Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?

I haven't been able to find a study on fertility, but it would be important to note the difference between radiation considered.  The dangerous radiation discussed in both of your links are cosmic rays as you noted.  Our main defense against this sort of radiation is the earth's magnetic field.  The hole you are talking about is in the ozone layer, which is much more important in UV protection than cosmic ray protection.  The amount of incident cosmic rays is slightly more at latitudinal extremes due to the deflection away from the equator by the magnetic field, but this is only 1.5 to 2 times greater, see fig. 8.

Unless we figure out how to punch a hole in the magnetic field as well, the main threat in the arctic is skin cancer from UV, not infertility from cosmic rays.


How does a jumping spider manage to "jump" on the ceiling?

You are right - most jumping spiders have draglines they secure to the surface before they jump.  They can't defy gravity, but they can recover from a miss if they do this.

  Disturb a jumping spider on a wall, and watch it seemingly defy gravity: it will jump horizontally out into the air, then return to the wall.  This seems fantastic until you spot the major ampullate dragline.  It essentially becomes the bob at the end of a pendulum string.

the book goes on to explain that the dragline is used as an airbrake and a spring to help the spider control the jump, which might make it seem to do unnatural things when jumping from a ceiling.  You might want to get a video of this if you can.

Some of the references in another book here, point to other uses of draglines - the spiders can tell each other's species by them, attract a mate.


Why isn't Fluorine, or Neon, the final electron acceptor in cellular respiration?

One of the main reasons that modern(!) biology uses oxygen as an electron acceptor is availability.

Around 2.45 billion years ago, oxygen (O$_2$) started being built up in the atmosphere (which actually killed off a lot of the lifeforms/bacteria at that point). Since then, oxygen consuming lifeforms were able to establish themselves. Before that, most organisms probably used mainly (elemental) hydrogen as electron acceptors.

Apart from not really being available in the atmosphere, there are other reasons why fluorine or neon don't make for good biological electron acceptors:

While elemental fluorine (F$_2$) is indeed extremely electronegative, this makes it so reactive that it:
a) could not be controlled by biology [the reactivity of oxygen is why it killed so many bacteria in the first place] and
b) just does not occur (or at least remain in) in the elemental state in nature (there is no measurable F$_2$ in our atmosphere).
Neon (and other noble gases) are in theory also quite electronegative, actually so much so, that they never* occur without their electrons and therefore don't react at all.

*It's somehow possible to form noble-gas compounds, but it requires very specific chemical reaction conditions, that mostly occur under controlled man-made conditions (and are not good for biological life forms).


Do all IgG autoantibodies lead to autoimmune diseases?

As usual with biology, it's not that simple. There are autoantibodies present even in people without any signs of autoimmune disease. The immune system is a complex network of positive and negative regulatory cells and molecules - looking at a single component is unlikely to determine the state of the system. This is a major reason that it has been so difficult to figure out how to selectively act on the immune system to stop or prevent an autoimmune disease without compromising normal immune function.
Here's an article that expands on some of these aspects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703183/
For example, note "Despite the physiological elimination (negative selection) or functional inactivation (anergy) of high-affinity, self-reactive T and B lymphocytes in the thymus and bone marrow, respectively, there is compelling evidence that low-affinity, potentially autoreactive cells persist and that low-affinity reactivity to self-antigens is required for survival of T and probably B lymphocytes in the peripheral immune system."
It's also important to keep in mind that affinity of Abs and receptors for antigens usually depends on additional 3rd party molecules involved in the interaction, and that a single molecule may present very differently in different situations (for example, damage or inflammation may alter some self molecules into a previously unseen configuration that stimulates self-reactivity).


Is human zygote unicellular or multicellular

A zygote is produced when the gametes, a sperm and egg cell, combine with each other. This is unicellular. That one cell then duplicates into two cells, and then four cells. People don't really have a need to name this stage, but anyone would understand it if you just called it two-cell or four-cell within the context of zygotic development. As more cells are created (16+), the solid mass of undifferentiated cells is called a morula. This occurs around 3-5 days after fertilization. This then becomes a sort of hollow sphere of cells. These cells are now called blastomeres and the whole structure is called a blastula. When you hear a cell name with "blast" in it, it typically means it is a precursor to some other type of cell. In this case, those 16 or so cells are the precursor to a future human's entire body.


Does ATP production increase with oxygen availability?

The factors limiting ATP production are the rate of fuel (glucose, fats, amino acids, etc.) metabolism and its efficiency (ATP molecules per fuel molecule).
It is possible to produce ATP with zero oxygen by the glycolytic pathway; if this were not true, there would be no anaerobic organisms on Earth (which there clearly are). Muscle can do this too for short periods of time, producing lactic acid. In fact, many researchers believe that this pathway can produce ATP the fastest of any route of glucose consumption, even though it is least efficient. In other words, the number of ATP per glucose is small (only 2), but glucose "flows" through this pathway so fast that it is still generated faster than by respiration, which produces 30-32 ATP per glucose, but can process far fewer molecules of glucose per second. The actual rate of ATP generation by mitchondria is only limited by O2 concentration, in a chemical kinetics sense, in hypoxia, i.e. when a tissue does not have adequate blood supply, as in certain tumors.
The main effect of oxygen availability is likely size scaling--if you have more O2, you can get it through a larger body more easily. It's not that the muscle cells themselves generate more energy, it's that you can supply more muscle fibers that are farther from the lungs/gills/whatever. That's why in the carboniferous period on Earth, where there was considerably more O2, many animals (particularly invertebrates) were much larger than they are today.


How to do a nucleic acid or genome and amino acid search

In my experience the most popular sequence database is https://www.ensembl.org/ (other databases are available, eg. NCBI).  If you have a sequence of either nucleotides or amino acids that you want to find matches for then the BLAST/BLAT search is probably what you want.


What is the mechanism of oxygen uptake in E. coli?

This question got me thinking about what are the metabolic enzymes that take oxygen up in E.coli. I searched the metacyc database for reactions that consume molecular oxygen and there are only 3 that take in oxygen and one that produces oxygen.

All three consumers of oxygen in E.coli are the oxidation of ubiquinone by at two sites in cytochrome-bcl or by cytochrome-bo.  All of these export protons to create the gradient that drives ATP formation by F₀F₁ ATPase in the periplasm (the region between E.coli 's inner and outer membrane).

On the production side, superoxide dismutase reduces superoxide to oxygen to control oxidation damage.  Apparently the innards of E.coli are somewhat oxygen tolerant.


Optogenetics - How do microbial opsins work?

There is nothing special about the use of rhodopsin when compared to making a cell express any transgene. This question can then be read as:

  What is the process in which a cell population is targeted and implanted with a gene of interest?

There are many ways, which depend on the specific cell type and on whether you want to do it in vitro, in vivo and in which species, and it would be very complex to explain them all in detail here, so I will limit myself to two approaches that are popular when doing optogenetics in rodents: viral infection and transgenesis.

Viral infection uses an inactivated virus to deliver the transgene. Essentially you engineer a piece of DNA with the gene for the bacterial opsin of interest and you put it in a viral envelope, that is a series of proteins that form the "body" of the virus and that contain its genetic material.
You then inject the virus in the desired zone (e.g. in a specific brain nucleus) and wait for it to infect the cells around the injection site. A week later those cells will express the transgene.

For (at least, I think) historical reasons the first type of viruses used for this approach were lentiviruses. These, however, are a tad more complex to handle (especially as they require specialised rooms where they can be handled safely) so adeno-associated viruses (AAV) are becoming more and more popular.

Note that the virus is inactivated, that is, it cannot replicate, just infect the cells around the infection site, but it will not be able to spread around. This is both for safety reasons and because you want the infection to be confined to the specific region where you injected the virus.

As I was saying before, instead of putting a bacterial opsin you can put whatever gene of interest, the procedure is the same. As for the opsins, the first two that were used were the channelrhodopsin-2 (ChR2), a channel sensitive to blue light and that can be used to depolarize (=excite) the cells and the halorhodopsin (NpHR), a chloride pump sensitive to yellow light that will, conversely, hyperpolarize (=inhibit) the cells.
There are nowadays tens of variants of these and other opsins that can be used to drive cell activity with lights. Many of these are described in this (beware! Quite technical) review:

Optogenetics in neural systems - Yizhar et al., Neuron 2011

Transgenesis works instead by generating an animal that carries the opsin (or any other gene) in its DNA. This can be done in various way, such as by microinjection of embryonic stem cells carrying the transgene.

You can find a fairly detailed explanation of the process here: Transgenic Cells and Gene Knock-outs, well summed up by this figure (taken by the same page):

Transgenic mice generation http://9e.devbio.com/images/ch02/wt020302-2.jpg

But how do you get cell-type selectivity?
In front of the gene for the opsin you also will have to put another sequence, called promoter. The promoter is a sequence that is specific to each gene and that is used to determine which genes a cell will or will not transcribe. For instance, the promoter for the gene coding for a protein only present in muscles will be used by muscle cells but not by neurons. You can even get more specific, for instance by using promoters that are typical of a subset of cells and not other (e.g. glutamatergic neurons use a different set of promoters than GABAergic neurons, although these two sets will -at least in part- overlap). However, this means that if you want to change the cell type you are working on you will have to change the DNA vector you are using.
A commonly used approach to avoid this is that of using Cre-dependent vectors (note that this can be used both for viral infections or for transgenic animals).
Essentially you will have a mouse line which expresses a protein derived from the P1 phage, called Cre recombinase, only in the cell type of interest (again, using a specific promoter). Cre has the property of cutting DNA next to specific 34 base-pair-long sequences called loxP (with sequence ATAACTTCGTATAGCATACATTATACGAAGTTAT). Essentially, if you have loxP-[some sequence in the middle]-loxP and Cre recombinase is around, it will cut away the sequence in the middle, leaving only a loxP sequence.
Hundreds of different Cre-expressing mouse lines are commercially available nowadays, to target many different cell types in different organs.

Now, you just need a construct that allows you to express the opsin in a Cre-dependent manner. This is what was done by the group of Hongkui Zeng, and reported in this paper:
A toolbox of Cre-dependent optogenetic transgenic mice for light-induced activation and silencing. - Madisen et al., Nat. Neurosci. 2012

Without going into too much details, the idea is to flank a STOP sequence with two loxP sites. This will block transcription (that is what a STOP sequence does) unless Cre-recombinase is present.

Essentially:

Source: myself, CC-by-sa licensed, feel free to reuse it

Note that in the scheme, ROSA26 is an ubiquitous promoter, that is, a promoter used by all cells, so in this case the specificity is given by expression of Cre recombinase and not by the promoter of this construct. Also, a fluorescent reporter (e.g. GFP) is inserted to be able to visualize where the opsin is expressed.

By breeding these mice with the Cre-line(s) of your choice you can then express the opsins in the cell type of your interest.


What species is this orange mushroom in Romania?

This is most likely Kuehneromyces mutabilis or sheated woodtuft. It is quite common in Romania where it is named Gheba ciobanilor.

Quote from Wikipedia about the diagnosis:

  The clustered shiny convex caps are 6–8 cm in diameter. They are very hygrophanous; in a damp state they are shiny and greasy with a deep orange-brown colour towards the rim; often there is a disc of lighter (less sodden) flesh in the middle. In a dry state they are cinnamon-coloured.
  The gills are initially light and later cinnamon brown, and are sometimes somewhat decurrent (running down the stem).
  The stipe is 8–10 cm long by about 0.5–1 cm in diameter with a ring which separates the bare, smooth light cinnamon upper part from the darker brown shaggily scaly lower part. This type of stem is sometimes described as "booted".
  This species always grows on wood, generally on stumps of broad-leaved trees (especially beech, birch and alder), and rarely on conifers.
  It is found from April to late October, and also in the remaining winter months where conditions are mild. It is often seen at times when there are few other fungi in evidence.

Further details can be found here in English

or here in Romanian


Can I elute my GFP-tagged protein off anti-GFP antibody using a peptide?

I found a paper that describes a method to purify GFP fusion proteins using affinity chromatography: "Purification of GFP fusion proteins with high purity and yield by monoclonal antibody-coupled affinity column chromatography" (1). Unfortunately I don't have access to the full text, so I can't check how exactly they elute the GFP fusion protein from the column. They describe a specific monoclonal antibody they use, there should be information on how to obtain it in the paper.

Abstract:

  GFP has often been used as a marker of gene expression, protein
  localization in living and fixed tissues as well as for protein
  targeting in intact cells and organisms. Monitoring foreign protein
  expression via GFP fusion is also very appealing for bioprocess
  applications. Many cells, including bacterial, fungal, plant, insect
  and mammalian cells, can express recombinant GFP (rGFP) efficiently.
  Several methods and procedures have been developed to purify the rGFP
  or recombinant proteins fused with GFP tag. However, most current GFP
  purification methods are limited by poor yields and low purity. In the
  current study, we developed an improved purification method, utilizing
  a FMU-GFP.5 monoclonal antibody (mAb) to GFP together with a
  mAb-coupled affinity chromatography column. The method resulted in a
  sample that was highly pure (more than 97% homogeneity) and had a
  sample yield of about 90%. Moreover, the GFP epitope permitted the
  isolation of almost all the active recombinant target proteins fused
  with GFP, directly and easily, from the crude cellular sources. Our
  data suggests this method is more efficient than any currently
  available method for purification of GFP protein.

(1) Zhuang R. et al., Purification of GFP fusion proteins with high purity and yield by monoclonal antibody-coupled affinity column chromatography. Protein Expr Purif 2008, 59(1), 138-43


Inability of vultures to digest diclofenac

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618889/

  Post-mortem examination revealed extensive visceral gout in all diclofenac-treated birds (see electronic supplementary material). Histological examination revealed significant lesions in the kidneys, liver and spleen with extensive uric acid crystal deposition.

Via: https://repository.up.ac.za/bitstream/handle/2263/26027/Complete.pdf?sequence=7

  From the mechanistic studies both diclofenac and meloxicam were directly toxic to chicken and vulture renal tubular epithelial cells following 48h of incubation. It was later shown that this toxicity was associated with an increased production of reactive oxygen species (ROS), which could be temporarily ameliorated by pre-incubation with uric acid due to its anti-oxidant activity. When cultures were incubated with either drug for only two hours, meloxicam showed no toxicity in contrast to the cellular toxicity present for diclofenac. In both cases no increase in ROS production was evident. In addition, diclofenac influenced the excretion of uric acid by interfering with p-amino-hippuric acid channels. The effect on uric acid excretion persisted after the removal of the diclofenac. It was therefore concluded that vulture susceptibility to diclofenac results from a combination of an increase in cellular ROS, a depletion of intracellular uric acid concentration and most importantly the drug’s long half-life in the vulture.

The second link posits three mechanisms for the cause of renal failure in vultures (ref., pg. 26):

Ischaemic nephropathy with secondary visceral gout
Organic Anion Transporter antagonism
Secondary renal toxicity with or without toxic activation


What enables azacitidine to incorporate into both DNA and RNA?

If you look at the very beginning of the Wikipedia page, you'll see that azacitidine is an analog of cytidine, the C letter of both DNA and RNA fame. Decitabine is a deoxy derivative, and hence would only be incorporated into deoxyribonucleic acid, or DNA.

Reading further, by structure azacitidine is ribonucleoside derivative, and is preferentially incorporated into RNA. However, it can be metabolized to 5-aza-2′-deoxycytidine-triphosphate and so be incorporated into DNA.


Are all protein composed of all the amino acid (in animal) or are there less diverse protein?

Trp-Cage is a protein found in Gila monsters, and it is only 20 amino acids long and there are plenty of repeated amino acids so this does not use all 20. But there must be plenty of other examples, there is no reason why physically a protein must use all available amino acids.


Infrared wavelengths are EM waves of longer wavelengths than visible light. Also, visible waves are more energetic than IR waves.

Because of this, Visible light has the ability to excite organic receptor molecules in our eyes called Rods and Cones. These molecules stimulate cell responses and in turn excite cell responses in our nerves called an Action Response. Still unclear to most scientists is how the brain composes these action responses into an image, though a great deal of research is being done to date.

The reason why "nothing happens" when we aim infrared lights into our eyes (which I still wouldn't suggest) is that the photoreceptor molecules that we use to see don't have the necessary bonding configuration to accept the energy from these impinging EM waves.
 However, don't go thinking that nothing happens. Infrared radiation is a type of radiation that is usually a measurable heat source. IR is one of the broader parts of the EM spectrum. My point is to say, that when you "radiate" some thing with an IR source:
1) You don't know if it is also radiating other EM waves unless you know the specs.
2) You're still exciting molecules with that energy even if it isn't causing a seen effect. I highly doubt anything will happen unless you have a very high powered IR source. You shouldn't really ever focus high power lasers of any source onto your body, because higher intensities could inflict damage.

To Learn more about IR radiation:
http://coolcosmos.ipac.caltech.edu/cosmic_classroom/ask_astronomer/faq/radiation.shtml

IR (InfraRed)
EM (ElectroMagnetic)


DNA content in plant seeds vs. fruit flesh

It depends on the seed and fruit you're talking about.

The amount of DNA in your crushed up sample of plant matter depends on only one thing--how many cells are in your sample. Look at this diagram of a kernel of corn (U of Indiana):

There are different cell densities in each area--in the endosperm, the cells can be huge (and therefore have a lower density of DNA when compared with the embryo).

Let's look at a stained mustard seed (U of London):

As you can see, the cells here are very dense. More dense means more DNA per unit sample.

As far as fruit is concerned, the same rule of thumb applies. Verner, 1938 shows some cool apple tissue histology that might give you an idea of cell density in fruit tissue (again, it will be different in different fruits--search for "fruitname histology" if you're interested).

However, now that we've talked about density, we need to actually think about getting the DNA out. The extraction process is actually much more important in terms of your final yield.

Many plant seeds contain polyphenolics, which can cause DNA degradation. This protocol (Cornell U) details many of the possible shortcomings:

  These compounds have also been reported to cause difficulty in DNA purification in other plant species; polysaccharides (Murray and Thompson, 1980; Fang et al., 1992); polyphenolic compounds (Katterman and Shattuck, 1983; Couch and Fritz, 1990; Howland et al. 1991; Collins and Symons, 1992); and sticky and resinous materials (Webb and Knapp, 1990).

These contaminants can degrade DNA, but also render it unusable in PCR amplification and endonuclease digestion (Kim et al. 1997, Cornell U, EPICENTRE Biotechnologies).

Overall, there are definitely species-specific differences in fruit/seed plant DNA content. Practically, however, the most important factor in DNA yield and viability for future experimentation is sample purity and contamination. Specific fruits and seeds may contain one or more of the above contaminants, so the answer to "Seeds or fruits?" definitely depends on the species of plant you're working with.


Output of clustalo on (1.2.1) on ubuntu 14.04

You just need to specify the output format with the outfmt flag.

clustalo -i sequence.fasta -o output.clu -outfmt=clu

should give you the desired output.

How to share data?

Try using an abbreviated example which people can copy&paste, for longer data you could use something like http://pastebin.com/ but the URL might expire.

    gi|1709777|sp|P51780.1|PRIO_TRIVU MGKIQLGYWILVLFIVTWSDLGLCKKPKPRPGGGWNSGGSNRYPGQPGSPGGNRYPGWGHPQGGGTNWGQPHPGGSNWGQPHPGGSSWGQPHGGSNWGQGGYNKWKPDKPKT

    gi|1709773|sp|P52114.1|PRIO_MUSPF MVKSHIGSWLLVLFVATWSDIGFCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWGKPSKPKT

    gi|1709774|sp|P49927.1|PRIO_PIG MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWNKPSKPKT


How long human can survive with just drinking water everyday

About 52 to 74 days according to hunger strike wiki page.

This wiki page bases its data on 8 persons who died due to hunger strike:
Days survived by each person: 66, 59, 61, 61, 61, 46, 71, 73, 62, 60.


How does the eye know whether to focus further out or nearer in order to bring a blurry object into focus?

The neurology of vision is an extremely complex subject and is difficult to describe with any brevity, because there is so very much going on in so many parts of the brain. It is estimated that about 50% of the pathways of the brain, and about 30% of the cortex are involved in vision (where only 8% of the cortex is devoted to touch, and 3% to hearing). Some research estimates that eighty to eighty five percent of our perception, learning, cognition and activities are mediated through vision.1

The ability to accurately focus on an object, sustain that focus, and to change focusing when looking at different distances is called accommodation. That happens with the pupil size, the lens shape, etc. but it doesn't tell us how the brain chooses on what to focus. The short answer is that it's much more than focusing like a camera lens. We have retinal areas that simultaneously pay attention to further and closer areas, light/dark, edges, and more, all going on at once. That and much more information carried to the brain is processed, and efferently focus is honed. It's even more complex when two eyes are involved.

There are so many aspects to sight that an enormous number of kinds of optical illusions exist. They are involuntary. That's why they're fun. In fact, if you weren't tricked, it would indicate a problem in part of your brain. Here's one that relies on processing contrast:

As you scan looking at the white dots, your peripheral vision seems to be able to see black dots, but it's clear on scanning them one row at a time that there are no black dots.

In the following illusion, the red vertical lines are parallel.

The following are summaries of the neuroanatomy of vision.

Eye, Brain and Vision
Anatomy and physiology of the afferent visual system

1 Vision Is Our Dominant Sense


This is indeed a Stag Beetle (Family Lucanidae); in particular a member of the genus Lucanus.  Looking at the bugguide.net page for the genus here your specimen is most likely Lucanus capreolus, though Lucanus placidus also looks possible -- the two species are very close in appearance, though the former does seem more likely based on distribution.  Consulting The Generic Guide to New World Scarab Beetles here confirms that L. capreolus is featured here -- the femora (the first long segment in the leg, and the first we can see -- look at the right front leg) are bicolored (darker at the tips) -- the femora of L. placidus would be solid dark brown to black.


What is the best way to calculate the biological diversity of samples from bacterial/viral OTU tables?

I mostly concur with @Nathan's answer, and in particular with the references he provided.

As Shannon & Simpson indices can be hard to interpret and can be non-intuitive, I prefer using Hill diversities as suggested by Nathan (the Jost 2006 and 2007 refs are great to read up on this). The main argument is that Hill diversities give effective number of species that are comparable between samples and follow the duplication principle.

Hill diversities rely on a unified formula (see this wikipedia article) with one parameter, q. Increasing values for q correspond to increasing weighting of taxa abundances in the diversity calculation:

D with q=0 does not account for taxon abundance, so is just the number of taxa, or richness
D with q=1 is not defined, but asymptotically approximated by e^H where H is the Shannon entropy. D_q1 is the effective number of species with abundance weights.
D with q=2 corresponds to the Inverse Simpson index (1/D_Simpson). D_q2 weighs more abundant taxa even more strongly.

One can choose any value for q (with q=1 with the limit e^H), and comparing diversity estimates for varying q can give you an idea of sample evenness. Setting q=∞ gives the Berger-Parker index (the fraction of individuals in the sample belonging to the most abundant species).

Importantly, for alpha div analyses on (16S/18S-based) OTUs, I would always generate rarefaction curves first, and then generate diversity estimates at a common, rarefied number of reads per sample.

You can do most of this using the R package vegan. The phyloseq package provides various alpha div estimates in one command, but no Hill diversities. I've written a few simple functions to perform rarefaction and calculate (rarefied or non-rarefied) Hill diversities from an OTU count table matrix:

function.rarefaction.R

function.alpha_diversity.R


Why are haemorrhoids more common in humans than in animals?
This is due to the majority of animals, including apes, are on all fours. Only the human species stands and walks straight up with two feet. Therefore, the blood in the body has enhanced arduousness in circulating and travelling back to the heart. A justification for the commonness of hemorrhoids in humans, is there is a higher frequency of blood congestion which then further leads to hemorrhoids.
There are animals which can get haemorrhoids

Cats
Dogs
Apes
Horses

The reasons and causes why animals can also get hemorrhoids is similar to humans, besides the structural reasons. This may include:
In Horses

The horse may strain while delivering young ones

When the bowel movements are disturbed, as in constipation, it leads to an increase in pressure applied to the rectum region. Unlike humans, the increased pressure from constipation does not come from straining to get the excrements out, but from the impaction of the excrements within the horse and the resultant pressure that causes.  This in turn leads to expansion of the blood vessels around the anus and this may cause hemorrhoids and eventually bleeding.

In cats

One of the main reasons behind the occurrence of cat hemorrhoids is heredity, which plays a major role in deciding who would and who would not get afflicted with this condition.
Diets low in fiber and liquid content are the main cause of constipation, which in turn leads to excess pressure being applied during defecation and straining when bowels are passed. Too much pressure in the rectum and lower abdomen causes blood vessels in this region to expand, thus leading to the creation of lumps called hemorrhoids.

There have also been some investigations in which haemorrhoids were induced by ligation of the inferior haemorrhoidal vein into apes. The outcome of this was that after a certain amount of days, there were hemorrhoidal piles in the anus in fifty percent of the animals. The outcome was unremarkable. There was no bleeding and all animals showed no signs of pain or suffering.
References:

"Horse Haemorrhoids, Horse Hemorrhoids, Horse Haemorrhoids, Horse Piles - Web. 01 Mar. 2016.
"Result Filters." National Center for Biotechnology Information. U.S. National Library of Medicine, Sept.-Oct. 2006. Web. 01 Mar. 2016.


Would anything limit an "invasive species" T. rex introduction now besides equilibration with available prey or intervention by humans?

Lots of things could impact a reintroduced invasive species.

Disease/sickness: although no close relatives are present that is not a guarantee,  many diseases jump species. Parasites likewise could cause problems, especially newer parasites the dino may not have a good defense for. Even modern Fungus could pose a problem for eggs.

Predators: While an adult t-rex is predator proof eggs and newborns are not. Rats and other small mammals as well as many birds have been the demise of many ground nesting birds.

Poisons: there are plenty of animals and plants that are poisonous enough kill a t-rex that the rex may not recognize as dangerous. Remember there are a lot of things around a t-rex did not evolve with. This is more dependent on location, a t-rex dropped in Australia might kill itself with its first meal.

Human stuff: I am not talking about humans killing them. I am thinking of the things humans make killing them. things like walking into power lines, eating weird plastic human garbage, car accidents ( a car moving at speed could easily cripple a rex), even something as simple as getting hit by trains


Is there a downloadable list of all species along with their traditional classification?

ITIS
To expand on the answer from @Rodrigo, the Integrated Taxonomic Information System seems to be a reasonable answer. It gives you a database of every taxonomic node in the Tree of Life™ and each node has a Taxonomic Serial Number (TSN). You can download the data as a database or even just use the tables as pipe-delimited text files.
For example the file vernaculars tells us that the TSN for European frog is 173444. By looking in the file longnames, we can see that the complete name for 173444 is Rana temporaria. Finally, the file hierarchy, tells us that the complete hierarchy for 173444 is:
European frog:
→ Animalia
→ Bilateria
→ Deuterostomia
→ Chordata
→ Vertebrata
→ Gnathostomata
→ Tetrapoda
→ Amphibia
→ Anura
→ Ranidae
→ Rana
→ Rana temporaria
You may download the ITIS data in several different formats from https://www.itis.gov/downloads.
Example data from some of the files.
If you downloaded the MySQL Tables data from https://www.itis.gov/downloads/itisMySQLTables.tar.gz, here are some of the useful files you'll find.
vernaculars
The first two fields of vernaculars contain the TSN (Taxonomic Serial Number) and the common name for a node. Some common names map to a single TSN and not all TSNs have common names. Some examples:
50|bacteria|English|N|2015-03-02|159942
14092|mushrooms|English|N|2004-01-28|11529
14092|pore fungi|English|N|2004-01-28|11534
14092|rusts|English|N|2004-01-28|11539
183798|Domestic Cat|English|N|2007-08-15|111781

You can read the file dropcreateloaditis.sql to see what the other columns mean.
longnames
The file longnames contains only two fields, the TSN and the complete "scientific" name of the item. For example:
50|Bacteria
14092|Basidiomycotina
183798|Felis catus

hierarchy
The first field of the file hierarchy is the entire hierarchy, from tip to tail, for the TSN in the second field represented as a sequence of TSNs separated by a hyphen (-). E.g.,
50|50|0|0|14789
555705-936287-623881|623881|936287|2|415
202423-914154-914156-158852-331030-914179-914181-179913-179916-179925-180539-552304-180580-552363-180586-183798|183798|180586|15|0

Of course, those TSNs can be looked up in the longnames table to convert to something human readable. Using that, here is what the first field of the last line above actually says,
Animalia → Bilateria → Deuterostomia → Chordata → Vertebrata → Gnathostomata → Tetrapoda → Mammalia → Theria → Eutheria → Carnivora → Feliformia → Felidae → Felinae → Felis → Felis catus

synonym_links
The synonym_links file contains a list of obsolete TSNs and the current TSN which should replace them. For example, the TSN for the vernacular mushrooms is given as 14092 (Basidiomycotina). However, that TSN is not in the hierarchy file. Instead, synonym_links points us to use 623881 (Basidiomycota), which works. Here are some synonym entries:
51|50|2015-03-02
14092|623881|2004-01-28
552455|180586|2007-08-15

Example script
If you have access to a UNIX machine (MacOS may work), you can look up any common name by using a simple script I wrote. It will print a taxonomy, just like for European frog above. You can cut and paste the following commands into your terminal to try it out.
① Download the data
    wget https://www.itis.gov/downloads/itisMySQLTables.tar.gz
    tar -axvf itisMySQLTables.tar.gz
    cd itisMySQL*/

② Download my lookup.py script
    wget https://tinyurl.com/yyld2mm4 -O lookup.py
    chmod +x lookup.py

③ Run the script giving it a common name
    ./lookup.py human
    ./lookup.py domestic cat
    ./lookup.py love-lies-bleeding

④ Sample output
    human:
     → Animalia
     → Bilateria
     → Deuterostomia
     → Chordata
     → Vertebrata
     → Gnathostomata
     → Tetrapoda
     → Mammalia
     → Theria
     → Eutheria
     → Primates
     → Haplorrhini
     → Simiiformes
     → Hominoidea
     → Hominidae
     → Homininae
     → Homo
     → Homo sapiens


When salivary amylase breaks down starch, are those substances tagged or destined for a particular use in the body

Salivary amylase breaks starches brown into shorter chain of sugars. In the beginning of the small intestine, this process is continued by pancreatic amylase. Other enzymes at the surface of the intestine's lining complete the process resulting in simple sugars which absorbed into the circulatory system. Some of these sugars, if there is an excess in your diet, will be converted to fat and stored.

The rest of the sugars will ultimately be taken into cells and undergo a process termed cellular respiration. The bulk of these sugars will be broken down and used to create (recharge actually) ATP, a substance that just about any process in the cell requiring energy can use for energy. The atoms in the sugars used in this process end up as carbon dioxide, which you breath out, and water. But a certain percentage of the sugars only get partially broken down. These fragments can be used to synthesize many different substances depending on what's needed in the cell at that time.


How is excess semen removed if ejaculation does not occur?

Well as far as my knowledge goes in this aspect..

If sperms are not ejaculated then they are simply reabsorbed by the epididymis and recycled.
I would say the first website you have linked up there is what is a more appropriate explanation.


Can a gene be split between different genomic locations several kb appart?

Yes you can have exons and introns of the same gene separated by hundred (even thousands!) of kilobases.

Here is an example for the human genome:
"On average, there are 8.8 exons and 7.8 introns per gene. About 80% of the exons on each chromosome are < 200 bp in length. < 0.01% of the introns are < 20 bp in length and < 10% of introns are more than 11,000 bp in length."

Source: https://www.ncbi.nlm.nih.gov/pubmed/15217358

For the splicing process, it is not really a problem for the distance. Let me reframe the questions by challenging the assumption you are making: long distances in a sequence correspond to long distance in space.

Actually, DNA/RNA molecules are can have a lot of tertiary structure for example, G quartets for DNA, hairpin structure for RNA.

Source: https://upload.wikimedia.org/wikipedia/commons/5/5d/ATPC_secondary_structure.jpg

Long sequence distances are a poor indication of the real distance in space. Thus although from an engineering point of view it is incredible what molecular splicing can achieve mechanistically speaking. As far as I remember, the length for the intron/exon is important for the efficiency/timing of the splicing process (I might be wrong here on the specifics).


Can "human exclusion zones" in national parks for preserving Wolves and Grizzlies be a good idea?

I think it is a neat idea that should be discussed.
Not just for wolves or large predators but for all wildlife situations
There should be small habitats for all wildlife to refuge scattered around. Of course national parks, reserves and refuges are there for this purpose, but humans have become far too abundant on this planet to coexist anymore, and maybe we need to take it a step further? Again, it's something that should be discussed and awareness made of the issue.

And by far the best reason for this if nothing else is to have a scientific "control" spot for environmental research. It is important to have a control in all experiments, and to have a human exclusion zone helps create that control. If we had that, maybe someone could actually prove how much humans really are screwing up the planet, or maybe someone will prove they aren't :D


What is the known maximum ranging distance of a bat's sonar?

This paper finds some species can detect as far as 67 meters, but the range varies between species.

Note that the bats can actively change their range of detection and trade off range for resolution (low range with high speed resolution for hunting in closed, cluttered spaces or high range with low speed resolution for hunting in open spaces), as explained in Wikipedia's article on Animal echolocation.

Cool stuff.


How does gas equilibration occur in the alveolus, numerically?

There is no known mechanism for exchange of $\ce{O2}$ and $\ce{CO2}$ in a one-for-one fashion. Their transport across the alveolar membrane takes place by diffusion alone: both of them attain their equilibria with blood independently.
Note that it is not necessary for inhaled and exhaled tidal volumes to be the same. In fact, under physiologic conditions, the exhaled tidal volume is slightly less than inhaled tidal volume. This is because humans normally produce slightly less $\ce{CO2}$ than they consume $\ce{O2}$. In other words, the respiratory quotient is less than $1$.
Thus, we see that the assumption of preservation of alveolar volume and pressure is not valid. Apart from inspiration and expiration, the diffusion of gases to and from blood also affects alveolar volume.

Reference and further reading:
Boron WF, Boulpaep EL, editors. Medical physiology. 3rd ed (international edition). Philadelphia: Elsevier; c2017. 1297 p. (I found this textbook an excellent resource for learning physiology in general and respiratory physiology in particular.)


Jamaican/Caribbean insect, plant identification keys/field guides

I've never been to nor botanized Jamaica or the Caribbean, but a quick Google search turned up the following references for Jamaican plants:

Iremonger, S., 2002. Guide to the Plants in the Blue Mountains of Jamaica. University of West Indies Press, 280p. ISBN: 9789766400316
Fawcett, W. and A. B. Rendle. 1910. Flora of Jamaica, containing Descriptions of the Flowering Plants known from the island. Longmans & Company. Found here.

You can also find a list of Jamaican species on Wikipedia and a list of medicinal plants in Jamaica here.


Why a continuous supply of energy is needed to support a weight?

For skeletal muscles, you'll find a discussion in the Physics SE: https://physics.stackexchange.com/questions/1984/why-does-holding-something-up-cost-energy-while-no-work-is-being-done

To make things short: while holding a position, muscles need to maintain a given length. However, internally, the muscle looks like a collapsible array of filaments, with myosin heads acting as crossbridges between them. Even when the muscle is not contracting, myosin heads unbind and rebind at some rate and would let the muscle relax -- unless you input more energy to compensate this with a further contraction.

For smooth muscle, according to this article, the rate of unbinding can be very slow:

  Once the contraction has occurred, the cross bridge attachments need
  to be released in order that the muscle can relax. Although less is
  known about this phenomenon, it appears to be related to
  dephosphorylation of MLC20. In some situations, the dephosphory- lated
  MLC20 is very slow to allow detachment of the actin from the myosin
  cross bridge, resulting in a prolonged contraction. This has been
  referred to as a ‘latch-bridge’ (Hai and Murphy, 1988). This
  phenomenon may be of great value especially for tonically active SM
  beds as it would allow them to maintain basal tone through holding in
  an isometric state without a great energy cost.

So as the muscle is not relaxing, no input of energy is needed to adjust its length to the desired one. I assume a disadvantage of that is that the reaction time of the muscle is slower.


Can cats use ketone bodies as only source of energy?

You are correct that cats consume a lot of protein, and it's safe to assume a large share of this is broken down to amino acids, which are then oxidized to produce energy. But amino acids in general are not catabolized via glucose; instead, they are converted into compounds that feed into the TCA cycle via other biochemical routes.

Almost every of the 20 proteinogenic amino acids have their own specialized catabolism pathway, so this is a large topic. The general theme is that the amine nitrogen is first removed by a transaminase to yield a keto-acid, which is when converted into a carbohydrate that can enter the TCA cycle. To give but one example, leucine is converted in the mitochondrion by a series of CoA-coupled intermediates into acetyl-CoA and acetoacetate (a ketone body; see below). The acetoacetate in turn yields two more acetyl-CoA. A description of this pathway is found at the HumanCyc database. This is a great resource for learning amino acid (and other) biochemical pathways, and provides literature references.

Some amino acids are indeed used for gluconeogenesis, mainly by the liver, but this is not a requirement for their catabolism by most tissues. (It would be energetically inefficient to first generate glucose and then break it down again!) An exception is the central nervous system, which does require glucose and cannot subsist on fat or amino acids (for reasons that, to my knowledge, are still not well understood). So in order to support the CNS on amino acids, the route your describe via gluconeogenesis does occur.

Ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate) are the main alternatives to glucose accepted by the CNS. Gluconeogenesis is energetically expensive in the long run, and if deprived of dietary sugar for a long time, the body will increase its usage of ketone bodies instead of glucose. However, ketone bodies can never fully replace glucose: even during prolonged starvation in humans, blood glucose is kept > 2mM. The CNS would not function otherwise. I'm not an expert in cat physiology but I would bet the situation is similar.


Analogous organs: coevolution or opportunism?

I think the question you have to answer is a bit badly phrased. Overall, I mainly agree with you, except for point A. Here are my comments for each points:
A
co-evolution is defined for the evolutionary dynamic between two lineages. It is typically not used to talk about two body parts. Consider for example the definition from Understanding evolution:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution.

, wikipedia

In biology, coevolution occurs when two or more species reciprocally ("co-") affect each other's evolution.

or dictionnary.com

evolution involving a series of reciprocal changes in two or more noninterbreeding populations that have a close ecological relationship and act as agents of natural selection for each other, as the succession of adaptations of a predator for pursuing and of its prey for fleeing or evading.

I would note that the term coevolution can sometimes be used in its border line case as in this paper for example. It is particularly confusing as the term co-adaptation is sometimes used to talk about the interaction of two phenotypic traits. But stil, I would NOT check A
B
I agree with you! The conclusion is not valid from the premise (which means that it is not necessarily true, so even if the conclusion may be true, it cannot be concluded from the premise)
C
I agree with you! The statement is a bit unclear.
Typically, evolution is opportunistic would mean that throughout evolution history, a lineage may well evolve to reuse an existing gene for another purpose (neofunctionalization for example) which is very likely what happened here.
D
I agree with you! The conclusion is not valid from the premise.
In short
I would check C.


What is the difference between the evolution of fins in whales and fish?

I agree with you that the question is ambiguous, and also that the most sensible answer would be C.  However, one could make a more or less reasonable argument in favor of several other answers, too.

  a. The common ancestor of whales and fish possessed genes for fins.

Technically, this statement is true.  At least some of the fins of whales and fish are even distantly homologous, even though the lineages leading to tetrapods (including whales) and to ray-finned fishes diverged quite early in their evolutionary history.

(Specifically, the flippers of whales are modified tetrapod forelimbs, which are homologous to the pectoral fins of ray-finned fishes.  Whether one should also consider the tails fins of whales and fish to be homologous is a bit more debatable: the actual fin structures are very different, and presumably share few if any developmental pathways, but the tail and the spinal column which they attach to and are powered by is clearly a shared feature of both groups.)

However, while shared evolutionary history may explain why fish and whales have similarly placed flippers / pectoral fins, and why they both have a flexible spine that supports undulatory swimming with the help of a tail fin, it does not explain the convergent evolution of whales' forelimbs (which were formerly adapted for walking on land) into fin-like flippers.  So in that sense, while perhaps partially correct, this answer is also quite incomplete.

  b. Whales and fish possess the same mutations in their genomes.

It's hard to even tell what this statement means.  Insofar as it's a restatement of the fact that whales and fish share some of their evolutionary history (up to the divergence of the bone-finned and ray-finned fishes), it's no more or less correct than statement A above.

However, I suspect that the intended meaning of this statement is that whales and (ray-finned) fish would've separately evolved the same "fin-making" mutations after their lineages diverges, which is both clearly incorrect and also, even prima facie, statistically very unlikely.  So I would rule this one out.

  c. Fins evolved in whales and fish because they both use them to swim in water.

This statement is written using teleological language, which some may consider misleading, as it could be misinterpreted as implying that evolution was a directed process: it could be interpreted as saying that whales needed to be able to swim, so they chose to evolve fins (or that some guiding consciousness granted them fins).  This is, of course, incorrect — or, at least, we have no scientific evidence of there being any such conscious force guiding evolution, or of any organism (with the arguable exception of humans) being able to deliberately direct their own evolution.

However, it's quite possible to interpret this statement in a way that makes it perfectly correct: as both whales and fish move around by swimming, possessing fins (or something similar to fins) is an advantageous trait for them, and has thus been favored by natural selection.  If pressed, I would thus choose this one as the most correct answer out of the given options.

In particular, note that the argument made by AliceD that "they have to develop fins first before they can use them" is not really true: the ancestors of both whales and fish were swimming long before they evolved fins, and thus the selection pressure in favor of having fins (or fin-like structures) was already present before the fins themselves evolved.

In particular, the first aquatic ancestors of whales are believed to have swum much like modern-day otters and seals, using their flipper-like limbs as makeshift fins.  While there's no discrete transition point where one could definitely say that whale limbs turned into proper fins, it is clear that the fins, and their direct evolutionary predecessors, were being actively used for swimming, and that this fact directly drove their evolution into the actual fins that modern whales have.

  d. Fins evolved in whales and fish because of different mutations that occurred in their genomes.

While technically correct, this statement is so vague that it's all but meaningless.  All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages.

Certainly, it would be silly to claim that "different mutations occurring in their genomes" is an explanation of why whales and fish evolved fins: humans also constantly have different mutations occurring in our genomes, but we clearly don't seem to be evolving fins.  Neither are pigs or bumblebees or sunflowers, even though all of those species (and, of course, all others too) are also constantly experiencing different mutations in their genomes.

Really, this answer reminds me of the story about a person in a car who gets lost and stops to ask a passerby where they are; the passerby, after a moment's thought, replies "you're in your car."  While technically correct, that answer is absolutely useless — and so is this one, too.

  e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

Again, this answer could be interpreted as basically a restatement of answer A, and thus as being partially correct.  However, it completely ignores the convergent selection pressure described in answer C, which is responsible for the more recent evolution of whale flippers into something resembling fish fins more than, say, human hands or the feet of hippopotamuses (currently believed to be the closest living relatives of whales and other cetaceans).  Thus, I would not pick this answer, for the same reason that I wouldn't pick answer A.


What is positive and negative supercoiling?

According to this powerpoint from the SIU School of Medicine:

Right handed supercoiling = negative supercoiling (underwinding)
Left handed supercoiling = positive supercoiling

And from this Boston University webpage:

If DNA is in the form of a circular molecule, or if the ends are rigidly held so that it forms a loop, then overtwisting or undertwisting leads to the supercoiled state. Supercoiling occurs when the molecule relieves the helical stress by twisting around itself. Overtwisting leads to postive supercoiling, while undertwisting leads to negative supercoiling.

And finally from wikibooks:

Positive and Negative Supercoilings

Positive supercoiling is the right-handed, double helical form of DNA. It is twisted tightly in a right handed direction until the helix creates knot.

Negative supercoiling is the left-handed, double helical form of DNA.

Although the helix is underwound and has low twisting stress, negative supercoil's knot has high twisting stress. Prokaryotes and Eukaryotes usually have negative supercoiled DNA. Negative supercoiling is naturally prevalent because negative supercoiling prepares the molecule for processes that require separation of the DNA strands. For example, negative supercoiling would be advantageous in replication because it is easier to unwind whereas positive supercoiling is more condensed and would make separation difficult.
Topoisomerases unwind helix to do DNA transcription and DNA replication. After the proteins have been made,the DNA template supercoils by the force to make chromatin. RNA polymerase also influence DNA strand to have two different supercoiled directions. The region RNA polymerase has passed forms negative supercoil while the region RNA polymerase that have not passed forms positive supercoil. By these processes, supercoils are generated.

In the following image from web-books:

 (a) Positive supercoils (the front segment of a DNA molecule cross over the back segment from left to right). (b) Negative supercoils.
This video, titled "super coil (positive and negative) formation of DNA" should help you visualize this.


What wasp like insect breeds in clay pots with dead spiders?

It's some sort of potter wasp/mason wasp (Eumeninae). The spiders are paralyzed and brought there as food for its larvae.
Here is an example of an opened nest I found on Bugguide.net that looks similar to yours:

I don't know if it's possible to say what species it is from the nest.


It can't be confirmed but it sounds like a pelican.


What are negative and positive after potentials?

Yes, you are correct. The negative current is hyperpolarising the axon and the positive current is returning it to baseline from a hyperpolarised state.

They are often referred to as inward/outward (negative/positive respectively) currents as well, due to the direction of the flow of ions. Which is further compounded when you start looking positive/negative ions.

Inward currents are inflow of +ve charge, or outflow of -ve charge.
Outward currents are vice-versa.


From the source that Amory cites :

  You know that the number of offspring is shown by Pascal's triangle,
  right?

  For two alleles you have 1 : 2 : 1

  For three alleles 1 : 3 : 3 : 1

  For four 1 : 4 : 6 : 4 : 1 etc.

  So, if 4 in 1000 are 12 and 36 cm
  tall, that means that every in 250 plants is tall like that. And on
  which level of Pascal's triangle you have sum of 250? For two alleles:
  1 + 2 + 1 = 4 For threee: 1 + 3 + 3 + 1 = 8 For four: 1 + 4 + 6 + 4 +
  1 = 16 etc. until 1 : 8 : 28 : 56 : 70 : 56 : 28 : 8 : 1 Here you see
  that you have 9 options of height. The difference is 36 cm - 12 cm =
  24 cm. 24 cm /9 = 3 cm, so 1 plant will 12 cm, 8 plants will be 15 cm,
  28 plants will be 18 cm, 56 plants will be 21 cm, 70 plants will be 24
  cm (i.e. "the majority of F2 are like P1 and F1") and 56 plants will
  be 27 cm tall out of 250 plants. Thus C is the closest.


Can IVF decrease the probability of trisomy in the fetuses of older mothers?

Trisomy is due to non-disjunction in meiosis (the process in which eggs and sperm are created). This happens before fertilization.

Trisomies are more frequently seen in children of older women.  It's not fully understood why this happens, but it is likely related to the fact that the oocytes do not complete meiosis (and become eggs) until ovulation.  Here's an interesting paper that examines the physical causes of non-disjunction, but you might want to read up a bit more on meiosis (depending on your background) before tackling it.

You might screen for nondisjunction, but I don't think it's possible without killing the cells.  See the Wikipedia page on karyotyping, which explains how an amniocentesis might be used for a prenatal genetic diagnosis.  I don't know the regenerative capabilities of the human blastocyst, but if you had enough cells for a test, I don't think the blastocyst would develop normally.


Does our brain contain an innate function about closing only one eye?

I'm only a 17 years old student but i guess this is the answer(its just what i guess, haven't seen it in any books or research):

This is a picture from the book Life.
When both eyes are working they send signals to brain.
signals from things on the left side are sent to right side of brain and signals from things on the right side are sent to left side of brain(coming from both eyes).
as you can see both eyes participate in sending signals to right and left hemisphere.

On the right side of picture you can see visual cortex of right hemisphere , it has signals coming from both left and right and makes the thing we see.

While seeing through only one eye (or when you cut optic nerve from one eye) there is still signals coming to visual cortex from the other eye and that makes image of what you see.(when you close one eye there is still little signal from it if you are facing a bright light source, but signal from the other eye has more effect as its more powerful( try it by closing one of your eyes and put a torch in front of only the closed eye, if the torch is bright enough you can see bright thing there))

when you close both eyes the signals coming from both eyes are almost the same and if you face a bright thing, you almost see it.

i just guess that's the mechanism :)


The smell of the shield bug (aka stink bug)

Shield bugs (also known as stink bugs) are a group of insects in the superfamily Pentatomoidea. As summarized by this article from Rice University, the components of the chemical odor of these insects consist primarily of long chain alkanes, aldehydes, and esters. Esters are to be expected as they're the primary components of many odors. This article also includes other ecological info about the shield bugs' stink, as well as links to some references (including this peer reviewed journal article by Krall et all (1999)).

Another article mentions a 2006 study from Clemson University that identified 2 of the aldehydes in stink bug odor as trans-2-decenal and trans-2-octenal.


From my research, I can deduce that the cranial volume for males is

  560 cm3 (34 cu in)

and

  465 cm3 (28.4 cu in) for females

Note: These skulls are approximately half the volume of modern human skulls average Homo erectus skulls are

  900 cm3 (55 cu in)

I don't think you would need the area for 3-D printing, but you can use the volume!


Identity by descent among unrelated individuals

The definition of IBD is always the same - an allele or segment of alleles which is shared between two individuals because of descent from a common ancstor.
In the context of this paper, the authors are referring to segments of the genome between individuals which are IBD. In this case, they are looking at recently isolated populations who are likely to share longer stretches of IBD with one another. This is the case because each individual within a relatively isolated population is likely to be, on avergae, more related to another individual than in an outbred population. In general, it it much easier to detect longer segments of IBD than shorter segments, and this is why they choose to study isolated populations. Also, you can be much more sure that longer IBD segments will share a common ancestor with one another.
More specifically, they define a 'large' IBD segment is one which is longer than L centimorgans of length. Additionally, they define 'IBD-sharing' level between two individuals, as the probability that a randomly chosen genomic position on homologous chromosomes from each of the individuals lies in a large IBD segment shared by the two individuals. Thus IBD sharing takes values between 0 and 1.
There are several different methods, such as PLINK, fastIBD and GERMLINE which can identify IBD segments and their corresponding lengths from genotype data.
If you are interested in a relatively accessible guide to understand the principles of both single locus and segmented IBD, then I would recommended checking out Graham Coops's population genetics notes, section 2.2.


same SNP rs# referenced to be found in two different genes

The NCBI dbSNP entry shows rs7442295 to be in the gene SLC2A9, not SCL2A9 stated in the original question.

As the Wikipedia article for SLC2A9 says, synonymous names for SLC2A9 include:

  solute carrier family 2 (facilitated glucose transporter), member 9, GLUT9, GLUTX, UAQTL2, URATv1, solute carrier family 2 member 9

So GLUT9 and SLC2A9 refer to the same gene, and the two papers are not in conflict about the location of the rs7442295 SNP.


What are the factors that control the speed of propagation of neuronal signals?

The diameter of axons also makes a difference, the thicker the axon, the faster the rate of action potential conduction. This is seen in invertebrates, such as squid. Squid have giant axons (up to 2mm in diameter), which exhibit rapid conduction rates. See Wikipedia 'squid giant axon', in which it says up to 1mm, but I have measured 2mm myself. These are not found in mammals.

Original research on squid giant axon  was by Cole & Curtis (The Journal of general physiology, 1939). For more recent research see Hartline & Colman (Curr Biol. 2007 Jan 9;17(1):R29-35.).

Work by Hodgkin, Huxley and Katz (The Journal of physiology, 1952,  116(4): 424–448) using squid giant axons lead to the elucidation of the mechanism of action potential conduction and a Nobel prize. Academic summary here: http://jp.physoc.org/content/538/1/2.full

Wikipedia: see the Goldman equation (Goldman shared the Nobel Prize with Hodgkins and Katz). This is more frequently known as the Goldman-Hodgkin-Katz  equation in UK publications.


Why cooked food considered nutritious if proteins decompose at much lower temperatures?

Cooking is just a form of digestion.

  What is digestion?

Digestion is the process of breaking down big molecules into smaller molecules. When you cook food you break down big molecules into its small components.

  Why do we digest food?

Think about a long sequence of DNA for example. You eat corn and you have in your body a long sequence of corn DNA. What can you do with that long molecule....well, nothing. You need to break this long molecule down in order to be able to assimilate the constitutive nutrients. With those nutrients, you can now make up your own DNA. In other words, we need to break the big Lego castle that is food to get the building blocks in order to rebuild a spaceship. Digestion refer to the first process (breaking up the Lego castle). We refer to the part of the metabolism who breaks things down as catabolism and we refer to the part of metabolism that build things up as anabolism. Note that catabolism + anabolism = metabolism.

  Why do we cook then instead of digesting by ourself

Digestion takes much energy and require the organism to have the right organs and to have the right matter (enzymes and stuff). We can save up energy (and the other stuff) by digesting the food outside our body. One could say that humans, (just like spiders for example) are performing external digestion.

  Why cooked food considered nutritious

Cooked food don't have more nutrients than raw food. It is actually likely that in the process of cooking you would lose some nutrients going in the water that you throw away typically.

The big difference is that nutrients in cooked food are easy to assimilate which might end up being more healthy depending on the specific food source. Cooking may also destroy potentially toxic products.

Note that in response to the cooking behaviour, human gut has evolved to be shorter than it was in our ancestor.


This is a really wonderful phenomenon. Ants disperse far and wide, but when one of them finds food, it brings it back to the nest, and in doing so leaves a pheromone trail. The next scout follows this trail, and finds the food, and then leaves a second pheromone trail over the first one. As this continues, the trail gets stronger and recruits new ants to haul off the bounty. You can have fun with this. Take your finger and rub across the trail to erase it. Or place a piece of tape over it. This will confuse the ants for a while, until they make a new pheromone trail. If you have some time, break up a potato chip, or some other bait, and put it on the cement. Watch the first scout find it, and then leave a trail behind. Soon there will be many.


How does prolonged exposure to high frequency noise affect hearing?

The ear uses a series of hairs to parse out sound frequency in the cochlea.  When the cochlear hairs die, we lose some frequency response.

As we get older, even without exposure to loud noises, the higher frequency responses tend to lose their response first.  But loud noises have been linked to hearing loss and high tones are often lost first.

Hot off the presses: there's been some success in regenerating the cells which respond to sound in our ears.

I want to add @Armatus has a good point.  Ultrasonic sounds - above hearing range - seem to not adversely affect hearing at all.  Will humans and animals be harmed by frequencies outside their hearing range?


It might be an imported cabbageworm:

or a green-veined white:

Both exist where you are, and the former is more common than the latter. I can't tell them apart, but consulting the pages might help.


The human diploid genome is ~6.5 billion bp, so you need to find the length of a sequence that has a probability of occurring only once (assuming the sequence is completely random):

$4^n=6.5\cdot10^9$

$n\cdot log(4)=log(6.5)+9$

$n=\frac{log(6.5)+9}{log(4)}$

$n\approx16.30$

According to this article, each finger of a ZFN recognizes 3 bp, which means you'd need $\frac{18}{3}=6$ fingers to probabilistically recognize a unique site. Interestingly, the article also says:

  The requirement for dimerization is a great advantage for this reason: because a monomer is not active, cleavage does not occur at single binding sites. The cleavage reagent is assembled only at the target if the fingers have adequate specificity, and the combined requirement for binding two proteins brings the overall specificity into a very useful range; e.g., two three-finger proteins specify the location of 18 bp, which is sufficient, in principle, to pick out a single target, even in a complex genome.


Why does vacuum sealing of foods prevent spoilage from anaerobic bacteria?

I do not understand why anaerobic bacteria, that don't require and cannot survive in air, do not proliferate and thrive in the vacuum sealed food containers

They do. Vacuum sealing can prevent aerobic bacterial growth but does not prevent anaerobic growth.
Botulism is a particularly dangerous consequence. If food containing C. botulinum spores is sealed without being properly treated (usually by heating) or otherwise by being inhospitable to bacterial growth (often due to acidity or salt), dangerous botulinum toxin can accumulate and be dangerous or fatal when the food is later eaten.


Triangulation number of the SARS CoV-19 virus

Coronaviruses, like many viruses with a lipid membrane, are pleomorphic. The individual particles don't have a consistent shape. Here is a cryo-electron micrograph of SARS-CoV-1:

It might not be obvious, but each particle seen here is unique, they are not different rotations of identical copies. Since there is no consistent symmetry, there can be no triangulation number.

The image is from the following reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1563832/


What is this discarded exoskeleton from?

I can't be certain, but it is probably the pupal shell of a crane fly (daddy longlegs, Tipula palidosa). Here is an image to compare, and you can find lots more with a Google image search.

In the UK at least, these are colloquially referred to as leatherjackets and if you find one in soil before the adult has emerged it will often twitch.


" ... you can get started for around $500 or less with a little improvisation and patience." -- How to Set Up Your Own DIY Bio Lab

The $500 is pretty minimal and you won't get much done with that -- they mention other equipment (like a PCR machine) -- and you'd need to be extremely handy to be able to build all the equipment by hand.  More likely you're looking at thousands or several thousands of dollars.

Several sites give guidance:

A How-To For DIYbio Lab Equipment
Genome at Home: Biohackers Build Their Own Labs

Getting reagents may not be easy; I don't know how readily companies sell to individuals.

Don't forget that some experiments may require approval by animal care committees etc, unless you want to be arrested for animal abuse.

You might look into biohacker collectives, which are shared spaces where multiple "hackers" can use common equipment.


New earliest life found, what are the implications?

Not a lot, the sample is not conclusively biotic in origin nor is it necessarily much older than known fossils, 3.7 billion vs 3.5 billion. The sample is a few simple hematite filaments, complex hematite filaments do form as a byproduct of oxygen using (aerobic) bacteria, they can also be formed by metamorphic processes. Subscribing these filaments to life and proposing oxygen must have been present far earlier than any evidence supports based on this is wishful thinking at best.

If it were correctly identified and as old as possible it would have only a small effect, it would make finding life on other planets more likely becasue it would mean life forms basically as soon as you have persistent liquid water. It might indicate oxygen earlier than suspected but that seems unlikely.


Can you force human body to mass produce specific proteins?

Yes, using recombinant DNA technology, one can take engineered DNA which has been put in an expression vector, induce it by one of various mechanisms to enter cells grown in culture (they can be from human, mouse, monkey, plant, bacteria, yeast, you name it), and the cells machinery will take over, transcribing and then translating it into protein.

  does this not mean we can force cells to produce specific proteins we want? Purely hypothetically, ethics aside.

Absolutely, and this is done on a regular basis - sometimes at industrial scales, as a matter of fact. Examples of well-known recombinant proteins include insulin, the blood clotting factor VIII, and therapeutic monoclonal antibodies.

  I also can't quite understand "what" uses that DNA to create proteins

This is an extremely broad question, but Wikipedia's Introduction to Genetics may help explain some of these ideas using less technical terms.The quick answer is that it is the cell's transcription and translation machinery mentioned above that do the heavy lifting. Very briefly, DNA is transcribed into messenger RNA or mRNA, which is then targeted to the ribosome for translation in protein. Think of the DNA as the main instructions for the shop, the mRNA as the working templates distributed to many workers, the ribosome as the machinery which takes the template and produces the finished goods, the protein.


How diverse are dogs in their traits other than appearance?

Dogs are highly diverse in their patterns of copy number variation (variation in the number of copies of different genes). This has been shown to be probably related to the diversity in morphology. It would thus presumably also affect other traits such as those that you list, and it seems to at least have been shown for disease susceptibility. Interestingly, wolves have less copy number variation on average than dogs (citation).


At first I was thinking Trichoptera, but the antenna were not long enough and I noticed your size is quite small (~5mm).

The small size and body stance made me think of the order Neuroptera (the net-winged insects).

Specifically, this specimen reminds me of the family Coniopterygidae (or the dustywings).

  A distinguishing feature is that like many other Neuroptera, dustywings carry their wings nearly side-by-side when at rest, whereas whiteflies carry them almost flat across the back  [the last part being related to the OP's original thought that their specimen was a whitefly]

Interestingly, unlike many other net-winged insects, the dustywings do not actually have "net-winged" venation -- just like the OP's specimen.

If this is in fact a dustywing, according to Wikipedia:

  These tiny insects can usually be determined to genus with a hand lens according to their wing venation, but to distinguish species, examination of the genitals by microscope is usually necessary.

Just as a reference, according to here and here, a similar looking species called Conwentzia pineticola lives in the UK. You can see a picture of this species below:

 Source: NatureSpot

Comments on appearance and characteristics:

From Catherine A. Tauber et al. (2009) in Encyclopedia of Insects (Second Edition):

  The Coniopterygidae is generally a very homogeneous family characterized by very small adults (forewing length 2–5 mm) with bodies covered by white waxy (“dusty”) secretions.

The family name means "dusty wing" [source] due to the usually conspicuous whitish dust of waxy scales on the wings of these insects. I can't tell if this "dusty" nature is apparent in your picture or whether your picture is simply blurry.

Regarding the antenna, Tauber et al mention:

  Adults have chewing mouthparts, large compound eyes located laterally on the head, and multiarticulate antennae that are usually filiform (thread-like) or moniliform (with bead-like segments).

You can see a similar looking (and similar sized) specimen from the U.S. here and one from Spain here. Additional images on bugguide.net seem to suggest that your specimen is in the subfamily Coniopteryginae.


Do goldfish really have a 5 second memory span?

My answer might sound unscientific, since I haven't had tanks filled with goldfish. However, I have had fish and other pets over the years, including cats, turtles and a very sick lizard. I have a scientific background, and on this strength, I will report based on personal observation, albeit with a small sample size.

My fish always "knew" me. When I approached the tank, they knew it was their "feeding person", and even when they were not getting fed, left what they were doing aside and came to the surface to "greet" me, or more likely, impending food. I even experimented by asking others to walk up to the tank and saw that most of them did not respond in a similar fashion, although sometimes they did. With me, I enticed the same reaction every time, even  after a new tank was populated or new additions were made.

This makes me conclude fish, and goldfish, which I did keep, have "better than expected" memory.

When they are put in a new tank - well, I suggest you move to a well crowded city that is new to you, and see how long it takes for you to get your orientation right.

Hope it helps.


If hermaphrodite C. elegans can reproduce with females?

Since only the male tail is equipped with various specialized sensory and copulatory structures that enable him to locate the vulva and successfully inseminate the hermaphrodite.  Hermaphrodites can self-fertilize, but only males can cross-fertilize a hermaphrodite.

sources: Wormbook: Male development
C. elegans II (2nd edition): Sexual Dimorphism


How are fluorochromes conjugated to proteins such as antibody?

Fluorochromes are covalently bound to the antibodies to form stably labelled molecules. This paper describes it in great detail, from the abstract:

  Fluorochromes can be covalently conjugated to antibodies through
  reactions with thiol or amine groups. Typically, fluorochromes
  containing isothiocyanate, succinimidyl ester, or sulfonyl chloride
  reactive groups are conjugated to amines on the antibody molecules.

These covalent bonds are stable at room temperature and are also at -20°C. It's more likely that repeated freeze-thaw cycles damage the antibody.


What is the average Leg-to-Foot Length/Width Ratio?

A brief study I conducted of my peers (10 people of varying genders, ages, and races, all about average body type) revealed a rather consistent foot-to-leg length ratio of 1:3 for males and females (variance is insignificant), and width of 2:3 for males and 1:2 for females.


Does fat on our heart come from the fat that we eat?

Fat is, in molecular terms, triacylglcerol. In order to be absorbed in the small intestine triacylglycerol molecules are broken down by lipases into fatty acids and monoacylglycerols. Once these have got across the enterocyte membrane they are reassembled into triacylglycerols and packed up into a special class of lipoprotein particle, a chylomicron, which enters the bloodstream via the lymphatic system.

The triacylglycerols in the chylomicrons are then able to be passed around through the system of lipoproteins (LDL, VLDL etc.) and pretty much can end up anywhere, including fat cells (adipocytes) or they can be metabolised as fuel molecules

So, because of that initial digestive step I would say that a single intact dietary fat molecule cannot end up as a body component directly, but complete metabolism of the components of the fat molecule is not necessary for these to contribute to body fat.


Can gene-gene interactions result in gene expression?

I don't know anything about your algorithms. But i will try to explain your the format of data that was given to you. I don't know your background in Biology, so i will assume it is not your expertise field and will make some simplifications of the subject.

What is gene expression?
To understand what is a gene expression, you need to understand what is a gene:

  A gene is a sequence in the DNA (composed of 4 bases A,T,C and G) that can be transcribed by a protein, in your context we will say it always start with a start codon (a codon is a triplet of DNA bases) and stop with a stop codon. It is usually around a thousand bases long. The transcription will give you a RNA, and that RNA can be translated (note the difference with transcribed) into a whole new protein.

Now the gene Expression is a measure of the amount of RNA from the gene you are looking for. In a cell you can have around 10000-100000 copies of that RNA; the raw count is not really stable as you can have extract two cells or three and it will change your "expression". Most of the time we normalize the count by the count of a bunch of known genes called housekeeping genes. The particularity of these genes is that their expression is quite stable.

  The figures you have are a ratio between RNA copies of your gene of interest and RNA copies of a stable gene (in term of expression).

What does G1(-/-) and wt mean?

Usually when we (biologist) call a sample wt it means wild type, in other words, a normal individual. G1(-/-) means that this sample is from an individual with the G1 gene inactive (could be obtained by genetic modification).

What is a gene-gene interaction?
An example of interaction first: let's imagine a gene coding for an enhancer (booster) of transcription. the presence of this gene allow another gene to be expressed in the cell, if this gene isn't present or isn't transcribed, the other gene won't be expressed either.

How can we see interaction there?

Let's look at line one, the control (normal individual), We see that G4 (column) is almost unexpressed (0.07). In normal conditions, this gene is not expressed. Now let's look at mutant G1(-/-) and G6(-/-), we see the expression of G4 is rising (0.37;0.23) compared to the control (wt).
We can suppose than G1 and G6 are acting as inhibitors of the G4 gene.


Let's break down the phrase as one of the commenters mentioned:

"proximal": in the context of chromosomal position, this means closer to centromere, whereas "distal" means further from the centromere (the middle part of the chromosome).
"deletion": referring to the genes that were deleted as a result of the chunk of the 21st chromosome being missing.
"breakpoint": points at which the chromosomes was broken leading to the deletion.

Putting it all together, this says that the deletion breakpoint closer to the centromere falls within the NCAM2 gene, whereas the deletion breakpoint further from the centromere falls within the GRIK1 gene, with the other 17/19 genes falling between the two.
To verify this interpretation, we can use the USCS Genome Browser as mentioned. We can see that if we compare the position of the NCAM2 gene and the GRIK1 gene on the 21st chromosome, the former is closer to the centromere than the latter. We can also do a spot check to verify that ADAMTS1 one of the other 19 deleted genes, lies between the two of them.


What does T and the numbers mean in T coliphages?

The "T" stands for "Type" as in type 1, type 2 etc. To quote Wikipedia on Escherichia virus T4 (emphasis mine):

Bacteriophages were first discovered by the English scientist Frederick Twort in 1915 and Félix d'Hérelle in 1917. In the late 1930s, T. L. Rakieten proposed either a mixture of raw sewerage or a lysate from E. coli infected with raw sewerage to the two researchers Milislav Demerec and Ugo Fano. These two researchers isolated T3, T4, T5, and T6 from E.coli. Also, in 1932, the researcher J. Bronfenbrenner had studied and worked on the T2 phage, at which the T2 phage was isolated from the virus.[39] This isolation was made from a fecal material rather than from sewerage. At any rate, Max Delbrück was involved in the discovery of the T even phages. His part was naming the bacteriophages into Type 1(T1), Type 2 (T2), Type 3 (T3), etc.

It turns out Wikipedia is incorrect: The original use of Type as a designation for these viruses comes from a paper published in 1945 (PDF) by M Demeric and U Fano: BACTERIOPHAGE-RESISTANT MUTANTS IN ESCHERICHIA COLI Genetics 30:119. In this paper they collected phages from Luria (of LB/Luria Broth (actually properly known as lysogeny broth)) and Delbruck amongst others and collated them all for comparison. Delbruck references them in his review article (PDF, possible paywall, summary here), also from 1945.
I could find no evidence for why the phages were numbered as they were, though strains from Luria (actually previously from his supervisor as P28 and PC) were labeled T1 (Luria alpha) and T2 (Luria gamma), so it is possible that it was simply in order that they were received or possibly in order of discovery amongst the several groups working on these viruses.
The T-even phages were grouped because of structural similarities, and are now strains of the species escherichia virus T4 in the genus Tequatrovirus (see link for taxonomy).


Finding for evolution, comparing past flower numbers with present

Has there been evolution in this population?

If $p$ differs in the population, then yes. If you $p_1$ and $p_{10}$ (the two different estimates at generation 1 and generation 10) are equal, then any deviation is caused by sampling error. Hence set $P_1 = P_{10}$ as the null hypothesis and performs a chi-square test.

Is natural selection involved?

For this we have to know the generation time and the population size. We can assume the generation to be of one year (10 generations). The population size $N$ could be estimated from genetic data of the sampled butterflies. The expected loss of genetic diversity per generation is $\frac{1}{2N}$ but you will need to consider any possible path by which one can go from $p_1$ to $P_{10}$ using a series of binomial distribution and sum up their probabilities. That being said, it is a little bit computationally expensive if $N$ is large but some Markov Model theory might give you some simplifications.


Q1: Yes, the CIGAR string operation 'M' means you can have both matches and mismatches. For example if you have a CIGAR string 10M, then you could have 10 bases that matched perfectly or you could have 5 matches and 5 mismatches. In this case, you have what are known as SNPs (or single nucleotide polymorphisms).

Q2: In your case, you have 99 matches, 170661 skipped regions in the reference genome, and 26 matches.

Q3: If you want to find out how many matches or mismatches there were, you'd have to take the reads from your SAM file, align them to their position in the reference genome, and compare them base pair by base pair to see if their nucleotides match. You can take advantage of the positional information found in field 4 of the alignment to accomplish this.

You can write your own code to accomplish this or use  something like Samtools, which I believe comes with a variant caller.


Why do people feel pleasure when using roller coasters / centrifuges?

Riding roller-coasters usually (unless you are psycho) induces a release of adrenaline and other chemicals, like endorphin (your bodies pre-emptive effort to combat any possible pain and stress you may be about to experience), into your body. Endorphin is a strong chemical, specifically released to make you feel relaxed and confident. Obviously this explains the natural high you may get from riding a coaster.

However, every now and then you get that person who ruins it for everyone by having a heart-attack. This person's body was not conditioned for this type of stress, and clearly they did not enjoy their ride much. Elevated blood pressure,
erratic heartbeat and palpitations...they should have instead taken a ride on the log flume. For the rest of us thrill-seekers, this type of gung-ho, take-all-comers attitude gives us a confidence boost by wiring our brains to not be overly stressed in actual emergencies.

Imagine the people out there who have grown up in small towns. You may have heard how such people can have a difficult time adjusting to the hustle and bustle of city life, especially in larger cities. This has to do with everything from their metabolism and diet, to their sleep cycle. Their body simply needs to get used to the new environment. The same goes for new combatants. Military's try their best to simulate combat for new trainees. The better the simulation, the better prepared people will be for combat. The first few combat situations for people are obviously going to be the most dangerous, being a truly foreign experience for most peoples bodies.

Physiologically it's going to push your body to the limit. After all, you sense your life is in serious danger. But as many people deal with this stress, they can start to acclimate until they ideally stay fearful, but become extremely focused on the fight. The adrenaline rush (and again, other chems) is part of what you need to get used to. If your body has a naturally stable system when exposed to these chemicals, or you have trained it to be so, then you are at an advantage compared to your peers.

https://www.psychologytoday.com/blog/threat-management/201001/adrenaline-rushes-can-they-help-us-deal-real-crisis

http://www.faqs.org/health/topics/15/Risk-taking-behaviors.html


Does some form of self organizing map exist in the brain?

These are great questions.  The SOM was absolutely biologically inspired.  Sure, there are many examples.

Examples of self-organizing topographical feature maps in the human brain include the the sensory homunculus, retinotopic maps, and the entorhinal cortex.  There are even maps such as these in the midbrain auditory nucleus of the barn owl as well as the auditory cortex of the mustache bat.

As to how they work and organize in nature, that is still an active area of research, and it seems like there are no experimental conclusions that suggest the existence of  universal rules for self-organization of sensory maps in the brain.  As far as I know, however, Kohonen's theory that these maps organize via a combination of lateral inhibition and Hebbian learning has not yet been displaced by a more modern idea.


Do Termites and Silverfish metabolize cellulose the same way?

It has been known for 40 years or more that some insects such as termites digest cellulose by synthesizing their own cellulases, whereas others have a symbiotic relationship with gut micro-organisms that perform this digestion (see Martin, Comp. Biochem. Physiol. (1983) 75A 313-324  — requires subscription — or this short popular science article).
What is the situation for silverfish — Lepisma saccharina? Today the evidence that generally determines whether an insect can digest cellulose itself is the presence of the genes for the cellulase enzymes in its genome. There is a relatively recent review of this in Annu. Rev. Entomol. (2010) 55 609–32 — again requiring subscription for access — in which the species in which these genes have been detected are listed. I know nothing about organismal biology or taxonomy, and can only summarize the species represented there for others to comment on:

Orthoptera
Blattaria
Phthiraptera
Hemiptera
Coleoptera
Hymenoptera

This doesn’t seem to me to include Lepismatidae (which Wikipedia tells me is the family), but what do I know. (I only know the genes aren’t present in fruit flies.) However some earlier indirect experiments studying the effects of antibiotics on insect cellulase levels suggest that Lepismatidae may have their own cellulase.


I think this thread will become a jungle very fast and very soon, so I suggest you to have a look at the cancer research reviews of the last 2 years to get a grasp. Have a look at cancer hallmarks and at other important key concepts, you will most certainly answer your question yourself :) I am not a cancer researcher so I cannot comment on the topic in a detailed fashion (I work on plants), but that's what's going to happen.

In general, I'd say that what we don't know about cancer is a "common ancestor" of all types of it that will enable us to tailor a one-sized cure.


Resources for finding all drugs of a certain class

The WHO has their own methodology, the Anatomical Therapeutic Chemical (ATC, thank you commenter) classification system, for organizing such data (its impetus is comparing results between studies).

Also, if you have $900 sitting around, you can get a subscription for the United States Pharmacopeia.  I'm not sure if that can be spread across multiple subscriptions for an organization like the Red Book David mentions.


Can someone help me identify this queen ant?

The small space between the thorax and the abdomen indicates this queen has only one petiole segment (no post-petiole). The large size and absence of an elongated first abdominal segment indicates the subfamily Formicinae. The morphological features necessary to go further with a formal identification are not visible, but from the general aspect of the ant it is likely to be a Lasius or a Formica.

See ref below:

  Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


Do Colorblind People Have Stronger Sensitivity in Their Other Remaining Cones?

Kudos for Delta-S in Reddit for enlighten me. Original post is here.

The answer is no, color blind people don't have stronger sensitivity in their other remaining cones. This goes back to the Photopic Sensitivity Graph below.

As you can see, human vision are most sensitive to green. All responses of green cone are within the photopic sensitivity as well as most response of the red cones. And despite few responses of red cones are outside the Photopic sensitivity, the peak sensitivity of red cones is very close to the peak of Photopic sensitivity (560nm and 555nm).

Peak Photopic Sensitivity: 555nm
S cones peak  : 420nm
M cones peak  : 530nm
L cones peak  : 560nm

So, in case of Deuteranopic, depending on which wavelength is loss (defected) from their eye, if it closer to the red response then they will likely to experience luminance loss as well. However, if the green cone that is defected is far from the red response, the red cones still have possibility to maintain the luminance they can achieve.

Unfortunately in the paper, it's not mentioned which sensitivity wavelength was defected from the unilateral participant. It is only mentioned "result indicate that she was deuteranopic".


Is there a list with common mistakes in database entries?

Microsoft Excel has a nasty habit of thinking it knows your data better than you do, and when it sees gene names like Mar3 and Sept7, it tries to be helpful and convert them to dates.

So anytime someone puts a long gene list in to Excel and takes it back out again, you see those genes and their relatives converted to dates.

This has been known for years, but you still see it in lots and lots of published papers.

According to http://dx.doi.org/10.1186/s13059-016-1044-7, almost 20% of article supplementary material gene lists made with Excel contain such errors.


This is indeed a polychaete worm, and likely a member of the beachworm family Onuphidae.

From the Marine Education Society of Australasia  :

  Polychaetes are particularly common on and in muddy and sandy shores. Their most obvious feature are the pairs of parapodia appendages. One pair comes from each body segment. These parapodia are used for crawling and swimming. "Para" means "like", and "podia", "pod" or "ped" means "legs". These parapodia are often tipped with hardened spine-like setae or dorsal cirri.

You can find some good informaiton on beach worms here, and information on the distribution, abundance and
population dynamics of various species here.

I'm sure a quick message to Dr. Pat Hutchings, the Austrtalian Museum's polychate expert, would prove to be be your best chance to get a species identification.

For those interested in additional polychaete identification, you can download a digital ID key.


Phosphorylation can occur on specific amino acids only, what you have called phosporylation sites. These amino acids are Ser, Tyr, Asp, Thr and His. In theory any of these amino acids may be phosphorylated, but in reality it may not actually occur for a number of reasons. Some of these are because of the change in overall charge of the protein which can influence the 3D conformation, or the amino acids are not accessible to specific kinases, etc. If you ask for the purposes of doing a Western blot, then the antibody specification sheet should indicate whether a phosphorylated form exists and there should be a reference to the literature describing this modification.


How can I detect transcription factors and preferably master TFs (master regulators) in an organism?

The easiest approach to find transcription factors for any given organism would be based on sequence homology with other transcription factors. In order for this to work your organism of interest does have to be sequences, you can check this (e.g.) on the NCBI genomes page. By comparing the genome or the genes of your organism with other known (fungi) transcription factors, you can find most of the transcription factors of that organism.

  Does NGS applicable to find TFs and preferably the novel ones?

Both NGS and ChIP-Seq only allow you to determine DNA (or RNA if you reverse transcribe first) sequences. Therefore these techniques alone will not help you in identifying which TFs act on your genes.

  I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

I can't currently think of any 'classical' or standard experiments to determine which TFs bind to a given gene or promoter. One possibility would be to use CoIP (co-immuno precipitation) on the RNA polymerase complex and use Mass-spectronomy to identify the TFs in that complex. The problem with this is going to be, that you need a way to only get the RNA polymerase complex for your genes of interest and not all the other ones in the cell. Maybe you can use columns with DNA probes that can hybridise with your genes instead of standard antibody based CoIP.

Another way to determine which TFs bind the promoters of your genes is to analyse the respective promoter sequences. However, without knowledge of most (or at least some) of the binding sequences of the TFs in your organism, this will most likely not work very well. Edit: As @AlanBoyd commented there is a database for fungal transcription factors. However, it seems like they mainly annotate which fungi genes are transcription factors, but do not cover binding motifs of these factors.