Is this a valid principle of curing HIV?

HIV hides in a number of known cells and unknown cells. Although most of the damage of HIV is caused by its infection of shorter lived cells, long lived cells which it infects includes anything with adequate receptors including memory T cells, dendritic cells, macrophages and some glial cells too. These cells are found widespread in the body from tissues to the blood stream. HIV also infects an as of yet unknown pool, which is thought to be the cause of rebound after HART (Highly Active Retroviral Therapy) is stopped.

The constant parts are not exactly there. Every part of HIV can essentially mutate and does. In functional HIV particles (which surprisingly make up a tiny proportion of total HIV particles in an infected individual), the epitopes you mentioned are mostly constant.

Destroying them is impossible as of yet and hence no cure for HIV. It is hard to destroy a particular protein. We could make HIV that doesn't make these proteins (it would then rapidly mutate until it did, or be non-functional to the point it was an awful vaccine not inducing a particularly adept CD8 response). Otherwise we could block either these proteins themselves or that which they bind. There is a group of individuals with the delta 32 mutation which blocks CCR5 preventing infection, however this is rare. For the most part most individuals are susceptible as CD4 and CCR5 are highly conserved amongst humans. We would benefit therefore from inhibitors of these proteins themselves, however due to glycosylation generally our antibodies are terrible at inhibiting the glycoproteins. Reverse transcriptase inhibitors exist and are in fact very important as part of HART.

HIV came from chimpanzees. In their natural host the HIV equivalent (SIV) doesn't cause immunosuppression. HIV doesn't infect quite a few primates due to restriction factors which do not exist in humans or do not target the same things. Then of course there's the matter of the lack of the correct receptors. There's ongoing research if there's a chemical that does cure HIV however there isn't a subset of individuals where this occurs to study. HIV resistance is normally due to elite control of the virus due to specific genetic features that make the immune system target the best least variable, most deleterious (if HIV mutates them to escape) epitopes. If we could get everyone to respond to these epitopes that would be great (see a billion vaccine trials for HIV) otherwise if we could flush out the cells where it hides latently integrated (our current therapy and the immune system can only target cells where HIV is constantly replicating).


Why does breathing increase in higher temperatures?

As you can see on the diagram below, oxygen solubulity in water drops by increasing temperature, so your fish has to breath more to get the same amount of oxygen.

ref

You can find more info about why gas solubility is temperature dependent here:
Chemistry (Averill & Eldredge) / Effects of Temperature and Pressure on Solubility.


At the moment, the youngest diagnosed Huntington's case was 2 years of age. This paper appears to discuss not only this boy's onset, but also the diagnosis of symptoms in the early-onset disease.

Here they research a link between age-of-onset and the length at which the repeats are.

The thing is that these repeats won't just constantly get longer. There is "slippage" during replication which causes the repeats to get longer, but it also causes the repeats to get shorter. It's possible that mom's bad chromosome may have been inherited but because of the slippage, it no longer produces Huntington's symptoms.

This image doesn't show actual mechanics of it happening, but it shows how the repeats can be added and subtracted.

As it turns out Kayser et. al decided to look at chimps and humans to discover which of two proposed mechanisms are more likely. Their findings suggest the slippage is closest to the "heterozygote instability model".

The model suggests:

  heterozygous loci might have a higher mutation rate due to mismatch repair events that occur during synapsis

To answer your question in short:

It appears that the "minimum age" so far is 2, however, that does not mean that it hasn't occurred earlier. Huntington's is characterised by a change in motor skills, and if the change occurs before birth it might not be noticed. In theory, it is possible that Huntington's symptoms can start pre-birth.


Why won't this spray kill this bug (household insecticide); could it be so selective?

It's a tiny baby cockroach.  Sorry.

http://animalia-life.club/other/german-cockroach-nymph.html

I looked up your chemicals; the first (metofluthrin) is mosquito repellant and the others are for fleas and mosquitoes.  The combo makes me think that this is something intended for spraying on the body or on animals.  It is not strong enough.

You need to get a bigger boat.  Get a spray made for roaches.


How selfish is Dictyostelium slug formation?

Joan Strassman's work is probably the route to go for this.

The short of your answer is that several things mediate who ends up where in the slug:

  Cheaters are limited from exploiting other
  clones by high relatedness, kin discrimination, pleiotropy, noble
  resistance, and lottery-like role assignment.

Here's the most relevant paper:

Strassmann, J. E., & Queller, D. C. (2011). Evolution of cooperation and control of cheating in a social microbe. Proceedings of the National Academy of Sciences, 108(Supplement 2), 10855-10862. [pdf]


How can we move our lips even though they don't have any bones?

Because of the Orbicularis oris muscle, it's a complex of muscles in the lips that encircles the mouth, It forms the greater part of the substance of the lips, lying between the skin and the mucus membrane, and extending from the edge of each lip to its root.


The key here is that it is a question about mitochondrial DNA. mtDNA in humans is inherited maternally (from the mother). Both sons and daughters inherit mtDNA, but only the daughters will pass it on to the next generation.

A child's mtDNA has to come from his or her mother, and all of a person's mitochondria are genetically identical. Therefore, children of an affected female will almost certainly have the abnormal trait, while children of an affected male will not.


In many cases the chromosomes do undergo some dispersion, they do not reach the extremely extended state of the interphase nucleus, this all happens in telophase -I. It would be correct to refer to the stage between two meiotic divisions as interkinesis which is generally short lived.

The prophase-II is initiated immediately after cytokinesis, usually before the chromosomes have fully elongated.


Melanin is a potent inhibitor of PCR - when you use B16 cells (or any other cell line that produces melanin) you have to purify your sample from it. Unfortunately a simple Phenol-Chloroform extraction or an ethanol precipation won't do the magic, since melanin co-precipitates with the nucleic acids.

I recommend following the following paper: "CTAB–Urea Method Purifies RNA from Melanin for cDNA Microarray Analysis".

The protocol derived from the paper can also be found here.


After mutations, which probably is the source of most variation.  The classic biological model of variation comes from accidents of history and environment.

Many mutations disappear over time because they aren't helpful (advantageous).  The reasons variations persist for more than a few generations is that our differences have helped us to live successful lives and (in biological terms of success) have offspring.  In europe the lactate dehydrogenase gene and others like it that help people digest milk is active through adult life as the result of domestication of milk producing animals,  in asia, this trait is rarer or non existent as agriculture does not produce milk there (in most cases).

This is a broad difference, but its true in smaller ways for all of our individual traits, or so the theory goes.  Individual family traits are helpful to create stronger family bonds, so even something like distinctive dimples or foreheads have claim to being an advantageous trait.  Its possible that blonde hair is the product of such an advantage - its a strong signal to paternity if the father is blonde for instance.

Another answer to your question I think, is that there are probably mechanisms in the cell or in mate selection that increase or decrease variation in the community at given times of stress.  For instance, snakes are among the animals who have a particular ability to select gender depending upon the conditions the female is experiencing.  more males may increase variation in the community - fewer males and more females will decrease it.  (not by a lot mind you, but a bit).

Additional response added as requested:

I see what you are getting at - why do children seem like such individual and unique things sometimes?

In sexual reproduction, the offspring are the product of the shuffling of the parent's genomes through meiosis, where the pairs of chromosomes we have are combined to make a single chromosome that will be half of the children genome.

This process can result in completely novel combinations of genes while conveying many likenesses from the parent.  I would guesstimate that this is the major cause of the uniqueness of offspring/children.

Also in mammals there are some cell lines which splice families of genes which will cause offspring to be potentially quite different from either parent.  Immune genes for instance are created from scratch from a bunch of genes that the parents give.  Making each offspring unique but also the product of the parent's genetic repertoire.  This can be significant as it affects health and also to some extent attraction - studies have shown that people who smell attractive to us are immunologically distinct from us.

@David mentions epigenetic variation, which is a more recent significant development.  During our life, the germline (sperm/egg) DNA may be chemically labelled depending upon environmental conditions we experience.  A famous example is experiencing famine conditions, which caused the children to be born on the small side amongst other effects.   More recent studies have shown that this is a widespread mechanism to control cells in our body during our lifetime as well as communicate to our offspring how life is.  It is expected that this labeling does not affect us forever - the epigenetic labels change over the course of a generation quite often (we believe).


Theoretically, any treatment can cause death. Drinking water can be lethal and oxygen is highly toxic and a strong oxidizer.

To quantify toxicity we usually use Median Lethal Dose (LD50) metric. That is a dose at which half (50%) of test group is going to die.

To answer "Why didn't people taking up the Ice Bucket Challenge die?":

Dose that people used was not high enough to cause any significant increase in mortality. Maybe some people did die, but it was just masked by other news (to some degree)


Basic step by step methods for PCR & Gel electrophoresis class

I've run a test following this protocol to the letter...

PCR step by step:

Collect all ingredients (excluding TAQ) from the refrigerator and keep cool (on ice). Leave the TAQ in the freezer until required.
Make master mix by adding all ingredients (excluding TAQ) using fresh pipette tips for each ingredient and using the volume specified
in the PCR reaction mix recipe.
Vortex & lightly spin down on a centrifuge.
Add the required amount of TAQ to master mix (insert in to the liquid) and mix using the pipette to draw some liquid up and down.
Add master mixes to labeled PCR tubes in the required volumes as specified by the protocol.
Add DNA to PCR tubes (using fresh pipette tips for each DNA sample) again using the volume specified in the protocol. Label your tubes
carefully (and on both the lid and tube).
Lightly spin down the PCR tubes on a centrifuge.
Run PCR in the thermocycler according to your protocol.
Collect samples from thermocycler and place in fridge until needed.

Gel Electrophoresis step by step:

Make 1xTAE (enough to make the agarose gel and to place in the electrophoresis apparatus).
Make an agarose gel (about 5 mm thick) by melting agarose and 1xTAE in the microwave; allow the liquid to cool a little before adding it
to the mold.
Once the gel is cool, place it in the electrophoresis apparatus, cover it with 1xTAE (just covering the gel) and then remove the comb.
Collect the PCR products from the fridge/thermocycler.
Make spots of loading dye on parafilm. The loading dye is premixed with GelRed so your samples show under UV light.
Add one sample to a spot, mix it by drawing the liquid in and out of the pipette tip, and then carefully add to a well in the agarose
gel. Take care not to puncture the gel or spill any of the liquid out
of its well. Discard the pipette tip.
Repeat the previous step for each sample and for a negative control (master mix and milli-q water instead of DNA). Use a fresh tip for
every sample.
Load PCR Ladder, also mixed with loading dye, in to a well.
Connect the electrophoresis apparatus to a power supply, with negative electrode (black) nearest to the wells containing the
samples.
Set the power to run 80-120 volts.
Wait until about a finger-width gap appears between the blue and purple bands (approximately 20-30 minutes).
Disconnect the power and collect the gel carefully from the liquid.
Take the gel to the UV camera and take a picture. Large DNA molecules move through the gel slowest so will be nearest to the
wells.

And got a perfect result...

The order is Control, female, male, female, male, female, male, ladder. Males have one band, females have two. The final pair didn't show too well on the picture but were clear enough on the screen in the camera room. Thanks for the tips everyone! Sorry the picture is low quality.
Feel free to recreate these guidelines but remember to credit the Biology Stackexchange Community!


No. For instance, Broca's area exists only in the frontal lobe of one hemisphere, usually the left. (it's responsible for speech, btw)


Is it one queen bee per hive or per colony?

Every beehive contains one colony, and every colony has one queen. (Of course there are exceptions, like if a queen dies or is about to be replaced, but I don't think that's what you're asking.)

A swarm is a specific thing, when the queen and part of a colony has taken off from the original colony to form a new one.

I think Wikipedia works well if you need more information on beekeeping terminology:
https://en.wikipedia.org/wiki/Beehive

https://en.wikipedia.org/wiki/Swarming_(honey_bee)

Edit: To clarify, I only have experience of keeping European honey bees (Apis mellifera).


Steroid hormones: how do they travel through the cytoplasm (not just the blood plasma) if they're hydrophobic?

Firstly not all steroid hormones travel inside the cell and regulate the gene expression.
Basically there are two pathways- direct and indirect.
Steroid hormones are lipid-soluble, which allows them to cross the extracellular membrane to the inside of the cell.

Classical models of steroid action suggest that steroid hormones bind to specific nuclear receptor proteins once inside the cell. Reference

Once inside the cell, a steroid hormone binds with receptor proteins in the cytoplasm. The steroid hormone and its receptor form a complex, called a steroid complex, which moves into the nucleus where it influences the expression of genes.
Reference

In the indirect pathway,

The traditional nuclear steroid receptors can also indirectly regulate gene transcription by serving as signal transduction proteins that interact with various signaling pathways in the cytoplasm of a cell. In particular, ER can activate kinases, enzymes that phosphorylate and thereby activate other proteins. This sets in motion a signaling cascade that eventually ends in the nucleus with the induction of gene transcription.
Reference


Comparison of examples in incomplete dominance and Co dominance

Mosaic dominance

I think your confusion comes from the statement

  incomplete dominance is also known as "mosaic dominance"

I had never heard of mosaic dominance before and I could not find much on this concept. I found a few papers but they either referred to mosaicism (see below) or they did use this term only a few times without defining it. There is an entry for mosaic inheritence in the online medical dictionnary though (here). The definition they give is

  inheritance in which the paternal influence is dominant in one group of cells and the maternal in another.

It is a little vague to me as 1) the phrasing is a little unusual and 2) it does not specify the underlying mechanism. If anything, it feels like a synonym of codominance and not of incomplete dominance.

Mosaicism is a thing in genetics but it is mainly unrelated to the concept of dominance as it refers to genetic polymorphism among cells within an organism.

Where did you read about mosaic dominance? Can you please give a direct quote?

If anything, mosaic dominance sounds like a synonym of codominance and not a synonym of incomplete dominance.

Codominance vs incomplete dominance

Outside the above issue, I think you pretty much define these two terms through your examples. You might want to have a look at the post (although it is a post who did not get much attention)

How is incomplete dominance different from codominance?

In short, codominance implies that the specific phenotypic effect of each allele is being visible in the heterozygote, while incomplete dominance implies that the heterozygote has a phenotype that is somewhat intermediate between the two homozygote phenotypes.


From the general body plan, it looks like it's probably a robber fly. Here's a page of specifically Kentucky robber flies – it's possible yours could be a Bearded Robber Fly.


Help identifying what this is in Crayfish gills?

My best guess would be Trematoda which is a fluke worm that infects mollusk. I would think this is the larval stage of cercaria which is free swimming and develops in the mollusk and then moves on to infect others.

Here are some different images of a cercaria:

In this YouTube video you will see what is known as a "Rat King" which is just a ball essential of Trematoda. Here is a screenshot


Why is mRNA used as a biomarker for cancer over tRNA or rRNA?

mRNAs encode specific genes and perform specific functions whereas the other two perform housekeeping functions in all cells. Changes in their expression are related to global changes in the cell.

The expression of rRNA and tRNA is affected in certain conditions such as stress and also possibly cancer (may be due to high replication rates). However, even if they are affected in cancer you cannot use them as markers for specific cancers as they are present and highly expressed in all cells.

Therefore specific tumour suppressor genes and oncogenes are studied.


How do bats survive their own coronaviruses?

It's common for the reservoir host of a zoonotic virus to be tolerant of it. MERS coronavirus appears to cause mild or no disease in dromedary camels ( source ), but kills about 35% of confirmed infected humans. ( CDC ) Sin Nombre hantavirus seems to be mild in the deer mice that spread it, despite ~36% fatality rate in humans. ( source ) Mosquitoes are efficient vectors for flaviviruses like dengue and zika in part because they have adaptations we lack that protect them from the virus. ( source ) Also, human communities are host to several viruses: about 90% of people have a herpesvirus infection ( source ) with similar numbers for polyomaviruses. ( source ) Very few of these infected individuals show symptoms.
The wide prevalence of these asymptomatic infections shows that the virus is successful when it can replicate while the host remains healthy. In general, virus reproduction kills cells, and when cells die faster than the host can replace them, this causes symptoms up to and including death. The host's immune system supresses virus activity, and a virus that can't evolve ways to avoid immune supression will be wiped out. But if the virus gets so good at avoiding the immune system, it will kill the host, which is bad for the virus. So both host and virus tend to evolve to a point where the immune system wins most, but not all of the time. There is a lot more to it, but I'll stop here.

In conclusion, we don't really need to look for special properties of bats to explain their tolerance of coronaviruses, even though, as iayork points out, there are reasons to expect bats might be more resistant.


By what mechanism does elevated homocysteine level cause endothelial dysfunction and damage?

In addition Alan Boyd's answer homocysteine interferes with Glutathione synthesis by reducing the catalytic efficiency of GCL (Glutamate–cysteine ligase), the enzyme which performs the rate-limiting step in GSH synthesis.

  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267299/

  Results of the present study are the first to suggest that the relatively high levels of homocysteine that accumulate during aging can interfere with de novo GSH synthesis. Although the precise nature of the underlying mechanism is at present unclear, our results demonstrate that physiological concentrations of free homocysteine can inhibit the efficiency of cysteine utilization by GCL in a competitive manner. Homocysteine has been shown to bind GCLc at the active site in vitro [25] as well as in vivo [35], forming γ-glutamylhomocysteine [36], which is then rapidly degraded enzymatically. An additional mechanism by which an age-related increase in free homocysteine can inhibit the catalytic efficiency of GCL in a competitive manner is described in [35]. It is possible that an aging-related increase in the competition between cysteine and homocysteine for the cysteine binding site of GCL might lead to a decrease in GC synthesis.

Low glutathione means a reduced ability to detoxify and deal with oxidative stress and a more oxidised redox state which has many implications

Further reading:

Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage
http://www.sciencedirect.com/science/article/pii/S2213231713000244

Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability
http://content.onlinejacc.org/article.aspx?articleid=1125915


How does the immune system distinguish between a TH1 and a TH2 response?

From what I have read, the Stage 3 differentiation depends on the surrounding cytokine environment. IL-2 does not specifically promote T-Cell differentiation, it is a general growth factor which promotes proliferation, and is secreted by both profiles.

Differentiation of T-Cell into Th1 is controlled by Interferon Gamma, the production of which is stimulated by IL-12, which is secreted by many APCs (upon stimulation by IFN Gamma produced by cells, in a self-feeding loop). IFN Gamma also suppresses IL-4 production.

Th2 cells are promoted by IL-4. It is not exactly known which cell initially produces IL-4, but it could be basophils. IL-4 then acts in a self-promoting loop, which encourages T-Cells to produce IL-4 as well as other effector cytokines, and also stimulates IL-10 production, which suppresses production of IFN Gamma and IL-12.

Thus, each pathway is self-promoting and suppresses the other pathway, ensuring that the immune response is set in stone.


Can systemic intravascular thrombosis cause brain infarction?

No, a thrombus would be much too large to pass through the highly selective blood brain barrier.  However, there are some cases where intra-vascular thrombosis can cause stroke.

One example would be non anti-coagulated atrial fibrillation, where the inefficient beating of the heart causes blood to remain stagnant in the left atrium.  This can cause a thrombus to form within the atrium which can then throw off emboli, some of which may enter the cerebral circulation. These may then partially or fully occlude one of the arteries in the Circle of Willis (the brain's circulation system), however the blockage is proximal to the blood brain barrier.

See Management of atrial fibrillation (GY Lip,2007) or for those hitting a pay-wall the professional reference section on AF


"Soft bodied" can come from a number of conditions, but generally, soft bodied insects are kept in ethanol. Adult insects should not need any kind of treatment before being pinned. Nymphs and immature insects should be in ethanol, and I suspect this is what you have. However, they can be freeze dried for a nice effect. One technique that works for females that are full of fatty eggs (such as Orthoptera) is to make an incision on the ventral side with an exacto-knife, and scrape out the contents of the abdomen. Then stuff with cotton, and close the incision. I think you likely have immatures, which should be in ethanol, but this technique would work if you are careful.


Human population growth - where can I find the data?

National censuses are collected, published and disseminated primarily by each country's census or national statistical office (NSO) or its equivalent. Census data are published in each country's vernacular, and as appropriate, many offer English as well as other language versions.
Statistical offices of international agencies (e.g. United Nations, statistical organizations for member states like the ASEAN, Eurostat, and OECD), also publish statistical data including population figures. The most consistent data in terms of format and frequency, whether online or in print are usually generated from them.

The US Library of congress provides some interesting links here:
http://www.loc.gov/rr/business/census/intlcensus.html
Also Cornell provides a few resources also:
https://www.ciser.cornell.edu/ASPs/datasource.asp
If you still need some information, your best bet is to then contact social scientists and ask for their opinion.


what benefits does lab procedure Realtime PCR have in gene silencing experiments?

RT-qPCR amplifies mRNA molecules present in a cell, if you have the right primers for it. The whole point of RNAi (the "gene silencing" that I think you're referring to) is downregulating the expression of a specific gene, so you'd expect the mRNA transcript of said gene to be not present (rather, present at very low concentrations at any given timepoint) if indeed the interference has worked.

Therefore, after RNAi has been performed, you can check by qPCR that there are indeed very low levels of the specific mRNA present in the cell. You might want to also perform a Western Blot against control cells transfected with scramble siRNA (where nothing should be downregulated, think of it as an "empty" siRNA), to check that protein levels are indeed much lower than in "regular" cells.


What is the meaning of "gap" in G1 phase?

The $G_1$ gap is the period between the last cell division and that start of DNA replication (synthesis). That's what "gap" means here. A period of time between two events. It's often described as time spent synthesizing proteins, but I prefer to think about it as the period before the signal to start synthesis lands. A cell can do any number of things in the meantime: synthesize proteins, grow, interact with other cells, move, differentiate, enter and exit $G_0$...

Albert's has a good chapter on the overview of the cell cycle and on the control system


Why are omega-3 fatty acids so easily oxidized when they're incorporated in cellular membranes?

I think the explanation for this description of fish oils as "easily oxidised" can be found in the Introduction to the actual paper (Nutrition 27 (2011) 334–337) that is cited in the article linked to in the question.

  Fish oil contains high levels of eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3), which are omega-3 polyunsaturated fatty acids. EPA, DHA, and fish oil have been shown to have protective effects against coronary heart disease, thrombosis, inflammatory processes, carcinomatosis, and metabolic syndrome. Therefore, fish oils and components of the oils are marketed as health supplements. However, the effects of omega-3 polyunsaturated fatty acids on aging and lifespan are unclear compared with those of omega-6 polyunsaturated fatty acids contained in safflower oil and soybean oil. EPA and DHA are oxidized easily compared with linoleic acid (18:2 omega-6) and oleic acid (18:1 omega-9) in vitro .

In other words, the fish oil omega-3 fatty acids EPA and DHA have, respectively, 5 and 6 double bonds, whereas the omega-6 fatty acids in safflower oil, linoleic acid and oleic acid have, respectively, just 2 and 1 double bonds. So the fatty acids in fish oil are more prone to oxidation simply because they have so many more double bonds.

Incidentally, as you can see from the two structures below, both of the omega-3 fatty acids, EPA and DHA, also have an omega-6 double bond.

EPA:

DHA:


enhancers in cell-type-specific signatures

Enhancer is a just a term for a regulatory region distant from a gene that contains specific sites where transcription factors bind. As it happens, a single enhancer can contain DNA binding sites for multiple transcription factors.

For example, an enhancer called TESCO, which regulates a gene called SOX9 (involved in sex determination) has binding sites for many different proteins (confirmed or putative): SRY, SF1, SOX9, ESR1, FOXL2 and likely many more that I haven't heard of. This allows complex regulation of SOX9 through protein-protein interactions.


X Linked Hardy Weinberg Equilibrium Problem

I make it 8%. Here is my reasoning.
The gene is X-linked.
40% mutant males, so freq(mutant allele) = p = 0.4, and freq(wt allele) = q = 0.6
To get a mutant female we have to have a mutant male parent, probability = 0.4
Of these matings one half will produce a female offspring so 0.4*0.5 = 0.2
i.e. 20% of matings derive from a mutant male and produce a female offspring.
Now look at the female mate:

probability(mutant) = p2 = 0.16
probability(carrier) = 2pq = 0.48
probability(wt) = q2 = 0.36

so our 20% of matings that have the potential to produce a mutant female offspring partition as:

mating with a mutant female: 0.2 x 0.16 = 0.032 mutant female offspring
mating with a carrier female: 0.2 x 0.48 = 0.096 of which:
0.048 mutant female offspring
0.048 carrier female offspring
mating with wt female: 0.2 x 0.36 = 0.072 carrier female offspring

(sanity check - 0.032 + 0.096 + 0.072 = 0.2)
Thus the probability of random mating producing a mutant female is 0.032 + 0.048 = 0.08 (8%)
Incidentally there is another way of thinking about this. Note that the H-W frequency of mutant females in the population is 16%. One of the assumptions of H-W is random mating. So the probability of a random mating producing a mutant female = p(female) * p(mutant if female) = 0.5 x 0.16 = 0.08
So - where have I gone wrong?


How correlated is the chirality of different molecules?

Hypothetically if an alien species were found , and if they contained similar biochemical polymers (DNA with A,T,C,G , Protein with 20 Amino acids etc) then we MAY be able to conclude that they share an origin with us. (Just similar chirality does not necessitates the theory of same origin)

Does the chirality of a single compound more or less determine the chirality of all other compounds in an entire biochemistry?

Yes. As Chiral molecules are almost always produced/purified from chiral medium (containing other chiral molecules and/or chiral physical attributes e.g. polarized light).
Therefore (Assuming that the reaction is enantioselective and you want pure chemical with a specific stereochemistry) the configuration of the chiral center of a new molecule does depend on the reagent chirality. Still this relation is not constant and differs from one reaction to another. For instance textbook SN2 reaction leads to inversion of configuration while Williamson ether synthesis reaction maintains the chirality.
A non-racemic mixture of a chiral compound is resulted from previous non-racemic mixture and so on. therefore the stereochemistry of the first non-racemic mixture determined the S/R , L/R ,(-/+) chirality of the entire life per se whose identity may never be fully understood.


Looking for book or article that derives formula for estimating the "average heterozygosity"

$H=4N\mu$ is the formula you're trying to derive.

It is an approximation coming from an infinite site model and applies to diploid populations only. For haploids, it becomes $H=2N\mu$. The value $4N\mu$ or $2N\mu$ is often also called $\theta$ as it is a value that appears in many places in the field.

There are a number of ways to derive it. It can be derived from coalescent theory or from classical fixation index stuff from Wright.

Any good intro book to population genetics should derive this formula. (see for example in Gillespie's book). You will find more book recommendation at Books on population or evolutionary genetics?.


Why are not both alleles knocked out at the same time in knock out mouse?

It is a simple matter of probability. If the probability of replacing one allele is p then the probability of two alleles getting replaced would be p2 (note that the latter will be smaller because probabilities are less than one).

If you have a selectable marker such as GFP then you'll end up selecting both heterozygotes and homozygotes but the frequency of the former will be much higher especially when you consider the fact that the probability of homologous recombination mediated knock-out/in is very low in mammalian cells (10-7 – 10-5). Therefore, inbreeding is an easier way to obtain homozygotes than screening the ESCs. Moreover, selective breeding is inevitable because in the first round will just produce chimeras (not all ESCs are replaced with the modified ones).

Technologies like CRISPR are now being used to accelerate the rate of gene replacement.


To what group does coconut plant belong?

In terms of taxonomy and morphology:

  Although coconut trees display considerable morphological diversity,
  they are considered taxonomically a single species (and the only
  species) within the genus Cocos. Based on stature and breeding,
  coconut cultivars can be divided into two groups: tall and dwarf.
  The former typically grows up to 35 to 40 meters and is mainly
  outcrossing, whereas the latter can only grow up to 25 to 30 meters
  and usually is selfing. Dwarf coconuts, which are less common than the
  tall variety, are usually found growing close to humans and have
  traits that likely result from human selection.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074736

I've found little information about whether or not they are halophytes, hydrophytes, xerophytes,or mesophytes - but according to a Google Book, a number of crops are widely cultivated in non-saline soils, including Cocos nucifera (coconuts). Another Google book with a lot of information about coconuts states this: Some experiments show that a small quantity of salt added to the tree roots is beneficial.

Cocos nucifera also love sunlight, so they can be considered heliophytes.


When birds fly in V-formation, how is it decided which bird gets to be the 'lead bird'?

There is an advantage for birds to fly in a V-Formation as stated by Portugal et al, 2013:

  As a bird flaps, a rotating vortex of air rolls off each of its
  wingtips. These vortices mean that the air immediately behind the bird
  gets constantly pushed downwards (downwash), and the air behind it and
  off to the sides gets pushed upwards (upwash). If another bird flies
  in either of these upwash zones, it gets free lift. It can save energy
  by mooching off the air flow created by its flock-mate.

There is no advantage to the lead bird though, only the birds behind will get these free lifts by being in the upwash zones.

A study on Ibises determined that there was no clear lead bird and birds cycled between positions. Flying in a V-formation is a collective effort, there would be no benefit to always being in front, so the birds take turns. I would assume the same aerodynamics and the cycling of lead bird apply to all birds that generally fly in V-formations such as Geese. Otherwise the lead bird would just exhaust itself and not have enough energy to complete the migration, it would be the same situation as if the bird was flying alone.

  By carefully observing the flock, the investigators learned that the
  amount of time a bird is leading a formation is strongly correlated
  with the time it can itself profit from flying behind another bird.

  By working together, a flock of birds is greater than the sum of its
  parts. By not being selfish, individual birds can reap the collective
  advantage of aerodynamic wash-up, while also allowing for larger
  flocks, which result in yet more time for an individual to be in a
  backdraft situation.

Additional Reading:

http://phenomena.nationalgeographic.com/2014/01/15/birds-that-fly-in-a-v-formation-use-an-amazing-trick/

https://io9.gizmodo.com/why-birds-take-turns-at-the-front-when-flying-in-v-form-1683465294

References:

Portugal, Hubel, Fritz, Heese, Trobe, Voelk, Hailes, Wilson & Usherwood. 2013. Upwash exploitation and downwash avoidance by flap phasing in ibis formation flight. Nature http://dx.doi.org/10.1038/nature12939


Epistasis Across Chromosomes and Individuals 'Homozygous for Interactions'

Question 1: The phenomena you describe in which it matters whether you have one or two copies of an allele (e.g., the AA phenotype being different than the Aa phenotype) are known as dominance effects. Dominance effects can interact with epistatic effects (in which the phenotypic effect of one locus depends on the genotype at the another locus).

One good example is the interaction between the Agouti locus and the Mc1R locus in the oldfield mouse (Peromyscus polionotus) in determining coat color. Dark-color homozygotes for the Agouti locus have dark coats irrespective of the allele at the Mc1R locus, whereas color in Agouti heterozygotes or light color homozygotes depends on genotype at the Mc1R locus. The figure below, from Steiner et al (2007), illustrates:

Question 2: Epistatically interacting loci need not be on the same chromosome. The loci discussed above provide a perfectly good example. Mc1R is on chromosome 1, where as Agouti is on chromosome 7, yet they interact epistatically.


Is the amount of cholesterol the body produces affected by how much cholesterol you take in with food?

Here's a study in which they measured a decrease in endogenous cholesterol synthesis after various amounts of dietary cholesterol: Dietary Cholesterol Feeding Suppresses Human Cholesterol Synthesis Measured by Deuterium Incorporation and Urinary Mevalonic Acid Levels (Arteriosclerosis, Thrombosis, and Vascular Biology, 1996):

  The objective of this study was to measure the response of cholesterol
  biosynthesis in subjects to three different amounts of dietary
  cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per
  2800 kcal. Individuals with low (n=7), normal (n=12), and elevated
  (n=11) plasma cholesterol concentrations consumed in random order
  solid-food test diets (15%, 55%, and 30% of energy as protein,
  carbohydrate, and fat, respectively) at each dietary cholesterol
  level. The three diets were consumed for 4 weeks each, and each
  dietary phase was separated by a 4-week washout period. During the
  final week of each diet, 0.7 g D2O was given per kilogram of body
  water and deuterium incorporation into the erythrocyte cholesterol
  pool was measured for 24 hours. Urinary mevalonate levels were also
  determined in samples obtained during two consecutive 24-hour periods.
  Both techniques provided measurements of whole-body cholesterol
  biosynthesis. In all subjects the cholesterol synthesis rate as
  measured by deuterium incorporation was significantly lower (P<.05)
  after the transition from low- to medium- and low- to high-cholesterol
  diets. Urinary mevalonate excretion decreased after the change from
  the medium- to high- (P<.05) and low- to high- (P<.01) cholesterol
  diets. Although correspondence between the two methods was poor, they
  both indicated some suppression of cholesterol synthesis by dietary
  cholesterol. The response of cholesterogenesis to different amounts of
  dietary cholesterol was related to the rate of synthesis under
  depressed conditions of the low-cholesterol diet. These findings
  indicate modest downregulation of synthesis in response to dietary
  cholesterol in humans, independent of plasma cholesterol levels.

  Metabolic responses to increased dietary cholesterol potentially
  include reduced endogenous synthesis, decreased absorption, and
  increased biliary excretion of cholesterol.

In some people, who are cholesterol hyperresponders, dietary cholesterol does not effectively suppress endogenous cholesterol synthesis, so it results in elevated blood cholesterol levels (Comprehensive Biotechnology, 2011). In one study, a decrease in dietary cholesterol intake resulted in a decrease of blood cholesterol in hyperresponders but not in hyporesponders: Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol (Clinical Nutrition, 1986):

  In this study we addressed the question whether hypo- and
  hyper-responders to dietary cholesterol differ with regard to the
  flexibility of endogenous cholesterol synthesis after changes in
  cholesterol intake. Whole-body cholesterol synthesis was measured as
  faecal excretion of neutral steroids and bile acids minus cholesterol
  intake. In addition, we determined serum concentrations of lanosterol,
  a precursor of cholesterol and a possible indicator of cholesterol
  biosynthetic activity. The study was carried out with 2 hyper- and 4
  hypo-responders; these subjects had shown a consistently high or low
  response of serum cholesterol to a decrease in dietary cholesterol in
  two previous experiments.

  The subjects received controlled high- (on average 697 mg of
  cholesterol per day) and low-cholesterol (109 mg/day) diets for
  periods of 4 weeks in succession; cholesterol was the only dietary
  variable. The two hyper-responders again showed a significant decrease
  in serum cholesterol. There was essentially no decrease in serum
  cholesterol in three of the four hypo-responders. The decrease in
  cholesterol intake caused an increase in cholesterol synthesis in five
  out of the six subjects.

In conclusion, in most people, dietary intake of cholesterol does not increase blood cholesterol levels because of decreased absorption and endogenous synthesis and increased excretion of cholesterol.


Looks like some species of tadpole shrimp. I couldn't tell you what species. There's really no other basis for identification other than these are extremely unique. As you can imagine, they're endemic to a variety of wetland environments. The take home point, however, is it's a crustacean rather than an insect.


Retraction of claws is a feature of the cat family, Felidae along with some civets that helps them keep those sharp by preventing unwanted wear.These claws are important for the members of cat family, including domestic cats that hunt preys by grasp attack rather than bite.

However cheetah among the big cats that usually hunt through bite-attack, has evolved to have semi-retractable claws that help it generate traction.

In pet cats it has offered another advantage:
Retraction keeps them from getting tangled in fabrics.

Sources:

Wikipedia
Russell AP, Bryant HN. 2001. Claw retraction and protraction in Carnivora: the cheetah (Acinonyx jubatus)
as an atypical felid. J Zool ,Lond 254:67-76.


What does "rapamycin-sensitive oncogenic transformation" mean?

The mammalian target of rapamycin (mTOR) is a Ser/Thr protein kinase that functions as an ATP and amino acid sensor to balance nutrient availability and cell growth. When sufficient nutrients are available, mTOR responds to a phosphatidic acid-mediated signal to transmit a positive signal to p70 S6 kinase and participate in the inactivation of the eIF4E inhibitor, 4E-BP1. These events result in the translation of specific mRNA subpopulations. mTOR is phosphorylated via the PI3 kinase/Akt signaling pathway and also autophosphorylates under translationally repressive conditions. mTOR plays a key role in cell growth and homeostasis and may be abnormally regulated in tumors. It is currently under investigation as a potential target for anti-cancer therapy.

The mTOR signaling pathway shows how mTOR is involved in numerous cell processes that can be dysregulated in cancer, including cell growth, proliferation, angiogenesis, autophagy, and various kinds of metabolism. "Rapamycin-sensitive oncogenic transformation" therefore means that the transformed cells still have intact "wild-type" mTOR complexes that can be down-regulated by the tumor-specific administration of rapamycin analogues, hence inhibiting the above-mentioned processes and arresting or killing the cells.


What do the intervals between groups of arrays in microarray gene expression data images mean?

The borders provide visual cues for the image analysis software to know which spot is which. The spots are also not printed all at once, but by a series of print heads, and the spaces allow for a small amount of error in the alignment of the print heads. It also allows for humans to more easily eyeball the results - the chip map can be printed in groups, and if you're looking to see what gene X did in your experiment, and know it's in the 2nd row, in the 2nd block, row 8, column 4, you can find it more easily than just knowing it's in row 73, column 27.


Isn't biological immortality strictly speaking impossible?

Good question.

There are many organisms that are technically biologically immortal. However, I would like to point out that the definition of biological immortality is this:

  ...cells that are not limited by the Hayflick limit, where cells no
  longer divide because of DNA damage or shortened telomeres.

(That's from here.)

So biological immortality doesn't really cover disease or physical trauma, which would actually include damage to DNA. I know what you're thinking: But wait, doesn't biological immortality literally mean cells that don't die because of DNA damage? Nope. Close, but no. Look back up at the definition. You probably caught it this time (by the way, it's not listing two different reasons (DNA damage and shortened telomeres), just rewording the Hayflick limit (DNA damage aka. shortened telomeres)). Biological immortality does not mean that the cell will not die because of excessive mutation (which would fall under physical trauma mind you, be it from chemicals, radiation, or just plain mistakes during replication), it means that the cell will not die from excessive programmed mutations, aka. its Hayflick limit, aka. telomere degradation. A molecular biology course summary from Berkeley says:

  However cells that express telomerase still undergo cellular senescence in response to DNA damage, oncogenes, etc.

Ok, sidetrack time (go ahead and skip this part if you already know what telomeres are). A telomere is a repeated DNA sequence at the end of a chromosome that protects the coding regions from deletion (the reason for these deletions is complex and off topic, but long story short, RNA primers cannot attach to the very end of a chromosome, so a little of the lagging strand is lost during every replication). So the telomere takes the hit instead of the important coding DNA further up the chromosome (see this article.) As you can imagine, there is only enough telomere to go around, so cellular aging exists unless the organism has active telomerase, which is an enzyme that adds telomeres every time they are lost (see this article).

So, short answer, biological immortality is very possible in its actual definition (see above).

Concerning your definition (immortality regarding all mutations, programmed or otherwise), an organism comes to mind: Physarum polycephalum. It is biologically immortal in the way we have just defined, but also avoids DNA mutation by sharing DNA (constantly comparing and fixing sequences) among thousands to millions of nuclei through homologous recombination, which repairs DNA mutations at a freakishly high efficiency when you include millions of strands bearing what should be the same sequence (see this article). Physarum polycephalum is a slime mold, meaning that when cells meet each other, they fuse. This particular slime mold actually prefers to be a plasmodium, which is a constantly growing mass that is technically a multinucleated single cell but can grow to be potentially infinitely large as far as we can tell. Because of its extreme ability to correct mutations, this organism has been referred to as, exactly like you said, an "evolutionary dead-end." I'm sure it still sustains some mutations over a very long period of time, but you might want to check it out nevertheless.


There are different opinions on this, since it's about usage. You could make an argument that, if you're talking about a B-cell clone, it is the product of a specific VDJ recombination (a mature, but naive B-cell), and refers to B-cells that produce antibody to one antigen. However, the term was originally proposed in this context:

  ...the expendable cells of the body can be regarded as belonging to clones which have arisen as a result of somatic mutation or conceivably other inheritable changes. Each such clone will have some individual characteristic and in a special sense will be subject to an evolutionary process of selective survival within the internal environment of the body.

In this case, I'd argue that, when the BCR sequence changes in progeny from that original naive B-cell (as in affinity maturation), you end up with different clones.

You do have to be careful, though, because people use this term differently.


In my experience, transduction efficiencies skyrocketed when I applied a spin-infection procedure. A 30 min low speed centrifuge with the virus changed a lot. Here is the TRC protocol for this: http://www.broadinstitute.org/rnai/public/dir/download?dirpath=protocols/production&filename=TRC%20viral%20infection%20200909.pdf


Can someone identify the species of this frog/ toad?

Looks to me like an Indus Valley bullfrog (Hoplobatrachus tigerinus).
Your specimen would be a bit small, but the species is nocturnal, the area fits and the patterning looks like a decent match as well:

(taken from the Wikipedia page)


One source for this estimate is Megias et al. 2001, an electron microscopy study in CA1 of the rat hippocampus.

I plot their data from Table 3 in the following graph.

The X-axis is not in micrometers. Rather it represents dendritic subclasses. $Ori$ stands for Stratum Oriens, $Rad$ for S. Radiatum, $L-M$ for Lacunosum-Moleculare, $T$ for thick dendrites, $t$ for thin dendrites, $prox/med/dist$ for proximal, medial, and distal, respectively. Stratum Oriens represents basal dendrites that are close to the cell body, stratum Radiatum apical trunks, and stratum Lacunosum-Moleculare the apical tufts. The approximate locations of the layers in reference to the cell body are (in micrometers): $Ori = (-100, 0)$, $Rad = (100, 350)$, $L-M = (350,550)$. The Y-axis represents the total number of synapses, both excitatory and inhibitory.


Why are sperm cells not attacked by the female immune system?

Studies show semen does mount a considerable immune response in the female mucosa, however:

  Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


Why is the Kakapo more attracted to humans than its own kind?

The male kakapo (Strigops habroptila) in that video is called Sirocco. Kakapo were (and still are) very close to extinction, so in the 1980s the Kakapo Recovery Programme was launched. As part of this programme, rangers monitor all known kakapo in the wild, visiting their nests and generally ensuring they are in good health. When Sirocco was a young chick, a ranger discovered him in his mothers nest with severe breathing problems. He was brought back to the Kakapo care hut and raised by humans. As a result of this, he imprinted on his carers (see his website!).

Imprinting is common in birds, and takes several different forms. The most well-known form is filial imprinting, where young birds (and some other animals) develop a strong fixated image of who their mother is. They then learn their behaviour almost exclusively from the animal they fixated on. This is well studied in geese, for example by Konrad Lorenz.

However, Sirocco was demonstrating sexual imprinting. This is where young animals (including humans, see e.g. Bereczkei et al., 2004) learn which characteristics are sexually desirable by fixing an image of their parent(s). In Sirocco's case, he imprinted on a human and subsequently saw humans as his species, and therefore potential mates.

The exact purpose of sexual imprinting has been widely discussed (e.g. see Immelmann, 1972). Lorenz suggested that it allowed animals to recognise their own species. However, some imprintable birds will show a preference toward individuals resembling the one they imprinted on, but when introduced to their own species will still recognise them as potential sexual partners. It may therefore be the case that imprinting allows a juvenile firstly to supplement a genetic predisposition toward its own species, but secondly to recognise closely related and less related individuals. Bateson (1978) suggested that this would enable a sexual strategy of choosing mates which are sufficiently unrelated so as not to cause inbreeding depression, but sufficiently related so as not to cause outbreeding depression, and he found an example which bore out the predicted behaviour in Japanese quails.

Sirocco seems not to have the genetic ability to recognise his own species, and according to his website does not associate with other birds.

 Bateson P. 1978. Sexual imprinting and optimal outbreeding. Nature 273, 659 - 660.
 Bereczkei T, Gyuris P, Weisfeld GE. 2004. Sexual imprinting in human mate choice. Proceedings of the Royal Society of London, Series B: Biological Sciences 271: 1129–1134.
 Immelmann K. 1972. Sexual and Other Long-Term Aspects of Imprinting in Birds and Other Species. In Advances in the Study of Behavior, Vol. Volume 4 of, pp. 147–174, Academic Press


The saying that you are referring to is from Carl Sagan, when he stated that:

  "We are a way for the universe to know itself. Some part of our being knows this is where we came from. We long to return. And we can, because the cosmos is also within us. We're made of star stuff,"

Quote source

In answer to your question, yes, we are 'repurposing' the elements that make us up, as are all living and non-living matter.

Chris Impey, professor of astronomy at the University of Arizona is quoted in the article Are We Really All Made of Stars? (Melina, 2010) as stating:

  the fact that the carbon, nitrogen and oxygen atoms in our bodies, as well as atoms of all other heavy elements, were created in previous generations of stars over 4.5 billion years ago. Because humans and every other animal as well as most of the matter on Earth contain these elements, we are literally made of star stuff

The elements that make up the cells etc in humans and any life forms, as with the materials that make up the Earth itself were ultimately formed by nucleosynthesis processes (mostly fusion and neutron capture) in stars, explained in the webpage Origin of the Chemical Elements as being:

  the early Universe consisted almost entirely of the element hydrogen, with a small amount of helium present too. Hydrogen, therefore, is thought to be the starting material from which all other elements have been built. This is consistent with the very high abundance of hydrogen in the solar abundance profile. The process may be thought of as a series of fusion reactions which weld together simple atomic nuclei to build increasing complex atomic nuclei.


Difference between sexual and asexual spore

In the same wikipedia page of spores you cited, you can find that they have said:

  Fungi commonly produce spores, as a result of sexual, or asexual, reproduction. Spores are usually haploid..

Again,

  Vascular plant spores are always haploid.

So, sexual and asexual spores have no difference in ploidy- both are haploid. (There are exceptions- zygospores in fungi are diploid)
Now, coming to mode of formation, they are different. For example, in Ascomycetes, sexual ascospores are produced endogenously whereas asexual conidiospores are produced exogenously.

Spores that are formed by the process of meiosis are sexual spores and when formed from mitosis are asexual. The term 'sexual' means meiosis is involved.


Use of pigs for obtaining transplant organs

Monkeys and many other primates are too small to provide organs that will provide the needs of a human host. The fact that primates are so close to humans physiologically is not always a win as transplanted organs will bring diseases into the host that can be quite dangerous.

Besides, because even human human transplants induce immune rejection of organs. Its typical that immune suppressants will be a lifetime treatment for the patient.

Finally, the cost of a pig organ is negligible and their organs are about the right size, and I would bet that activists don't protest pig transplants nearly as much as primate donors.


How does your body know when it is infected so it can invoke a fever?

During infection certain macromolecules present in the pathogens (pathogen associated molecular patterns) such as lipopolysaccharide launch the innate immune response, through toll like receptors. This leads to production of pro-inflammatory cytokines and also other inflammatory mediators like prostaglandins, thereby causing inflammation and fever.


Response of the gustatory receptor neurons can be measured using standard electrophysiological techniques, under different conditions(exposure to substances). For example see this article.

However, it is difficult to say if a person feels sweetness or not or how the substance produces complex taste perceptions in some people.


Could someone recommend a book for surveying species?

Judging from your response to Gurav in the comments, it sounds like introductory zoology and plant biology texts would fit the bill.

For zoology, we teach from Hickman et al's Integrated Principles of Zoology. It outlines the major phyla, their defining characteristics, with plenty of specific examples scattered throughout. There are nice little problem sets throughout, and it goes into a solid amount of detail for a first or second year zoology course.

For plants, I've used Graham et al's Plant Biology, which takes a similar general approach. Though it's perhaps a bit broader, and less species-focused.

Both of these books outline the major relevant groups, and use 'representative' species to illustrate various biological points throughout. They might be a good place to start!


See this paper "Divergence time estimates for the early history of animal phyla and the origin of plants, animals and fungi" for information on the divergence estimates (I'm not sure if there are more recent papers discussing this).

Plants, animals and fungi are eukaryotes, distinct from eubacteria and archaebacteria, which are prokaryotes. The difference being in the composition of the cell, particularly a nucleus contained within a membrane for eukaryotes, along with other membrane bound organelles, e.g. chloroplasts. They all share a common ancestor, according to this paper, that split 1.576 Bya (billion years ago) +/- 88 Mya (although it states the relationships are unresolved - it is often difficult to resolve relationships so deep in a tree). They form distinct groups known as Kingdoms under Linnaean based biological classification; the Fungi, Plantae and Animalia. Thus, in answer to your question, no, animals did not evolve from plants.

Plants have chloroplasts in their cells, which provide the ability to produce energy via photosynthesis. It is thought that the chloroplast resulted from a symbiotic relationship between early plants and a cyanobacteria in that they both relied on each other for survival and so coevolved. Animals don't contain chloroplasts and instead contain an organelle called the mitochondria (although most plants also have mitochondria), which is also thought to have been a bacterial endosymbiont, probably related to rikettsias.

Protists also contain chloroplasts. The protists are intermediate between all three groups and have been notoriously difficult to classify, being placed into a fourth Kingdom, the Protozoa, although this grouping has been contested. The current Cavalier-Smith system was proposed in 2004 and classifies life into 6 Kingdoms.

Chloroplasts are thought to have evolved from a single endosymbiotic event in Archaeplastida, although there are evidence to suggest some secondary endosymbiotic events. Check out this paper for more information; figure 1 shows the relationships between the different groups and the endosymbiotic events. The Opisthokonts are the origin of the Fungi and Animalia kingdoms.


Why does the blood not clump and result in death?

Some people do die from graft vs host disease after bone marrow transplants involving ABO incompatibility, but not usually from blood clots.

Foreign red blood cells don't usually form significant clumps (or clots) as a result of an antibody interacting with a surface cell antigen. They can form tiny clumps, however, that are not life threatening, but simply plucked out of the bloodstream by macrophages.

The typical reaction consists of foreign red blood cell detection and destruction (broadly called hemolytic anemia.) So anemia is a problem, but normally not significant clumping/clotting.

Safety and impact of donor-type red blood cell transfusion before allogeneic peripheral blood progenitor cell transplantation with major ABO mismatch.
Blood transfusions and the immune system
Consequences of ABO incompatibility in allogeneic hematopoietic stem cell transplantation.


Can germs develop surfactant resistance in a harmful way?

Never say never indeed!
a three part answer to the question:

Bacteria can develop resistance.  These researchers did a screen for Staph and Pseudomonas which survived a detergent/soap treatment and indeed were able to select for many strains.  I'm not sure that their explanation of why they are resistant is a final answer, especially for the Pseudomonas strains which have no hypothesis at all.

Nearly all bacteria do this all the time #1  Most bacteria can go into spore or plaque forms which basically hibernate.  These plaque colonies are matrices of crosslinked bacteria and are resistant to extremes of conditions in the environment or lack of food.

Even Normal Resistance is a relative thing.  Alcohol sanitizers kill 99.9% of bacteria.  That sounds like a lot but that 0.1% can come back to full strength in a relatively short period of time.  0.1% is still millions of individuals surviving after a shower.  Resistant bacteria have a higher proportion of survivors and should improve the bounce back rate.  So resistance is a term which you need to define for a given situation.

Surfactant (soap) resistant bacteria can be nearly any sort of bacteria and a certain percentage of them are ready for a scrub down at any given time.  To get a surface completely free of bacteria takes a good deal of work.
As far as a danger to human health - resistance to being killed by soap is a real problem because the few of them which also have resistance to antibiotics and are pathogenic will be pretty much unstoppable.  Its not likely that surfactant resistance will itself make a bacteria pathogenic (never say never!) but if such a 'triple threat' emerges we'd all be in trouble.


Why does tetracycline have such a broad spectrum of activity?

This is a tricky question. First of all, I wouldn't call tetracyclines "uniquely" broad spectrum. They are broad spectrum, but there are other drugs with equally broad coverage absent acquired resistance (e.g., imipenem and chloramphenicol), and current clinical use of tetracyclines is limited somewhat by the spread of resistance.  They don't have any major class limitations, though. Again, absent acquired resistance, tetracyclines are effective against gram positive aerobes and anaerobes, and gram negative organisms, as you seem to be aware.

Tetracylines access their target on the 30S subunit of the bacterial ribosome (blocking the A site, as you said) by passive diffusion through porins of the outer membrane of gram negative bacteria, and active transport across the cytoplasmic membrane of gram negative and gram positive bacteria, but the mechanism for that active transport is still unknown. This is quite a good review despite being quite old. Now, some 30 years later, we have still not identified the exact mechanism, as you can read in Goodman & Gillman's most recent edition (13th), Ch. 59, crossing the cytoplasmic membrane requires metabolic energy, but the process is not well understood. Because of this, we can't point to a specific structural or chemical characteristic. For chloramphenicol, it would be the ability to diffuse across the cytoplasmic membrane; for tetracycline, we don't know. I suspect part of the reason for this is that people are now more interested in pumps removing tetracyclines from the cell than those that accumulate it, so it's more of a question about research priorities than some transport mechanism that is particularly difficult to detect.


Do Red blood cells(mammals) really have no organelles?

Yes. This is true. During the final stages of red blood cell formation in the bone marrow, the nucleus and several other organelles are broken down and/or expelled from the cells. In the process they decrease markedly in size, from about 24 to about 7-9 micrometer. Presumably this makes them small enough to pass through the smallest capillaries. Lacking those organelles also limits their life expectancy to approximately 120 days.


If you have a sequence, run a nucleotide BLAST search at NCBI, specifying Triticum aestivum (taxid:4565) as the organism.
The miRBase page for Triticum aestivum has details of wheat microRNAs, and a page where you can do a sequence search with either BLAST or SSEARCH (as @WYSIWYG kindly pointed out).
Perhaps the Triticum aestivum page at PlantGDB may help.


Is there a durable surface that ants can't pass?

I've found that ants do not walk through petroleum jelly. It is also convenient, as it isn't too messy, and can be whatever shape you want. I use it to keep ants from climbing into my hummingbird feeders. Make sure the area you treat is wider than the ant is long.


List of proteins by number of amino acids / chain length

You can find the data you need in the Protein Data Bank.

  Since 1971, the Protein Data Bank archive (PDB) has served as the
  single repository of information about the 3D structures of proteins,
  nucleic acids, and complex assemblies.

  The Worldwide PDB (wwPDB) organization manages the PDB archive and
  ensures that the PDB is freely and publicly available to the global
  community.

Each of the PDB member organisations provides the same data with a different interface:

PDBe,
PDBj,
RCSB.

In general, you either query the database through one of the web interfaces, or you download all the data and search it locally. In this case, the RCSB website has the option you asked about (sorting by the residue count):

Alternatively, you could download:
ftp://ftp.wwpdb.org/pub/pdb/derived_data/pdb_seqres.txt
and parse it and sort it as you wish.
This file has sequences of all chains in the PDB entries.

But since your goal is to find the relationship between the sequence and the folded structure, you should probably start from reading about the protein folding problem and about methods used in protein structure prediction.


How can rapid growth cancer get nutrients in vivo?

Long back in 1971 Falkman and others put forward new therapeutic implications of targeting blood vessels supplying nutrients to tumors.   Treatment you are mentioning is called 'Anti-angiogenic therapy '. However current challenges in this therapy are resistance to antiangiogenic agents and non specificity. Plus there was huge 'normalization effect' which was actually helping other blood vessels around tumor. To answer your question, Cancer cell makes their own blood vessels instead relying on host machinery. There are many other factors also why this kind of treatment is not successful yet.


Can citric acid be used as fungicide in banana based fly (Drosophila melanogaster) food?

I have no data on the fungicidal and insecticidal properties of citric acid at various concentrations (and you may be hard pressed to find a good study on this), but I have worked in some fly labs and I understand the composition of fly food only peripherally. The most commonly and most abundantly used fungicide in a lot of fly labs is methylparaben (trade names Tegosept or Nipagin in Europe). I imagine food recipe-makers have arrived at this solution through trial and error over the years; this is as much an art as it is a science, in balancing the ingredients with humidity, temperature, species and genotype with desired generation time. Methylparaben is used with and without propionic acid for Drosophila melanogaster. Do you have methylparaben in your fly food? Also, I think citric acid is not commonly used, again I imagine because technicians probably found it inferior to its alternatives.
The National Drosophila Species Stock Center at Cornell uses methylparaben with its banana food recipe.
Alternatively, please take a look at the variety of recipes Bloomington Drosophila Stock Center uses. To my knowledge they supply and stock the largest collection using the most recipes.

Fly foods
Alternative recipes


Calculating Protein Concentration from Kilo Units (KU)

From the page linked from your link:

  Unit Definition

  One unit will convert 1.0 μmole of phospho(enol)pyruvate to pyruvate
  per min at pH 7.6 at 37 °C.

So, the unit is defined by activity, and there is no way to know how many molecules or milligrams of protein are included


ECG detection using minimal number of electrodes

You could try to dig into the specs of the new/upcoming Withings ECG smartwatch for some insights https://www.withings.com/uk/en/move-ecg


Yes, mantises hunt cicadas...

Mantis eating cicada. Source: Dreamstime.

...and yes, orioles hunt cicadas too...

Oriole eating cicada. Source: Bird Ecology Study Group.

.., and what may be more relevant to your idiom: orioles prey on mantises.

Oriole eating mantis. Source: Sustainable Adventure.


Why do people in the scientific community use terminology such as renal, hepatic, cardiac instead of kidney, liver and heart?

Medicine is not my field, but I want to point out two things:

The former words have latin (or greek) roots, and historically latin was the international language of science. Therefore, nomenclature in different scientific fields are often based on latin.
The former words describe tissues and the related functions/processes (e.g. renal = kidney + related tissues + processes carried out by the renal system), while the latter are names of organs. Therefore, the former words are more suitable and precise when you want to describe these processes. For instance (as far as I know), Hepatic disease can be be caused by problems outside of the liver as such, e.g. blockage in the hepatic vein.

Users more knowledgeable in medicine are welcome to fill in or correct me if I'm mistaken.


Short answer
It all depends on the time window you are talking about. After having been detached from the mother plant, a leaf will typically keep on photosynthesizing for a few hours or so.

Background
Cutting of the stalk of the leaf results in impaired water flow and wilting. As soon as a leaf is detached from the plant, it will also be cut off from hormones, minerals and other nutrients. The result of this is that senescence (and death) sets in straight away. However, leaves will typically stay green and moist for hours or even days, dependent on the conditions it is stored. Hence, in practice, photosynthesis can be measures at least a few hours after a typical leaf is picked (source: Science and Plants for Schools).


Why are the results of local BLAST and miRbase BLAST different?

The main problem I could identify is that your scoring matrix is not the same; as you said miRbase uses match score of +5 and mismatch penalty of -4.

The BLASTN defaults can be found here. However, I ran the local BLAST using the exact command that you mentioned and the default values that it used were:
reward = +1
penalty = -2

Matrix: blastn matrix 1 -2
Gap Penalties: Existence: 0, Extension: 2.5

The other reasons could be the difference in the database itself (the sequences used) or the version of BLAST used in the two cases.


Which will produce more oxygen? A few large trees or a greater number of smaller plants?

Ignoring parameters such as:

Leaf shapes
Difference in photosynthetic efficiency due to other metabolic factors
Unequal illumination of leaves
Nutrient content of the soil

Photosynthesis rate of a plant1 depends on the [total number of leaves] × [surface area of a leaf].

Assuming that a tree occupies same ground area as a shrub, there will be same number of trees as shrubs.

A tree is taller and can bear more number of leaves and if we assume that the surface area of the leaves are similar between trees and shrubs then the tree would carry out more photosynthesis.

However you say that the number of leaves is the same; in this case both will carry out same amount of photosynthesis (the shrub may outlive the tree though, as the latter won't be able to support its huge size with same level of photosynthesis as the shrub).

A note on phtoplanktons and algae: One reason amongst a few for why they are efficient at photosynthesis is because the number of photosynthetic cells per volume is higher in them.

1 I am using the term plant to denote all plants. Big trees are called trees and small plants are called shrubs, for convenience.


I think you pretty much nailed the problem. If I understand correctly, you are just confused about the approximation that your textbook does, an approximation that is correct but not needed. Let me restate the solution to the problem first.

Resolution of the problem

As you said the frequency of sick people $\frac{1}{300} = 2pq + q^2$ in this case, where $q = 1-p$ is the frequency of the (dominant) allele causing the disease. It is a simple quadratic equation with one unknown so one doesn't even need to make any approximation to solve for $q$ (or for $p$). Rearranging the equation and expressing $p$ in terms of $q$ (p=1-q), you'll find that $q ≈ 0.00167$.

Are the results intuitive?

Note that the frequency needed to create a frequency of $\frac{1}{300}$ sick individuals is $\sqrt{\frac{1}{300}} ≈ 0.05$ if the allele causing the disease is recessive while it is only about $0.0016$ (31 times less frequent) if the allele causing the disease is dominant. It shows that indeed a lower frequency of a more dominant allele is enough to create more sick people.

Is the $q^2$ term negligible?

Given that $q ≈ 0.00167$, the term $q^2 ≈ 10^{-6}$, while the term $2pq ≈ 10^{-3}$. So, indeed the term $q^2$ is rather negligible compared to $2pq$.


Actually there is some confusion here, and that's quite excusable, because it's extremely common reading that monoploid and haploid are synonyms and have the same meaning. However, they are different terms. According to Hartl and Ruvolo (2012):

  The potential confusion arises because of diploid organisms, in which the monoploid chromosome set and the haploid chromosome set are the same.

As we, human beings, are diploid organisms, it's easy to see why haploid and monoploid ended up being considered as synonyms.

However, a more precise terminology would be:

Monoploid: the total number of chromosomes in a single complete set of chromosomes (this does not change whether we are talking about a somatic cell or a gamete).
Haploid: half of the total number of chromosomes in a somatic cell. The haploid chromosome set is the set of chromosomes present in a gamete, irrespective of the chromosome number of the species.

That being said, diploid and haploid are not antonyms nor mutually exclusive terms. A cell can be diploid and haploid at the same time. Let's exemplify this with organisms that perform gametic meiosis:

Human beings have diploid somatic cells, with 46 chromosomes. When a somatic human cell perform meiosis, it produces haploid cells which are monoploid. Human gametes are haploid and monoploid.

In wheat (Triticum aestivum), somatic cells are hexaploid, having 42 chromosomes (that is, 6 full sets of 7 chromosomes). When a wheat cell perform meiosis (producing micro and mega spores, and later on gametes), it produces haploid cells which are triploid. Wheat gametes are haploid and triploid.

The same whay, a tetraploid organism would produce, by meiosis, a cell which is haploid and diploid. Thus, depending on the number of chromosome sets in the somatic cell of a given species, you can say that a gamete is diploid (as stated in this other answer).

In a nutshell, a gamete that was produced by meiosis (there are life cycles where the gamete is not produced meiotically) is always haploid, regardless the number of chromosome sets it has (which will determine if it is monoploid, diploid, triploid, hexaploid etc...).

Sources:

Hartl, D. and Ruvolo, M. (2012). Genetics. 1st ed. Burlingham, Mass.: Jones and Bartlett Learning.
Genetics-notes.wikispaces.com. (2017). genetics-notes - Ploidy. [online] Available at: https://genetics-notes.wikispaces.com/Ploidy [Accessed 1 May 2017].


This is a question that has been the focus of study for the last century (e.g., Amodel of cell size regulation - Ycas et al, J. Theoret. Biol. (1965) 9, 444-470). Cell size regulation may be in part determined by ribosomal activity (through mTor regulation) and is a critical checkpoint in cell division.

How the cell senses its size, however, is not understood. In 2009, two reports suggested that protein gradients could be responsible for the sensing of cell size. You can read a commentary about those articles in Cell size control: governed by a spatial gradient. - Almeyda and Tyers, Dev. Cell. (2009) 17(1), 3-4:

  The phenomenon of cell size homeostasis, whereby cells coordinate
  growth and division to maintain a uniform cell size, has been an
  outstanding issue in cell biology for many decades. Two recent studies
  in Nature in fission yeast demonstrate that a gradient of the polarity
  factor Pom1 is a sensor of cell length that determines the onset of
  Cdc2 activation and mitosis.

These articles demonstrate one way in which cells may sense their size, but most probably several other mechanisms are also in place.


What percentage of individuals infected with COVID-19 don't have symptoms?

The proportion of individuals infected by SARS-CoV-2 who remain
asymptomatic throughout the course of infection has not
yet been definitely assessed.

The COVID-19 epidemic, Tropical Medicine & International health (2020)

The asymptomatic ratio is thus estimated at 41.6% (95% confidence interval (CI): 16.7%, 66.7%) among evacuees. Because fourteen days have elapsed since their departure from Wuhan—longer than the 95th percentile estimate of the COVID-19 incubation period (Li et al., 2020; Linton et al., 2020)—there is very little probability that the five virus-positive asymptomatic individuals will develop symptoms. Should one of the five becomes symptomatic in the future, the overall asymptomatic ratio would decrease to 33.3% (95% CI: 8.3%, 58.3%).

Estimation of the asymptomatic ratio of novel coronavirus infections (COVID-19), International Journal of Infectious Diseases (2020)

Our estimated asymptomatic proportion is at 17.9% (95%CrI: 15.5–20.2%), which overlaps with a recently derived estimate of 33.3% (95% confidence interval: 8.3–58.3%) from data of Japanese citizens evacuated from Wuhan [13].

Estimating the asymptomatic proportion of coronavirus disease 2019 (COVID-19) cases on board the Diamond Princess cruise ship, Yokohama, Japan, 2020, Eurosurveillance (2020)

Table S1. Model parameters. All time periods are given in days.
Parameter                     Baseline              Distribution  Reference/reason
                              (alternative values)
...
Pr(Asymptomatic | Infection)  0.178 (0.1, 0.5)      Beta          Mizumoto et al. (13) (lower, higher)

Estimating unobserved SARS-CoV-2 infections in the United States (preprint) (2020)


how to reconcile PDB structures' sequences via Uniprot references?

None of them is integrase:

P12497
Protein    Gag-Pol polyprotein
Gene       gag-pol
Organism   Human immunodeficiency virus type 1 group M subtype B (isolate NY5) (HIV-1)

P14350
Protein    Pro-Pol polyprotein
Gene       pol
Organism   Human spumaretrovirus (SFVcpz(hu)) (Human foamy virus)

Even if you meant the integrase product of the polyprotein, the second one is not even HIV.

From Wikipedia:

  Human Foamy Virus (HFV) is a retrovirus and specifically belongs to
  the genera Spumavirus. The spumaviruses are complex and significantly
  different from the other six genera of retroviruses in several ways.
  The foamy viruses derive their name from the characteristic ‘foamy’
  appearance of the cytopathic effect (CPE) induced in the cells.[1]


Is it possible that the recipient of a heart transplant would display some of the donor's personality traits, as if the heart has memories?

Although there is clearly no feasible mechanism for such a phenomenon, there is good evidence that transplant patients can believe in some sort of transference of qualities from the donor. See for example (my emphasis):

Inspector, Y. et al. (2004) Another Person's Heart: Magical and Rational Thinking in the Psychological Adaptation to Heart Transplantation. The Israel Journal of Psychiatry and Related Sciences 41: 161-73.
Abstract
The goal of this study was to examine heart transplant recipients' psychological adaptation to another person's heart, with particular emphasis on recipients' attitudes toward graft and donor.
Thirty-five male heart recipients were examined by: the Symptom Distress Checklist (revised) (SCL-90-R); the Depression Adjective Checklist (DACL); a Post-Traumatic Stress Disorder Questionnaire (PTSD-Q); a Heart Image Questionnaire (HIQ); and a Semi-Structured Interview (SSI), aimed at eliciting attitudes and fantasies regarding the transplanted heart.
All instruments indicated high levels of stress even several years after the transplant, but, simultaneously, 73% of recipients felt that acquiring a new heart had had a dramatic influence on their lives with a new appreciation of the preciousness of life and a shift of priorities, toward altruism and spirituality. Sixty percent returned to work after the transplant but some had to adapt to a changed attitude from those around them who regarded them as anything from mystical creatures to vulnerable or still-sick individuals. While all recipients possessed a scientific knowledge of the anatomy and physiological significance of the heart (as revealed in the HIQ), many endorsed fantasies and displayed magical thinking: 46% of the recipients had fantasies about the donor's physical vigor and prowess, 40% expressed some guilt regarding the death of the donor, 34% entertained the possibility of acquiring qualities of the donor via the new heart. When asked to choose a most and least preferred imagined donor, 49% constructed their choices according to prejudices, desires, or fears related to ethnic, racial or sexual traits attributed to the donor.
This study confirms the intuitive idea that heart transplant involves a stressful course of events that produces an amplified sense of the precariousness of existence. Simultaneously, it gives rise to rejoicing at having been granted a new lease on life and a clear sense of new priorities, especially with regard to relationships. Less expectedly, this study shows that, despite sophisticated knowledge of anatomy and physiology, almost half the heart recipients had an overt or covert notion of potentially acquiring some of the donor's personality characteristics along with the heart. The concomitance of the magical and the logical is not uncommon in many areas of human existence, and is probably enhanced by the symbolic nature of the heart, and maybe, also, by the persistent stress that requires an ongoing, emotionally intense, adaptation process.

Another study is reported in:
Bunzel B, et al. (1992) Does changing the heart mean changing personality? A retrospective inquiry on 47 heart transplant patients. Qual Life Res. 1:251-6.
To actually investigate this further I suppose it would be necessary to set up experiments in which patients had transplant operations in which (unknown to the patient) no transplant actually took place, with the expectation that these individuals would display the same magical thinking. Grant application?


What is meant by Physarum polycephalum having 720 sexes?

It is true that many/most unicellular organisms such as e.g. bacteria or fungi have no need for sex to reproduce, and can divide by simple cell division. However, sex (defined rather broadly) is a universal feature of life. For example see this review article by Rosie Redfield, which examines exactly what we mean by "sex". The broad definition is just recombination of genetic material, which is a universal (or nearly so) feature of organisms.

It's a little hokey to say that Physarum polycephalum has 720 sexes, as "sex", the idea of a specific category of individuals with regard to reproduction, is different from the biological idea of "sex", when we say "yeast have sex".

What Physarum has, like fungi and other similar organisms, is not really sex, but mating type (see here). Mating type really has nothing to do with what kind of sex organs a fungus has, but rather what fungi have sex with. Certain mating types only have sex with certain other mating types. But this isn't really a one-to-one correspondence like male-female. It's much weirder than that.

There are both "heterothallic" (sort of "single-sexed") and "homothallic" ("hermaphrodite") mating types of the protist, and each organism has a mating type. The homothallic ones don't need other individuals to have sex and make offspring. The heterothallic ones do need other individuals. These mating types are defined not by a sex chromosome like in humans, but by a single gene. When they say 720 sexes, what they mean is that we have found 720 different DNA sequences at the mating type gene which have somewhat different mating behaviors.

I think that your evaluation is correct that the journalists are being pretty inexact here. But I think also that it's important to recognize that basically all of biology is sexual, one way or another.


Fruit colour related to the dissolving of pectin

During ripening, pectinases are produced which break down pectin and render it soluble. Color change is also associated with fruit ripening.

Hence the correlation.


What Freshwater Fish Are Affected By Magnetic Fields

Sockeye salmon species definitely do, although admittedly the interesting salmon are those that spend significant time in the ocean.
Here's some evidence that carp can.
Raindbow trout are also capable.
Zebrafish are also able.
Japanese eels too, of which some are freshwater.


Is epilepsy more heritable from maternal side?

Epilepsy is a neurological disorder characterized by hypersynchronous discharge of neurons .i.e abnormal electrical activity in the brain. Epileptic seizures caused primarily due to i) inhibition of inhibitory neurotransmitter systems such GABA neurotransmitters or ii) Enhancement of excitatory neurotransmitter systems such as nAchR. These conditions arise due to head injury, trauma and genetic factors. But there is no evidence as of now regarding Mitochondrial DNA taking part in inhibitory and excitatory systems. so, epileptic seizures are not specific in inheriting from any side (Maternal or paternal side) as far as pathophysiology of epilepsy is concerned.


Is it true to say that the genome of trees includes or at least "encapsulates" the genome of mushrooms?

No.

Evidence: If you go to the TreeGenes site and examine those tree genomes that have been sequenced you won’t find any fungal chromosome sequences. (And vice versa.)

Reason: Although trees and mushrooms may develop symbiotic relationships they are independently viable (at least the trees), and even two organisms that can only survive in a symbiotic relationship have separate nuclei with separate chromosomes. They are distinguishable, so they are distinguished.


Why it seems that principles of chemistry are not being applied in this biochemical process?

From the link given by @Kendall

Such a gradient can be maintained because the thylakoid membrane is essentially impermeable to protons.

I think this solves your dilemma of 'why not maintaining equilibrium' totally.

The reason for this difference is that the thylakoid membrane is quite permeable to Cl- and Mg2+. The light-induced transfer of H+ into the thylakoid space is accompanied by the transfer of either Cl- in the same direction or Mg2+ (1 Mg2+ per 2 H+) in the opposite direction. Consequently, electrical neutrality is maintained and no membrane potential is generated.

It precisely shows why electrical equilibrium is not disturbed due to pH disturbance.
Finally:

2 H2O + 2 NADP+ + 10 H+stroma => O2 + 2NADPH + 12 H+lumen
12 H+lumen + 4 ADP + 4 Pi => 4 ATP + 12 H+stroma


They are doing a peptide competition assay (see abcam protocol).

The antibody is incubated with a purified sample of the antigen and used in a normal Western-Blot of cell lysates. Any cross-reactivities of the antibody would still be visible as only the interaction with the epitope of interest is blocked. So all bands that disappear after such treatment are indicators for the substance that was used for blocking. A Western-Blot with non-blocked antibody is normally used for comparison.

In the experiment you mentioned, they vary the principle a bit, as they are comparing two blots - one blocked with a succinylated library, one with a non-succinylated one. As the band disappears after treatment with the succinylated library, they confirm that their antibody is specific against succinylated proteins - at least in these three cases.


most different human tissues with respect to gene expression profiling

You can navigate the GTEX project. PCA section.

https://www.gtexportal.org/home/histologyPage?tab=PCA

You have different samples for many tissues. Currently you can navigate it tissue by tissue but perhaps there's a way of visualizing the whole dataset (or you can ask for it).


Blood antibody tests for Chlamydia trachomatis can be done, but they are far less reliable than amplification:

  According to our results, serologic testing for Chlamydia can exclude active infection of the lower genital tract with a high reliability (> or = 95%). However, detection of C. trachomatis can only be reliably achieved by nucleic acid amplification assays.

Low correlation of serology with detection of Chlamydia trachomatis by ligase chain reaction and antigen EIA


Everyone has a mix of ongoing oscillations, of brain waves, at any given point. Some frequencies of waves are more or less likely to co-occur with other types of waves.

In general, brain activity follows roughly a power law distribution - that is, there is more power at lower frequencies and that power decreases in a predictable way as you go to higher frequencies.

When researchers talk about brain waves at a particular frequency, they are talking about a deviation from power law at that frequency - if they say "gamma waves" what they really mean is "there is more energy at gamma frequencies than we would expect if things were random."

Some of these deviations are predictable with changes in brain state - for example, low frequency (delta) activity is greater during sleep, and higher frequency (gamma) activity is higher during cognition.

It should also be understood that these terms really come from a method of data analysis such as Fourier analysis that breaks a signal down into component frequencies. It isn't necessary that a signal is actually produced by combinations of sine waves to break that signal down into component sine waves and describe it that way.


In what "space" does egg mature in Kiwi?

In birds, eggs mature post-fertilization in the magnum and "shell gland", sometimes called a uterus.

I can't find anything to suggest a kiwi is any different, despite their large egg size. An exception is that kiwi have two functional ovaries (yet the join in one functional oviduct and the rest of the reproductive system is only present once) (Ballard & Cheek, 2016). Given this source mentions this specific difference, it seems unlikely they would have omitted any other important differences.

This course page may be useful for bird reproductive anatomy more generally: http://people.eku.edu/ritchisong/avianreproduction.html

Ballard, B., & Cheek, R. (Eds.). (2016). Exotic animal medicine for the veterinary technician. John Wiley & Sons.


I couldn't find anything about diplobacilli, but I did find some information on Streptococcus pneumoniae, which has been extensively studied. S pneumoniae (R6 strain) normally occurs as diplococci. Electron micrographs—see here and here—show that the two cocci of a pair share a portion of cell wall. This is a result of incomplete separation during cell division. Also, mutations in peptidoglycan-hydrolysing enzymes have been shown to produce longer chains of cocci.
Presumably, something similar holds for diplobacilli.
Calling these bacteria 'multicellular' might be inappropriate, because multicellularity implies at least some division of labour: the cells perform different functions in a cooperative manner. Diplobacilli (such as Moraxella lacunata) or diplococci have not been shown to have such a division of labour, as far as I know.


Does Povidone-Iodine that penetrates through the skin stays in the body (cells, liver etc)?

Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated.

Though Providine-Iodine is not absorbed as is, Iodine is.

From the Lexicomp drug information for prescribers:

  Absorption: Absorbed systemically as iodine; amount depends upon concentration, route of administration, characteristics of skin

Other pharmacokinetic properties are as for Iodine. It may be taken up by the thyroid. Clearance is primarily unchanged (as Iodine) by the kidney.

The absorption through the skin as iodine and elimination by the kidneys are the reasons for the prescribing precautions:

Use with caution in patients with burns (excess absorption)
Use with caution in patients with renal impairment (impaired excretion)
Use with caution in patients with thyroid disorders (taken up by the thyroid)

This case report of Iodine toxicity following prolonged povidone iodine administration is available on pubmed central. It's from the 80s, but it is still relevant and the comments section has a good overview:

  The reports of iodine absorption from topical povidoneiodine
  solution suggest that absorption is enhanced when the
  compound is applied to denuded skin, mucosal surfaces with
  high absorptive capacity or extensive areas of intact skin. The
  evidence for iodine absorption includes documented serum
  iodine concentrations and thyroid function abnormalities.


This is a bit hard - most possible answers you still aren't going to like, but I'll give you three suggestions.

It sounds like you want to take something with a mathematical model and try to modulate it with molecular biology.

It seems unlikely that I can really give you a specific project, but there are four sources  I will recommend you look at.

I think I'd suggest the further limiting assumptions:

you want to work with E coli - its the easiest and most readily available organism to work with.
you want to work with a system that is self contained within a single plasmid - so it relies only upon 2 genes to act, 3 at the outside or you will have issues getting it all to work.
you want a mathematical system that already has a well fit model that  you will peturb.  building a new model might be a bit of a big first off project.  (but who am I to tell you what to do - these are just suggestions).

The First suggestion I have is Jeff Hasty at UCSD.  He has focused a lot on oscillating gene circuits.  He has simple systems that might be reproducible with a small lab, most recent work that combines a GFP oscillator with LUX is pretty cool. Both oscillators and LUX are independently good systems to work with. .  I've been a science fair judge and I can tell you, just reproducing one of his systems would be an impressive lot of work

Another body of work to look at is Adam Arkin. He has looked at lots of circuitry component candidates.  Articles such as "The hunt for the biological transistor" might get you thinking.  This is a broader body of work, and so it might take a while to get an idea from it.

Third, if this is boring to you and you want to look more broadly, you can look through the iGEM competitions.  These are projects with oscillators and bio synthesis systems which sometimes have mathematical models associated with them.  The big advantage here is that you might be able to start or join an iGEM team and then some or all the plasmids will be made already - mol bio gets very expensive if someone doesn't gift you some materials.


I'm trying to answer my own question. I did a bit of searching, and I found out that my insect resembles the Mupli beetle the most. From Wikipedia:

  The Mupli beetle, Luprops tristis (ഓട്ടുറുമ in Malayalam), is a plant detritus eating Darkling beetle found in parts of India. The adult beetle is black and around 8 millimeters (0.31 in) long.

I hope someone can verify if my findings are correct or not.


Gooseneck barnacles
It appears to be a cluster of goose barnacles washed up onshore. This is based on the thick, distinct pedicle and the general shape of the asymmetrical valves. Without more information, that’s as accurate as I can probably get you.