What in soy are people allergic to and will these allergens be passed along if an animal that has eaten soy is consumed?

There are multiple soy protein allergens.  This has a pretty good review in the introduction.  Here is a list of some of the allergens (same paper).

Chickens on soy diets do lay eggs with higher concentrations of soy isoflavones than chicken on non-soy diets. (Edit: higher concentrations of soy isoflavones are also found in chicken tissues -- see ref 4 below.) References (originally found here) are:

Saitoh, S.; Sato, T.; Harada, H.; Takita, T. Transfer of soy isoflavone into the egg yolk of chickens. Biosci. Biotechnol. , Biochem. 2001, 65, 2220-2225.
Saitoh, S.; Sato, T.; Harada, H.; Matsuda, T. Biotransformation of soy isoflavone-glycosides in laying hens: intestinal absorption and preferential accumulation into egg yolk of equol, a more estrogenic metabolite of daidzein. Biochim. Biophys. Acta 2004, 1674 (2) 122-130.
Lin, F.; Wu, J.; Abdelnabi, M.; Ottinger, M.; Giusti M.M. Effects of dose and glycosylation on the transfer of genistein into the eggs of the japanese quail (Coturnix japonica). J. Agric. Food Chem. 2004, 52, 2397-2403.
Vargas Galdos, Dante Miguel Marcial. Quantification of Soy Isoflavones in commercial eggs and their transfer from poultry feed into eggs and tissues. Thesis. Ohio State University, Food Science and Technology Graduate Program, 2009; http://etd.ohiolink.edu/send-pdf.cgi/Vargas%20Galdos%20Dante%20Miguel%20Marcial.pdf?osu1236706764.

However, I do not know whether this is enough to cause an allergic reaction if consumed. (There's plenty of anecdotal evidence, but no clinical studies that I know of.)


What is the function of multiple nuclei in syncytial cells?

A mononucleate's size is limited by its nucleocytoplasmic ratio, and protozoa like being big.

The solution? Multiple copies of the same genes in huge nuclei, or multiple individual nuclei.

Multiple nuclei are common in any large, complex cell. There is nothing specific to the presence of cilia that require multiple nuclei, and ciliates are not the only multinucleate protozoa (the amoeboid Chaos genus can contain up to a thousand). The reason large, complex cells require this is simply because they are so big. Such a huge size requires, in addition to more complex nuclear regulation, a high total protein turnover, which in turn requires a high transcription rate. Even with mRNA being translated by numerous ribosomes, the amplification factor is still limited. Having multiple nuclei increases the rate of mRNA production, which increases the total synthetic capacity of the organism. When only a specific gene is required to be transcribed at a high rate, that individual gene may be duplicated many times. This is often seen in the nucleolus, which contains many copies of the same genetic material required to create the huge amount rRNA needed for ribosome biosynthesis:

Many protozoa are large because they are packing as much complexity into a single cell as they can, even to the point of having a backbone-like structure or simple photosensitive "eyes" (though not all protozoa are large). Many adaptions are required to allow single-celled organisms to grow to this size, such as a more complex cytoskeleton, a dedicated feeding apparatus, a contractile vacuole, etc. Multiple copies of genetic material is just another required adaptation. This adaption can manifest itself in various ways. Some organisms have multiple copies of the same nucleus. Others fuse these nuclei into a single, large nucleus (a macronucleus), keeping a limited number of micronuclei around for sexual reproduction:

Multicellular organisms tend to have multiple nuclei in specific cells for the same reason. Many types of cells, for example, require an extremely high rate of protein turnover and are very large (such as skeletal muscles), so they have multiple nuclei. This occurs when a single nucleus is no longer sufficient, even at peak capacity.

I would like to point out that what you are describing is a coenocyte. A syncytium is a multinucleated cell which has arisen from the fusion of multiple cells and their constituent nuclei (karyogamy), whereas a coenocyte is a cell which had undergone multiple rounds of nuclear division, without accompanying cytokinesis.


Methanol is rapidly absorbed not only after oral ingestion but by inhalation or after cutaneous exposure and becomes oxidised in the liver to formaldehyde and to formic acid, metabolites which are more toxic than methanol itself and which inhibit mitochondrial ATP production.

  Histopathologically, circumscribed myelin damage behind the lamina cribrosa of the optic nerve has been reported. The electrophysiological changes following acute methanol ingestion suggest that methanol affects photoreceptors, Muller cells, and the retrolaminar portion of the optic nerve.

Source : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771266/

Several years ago there were numerous cases of blindness and death due to Methanol in Estonia.

If you ask : What exactly happened?

Waste from wood (sawdust, shavings), and other cellulose-containing materials (paper, rags, etc.) can be processed by applying excessive heat and acids, resulting in degraded cellulose into sugar (glucose). Sugar obtained is fermented to get ethanol. However as a side-effect, some methanol is produced as well. This compound is not safe to drink. Basically, someone sold it (illegally) as an ethanol drink (I am not sure if they stole it and tried to monetize it this way.).

There was a (stupid) joke that somewhat popularized knowing about this problem:

  (roughly translates to) "Guys, let's drink faster, it is getting dark."

Other impurities in the alcohol could have similar effect, but I can confirm at least the methanol part.


This is the Japanese cinnamon, Cinnamomum tenuifolium, or "Yabu Nikkei" in Japanese. It smells like cinnamon and is found from the middle of Honshu (Fukushima prefecture and southward) throughout Shikoku, Kyushu, Okinawa, and into China. It is the native and more commonly found cinnamon species in Japan that grows wild in forests. The other species is Cinnamomum sieboldi, which was introduced to Japan in the early 18th century from its native Indochina via China. C. tenuifolium is distinguishable from C. sieboldi by its much more symmetrical arrangement of leaves, as depicted in your photograph.

This page also details the differences and similarities to other related species in Japan, however it is only in Japanese:

Camphor/Cinnamon species in Japan.


How it is determined that a particular gene or set of genes is responsible for a trait?

In the below list of technics, I am assuming we are talking about haploid individuals (to avoid discussion about dominance relationship) and assuming no epistasis but the technics can 'easily' be extended to include these cases. I also assume we are talking about coding regions.

Note that I am more of a biostatistician / population geneticist than a molecular geneticist, so I am pretty sure I will unwillingly bias my list toward what I know most. There is a lot to say about every single technic but of course, this cannot be covered in a single StackExchange post.

Technics

Statistical association (observational study) with existing variance in natural population. Do carrier of a given allele have another trait value than the carrier of the other allele. Possible confounding variables include population structure and linkage disequilibrium.

Population structure: To deal with this confounding variable, we can make a genetic PCA and include the first two axes as covariate in a type I sum of squares regression. We can also use tools such as STRUCTURE to infer the population structure and then use the inferred groups as a nominal covariate.
Linkage disequilibrium: We typically consider a number of marker that we try to associate to a specific phenotypic trait. It is impossible to tell whether the observed association is directly caused by the marker we observe or by a tightly linked marker. For further investigations below technics must be considered.

Statistical association (experimental study). It is possible to create the treatment groups by knocking out (or other technics such as the now popular CRISPR technic) specific gene in out in some individuals and look for a statistical association. The advantage of such manipulation is that we can create the optimal level of genetic variance we need to increase our statistical power.
Transcriptome analysis. Making sure the coding region is being expressed in the tissue of interest. E.g. if you expect a given gene to affect myosin tertiary structure, you might want to make sure the coding region is indeed expressed in the muscles and not only in the brain!
Protein action. It is also possible to study the specific action of the protein coded by the coding region of interest. Such studies typically require the study of an entire biological pathway and is often demanding and quite expensive. Here the methodology are diverse but they're discussion is both outside the scope of the question and outside the scope of my knowledge.

Example - Genetic Basis of Color Adaptation in mice

In a comment, you asked

  Is there any research paper, review paper or blog which covers entire details how the association and mechanism was established for any of those discoveries?

In most study cases, not all of the above steps are being considered. Also, even if it is the case, such study will be covered by several peer-reviewed papers and not a single one. I don't know of any peer-review paper that explains the whole process for a particular case but those probably exist.

There are documents that explain such process for layman. For example From Darwin to DNA: The Genetic Basis of Color Adaptations by Hoekstra is a standard reading for undergraduate that will interest you. It is easy and pleasant to read. Quoting from this article

  In this essay, we will take a journey — into the laboratory and the field — to understand the genetic basis of adaptation in natural populations of mice, and the phenotype we will focus on is the color of their fur.

The gene of interest in this paper is melanocortin-1 receptor (Mc1r). Depending on what level of understanding you want to reach, the article might be a bit too introductory but it refers to some good peer review papers that will allow you to further your knowledge.


Are there any papers arguing against vaccination in French?

I wish you good luck, as 99.99% of the anecdotal claims out there that conclude vaccination is bad are based on unfounded rumors.

Note that much of the negative public opinion is based on a fraudulent (and retracted) paper by Wakefield in The Lancet (1998). Unfortunately for you, however, it is in English.

My French is a bit rusty, but if you go to Google Scholar and type in a search term like vaccination results in autism (les résultats de la vaccination dans l'autisme) or Wakefield vaccination autisme something might pop up in French that advocates against vaccination.


What would happen if we had a device that produced oxygen inside of our lungs?

You might need to narrow your parameters a bit.

Just things to consider:

Our lungs are not hollow organs that can accommodate an oxygen producing machine. They are basically narrow tubes that get smaller and smaller until they end in a tiny balloon-like structure - about 700 million of them. Where would the machine go?
100% oxygen is toxic to the lungs, as it is to many other things as well.
How would the oxygen diffuse to all the other areas of the lung that need oxygen? Diffusion is a complicated process in a structure like the lungs.
from what would it produce oxygen? For example, would it extract it from water? How would the body deal with the loss of moisture from the air in out lungs? Where would the excess hydrogen go?
Hydrogen is highly flammable around 29%. Would we become fire-breathing?
How would the machine not hyperinflate and thus injure the lung?
How would we get rid of CO2? We would still have to breathe in and out.
Etc.


Is there in vivo evidence of Amyloid beta toxicity?

From a quick search, it seems that there is plenty of solid evidence for in vivo toxic effects. A couple of papers here and here.


Forming a cladogram from a table of information

I think the clue is at each step to look for the trait that is shared by most of the remaining taxa.

In your example: 9 out of 10 taxa are vertebrae. So you are correct to pick this trait first and outgroup Lancelets.

Looking at the remaining 9 taxa:
8 have jaws, and a different set of 8 swim bladders or lungs
At this point you can pick one of those traits, as far as I know.
You chose jaws and outgrouped Lampreys.

In the remaining 8 taxa, the characteristic that is shared by most of them (7), is having swim bladders or lungs. Thus, you can outgroup Sharks here.

In that way, you can go on for the remaining traits and taxa.


How to inhibit formation of specific antibodies (to antisera)?

If you are referring to reducing the titer in the immunized animal, you could give the animal a drug that has immunosuppressive properties. Velcade (PS-341) is a drug that effectively reduces plasma cell counts. There are many immunosuppressive drugs available.

If you  want to reduce the antibodies affinity, you are undertaking a much more delicate process. Affinity can be transiently affected by introducing a  unfavorable environment for the antibody. You can accomplish this by changing the temp, salt conditions, pH or introducing a denaturing agent like guanidine HCL.

Changing any of these conditions in just a little excess could also result in a permanent reduction in affinity.

If you are attempting to tailor the affinity constant of the Ab by changing the architecture of the antigen, you are correct this can be done using site directed mutagenesis. However I think it would be more effective to perform a random mutagenesis and then screen the mutants for the Ka value you want.

Lastly the antigen could also be post-translationally modified. After performing in vitro transcription and translation you could modify your antigen using different strategies such as ubiquination, phosphorylation, prenylation etc... All these could potentially affect Ka as well.

A Hybridoma system to produce a monoclonal antibody should also be explored. Here is a reputable company that produces monoclonal antibodies:

http://www.sdix.com/Products/Custom-Antibody-Services/Ab-Production-and-Services/mAb-Antibody-Development/Hybridoma-Development.aspx


I'm impressed to stumble upon someone who can do that with his tongue. And mainly because I can do that myself!

Looking at the images and feeling with my tongue, this rugged area you mention is definitely too close to the nose to be the adenoids.

So I googled a bit (well, more like a lot) and I found this cool webpage which details that area.
http://www.theodora.com/anatomy/the_pharynx.html
and I found this snippet of text:

  Above the pharyngeal tonsil, in the middle line, an irregular
  flask-shaped depression of the mucous membrane sometimes extends up as
  far as the basilar process of the occipital bone; it is known as the
  pharyngeal bursa.

I've found stones in my tonsils but never in my adenoids. What I've sometimes found was dried mucus adhered to it when waking up in the morning.
I believe those stones might be rests of food (which can't really get up there).
Maybe this green mucus you found was just dried mucus? Maybe a little infection on a particular day?
I hope you get the answer, since it's passed a quite long time since you asked :)


How to compare Smith–Waterman algorithm implementations?

There are only two possibilities for Smith-Waterman alignment with a given cost matrix. It's either right or it's not.

Honestly, whatever you're using, it's really really unlikely that a pure Smith-Waterman implementation is wrong. It's not that complicated, really. There are a lot of heuristic improvements on Smith-Waterman, but if you're both a) sure you don't want to test them b) sure they're not being used, you can always generate lots of random sequences and align them in pairs. If any pair doesn't align with the same score in the same way, something is wrong and you should investigate further.


In a fitness landscape, is fitness relative or absolute?

By experience, most of the time, authors are talking about relative fitness. To
confirm my feeling, I looked at the three randomly chosen theory papers from the first page of results that Google Scholar returned when searching for fitness landscape and they all use fitness as a relative measure. The papers are Derrida and Peliti (1991), Merz and Freisleben (2000) and Woodcock and Higgs (1995).

However, I do not think this is in the definition of a fitness landscape. One could work with absolute fitness and still call his model a fitness landscape. I think that therefore the answer is specific to every model considered. Note that even the "landscape axes" for which a fitness value is assigned can be of different nature. Typically, one can associate phenotypic or genotypic and/or even environmental axes.


Additive genetic variance with $n$ alleles

Well, the total genetic variance is just, by the definition of the variance,
$$
\sigma^2 =\sum_{i,j} f_i f_j (w_{ij}-\bar{w})^2
$$
(using $f_i$ and $w_{ij}$ for frequency and fitness, respectively), and
$$\bar{w} = \sum_{i,j} f_i f_j w_{ij}$$ is just the average fitness.

You can calculate the additive genetic variance for different loci by simply assuming that there is no dominance effect, i.e. the alleles are independent. If it helps, think of it as a quantitative trait in a haploid organism. Thus,

$$
\sigma^2_A =\sum_{i,j} f_i f_j (w_iw_j-\bar{w}')^2 = \sum_i f_i(w_i-\bar{w}')^2.
$$
with
$$
f_i=\sum_jf_{ij};  w_i=\sum_j f_{ij}w_{ij}; \bar{w}' = \sum_i f_i w_i;
$$


Why does fever above 102 herald a cancer patient's death?

I'm not sure I agree with that, but if I had to support that assertion, I would say that while patients with COPD, CHF and neurodegenerative diseases may die of hypoxia (no fever there), patients with cancer more often die of opportunistic infections.

In patients being treated with chemotherapy (and for some time afterwards as well), myelosuppression - that is suppression of white blood cells vital to fighting infection - is a major risk factor, and is the major dose-limiting factor of systemic chemotherapy.

However, as I stated, I don't agree that fever is a predictor of end of life in cancer patients.

In one large study of terminally ill cancer inpatients, infection was the cause of death in only 15% of patients. More common causes included congestive heart failure (24%), renal failure (30%), liver disease (30%), cerebrovascular disease (30%), pulmonary embolism (25%) - very common in cancer patients - and lung disease. (Overlap exists because of comorbidity.)

Another study of hospice patients found the major problems in terminal cancer patients were the presence of cognitive failure, weight loss, dysphagia, anorexia and dyspnea to be independent survival predictors in this population (which somewhat supports the above study.)

The National Cancer Institute's Last Days of Life–Health Professional Version does not even list fever as a predictor of end of life (EOL).

Among a few others, the late signs found highly specific for impending death in 3 days involved instead signs of cardiac, cerebrovascular, respiratory, and renal failure.

Similarly, a study in the journal Supportive Care in Cancer found that according to palliative care experts (78 professionals, including physicians, nurses, and others):

  changes in the following categories (each consisting of up to three phenomena) were considered highly relevant to clinicians in identifying and predicting a patient's last hours/days of life: "breathing", "general deterioration", "consciousness/cognition", "skin", "intake of fluid, food, others", "emotional state" and "non-observations/expressed opinions/other".

Coley's toxins have to do with treatment of cancer. I'm not sure that they have anything whatsoever to do with death from cancer.

Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients
Invasive fungal infections in patients with hematologic malignancies in a tertiary care cancer center: an autopsy study over a 15-year period (1989-2003)
Last Days of Life–Health Professional Version
International palliative care experts' view on phenomena indicating the last hours and days of life.


So far, you're right in that there is no hard method of determining cephalopod sex determiners.  Male and female share the same number of chromosomes, but are morphologically different, with the male developing a special arm for transferring spermitangia and the females often being larger than males (1).

Most research papers seem to focus on just being able to tell the sexes apart by behavior/anatomy (2) and have not yet broached on the How, except to note that they do not seem to have specific markers, which you've already noticed (1).

You can tentatively run with this, and keep an eye out for new research in Google Scholar, and decide that your race uses environmental signaling (3) to determine their sex.  Given how real life nature goes, you'd probably be in the clear as certainly one cephalopod species will use that method to determine sex. It also can segue into sequential hermaphrodism if you're interested in going in that direction.  It would certainly bring a novel element to your sophonts, rather than making an octopus "human". (Hypothetical extrapolation based on the previous version of this question in Worldbuilding.stackexchange)

But, to give you some ideas for environmental factors.  Some species of Daphnia will make parthenogenetic males when three factors meet: a short photoperiod, shortage of food and a high population density (4). The ever popular crocodiles have temperature dependent sex-determiners, with a narrow "sweet spot" to get a 50/50 male/female clutch (5). The green spoonworm determines it's sex as a larvae, if it lands on the seafloor it becomes female, if it lands on a female it becomes male and lives as a parasite inside of her.

Until further research, develop some form of environmental conditions that can be met naturally, or generated by intelligent octopi for what you want this question to answer.

(1) Coe, W. R. (1944). Sexual differentiation in mollusks. II. Gastropods, amphineurans, scaphopods, and cephalopods. The Quarterly Review of Biology, 19(2), 85-97.

(2) Mercer, M. C., Misra, R. K., & Hurley, G. V. (1980). Sex determination of the ommastrephid squid Illex illecebrosus using beak morphometries. Canadian Journal of Fisheries and Aquatic Sciences, 37(2), 283-286.

(3) Rider, C. V., Gorr, T. A., Olmstead, A. W., Wasilak, B. A., & LeBlanc, G. A. (2005). Stress signaling: coregulation of hemoglobin and male sex determination through a terpenoid signaling pathway in a crustacean. Journal of experimental biology, 208(1), 15-23.

(4)Kato, Yasuhiko; Kobayashi, Kaoru; Watanabe, Hajime; Iguchi, Taisen (2011). "Environmental Sex Determination in the Branchiopod Crustacean Daphnia magna: Deep Conservation of a Doublesex Gene in the Sex-Determining Pathway". PLoS Genetics. 7 (3): 1–12. doi:10.1371/journal.pgen.1001345. PMC 3063754 Freely accessible. PMID 21455482.

(5) Janzen, Fredric J.; Krenz, James G. (2004). "Phylogenetics: which was first, TSD or GSD?". In Nicole Valenzuela; Valentine A. Lance. Temperature Dependent Sex Determination in Vertebrates (PDF). Smithsonian Institution. pp. 121–130. ISBN 978-1-58834-203-4.


Why are plants referred to by their Latin species names, and not by their popular names?

The use of a genus-species notation gives more exact information. For example there are multiple species of chamomile: There is Roman chamomile (Chamaemelum nobile), German chamomile (Matricaria recutita, or Chamomilla recutita) and Dyer's chamomile (Anthemis tinctora). The first two species are appraised for their medicinal properties and help to calm upset tummies and to aid sleep, among other things. The latter species, however, does not have these properties and is used for dyeing. This illustrates the fact why 'chamomile' alone is insufficient.

Popularly, classifications of living organisms arise according to need and are often superficial. Anglo-Saxon terms such as 'worm' have been used to refer to any creeping thing including snakes, earthworms and intestinal parasites. The term 'fish' is used in shellfish, crayfish, and starfish. However, there are more anatomical differences between a shellfish and a starfish than there are between a bony fish and man.

In science it has been the convention to use the genus-species notation since Carl Linnaeus introduced it in the 1700's. This formal classification serves as a basis for a relatively uniform and internationally understood nomenclature. A uniform classification system simplifies cross-referencing and retrieval of information. The Linnaean taxonomical system aids in this purpose and is widely used. The genus-species system can be extended by including subspecies and varieties. Many (plant) species don't even have an (English) trivial name. Taking your lavender example: there are some 39 Lavendula species known and obviously, many of them don't have a trivial name. Here one has to fall back to the Latin names to be sure what it is.


1) Can two different proteins have the same mRNA?

This isn't clear enough to give you an answer:

Can two different proteins be made from the same mRNA molecule?

Yes, polycistronic mRNAs can encode several proteins which are translated separately (we can engineer this using internal ribosome entry sites, IRES).
Yes, different proteins can be translated from one open reading frame by failure of peptide bonding between two amino acids (we can engineer this using 2A peptide sites).
Yes, identical proteins can be translated from one mRNA and then modified differently after translation to yield different "final" proteins.
Yes, identical polypeptides can be translated from one mRNA and then incorporated in different protein complexes.

Can two different proteins be made from the same mRNA code?

No, not made in the sense of translated.
Yes, as above, identical proteins/polypeptides can be made and treated differently after translation.

2) Is it possible that the gene types which encode the synthase are the same?

Gene types? Do you mean genotype, i.e. allele? What synthase? Sounds like a homework question to me.


Allergies - congenital situations or created and developed over the years?

Allergies are caused by one's immune system.  If you had never been exposed to the allergen, you would not experience any symptoms.  So they are not innate or inherent.

Why do people develop food allergies after repeated exposure?  I have not read any convincing explanations for the biology behind this.  When you look at the heavy-chain switching that takes place in B-cells, the IgE that are responsible for allergy symptoms are the terminal switch, so those antibody variable regions have already been selected during your life history up until that point.


Why are there exactly 207 morpho-electrical types of neurons?

This is just that one author's opinion - it is telling that both sources you have for the number come from the same author. Henry Markram has a leadership role in the Blue Brain Project, a project to create a very detailed computer simulation of a chunk of neocortex to answer various questions. In the context of this project, it is somewhat necessary to make some decisions about numbers of cell types so that they can be incorporated in the model. People can bicker all day long about which types are actually unique types, though.

As far as the mathematics of having 55 morphological types and 11 electrical types, yet only 207 morpho-electrical types rather than 605, the answer is that the matrix is sparse. To get 605 types, you would need to observe all 11 electrical types within each of the 55 morphological categories. If not every electrical type is observed for a given morphological type, you will have less than 605 total. In some cases morphological types are specifically associated with particular electrical types.

You should also read about the concept of lumpers and splitters - in summary, in any context of classification without clear distinctions, different people will come up with different boundaries. It isn't really possible to argue "right" versus "wrong" in this context, because doing so requires weighting different values. Lumping may be beneficial for the sake of simplicity and generalization but miss some details; splitting may allow for more nuance but also risks not seeing "the forest for the trees."


How do aerobic Rhizobium bacteria survive in root nodules while fixing atmospheric nitrogen?

TLDR
One hypothesis for survival is nitrate respiration.

Long Answer
Ampount of oxygen available in root nodules is controlled by the host plant by two ways:

By presence of leghemoglobin
By the diffusion resistance
Under anaerobic condition the bacteria survives by making use of denitrification process which could be used to produce ATP under anaerobic conditions.

It is known for a while that, beside nitrogenase activity, in many symbiotic associations between legumes and Rhizobium the activity of nitrate reductase also exists 12. Most of the nitrate reductase ativity has been found to be concentrated in infected bacterial body i.e., bacteriod3. The bacteriod uses the process of conversion of nitrate into nitrite for creating a proton gradient which is inturn used for generation of ATP.
Reference.


What is the difference between abiogenesis and spontaneous generation?

One important difference is that spontaneous generation is a form of "mechanism" by which a certain species is "born", so it is repeated many times. For such complex organisms this would be part of their "life cycle". It would also need to be a regulated, robust process.

Abiogenesis, on the other hand, would create an organism which from that point on does not rely on abiogenesis in any way, so it would be a unique event. Abiogenesis is highly probabilistic which is why it would result in very simple organisms.


How can I determine where meiosis occurs in the life cycle of a plant?

All of these terms are just names for things that existed long before someone named them, and although you can figure out some of the ploidy from the diagram, you need to know the terms/definitions to complete it all.

Sporophytes are just the name for the diploid cells of a plant/algae that reproduces through a haploid life stage called a spore. You could consider the zygote almost like it is a "special sporophyte" from the perspective of ploidy: it's only special because it's the first cell assembled from two haploid cells. All of the other sporophytes are produced from mitosis from either another sporophyte or from the original zygote.

Being diploid is nice because you have two copies of every gene, which is more robust to mutations (while also maintaining genetic diversity for later generations), and, crucially, it lets one organism make a variety of haploid spawn for sexual reproduction.

Maybe you are wondering just about the terms haploid/diploid, and why "2N" vs "N"? The important thing is it isn't just the total number of chromosomes, it's the number of COPIES of each chromosome: with N you have just 1 of each, with 2N you have two of each. The important thing is that they are homologous, it doesn't matter if N is 1 or 2 or 40.


Can someone tell me if the example I wrote below is one possible answer?

No your answer seems correct, but are you sure they aren't asking you to delete the two bases at the absolute 5' end? In that case it becomes:

5’- EBI GBO YSA WTH ECA TEA TTH EHO TDO G – 3’

But if they're asking you to delete any two near the end, then you're correct.


What is working definition for female infertility?

Infertility is defined as the inability to conceive after one year or longer of intercourse without the use of contraception or therapeutic donor artificial insemination.

That definition does not include a state of permanence.  That is, with treatment, fertility can indeed be achieved in many cases.

  You may want to consider the term sterility as a definition, which has a permanence to it. But even then, if you consider tubal ligation (female sterilization) or a vasectomy (male sterilization), then you'll quickly conclude that sterilization can be reversed.  At that rate, you may want to state "irreversible sterility" where a genetic basis cannot be overcome with treatment/intervention.  Even then definitions may vary.

As you've discovered, even some genetic-based infertility can be overcome with IVF.  In terms of your genetic interests, the condition of XX male syndrome, resulting from loss of the SRY gene during crossover, causes the inability to produce any sperm (azoospermia).  There is no existing treatment for that or even a reasonable theoretical one.

This could get more complicated/interesting as new medical therapies mature.  If one were to clone a human for example, is that a type of reproduction? Likewise, there is gene therapy, which could overcome some types of genetic-based sterility.

Sources:

http://medical-dictionary.thefreedictionary.com/Infertility
http://medical-dictionary.thefreedictionary.com/sterility
http://www.acog.org/~/media/For%20Patients/faq011.pdf


How many human proteins have a solved 3D structure?

6405 proteins mapping to 5220 genes, according to Ensembl.

In Ensembl's BioMart, you can select the PDB ID as external reference. Export the results and count the unique proteins/genes that have a PDB ID.


Does any organism use both photosynthesis and respiration?

tl;dr: Yes, all plants breathe.—

I'm not sure whether I understand the question correctly; because all plants use respiration! Some of the organic high-energy substances produced by photosynthesis are later "burnt" to produce energy in the same "respiration" process used by animals, producing CO2.

The difference to animals is that green plants synthesize their carbs (including the ones they burn for energy), fat and proteins from thin air, so to speak, while animals must eat them.

These antithetic processes, photosynthesis and respiration, are often tied to the day-night cycle. When light is available, the plants-only photosynthesis dominates so that the plant consumes CO2 and emits oxygen; at night, when photosynthesis becomes impossible, the usual common-place respiration causes the plant to consume oxygen and emit CO2, just like animals.

Only as long as the plant is growing, this cycle is tilted towards photosynthesis so that more oxygen is emitted than absorbed: the excess carbon and hydrogen is sequestered in the plant's growing biomass. But when the plant dies, all this high-energy biomass is burnt by animals and micro-organisms, making the overall balance carbon- and oxygen-neutral.2

So how do plants breathe — or rather, exchange gases with the atmosphere in general — if they don't have lungs or gills? The key is the large surface area of typical plants with leaves. Seen in this light, a tree looks well-designed for filtering stuff out of the atmosphere. Consider these two images. The first one is a lobe of a human lung3. The second one is a tree... or is it?

I found John W. Kimball's page about gas exchange in plants accessible and full of interesting information. Central to our discussion are three facts:

A plant's living cells, including the ones in the stem, are never far from the surface.
The rate (or "speed") of respiration, i.e. oxidizing carbohydrates, is lower than in animals. (Plants do not perform physical labor with muscles and do not have a brain, which are the two main energy consumers in the human body.)
Photosynthesis happens mostly in the thin leaves.

Because of these factors — smaller amounts of gases per time over shorter distances — plants do not need high-volume, long-distance gas transport in the fashion most large animals do, with blood circulation. The gas travels between and through the cells as needed, guided and regulated by mechanisms detailed in Kimball's text. The fluid traveling through the stem provides (lots of) water to the leaves in the upward direction and nutrients to the living cells downward, but apparently does not carry (much) gas.

The Arbor Day Foundation has a nice page detailing a tree trunk's structure with information about each layer's function. (I didn't know that the cells in the heartwood — the inner part of the trunk — are dead and do not participate in the transport of nutrients or water.1)

Your question seems to be triggered by a perceived similarity between the molecule giving blood its red color, hemoglobin, and the molecule which gives plants their green color, chlorophyll.

True, both are organic molecules with metal atoms embedded, but they are quite different, even apart from their color. Hemoglobin is a protein with a fairly complex spatial structure; look at the image on the Wikipedia page. It weighs as much as 64,000 hydrogen atoms, i.e. it has a molar mass of about 64,000 g/mole. Chlorophyll is also an organic molecule, i.e. it has carbon chains and rings, but it is not a protein. (In living cells Chlorophyll molecules are embedded in a protein complex, arranging them to work together; that is a different thing.) It does not fold in space, partly because it is not as big. Its molar mass is only close to 900 g/mole, almost 80 times lighter than hemoglobin. A model of one variety can be found on its Wikipedia page, too.

The jobs the two molecules do also are fairly different, even though both have to do with oxygen.

Hemoglobin has a transport job. It binds oxygen efficiently. The spongy, blood-heavy lung tissue absorbs oxygen, which dissolves in the blood and is bound to the hemoglobin swimming around in it. There is a lot of hemoglobin in our blood, increasing the blood's capacity for oxygen transport by a factor of 70 compared to just dissolving oxygen in water (and it dissolves actually quite well in water!). Thus, hemoglobin does not synthesize anything but simply transports gases, mainly oxygen, through the body to where they are needed. Some athletes dope by collecting their own hemoglobin and re-injecting it before a competition, thus increasing oxygen supply for their muscles.
Chlorophyll does not transport molecules but instead does some heavy chemical lifting. It absorbs light to harvest its energy through the mechanism called photosynthesis. The details are fairly complicated, but the big picture is not: It is a reversal of respiration, or chemically a reversal of oxidation, called reduction: Oxygen is separated from the hydrogen in H2O and carbon in CO2 and given off to the air. Doing this consumes the same amount of energy which is released during oxidation (be it by fire or by metabolization in the plant). The emerging oxygen-poor(er) compounds can be oxidized later elsewhere to release that energy, or can be used as building blocks for new cells.

1 My girlfriend thinks I'm stupid not to know that ;-).

2 Unless it is buried and taken out of the biosphere, fossilizing to peat and eventually coal, tar and mineral oil. Then the net CO2 balance of a plant's life is indeed negative, i.e. the plant has removed CO2 from the atmosphere; until somebody excavates the fossil fuels, re-injects them into the biosphere and and restores former CO2 levels and all the tropical climate which made the old jungles grow so well.

3 From wikipedia, https://upload.wikimedia.org/wikipedia/commons/a/a1/Lungs_diagram_detailed.svg. By Patrick J. Lynch, medical illustrator, via Wikimedia Commons. The "tree" is actually the same lobe, rotated and colored.


There are several ways to infer into the propagation delays of auditory system in vivo that is applicable to humans (i.e. leaves the subjects intact).

One of them is so-called ABR that stands for Auditory Brainstem Response. As it is clear from its name this method allows you to derive the brainstem response to an auditory stimulus (so, you can track the auditory pathway up to its input into thalamus), but its resolution is so fine that you can separate single components ("waves") for the following path segments (from Wikipedia):

Wave I – generated by the peripheral portion of cranial nerve VIII
Wave II – generated by the central portion of cranial nerve VIII
Wave III – generated by the cochlear nucleus
Wave IV – generated by the superior olivary complex/lateral lemniscus
Wave V – generated by the lateral lemniscus/inferior colliculus

So, it takes only 10 ms for the signal to reach the input into thalamus. This correlates well with some auditory signal based activities, like startle reflex, which was also shown to have about 10 ms latency.

I tried to search for some electrophysiological recordings from auditory cortex (temporal lobe) paired with auditory stimuli, but the first paper I came accross that is available for free (and which I can also link from my answer) is this work done on monkeys.

If you look at Figure 1:

This is the results from multiunit recordings and you see that the initial activity in the cortex starts approximately 20 ms after the stimulus onset with a short activity pattern, followed by some short break and then longer period of activity with broader frequences spectrum.

In my opinion the delays in signal propagation are not due to complex signal processing in the olivary nucleus or any other brainstem structures, rather they are due to electro-chemical transformations in CNS synapses.

The initial arrival of the signal into the cortex does not mean the perception of the sound, it definitely takes hundreds of millisecond until the conditioned cortex-mediated response to this stimulus.


It is certainly a scarab, in subfamily Cetoniinae. It looks very much like a White Spotted Fruit Chafer, Mausoleopsis amabilis http://www.projectnoah.org/spottings/11819281


I believe your textbook is referring to the fact that you only perform the complete beta oxidation eight times.  Because there's a carboxylic acid at the terminus of a fatty acid chain, the cell takes a slightly different route and reacts it with ATP, which generates a fatty acyl adenylate and pyrophosphate (PPi).  This AMP can subsequently be displaced in an attack by CoASH, at which point the beta oxidation process can proceed in full to begin cleaving off acetyl-CoA.

Here's a visual representation of this activation process, too.


Why isn't the p16-INK4a gene involved in apoptosis expressed in heart or liver tissues?

p16-INK4a is a part of a very important checkpoint mechanism. It's the "bad guy" in the context of aging because it induces senescence, and too much senescence leads to aging-related  tissue degradation.

But senescence is important. It's one of the responses cells take when something goes wrong-- DNA damage, viral infection, telomere depletion, that sort of thing. Senescent cells have stopped proliferating. We have a word for cells that don't stop proliferating, and that word is "cancer". So, p16-INK4a is a major tumor suppressor. A universal p16-INK4a knockout would have a much harder time shutting down the proliferation of cells that had undergone DNA damage, and would therefore be much more prone to cancer. You'd have very young-looking tissues filled with tumors.

So, the headline question is why INK4a is not expressed in the heart or liver if it's so important. This is speculation on my part, but I think it's because those tissues are especially prone to being damaged by fibrosis, and a build-up of senescent cells would lead to increased fibrosis. Senescence is just one possible response to DNA damage, though. Another is apoptosis. If the senescence-induction pathways aren't active in heart and lung tissue, I'd expect the apoptosis-induction pathways to be pretty active.


Does RNA serve as the genetic material of some plants and animals along with viruses?

There are no animals or plants with RNA genomes. There was a mistaken belief in the 1920s that plant genetic material was RNA whereas animals had DNA, but this was finally disproved by JN Davidson in the 1940s.


An artifact in biology usually refers to experimental error or other spurious results. In the context of microbiology, you will get artifacts if, for example,  you sneeze on the plate you are growing a colony on.

The term is generally used for any result that is not actually true but stems from bad analysis or experimental procedures. Take, for example, this definition from biology-online.com:

  Something artificial, a distortion that does not reflect normal anatomy or pathology, not usually found in the body. For example: in radiology, the appearance on an x-ray of a surgical metal clip that obscures the clear view of an anatomical structure.


How to determine whether changes of an allele's frequency are due to genetic drift or selection?

Is there a way to disentangle selection from drift

Yes, there are actually many ways...so many so different ways that it is impossible to correctly answer this question. Hopefully, below answer will give you some appreciation of why there is such a diversity of methods and wil give you sources to further your knowledge on the question.

It depends upon the data you have

The answer very much depends on the data you have in mind. Are you looking at a

panmictic population
a structured population
are you comparing a large number of lineages along a phylogeny
do you have information about a proxy for fitness in this population
can you perform an evolution experiment (depends a lot on the generation time)
do you have genetic data that are temporally separated
...

Also, what type of selection are you thinking of?

balancing selection
Are you trying to find epistasis for selection
Are you looking at some form of balancing selection
Local selection
...

Also depends upon whether you have data about potentially correlated variables such as

phenotypic data
ecological data

There are tens (or even hundreds of methods esp. when having data about related lineages) under each bullet point above, so your question is definitely quite broad.

Source of information

Statistical tests that test to the null that there is no selection are often called "test of selective neutrality". You might want to read Nielsen 2001  and Nielsen 2005 to get an overview of tests of selective neutrality in panmictic populations.

You might want to have a look at this answer, this answer and especially this answer.

What does it take to understand the methods for disentangling selection from drift?

Understanding the tests of selective neutrality can be a bit demanding as it requires having good knowledge in classical statistics, bayesian statistics, MCMC, Approximate Bayesian Computation and even machine learning algorithms. It also requires good knowledge in population genetics (typically incl. coalescent theory) and statistical phylogenetic.

A specific example

Unfortunately, I can't think of any specific example of a test which is really easy to grasp without a priori knowledge. A classical, not too hard and historically example test for neutrality in panmictic population is the used of Tajima's D (which derivation require basic knowledge in branching processes). You might want to learn about it to have a specific example. I recommend Gillespie's book Population Genetics: A Concise Guide to learn about this test. More book recommendation can be found here.


Can Palisade Cells Survive Independently?

Yes they can. In 1902 Haberlandt reported single palisade cell culture from leaves in knop’s salt solution. Now there are many different methods of plant tissue culture

for PLANT TISSUE CULTURE see


You have it wrong. Coronaviruses are part of a family of viruses that are called "enveloped viruses". These all have an "envelope" comprised of a lipid layer derived from the host cell as the virion exits. The envelope is distinct from the spike. The spike protein is produced by the virus during replication and is not found naturally in a host cell.
This does not pretend to be "food" at all, but it can help evade host immune responses by hiding the other virion capsid proteins.


What is the consensus in the scientific community over COVID-19's mode of transmission?

The terminology really depends on the scientific field. You also have to be aware that sometimes terminology is simplified for the purposes of presenting information to the general public.
A droplet can really mean anything from a few micrometers up to several millimeters and it does not necessarily have to be spherical. The key point is that the virus may spread through droplets.
Aerosols typically refer to small solid particles or liquid droplets, maybe less than 20 micrometer in size, but again, it depends on the field.
In quiescent air, any heavy (more dense than air) particulates (solid or liquid) which are about 1 micrometer  or less will remain suspended in the air for several hours due to Brownian motion and also the fact that their gravitational settling velocity is small.


Revised Answer

The additional pictures point to something in the genus Prunus.  Note that there are extrafloral nectaries at the base of the leaves, and feathery stipules are visible (see here for annotated picture of a different species).  Since it has a weeping habit, and doubly toothed leaves, I think what you have there might be a Japanese Weeping Cherry Prunus subhirtella var. pendula (but other names seem to be in use).  Some info here which seems consistent with your specimen.

Original Incorrect Answer

I think you are probably looking at Ulmus glabra "Camperdownii" or a similar cultivar.  This is a "weeping" elm variety that is produced by grafting; all plants are descendants of a single tree. Wikipedia gives the full background.  Your specimen has somewhat more pointy leaves than many of the images for Camperdown Elm I found online, but apparently there can be some variation.

EDIT: The fruit picture (added after my answer) clearly rules out my answer!  Also looks like there are nectaries at the base of the leaves.


Perception of artificial light - flickering

It's difficult to give an exact answer without actually observing the light and performing measurements. I have a theory, though.

Your peripheral vision is hyper-sensitive to changes in light - an evolutionary trait that provided quicker reactions to predators sneaking up on you. As such, even the tiniest fluctuations in light can be registered with your peripheral vision; much more so than your primary field of vision. In this case, it may well have been that the light was flickering very subtly, or at a very high frequency, which your primary field of vision could not pick up. When your peripheral vision was in play, it immediately spotted the flicker.

This is reliant on a principle called the flicker fusion threshold, which essentially states that there is a threshold of various light properties (including flicker frequency, colour, intensity, etc.) at which an eye begins to distinguish a steady light from a flickering one. Research has demonstrated that species who have high rod density are good at picking up flickering, whereas species with low rod densities have a much poorer threshold. Cone density doesn't seem to factor in very much, since flickering is primarily a change of intensity rather than hue.

This transfers into the human eye, since we have a high rod density (and low cone density) at the edges of our retinas, i.e. in our peripheral vision. If you had the eyes of another species (as creepy as that would be) with a high rod density, you may well have been able to detect the flicker quite easily with your primary field of vision.

To directly answer your question - yes, I believe this is primarily the "fault" of the eye, rather than the brain. The brain has a role in identifying the flicker at a subconscious level, in terms of fight or flight response, but the eye is responsible for providing the elevated sensitivity at the peripheral.


The quick and simple answer:

Cramps of a hypokalemic origin are much more common than those of a hyponatremic origin because the Na-K pump is more effective at moving potassium in comparison to sodium.
At the onset of a muscle contraction, the presence of calcium triggers the opening of the Na-K channels in the membrane. Potassium is a calcium inhibitor, so as the potassium flows out of the cell, it eventually reduces the presence of calcium. This causes the closure of the Na-K channel (negative feedback mechanism). In a hypokalemic state, the lack of sufficient K doesn't inhibit the calcium channel, and in turn doesn't properly terminate the muscle contraction at the cellular level.

The continued presence of calcium, which has a lot to do with nerve impulses, means that the nerves keep firing, and in some cases such as a 'charlie horse', these impulses fire fast and continuously. The body at this point is reaching a small local state of metabolic acidosis resulting from the extremely high oxygen consumption, increasing levels of CO₂ (the acidosis component) and reducing blood partial oxygen levels. Since the oxygen is no longer as abundant as it was, it inhibits the bodies ability to locally produce the ribose and phosphate necessary for ATP. Less ATP = more myosin that can't be disconnected from actin = continued muscle cramp.


Why is the nucleus accumbens in that place?

The ventricle looks in a different place simply because the first image is a transverse section whereas the second one is a sagittal section.
In the sagittal version the striatum looks very far from the ventricle because it is a quite lateral slide, more medially it would look closer to it as it does in the first figure you show.

Here you can see a representation showing also a more medial transverse section.
source: Vertebrate brains and evolutionary connectomics: on the origins of the mammalian ‘neocortex’. Harvey J. Karten. (2015) DOI: 10.1098/rstb.2015.0060


Is prion a term used to describe the normal form of the protein as well as the disease causing form?

The normal isoform of the protein is called PrPC, which stands for cellular prion protein, while the infectious isoform is called PrPSC, which stands for scrapie prion protein.

According to Riesner (2003):

  The biochemical properties of the prion protein which is the major, if not only, component of the prion are outlined in detail. PrP is a host-encoded protein which exists as PrPC (cellular) in the non-infected host, and as PrPSc (scrapie) as the major component of the scrapie infectious agent. (emphasis mine)

If you search for "cellular prion protein" you're gonna find several papers that use the name prion protein to the normal isoform. Some examples:

Prado, M., Alves-Silva, J., Magalhães, A., Prado, V., Linden, R., Martins, V. and Brentani, R. (2004). PrPc on the road: trafficking of the cellular prion protein. Journal of Neurochemistry, 88(4), pp.769-781.
Ramljak, S. (2008). Physiological function of the cellular prion protein (PrPc_1hnc). 1st ed. Berlin: Logos-Verl.
Pantera, B., Bini, C., Cirri, P., Paoli, P., Camici, G., Manao, G. and Caselli, A. (2009). PrPc activation induces neurite outgrowth and differentiation in PC12 cells: role for caveolin-1 in the signal transduction pathway. Journal of Neurochemistry, 110(1), pp.194-207.
Martins, V., Mercadante, A., Cabral, A., Freitas, A. and Castro, R. (2017). Insights into the physiological function of cellular prion protein.

And many others.

Therefore, following this nomenclature, the answer to your question ("Would I be correct in saying 'The prion protein is normally involved in synaptic transmission but can turn into a disease causing form'?") is yes. The difference is the adjective: cellular or scrapie.

Finally, pay attention to this: you have two different questions here. In the title you say "Is prion a term used...", but in the last paragraph you say ""Is the prion protein normally involved in...". As extensively discussed in the other answer, the term prion alone (instead of prion protein) is normally used only when referring to the abnormal isoform. More on that here: https://www.cdc.gov/prions/pdfs/public-health-impact.pdf

Source: Detlev Riesner; Biochemistry and structure of PrPC and PrPSc. Br Med Bull 2003; 66 (1): 21-33.


If alcohol is a depressant, why does it makes certain people more hyperactive?

These types of reactions in pharmacology in general are called paradoxical effects.

The main effect of alcohol on the CNS is the potentiation of GABA receptors. GABA receptors are (mostly) inhibitory receptors in the CNS, so potentiation of GABA receptors mostly decreases brain activity by increasing inhibition.

However, you can distinguish between neural inhibition and behavioral inhibition. Some brain regions, like the prefrontal cortex, seem to primarily have inhibitory effects on behavior. That is, usually prefrontal cortex is active when suppressing actions. If you were to suppress the prefrontal cortex, you would get the opposite effect on behavior. When there is "inhibition of inhibition" the term often used is "disinhibition."

It isn't yet clear why exactly alcohol leads to behavioral disinhibition at lower doses, but this is one possible mechanism. In general, U-shaped dose-response curves are quite common in neuroscience, so alcohol isn't all that unusual in that sense.


Why is the mechanism of inheritance for this disease autosomal dominant?

I think this question is not possible to answer without knowing the frequency of the deleterious alleles in the population.  There's no way to assess whether incomplete penetrance is more or less likely than an undetected mutation in the mother's side.  Since the question doesn't mention the mother's family at all, and only the father's, that suggests to me that the question writers don't want you to think that anything is wrong in the mother's side.  That would make it dominant with incomplete penetrance.


Black panther refers to melanistic examples of either leopards (Panthera pardus):

or jaguars (Panthera onca):

It is not typically used to refer to (the rare/historic/unconfirmed) examples of melanism or pseudo-melanism in other species of Panthera (e.g. black tigers).


There is little hard evidence on whether smoke acts as a mosquitoe repellent. A literature review done by the WHO (Biran et al, 2008) on smoke and malaria show that evidence is mixed, at least when it comes to long term protection and protection from blood meals from firewood smoke. Their review also notes that few scientific studies have been done on the topic, and they report results from one experimental and a couple of observational studies. However, they do note that burning particular plant materials (based on traditionally used plants) may be effective (see e.g. Pålsson & Jaenson. 1999).

These results also doesn't preclude that very heavy, temporary, smoke may be effective to get rid of mosquitoes ("... during camping is to stand in the fire's smoke...") - that this can be effective is certainly my personal experience as well.


Are there any organisms that are made of more than one (~5-12) cell?

There's Trichoplax adhaerens, a Placozoa, made of a few thousand cells. Then there is Dicyema japonicum, a simple mesozoan, made up of 9 to 41 cells. Arguably, the simplest multicellular organism is the algae Tetrabaena socialis, whose body consists of 4 cells. Then, there's the parasitic Myxozoa which have 7 cells.


Where did the term "vegetative nervous system" come from?

"Vegetative" doesn't only mean related to plants, but has other less common meanings.

  4 a (1) :  growing or having the power of growing (2) :  of, relating to, or engaged in nutritive and growth functions as contrasted with reproductive functions a vegetative nucleus
  b :  promoting plant growth the vegetative properties of soil
  c :  of, relating to, or involving propagation by nonsexual processes or methods
  Merriam-Webster

So the word "vegetative" refers to the growth/nutrition functions of the autonomic nervous system. The short answer is that he chose that word because, particularly at the time he chose it, that was an appropriate word to use to refer to the regulation of things like digestion. Since the autonomic nervous system has other functions, such as in sexual arousal, and because the term vegetative has other meanings, the term "autonomic" has completely replaced vegetative in this context.


How did plaques form in Salvador Luria's Bacteriophage experiment (discovery of restriction enzymes)?

This indeed a very interesting experiment. In the lecture, you can see that the obvious explanation for the initial inhability to grow in strain B indicates that the bacteria is resistant to the virus. However, ocassionally, a virus is able to form a plaque in strain B, which initially seems to indicate that it mutated. However, in a second passage from Strain A to Strain B of this initial "mutant", we observe that there are no plaques in Strain B. This indicated that something beyond the DNA (unlike a mutation) was at play, and eventually led to the discovery of these epigenetic markers (methylation) that are made by the machinery of the bacteria (thus, Strain A lacked such machinery, so it maintained the viral DNA but did not mark it as 'viral').

Because these experiments occurr in Petri dishes, where there are millions of cells (billions, in fact), there is always some probability that the restriction machinery does not work. This probability (small, but detectable) of no detection is what is observed in the "original" plaque formed in Strain B. In addtion, when the virus is just added, it is still not marked, so it needs some time to be marked (more cell replication cycles), and during this time the virus can be infective. Either of these possibilities will produce a small fraction of plaques in Strain B.


What is the fastest way to build an alanine scanning library?

The fastest will change as time passes and better technologies are developed.

I think the fastest method existing at the moment is Shotgun Mutagenesis (provided by Integral Molecular Inc).

This does not employ any new method of doing that. They just provide a set of plasmids, that has all the possible mutations. The set itself is generated by automated DNA synthesis.

So if you don't have a DNA synthesizer with you then simply order the kit from the company.


Why is only the donor's antigen seen during a blood transfusion?

Blood transfusions are done with erythrocyte concentrate and not whole blood. The antibodies are dissolved in the blood plasma. Grafting parts of the donor's immune system by transfusing white blood cells (the leukocytes) would cause even more problems than just agglutination in most cases. That's why care is taken to separate the red blood cells.


What percentage of human capillaries are located in the skin?

The first part of your second question permits a rough calculation.

The second question ( i ): For humans the skin has been defined as ending at the hypoderm, which is 2-3mm deep. The average human skin has been estimated to cover an area of 1.5-2 m$^2.$ We can use 2.5 mm and 1.7 m$^2$, respectively. This gives a volume of 0.00425 m$^3$ or 4250 mL in fluid volume. The information for this calculation is at the Wiki site on human skin.

One estimate of the average total volume of fluid in a human body is 40L. Of that, 5L is blood. So roughly 1/8 of the body's fluid is blood. To a good approximation, the body is about 60% water by weight. This is presumably a little less than the percentage of fluids generally but since these are rough numbers we can use it. So 60% of the skin is fluid/water, and 1/8$th$ of this is blood.

Of the 4.250 L of skin, 60% is fluid, of which 1/8 $^{th}$ is blood, so $(4.25) \cdot (0.60) \cdot \frac{1}{8} = 0.3188$ liters of blood at any given moment in the skin, subject to considerable variation no doubt. This sounds a little low but the definition of skin sort of forces this--it is only skin-deep.

One source gives an estimate of the energy expended to pump blood in a normal adult heart as 0.5-1.0 Joule per beat which at 70 beats/minute amounts to 100.8 kJ/day using 1 Joule.

So the heart is handling about 5 L of blood of which 0.3188 L is blood in skin, so very roughly we could estimate that $0.3188/5 = 0.0638$ or 6.38% of the work above goes toward supplying skin, i.e. 6.43 kJ/day of energy.

As a sanity check, if someone burns 1200 [nutritional] calories a day, which is about 5 MJ, we can see that keeping skin supplied with blood represents a small fraction of daily energy expenditure.

The title question: Like you, I found no study on point but that does not mean one does not exist. I can't see why anyone would do/fund such a study as the answer is unlikely to inform further work, answer any current questions, or solve any problems.

The last part of your second question (ii) Transporting blood to the capillaries and circulating the blood through capillaries are aspects of the same job. Dividing the work of the heart into skin/non-skin was already artificial. To further divide the work into segments this way requires some motivation because any answer would be a bad approximation.


Can elephants smell when they have water in their trunks?

Yes they can, as the G protein-coupled olfactory receptors detect presence of molecules and no receptors exist that are inhibited by competitive binding of water molecules.
Both you and an elephant can smell (with) water in the nose! Just try it! I am sure you can smell a difference between pure water and water with a tiny drop of perfume in it if you aspirate it though your nose!


Why doesn't the herbicide 2,4-D damage lawn grass?

According to this link from Purdue, the seed of the answer is this:

  The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.

But on the other hand, Song 2014 has this to say about 2,4-D:

  However, the underlying molecular mechanism of how auxinic herbicides selectively kill
  dicots and spare monocots is not
  understood yet (Grossmann 2000; Kelley
  and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport,
  and signal transduction
  are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has
  proposed that the selectivity of auxinic herbicide is because of
  either limited translocation or rapid degradation
  of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002;
  Kelley and Riechers 2007). Auxin transport is influenced by plant vascular
  systems (Mattsson et al. 1999;
  Scarpella et al. 2006). The difference in vascular tissue structure between dicots
  and monocots may contribute
  to the selectivity of auxinic herbicides. In monocot
  stems, the vascular tissues (the phloem and xylem) are
  scattered in bundles, and lack a vascular
  cambium; in dicot stems, the vascular tissues are form
  ed in rings and
  possess a cambium.

So in other words, we don't know yet. It seems to be very strongly tied to auxin transport, but we do not have the full mechanism of action; since auxin is such an important plant hormone, and the pathway is therefore highly conserved (that is, the genes tend to be nearly identical on the parts of the sequence that affect the phenotype), the general conclusion is that the pathway itself is not affected, but an accessory pathway clears up auxin in levels excess of any normal amount in monocots.

Edit: Whoops, got the author's first/last names mixed up.


Overlapping genetic information in eukaryotes

You might be interested in the INK4A locus (chromosome 9p), encoding both p19 and p16 genes, very close to p15. You can read a description here. All three proteins are known experimentally to exist.

Now, whether these are two different genes or the same gene with alternative splicing and start sites leading to different reading frames it's up to discussion. The point is that p19 and p16 share DNA coding sequence but not protein sequence nor function.


HLA typing between siblings to identify a genetic disorder

No, you can't conclude that.

First of all, two siblings being HLA identical tells you very little about the rest of their genome. HLA genes are closely linked, and each haplotype is transmitted in mendelian fashion as a single gene.  For non-linked genes (on other chromosomes, or further away on chromosome 6), they are as or nearly as likely to have the same genes as non-HLA identical siblings.

Further, the disease of interest may (is highly likely to) be multigenic and have incomplete penetrance. The heritability of common disorders generally varies from 20-80% (Cecil Medicine Chapter 41, the Inherited Basis of Common disorders).


How to find mutations related to disease for a protein?

I think I understand what you are asking so I will make a little guide to find what you need:
NOTE  the mutations you are searching for are probably on gene level so you can search your protein on Uniprot and then use the gene name to search on DisGeNET, you typ in the gene you are searching for:

Then you hit the search button and this will give you a result like this:

You can see that this site uses a sort of text-mining, in other words it is searching for the gene name associated with disease in articles. The score is an indication for how good the text-mining "worked". As mentioned in the manual:

  We have developed a score to rank the gene-disease associations
  according to their level of evidence. DisGeNET gene-disease
  association score takes into account the number and type of sources
  (level of curation, model organisms), and the number of publications
  supporting the association. The score ranges from 0 to 1.

Then you have to click the browse details... in the down right corner. This will guide you to another summary page like this:

(NOTE I omitted a lot of rows to avoid huge images in the answer, so there will be more rows in your result). Because you were interested in prostate cancer I will click on Prostatic Neoplasms:

You can click on the 3 to obtain the 3 articles where the combination of the CYP3A4 and Prostatic Neoplasms was found. This will give you a list like:

As you mentioned in your question

  "where do I find such papers"

You can easily click on the PMID this will guide you to the article, for example the first article:

  CYP3A4 polymorphisms--potential risk factors for breast and prostate
  cancer: a HuGE review(link).

I think this will help you to find the papers related to the protein + disease, you can further read the papers to find mutations which cause these diseases.


Examples of prey predator interactions where density of predator is very low and prey form groups when the predator attacks the prey for food

Many species of animals use flocking/ schooling/ shoaling/ etc as a mechanism to confuse predators. A few examples are tuna, starlings, goldband fusiliers. tuna and goldband fusiliers use their reflective scales to blind and confuse the predator, whereas starlings use sheer numbers to overpower and throw off their predator. The large groups tend to scare away far away predators.

The act of grouping is not dependent on whether or not the predator is endangered or not, but there would be cases where both the predator is endangered and the prey uses grouping. For example, several species of owl are endangered, which prey on starlings.

https://en.wikipedia.org/wiki/Collective_animal_behavior#Protection_from_predators

http://www.fcps.edu/islandcreekes/ecology/european_starling.htm

http://rsif.royalsocietypublishing.org/content/10/85/20130305


Based on your image I would rather identify it as an Eurasian Tree Sparrow. They are pretty similar to the House Sparrow, but have a distinct black spot below their eyes which is missing for the House Sparrows (image from the Wikipedia):


Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?

The article you linked is interesting, but as @Charles E. Grant mentioned in the comments, it’s not particularly reasonable to compare a non-tear repetitive stress injury (like epicondylitis) to a full muscle tear. Non-tear repetitive stress injuries persist because the offending frequent motion doesn’t stop. A muscle tear, however, will recruit an inflammatory response that will eventually be resolved by anti-inflammatory factors (Th2 cells directing the cellular microenvironment towards healing / scarring).

This healing process might not result in an optimal resolution of the initial injury, and it’s not unique to any particular body system. Rather, pretty much anything in your body that can be injured will first respond with a period of innate inflammation followed by fibrosis and resolution (whether or not that restores function / alleviates pain depends on a number of factors including injury severity, therapeutic management, and healing conditions e.g. if there were repeated injuries during the healing process).

With regard to gluteus minimus tears — it depends on the injury. If a patient persistently aggravates an already-torn muscle, they will have more inflammatory cells recruited to the injury. If they do a good job allowing the injury to heal (not re-aggravating the injury, receiving surgery if structural correction is required), the inflammatory process will resolve relatively quickly.


Why is the threshold between human embryo and human fetus defined as 8 weeks after fertilization?

An embryo is called a fetus at a more advanced stage of development
  and up until birth or hatching. In humans, this is from the eighth
  week of gestation. However, animals which develop in eggs outside the
  mother's body are usually referred to as embryos throughout
  development; e.g. one would refer to a chick embryo, not a "chick
  fetus" even at late stages.

wikipedia - embryo

I can answer what "more advanced" means with the following 2 pictures. I think you can see the difference. (Real photos were too disgusting for me.)

Figure 1 - 7th week embryo - source

Figure 2 - 8th week fetus - source

For the sake of blind people and google, the 8th week fetus has a face and a human form, while the 7th week embryo doesn't.

  From the 10th week of gestation (8th week of development), the
  developing organism is called a fetus.

  All major structures are already formed in the fetus, but they
  continue to grow and develop.

  Since the precursors of all the major organs are created by this time,
  the fetal period is described both by organ and by a list of changes
  by weeks of gestational age.

  Because the precursors of the organs are now formed, the fetus is not
  as sensitive to damage from environmental exposure as the embryo was.
  Instead, toxic exposure often causes physiological abnormalities or
  minor congenital malformation.

wikipedia - prenatal development

So the scientific explanation of the threshold is that the precursors of all the major organs are created by that time.


Genetic networks vs genetic architectures?

You can think of a genetic network as a network of interacting genes, turning each other on and off based on complex relationships and external stimuli. A genetic network is typically characterized in terms of graph theory--connectivity, density, etc.

The term genetic architecture, on the other hand, typically refers to a trait or phenotype and the characteristics of the gene(s) that contribute to that phenotype (this is what the Wikipedia article means by genotype-phenotype mapping). Characterization of a phenotype's genetic architecture involves describing how the phenotype(s) is/are related to the genotype(s). For example, for a particular trait or set of traits, is there a one-to-one relationship between gene and trait? Or do multiple genes contribute to a single trait? Or are multiple traits affected by changes in a single gene? The relevant terminology is discussed briefly in the Wikipedia article: polygeny, pleiotropy, etc.


Why did translation develop a specific codon for initiation?

It is not clear to me where initiation took place in the translation of artificial polynucleotides such as (UC)n which Khorana used in experiments that, following up the work of Nirenberg and Matthaii, helped decipher the genetic code. It may well have occurred at random positions rather than the 5′ end. Such a mode of translation would obviously have been wasteful if it occurred during early evolution as a mixture of products would be formed, many of which would be inactive and might even compete with the active species. If this were the original situation,  it is easy to see how a change to initiation at a specific point would be advantageous.

But why not start at the 5′ end? Contemporary eukaryotic initiation complexes recognize the 5′ end of the mRNA, even though they then scan further to find a specific initiation codon that will respond to the initiator tRNA. As there is no physical separation of  genes on a chromosome, it is obvious why transcription needs to start at a specific point within the DNA, but the need not be true for the translation of individual mRNA transcripts.

I can see two ways of approaching this question.

The first is from the standpoint of the contemporary ‘DNA World’. The arguments one can make  include:

In a general sense 5′-end initiation may be regarded as restrictive
in that it would not allow the 5’ end of mRNA to provide other
functions such as forming a secondary structure to regulate the ease
of translation.
5′-end initiation would preclude the polycistronic mRNAs we see in
contemporary bacteria.
In 5′-end initiation it might have been difficult to distinguish the
ends of mRNAs from other RNAs before the modification of bases that
we see in contemporary eukaryotic mRNAs had developed.
Likewise, as suggested by @John in a comment on the question, 5′-end initiation might have caused translation of fragments of RNA as they degraded.
The selection of a specific codon was secondary to the need for a
single initiator tRNA, which has been discussed in relation to
another SE question, although the arguments there relate to more recent stages in evolution.

However there is another approach which considers the situation in a putative ‘RNA World’.

The difference here is that — like some contemporary RNA viruses and bacteriophages — the genome might also have been the mRNA but without a system to produce many copies of the ‘plus’ strand for translation. Translation may have been on the genomic RNA.

To translate several proteins it would have been advantageous to have
several initiation sites on what would have been a polycistronic
messenger (rather synthesize a polyprotein like poliovirus).
The 5′-end of the RNA may not, in any case, have been available for
encoding protein as it might have another (e.g. replicative)
function, and it is also possible that part of what in contemporary
systems is a separate part of the translation apparatus was
physically incorporated into the genome.


Must I HPLC-purify my PCR Primers for amplicon sequencing with PacBio SMRT?

I am at the same stage as you right now. I am assuming that you are planning a 2-step amplification: first one with the universal primer and second one with the barcoded primers. So, this has been my rationale and experience on this.
HPLC purification
If you are generating your own primers and not buying the plate from PacBio it is better to get HPLC purified oligos. The idea behind using HPLC purified primers is that the oligo synthesis may produce truncated products (primers with deletions usually towards the 5' region) in little concentrations. According to IDT, each base addition has an approximate error rate of 1%.  Therefore, longer products have a higher probability of deletions; the number of expected errors would be 0.01 × length of the primer. For a 46nt primer (16nt barcode + 30nt universal sequence), the percentage of deletion-free products would be ~63% (Poisson probability of no deletions). So, you can expect 27% truncated products with approximately 1.2 deletions per product†. Therefore there is some likelihood that the truncated products may mess up your barcode. However, the probability of the deletions specifically in the barcode regions would be less than this estimate.
5' NH4-C6 modification
This modification makes prevents the ligation of the PCR products. You generate the final library by re-amplifying the PCR products of universal primer, with the barcoded primers. The product will also contain a little amount of the template, which you do not want to be ligated to the sequencing adapters. Again, this would be very less: for example if you take 2ng of the template and your yield is ~1.5µg (I typically get this much yield even with a colony PCR of 25 cycles) then the template contamination is less than 0.2% (ideally you should calculate this with number of molecules instead of mass but since the template and product would have almost equal molecular weight you can use the latter also).
Why 16-mer barcodes
You can use shorter barcodes too but you should make sure that they are different enough such that any sequencing error would not make it difficult for you to distinguish between your barcodes. PacBio has an error rate of 13% for a single read; it reduces if you do the Circular Consensus Sequences (0.13^n where n is the number of rounds). When you have a large number of samples then it is better to use longer barcodes as you can reliably distinguish between different samples. They also recommend that the barcoded primers have a 5' phosphorylation. This will further increase your cost. The 5' phosphorylation will increase the ligation efficiency. It is technically possible to use polynucleotide kinase to phosphorylate the products but the efficiency of T4-PNK varies with the 5' base (Houten et al, 1998). In this case I would recommend pre-phosphorylated primers.
Why 30-mer universal primer
I don't have a good knowledge about this but I guess the reasons have to probably do with the molecular biology rather than the data analysis part of it. Demultiplexing can be done manually and it is not very difficult. Technically, a 20nt sequence should also suffice (usual length of PCR primers). Under usual circumstances, I don't think you are going to save a lot by using a 10nt smaller primer. The total length of primer (universal sequence + the template specific sequence) may go down from ~50+ to ~40+. Many oligo-synthesis services have an upper bound for HPLC purification; they would PAGE purify the longer ones. For example, the company that I order from has a cutoff of 50. So, longer primers have to be PAGE purified which would reduce your yield and increase the price. But usually you can negotiate with the company to allow your 1-5nt longer-than-cutoff product to be HPLC purified.

Summary
Some of these modifications would just improve the efficiency marginally and may be skipped if your data is not likely to be affected by a slight drop in efficiency.
So this is my final recommendation:

HPLC purification: not necessary but recommended for long primers (at least the barcodes)
NH4-C6 modification: not necessary
5' phosphorylation of barcoded primers: recommended
Length of universal primer sequence: can possibly be shortened by 10nt but probably that is not likely to reduce the cost significantly.

However, you can significantly reduce your cost by asymmetric barcoding. For example, if you have 100 samples then the minimum number of barcode primers needed would be 20 (10 pairs). You can shuffle the forward and reverse primers to create 100 combinations.

† Explanation of the error rate probability
Let $\lambda$ be the error rate per base (0.01) and $N$ be total number of bases (46). The error will follow Poisson distribution and the probability of errors would be:
$$P(X=k)=\frac{(\lambda N)^k e^{-\lambda N}}{k!}$$
For zero error i.e. $k=0$ the probability would be simply $e^{-\lambda N}$ which would be ~0.63
The mean number of deletions for the 27% that contain errors would be (see zero-truncated Poisson distribution):
$$E(X|X>0)=\frac{\lambda N}{1-e^{-\lambda N}} \approx 1.25$$


Which books give data on how humans grow physically from birth till death?

The 'Illustrated textbook of paediatrics' by Lissauer et al. (ISBN 9780723438717) contains a section about the average growth of children from birth up until puberty. After puberty humans don't grow anymore unless there is a medical condition. However it is important to understand that growth is influenced by many factor including ethnicity, sex, socioeconomic status and health and therefore precise numbers are hard to find.

For the most accurate information you should look for scientific publications for you specific population.


What are these pathways called in Biology?

Short answer
Assuming you wish to have a common name for both of these (widely differing!) pathways I basically agree with @Chris, and I would go for general terminology, namely metabolic pathways.

Background
The pentose-phosphate pathway is neither anabolic nor catabolic so those terms won't do. The pentose-phosphate pathway is, however, closely linked to general metabolism to supply the body with C5 sugars. So metabolic pathway sounds right to me.

The other pathway is a sulfate reduction pathway, which is an anaerobic respiration pathway that uses sulfate as the terminal electron acceptor instead of oxygen. It is an entirely different pathway. However, it too is neither catabolic or anabolic, but still closely linked to metabolism. Hence, metabolic pathway is applicable here too.


What really happens when a body is tired?

Its still not clear why we need to sleep (as distinguished from the question of why our body gets fatigued in physical exertion).  A popular idea is that the brain needs to 'catch up' and reorganize itself given all the stimulus it has had from the previous day.  This 2010 National Geographic article says it all:

  I asked William Dement, the retired dean of sleep studies, a co-discoverer of REM sleep, and co-founder of the Stanford Sleep Medicine Center, to tell me what he knew, after 50 years of research, about the reason we sleep. “As far as I know,” he answered, “the only reason we need to sleep that is really, really solid is because we get sleepy.”

It is clear that we need sleep and that we become less reliable at tasks when we are sleep deprived.  eventually we become completely unable to function.

I'm not sure anyone can answer the last question - why does conscious effort help us to perform tasks?  one would have to understand/define the neurology of consciousness to answer that question.  That is still a bigger question that remains open I think.


What is the neural coding of rod and cone cells?

Indeed, brightness is a matter of photon count.

In any given rod, there are numerous photopigment molecules. There are about 1 billion rhodopsin molecules in any given rod, so although a change in conformation of any single rhodopsin molecule is a discrete event, you can consider the fraction of 11-cis- versus all-trans retinal (a photoreceptor's initial readout of brightness) to be effectively continuous, even more so because there is a <1 probability of a photon of light being absorbed by any rhodopsin molecule, so the discrete measure itself is an approximation of the 'actual' brightness/photon count.

Although it isn't perfectly analogous, because here we are talking about proportions rather than actual bitwise encoding, consider that computers are also able to represent fairly continuous values, but they are still always discrete approximations to those continuous values. A 24-bit computer monitor, for example, can actually only display 256 different intensities for each R, G, and B color stream (8 bits each).

The principle being discussed in the paper you describe is that once a rod (or cone) absorbs a photon, it loses any information about what the wavelength was, only that it was sufficient energy to activate the rhodopsin in that photoreceptor. There are several other questions and answers here on Biology.SE that discuss how wavelength (i.e. color) information can be extracted by differential activation of different cone types, for example:

Why can cones detect color but rods can't?

How do our eyes detect light at different frequencies?


Why are fruits so large compared to their seeds?

The short answer: Fruits are large compared to seeds because humans have made them large.

In the natural environment, there is a different set of evolutionary pressures. A fruit has to be able to successfully propagate itself using its seeds, while commercially farmed fruit is usually cloned via vegetative propagation. Therefore, the commercial farmed fruits do not need large seeds to propagate, since they are cloned by the farmers. In many cases, their seeds are actually nonviable (i.e. they will not grow when planted).

For example, this is a wild banana, before being selectively bred by humans. As you can see here, the seeds are enormous compared to those in commercial Cavendish bananas.

Similarly, this is a wild strawberry compared to its commercial farmed variant.

Fruits with large seeds don't appeal to consumers, and therefore farmers who sell fruits with large seeds will get a poorer return on investment.

Therefore, farmers who plant the fruits which appeal the best to consumers by being the easiest to eat (small seeds) will reap the greatest profits.


This is not a marsupial such as an opossum, since no marsupials are native to the region. It looks to be a rodent of some kind, probably a species in the Muridae family.

Which species is it is exactly is hard to tell, since there are many species in Muridae which look quite similar, but my best guess is that this is a Tamarisk jird. It could also conceivably be an escaped domestic gerbil or some type of mouse. The one that you found has more pronounced light areas on its coat than the photographs I found, but is within reasonable limits of what variation can be expected.

Here are some of the few pictures I was able to find that I could verify were of this species.

Klaus Rudloff (source)

Klaus Rudloff (source)


Can a pathogen be totally resistant to the human immune system?

I can't think of any pathogenic organisms that are completely resistant to the immune system. Some bacteria that cause chronic diseases (e.g. tuberculosis) are relatively resistant, and a handful of viruses (e.g. spumaviruses) are relatively invisible, but the nature of pathogen transmission would mean that completely resistant organisms would spread through a population pretty fast and we'd know about it.

Pathogenic prion agents, like scrapie and Creutzfeld-Jacob disease, are essentially invisible to the immune system, and can be transmitted; but they aren't pathogenic organisms. They might be the closest to your description though.


How to determine the most likely reading frame of a DNA sequence?

This is what we classify as a homework question, but as it satisfies the criterion of the poster demonstrating an attempt to answer it, I provide the following suggestion of an answer.

I assume that as it appeared in an introductory bioinformatics module the exam question is just testing reading frames (obviously) and the punctuation of the genetic code. The meaning is not entirely clear, but as one reading frame would start with the initiation codon ATG/AUG (reverse complement of: cat - 3′)† and end with the termination codon TAA/UAA (reverse complement of: 5′ - tta) that will presumably produce “the most likely protein translation”.

This is reading frame F4 in the output from EMBOSS Sixpack, below, in which termination codons are indicated by an asterisk.

      L  F  I  R  Q  R  H  A  R  H                                   F1
       Y  S  S  A  S  A  M  R  A  X                                  F2
        I  H  P  P  A  P  C  A  P  X                                 F3
    1 ttattcatccgccagcgccatgcgcgccat 30
      ----:----|----:----|----:----|
    1 aataagtaggcggtcgcggtacgcgcggta 30
       X  N  M  R  W  R  W  A  R  W                                  F6
      X  I  *  G  G  A  G  H  A  G                                   F5
        *  E  D  A  L  A  M  R  A  M                                 F4

The conceptual translation, reading N to C, is MARMALADE, which is obviously meant to be humorous and suggests that it is indeed the intended answer.

Open Reading Frames

The poster asks for clarification of the difference between reading frame and open reading frame. There is a Wikipedia entry for open reading frame but I provide an explanation of my own to relate it to the example.

There are always six reading-frames for the conceptual translation of a piece of double-stranded DNA, as shown in the example.

I would define an open reading frame as one that is not excluded from being translated by the punctuation of the genetic code. It has the theoretical potential to be translated considering only the punctuation of the code, although it may not actual be translated. It can start either with the first AUG after a termination codon (even though it cannot be certain that this is the actual AUG used) or the start of a sequenced fragment of DNA (with the assumption that an AUG is possible preceding the 5′ end of the fragment). It can end either with a termination codon or the end of the sequenced fragment (with the assumption that a termination codon will lie 5′ to the end of the fragment).

By these criteria, reading frames F1, F2, F3 and F6, above are completely open (even though the internal methionine could theoretically be an initiation codon), F5 contains the open reading frame GAHGAGG, and F4 is a complete open reading frame, perhaps excluding the termination codon (depending on your semantic definition of the precise end of an open reading frame).

† Reverse Complement

If we take a section of DNA written in the 5′-to-3′ direction — according to standard convention — and use the Watson–Crick base-pairing equivalences (A=T, G=C) to generate the complementary strand, this will be in the 3′-to-5′ direction. For the strand in the question,

5′ - ttattcatccgccagcgccatgcgcgccat - 3′

the complementary strand is:

3′ - aataagtaggcggtcgcggtacgcgcggta - 5′

As shown above.

For ease of translation manually — and for any computer program that manipulates sequences — one needs to reverse this to the  5′-to-3′ direction:

5′ - atggcgcgcatggcgctggcggatgaataa - 3′

This is the reverse complement. Now the starts of the three reverse reading frames are easy to read as:

ATG...
 TGG...
  GGC...


[Not really a precise answer (and I'm not a botanist after all).]

It's likely a lycopodiophyte. Looks like a Huperzia species, but it's impossible to tell exactly from the provided photo [if the species is not familiar, of course]. Of great help would be general appearance of the plant and form of sporangia.

You can try this key: Lycopodiaceae of North America.


Why is Cannabis Sativa considered a distinct form of Cannabis?

C. sativa was originally named by Linnaeus in 1753, long before the plant was commonly used for recreation (in Europe, at least), so the name probably reflects the fact that that species was cultivated for fiber (hemp), just as many plants have the Latin name Officinalis or officinale, meaning that they were used in medicine.  Later botanists considered other varieties to be sufficiently different to be different species or subspecies. (Including some interesting reasons based in the laws of the 1970s: https://en.wikipedia.org/wiki/Cannabis#Taxonomy )

It's also not true that all Cannabis is cultivated.  It can be found growing wild, either native or as a introduced plant, in many parts of the world.


What are the limiting factors of human stamina?

A few explanations at the cellular and molecular level:

First, for contraction to happen, muscles need signals from nerves. Replenishing the pool of neurotransmitters (used for each synaptic burst) takes a bit of time, and short-term exhaustion may happen at this level.

In the muscle cells, contraction is caused by a calcium release within the cell, from a cellular compartment called the sarcoplasmic reticulum. This reticulum can only contain so many ions, so if the muscle contracts a lot, it will eventually need to rest for a while to re-accumulate calcium in the sarcoplasmic reticulum to prepare for more contractions.

Muscles need molecular "fuel" (like ATP molecules) to contract/relax. After an intense or sustained effort, these molecules are partially consumed and the muscle simply runs out of energy; it needs a bit of time to resore the pool of metabolites needed to work properly. Conversely, muscle contraction also causes the accumulation of metabolites and ions like potassium, which partially inhibit muscle contraction. Fatigue occurs when these accumulate at high level, and they must be cleared before making new efforts.

For references see:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668469/ doi:10.1038/emm.2017.194 (general review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033663/ doi:10.1249/MSS.0000000000000923 (focuses more on muscle-neuron relationships)
https://www.ncbi.nlm.nih.gov/pubmed/9232550 Green, J Sports Sci. 1997 Jun;15(3):247-56.  (at the cellular scale)
https://www.ncbi.nlm.nih.gov/pubmed/7715628 Williams & Klug, Muscle Nerve. 1995 Apr;18(4):421-34.(more focused on calcium)