Recommendation of a comprehensive book on the history of medicine

While it's not meant to be a history of all of medicine, I thought the The Emperor of All Maladies touched on a good deal of the history as the author took us through how cancers were diagnosed and treated since long ago.

Great book, that was.


EDTA carbohydrates, phenol all have absorbance near 230 nm.  TRIzol reagent is a phenolic solution which absorbs in the UV both at 230 nm and ~270 nm

Guanidine HCL used for most DNA isolations will absorb at ~230 nm also

All these things will seriously inhibit your pcr, (and lower your ratio) especially the denaturing agents like guanadine.

All these DNA kits are different spins of a pretty similar process.

If you have a good steady centrifuge stick to the phenol & ethanol. Be certain you are drying your pellet well, but don't over dry it. I'll hear my pellet at 37 for 3-4 min to get rid of ethanol. Ethanol no good in pcr. If you hate doing ethanol precipitation (which I do) cause of invisible pellets, add a high grade bit of glycogen to your aqueous phase before the precipitation. This will make your pellet visible and is completely inert.

If your cleanup isn't the problem do an annealing  and Mg gradient and up your primer quantity.

May want to give me more info like the individual absorbance, pcr conditions, template size etc

Traditionally bead purifications gives really good purity, reason I use it for microarrays. But it's expensive and not necessary for pcr.

Charge switch is just changing the charge of the bead by changing the ph.


From the Wikipedia article on fungi (under Characteristics -> Shared Features):

  They have a characteristic range of soluble carbohydrates and storage compounds, including sugar alcohols (e.g., mannitol), disaccharides, (e.g., trehalose), and polysaccharides (e.g., glycogen, which is also found in animals).


Follow the instructions that came with your column for cleaning. The resin will probably be fine, but you'll need to thoroughly clean the column. My GE columns recommend washes of:

20% EtOH
30% Isopropanol
1M NaOH
1M NaCL
SDS in 0.1M Acetic Acid
Stripping buffer (EDTA)

Wash between each with several column volumes of distilled water. You may not need to do all of them. Then just recharge your column with a 100 mM Ni solution (or metal of choice)


Opinion:

the Jackson laboratory

http://jaxmice.jax.org/

Is the industry leader in transgenic mouse production. Their list of mouse strains is almost a db in itself but currently no db exists that I'm aware of. I take it your looking for something similar to what's available for c elegans:

http://www.celeganskoconsortium.omrf.org/


Is the phrase "transmembrane segment" equivalent to the transmembrane domain of a protein?

Yes
I'll admit defeat in trying to find the section in the text you linked - if there's any one thing Google can't do, it's search.  But questions like this are better put to Uniprot, which gives quite a bit of information.  Following that link, you'll see they identify 21 AA of transmembrane topology from 698 to 718, with a cytoplasmic domain afterward.  So the cytoplasmic tail is the intracellular domain.
In a sense there is a second transmembrane domain - the signal peptide from 1-19 - but because it is cleaved little attention is paid to it.  The extracellular domain starts at 20, with an N terminus outside the cell.
To quote Wikipedia, a transmembrane domain "usually denotes a single alpha helix of a protein".  You should probably listen to them on such an issue because nobody is more fixated on semantics (it's a sort of vote).  Philosophically, you can picture that multiple transmembrane segments could operate as a functional unit - but each of these segments would be separated by some region of extracellular or intracellular sequence from the next.  A "domain" in a protein is a self-contained unit in the primary sequence, not just a series of helices that turn out to be near each other, so that wouldn't work.  And in fact if you look at a GPCR paper they speak in standard terms of seven transmembrane domains even while analyzing how they function together.


What keeps mitochondria from multiplying out of control?

I'm guessing at the motivation for your question -- In the evolutionary history of eukaryotic cells, mitochondria were once free-living bacteria.  What prevents them from acting as intracellular pathogens and replicating out-of-control?
Yes, by endosymbiotic theory 1, mitochondria were once free-living prokaryotic organisms.  This is evident because they have their own DNA, undergo replication by fission, and have characteristics similar to proteobacteria.
However, some of the genes required for mitochondrial replication have been moved to the nuclear genome.  This means that, while mitochondrial replication is not necessarily tied to cell replication, factors encoded in the nucleus are necessary for mitochondrial replication.2

https://en.wikipedia.org/wiki/Symbiogenesis
Ali, et al. Nuclear genetic regulation of the human mitochondrial transcriptome. eLife 2019;8:e41927.


What are mutator genes which cause copying errors in other genes?

Most obvious examples are the genes directly involved in DNA mismatch repair (MMR) such as mutS, mutL, mutH, MLH1 and MLH2.


Did I understand the definition of "gross primary production" correctly?

Yes, you more or less got it!

If you have only 3 primary producers (say 3 plants) in a given ecosystem.

Plant A produces 2g of organic carbon per second
Plant B produces 5g of organic carbon per second
Plant C produces 1g of organic carbon per second

, then the GPP is 8g per second.

This produced organic carbon can be in the form of leaves, root or whatever tissue these plants are growing.

Note: the numbers chosen are irealistic both in terms of production per second and in terms of number of plants in an ecosystem.

  gC (grams of carbon assimilated) m-2 (m squared) year-1", what is meant by "grams of carbon assimilated" ?

The whole point of primary producers is to fix carbon. That is to take inorganic carbon (such as $CO_2$) and make it organic (such as $C_6H_{12}O_6$ aka glucose). This is why we are typically particularly interested in carbon and not so much in water.

For more info, you should have a look at an intro course to respiration and calvin cycle.

Note that if you remove water from an organism you are roughly speaking left with 75% of carbon, 10% of Nitrogen and the rest made of different elements.


How does bonding between non-complementary bases occur?

How do the two bases that aren't complementary remain bonded?

Non complementary bases can only form non-Watson-Crick bonds, which are very unstable and noticeably different.
Therefore any mismatch in the DNA of the genome will form a recognisable disruption of the DNA helix. This disruption is usually removed very quickly by the cells, since it makes DNA much more unstable.

Most cells have multiple mechanisms to detect and repair these sites, with one system specifically dedicated to DNA mismatch repair.
This system acts on mismatches directly after DNA replication, since at this point specific markers (sometimes DNA methylation, sometimes not fully understood) can differentiate between the newly synthesised DNA strand (which may contain an error) and the old one.

The repair mechanism will remove the mismatch and replace it with a properly bonded base pair, so that mismatches in the DNA are always short term issues - it is still possible though that 'wrong' mismatching base is replaced, which then (finally) leads to a mutation.

The error rate of DNA polymerase (1 in 10^7 sounds about right, this is the combination of the initial error rate and the DNA polymerase proof-reading mechansim) therefore has to multiplied with the error rate of this repair mechansim, which is around 10^3 (I can't find a source for this right now), to get a final error rate of DNA replication in cells.


Why does DNA need to be pure for restriction enzymes to act on it?

Some other macromolecules or other solutes may be present that could interfere with the affinity of the restriction enzyme. For example, there could be salts that denature or modify the conformation of the enzyme or inhibitors present that may interfere with the enzyme. Hope this helps.


What happens when we know that there is something that we forgot but we can't remember what it was?

It is a phenomenon known as room amnesia, some research has shown that your brain may use physical barriers like the room and doorways as a way to compartmentalize thoughts.
One article summarizes it here:

  The researchers say that when you pass through a doorway, your mind
  compartmentalizes your actions into separate episodes. Having moved
  into a new episode, the brain archives the previous one, making it
  less available for access. It’s as if you slam a mental door between
  what you knew and…what was I saying?

This is the research.


To understand Second messenger signalling in I/c and E/c

I think the schematic you have there and the one that @Masi posted are pretty good.  A better way of getting a grasp of intercellular signaling would be to study a specific hormone and understand how each of the elements in the block diagrams here could vary.

For instance take a look at this diagram from a journal article where they are tinkering with yeast mating factor, one of the first discovered extracellular signaling pathways.

alpha factor and 'ligand' (I assume its not known at this point) bind to their receptors Ste2 and hGPCR respectively.  They then activate G protein complexes and both activate the same kinase cascade Ste4/18 -> Cdc42 -> Ste20 -> MEKK/MEK/MAPK/Ste5 which then may activate Far1 (or not) and Ste12.  Far1 and Ste12 are migrated into the nucleus to activate genes for cell reproduction.

By actually filling out the boxes in your diagram you can see dozens of different paradigms for how cell signaling may work, and why the diagram you have needs to be so simple.  Hope this helps.


What are some possible causes that might explain why the global temperature has remained relatively constant in the last decade?

Not my field but I have a couple of thoughts:

According to your link, the blue line represents the change in the trend and the red bars are the temperatures. These have not remained that stable, it is the bar that gives that illusion:

A much more important point are the grey bars extending above and below each year's value. This is the range of uncertainty, the actual values could be anywhere within the range of those bars. Notice how the uncertainty decreases the closer you get to the current date.

I think a lot of the stability you observe is probably due to the line hiding the detail and the far lower precision of the older measurements.


Is identifying the genus of a fungus (mushroom specifically) enough?

Again, I would say: no, genus is not enough.

Another example: boletes (specifically, genus Boletus).

According to Wilderness College:

  One of the most common and well-known groups of edible wild mushrooms are the boletes or boletus species (Boletaceae) ...

But

  Many species in this group are edible, with only a handful being poisonous. The poisonous boletus species have red or deep orange pores. Outside of the few toxic species, some species of boletus are bitter or inedible.

For example, see here for a list of edible boletus mushrooms (e.g., B. edulis), while some examples of Boletus species to avoid include: B. huronensis and B. satanas

An additional issue to classifying all species in a genus as "safe to eat," is that our classifications are not always reflective of real taxonomic associations. In other words, some groups are not monophyletic and their evolutionary (and therefore physiological/nutritional) characteristics should not be assumed to originate from the same common ancestor .

This is apparently true of the boletes. From Wikipedia:

  Boletus has been found to be massively polyphyletic, with only a small percentage of the over 300 species that have been assigned to Boletus actually belonging there and necessitating the description and resurrection of many more genera

See for example: Nuhn et al. (2013)1

1: Nuhn, M.E., Binder, M., Taylor, A.F., Halling, R.E. and Hibbett, D.S., 2013. Phylogenetic overview of the Boletineae. Fungal Biology, 117(7-8), pp.479-511.


To my knowledge disease risk is not a generally acepted epidemiological term. You may want to look at the incidence rate or prevalence and follow the suggestions from the "See also" section.


Humans have Cannabinoid receptors. Does that mean we're meant to consume cannabis?

Receptors
Any drug or compound with specific effects has a receptor. You can read about this general concept in Goodman and Gillman's The Pharmacological Basis of Therapeutics. Chapter 1 introduces the concept, chapters 3 and 5 expand further. As far as the history of this concept is concerned, receptors mediating the specificity of action was first clearly articulated by Paul Ehrlich (in the context of dyes and toxins), and further developed by John Langley (and Ehrlich again in response). Cannabis and cannabinoids are not unique in this regard. Illicit and therapeutic drugs of all kinds have a target binding sites (receptors). In almost all cases, these receptors are bound by endogenous compounds as well.
Does having a receptor mean we should consume something?
There was a case to be made that having a great number of receptors that bind psychoactive compounds in cannabis means there is a physiologic role for some cannabinoid (especially given the pattern of expression) and suggested the existence of an endogenous cannabinoid before it was discovered. This was discussed in the nature paper that first identified the receptor and its functional expression and in the science paper that reported the discovery of endocannabinoids. Generally, it doesn't suggest that we are "meant to consume cannabis". Toxins and poisons also have receptors, and we certainly don't want to consume those.
As far as the name is concerned, the comment by @user137 is correct. Receptors are sometimes named by exogenous drugs that activate them, in particular when these compounds are discovered and studied before an endogenous ligand is found. Opioid receptors are another example.


Why does UVA penetrate deeper than UVB, though it's weaker?

Our skin contains quite a lot of water and I think this is answers the question: The absorption of UV light by this water goes drastically up when you shift to shorter wavelengts with a minimum absorption in the UV-A spectrum.
See this figure (from here):

So water has a very low absorption around 340-350nm (UV-A) and a very high absorption at shorter wavelength (UV-B and UV-C). This also explains why we get a lot more UV-A through the atmosphere than for harder UV-Radiation.


The chemical we are talking about here is called pheromone, trail pheromone to be specific.

  A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting outside the body of the secreting individual to impact the behavior of the receiving individuals.1

Pheromones are of mainly 9 types (13 exactly, but 4 not so common) which are:

Aggregation pheromones
Alarm pheromones
Epideictic pheromones
Releaser pheromones
Signal pheromones
Primer pheromones
Territorial pheromones
Trail pheromones
Sex pheromones
Nasonov pheromones
Royal pheromones
Calming pheromones
Necromones2

Ants, and many other animals, use trail pheromones to mark their trail as a guide for others in their gang. Other ants, catching the signal of trail pheromone, follow the way it goes and reach their gang leader. Trail pheromones are volatile compounds, so it is not very likely that you would see ants following the exactly same path tomorrow or a week later. All ants release trail pheromones, so as long as ants are going through that path, the trail signal will keep getting stronger and will also tell lost ants "Hey, bro! We are going this way. Don't you want to join us?" See, for example, here3:

In the beginning, different ants follow different paths, but as soon as an ant finds the shortest path, all ants join it on that path, due to which pheromones on other paths evaporates and finally, they all walk in straight line.

Of course, trail pheromones are very useful for organisms who have lost their way home, but you know, other organisms, like their predators, are not just sitting and watching them. Some predators can also catch pheromones and find out where the whole team is going, to attack them all at once. Such chemicals are known as kairomones. See this4:

  A kairomone is a semiochemical, emitted by an organism, which mediates interspecific interactions in a way that benefits an individual of another species which receives it, and harms the emitter.

Semiochemical is just a type of pheromone which a species X releases, but a species Y can also respond to its presence. Its just like when you walk on road and say "Whoa! Seems like a pizza delivery van just passed by" (obviously, smell of pizza is not by a pheromone ;)

The trail pheromones released by army ants can also be detected by a blind snake or a forest beetle, leading it right inside their nest. Obviously, all semiochemicals are not bad. Chemicals like synomones (helping both species) and allomones (just the opposite of kairomones) are also present5, but they are beyond this question's scope.

References:

 Medical Definition of Pheromone
Types of Pheromones - Wikipedia
Life in Wireframe - Ant Algoithms
Kairomones - Wikipedia
These Pheromones Get The Animals That Secrete Them Killed


How can a chromosome translocation in somatic cells lead to disease?

You have made an incorrect assumption-- that all the genes on both chromosomes necessarily remain intact. It's possible that they do, and the the translocation is harmless.

But the transition point could be within a gene. This would usually lead to that copy of the gene becoming inactive, which can cause diseases just like any other loss-of-function mutation.

Alternately, the translocation can fuse two genes in a pathogenic way. While this might seem fantastically unlikely, the fact that the translocations are non-random means that there are patterns that recur frequently. The BRC-ABL fusion (https://en.wikipedia.org/wiki/Philadelphia_chromosome) is one of the most common causes of childhood leukemia. The fusion protein is constitutively active because the regulatory domain of the original protein has been replaced.

Finally, a translocation could separate a promoter element from the gene it controls, which could cause aberrant expression of that gene. The promoter element could also wind up proximal to a different gene and cause aberrant expression of that gene.


The question is relatively broad and one should take into account that the brain not only consists of neurons, but also glial cells (supportive cells) and pre-mitotic neuronal stem cells. Furthermore, as critical fellow-scientists have indicated, developmental stage is very important, as the developing embryonic brain is very different from the adult brain.

However, after sifting through various publications, the answer to the question is actually remarkably simple: Yes, brain cells migrate.

In  the adult brain glial cells migrate in the brain (Klämbt, 2009). Glial cells are involved in a myriad of functions, but a notable example of migrating glial cells are the oligodendrocytes that migrate relative long distances to find their target axons onto which they wrap themselves to form the insulating myelin sheath (Tsai and Miller, 2002).

Neuronal stem cells migrate over long distances in response to injury (Imitola et al., 2004) and they migrate from specific stem-cell locations (e.g., hippocampus and subventricular zone) to other regions (Clarke, 2003).

Interestingly, post-mitotic (fully differentiated, not-dividing) neurons can also be migratory in the adult brain. Specifically, newly formed neurons can migrate over hundreds of microns in fish (Scott et al., 2012) and neuronal migration has been shown in the human cortex as well (Fox et al., 1998).

Not surprisingly, glial cells, stem cells and neurons also migrate during embryonic development. Most notably, post-mitotic neurons destined to fulfill peripheral functions have to migrate over relatively long distances from the neural crest to their target locations (Neuroscience, 2nd ed, Neuronal Migration).


Your question refers to differential gene expression and methods of Eukaryotic gene regulation. This is a very broad question for there are a lot of methods to control gene expression. They can function as transcription control, mRNA processing control, translational control, post-translational control and so on in eukaryotes. In prokaryotes, the methods include the operon model etc, which is much simpler than eukaryotes and multicellualr organisms but still quite complicated when studied in its entirety. Here and Here are few places where you can study differential gene expression. As an introductory text,  chapter 19 of Life:The science of Biology by Purves, Sadava, Orions and Heller(the link is to a supplementary-material site and not to the book itself), Otherwise, to elucidate all mechanisms here would become too long and in any case uncomprehensive.


This is Clerodendrum schmitii similar to C. wallichii (Bridal Veil). It is commonly called Chains of Glory and is native to Thailand.

It belongs to Verbenaceae family.

  Chains of Glory is a shrub to small tree, multi-stemmed, with hanging branches. Each winter it grows long, pendent, dark red racemes, 1.5 ft long, of delicate white flowers. The cascading white fragrant flowers are held in loose hanging clusters, similar to Bridal Veil. The white flowers on long dark red flower stalks look very attractive against the dark green leaves. Chains of Glory is native to Thailand.

(from flowersofindia)

  The genus is native  to tropical and warm temperate regions of the world, with most of the species occurring in tropical Africa and southern Asia, but with a few in the tropical Americas and northern Australasia, and a few extending north into the temperate zone in eastern Asia.

(from wikipedia)

Picture reference:

  Chains of Glory $^1$

 Bridal Veil $^2$

$^1$ (Source: tuoitre.vn)

$^2$ (Source: Cebuano wiki)


What is one Botulinum toxin medical unit?

1 unit is approximately 10 pg

Source

  One unit of MYOBLOC (botulinum toxin type b) corresponds to the calculated median lethal intraperitoneal dose (LD50) in mice. The method for performing the assay is specific to Solstice Neurosciences' manufacture of MYOBLOC (botulinum toxin type b) . Due to differences in specific details such as the vehicle, dilution scheme and laboratory protocols for various mouse LD50 assays, units of biological activity of MYOBLOC (botulinum toxin type b) cannot be compared to or converted into units of any other botulinum toxin or any toxin assessed with any other specific assay method. Therefore, differences in species sensitivities to different botulinum neurotoxin serotypes preclude extrapolation of animal dose-activity relationships to human dose estimates. The specific activity of MYOBLOC (botulinum toxin type b) ranges between 70 to 130 Units/ng.

UPDATE

10 pg of toxin (150 kDa) is 4 x 109 molecules


How much time does it take for an evolutionary change to take place?

How much time does it typically take for a new mutation to fix in an animal population?

The answer can really take any number. It will all depend upon the size of the population and the selection coefficient on the mutation. If we assume neutral mutations, then we can use Kimura and Ohta (1968)'s result. They showed that the expected time for a neutral allele to reach fixation (given that it will reach fixation) is

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$

where $p_0$ is the initial frequency and $N$ is the population size. Replacing $p_0$ by $\frac{1}{2N}$ and you get

$$\bar t\left(\frac{1}{2N}\right)=-4N\left(\frac{1-\frac{1}{2N}}{\frac{1}{2N}}\right)\ln\left(1-\frac{1}{2N}\right)$$

which can be simplified

$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(\frac{2N-1}{2N}\right)$$

Stick in any $N$ you want and you'll get your answer. Of course, this equations assume panmixie. In absence of panmixia, then it all depends upon the interconnectedness of the different populations. If some population are perfectly isolated, then a mutation will never fix in the entire species.

How much time does it typically take for a new mutation to happen and fix in an animal population?

The time to wait for the mutation to fix is typically quite negligible comparing to the time it takes for this mutation to happen. Let $\mu$ be the mutation rate. The number of mutations happening each generation is $2 N \mu$ and assuming they are neutral a fraction $\frac{1}{2N}$ of them will fix. Hence, the expected waiting time is $\frac{1}{2 N \mu \frac{1}{2N}} = \frac{1}{\mu}$. In humans, the average $\mu$ is of the order of $10^{-8}$ per site but there is a lot of variation among sequences.

So, if your mutational target is only a single site, then the expected time to fixation of a currently non-existing mutation is $10^8$ generations! If you are considering the entire genome as you mutational target is the entire genome, your mutation rate is of the order of $10$ and the expected number of generations is only $\frac{1}{10}$.


What is this fungus that is growing on my plant, and is it dangerous?

My answer won't apply if your plant isn't a cycad (a species from the genus Cycas) as only cycads are affected. Cycad aren't native to the Dominican Republic but have been planted as ornamentals in many parts of the world. If your plant's a cycad, I'm convinced that what your plant has is NOT a fungal but insect infection - something far more serious for your plant but not harmful for you or other people.

Please compare photos provided to make sure of identification. Even enlarging your top photo,  it's not quite focused or clear enough to be sure. It appears that your white 'fungus' is actually Aulacaspis yasumatsui or the Asian cycad scale insect. Athough native to southeast Asia, it's been spreading to many places where cycad are found. Whether it's reached the Dominican Republic yet, I don't know but its been in Florida since the mid-1990s and is found in a number of Caribbean countries. It's now a very serious pest of cycad worldwide, resulting in the death of many.

Here are some photos for you to compare. I did my best to find photos that show greater detail for you to check. If the photos fit what you have, you need to treat your plant to prevent it dying and for the infestation spreading to other cycad on the island. I've no experience with this but the information on how to deal with this pest comes from Central Florida Palm & Cycad Society so they should know the best way to treat this.

Treatment of Asian Scale

 Image from Forestry Images courtesy of Jeffrey W. Lotz

 Image from Central Florida Palm & Cycad Society


Why not use non-visual self-recognition to test for consciousness in an organism?

Reading the page you linked, I found this

  MSR test may be of limited value when applied to species that
  primarily use senses other than vision. For example, dogs mainly use
  olfaction and audition; vision is used only third. It is suggested
  this is why dogs fail the MSR test. (With this in mind, the biologist
  Marc Bekoff developed a scent-based paradigm using dog urine to test
  self-recognition in canines.[19][41] He tested his own dog, but his
  results were inconclusive.[42])

Emphasis mine.

19 Archer, John (1992). Ethology and Human Development. Rowman & Littlefield. ISBN 0-389-20996-1.

41 Stanley Coren. How Dogs Think. ISBN 0-7432-2232-6.

42 http://www.psychologytoday.com/blog/canine-corner/201107/does-my-dog-recognize-himself-in-mirror


Genomic instability of cancer cells in h&e image

Histologic diagnosis of tumors is made using the so-called  WHO blue books.

Different tumors show different patterns of cellular and tissual aberrations.

On h&e  karyorrexis and  pyknosis  are examples histological markers of nuclear aberration.

A recent  paper reviews the salient visual and subvisual morphological changes of cancer nuclei and their possible cause or etiology and significance.


Element of promoter responsible for expression power of gene

Tldr; In an in vivo context the answer is going to be dependent on DNA sequence and context.

Simplistically, Eukaryotic genes promoters can be segmented in to several parts. The first, a core promoter region where RNA pol II will bind. This isn't capable of a robust transcriptional response on its own and relies on proximal promoter regions, or more specifically transcription factor binding to the proximal promoters. Proximal promoters are usually 100 or so base pairs upstream of the transcription start site and will bind proteins that will assist in Pol II binding and activation (or silencing). Enhancers (and Silencers) are conceptually similar to proximal promoter regions with the exception that they can be a looooooooooong way away from the transcription start site in sequence space. See here:1.

So, if you just wanted to drive expression of a transgene in a cell line in the lab there are plenty of established cloned promoters and enhancer regions known to work such as SV40 or Gal4. This would be an example of "replacing the promoter". That's exactly what it is and why these sequences were chosen to be cloned.

If you are asking which regions are specific to activate or repress a gene in vivo and/or in context then it will be, of course, context dependent and you'll have to find out yourself if someone hasn't already. Generally, these regions of effect will be binding sites for sequence specific transcription factors  which interact with the core transcriptional machinery (or bind other proteins that do) to effect the rate of transcription. So, if the sequence is what can induce an effect, how can you find it? You can search for these sequence specific sites by analyzing your sequence of interest with a slew of computational tools for potential binding sites and directly assess any hits ability to increase/decrease expression as isolated units when cloned upstream of an appropriate reporter construct. I guess you could even go as far to CRISPR single base pairs in or out to "edit" any hits. Alternately, you could use a purely wet bench technique such as promoter bashing to similar effect - performing serial deletions to find out which part of your promoter is important for strong/medium/weak effects or activation/repression.

The Stark Lab developed a cool genome-wide approach looking at the ability of DNA to drive expression. Although, something worth bearing in mind is that in a normal in vivo situation everything is context dependent - one piece of sequence may be reliant on another close by (like the core promoter requires proximal promoters) or it may require one or more pieces of DNA that are distant in sequence space to be close by in 3D space (like distal enhancers).

People have also taken completely synthetic approaches to making promoters .

This would be easier to answer if your question was more specific.
HTH.


How isolated are different areas of the brain?

Well, to answer your question, both your hypothesis are true, at least partially true.

The brain has several known specialized connections called neural pathways that connect specific areas of the brain and are responsible for determined functions.

For instance, when you move your leg, the stimulus starts at the motor cortex and travels through the pyramidal tract to your leg and then back.

However, one can argue that the stimulus didn't start at the motor cortex. Why? you thought about moving, then made the decision and only then perform the real action of moving your leg.

And here's a more complex (and maybe humorous) example:

You see a dog running ferociously at you.
The stimulus travels through your visual pathway to your visual cortex.
The image of a dog forms in your brain.
It then travels to your Hippocampus.
You realise that's a dog and also remember a traumatic childhood experience with a dog.
The stimulus travels to your amigdala.
You feel fear
The stimulus activates the sympathetic system.
You're now prepared to fight or flight
The frontal lobe is activated
You decide to kick the dog
The stimulus goes from your motor cortex to your cerebellum
Your cerebellum "remembers" the karate classes you had as a kid
The stimulus goes to your leg
You kick the poor dog. He runs.
Nucleus accumbens is activated
You feel good with yourself

So, in short, the brain has pathways that connect specific areas of the brain but, in a sense, all parts of the brain are connected either directly or indirectly. Like the saying "all roads lead to rome!"

DISCLAIMER: I do not endorse animal cruelty.


Does eating beans of a mother cause flatulence on babies?

When the mother eat beans, the fiber (oligosaccharides) from them is not digested in the small intestine, so it travels to the large intestine, where normal intestinal bacteria break it down to some absorbable nutrients (like short-chain fatty acids) and gas that is largerly expelled (fao.org). Some gas can be absorbed into the blood and then removed by the lungs (PubMed).

This means that neither the fiber nor the resulting gas ends up in the mothers breast milk, so it cannot give gas to the baby.

Breast milk contains human milk oligosaccharides (HMO). HMO is undigestible, but bacteria in the infant's intestine can break it down and produce gas. However, the amount of HMO in the breast milk is not likely related to the amount of beans or other high-fiber foods the mother consumes, but is genetically determined (PubMed).


Fruit is discolored in the first place because, when certain compounds are altered (oxidized), they turn brown.

In a banana (and most fruit) those compounds are phenolic compounds, and polyphenoloxidase is the thing that oxidizes them.

In an undamaged banana, the phenolic compounds and the polyphenoloxidase (that can turn them brown) are physically separated.

When the banana is crushed/dropped/etc, the structure of the banana is damaged so that the phenolic compounds and the polyphenoloxidase come into contact.  The polyphenoloxidase oxidizes the phenolic compounds, and you get that brownish color.

A nice summary (which links to a more detailed reference) can be found here: https://www.scientificamerican.com/article/why-does-bruised-fruit-tu/


Your description is more or less correct, but so are both images. The bottom images shows the predominant form the amino acid would take at neutral pH (or any pH between ~2 and ~9.5). This is because the caroboxylic acid (-COOH) and amino (-NH2) groups are a weak acid and base and can lose or gain a proton (hydrogen cation), respectively. pH below the pKa of the functional group (~2 for carboxylic acid and ~9.5 for amino) favours protonation whereas pH above the pKa favours deprotonation. Also note that the "centre carbon" (the α-carbon) did not gain a proton in the second image, it's just drawn differently.

You could try this website for an overview of acid/base chemistry and perhaps these Wikipedia sections on zwitterions and isoelectric points with respect to amino acids, though there are many alternative sources of material available if you search for them. This question and answer may also be useful for you, at least eventually.


Can butterflies still fly after their wings are touched?

Both the Forewing as well as the Hindwing of Butterflies are made of thin chitin structures which are pretty thin and sensitive. If you touch the wing with to much force, it may break.

Then the upper side of the butterfly wing is covered with small scales - what you called the "dust". This can be seen in this figure (from here):

and also in this electron microscopy image (from the Wikipedia):

The scales have a number of functions, they are responsible for the butterflies color and pattern (which are important for finding mating partners as well as for camouflage) and they also seem to play a role in insulation and thermo regulation (see here for more details).

The scales play also a role in making the wings stronger and help improving the flight characteristics. When flying upwards the get pressed to the wing and act aerodynamically, what the wings are in downward motion, they help stabilizing the flight. See here for more details: "Butterfly wing scales : pigmentation and structural properties".

Some of the scales get lost during flying and collecting nectar, so taken together, loss of a big number of them will influence the flight characteristics of a butterfly. However, I think it is much more likely that such a rude treatment will damage the wings, which is obviously more harmful. So light touches will not do harm, more severe will.


Are there any photosynthetic catalysts in use other than chlorophyll?

There are photosynthetic organisms that use retinal-rhodopsin complex. However, the mechanism of photosynthesis is different in these organisms than those that employ chlorophyll dependent photosystems. In these organisms, the light causes the rhodopsin-like membrane proteins to pump proton out of the cell and create a proton gradient which in turn is used by the ATP synthase to make ATP.

See this post too Why are there no known photosynthetic archaea?

This mechanism of "photosynthesis" is not as efficient as the chlorophyll dependent one (page 22, Baltscheffsky, 1997†). Moreover, it does not produce NADPH.

† Baltscheffsky, Herrick. Origin and evolution of biological energy conversion. New York etc: VCH, 1996. Print. ISBN: 978-0-471-18581-9


What does the energy in an energy pyramid represent?

Each layer in the energy pyramid represents the stored energy in biomass in that layer. This energy is obtained from the previous layer. Because every layer uses a certain amount of energy needed for survival (combustion of sugars and fats through respiratory processes) obtained from the previous layer, each subsequent level is smaller than the previous one. Also, the autotrophs in the photosynthetic layer use up (solar) energy for living. The higher up you get, the more energy is cumulatively taken away to sustain life and growth of the previous layers. Therefore, it's a pyramid shape.

Energy pyramid. Source: Biocab


What areas of the brain are involved in doing arithmetic operations?

This is a part answer to your question.

According to "Arithmetic processing in the brain shaped by cultures" (Tang, 2006), the parts of the brain that are activated while doing arithmetic is to an extent, governed by culture, in the article, the authors assert:

  Using
  functional MRI, we demonstrated a differential cortical representation
  of numbers between native Chinese and English speakers.
  Contrasting to native English speakers, who largely employ a
  language process that relies on the left perisylvian cortices for
  mental calculation such as a simple addition task, native Chinese
  speakers, instead, engage a visuo-premotor association network
  for the same task. Whereas in both groups the inferior parietal
  cortex was activated by a task for numerical quantity comparison.

(The article also includes fMRI imagery examples).

It also seems that recognition of simple arithmetic starts at an early age, according to "Infant brains detect arithmetic errors" (Berger et al. 2006).


Yes, plants of all sizes can have cancerous growths.

Agrobacterium tumifaciens, the causative agent of crown gall disease, produces what is called a tumor. See this link for detailed information on these growths. Alternatively, use a plant physiology textbook to look up the above terms. (Here, is where a textbook is better than a single abstract in PubMed.)

I am certain that you have seen such growths on trees, such as this. Other smaller versions can occur on smaller plants - on stems and leaves, for example. The plant builds up tissue around the A. tumifaciens infection in an effort to isolate and contain the infection and its effects.


How do diving marine mammals avoid decompression sickness?

I think I got the answer....

  The primary anatomical adaptations for pressure of a deep-diving mammal such as the sperm whale center on air-containing spaces and the prevention of tissue barotrauma. Air cavities, when present, are lined with venous plexuses, which are thought to fill at depth, obliterate the air space, and prevent "the squeeze." The lungs collapse, which prevents lung rupture and (important with regard to physiology) blocks gas exchange in the lung. Lack of nitrogen absorption at depth prevents the development of nitrogen narcosis and decompression sickness.

Source: Scientific American


Monozygotic vs Dizygotic heteropaternal superfecundation

A normal singleton child is a result of the fertilization of an ovum (with 23 chromosomes) by a sperm (with 23 chromosomes). After fertilization, the cell (with 46 chromosomes) is called a zygote.  All normal human cells (other than ova and sperm) have 46 chromosomes.
Monozygotic twins (identical twins) occur when the set of cells resulting from the early divisions of a single zygote separate into two groups.  Each of these two groups of cells proceed to form a normal embryo, with resulting (if carried to term) in twins.  Since these twins came from the same zygote, they have the same 46 chromosomes and so are essentially genetically identical.
Now how could this monozygotic process occur with two fathers being involved?  Only by having two separate sperm combine with a single ovum.  This would result in the zygote having 69 (3x23) chromosomes.  This could happen, but would be an extreme case of aneuploidy (abnormal number of chromosomes). Such a genome is massively defective due to the presence of too many gene copies, and the embryo (whether singleton or twin) will be spontaneously aborted.  Only a few kinds of aneuploidy can result in a viable fetus, almost all having only a single extra chromosome (one of the smaller ones); the most common case is having 3 copies of chromosome #21, which results in Down Syndrome.
So, monozygotic heteropaternal superfecundation has not been observed because the resulting pregnancy is very unlikely to go to term. (It's just as unlikely when the two sperm are from the same man.)


Well, I’m not sure I should answer this, as your question is predicated by an incorrect supposition:

Acetoacetyl-CoA is a C3 unit.
3-Hydroxybutyryl-CoA / Butyryl is a C4 unit.

Not according to Kegg:

However, my answer is worthwhile if I explain how I found this out. One way to check this sort of thing is to go to the Kegg website and search for the compounds of interest, find the appropriate pathway (shown below) and then click to check compounds and reactions.

There is also the Metacyc website for metabolic pathways, and you can check the formulae on Wikipedia.


Where are epitopes located on HLA molecules?

T cells in a graft see both non-self peptides associated with the non-self HLA molecules, and can also see the non-self HLA molecules regardless of peptide. (MHC is a broader term than HLA, and I will use MHC here.)

  Surface expression of CD4 or CD8 is commonly used to identify T-cell subsets that recognize antigen presented by class II MHC or class I MHC, respectively. This holds true for T cells that respond to allogeneic MHC molecules that are directly recognized as foreign, as well as peptides from allogeneic MHC molecules that are indirectly presented by self MHC molecules.

--Contrasting Alloreactive CD4+ and CD8+ T Cells: There's More to It Than MHC Restriction

Recall that as T cells mature in the thymus, they undergo negative selection such that those T cells that spontaneously recognize self MHC molecules are deleted, but there's also positive selection that ensures the T cells can recognize MHC features in general. That leaves many T cells that could spontaneously recognize slightly different MHC molecules (i.e. non-self) that are not deleted. That means that in a transplant, there are a large number of T cells that can recognize the non-self MHC in a non-peptide-dependent manner.  There's also a much smaller number that can interact with the non-self-MHC but only in a peptide-dependent manner; this is just by chance, in that that particular T cell receptor happened to have the shape that sees that non-self-MHC and the peptide.

As for autoimmunity, that's all peptide-dependent, as far as we know, barring some of the really horrendous infant-onset autoimmunities that result from improper T cell maturation in the thymus.


Book recommendations: biological data analysis/error

There are many books that teach statistics and R together. I would personally not recommend these books. Learn the fundamentals and just google what command already exist in R to perform the analysis you need to do.

I would recommend Experimental Design and Data Analysis for Biologists by Quinn and Keough. It is general, applied and pleasant to read.

As you already have good basis in statistics, you won't need an intro textbook but for other users (and because I personally work with one of the authors) I would like to mention The Analysis of Biological Data by Schluter and Whitlock.


Why do musk deer have the smallest red blood cells and amphibians have the largest?

In the abstract of (Duke, 1963) we see that mouse deer (Tragulus) have the smallest erythrocytes, not musk deer (Moschus). The paper also explains the origin of the confusion. Mouse deer have 1.5 µm erythrocytes but those of musk deer are 3.6 µm (p. 240). In fact musk deer erythrocytes are the same size as goat erythrocytes at (2.5-3.9) µm (Weiss, D. (2010). Schalm's Veterinary Hematology. 6th ed. pp. 836–842). Whether smaller erythrocytes have since been found, I can't say.

I don't have a definite answer why mouse deer erythrocytes are the size they are but I'd posit a few factors. The size of the erythrocyte needs to approximately match the size of the capillaries so they can press tightly to the epithelium and increase the efficiency of gas exchange. Another factor affecting erythrocyte size is cell number. If you have smaller cells, you need a larger number of them to keep the same sum total volume (as in the figure below). So then factors affecting blood vessel size and the rate of erythrocyte production could possibly affect erythrocyte size.

Size also changes surface area to volume ratio (sa/vol) by the square-cube law and this changes characteristics of diffusion over the cell membrane. A larger erythrocyte may have more plasma membrane, which would allow more diffusion and transporter activity but this may also increase the erythrocyte's volume, which would limit the rate of gas exchange due to solutes needing to work their way out of the middle of the cell. Having a high sa/vol is dependent on morphology (hence, our erythrocytes are biconcave) but Duke claims that mouse deer erythrocytes are actually spherical. So, in theory, the cells' small size could be a compensation to keep their sa/vol high, despite not being biconcave.

Interestingly the size of the cells might not affect the sum total intracellular volume of the cells. In fact, sphere packing density is independent of the size of the spheres. If the cells were made larger, this would increase the size of the gaps between them by the same amount. This could indicate that the the total amount of solutes in the blood is independent of the size of the cells, which could explain the great variation in the size of erythrocytes.


This is a phasmid (Order Phasmatodea) from the Genus Monticomorpha. Its common name in Spanish is (insecto) ututo.

Here is an image of it:

Source: http://www.projectnoah.org/spottings/1847685515

They are found in Colombia, Ecuador and Peru. You can see that the distribution matches your place:

Source: http://phasmida.speciesfile.org/Common/editTaxon/Distribution/ShowDistribution.aspx?TaxonNameID=1199515

Identifying the species may be a bit more complicated. The Phasmida Species File page I linked above lists 8 species of ututos (with pictures), 5 of them occurring in Ecuador.


I agree with @Amory in the sense that Hamilton's rule is not a rule that applies to each specific individual and explain their behavior (or other traits). The Hamilton's rule describe the direction (and not the dynamic) of how a social traits evolve. A social trait is any trait which does not only affect the fitness of its carrier but also affect the fitness of other individuals in the population. Theoretically, all (or almost) traits are actually somehow social traits.

$RB>C$ is a simplistic way of looking at Hamilton's rule which might bring you to some confusion. This formula makes more sense to me by replacing $B$ by $\frac{dw(x,y,z)}{dx}$ and $C$ by $\frac{dw(x,y,z)}{dy}$. $w(x,y,z)$ is the fitness function of a focal individual expressing trait $x$ and interacting with an individual drawn from a subpopulation expressing trait $y$ (expected value of the probability distribution of trait expression of individuals in the subpopulation) in a population expressing trait $z$ (expected value again). In the particular case where there is no population structure $y$ equals $z$. $\frac{dw(...)}{dx}$ describes the partial derivative of the fitness function according to the variable $x$.

Therefore the Hamilton's rule can be rewritten as:

$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$ where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$.

Altruistic behavior evolves if (but not "if and only if") this rule is respected. Hope this reformulation of Hamilton's rule helps a bit understanding it.

In the special case where $R\cdot\frac{dw(x,y,z)}{dx}=\frac{dw(x,y,z)}{dy}$ then, the trait of interest is not selected (neither counter selected). Therefore the trait will evolve under genetic drift alone. While the allele frequencies are modified by drift, the Hamilton's rule might (or might not) differ from the equality and then the trait would not be neutral anymore.


Is the fixation rate always equal to the mutation rate for neutral alleles?

The answer to your headline question is that no, fixation rate is not always equal to the mutation rate for neutral alleles. For instance:

Fixation rates for neutral alleles are affected by changes in population size, given a constant mutation rate. In general, fixation rates are lower in growing populations (Waxman 2012).

This makes instinctive sense if you consider the single-generation fixation probability of a neutral allele which only exists at all but one copy in the population, i.e., the common allele (A) exists at 2N(t)-1 copies, whereas the less common allele (a) exists at 1 copy. To simplify, let's assume complete random mating. Under negative population growth (say N(t+1) = 0.9N(t)), there will be 0.9*(2N) places that the rare allele could possibly exist at t+1, and it has a 1/(2*N(t)) chance of filling each of them. Under positive population growth (say, N(t+1) = 1.1*N(t)), the rare allele could potentially occupy 1.1*(2N) places at t+1, but still has 1/(2*N(t)) chance of filling each of them. It is clear in this case that A has a reduced generation-wise likelihood of fixation under positive population growth than under negative population growth, simply because the rare allele has an increased chance of doggedly persisting. The finding applies to any allele near fixation.

If I have understood Kim and Stephan (2000) correctly, then overall fixation rates are also reduced by background selection. The main mechanism for this is that background selection purges linked neutral alleles, decreasing overall heterozygosity and thereby reducing the chance that a new, rare allele will become established. The same surely applies to selective sweeps, given linked neutral alleles.


I think you've got the solutions the wrong way round and that you should be applying the pressure on the non-pure solution, not the pure solution. Pure water is drawn in through the membrane so you have to put pressure on the non-pure solution to keep it out. Which textbook are you using? See the following quote from Voet et al. 5th ed. p. 30 and figure from Lehninger. Principles of Biochemistry p. 57.

  The osmotic pressure of a solution is the pressure that must be applied to
  the solution to equalize the flow of water across the membrane in both directions
  (the added pressure forces more water from the solution through the membrane);
  it is proportional to the concentration of the solute.


There is a difference between potential and risk. That's why different agencies came to different conclusions.

The IARC (International Agency for Research on Cancer, a body of the WHO) assesses the potential of a compound to cause cancer. They go through the research that point into this direction and if there is any hint that any dose of the compound might cause cancer they have to rate it accordingly. If you go through the IARC report on glyphosate, you find that a lot of the studies they looked into did not actually find a link between glyphosate and cancer in humans. Nevertheless, there are some studies that show that high doses of glyphosate can result in cancer in animals. So, the IARC had to conclude that glyphosate has the potential to cause cancer. They put it into the category 2A (probable carcinogens). In the same category you find red meat, hot beverages and being a hairdresser, because these things have the potential of causing cancer.

Agencies like the FDA, EFSA etc. are assessing the risk of cancer from "normal" glyphosate exposure. While it seems to be possible to get cancer from "too much" glyphosate, we are only exposed to a tiny fraction of that dose. While it's unavoidable that small amounts of glyphosate residues are found in our food, these amounts are most probably not harmful. At least, that's what most research concludes. The dose makes the poison. While eating fresh organic berries does not pose any risk to harm you, they naturally contain small quantities of chemicals that have the potential to harm you at high concentrations. Your body itself makes small amounts of compounds that have the potential to harm you (e.g. Formaldehyde).

That's why the debate is so heated. Environmental activists are taking the cancer potential assessment of the IARC and turn it into a risk for the consumer, which is untrue. If they would work with the same energy against other group 2A carcinogens, we would have to close down barber shops...

So, does glyphosate has the potential to cause cancer? Probably yes.
Does this provide a risk for the consumer/farmer? Probably no.


Is there a name for the behavioral phenomena of when animals like ants sacrifice themselves?

The term you're looking for is altruism. According to Wikipedia, altruistic behaviour "allows an individual to increase the success of its genes by helping relatives that share those genes." Someone correct me if I am wrong but this means that this behaviour evolved by natural selection because it ensures the survival of a species in most cases. The link about exploding ants is probably a nifty example of altruism.


How many birds in this population would be expected to have either red or white feathers?

The solution

$$p^2 = 202 / 630 ≈ 0.32$$
$$p = \sqrt{202/630}$$
$$(1-p) = 1 - \sqrt{202/630}$$
$$(1-p)^2 = \left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$$

There is a fraction of $202 / 630 ≈ 0.32$ of red birds. There is a fraction of $\left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$ of white birds. There is therefore a fraction of $0.32 + 0.188 = 0.508$ of birds that are either all white or all red. In a population of 630 individuals, it therefore represents $630 * 0.508 ≈ 320.53$. A result that is apparently rounded up at $321$ in your answer key.

Your mistake

You computed the number of birds that have both white and red feathers (WR) while the question was asking for either red or white feathers. You calculated the expected number of heterozygotes instead of calculating the expected number of homozygotes.

Of course the number of heterozygotes and the number of homozygotes should add up to the number of individuals in the population ($321 + 309 = 630$).


What's the best way to measure biodiversity?

A very good way to measure biodiversity would be to do environmental barcoding with high-throughput sequencing methods, and then use an algorithm that estimates genetic distance to get both species count estimates, and then calculate higher-level diversity, such as genera and families. Then you would repeat this procedure over several collections to obtain a species accumulation curve, so you could then estimate the asymptote. The future possibility of biogenereed organisms would not be worth reporting among the thousands of species at a given location.


Using egg whites as DNA destruction test possible?

Cooking DNA will absolutely not destroy it. Few things will actually destroy DNA. Bleach is one of the only common substances that will do it.

To test for DNA quantity you need to perform qPCR. The equipment is $20,000+.


Can one eye affect the other eye's low-light adaption?

Yes, but not in a really effective manner. Two things occur for an eye to switch to "night mode". The most influential change is that of seeing mainly with the "rod" visual receptors, as you noted. The second, relatively minor change is that of pupil diameter. In the dark, the iris constricts to produce a larger pupil, allowing more light into the eye. This can be done very rapidly, which is why any interruption in this mechanism is negligible.

The important piece of information you need to know is that for most people, each eye's iris acts sympathetically to that of the other. This means that if I were to shine a pen light into your right eye, causing your pupil to constrict, your left eye will do the same, even if no light is entering that eye.

So, if you were to wear an eyepatch over your left eye in a brightly-lit area, and then enter a dark room and remove the eyepatch, you would have far better vision in your left eye because that eye is operating primarily with rods. To answer your question, there was a tiny setback caused by the right eye in terms of pupil diameter, but this would be corrected within a fraction of a second.

Regarding your inference as to a "saturation effect", the answer is yes and no. If you were to wear contacts, with the lens covering the left eye being tinted dark and the lens on the right being clear, then at first it would appear that the light entering the right eye is affecting the vision of the left. This is simply a matter of focus, though. You're distracted by the larger amount of information that needs to be processed coming from the right eye. With proper focus, however, you would see that the left eye is operating independently in terms of light adaptation (aside from pupil diameter, as mentioned).

I hope this answers your question

Edit

I've been asked to add references. I'll not provide a reference for the use of rod receptors in low light as you have already acknowledged this fact, but I will provide a reference for the simultaneous pupil dilation. For the saturation effect, you can easily prove this to yourself at home. Skip the contacts and pop one lens out of a dark pair of sunglasses.

https://en.wikipedia.org/wiki/Pupillary_light_reflex


A basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism

Reading your updated question, I think you are interested about epistasis. Let me know if I am mistaken.

The concept of epistasis might be confused with the one of pleyotropy, so I will define both terms.

Pleyotropy occurs when one gene influences multiple phenotypic traits. Note: the phenotype, to make it simply is what a living things look like (its cells, proteins, shape of the face, size of the leaves, etc…). It is often thought in duality with the genotype which is the total genetic information contained in an individual that codes for the phenotype (Be careful, the environment is also an important factor influencing the phenotype, if you make sports you will have big muscles!)

Epistasis is when the effect on the phenotype of one gene depends on the presence of several (or only one) other genes. Wikipedia gives this (simplistic) example:

Here, two bi-allelic genes are involved. One gene that determines the hair color. The two alleles influence the phenotype such: one allele gives red hair and the other allele gives blond hair. Now There's another bi-allelic gene coding for baldness. One allele causes the bearer to be hairy and the other one causes the bearer to be bald. Therefore, if an individual carries the allele "Bald" in the "Baldness" loci, what this individual carries on the other loci is not important because it will result into the same phenotype anyway, he is bald. Now if in the baldness loci, the allele is "Hairy", then the expression of the other gene "Hair color" matters and therefore if the allele is "blond", the bearer has blond hair and if the allele is "red" the bearer has red hair.

The "Baldness" gene is called a modifier. One can also say that the expression the "Hair color" gene depends on the genetic background of the individual.

Now cases of epistasis are not always that easy and if they influence the fitness, this kind of epistatic interaction might have implications for their evolution.


Probability of number of boys and girls being born on a single day

I know this is kind of tedious and only practical when you are considering no more than 10 children  (which I think is a lot to parent), but anyway, I like to solve these problems with a binomial expansion.

So we have binomial probability so 2 options - either a boy (n) or a girl (g) at equal probability or 50% or 1/2.

(b + g)^n = a binomial expansion according to the coefficients of Pascal's triangle.
Where n = 4 children, then the row of Pascal's triangle is 4 in which the first row of pascal's triangle is technically row 0.

Equation: (b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)

Problem A)
So the probability that the number of boys and girls will be equal is

Probability((6(b^2)(g^2)), where (b^2)(g^2) means two boys and two girls, an equal number.
When b = 1/2, and g = 1/2, or well ... b + g = 1

6(b^2)(g^2) = 6[(1/2)^2 * (1 / 2)^2] = 6 * (1/2)^4 = 6 / 16 = 3/8

B) All four will be girls: Prob((1(g^4))

= 1(1/2)^4 = 1/16

C) At least one baby will be a girl:
That corresponds to 4(b^3)(g), 6(b^2)(g^2), 4(b)(g^3), and 1(g^4)

The probability that at least one will be a girl is

= (4 + 6 + 4 + 1) * (1/2)^4 = 15 / 16

D) Which combination of boys and girls is most likely?
That would be 6(b^2)(g^2), so when b = g = 1/2

Prob(most likely combination) = 6/16 = 3/8 or two boys and two girls.

Note that if you add up all the combinations, the result is 100% of all probabilities:

(b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
When b = g = 1/2, then basically:

(1 / 16) + (4 / 16)+ (6 / 16) + (4 / 16) + (1 / 16) = 16 / 16 = 1 = 100%

You did it right. But I suppose this is another way to evaluate a binomial like this.


Don't understand figures in this citizen-science mosquito ID project

In the second figure –
  What does the color scale and color coding represent?

Each color is an individual mosquito species,
arranged the same from top to bottom on all plots.
Here, on the left, all species are gathered on one plot,
with the y-axis now labeled “Species.”

The sounds of many mosquitoes apparently have statistical profiles
similar to each other,
so the individual plots
demonstrate how additional factors help distinguish species
in some such cases.

In the plot for “Time” (C),
the sun and moon merely accompany the species
whose differing circadian habits they illustrate.
It is only a coincidence
that the daytime species is plotted higher.

Just to complete the picture,
here is how these plots mark statistical profiles.


There can be many responses. They are important for alloimmunity (so by transfusion, transplantation, etc...), for recognizing pathogens, cancer, virus, etc... By T cell activation, the regulator T cells recognize these antigens as self, and prevent the autoimmune reaction.

I guess they were thinking on MHC1 and MHC2. MHC1 shows the inside of the cells, so e.g. by viral infection or cancer non-self oligopeptides (from degraded proteins) bind to MHC1. These non-self antigens are recognized by CD8+ T cells, which destroy the affected cells. MHC2 is used by APCs to present possible pathogens to CD4+ T cells in a similar way.


Isotretinoin and retinoid receptors in brain confusion?

The second study did not even examine the pharmacological effects the drug had on the brain. The researchers noted depression scores tended to increase while on the drug, but not in significantly significant way. Keep in mind the drug is clearing a disfiguring condition, so this novelty may interfere with the ability for measures to detect psychiatric issues.


Why does K+ going out of the cell cause hyperpolarization?

Adding K+ on the outside of membrane is not the same as transfering K+ from inside to outside.
When K+ is added to outside(hyperkalemia) the RMP becomes less negative(depolarisation)
When K+ is transfered from in to out RMP becomes more negative(re/hyperpolarisation)
We should not forget that most of the intracellular anions are nonpermeable protiens, so when K+ is transfered to outside they pull harder, and when K+ added outside, the pull decreases


The role of GC content in promoting or hindering transcription

This paper suggests the opposite in mammalian cells. Obviously, gene regulation is quite different in prokaryotes, so don't know how much confidence you want to put into that one.

This paper suggests more of the same, but includes some caveats related to prokaryotes that may pique your interest. They do a pretty in-depth dive of GC content near genes from many different species, but I haven't read it closely enough to give a good breakdown.


Is it firmly established, that mutations are sufficient for cancer?

Acquiring mutations (more than one) are the necessary (and sufficient) steps on the way to cancer. The current opinion is that cells need "multiple hits" to fully transform into a cancer cell. It is also called the Knudson hypothesis, the original paper is here.

For example melanocytes (the pigment cells in the body) which acquire the activating BRAF V600E mutation (which is an important step in getting a melanoma cell, this mutation is found in about 70% of all melanoma) is not enough to transform the cell. Other mutations are necessary to do this.

Among the things important for cells to become malignant are to escape the apoptosis mechanisms of the cells and also the immune system. Both are linked to the mutation, inactivation or epigenetic silencing of genes, so I would say genes are the key to cancer.

For further readings these two articles should be interesting:

Are oncogenes sufficient to cause human cancer?
Significance of multiple mutations in cancer


I think that the type of fMRI you are referring to is blood-oxygenation-level-dependent fMRI or  BOLD fMRI.

The principle behind MRI in general is the detection of proton signals from water molecules. The proton signal is generated by magnetizing the protons in tissue, which causes their spin to change. A subsequent powerful radio wave disrupts this spin and the following relaxation phase of the protons to the original state can be detected by MRI. Water, and hence protons are everywhere in the body, including the brain and the blood.

Deoxygenated hemoglobin (hemoglobin without oxygen) in blood changes the proton signal in its immediate surroundings due to the magnetic properties of deoxyhemoglobin. This is caused by the fact that deoxygenated hemoglobin is paramagnetic and decreases the proton signal. In fact, the paramagnetic influence of deoxyhemoglobin has been regarded as noise in structural MRI scans, before its use in BOLD-fMRI became clear. Oxygenated hemoglobin does not have this property.

Radiopaedia has a nice explanation as to exactly how the BOLD signal is used in BOLD fMRI, and I quote:

  When a specific region of the cortex increases its activity in response to a task, the extraction fraction of oxygen from the local capillaries leads to an initial drop in oxygenated haemoglobin [...]. Following a lag of 2-6 seconds, cerebral blood flow (CBF) increases, delivering a surplus of oxygenated haemoglobin, washing away deoxyhemoglobin and with it the attenuating effect on the MRI signal. It is this large rebound in local tissue oxygenation which is imaged, as it is accompanied by an increase in the MRI signal. The difference is used to generate the BOLD fMRI response.

So brain activity increases the BOLD signal by picking up oxygen-changes after an increased blood flow to that specific part of the brain.

So your statement [...] If there is more brain activity and therefore more oxygenated hemoglobin the signal should be less strong because the oxygenated hemoglobin does not react to the magnetic field is incorrect, because oxyhemoglobin attenuates the proton signal.


Why do protein solutions have to be alkalised in biuret test?

This is probably to prevent precipitation of copper hydroxide (see Itzhaki & Gill, 1964 - they suggest adding dilute copper sulfate slowly to the NaOH solution to avoid this). If you have the protein already alkalized and ready to react you'll get the color reaction before precipitate forms.

Commercial premixed solutions, like @canadianer mentioned in a comment, have tartrate present to prevent this (Geiger & Bessman, 1972 mention this).

It doesn't seem like it's strictly necessary to add NaOH first, but that's probably the most reliable way to do the assay without using an additional stabilizing agent.

Itzhaki, R. F., & Gill, D. M. (1964). A micro-biuret method for estimating proteins. Analytical biochemistry, 9(4), 401-410.

Geiger, P. J., & Bessman, S. P. (1972). Protein determination by Lowry's method in the presence of sulfhydryl reagents. Analytical biochemistry, 49(2), 467-473.


The distribution in the sensory epithelium indeed refers to the location of the different receptors. And indeed, you are also right that cones are concentrated in the fovea, and rods are mostly found more eccentrically in the retina (Kolb, 2012. I would say the free nerve endings are situated just below the epidermis, and the PCs in deeper layers of the dermis (Fig. 1). But check your notes on what your prof. wishes to hear about this.

Fig. 1. Skin receptors. source: Neupsy Key

The physiological response properties of receptors is not their output per se. It is the way they respond to stimuli, that includes their output, but also includes the sensation of physical stimuli through second messenger systems or otherwise, and eventually the output. Kolb (2012 goes into detail on the physiology of photoreceptors in quite some detail and for the physiology of touch receptors I would refer to Dougherty in Neuroscience online.

References
- Dougherty, Somatosensory Systems. in: Neuroscience online. University of Texas
- Kolb, Photoreceptors. In: Webvision. The Organization of the Retina and Visual System (2012)


It's definitely real ;)

Depending on your previous knowledge, this review from 1987 might be a good starting point.
http://science.sciencemag.org/content/237/4819/1154.long

To give you an idea of recent developments this article is an easy read. Be sure to browse the references.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/


Is there an equivalent to "Fields Virology" for Bacteria?

I might as well give this as an answer: the closest analog to Fields for bacteriology that I'm aware of are the two Bergey's manuals: Bergey's Manual of Systematic Bacteriology, and Bergey's Manual of Determinative Bacteriology. They deal with taxonomy and identification of bacteria (and even cyanobacteria and archaeans), with some emphasis on the medically important classes.


Bug Identification: what type of bug is this small ant-like bug?

It looks like a ground beetle (family Carabidae)


Nucleotide frequencies in Kimura's two-parameter model

If sufficient time has elapsed, there will be a large number of transversions present between the original base and the final state. The initial state will therefore not matter.

Say, you flip (turn over, not toss) a coin at random intervals. For short time and few flips, the initial state will matter. But if you go on flipping it for millenia, the final state will be essentially random -- you will not be able to tell what was there in the beginning.


I highly doubt that this is a sentry palm. It seems to be a golden cane palm, also known as areca palm or butterfly palm, Dyopsis lutescens.

Here is an image for comparison:

And here is a close up of the leaf:

This whole structure is just 1 leaf. What you called "leaves" in your question are actually just leaflets (or foliolum in Latin).


What is this insect? Seems to be in Indonesia

https://en.wikipedia.org/wiki/Creatonotos_gangis

Creatonotos gangis is a species of arctiine moth found in South East Asia and Australia. It was described by Carl Linnaeus in his 1763 Centuria Insectorum.


Are there transposons which create homozygous genotypes in offspring?

I study transposons for my PhD; I am not aware of any that preferentially insert through an active mechanism to an un-inserted allele.

There are tranposons such as R1/R2 which have a 'favorite' insertion site and will insert/compete for that sequence. That's kind of similar to your question but not generalizable.

The predominant factor I can think of which would cause such a thing to arise would be gene conversion in which the insert allele is used as a repair template for an un-inserted allele. Gene conversion is rare but can explain how the TE insertion is found on multiple haplotypes.

It's very unlikely that the alternative hypothesis occurs in which the same type of TE inserts at the exact same position in two different haplotypes and that TE doesn't have a preferred insertion site.


A question about the intersection of evolution and thermodynamics

Getting long for a comment

I can only comment that evolution does not proceed towards thermodynamic optimum. Adaptation is thermodynamic optimization but evolution is directionless. Otherwise the extant species would not suffer from tradeoffs (which they have even in their usual habitat). Establishment of a self replicating cell may be thermodynamically driven and given the conditions, irreversible; macroscopic evolution is like die roll where some states are randomly⁺ selected and eliminated.

⁺Not really random but a complex non-linear function which seems unpredictable

You can imagine a chamber with particles exhibiting brownian motion. Assume that particles have a random size distribution (lets say they are crystals of different topologies). Now if you keep a separator with few holes wide enough for a just one particle of a given size to pass. Then you'll end up getting only few particles of a narrower size distribution on the other side. This no way ensures that these were the most thermodynamically stable particles.


Simple answer: yes, this happens all the time.

A couple of notes:

Firstly, pretty much everything in biology is continuous. If a gene is expressed at a level of 1 protein per million cells, everybody would say it's not expressed, even though I guess you could argue the point. And don't underestimate how much regulation can affect expression -- you can easily have thousand-fold or million-fold differences between tissues and conditions.

Now, regarding the expression cascade: This is exactly what happens during the cell cycle. As the cell grows, there are genes that can sense the availability of nutrients and all the other signals that control initiation of cell division. Those then can turn on the genes first phase of the cell division cycle. Other regulators can sense whether that phase completed, and turn on the next set of genes, and maybe degradation signals for the genes from the first phase. And this then continues through the cell cycle.

Here's a figure from a paper that looked at gene expression in synchronyzed yeast cells (http://www.pnas.org/content/104/43/16892.full):


Are acid-fast bacteria Gram-positive or Gram-negative?

Taxonomic Classification:

The most salient acid-fast bacteria are Mycobacterium spp., which are part of a phylum of gram-positive bacteria called Actinobacteria. This classification is based on 16S rRNA sequencing. However, based on genetic conservation, this paper makes the claim that they are more closely related to gram negative bacteria.

Gram Reaction:

Acid-fast bacteria are characterized by cell walls rich in mycolic acids. This characteristic causes both poor stain penetration and high stain retention which forms the basis of acid-fast stains. However, it also means that crystal violet will not penetrate the cell wall efficiently. Thus their gram reaction is variable and they generally stain light purple. The result is dependent on technique as well as mycolic acid content variation between genera (Nocardia spp, for example, are less acid-fast and stain gram positive). Needless to say, their cell walls don't fit well with the classic dichotomy of thin versus thick peptidoglycan which the gram stain differentiates between.

Example Gram Stains:

For comparison, the left image is of Bacillus subtilis, a gram positive, non-acid-fast bacilli. In the middle is M. phlei and on the right is M. smegmatis, both of which are acid-fast but show a weakly positive gram reaction. Images from Napa Valley College.

B. subtilis is again on the left for comparison. In the middle is M. fortuitum staining positive but more weakly than B. subtilis. On the right is N. astroides which is partially acid-fast but stains strongly gram positive. Images from Microbe Canvas.


You should most definitely have a look at a very introductory course to evolutionary biology such as evo101 for example.

  Does evolution produce organisms perfectly adapted to their environment?

There is a lot to say about this question. The question is very broad and cannot be fully answered in a single post. The very very short answer is "no". I will very briefly develop this "no" below.

Concept of perfection

There are semantic (and hence philosophical) issues of the concept of perfection in this question but I shall not go into these issues. Typically, in the fact of sexual selection (and other arms race), the concept of "perfection" becomes very unclear (see S Pr's answer).

There is variation in populations

Evolution is all about genetic variance in populations. The fact that variance exists makes that necessarily there is no notion of perfectly adapted for a population (or for a species) as not all individuals are the same!

"Drivers" of evolution

Evolution is a change in allele frequency over time. There are a number of drivers of such changes, including natural selection, genetic drift and mutations.

While natural selection is a deterministic process, genetic drift and mutations aren't. There is hence constantly departure from a "hypothetical perfect" caused by genetic drift and mutations.

Mutations, while being a "random process" (see Are mutations random?), most mutations are deleterious, hence constantly inputting "imperfection" into populations.


Front row, left to right; Victor McKusick, Maurice Wilkins, James Watson, Walter Gilbert and John Kendrew.


How do electrons destroy DNA bonds in radiation?

I think you have a fundamental misunderstanding of the chemical reactions involved in radiation therapy. Neither photon based or proton based therapies "create electrons", but they do cause ionization by adding enough energy to existing electrons around atoms so that the electron is ejected from the atom, creating an ion or free radical, which can then undergo chemical reaction.

Photons, typically gamma rays, X-rays, and high energy UV, typically interact with water molecules and produce free radicals, including the dangerous hydroxyl radical. The hydroxyl radical can interact with proteins and DNA and damage those molecules, but has a very short half-life. Molecular oxygen can help increase the damage by reacting with the hydroxyl radical to produce Reactive Oxygen Species, ROS, which can also damage DNA or protein. However, many tumors have low oxygen concentration that reduces the effectiveness of photon based radiation therapy.

To overcome this, many patients receive proton based radiation therapy. Protons are much heavier than photons (I guess infinitely heavier than a photon, since photons have no mass) and therefore scatter to a much smaller extent. They just sort of plow through tissue and knock electrons out of orbitals as they collide with molecules such as DNA or protein. They don't rely so much on free radical generation or ROS, so low oxygen levels don't reduce their effectiveness.

The goal is damage the DNA to induce double strand breaks which are hard to repair in fast growing cancer cells. Because they grow so quickly, they are already stressed and their DNA repair machinery is less effective than in healthy cells. If their DNA can be sufficiently damaged, the cell will die.

For more information about these processes, please see these wikipedia articles on Radiation Therapy, Radiolysis, Linear Energy Transfer, and Free Radical Damage to DNA.


How to distinguish the Ct of the target gene from the Ct of the housekeeping gene? (very basic qPCR question)

You do not take readings from the same reaction, you split the sample. You would run each primer pair in their own reaction. You also want to run each reaction in triplicate so you can get some idea of the error.
So, a general plate set up might look something like this:

A1: Control sample, housekeeping primers; A2: Control sample, target gene primers
B1: Control sample, housekeeping primers; B2: Control sample, target gene primers
C1: Control sample, housekeeping primers; C2: Control sample, target gene primers

D1: Treatment sample, housekeeping primers; D2: Treatment sample, target gene primers
E1: Treatment sample, housekeeping primers; E2: Treatment sample, target gene primers
F1: Treatment sample, housekeeping primers; F2: Treatment sample, target gene primers

So in this scenario, the delta-delta Ct value comes from the following:

delta-delta Ct = ( Ct(treatment, target) - Ct(treatment, housekeeping) ) - ( (Ct(ctrl, target) - Ct(ctrl, housekeeping) )

If the PCR machine does not offer to do the delta-delta Ct analysis for you I recommend this blog which both explains it well and provides and excel spreadsheet so you can just drop you Ct values in.
HTH.


Correlating beta-lactamase expression to absorbance

In the β-lactamase test, an inhibitor of β-lactamase is added to a sample of the culture medium. The inhibitor binds to the enzyme and changes its color, which is in direct correlation to the concentration of the β-lactamase. More β-lactamase means more inhibitor binding and this results in more color development leading to a higher absorption. So higher absorption means more β-lactamase in the supernatant.


I'm not a physician, but I suspect the popliteal artery may not have been the vessel used.  The popliteal artery has a very important role in supplying the leg with blood, and maintaining the blood supply from it to the lower (distal) leg is sometimes reason for harvesting other vessels.
You described a very long cut, which sounds like what you would see for harvesting the great saphenous vein.  The great saphenous vein is the longest vein in the body, and dominates recent scientific publications in response to a query of ''coronary bypass harvesting''.  (There are publications in that batch evaluating newer endoscopic techniques in which the long cut can be avoided)  Wikipedia reviews the use of this vein reasonably well.


Cell life: division for immortality or reproduction with aging

First of all, in eukaryotes (as far as I'm aware), older cells can be distinguished from younger cells due to telomere shortening, so there is an ageing process. HeLa cells mentioned by @Gary Chou have a more active telomerase which mitigates telomere shortening, allowing cells to continue to divide indefinitely. I think it's a very interesting question whether this immortality eliminates any sense of "older" and "younger" cells from in HeLa cell culture. I suspect not, but I am not sure on the specifics.

In general this question will depend on how an organism divides (we're going to talk single-celled organisms from now on). For example, the yeast Saccharomyces cerevisiae is a budding yeast, which means that it divides by budding a smaller cell off of the larger cell. This clearly allows for an interpretation of "mother cells" and smaller "daughter cells." Indeed, as lots of research on ageing in S. cerevisiae has shown, beyond being larger, the mother cell undergoes replicative ageing: over time the mother cell is less capable of growth and division--she gets old!

Perhaps the most interesting case of all (and maybe the one you had in mind) is when the organism divides symmetrically, like the bacteria, which undergo binary fission. For decades, as far as scientists could tell, the two cells that were the product of one bacterium dividing looked identical, and all measurements seemed to indicate that the cells were "sisters," i.e. exactly the same, both newborn. So if in the right conditions bacteria could continue to divide indefinitely, it seemed that bacteria were immortal, since each division reset the ageing clock for each bacterium.

However, a seminal study in 2005 (1) changed this view. The researchers took time-lapse microscope movies of a colony of Escherichia coli from a single cell. E. coli is rod-shaped, so when it divides it has to synthesize two new ends or poles, one for each cell, so just after division each cell has a "new pole" that was made in the process of that division and an "old pole" which had originated before. In this study Stewart et al. kept track of the old poles in the growing colony, and they defined the age of a cell as the age of its old pole. They found that older cells (i.e. cells with older poles) displayed replicative ageing, just like yeast! They grew more slowly and were less capable of dividing. This was examined rigorously by Wang et al. (2) in a "mother machine" in which bacteria were able to grow in constant nutrient conditions (by flowing fresh media across them) in dead-end channels. The cell at the dead-end of the channel always inherited the old pole, and so was a "mother" to all future cells. They found that, while a cell line was able to grow for very long periods of time completely stably, after hundreds of generations there was an increased likelihood for the cells to display signs of stress. They attributed to the accumulation of toxic factors in the mother cell over time. So even in cells dividing by binary fission, there appears to be some difference between the two cells arising from the division, depending on how old the pole that they inherit is.

These effects in bacteria are small, and require watching many generations to reveal. Even in light of these results many researchers will still call the "mother" cell the cell about to divide and the "daughter cells" the cells that result from division, implying that there is no difference between "daughters." Stewart et al. claim that on the basis of their work this conception of bacterial division must be revised, and that instead of division producing two identical daughters,

  the old pole cell should be considered an aging parent repeatedly producing rejuvenated offspring.

Furthermore, they add a nice philosophical touch to their findings:

  These results suggest that no life strategy is immune to the effects of aging, and therefore immortality may be either too costly or mechanistically impossible in natural organisms.

(1): Stewart EJ et al. (2005) Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division. PLoS Biol. 3(2): e45

(2): Wang P et al. (2010) Robust Growth of Escherichia coli. Curr. Biol. 20(12): 1099-1103.


Can replication occur if DNA is methylated?

Absolutely.  It's a pretty cool process, actually.  Most (well...) DNA methylation occurs in the context of what are called CpG; that is, a C (Cytosine) followed by a G (Guanine).  Because C and G are the Watson-Crick pair for each other, the sequence on the opposite strand will also be CG.  Usually, both Cs are methylated, which turns out to be rather critical for maintenance of methylation.

DNA replication occurs through a semi-conservative mechanism, which means each old, original strand is copied and paired with a new strand.  The new strand has no methylation on it, however; it is at this point that the enzyme DNA methyltransferase (DNMT1, specifically) comes into play.  DNMT1 finds the CpGs methylated on one strand ("hemimethylated") and methylates the other strand, providing complete inheritance.  Here is a nice summary, and this is a review that (briefly) summarizes the evidence that CpGs may play a role in irigins of replication (the jury's still out).


What tool can I use to align multiple protein sequences to one reference sequence?

What you want to perform is commonly called a multiple sequence alignment.  As @Wayne_Yux said, the first step is to put all of your protein sequences in a single fasta file.  You can then use one of several online tools to apply different alignment algorithms to your protein sequence set.

A popular sequence alignment algorithm is Clustal, which progressively builds a multiple sequence alignment from all of the pairwise alignments.  genome.jp hosts a web-based alignment tool that allows you to choose from Clustal and other alignment types (1).  For alignment of many small sequences to a single larger sequence, you should use the "SLOW/ACCURATE" option (2).  After you upload your fasta (3) and execute multiple alignment (4), an aln file will be generated which you can download (5).

You can then take this aln file and upload it to a different tool that allows you to visualize alignments.  Personally, I like ESPript, which gives color-coded alignments in pdf or image formats.  Because you want to compare many sequences, it will probably be necessary to change the "Alignments output layout" parameters, e.g. change "Gap between blocks" to a smaller number to fit all of your sequences in one frame.


Why is the administration of exogenous Anti-D not harmful to the foetus?

I've had a difficult time getting anything definitive to support my answer to your specific question of safety, however, I thought I'd go out on a limb and give you my understanding. A recent review of what is known about this can be found at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809506/

I think you are on the right track with your 'dose-dependence' hypothesis. This is exactly what the makers of RhoGAM suggest, saying that the amount of antibody administered at 28 weeks into the pregnancy is sufficient to block any Rh antigen on Red Blood Cells that escape into the mother's blood, but insufficient to cross the placenta and be a problem. At this time the child will be large enough that any RhoGAM that does cross the placenta will not kill enough Red Blood Cells to harm the child.

Mom gets another dose of antibody after the delivery in order to ensure thorough coverage of antigen that results from mixing of blood at that time, however this dose is not a problem as the baby has already left the mother.

By the way, the rationale for the antenatal dose is that post-partum administration alone failed to prevent sero-conversion in almost 2% of Rh- women, putatively due to transplacental hemorrhaging.


Why Hfr cells are called high frequency recombination cells?

According to Luca Cavalli-Sforza, the scientist who coined the acronym Hfr:

  Recombination as observed at the beginning had a very low frequency. It stopped being rare when I found a mutant strain which I called Hfr for “high frequency of recombination.” I found it accidentally in 1949 while I was selecting mutations resistant to nitrogen mustard and radiation. The first two resistant mutants, which had undergone a rather heavy treatment in the process of selecting for resistance to nitrogen mustard, proved to be exceptional in their mating behavior. One was Hfr and it showed immediately its remarkable mating ability, which was higher than that of normal crosses by a factor of 1000 or more. I repeated the experiment two more times before believing it. The other mutation, as I later proved, was an F- (self-sterile) mutation of an F+
  (fertile) strain. (emphases mine)

Source: Forty Years Ago in GENETICS: The Unorthodox Mating Behavior of Bacteria


Why can myopic eyes focus on nearby objects, but not on distant ones?

There are four common refractive errors, namely nearsightedness (myopia), farsightedness (hyperopia), astigmatism (Fig. 1) and presbyopia.

Fig. 1. Refractive errors. source: Excimer Ophthalmologic Clinic

myopia (nearsightedness): The eye ball is too long, or the cornea too steep, causing light to focus in front of the retina and making distant objects appear blurry.

hyperopia (farsightedness): The eye is too short, or the cornea too flat, causing light to focus behind the retina and making near objects appear blurry.

Astigmatism: is caused by an irregular cornea or lens, causing images both near and far to be distorted or blurry.

Presbyopia: a common age-related problem that is caused when the natural lens in the eye loses its elasticity, making it difficult to focus on near objects (hyperopia).

Focusing of the retinal image is mainly regulated through the process of accommodation (Fig. 2). Accommodation is mediated mainly by changes in the shape of the lens. A more globular lens results in a larger refraction of the light to focus on near objects. A flat lens refracts light less and is suited for focusing in the distance.

The lens is held in place by the suspensory ligaments. The ligaments in turn are attached to the ciliary muscle (Fig. 2). When the ciliary muscle contracts, it shortens. This effectively moves it closer to the lens and so any tension in the suspensory ligaments is released as the ligaments go slack.  Slack ligaments mean the lens adopts a more globular shape.

When the ciliary muscle relaxes, this changes its position to increase the tension in the suspensory ligaments. Taut suspensory ligaments (caused by the relaxed muscle) will pull the lens into a long thin shape.

Fig. 2. Accommodation. source: PMG Biology

In the case of myopia, objects in the far distance are blurry. Objects far away tend to send near-parallel light rays onto the lens and the lens needs to be maximally flat and hence the ciliary muscles should be maximally relaxed. If in this case the image is still in front of the retina, the lens cannot relax any further and hence the image is blurry. Because there is enough dynamic range for the ciliary muscles to contract, there is not any problem with objects close by, because the lens is perfectly capable of assuming a concave (fat) shape.


Why do plants flower in different seasons?

Why plants evolve to flower at various times depends on several factors. I've taken these from the book chapter Kudo 2006.
1) Climate and other abiotic conditions.
Spring, and the onset of consistent above freezing temperatures, is the first opportunity for many plants to flower, but it may not be ideal for all. For example some locations are still very dry in the spring and plants require water from rain later in the year.
Late frosts, which can damage flowers, is always a risk. Some plants can suffer the occasional frost and loss of flowers, while others hedge against this by flowering later.
2) Pollination competition.
For plants which are pollinated by animals (mainly insects), the finite amount of pollinators results in competition among plants for this resource. If all plants flowered at the same time competition would be extremely high, and no amount of animal pollinators could successfully visit every plant. Thus some plants have evolved to start flowering later in time and potentially have less competition. Note that other strategies to increase pollination from animals could also be to have larger and/or more numerous flowers.
3) Herbivory
Flowers eaten by animals are a waste of resources for the plant. For example if an insect preys heavily on flowers, and is most active during a certain part of the year, plants would evolve to flower outside of that time.
4) Seed maturation and dispersal
The ultimate purpose of flowers are to reproduce, and the timing of flowering can influence that. Plants with large fruit, such as berries, need ample time before winter to mature and this necessitates early flowering so that there is enough time for animals to disperse the fruit.
Constraints
There are many limitations to everything above, and if a plant species evolves one strategy it generally limits itself in other aspects. For example the very first plants to flower in temperate environments may have low competition for pollinators, but they also risk being damaged by late frosts. A viable strategy may be to flower throughout the spring and summer, which some plants do, but they can only grow in environments with year round resources and likely cannot produce large fruit which animals can eat and disperse. Plants which flower in late summer or autumn likely need large roots to store the water and energy to do this.

Kudo, G. (2006). Flowering phenologies of animal-pollinated plants: reproductive strategies and agents of selection. In L. D. Harder & S. C. H. Barrett (Eds.), Ecology and Evolution of Flowers (pp. 139–158).


Do plants experience the following feelings

Wikipedia defines emotion as "any conscious experience characterized by intense mental activity and a certain degree of pleasure or displeasure."

Plants do not have a central nervous system and therefore no mental activity so they certainly don't have emotions in the sense that humans and animals can have emotions. However plants feel/detect being eaten and they can communicate this to other (related) plants by releasing volatile organic compounds.