text:
How are DNA virus cladograms actually calculated in practice? Is the procedure different for RNA viruses? Are these processes somewhat subjective?
The May 24, 2022 Bloomberg opinion piece Monkeypox Isn’t Looking Like a Covid-Sized Threat; It’s still early, but contact-tracing efforts and analysis of the virus’s genome offer hope that this outbreak can be contained. includes the following:

Why now, monkeypox?
Scientists are scrambling to answer this key question. Two strains, or clades, of monkeypox are known to exist, and the one currently circulating seems to be the milder West Africa one. (For more on that, see this explainer from Therese Raphael and Sam Fazeli.)

One challenge is that researchers lack a good baseline measure on the transmissibility of this clade of the virus. Over the weekend, Maimuna Majumder, a computational epidemiologist at Harvard Medical School, provided an initial analysis of the monkeypox virus’s R0 (R-naught) — the number of people expected to be infected by a single case. These findings, which have yet to be peer reviewed and are based on very limited data, suggest an R0 of 1.15 to 1.26 — low enough to imply that the virus can be kept in check by contact tracing, vaccination and isolation of infected people.

While the present chain of monkeypox transmission differs from earlier patterns, this clade of the virus is generally mild for most infected people (albeit with a long period of isolation and recovery). And, critically, vaccines and antivirals are available to address infections.

I'd never heard the term "clade" before. I've found News Medical/Life Science's (Last Updated: Jan 11, 2022) What are Viral Clades? which which introduces the concept of the cladogram and basal clade and uses the RNA virus SARS-CoV-2 as an example is somewhat helpful but it's more of an explainer than a procedure, consistent with the site's mission to be

a tight-knit community of scientific, medical, and life sciences experts that produce and share the latest information, in a readable, understandable way.

So I checked Wikipedia's Cladogram which has a general discussion but doesn't go into great detail.
So I'd like to ask:

How are DNA virus cladograms actually calculated in practice? Is the procedure different for RNA viruses? Are these processes somewhat subjective?

By "subjective" I mean do scientists producing cladograms have to make any decisions as to what genetic differences are important for the diagram, or would several groups working independently always arrive at identical diagrams from identical data sets because they apply a standardized methodology?

I understand that there are three question marks in the title and one might at first suggest this is multiple questions, but in this particular case I don't think it's better to break this up into three separate question posts because they are so closely related and answers will likely come from the same sources and require the same expertise to write and future readers will find them equally interesting. But if a potential answer author feels strongly otherwise I am certainly willing to consider a breakup.

potentially related: How can I classify the 3 clades(S, G, V) of the coronavirus that are found on GISAID? and in bioinformatics How can I classify the 3 clades(S, G, V) of the coronavirus without using protein data? As I'm not a bioinformaticist and not likely to understand answers written in bioinformatic-ese, I've chosen to post this here rather than there.

For what it's worth, clades are not something specific to viruses, but all biology. A clade is a group of organisms with a common ancestor; cladistics is the study of the ancestral relationships of organisms and classification by those relationships.

This question is slightly different than the suggested similar questions about the S,G,V clades. This question is about phylogenetic reconstruction generally, while the others were asking more how to identify an unknown sample within an existing phylogeny.

Too short for an answer, but consider that some people construct trees with BEAST2.

@Galen "...strict or relaxed molecular clock models." This is great, I'll read now, I think this will help me a lot. It seems that since there can be such flexibility in one's choice of clock models, one could argue that the answer to "Are these processes somewhat subjective?" is "Yes!"

How are DNA virus cladograms actually calculated in practice?
A cladogram, or phylogenetic tree1, is constructed by comparing similarities and differences between organisms, and placing those within an evolutionary model.2 In practice, especially for viruses and microorganisms, the analysis is performed on the organisms' nucleic acid or protein sequences.3,4 For example, a simple model might assume that all nucleic acid changes are equally likely; others might treat transitions and transversions differently; still others may have a unique substitution rate for each possibility, with the overall likelihood depending on the gene under analysis, position within the gene, frequency of each nucleotide, etc. The choice of model may be directly selected by the researcher, but is often selected from an analysis that balances model fit against over-parameterization. The researcher selects the tree that optimizes some aspect of the model, for example the likelihood that the selected tree could produce the observed data under the chosen evolutionary model.5,6
Is the procedure different for RNA viruses?
No, the procedure outlined above applies to both DNA and RNA viruses, although aspects of the model parameters may differ.
Are these processes somewhat subjective?
The same model, applied to the same data, will produce the same result (assuming a thorough tree search was performed), so that aspect is not subjective. However, model choice implies assumptions about the nature of biological evolution, and researchers may disagree on the validity of those assumptions.
That being said, the methods for analyzing viral outbreaks are very well characterized and it's unlikely two competent researchers will produce greatly conflicting trees. In reference to the monkeypox example, the two clades mentioned are strongly supported, to the point where it would be innaccurate to call them subjective.
Extra
It should be noted that for any given tree, the identification of clades is not at all subjective. Every node in a phylogeny represents an ancestor of a clade. However, researchers find some clades especially relevant to the study system, so they will call them out with a name or label. For example in monkeypox the West African/Central African clades are very relevant to most discussions.
The above generally applies to any group of organisms. Viruses and other microbes may differ in that we have access to specimens that were the actual ancestors of the current generation. For example, apart from what we learn from fossils, we can only infer the characteristics of the common ancestor of chimps and humans. However, for SARS-CoV-2 we have samples of the original isolate, even if viruses with that exact sequence are no longer present in the wild. When constructing a tree with this sample we would place that specimen at the node representing the ancestor of all current SARS-CoV-2, rather than at one of the tips of the tree.
Finally the phrase "basal clade" is nonsensical. All clades, by definition, contain an ancestor and all of its descendants. There are clades where the ancestor existed earlier in time and has more descendants than others, but then, that clade is itself just a part of a larger clade. The linked article states, "a basal clade is one closest to the root common ancestor", but of course, that ancestor had more than one successful descendant, and so both descendants are equally close to the root. The article also states, "The S clade... mutated to produce the V clade," but if the term is being used properly the V clade is a part of, and a subclade within, the S clade.7 Here is a longer discussion of why "basal" is usually an inappropriate descriptor of phylogenetic placement. (However, as mentioned above, for some microbes we do actually have samples of the ancestral strains, so "basal is a bit more meaningful there.)

1A phylogenetic tree is a broader category of analysis where the lengths of the branches in the tree have meaning. A cladogram only shows topological relationships, while a phylogenetic tree shows both topology and some magnitude of change (usually either evolutionary or temporal).
2A tree can also be produced by simple similarity clustering, which is fast, but can be positively misled compared to the true phylogeny.
3Phylogenies can also be constructed from other information, such as morphological similarities/differences, as in fossils, for example. Still, some evolutionary model is used to transform the similarity matrix into the phylogeny.
4Of course, the protein sequence can be derived from the nucleic acid sequence. Which is used usually depends on the nature of the question and the breadth of the organisms included in the analysis.
5This is the maximum likelihood method, Bayesian methods are also common.
6Selection of the optimal tree is NP-hard, and there exist many methods to tractably estimate the solution.
7SARS-CoV-2 has its clades named after specific mutations that "define" (are synapomorphies for) the clade. However, this isn't strictly informative, since there's no reason a member of that clade couldn't mutate back to the previous state, or that a member of another clade couldn't pickup an identical mutation.

This is very helpful, as are the linked papers, thanks! "...the procedure...applies to both DNA and RNA viruses, although aspects of the model parameters may differ" The nature of that difference could be the basis of a new question at some point, but I'll need to give it some careful thought.

Very nice answer.

Disclaimer: I'm not a bioinformatician, though I occasionally dabble in it, so I may well have some things incorrect. Please feel free to correct or make your own answer.
As I see it, you are asking how cladograms/dendrograms are generated for viruses.
The answer is basically that you take the genetic sequences and compare them for changes in sequence and conserved regions. The more similar the sequences are, the greater the likelihood that they are closely related and they should come out on the same branch or leaf of the tree. Conversely, the more changes in a sequence (compared to a reference) should have greater divergence and come out in a different branch of the tree.
Edited to add regarding "more similar": Similarity in sequences is based on a few parameters, but is largely based around conservation of energy. So, if you had 3 DNA sequences (AA codes underneath)
AATTCCGGG
AsnSerGly

AAATCCGGG
LysSerGly

AACTCCGGG
AsnSerGly

Compared to 1 as reference, 1 and 2 are more similar because they conserve the A/T pairing (lower energy), whereas 3 substitutes a C, which results in a C/G substitution pairing (higher energy). Of course, if you were looking at this from the possibility of translation into protein (no frame given), then 3 actually makes more sense given that it retains the coded amino-acid sequence. Substitution matrices for these sorts of things have been worked out that produce odds-ratios for a particular substitution type. The commonly used ones are PAM (Point Accepted Mutation) and BLOSUM (BLOcks SUbstitution Matrix).
The procedure to generate a cladogram is essentially the same for any organism that you care to analyze and follows these basic steps:

Sequence
Assembly
Alignment
Tree building

Now, while this all sounds good and easy, it really really isn't. The first two of those steps are more or less unambiguous, though with the advent of single-molecule sequencing these have changed a bit too in the past 10ish years. The latter two are dependent on exactly which alignment algorithm you use. There are quite a few different alignment algorithms out there, many of which are now considered out-dated or have been superseded by a newer one.
If you want to have a go at some basic alignment and tree-building, I recommend using Clustal Omega, which is a web-server where you can put your sequences (in DNA, RNA or protein) in FASTA format, and hit the button. Grab a few sequences for the mRNA/CDS (because this cuts out the introns) for a gene from different species from GenBank and have a go. It should have an alignment output and a tab on the output with a cladogram.
It also depends on exactly what sequence and what form you use for analysis. For instance, to take a recent example - The trees and all of the variant names you see for SARS-CoV-2 (e.g. these ones at nextstrain.org) are based off the genomic sequences for the spike protein only. If you used the sequence for the RNA dependent RNA polymerase (RdRp) you would get a different picture (almost no divergence because these are highly conserved, so highly you can use these to find novel viruses that infect all clades of life), and these trees would also be different to those generated if you used the whole genome. In addition, you can convert the genomic sequences into protein, and you might well get a more conservative tree out - because of the redundancy in the codons for each amino-acid.
As with much in biology it also has to do with exactly what you use as reference sequence(s) and how divergent those are from your target. For instance if you were to attempt to build a tree of all Humans (Homo sp.), you might use Chimpanzee (Pan troglodytes) as an out-group (reference), but you could also use Orangutan (Pongo pygmaeus) or Gorilla (Gorilla gorilla), or a combination of these, and you likely would get slightly different results each time. Appropriate choice of out-group is one of the hard questions in this sort of analysis.

Accidentally posted before finished...

@uhoh If you have three sequences 1: AATTCCGG 2: AAATCCGG and 3: AACTCCGG then 1 and 2 are more similar (conserved base pairing) than 1 and 3 or 2 and 3, though this might not hold-up if you went to the protein sequence because of the codon redundancy... Just one of the problems...

yep, in addition to substitutions there are also additions and deletions of single base pairs and complete codons, and those can happen in areas that vary in the amount of impact on expression rate and on the nature and activity of the resulting protein (if that's what the stretch is doing). It still seems quite hard to unambiguously define or decide what "more similar" means with all this going on, which is why I ask about the subjectivity.

The similarities have been worked out over time and basically it uses an odds-ratio for the positional changes. Substitution matrices are available. The common ones are PAM and BLOSUM

thanks for the edit!


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Zayed et al. (2022) "Cryptic and abundant marine viruses at the evolutionary origins of Earth’s RNA virome"; expressed sequences or transcribed?
Phys.org's Ocean water samples yield treasure trove of RNA virus data summarizes Zayed et al. (April 7, 2022) in Science Cryptic and abundant marine viruses at the evolutionary origins of Earth’s RNA virome.
The Phys.org summary includes the following paragraph:

In these current efforts to detect RNA viruses, there were no viral particles to study. Instead, researchers extracted sequences from genes expressed in organisms floating in the sea, and narrowed the analysis to RNA sequences that contained a signature gene, called RdRp, which has evolved for billions of years in RNA viruses, and is absent from other viruses or cells.

When I hear expression I think of a polypeptide final product, although it is certainly a multistep process. My understanding is that the data analyzed by Zayed et al. were RNA sequences extracted from the seawater, and not protein.
I'm thinking that "transcribed" or perhaps just "present" should have been used (depending on the details of the methodology) instead of "expressed" but I'm not sure of that at all. Wikipedia's Orthornavirae describes the transcription so I know that one does not have to start with DNA to invoke the term transcription:

The RdRp is used to transcribe the viral RNA genome into messenger RNA (mRNA) and to replicate the genome

This is the extent of my understanding here, so I'd like to ask:
Question: In Zayed et al. (2022) "Cryptic and abundant marine viruses at the evolutionary origins of Earth’s RNA virome" did the study look at "expressed" sequences, or "transcribed", or both, or neither?

Related:

In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to? (2019)

Pardon me for not specifically answering with regard to marine viruses; I think the crux of an answer depends on addressing your misconception!

expressed sequences or transcribed?

This is semantics, and important semantics to be familiarized with in biology research.
The word expression is not the most strictly defined word, and is used differently and in a context-dependent fashion. For example, in such research as you point to, one often studies gene expression by looking at the transcriptome independently, to "gauge which genes are expressed", without assurance of translation of said RNA into protein, nor assurance of localization, or function, or even maintenance of said protein. The life history of every protein certainly goes beyond the central dogma of molecular biology, and many simplify the picture into only gene transcription and translation, but these are just proxies (or rather stages) of gene expression. Translation itself is no guarantee of final function (i.e. points or stages at which it may be easy to quantitatively measure expression, which can only be indicative).
Expression is most often associated with the process of active use of a gene, of it being 'put into play'. This is unfortunately complicated by the fact that being 'put into play' requires passage through a lot of hoops. It is NOT synonymous with transcription, or a gene that crosses the transcription + translation hurdle.
Real life use
Colloquially, you can say a gene will be expressed when a signal reaches the nucleus that will put a cascade of transcription factors into motion that will eventually assemble transcriptional machinery to transcribe a gene. Hormones can 'cause' gene expression. Alternatively, you can say expression can occur when ribosomes are unblocked or assembled, or post-transcriptional silencing machinery is lifted to re-allow translation of specific mRNA strands. Yet further, a gene is clearly not 'expressed' if the protein is non-existent, and this can come about through improper folding or swift removal or mislocalization, and so on. There are many contexts in which you can use this flexible word, and it always has a connotation of gene information flow, rather than a mechanism which is responsible for gene information flow. Today, the word expression is often used more frequently on the transcriptional side of things, where we have an easier time using robust and longer-established techniques (e.g. RNA-seq) and talking about results than on the protein translational side of things, which require further insights into post-translational modifications, trafficking, integration into membranes, protein folding chemistry, export, all that jazz. However, do not forget that proper insulin gene expression really ultimately means that the resultant protein-hormone insulin is in active circulation in the body... and NOT that insulin-coding mRNAs are present abundantly in the cytoplasm of beta cells of the pancreas.
Take-home lesson: remember, the central dogma (DNA->RNA->protein) is an organizing concept, and many words refer to it, but these same words may not be comprehensive or technical or stringent enough to describe particular events, only our conceptualization of them.
tl;dr
Transcription is a specific term (copy-reading of DNA into mRNA strands) while expression is a conceptual term (which points to but does not completely encompass information flow from DNA into protein, eventually)

"Transcription is a specific term (copy-reading of DNA into mRNA strands)..." and yet in my question I cite Wikipedia's Orthornavirae: "The RdRp is used to transcribe the viral RNA genome into messenger RNA (mRNA)" so does the misconception belong to the Wikipedia article's authors? It looks like you're contradicting that by invoking "copy-reading of DNA" as a necessary part of transcription and saying that without DNA the word "transcription" should not be used.

@uhoh Transcription of DNA is not defined in terms of the functionality of the product of the process — only that it is RNA.  Whether or not your quotation from the anonymous author of the unedited Wikipedia article correctly reflects its intent, it is plain wrong as a general definition. Transcription of DNA is the production of the RNA complement of a section of DNA. Note that I avoid the word “copy” in my definition as it does not correspond to normal English use. I avoid mRNA because tRNA rRNA, etc. are also transcription products, as well as pre-mRNA.

@David Thanks. The purpose of my first comment is only as follows: the answer begins by addressing me personally; "I think the crux of an answer depends on addressing your misconception!" I am simply pointing out that it's not my conception, it's what I found reading as part of adding some research to a question. So the answer should start by finding fault in the sources I've cited rather than going after me personally.

@David Also, answers should address "expression" in the context of the linked paper in Science (and as far as I can tell, this answer doesn't address this conclusively). I hope to have my hands on it later this morning, but like the Cell paper cited in my earlier question that you so aptly answered, I am not sure I will be able to understand the present paper to the extent necessary to say for sure if "expression" in this context applies or not.

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Has this 2018 report of nematodes frozen for 30 to 40,000 years been confirmed? Has Carbon 14 dating confirmed their age?
Gizmodo's 2018 article Russian Scientists Claim to Have Resurrected 40,000-Year-Old Worms Buried in Ice says:

A team of Russian scientists is lining themselves up to be the opening cast of a John Carpenter film. Earlier this month, in the journal Doklady Biological Sciences (Viable Nematodes from Late Pleistocene Permafrost of the Kolyma River Lowland), they announced they had discovered ancient nematode worms that were able to resurrect themselves after spending at least 32,000 years buried in permafrost.
The discovery, if legitimate, would represent the longest-surviving return from the cold ever seen in a complex, multi-celled organism, dwarfing even the tardigrade.
[...]
It’s definitely not out of the question that these worms could have been revived after so long, according to Robin M. Giblin-Davis, a nematologist and acting director of the Fort Lauderdale Research and Education Center at the University of Florida.
“Theoretically, it is possible that if the organisms are protected from physical damage that would compromise their structural integrity during their frozen internment, they should be able to revive upon thawing/rehydration for very long periods of time,” he told Gizmodo via email.
At the same time, the team’s findings could still be a dud. “The biggest issue is the potential for contamination of ‘ancient samples’ with ‘contemporary’ organisms,” he said.
While the researchers do admit the possibility of contamination in the paper, they say it’s unlikely. They cited strict procedures to ensure complete sterility. And given that the ice samples were buried 100 feet and 15 feet down, respectively, they argue it’s implausible modern day nematodes could have wormed their way that deep.
The researchers identified some of the worms in the 32,000-year-old sample as belonging to the genus Panagrolaimus, and some of the worms in the 40,000-year-old one as part of the genus Plectus. Byron J. Adams, a nematologist at Brigham Young University who has studied nematode species capable of surviving extreme conditions, said the researchers’ claims seem credible, based on what we know about the biology of some modern-day nematodes.
“I’d love for it to be true,” Adams told Gizmodo. “We see what we think are prolonged stasis in Plectus and Panagrolaimus in Antarctica but have difficulty carbon dating them.”

and contains the image shown below.
Question: It's now been three years; has this July 2018 report of nematodes frozen for 30 to 40,000 years been confirmed? Has Carbon 14 dating confirmed their age? Since this period is many half-lives, there should be very little remaining Carbon 14 and and at least their approximate age should be straightforward to confirm and contamination with "contemporary organisms" fairly easy to rule out.

Selected images of the frozen worms said to be recovered from ancient permafrost samples dating back at least 32,000 years ago. Image: Shatilovich, et al. (Doklady Biological Sciences)

Background and relevance:
See Space SE's What precautions are planned to prevent samples returned from Mars crashing and releasing organisms on Earth?

Genesis crash site scenery; An earlier sample return mission broke open upon impact and exposed contents to the environment
This now has renewed interest because of another long-permafrost-preserved animal's ability to survive:

This animal survived 24,000 years frozen in the Siberian permafrost
Frozen in Siberian Permafrost for 24,000 Years, Microscopic Animal Comes Back to Life

“The takeaway is that a multicellular organism can be frozen and stored as such for thousands of years and then return back to life—a dream of many fiction writers,” said (Stas) Malavin. (a co-author of the study A living bdelloid rotifer from 24,000-year-old Arctic permafrost)

From Wikipedia's Bdelloidea:

The main characteristics that distinguish bdelloids from related groups of rotifers are exclusively parthenogenetic reproduction and the ability to survive in dry, harsh environments by entering a state of desiccation-induced dormancy (anhydrobiosis) at any life stage. They are often referred to as "ancient asexuals" due to their unique asexual history that spans back to over 25 million years ago through fossil evidence.

Asked in meta: How to tag questions about animals or other living things surviving being frozen for a long time? Is a new tag needed or just adjust cryonics tag?

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Species ID of this giant brain-shaped mushroom? How do its spores escape, there's no "puff" for this puffball!
After several days of rain then a few warm sunny days in northern Taiwan in August, I came across this giant mushroom growing in an open field that's only occasionally mowed.
This mushroom about 18 cm tall and the cap is 20 cm wide. The the very thick base is also 15 cm wide.
The color is beige and white. The cap is wrinkled giving the very rough appearance of a brain.
There were no obvious places for the spores to come out.
There were older ones that had fallen over and had turned dark brown to black.
They feel quite dense.
Questions:

Can this mushroom be identified?
How do its spores escape?

Following up on the helpful comments I've gone back and taken some additional photos of other mushrooms in this large group.
The first was still white, the second had fallen over and turned brown.
I'm thinking that there is something wrong here, there's no evidence of a "puff" or big dramatic dispersal event. They just turn brown, fall over, then turn black.
It seems like a lot of work to go through to make such a huge puff ball, but then not really ever "puff"!

First google result for "brain shaped mushroom taiwan" suggests Calvatia craniiformis, which has variable morphology but many pics look similar to your specimen, e.g. https://www.shutterstock.com/image-photo/skull-puffball-species-giant-white-mushroom-1398120314

@Luigi Thanks! I've posted this for a friend, and since posting they've been searching in Chinese and come across both  C. craniiformis and  C. lilacina found here. Looks like we're getting close. There is actually cooking instructions but I'm not going to be doing that :-) https://i.sstatic.net/zPtRs.jpg

https://www.marylandbiodiversity.com/view/4990

Puffballs break open when mature relapsing dust-like spores. When mature they are mostly hollow . When stepped on they make a puff of spore, I guess that is the source of the name.

@blacksmith37 I ran across this image      https://en.wikipedia.org/wiki/File:Purchawka_olbrzymia_i_widelec.jpg of Calvatia gigantea which is said to be a "puff ball" but certainly looks solid in cross-section, and the mushroom in my question feels quite dense and solid, even the ones that turn black, die and fall over intact. I think there's something different going on here. https://commons.wikimedia.org/wiki/File:Old_Giant_puffball_Calvatia_gigantea.jpg I don't have any photos of the dead mushrooms I saw near this one.

@blacksmith37 I'll try to add a photo of a dead, fallen-over mushroom in a day or two when I can get back there. In the mean time here are more cross-sectional images https://www.mushroomdiary.co.uk/2015/09/giant-puffball-calvatia-gigantea/ and also https://doorcountypulse.com/door-to-nature-mushrooms-galore/ There are plenty of slicking and cooking recommendations but I'm not going to be partaking in that.

"A giant puffball is edible if the inside is totally white and even-textured" It sounds like these are not hollow at all.

@uhoh all puffballs are solid when young, hollow when mature.

I found some record size giant puffballs ( like 18" diameter). fried a few slices in butter; tasted like fried butter .  So little or no flavor.

@jmster I've added some photos

@blacksmith37 ditto Do puffballs this big rely on being stepped-on to reproduce?

If this is indeed a giant puffball, the puff comes out of tiny pores in the sporangium (the bit you see), especially as it rolls and breaks apart after maturity. IIRC one of the Attenborough doco's had great footage of this, possibly Private Life of Plants.


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Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C? (but not much higher)
Background
Discussions below several recent posts in Space SE (links below) indicate that bacterial spores are a serious problem when considering how to prevent a future spacecraft mission to subsurface ocean worlds like Europa or Enceladus, ice-crusted moons of Jupiter and Saturn believed to have substantial liquid water oceans below.

Is there any demonstrated or even proposed technology that can sterilize a spacecraft with 100% certainty and yet leave it electronically functional? The answers posted are essentially "No"
Who decided that a <1 in 10,000 probability of contaminating the europan ocean by a viable Earth microorganism was legally and ethically sufficient? The answer seems to be "nobody" and the value comes from a temporary guideline from the early 1960's. "Legally and ethically" comes from a block quote from a 2016 document.
This answer to Why are we trying to prevent life from spreading via landers rather than actively encouraging it?
This answer to Why aren't there any robotic missions on Europa or Enceladus? where item #5 and exchanges in comments lead to a meta post. That absolute sterilization is considered currently unachievable for a working spacecraft poses the challenge of deciding what is sufficient and acceptable. It's a head-scratcher of a quandary.
Are any space agencies working on a 100% reliable sterilization technique for spacecraft bound for subsurface ocean worlds?

The 2018 Extremophiles paper:
All that discussion of bacterial spores lead me to Beladjal, L., Gheysens, T., Clegg, J.S. et al. Life from the ashes: survival of dry bacterial spores after very high temperature exposure. Extremophiles 22, 751–759 (2018). https://doi.org/10.1007/s00792-018-1035-6 (also downloadable from researchgate).

Abstract
We found that spores of Bacillus amyloliquefaciens rank amongst the most resistant to high temperatures with a maximum dry heat tolerance determined at 420 °C. We found that this extreme heat resistance was also maintained after several generations suggesting that the DNA was able to replicate after exposure to these temperatures. Nonetheless, amplifying the bacterial DNA using BOXA1R and (GTG)5 primers was unsuccessful immediately after extreme heating, but was successful after incubation of the heated then cooled spores. Moreover, enzymes such as amylases and proteases were active directly after heating and spore regeneration, indicating that DNA coding for these enzymes were not degraded at these temperatures. Our results suggest that extensive DNA damage may occur in spores of B. amyloliquefaciens directly after an extreme heat shock. However, the successful germination of spores after inoculation and incubation indicates that these spores could have a very effective DNA repair mechanism, most likely protein-based, able to function after exposure to temperatures up to 420 °C. Therefore, we propose that B. amyloliquefaciens is one of the most heat resistant life forms known to science and can be used as a model organism for studying heat resistance and DNA repair. Furthermore, the extremely high temperature resistivity of these spores has exceptional consequences for general methodology, such as the use of dry heat sterilization and, therefore, virtually all studies in the broad area of high temperature biology.

Here are two separate excerpts from the Results and discussion section that seem germane to my question:

These observations showed that extensive DNA damage occurred in the spores during exposure to extreme heat. While no germination of inoculated spore ashes occurred immediately after heating, continued incubation did indeed result in germination and vegetative cell growth (Fig. 1c). That result, together with the fact that DNA was present in the spores, suggests that spores of B. amyloliquefaciens contain a very versatile and efficient DNA repair mechanism able to “reverse” the heat-induced damage, resulting in spore germination and the production of vegetative cells.

Remarkably, activity was found for these two enzymes immediately after heating, showing clearly that these proteins survived extreme temperatures within the spores of B. amyloliquefaciens. Moreover, we also found that both enzymatic activities were preserved at the same levels, over two generations (Fig. 5). We assume it is very likely that spore proteins are responsible for the repair of damaged DNA after extreme temperature exposures.

My current understanding is that it is proposed that the spores contain proteins that are ready to repair the substantial DNA damage caused at 420 °C as soon as the spores are incubated.
Question
Is it known how some heat-resistance Bacillus spores repair their DNA after having been heating to 420 °C? Do spores so treated then incubated first absorb enough water to provide mobility for these proteins to start moving around and repairing the DNA? Do they require energy to do this? If so, is the energy source stored in the spore or absorbed from the incubation medium?

Fig. 2 Quantitative survival of dried spores after heating at different temperatures

Here's a good place to start:  doi: 10.1128/MMBR.05020-11 https://dx.doi.org/10.1128%2FMMBR.05020-11
DNA Repair and Genome Maintenance in Bacillus subtilis


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Is this a real "double microscope" with two stages and two sets of objectives? Is it used in biology?
In this US late night TV broadcast1 a set has been created with some "science objects" for visual impact, and right in the center is an unusual looking optical microscope.
The bottom looks like two separate microscope bodies, each with its own stage and objective turret, but on top there is a long optical block which presumably contains several mirrors or prisms and the illumination system, topped with a binocular eyepiece.
Question Is this a real "double microscope" with two stages and two sets of objectives, as opposed to something that has been created for TV visual impact alone, and is this or something similar ever used in biology?
 (cropped, zoomed and sharpened)

1Jimmy Kimmel Live, June 2, 2021

For me this doesn't make sense. Two sets of oculars is not uncommon in a teaching environment but the other way round?'

@Chris a "comparative biology microscope" perhaps?

That could work. Use two samples and then overlay images.

@Chris: But far easier to do it with two scopes with digital cameras, feeding the images into a computer.

@jamesqf four pieces of equipment (microscope, camera, computer, monitor) is not always abetter solution than one; some folks really prefer looking through a microscope directly than watching it on TV in a brightly lit room. The eyepieces may offer a 50° apparent FOV with black everywhere else, whereas staring at a monitor might offer half of that or less plus a room full of distractions. Imagine buying a nice pair of binoculars then putting a camera on them and viewing through your laptop, nobody does this because it's absolutely worse than simply looking through the binoculars.

@uhoh: I suspect the reason people don't put digital cameras on binoculars is that they don't want to carry the laptop around in the field.  As for the folks who prefer looking directly through the microscope, I would guess they don't wear contacts and/or suffer from eye floaters.  And then there's the issue of cost: unless someone else is paying for your equipment, an off-the-shelf microscope & digital camera are likely to cost a lot less than a special-purpose dual microscope - plus you can use them for other things.


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What is, (and what isn't) "kinetic replication" as it applies to molecules and to living organisms?
CNN's World's first living robots can now reproduce, scientists say describes "xenobots"; clusters of stem cells that move around and by this motion occasionally push enough free stem cells together such that they form a new one, at least that's my understanding.
The article says:

"Most people think of robots as made of metals and ceramics but it's not so much what a robot is made from but what it does, which is act on its own on behalf of people," said Josh Bongard, a computer science professor and robotics expert at the University of Vermont and lead author of the study.
"In that way it's a robot but it's also clearly an organism made from genetically unmodified frog cell."
Bongard said they found that the xenobots, which were initially sphere-shaped and made from around 3,000 cells, could replicate. But it happened rarely and only in specific circumstances. The xenobots used "kinetic replication" -- a process that is known to occur at the molecular level but has never been observed before at the scale of whole cells or organisms, Bongard said.

Interestingly the CNN article actually links to the new paper in PNAS Kinematic self-replication in reconfigurable organisms which uses "kinematic" rather than "kinetic".
There is no easy to find Wikipedia article titled "kinetic replication" and the phrase does not appear here in Biology SE nor in Chemistry SE.
I found the 2009 PLOS Computational Biology article Investigating the Conformational Stability of Prion Strains through a Kinetic Replication Model which relates the structural stability of the prion aggregates to the rate of replication.
I also found the 1996 Biophysical Chemistry paper Prionics or The kinetic basis of prion diseases.
And in Journal of Physics A: Mathematical and Theoretical (2015) there is Hidden percolation transition in kinetic replication process.
Nothing jumps out to me as a clear definition.
I found searching for the term to be somewhat confounding because the word "kinetics" relates to the measurement of reaction rates as well as to focus on the actual physical interaction between individual molecules (or organisms) which I think is what's being referred to here. Lots of search results including "kinetic" and "replication" but very few on the combined term.
So I'd like to ask for an answer that explores the term "kinetic replication", hopefully cites a formal definition or at least outlines a generally accepted one, and offers a way to distinguish when the replication of a molecule or an organism is "kinetic replication" and when it isn't.
Question: What is, (and what isn't) "kinetic replication" as it applies to molecules and to living organisms?

I chose the replication tag but it automatically switches to dna-replication which I am not sure applies here.

I upvoted because: nice find. I suspect the answer may lie in a whimsical comment coining the term made to a journalist more than a hard-science definition. Google Ngram shows 0 results.

@ARogueAnt. I updated a few minutes ago to add the link to the PNAS article which uses "kinematic self-replication" (a robotics term) rather than "kinetic replication". I'm surprised Ngram didn't at least pick up the two papers I've linked to, do they only search in books or do they also check journal articles?

I'm not certain. The reference which leapt out at me was to the superpower of one of the X-Men, hence the whimsey.

It seems to me, having watched the video in the CNN link, that what is being referred to might be autocatalysis: the concept that the product of a reaction can catalyze the same reaction.  Auto-proteolysis is a great example. Despite what Wikipedia says, autocatalysis as an explanation for the origin of life long predates 1995. See this video for a great explanation by Manfred Eigen, who received the Nobel prize in 1967

@user338907 excellent video and explanation, thanks!

@user338907 nobody has posted an answer yet, perhaps that link and a very brief summary of a few key points will work an an answer?

The short answer to your main question: "what is a kinetic replication?", is that all known mechanisms of replication can be labelled kinetic because they are dynamical processes involving molecular motion.
The second and the third paper you cited use the term "kinetic" in the context of chemical kinetics. That is, studying the reaction rates of many (different) chemical molecules. I would assume that most biological papers would use the term "kinetics" in a similar context (bio- chemical kinetics).
However, the first paper you cited talks about something different. The term they use is "kinematic" which is deliberately intended to describe a unique phenomenon pertaining to physical motion of cell structures.
See the significance statement of the paper:

Some molecules also replicate, but by moving rather than growing:
They find and combine building blocks into self-copies. Here we show
that clusters of cells, if freed from a developing organism, can
similarly find and combine loose cells into clusters that look and
move like they do, and that this ability does not have to be
specifically evolved or introduced by genetic manipulation.

In classical physics, kinematics pertains to study of motion and this paper also refers to physical motion of cells.
Chemical kinetics is also based on movement of molecules but these movements can also cause new chemical bonds to form. Thus the changes do not merely occur in spatial co-ordinates. The PNAS paper authors present an example model of self perpetuation (also called replication) that is primarily based on spatial reorganization. Their results do not talk about any chemical changes occurring in the cells. Perhaps they do occur (my guess; like change in expression of cell adhesion molecules) but the overall mechanism still appears to be mostly physical.
Coming back to your original question. I don't think anyone really uses the term "kinetic replication" and that's the reason you could not find any references to it. The CNN reporter indeed made a typo when referring to the PNAS paper.

Luckily I'm at home at the moment because when I got to the last sentence I laughed out loud. :-) Well if a CNN typo caused me to learn some new things, then I can be happy about it. I'll need one more cup of coffee before I can take in the full extent of your answer, but I can say right now thank you for taking the time to write such a clear and comprehensive answer!


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How does rate of evolution/innovation scale with population size?
I understand that there will be many other factors that affect rate of evolution/innovation. However, other things being equal, how will the rate of evolution vary between two populations of different sizes? Does doubling the population size double the rate of introduction of new traits?
Is this answerable for evolving life in general, or do different forms of life have different scaling laws? For example, is it different for sexual and asexual life?

I'm no evolutionary biologist but surely the rate (meaning the frequency) for a given mutation won't change if two populations are of different size, but the likelihood of observing it at a given time probably will. Obviously I'm assuming any mating won't change/affect the rates. But I could be totally wrong!

@Bez you mean the rate for an individual will be the same, but its rate of occurrence in the population will be proportional to the population size?

Yes! that sounds about right!

@Bez I can see intuitively that the rate of appearance of a given mutuation (good/bad/neutral) will be proportional to the population size, but it isn't clear to me whether the same will apply to new traits being adopted. For example, if a trait requires 3 separate mutations to occur in a specific order, will its probability of occurring still scale linearly?

It still should since you can calculate the probability of a sequential mutation just as you can calculate what are the chances of getting a 4, 5 and 6 in that order after throwing the dice exactly 3 times! The higher the number of throws, the higher its probability of occurrence but the overall chances of getting that particular order won't change! Obviously I'm discarding the concept of selection pressure etc!

One thing I expect to make a difference is the time taken for a new trait to spread sufficiently, before the next trait that builds on it can occur. Would doubling the population mean that the next trait occurs in half the time, but subsequent traits take longer?

Let us continue this discussion in chat.

Interesting question (+1) but not that easy to answer. I'll give a try!
First, the rate of evolution and rate of adaptation are two different things.
There are two main thing processes that quantitatively differ in populations of different sizes. 1) population-wide mutation rate and 2) genetic drift.
1. Population-wide mutation rate
Large populations create more mutations at each generation and therefore if the rate of evolution or the rate of adaptation is limited by the genetic variance, then one can expect large population to have higher rate of evolution and higher rate of adaptation.
--> Large populations may have higher rate of evolution and higher rate of adaptation
2. Genetic drift
However, small population have higher drift, resulting in a higher probability of fixation for new neutral (or slightly deleterious) mutations. It results that a small population will fix (fixed: frequency = 1) a higher proportions of the new mutations through time than large populations.nActually the probability of fixation of a neutral mutation is \frac{1}{2N}. Therefore, the rate at which neutral alleles fix is $\mu\cdot 2N \frac{1}{2N} = \mu$, where $\mu$ is the mutation rate. So, the rate of fixation of neutral alleles is independent of the population size.
--> Small populations have more drift but this doesn't necessarily yield to higher rate of evolution
Other and comments
Shifting balance theory
If adaptation is limited by the genetic architecture, that is, only mutation of very big effect on phenotype can be advantageous, then small population have the advantage to be able to accumulate slightly deleterious mutations, so that they can get off a local peak on the adaptive landscape and eventually manage to evolve toward a new higher fitness peak.
--> Small population may have higher rate of adaptation
Population-wide mutation rate vs genetic drift
Weighting the relative importance of rate of production of neutral (or quasi-neutral) mutations (See population-wide mutation rate above and the probability of fixation of neutral (or quasi-neutral) mutations (See Genetic drift above) depends also on the probability distribution of mutational effects (=probability distribution of the effect on fitness of a given new mutation).
Ceteris Paribus
The comparison between large and small populations are dependent on the state of other parameters. So even when saying all else being equal (ceteris paribus), we need to know what these other parameters are equal to, in order to answer the question because there are interactions between populations size and other parameters in explaining the rate of adaptation and rate of evolution.
Other impact of population size on genetic features
Population size has many impacts on various genetic features, such as pattern of genetic diversity, distribution of per locus Fst between subpopulation, and other things. This paper is likely of interest

There is probably other processes I forget about. Also, there is probably some sources that offer some quantitative measure of the general effect of population size on adaptation.

On point 2: for strictly neutral mutations, the increase in fixation probability ($1/N$) in small populations is exactly canceled by the reduction in the mutation flux ($N\mu$), so the rate of evolution is independent of population size.

@DanielWeissman I'd be interested to see an answer expanding on this.

@Remi.b I'm not sure I understand your comment. Drake's Rule refers to the product of the per-base mutation rate and the genome size, not the population size.

Oops. You are totally right! Temporary brain malfunctioning! To defend myself more than I should, I would note that I would expect a rough tendency for species with small genome size to have large population size. I deleted my comment above. Thanks!

It looks like that we humans can’t estimate this for now (to answer this in binary way Yes/No). Is it?

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Looking for a gene in my raw genetic data. What are the possible causes for this?
Obviously, I barely know what I am talking about.
But I want to find the "MUC5B promoter polymorphism rs35705950" in my RAW genetic data from 23andMe. (see this paper  http://www.ncbi.nlm.nih.gov/pubmed/23695349)
I think rs35705950 is the SNP number...   When I search I get no results.
When I search for MUC5B I get 9 results, but the SNP numbers doesn't match.
My question(s)
Is it possible that I just don't have this gene (rs35705950)?
Does 23andMe not have ALL of my genetic information?
Am I doing something wrong or misunderstanding what I am looking for?

Let's set things straight. The genomes of humans are highly similar and in general everyone shares the same genes. SNPs, or Single Nucleotide Polymorphisms, are single basepair positions in the genome in which there tend to be differences between people. This means, that instead of measuring the whole genome sequence for a person, which is very expensive and difficult, we can just examine a subset of the genome (the SNP positions) and capture most of the unique characteristics of that genome.
23andMe do exactly that. They measure a large set of SNPs (but not all of them), and thus give you some useful information about your unique DNA sequence. So you would need to look in the output given to you by 23andMe and see if they measure the SNP in question (rs35705950).
What do SNPs have to do with genes then? Well, if one of these SNPs occurs inside a gene, it could affect the gene, for example by producing a slightly different protein that could lead to some phenotype. So, studies link SNPs to different phenotypes such as disease or hair color. Usually the link is not one-to-one, but given as a probability.

In short, rs35705950 is not a gene, but rather a SNP, a SNP that occurs within the gene MUC5B. 23andMe measures a selected subset of human SNPs, less than 0.1% of the genome.

So I suppose 23andMe does not have the data for this SNP, given that I cannot find it in the RAW data search.  Are there other services that would sequence your entire genome or a given SNP?

Sequencing your whole genome would be thousands, if not ten thousand dollars.  That's not what you want.  There is a Taqman assay designed for it, which is good, but I don't know how you would find a commercial lab to run the assay for you.

@Blankasaurus checking a specific SNP would be trivial for a molecular biologist, this is the type of thing you do in an undergrad molecular biology lab course. I am pretty sure you could pay some company to do this as well. Basically you can take some saliva, extract DNA, and use PCR (Polymerase Chain Reaction) to amplify the region of interest, and then sequence it using Sanger sequencing.

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Why should plants transform glucose into sucrose before transporting it to other parts?
I've learned that plants transform glucose into sucrose before sending it into phloem. But the process seems to be complex and energy comsuming. Why should plants do it? Is it really necessary?

Glucose, fructose and galactose are the three dietary monosaccharides. Glucose and Fructose are  simple monosaccharides found in plants. A monosaccharide is the basic unit of carbohydrate and the simplest form of sugar, glucose are aldose and Fructose are ketose.

If the carbonyl is at position 1 (that is, n or m is zero), the molecule begins with a formyl group H(C=O)-, and is technically an aldehyde. In that case, the compound is termed an aldose. Otherwise, the molecule has a keto group, a carbonyl -(C=O)- between two carbons; then it is formally a ketone, and is termed a ketose. Ketoses of biological interest usually have the carbonyl at position 2.
  http://en.wikipedia.org/wiki/Monosaccharide

Whereas Sucrose is a disaccharide composed of glucose and fructose. A disaccharide is more complex than monosaccharide, more complex compounds like oligosaccharides and polysaccharides exists. Sucrose synthesised within the cytosol of photosynthesizing cells is then available for general distribution and is commonly trans located to other carbon-demanding centers via the phloem.
Sucrose and starch are more efficient in energy storage when compared to glucose and fructose, but starch is insoluble in water. So it can't be transported via phloem and the next choice is sucrose, being water soluble and energy efficient sucrose is chosen to be the carrier of energy from leaves to different part of the tree. Another problem exists,   glucose is highly reactive and this may result in some intermediate reactions while transporting glucose. Being a complex structure, sucrose is not as much reactive as glucose. So plants uses the sucrose as a medium to transfer energy. Inside the cells, sucrose is converted back to glucose and fructose. Energy is yielded when it is needed. So plants transfer glucose and fructose in the form of sucrose in order to:

Increase energy storage
Efficient energy transfer
Removing in between reactions

References

Carbohydrates
Sucrose & Starch Biosynthesis
Sucrose Metabolism
Sucrose and starch synthesis
Disaccharide

there is no free glucose in the photosynthesis. Stop to spread that myth. The net product is G3P. The end products of photosynthesis are sucrose and starch, but never glucose. Do you test glucose in the leaves? No... it is always for starch. ;) The G3P is converted to sucrose and other molecules, for example, thiamine. Glyceraldehyde 3-phosphate occurs as a reactant in the biosynthesis pathway of thiamine (Vitamin B1), another substance that cannot be produced by the human body. Part of sucrose is then translocated to the phloem. Starch is stored in the stroma of chloroplasts. It is also stored in the amyloplasts in the roots, stems cells after sucrose suffers a conversion to starch.

Welcome to Bio. Could you post a reference to support your statement?

See very first statement in https://en.wikipedia.org/wiki/Calvin_cycle

During Calvin cycle, 3 molecules of CO2 combine with RuBP acceptors to form 6 molecules of G3P. 1 G3P molecule exits the cycle and goes towards making glucose while the other 5 are recycled, regenerating 3 RuBP acceptor molecules.
Plants do synthesise glucose.

This seems more like a comment to the foregoing answer. Some link would come in handy. Thank you!


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Are carbohydrates an essential component of human diet?
Are people able to satisfy all the needs of a healthy diet without consuming carbohydrates?
My question includes the assumption that a person has no health condition that would prevent them from meeting their caloric needs with only fat and protein.
I'm also not asking about the practicality of eliminating all carbohydrates.  If a person could consume no carbohydrates whatsoever, this other question would clearly matter a lot, but I'm not asking it.
If there are essential dietary components that happen to be carbohydrates, but are not converted into glucose, I'll say up front that it wouldn't satisfy what I"m asking.  However, it would be interesting footnote on an otherwise correct answer.

While it's possible to live that way for some period of time, your body will be dying of stress. Your liver and kidneys will be first to fail. Your brain and muscles will struggle as well. Regarding your last paragraph, dietary fibers (comprised of different carbohydrates) are essential to maintain healthy digestive system and microflora, and the later has a tremendous impact on your immunity.

@Christiaan it won't. Beta-exidation of fats produces acetyl-CoA that fuels the citric acid cycle when there are no sugar resources left.

@EliKorvigo, thats interesting. Will look into that, thanks.

@Christiaan sorry for the typo, it was supposed to be "beta-oxidation".

http://ajcn.nutrition.org/content/75/5/951.2.long Check this out.

@243 interesting article from Journal of Nutrition - I've never though of carbs as being essential - given that fatty acids can supply power via beta-oxidation and all the amino acids are either ketogenic, glucogenic, or both - and thus can supply the TCA cycle via anapleurotic reactions. Sounds like the Inuit populations with almost no carb intake do just fine - suggesting that dietary carbohydrates are not required for life - very interesting

From a theoretical perspective this is a very interesting question, mostly because it is difficult to completely abstain from carbohydrate intake on a normal diet. Even the popular low carb diets of the late 1990s and early 2000s (e.g. Atkins Diet, South Beach Diet) were just that, they were Low Carb, Not No Carb.
We know there are essential dietary nutrients for humans, like essential fatty acids and essential amino acids. The reason that these must be obtained in the diet is because humans do not have the enzymes to synthesize these nutrients de novo (aka, "From Scratch").
From a biochemical perspective we know that fatty acids and acetyl-CoA cannot be converted back into glucose or other carbohydrate intermediates. This is because of the irreversible biochemical reaction catalyzed by pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA. Thus, fatty acids (lipids) can be oxidized to acetyl-CoA (for the TCA/Krebs Cycle) but cannot be further converted to glucose within the body.
In terms of protein, however, amino acids are either glucogenic, ketogenic, or both. If amino acids are ketogenic, then this means they can be converted into acetyl-CoA for the Krebs Cycle. If amino acids are glucogenic, then it means that they can be broken down into glucose. The breakdown of amino acids can be used to synthesize glucose or for anapleurotic reactions of the Krebs Cycle.
As stated in the editorial noted in the comments of this question (From the American Journal of Clinical Nutrition), there are daily "requirements" for carbohydrates. However, it does not appear that any diseases are unmasked by very low to zero carbohydrate absorption (which is most closely occurs in the Inuit populations whose diet is entirely fat and protein).
So, if you ask the question "are carbohydrates essential components of a human diet?" the answer would be probably not. However, as mentioned above, carbohydrates are ubiquitous and it is impossible to abstain from all carbohydrate intake.

Below is a picture freely available online from this website (from Lehninger Principles of Biochemistry, 5th Edition) of the glucogenic and ketogenic amino acids and the metabolic intermediates to which they can be converted. This is how Krebs Cycle intermediates can be generated from amino acids and are not dependent on dietary carbohydrates.

Wouldn't ketogenesis on such a scale (for all glucose needed) lead to severe ketoacidosis?

@YviDe at first thought you might think so... but according to the article from American Journal of Nutrition it sounds like the Inuit populations live virtually as close to zero carbohydrates as you can get. It doesn't sound like they have any 'problems' like ketoacidosis. Prolonged starvation would also be a similar state - check out this great review from George Cahill...(http://www.med.upenn.edu/timm/documents/ReviewArticleTIMM2008-9Lazar-1.pdf)  I would guess that the development of ketone bodies would be gradual enough in a conversion to fats and proteins that the body could buffer it

Interesting. Is there data on the actual carbohydrate content of the Inuit diet? Meat does contain some carbohydrates, e.g. muscle and liver tissue contains appreciable amounts of glycogen, and all animal cells are thought to have a few % carbohydrate content in the form of ribose, glycoproteins, etc.

@Roland I don't think there is specific data on Inuit... but that American Journal of Nutrition article referenced above in the comments to the question is kinda interesting - I agree with you, though, some carbohydrates are everywhere

For completeness, it should be noted that the irreversibility of the pyruvate→acetyl-CoA reaction does not, in and of itself, preclude the conversion of fatty acids and acetyl-CoA into carbohydrates; plants do just that by short-circuiting the Krebs cycle into the glyoxylate cycle and releasing the extra two carbons as glyoxylate (which can then combine with acetyl-CoA to form malate, which can be turned into oxaloacetate, which can be used for gluconeogenesis) rather than carbon dioxide.  However, as almost all animals lack functional (1/2)

versions of the two enzymes required for the glyoxylate cycle to proceed, it is true for most animals that fatty acids and acetyl-CoA cannot be converted into carbohydrates.  (2/2)


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Identify this wild plant with brilliant scarlet red flowers
Location is Virginia, USA
They seem to last all summer

Possibly a species of Monarda?  AKA bee balm... https://www.wildflower.org/plants/result.php?id_plant=MODI

It looks like some kind of Lobelia. A close up of the flower itself would be very helpful.
I believe it is a Cardinal Flower:

This 1-6 ft. perennial has showy, red flowers in 8 in., terminal spikes. Each flower has three spreading lower petals and two upper petals, all united into a tube at the base. Erect leafy stems, often in clusters, with racemes of flowers resembling flaming red spires. The lower portion of the erect stem is lined with lance-shaped leaves.

That's it!  Thank you.


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How does the stomach handle continuous eating?
In biology class, we learned this familiar story:  Food enters the stomach, the stomach churns it with acid and enzymes, and then, somehow, the stomach senses when the stew is ready and releases it into the small intestine.
But this simple narrative implicitly assumes that all the food of a meal comes into the stomach at about the same time, and only then does the digestion process begin.  This is often not the reality.  What happens when we eat continuously over many hours, such as at a Super Bowl party, or an all-day summer barbecue, or a long afternoon at an all-you-can-eat crab shack?
Does every new bite cause the stomach to reset its process to zero?  "Uh oh, detecting fresh, undigested food...  better start over..."  But if the stomach resets to zero with every new bite, wouldn't it eventually grow overfull?
Or does the stomach eventually get fed up with all the new introductions and just start releasing whatever it has into the small intestine, ready or not?  In that case, when and how did it decide to proceed with incomplete processing?

First of all, the stomach releases the digested food continuously. Simply put, during digestion the pylorus regularly opens a bit so that small food particles (< 1-2mm) are able to leave the stomach – it's not a batch process (see also this question).
However, because humans tend to ingest a lot of indigestible materials (e.g. bones), there is a need to pass the larger indigestible particles – and this process only happens after all digestible food has left the stomach and thus is "reset" every time you ingest new digestible food.
So if you would continuously ingest food that contains indigestible parts (e.g. mice or other small mammals), the larger bones of those mice would accumulate until you take a longer break and the stomach could complete it's digestion – but for normal food, this does not matter since it will be broken down enough to leave your stomach continuously.

Source: According to Estimation of gastric residence time of the Heidelberg capsule in humans: Effect of varying food composition, 1985 (PDF), the  interdigestive migrating myoelectric complex (IMMC) is responsible for the emptying of of large undigested particles:

Recently, Hinder and Kelly (1), using radiolabeled techniques, demonstrated differences in the gastric emptying patterns of a liquid, a digestible solid, and an indigestible solid in dogs. Based on such experiments, it has been suggested that the emptying of large (>1 mm) indigestible objects from the stomach
  is dependent on the interdigestive migrating myoelectric complex (IMMC)

Furthermore the study shows that the IMMC gets triggered only after all digestible matter has leaved the stomach:

The longer GRT of the Heidelberg capsule compared with the t1/2 of the 99mTC-DTPA is consistent with the finding that large nondigestible solids are emptied by the IMMC once all of the digestible materials have passed through the pylorus into the duodenum

and

the interdigestive migrating myoelectric complex can be markedly delayed by frequent feedings with solids, and the interdigestive migrating myoelectric complex is delayed by both liquid and solid meals

and

Feeding has been shown to interrupt the IMMC; resumption of myoelectric activity is necessary for the passage of large nondigestible particles such as the Heidelberg capsule

Does the stomach need to start over after every bite? No. When the stomach digests food and some new food comes in, it just continues to digest the old and new food. The stomach releases small particles first and continues to crush large particles.
In the stomach and small intestine, there are mechanoreceptors and receptors that detect gastric acid, amino acids, etc., which stimulate the release of gastrointestinal hormones and the vagus nerve, which all together act as brakes or accelerators of stomach emptying (Nutrients, 2016).
In both continuous and "few meals a day" pattern of eating, the stomach emptying can be greatly affected by various food factors:

Consistency. Liquid foods empty faster than solid foods.
Particle size. Small food particles empty faster than the bigger ones.
Volume. Greater volume of food will stimulate gastric emptying sooner than a small volume.
Energy value: 300 Cal meal will empty faster than 600 Cal meal; the stomach tends to release a certain amount of calories per time
Water and drinks up to ~7% of sugar empty faster than those with >8% sugar (regular fruit juices and sodas)
Macronutrients:
Fat and soluble fiber (such as glucan from barley or pectin from apples) can slow gastric emptying.

Human factors that can slow down gastric emptying:

Psychological factors, such as anxiety
Physical factors, such as exercise
Diseases, such as diabetic neuropathy
Medications, such as antacids and opioids

Other sources:

Gastric Emptying, Claudia Cheng (Department of Anesthesia and Intensive Care, Faculty of Medicine, The Chinese University of Hong Kong)
Advances in the physiology of gastric emptying (Neurogastroenterology & Motility, 2019)


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Is olfactory input processed by the thalamus?
Is olfactory input processed by the thalamus? I know olfaction is the only sense that can bypass the thalamus, but are there cases where the input can project to the thalamus?

Short answer
Third-order olfactory neurons project to the thalamus and mediate conscious perception of odors.
Background
The human olfactory system is schematically depicted in Fig. 1. The olfactory system is indeed interesting, as it is the only sensory system in which the primary receptor cells project directly to the brain. The olfactory cells in the nasal sensory epithelium project via small, unmyelinated axons via the first cranial nerve to the olfactory bulb in the brain.
In the olfactory bulb, so-called mitral cells project to the olfactory cortex via the olfactory tract. Medial fibers project to the anterior olfactory nucleus and septal areas. Some others cross over to the contralateral olfactory bulb. Lateral fibers contact the primary olfactory cortex.
Now it becomes interesting - third-order neurons in aforementioned regions send projections to the dorsomedial nucleus of the thalamus, the basal forebrain, and the limbic system.
The thalamic connections are thought to mediate conscious perception of odor perception. The amygdala and the entorhinal area are neural components of the limbic system and may be involved in the affective and aversive components of olfaction.

Fig. 1. Olfactory pathway. source: Medscape


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Is curling the fingers considered digit flexion?
Is curling the fingers considered finger flexion and straightening the fingers considered finger extension? I feel like this is correct in everyday language, but I am not sure if it is correct in anatomical terms.

In the vertical plane, bending of the fingers is indeed referred to as flexion, while straightening is called extension. In the horizontal plane, spreading the fingers is called abduction, and approximation is called adduction (Fig. 1).

Fig. 1. Finger movements and terminology. source: US Dept. of Veteran Affairs


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Are humans more adapted to "light mode" or "dark mode"?
I was discussing with a colleague about using dark-mode vs. light mode and remembered an article arguing that humans vision is more adapted to light-mode rather than dark-mode:

I know that the trend “du jour” is to have a dark mode for pretty much
everything, but look around the world is not dark with a bit of light,
it’s actually the contrary. And as the human has evolved its vision to
adapt to this reality, it’s asking extra efforts on many people.

Unfortunately, no reference is provided to support this claim, so I am wondering if this is just an opinion or there are some studies to support this.
Wikipedia seems to confirm this somewhat since we are adapting much faster to "light mode" transition than to dark mode one:

This adaptation period is different between rod and cone cells and
results from the regeneration of photopigments to increase retinal
sensitivity. Light adaptation, in contrast, works very quickly, within
seconds.

Also, some studies confirm that working using light mode is on average more efficient than using dark mode:

light mode won across all dimensions: irrespective of age, the
positive contrast polarity was better for both visual-acuity tasks and
for proofreading tasks.

I am looking for arguments coming from evolutionary biology to confirm (or not) the assumption that human evolution favors light mode.

Meh, this evo thing is probably the wrong angle here. If you're looking at something dark in an otherwise fairly bright (room) environment, it is actually tiresome.

As an aside, you're less sensitive to flicker in a dark environment. https://www.sciencedirect.com/science/article/pii/B9780123742032002359 (see full text) So if that bothers or tires you (which is plausible with screens), then dark mode in a dark environment does help in that regard.

@Fizz: Yes, the world does not have a raster scan running through it :-(  Not so bad with LCD/LED displays as it was with CRTs (which would give me splitting headaches if I worked for a prolonged period in "light mode".  But the evolutionary biology arguments are beside the point: it is observed fact that many people do prefer dark mode.

Challenge: "Adapted to" is insufficiently specified. Visual resolution will be higher with a brighter display due to pupil constriction, but night vision will be impaired.

The "some studies" are wrong. Astronomical citings routinely have greater precision than the lens rules calculated in bright environments say they should have. Optical resolution simply is better with withe on black.

Even if the article’s conjectures were to hold, they would do so for quite other reasons than that “the world is not dark with a bit of light”. Yes; and the world is also experienced predominantly as indirect reflected light rather than direct projected light. Conditions rightly described as “optimal” in one environment (the great outdoors) may legitimatey differ in another (my home study). Even if my study is objectively sub-optimal, it may be beyond my means/power to make it so; thus, in the dark vs. light debate, one does not take all — providing both is important for accessibilty.

Most of us programmers who practically spend our life behind monitors, we prefer dark mode right from the start. It's better for the eyes, it doesn't take a lot of research, a white background is simply annoying. You can't focus, you turn on every light source in the room to help your eyes but still, white screen is disturbing and your eyes get tired a lot sooner. Dark mode is there for a reason. We've been using it since the age of Unix and MS-DOS, it's nothing new, it's only reinvented, as in, finally everyone else realized it too. It was a long lasting fight to convince people that no matte

"we are adapting much faster to "light mode" transition than to dark mode one" Of course: It's better to not see anything for 10 seconds than to have pain in the eyes for 10 seconds.

We should not forget that not all humas are equal. People from the autism spectrum (about 1% of all humans) tend to have a sensory processing disorder which can mean that bright light appears unpleasant. So even if light mode would be the better choice for most, it is not necessarily the best choice for all.

Found myself revisiting this in the wake of 2 developments: 1. I learned those w/ astigmatism can find dark-modes unusable due to the ‘starburst effect’, which light-modes don’t provoke as much due to diffs in pupil dilation. 2. My own eyes now hate light-colored backgrounds (especially on IPS displays). Bloodshot within minutes. No idea why; it’s never been an issue before! Since I’m now experiencing physical discomfort w/ lighter colors, I’m using dark-modes for respite… I stand by my earlier claim: it’s an accessibility issue, not mere style preference. One size does not fit all.

A question that requires quite a lot of guts to ask on this site :) Nonetheless, and risking sparking a debate, there are a few arguments that spring to (my!) mind that can support the notion that we thrive better in 'day mode' (i.e., photopic conditions).

To start with a controversial assumption, humans are diurnal animals, meaning we are probably, but arguably, best adapted to photopic (a lot of light) conditions.
A safer and less philosophical way to approach your question is by looking at the physiology and anatomy of the photosensitive organ of humans, i.e., the retina. The photosensitive cells in the retina are the rods and cones. Photopic conditions favor cone receptors that mediate the perception of color. Scotopic (little light) conditions favor rod activity, which are much more sensitive to photons, but operate on a gray scale only. The highest density of photoreceptors is found in the macular region, which is stacked with cones and confers high-acuity color vision. The periphery of the retina contains mostly rods, which mediate low-visual acuity only. Since highest densities of photoreceptors are situated at the most important spot located at approximately 0 degrees, i.e., our point of focus, and since these are mainly cones, we apparently are best adapted to photopic conditions Kolb, 2012).
An evolutionary approach would be to start with the fact that (most) humans are trichromats (barred folks with some sort of color blindness), meaning we synthesize our color palette using 3 cone receptors sensitive to red (long wavelength), green (intermediate) and blue (short). Humans are thought to have evolved from apes. Those apes are thought to have been dichromats, which have only a long/intermediate cone and a blue cone.  It has been put forward that the splitting of the short/intermediate cone in our ape ancestors to a separate red/green cone was favorable because we could better distinguish ripe from unripe fruits. Since cones operate in the light, we apparently were selected for cone activity and thus photopic conditions (Bompas et al, 2013).

Literature
- Bompas et al., Iperception (2013); 4(2): 84–94
- Kolb, Webvision - The Organization of the Retina and Visual System (2012), Moran Eye Center
Further reading
- Why does a light object appear lighter in your peripheral vision when it's dark?

The di/trichromat approach really isn't all that relevant to computer displays, unless you're really into syntax colorization.  (Something I detest, but tastes differ.)  What matters is contrast between light and dark, and you could probably have readable displays at intensity levels where only the rods are activated.  The example I like to use is stars on a dark sky. Tt's easy to see individual stars, or lighted pixels, on a black background, not so easy to pick out a few dark pixels on a white display.

This answer gives some interesting thought directions, but they don't really have anything to do with dark mode vs light mode. Dark mode isn't dark in the sense that the range of brightness is lower, but in that the bright features are smaller. In practice, it is perfectly possible to use dark mode in photopic vision. Vice versa it is even possible to use light mode in scotopic vision, though that requires turning the total luminosity way down (which I'm pretty sure is worse for the eyes than scotopic dark mode).

@jamesqf, I agree, but the fact we can operate well in the dark  doesn't take away the fact we do better in daylight overall. In the end, evolution will not have favored spotting stars in the sky, or pixels on a dark screen. I chose to approach the question from a scientifically more likely angle.

@leftaroundabout I personally want my screen to be generally similar to ambient brightness, easier to ignore surroundings (= light mode during day and dark mode during night with lights off). From this answer we should preferably be in a well-lit environment. Then the question becomes - should the features be even brighter, or darker? Tech to make them darker is trivial (just not turn those pixels on) while not many screens let you make them even brighter - though it would be interesting to see what is better in that case.

@jamesqf the brightest stars are seen with cones. This is easy to understand if you remember that you can see e.g. Sirius looking at it directly, with your fovea. OTOH, it takes significantly more effort to view very dim stars (that can stimulate only rods): one needs to use the averted vision technique, which not only gives smaller resolution, but also is a bit uncomfortable: one has to train to avoid the temptation to look at the object directly, since in that case it will become invisible.

@AliceD I'm sure spotting night predators in the dark would have been quite important to early apes and humans. Cats and wolves are very easy to spot for humans in the dark. It's also handy for things like finding water, and in general, specular reflections are a typical example of light-on-dark objects of interest. And of course, there's considerable variation in what different people find comfortable or efficient; I feel people overly focus on finding the "one best thing". If dark-on-light works for you, great; if it doesn't, also great. It's not as if there isn't choice.

@AliceD: As usual, the problem with saying "we do better" is that we differ.  The demonstrated fact that a significant fraction of computer users prefer dark mode demonstrates that, I think.  And I would bet that a good many of those who say they prefer light mode have never given dark mode a real chance :-)

@jamesqf I personally highly prefer dark mode as it is more relaxing to the eyes and mind. But the visual system hasn't evolved for 10-hours-per-day-screenwork. I guess that's the point of my post. I've never attempted to defend 'use light mode when behind the screen'. I've just attempted to write an answer that highlights the evolutionary backgrounds of the visual system, without stepping into an opinion that cannot be backed up by literature.

Humans are thought to have evolved from apes... replace this with Humans share a common ancestor with apes, and.... Our evolutionary history is more fleshed out than just a "thought"

@jamesqf I don't think it's clear-cut. I've always found that light-on-dark themes cause me more eyestrain when dealing with text.

@ssokolow: As I said, people differ, and one size, or one color scheme, obviously doesn't fit everyone.

@Isaac and more recently, "Apes" is used as a monophyletic group, including humans and other hominids. So Humans are apes.

Scotopic periphery vs. photopic fovea seems like it may correspond to my preference for "dark lite" themes, where only the UI elements are dark, while content areas remain light.

From experiments it seems you should better use dark mode if you want to prevent myopia:

Using optical coherence tomography (OCT) in young human subjects, we
found that the choroid, the heavily perfused layer behind the retina
in the eye, becomes about 16 µm thinner in only one hour when subjects
read black text on white background but about 10 µm thicker when they
read white text from black background. ... Therefore, reading white
text from a black screen or tablet may be a way to inhibit myopia,
while conventional black text on white background may stimulate
myopia.

https://www.nature.com/articles/s41598-018-28904-x

So although humans are commonly awake during the day and sleep at night it seems that this fact is actually irrelevant when it comes to the effects of dark/light mode for the health of your eyes.

This makes sense. I've been using white text on dark backgroun since the early nineties - not because it was something the cool kids did (none of them did it back then :) ) but because when most pixels on your screen are at RGB 255,255,255 - i.e. full intensity white - it's like staring into a floodlight all day - something I didn't think was a healthy option. A few people asked why my screen looks weird and I explained my eyes never get tired this way and some switched to dark backgrounds on their PCs and were amazed at the difference to their eye fatigue.

Both.
More specifically, we're a kitbashed light-mode version of a primarily dark-mode group of animals. Mammals famously have terrible color vision, most mammals are dichromats (red color-blind) whereas most other animals like fishes, amphibians, reptiles, and birds are trichromats or even tetrachromats (seeing into the ultraviolet spectrum). In their evolution mammals got rid of a lot of their cones and replaced them with rods, giving them much better dark vision at the expense of not being able to see good colors. But this was back in the Mesozoic, when most mammals were nocturnal, crespuscular, or burrowing, and color vision wasn't a huge deal.
Primates then re-evolved color vision by duplicating and repurposing a cone for green some time in the Eocene. It is thought that they did this because it helps in identifying ripe fruits, which are often some shade of red, orange, or yellow, from green unripe fruit. We also lost our tapetum lucidum, which is the reflective layer of the eye that you see when shining a light in most animal's eyes that greatly enhances night-time vision. No one knows why, it may be genetic drift. Unfortunately our color vision isn't great, so we're kind of stuck in this awkward intermediate between other mammals, which can see great in the dark but have no color vision, and birds and reptiles, which have amazing color vision but are borderline blind in the dark (owls being the obvious exception).


text:
Do the BLAST scores have any relation between them?
Is there any relation among the BLAST scores (E-value, similarity, identity, gap, bit score)?  Is the e-value score for an alignment proportional to other scores, such as similarity score (i.e. the lower the e-value, the higher the similarity)?
Thank you!

This answer might be useful: http://biology.stackexchange.com/a/40862/16651

Yes there is a relationship between them but you may not be able to observe correlation between some of them.
Number of matches and score are definitely proportional, however higher similarity would translate to higher score only if the lengths of the scoring pairs are the same. Gap would have a negative effect on the score but it totally depends on what your scores/penalties are (see BLAST help and documentation).
E-value is basically the likelihood of two random sequences having a certain match score from a given database. So whether or not it is low for a hit depends on the score distribution of the database. Lower E-value does not mean higher similarity. It means that a hit of this score has a low likelihood to be found by random chance. The score distribution is generally skewed towards low scores and so high scores usually have low E-value but what a "high" score is totally dependent on your queries and therefore this statement cannot be generalized.
From BLAST docs:

$$E=K.m.n.e^{-\lambda.S}$$
This formula makes eminently intuitive sense. Doubling the length of
  either sequence should double the number of HSPs attaining a given
  score. Also, for an HSP to attain the score 2x it must attain the
  score x twice in a row, so one expects E to decrease exponentially
  with score. The parameters K and lambda can be thought of simply as
  natural scales for the search space size and the scoring system
  respectively.


text:
Bigger animals needs bigger amount of oxygen?
Bigger animals, like Elephants, or Dinosaurs for example, are in need for more oxygen than the amount of oxygen that small animals need? (humans, dogs, cats, etc)
Thanks in advance.

If all animals need the same concentration of oxygen throughout their tissues, larger animals need more O2 because they more tissue, but metabolism is probably more important than size alone. One thing to consider isn't so much the amount of oxygen but the diffusion of oxygen. Large animals have trouble getting oxygen to all of their tissues, so they have lungs, hemoglobin, and efficient circulatory systems to move the oxygen in and CO2 out. Small animals have less tissue to diffuse through, so they can rely more on simple diffusion of atmospheric oxygen through their bodies.

I'm not an expert but I think it's pretty obvious.. Bigger animals do require more energy and thus more oxygen for cellular respiration. They also have bigger lungs, although the rythm of the breathing is slower.

Animals with the same metabolic rates need the same amount of oxygen per unit body mass, larger animals have slower metabolisms than smaller ones (that's also why they need less food per unit body mass).  1 ton of rats use more oxygen than 1 ton of elephant. bigger animals need better ways to distribute the oxygen, that is better ways to absorb and transport it. One of the reason Sauropods got so big was they have a much better breathing mechanism than mammals.


text:
Are there any similarities in the DNA of a humans and animals?
As the title says, i've been wondering if there are any similarities between the DNA of humans and the DNA of animals?
Like, maybe monkeys are more similiar in their DNA to humans, than dogs are (to humans)?
Thanks in advance, sorry if there are any english mistakes.

see: http://biology.stackexchange.com/questions/20038/same-dna-vs-genes

Genome-wide variation from one human being to another can be up to 0.5% (99.5% similarity)

Chimpanzees are 96% to 98% similar to humans, depending on how it is calculated. (http://genome.wellcome.ac.uk/doc_WTD020730.html)

Cats have 90% of homologous genes with humans, 82% with dogs, 80% with cows, 79% with chimpanzees, 69% with rats and 67% with mice. (http://genome.cshlp.org/content/17/11/1675.full)

Cows (Bos taurus) are 80% genetically similar to humans (http://www.sciencemag.org/cgi/content/full/324/5926/522)

75% of mouse genes have equivalents in humans (http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1000112), 90% of the mouse genome could be lined up with a region on the human genome (http://www.genome.gov/page.cfm?pageID=10005831) 99% of mouse genes turn out to have analogues in humans (http://www.nature.com/nature/journal/v420/n6915/full/420509a.html)

The fruit fly (Drosophila) shares about 60% of its DNA with humans (http://www.genome.gov/10005835).

About 60% of chicken genes correspond to a similar human gene. (http://www.sciencedaily.com/releases/2004/12/041208230523.htm)


text:
Determining break/border of movement
A population given inhabiting an area. I can trace every individual and I've got the hypothesis there is a break in distribution like individuals born in the upper half of the area will rarely move to the lower half and vice versa.
Tracking each individual how can I determine the line/border which divides the population in a upper and lower half. What's the math or algorithm behind to draw this imaginary line?

Make sure to not let your hypothesis cloud your analysis. What if there are three, or five populations with distinct moving patterns?

Even if there are more than two populations the general question is still to determine if there is a break in distribution and how "geographically" locate this.

You should look into ordination techiques, to which you can apply different clustering techniques. Take a look at the R package vegan, which can do but ordination and calculate clustering.

There are a lot of approaches to this kind of problem. Starting with the simplest approach I think you'd benefit from using a K-means classification, with K=2 (or higher numbers to address @Luigi's concerns about model bias.) Once you've defined the geometric center of each population, you can treat them as foci, and use the equidistant points between each focus to define the boundary of interest. That does import another assumption (that the boundary is equidistant to the two points).
A more sophisticated way to divide two clusters is with a support vector machine but because this is a machine learning approach, you'd need to manually annotate a number of training data sets as "group 1" or "group 2." But after training, the SVM will define the optimal boundary (hypersurface) between these groups.
The two types of approaches (clustering versus machine learning) differ in where the manually-imported assumptions lie. One can combine them fruitfully -- using K-means to define the populations and SVM to define the dividing boundary.


text:
Relative sweetness
I have noticed that when I eat something sweet, then afterwards, I eat something else that is sweet, the second sweet food is not as sweet as it usually is. I am pretty sure many others have a similar experience before too. Why does this happen?

Our senses generally adjust their sensitivity according to the signal strength, e.g. by neural adaptation.

@augurar good call on neural adaptation. I originally mistakenly called it "habituation" in my answer, which it turns out is slightly different.

What you describe is an example of neural adaptation, whereby neural response to a consistent stimuli becomes reduced with repetition. This occurs not just with sweetness (as shown empirically in this study on sucrose consumption by rats), but with many other types of stimuli (the feeling of clothes on your skin, the particular smell of your own home) as well.
In general, our senses are tuned to detect relative changes in our environment rather than absolute values. For example, if I were to place an unmarked 10 kg weight in one of your hands and a 12 kg weight in your other hand, you might have some trouble telling me what the exact mass of each weight is. You would have no trouble whatsoever telling me which weight was heavier. Neural adaptation allows us to maintain the ability to make these kinds of distinctions over a wide range of stimuli intensities.
There is no scientific consensus as to the exact mechanism of neural adaptation (and there probably isn't just one), but there are many candidate processes at the level of individual neurons, such as long term depression. Grill-Spector et al published a widely cited paper a few years ago called "Repetition and the brain: neural models of stimulus-specific effects" in which they put forth several potential mechanistic models of neural adaptation.


text:
Applications of shortest path problem
The shortest path problem is the problem of finding the shortest path between multiple nodes. What are the applications of the shortest path problem in biology?
A simple google search gives me this - http://mutage.oxfordjournals.org/content/30/2/191.full.pdf
This, unfortunately is under a paywall.
Apart from that article, I can't find anything else useful.

Why the downvote?

There are several applications. This question is too broad. (Not my downvote btw)

@WYSIWYG like? A simple google search doesnt give me anything...

look for "bioinformatics" instead of "biology". ;-)

The classic application is analysis of graph data. For example, protein-protein interaction networks or gene regulatory networks and the like. There are various types of data that can be presented in the form of a network and network analysis is an integral part of Systems Biology.
Another example is determining the similarity of functional annotations from the Gene Ontology. One of the ways of doing so is finding the shortest path between two nodes in the GO graph.
Or, for a more concrete example, I recently published a paper where I examined various features of a particular group of proteins. One of the pieces of information I used was how central these proteins were to the network and, for this, I measured how often they served as a node in the shortest path between two others.
The simplest way for you to find more example is to go to PubMed and search for "shortest path":
https://www.ncbi.nlm.nih.gov/pubmed/?term=shortest+path

Thank you for your answer... Can you please give me a link to your paper?

@TanMath here you go, but it won't help you much. The shortest path analysis was a tiny part of the work, I only mentioned it because I happened to have done this recently. Your best bet is to go on PubMed and search for "shortest path".

Hace you seen my latest question about influenza? Do you know anything about that?


text:
How semi-synthetic cell with artificial DNA works
I know that by now this is old new but I heard that a cell that used a synthetic pair of nucleotides, called X and Y, have been made. My question was, how did the cell understand the X and Y nucleotides during translation and how was it even represented in mRNA? It must have been represented differently, possibly using X and Y nucleotides only. That's the only way I can think of that causes the cell to make 172 amino acids instead of the usual 20. By the way I read this in the Discover magazine, January issue.

The altered E Coli still only made use of the regular 20 amino acids (presumably).
Looking at the original citation, Malyshev et al didn't characterize the RNA in their altered E Coli at all. All they did was add free X and Y to the E Coli's growth medium and add a gene to the E Coli that expressed an algal nucleotide triphosphate transporter. Malyshev et al then demonstrated that replication (copying of the DNA) proceeds normally and in such a way as to preserve the X and Y content.
So no information as to whether any of the products downstream from the DNA (ie mRNA, proteins, etc) were affected by their modifications.