I found this on the beach at Breamlea in Vic Australia and wondered if you could tell me what it is please

It's a swim bladder, probably a porcupinefish swim bladder. They can be found washed ashore still inflated. They've been described as "molar shaped". (Picture from Australian Museum.)


Differences between right and left handed people

According to this Psychology Today article: 3 Myths and 3 Facts about Left-Handers (with numerous links to many papers throughout the article), there are no particular difference between left and right handed people in terms of intelligence, personality, creativity or mortality.

There seems to be a noticeable difference in the number of people having the language centre being in the left hemisphere of the brain (95% for right handed people vs 70% for left handed people).


How old does a baby have to be before it can retain memories?

Surely an important question. But there are different kinds of memory (classified mainly as declarative and procedural) which you don't specify exactly in your question. Wikipedia and Scholarpedia list here many known facts. I will give you some short hints and links for introduction and overview instead of pasting that stuff here.

You are probably referring to autobiographical or episodic memory, that is memorizing consciously particular events within one's own life within a context. And for this type of memory researchers agree that self-awareness seems to be a necessary precondition. The existence of this cognitive ability can be checked by the mirror test. Human infants pass this test normally around a age of 18 months (also some animals). The cognitive self develops between 21 and 24 months and marks the end of infantile amnesia.


Where would vegetarians/vegans get a substitute of hemo/myoglobin from?

The following informations is taken this source. It also lists some references. If this doesn't answer your question let me know in the comments.

Iron is found in food in two forms, heme and non-heme iron. Heme iron, which makes up 40 percent of the iron in meat, poultry, and fish, is well absorbed. Non-heme iron, 60 percent of the iron in animal tissue and all the iron in plants (fruits, vegetables, grains, nuts) is less well absorbed. Because vegan diets only contain non-heme iron, vegans should be especially aware of foods that are high in iron and techniques that can promote iron absorption. Recommendations for iron for vegetarians (including vegans) may be as much as 1.8 times higher than for non-vegetarians.

Some might expect that since the vegan diet contains a form of iron that is not that well absorbed, vegans might be prone to developing iron deficiency anemia. However, surveys of vegans have found that iron deficiency anemia is no more common among vegetarians than among the general population although vegans tend to have lower iron stores.

The reason for the satisfactory iron status of many vegans may be that commonly eaten foods are high in iron.For example, you would have to eat more than 1700 calories of sirloin steak to get the same amount of iron as found in 100 calories of spinach.

Another reason for the satisfactory iron status of vegans is that vegan diets are high in vitamin C. Vitamin C acts to markedly increase absorption of non-heme iron. Adding a vitamin C source to a meal increases non-heme iron absorption up to six-fold which makes the absorption of non-heme iron as good or better than that of heme iron.

Fortunately, many vegetables, such as broccoli and bok choy, which are high in iron, are also high in vitamin C so that the iron in these foods is very well absorbed. Commonly eaten combinations, such as beans and tomato sauce or stir-fried tofu and broccoli, also result in generous levels of iron absorption.


How do scientists transfer the specific DNA in Optogenetics?

Well for one, just having a gene doesn't mean you can make it work as intended, and indiscriminately tweaking the genetic material can produce unwanted effects. For example, if I overexpress p53, a common tumor suppressor gene, the cell undergoes apoptosis (1). If I break/delete the same gene, the cell might undergo apoptosis or it might become cancerous. Human development is of course regulated by hundreds of genes at a time, however, so legs on a butterfly is far more complex than just a single gene.

A common approach for inserting genes into a host genome is the lentiviral transfection. Generating a lentiviral vector is detailed here. A similar strategy for transfection using HEK293 for viral production is described in the following paper. I have no knowledge of optogenetics but I tried my best to find a paper in the field that employs the method in practice. In case you have no access to the article,

Viral Production

  HEK293T cells (ATCC, UK) were cultured in Iscove’s modified Dulbecco’s medium (Sigma-Aldrich, Germany) supplemented with 10% (v/v) FCS (Sigma-Aldrich) and penicillin–streptomycin–glutamine (Sigma-Aldrich) in 5 × 150 mm dishes. After 80% confluency was reached, cell were transfected in serum-free medium with the helper plasmids pRV1, pH21 and pDFΔ6 and pAAV1/2-hSyn-BLINK-IRES-eGFP or pAAV1/2-hSyn-IRES-eGFP at a molar ratio of 1:1 with CaCl2. On the next day, the medium was replaced with serum-containing medium, and 48 h after transfection cells were harvested, pelleted and resuspended in lysis solution (150 mM NaCl, 20 mM Tris, pH 8).....

Culture & Transfection

  Hippocampal neuronal primary cultures were prepared from embryonic day 18–19 (E18– E19) rat hippocampi as previously described43. All the experiments were approved by the Institutional Animal Care and Use Committee of University of Milan and by the Italian Ministry of Health (#326/2015). Neurons were transfected at 7 days in vitro (DIV7) via the calcium-phosphate precipitation method with 4 μg of plasmid DNA for GFP for the experiments assessing the axonal and dendritic distribution of BLINK2 reported in Fig. 2c. Neurons were infected with AAV1/2-hSyn-BLINK2-IRES-eGFP at DIV10 and fixed at DIV12 for the immunocytochemistry assays.

There's more to the method, but in short they transfect the 293 cells with these plasmids that create a functioning virus enclosing their plasmid of interest, and then they harvest the virus and use that to further transfect their neural cells with the gene(s) of interest.


This plant has been identified as Viscaria oculata.


Does sex-chromosomes exist in all the cells in a human body?

Like the other answer already said: yes, all cells in the human body contain all 2x 23 chromosomes (with the exception of cells that loose all nuclear DNA during maturation, like red blood cells, or cell produces by meiosis, which contain only a single set of 1x 23 chromosomes).

However, the more interesting part of your question remains to be answered:

  Then a cell of a male and a cell of a female are always different and never be the same?

Technically it is true, that cells from a male and female can never be the same, however that difference is vanishingly small.

Genetically the difference is that female cells have two X chromosomes and male cells have one X and one Y. However:

in all female cells one of the two X chromosomes is permanently silenced (turned off), so essentially they also have only one (active) X chromosome.
the male exclusive Y chromosome is tiny. Size wise it is ~1% of the human genome, but it only has ~200 genes (of which only a portion is protein coding), which is even below 1% of all human genes (there are ~25.000 protein coding genes, around twice that much in total). Many of these genes are also only used/active in male exclusive organs.

These two points taken together mean that the majority of male and female cells do actually have the same active genes - and are therefore "the same" (there are of course many many other factors in biology, including individual differences, that require putting this into quotes).


You assume that the undigested plasmid is supercoiled, but more probably it is in the relaxed circular form due to single strand nicks. This form migrates slower than linear DNA.


Why is the start of my coding sequence ATG and not TAC?

This image from the Kahn Academy article 'Overview of transcription' might help:

Essentially, the sense/coding strand of the DNA encodes the sequence that is transcribed. The RNA polymerase binds to the antisense/template strand, for which the code is indeed TAC, but when it then transcribes this strand it is again complemented, giving us the AUG that is recognised by initiator tRNAMet (also known as tRNAfmet), as shown in this diagram from the Kahn academy article on 'tRNA and Ribosomes'.

(Note that this diagram is actually showing Met in the middle of a sequence, rather than the start. fMET binding looks slightly different.


Exact definition of single nucleotide polymorphism (SNP)

In genetics, a SNP (Single Nucleotide Polymporphism) is the substitution of a nucleotide with a different one.
A SNP can have phenotypic effects or not.

A mutation, in genetics, is any kind of inherited change in DNA. Mutation types are: SNPs, indels, structural variants, translocations and so on.

Sometimes researchers (especially in the field of medical genetics) call "mutation" (meaning "pathogenic mutation") a SNP which is responsible of a disease (especially in case of a Mendelian disease). Since mutations causing severe Mendelian diseases are usually rare, several people use the arbitrary threshold of 1% to discriminate between a "SNP" and a "mutation".

So, probably your professor is stating that SNPs cannot cause a Mendelian disease because he uses the last definition I gave. However, while this definition may be useful for medical genetics purposes (i.e. I also agree that a very common variant is unlikely to be causing a rare Mendelian disease), it is arbitrary, if not wrong.


Evolution is largely random, because most of the processes that drive evolution are random. A few ideas you should understand to realize why it is so random.

Most people are only aware of natural selection when it comes to evolution, and think that natural selection has a goal of creating new, increasingly sophisticated forms of life. None of this, of course, is true. Evolution is not only natural selection, there's also genetic drift, gene flow, and mutation, which are random. Natural selection is not technically random, but it's not the biggest player. Secondly, natural selection does not have any goals and does not move forward, create more complex life, invent adaptations, or does anything of this sort. Natural selection is not designed to produce perfection, it just acts upon whatever variation is present in population, and favours individuals that are more successful in reproduction. Case study: 98% of our DNA doesn't code for any proteins, and presumably most of this DNA is junk. Does it sound like perfection to you, like we are the ultimate species?

The reason I tell you all this is because, in my opinion, when asking this question of "inevitability", you assume that there's some guiding hand that leads evolution towards some end-point, a climax. But there is no such guiding hand, and it takes a number of incredibly unlikely events to occur in a specific order for: Earth to be created with such conditions, life to start on Earth, collective learning to evolve in some form of live, agricultural revolution to occur so this form of life can thrive, etc. If at any stage something went different, everything would be different.

Final thoughts, why are you so sure that humans won't go extinct just like 99.9% of all the species that ever existed on Earth? A typical species goes extinct in about 10 million years, and we've been around for only 200,000 years. If you accept this possibility (which is real, in my opinion), suddenly, it doesn't seem that intelligent life, and we as its representatives, is some inevitable end-point in evolution, does it?

Edited: As to your last (new) question, "if randomness in evolution exists, are we still able to describe the general trends in evolution?". Firstly, of course randomness exists in evolution! Mutations are caused by errors in the process of DNA replication, genetic drift is caused by random sampling by definition. Secondly, there is no universal trend to more complicated organisms being evolved, as I mentioned above. Some organisms do get more complex, but some organisms haven't changed much over very long time, some are "living-fossils". Once again, evolution has no goal to create more complex life -- if, say, nautiluses or horseshoe crabs are capable of surviving and reproducing in the niches they occupy -- there's nothing else needed for their existence. Furthermore, fitness is linked to the environment, which is dynamic -- many complex species went extinct during global changes in the environment, whereas what you might call as "primitive" species of unicellular bacteria survived.


Which method of seed dispersal is the most common among the seed plants?

This paper from Herrera (1989) investigates the role of endozoochory in Angiosperm diversification, and it has a table that can help answering your question, since it deals with all seed plant families:

As you can see, among Gymnosperms there is no question: endozoochory is the most common mechanism of dispersal.

Unfortunately, things are a bit more complicated among Angiosperms. Exclusive endozoochory is not the most common mechanism (27.1% versus 72.9%). However, if we take into account that the plants that perform endozoochory are actually the sum of the first and second ("mixed") columns, the total is 50.9, which is more than 50%. Of course, there is a mathematical possibility that another method, together with the "mixed" column, also surpass 50%.

Finally, it's worth mentioning that the authors are calculating the frequencies of endozoochory only. If one adds epizoochory to that number (zoochory = epizoochory + endozoochory), the frequency of zoochory is even higher.

Source: Herrera, C. (1989). Seed Dispersal by Animals: A Role in Angiosperm Diversification?. The American Naturalist, 133(3), pp.309-322.


CAG is a synthetic, ubiquitous promoter which combines elements of the CMV early enhancer, the chicken β-actin gene, and the splice acceptor of rabbit β-globin. According to the researchers who created it:

  The elements which constitute the pABWN vector, the CAG promoter, the weak neo unit, and the BPV fragment have only low specificity to cell types or species. Therefore, this system can be applied not only to L cells or CHO cells, but to a wide variety of cell lines. The pABWN vector should be very useful for producing large amounts of valuable proteins in mammalian cells, for changing the phenotype of host cells by overexpression of some normal or mutated genes, and for disrupting the function of targeted genes by overproduction of anti-sense RNAs.

In the paper you cite, CAG-ChR2 is used to activate all neurons in the vicinity of the light stimulation, for example in Figure 2Ab, where the panel is labeled "PYR+INT activation."


How does the colinearity of the HOX genes determine the body plan of an organism?

Quoting from some parts of Sean Carroll's book - Endless forms most beautiful, I have tried to provide you with an answer but, remember that this can never suffice for the reading of this great book.

Yes, we do understand how the hox genes' expression is regulated.

From page 126-127

  ......The establishment of these Hox zones and their subsequent action
  in sculpting the different forms of repeated parts is the fundamental
  genetic logic upon which the modular forms of large,biletarian animals
  is built.

  The genetic logic relies on genetic switches at two levels. One set of
  switches belongs to the Hox genes themselves. these switches activate
  each Hox gene in different zones that will become different modules of
  the animal. Another set of switches contain signature sequences that
  are recognized by Hox proteins and that control how other genes are
  expressed in different modules.

  In both arthropods and vertebrates, the Hox genes are developed in
  zones along the main body axis. The distinct zones of each Hox gene's
  expression domain are governed by genetic switches, and seperate
  switches control Hox gene patterns in different tissues such as the
  ...... Because of the logic of the genetic switches, the cells that
  belong to one module express different Hox proteins or combinations of
  Hox proteins than those in adjacent modules....

Let us take an example of Ubx gene which leads to formation of wings in the 2nd and 3rd thoracic segments of  drosophila. This gene is turned off in the first thoracic segment  but in the second and third segments, it is turned on. This regulation can be achieved because of the genetic switches which in turn can be switched on or off by activators and repressors. These activators and repressors are unevenly distributed in the embryo and so regulation of switches in different parts of the embryo is possible.


Literature about industrial enzyme application

I'll give you examples I have encountered in talks. There are too many variations and types of applications for me to break out in a comprehensive way.

Example 1: enzyme production.  this sort of application is about optimizing the amount of a desirable enzyme or protein produced from a liquid culture.  Sorry if this is too close to cell growth, but its terribly important.  Small cell cultures are used in research and the genetics of the cells (usually e coli or yeast, but also often a fungus that's been found somewhere) to improve the amount of the desired protein.  The protein may be secreted, which makes it much easier to purify.

Once a good strain is found, the culture is scaled up to thousands of liters, often many kilos of pure enzyme can be produced this way.  Examples: the enzymes that break down fabric for acid washed jeans, the proteases and cutinases which are included in laundry detergent
and insulin.

Example 2: glucose isomerase.  This enzyme is used to produce high fructose corn syrup.  The enzyme itself actually changes fructose into glucose, but by le Chatlier's principle, a glucose syrup under high pressure will be converted to fructose by the enzyme.  This enzyme, produced by an industrial process like that described in example 1 is immobilized onto a resin and packed into large industrial sized columns.  I seem to remember from the talk that they were similar in size to an oil barrel.  Large amounts of glucose rich corn syrup are passed through the column; it comes out about 40% fructose.

Another example (3)  along those lines might be how to use an enzyme with a product.  In an industrial manufacturing process like enzyme denim treatment, the fabric may be washed in a solution including the enzyme.  The process has to be careful to control the amount of enzyme the denim is exposed to and to optimize the conditions so that none of the fabric is ruined but comes out consistently.  The enzyme might be killed by a pH change or heating.  This is essentially chemical engineering and there are courses about this sort of thing at most major chemE departments now.


GULO encodes L-gulonolactone oxidase which catalyses a step in the biosynthetic pathway to ascorbic acid (vitamin C).

I did a BLAST search at NCBI using the mouse GULO protein as probe, excluding mammals, and I saw highly significant hits in reptiles, birds, sea urchins, fungi and bacteria. I conclude that this enzyme, (or very close relatives) is ubiquitous.

Humans (and other primates; also guinea pigs and the Dalmatian coach hound) have a defective GULO gene and so require dietary ascorbate.

Since the gene is non-functional in humans it isn't expressed in the foetus.


Where to begin studying Biology in earnest, with preferably free sources?

Before getting into veterinary and mammalogy, you might want to start with the basics. As many people have mentioned, Campbell and Reece is one of the best textbooks to start a foundation in biology. If you live near a public library you might find a 6th or 7th edition to borrow. Amazon has a few 7th editions for cheap as well. Although it is an introductory biology book, it will give you a wonderful tour of cellular and molecular biology that will make it much easier when studying animal physiology (which they also covered in the later chapters to a limited extent).

Free Biology Text Books:

Boundless Biology: Boundless is a company that has many free textbooks for high school level biology to help teachers in have a free online textbook.

I have also found a list of free biology text books here that might be of use.

Free Mammology Textbook:

As part of a National Science Foundation Grant, the Northwest Center for Sustainable Resources created *Introduction to Mammology*. It is a free textbook that was developed for a two-year Wildlife Technology program. It also contains information related to the lab portion of the program, but you can skip those and focus on the material.

Free Online Coursework:

Coursera: A few people have already mentioned Coursera, which is a Massive Open Online Content (MOOC). Here, you can find many courses across a wide range of biology topics (and others!). You can enroll in a course (for free) and many times they come with accompanying free textbooks as well (at least that is what I have experienced).

edX: Another MOOC that was started by Harvard.

Khan Academy: Another great website for explanations of certain aspects of biology. As Tyto alba stated, there are some errors in the videos.


What is the difference between kingdoms protistae and protoctistae?

First, just a correction: it's "Protista" and "Protoctista", not "Protistae" and "Protoctistae".

They mean the same thing. Those are just different names proposed by different taxonomists for describing the same group of organisms.

Protoctista (or Primigenum) was proposed by John Hogg in 1860.
Protista was proposed by Ernst Haeckel in 1866.

However, as it is common in taxonomy and nomenclature in general, things sometimes get a bit more complicated: some biologists, like Lynn Margulis, don't treat those two terms as synonyms. Particularly, I don't use her nomenclature.

Source:

Jstor.org. (2017). Protozoa, Protista, Protoctista: What's in a Name? on JSTOR. [online] Available at: http://www.jstor.org/stable/4331095 [Accessed 12 Sep. 2017].


Advanced Higher Biology 2017 - EPT Index

Well, you made a mistake: The numbers in the second table are irrelevant to the question as it is not about taxa but about individuals. And the ETP number is calculated from number of EPT taxa (and not individuals).

The correct answer was 3*100/7 = 42.9% ==> B good quality of water.


This is really sounds like a guideline, a starting place, not necessarily your best protocol.

In practice its hard to be more specific as MS says.  The pH of the buffer will affect the charge of the protein, and to a lesser extent the DNA.

Also the protein may have an ideal pH for binding which you could guess is in the range of 7.0-7.4, but might find that the strongest binding depends on unexpected pH and salt concentrations, or the addition of a small molecule.

The affinity of araC for instance is greatly increased by the presence of arabinose in sufficient concentration.

lac Repressor, in contrast releases itself from DNA in the presence of IPTG or  lactose.


When is really necessary to visit field to observe sample collection process?

After being a lab tech, just because they should report everything, doesn't mean that they are doing exactly what you think/wish. I would say it is important so you can see if the process of sample collection and processing is exactly what you need for your thesis. I had to follow a written report on how to feed a certain insect, after a few nights the post doc came in and realized there was something missing from the report and we were feeding the insects one the wrong side of the leaf. May not happen to you, but I think its always good to verify.


What nutritious insects exist to farm that require the least attention?

The silkworm Bombyx mori is farmed for silk, but the pupae are also eaten across the Far East. Since these insects (larvae) have been domesticated for centuries there are well-established procedures for growing them.


Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients?

This is a big question and a very active field of research. I'm not deeply into this litterature, but you should look into the the different scaling relationships (often power laws) that have been described on metabolism vs body size, species-area relationships and species richness vs biomass. Also consider that energy-use by species in a community is considered a zero-sum game both in the neutral model (Hubbell, 2001) and in Red Queen models of evolution. You will probably not find a definite answer to your question though, but there are some interesting intersections of ideas out there. As others have suggested you also need to consider and take into account differential historical extinction rates, and how this will influence current patterns (Mittelbach et al. 2007).

Points of entry could be:

Gaston. 2000. Global patterns in biodiversity (essential reading!)
Chave. 2013. The problem of pattern and scale in ecology: what have we
learned in 20 years?
Venevsky & Veneskaia. 2003. Large-scale energetic and landscape factors of vegetation diversity
Mittelbach et al. 2007. Evolution and the latitudinal diversity gradient: speciation, extinction and biogeography
Marquet et al. 2005. Scaling and power-laws in ecological systems

A couple of caveats/ideas though; first of all, it has been argued that the latitudinal gradient of species richness is likely to be due to many different mechanisms in different taxa (see Gaston, 2000). Here you are looking for a hypothesis to explain not only this single pattern, but all three of them, which makes a single explanation even less likely. Second, many non-exclusive explanations have been put forward for the latitudinal gradient. Even if we don't know which ones of these that are the true mechanisms, some are clearly incompatible with being explanations for all the three patterns you mention, while others might be applicable to all of them. For instance, environmental stability in the tropics is one suggested mechanism for the latitudinal gradient, but this doesn't make much sense for a gradient along ocean depth (deep sea has arguably been a more stable environment both over shorter and longer time-frames). It might be relevant for an altitude gradient though. Going through different hypothesised explanations for the latitudinal gradient in this way (from what I know, the best studied of these gradients) could give you a list of ideas that are most interesting to target (maybe somebody has already done this though).

I hope this helps.


Are there dextral/sinistral higher animals?

Handedness has been studied in several different species of toads. As basal tetrapods, the authors argue that these taxa are unlikely to be influenced by human hand dominance and are thus a better model for studying the evolution of handedness.

Bisazza et al. (1997) studied "pawedness" in Bufo bufo, B. viridis, and B. marinus in wild-caught animals by determining which forelimb was used to remove a piece of paper from the animals' snout or a balloon placed over its head.

The results were mixed. B. bufo preferred the right forelimb in both tests, but B. viridis and B. marinus did not. B. marinus did preferentially turn its head left in another experiment, using the right forelimb for support.

A subsequent study by Malashichev and Nikitina (2002) showed that Bombina viridis is "lefthanded," while Bombina bombina is "ambidextrous."

So based on these studies, lateralization appears to have a long evolutionary history.


Do lunar rhythms have really impact on plant growth?

Great question! The way I will do this is by explaining a bit about what moon planting is, then I will go through the articles I have found one at a time, to provide the different persepctives on moon planting, as it is called.

What is moon planting?

Moon planting is a methodology of planting, in which the lunar cycles are used as guides to know when to plant.

How might it work?

The first article is a great article about a gardener who tried to do moon planting, but it did not work for her, until she realized she did it wrong. Then, she found out the logic behind why lunae planting works. It really doesn't have to do with lunar cycles. Here is her explanation:

  Let’s look at a possible scenario. Gardener I is a moon planter; Gardener II isn’t. Both gardeners wait till spring to plant their beans. (No sensible cool climate gardener will plant beans in winter. It’s too cold for them to germinate, and many seeds will rot or be taken by ants.) But come the first warm spell Gardener II succumbs to one of the great spring urges and plants the beans at the first hint that spring has arrived. Gardener I, on the other hand, waits till the next good moon planting time before planting the seeds. Early warm spells are usually followed by another cold one… and again seed planted too early may rot. Even if it doesn’t, plants that suffer any set-back when they are young usually don’t do as well as plants that have flourished right from the start. (The set-back can be from cold, boggy soil, snail or scale attack — the effect is the same). So counterintuitively, beans that are planted later in spring will probably do better than beans planted too early.

The opposite works too when planting in autumn. By the lunar planting schedule, it is better to grow earlier, and since the soil is warmer, the plants will grow better.

In the second article, the author reviews the research done on the effect of lunar cycles on reproduction, germination, and more. However, only the work of a researcher, L. Kolisko, shows evidence for the benefits of lunar planting. Therefore, the conclusion was lunar planting are not significant to affect crop yield.

However, in another article, it shows that there are many cycles in plants that are affected by the lunar cycles and that for some organisms, the lunar cycles do affect reproduction, germination, and production of different metabolites. Therefore, lunar planting might have an effect in that way as well.

Conclusion

The conclusion is that lunar planting may actually work, but many scientists are debating about it. So in reality, we aren't 100% percent sure about it, because there is evidence supporting it, and evidence contradicting it.

References

http://danfingerman.com/skeptic/Moon_planting.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/beeson_1946.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/schad.pdf


What can cause incompatible sticky ends to be ligated?

The answer from @Armatus got me looking at star activities again. EcoRI is prone to exhibit star activity in non-optimal buffers. In the case of this enzyme this tends to be a relaxation of site specificity, so HAATTC and GAATTD would be possible cut sites. The cleavage at such sites produces the standard sticky end.

So, what if there is a star site near to the XmaI site such that a digest at the true EcoRI site and also at the star site removes the XmaI site and so allows recircularisation. If the configuration was, for example:

....GAATTC.................[XmnI].GAATTD...GGATCC....

the ligated product would have neither EcoRI nor XmnI sites.


Microsatellite shifts (peak calling) GeneMapper! Thesis help!

Your markers are probably fine, especially because you keep seeing the same allele in multiple individuals. Dinucleotide repeats do not always copy perfectly. More likely, remember that the primers you use to amplify your microsatellites bind outside of the actual repeat region. You could have an insertion/deletion in the region between the primers and the repeat region, changing your allele sizes from to even to odd (or vice versa).


If two definitive ovums are fused will they form an organism?

No, it is not possible. The reason is the genetic imprinting, which takes place on the parental DNA in the egg and the sperm. Here small modifications are added to the DNA which marks them as silenced. So some genes are expressed from the mother (while the fathers copy is not expressed) and vice versa.

There are even genetic diseases which are caused by imprinting. One example is the loss of a gene region on chromosome 15. Depending in which copy its lost, either the Prader-Willi Syndrome or the Angelman Syndrome occur. PWS is inherited via the father, Angelman via the mother. Another interesting article on imprinting can be found here.

If you combine two eggs, some genes, which are not imprinted in the father, will not be expressed in the developing embryo which will finally lead to death of it. However, researcher deleted the maternal imprinting in mice and mimicked the from the father and made off-springs from two mothers possible. This is something which is ethically very problematic in humans. The article can be found here:

Birth of parthenogenetic mice that can develop to adulthood


How do axon terminals report to the soma?

We can consider the classical example of Long Term Potentiation.

CREB is a transcription factor which is activated during LTP by phosphorylation.

Your reasoning about the delay between signal and transcriptional response is correct and thats why neurons have local translation factories near the dendritic spines and gene regulation (fast responses) is mostly post-transcriptional. (there is no article which says exactly so but you can refer so some articles  which report that miRNA-repressed genes are reactivated upon certain signals. They hint that post translational regulation is very important in neurons)

http://www.cell.com/neuron/abstract/S0896-6273%2809%2900939-8

http://nar.oxfordjournals.org/content/40/11/5088


Why are protein-coding regions rich in GC?

Transcription factors generally bind to promoters, enhancers, silencers, and other regulatory regions that lie outside coding regions, through there are "duons" which code for amino acids and also bind TFs to regulatory effect. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967546/
One paper suggests GC content helps balance recombination events with genetic stability, and so there may be an evolutionary benefit from organisms that undergo sexual reproduction having GC-rich coding regions. https://www.frontiersin.org/articles/10.3389/fpls.2016.01433/full

In eukaryotes, meiotic exchange of genetic information, or recombination, between homologous chromosomes is a critical step in generating genetic diversity required for adaptation. Recombination is also a crucial tool in plant improvement efforts. Local genome architecture is sculpted by the recombination process, and genome architecture, in turn, drives recombination. This interplay helps to create variability in genomic space, defining relatively stable and plastic genomic regions. This fluctuation in genomic stability is critical for balancing adaptation and stability on the phenotypic level.
Recombination has direct implications for GC patterns and vice versa. GC content refers to the percentage of guanine and cytosine bases in a DNA sequence, as opposed to adenine and thymidine bases. There have been many studies substantiating the positive correlation between recombination and GC content (Ikemura and Wada, 1991; Eyre-Walker, 1993; Fullerton et al., 2001; Galtier et al., 2001; Marais et al., 2001; Duret and Arndt, 2008; Haudry et al., 2008; Escobar et al., 2010; Muyle et al., 2011). Crossovers have been found to be correlated with high GC content in rat, mouse, human, zebrafish, bee, and maize at a broad scale (Jensen-Seaman et al., 2004; Beye et al., 2006; Gore et al., 2009; Backstrom et al., 2010; Giraut et al., 2011), while other studies detected strong correlation only at a fine scale (∼5 kb for yeast, ∼15–128 kb for human) and rather weak correlation at a broad scale (∼30 kb for yeast, ∼1 Mb for human; Gerton et al., 2000; Myers et al., 2006; Marsolier-Kergoat and Yeramian, 2009).

GC-richness may offer the ability for organisms to create offspring that evolve to changes to the environment and fend off parasites, while also being viable enough to procreate, themselves.


Short answer
The causes of ALS are not well known. Some familial types are associated with toxic proteins, susceptibility to toxins and defective protein metabolism. My personal 2-cents is that metabolic and toxicologic defects tend to cause cumulative tissue damage over time, perhaps explaining the delayed onset.

Background
Amyotrophic lateral sclerosis (ALS), is a progressive, fatal disease characterized by the gradual degeneration and death of motor neurons.

In 90 to 95 percent of all ALS cases, the disease is sporadic, meaning that it appears apparently at random. Individuals have no family history of ALS, and their family members are not considered to be at increased risk for developing it.

About 5 to 10 percent of all ALS cases are inherited. About one-third of all familial cases result from a defect in a gene known as “chromosome 9 open reading frame 72,” or C9orf72. The function of this gene is still unknown. Another 20 percent of familial cases result from mutations in the gene that encodes the enzyme copper-zinc superoxide dismutase 1 (SOD1). In case of mutations in the SOD1 gene it is though that mutant SOD1 protein is toxic.

Other inherited forms are believed to change in the processing of RNA, that may lead to ALS-related motor neuron degeneration. Other gene mutations implicate defects in protein recycling. And still others point to possible defects in the structure and shape of motor neurons, as well as increased susceptibility to environmental toxins.

Source: NIH - ALS Facts Sheet


It's definitely a bird pelvis (synsacrum). Based on the size (~30 cm), it came from a very large bird. Unfortunately, comparative images of bird pelves are rare on the internet. Some possibilities (large birds of Sweden possibly found on the coast):

Great northern loon
Golden eagle
Common crane

A loon skeleton (from http://paolov.wordpress.com/2011/08/05/friday-mystery-object-107/) shown below.


Where in the world does blue eyed whites originate from?

According to this discussion, blues first appeared exactly where one would expect - in northern Europe.

The interesting thing is the survival value (if any) that blue eyes offer. One theory is that blue eyes are merely a side effect of light skin. The other theory is that blue eyes are simply sexy and irresistible.


Are both (partial) copies of DNA transcribed in S and G2 phases of cell cycle?

I can't unequivocally say, at least without further literature review, that both sister chromatids are transcribed equally everywhere, especially since the cell does have mechanisms to differentiate between the old and new DNA strands (such as methylation state). It would be conceivable to expect, however, that the same regulatory factors that were present before replication have the same effect on newly synthesized DNA as they did on the old. Here are some electron micrographs showing transcription from both chromatids at some locus.

McKnight SL, Miller, OL Jr. 1979. Post-replicative nonribosomal transcription units in D. melanogaster embryos. Cell 17:551-563

Here you can see RNA (solid line in schematic, b) of increasing length branching from both sister chromatids (dotted line):

A similar image but this time showing the replication fork (arrow):

This image shows RNA free gaps (arrows) in a single transcription unit, which are symmetrical between the two chromatids:

From which they conclude:

  The observation that fiber-free gaps often occur at symmetrical positions on sister chromatid transcription units suggests that the two identical transcription units respond similarly to the mechanisms that control RNA polymerase chain initiation. These cannot now be specified, but could include the local supply of RNA polymerase or other controlling molecules.


Help me understand my membrane potential assignment

If there is passive transport for each ion, then every ion will diffuse over the membrane until the concentrations will be the same, and the membrane potential will be zero. So there is active transport in the cell, which maintains the resting potential which is -63mV.

So with the current concentrations the membrane potential will differ from this -63mV, and so the cell will change the ion levels to change the current potential to be equal to the resting potential.

I think you should try to simply summarize the Nernst potentials. It won't be so accurate as the Goldman equation, but you don't have the relative permeabilities of this cell type, so the questioner probably does not wait the Goldman equation from you.

I would solve it this way:

Em = RT/zF * ln(out/in)

R = 8,314 J/molK
T = 37 + 273 = 310K
F = 96485 J/molV

RT/F = 26,712mV

ENa = 26,712mV*ln(136/45) = +29,543mV
EK = 26,712mV*ln(6/100) = -75,152mV
ECl = -26,712mV*ln(140/13) = -63,486mV
Em = ENa + EK + ECl = -109,95mV

Emr = -63mV
Emr - Em = -63mV + 110mV = +47mV

So we have to increase the membrane potential. Decreasing intracellular K+, Cl- concentration and increasing intracellular Na+ concentration can do that.

Concentrations: extracellular 136 Na, 6 K, 140 Cl, intracellular 45 Na, 100 K, 13 Cl. So possible passive transports are increase Na+, decrease K+, increase Cl-.

Conclusion the passive transports will be increasing Na+, decreasing K+ the active transport will be decreasing Cl-.

Note that I haven't used these terms for 5 years, so if you can consult with somebody else about this, then ask him/her whether this is correct.


Complexity is a lure. Evolution isn't defined by complexity, but by adaptation to one's environment, as you mentioned.

Evolution is an ongoing, non-deterministic process. There's not one definite evolutionary "path" that brings a unicellular to a modern human being. Nor is there a predictable evolutionary path that brings a dog into becoming a human. You also have to acknowledge that, because evolution is ongoing, the dog of yesterday is not the dog of tomorrow. That applies to all the living.

Is it possible that given the right amount of time and the ideal environment the modern human could evolve into the modern dog?

Yes, it is possible.

Is it probable? No.

The chances are that if humanity were to find itself in such an exotic environment - to which dogs are 100% adapted, but humans 0%, which just shows how unprobable such an environment is - it would become extinct before it has a chance to adapt, much like a lot of other species have done.


What does orbital mean in orbital frontal cortex?

Orbitofrontal cortex: the area of the cerebral cortex located at the base of the frontal lobes above the orbits (or eye sockets), involved especially in social and emotional behaviour.


In plants, there are three types of tissue: meristematic, simple, and complex.

Meristematic (embryonic and totipotent)

Simple (composed of only one type of cell), such as

parenchyma
collenchyma
sclerenchyma

Complex (composed of more than one type of cell), such as

dermal (protective covering)
vascular (conducting tissue)
xylem (conducts water and dissolved minerals)
phloem (conducts water and dissolved organics)
ground (bulk of the body; primarily parenchyma, collenchyma &
sclerenchyma)

With this information in mind, let's take a look at what the source you provided says that makes up Xylem tissue.

  "[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels

Here are the roles of said cells in Xylem:

Xylem parenchyma are cells specific to storage and short distance transport.
Sclerenchyma Cells (xylem fibers) are specific to support and protection.
Vessel Members (which are conducting cells) are specific to water, mineral transport, and support mostly in advanced angiosperms.
Tracheids (which are also conducting cells) are specific to water, mineral transport, and support mostly in gymnosperms and lower angiosperms.

I hope this information helped you understand why Xylem is not an organ, but rather a complex tissue of plant.

References:

http://facweb.furman.edu/~lthompson/bgy34/plantanatomy/plant_cells.htm

http://www.bio.miami.edu/dana/226/226F09_5.html


Most likely a member of the genus Staphylea. Since you are in Pittsburgh, PA, it's most likely Staphylea trifolia L., or an introduced species.


Identifying internal structures of dissected fish

Since I can't actually look at and handle the yellow structures, it is difficult for me to provide any information on them.

As far as the white structures you mention on the first picture, I believe those are most likely muscles.
As for your third question. That does appear to be all one structure; and yes, going on that assumption, the entire structure would be the swim bladder.


Why can't I read everything in my field of view?

The field of view is determined by the light-receptive parts of the eye: the retinae (Kolb, 2012). The fovea is the region with the highest resolution. It is located in the central part of the retina and covers only about 2 degrees of the field of view (Lauweryns, 2012). The total field of view is roughly 180o (Fig. 1).

Fig. 1. Schematic of the human field of view showing the foveal region. Source: Medical Dictionary.

The reason for the regional differences in retinal resolution (referred to as visual acuity) is that the cone photoreceptors are densely packed in the foveal region, while rod photoreceptors predominate the retina outside the fovea region (Fig. 2) (Kolb, 2012).

Fig. 2. Distribution of rods and cones. Source: Webvision.

The cones sense color and are specialized to work under well-lighted (photopic) conditions. In contrast, rods are hardwired to converge onto a single optic fiber to collect responses for dim lighting (scotopic, or night vision). Because many rods (tens of rods) connect to a single optic nerve fiber, the spatial acuity is dramatically reduced (Fig. 3). Hence, you can read with only a few degrees of your vision. While reading, your eyes continuously scan the page for the next word to center it onto the foveal region.

Fig. 3. Many rods converge onto a single ganglion cell, while one cone synapses onto a single ganglion cell. Source: Slideshare.

This is the big handicap that people with age-related macular degeneration face. The macula (that includes the foveal region, see Fig. 1) degenerates and the cones are lost. Hence, they loose their high-acuity region and cannot read anymore without using magnifiers or other low vision aids.

References
- Kolb, Webvision - The Organization of the Retina and Visual System (2012)
- Lauweryns, Brain and the Gaze: On the Active Boundaries of Vision (2012)


Why is DNA Shuffling more efficient than Point Mutation?

You should read this paper. Here is the gist of what you are interested in:

Because most point mutations are deleterious or neutral, the random point mutation rate must be low and the accumulation of beneficial mutations and the evolution of a desired function is relatively slow in such experiments. For example, the evolution of a fucosidase from a galactosidase required five rounds of shuffling and screening before a >10-fold improvement in activity was detected4. Naturally occurring homologous sequences are pre-enriched for 'functional diversity' because deleterious variants have been selected against over billions of years of evolution...
Although shuffling of a single gene creates a library of genes that differ by only a few point mutations1, 2, 3, 4, 5, 6, the block-exchange nature of family shuffling creates chimaeras that differ in many positions. For example, in previous work a single beta-lactamase gene was shuffled for three cycles, yielding only four amino-acid mutations3, whereas a single cycle of family shuffling of the four cephalosporinases resulted in a mutant enzyme which differs by 102 amino acids from the Citrobacter enzyme, by 142 amino acids from the Enterobacter enzyme, by 181 amino acid from the Klebsiella enzyme and by 196 amino acids from the Yersinia enzyme. The increased sequence diversity of the library members obtained by family shuffling results in a 'sparse sampling' of a much greater portion of sequence space15, the theoretical collection of all possible sequences of equal length, ordered by similarity (Fig. 4). Selection from 'sparse libraries' allows rapid identification of the most promising areas within an extended sequence landscape (a multidimensional graph of sequence space versus function)


Looks most likely to be a Gulf Toadfish, Opsanus beta, judging from its size, location caught, and other similar identifying features.

More detailed species information at:
Opsanus beta on FishBase.org


RT-PCR: Not seeing how it can measure mRNA expression levels

There might be a confusion of terminology. There is real-time quantitative PCR, which can sometimes be called RT-PCR. There is also reverse-transcriptase PCR, which is also confusingly called RT-PCR. To try to reduce confusion, real-time quantitative PCR is also called RT-qPCR or qPCR.
What you describe in your question is the reverse-transcriptase type of PCR. This is used for amplification, not quantification, of starting material.
QPCR or quantitative PCR, on the other hand, uses fluorescent dyes to measure the amount of amplified gene product. Standards provide a baseline measure of how much genetic material you should expect to see over time, at each PCR cycle, for a given amount of measured fluorescence. Measuring fluorescence of your own sample over time, and comparing it against the standard, gives you an estimate of what you started with, initially.


Are there biological reasons why life expectancy is lower for men in most countries of the world?

There are both biological and  social factor for that:
Biological

Females have two X chromosomes. When mutations in genes of the X chromosome occur, females have a second X to compensate. Males, on the other hand gave just one chromosome X and all genes its genes express themselves, even those lethal or deleterious.
Females have better resistance to biological aging and hormones and the role of women in reproduction are known to be associated to greater longevity (e.g. estrogen offers some protection against heart disease because it facilitates elimination of bad cholesterol while testosterone has been linked to violence and risk taking).
The female body evolved to accommodate the needs of pregnancy and breast feeding hence deals better with making reservation. This ability has been linked to a female's better ability to cope with overeating and eliminating excess food

Social
This "advantage" women seem to have was once nullified by the status and life conditions they had back then, as the risks and the burden of pregnancy and the lack of attention to health and rights women had in a way more misogynist world.
Given the economic, social and political changes that the world experienced, a general progress in female life conditions took place and women have not only regained their biological advantage, but have gone beyond it, achieving higher life expectation. Social and comportamental factor are involved in this higher longevity:

Women tend to engage in fewer risky and bad for health behaviors than men do, e.g. men have more problems than women with alcoholism, smoking and road accidents.
The world is still very sexist and the gender roles to be played would expose men to higher risks. Regarding to work, for instance, although women nowadays participate in the work force, their professional activities remain different and are less prejudicial to their health (on average).
Also regarding to  very sexist gender roles, men are expected to be strong and manly and powerful and women are expected to be gracious young and beautiful. As a result of that, women are more attentive to their body and health, engage themselves in more healthy activities and benefit more from medicine and science. Men on the other hand submit their bodies to challenges from early ages and tend to neglect their bodies needs.

You can have access to detailed statistics (male/female, country by country, life expectancy and other health data) here:
http://www.who.int/gho/publications/world_health_statistics/2016/Annex_B/en/
And also, read more about the issue here:
https://www.scientificamerican.com/article/why-is-life-expectancy-lo/
http://www.who.int/mediacentre/news/releases/2016/health-inequalities-persist/en/
https://en.wikipedia.org/wiki/List_of_countries_by_life_expectancy#cite_note-10


Is there a reliable estimate of the number of cells on Earth?

Okay so I looked around a bit, and there are surprisingly few papers related to this question.

This paper is the best I cold find, but it's almost 20 years old. There's also this one, which slightly updates the other one, but they both focus on bacteria. For those the total number is estimated to be somewhere in the range of $10^{30}$.
For humans the latest published number is $3.72 \times 10^{13}$, so even with a few billion in total ($10^9 \times 10^{13} = 10^{22}$) we probably don't even matter for the total cell count. Since smaller more abundant animals have a much lower number of cells, they probably don't matter either.

Now to the only thing I'm not sure about: plants

The number of plants on earth is really elusive, only more elusive is the number of cells per plant. This study claims around 3 trillion ($10^{12}$) tree's on earth. Since tree's are bound to have (many) more cells than humans, we're probably getting closer to the number of prokaryotic cells by now (I guess the number of 'tree cells' will be somewhere around $10^{27}  - 10^{30})$.
So far I didn't find anything about grasses or other plants (neither numbers nor cell counts), so it's really hard to say whether these matter or not.
This study seems to give an average number of cells per growth ring in tree's, but I'm not sure how to get a number of cells / tree from that.

In total the estimated number of bacteria ($10^{30}$) is probably a good measure for the number of cells on earth. Even if plants manage to come to that level, the order of magnitude will probably not change (by much).


The macromolecule concentration within E Coli is estimated to be around 0.3-0.4 g/ml [1]

The concentrations of your substrate in respect to your enzyme are generally fairly analogous to in vitro studies compared to in vivo studies. However, this is heavily based on the assumption that the diffusion constants for both molecules stay consistent. In many cases that is true and errors can be corrected for using PEG to imitate the crowding effect. And yes, people have begun to look at the question [2]

However, for larger macromolecules like DNA and chromosomes that do see effects from subdiffusive transport, the molecules don't obey diffusive random-wal behavior [3]. The classic model system is the lac repressor which exhibits non-diffusive kinetics due to its interactions with DNA.

http://www.ncbi.nlm.nih.gov/pubmed/1748995
http://www.ncbi.nlm.nih.gov/pubmed/21237136
http://prl.aps.org/abstract/PRL/v104/i23/e238102
http://www.ncbi.nlm.nih.gov/pubmed/7317363


Hominidae is to hominid as Poaceae is to what?

Since Poaceae is the plural of Poacea in Latin - like aquae is the plural of aqua - I would say a Poacea, but I'm not a native English speaker so I don't know if this form would be acceptable in English. My guess is that you will have to use the long form a member of Poaceae. In languages like Italian and French it's easier because the Latin nomenclature and grammar are translated. So in Italian you will say una Liliacea for the singular and due Liliacee for the plural, while in French it would be une Liliacée and deux Liliacées respectively.


Do we know if dogs are asymptomatic transmiters of sars-cov-2?

It may be too early to tell.

Testing of dogs in Wuhan found no infected dogs
"487 dogs including 90 beagle dogs, 147 pet dogs and 250 street dogs during the outbreak of SARS‐CoV‐2 were also tested serological negative."
from https://onlinelibrary.wiley.com/doi/full/10.1111/tbed.13577

This article mentions deliberate infection of five dogs. on this very small sample they suggest that dogs are not likely to become carriers.

"Coronavirus can infect cats - dogs, not so much."
https://www.nature.com/articles/d41586-020-00984-8

found by searching "dog" on LitCovid at https://www.ncbi.nlm.nih.gov/research/coronavirus/


How does DNA resolve on size exclusion resin?

It works pretty well and can be used to desalt DNA. The DNA runs a bit different than proteins since it is more a long stretched molecule while a lot of proteins are globular. See this references (the first is about the behaviour of DNA on superose):

Size-exclusion chromatography of DNA restriction fragments. Fragment
length determinations and a comparison with the behaviour of proteins
in size-exclusion chromatography.
Size exclusion chromatography of DNA and viruses: properties of
spherical and asymmetric molecules in porous networks
Size exclusion chromatography of plasmid DNA isoforms


What is the name of this flowering plant?

It looks like a variety of canna lily. There are several flowers that have opened on the tip of your plant, as in the photo below.


How is the "fine mapping of pelvic regulatory region" done in this paper?

I'll try to help clarify the picture, but given that I have not read the paper, I am not too clear on the context.

A. IT compares the DNA of the stickleback (the SALR), medaka, and zebrafish. If there is a red peak, there is relatively high sequence identity (or similarity), indicating similarity (in evolutionary ancestry in this context?). Gray is repeating sequence, perhaps due to duplication or some kind of evolutionary history. For microsatellite markers, I believe that the paper is referring to the use of microsatellites (small tandem nucleotide repeats) as markers to compare the three.

B. Reporter genes are expressed and help the researcher identify something (by giving information, such as fluorescence etc.) (eGFP indicates green fluorescent protein e= enhanced)

C-H. These are just pictures of the fishes. Note the fluorescence (green). It indicates some expression (of the gene of interest). The absence or presence of the fluorescence indicates something, based on what the eGFP was attached to.

Hope this helped! But you need to do the analysis yourself, or at least I can't :P


Evolution- Variations, adaptations and selective advantages

I would define variation as something a little less specific. When talking about evolution I would consider it to mean any phenotypic variation that exists. I say phenotype because that is what selection "sees" but there can be genetic variation without phenotypic variation (see synonymous mutations). The trait could be physiological, morphological, behavioral or a life history trait (a trait which, all else remaining constant, affects fitness e.g. Lifespan or development time). This is also not necessarily just within species too, comparing homologous trait between two species could reveal between-species variation. For example, in one species every individual might day at exactly 100 days old, in another it may be 102 days, there is no variance within species but there is variance between. The phenotypic variation can be a result of genotype, environment, or a genotype-environment interaction.
If a trait positively affects fitness it is an adaptation, it is a trait that offers some kind of benefit over other current or previous incarnations of the trait. The variance for that trait can be zero - a highly adaptive trait is likely to spread rapidly and variation for that trait would zero if it was entirely genetically defined and fixed in the population but that trait would still be considered an adaptation. I would define fitness as the lifetime reproductive success of your evolutionary unit, commonly thought to be the gene. If a variant of a trait increases relative fitness it provides a selective advantage, and any genes (alleles) causing that trait should spread through the population at the expense of other alleles.
It is important to remember that not every biologist will define these in the same way, there is some debate about definitions in biology.


There are 5 species of Malaria the can infect humans, and Chimpanzees and gorillas have also been found with 5 species, including vivax and falciparum.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4089193/

The parasite can go dormant in the liver for days to years, causing no symptoms and remaining undetectable in blood tests. They form what are called hypnozoites (the name derives from "sleeping organisms"), a small form that nestles inside an individual liver cell. The hypnozoites allow the parasite to survive in more temperate zones, where mosquitoes bite only part of the year.

Cows are known to carry falciparum protozoa, which has at least four reservoir species. (cows, chimps, gorillas, humans) Human with sickle cells also act as a reservoir in a different way, perhaps more or less invisible or innocuous, i haven't studied recent research, and sickle cell may also have some effect in cows and chimps and gorillas.


Calories burn rate calculation — scientific studies

Disclaimer: Not my field but I'm doing my best.

We often measure the calories consumed indirectly by measuring the quantity of oxygen consumed. As we have a reserve of ATP(ATP is a molecule, a stock of ATP is some kind of battery of our body) in our body, at very short term the oxygen consumption is not necessarily perfectly correlated with energy use but at a longer term it works perfectly fine. Seek for further information on the Citric Acid Cycle to understand why the oxygen consumption is directly related to the energy created (which is itself at a long enough term directly related to energy use). If I am not mistaken a bunch of seconds should probably be a long enough term (time to consume all ATP at the start of an important effort) but I would appreciate if someone could give a reference for that.

For small animals we often put the animal in a chamber and calculate the energy consumption by measuring the volume of CO2 that they expire. For this purpose we have to measure the volume of CO2 at the entrance and at the exit (of the chamber) to measure the difference. For humans, we often put a mask on the face of the "cobaye". We allow him to breath normally without doing any effort for a while and then we ask him to run/bike/whatever on a home trainer.

I don't know much about such studies but it is important to 1) know the variance in energy consumption in the population for a typical exercice 2) understand that lab condition probably differ in various ways from person-to-person real life condition (no wind, no dust, stress of the experimentator, discomfort of the mask, ...).

As I have no idea concerning the variance in the population I cannot tell how representative are the summary values that we can find on many popular websites but I would tend to think that given the experimentation, these numbers has probably been fairly accurately measured.


Wikipedia has your answer:

  It seems paradoxical to treat an extreme diuresis with a diuretic, but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering GFR [glomerular filtration rate] and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.

The source for that is an editorial from 2004 that has some good other sources, including what appears to be the 1959 original paper finding this seemingly-paradoxical result.

  Thiazide diuretics inhibit the NaCl co-transporter (NCC/TSC) in the renal distal convoluted tubule (DCT). The DCT is water impermeable and considered to be part of the diluting segment. Therefore, the water-preserving effect of thiazides is unlikely related to a direct effect on the DCT. In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion. The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption. Hence, less water and solutes are delivered to the distal tubule and collecting duct and are lost as urine.


How deep does water have to be so a mosquito can lay viable eggs in it?

Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (reference). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (reference). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (reference).


In order to make your reasoning clearer, you should use more formal notations and explain your thinking step by step. Here's a proposition.

Let's use the following notations :

$C$: the total number of couples (mixed and not mixed)
$r$: the reproductive success
$F1_h$: the number of hybrids in the F1 generation
$F1_{nh}$: the number of non hybrids in the F1 generation

You are looking for the percentage of hydrids in the F1 generation, which is:
$x = \frac{F1_h}{F1_h + F1_{nh}}$

You know that $10~\%$ of the couples are mixed couples and that their reproductive success is reduced by $50~\%$. This can be written:
$\begin{cases} 0.9\cdot C \cdot r = F1_{nh} \\ 0.1\cdot C\cdot \frac{r}{2} = F1_h \end{cases}$

Thus: $\displaystyle x = \frac{F1_h}{F1_h + F1_{nh}} = \frac{0.05\cdot C\cdot r}{C\cdot r\cdot 0.95} = \frac{0.05}{0.95}$

This is indeed the result you suggested. So the correction you were given might not be correct. Or maybe there was some more information in your homework that you ignored...


Do all polygenic traits involve epistasis?

A polygenic trait is a phenotypic trait for which the variance in the population is explained by two or more loci. Epistasis is a case there is a statistical interaction between several loci on the value of a phenotypic trait.

The several loci underlying a polygenic trait might be purely additive (no interaction) and therefore a polygenic trait does not necessarily involve epistasis.


Is there any relation between weight class and extreme lifting performance in O-lifting?

I suspect that such might partially result from both an inherent advantage and a coincidental advantage of lower height.  The former would be an effect of strength being roughly proportional to the cross-sectional area of muscle (square of a linear measure) and mass being proportional to the body volume (cube of linear measure).  This would make a 182cm person 10% stronger by body weight than a 200cm person of the same build (when one might initially think that having the same build would imply the same strength per unit weight).

The second advantage might be from taller individuals tending to have a more slender frame.  A more slender frame might be associated with lower muscle bulk (cross-sectional area) even with intensive training (more "ectomorphic"?).  Since there is a limit to thickness, to increase mass height must be increased, and if taller individuals tend to be more slender in build then as mass increases the build would tend to become more slender reducing muscle cross-sectional area (strength) in proportion to mass.


Is there a metric for “evolutionary agility”?

Yes, there is a measurement laid out by Haldane (1949) called 'Darwins'. One Darwin is given an $e$ fold change in a trait over the period of 1 million years.
As to your second point, yes there are different variables which control the rate of adaptation within a population. The classic factor is genetic variation, as given by Fisher's (1958) fundamental theorem of natural selection, which states:

The rate of increase in fitness of any organism at any time is equal
to its genetic variance in fitness at that time

So broadly speaking, individuals with more additive genetic variation will adapt more rapidly.
Of course, there are many other factors such as generation time, effective population size and mutation rate will influence the response to selection. However, such as in the case of generation time, the relationship is not necessarily a simple one (Gandon and Mikalakis, 2002).
EDIT
After re-reading your question, I think I perhaps misunderstood it.
I suppose the term you are looking for is 'evolutionary potential', which is defined by Steeves et al (2017) as:

The capacity of a population to evolve in response to environmental
change.

There is a nice chapter in this book which gives a good overview of the topic. The chapter may perhaps be available for free on certain websites.
References

Haldane, John Burdon Sanderson. "Suggestions as to quantitative measurement of rates of evolution." Evolution (1949): 51-56.
Fisher, Ronald Aylmer. The genetical theory of natural selection. Рипол Классик, 1958.
Gandon, Sylvain, and Y. Michalakis. "Local adaptation, evolutionary potential and host–parasite coevolution: interactions between migration, mutation, population size and generation time." Journal of Evolutionary Biology 15.3 (2002): 451-462.
Steeves, Tammy E., Jeff A. Johnson, and Marie L. Hale. "Maximising evolutionary potential in functional proxies for extinct species: a conservation genetic perspective on de‐extinction." Functional Ecology 31.5 (2017): 1032-1040.


Resting and action membrane potential..?

Answering the question: "Why is a negative membrane potential important?"

I don't think cells have strong feelings about being slightly negative inside its membrane. I'm guessing these are the driving factors:

the cell membrane is nonpolar, so charged particles can only pass via transport proteins. This makes ion gradients an easy way to maintain a source of (literally, in the physics sense) potential energy.
the cell needs to control its environment and send signals to other cells. The particle gradient (sodium, for example), allows it to accomplish these tasks: bring in glucose by co-transporting with sodium, send an action potential by triggering voltage-gated ion channels.
Therefore, the Na/K pump is a way to "charge" the ability of the cell to perform various types of work in the future.

To risk an analogy, a cell having a membrane potential is like you charging your cell in the morning. You aren't quite sure what exactly you'll be doing with your phone all day, but it will be many different tasks and all will be doable because you've got a controlled energy source.


How do animals/plants change for each season?

There are various parameters that describe change of seasons such as day length, temperature, humidity. But it can be assumed that most of these parameters ultimately depend on one parameter- day length.

The response of plants towards the length of day/night cycle is called photoperiodism (which dictates spring flowering).

This article explains the effect of a gene called CONSTANS(CO) on spring flowering. CO is post transcriptionally regulated by cryptochromes and phyochromes.

  The circadian rhythm in CO mRNA abundance was proposed to represent a photoperiod response rhythm, in which exposure to light coincides with CO expression only under LDs (Long Day) and thereby triggers flowering.

  ......

  We propose that early in the day phyB promotes the degradation of CO whereas in the evening cryptochromes and phyA antagonize this degradation and stabilize CO protein,

However, my knowledge of plant molecular biology is not that great and I would advise that you refer the mentioned article and the cross references cited in that.


Is there logic in this sentence? "Authors discovered a gene as one of the genes evolved through natural selection"

Yes, the statement in the news article is not correct; however, it (probably accidentally) isn't quite as nonsensical as it sounds.

The actual paper that the news article is trying to describe is unsurprisingly more accurate.

  Here, we found a gene, SLC18A1 (VMAT1: Vesicular monoamine transporter 1), as a positively selected gene in the human lineage. This gene has a human‐unique variant (Thr136Ile; different from other mammals (136Asn)) whose association with several psychotic symptoms has been repeatedly indicated. Moreover, our analysis showed that this variant has been maintained in non‐African populations by balancing selection and had originated around 100,000 years ago, typically regarded as the timing of Out‐of‐Africa migration.

--Positive and balancing selection on SLC18A1 gene associated with psychiatric disorders and human‐unique personality traits

Here instead of talking about "natural selection", the authors refer to "positive selection" and "balancing selection", two sub-categories of natural selection. Since much of the genome is under negative selection, it's worth noting alleles that are not.

  Didn't all genes evolve through natural selection?

The reason the news article is not nonsensical is that natural selection is not the only force that acts on genomes.  We've known for 50 years that drift is an important factor that influences genetic evolution (wikipedia: Neutral theory of molecular evolution, Nearly neutral theory of molecular evolution).  However, it's pretty clear from the article that the author is unaware of these concepts and probably doesn't understand the significance of the paper.


Is the common house gecko poisonous to touch?

They are completely harmless. There are no poisonous lizards in India, and only one species of poisonous lizard in the world (Heloderma suspectum, from Mexico and SW U.S.). A gecko's skin is not toxic. They don't inflict a painful bite. The best way to hold a lizard without harming it is by the base of a hind leg.


What did Darwin mean by "degraded flowers"?

Perfect flowers have both male and female parts.
"Degraded" isn't used anymore - just "imperfect".

"A bisexual (or “perfect”) flower has both stamens and carpels, and a unisexual (or “imperfect”) flower either lacks stamens (and is called carpellate) or lacks carpels (and is called staminate). Species with both staminate flowers and carpellate flowers on the same plant (e.g., corn) are monoecious..."

ref https://www.britannica.com/science/perfect-flower

Found by searching for "perfect flower"


Difference between vacuolar and symplast pathway

The vacuolar pathway involves the movement of water between vacuoles of neighbouring plant cells. The symplast pathway, on the other hand, involves the movement of water from the cytoplasm of one cell to the cytoplasm of a neighbouring plant cell without it entering a vacuole inbetween, so the symplast pathway has no vacuole to vacuole movement.


How strong of an electric field is dangerous to adult humans?

Research published by WSU Professor Emeritus of Biochemistry and Basic Medical Sciences, Dr. Martin Pall, bears directly on your question about potassium channels.

https://www.researchgate.net/project/microwave-frequency-radiation-acts-via-voltage-gated-calcium-channel-activation

He has concluded that weak EMFs cause cascading health impacts that derive from false electrical signaling of voltage-gated ion channels, and that these impacts include heart disease and the dreaded social bugbear elctrosensitivity (microwave disease).


Is Pars intermedia functional in humans?

Both- the textbook and your teacher are right.

The most obvious function of the pars intermedia in lower vertebrates is the secretion of melanocyte-stimulating hormone (MSH) for the purpose of pigmentary control.
In human fetal life as well, this area produces MSH which causes the release of melanin pigment in skin melanocytes.
In adults,

The human pituitary has no distinct pars intermedia (PI). Instead, the proopiomelanocortin (POMC) producing, adrenocorticotropin (ACTH)- and β-endorphin-immunoreactive PI cells are incorporated within the pars anterior, thereby participating in the formation of the pars distalis.

Edit:

POMC is cut (cleaved) to give rise to multiple peptide hormones. Each of these peptides is packaged in large dense-core vesicles that are released from the cells by exocytosis in response to appropriate stimulation:
α-MSH produced by neurons in the ventromedial nucleus has important roles in the regulation of appetite (POMC neuron stimulation results in satiety) and sexual behavior, while α-MSH secreted from the intermediate lobe of the pituitary regulates the movement of melanin produced from melanocytes in skin.

Sources:

https://link.springer.com/article/10.1007/BF02738816
https://pubmed.ncbi.nlm.nih.gov/6912095/#:~:text=Abstract,the%20purpose%20of%20pigmentary%20control.
https://en.wikipedia.org/wiki/Pars_intermedia


I would suggest putting them in the ground and watering them (Factors affecting acorn production and germination and early growth of seedlings and seedling sprouts).


What is the biochemical reason for mental fatigue?

This is not the biochemistry, but the brain regions involved are described in this article about an fMRI study: http://www.sciencedaily.com/releases/2012/12/121210101630.htm

EDIT:

From what I can tell, mental fatigue is attributed to low oxygenation levels.  Here's a study that examines the effect of creatine in preventing mental fatigue: http://jtoomim.org/brain-training/watanabe2001-creatine-reduces-mentalfatigue.pdf


Are our ears more sensitive to low or high pitched sounds?

Short answer
Our ears are most sensitive to the mid-frequencies.

Background
There are different ways of assessing sound level. The physical one simply determines the physical sound pressure level (SPL) in which all the frequencies weigh equally. This is referred to as C-weighting and is expressed in dB SPL.

Our ears, however, are most sensitive to intermediate frequencies, peaking at around 4 kHz (Fig. 1). The frequency weighting that takes this into account is dBA weighting.

The reason why we are most sensitive to mid-frequencies can be sought in the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.

Normal equal–loudness-level contours for pure tones. source: Duncan (1996)

Reference
- Duncan, High Performance Audio Power Amplifiers
For Music Performance and Reproduction (1996): 1-18


What are some examples of interbreeding between species that are separated by 5 million years or more?

I depends a little bit about what you mean by interbreeding. In any case, my answer won't be fully satisfactory.

Horizontal gene transfer

If you are referring to any exchange of genetic materials than, you can have a look at Salzberg et al. (2001) who report 40 genes that were horizontally transferred from bacteria.

Elysia chlorotica is sea slug which is able of photosynthesis thanks to a horizontal gene transfer (Schwartz et al., 2014)

Typical interbreeding

If you are thinking about some kind of more common type of inbreeding, then you might want to consider

mule who is the hybrid between a male donkey and a female horse. Donkey and horse share a common ancestor that is about 4.5 millions years old (according to Live Science). Mules are often sterile but some of them have been fertile (Rong et al. 1988; see also this article from the Denver post; thanks @iayork)

Platanus × acerifolia is a hybrid between Platanus orientalis and Platanus occidentalis. Platanus are a rather old genera with fossils of 115 millions years old found (from wiki). However, I don't know how old is the common ancestor between P. orientalis and P. occidentalis

There are plenty of other examples in wikipedia > hybrid but I failed to find good estimate of common ancestry for those who may have had a common ancestor older than 5 millions years but it probably exist given that the mule example is already 4.5 millions years old.


I’m not sure that this is on topic, as you really could have found this information yourself.

You don’t quote a source for your info about this, which doesn’t help you or anyone interested in this topic. Here is a Nature News article.
If you click on the link in that article you get to the Cello site. You need to choose a name and password to gain entrance, but are not asked for any personal information. All they will have is the IP number of your computer.

The info on this site will not mean much to anyone not involved in synthetic biology.


What factors affect the likelihood of auditory stimuli causing arousal during sleep?

The other day I was reading "Sleep soundly every night,feeling fantastic everyday" by Robert S. Rosenberg.
Somewhere in the books it was written as:
"Sound: You need your bedroom to not only be cool and dark, but also quiet. If a dripping faucet or the barking of a neighbor’s dog is interfering with your sleep, try earplugs, earphones, or generating white or pink noise to even the sound field so your ears won’t focus on the background contrast of environmental sounds. There are machines available to do so, but for some the sound of a fan will do the trick. If your partner’s snoring is keeping you awake, you should encourage him or her to be checked by a doctor for sleep apnea. Treatment can improve your sleep and also might save his or her life."

by searching more I found out that the difference between the range of frequencies from moment to moment is a more important factor than a sudden loud noise.

The idea behind white or pink noise or the natural ones like the sound of fan is that they produce a broad range of frequencies at the same level.And by doing so they can reduce or at least mask the disruption.


Unlikely that you have a mercury problem. I have had about 6 mercury thermometers broken in my house over a few years ( the places I kept them were not safe from a housekeeper).I don't know if she did anything to clean up; I except only sweep up broken glass. These were laboratory thermometers ,so typically over 12 in. long. No cats but dogs, no symptoms yet.


What does it mean for a distribution to be "consistent with a two rate-limiting stochastic steps"?

The rate limiting step of a reaction is the slowest component of the reaction. So if there are two steps in a reaction, each of these steps will have a rate, and the slowest of those two rates will determine the overall rate of the whole reaction.

As a simple example, consider the equation

$A + B + C\rightarrow AB+C\rightarrow ABC$

If the rate of $A+B \rightarrow AB$ is fast, but the rate of $AB+C \rightarrow ABC$ is slow, then the overall reaction will still be slow.

The figure in your question is showing the distribution of the burst durations, and highlighting the fact that the calcium level has no effect on the burst duration. The second quote is a bit confusing, this is my interpretation:

The functional form which they fitted to the distribution indicates that the expected burst duration is about 70 seconds. I'm not completely sure which stochastic steps they are referring to, maybe translation and subsequent localisation (I think transcription would happen on a different timescale and so could be ignored in this case).

By the way, this paper is a really excellent example of an organism harnessing stochasticity to its advantage in order to synchronise its response to a stimulus (calcium in this case). I just think that it is so cool that the mean response to the signal level can be different to the response to the mean signal level - so counter-intuitive to me. And so much fun!!


Contrary to oceans, deep lakes are always isolated from other deep lakes by land. Therefore, one might expect different fauna in every lake, with possibly a lot of endemic species. So it may be hard to study deep lakes in general.

The ancient and deep lake Ohrid, in the former yugoslav republic of Macedonia, has been researched relatively well. Here's a reference which will get you started. Or search "lake ohrid fauna".


Imagine a covalently closed circular double-stranded DNA plasmid. In its "natural", or "relaxed" state you could spread it out, flat, on a suitable surface.

Now imagine cutting one of the strands of the DNA (i.e., cutting the sugar-phosphate backbone, the way that an endonuclease would, leaving a nick, the 5'-end of the nick has the phosphate, and the 3'-end of the nick has an -OH group), and rotating that nicked strand in a clockwise direction, several times, around the other, intact, DNA strand.  This does not involve breaking any of the basepairs, or unravelling the strands, you are just twisting it around.

Now imagine sealing that nick, by ligating the 5' phosphate to the 3' OH.  At this point the dsDNA helix is slightly "overwound", and will no long lie completely flat. It has begun to be supercoiled; these are positive supercoils.

If, alternatively, you had rotated the nicked DNA strand several turns in the counter-clockwise direction before re-sealing it then that molecule would also start to be supercoiled, but it would be "underwound" with negative supercoils (and it would also no longer lie flat on the surface).

There is an enzyme called DNA topoisomerase I that cuts, and re-seals, one of the two strands like this.  Another enzyme called DNA topoisomerase II cuts both strands before introducing supercoils.


Fold coverage is often derived with respect to a genomic locus, not a read. In sequencing experiments, fold coverage of a genomic loci (coordinate along a reference assembly) will be the number of aligned reads that overlap the position.


Your updated question, as I said in a comment is much more precise but also describes a biologically and thermodynamically absurd scenario that betrays deep misconceptions about how cells work and what they need to work. Having said that I've realized it has an answer, so I'll give it:

  Would we then consider such a thing a genuine living organism and if so why?

As in every case in science where previously-sharp categories become fuzzier through the discovery or creation of entities that fall in previously-empty intermediate zones, "we" would debate ardently about whether those things should be considered "genuine living organisms" or not. There would be several possible outcomes to these debates:

1) All of the new intermediate entities demonstrate that in the space of characteristics things can have, the old category as previously defined no longer forms a sharp cluster, but a sharp cluster still does exist that is pretty close to that old category; in that case the old category gets a new definition, and as a result some entities might change their classifications, or not. Real-world example of this kind of definition change (though not necessarily caused by the appearance of intermediate steps): how stars and planets went from their antique definitions of "stays put in the sky vs moves around" to their current very-different definitions.

2) The new entities demonstrate that what was thought to be a sharp cluster in the space of characteristics is just... not. A clear, universal, unambiguous definition is thus impossible. One possibility is that the cluster dissolves entirely; the category as a whole is thus abandoned (many abandoned taxonomic terms can be seen as examples of this).

3) The old sharp boundaries no longer exist, but there is still a definite cluster in the space of characteristics that can be pointed to, it just has fuzzy borders. Like colors, which blend into each other but we still know there is "red" and "blue" and they're not the same. In that case, like with colors we might abandon the edge and focus instead on doing like we do with colors; defining the entity by looking at what "a good representative of this category is" and "what an ambiguous representative of this category is", thus giving a reliable idea of where the cluster is, where it isn't, and where the boundary is, even if it's fuzzy.

4) Sometimes you do need sharp definitions though, especially in science. In that case there are two possibilities:

4a) Use different definitions in different contexts, depending on which characteristics of the cluster interest us at any given point. "Species" is an excellent example of this; a paleontologist, a vertebrate biologist, a plant biologist, and a bacteriologist will use the same word to talk about similar concepts (a grouping of organisms with specific ecological and evolutionary significance), and they will use different criteria to determine what a species is in each case, meaning they have different definitions.

4b) Settle on an arbitrary boundary based on certain criteria that cuts through the fuzziness, with the understanding that it is arbitrary, other criteria would have yielded a slightly different boundary and different classifications for given entities that exist in the fuzzy zone, but it is useful for whatever purpose to have that boundary and thus a boundary will be chosen. Debate might continue a long time over where the boundary is, and potentially involve different people using different boundaries as in 4a, or not. Classic recent example is the definition of planet, and the process that led Pluto to no longer be considered one. This can also involve the creation of new categories, like "dwarf planet" in the case of the redefinition of "planet".

So to answer your question "would this be considered genuine life?", the answer will be "yes", "no", "it depends" or "neither" depending on which of those outcomes the debate ends up settling on. And we cannot know which outcome it will be, because the choice that will be made will entirely depend on what the space of characteristics will be like that makes a currently-sharp boundary fuzzy... And obviously we do not already know what the space of characteristics is like because those discoveries or inventions that will prompt us to revisit what we think of as "life" hasn't happened yet ! (well, not the ones you posit. Obviously the definition of "life" itself has already undergone the processes I describe many many times as it got better understood !).

(note I'm not even getting into the vernacular, and whether it will follow scientific usage or not and at what rate if so. It's interesting to note it still in many ways hasn't caught up with (or is just unrelated to) today's biological definition of "life" !)

(I will also add that I cannot posit an outcome even based on the specific scenario you describe, for two reasons: first, the decision would be a communal one made by professionals in the field, and I am a single person and not a professional biologist. Second, the specific scenario you describe already goes against everything we currently know about life, so, yeah.)


Are there evolutionary advantages for the bee sting to kill the bee?

Fitness of the colony vs fitness of a single worker

Bees have a division of reproductive labour (they are eusocial). Only a queen reproduce (and the males called drones) while the workers dedicate their existence to ensure the survival of the colony. If committing suicide will be of any help to the colony then one would expect a bee to do so. What I just said is an oversimplification of the structure and mating systems of bee colonies.

You should have a look at the field of social evolution to have a better understanding of what's going on with bees!

What is the cost?

Above I argued why nobody really cares much if a single worker dies. This being said, if the bee survived to stinging, then it could eventually keep protecting the colony as it was doing before stinging. So why does it has to die? Clearly, there must have a cost to not die. It seems very plausible to me (but cannot offer an evidence for it) that there would be a strong physiological cost to create a stung that that would not kill its carrier. Such physiological cost (even if mild) can by large outweigh the cost of losing a single worker for the colony.


Asides from just eyeballing the change in color/consistency, Wikipedia suggests using iodine for a qualitative measurement (though without reference):

  Iodine (I) can be used to determine whether fruit is ripening or rotting by showing whether the starch in the fruit has turned into sugar. For example, a drop of iodine on a slightly rotten part (not the skin) of an apple will stay yellow or orange, since starch is no longer present. If the iodine is applied and takes 2–3 seconds to turn dark blue or black, then the process of ripening has begun but is not yet complete. If the iodine becomes black immediately, then most of the starch is still present at high concentrations in the sample, and hence the fruit hasn't fully started to ripen.

A quantitative method applicable to many kinds of fruit is going to be tricky. If you have a spectrophotometer you could measure the changes in light absorption as the fruit ages. You will probably want to measure the absorptions of control fruits as they age and then compare them to fruits from whatever experiment you perform.

Another possibility is measuring ethylene and/or carbon dioxide production. As fruits ripen they produce more of both these gasses, but this increase does not follow a neat linear correlation with time to put it lightly. Non-climacteric fruits, if you use them, may also be problematic here as they do not show such increase in gas production.

Merzlyak, M. N., Gitelson, A. A., Chivkunova, O. B., & Rakitin, V.
Y.    (1999). Non‐destructive optical detection of pigment changes
during    leaf senescence and fruit ripening. Physiologia plantarum,
106(1),    135-141.
Burg, S. P., & Burg, E. A. (1962). Role of ethylene in fruit
ripening. Plant Physiology, 37(2), 179.


Is it the sphincter that flexes when a human pushes a bowel movement?

The pressure that you apply when you push during a bowel movement derives from an increase in the pressure of the abdomino-pelvic cavity.  You generate this pressure by closing the glottis (the opening to the lungs) and contracting the anteriolateral abdominal muscles (i.e., the external oblique, internal oblique, and transversus abdominus).  This reduces the volume of the (now sealed) abdominopelvic cavity and increases pressure helping to drive feces from the rectum.  This is mechanism is also used to expel urine and during childbirth.

If you do this with the glottis open, then you forcibly exhale because the increased pressure of the abdominopelvic cavity is transferred across the diaphragm and into the thoracic cavity compressing the lungs.


Why are some menstrual cycles irregular?

There's two phases of a menstrual cycle, before ovulation known as the follicular phase and after ovulation known as the luteal phase. The second phase is not very variable, it's the same length almost always as it is governed by how long the corpus luteum (remnants of the follicles after the ovum bursts out) survives. The first part is variable and is what causes periods to be irregular. In this phase the eggs mature. The body picks several eggs to mature but only one will "win". However, how fast it wins changes. It all depends on how fast it grows and much it manages to suppress growth of the other eggs and that in turn depends on the quality of the egg. But then this also branches out, as it is controlled by levels of hormones this is heavily affected by stress and diet among other things.

It's unfortunate that the first phase is variable otherwise knowing which day you were going to ovulate would be easy.


Do beneficial viruses exist? If so, what examples are there?

Do they exist? Yes

What are they called? Marilyn Roossinck calls them viral mutualistic symbiotes. She has an excellent review here.

What are some examples?

My personal favorite is GB-Virus C, or Hepatitis G, which appears to slow the progression of HIV using a number of different mechanisms:

  Box 1. Summary of the effects of GBV-C infection in HIV-positive individuals

  GBV-C infection downregulates HIV entry co-receptors CCR5 and CXCR4, and increases secretion of their ligands RANTES, MIP-1α, MIP-1β and SDF-1.
  In vitro GBV-C NS5A and E2 proteins inhibit X4- and R5-tropic HIV replication, and NS5A protein downregulates CD4 and CXCR4 gene expression.
  HIV-infected individuals positive for GBV-C E2 antibodies have survival benefit over HIV-infected individuals with neither GBV-C viremia nor E2 antibodies; in vitro GBV-C E2 antibodies immunoprecipitate HIV particles and inhibit X4- and R5-tropic HIV replication.
  GBV-C induces activation of interferon-related genes and pDCs.
  GBV-C promotes Th1 polarization and the NS5A protein contributes to this effect.
  GBV-C infection reduces surface expression of activation markers on T lymphocytes, suggesting its role in T cell activation signaling pathways.
  GBV-C protects the T cell from Fas-mediated apoptosis and as a result of its effect on immune activation may also play a role in protecting lymphocytes from activation-induced cell death.
  GBV-C viremia reduces IL-2-mediated T cell proliferation suggesting a significant interaction between GBV-C, IL-2 and IL-2 signaling pathways.

Endogenous retroviruses

As @mbrig recalls in the comments, there are a number of retroviruses that have inserted themselves into the germ line. Those are called endogenous retroviruses, and they interact with the host genome in a number of ways. Some are even translated:

  Proteins produced from ERV env genes have also been demonstrated to function as restriction factors against exogenous retroviral infection