What is the base cancer rate for an arbitrary carcinogen?

To answer this question in its entirety we have to split it into two questions:

  What are the underlying mechanisms of carcinogenity?

One of the main mechanism behind carcinogenity is the mutagenity of the cancerogens, i.e. the ability to cause mutations, that are abberations of the cell DNA leading to uncontrolled proliferation. This classical paper investigates the relation between cancerogenity and mutagenity.

One should mention here that there are many types of mutations possible, mutations are not equally dangerous for cells and some mutations can be successfully repaired using the intact strain.

Therefore the following parameters of the source substances need to be measured to estimate the cancerogenity:

Substance concentrations or absolute amounts (both being indirect measures of their chemical activities, the lower concentration is needed for causing cancer the higher is the chemical activity and vise versa).
Substance radioactivity (for the mutagenesis due to radiation).

  How can we measure the carcinogenity of different substances?

The most general approach here is to introduce certain amount of cancerogen into the animal body or to the cultured cell and to see the effect. The effect is calculated as the percentage of cells that undergo the transformation from normal into cancer cells. Two metrics are available here:

  DT = Tumorigenic Dose (the amount of substance causing certain
  percentage of cancer in treated animals, all treated animals are taken
  for 100%)
  CT = Tumorigenic Concentration (same, but adjusted for
  concentration and used in cell cultures).

(They are written CT and DT because in science people tend to used Latin abbreviations where the adjective actually follows the noune).

The common metrics are DT5/CT5 (5% cells/animals get cancer) and DT50/CT50 (50% of the animals). Those are similar to other common metrics, the most common is LC50/LD50 -- lethal dose for 50% of the animals/cells.

Unfortunately I couldn't not find any pre-compiled list with most known cancerogens and their TD/TC values. These seem to be interesting primarily for scientists. But going back to your question: you are absolutely right: some cancerogens are much more potent in causing cancer than the others!


Do cockroaches have less health issues than humans?

AndroidPenguin, where did you read that our immune systems are far better than those of 'a cockroach'? This seems pretty strange to me, but I'd be interested in reading a study that compared human and cockroach immune systems if you can provide a reference.

Victor, with respect to cockroaches, there are numerous species of cockroaches. Here's a page about cockroaches with a link to publications on cockroaches and a phylogenetic tree of the families and subfamilies.

http://www.bio.umass.edu/biology/kunkel/cockroach.html

All those species tend to occupy distinct niches with distinct traits. With respect to cockroach evolution, sewers are too new a phenomenon to have had an influence on cockroaches. Rather cockroaches have been successful in adapting to this novel 'habitat'. The same holds for rats and other denizens of sewers. Sewers are a very nutrient rich environment, and as in many nutrient rich environments, a few species tend to possess the right traits (whatever those may be) to survive and out-compete other species. To take an example from coral reefs, when coral reefs suffer from eutrophication, this leads to a growth in phytoplankton and a reduction of the euphotic zone that can lead to the death of all but the most resistant corals. Likewise in the terrestrial environment, only the most tolerant or opportunistic species tend to survive in highly perturbed and nutrient rich environments like sewers. With respect to cockroaches getting cancer, I've never read anything about insect cancer, but I imagine in theory that they could get cancer. I'm not sure, however, of the impact given the much shorter life spans of insects. It's an interesting question though.


What is the mechanism of antiperistalsis that occurs during vomiting?

Emetic agents in the bloodstream stimulate chemoreceptors in area postrema and nucleus tractus solitarius [1].
Nucleus tractus solitarius is connected to motor neurons in ventral medulla and hypothalamus [1].
Esophageal and gastric peristalsis is inhibited. Small bowel peristalsis is reversed. Esophagus and stomach don't have antiperistaltic movements [2].

  Why the peristaltic waves normally don't propagate in anal to oral direction?

Because of the mechanism of descending inhibition. Distension of the esophagus and intestine causes a reflex action that leads to circular muscular contraction just above the bolus/chymus. Longitudinal muscle also contracts (shortens) [3].

Reference:

Hornby PJ. Central neurocircuitry associated with emesis. Am. J. Med. 2001 Dec 3;111 Suppl 8A:106S-112S. PubMed PMID: 11749934.
Brizzee KR. Mechanics of vomiting: a minireview. Can. J. Physiol. Pharmacol. 1990 Feb;68(2):221-9. PubMed PMID: 2178746.
AUMSA. Digestive Physiology. May 2012. CC-BY-SA-3.0


How can one create images like those in the PDB ‘Molecule of the month’?

Those (really cool) pictures are created by David Goodsell using custom-written software.
From an interview to the artist:

PDB: How do you create the illustrations?
Goodsell: Most of the pictures are created with a computer program that I developed back when I was doing postdoctoral work with Dr. Art Olson here at The Scripps Research Institute. I've been using this style of illustration--with flat colors and black outlines--for about 10 years now. I like the way that this style simplifies the molecule, giving a feeling for the overall shape and form of the molecule, but at the same time you can still see all the individual atoms. On the last page of each Molecule of the Month--"Exploring the Structure"--I always use RasMol, to give visitors an idea of the kinds of pictures that they can create themselves with off-the-shelf software.

There are good tools around if you want to replicate that look. Although it may take a bit of tweaking (and possibly programming) I would surely give PyMOL and Bioblender a try.


Why does size decrease across the sequence of human chromosomes?

You nailed it!

Nomenclature

Autosomal chromosomes

Chromosomes are numbered based on their size (in base pairs).

Sexual chromosomes

Sexual chromosomes (when they exist) are defined as the largest number regardless of their length. Note that the definition of a sex chromosome can sometimes be a little bit troublesome (see this book).

Exceptions

It sometimes happens that the first approximation of the length of a chromosome is inaccurate and that chromosomes are therefore numbered wrongly. In such case, when we realize the mistake, we just keep numbering the chromosomes the same way we did before even if it doesn't follow the standard nomenclature! This is, for example, the case of chromosomes 19 and 20 in Homo sapiens as you can see on your barplot. Chromosome 20 is actually a little bit longer (by about 4.5 Mb) than the chromosome 19. There are many other types of exceptions as well. Thanks to @Dexter  pointing out int he comments that in Drosophila melanogaster (model organism) the sex chromosome is numbered before the automosomes (autosome = non-sexual chromosome).


How do you compare unpaired biological replicates?

Calculating fold change is pretty straightforward but you cannot do one on one comparison because they (control and treated) are not really paired (same sample). That's why IPA gives you six results (FC for each pair). However, you can calculate fold change between two genes because they are from the same sample. Note that fold changes are quite dangerous and can lead to misinterpretation of data (for example 1/2 would be same as 100/200). You should use them cautiously.

I think, in this case, you can simply apply a t-test. This will tell you if your two groups i.e. treated and control are significantly different from each other. You would not be calculating fold changes here. If you had more number of groups then you can go for one-way ANOVA.

I am not sure what output you really want after the analysis but I think the main goal is to say that control is different from treated.

Since you have multiple genes (variables) you can either go for a multivariate t-test, which will tell you if the control is overall different from treated, or many univariate tests which will tell you how each gene differs between the two groups. There are some methods such as Bonferroni correction which can be used to improve the prediction of multivariate tests.

When you have established that a certain gene is differentially expressed, using t-test, you can report the fold change of the averages.


Difference between intervertebral and vertebral foramina

They are actually different.

(source: emory.edu)
INTERVERTEBRAL FORAMINA is actually spaces between adjacent vertebrae which gives passage for spinal nerves to exit.
Whereas, VERTEBRAL FORAMINA forms vertebral canal.
Source:
Organization of the Nervous System: An introduction for students in the Human Anatomy Course


What is meant by a muscle fiber being glycerinated?

From: http://www.acad.carleton.edu/curricular/BIOL/classes/bio126/Documents/Lab_5.pdf

  Glycerination disrupts the membranes of the muscle cells, ruptures mitochondria, and leaches out soluble constituents such as ATP and inorganic ions. However, glycerinated muscle retains the organized structural array of myosin thick filaments and actin thin filaments, actin-associated proteins like troponin and tropomyosin which regulate contraction, and the functional capacity for contraction.

I would expect that because the sample has lost ATP and inorganic ions, you would need to supply ATP (the source of energy), $Mg^{2+}$ (which is necessary for ATP hydrolysis) and $Ca^{2+}$ (to induce the contraction).


What happens to glucose taken up by the liver in type 1 diabetes?

1) Hepatic glucose intake may not be much greater in hyerglycemia than in normoglycemia:

Regulation of Hepatic Glucose Uptake and Storage In Vivo (Advances in Nutrition, 2012):

  ...neither hyperinsulinemia nor hyperglycemia can independently induce
  much net hepatic glucose uptake.

2) Glucose can be used for de novo lipogenesis in the liver despite the lack of insulin:

De Novo Lipogenesis and Cholesterol Synthesis in Humans with Long-Standing Type 1 Diabetes Are Comparable to Non-Diabetic Individuals (PLoS One, 2013):

  Fasting total hepatic lipogenesis (3.91±0.90% vs. 5.30±1.22%;
  P = 0.41) was not significantly different between diabetic and control
  groups...


This isn't fully understood but one theory is that they live in soil feeding off dead things and so are in competition with bacteria and other fungi for resources including space.  The antibiotic compounds they produce have been described as a sword and shield.  Some compounds are offensive (sword) and attack other fungi and bacteria while other compounds protect a species (shield) from the compounds of other organisms seeking to do the same thing to them.  This is only half the story really, fungi also excrete compounds that look similar to antibiotics but have no known function.  Still other compounds have seemingly no effect on other organisms but when taken by humans and other mammals lower cholesterol in the blood. Strange thing for a fungus to produce.


My question, Is it just visual perception or special mechanism for detection of acceleration?

Acceleration is a synthesized conclusion from a multitude of systems.

Most prominent is the Endolymph system you already mentioned:

As you accelerate, the endolympth and the otoliths within (small, calcified deposits) pass over the hair cells and produce action potentials which travel to the brain. The higher the magnitude of acceleration, the more action potentials will be sent.

This is also where dizziness comes from, as the endolymph and otoliths do not come to rest at the same rate, momentarily giving the brain two different interpretations of what acceleration you're experiencing.

There is also the Doppler Effect:

Based in the cochlear system of the inner ear this time, instead of the vestibular system, the doppler effect is interpreted by the brain and gives a very rough interpretation of both velocity and acceleration (if the velocity of the object happens to be changing).

Then there is the entire visual side of things. Motion blur and the speed at which the perception of objects change size are large contributors to our sense of visual acceleration, but almost all of this is done via complex manipulation of visual data in the occipital and frontal lobes.

There are also countless minor contributors: skin and join tension (the sensation of weight due to acceleration), ease of breathing, sensory cells in your hair if your hair is exposed to the open air while acceleration, blood pressure sensors (and numbness when the body can't compensate), etc.

  In any of these cases, why I was feeling more acceleration while siting opposite than in direction of acceleration?

My guess would be because your body is more visually attuned to facing the same direction as the acceleration, and when you were facing the opposing direction your mind overcompensated in an effort to protect you since you probably don't get a lot of opportunities to rapidly accelerate backwards over distances of more than a few feet.

Your brain might also have been panicking a bit because you couldn't see where you were going (usually very bad), and the heightened sensory state made the magnitude of the acceleration feel greater.

These are my best guesses, however. If someone has an academic source, please feel free to edit this answer!


Four quick flaws:

1) Environments are always changing. The fitness space is dynamic, and includes both biological and non-biological players, the former which are also ever-changing. Given a sufficiently stable ecosystem, one would expect an equilibrium among species to develop (though it could be cyclical). However even if the environment stays constant, novel mutations could always increase the fitness of a given species, which could then affect the fitness of all the other species. Also, natural selection is not the only factor that influences evolution, and other factors can add dynamic instability.

2) You are conflating genetic algorithms with evolution. Genetic algorithms use selection to solve a minimization problem and are typically bounded within fairly rigid constraints. They are motivated by biology, not models for biology.

3) You are conflating complexity and fitness. Complexity can be more fit or it can be less fit. Evolution only selects for fitness, not for complexity.

4) Do organisms continually increase in complexity? Depending on how you define it, they may not. Thinking about humans as a "goal" of evolution or something like that is a feature of creationism or intelligent design, not biological evolution. Some of the most successful organisms on Earth in terms of number of individuals or even biomass are some of the simplest.

There may be others as well.


That one is Greek origin from aneimon or "naked, unclad, without clothing" which is to refer to the panicles of the sporangia.


Generally, ethylene production is used to gauge fruit ripeness.  This paper (PDF download) outlines an experiment measuring ethylene production from Hass avocados at different temperatures over several days.  It appears they used gas chromatography to measure both ethylene and CO2 concentrations.


What kind of red and black insect is in the photo?

This is a nymph of some species of Hemiptera, or true bug.

Specifically, this appears to be the nymph stage of a wheel bug (Arilus cristatus) or some other species in the family Reduviidae.

 Source: David Larson

 Source: Debbie Roos 2005

Here is a picture of an adult (with name-sake dorsal wheel):

 Source: Donald W. Hall

You'll notice that the nymph is quite different looking:

  Nymphs have been described in detail by Readio (1927). Smaller nymphs are bright red with black marks. The last instar nymphs are darker. Nymphs lack the "wheel" or crest. For a diagnostic key to identify nymphs of the family Reduviidae to genus (including Arilus), see Fracker and Usinger (1949). [Source].

If you're truly interested in accurately  IDing to genus/species, you might check out Fracker & Usinger 1949$^1$, Herring & Ashlock 1971$^2$, or papers that cite their work.

You can find more information about A. cristatus here.

Citations:

Fracker S.B. & Usinger, R.L. 1949. The generic identification of Nearctic reduviid nymphs (Hemiptera). Annals of the Entomological Society of America 42: 273-278.
Herring, J.L. & Ashlock, P.D. 1971. A Key to the Nymphs of the Families of Hemiptera (Heteroptera) of America North of Mexico. Florida Entomologist 54: 207-212.


How Do Acid and Base Loving Plants Get Enough PO4?

Fixation of phosphorous occurs when the chemical equations tip in favour of less soluble compounds. Plants are able to absorb Orthophosphate ions, such as H2PO4- and HPO42-.

Orthophosphate is most available to plants at pH values near neutrality. It is believed that in relatively acidic soils, orthophosphate ions are precipitated or sorbed by species of Al(III) and Fe(III). In alkaline soils, orthophosphate may react with calcium carbonate to form relatively insoluble hydroxyapatite:

3HPO42- + 5CaCo3(s) + 2H2O -> Ca5(PO4)3(OH)(s) +5HCO3- + OH-

Environmental Chemistry, Seventh Edition -Stanley E. Manahan
This does tend to make it more difficult for plants to obtain their phosphorous when it is stuck to something that they cannot absorb, but it is not hopeless. These equations are equilibria, so they can be made to go both directions by adding or removing reagents from each side.

The plants will pull from the left side of the equations by removing the orthophosphate ions. More will be released to maintain the equilibrium.
In acidic or basic environments, rainwater will serve as a base or acid to push the equations from the right.
Decaying organic matter releases orthophosphates that the plant can absorb.

In this way, plants living in acidic or basic environments would still obtain enough phosphorous.


What is the current consensus, if any, about why long term potentiation is not clearly correlated with learning?

I'm going to answer your general inexact question with a general inexact answer. The consensus is that LTP is correlated with learning.
To clarify in more detail, studies have shown that when an animal performs a learning task that involves the hippocampus(which is important for memory), and the animal effectively learns, less LTP is seen in-vitro in brain slices from these same animals. LTP is said to be occluded or blocked since potentiation of those synapses have already maximized through the in-vivo mechanisms. This can be interpreted as learning affecting LTP or at least both acting on the same basic mechanisms of the synapse(strengthening and weakening).

See for ex.
Learning induces long-term potentiation in the hippocampus.", Jonathan R Whitlock, Science (New York, N.Y.), 2006;313(5790):1093-7


The pigmentation of hairs is achieved by the follicular melanocytes (specialized pigment cells) at the base of the hair shaft. These cells produce the pigment which is subsequently transported into the cells which produce the hair and integrated into the hair matrix.

Besides genetic reasons, there are two major ways of losing this pigmentation. First, as a part of the normal hair cycle, the hair grows for a while until it falls out and the hair follicle regresses. In this process the cells in the hair follicle die, including those which made the hair as well as of the melanocytes. In this step of the hair cycle the hair follicle changes its morphology. When a new hair cycle starts, the pigment cells in the hair follicle are replenished from a stem cell population called melanocyte stem cells. These cells are located in the hair bulge (marked in red in the figure below). The cells then start to proliferate to multiply their number. A few of these cells stay stem cells (to be able to repopulate the pigment cells after the next hair cycle.) Others differentiate into melanocytes which subsequently migrate towards the bottom of the hair bulb (shown in green in the figure).

Over time, the number of stem cells gets lower, and at some point there are none left. This leads to a situation where the pigment cells are not replenished at the beginning of a new hair cycle and the hair stays unpigmented. As this is a continuous process, the pigmentation gets weaker before it is completely lost. As far as this process is understood to date, this depigmentation is irreversible.

There are two very interesting papers about this topic:

Melanocyte Stem Cell Maintenance and Hair Graying
Melanocyte stem cells: biology and current aspects.

The other reason for losing pigmentation (temporarily or permanent) is the generation of so called "reactive oxygen species" (Hydrogenperoxide) in the cells of the hair follicle, which then destroy the pigment. This is basically the same reaction which is used to bleach hairs, but in this instance from inside. This reaction can have numerous causes, among them are vitiligo and stress. The reason for the build-up of the hydrogenperoxides is that enzymes, which usually break them down before they can cause harm are either mutated or downregulated. If the level of these enzymes (the catalases) goes back to normal, pigmentation is also getting back to normal. This has been tested experimentally with people who suffer from the pigmentation disease vitiligo.

Oxidative Stress in Ageing of Hair
Basic evidence for epidermal H2O2/ONOO−-mediated oxidation/nitration
in segmental vitiligo is supported by repigmentation of skin and
eyelashes after reduction of epidermal H2O2 with topical
NB-UVB-activated pseudocatalase PC-KUS


What is the carbohydrate found in almonds, cashews, pecans, hazlenuts and pistachios?

Firstly you must realize that all the above mentioned nuts are actually the seeds of plants.

So the question now is which carbohydrate is mainly found in seeds of plants.

During the double fertilization of angiosperms, one sperm fertilizes the egg to form the embryo while the other fertilizes the endosperm nucleus to form the endosperm which acts as the nutrient storage for seeds.

The major carbohydrate for seed endosperm is Starch, often stored as granules for their property as being insoluble and compact.

However there are other carbohydrates such as free sugars, glucofructans and hemicelluoses present.

Hope this helped.

References
https://link.springer.com/chapter/10.1007/978-1-4615-2672-8_8


Beetle identification - Kakadu NP, NT, Australia

After a hint from @fileunderwater I also think now that it is much more likely that this beetle belongs to the family of the Scarabaeidae which contains some 30.000 species worldwide. Scarabaeidae and Trogidae (what I thought was right before) are part of the same superfamily, the Scarabaeoidea.

The way the antennas are shaped as well as the body shape and the way the legs are ordered looks pretty much like this, even better than for the Trogidae. Have a look at this poster which shows a lot of different varieties (from here):

Some more information and real images can be found here and here.


I found the same cultivar of banana being sold in a market while on a recent trip to Sulawesi, Indonesia. I was told by the owner that this cultivar is locally known as the pisang kepok, or alternatively the Saba banana. This cultivar is thought to originate from the Philippines.


As you note yourself, this depends strongly on the vessel that you are studying. I found this table in reference 1:

It lists speeds between 34 and 45 cm/sec for the inferior vena cava and 12 to 16 cm/sec for the superior vena cava.

For the capillaries I found this table in reference 2, which measured the blood velocity in cats. Nevertheless I think this approach is also useful for an approximation for humans since the capillary system should be comparable:

It lists velocities between 0,2 and 2,7 mm/sec.

References:

Velocity of blood flow in normal human venae cavae.
Regulation of blood flow in single capillaries.


This is a kind of neuroptera larva https://www.google.com/search?q=neuroptera+larva.

The smooth jaws discard an antlion https://en.wikipedia.org/wiki/Antlion.

Is more like a chyrsopidae https://www.google.com/search?tbm=isch&q=neuroptera+larva&chips=q:neuroptera+larvae,g_1:chrysopidae:qWI0Ngq4zAQ%3D. They like to camouflage with debris found around them.


Yes! Many mammals, including cats and humans, produce DMT in small amounts.
DMT has been detected in blood and urine and is produced by the enzyme indolethylamine N‐methyltransferase (INMT). These do bind to serotonin receptors. Serotonin receptors are actually expressed in multiple tissues outside of the brain. However, DMT does cross the blood-brain barrier (ref), so it's possible that endogenous DMT has some neuroactive effect (I really don't know). Good question.
This 2016 paper states (referring to a 2012 review) that it was identified in urine, blood, and CSF:

A review by Barker in 2012 assessed 69 studies that reported endogenous DMT detection and quantities reported in urine (29 studies), blood (11 studies), and cerebrospinal fluid (4 studies) from 1955 – 2010 primarily comparing detection levels within healthy controls and schizophrenic patients. DMT in urine was examined in 861 individuals (635 patients), 276 patients and 145 controls were positive for DMT.

I think that's the most direct answer to you question I could find.
I didn't find anything on cats specifically, but that's likely to be similar.
This earlier 2004 paper states that it was only found in urine, but the previous study refers to studies before 2004, so I don't know why these two seem to contradict:

In mammals, endogenous bufotenine and DMT have been identified only in human urine. The DMIAs bind effectively to 5HT receptors and their administration causes a variety of autonomic effects, which may reflect their actual physiological function. Endogenous levels of bufotenine and DMT in blood and a number of animal and human tissues were determined using highly sensitive and specific quantitative mass spectrometric techniques.

Here's the entry for INMT on Kegg, and the Human Protein Atlas lists where INMT is expressed. Weirdly, that enzyme is highly expressed in the human lung.


What percentage of RNA splicing happens during transcription?

I don't think it will be possible to give a conclusive answer to this question, because a) it's a matter of active research and b) the rate / percentage of transcripts that are fully spliced co-transcriptionaly is almost certainly not constant but will depend on a lot of factors & regulatory mechanisms.

Another important detail is that this analysis / paper is based on mRNA sequencing, which uses oligo-dT primers to enrich for polyadenylated mRNA molecules. However, oligo-dT primers can also bind to stretches of A's inside of RNA molecules (this process is called internal priming) and since such stretches are more common in introns compared to exons this may contribute to the abundance of intronic reads in mRNA sequencing data (I don't have a good literature source for this specific case, but it's a known 'issue' for sure).

Maybe some of these reviews are also helpful (not sure if all are freely available):

Splicing and transcription rates in living cells
Environmental influences on RNA processing
Co-transcriptional spliceosome assembly and function


No.

No higher order organism has enough proteins that are stable at 100 degrees C to survive. Proteins denature at higher temps and all cellular functions that depend on them cease.

Some thermophillic bacteria have evolved proteins that are stable above 100 degrees C over eons of evolution.


does small different between 16s ribosomal DNA leads to diffrence into protein products?

The 16s ribosomal DNA does not code for any protein, it codes for the 16s ribosmal RNA, which is part of the (small subunit of the) ribosome.

The differences will most likely not affect the ribosome much, but to be sure you'd have to check the exact position of the mutations in a reference structure and see if they are at important positions (i.e. binding of the Shine-Dalgarno sequence)


Is there an animal which, when eaten by other animal, poisons the predator and gets out of it's stomach?

The closest I can think of with that hint is a Middle Eastern beetle that hunts frogs and other amphibians:

  In almost 400 face-offs, the amphibians only managed to get the larvae in their mouths seven times. Even then, they soon spat out the larvae, which quickly turned on them (first video below). One toad even managed to swallow a larva, which moved inside its stomach for two hours. For some reason, the toad eventually regurgitated its catch, and the larva, apparently unharmed, killed and ate the animal that had just eaten it (second video below).

However, it's only a pseudo-fit to the clue. The beetle doesn't hunt American bullfrogs, but ones native to its area of the world.


Which server to use for volume and accessible surface area calculation of proteins

You can use PDBSum and PDBe-PISA servers for calculating accessible surface area and buried surface area and Castp server for finding pockets within your protein molecule. If your protein is globular, you can measure the diameter in pymol and calculate its volume. Hope it helps.


Are there any scientifically based predictions or theories of future human evolution?

Its pretty much impossible to predict what will happen in the evolution of species.  Evolution is a parallel search with millions (or in the case of humans 8+ billion) of threads.  Our adaptive capacities have never been fully understood and will always surprise us I think.

Of course that doesn't stop people from trying!  The prediction you mention is based on one man's ideas of dominant selection pressures on humanity now... for a men's TV show.  In Dr Curry's scenario, technology users, and economic disparity, producing Eloi and Morlock like dimorphism as in the HGWells book "Time Machine". This seems like hogwash to me.  All socioeconomic classes try to find high quality partners and height and attractiveness will be hard to stamp out in a large segment of humanity.

Economic elites breed slowly and even if they will try to skim the evolutionary cream of humanity off the top, there will be plenty of beautiful, tall and smart people who will lack economic opportunity in my opinion.

There have been more serious, IMHO, questions about whether medical technology, which lets the sick recover and may even compensate for genetically problematic traits.  There are no inoffensive examples I can think of so I'll take male pattern hair loss - apologies.  If medicine allows all men (and women) to grow a thick shock of hair regardless of our genes then the baldness traits might spread through the species.  Sure it could happen, but then most bald and balding people end up having children now anyway.

In fact since civilization has started feeding the hungry, making the hunting of wild beasts less important, causing the shrinkage of the male physique (we used to be much more muscular), inventing medicine and schools where smarts can be selected for, and giving us all more choice when it comes to mates, evolution has accelerated for human beings. The authors specifically cite social factors as being more important in our evolution now.


In a sugar such as a disaccharide are both ends of the sugar known as reducing ends?

No, in dissacharides the reducing end is situated only on one monosaccharide which is having free anomeric carbon. This carbon does not take part in glycosidic bond formation and can form open chain.

Check out:
https://chem.libretexts.org/Courses/Sacramento_City_College/SCC%3A_Chem_309_-_General%2C_Organic_and_Biochemistry_(Bennett)/Text/14%3A_Carbohydrates/14.6%3A_Disaccharides


Is it possible for a person to eat so many carrots that one turns orange?

Beta-carotene, the pigment that gives carrots their orange colour, can accumulate in the skin if taken in excess amounts. This condition is called carotenosis. Since beta-carotene is a lipohilic (fat loving: dissolves in lipids), its absorption is facilitated by dietary fats [1].

There is one report that says that excessive consumption of beta-carotene containing fruits and vegetables can lead to carotenosis [2].

Also have a look at this Scientific American blog.

Prince, Martin R., and Joan K. Frisoli. "Beta-carotene accumulation in serum and skin." The American journal of clinical nutrition 57.2 (1993): 175-181.
Wageesha, Nekadage Don Amal, et al. "Studies on hypercarotenemia due to excessive ingestion of carrot, pumpkin and papaw." International journal of food sciences and nutrition 62.1 (2011): 20-25.


All the mitochondria of an individual are originating from the mother. This means that if the mother is afflicted by a mitochondrial disease, the offspring will also be affected. This is why the three parent model is being considered in some cases (1).

(1) Pritchard, C. (2014, September 1). The girl with three biological parents. BBC News. From http://www.bbc.com/news/magazine-28986843


Was 14,000+ year old DNA "laying around in cave dirt" protected from degradation, or is it just naturally this robust?

To be clear they are not finding long DNA strands but short fragments. DNA becomes more robust the shorter it gets. Fragments can last millions of years. The local chemical conditions have a huge influence on how long DNA lasts the oldest being hundreds of millions of years old under ideal conditions.

The ones the archeologists are finding are not even close to enough to rebuild an intact strand but it can be used for matching. Of course contamination is a big problem, anything that dies leaves DNA in the soil. With humans it becomes especially problematic becasue the archaeologists themselves are a major source of contamination.

For an indepth look at contamination protocols, some of which as still questionable, can be found here. Sorry its behind a pay wall.

Likely they are referring to deamination cytosine substitution, which creates mismatched pairs of DNA and occurs more and more as DNA ages.


What's the smallest flier that migrates?

The marmalade hoverfly (Episyrphus balteatus) flies to Southern Europe and back every year.

It's difficult to track and find them compared to birds and butterflies, here is a study witch citations: https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1570-7458.2007.00568.x?purchase_referrer=scholar.google.fr&tracking_action=preview_click&r3_referer=wol&show_checkout=1

it is now known that large numbers of E. balteatus migrate South during the autumn period. Therefore, it has been sug-gested that a comparable migration to the North helps tore-establish E. balteatus populations in northern Europe during the spring. There are many records to show that some hoverfly adults are active so early in the spring that they could not possibly be long-distance migrants. Nevertheless, although some adults remain active late into the autumn, few authors have managed to find females in overwintering sites

studies have suggested that E. balteatus migrates in large numbers during late summer and autumn to the Mediterranean area and only return to central and northern Europe during the following year(Aubert et al., 1976; Gatter & Schmid, 1990; Kehlmaier & Martínez de Murguía, 2004; Hondelmann et al., 2005).

https://www.sciencenews.org/article/flying-insects-tell-tales-long-distance-migrations


Can any plant regenerate missing tissue?

In general, plant cells only undergo differentiation at special regions in the plant known as meristems. Two of the primary types of meristem are the root apical meristem (at the tips of roots) and the shoot apical meristem (at shoot tips)^. Within the shoot apical meristem the plant cells divide and begin to differentiate into different cell types (such as different cells of the leaf, or vascular cells). Later growth (of, say, a leaf) is largely a result of cell expansion (although cell division does still occur, but drops off as the leaf expands). Therefore, if you punch a hole in a leaf, it probably won't be filled in because the cells in that leaf have finished growing and dividing.

However, as a shoot grows, more meristems are created. These are found in the axillary buds, just above where the leaf meets the stem. The meristems in the axillary buds can grow to form branches. Different plants obviously make different numbers of branches, but there is a common control mechanism known as apical dominance, where the meristem at the tip of the shoot suppresses the growth of the lower axillary buds. This is why a shoot with no branches can be made to grow branches by cutting off the tip (gardeners often do this to make "leggy" plants more bushy).

All of that was a long explanation to say, no, a plant doesn't normally^^ regenerate in the sense of filling in cells that have gone missing. However, if you cut off a shoot, the next remaining bud might begin to grow and, in a sense, replace the part that was lost. In that case, an existing bud is recruited to form a new branch and replace lost functionality, but I wouldn't say that qualifies as regenerating missing tissue.

^There are other types of meristem as well.

^^If you torture plant cells enough you can force them to become "stem cells" and thereby make an entirely new plant, but this is rare in nature.


What are the limiting factors for gene length and number of exons?

This question drops firmly into the lap of molecular evolution and the constraints that are placed upon genes by the forces of mutation, selection, drift and recombination.

There are numerous situations, particularly gene duplication, that can result in a gene that is free from the selective constraints of it's parent, many of which will accumulate so many deleterious mutations as a result of stochastic processes that they will become non-functional e.g. psuedogenes. Some can be altered and rearranged, accumulating exons and introns, and if they infer a fitness benefit on the organism, may be moved to fixation within a population.

Evolution is a population genetics process, and there are many variables which can effect the outcome, not least the difference in populations size. The genomes of larger populations (such as those of bacteria) appear to have much smaller genomes, and of course no (at least not spliceosomal) introns, perhaps as a result of increased fitness due to the decreased generation time of an organism with a more slender genome. It would be a good idea to read The Origins of Genome Architecture by Michael Lynch, as I think he answers your questions, better than I can.

Many of the genes you retrieve from EnsEMBL will of course have experimental evidence to support them. The genes that are predicted in the pipeline can be looked upon with less confidence, but you can of course look at the alignments with closely related species to see if you think the introns/exons are indeed viable. An example of a gene with 79 exons is the Dystrophin (DMD) gene, the longest annotated gene at 2,217,347bp (see Roberts et al, 1993 and Nishio et al, 1994).


Is this tall, white tree in central Australia a kind of Eucalyptus?

This is Eucalyptus apodophylla, the so called whitebark.

Further information can be found here


How do detergents interfere with protein assays?

Depending on the detergent, its concentration, and the exact assay being performed, it can affect both the protein and the assay reagent(s). Some detergents will bind the (usually colorimetric) reagent, or otherwise chemically react with it, giving high background to your assay and sometimes completely masking the specific signal of the assay itself. Many modern protein assays are tolerant of a fairly low level of various detergents, perhaps some but not others, and this underscores the necessity of running a buffer/diluent-only control to verify the background of your measurements. Other assays, like Bio-Rad's DC Protein Assay or the Pierce Detergent Compatible Bradford Assay Kit from ThermoFisher, are engineered to tolerate a certain (often fairly high) level of detergent without increasing the background of the assay.


From a study titled "Production of Penicillin by Fungi Growing on Food Products: Identification of a Complete Penicillin Gene Cluster in Penicillium griseofulvum and a Truncated Cluster in Penicillium verrucosum", moulds on food items were analyzed for fungi that could produce penicillin. The conclusion drawn was

  Among different fungal species belonging to the genus Penicillium that
  are currently used as starter cultures in the food industry or that
  are frequently isolated from cured meat products, only P. griseofulvum
  (in addition to the previously reported P. chrysogenum and P.
  nalgiovense) was found to produce penicillin and possess the three
  penicillin biosynthetic genes (pcbAB, pcbC, and penDE).

Even penicillin should be avoided as the paper states that

  The presence of penicillin in food must be avoided, since it can lead
  to allergic reactions and the arising of penicillin resistance in
  human-pathogenic bacteria.

During world war two, a strain of Penicillium chrysogenum was isolated from the mould growing on a cantaloupe (reference) for the development of penicillin. This was after searching through many mould families developing on different food items so penicillin strains do develop but are rare.

The problem faced is that moulds cannot be differentiated from each other through sight nor is all penicillin moulds safe (reference). Whatever be the case, I hope that you didn't venture to try and eat that beetroot.


Need of X or Y chromosome protein after meiosis

X chromosome has many important genes required for general housekeeping. So we need not really talk about X-chromosome genes. Here is a list of genes present on the X-chromosome.

@Armatus, if all those genes were on autosomes then presence of Y wont be mandatory for male development. There are autosomal genes that are involved in sexual development for e.g. Anti-Mullerian Hormone gene is present on chromosome 19. However, there must be a master regulator that is male specific and since sex determination is chromosomal in mammals, the Y-chromosome must encode that master regulator.

Sry, encoded in Y-chromosome, is one such protein that is absolutely essential for male sexual development. Having said that, it could be very well possible that the basic genes required in the process of spermatogenesis are autosomally encoded. In fact it is so. I just took the list of genes that were associated with sepermatogenesis in KEGG and checked their chromosomal locations. They are all autosomal.

Gene --- position
SPATA1  ---  1p22.3
SPATA25  ---  20q13.12
SPATA32  ---  17q21.31
SPATA9  ---  5q15
SPATA19  ---  11q25
SOHLH1  ---  9q34.3
SPATC1L  ---  21q22.3
SPATA18  ---  4q12
SPATA2  ---  20q13.13
SPATA21  ---  1p36.13
SPATA2L  ---  16q24.3
GMCL1  ---  2p13.3
SPATA7  ---  14q31.3
SPATA5  ---  4q28.1
SPATA6L  ---  9p24.2
SPATA4  ---  4q34.2
SPATA24  ---  5q31.2
SPATS2L  ---  2q33.1
SPATA16  ---  3q26.31
SPATA6  ---  1p33
SPATA12  ---  3p14.3
SPATS1  ---  6p21.1
SPATC1  ---  8q24.3
SPATA22  ---  17p13.3
SOHLH2  ---  13q13.3
SPATA13  ---  13q12.12
SPATS2  ---  12q13.12
SPATA20  ---  17q21.33
ASUN  ---  12p11.23
SPATA8  ---  15q26.2
SPATA17  ---  1q41
SPATA3  ---  2q37.1
SPATA5L1  ---  15q21.1
GMCL1P1  ---  5q35.3
SPATA41  ---  15q26.3
SPATA42  ---  1p13.3
SPATA33  ---  16q24.3


What happens to a virus SARS-CoV-2 on an object?

Those articles simply refer to the viability of the virus, i.e. whether it can still infect a host thereafter. (Sometimes this is referred to as "survival" of the virus.)
A unviable virion is not quite the same as it being "not there" at all, although it is so from the perspective of a host that doesn't get infected.
Those viability [in the environment] studies use a quantitative measure of how much of the virus (i.e. how many virions) are still viable after some time on some surface (or even in "the air"), e.g.

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. [...]
SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces [...], although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel).

So they are measuring the time to some [chosen] statistical threshold of viability. For reference as to their particular method:

The TCID50 (Median Tissue Culture Infectious Dose) is one of the methods used when verifying viral titer.
TCID50 signifies the concentration at which 50% of the cells are infected when a test tube or well plate upon which cells have been cultured is inoculated with a diluted solution of viral fluid.

Which part of the virus machinery breaks first might depend on the environment. On copper, for example, it has been found that for "common cold" coronaviruses (e.g. HuCoV-229E):

Exposure to copper destroyed the viral genomes and irreversibly affected virus morphology, including disintegration of envelope and dispersal of surface spikes. Cu(I) and Cu(II) moieties were responsible for the inactivation, which was enhanced by reactive oxygen species generation on alloy surfaces, resulting in even faster inactivation than was seen with nonenveloped viruses on copper.
[...]
Coronavirus was exposed to metal surfaces and recovered, and the positive-stranded viral RNA genome was extracted and purified. A one-step reverse transcriptase real-time quantitative PCR (RTqPCR) was performed to detect a 139-bp region of ORF1 within nonstructural protein 4 (nsp4). Virus that had been exposed to copper and brass surfaces demonstrated reduced copy numbers of this fragment with increasing contact times. [...] . Comparison of the entire viral genome by agarose gel electrophoresis confirmed that nonspecific fragmentation occurred on copper and brass, with fragments becoming smaller with increasing contact time.

See also related q here on virus survival in small droplets, where a different inactivation mechanism is suspected.
In general, all viruses start to degrade outside their hosts at temperatures above -20C, even in the absence of some more specific environmental stressors (like unfavorable humidity, reactive surfaces like Cu, etc.) In suitable hosts, this temperature-based degradation is more than offset by the virus' multiplication.


Tracing it backwards this was the earliest reference I found via google scholar, it's from 1988 and uses the $r B C$ notation in the format we are used to.

  Hamilton's rule states that for a social
  action to be favored under natural selection, rb - c > 0, where c is the cost to the
  actor in terms of the effect on (usually a reduction in) his expected number of
  future offspring, bis the benefit to the recipient in terms of the effect on (usually
  an increase in) his expected number of future offspring, and r is the relatedness of
  the actor to the recipient

However, I've traced back a bit further by going through the references and found this Michod paper from 1978 where they defined terms $b_i$ and $c_i$ as the

  "fitness effect of genotype $i$'s behaviour on others"

and,

  "fitness effect of genotype $i$'s behaviour on self"

respectively, which was the first such notation I could find which could be interpreted as $b$ = benefit via the increased fitness of others and $c$ as a cost to self.

As far as I can tell this leaves a 14 year gap between Hamilton's long version and the beginnings of the current notation by Michod in 1978, with the first "rB - c > 0" type of notation appearing in 1988. Obviously my search is not exhaustive - many papers from this period will be hard to find and text search (e.g. using "rB" as a search term) - but it's a good start. If I find an older reference any time I will update.


Identifying a mushroom. (Pyrenees near Gavarnie, France)

This is almost certainly the parasol mushroom, Macrolepiota procera. The parasol mushroom is edible, but many other often resembling mushrooms are not. Never eat a wild mushroom unless you're an expert or consulted one.
 https://en.m.wikipedia.org/wiki/Macrolepiota_procera


How exactly is glyceraldehyde 3-Phosphate reverted to ribulose 1,5-bisphosphate for the continuation of the calvin cycle?

You need to account for free phosphates (Pi) that derive from ATP and are released in phosphatase reactions. The regeneration of 3 ribulose-1,5-2P has the overall reaction

5 glyceraldehyde-3P + 3 ATP $\rightarrow$ 3 ribulose-1,5-2P + 3 ADP + 2 Pi

So in total eight phosphates (here counting ATP as 1) are redistributed, 6 of which end up in ribulose-1,5-2P, and two are released as free phosphates. (These Pi are then recaptured during ATP synthesis in the light-dependent reactions.)

The above is a summary reaction of course; the complete scheme involves 10 enzymatic reactions that rearrange carbons in various ways to form 5-carbon sugars from 3-carbon ones (which takes a bit of juggling of atoms). Release of free Pi occurs in the fructose biphosphatase and seduheptulose biphosphatase steps.

A detailed account can be found in any major biochemistry textbook, like Stryer's Biochemistry. Online resources like MetaCyc can also be helpful.


Reconstruction of wildlife distribution based on poorly-sampled data

The problem of how to infer species distributions from scattered species occurrences is common in ecology, and there exists a number of methods to construct distribution maps. As a start, you should have a look at Species Distribution Models (SDMs) using regressions models or Maxent, and the paper by Elith et al (2009) is a good starting point and a standard reference. SDMs using maxent is now a common approach, which integrates species occurrences as point data along with environmental layers (e.g. temperature, moisture and topography) to predict species distribution maps, and this can also include absence data or "pseudo-absence" data (randomly sampled data from a region of interest). The maxent software is described and can be downloaded here: http://www.cs.princeton.edu/~schapire/maxent/
A common criticism against distributions produced by Maxent is however that they ignore e.g. species interactions, and they only considers the species occurences and the environmental variables that has been included in the model.

In your "Note", you touch upon the issue of detectability, which is an important issue that has received much attention recently. The problem is largest when you only have presence data, and to have real presence/absence data is preferable. Even if you don't have real absenses (the species has been searched for but not found), an estimate of sampling effort in different areas is still very useful, since this means that you can at least evaluate whether absenses is due to "real" absense or lack of sampling. In your case, the movement paths of characters could be used as a measure of spatial "sampling effort". The main issue with detectability in studies of distribution of species trends is if there is trends or bias in detectability, which means that apparent changes over time or patterns in distribution might be due to differences in detectability and not real differences between areas or over time. This could for instance be the case if observers are more likely to spot a species in one type of habitat (open savannah) then in another type of habitat (closed forest). Useful starting points for issues of detectability are Dorazio (2014) (technical though) and Kery et al (2010).


It's a mallow.

The leaves - they look like maple leaves - and the flower are identical.

Mallows are from the family Malvaceae, which includes food plants (okra, cocoa beans, kola nut), economic plants (cotton), and ornamentals (e.g. hibiscus) One species of this family (Althaea officinalis) is actually the original ingredient to make marshmallows.

I'm not sure which mallow it is (there are 243 genera with 4225+ species), but it's a common weed wildflower all over the world.


Testing monophyly from per site log-likelihoods without optimising branch lengths

If you have the budget for it, I highly recommend Geneious for topology work.  It was a real saver for me on an epi paper last year.

Anyway, they allow for testing per-log likelihood without adjusting edge length.  If you want to throw up some dummy data somewhere I can throw up an example.
I have no connection or stake with the company, just happy with it.


Why is one testicle larger than the other?

I would strongly question whether the underlying claim that testicular asymmetry is generally true. While there is no known clinical significance of testicular asymmetry, most men probably have no noticable difference in testicular size. There have been a number of studies over several decades, and findings have been inconsistent.

Braus (1956) stated that the left testis was heavier and lower; Chang et al. (1960) determined on study of cadavers that the right testis was generally larger than the left.

A 2008 study in 0 to 6-year-old boys found no difference in testicular volume measured ultrasonographically.

Age or level of sexual activity may also play a role; it is known that testes get larger during sexual activity.

The reason for testicular asymmetry is unknown. It has been reported in many different species (see Yu, 1998). The most common explanation provided in humans is that the right testis is more commonly larger than the left due to a difference in vascular anatomy: the left testicular vein empties into the renal vein while the right testicular vein empties into the inferior vena cava. However, anatomy alone would not explain testicular asymmetry in other species as well, so there is no doubt more to this than presently understood.


What is the length of anaerobic biodigestion stages?

To give timescales for the different processes is very difficult because the speed (in g/d product yield) depends greatly on the number of bacteria, so first you'd have to modl the bacteria growth. I assume you don't want to go that road.

Also note that not all of the substrate is in the same state of fermentation at the same time, more so if you have bigger lumps. Like whole carrots.

One industrial batch-style fermneter I know of uses total retention times of 3-4 weeks, and they mix half the digestate into the fermenter again to provide for inocculum.


Iron deficiency anemia symptoms explanation

The molecular basis of copper-transport diseases in Trends in Molecular Medicine, Volume 7, Issue 2, 1 February 2001, Pages 64–69, has a link to a 1973 paper by JM Gillespie entitled "Keratin Structure and Changes with Copper Deficiency," stating

  Menkes patients are often diagnosed from their unusual hair structure – termed pili torti – also known as kinky or steely hair, caused by reduced keratin cross-linking, a process that is catalyzed by an uncharacterized copper oxidase.

I haven't been able to find anything further, but since iron and copper levels can both be affected in anemia, this may be the link you're looking for. There may also be other enzymes involved that use iron-mediated catalysis. Since there are so many different kinds of keratins (the major protein that makes up hair and nails, among diverse other functions in the body), there may easily be multiple cross-linking and assembly pathways.

Other websites I found have also claimed that anemia-associated pathologies with hair and/or nails may be related to reduced oxygenation as a result of low iron levels, but they don't give any citations, and given the nature of the sites (nail care, fashion, etc.) it may just be an educated guess.


Have skeletons of "failed" animals been found yet?

Short answer
The dodo and Irish Elk, both going extinct relatively recently, are examples of species that have yielded skeletons and went extinct, at least partly, due to maladaptations.

Background
Extinct animals are an example of an answer to your question, barred those species did not go extinct through a cataclysmic event of course. No species can evolve into a meteor-resistant species. The term you are looking for is, I think, maladaptation.

For example, the Irish elk (Fig. 1) has been proposed to have gone extinct at least partly through a maladaptation. The male Irish elk was grew the biggest antlers ever recorded, (over 10ft (3 m) wide. Irish elk became extinct 10,600 years ago, and the male antlers have been proposed as a possible reason, although this is debated (source: Wikipedia). For example, males might have suffered because they got entangled in thickets. The climate changed at the end of the last Ice Age, causing the woodlands in which elk live to shrink. And food shortage might have resulted in a lack of nutritional support for the hefty antlers. However, extinction of an entire species is always caused by a multitude of cooperative factors, so the antlers alone can't be blamed (source: Love Nature, Wikipedia).

Also the dodo (Fig. 2) can be an example of an answer to your question. While not caused by a natural phenomenon, some animals simply become maladapted due to human influences. The dodo is the classic example. The dodo went extinct in the 1600's. It was adapted to life without ground-dwelling predators, as it nested on the ground and couldn't fly. The plump, slow, flightless birds were unable to escape from the sailors and their dogs, rats and pigs who landed on Mauritius (sources: Smithsonian, Love Nature).

Fig. 1. Skeleton of Irish Elk. source: Love Nature

Fig. 2. Dodo skeleton. source: Physiology

Sources
- Love Nature
- Smithsonian
- Wikipedia page on Irish Elk


Rod and cone photoreceptors are neurons?

Photoreceptors are considered neural based on embryonic origin: they derive from neuroepithelial cells like neurons do.

Neuroepithelial cells also produce non-neuronal cells like some glial cells.

It doesn't make much sense to worry too much about whether a rod/cone photoreceptor is a neuron or not. They don't have long axons or dendrites, but they need not have either to be called a neuron. They make synapses, but these synapses are highly specialized and different from other types of neurons; that isn't sufficient to not call them a neuron. They don't fire action potentials, but they need not fire action potentials to be called a neuron. They do release neurotransmitter, but there are other cells that also release neurotransmitters that are not considered neurons. Ultimately, deciding whether a cell is a neuron or not is a matter of semantics, not biology.

Most texts I am familiar with consider them neurons because of their neural origin, which differentiates them from other sensory cells that derive from other tissue.


Is transplantation of neurons between species possible?

Short answer
Neural xenografts can survive and form functional connections in the host.

Background
Across-species (xenogeneic grafting) grafting of cerebral cortex from a fetal rat to an adult mouse brain and vice versa, have shown that immunocompetent hosts can reject a graft in less than 30 days. Rejection results in destruction of  the graft tissue presumably by macrophages. Immunosuppression can be used to prevent graft rejection (Mason et al., 1986).

A review article on this topic shows that in the absence of immunosuppression, neural xenografts (donors were fetal to adult-aged) in a rat host brain survive in 37% of the cases in case of a mouse donor, 16% in case of a hamster donor, 9% in case of a rabbit rabbit, 7% from a pig donor, and 0% when human donor tissue was used. Hence, species-separation seems to be a determining factor in xenograft rejection. Induction of MHC-I and MHC-II expression in the xenograft mediates graft rejection in the brain. Hence, despite the fact that the brain is immunopriviliged because of the relative low expression levels of MHC class proteins, it is still sufficient to reject grafts (Pakzaban & Isacson, 1994).

Xenografts have been shown to generate functional afferent and efferent axonal connections with the host brain when grafts of the striatum, substantia nigra, hippocampus and retina were homotopically transplanted.

Functional (behavioral) studies have confirmed these physiological studies. Rats with Parkinson's disease could be successfully treated with substantia nigra grafting from mouse, hamster, rabbit, pig and even humans. Similarly, retinal xenografts have resulted in functional pupil responses, hippocampal xenografts have restored learning deficits, and suprachiasmatic nucleus xenografts have been shown to restore circadian rhythms (Pakzaban & Isacson, 1994).

References
- Mason et al., Neurosci (1986); 19(3): 685-94.
- Pakzaban & Isacson, Neurosci (1994); 62(4): 989-1001.


How did life survive in the Snowball Earth theory?

First, the "snowball earth", despite favoured by many scientists, is not a theory in the scientific meaning of the term, but a hypothesis, because it is not widely accepted: https://en.wikipedia.org/wiki/Snowball_Earth#Scientific_dispute. Some models show sea ice at the equator, while some more sophisticated climatic models failed to form sea ice to the equator.

But let's talk about the most famous "snowball earth" event, the Huronian Glaciation. It happened just after the "Great Oxygenation Event": the massive amounts of oxygen (O2) released in the atmosphere decreased methane concentration, and temperatures plummeted. It's supposed that Earth's surface became entirely or nearly entirely frozen.

  How was it possible for life to survive this extreme state?

It's worth mentioning that, by that time (2 and half billion years ago), there were only unicellular organisms (and probably no eukaryotes, just bacteria). There were no pluricelular organisms nor life on land (outside water). Thus, having in mind that there were still a lot of liquid water (under the ice), it's easy to see those bacteria surviving. Sure, many species have become extinct, but not all life forms were threatened.

About the Huronian glaciation:

http://link.springer.com/referenceworkentry/10.1007%2F978-3-642-11274-4_742
http://www.sciencedirect.com/science/article/pii/S1674987113000297


Does sodium lower the harmful effect of potassium on kidneys?

Chemically speaking, sodium and potassium are very, very similar, and also pretty common, and our body needs both.

Due to their similar electrical properties in particular, they are used as kinds of 'counters' in some processes in the human body, as they can be distinguished to some extent by other processes, and the balance of the two is important.

What it is important to note, however, is that more potassium than sodium is needed, so an overly-high-potassium diet is rarely considered a health risk, even if only due to it being infrequent. People tend to be potassium-deficient rather than sodium-deficient.

Generally speaking, unless you are consuming way too much of both, having a potassium surplus is less problematic than a sodium surplus, and harmful effects certainly don't "stack", at least not trivially. Rather, extra potassium will tend to offset extra sodium, ameliorating rather than aggravating health effects.

Even so: All of this can vary wildly with general diet and other factors, so the prudent thing to do regarding ones sodium/potassium balance is to see one's doctor and have blood work done.


In the induced fit model for enzyme action, does the enzyme active site change slightly after products form?

I understand now that they are highlighting how during the transition state the enzyme was induced to change shape, but once products formed and left active site, there was further changing of shape of the enzyme active site so it could return back to its original shape - therefore it could be reused again, as in line with the role of an enzyme/ catalyst.


How many molecules are generally required for cell signallng processes for given cases?

A cell can interact with other cells in zillions of ways. You can send information from one cell to other cells via neurotransmitters, hormones, pheromones, electric signals, magnetic resonance ,leukotrines etc.

In general a single type of molecule is enough to send such information. Like you require only Acetylcholine(Ach) as neurotransmitter to transmit various nerve impulses.
But, even for a single type, you require thousands of molecules. Like 1 molecule of Ach can do almost nothing and would immediately be broken by Acetylcholinesterase. You require 1000s of such molecules.

You can modify the communicating information via different types of transmitters. You can use GABA or glycine to supress any information exchange or use dopamine to enhance it. But again you will need many molecules of GABA or Glycine.

For visual pathway,  you can use no. of types of transmitters like glutamate, glycine, gaba, dopamine, acetylcholine, substance P etc.
Neurotransmitters for visual pathway.

Hormones are transmitters that are required in small quantities. But,  again you require certain concentration. There is normal blood concentration of various hormones like 80 pg/ml for calcitonin.

Quorum sensing use transmitters like AHLs. Again a certain threshold value is required for them to act.

Again,  to produce these transmitters you have to go through a rigorous process of transcription, translation and post-translational modifications.
So, for cell to communicate a rigorous process is used.


What evidence is there on the medical effects of circumcision?

This question has already been answered over at the Skeptics site in great detail.

See Does circumcision reduce HIV risk? and Does circumcision lead to a net increase in quality of life?. The answers are well-sourced and there are answers addressing both sides of the issue.


How to create a 3D density map of a system of varying number of particles?

R packages misc3d and rgl. The function image3d in misc3d does what you need and is very parametrizable via rgl (change the transparency, the view angle, axes, etc...). I used it with fairly big arrays (~10000000 data points/plots) and it produced great 3D density plots.

Both R (e.g. package biOps) and Matlab (image processing toolbox) have very powerful tools for image analysis if you need to get for example RBG levels in your plots but as far as I understood, you have the 3D arrays containing the interaction values, right?

Matlab proposes similar tools if you prefer Matlab (don't remember the exact functions) over R and both will require a fair amount of RAM as the data must be loaded in the environment.

As your system is time dependent you can also create movies fairly easily if you wish so (e.g. rgl's movie3d function).

Here a quick example of a 3D density plot:


Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective?

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

Not back then.

https://emedicine.medscape.com/article/966220-workup

Although the diagnosis of measles is usually determined from the classic clinical picture (see Clinical), laboratory identification and confirmation of the diagnosis are necessary for the purposes of public health and outbreak control. Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M (IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation.

None of this existed in 1970.


How Mitochondria differs from Prokaryotes(probably regarding energy production)?

If you mean "why do we have mitochondria instead of our cells doing the work themselves"
Then I can think of several answers.

First, oxidative phosphorylation must take place within an organelle, and requires specialized cellular machinery to occur.

So either a prokaryote can wait a couple million years to evolve these structures, or it can ask its friend to do it, and HE is specially evolved to do just that.

Like the way you hire a plumber when your toilet gets clogged, instead of going to plumber school yourself.

Also, oxidative phosphorylation has to do with oxygen.

Oxygen, when busted apart, can form unstable molecules called free radicals that are essentially bleach.

These molecules zoom around smashing up anything they touch including DNA.

So the host cell says "better you than me!"
Remember how I said you need an organelle for oxidative phosphorylation?

This is why. So all the "bleach" gets contained.

Two very good reasons why we evolved to rely on a separate organism instead of just making our own breathing organelle.


Why are the pulmonary vein and artery not like the rest of circulatory system?

It is true that nearly all arteries carry oxygenated blood and nearly all veins carry de-oxygenated blood, but that is not what defines them. Arteries are blood vessels that carry blood away from the heart, and veins carry blood towards the heart. If you look at the situation in that light, the naming makes sense: the pulmonary artery is carrying de-oxygenated blood away from the heart to the lungs, and the pulmonary vein is carrying the re-oxygenated blood back to the heart, to be pumped through the rest of the body.


How to know if a woman is fertile without actually making her pregnant?

Of course. There's several fertility tests available to determine the quality and quantity of egg reserve, and whether or not the there are abnormalities in the uterus.

However, some of them are invasive procedures, and all of them should be performed by a professional. I doubt the layperson would know what they're looking at on an Ovarian Ultrasound.

If you're asking whether there's an "easy" way that doesn't involve a trip to a doctor - then I would say 'no.' Casual inspection would only reveal any abnormalities in the vagina and the opening of the cervix, and hormone tests are only partial indicators.

Then again, if a woman has reached physical adulthood and is under the age of 38 then the chances of being infertile (or have difficulty conceiving) are quite low - about 3% to 10%. Infertility is usually much more of a concern to women who wait until after the age of 35 to have children, as there is a definite biological window (the number of eggs the woman was born with) to consider that starts to close as a woman nears her 40's.

It's also important to note that trouble conceiving can stem from either partner, and there's about a 40%-50% chance in a couple trying to conceive the male has an 'issue' and the woman is perfectly healthy.


Osteoarthritis results from the gradual degradation of articular cartilage. When the cartilage is damaged extensively, e.g., all the way through the cartilage and into the bone, an inflammatory response ensues in the bone. This often happens when bone is rubbing against bone.

One of bone's responses to injury and inflammation is the production of new bone. In this case, the bone, called osteophytes or bone spurs, is produced pathologically (i.e., not like the bone laid down normally during growth). Heberden's nodes are the names given to these osteophytes at the distal interphalangeal joints, but the process is basically the same at other joints in the digits, ankle, etc.


what is the difference between early blight of potato and late blight of potato?

Some Differences are listed here

Please consider reading these articles (article 1, article 2)


The incus is there in humans because it is there in our mammalian ancestors, and it is there in our ancestors because the mammalian three-bone ossicle system was inherited from early amniotes.

The synapsid ancestors of mammals had the ancestral jaw articulation between the articular (later called malleus) and quadrate (later called incus). This is the bottom image below. There are fossil species with a transitional form in which there are two jaw joints (e.g., Pachygenelus). In extant mammals, the jaw joint lies between the dentary and squamosal (part of the temporal bone), while the old articular and quadrate are part of the ossicle system (top image below).

There is a lot of material on the web about this:

http://crompton.oeb.harvard.edu/publications/transformation-quadrate-incus-through-transition-nonmammalian-cynodonts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552421/
http://www.zoology.ubc.ca/~millen/vertebrate/bio204_labs/Lab_3__Skull.html

So in short, the incus is there because there was no other way for the mammalian ear to evolve from the ancestral system. It doesn't have a purpose per se, except that it's always (at least going back to jawed fishes) been attached to the stapes and articular (malleus).


How a vegan can consume all the needed varied proteins / amino acids?

Proteins are made up of amino acids. It isn't particular proteins that are necessary in diet, but particular amino acids. For humans, these come primarily from breaking down the proteins in foods we eat.

Essential amino acids are the amino acids that humans cannot synthesize; other amino acids can be synthesized from these, but they do not need to be part of the diet. Not all sources of protein have sufficient quantities of all of the essential amino acids. When people refer to a protein source as "incomplete" they mean that particular source is low on one or more of the essential amino acids.

Meat products are typically "complete" because they contain all of the essential amino acids together. Therefore, if you subsisted on various foods but only got your protein from one animal source, you would be okay.

Some plant products do not have all the essential amino acids in large concentrations. However, if you combine protein sources from different "incomplete" plant sources that together cover these deficiencies, there is no disadvantage compared to a single "complete" source.

You also have a fairly substantial reserve of amino acids in the form of all the proteins in the body, which are constantly broken down and recycled. The daily protein intake is just a tiny fraction of the total amino acid content in the body.

Here is a paper that talks about some of these issues, and addresses some of the myths about balancing proteins. The quick summary is that problems develop if you get your sole protein from a source that is low in a particular essential amino acids over a long time period, but there is no need to ensure every meal contain all the amino acids.

It is possible for people on unusual protein diets, such as vegans, to develop a particular amino acid deficiency. There are many many guides on the internet for protein sources to mix to avoid this problem. A common combination is a legume (beans, peanuts) and a grain (wheat, rice). There are also some vegetable sources that provide complete protein nutrition - soy, for example, mostly works as long as it is not truly the only source.

References:

Young, V. R., & Pellett, P. L. (1994). Plant proteins in relation to human protein and amino acid nutrition. The American journal of clinical nutrition, 59(5), 1203S-1212S.


What are the units of the band intensities in a western blot image?

The units in your case are arbitrary units.
For instance, you may have taken a photo of the bands with a camera that saved a gray-scale file with an 8-bit depth. That means that the brightness values of each pixel have 256 gradations (or 2^8 values of brightness possible between minimum/blank and maximum/saturated). The program only takes the pixel brightness value anywhere between black (0) and fully white (256) and simply performs the calculations so. There is no real connection between actual band intensity and the output from ImageJ or any software.
Alternatively, you can also have relative units. Say you have a reference: a positive or a negative control. If your reference has a brightness of 10, and your band has a brightness of 7, you could express the band intensity as "0.7 relative units"; here you have to specify your reference, i.e. what you are calibrating your relative units to, hence the term relative.


What is the difference between different brain regions

The wiring is different as you mentioned. However, perhaps the most important is the brain knows where it's input is coming from. The brain knows where each fibre innervates and thus can compile and present this data to our conscious mind. We show if we stimulate the brain directly, than we feel a sensation in the part of the body that portion of the brain is responsible for. Plasticity means our brain can change what feeds into where, this is most commonly where we learn a motor skill. If we play the piano for example the part of the cortex feeding to this area increases.

Another way is the type of chemical transmitter and receptor. Dopamine is primarily used for things that cause us pleasure for example. However dopamine can affect our movement if it is secreted in from the substantia nigra, as this feeds into the motor cortex. Furthermore, neurotransmitters can be excitatory or inhibitory and this is an analogue rather than binary signal. All of these fine tune, and the position at which they inhibit and the location and the feedback from which they obtain their signal all indicates from where the brain is getting the information or to what it is responding to.

In summary it is wiring, signalling and location. However the components are incredibly similar but it isn't the small differences that have a profound effect.


Is there a circadian component to hunger?

Yes, absolutely. A major focus of understanding obesity, diabetes and other metabolic disorders are targeted to understanding the circadian (and other cyclical nature) systems in neurobiology and endocrinology. I can speak within the study of diabetes, there is an observed diabetic "dawn effect" in which there is an early morning (dawn) spike in blood glucose. The exact mechanism for this spike in blood glucose is not fully known, but the general circadian nature is intriguing and would suggest a dominant hormonal cause.

Some other review articles may be found here. An overall review of homeostatic balance as it relates to the central nervous system and apetite regulation. The second review more closely focuses on the biochemistry and endocrinology of central and peripheral regulation on food intake and physical activity.

Berthoud HR, Morrison C. The brain, appetite, and obesity. Annu Rev Psychol. 2008;59:55-92.
Lenard NR, Berthoud HR. Central and peripheral regulation of food intake and physical activity: pathways and genes. Obesity (Silver Spring). 2008 Dec;16 Suppl 3:S11-22.


Are there histones present in the cytoplasm?

In early embryogenesis, cell division called cleavage occurs every 30 min and there is no transcriptional activity. Oocytes have accumulated important gene transcripts and synthesize the proteins at right times. However, histone is one of the most abundant proteins and it would be difficult to supply enough histone proteins during early embryogenesis while oocytes translate other gene transcripts regulating differentiation.

This is my speculation, but the article calls cytosolic histones "stockpile". Just in case, I don't mean that I deny some other roles of histones in cytosol if there are any.


What is this insect? 6 legs and red body

These appear to be the nymphs of the red-shouldered bug (Jadera hematoloma), which eat the seeds of the Sapindaceae family (Soapberry family) throughout South America, Central America and the southern parts of North America.
There is a close-up picture of one of these at bugguide.net, and further images here on the same website.


How does Oedipus complex fit in the evolutionary theory?

It doesn't.  The Oedipus complex is one of Freud's theories to explain human behavior, not something that is endorsed by the fields of psychology or psychiatry.  Freud had a lot of interesting theories, some of which remain core concepts in psychology, and some of which have been marginalized or rejected.

There are some professionals who feel it has merits for consideration, to one degree or another, but if you look at publications by the APA (American Psychological Association) and Psych.org (American Psychiatric Association), you won't see in their practice guidelines.

APA: http://psycnet.apa.org/journals/pst/32/4/535/

Wikipedia: http://en.wikipedia.org/wiki/Oedipus_complex#Criticism

If you're asking how might it fit with evolution if it were to be true, that's more of a philosophical question - which perhaps is the better angle from which to approach the question.

In "survival of the fittest" - "fittest" is better described as "those who most successfully reproduce and produce offspring that are also highly successful in reproducing."

Reproducing with one's immediate family results frequently in severe birth defects, the opposite of "fit."  Those who want to reproduce with their mother but don't, and reject all other mates, will not reproduce.  Not "fit."  The only possibility similar to the oedipal complex is that males choose mates that are like their mothers.

What is true is that we often marry someone similar to our parent - but it is not a result of an actual oedipal complex.  Freud wrote the oedipal complex in part to try to explain this phenomenon.  But there are better explanations - we are attracted to that with which we are most familiar, to that which makes us feel comfortable, to that which makes us feel warm and fuzzy.  Our definition of beauty is largely shaped by family faces - because that is what you are surrounded with as your mind develops.  Etc etc.


Could someone help me identify this insect from Malaysia?

That is Catacanthus incarnatus (Pentatomidae). http://cyy4993.blogspot.com/2012/11/stink-bug-pentatomidae-catacanthus_17.html
http://eol.org/pages/3685880/overview


What characteristics of the protein folding process ensure that the energy landscape is a funnel?

Naturally occurring proteins are evolved such that this is the case

Natural proteins only occupy a very small amount of sequence space. For a 200 aa protein, there are $20^{200} \approx 10^{260}$ possible sequences. There are nowhere near that many naturally occurring protein sequences, even if you take into account all the different alleles in the different organisms in the world.

What happens when you synthesize and express a random (non-natural) protein sequence? You get junk. It doesn't fold or it aggregates or something else happens. You don't get a stably folded protein. Heck, you don't even need to have a fully unnatural protein. You can take a naturally occurring protein and make a few mutations in it, and end up with non-folded junk.

Evolution has a very strong selective pressure to make sure proteins can fold properly and beat Levinthal's paradox. If a protein can't fold, it can't perform any function in the cell, and thus there's no selective pressure to maintain expression. (The promoters get trashed, and the DNA gets mutated away to "junk" DNA.) Only if the protein is stably folded is selective pressure maintained. So you get the one-in-a-million sequences which does have a decent folding funnel.

So it's not that there isn't protein sequences out there with a flat energy landscape, or an energy landscape with lots of local minima. It's just that whenever such a protein forms, it can't fold. And if it can't fold, it's freed from evolutionary pressure and disappears from the gene pool - either because the organism that holds it can't survive without it, or because random mutations wipe it out with random noise. It's survivorship bias -- you see proteins with a reasonably well-formed folding funnel because they're the only ones you would see.

(There are proteins out there with less-than-robust folding funnels, or with alternative energy states. A brief search of the literature will turn up a number of examples where protein folding requires cofactors or chaperones. Or where a protein has two different folded states, depending on environmental condition. Or where the most commonly folded state is only a meta-stable state, and there's a more stable conformation which the protein will convert to, if given a chanvce - amyloid fibrils being the most common example. These are refinements on the general principle. You don't need a rock solid folding funnel, you just need one "good enough" for the organisms' purpose.)

You can see some of this in the "de novo" protein designs that come out of labs like David Baker's. They're able to take a protein topology and use a computer to design a sequence "from scratch" which folds to that topology. But far from all of the sequences which their computer program spits out actually will fold. Only a small fraction of such designs will actually fold into a compact protein.

But one of the things that they've found which improves their success rate is to check the designs by "forward folding". That is, the computer spits out a design which it predicts will be a low-energy sequence for that structure. But just having a sequence which is predicted to be "low energy" isn't enough. As an additional step they run the sequence through a folding simulation to see if the sequence they designed also has a clear preference for the designed state. Roughly speaking, checking if there is a clear "folding funnel" which will drive the protein toward the desired folded state. By doing this subsequent computational check, they're able to greatly increase their success rate when the proteins are actually expressed.


How to introduce predators to a simulated ecosystem?

What you're trying to do sounds really cool. I feel that you can do the following:

1) Increase reproductive period of predators

2) Increase prey to predator ratio (see Lotka-Volterra equation)

3) Make the reproductive speed/ ability of an individual to be in relation with the number of energy 'points'

What kind of set-up are you working with, a unicellular model or a larger scale?

Maybe you could start with a solely herbivorous setup, but give all individuals the ability to harm/sap a small amount of energy out of another individual.

Is there some way you could send me your project? I want to have a look at it


Are There Exceptions to Animal Cells not Having Cell Walls?

Humans, as well as the rest of the metazoans (i.e. animals), absolutely do not have cell walls. What humans do have is extracellular matrix (ECM), which is the sort of fibrous, sort of gel-like material in which cells in many of the tissues are embedded. Collagen is a major component of ECM.
From the old copy of Alberts that is hosted on the NCBI website:

Tissues are not made up solely of cells. A substantial part of their volume is extracellular space, which is largely filled by an intricate network of macromolecules constituting the extracellular matrix (Figure 19-33). This matrix is composed of a variety of proteins and polysaccharides that are secreted locally and assembled into an organized meshwork in close association with the surface of the cell that produced them...
Two main classes of extracellular macromolecules make up the matrix: (1) polysaccharide chains of the class called glycosaminoglycans (GAGs), which are usually found covalently linked to protein in the form of proteoglycans, and (2) fibrous proteins, including collagen, elastin, fibronectin, and laminin, which have both structural and adhesive functions.


Muscles are designed to contract i.e., when they tense they get shorter. Their stretch is a passive process, typically facilitated by antagonist muscles in case of skeletal (striated) muscles. Consider the biceps and triceps antagonists in the upper arm in Fig. 1:

Fig. 1. Left: The biceps actively contracts to bend the arm and is called the agonist. The triceps is inactive and is passively stretched by the biceps, called the antagonist. Right: To stretch the arm, the reverse happens, i.e. the triceps contracts and is now called the agonist. The biceps is now inactive and is called the antagonist and it is passively stretched by the triceps. Source: Pilates Studio

At the molecular level, the tensing of muscles can be readily seen as contraction, as opposed to stretching (Fig. 2):

Fig. 2. Muscle fibers contract actively and stretch passively. The passive stretched state is depicted in the upper panel. Under the influence of ATP (active part) the muscle fibers condense and the muscles contracts. source: Emaze Presentations.

Further Reading
- Do both ends of a muscle contract?


PEG-silane treatment: why incubate for 18 hours at 60 degrees Celsius?

The binding of proteins (and cells) to glass (or silicon) surfaces can be prevented by coating the glass with polyethylene glycol (PEG) groups. PEG-silane is a reagent used to create this coating.

PEG-silane (the image shows a methoxy- version) (image taken from here; no connection)  will coat glass surfaces because the silane portion (right hand end of the structure shown) will react with -OH groups on the glass surface.

I can't help with the part of the question about time and temperature of incubation, but it seems longer and hotter than protocols I have seen. Perhaps the indium tin oxide (ITO) coating on the slides has something to do with it?


This article analyses the exchange of DNA during the process of grafting

Exchange of Genetic Material Between Cells in Plant Tissue Grafts - Stegemann and Bock, Science 2009

Quoting from the article:

  Although the grafted tissues fuse and establish vascular connections,
  the stock (the lower part of the graft) and scion (the upper part,
  usually supplying solely aerial parts to the graft) are thought not to
  exchange their genetic materials. But grafting (whether natural or
  assisted) provides a path for horizontal gene transfer. Gene transfer
  is confined to the graft site and no long-distance transfer may occur.
  Analyzes indicating that large DNA pieces or even entire plastid
  genomes are transferred. Only plastid genes may be transferred, no
  transfer of nuclear genes occur. Plant cells are connected via
  plasmatic bridges called plasmodesmata, but the passage of large
  macromolecules requires the action of specific plasmodesmata-widening
  proteins. Whether large DNA pieces or even entire organelles can
  travel through plasmodesmata requires further investigation.

  Finally, although our data demonstrate the exchange of genetic
  material between grafted plants, they do not lend support to the tenet
  of Lysenkoism that “graft hybridization” would be analogous to sexual
  hybridization. Instead, our finding that gene transfer is restricted
  to the contact zone between scion and stock indicates that the changes
  can become heritable only via lateral shoot formation from the graft
  site. However, there is some reported evidence for heritable
  alterations induced by grafting and, in light of our findings,
  these cases certainly warrant detailed molecular investigation.


What is the evolutionary purpose of the topology of the human ear?

Humans do not have the ability to move their outer ear in response to sound. Many animals can do that, and use it to determine the source of the sound waves. Thus, human outer ears are equipped with many "hills and valleys". It does not provide amplification (because the waves can lose their energy bouncing around the ridges), but rather gives the brain more information about the sources' location in space. The brain calculates that location by determining minute differences in the time it takes for the sound to reach sensory cells in the inner ear on both sides. The shape basically attenuates the raw information. That way you get different properties of the sound wave that enters your ear depending on the angle at which it fell on you outer ear.


probability of hairpin vs self-dimer formation?

I have tested a similar design to this. With a duplex protocol the chance of forming a hairpin is much higher than that of forming self-dimer, even at concentration of 25 μM. You can run a 3-5% agarose gel to test the outcome.


I'd argue that this relates to species-specific strategies of seed dispersal, so the answer depends on which species you're asking about. Here's an answer for chili peppers, which I think illustrates how complex and idiosyncratic these strategies can be.
As I mentioned in this answer, the seedsavers' manual Seed to Seed has great info on most plants, including the genus Capsicum (chili peppers). They say to clean the seeds from the peppers, and then dry them thoroughly but not in direct sun.
The Tewksbury lab has done someone amazing work on Capsicum evolution and seed dispersal from a biological standpoint. As published in Tewksbury and Nabhan 2001 (behind paywall, but described well in this Science in the News article) Capsicum fruits have evolved specifically to be eaten by birds, who do not have the receptors that make the fruits taste spicy to us and other mammals.
Essentially then, what you're trying to do when you hand-germinate seeds is to mimic the process of the fruit being eaten and passing through a bird gut. Tewksbury and Nabhan found that seeds from fruits eaten by birds actually germinated at a slightly higher rate than their control group of hand-processed seeds. In contrast, seeds eaten by mammals (who in normal settings totally avoid these spicy chilis) were destroyed and did not germinate.
Seed dispersal mediated by birds and other animals is one way that plants can be motile.

 Tewksbury JJJ, Nabhan GPG. 2001. Seed dispersal. Directed deterrence by capsaicin in chilies. Nature 412: 403–404.

Whealy K. 2012. Seed to Seed. Chelsea Green Publishing (p. 152)


Hummingbird hawk-moth (Macroglossum stellatarum). For what it's worth, there are also a variety of sphinx moths around the world.

Here's a photo from the linked Wikipedia page. As you can see, it looks very much like the one in yours:


Pseudoautosomal regions of the X chromosome showing heterozgyosity

A normal male can show heterozygosity in the "X" results of a 23andMe SNP test despite having only one X chromosome.  This is because there are very short regions at the ends of the Y chromosome, called pseudoautosomal regions, that match up with equivalent (homologous) regions at the ends of the X chromosome.

Because the pseudoautosomal regions of the Y are homologous to the matching regions of the X, the SNP results for those areas cannot be distinguished in the SNP tests, so the results appear along with the X results in "X" chromosome file.  The results in those two areas of the file can be either homozygous or heterozygous at each location.  Most of the locations in the "X" file are for  locations outside of those regions, so most of the file entries cannot report heterozygous results.


that sounds like a fun experiment!  But unfortunately you are right, the size difference is shaped by genetics as well as an environmental condition that might be hard to pin down.
For the genetics, It would indeed take millions of years (or at least 100,000s) for the genetic adaptation to kick in to create that change.
As for the environmental conditions, another source of gigantism is being on an island.  As the small number of species expand to fill out all the niches in the tank, they may get larger simply because the environment allows it with no predators.
The tank would have to be enormous to get those niches I think. This paper describes an archipelago of islands and shows that you tend to get smaller animals more easily with smaller islands, and larger species need larger islands.  Large here is millions of square meters.
Both of these processes take many generations. This is not my field but this paper studied 200 generations of plants and showed only migration and lifespan changes.  Size adaptations that come with changing ecological roles might have to take 1000s of generations. We'd have to freeze ourselves to see the giant slugs.  I'm sure there's a better answer out there, but this is what i found so far.


Where can I obtain the sequence of the E. coli ribosomal RNA precursor?

Generally most organisms have multiple copies of the genes/regions coding for ribosomal RNA (since it's needed quite a lot). Additionally these regions can be repetitive or otherwise similar to sequence or place correctly in the genome, therefore it's generally harder to find good genomic sequences for rRNA compared to other genes.

Based on your link, it seems that you are looking for the rRNA of E.coli; the GeneBank entry corresponding to the fasta file you linked contains the annotation of the full genome and has 7 entries for sets of ribosomal RNA (named rr[slf][A-H]*).
If you take any of the sequences spanning one of these regions you should get the sequence of the full precursor. However, there are things you should be aware of:

there will likely be minor sequence differences between all 7 regions
Apparently most of the e.coli rRNA operons also have tRNA genes mixed into them (these are different for all 7 operons)
replacing the genomic T with U will make the sequence look like RNA, however ribosomal RNA is often also edited post-transcriptionally, so the sequence you get may not fully match the mature rRNA sequence.

Another website that gives a better readable overlook over the rRNA operons in e.coli is this, it also contains source links & seems to match the genbank entry from what I can see.

  Example on how to find rRNA region from the geneBank entry:

  This is a (shortened) part of the annotation of the GeneBank entry, which shows the 'A' ribosomal genes :

gene  4035531..4037072
  /gene="rrsA"
rRNA  4035531..4037072
  /gene="rrsA"
gene  4037141..4037217
  /gene="ileT"
tRNA  4037141..4037217
  /gene="ileT"
gene  4037260..4037335
  /gene="alaT"
tRNA  4037260..4037335
  /gene="alaT"
gene  4037519..4040423
  /gene="rrlA"
rRNA  4037519..4040423
  /gene="rrlA"
gene  4040517..4040636
  /gene="rrfA"
rRNA  4040517..4040636
  /gene="rrfA"

  As you can see the genes in the region/opernoccur in order rrsA, ileT, >alaT, rrlA, rrF (the fact that this is an operon can not be inferred from the GeneBank entry) and if you take the corresponding region of the fasta sequence (nucleotides/characters 4035531 to 4040636) you'll get (most of) the primary transcript sequence.
  Since promoter & terminator Sequences are not annotated in GeneBank (or any/most other genome assemblies), you can't easily get the sequence before the first and after the last gene. One  potential source for these might be the other ressource I linked, which lists some sources for terminator sites.

* This is expressing all names as regex. i.e. for rRNA operon A there are rrlA, rrsA & rrfA; same for B,C,...