Mutation of DNA can be caused by an exogenous or endogenous source. Many external factors like irradiation or chemicals induce mutations. Some endogenous mutations arise from oxidative stress, insufficient DNA repair or spontaneous mutations on the molecular level.

There are many mechanisms for DNA repair like base excision repair, nucleotide excision repair, homologous end-joining or nonhomologous end-joining (Löffler, Biochemistry and Pathobiochemistry).
But it is more difficult for the cell to repair the mutation if it is present in both DNA strands.
According to your second question:

  DNA polymerase could just skip a section of the DNA or add in extra bases

DNA polymerase cannot reconstruct what was the original strand or the orientation of the strand. To prevent cell death, some DNA repair mechanisms include alteration in the genome. The DNA polymerase can reads through and the mutation will be replicated when the cell divides. Consequently, the key question is how the effects of the mutation influence the ability of the cell to survive.


Are there examples of animals that live in groups, where all have the same role?

Yes, there are many examples. Those species are said to be gregarious. See below for examples.
Level of sociality
When it comes to social behaviour, it is common to categorize species into one of four categories: Solitary, gregarious, presocial, and eusocial.
Note that definitions may vary among authors and that there are limit cases that make the question of categorizing much richer than the simple definitions I am using below.
Solitary
Solitary species are species where individuals mainly live alone and are independent of each other (They may still meet to mate, though).
Examples: fox, polar bear
Gregarious
Gregarious species are species that gather into a group but do not share any labour. Each individual is selfish. Such gregarious behaviour can be driven by safety (typically during migration), to taxis toward a resource, or any other reason that may cause these individuals to gather!
Note, when you say "have the same role," it is clear that different individuals may use different life strategies (like typically territorial males vs. sneaker males in birds).
Examples: wildbeest (during migration), many insects attracted to a given lightsource.
Presocial
Presocial species are species that are gregarious and have a separation of labour but no separation of the the reproductive labour.
Examples: Humans, many hymenopterans, vampire bats
Eusocial
Eusocial species are species that have a separation of labour including separation of the reproductive labour.
Examples: Termites, ants, naked mole-rat


Which Geologic time scale is the most accurate?

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".

The ICS International Chronostratigraphic Chart, ambiguously, puts "Eonothem/Eon" over both the "Precambrian" column and the "Hadean - Archean - Proterozoic" column, with the next column over being "Erathem/Era", which corresponds to what's in the other periods.

It seems clear that 1) the Hadean, Archean and Proterozoic are considered "Eons" like the Phanerozoic is (with their sub-divisions all being called "Eras"), 2) the Precambrian is a larger period of time that encompasses the Hadea, Archean and Proterozoic, and 3) there might be some disagreement as to how to name the period of time the Precambrian is; Wikipedia says "Supereon", which makes sense, but the ICS chart doesn't include that word and seems happy to have it share the name "Eon" with its immediate subdivisions. But the name is just a name, the more important things are how the different periods relate to each other, which is covered by 1) and 2).


Identifying Promoters in Non-homologous Sequences within the Same Organism

Why does the same promoter within the same organism have such varied sequences?

While there may be other reasons, the fact that the same species has several genes encoding GPD proteins is an indication that this enzymatic activity is important for different mechanisms, times or conditions. For example, I mentioned in a comment to one of your previous questions that the three GPD-encoding genes in budding yeast (TDH1, TDH2 and TDH3) are expressed during different growth phases. Therefore, although the proteins encoded by these genes might share both sequence homology and function, their promoter regions most likely will not. We even expect their promoters to be different, to allow for such differential expression. Put differently: if the three TDH promoters were all highly similar, we would expect them to also be active at the same times, effectively rendering the three genes redundant.
There is therefore no reason for assuming that promoters driving the expression of two different genes will share any homology, just because the encoded proteins happen to share function.

If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?

The only way of knowing exactly what region upstream of a gene that regulates it's expression (i.e., what functional elements that defines its promoter) is to characterize the promoter region. This is way beyond the scope of your work. What we tend to do in budding yeast when we clone an uncharacterized promoter, is to simply take 1000 bp upstream of a gene's start codon, and assume that this includes all elements necessary for proper regulation of the gene in question (e.g. possible transcription factor binding sites (TFBSs), transcriptional start site (TSS), etc). 1000 bp is a relatively safe length in budding yeast, since the distance between genes rarely exceeds this, and we tend to assume that promoter regions don't overlap neighboring genes' coding regions. But this might be different in your species. Also, if you know the location your gene's TSS, this would be a safer reference point than the start codon.

Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

My guess is that the authors that cloned the GPD promoter from Lentinula edodes either already knew that this specific gene is highly expressed and therefore selected its promoter; alternatively they might have cloned all GPD promoter variants, and then simply published the one that they saw worked best.
If you don't have any information about the expression of the GPD-encoding genes from your species, any decision as to which promoter to choose will inevitably be more or less guesswork. It seems to me that the evolutionary distance between Lentinula edodes and Psilocybe cubensis is way too large to make any direct inferences. Nevertheless, with the lack of better options here is what I suggest:

Try to identify which of Psilocybe cubensis's GPD proteins is most similar (in terms of sequence homology) to the protein the authors chose for their Lentinula edodes GPD promoter. This might indicate that these are direct orthologs, and with a bit of luck may also share similar relative expression patterns and/or levels. You could also do a similar matching with the Tdh3 protein from budding yeast, since TDH3 is indeed a very strong promoter (article behind paywall, but easy to find elsewhere). If you still don't know which of the promoters to choose, proceed with both candidates and see which one works best (although that means doubled cost and effort).

Once you have identified your candidate GPD gene, you define an appropriate region upstream of your gene’s coding region as the promoter region. This can be arbitrarily picking 1000 bp, or the entire intergenic region, as @Cholpisit suggests.

Design your primers for cloning this region into your target vector, upstream of GFP.


How important is getting enough glucose for maximal brain performance / cognition?

In short: skipping a meal lowers blood glucose levels, which can reduce cognitive performance, for example, memory.

Let's say that between meals you are in fasting state for 8 hours during which you do some desk work and some moderate exercise for 1.5 hours. With such level of physical activity, your last meal and your glycogen stores should provide enough glucose for all your body needs, including the brain. So, during this time, you do not need any ketones or lactate as additional source of energy. According to Medical Hypotheses, 2014:

  Estimated amount of glycogen in the human organism is about 200–500 g,
  and in certain specific conditions could reach up to 1.0 kg, which
  seems to be optimal for human organism. This amount is definitely
  sufficient for keeping optimal concentration of glucose in the blood
  during usual fasting periods not exceeding 24 h (between meals, during
  sleep, in case of exercise, etc.)

Skipping a meal can lower your blood glucose levels. According to WebMD:

  Normal blood sugar levels are less than 100 mg/dL after not eating
  (fasting) for at least eight hours. And they're less than 140 mg/dL
  two hours after eating.

  During the day, levels tend to be at their lowest just before meals.
  For most people without diabetes, blood sugar levels before meals
  hover around 70 to 80 mg/dL. For some people, 60 is normal; for
  others, 90 is the norm.

Blood glucose fluctuations related to meals:

Image source: Wikipedia, Creative Commons License

In some studies (AJCN, 1998), skipping breakfast was associated with lower blood glucose levels and worse memory test but not intelligence test results:

  This article compares the findings of three studies that explored the
  role of increased blood glucose in improving memory function for
  subjects who ate breakfast. An initial improvement in memory function
  for these subjects was found to correlate with blood glucose
  concentrations. In subsequent studies, morning fasting was found to
  adversely affect the ability to recall a word list and a story read
  aloud, as well as recall items while counting backwards. Failure to
  eat breakfast did not affect performance on an intelligence test.


How does de-myelination occur in multiple sclerosis?

T-cell migration to the brain is very limited and occurs at a very low level in healthy conditions, however during diseases the number of T cells passing through the blood-brain barrier is elevate due to increased expression of traffic signals and adhesive molecules.
I've found two good articles on how T-cells migrate through blood-brain barrier:

J Neural Transm (2006) 113: 477–485
Molecular mechanisms involved in T cell migration across
the blood–brain barrier, B. Engelhardt

and
 D. W. Miller, “Immunobiology of the blood-brain barrier.,” J. Neurovirol., vol. 5, no. 6, pp. 570–578, 1999.

During T-cell maturation, those that react too heavily to antigens of the body are killed to avoid having T-cells that would kill the body's own cells. But in rare cases this process fails and auto-reactive T-cell get released from the thymus (This short paper is good for starters). So the (simplified) reason why T-cells attack oligodendrocytes is that they falsely recognize them as pathogens, and therefore kill them. The loss of oligodendrocytes results in loss of myelin sheats.

Also in this paper (it holds many info on demyelination and multiple sclerosis) it is shown that even non-specicfic T-cells can open the way for antibodies through the blood-brain barried, and this results in extended demyelination.


How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?

Specific antibodies are typically detected using ELISA.

The way you make a test for an antibody to a particular pathogen is not by using secondary antibodies to the specific part of the target antibody, but by using the antigen.

Different kits work differently, but the general idea is that you have antigen stuck to a surface, you put the sample on that surface. If there are antibodies to the antigen, they stick to it. Then you wash everything away and add a tagged antibody that binds to generic human antibodies.

See also https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic


Yes, the human body "converts" water.

Out of the hundreds of chemical reactions going on in the human body, there are reactions which take water as an input and "react it away" into something else. There are also reactions which create water out of other molecules.

Example 1: Hydrolase reactions. They have the form of

  A–B + H2O → A–OH + B–H

You get water as input, and something else as output.

Example 2: Peroxidases "defuse" the highly reactive hydrogen peroxide, producing water. For example, look at the L-ascorbate peroxidase, which catalyzes

  L-ascorbate + H2O2 → dehydroascorbate + 2 H2O

Beside these reaction, there is also a lot of water which doesn't react and is simply excreted after having served its purpose. So, while some water is "converted", some other part "passes through".

The reactions are balanced in such a way that normally, you excrete the same amount of water as you drink, as explained in Amory's answer. But despite this balance of the amount, you cannot claim that the water just passes the body unchanged. Some molecules of it are used up, and others are created de novo.


When forming an enzyme-substrate complex in a spontaneous reaction, why free energy increases?

This increase is the activation energy:

https://en.wikipedia.org/wiki/Activation_energy


How are DNA polymerase error rates measured?

According to their website New England Biolabs use a version of the approach pioneered by Wayne Barnes, as described in:

  Kermekchiev, M.B., Tzekov, A and Barnes, W.M. (2003) Nucl. Acids Res. 31, 6139–6147

This is basically an assay for the mutation rate in a PCR-amplified lacZ (β-galactosidase) gene, assayed by transforming E. coli, plating on the chromogenic β-galactosidase substrate Xgal, and then scoring white colonies as mutated genes. Also according to NEB, Agilent Technologies use a similar mutational assay, but based upon the lacI (lac repressor) gene.


Why is haemophilia unviable in later stages of life?

I think what they mean is that those affected with haemophilia rarely survive to the adult life. This is less of a constraint for women, since a woman carrying only one recessive gene will not be affected by this disorder.


Why do hot water baths affect only males' fertility? Why not females'?

Well, the answer by @An J has already explained the prima facie of your question which is: sperms need lower temperature for development. But I will be explaining in my answer: Why do the sperms actually need a lower temperature for their development?

This is a debatable subject, but there have been several models or hypothesis about this. I found this literature on it, and it summarises the thing excellently. Hope it helps:

  Throughout the Cenozoic, the fitness benefits of the scrotum in placental mammals presumably outweighed the fitness costs through damage, yet a definitive hypothesis for its evolution remains elusive. Here, I present an hypothesis (Endothermic Pulses Hypothesis) which argues that the evolution of the scrotum was driven by Cenozoic pulses in endothermy, that is, increases in normothermic body temperature...

  The model argues that stabilizing selection maintained an optimum temperature for spermatogenesis and sperm storage throughout the Cenozoic at the lower plesiomorphic levels of body temperature that prevailed in ancestral mammals for at least 163 million years. Evolutionary stasis may have been driven by reduced rates of germ‐cell mutations at lower body temperatures...

  The fitness advantages of an optimum temperature of spermatogenesis outweighed the potential costs of testes externalization and paved the way for the evolution of the scrotum. The scrotum evolved within several hundred thousand years of the K‐Pg extinction, probably associated initially with the evolution of cursoriality, and arguably facilitated mid‐ and late Cenozoic metabolic adaptations to factors such as climate, flight in bats and sociality in primates.

About the function of the scrotum from the article

  The scrotum is a sac‐like thermoregulatory structure that houses the testes at a temperature lower than the core body temperature (Tb; Moore, 1926; Wislocki, 1933; Ruibal, 1957; Setchell, 1998). The cremasteric muscles in the scrotum contract and relax to draw the testes closer to or allow them to dangle further away from the body in order to maintain the testes at an ‘optimal’ temperature for spermatogenesis (sensu Moore, 1926; Tsperm) and sperm storage of 34–35 °C (Setchell, 1998; Gallup et al., 2009; Mawyer et al., 2012). In humans, the scrotal temperature is maintained about 2.7 °C lower than the Tb (Momen et al., 2010). Notwithstanding the relative fitness benefits of a cooled epididymis vs. the cooled testis, four nonmutually exclusive hypotheses currently dominate explanations for the evolution of the scrotum: the Cool Spermatogenesis Hypothesis (Moore, 1926), the Galloping Hypothesis (Frey, 1991), the Mutation Hypothesis (Short, 1997) and the Activation Hypothesis (Gallup et al., 2009).

Cool Spermatogenesis Hypothesis

  ...argued that Tsperm and the maintenance of sperm viability during storage in the epididymis is about 34–35 °C (Moore, 1926; Appell et al., 1977). Scrotal temperatures that approach those of the core Tbcompromise fertility (Moore, 1926; Bedford, 1978b, 2004; Setchell, 1998), particularly if evaporative cooling of the scrotum is impaired (Momen et al., 2010).

The Galloping Hypothesis

  ... (Frey, 1991)proposes a trade‐off between testes vulnerability (fitness cost) and the avoidance of strong intra‐abdominal pressure fluctuations during galloping which impair spermatogenesis in abdominal testes (fitness benefit).

The Mutation Hypothesis

  ... maintains that the testis is a ‘hot spot’ for germ‐cell mutations and that the lower temperatures of the scrotum reduce the rates of mutation on the Y chromosome through mutagenic metabolites (Short, 1997).

The Activation Hypothesis

  ... storage of sperm at a lowered temperature ensures that they undergo ‘thermal shock’ during ejaculation into the higher temperatures of the female, which increases their motility and hence the probability of a successful insemination (Gallup et al., 2009).


A question about cancer antigens and their mechanism

This is a hard question to answer because each type of cancer is a whole different game at the molecular level, however there is something you might be interested in called "hallmarks of cancer" (image 1) which are key features for cancer to thrive. They were originally described by Hanahan and Weinberg (2000) and have been revisited by Fouad and Aanei (2017) in an updated review. The hallmarks of cancer aren't specific genes themselves, but rather broader categories that englobe certain types of genes.

If you want to look at specific genes, we could talk a bit about what more purely data driven approaches have found. There is a very interesting work by Kandoth and collaborators (2013) that presents data from The Cancer Genome Atlas (TCGA), which is a database of different kinds of genomic features from several different cancer types. Among the results of this work (specifically on figure 2 which I include here as Image 2) you can see a table of 127 significantly mutated genes across 12 different cancer types. One gene that is well known in medical literature for being frequently mutated in almost any cancer type (situation which is also observed in the aformentioned table) is TP53 which encodes a protein that is key for genome maintenance in normal cells by participating in DNA damage and repair (which is a cancer hallmark under the "altered stress response" category). In the table you can also spot tissue-specific cancer genes such as APC in colon/rectum cancer and VHL in renal cell carcinoma.

Just to make sure you can understand the table, the gene names are presented in the right (rows) and the names of the cancer types are presented at the top (columns). The description for the cancer types abbreviations can be found here. To the left of the table there is a functional classification of the genes so you can know more or less what a given gene does in a quick manner. The values presented are simple frequencies (divide the number of samples of a particular cancer type that have the mutation over the total number of samples of that same cancer type) expressed as percentages (so they are already multiplied by 100). The final column (Pan-Cancer) shows the same idea, but taking all samples from all cancer types into consideration for the frequency calculation.

So for answering your question regarding if there is a common feature in all types of cancers: strictly speaking at the gene level no, since even the TP53 mutation which is the most common amongst all cancers might not be present in some cancers; however, looking at it by categories of genes (as one or some of the 7 hallmarks) reveals that all cancers apply similar strategies to thrive (they exhibit different mutated genes, but these genes frequently belong to the same biological pathways and participate in similar functions). I hope you find this useful (:

Image 1: 7 hallmarks of cancer (2017 review).

Image 2: frequency of mutation by gene and cancer type.

References:

Fouad, Y. A., & Aanei, C. (2017). Revisiting the hallmarks of cancer. American journal of cancer research, 7(5), 1016–1036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5446472/
Kandoth, C., McLellan, M. D., Vandin, F., Ye, K., Niu, B., Lu, C., … Ding, L. (2013). Mutational landscape and significance across 12 major cancer types. Nature, 502(7471), 333–339. doi:10.1038/nature12634
National Cancer Institute. TCGA Study Abbreviations. Retrieved from https://gdc.cancer.gov/resources-tcga-users/tcga-code-tables/tcga-study-abbreviations


Why doesn't HDL cause diseases like LDL?

Thank you for the fascinating question! It was tough to research but very worthwhile.

LDL is actually not such a bad molecule. It is formed from VLDL/IDL after VLDL/IDL distribute triglycerides, phospholipids, cholesterol and cholesterol esters to peripheral cells. With less to give, LDL subsequently tries to be helpful by providing any needy peripheral cell with leftover cholesterol necessary for plasma membrane synthesis and other cellular functions. In fact, even endothelial cells, which line the vasculature, have LDL receptors to welcome any cholesterol packages from LDL. Another function of LDL is to make HDL even ‘healthier’ by removing cholesteryl ester from HDL molecules in the periphery and returning it to the liver.

Remember that LDL does not contain exactly the same components as its precursors. LDL does not have the ApoE & C proteins that VLDL and IDL have. LDL has only ApoB-100 and a concentrated level of cholesterol. LDL-family receptors generally recognize ApoE and ApoB, which are located on VLDL and IDL, thus easily pulling them into the liver out of the bloodstream, via endocytosis. Because LDL contains only the ApoB protein, it is less easily recognized. Thus, more LDL lingers in the blood. This is supported by the lengths of their half-lives--- with VLDL and IDL half-lives being about 6 hours and LDL half-life being about 3 days.

Where disease comes in is with an imbalance of fat in our diet. This is explained in detail by this extensive article on Managing Dyslipidemia: The Triglyceride/High-Density Lipoprotein Axis. The article explains that disease cannot solely be blamed on LDL alone. A high fat diet leads to elevated triglycerides in the blood stream, which increases blood viscosity, interference with endothelial function, stimulation of arterial inflammation, and interference with normal blood coagulation. These conditions can predispose to atherosclerotic lesions. In addition, there is an up-regulation of protein ApoC-III, which subsequently increases the half-lives of VLDL and IDL particles. It even increases the activity of an enzyme called cholesteryl ester transfer protein (CETP), which can exchange cholesteryl ester in HDL and LDL for triglycerides in VLDL and IDL, and vice versa. This leads to change in composition of HDL and LDL, making them more triglyceride-rich, physically smaller, and less interactive with their respective membrane receptors. With HDL even smaller, it is also easily filtered through the kidneys, leading to lower levels. All this means there is more circulating LDL in the blood.

LDL enters the endothelium via breaks in the endothelial wall created naturally (by dying or dividing cells) or through injury (by inflammatory processes including infections, chemical exposures) or it leaks in through junctions between endothelial cells when there is high intraluminal pressure (such as in hypertension). From there, LDL can become oxidized and ingested by macrophages, forming foam cells, which can rupture spewing its contents into the surrounding arterial wall, leading to the beginning of atherosclerotic lesion.

Why can’t HDL cross through endothelial wall, too? Actually, it can! According to the above-mentioned article, “HDL particles [in its native form] appear to have the potential to delipidate cholesterol from foam cells” at the site of a lesion. With HDL being smaller, it can enter the endothelium to interact with foam cells. Its interaction, however, is the opposite of LDL. Cholesterol is transferred back from the foam cell to HDL, reversing the oxidized LDL-induced process. In addition, “HDL protects LDL from oxidation by [using] metal ions” before oxidized LDL can lead to further damage. This mechanism is still unknown.

Why can’t HDL become oxidized, too? Indeed, this can also happen! However, it appears again than oxidized HDL behaves oppositely to oxidized LDL. “Oxidative tyrosylation of high density lipoprotein by peroxidase enhances cholesterol removal from cultured fibroblasts and macrophage foam cells [5].” There is a caveat though. This function seems to depend on how HDL is oxidized. If oxidized by copper or hypochlorous acid, HDL “loses its ability to remove cholesterol from cultured cells [6].”

In short, given the very same conditions including oxidative environment and entry into the endothelial cell, HDL inherently behaves oppositely to LDL. This likely is related to their inherently different composition, but we have yet to understand how this occurs at a molecular level. However, HDL could technically be 'bad' under the right oxidative conditions. In the end, LDL is given a bad reputation because its relatives IDL/VLDL easily escape into other cells via receptors and HDL concentration is lowered partially by renal filtration.

References:

Mera, Steven L. Understanding Disease: Pathology and Prevention.
http://www.ncbi.nlm.nih.gov/pubmed/19592615
http://www.nature.com/nrmicro/journal/v8/n2/fig_tab/nrmicro2269_F1.html
Libby, P (2006). "Inflammation and cardiovascular disease mechanisms". American Journal of Clinical Nutrition. 83(suppl) (2): 456S–460S. 994471841.
http://www.medscape.org/viewarticle/582014
http://atvb.ahajournals.org/content/23/9/1488.full#ref-16


Are there known genome sequencing issues in E. coli?

Generally, gaps in genomes occur due to failure of de novo assembly -- the DNA can be sequenced accurately, but cannot subsequently be placed into a contiguous assembly due to alignment ambiguity with adjacent sequences.  In eukaryotes, telomeres and centromeres are difficult to assemble from short reads because they are highly repetitive. In bacteria, repetitive regions of the genome can cause similar problems when assembling from short reads.  Such regions include CRISPR arrays, integrated mobile elements (e.g. transposons), and gene duplications.1,2
So, what made a short-read no-gap assembly of E. coli strain C difficult, specifically? Alignment of the original short-read assembly 3 to the long-read reference 4 with Mauve 5 gives positions and length of gaps.

The first gap in the ordered short-read assembly (left-most red line in the figure) occurs at position 15,085 in the first contig and is 320 bp long. Looking at the same region in the long-read assembly, this closely corresponds to a 236 bp tandem repeat (CTGG × 59) at position 14,848. The authors of the short-read paper used 150 bp paired-end MiSeq reads to create their assembly, which, after adapter trimming, would likely not give enough sequence context flanking the repeat region to span it with a single read, thus creating a gap. This is just one example, and the rest of the gaps could also be repeats or other aforementioned mobile elements.

Treangen TJ, Abraham AL, Touchon M, Rocha EP. Genesis, effects and fates of repeats in prokaryotic genomes. FEMS Microbiol Rev. 2009 May;33(3):539-71.
Ricker N, Qian H, Fulthorpe RR. The limitations of draft assemblies for understanding prokaryotic adaptation and evolution. Genomics. 2012 Sep;100(3):167-75.
https://www.ncbi.nlm.nih.gov/nuccore/MNKV00000000
https://www.ncbi.nlm.nih.gov/nuccore/CP029371
Darling AC, Mau B, Blattner FR, Perna NT. Mauve: multiple alignment of conserved genomic sequence with rearrangements. Genome Res. 2004 Jul;14(7):1394-403.


What is the difference between monoecious and homothallic?

The difference is that they come from different scientific traditions and describe the same idea for different kinds of organisms. Homothallic is applied to fungi and algae, whilst monoecious is applied to plants (and sometimes invertebrates). This use of different words to describe the same phenomena in different types of organisms is unfortunately quite common. You could also had hermaphrodite as another example for organisms with both male and female reproductive parts. One can point to crude phenotypic differences to justify the distinction in terms but the underlying concepts are the same.

I note as well that the separation into different types of organism used is usually based on older classification systems rather than reflecting any biological reality.


What is the precise mechanism by which exercise reduces chance of cancer?

Vigorous exercise (even for five minutes) causes increased DNA damage http://www.ncbi.nlm.nih.gov/pubmed/20839226. The increased DNA damage would stimulate the defenses including the immune system (e.g. natural killer cells) http://www.ncbi.nlm.nih.gov/pubmed/16618710, and the boosted immune system would eliminate cancer cells, reducing cancers based on the immune suppression model of cancer http://www.ncbi.nlm.nih.gov/pubmed/27928220. The reduction of cancers with increased exercise (physical activity) has indeed been observed http://www.ncbi.nlm.nih.gov/pubmed/18506190.


Haidinger's brush: Is this a by-product of the eye's physics, or are there any evolutionary grounds for it?

According to the link you provided, the phenomenon Haidinger's Brush seems to be associated with the macula of the retina. The yellow color of the macula may explain the yellowness of Haidinger's Brush. This suggests to me that the brush may be an artifact of the structure of the eye, and others have claimed that Haidinger's brushes probably do not have any ecological significance (Greenwood et al. 2003). If the brushes do not have an ecological significance, then they are very unlikely to have any evolutionary significance.

The brushes may be visible to other primates, such as Macaques (Snodderly et al. 1984), as they have a macula structure very similar to the human macula. This leads me to think the phenomenon would also be potentially visible to other primates such as chimps and gorillas. If so, then our nearest ancestor (forebearer) that could potentially see the brushes would be the common ancestor of humans and chimps.

For a broader review of polarized vision and underlying evolutionary hypotheses, the paper you linked to by Cronin et al. (2003) is a good review. I also came across a book, Polarized Light in Animal Vision. Polarization Patterns in Nature. by Gábor Horváth and Deszö Varjú and published by Springer. The front matter and table of contents are available here.  It appears to be a very thorough review of polarization vision in animals.

Literature Cited

Cronin, T.W. et al. 2003. Polarization vision and its role in biological signaling. Integrative and Comparative Biology 43: 549-558.

Greenwood, V.J., et al. 2003. Behaviorial investigation of polarisation sensitivity in the Japanese quail (Coturnix coturnix japonica) and the European starling (Sturnus vulgaris). Journal of Experimental Biology 206: 3201-3210.

Snodderly, D.M., J.D. Auron and F.C. Delori. 1984. The macular pigmnent. II. Spatial distribution in primate retinas. Investigative Ophthalmology and Visual Science 25: 674-685


How does hypochlorous acid inactivate viruses?

The other answer by @CMosychuk talks about the general aspect related to use of hypochlorous acid. I will discuss here its molecular mechanism of action.

Hypochlorous acid (HOCl) is a very powerful oxidizing agent. In aqueous solution, it dissociates into H+ and OCl- as:

$$\ce{HOCl \leftrightharpoons H^+ + OCl^-}$$

However, HOCl also destroys viruses by chlorination. It acts on anything, from lipids to nucleic acids. For example, Hawkins et al ,2002 describe in detail the effects of HOCl on nucleic acids. HOCl, by direct chlorination, leads to the formation of chloramines, and ultimately nitrogen-centered radicals. These radicals often react with each other to form dimers. Also, they have reported formation of single- as well as double-stranded breaks on application of HOCl on plasmid DNA. See this image:

These reactions render the nucleic acid useless and the virus harmless. In a similar manner, HOCl also reacts with polypeptides, ultimately leading to their fragmentation. See these images (from here):

Also, as mentioned in the other answer, application of HOCl has been shown to promote denaturation and aggregation of proteins. The linked paper also talks about HOCl's effects on other biomolecules, such as carbohydrates, but those effects would be out of scope here.


What Biology topics are linked to the Nitrogen Cycle?

The nitrogen cycle is a highly biological process. Nitrogen gas is ~75% of the earth's atmosphere and N2 is the most chemically stable form of Nitrogen for conditions in the Earth's crust.

Nitrogen is one of the four most essential and universal elements to terrestrial life (Carbon Hydrogen and Oxygen being the others).  Nitrogen fixation, the name given to the various processes which make chemically reactive forms of Nitrogen available to living things. Ammonia (NH3 / NH4+) and Nitrites / Nitrates (NO2-, NO3-) are chemically unstable compared to N2 and the conventional biosynthetic processes in the cell can use any of these forms to make proteins, nucleic acids and other biologically active molecules necessary for life.

Ammonia and similar compounds like Urea come from the biological byproducts of  living cells - waste.  These are readily recycled in the soil by plants and microorganisms and I imagine some animals and insects.  Nitrogen is a limiting resource for living things and most biomes are pretty efficient at recycling reduced nitrogen from primary (NH3) secondary (NHR2), tertiary (NR3) and quaternary amines (NR4).

But the biosphere has a great demand for bio-useful nitrogen and in most places on earth in deep water and soil microorganisms can break down N2 directly into nitrates/nitrites. This happens deep underwater or underground because the enzymes which perform this activity are delicate and ruined by O2.  This process is entirely performed by anaerobic microorganisms. In recent decades, the ecological importance of subterranean microbial communities has become better appreciated for the complex structure and ecological roles it plays.

An interesting side note to this is that up to the early 20th century, the growth of life and human civilization was really limited by the intense labor required to grow food.  While hydrogen oxygen and carbon are essentially free - obtained from water, atmospheric oxygen and CO2 by plants, Nitrogen was the limiting factor in many cases to growing more crops or animals for food.

The Haber process, which converts nitrogen and hydrogen gas under high temperature and pressure into ammonia over a catalyst was such an important discovery - it allowed the industrial preparation of effective fertilizers and was instrumental in creation of the green revolution.


Do electron microscopy change the structure of the specimen due to the vacuum step?

There are several different ways to deal with the difficulties of imaging biological samples in vacuum. I'll go over the ones I'm familiar with.
TEM - plastic sections
The water in the specimen is gradually replaced with a resin which then solidifies, and slices about 100 nm thick are cut from the specimen and put into the TEM column at high vacuum. The chemical composition of the specimen is radically altered, but the shape of cells and even the arrangement of organelles inside can be preserved if the treatment is done well. Here's a representative image for this technique from http://www.cellimagelibrary.org/images/7722. You can see the endoplasmic reticulum with ribosomes and mitochondria.

TEM - CryoEM
The specimen is cooled so fast that the water in and around it solidifies without forming ice crystals, which would otherwise disrupt membranes, etc. The specimen is nearly identical to its natural state. These 'vitrified' specimens can be put directly into the microscope column, but they need to be maintained at liquid nitrogen temperatures. The size of specimen that can be cooled rapidly enough is limited to about 300 microns thick. A standard TEM beam doesn't penetrate well through samples more than about 200 nm thick; cryo specimens can be cut similar to plastic sections (though it's much harder than at room temperature), or by focused ion beam milling. Here's a representative image from https://www.pnas.org/content/117/16/8941 showing flagellar motors:

Environmental SEM
Larger specimens can be imaged without dehydration or coating in an environmental SEM (ESEM). This microscope has a high-vacuum chamber for the electron gun and lenses, and a low-vacuum chamber containing the specimen and detectors. This method can image larger samples, up to about 10 mm, close to their natural state, but isn't as high-resolution as the TEM methods. Here's an image from https://forschungsinfrastruktur.bmbwf.gv.at/en/fi/fei-esem-xl30-scanning-electron-microscopy_540 showing a small fish, you can judge for yourself how well the structure is preserved:


Are all non-breeding naked mole rats the same sex?

Naked mole rat colonies contain individuals of both sexes, with one breeding female and one to three breeding males, and the rest non-breeding individuals of both sexes.

The other individuals in the colony have an additional caste system that seems to depend on size but not sex (i.e., there does not seem to be a hierarchical relationship between non-breeding males and females).

Non-breeding females, but not males, have suppressed reproductive tracts. In the absence of a queen, some non-breeding females' reproductive systems will begin to activate, until one becomes dominant and the others return to being non-breeders.

References

Clarke, F. M., & Faulkes, C. G. (1997). Dominance and queen succession in captive colonies of the eusocial naked mole–rat, Heterocephalus glaber. Proceedings of the Royal Society of London B: Biological Sciences, 264(1384), 993-1000.

Jarvis, J. U. (1981). Eusociality in a mammal: cooperative breeding in naked mole-rat colonies. Science, 212(4494), 571-573.


What prevents backflow of blood from right atrium to vena cava during atrial systole

Pressure differences. Atrial contractions are much more gentle than ventricular ones, and in normal circulation the venous pressure in the vena cava often stays higher than the right atrium, even during atrial systole. If the pressure in the atrium does rise above the vena cava pressure at the peak of systole, there can be some backflow, although it is slight and brief in normal physiology.

The major veins are typically somewhat distended so they are constantly pushing blood into the right atrium. Blood continues to flow from the veins into the right atrium and from the right atrium into the right ventricle throughout ventricular diastole, including during most of atrial systole.

References:

Anderson, R. M. (1993). The gross physiology of the cardiovascular system. Robert M. Anderson.

Wexler, L., Bergel, D. H., Gabe, I. T., Makin, G. S., & Mills, C. J. (1968). Velocity of blood flow in normal human venae cavae. Circulation Research, 23(3), 349-359.


Human perception of time depending on age

This is not really a biological answer, but a psychological one:

One important fact to consider is that the perception of time is essentially a recollection of past experience, rather than perception of the present.

Researchers who study autobiographical memory have suggested that part of this effect may be explained by the number of recallable memories during a particular time period. During one's adolescence, one typically has a large number of salient memories, due to the distinctness of events. People often make new friends, move frequently, attend different schools, and have several jobs. As each of these memories is unique, recollection of these (many) memories gives the impression that the time span was large.

In contrast, older adults have fewer unique experiences. They tend to work a single job, and live in a single place, and have set routines which they may follow for years. For this reason, memories are less distinct, and are often blurred together or consolidated. Upon recollection, it seems like time went by quickly because we can't remember what actually happened.

In other words, it can be considered a special case of the availability heuristic: people judge a time span to be longer in which there are more salient/unique events.

Incidentally, (and to at least mention biology), episodic memory has been shown to be neurally distinct from semantic memory in the brain. In particular, a double dissociation has been shown for amnesics who suffer from semantic or episodic memory, but not both.

My apologies for the lack of citations, but a good bit about autobiographical memories can be found in:

  Eysenck, M.W., & Keane, M.T. (2010). Cognitive Psychology: A
  Student's Handbook.

You may also be interested in some responses or references to a related question on the Cognitive Science StackExchange:

Perception of time as a function of age


What causes tissues manifest the various forms that they do?

This is a subject of active research. All the cells in the zygote are identical up to 8 cell stage. At the next division resulting in 16 cells formation it is called a morula.
The zygote has totipotent cells meaning each cell has the ability to develop into full organism by itself if it separates from the zygote (this is how identical twins are born).
Human zygotes are totipotent till at least 4 cell stage. In other primates experiments have demonstrated totipotency upto 16 cell stage.
The totipotent cells differentiate into pluripotent cells and then into various distinct cells belonging to different systems. This process is very complex and a lot of embryological factors and chemicals come into play.
The embryonic factors cause migration (called embryotaxis) and differentiation of the embryonic cells. Some of the factors are sonic hedgehog, wnt, insulin like growth factors, Hox, etc...
Different factors cause differentiation into different cell lines. These factors also cause the organs to attain specific shape and structure, thus the heart is shaped as a heart and the liver is shaped as a liver and so on.
Once the cells differentiate into a particular line, the stem cells of that region generally differentiate into that particular line due to the paracrine influence in that locus, even though these stem cells can differentiate into other cell lines when appropriately stimulated (thus demonstrating pluripotency). So intestinal stem cells would differentiate into goblet cells, surface epithelial cells, Enterochromaffin cells, etc... which are present in that locus.

For more see here:

http://www.sciencedirect.com/science/article/pii/S009286740800216X
http://www.embryology.ch/anglais/iperiodembry/controle01.html
https://www.bio.cmu.edu/labs/ettensohn/pdfs/dvg22746-2.pdf


Why are de novo genetic mutations usually NOT inherited?

A germ line mutation will be passed to the offspring only if

the individual reproduces
the individual reproduces after the mutation has occurred in the germline. Indeed if the mutation appears in the testes 5 years after the individual has reproduced then the offspring will never carry this mutation. Note that female mammals make a big storage of ovules early in life while mammal males do not. As a consequence the number of new mutations transmitted to offspring is age-dependent in males but age-independent in females. See this post for more info
the gamete that is transmitted is descendent from the individual cell who had the mutation. There is of course many lineages of gametes and their pattern ancestry will affect what fraction of gametes carry a given mutation.
the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis). Of course, there is always segregation who decreases the probability of a new mutation to be transmitted by half.

Of course, there are also all the mutations occurring outside the germ lineages (somatic lineages) which won't be transmitted but you specifically asked for germ line mutations.


Short answer

As said @Biogirl, "This pedigree can not lead to one absolute answer". We miss information in order to answer this question.

Long answer

Should we make the assumption that the allele causing the disease (A) necessarily come from the lineage you draw or can it come from the partners of the second generation (offspring of GrandParents)?

Then, depending on your answer to this question...

If yes (= if the allele causing (A) comes from the GrandParents):

This genealogy is impossible if the type of inheritance is as simple as you suggested (either recessive or dominant, no epigenetics, no epistasis, no effect of the environment, no protein-mediated disease via the vomb,... even if it can be autosomal, sexual or mitochondrial genes)

If no (= if the allele causing (A) do not come from the GrandParents only)

Everything is possible (from the space of possibilities that you suggested)

some possibilities would be more probable than others (depending especially on the allele frequencies)


Predicting progeny of recessive mutations using recombination

First, the recombination equation is:

cM = recombinants/(recombinants AND parentals) * 100

Let's assign the following genotypes for clarity's sake:

RR = black bristles
Rr = black bristles
rr = red bristles
SS = pebbly eyes
Ss = pebbly eyes
ss = shiny eyes

F1 cross: rrSS x RRss = RrSs (all progeny)
F2 cross: RrSs (F1) x rrss = ?

You would have the following gametes:

Parent 1, RrSs = RS, Rs, rS, rs
Parent 2, rrss = rs, rs, rs, rs

Draw your punnet square and you get the following genotypes of the offspring.

So your GENOTYPES of your F2 cross will be RrSs, Rrss, rrSs, rrss

Let's translate those to phenotypes.

RrSs: black pebbly (parental)
Rrss: black shiny (recombinant)
rrSs: red pebbly (recombinant)
rrss: red shiny (parental)

Now let's look at recombination frequency.

15cM = (recombinants/(recombinants+parentals)*100
recombinants/(parentals+recombinants) = 15/100

This tells you for every 15 recombinants, you have 85 parentals. If you scale this up to 1000, that's 150 recombinants for every 850 parentals.

Your 150 recombinants comes from 75 black/shiny and 75 red/pebbly.

Your 850 parentals ceoms from 425 black/pebbly and 425 red/shiny.

Anyways that was my attempt which appears to be directly opposite to what your answer key says. Did you copy it down correctly?


Area under the curve in a drug concentration curve

This definition of AUC is non-standard.
The usual definition does not involve the MIC or 24h: it is the area (~ integral) of the plasma concentration curve as a function of time, from first administration time $t_0$ time to infinity. (You will sometimes see it subscripted as $\mathrm{AUC}_{0 \to \infty}$)
In the case of so-called time dependant antimicrobials (beta-lactams, macrolides, vancomycin), the bacteria are inhibited from replicating as long as the concentration stays above the MIC (minimal inhibitory concentration). Often a second threshold, the MBC (minimal bactericidal concentration) is defined corresponding to the required concentration to kill rather than just inhibit replication.
As you stated, the second strategy has indeed a longer duration above MIC. It is more effective from a purely kinetic standpoint. Whether than translate to clinically relevant effects depends on the antibiotics, the bacteria and the tissue under consideration.
A second point is whether a higher AUC is beneficial if the time spent above MIC or MBC is the same (nb: not the case here). However this also depends on factors beyond just pharmacokinetics.
As an aside, some antimicrobials like the aminoglycosides display a "concentration dependant" effect where the peak drug concentration determines the effect, dictating different dosing schedules.


This may be, though not sure, one of the supporting bones of the dorsal spine of the black drum,

Pogonias cromis also known as drum or drummer.
It is the only species in the genus Pogonias.
Reference

Freshwater drums are native to Ohio, preferring habitats of deeper pools of rivers and in Lake Erie with clear water and clean bottoms. They spawn from April to late summer.
Reference

Pogonias courbina is distinguished by the following characters: the occurrence of character-
istic thickening of the dorsal spines VII to XI in all specimens larger than 250 mm SL; all pter-
ygiophores in the dorsal-fin laminar, thin; anal-fin pterygiophores slender excluded those of
spines; lateral projections of gas bladder with few finger-like projections; genetic distance
between both species 1%

An important site that helped me to identify this-
https://txmarspecies.tamug.edu/otherdetails.cfm?scinameID=black%20drum%20pterygiophore


Where can I find comprehensive data on animal distribution?

I like your question a lot! I think what you're trying to achieve is the best way of solving your problem. Unfortunately, although I do have a few links for you that might get you a little bit further, a perfect solution is, I fear, not available. Tides are extremely complicated and depend on many factors. Some of these are large scale effects such as the relative positions of earth, sun and moon, but others are more local, such as ocean currents or the shape of the coast. Especially the latter can make a surprisingly large difference on a relative small spatial scale. Luckily, it is possible to come a long way and have very decent approximations.

The best option, as far as I'm aware, is to use XTide, a software program that can calculate tides at thousands of locations worldwide, making use of actual measurements as well as mathematical models. This will give you by far the largest amount of information, and the most detailed information. better still, it's open source software and completely free. The drawback is that it is complicated to use. Also, if you are a windows user, it is even more tricky as this is an X-windows program, developed for UNIX and UNIX-like operating systems (it should run fine on linux and macos). It is definitely possible to run it on windows, but I wouldn't recommend it for the faint of heart.

My second option would normally be to use rtide, an add-on package for the statistical program R, though in your specific case it's probably not good enough. The rtide package is fairly easy to use if you're familiar with R, and runs equally easily on all operating systems supported by R. The drawback is that it doesn't give as much detail as XTide, and it is based on data from a mere 637 stations, all of which are in the USA, so it's only of limited use for the Pacific Northwest. In addition, it takes more work to calculate certain variables such as the tidal range than to do the same calculations in XTide

A third option would be to use a website like https://www.tide-forecast.com/ where you can click your way to the relevant data. The number of stations they cover is even smaller than those offered by rtide, but they do cover the entire world. If you do not want to go the XTide way, then combining rtide with https://www.tide-forecast.com/ would probably be the best way to go: the former gives you a large number of stations in the Pacific US, while the latter will add some stations in the rest of the Pacific Northwest.

I hope this helps!


Systems identification in small neural network

For very small systems like the worm c.elegans it must be possible to record from all neurons at the same time, at least optically.

While it is true that whole organism optical recording is technically possible in C. elegans, I'm not aware of any published work  where all neurons were identified and recorded from simultaneously and then combined with connectivity data in a systematic way.

I should note, that this isn't limited to C. elegans. Florian Engert's lab has published whole-organism recordings from zebrafish as well. At the moment, though, there are still technical challenges to work out before we get the input-output relationships you desire on a whole organism level. First off, the recordings aren't truly simultaneous, in the sense that it still takes time to build up 3D images from z-stacks. Second, the image processing to label neurons is not yet robust.  And finally, the most popular optical indicators  are based on calcium levels and thus provide only a proxy for membrane potential and furthermore they have limitations in time resolution, range and accuracy.

The field, however, is progressing rapidly and I suspect that these challenges will be overcome in the next few years.

  What are the best databases to ask such questions?

There are no database yet for C. elegans neural activity,  likely because the number of groups publishing optical recordings in C. elegans is still fairly small. But as more labs pick up the technique, I think the value of a database will become more obvious to the community and the OpenWorm project is providing some well-needed leadership in this area.

Finally, I should point out that in the end we may find that neural activity and connectivity provide only one part of the story. It is likely that in C. elegans neuromodulators and other "unwired" connections between neurons could play very important roles as well.


The key is specialization: e.g. some cells specializing in getting food, others in producing something sticky to keep them together. Which cell does what is usually determined by chemical signals: depending on their specialization they produce particular chemical compounds. So if a non-specialized cell notes that one compound is rather low because the specialized type of cell producing it is in low supply then it specializes that way.

While initially all cells are capable of reproduction, at some point there also will be cells specialized for reproduction, whereas the others lose the ability to reproduce to better concentrate on their specialized duty. Hence the other cells do not have an independent existence anymore but exist only as part of the larger organism. When such an organism is then to be considered a separate pluricellular entity is a matter of definition: if it is an entity independent of the original (e.g. capable of moving away)? if sexual reproduction happens?

Wikipedia also has some things to say.


Exact definition of 'convergent' and 'divergence' in cell signalling?

In my experience those terms are primarily used intracellularly, but I wouldn't argue that it is wrong to use them more broadly, it's just that essentially everything released extracellularly is going to have some level of divergence, so it makes more sense to use a separate classification scheme (i.e., endocrine/paracrine). Between cells, the terms are also used in other contexts such as the nervous system to refer to inputs from multiple neurons synapsing on one neuron (convergence), and outputs from one neuron synapsing on many targets (divergence).

Convergence just means multiple signalling pathways converging on the same target: like multiple pathways that can activate phospholipase C.

Divergence just means that one effector, which could be a protein such as a kinase or a second messenger like IP3, has multiple targets.

You are quite likely to get both convergence and divergence within any given signalling pathway. In my opinion, this is one of the ways that biology is not taught well in schools: textbooks might make it seem like convergence and divergence are these concrete, specific classifications, but they are really just descriptive terms. Phospholipase C pathways are a great example that displays both. If you are talking from the perspective of activation of phospholipase C, you are probably talking about convergence because there are so many ways to activate phospholipase C, but at the same time, if you talk from the perspective of the G protein subunit that is activating phospholipase C, that G protein probably has other targets as well, so that's divergence. And downstream of phospholipse C you have divergent effects of DAG and IP3.


Why are there three stop codons but only one start codon?

Disclaimer

It is important to realize that it is not possible to answer questions of this sort (the evolution of translation)  in anything other than a speculative manner. Please bear this in mind, especially if you find the speculation below persuasive.

Summary

It is suggested that the redundancy of termination codons is largely similar to that for ‘elongation codons’ decoded at the A-site of the ribosome, although protection against suppressor tRNAs may also be a factor. The consideration here is, therefore, mainly focussed on the question why there is only a single codon for methionine (initiation and elongation), and I suggest this may have been a combination of the late appearance and infrequent usage of methionine, together with the particular requirements for an initiation tRNA at the P-site of the ribosome, where standard wobble is apparently not possible.

Disposing of a Red Herring

Although alternative initiation codons are sometimes used, this usage differs in prokaryotes and eukaryotes, is very limited, and is not seen with the use of methionine in elongation. I would therefore consider this does not invalidate the question, but perhaps rephrase it as:

  “Why does the genetic code have only one codon assigned to methionine,
  the initiation codon, whereas other amino acids and termination have
  generally more than one?”

Time of appearance of and extent of use of Methionine

It is generally thought that genetic code initially encoded a small number of amino acids, and that this number increased over time. Methionine is one of the most complex (and energetically expensive) to synthesize (see Wikipedia entry), so is likely to have appeared late. One can argue that most of the codons would have been ‘taken’ (assigned) by that time. This argument is consistent with the situation for tryptophan, the other amino acid which has only a single codon, and which is also synthetically complex. Furthermore, these are the two least abundant amino acids so on can argue that their number of codons reflects their relative usage.

Admittedly, there need only be one stop codon per protein, but it is possible that the mechanism of termination evolved before that of methionine-specific initiation. (Initiation might originally have been from the 5′-end of the mRNA.) There is also the question of protection against suppressor tRNAs, but I shall delay discussion of this until the end.

The unique features of the initiator tRNA

Elongation involves several dozen amino acyl-tRNAs being recognized by an elongation factor which binds them to the A-site of the ribosome, at which 3′-codon wobble occurs where the redundancy of the genetic code allows and the anticodon of the tRNA has evolved appropriately.

In contrast initiation involves exclusive recognition of a special tRNA by initiation factors but not elongation factors, and subsequent binding at the P-site The tRNA has unique structural features that allows it to be N-formylated — structural features that are retained in eukaryotic initiator tRNA, even though there is no transformylase in eukaryotes. (see this SE Question]

This uniqueness may explain why there is only one tRNA for initiation. However one might ask why there is a not a group of methionine codons (e.g. AUA as well as AUG) recognized by the same initiator tRNA through wobble. The reason for this would seem to be that the P-site does not allow third position wobble (as I explain in the answer to a related question), so the initiation met-tRNA would be codon-specific.

Loose Ends

Although perhaps straying a little from the question, one might still ask why there are not alternative elongation codons for Met — e.g. AUA, which could have been ‘stolen’ from Ile, which already has AUU and AUC. In fact in mammalian mitochondria this codon reassignment has happened, but unfortunately does not help explain things. In mitochondria there is only one tRNAmet for both these codons, consistent with the simplification of tRNAs for the small mammalian mitochondrial genome. Initiation requires the formylation of the methionine.

I will finish by returning to the question of multiple termination codons, which are not really consistent with my suggestion that the extent of redundancy reflects usage. Although termination codons, like elongation codons, are recognized at the A-site they are recognized by protein release factors rather than tRNAs. This means that they will be affected differently by a mutation in a tRNA that alters the anticodon. For an amino acid codon, an altered non-cognate tRNA would only cause some misreading and an altered cognate tRNA might be neutralized by wobble or by duplicate or redundant tRNA genes. AS termination codons are not normally decoded by tRNAs, a suppressor tRNA would cause read-through at all the suppressed codons. The presence of two alternatives means that termination would be likely to occur within about 30 codons 3′ to the original termination codon. Variation in the length of the N- and C-termini of proteins is common among related species, and thus need not be deleterious to the cell.

Related SE Questions

‘Wobble’ in Initiation and Elongation — I have contributed an answer to this.
Why is AUG the Initiation Codon? — I will respond to this presently.
Redundancy of the Genetic Code — I have contributed an answer to this.
Initiator and Elongator tRNAs in Translation — I have contributed an answer to this.


Inbreeding of selfing and outcrossing plant

I don't think it's a terribly rigorous statistical argument, so much as a toy model arguing that there can be a reproductive advantage to selfing in an outcrossing population. Here is the logic as I see it:

Ovule and pollen represent the female and the male reproductive gametes in a monoecious plant (monoecious means that it has both male and female reproductive organs in the same individual).
In sexual organisms that do standard sex (i.e. not a complicated variety of sex), both ovule and pollen (gametes) are necessary to generate a fertilized offspring (zygote).
In outcrossing individuals, pollen is broadcast to fertilize other individuals (1 pollen gamete) and ovules receive pollen from other individuals (1 ovule gamete). Total: 2 gametes
In selfing individuals in an outcrossing population, selfing individuals guarantee that they fertilize their own ovules. Thus, they replace the pollen of other individuals (1 pollen gamete + 1 ovule gamete).
Selfing individuals still broadcast pollen to fertilize other outcrossing individuals (+1 pollen gamete). Total: 3 gametes

The key is in looking at the figure and understanding what it's arguing.
Again, these are not really rigorous ratios, details will be determined by exact biology of any case in real life. As far as I can tell from the text, the argument is not "these are the exact ratios in all organisms", but rather that "selfing gives the advantage that a selfer contributes all of the same gametes as the outcrosser, plus the male gametes to fertilize its own male gametes".
Secondary note: this model is only true when the proportion of selfers in the outcrossing population is very small. Note that as the proportion of selfers increases, everyone is just fertilizing their own ovules, and the net contribution goes back down to 2 gametes per generation. So this does not describe an equilibrium case for population composition. [As noted in comments, it is likely the case that it is equilibrium for population size, e.g. number of individuals.]
For more theory about this, you can read about the evolution of self-(in)compatibility. Here is a somewhat recent review. Evolution of self-compatibility in plants is extremely dynamic, as you might expect from the arms-race aspect.
Update:
Pulling up some notes from the comments on the assumptions of the model:

I think that this example works when population number is at equilibrium, but population composition (e.g. selfers vs. outcrossers) might not be at equilibrium.
I think that for the amount of pollen, we have to assume that all organisms contribute an equal, infinite amount of pollen. So selfers fertilize their own, and then also dump pollen into a pool into which outcrossers also dump infinite pollen.
However, there are only a few ovules; every individual contributes one. That is, outcrossers and selfers contribute one ovule per individual.
On average, everyone's pollen will be sampled roughly once (actually a little less) if every non-selfed ovule takes one pollen from an infinite pollen pool of uniform composition.
As number of selfers in the population increases, less and less of the common pool of pollen will be sampled.
If everyone in the population is a selfer, there will obviously be no outcrossing, because everyone just fertilizes their own ovule. This is the equilibrium state, if selfing is heritable and this stated advantage to selfing holds.


Why are some organisms able to regenerate?

All organisms, including humans, have the ability to regenerate something in the body. But the process is much more developed in lower organisms such as plants, protists -- unicellular organisms such as bacteria, algae, and fungi  and many invertebrate animals such as earthworms and starfish. These organisms can grow new heads, tails, and other body parts when injured.
Scientists don't know why mammals don't have the same ability to grow new limbs. But they think it is because mammals have more complex biological structures; limb regeneration would require sophisticated controls to ensure that limbs and organs don't grow out of control. Humans, for example, are already equipped with safety mechanisms to ensure that individual cells don't grow uncontrollably. But these mechanisms wear down as a person ages and cancer is often the result.
Nevertheless, mammals do regenerate skin, muscle, and blood. Scientists are just beginning to learn about other types of cells, such as those in the brain and blood, that also regenerate. Further study of the phenomenon might lead to a way of growing replacement organs and limbs outside the body.
Not all organisms regenerate in the same way. In plants and organisms like hydra and jellyfish, missing parts are replaced by reorganizing neighboring tissues into whatever parts have been cut off. Animals with more complex bodies usually regenerate parts by producing a specialized bud, or blastema, at the site of amputation. The blastema supplies the tissue necessary for the regenerated part.
The regenerated body part is not always the same as what was lost. Many insects regenerate abnormally small legs from which some segments may be missing.
Tadpole tails, for example, typically grow back to about only half their original length. And regenerated parts often differ in details. A regenerated lizard tail, for example, contains a cartilaginous tube instead of the vertebrae in the original.


You almost said it all! Here are two ways to think of this problem

Finding the missing probability

Let's denote the fraction yz genotype in the population with $f(yz)$. The sum of of fraction of all genotypes must be equal to 1. In equation it means

$$f(aa) + f(aA) + f(AA) = 1$$

Here, of course I don't make a difference between $f(aA)$ and $f(Aa)$ (whether A is inherited from the mother or from the father). Knowing as you said

$$f(aa) = p^2$$

and

$$f(AA) = q^2$$

and feeding this value back to the first equation result into

$$p^2 + f(aA) + q^2 = 1$$

Solving for $f(aA)$ yields to

$$f(aA) = 2pq$$

Directly calculate the probability

Another to reach this result is to ask the following questions

  What is the probability that the maternal allele is A?

The answer is $q$

  What is the probability that the paternal allele is a?

The answer is $p$

  What is the probability that the maternal allele is a?

The answer is $p$

  What is the probability that the paternal allele is A?

The answer is $p$

Therefore, $$f(aA) = pq + pq = 2pq$$


More than two alternative forms (alleles)of a gene in a population occupying the same locus on a chromosome or its homologue is known as multiple alleles.

Multiple alleles arise due to mutations of gene.A gene can mutate several times by producing a series of alternative expressions.Different alleles in a series show dominant-recessive relation or may show co-dominance or incomplete dominance among themselves.

In Drosophila,a large number of multiple alleles are known.One of them is the series of wing abnormality ranging in size from normal wings to no wings.The normal wing is wild type.The extreme expression with no wings I.e is just stumps is due to one allele 'vg',in homozygous condition .

For reference.
http://eagri.tnau.ac.in/eagri50/GBPR111/lec04.pdf


Sugar metabolism in preserved/cryopreserved livestock semen

The sugars that you mention are primarily used as a "cryoprotectant" and thus to reduce physical damage to the cells while frozen.  The sugars are not used to provide energy to the sperm as the enzymes will not function in the temperatures and conditions of a frozen environment. The addition of sugars is typically used with other types of cells/tissues in their cryopreservation as well.  The abstract in the link below summarized this.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/raq.12195


Are there specific conditions that allow humans to see ultraviolet wavelengths

You will be interested in Aphakia, which is the lack of an eye lens usually through surgery but sometimes from birth.  These individuals supposedly see UV as a whitish-blue or whitish-violet:

  This appears to be because the three types of colour receptor (red, green and blue) have similar sensitivity to ultraviolet, so it comes out as a mixture of all three - basically white, but slightly blue because the blue sensors are somewhat better at picking up UV.1


This is a good experiment!

3 types of food: ok
9 tanks: ok
Apply different treatment randomly - no!  You are right - no way to tell with random.  It is like comparing McDonalds to vegan diet - you have to stick with your diet to be able to tell a difference in the end.  So Tank 1,2 and 3 get food A.  Tank 4,5,6 get food B.  Tank 7,8,9 get food C.  Each tank gets only that food type.
You need to add the same weight of food to each tank.  More food = more weight.  I am not sure how much is a reasonable amount; it depends on your fish.  Get out what looks like a reasonable amount and weigh it.  That is how much food each tank gets each day.  You could weigh a bunch of quantities and set them aside - maybe in an old egg carton?  That will make it easier to feed the fish each day.
Have the same number of fish in each tank. 3?   Ideally fish are same species and all about the same size to start because different size fish might not all gain weight at the same rate.  I am picturing 11-cent goldfish.  3 per tank makes 9 / food type and 27 in all which is good.
You can gauge growth by fish weight.  When it is time to weigh the fish, fill a bowl with aquarium water, put it on the balance and zero the balance.  Now you will get the weight of whatever you add to the cup because balance is ignoring weight of cup and water.  Sweep a fish out of the tank into the bowl and weigh it.  Then dump it back in and repeat with next fish.

If you can tell the fish apart each one can be weighed separately and I think should also be named with a name that starts with the letter of its tank because that is fun.  For example TankB4 will contain Burr, Black Beauty and Buzz.  Tank C7 will have Clyde, Caesar and Coco.

Keep track in your lab notebook of each fish and its weight
Take a photo of each one when you start and one when you are done.  This will make a great poster.

You can weigh fish every day or maybe every 3 days if you think handling them is too stressful.
You can track weight for each fish, average weight for each tank, and average weight for all 9 fish (3 fish / tank x 3 tanks / food type) over time.  You will graph each of these.  You can use Excel or do by hand.

If a fish or 2 die your data will still be good.

Good luck!  I hope you will come back to this idea and post an image of Aloysius, Angel and Aesop, the fish from tank A1.


How much does donating blood affect the amount of oxygen in your blood stream at high altitude?

The oxygen-carrying capacity of the blood is:

  amount of haemoglobin * % saturation

The average blood donation is approximately 10% of total blood volume. . Since the donation will have no effect on the % saturation, the oxygen-carrying capacity at each altitude will go down by 10%.

By inspection of the graph in the question, the % saturation goes down by 10% at 10,000 feet. So I conclude that donating 10% of blood volume is equivalent to ascending to 10,000 feet in terms of the effect upon the blood's oxygen-carring capacity.

Response to OP comments:

1) Anyone living at 5,000 feet will have adapted to that altitude in two ways. First of all the erythrocyte levels of 2,3 bisphosphoglycerate will be elevated to maintain unloading of oxygen from haemoglobin in the tissues. Secondly, the number of red cells per mL of blood will have increased, to restore oxygen delivery. Incidentally this increases blood viscosity which is deleterious in the long term. Tibetans living in the Himalaya have adapted genetically to prevent this effect on their blood viscosity.

2) The effect of air pressure is already included in the graph, since it shows the actual degree of saturation of the blood.


Are there parasitoids of mosquitoes ? (other than nematodes)

It happens I just found an answer to my question in a recent review book by George Heimpel and Nicolas Mills. It appears that for now we do not know any  parasitoid of mosquitoes.

Quoting chapter 1 :

  "Most insect herbivore species are attacked by
  one or more parasitoid species, but some major
  arthropod pest groups appear to be entirely free
  of parasitoid attack. For instance, we know of no
  parasitoids that attack mosquitoes or other biting
  flies with aquatic larval stages, and no parasitoids
  that attack phytophagous mites or adelgids."

Source:
Heimpel, G., & Mills, N. (2017). Definitions and Interactions. In Biological Control: Ecology and Applications (pp. 1-18). Cambridge: Cambridge University Press. doi:10.1017/9781139029117.003


Usually the tracrRNA is a part of the CRISPR locus and is encoded in the the vicinity of the CRISPR array (e.g. upstream or downstream of the cas genes or the array).

http://www.genome-engineering.org/crispr/wp-content/uploads/2013/01/crispr_processing1.jpg


How does the DNA cross through bacterial cell wall during electroporation?

The bacterial cell wall is quite porous, and is not considered a permeability barrier for most small molecules. It mainly functions as structural support and to resist turgor pressures.
The average pore size of relaxed peptidoglycans were measured to have a radius in a range of about 2.0 to 2.5 nm, regardless of thickness (i.e. Gram + and Gram - bacteria have similar pore sizes), but when stretched under turgor pressures, peptiglycan is permeable to globular proteins of 50 kDa or more, while hyperosmitic shock of bacterial cells can trigger the release of proteins up to 100 kDa in size (Vollmer et al., 2008). That equates to ~6.5 to 8.5 nm in diameter by one method of estimation.
A single strand of DNA double helix is around 2 nm in diameter, so it stands to reason that even a circularized plasmid could potentially pass through pores just a little more than 4 nm wide.
Reference:
Vollmer, W., Blanot, D., & De Pedro, M. A. (2008). Peptidoglycan structure and architecture. FEMS microbiology reviews, 32(2), 149-167.


What are key factors when evaluating and comparing miniprep columns?

Storage conditions and shelf life are some of the things that you should consider in comparing columns.


Can we really 'discover' 85% of mammalian viruses?

For some statistical models, see e.g. The Mathematics of Biodiversity (Part 1) by John Baez.

However, in terms of new species, such statistical methods may not suffice - usually also our tools for discovering change. So it might be more accurate to extrapolate number of some kind species we know as a function of time.

For extrapolations (though not for viruses) see e.g.:

Camilo Mora et al., How Many Species Are There on Earth and in the Ocean?, PLOS Biology (2011).

In any case, for viruses (and many other fast-multiplying asexual creatures) defining number of species can be anywhere from tricky to impossible (for fundamental reasons, not only - practical). At best you can try to estimate their time to the last common ancestor. See also links in this discussion on Azimuth.


Hyperparasitism is one possible term. According to the linked article it is commonplace in certain types of insects, but also in fungi. Apparently the cases of at least three levels are known: a fungus on a fungus on a fungus on a tree.


Influence of temperature on protein binding and decay rates

Let's do your second one first, you want to find the rate of binding:

Yes you are right you need to calculate for km

I think I found the paper that ties temp into the reaction rate:

statistical approach called response surface methodology (RSM) is used for the prediction of the kinetic constants of glucose oxidase (GOx) as a function of reaction temperature and pH. Lineweaver–Burk transformation of the Michaelis–Menten equation was utilized as the integral part of the RSM algorithm. The effects of variables, namely reciprocal of substrate concentration (0.033–0.5 mM−1), reaction temperature (14.9–40.1 °C) and reaction pH (pH 4.4–8.5) on the reciprocal of initial reaction rate were evaluated and a second order polynomial model was fitted by a central composite circumscribed design (CCCD).

Biochemical Engineering Journal
August 2005, Vol.25(1):55–62, doi:10.1016/j.bej.2005.04.001
A new approach for determination of enzyme kinetic constants using response surface methodology
İsmail Hakkı Boyacı

For the decay

I'm still working on the first I'm suggesting to check this out but need sleep I can read it tomorrow

http://www.eastcoastbio.com/productcart/pc/stability_testing.asp


Does bioluminescence communcation occur on macroscopic level?

Almost certainly. In the deep-sea, some species of laternfishes (Myctophidae) show sexual dimorphism in their light organs. Males have large light organs. The females are much smaller. Here is a brief summary, based on an interview with Dr. John Sparks at the American Museum of Natural History.

Sparks is discussing his recent publication with colleagues (Davis et al. 2014) that suggests that bioluminescent communication may actually facilitate speciation in some deep-sea fishes.

There are probably more instances of communication using bioluminscence in deep-sea organims but, to my knowledge, the Davis et al. paper provides the best evidence so far.

  Davis, M.P. et al. 2014. Species-specific bioluminescence facilitates speciation in the deep sea. Marine Biology 161: 1139-1148. (open access)

On land, Stoltz et al. 2003 has demonstrated that positive selection has acted on bioluminescent color in Jamaican click beetles. The male beetles use the flashing to attract females for mating. Some males emit yellow light while males in a separated area have orange light.

  Stoltz, U. et al. 2003. Darwinian natural selection for orange bioluminescent color in a Jamaican click beetle. Proceedings of the National Academy of Sciences USA 100: 14955-14959.


Genes related to senses and their variation across animals

There are two notions I could think of

There might have a trade-offs about where to spend ressources (energy and nutrients). If an organism spend a lot of ressources in, say, vision (incl. the part of the brain that deal with interpreting the input), then there won't be much left for other things.
When a sensory system is well enough developed that the other sensory systems would bring up only marginal benefits, it is better to just not spend unecceesary ressources on building these other sensory systems.

Please note that

The above two hypotheses are just guess work from me and I did not support any of what I said with an actual evidence.
I assumed that there is a negative correlation between the "quality of the different sensory systems" (whichever way that would be defined) but I don't know whether this is true or not.


Do you produce more sperm after 1 week of abstinence vs 1 year of abstinence

There is an increase by abstinence.

  The within-subject variability of the semen sperm count (n), volume
  (v) and the total number of spermatozoa (N) was studied on 220
  ejaculates from 36 normal subjects after an abstinence of 7 days or
  less.

  The three semen characteristics for a given subject were highly
  correlated with the length of abstinence: for an increase in
  abstinence of 1 day there were mean increments of 13 × 106/ml for n,
  0·4 ml for v, and 87 × 106 for N.

1979 - Within-subject variability of human semen in regard to sperm count, volume, total number of spermatozoa and length of abstinence

  Semen analysis was performed on six men after various sexual
  abstinence periods (from 2 to 18 days). The variations in semen
  parameters were analyzed statistically as a function of the duration
  of abstinence.

  Lengthy sexual abstinence was found to affect all semen
  characteristics. Semen volume and concentration and total sperm count
  showed significant increases, whereas motility and normal morphology
  decreased significantly with duration of abstinence. Significant
  changes in the percentage of normal sperm forms were observed after
  more than seven days' abstinence.

  The study indicates that the influence of long sexual abstinence on
  semen quality varies with the variable considered. With regard to
  fertility, a long abstinence period might induce senescence of
  spermatozoa.

1994 - Effect of long abstinence periods on human sperm quality.

Sperms can die of "old age", as the previous quotes mentioned long abstinence period induces senescence. It is hard to find anything about their lifetime, it is at least 7 days I think.

  For humans, entire process of spermatogenesis takes 74 days. Including
  the transport on ductal system, it takes 3 months. Testes produce 200
  to 300 million spermatozoa daily.

according to wikipedia

So there is a constant rate of sperm production.

I think the following differential equation can describe the change of the sperm count:

$$ \dot{x} = μ - Dx $$

where

x is the sperm count
μ is the production rate regulated by testosteron (about 250 million per day)
D is the death rate which depends on the age of the population (depends on the lifetime, production rate, elapsed time)

So there will be a maximum amount by abstinence. By that amount

$$ μ = Dx $$

so

$$ x_{max} = μ /D $$


Why do fat people and thin people get hungry at the same time?

I am not sure your statement is true, fat and thin people may not always get hungry at the same time. You cannot simply compare these two categories as they contain subcategories including people "feeling hungry" because of disorders related to their mental health, physiology, diseases,...

The term you are looking for is "appetite regulation" and reading the wikipedia page will give you an overview of this subject and why your question is too broad to be answered. https://en.wikipedia.org/wiki/Appetite#Regulation


Can the Hebbian theory apply to Inhibitory Neurons

≈Yes, it's easy to conceptualize at a simple ganglionic circuit. A really good example is (I believe from Kandel's lab)demonstrated by Aplysia's gill withdrawal reflex. Repeated stimulation causes reduced EPSPs in motor neurons that innervate muscles that cause the withdrawal reflex. However when you apply a electric shock to the tail, the snail will immediately regain withdrawal reflex sensitivity. The tail sensory neuron response activates the serotonergic facilatory interneurons which have multiple IO with sensory and motor neurons.

And don't forget, interneurons can inhibit other interneurons leading to disinhibition.

For most LTP work you're probably ok using Hebbian models. Make sure to keep in mind that in more complex systems like cortical circuits.  there are some modes of communication that don't always play well with Hebb's Laws: gliotransmission, retrograde transmission, neuropeptides/GPCRs, and activation of perisynaptic receptors/receptors on adjacent cells.


Yes, stretch means sequence in this context.  See definition #5 for stretch (noun) on Wiktionary:

A segment or length of material.

So, the "stretch of amino acids" in the article refers to the peptide sequence portion of the lipopeptide prophylactic.


Genotype of children conceived after stem cell transplant?

Spermatozoa are produced in a process called spermatogenesis. They come from germ cells, which in the human males are located in the testes. These are not affected by stem cell transplants.

In females, the equivalent oocytes are already present at birth. They undergo meiosis later, but since their genetic composition is already set at birth, they, too, are not affected by stem cell transplants.

This might make the process clearer: Primordial Germ Cells and Sex Determination in Mammals

  In all vertebrate embryos, certain cells are singled out early in development as progenitors of the gametes. These primordial germ cells migrate to the developing gonads, which will form the ovaries in females and the testes in males. After a period of mitotic proliferation, the primordial germ cells undergo meiosis and differentiate into mature gametes—either eggs or sperm

A stem cell / bone marrow transplant only affects the bone marrow, where the blood cells are produced.


Do animals get sick from eating dirty food or eating off the floor?

I'm sure it varies wildly based on the animal and what they're eating.  In general, if in the course of an animal's natural feeding process it picks up a little dirt, it has evolved to cope with that.  Animal's behaviors and guts have evolved to fit their food source and lifestyle.  For a behavioral example, seals will eat rough rocks to help breakdown bones (and barf them up when they get too smooth).  Guts have evolved symbiotic relationships with microbes that are specifically adapted to the food source, termites have microbes to help them break down wood, whereas we don't have the microbe population to pull that off.  Interesting side note: it was found that one of the gut microbes in some Japanese people has gotten a horizontally transferred gene from a bacteria that lives on seaweed, probably helping them break down seaweed.

There could be a problem when the body is challenged with dirt that contains uncommon substances that the body isn't adapted to.  I'm sure if a cat rolled around in soil contaminated with a lot of arsenic it probably wouldn't be doing very well after licking off all the dirt.

This does bring up an interesting current medical hypothesis called the Hygiene Hypothesis.  Basically, these things you are talking about, utensils, antibacterial soap, etc. are all very very recent developments in human evolution.  As a result, proponents of this hypothesis think that our bodies are adapted to challenges by microbes and parasites, and depriving our bodies of that exposure when we are young totally screws up the development of our immune systems.  This would explain why we see a huge increase in allergies and autoimmune diseases in the developed world, our immune systems are totally miscalibrated, and freak out over harmless things like pollen (allergies), or worse, attack self-antigens (anti-insulin antibodies in type I diabetes).  Human children are animals, and baby animals should play in the dirt!


It looks like combretaceae, or a species related to it.


If we sequenced the genome of every species, would all phylogenies agree?

Horizontal gene transfer

Don't expect to have a tree! Horizontal gene transfer happens and therefore we would end up with a network, not a tree.

Gene trees

Different DNA sequences have different evolutionary histories. See, in particular, the question of incomplete lineage sorting. This means that one may compute a tree for a given DNA sequence that must disagree with the tree of another sequence. So, don't expect a perfect species tree where all sequences will agree on.

Note that the two points "Horizontal gene transfer" and "Gene trees" are highly related. So much so that they could fit together.

Not all individuals have been discovered

If by saying of every organism, you meant "of every organism that we encounter", then we still have the issue of organisms that we have never encountered. If you meant "absolutely every individual that exist", then this is a non-issue. It also matters as to whether you mean every individual of every species or just one individual per species.

Also, it is slightly unclear whether, in your hypothesis, we can sequence all dead individuals! Extinct lineages would still not be resolved if we cannot sequence them.

Massive mutational events

It is possible that very large mutational event could prevent us to see the exact relationship between individuals. But that would only interfere on an extremely fine scale phylogeny (intra-species level).

Methodology

If we really sample all the individuals, the detail of the methodology may not matter much. It will still need to be decided whether we want to consider AATC closer to AA.C or to AGTC (where . indicates a deletion). Again, this will likely only matter on a very fine scale (intra-species level).

Computational power

Of course, if we sequence every nucleotide that exists on earth, we would never have the computational power to even store the data. Not talking about actually processing it. We would not either have the computational power to process the sequencing (nor the necessary amount of products to allow for the sequencing to happen).

If you meant to fully sequence only one individual per species (and then again the arbitrary nature of the concept of species will complicate things up), then we might have the computational power (see @KonradRudolf's comment)

The concept of species can often be misleading. You might want to read the post How could humans have interbred with Neanderthals if we're a different species? for a discussion on the concept of species.


Posted due to certain inaccuracies in comments and answers provided to this question regarding the Human Immunodeficiency Virus.

It should be noted that while it may not affect the ability for macrophages in the dermis to phagocytose the heavy metals found in the inks used in tattooing, and thus not interfere with the fixing of a tattoo in an HIV+ person, the Human Immunodeficiency Virus, the virus responsible for Acquired Immune Deficiency Syndrome (AIDS) does in fact have the ability to infect any cell type that expresses the cell surface glycoproteins CD4 and CCR5.

Cells that express CD4 and CCR5, barring mutations seen in the bone marrow received by the Berlin Patient (Timothy Ray Brown), among them CD4 "Helper" T-Cells, Macrophages, and certain Dendritic Cells, are all capable of being infected by the HIV virus.

Glycoprotein 120, found on the surface of the HIV envelop, binds with high affinity to CD4. The coreceptor CCR5 then binds to the gp120 CD4 complex and allows the HIV envelop to fuse with the plasma membrane of the host cell. The fusion then delivers the viral nucleocapsid and associated proteins into the cytoplasm of the cell and the infection takes place.

If I had to venture guess, I would say that as Macrophages tend to be present within the dermis of the person for extend periods of time, there is likely enough of a population present in the skin to have the macrophages necessary to fix the inks used in tattooing.


Z value is a fitted constant and it ranges between 0.1 to 0.3 regardless  of the region or taxonomic groups.i.e. the slope is almost similar .Among larger areas like continent,the slope tends to be much steeper.becoz, Larger the area larger will be number of species(species richness),for larger areas the Z values tends to be 0.6 to 1.2.(NOTE:if Z is less,lesser area is enough to capture more species).


Concentration dependent cellular processes

There are several, but I guess the most well known is the neuron action potential, where the concentrations of Na+, K+, and Cl- ions determine the membrane potential of the cell. When the potential reaches a certain level, it triggers the action potential. You can read about this in much more detail on wikipedia, https://en.wikipedia.org/wiki/Action_potential .

But to be pedantic about it, almost every cellular process is concentration dependent.


What you are suggesting is an organic photosynthesizer,but that's not necessary when you already have plants that have genetically adapted for millions of years just to be suitable for this very purpose.
 Of course,artifical photosynthesis already exists,essentially using the same process;photons,chloroplasts,calvin cycle,photosystems 1 & 2,etc.It utilizes the general concept with photoelectrochemistry,so basically just replacing the organic tools with artificial photoelectric cells,which also uses h20 and light.What you are asking is why we have not developed genetically engineered organic matter to produce higher efficiency.As a matter of fact,GMO plant's already exist with immunity,though I have not heard of GMO that catalyzes photosynthetic reactions,and best not,because genetic engineering is still at it's best a new field that is too complex,for example,the general GMO is to incorporate the bacterial enzyme cas9 to cleave away specified DNA to alter an organism's genome,such as inhibiting receptors to cannabinoids,or to fight pests with substances that are not harmful to humans,etc.But it has consequences,such as permanence of that edited genome,so if the organism/plant reproduces,the progeny would also exhibit the same GMO properties.
 Photosynthesis is a complicated series of reactions that uses complicated enzymes and such.For example,the enzyme rubisco that changes co2 to energy rich molecules such as glucose,from highly unstable phosphoglycerates.Artifical photosynthesis is quite new,but it also uses the same fuel;co2,h20,and light,not sure if it uses biological nutrients like soil,but the process also uses Nicotinamide adenine dinucleotide phosphate,or NADP+.It is used for anabolic reactions,so it builds up molecules,vice versa are catabolic reactions,which is when enyzmes break down lipids and molecules in metabolism.Albeit I do not know for sure if this molecule has the same purpose in artifical photosynthesis,but for general photosythesis,yes.NADP+ also absorbs electrons for independent and dependent reactions to generate ATP and NADPH,etc.
 I hope this simplifies some things.CONCLUSION:we do have artifical photosynthesis,but gmoed photosynthesis may be harmful to a plant's heredity if we damaged it's genome,causing potential harm.
  Artifical is quite similar to organic,so I guess you say they are biopanels,using h20,co2,and light.


Regarding different nucleotides on a DNA strand

These are IUPAC codes for so-called "degenerate" or ambiguous bases, alternatives to the usual A, T, C, and G nucleotides (for DNA). The N code represents any base, while M and K map to A or C, and G or T, respectively.


It might be a juvenile lined snake (Tropidoclonion lineatum). The What Snake Is That page for Missouri says they are native. In your photo, I see very faint black stripes with a central tan line, which matches a lined snake. Photos of juveniles seem to be rare though.

Lined snakes grow to about 2 feet long and are non-venomous. According to this natural history page, the only venomous snakes in Missouri are pit vipers (of which 5 are native).


Encyclopedia of Life includes information on synonyms (see link for Apatosaurus) - not a list but searchable and often with references and background info. After a quick google search I also found this list from dinosaurcentral.com, but I don't know how credible and updated it is and it seems to lack references.


Is there a type of amnesia that separately affects long-term memory?

If I understand your question correctly, what you are describing is retrograde amnesia.  This is further subdivided into pure, focal and isolated.

From the site:

  Typically, episodic memory is more severely affected than semantic memory, so that the patient may remember words and general knowledge (such as who their country’s leader is, how everyday objects work, colours, etc) but not specific events in their lives. Procedural memories (memory of skills, habits and how to perform everyday fucntions) are typically not affected at all.


Absorption, distribution, metabolism, excretion, and toxicity ADMET can be somewhat computationally defined but is largely secretive due to the money involved in drug discovery. FAF-Drugs2 will do basic ADMET. The Schordinger Suit provides a more indepth ADMET for a fee.