to layer some isopropanol on top of the gel as this prevents oxygen getting in and inhibiting polymerisation.

Oxygen can also lead to oxidation of protein products, which might be crucial if you then want to extract the products and use them for something else (e.g. Sun & Anderson, 2004).

Finally, having bubbles in your gel can distort the results and make them less reproducible, as the bubbles will not form consistently with each repetition and they disrupt the physical medium of the polyacrylamide. So another purpose of degassing is to ensure repeatability.

The Bio-Rad acrylamide polymerisation info sheet has the best info I could find:

  The formation of polyacrylamide gels proceeds via free radical
  polymerization. The reaction is therefore inhibited by any
  element or compound that serves as a free radical trap
  (Chrambach 1985). Oxygen is such an inhibitor. Oxygen,
  present in the air, dissolved in gel solutions, or adsorbed to
  the surfaces of plastic, rubber, etc., will inhibit, and in extreme
  cases prevent, acrylamide polymerization. Proper degassing
  is critical for reproducibility. Therefore, one of the most
  important steps in the preparation of polyacrylamide gels is
  the evacuation, or “degassing” of gel solutions immediately
  prior to pouring the gel. This is done by placing the flask of
  gel solution in a vacuum chamber or under a strong aspirator.
  In some cases, a vacuum pump may be required.

  Buffer stock solutions and monomer stock solutions are usually
  stored at 4°C. Cold solutions have a greater capacity for
  dissolved oxygen. The process of degassing is faster and
  more complete if the gel solution is brought to room
  temperature (23–25°C)‚ before degassing begins.
  Furthermore, if a cold gel solution is placed under vacuum,
  the process of evacuation tends to keep the solution cold.
  Pouring a gel with a cold solution will have a substantial
  negative effect on the rate of polymerization and on the
  quality of the resulting gel.

  Polymerization in which riboflavin is used as one of the
  initiators calls for degassing. The conversion of riboflavin from
  the flavo to the leuco form (the species active in initiation)
  actually requires a small amount of oxygen (Gordon 1973).

  This explains why polymerization initiated primarily by riboflavin
  can be completely blocked by exhaustive degassing. However,
  oxygen in excess of that needed to convert riboflavin to the
  active form will inhibit polymer chain elongation, as it does in
  reactions initiated only by ammonium persulfate and TEMED.
  Thus, while degassing is still important for limiting inhibition,
  it must not be so extensive that it prevents conversion of
  riboflavin to the active form. For polymerization initiated by
  riboflavin/TEMED, or riboflavin/TEMED/ammonium persulfate
  systems, degassing should not exceed 5 min.

  A consequence of the interaction of riboflavin with oxygen is
  that riboflavin seems to act as an oxygen scavenger. This is
  supported by the observation that the addition of riboflavin
  (5 µg/ml) to stacking gel solutions containing ammonium
  persulfate/TEMED initiators results in cleaner, more uniform
  polymerization at gel surfaces exposed to oxygen (such as
  combs). The same effect could likely be achieved by more
  thorough degassing of solutions without riboflavin.

  Whether using chemical polymerization (ammonium
  persulfate/TEMED) or photochemical polymerization
  (riboflavin/TEMED or riboflavin/TEMED/ammonium persulfate
  initiators), reproducible gel quality and separation
  characteristics require careful attention to gel solution
  temperature before degassing, and to degassing time,
  temperature, and vacuum. These parameters should be
  kept constant every time gels are prepared.

Sorry for the long quotes, but they are pasted here in case the original sources disappear.

References:

Sun, G. & Anderson, V.E. (2004) Prevention of artifactual protein oxidation generated during sodium dodecyl sulfate‐gel electrophoresis. ELECTROPHORESIS. [Online] 25 (7‐8), 959–965.


Why am I getting low transformation efficiency with DB3.1 E.coli cells?

How are you storing the cells?  Competent cells can be very finicky.  In my lab, we usually flash-freeze them with ethanol/dry-ice and store at -81 degrees (long-term use) or we store them surrounded by ice at 4 degrees (short-term use).


Isotropy of sarcomere bands in skeletal muscle cells

This is sort of technical answer, but I hope its helpful I hope.

All these bands in the sarcomere are anisotropic.  Isotropy would imply that the structure/properties of something is equally ordered or coherent in all 3 directions.  The sarcomere has definite structure along its longer axis so the H band is anisotropic.

Since the H band is a small structure compared to the actin and myosin components of the sarcomere, much of the signal that one measures via diffraction or polarization experiments is from those two fibers and less information would be discernible from the anchoring portion (H band) of the myosin filament.

In the case of the A and H bands, which are identified by electron microscopy, the structure along the sarcomere axis is not very strong - they are thin sections of the sarcomere and tend to function structurally to connect the actin and myosin axes.

Because of this the information that you might get from A and H band segment studies will be that 'these bands are not very ordered along the axis of the sarcomere'.  That's not a lot of information, and we know this from other experiments.  But it is information nonetheless because they have some spatial organization.


Via deep scientific analysis (i.e. trying it myself 5 seconds ago), I have determined that you can in fact speak while breathing in, it just sounds funny.

Think of the vocal chords as being like the body of a flute. As air passes by them, they vibrate and make sounds. Through careful modulation of their shape, specific sounds can be reproducibly made (this is equivalent to opening and closing the stops on the metaphorical flute). The way the pressure in your throat changes when you inspire (breathe in) is very different from the way in which the pressure changes when you expire (breathe out). These pressure differences are a large part of the reason why you sound different when you speak during inspiration as opposed to expiration, just like breathing into a flute differently would produce different sounds (although potentially the same notes).

Other physiological, neurological, etc. effects probably also cause differences in the vocal cords during expiration/inspiration and thus also contribute somewhat to the differences in the sound.


What is meant by 'topologically continuous' in the context of cell compartmentalisation?

What "topologically continuous" appears to mean in this context is that materials can flow between them.
So far as I am aware, this is not a well-defined mathematical term, which is part of what makes this confusing. In topology, some spaces are continuous and others are not, but the meaning of "continuous" in topology is rather more general than the authors usage here.


I am pretty sure that it is a moldy core rot which would be caused by a fungus that infects the apple during the flowering stage. The fungi is also referred to as "apple fuzz".

From SF Gate

  fungus sometimes does enter apples at the blossom end and damage the core, especially if weather is wet, a condition called "moldy core,"

From PennStateExtension

  Moldy core is caused by several different fungal pathogens. Many cultivars of apples are affected, including Delicious, which is very susceptible. Moldy core may develop into dry core rot if the pathogen penetrates into the core flesh, but the fungus is generally restricted to the core or carpel region.

The Disease cycle

  The moldy core fungi colonize the flower parts as soon as the blossoms open. The fungi then enter the developing fruit through an opening in the calyx. Moldy core is primarily a problem during years with light fruit set or when dry weather in early summer is followed by heavy rains in late summer. In addition, wet weather during bloom may cause conditions favorable for the fungi to produce spores.

What kind of fungi is it?

Mycelium

Geographical range

The fungi is mostly found in the apple sorts “Delicious” and “Idared”. Idared's origin is from Idaho, and delicious is originally from Iowa, USA.

Is it dangerous to my health?

Not more dangerous than usual mold would be to your health. You can find more information here. On some forums online I read about people consuming the white fuzz, and did mostly not complain about any problems. However, I read about one case where the fungi evoked an allergic reaction.

Picture

Further reading

Principles of Forest Pathology page 558


Does biofuel production by microalgae need an extra source of CO₂?

Maybe this is easiest understood comparing to our current rate of CO2 consumption to the possible industrial CO2 absorption rate.

Human non biological CO2 production is 29 Gtons.  A little more than four tons of carbon per human being each year.  The natural carbon cycle on the planet through CO2 is otherwise about 788 Gtons.

Is it possible to grow enough algae to balance our current rate of industrial production? I think so - it would be an additional 2% of the current carbon cycle.  In a first pass, that implies turning 2% of the non-productive earth surface into an average patch of ocean or forest/jungle.

This is possible, but it would be expensive.  we're talking about flooding a desert basin for algae production. (numbers are from google).

2% * (area of earth surface = 197million miles^2) = 3.9 M miles^2.

Sounds doable, but remember that 70% of the earth's surface is already water and producing algae at a pretty good clip.  We'd be using ~6% of all the land for the algae farm:

For comparison,  3.9M miles^2 is larger than the continent of Australia.  (2.97 Million miles ^2), and bigger than the Sahara desert (3.6 M miles^2).

just to get into the questions raised in the comments.... To DEPLETE the CO2 level in the atmosphere, we'd have to produce more fuel from the algae than we use - which seems to be impractical from a market standpoint - the fuel would be sitting around in warehouses while the plants die.  I can't imagine anyone making any money from this, and it would be expensive... so it'd be a strange set of circumstances that would deplete the atmosphere from carbon dioxide.  Also more oxygen probably would encourage more combustion and more animals too... so hard to see this happening.


Bio-fuel efficiency as aviation gasoline

The term biofuel refers both to the source of the fuel, as well as (currently, at least) the compounds contained in it. If the production quality is strictly controlled, eventually there should be no detectable difference between a fuel mixture derived directly from biological sources, and one derived from petroleum products (which, technically speaking, are of biological origin themselves, just a few million years removed). However, due to technological limitations, biofuels and petroleum-based fuels do have different chemical components today.

The reason we hear of differences in mileage or "energy density" in biofuels used to power automobiles as compared to gasoline/petrol is because they are not the same mixture of chemicals. This page goes into detail (the whole site is actually quite clear with its explanations), but the basic difference is that petroleum products are essentially 100% hydrocarbons (only containing hydrogen and carbon atoms) while nearly all biofuels contain oxygen as well, which has numerous effects on the fuel's physical and chemical characteristics, altering everything from polarity to reactivity to stability over time to the types of byproducts (and pollutants) produced during combustion.

There is much more to the story, but the basic answer to your question is yes, biofuels could replace petroleum-based products for aviation and many other types of fuels, and not impact the maximum speed of the aircraft. It may require engine modification, and the energy density may not be exactly the same (possibly reducing range), but for the long-term health of our planet we MUST reduce and eventually eliminate our use of petroleum.

By the way, the Aviation or Chemistry StackExchange sites would likely be able to provide you with much more in-depth answers, as ultimately this question is better suited to either or both of those sites than Biology, which would be more concerned with the production of biofuels by living organisms.


I'll kick this off with an attempt at a definition: a selection regime is

the set of selective pressures on a population

As in, "alteration of selection regime resulting from harvest" (Mooney & McGraw 2007)

or "Human-induced nutrient input can change the selection regime and lead to the loss of biodiversity. For example, eutrophication caused speciation reversal in polymorphic whitefish populations through a flattening of littoral–pelagic selection gradients." (Hirsch et al 2013)

 Hirsch PE, Eckmann R, Oppelt C, Behrmann-Godel J. 2013. Phenotypic and genetic divergence within a single whitefish form - detecting the potential for future divergence. Evolutionary Applications 6: 1119–1132.
 Mooney E, McGraw J. 2007. Alteration of selection regime resulting from harvest of American ginseng, Panax quinquefolius. Conserv Genet 8: 57–67.


Why do plants store energy as carbohydrates and not as fats?

The question was:

  Why would plants store their energy as carbohydrates and not as fats, if fats are a more efficient energy store?

But before trying to answer it you have to be quite clear what is meant by efficient. Without qualification this term is meaningless. A little reflection will tell you that whatever positive properties are implied by ‘efficiency’ may have different importance in relation to the very different modes of existence of animals and plants. One will also want to test any explanation on the exceptions — the instances where animals store carbohydrates (generally polysaccharides) and plants store fats. With this in mind I argue as follows:

1. Carbohydrate is the straightforward solution

Plants synthesize glucose from carbon dioxide, animals take in carbohydrates in their diet and break them down to monosaccherides. Hence, storing excess as polysaccheride (glycogen in animals, starch in plants) involves developing and using a relatively simple polymerization/depolymerization system. One would therefore assume it to be the default. The question is then, “in what circumstances is it advantageous to store surplus as fat?”.

2. Fat is a more concentrated energy store, so is used to minimize weight

Dull eh? But that’s the answer. The following extract from Berg et al. explains this clearly (triacylglycerol is the chemical name for triglyceride or fat):

  Triacylglycerols are highly concentrated stores of metabolic energy because they are reduced and anhydrous. The yield from the complete oxidation of fatty acids is about 9 kcal g–1 (38 kJ g–1), in contrast with about 4 kcal g–1 (17 kJ g–1) for carbohydrates and proteins. The basis of this large difference in caloric yield is that fatty acids are much more reduced. Furthermore, triacylglycerols are nonpolar, and so they are stored in a nearly anhydrous form, whereas much more polar proteins and carbohydrates are more highly hydrated. In fact, 1 g of dry glycogen binds about 2 g of water. Consequently, a gram of nearly anhydrous fat stores more than six times as much energy as a gram of hydrated glycogen, which is likely the reason that triacylglycerols rather than glycogen were selected in evolution as the major energy reservoir. Consider a typical 70-kg man, who has fuel reserves of 100,000 kcal (420,000 kJ) in triacylglycerols, 25,000 kcal (100,000 kJ) in protein (mostly in muscle), 600 kcal (2500 kJ) in glycogen, and 40 kcal (170 kJ) in glucose. Triacylglycerols constitute about 11 kg of his total body weight. If this amount of energy were stored in glycogen, his total body weight would be 55 kg greater.

The animal exception — glycogen

A limited amount of fuel is stored as glycogen in animals. The increased weight load is offset by the advantage of rapid mobilization and the fact that glucose is obtained (animals cannot convert fatty acids to glucose).

The plant exception — oils in seeds

Plants do not walk around, so weight is not generally a consideration that would induce them to store their reserves as fat. They can develop large tubers under the ground, for example. However there is an advantage to minimizing weight in the energy reserves required for the development of seeds — it allows for easier spreading in the wind or through animal consumption. Thus one can rationalize why the energy reserves in seeds are oils (lower melting point triglycerides on account of their greater unsaturation).


Test of antibiotic A for sensitivity as surrogate of antibiotic B

This is not a proper answer as such and it's based on a bit of an 'educated guess' but it was too long for a comment.
I did however, find this article. Unsurprisingly, one of the big drivers of using surrogate antibiotics is down to availability and cost. Some antibiotics, while known about, may not be produced commercially at scale, or be widespread enough for testing facilties around the world to use. Consequently, the WHO can maintain a list of antibiotics with complementary 'cross-talking' modes of action, so that a resistance mechanism can be probed without needing the specific antibiotic.
Another reason for using a surrogate might be to avoid some of this cross-talk. I.e., if you wish to know the effectiveness of (say) imipenem, and you know imipenem and meropenem have the same mode of action, but perhaps the bacteria has a second resistance pathway that  is specific for imipenem - you could use meropenem as a surrogate, knowing that it won't be degraded/removed by pathway 2, and you can still probe the mode of action.*
*(This is a contrived example, I have no idea if you'd ever use those 2 antibiotics in this manner.)
It seems like, from reading online, the real drivers to use surrogate testing however, are purely as an interim measure due to the enormous lag phase between discovery of new drugs, testing, scale up, administrative approval, and then general market availability.


Okay, to identify to Order level you can use the key here (although it's actually not as user-friendly as I'd expect; I might suggest they revise it). The key characteristic is that the forewings are uniformly hardened. So, starting at question 1:

"Insect has wings" - yes; go to 2.
"Two pairs of wings" - yes (wing cases/elytra are the first pair); go
to 7.
"Fore wings hard or leathery" - yes; go to 8.
"Fore wings of uniform texture throughout" - yes; go to 9.
"Fore wings (elytra) hard and veinless, meeting in centre line" -
yes; go to 10.
"Abdomen without forceps: elytra commonly cover whole abdomen =
Coleoptera [beetles]".

So we know it's a beetle.

There's a key to beetle families here. Starting at question 1:

antennae are "clubbed or thickened" so go to 5.
"Elytra covering all of abdomen" yes, go to 7.
"Head not stretched forward into a beak" - go to 9.
"the last few segments [of the antennae] clearly wider than the rest" - no, so go to 24.
the elytra (wing cases aren't "soft (easily bent, folded or even
rolled up)" so go to 28.
this is a tricky one, but basically you can (just) see that all the tarsi (feet) have the same number of segments, so we go to 29.
29: "      Beetle usually elongate and parallel-sided; antennae very long often longer than head and body; most antennal segments very elongate (at lease twice as long as wide)" - sounds like our beetle, so that makes it a longhorn beetle. (Some of the other criteria - eye nothces etc - only apply to some species, but this key is a UK-specific one).

So we have a longhorn beetle (Coleoptera: Cerambycidae). In theory you shouldn't need to geographical location to get this to species level as it could be an introduced species etc; in practice most keys are specific to certain geographical regions so you might need to provide the collection location to get it to species level. You could start by Googling "longhorn beetle identification key" and give it a go though.


How does the brain alter/inhibit muscle reflexes?

how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

A: At multiple places within a hierarchical system:

In a  simplified way, the Motor cortex is the executor of movement via projections to the brain stem and spinal cord, this is accomplished via excitatory signals to a muscle, the agonist, and inhibitory signals to the antagonist, so in one sense, spinal interneurons would be the answer, since they interface with the motor cortex and alpha motor neurons at the muscle site.

There are also feedback loops all over the motor hierarchy, premotor and supplementary motor cortex regions for instance help plan the movement direction, we don't seem to code a target in the strict sense, but rather a movement direction and then correct via sensory feedback.

The cerebellum projects to premotor, motor cortex and the brainstem, and receives projections from premotor areas, it is involved in stopping and timing movement,the brakes for action if you will.

The circuitry of the Basal Ganglia  which loops with premotor and projects to the motor provides the go, no go and graded modulation via inhibition to the motor cortex, which in turn affect less spinal interneurons, so in another sense this circuitry would be responsible.

  Can it alter the weighting of inhibition in antagonistic muscles?

Yes, via spinal interneurons (Henshaw cells, Ia inhibitory interneurons and Ib inhibitory interneurons)

  As well as 'set the length' for a stretch reflex to target?

Yes, via a the motor,basal ganglia,cerebellum motor hierarchy, although as mentioned, there is no target but rather a direction vector and feedback that tells you when to stop the movement, i.e. you reached your target. ( Higher cognitive areas do seem to have a representation of the target though).

  Or does it somehow control both 'with one value'.

Depends on the interneuron, but basically they serve as information relays ( they also convey sensory information )

  Where and how exactly does it interject into the feedback loops?

As mentioned there are multiple feedback loops, the brain is not a unit, but a system and as such I would rephrase the question as which subsystems, brain regions, neuronal tracts and neurons create feedback loops in the motor system.

  I am trying to understand it more from a programmers pseudocode

I am a software developer myself, so let me try switching hats, this is one scheme:

If all you want is to control agonist/antagonists, tie up 2 or more variables together such that when one goes up, the other goes down, and presumably change 2 effectors ( virtual or real ) and their position relative to each other,

If you want specific control, you would then need to send 2 channels of information and modulate both variables, if you just send one to either one, the other will respond based on the above configuration.


Why is polyploidy much more common in plants than in animals?

Polyploidy is common in plants than in animals because in animals sex determination mechanism involves number and type sex chromosomes. Polyploidy will interfere with this mechanism and hence it is seen rarely in animals. I believe its probably because an animal progeny with multiple sex chromosomes won't be able to reproduce more of its kind unless it can also reproduce asexually (which is seen in plants as mentioned below).

Plants, on the other hand do not have any such sex determination (based on number or type of chromosomes) and majority of them can also reproduce vegetatively. This vegetative propagation enables multiplication of polyploid plants. Sexual reproduction will result in loss of desired polyploidy as per the principle of segregation. However, if a polyploid plant can produce a viable progeny sexually, it might have a different ploidy than its polyploid parent which won't happen if the parent reproduces asexually. Hence, polyploid plants can be classified as sterile and fertile polyploids (the reference will give a detailed account on this mechanism).

Refer the section of Polyploidy (page 115, Chapter 6) of this book (Principles of Genetics, Snustad and Simons, 6th edition)

When it comes to gene dosage, animals do show gene compensation of X-linked genes by various methods. Example- formation of Barr Body in human females (Note that this has nothing to do with polyploidy, but happens since females have one X chromosome more than males). Whereas gene dosage in polyploid palnts has been exploited for improved agricultural yields as they have shown better productivity than their diploid couterparts.


Concept of mean systemic filling pressure

You've misread the linked article if you take this to mean there is some place that is unaffected by cardiac activity. It's just that there must be some place that is equal in pressure to the MCFP. The actual position fluctuates throughout the cardiac cycle.
The reason, though, that some place must be equal to MCFP is that pressure is continuous. Somewhere in the vasculature (i.e. proximal arteries) is definitely greater than the mean; somewhere else (i.e. proximal veins) is definitely less than the mean. Because the pressure varies continuously the function must pass through the mean at some point along the vascular path. This isn't anything special about biology, just mathematics.


Does amylolysis occur in vegetables if stored below 0⁰ Celsius?

Yes. Freezing would practically stop all biochemical reactions. Household freezer can maintain -15⁰C so that would work. However, freezing also damages the cells if cryoprotectants are not used. But I guess that is not your concern.


It almost definitely wasn't 10 inches, but there are some pretty big spiders in Mexico. There is a species of spitting spider with a 9 inch legspan but it lives in South America not Mexico.
Scytodes globula

The cellar spider has a legspan of up to 3.6 inches and a comparatively small body with long skinny legs and no visible hair, but I can't see how that would be confused for 10 inches.
Pholcus phalangioides

The giant crab spider fits that description to some degree. It has a legspan of up to 4 inches.
Heteropoda venatoria

The golden silk spider is very large with long skinny orange and red legs.
Trichonephila clavipes


Pink individuals of the katydid species Amblycorypha oblongifolia are a relatively uncommon but natural phenomenon with a long history of research.

It looks from popular press accounts (Science Friday, Scientific American) that the pink coloration may be caused by a dominant allele, and is only rare because of a high selection pressure against pink individuals (i.e. they're much less good at hiding among leaves, and are eaten before they can reproduce).

Photo by Richard Whitby, via flickr.com/blueboat2 (cc-by-sa 2.0)


Coalescent theory - independence of coalescent times

As long as members of a generation "randomly choose" their ancestor in the previous generation the law of independent probability (your equation) will hold.
Any study of coalescent theory begins with the Wright-Fisher model. The assumptions are:

finite diploid population of constant size N,
non-overlapping generations (simultaneous reproduction),
random mating,
no mutation, selection, or migration.

These assumptions are consistent with independent non-identically distributed waiting times. An example of an assumption under which independence no longer holds:
Individual B's random choice in generation 2 of ancestor A in generation 1 reduces the probability that individual C in generation 2 will choose A. In other words, the likelihood that A will give its genes to the next generation falls off with each new recipient. Then the independence no longer holds.
See, e.g., Deonier, Computational Genome Analysis (2005, Springer) at pp. 392 ff.
J. Wakely's paper Coalescent Theory: An Introduction (Systematic Biology, 58:1, Feb. 2009) may be one of the best overviews of this immense topic available. He mentions Kingman's 1982 mathematical proof (which I haven't gone through) of the coalescent process (Stochastic Processes and their Applications 13 (1982)--available as a free download from ScienceDirect).


How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?

It is useful to think in terms of the proportion of genetic material that an individual gets from each parent and the amount of this genetic material that will be shared with another individual (on average), and then sum this together i.e. as:

$ relatedness = prop_{mother} * shared_{mother} + prop_{father} * shared_{father} $

A female will share 50% of the genetic material from the mother's side and 100% if the material from the father's side with her full sisters: $0.5*0.5 + 0.5*1 = 0.75$

A female will share 50% of the genetic material from the mother's side and 0% if the material from the father's side with her brother: $0.5*0.5 + 0.5*0 = 0.25$

A male will share 50% of the genetic material from the mother's side with his sister (and doesn't get any from the father's side).

A male will share 50% of the genetic material from the mother's side with his brother (and doesn't get any from the father's side).

Remember also that this only holds if the female has only mated once.


There's this database of genetic/drug interactions, which I think is pretty much exactly what you're looking for.

Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'.

Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way.

Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.

There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.

There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.

Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.

There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.

Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.

In the miscellaneous category:  Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the EPR effect, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic.

It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.

The preparations/solvents of chemotherapy agents can also be significant. Cremophor was used to suspend some anticancer drugs, but recent developments imply that might be on its way out.


What is the role of tracrRNA in CRISPR-cas9?

Your two questions are related and you are correct in your supposition that the Cas9 protein associates to a specific RNA sequence. That of the tracrRNA processed with the crRNA into a gRNA. This is achieved without any other aid so could be considered to  do so automatically. How specific the tracrRNA sequence needs to be is an interesting and often overlooked question.

When comparing tracrRNA from different species it is clear that there is not a lot of sequence conservation but they are predicted to be contain similar secondary structures.

Matching tracrRNA and Cas9 from closely related species does result in in vitro DNA cleavage but this does not work with more distantly related species. Nevertheless they are remarkably versatile and this has been exploited in a number of exciting genome engineering applications where additional structures are added without compromising the binding of the RNA to the Cas9.

The tracrRNA and the crRNA together form the gRNA which targets the Cas9 protein to the location of cleavage. In the endogenous bacterial systems the gRNA takes the form of a processed RNA duplex but in the genome editing implementations this takes the form of a single chimeric RNA with the two components already fused together.

When it comes to actual cleavage of DNA it is important that the Cas9 is in the correct conformation and changes in this are known to occur when binding to the target DNA. Recent work suggests the tracrRNA plays a role in maintaining the Cas9 protein in an active form allowing it to be able to target DNA.

It likely also contributes to the overall stability (and thus efficiency) of the CRISPR-Cas9 complex.

Ultimately the tracrRNA is an essential component of the CRISPR-Cas9 system via it's role in both guiding the Cas9 protein to its target and aiding it's function.

The following references might be of interest to you:

The tracrRNA and Cas9 families of type II CRISPR-Cas immunity systems

Guide RNA engineering for versatile Cas9 functionality

Structural roles of guide RNAs in the nuclease activity of Cas9 endonuclease


The technical answer is: Because the coloration of skin and hair is done by the two forms of melanin: Eumelanin, which is dark brown to black and Pheomelanin which is yellow to red. This enables colors from white (not pigmentation) to black (dense eumelanin pigmentation) and also colors in between by different ratios of the two pigments.

The evolutionary answer is that it obviously made no evolutionary advantage to have other colors. If you look closer at this, you will see that most habitats are not green or only for a part of the year. If you think about african plains, these are mostly brown, something like artic landscapes are only green for a very short timeframe in the summer, for the rest of the year these are white to brown. And even tropical rainforests are mostly dark to brown on the ground. They would clearly stick out of the environment with green colored hair.

For all these different habitats the animals living there have adapted their hair color. It is not uncommon for artic animals to change their hair color with the course of the year, dark to brown in the summer and white in the winter (artic foxes and snow hare) for example. Animals which live in deserts will have a paler color than those which live in dark colored mountain areas.

See this article for more information: "The Adaptive Significance of Coloration in Mammals"

Also interesting in this context is this article which looks at the reason for zebra stripes: "The function of zebra stripes"


How does a cell create/gain its initial ribosomes for protein synthesis?

From the comment section:

Cells divide and when they do the two daughter cells will not only have copies of the DNA but also of the organelles, the cellular machineries and the cell membrane which implies that yes the daughter cells receive also ribosomes. The replication happens during the interphase.


What is this plant with pink flowers and maple tree shaped leaves?

It's a Japanese Anemone (Anemone hupehensis); if I had to guess, I'd guess it was the cultivar "Robustissima".

I used to grow these when I had gardens. Absolutely you can divide them! Wait until the spring if you can; if you have to divide in the fall, wait as long as you can to do so.


Reason for the source of fetal bovine serum

The reason fetal bovine serum (FBS) is used is because it supports a wide variety of cells and really supports their growth.  It has a high concentration of growth factors, but also a low concentration of antibodies.  So it promotes growth in almost any cell or tissue type without also having antibody reactions with it.

Adult cows blood will have the opposite concentrations, higher levels of antibodies and lower levels of growth factors as they have already grown.

There are currently several research projects looking for a alternative or synthetic FBS, but nothing has worked as a total replacement.  There are a few substitutes for specific purposes, but nothing with the diversity of uses that FBS has.


How difficult is it for wild birds to find food?

If you live in the Costa Rica rainforest then your parrot may be better off living outside in the jungle.If you live in downtown New York City then your parrot is better off living inside with you.Starvation , predation and accidents(especially in urban areas) are three main causes of early death in many species.


Is end-systolic volume (ESV) the same as residual volume?

The ESV is the residual volume of blood remaining in the ventricle after ejection.
It is the minimum volume of blood in the ventricles (residual volume).
Note that you can also have residual volume of air in the lungs after exhalation.


Why does a tumour's genome change depending on the environment?

Tumor cells can have very unstable genomes, as much of the error repair machinery is damaged or missing. Since the cells are rapidly dividing and the DNA gets duplicated each time a cell splits, more and more mutations accumulate as the tumor grows and metastasizes. Just like in evolution as a whole, mutations that are either neutral or help the cell survive better in its environment are kept, whereas cells that develop deleterious mutations (perhaps killing the cell outright, making it more visible to the immune system, or just giving it a growth disadvantage as compared to neighboring cells) either die out or get outnumbered by other cells. This is why, over time, tumors can become resistant to therapies intended to kill them, as their cells accumulate mutations that help it evade the treatment and keep growing. There may be a disadvantage that the cells might grow more slowly than the original ones, but since the original ones were killed by the treatment, the resistant ones survive. So, this means that a tumor is rarely homogeneous, with all the cells having the exact same genome. Deep sequencing using next-generation methods is being used to gather information on all the different mutations throughout a tumor, which can help doctors learn which mutations are most common and prescribe patient-specific combination therapy which can kill all the various cell populations at once.

So why are metastatic and xenografted tumors different from the parent? Metastases can arise from single cells or very small clumps of cells, and xenografts are generally made with very small pieces of tumor, so both may start with a different set of mutations than is common in the original tumor. As they grow and divide, as described above, they will become different from their parents. The surrounding environment definitely affects this: the amount of oxygen present, degree of vascularization and blood supply, number and kind of immune cells present, etc. With all these and more factors, a metastasis or xenograft will evolve differently than its parents.


Is there any way bicondylar/bigonial, bizygomatic or bitemporal breadth can change in adults?

Acromegaly (pituitary gigantism) is a disease that causes enlargement of the bones of the face.  There is interest in computerizing facial measurements to catch subtle enlargements and prompt testing for the disease.

https://www.researchgate.net/publication/261409008_Three-dimensional_facial_analysis_in_acromegaly_a_novel_tool_to_quantify_craniofacial_characteristics_after_long-term_remission

  Sixteen patients in remission of acromegaly for over 24 months (50 %
  male, mean age 56.0 ± 10.7 years, mean body mass index 29.3 ± 5.5
  kg/m(2)) were compared to 16 matched control subjects. A 3D cone beam
  computed tomography scan and 3D stereophotograph of each individual
  were acquired and analyzed using 3D cephalometry. In addition to an
  accurate quantification of the classical craniofacial characteristics,
  3D cephalometry, shows that many typical soft tissue deformities
  persist, even after long-term remission. Furthermore, we found that,
  compared to controls, the patients in remission of acromegaly have a
  wider face at the level of the zygoma and longer maxilla (p < 0.05)

Apocryphally, enlarging hat size goes along with acromegaly.

Pagets disease of bone causes enlargement of the skull and also an increase in hat size (so bitemporal dimension); the hat size increase was one of the chara eristics first described in the disease.

Thalassemia is a group of blood diseases characterized by ineffective red blood cell production.  The body compensates by making more marrow anywhere it can.  Some people wind up with expanded bones in the skull or maxilla as a result.

https://www.slideshare.net/ismahharon/thalassemia-is

These are all systemic diseases that affect the bone.  Of course one can have a tumor of bone (primary or metastatic) that expands it and changes the shape of the face or the head.


Are humans not sexual dimorphic? Can genetic XY but SRY not expressed become pregnant?

If you're asking if humans are a sexually dimorphic species, the answer is "yes".
If you're asking based on the viral response of the science teacher, then the answer is still, "yes".  What is described above are chromosomal abnormalities, or other disorders of development, but they are still describing sexual dimorphism in the phenotype. However, the answer itself is incomplete, as it's written out of political motivation.
Whilst true that a person can present, phenotypically, the opposite of their genetic sex, this isn't akin to them "being male/female" counter to their allosomes.  Of course, this in itself can prove to be a contentious issue - how is sex defined?  Under normal circumstances, phenotype is the obvious way of knowing. If someone has the external genitalia of a male, they can be assumed to be male, and vice-versa for females.  When it comes to chromosomal abnormalities, there is an "error" in devlopment, where the genotype is not properly expressed in the phenotype, and so while presenting as one sex, the "true" sex as determined by the genotype is the opposite.  It should also be noted that sexual characteristics can be ambiguous certain cases, creating abnormal sexual presentation, such as in hermaphroditism/pseudohermaphroditism, or "intersex" (the quote mentions 5-alpha-reductase deficiency, which is associated with male pseudohermaphroditism).

The problem with the quote above (at least in the way it is written) is it appears to suggest that chromosomes have little to do with phenotype, as in sex determination, and that this carries over to gender dysmorphic patients.  These are both mostly false.  Gender dysmorphic patients generally do not have any allosome abnormalities, and the reason that the given examples are deemed "errors" (eg XX male syndrome; 47,XXY) is because that is what they are, as well as being rare.  The typical effect of these problems is that the patient is infertile, (i.e. they are not sexually functioning, and have reduced biological fitness).

In short, the teacher is correct in the examples used, but overstating them with regard to the general population, and with regard to transphobia and gender dysphoria.  Humans are indeed sexually dimorphic but as with any complex biological system, errors expressing genotype can occur.


Do all parts of a plant contain the same type of cell?

The diagram shows an exemplary plant cell . Except for the raphide/druse crystals, which I do not know, all of these components are definitely present in every plant cell. Do note that this diagram is only an example and while it describes the basic components present in the cells, details can vary, since plants can have highly specialised vacuoles or plastids (like chloroplasts) in special cell types.

As @AlanBoyd pointed out, there are some specialised cases like the Sieve Tube cells, that do not have a nucleus. But in your average cell, you should find all of the components described in the diagram.

The differences between cell types are typically caused by the expression of different genes, that change the behaviour of each cell, and not directly by a change of how the cell is build up.


What did the ancestors of textile moths eat?

Modern textile moths actually eat a wide variety of material, including fur, feathers, shed exoskeletons, bran, and grain. humans just pay more attention to them when they eat textiles. They prefer human handled material because we tend to create larger concentrations than occur in nature.

if you are interested in changes in biology in response to humans you may want to look at starch digestion in dogs, nylon eating bacteria, and body lice.


What happens to the complementary base when the other undergoes a base substitution mutation?

Consider a stretch of DNA

A T C C T C
T A G G A G

Let's say that during replication a nucleotide get switched

A G C C T C
T A G G A G

Now, this does not work. The cellular machinery will find this location and try to solve it. It will either resolve it as

A T C C T C
T A G G A G

and no mutation would have happened. Or it will solve it as

A G C C T C
T C G G A G

and a mutation just happened.

You might want to read about DNA repair mechanisms.


As a preface, this isn't a comprehensive answer for everything. As MattDMo points out, some of the original answer was poor in it's presentation. In my update there's some supporting information to some expert testimonial, but this is mainly targeted at adult cases rather than pediatric cases, i.e. why would cardiac cancer be rare in an adult with no prior history of cancer. There's a reference #5 at the bottom which goes into some of the genetic conditions that result in rhabdomyocarcoma.
Cardiac muscle cells do not divide particularly often (though they may divide: Evidence for cardiomyocyte renewal in humans). This would be a good mechanism of resistance of heart tissue to a more typical or rapid cancer development, compared to say, the endothelium of a vessel or an interstitial/connective tissue cell. Not to say heart tumors are impossible, either, as rhabdomyocarcoma is a good example of a cardiac tumor. Moreover, here's an excerpt from this article on heart cancer:

“There’s not a lot of fatty tissue [in the heart],” Gaynor said. Even more, “the heart’s enclosed in a membrane,” he explained. Known as the pericardium, this fluid-filled sac may itself become engulfed by cancer, with tumors metastasizing to the outside of it, but still it does its job of protecting our precious hearts.
So, even though cancer can happen anywhere there are cells, your heart remains virtually immune due to its muscular nature and the assistance of the pericardium. Smart heart.

And then from Cancer Prognosis: Role of BMI and Fat Tissue,

Many prospective clinical trials have linked excess body weight—typically represented as a BMI of 25kg/m2 of body surface area or greater—with a higher risk of development of cancers, including postmenopausal breast cancer in women and esophageal, colon, pancreatic, endometrial, and kidney cancers in both sexes. The number of obese Americans will increase by an estimated 65 million by 2030, increasing cancer diagnoses by 500,000 (Lancet 2011;378:815–25).

So fat content has it's role in progressing cancers, determinately. Let's explore this part. The adipocyte isn't simply a storage for fat, it has it's own host of proteins it produces and secretes. In obesity, the adipose tissue becomes dysregulated in it's secretion of adipokines [1]. The book Adipose Tissue and Cancer by M. Kolonin, the author notes that two major adipokines, leptin and adiponectin, play a major role in tumorigenesis by induction of cell survival and proliferation pathways [2]. Also duly noted, increased circulating insulin and insulin-like growth factors due to insulin resistance results in mitogenic effects on tumor cells.
White adipose tissue has been shown by Pedro et al. to increase bioavailability of sex hormones such as estradiol, through increased aromatase activity and  "increased insulin and bioactive IGF-1 levels which downregulate the concentration of the circulating sex hormone-binding globulin, resulting in an increased fraction of bioavailable estradiol, but decreased testosterone production." The same study has a section on inflammation induced by adipose tissue in section 3.2, the entire article is rather long but they sum up some of the information into a figure,

Source: Pedro et al.
Generally speaking, and in reference to the expert testimonial above from Dr. Gaynor, the heart isn't a very fatty organ, and it's protected from the surrounding adipose tissue by the pericardium. You could also argue that the fast flow of blood through the heart would leave a smaller fraction of circulating tumorigenic molecules for ready uptake by cardiac cells.
Being said, and while I haven't any data for the molecular pathogenesis for cardiac tumors, nondividing epidermal cells have been shown to enter a proliferative state in response to inflammation [3]. We also see that adipokines have been implicated in heart disease due to pro-inflammatory effects [4]. My concession here is that the rarity of cancers in adult cardiac muscle cells is because this process is very slow, and it's aided in part by the sort of environment the heart finds itself in. We often see cases of cardiac tumors in children due to errors in development [5].


How prominent is the gene-centric view of evolution among professional researchers?

What do you mean by gene-centric view of evolution

I am not totally sure you know what really means the gene centric view of evolution. Everybody agrees that selection (also) acts on genes and that selfish genetic elements exist. I think that what one calls the gene centric view of evolution is nothing but the modern synthesis of evolution (following the work of Ronald Fisher, Sewall Wright and some others such as Motoo Kimura).

Or maybe by gene centric view you refer to the concept of level of selection.

Some people however argue that because of the gene centric view of evolution, we tend to underestimate the importance of some parameters in evolution and some are willing to rename the evolution theory into Extended Evolution Theory according to new insights about how parameters such as developmental bias for example influence the evolution of populations.

Modern snythesis of evolution theory

You will find more information in this recent article that you may appreciate reading if it is not too complicated. I personally endorse the "No, all is well" opinion. It is important to understand that those who criticize the gene centric view in this article are NOT saying that selection do not act on genes neither that selfish genetic elements do not exist (thinks that R. Dawkins talk about in his books). They totally agree with those things. They just argue that the fisherian view of evolution in not enough and that according to recent findings we may want to rename our theory. The "no, all is well" opinion totally agrees with the importance of these new insights that do not come from what one may call the gene-centric view of evolution but they just don't think it is worth renaming the theory for that because our knowledge in evolution is just growing as it has always been growing and it doesn't seem that we are currently living a revolution in our understanding of evolution. I think that the main revolutions that happen to occur in evolution these days mostly have to do with the methodology of testing rather than with the theory itself. These revolutions have to do with increased computer power, better statistical methods and faster and cheaper sequencing.

Level of selection

Now, by gene-centric view of evolution you may refer to the concept of level of selection. To my knowledge everybody agree that selection occurs at different levels. Again, NOT everybody agree on the relative importance of selection acting at different level. The vast majority of research focus at evolution at the gene level, sometimes implicitly only.

To conclude, we all agree on the theoretical principles (I think) but not everybody agree on the relative importance of the different mechanisms. In saying this, I don't mean that everybody agree with everything that is written in R. Dawkins books!


How can one identify an organism from its dissymmetry ratio?

It depends what lineage (bacteria, virus, eukaryotes) you are interested in and what level of accuracy you are hoping to reach.

We know the (A+T)/(G+C) ratio for a handful of eukaryotes only. So if you were thinking about eukaryotes, there is no need to look much further. You cannot match a (A+T)/(G+C) ratio to a species because we don't know the (A+T)/(G+C) for the vast majority of species.


What is this white/translucent with brown back, larva/worm creature I found, in the UK, on my lettuce?

It's a kind of hoverfly larva (don't know which one, maybe Episyrphus balteatus), they eat aphids on cabbages.

Image on wiki commons


To which distinctions does the term "hymenoptera" refer?

I don't have a definitive answer, but I suspect Hymenoptera is "just a name," albeit a name that has lasted through the phylogenetic nomenclature revolution.

Hymenoptera was erected by Linnaeus in the 10th edition of Systema Naturae (1758). The description of Hymenoptera (membrane wing; p. 553 [hope your Latin is better than mine]) follows that of Lepidoptera (scale wing) and Neuroptera (net wing) and precedes Diptera (two wing).

Classical taxonomy, which Linnaeus was more or less inventing at the time, was based on shared similarities. Those insects which Linnaeus thought more similar to each other than to other insects (e.g., ants, wasps, bees) all shared the characteristic of having a membrane based wing. The scaly wings of moths and butterflies made them more similar to each other.

He needed names for these groups, so he chose logical ones based on outward appearance of the wings: scaly, netted, membranous, or paired. That fact that these major groupings have more or less stood the test of time suggests that Linnaeus picked a good characteristic on which to name his classification of the major groups of insects.


How much vitamin C has a noticeable effect on E.coli k12

I found a 'short communication' paper by Akira Murata et.al where they did In Vitro testing of Vitamin C on L. casei showing no inhibition of growth, and also tested on E.coli and B. subtilis and found that Vitamin C inhibited the growth. Also I believe Suzanne Humpries stated the same thing somewhere in this 1.5 hour long video, indicating she may posses more knowledge as to studies.

  Ascorbic acid did not inhibit the growth of L. casei even at high
  concentrations, and rather stimulated the growth at certain
  concentrations (2~3 X 10- 2 M). This observation indicates that
  ascorbic acid can be used as an antiviral agent.

  In E. coli and B. subtilis, unlike L. casei, a high concentration
  of ascorbic acid acted so as to lessen their growth rates (Fig. 3).
  Particularly, in B. subtilis W23, cell lysis was observed about 100
  min after the contact with ascorbic acid and, moreover, when a drop of
  the lysate was placed on a plate seeded with B. subtilis 168 and
  incubated overnight at 30oC, there appeared a clear zone around the
  placed lysate. Since B. subtilis W23 is known to possess an inducible
  defective phage PBSZ able to kill B. subtilis 168,3 ' 41 the observed
  result maybe ascribed to the induction of the defective prophage from
  B. subtilis W23 by action of ascorbic acid. Lwoff and Siminovitch51
  reported once that the lysogenic phage in B. megaterium was induced by
  treatment with ascorbic acid.


As far as I understand your question, the "development" of eukaryotic cells can be linked to the endosymbiotic theory Symbiogenesis.

This diagram only depicts a possible trajectory of evolution which is still unknown.

A cell that respired anaerobically took in a bacterium that respired aerobically, supplying both itself and the larger cell with energy in the form ATP. This created a competitive advantage for the larger cell because aerobic respiration is known to be more efficient than anaerobic respiration. Unhurriedly, the aerobic bacteria evolved into mitochondria and the larger cell into a heterotrophic eukaryote.
A heterotrophic cell took in a smaller photosynthetic bacterium, which supplied it with organic compounds, thus making it an autotroph. The photosynthetic prokaryote evolved into chloroplasts and the larger cell into photosynthetic eukaryotes.


Why darwins, a measure of evolutionary change, is calculated on the log scale?

There are several purposes for log transformations, but one of the most common that occurs in biology is when changes are relative aka multiplicative. See for example this answer from CrossValidated.

If I told you that one lizard has a tail 5 cm longer than another lizard, that doesn't actually tell you much about how different it is. If the first lizard had a tail 1 cm long, that's a pretty massive difference! If the first lizard had a tail that was 100 cm long, the 5 cm difference is pretty minor.

Taking the log shows this:

Big (relative) change:

$log_e(6) - log_e(1) = 1.8$

$6 - 1 = 5$

Small (relative) change:

$log_e(105) - log_e(100) = 0.049$

$105 - 100 = 5$

The simple differences are both 5, but the log differences show you a big change versus a small one.

Logarithms are also more convenient than ratios for rates of change because they are easy to manipulate to predict change over any time interval assuming a constant relative change over time.

Taking the 6cm vs 1cm example above, lets say we want to guess the change when only half of the time is elapsed. If we take half of 1.8 = 0.9 and solve the following for X:

$log_e(X) - log_e(1) = 0.9$

$X \approx 2.5$

So we'd expect after only half the time, the length would have been about 2.5 cm.

$2.5/1 \approx 6/2.5$ meaning that the relative change for each subdivision of time is equal.

You could try this for any dt, too, and plot out X as a function of time with any dt when you use logarithms. You can't do this directly with a ratio like "6/1" because you can't directly subdivide that "6/1" into smaller time intervals (trying to do so would take you into the world of logarithms again :) ).

test <- function(time,x1,x2) {
  out = exp(log(x1)+(log(x2)-log(x1))*time)
  return(out) }
time = seq(0,2,0.01)
plot(time,test(time,1,6),
     xlab = "Time",
     ylab = "X",
     type = "l",
     main = "Change in morphology through time")
points(x = 1,
       y = 6,
       pch = 21,
       bg = "black",
       col = "black")

Ultimately, what matters most is what thing you are measuring and how you want to interpret a particular type of change. For things like lengths or average counts, often a relative multiplicative change makes the most sense.


Why is the ribonucleoside derived from thymine, 5-Methyluridine, abbreviated m5U and not T?

From the standpoint of modern molecular biology, one can say that the table in the Wikipedia article would be better if — in the first instance at least — it left blank the entries for the ribonucleoside corresponding to the base thymine and the deoxyribonucleotide corresponding to the base uracil. This is because the thymine ribonucleoside is not a normal constituent of RNA, and the uracil deoxyribonucleoside is not a constituent of DNA.

It would also be more honest if the article explained that the abbreviations used in DNA and RNA databases employ the single letter to represent a deoxyribonucleoside monophosphate residue or a ribonucleoside monophosphate residue, as the case may be, and that only the chemist or student of nucleotide metabolism is likely to be concerned with the abbreviations presented.

It is in metabolism (for which these were named) that the abbreviations make sense. ATP is adenosine triphosphate, so the ‘A’ has to represent the nucleoside, adenosine, and dTTP, deoxy-thymidine triphosphate, is the metabolite that is a DNA precursor used by DNA polymerase. The reason that dU justifies inclusion is that dUMP exists in cells — as a precursor of dTMP (which is then converted to dTTP).

So finally to your Q1 about 5-methyluridine. The answer is that, as far as I am aware, this does not occur in cells as the free nucleoside or the free related base or nucleotide. It can only be considered as occuring at a particular positions in certain transfer RNAs (and ribosomal RNAs) where it is produced by the enzymic modification of the uracil ring by a 5-methyluridine methyltransferase. So in the metabolic era, before the detailed chemical analysis of minor bases in structural RNAs, there was never any reason for biochemists to refer to 5-methyluridine and consider its abbreviation.

You may or may not be aware that there are many minor bases of this type in different tRNAs, all produced by enzymic modification of the four bases occuring in an initial RNA transcript synthesised by RNA polymerase. There are over half a dozen different modifications of uracil, so it was far more meaningful for the scientists working on them to distinguish them with abbreviations that indicated their chemistry, rather than assigning arbitrary single letters to them. The fact that one could logically employ T as an abbreviation for 5-methyluridine would have been of no practical use, and, because of the association of thymine with DNA, could well have led to confusion. Hence, the committee standardizing nomenclature would have been faced with a fait accompli. In such circumstances realism prevails over idealism. (And in any case the names of the bases are a mess — how many students have been confused by adenine/adenosine but cytosine/cytidine.)

Regarding your second question: people don’t talk very much about m5U and U, but when they do they naturally distinguish between them because they are different molecules. Specifically, the databases for tRNA structures will distinguish clearly the different modified bases.


Why do haemophillic females $X^hX^h$ die before birth?

Haemophiliac females are rare but they can survive just like affected males do. However, the case is slightly more complicated in women because of menstruation.

I could not find an article from any medical journal but this site seems authentic enough for a reference.


I could not find a peer-reviewed paper, but there is a widespread popular belief that adult cats only meows to communicate with humans but never with other cats. Meowing allows a cat to obtain the attention of its human owner and eventually get what it wanted.

See this webpage from the american society for prevention of cruelty to animals for example or this quora post.


Can you tell me what species of insect this is?

This looks like a horsefly (family Tabanidae, in Italian "tafani"), maybe Tabanus bromius but I'm not sure. If it's so, be careful: they bite and their bite is painful. Here you can find some quick suggestions about horseflies and their bite.

However, as you live in a city, don't worry too much: as the female horseflies feed on horse and cattle blood, they are normally present in the countryside, so those that you saw are exceptions more than the norm!


Yes, it can be done to a certain degree.

Cementum is capable of repairing itself to a limited degree and is not resorbed under normal conditions. Some root resorption of the apical portion of the root may occur, however, if orthodontic pressures are excessive and movement is too fast. Some experts also agree on a third type of cementum, afibrillar cementum, which sometimes extends onto the enamel of the tooth.

Cementum is produced by cells called cementoblasts.

more here:
http://en.wikipedia.org/wiki/Cementum


Phospholipid Bilayer structural reversal

This would have quite dramatic consequences. The layers are ordered in the way they are, because of their polarity. In the way they are ordered, the hydrophobic tails are inside and directed towards each other, the hydrophilic heads are orientated to the outside and inside. Since both sides of the membrane are surrounded by aqueous solutions, this is necessary to allow a contact between solution and cell membrane and to allow an exchange of molecules between them. If the layers would be oriented the other way, this contact and exchange wouldn't be possible. Proteins channels in the membrane wouldn't be possible as well, since the intermembrane domains are composed preferrably of amino acids with hydrophobic sidechains, while the domains on the outside of the membrane contain more hydrophilic amino acids.
A turn like this would need a completely different composition of life - meaning it couldn't be based on water like it is.