As you correctly point out, designing an optimal primer pair for 16S-rRNA sequencing is a tricky affair because even the less-variable regions are not same between different strains and species. Sambo et al (2018) have even developed a bioinformatics software for optimal design of primers for 16S-rRNA sequencing for multiple bacteria.

  We propose here a computational method for optimizing the choice of
  primer sets, based on multi-objective optimization, which
  simultaneously: 1) maximizes efficiency and specificity of target
  amplification; 2) maximizes the number of different bacterial 16S
  sequences matched by at least one primer; 3) minimizes the differences
  in the number of primers matching each bacterial 16S sequence. Our
  algorithm can be applied to any desired amplicon length without
  affecting computational performance.

There is diversity in the 16S-rRNA genes within the same species i.e. the different copies are not exact duplicates (Větrovský & Baldrian, 2013).

  Větrovský & Baldrian (2013)

Interestingly, the different rRNA operons in E.coli have different promoters and are even differentially expressed during stress conditions (Kurylo et al., 2018).

However, Kitahara et al. (2012) found that 16S-rRNA genes isolated from soil samples, in place of the original E.coli gene, could support its growth. In other words E.coli is highly robust to mutations in its 16S-rRNA.

  After counterselection, ∼200 clones of KT103-derivatives (carrying
  pRB103 whose 16S rRNA gene was substituted with foreign genes) were
  obtained, from which 33 nonredundant 16S rRNA genes (A01–H03) were
  identified. Through multiple alignment of E. coli 16S rRNA and our
  metagenomically retrieved 16S rRNA sequences, it was found that at
  least 628 (40.7%) of the 1,542 nucleotides were variable, indicating
  marked mutational robustness of the 16S rRNA. Strikingly, the
  functional 16S rRNA sequences (except A10 and F02, which were 99.0%
  identical to E. coli 16S rRNA) obtained in this study showed only
  80.9–89.3% identity to E. coli 16S rRNA, which was well below the value reported thus far (Proteus vulgaris 16S rRNA, 94% identity to E.
  coli 16S rRNA)

For your question

  But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB,
  rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a
  particular operon used for the 16S position notation?

I don't think any one of them is considered the reference. The complete E.coli 16S-rRNA sequence reported in NCBI seems to consider a "consensus" of different reported sequences:

  [5], [7] contain updated sequence data for the original work by the
  same laboratory [4]. There were too many discrepancies between [4] and
  [5], [7] to list each revision in our sites table. The sequence shown
  is from [7]. [4], [5], [7] point to a number of cistron
  heterogeneities. There is uncertainty, however, with regard to
  assigning these various heterogeneities to specific cistrons. The RNA
  method used by [4], [5], [7] gives the average of all the cistrons
  present in the cell [7]. The heterogeneities are classified by their
  relative proportions into major, minor and undetermined species. The
  sequence shown corresponds to the major species. The heterogeneities
  were annotated as variations in the sites table. It is not known which
  of the residues 'c' (base 633) or 'a' (base 641) undergoes a deletion,
  giving rise to the minor component 'atctg'. [7] suggests the existence
  of one or two mutated cistrons among the known seven cistrons of
  ribosomal RNA. With the exception of a single base deletion, this
  sequence is identical to the current 16S rDNA sequence for the E.coli
  rRNB gene.

The NCBI page also lists different polymorphisms and base modifications in the 16S-rRNA within and between different strains/"species".

NCBI has several partial sequences as well. When I checked for P.aeruginosa and B.subtilis, I could find only one or two complete sequences (rest were partial). Moreover, each entry indicated the strain that it was obtained from. Therefore I assume there is no single reference sequence.

I guess that people do consider the different variants while doing phylogenetic analysis (or simply just look for conserved "signature" sequences for a given species). I am sure that there are computational algorithms for doing the classification in an optimal manner (see Chatellier et al., 2014). Since, I don't have an expertise in this area I cannot say anything conclusively about the routine practice. In fact there is still ongoing research in improving the analysis (for example, Yang et al., 2016 and Sambo et al., 2018).


Number of reading frames in nucleotide sequence

Every nucleotide sequence has six possible reading frames, because each codon (determining one amino acid) consists of a base triplet (3 frames), and there is a complementary strand which could be coding (3 reverse frames).

To find the possible open reading frames contained in your sequence, you have to look for start codons. That is: ATG. But, as said the complementary strand could be coding. So if your known sequence contains CAT, that would be ATG on the opposite strand and might also be an open reading frame.

Count them now and then read on to compare answers.

Your specific sequence contains four start codons (3x ATG and 1x CAT, which makes ATG on the complementary reverse).

5' ... AT ATG A ATG ATG A CAT ... 3'

3' ... TA TAC T TAC TAC T GTA ... 5'


Take a look at some pictures of eagle and owl and observe their beaks. It will help you in concluding which might have the widest binocular vision angle.


What is the convention for indicating genomic primer sites?

There is no such convention. People, mostly name their primers arbitrarily (or just FP and RP) and mention in the text about their binding sites.

In general, in the context of specific genes, the positions are described with respect to the transcription start site (TSS).


Do acetic acid bacteria use the electron transport chain when converting ethanol to acetic acid?

Yes

I find it somewhat ironic that in a response a recent post from the poster concerning itself with the precise definition of ‘fermentation’ I argued that this was a semantic question because of the use of the term in the English language before any biochemistry was known. I now discover that the term is used in an even looser sense than I was aware of — in an aerobic context. The conversion of ethanol to acetic acid by acetic acid bacteria is apparently referred to as oxidative fermentation as explained in this extract from a paper in The Journal of Bacteriology:

  Acetic acid bacteria are obligate aerobes that belong to the α-Proteobacteria and have a strong ability to oxidize ethanol, sugar alcohols, and sugars into their corresponding organic acids. Such oxidation reactions are traditionally called oxidative fermentation, since they involve incomplete oxidation of these compounds. These bacteria accumulate the corresponding incomplete oxidation products in large quantities in their surrounding environment.

The biochemistry is summarized by Gómez-Manzo et al.:

  Ethanol fermentation by acetic acid bacteria is carried out by two sequential reactions catalyzed by pyrroloquinolinequinone (PQQ)-dependent alcohol dehydrogenase enzymes (ADH) and aldehyde dehydrogenase (ALDH), which are located in the cytoplasmic membrane [6] and transfer electrons to ubiquinone Q10 [7]. PQQ-ADH is a periplasmic quinohemoprotein-cytochrome c complex and catalyzes the first step of ethanol oxidation by transferring electrons to Q10 and producing acetaldehyde which usually is the substrate for another enzyme (ALDH), and converted to acetic acid during the second step of ethanol fermentation.

The fact that the reduced pyrroloquinolinequinone is re-oxidised by ubiquinone, indicates that the conversion of ethanol to acetic acid requires the electron transport chain in the bacterial membrane to continue, and that the ultimate electron acceptor is oxygen.


...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).

Yes and no. Enhancers are in fact sometimes palindromic, so they're mirrored on both strands of the DNA.

  This is unlike a protein-coding DNA gene, which might need to be on both DNA strands

No. Protein-coding DNA is always on one strand only because transcription doesn't suddenly switch strands.

  in a so-called homozygous state, in order to surface as a phenotype - like the classic case of blue eyes.

No. Homozygous means on both chromsomes and has nothing to do with strands or the need for an allele to be homozygous to produce its phenotype because it's recessive.

  And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands. The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

This is completely all over the place and makes no sense to me. Either "strands" is used in the correct way, in which the previous statement is wrong, or "strand" is used as "chromosome", in which case there is no reason why an enhancer should only be on one chromosome. Just like the gene, it can be hetero- or homozygous. The statement about "having to wait for a change on both DNA strands" is more relevant to whether something is dominant or negative. Regardless, I don't think it's possible to make any statements here about enhancers allowing for evolution to progress faster.


Though I don't come across graphs like these too often, I guess the answer should be A because...

From the graph, it is clear that Leaf 1 has more mass than Leaf 2 after 5 hours. This means there is a lower rate of transpiration in Leaf 1, which can definitely be explained by a thicker cuticle (since the thicker the cuticle, less is the water lost). Hence choice A is correct.

Now, look at choice C. Like you said, in leaves where stomata are protected by hairs, there will be lower rate of transpiration. Then, obviously Leaf 2 should have a higher mass than Leaf 1, right? But this is not the case (as per the graph). Hence, choice C is incorrect.


Glaucus atlanticus consumes and reuses the nematocysts of jellyfish siphonophores. Perhaps not quite what you were looking for, as the animal doesn't simply concentrate the toxin, but actually co-opts entire stinging cells.

Further to your mention of dinoflagellate toxins being concentrated by fish, I seem to recall reading something about some toxins being modified in vivo into more toxic derivatives, but cannot find any mention of it.


Neuroscience and learning of a single neuron

No, you cannot teach a single neuron an alphabet.

In general, the way the brain learns and stores information is by adjusting the strength of connections between neurons. Therefore, there is not really any information in a given neuron, but in the pattern of how it's connected to other neurons.

For the example of the alphabet, there are a lot of different pieces of information to tie together: there will be different neurons that respond to the visual shape of a letter, the word that names the letter, the sounds that the letter represents in spoken language, the words that contain the letter, etc.

A general neuroscience textbook like Purves is a good place to start learning about how brains work. You might also learn about how artificial neural networks learn. They are definitely different from biological nervous systems, and the learning mechanisms vary, but they share some characteristics such as the information being represented in the strength of connections between units, usually called weights in an artificial network.


What's the name of this green fruit with little pikes fallen from a city tree on the pavement?

It is horse chestnut it is very common to plant chestnut trees in public parks and a lot of people do have them around their property and by the side of many roads.
What you have in your picture is the fruit and the leaves on the ground confirms that this is horse chestnut.
Source https://en.wikipedia.org/wiki/Aesculus_hippocastanum
The nut is poisonus and the toxin can cause loss of coordination and tremors in horses if they eat the nuts.
Touching or handling the nuts do not cause any adverse effect to humans they are only dangerous to humans if they are eaten.
Horse chestnut contains alcaloid saponins and glucosides that have a toxic effect on mamals.


What are the consequences of voluntary total celibacy?

I was told in my undergraduate degree that males produce sperm all the time, and that under conditions of no sexual stimulation, that sperm is excreted involuntarily every 15-16 days, at night, while dreaming. I was also told that the renewal rate of sperm is higher under regular sexual stimulation, which increases the fertility of the sperm that is excreted.


It very much depends on the river and location along that river. if there is a city upstream who is defecating into the river, you'd better not drink from that river. But drinking from the same river upstream of this city could be totally fine.

Disease transmitted through the faeces were very common in the the 19th century especially in cities that had no system of evacuation of wastes. Now, of course the prevalence of such diseases depends on the type of society and therefore on the era and location.

Generally speaking, it is always best to carry tap water (or bottled water) on you. If you have to drink from a river, be cautious, talk to local people, think of what could live upstream (people, cattle, ...) and always use a good filtration system before drinking from any river.


Why are there inverted repeats in response elements?

Starting with prokaryotic (i.e., bacterial) transcription factors--which were the first to be characterized in depth, this type of pattern was noted.  Even for the "classic" Type II Restriction Endonucleases used for molecular cloning have palindromic recognition sequences.  In all three cases the answer is that the sequence-specific DNA binding protein binds as a dimer, and so each monomer is recognizing a "half-site" (one of the inverted sequences).


The whole process is called osmosis. In it there is the flow of liquid along a concentration gradient. Water then flows from the side which contains the low concentration of dissolved molecules (this can be salts or sugar for example) to the side with the higher concentration until it reached equilibrium. This principle is shown in the image below (all images from the Wikipeadia article on osmosis):

The blue dots are the dissolved material, the concentration is high on the right side and lower on the left. Through the dotted line in the middle (which is a semi-permeable membrane) only the solvent can pass to reach a concentration equilibrium. There is a pretty cool osmotic pressure simulator available on Molecular Logic which can also help understanding the principle.

And this is exactly what happens to the yeast cells. The sugar crystalls get dissolved (at least partly) by some of the humidity from the yeast block (this will not work with dried yeast) and form a highly concentrated sugar solution (also called hypertonic). The sugar concentration inside the cells is relatively low (called hypotonic). This leads to the effort to balance the concentration inside the cell and outside of it which then leads to a massive efflux of water from the cells. This goes so far, that the cell membranes break and the interior of the cells is released (nucleus, DNA, proteins and so on) and the sugar is completely dissolved in the released water. The reason why this mixture is so "gooey" afterwards is the DNA, which forms long, thick strains.

This method can be used in the lab to break up cells relatively gently without applying too much force.

When baking you should make sure, that your yeast is not coming directly into contact with undissolved sugar (or salt which works the same way), as this will kill a part of your yeast cells. However, for baking you usually dissolve the yeast in water or milk, so there is a huge excess of water which dissolves the sugar (or salt) and protects the cells. Addionally your yeast is much better distributed in the dough and gives better results.


The classical division of humans and animals has always been self-centered and artificial. Humans are animals, competing with other organisms under exactly the same rules. Evolution involves trade-offs, strategies, and adaptation. Humans have been set on a path to use their brains to compete, rather than claws. But the concepts are the same. It happens that this is a very effective strategy, such that humans now dominate virtually every ecosystem on Earth, to the point that some are now calling the age we live in as the "Anthropocene". Humans are the apex predator. We now have no natural enemies, however as vectors of disease, mosquitos control our populations more than any other animal.


How does a metronome help in controlling breathing rate?

The paper in question used metronome to aid test subjects control their breathing rate. This seems like a good approach, much better, than asking "please, breath with 0.1Hz frequency".

  The subjects were asked to remain at rest in a supine position for 10 min, and then to control their respiratory rate with the help of a metronome at different breathing rates: 6 (near 0.10 Hz), 10 (near 0.16 Hz) and 16 (near 0.27 Hz) breaths/min.

Metronome is a device that produces any perceivable ticks (sound clicks or, maybe, light flashes can be used) with given and constant frequency. So patients were asked to synchronize their breathing with metronome clicks.

Only precaution in mentioned experiment is that high frequency of breathing can cause voluntary hyperventilation. Or if preset frequency is low and patient is trying to follow it, hypoventilation might occur. Fainting seems among the worst of consequences in both conditions (if person is relatively healthy).


plant crossing for creating breeding population

A cross was done among plant with the desired trait to create the breeding population. The breeding population was usually phenotypically selected for desirable traits.

That phrase is confused. To phenotypically select from a breeding population, you first have to generate the breeding population, which requires an initial cross of desired plants. The generations are generally labelled as F1 F2 F3 and checked for statistics. They can back-cross the mother plant onto herself. The selection refines itself as the number of crosses of the most desirable plants increases in generations.

Hybrid populations are often stronger and have a wider gene base, so if you want big fruit for a tree, you can cross an asian one with a european one, it might be more resistant and vigorous, gain stronger roots, better low N performance, and better structre from one plant, which is then mixed with the desirable traits for example of yield or mould resistance. The wider the gene base, the more potential diversity of individuals can be chosen which also contain the alleles from the desired traits, and the selections start with more options. The goal is to maximize the desired pheno's.

http://www.nature.com/nature/journal/v537/n7622/full/nature19433.html?foxtrotcallback=true


Why is the resting membrane potential of excitable tissue not affected by the extracellular sodium concentration?

I cannot imagine anyone being able to explain it more clearly than this webpage. Your question is addressed in the middle of the page.

It's easier to split the idea into two separate, but parallel ideas: electrical potential and chemical potential. Both sodium and potassium contribute to resting potential. Sodium affects the voltage (electric potential) across the membrane. However, their chemical potentials (difference-across-membrane) are separate. The key idea is that there is a difference between resting membrane potential and potassium equilibrium potential.

I quote a helpful thing to keep in mind:

In a neuron, the resting membrane potential is closer to the potassium equilibrium potential than it is to the sodium equilibrium potential. That's because the resting membrane is much more permeable to K+ than to Na+.

    If more potassium channels were to open up—making it even easier for K+ to cross the cell membrane—the membrane would hyperpolarize, getting even closer to the potassium equilibrium potential.
    If, on the other hand, additional sodium channels were to open up—making it easier for Na+ to cross the membrane—the cell membrane would depolarize toward the sodium equilibrium potential.


Evolutionary term for multiple, related adaptations

Co-adaptation

The term you are looking for might be co-adaptation. Co-adaptation is kind of a generalist term that fits many scneario, its definition (source: wikipedia > co-adaptation)

  In biology, co-adaptation, or coadaptation is the process by which two or more species, traits, organs, or genes undergo adaptation as a pair or group. This occurs when two or more characteristics undergo natural selection together in response to the same selective pressure. While the parts may be functionally independent they are only beneficial when together, sometimes leading to increased interdependence. Coadaptation and its specific examples are often seen as evidence for the broader process of coevolution.

You seem to be thinking about a chain of adaptations, where the first adaptation changes the selection pressure on another trait causing another adaptation. For this purpose co-adaptation is not the perfect term but I am afraid there is no perfect terms. You might want to consider the following ones though that help you express your ideas.

Structural interdependence

Ziegler et al. 2009 talk about structural interdependence and interdependence of internal organ.

Phenotypic space

Of course, you can use the frameworks of the phenotypic space (as in Pigliucci 2007) and of fitness landscape to talk about how a change in a given phenotypic trait affect selection pressures at other traits.

Phenotypic constraint

A phenotypic constraint (as in Pigliucci 2007) is a case of fitness valley in fitness landscape in the correlation between two of more phenotypic trait, hence causing a trade-off. Absence of such constraint are cases of interest to you

Phenotypic plasticity

It is common to talk about the ability of a specific phenotypic trait to vary to fit into the broader context of the whole body as phenotypic flexibility or phenotypic plasticity. There is a difference plasticity and flexibility for many but I don't think all authors use the exact same definition.

Phenotypic plasticity

  Phenotypic plasticity refers to the changes in an organism's behavior, morphology and physiology due to its adaption to a unique environment.2 Fundamental to the way in which organisms cope with environmental variation, phenotypic plasticity encompasses all types of environmentally induced changes (e.g. morphological, physiological, behavioural, phenological) that may or may not be permanent throughout an individual's lifespan. The term was originally used to describe developmental effects on morphological characters, but is now more broadly used to describe all phenotypic responses to environmental change, such as acclimation or acclimatization, as well as learning.5 The special case when differences in environment induce discrete phenotypes is termed polyphenism.

Exaptation

This is a poorly related term but it may eventually be of interest to you. The definition from wiki > Exaptation

  Exaptation [..] and the related term co-option describe a shift in the function of a trait during evolution. For example, a trait can evolve because it served one particular function, but subsequently it may come to serve another. Exaptations are common in both anatomy and behaviour. Bird feathers are a classic example: initially they may have evolved for temperature regulation, but later were adapted for flight. Interest in exaptation relates to both the process and products of evolution: the process that creates complex traits and the products (functions, anatomical structures, biochemicals, etc.) that may be imperfectly developed.

Phylogenetic signal

Phylogenetic signal is used way more often than the term exaptation. It is however also quite unrelated to what you are looking for but I added it because... well we never know what you'll find helpful!

  Phylogenetic signal is a measure of the statistical dependence among species' trait values due to their phylogenetic relationships.

For example, the existence of 4 limbs in vertebrates is a phylogenetic signal (see Why don't mammals have more than 4 limbs?)


What Effect would Cannabinoids have on the Acute Porphyrias?

Yes, they can induce an acute attack.

  Drugs metabolised by cytochrome P450 (CYP) such as analgesics may induce acute attacks in patients with hepatic porphyrias. In recent years, preclinical and clinical studies have suggested that cannabinoid pharmaceutical preparations may be potentially useful in the treatment of pain [1].

There is even a clinical case about acute intermittent porphyria in a marijuana user:

  Mr. G is a 55 year old Caucasian male with a past medical history significant for acute intermittent porphyria (AIP), chronic back pain, renal insufficiency, hypertension, and nicotine dependence. The patient has presented to the hospital with multiple AIP exacerbations since diagnosed eleven year prior to the current case. [...] Urine drug screen was positive for cannabinoids, which he admitted to frequent marijuana use [2].

But an experimental study on mice failed to prove that:

  Our findings indicate that CP-55,940 (a cannabinoid CB1 receptor agonist) and its metabolites do not behave as porphyrinogenic drugs and may potentially be safe for treating pain in patients with acute porphyrias [1].

References:

Fontanellas A, Manzanares J, García-Bravo M, Buzaleh AM, Méndez M, Oliva JM, Batlle A, Palomo T, Enríquez de Salamanca R. Effects of repeated administration with CP-55,940, a cannabinoid CB1 receptor agonist on the metabolism of the hepatic heme. Int. J. Biochem. Cell Biol. 2005 Aug;37(8):1620-5. doi: 10.1016/j.biocel.2005.02.010. PubMed PMID: 15896668.
Ware SK. Acute Intermittent Porphyria With Psychiatric Manifestations: A Case Report. Ment Health Clin. 2013;3(5):100. Available at: http://cpnp.org/resource/mhc/2013/11/acute-intermittent-porphyria-psychiatric-manifestations-case-report. Accessed July 27, 2014.


Using an analytical balance (0.0000 precision) to measure µg (micrograms)?

As others have said, that mass is too small to measure with a standard analytical scale. There are two options you could use:

Make a larger volume of your 200 ug/mL solution.
Make a concentrated stock such as 20 mg/mL. This a 100X stock; you can make 1 mL of 200 ug/mL proteinase K with 10 uL of stock and 990 uL of buffer. Small volumes are easier to measure than small masses (with a micropipette).


Spider identification: male black widow?

I think it's unlikely.  Without a photo, it's hard to be sure of anything, but Black Widows don't have reddish legs or enlarged fangs, and it's hard to think of any circumstances in which they could be called "very quick".
Your description might fit a spider called Dysdera crocata (here's a link: https://bugguide.net/node/view/3388 ), but that's purely a guess on my part.
The problem with trying to ID something from photos when you're not very familiar with it, is that you may not be sure what to look at to distinguish it.  If you can't get a photo, make sure you include the most detailed possible description, including anything about it, no matter how seemingly insignificant.  What it was doing, where it was, etc., etc.


Have some humans evolved to be less attractive to mosquitoes?

We now know based on a twin study that attractiveness to mosquitos is heritable (with a fairly high heritability of 0.62). Based on a genome-wide association study (GWAS) [which is probably the study referenced in the youtube video] we have found some of the genetic loci that control attractiveness; in particular, 15 single-nucleotide polymorphisms (SNPs) relating to (self-reported) attractiveness, were discovered in the latter study. These SNPs were in regions of the genome related to the immune system (which isn't surprising since immune system genes are closely linked to human odor profiles).

However, figuring out (a) whether these genes have been under selection (by looking for signs of genetic hitchhiking or unusual ratios of synonymous to non-synonymous substitutions) and (b) whether that selection is due to mosquito avoidance will probably a great deal more work - and may be very difficult given that the immune system is under selection for many different characteristics simultaneously ... the GWAS study says its results

  illustrate the complex genetic and immunological landscapes underpinning human interactions with mosquitoes ...


What is the difference between Leloir and Non-Leloir glucosyl transferases?

LeLoir glucosyltransferases use uridine-diphosphate (UDP) 'activated' sugars as substrate, for example UDP-glucose, where 'LeLoir' refers to the LeLoir pathway, the metabolic pathway that inter-converts glucose and galactose (or, more strictly, the inter-conversion of UDP-glucose and UDP-galactose)
Non-LeLoir glucosyltranserases use sucrose as substrate and do not require the sugar to be be conjugated to UDP (or to be 'activated' in any way), and as such are very useful in the biotechnology industry.
See
A new pathway for the synthesis of oligosaccharides by the use of non-Leloir glycosyltransferases)

LeLoir was an eminent Argentinian biochemist.
For the enzymes of the LeLoir pathway,
The Leloir pathway: a mechanistic imperative for three enzymes to change the stereochemical configuration of a single carbon in galactose
by Perry A Frey is IMO definitive (and the pdf is freely available).
(Glucose and galactose are epimers: they differ only by the configuratation at C4. A key enzyme of the LeLoir pathway is UDP-glucose 4-epimerase, which contains a tightly bound NAD(+) and epimerization proceeds by oxidation/reduction (strictly, hydride abstraction/addition) at C-4, where the tightly bound NAD(+) is transiently reduced during catalysis: ie, NAD acts a (transient) hydride 'repository'! To the best of my knowledge, no enzyme has ever been found that directly catalyses the epimerization of glucose to galactose (although there appears to be no thermodynamic reason why this is not possible): the sugar must be conjugated to UDP in order to be a substrate for UDP-glucose 4-epimerase)


It looks like as in fishes, the lack of an intrinsic cause of death in turtles in general is seen:

  Like in fishes, the reptiles appear to show three types of senescence. The African skink, Mabuya buettneri, shows rapid senescence similar to death at mating observed in Salmon and marsupial mouse. Most of the lizards and snakes undergo gradual senescence comparable to the pattern exhibited by a majority of vertebrates. On the other hand, turtles, tortoises and crocodiles continue to grow throughout life and are thus credited with slow or negligible senescence.
  Patnaik 1994 Gerontology 40(2–4):200–20.

The main article by Congdon, the researcher who the Discover article profiles, also seems to be fairly definitive about this lack of senescence (or negative senescence?) in Blanding's Turtles specifically:

  Survivorship, reproductive frequency and size-adjusted mean clutch size were all higher in the Oldest age group compared to the younger age groups.
  Congdon et al 2001 Experimental Gerontology 36(4–6): 813–827


All cells in a person’s body have roughly the same DNA. As you point out correctly, mutations can happen in any cell at any time. They are frequently caused by

UV radiation
Chemicals (think of the correlation between the development of lung cancer and smoking)
Replication of DNA during cell division
Integration of foreign (e. g. viral) genomic material
On purpose by the body’s own enzymes

That last point brings us to cells of the immune system, some of which (classically T- and B- Lymphocytes, but there is emerging evidence for others) generate variance within their genomic DNA on purpose.

Red blood cells lack a nucleus altogether.

Gametes only have half the body’s genome, as you already pointed out.

Finally, although having the same base sequence, epigenetic modification of DNA molecules by, for example, Methylation makes DNA chemically different even between cells of the same type.


Richard Goldschmidt's “systemic mutations”?

His notion of systemic mutations involved the postulation of massive chromosomal rearrangements (not mere recombination/crossing-over) as mediators of speciation in one-step. While whole genome duplications have been shown to induce speciation (see, for example, cryptic speciation in Hyla versicolor) they are not large scale rearrangements as he suggested. Additionally, while there is evidence for multiple large scale chromosomal arrangements at once in cancers (Chromothripsis) , there is no evidence of a similar process resulting in immediate reproductive isolation.


What would be the estimated cost sequencing?

Most NGS approaches should enable you to sequence all those plasmids at very low cost-per-base values (Please see here for more on prices). The challenge in sequencing them all, if there are sequences common to all your plasmids, will be to get adapters for each sample/plasmid so that reads can be mapped back to the correct plasmids.


A mathematician's confusion regarding parametric $t$ tests for gene expression data

I understand this in the following way:

For each probe you have two sets of measurements, one for ER+ and one for ER-. What you do is a T-test (to my understanding is that the "parametric" just emphasizes that T-test is a parametric test) on these two sets, testing if their mean is significantly different (they refer to this as "separated"). You repeat this test for all 7650 probes, and you get a set of 7650 p-values. You then do some multiple testing correction, such as a Bonferroni correction (I haven't checked in the paper if they did it, but they obviously should). Finally, they find that 606 of the p-values are significant (for some choice of threshold), suggesting that they can "separate" ER+ from ER-.

As a computational biologist I would advise you to look specifically at bioinformatics papers if you are looking into developing new methods, since the analysis in "pure biology" papers can often be lacking and would not give you a good perspective of state-of-the-art analysis methods. Specifically for the question of separating groups from gene expression you should look into the field of Machine Learning, as it had been widely applied to this problem.


Bacteria trapped in crystal inclusions found 'alive' after 50,000 years - what were they eating all that time?

The question is interesting, but I must say it is too early to say anything. But let me tell you what I can.

Dormancy, first of all, is a state in which all metabolic activities of an organism temporarily stop or slow down, and when saying all, I literally mean it. Dormancy can be considered, in layman's terms, as molecular level of hibernation. Any organism, in dormant state, does perform all kinds of activities, but in super slow motion. Again, we don't know anything about those microbes, so I can just tell the currently known mechanisms by which those microbes could have survived. Gypsum i.e. $CaSO_4.2H_2O$ contains sulfate ($SO_4^{2-}$), so those microbes (let me call them X from now) must be sulfur metabolizing ones to survive. Now, known mechanisms of sulfur metabolism include:

sulfur oxidation
sulfate reduction
sulfite reduction

which are summarized as:

source

Now, with sulfate already available from gypsum (considering dissociation) as:

$CaSO_4.2H_2O \rightarrow Ca^{2+} + SO_4^{2-} + 2\hspace{1mm}H_2O$

The reactions it can perform are sulfate reduction and sulfite reduction. Some of the mechanisms are:

source

In the presence of $CO_2$, glucose can also be formed as:

$12\hspace{1mm}H_2S + 6\hspace{1mm}CO_2\hspace{1mm}\rightarrow\hspace{1mm}C_6H_{12}O_6 + 6\hspace{1mm}H_2O + 12\hspace{1mm}S$

The required $CO_2$ might come from respiration. During dormancy, this process is highly slowed down, so that X may have survived such a long time by just this process.

Again, this is just the known mechanism, X may have evolved other, possibly even more efficient, mechanism. The above example was just to suggest how X could have survived in gypsum crystals for as long as 50K years. We don't know anything about X yet. From the article you cite:

  If confirmed, the find is yet another example of how microbes can survive in extremely punishing conditions on Earth.

meaning we don't even know yet whether they are really viable or not.

  The life forms—40 different strains of microbes and even some viruses—are so weird that their nearest relatives are still 10 percent different genetically. That makes their closest relative still pretty far away, about as far away as humans are from mushrooms, Boston said.

Now, viruses ain't alive. And 90% similarity means a lot of difference, which means they almost certainly have different mechanisms for survival. At last, I would again remind that it is too early to say anything unless some scientific studies are performed and published.

P.S. talking about energy source, even the heat and radiation from environment could be used as a source of energy. Obviously, harnessing energy directly from external heat is pretty difficult, but when one finds fungi using radiation for growth, then you never know!


No not white or grey generally, it's a mix of other colors, they often have low resolution of a particular color.

Here's a page where you can mouse over a color wheel and see a version in color blind mode:
http://www.archimedes-lab.org/colorblindnesstest.html

The first type of cone is primarily sensitive to short wavelengths (blue), another to medium wavelengths (green) and one to long wavelengths (yellow). The yellow cone is usually referred to as the red cone. While its sensitivity peak lies in the yellow wavelength band, it is also quite sensitive to red. A single cone cannot detect color, as it provides only a scalar number indicating the total light energy it absorbs. For example, the red cone by itself cannot distinguish red from yellow, green or orange. Red is detected by a combination of high activation of the red cone, low activation of the green cone and no activation of the blue cone. This page has a very comprehensive graphs and a first hand account of Tritanomaly

Evolutionary gene mechanisms have a particular knack of varying vitally important organs and functions, arm length, walking gait, hair type, color, and colorblindness is perhaps an expression of high variance to a survival critical and modular organ which animals have a high variance in depending on their habitat and survival requirements.


Does the SMUG1 enzyme break single-stranded DNA?

I think you needed to click just one more link: https://en.wikipedia.org/wiki/Base_excision_repair

It just cuts out the base so there's an empty spot on the ribose. I was looking for a picture and the top hit was actually this site (at A):

What is the mechanism of monofunctional glycosylases?


Ways to cause membrane damage to microalgae and yeast?

To get to the membrane of these species you first need to get past a formidable cell wall. The methods listed below are therefore more aimed at making cells permeable but the membranes must sustain some damage in the process.

At our lab we regularly use glass bead transformation for microalgae
transformation. The microabrasion allows DNA to go in so I imagine
the membranes must be damaged somehow.
I've also used hypotonic media (depending on the strain) to swell
cells close to their bursting point. I imagine they become rather
permeable at this point since they let several dyes in that are
otherwise excluded.


What is the difference between transformation and transfection?

If you are interested in the history of molecular biology this is an interesting question.

Basically transformation came to be used to describe experiments in which the phenotype of an organism was changed by the uptake of DNA, and because of the way this developed in  bacterial systems this DNA was usually a plasmid. Then it became possible to use purified phage DNA to infect cells, whereupon the 'transformed' cells produced phage particles - for obvious reasons this was called transfection.

When efforts turned to getting the same techniques working with cultured animal cells many of the vectors were based on viral genomes (e.g. SV40) and these workers referred to this as transfection. At this point the distinction between the two terms became meaningless, and usage tends to be for historical reasons. Interestingly in molecular manipulations of yeast, where there are no viruses, the transfection word is rarely used.


protocol for pulldown of DNA breakpoints?

The paper you cite says that the break points are single stranded DNA which have specific proteins bound to them.

I'm not an expert here, but if thats the cause of meitotic break points there are some interesting possibilities for detecting them:

you could detect them with a tiling array.  - that's an micro array which has an oligomer every 40 bp or so of the genome.  The array could be used in a CHP experiment that detects the same proteins as in this paper.

Its possible that the array could possibly hybridize the single stranded DNA from the genome too if the conditions were right.  This sounds noisy though.

On the cheap side it might be possible to use PCR to copy the single stranded DNA from a chromosomal DNA prep.  if the oligos you use are labelled with streptavidin say, you could isolate it , re amplify it and sequence cheaply.

any of these sound like a good bit of work :)


I think, the graph you indicated, might saying the following matter:
Let's take an example. " Some snails and fish  go into aestivation  to avoid summer-related problems-heat and dessication."  Now, when summer comes after the season Spring, the temperature gradually rises. The fishes can generally  withstand upto a threshold limit of temperature, and conforms upto this threshold limit. When their   comfortable weather breaks due to rising temperature, then they enter Aestivation and the graph now starts paralleling the X-axis.
Look, the graph doesn't parallel to the " Conformers' line" from the origin, but deviates with a little angle from that line : that implies the organism was trying to regulate against the external environment at first.
Undoubtedly, it's my own opinion, may carry some shortcomings generally.


Failed attempts at changing ecosystem in order to preserve it?

Perhaps not quite what you had in mind, but it seems like the introduction of the mongoose into Hawaii is close. In the late 19th century sugar planters introduced mongooses into Hawaii in an attempt to control rat populations. It turns out that rats are mostly nocturnal, and mongooses are mostly diurnal, so the two species rarely interacted. The mongoose population boomed and had a huge negative impact on native bird and turtle populations, since the mongooses would eat the bird and turtle eggs.


How much variation is there between DNA molecules from the same organism

The phenomenon is called mosaic single-nucleotide variations (SNVs) in somatic cells and it is an active area of scientific research (e.g., Abyzov et al., 2017, Genome Res. 27: 512-523):

  We estimate that on average a fibroblast cell in children has 1035
  mostly benign mosaic SNVs.

  Similar analyses in adults revealed no significant increase in the
  number of SNVs per cell, suggesting that a major fraction of mosaic
  SNVs in fibroblasts arises during development.


How does a decrease in free Ca2+ result in nerve/muscle overexcitability?

The thing is that the Voltage Gated Channels,they are closed in resting state because Ca2+ is bound to it.So,in the resting stage,Ca2+ somewhat blocks the Na+ - K+ channel.But since there is low Ca2+ so there won't be much Ca2+ for guarding of channels and so it will lead to an increase in permeability.See the photo and imagine the gate being guarded by a Ca2+.I hope this helps.


Identity of strange bird with fish net tangled around one foot

This could be an immature black-crowned night heron, Nycticorax nycticorax.
Lines of evidence:

pale yellowish bill
thick neck
hunched back
orange eyes
head feather patterning consistent with "black crown" in adults

See these photos and captions published by the Cornell Lab of Ornithology:

Juvenile Black-crowned Night Heron
Thick-necked heron with a thick bill. Juveniles are brown and streaky overall. Note pale yellowish bill.
© Evan Lipton

Immature Black-crowned Night Heron
Immature birds have a mix of juvenile and adult plumage. This individual has faint streaking on the chest, a dark gray cap, and a nearly complete dark gray back.
© Alex Lamoreaux

Adult Black-crowned Night Heron
Stocky and compact heron. Often tucks neck into its body creating a hunchbacked look. Adults have a black cap and back that contrasts with its whitish to pale gray belly and gray wings.
© Jeff Timmons

Note the fishing line tangled around the adult bird's feet.  Must be a common trait!


Updated Answer:

Why it's not the egg sac of Argiope aurantia:

Upon knowing your location to UK, we can rule out quite a few spiders, especially the Argiope aurantia since it is endemic to Northern and Central America.  The spider's egg sacs are also noticeably smaller than "a hen's egg" as this post describes.

Why it's not a gall:

We can rule this out since it appears to be located on a wooden fence post.  Galls require living plant matter to grow.

Why it's not a wasp nest:

There are not wasps that produce threadlike materials. Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no webbing or threadlike material.  In the picture, we can clearly see some white 'webbing' between the gap of the fence posts directly underneath the mass.

So I really think it is an...

Aethalium of a slime mold:

Given the location, described area, spreading pattern in the picture, and apparent spongy texture of the mass, this looks to be the aethalium (or fruiting body) of a slime mold.  My guess would be in the genus Reticularia or Enteridium, which are typically seen in its reproductive phase as a white 'swelling' on standing dead trees in the spring, or on large pieces of fallen wood.  For example, Enteridium lycoperdon are common throughout the UK and are commonly associated with pine trees, the most common wood used to make fences in the UK.

*This post was edited from my original response.  Please refer to the edit history concerning the previous answer.


Are there endoscopic technologies for blood vessels?

Blood is hard to see through, so visualization with a camera isn't used (to my knowledge). However, Intravascular ultrasound can be used, though it is expensive and not all that common. Instead, angiography is usually used, by filling the vessels with a radio-opaque dye

There are also many techniques used to treat vascular conditions, like balloons/stents to open and keep open blocked or partially blocked vessels, or to repair valves. You can read more about Interventional cardiology or minimally invasive procedures.


dN denotes deoxyribonucleoside (where N can be A, T, G or C). If there is no d prefix, then it denotes a ribonucleoside.

Regarding the difference between poly and oligo:

The former refers to having a large number of monomeric units whereas the latter means having a few monomeric units. There is no strict definition of the boundary between poly and oligo. Poly-A tails are typically about 70-80nt long in yeast (Eckmann et al. 2010). So it logically follows that anything shorter than that should be called an oligo-A. Chemically synthesized stretches of DNA are often referred to as oligos even though nowadays one can synthesize more than 80nt long DNA/RNA. Moreover, a stretch of As in some mammalian mRNAs smaller than the usual length of ~150-250 is still referred to as a short poly-A tail instead of an oligo-A tail (Jalkanen et al. 2014; there are many more examples).

Additionally, even if the cutoff is, let's say, 100 units, it doesn't apply to proteins. A protein with 100 amino acids is still considered a polypeptide and not an oligopeptide. For peptides, the cutoff is generally around ~30.

So, I would conclude that the usage of these prefixes is quite contextual.


Let’s first consider what the Central Dogma[1] actually says. It is precisely summarised in the following figure[2]:

solid arrows represent transfer of information that has been observed directly; dashed arrows represent potential, not yet observed, transfer of information

In the time since the original formulation of the Central Dogma in 1958, we have been able to contribute evidence for one of the dashed lines: RNA→DNA is performed in vivo via reverse transcriptase. By contrast, note the absence of any arrows originating from “protein”. The idea of the Central Dogma was that proteins were an information transfer sink: information could only flow in, not out.
And Crick and his contemporaries had good reasons for assuming such an information sink: translation from RNA to proteins is lossy  because the genetic code is degenerate. A given amino acid can be encoded by more than one codon.
This doesn’t mean that polypeptide chains couldn’t be reverse translated into “a” RNA representation. But it wouldn’t necessarily be the original RNA. Stated like this, it’s obviously possible: we can in fact take a polypeptide chain, sequence it, and synthesise a corresponding RNA.
However, this doesn’t happen in nature — at least, it hasn’t been observed so far, and there are good reasons to assume it doesn’t happen at all. In fact, Crick’s paper[1] explains:

The transfer protein→RNA … would have required (back) translation, that is, the transfer from one alphabet to a structurally quite different one. It was realized that forward translation involved very complex machinery. Moreover, it seemed unlikely on general grounds that this machinery could easily work backwards. The only reasonable alternative was that the cell had evolved an entirely separate set of complicated machinery for back translation, and of this there was no trace, and no reason to believe that it might be needed.

The “complicated machinery” Crick mentions here consists of two distinct parts: On the one hand the ribosome, and on the other hand the aminoacyl tRNA synthetases (aaRSs, singular aaRS). The latter is essentially the physical embodiment of the genetic code in the cell. The former is the machinery necessary to decode RNAs using the codon adapters (= tRNAs) charged by the aaRSs.
Crick correctly notes that, in order to allow the transfer protein→RNA, the cell would require a system analogous to the ribosome and all the aaRSs, redundantly encoding the exact same information. And it would need to ensure that these two distinct encoding systems (translation and reverse translation) never get out of sync with each other.
It’s worth contemplating, briefly, why the cellular translation process isn’t simply reversible, given that it’s an chemical process, and thus pretty much by definition reversible in theory. The reason for this is that translation happens in two entirely distinct, and physically separate, stages: the charging of individual tRNAs with their corresponding amino acids by an aaRS, and the actual mRNA translation by the ribosome.
Simply reversing the ribosome activity would result in a polypeptide being digested from one end, yielding individual amino acids. However, the ribosome actually has no facility for capturing these amino acids, they would simply diffuse away without being attached to a tRNA, let alone the right tRNA. A successful reverse translation would have to physically couple each type of aaRS in turn to the ribosome to ensure that terminal amino acids would pair with the correct tRNA, which, in turn, would pair with a codon. There are two fundamental objections to it, which render it impossible:

Codons, which could be combined into mRNA chains, don’t swim around individually. In fact, short RNA chains are highly unstable and are quickly degraded. By contrast, individual ribonucleotides can be combined into chains — that’s what polymerases do all day, after all. But the ribosome doesn’t possess polymerase activity, and the tRNA anticodon would not provide sufficient physical support to enable a polymerase to dock to it and start synthesising a secondary strand.
Steric hindrance prevents the aaRS enzymes from interacting with the tRNAs while they are being held by the ribosome: the ribosome and the aaRSs would have to physically overlap.

It’s hard to get definitive answers in science purely from theoretical considerations, but this one’s as certain as you’re likely to get: cellular translation using the ribosome is a non-reversible process. Reverse translation, if it existed, would therefore require a separate machinery.


Genetics: pedigree following a rare trait autosomal recessive

Question 1

Okay, so I'll go through my own process for you here step by step, moving down the tree.  Here's an annotated version of your diagram with my own thoughts (it's been a while since I've done this but should hopefully be accurate):

Generation 2:  As you realised, the trait is autosomal recessive so the female (II:2) has the genotype aa.  The male is considered wild type unless informed otherwise, giving him a genotype of AA.  I think you had worked all this out, but they are shown in red on the diagram.

Generation 3: Using the two genotypes of the parents from II (red), we know that all the progeny in generation III are carriers - i.e. Aa genotypes.  This is indicated for III:6 in orangey-brown.  I think you also worked this out successfully.  However in your original chart, III:7 is noted as Aa.  III:7 is from outside of the affected family and would therefore again be considered to have be wild type and therefore instead have the genotype AA - shown in purple.

Generation 4: In order to work out the potential genotypes of IV:1 we have to do a cross between the two parents III:6 and III:7 - which works out as follows:

        |          Male          |
        |     A            a     |
        |------------------------|
F       |                        |
e     A |    AA            Aa    |
m       |                        |
a       |                        |
l     A |    AA            Aa    |
e       |                        |

As you can see, there is a 50% chance of IV:1 being healthy AA and a 50% chance of being a carrier Aa - shown in green.  As IV:2 is affected, we know his genotype is aa (pink).

Generation V:  Now for answer to your first question.  If IV:1 had the AA genotype then the child could never be affected, reducing the odds to 50% immediately. Of this remaining 50%:

        |          Male          |
        |     a            a     |
        |------------------------|
F       |                        |
e     A |    Aa            Aa    |
m       |                        |
a       |                        |
l     a |    aa            aa    |
e       |                        |

50% of the offspring would be affected.

Therefore the probability of V:I being affected is $\frac{1}{2} \times \frac{1}{2} = \frac{1}{4}$

Question 2

The second question seems very odd to me.  If IV:2 was unaffected in the literal sense of the word they would be wild-type AA.  This would make the probability of them having an affected child as 0.

As this isn't one of your options, I assume they mean that IV:2 is a carrier (Aa).  We are this time therefore crossing either AA or Aa (IV:1) with Aa (IV:2).  Again, if IV:1 is heterozygous dominant (AA) none of her children will be affected.  This means the odds are again reduced by a half.  In the case that she is heterozygous Aa then the cross becomes:

        |          Male          |
        |     A            a     |
        |------------------------|
F       |                        |
e     A |    AA            Aa    |
m       |                        |
a       |                        |
l     a |    Aa            aa    |
e       |                        |

Giving 25% healthy, 50% carrier and 25% affected.

As you're looking for affected children: $\frac{1}{2} \times \frac{1}{4} = \frac{1}{8}$


References concerning the relative population sizes of predator and prey

You are indeed correct that the prey of predators are usually more common than their predators, especially if you focus on "true" predation (i.e. remove parasitism and parasitoidism). As a rule of thumb, the energy conversion between trophic stages is 10% (first proposed in Lindeman, 1942), which sets one sort of bound on the density relationship between predators and prey. The relationship is extremely variable though, which is easily understood if you consider the density relationships of hares and foxes vs. whales and krill.

For a general reference, Hatton et al (2015, "The predator-prey power law: Biomass scaling across terrestrial and aquatic biomes") might work, even though it is mainly framed in terms of biomass. However, the paper clearly states that biomass and density usually go hand in hand. The main result of the paper is that the biomass relationships between predators and prey collapse to very regular power laws (exponent 3/4) across ecosystems.

As mentioned above, and depending on who you ask, parasitism and parasitoidism are sometimes seen as types of predation. There, the density relationships between "predator" (parasitoid) and "prey" can be very different, especially at certain points in time or at certain lifestages. For instance, in insects it is not uncommon for one "prey" (host) to give rise to a large number of newly hatched "predators". This means that the number of parasitoids can probably outnumber the number of hosts, at least at smaller spatial scales, at some time periods (e.g. late summer, before the parasitoid is hit by high winter mortality).


What is the point of being selection-free?

Urnov et al. are trying to effect gene therapy - where a mutation causing a genetic form of severe combined immunideficiency (SCID) (also known as the bubble boy syndrome). Affected SCID patients can have little to no immunity to infection what so ever.  SCID in this case is caused by a single site mutation in the IL2R-gamma gene.

Their method is to use a DNA binding protein (containing zinc finger domains that bind the DNA) which attracts a DNA repair enzyme.

The result is that 18% of the cells have the SCID gene repaired.  This would have been a trivial result if they had applied selection, which generally refers to any method which eliminates cells which were not affected (in this case having their DNA repaired) by a transformation like their treatment.  They claim that 18% of all the cells were repaired (I assume this is in a cell culture).  This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ, which should be enough to restore immune function.

While its possible to apply a selection method to gene therapy, it would be far better if you did not.  Cancer chemotherapy for instance is a selection based treatment for instance, relying on toxins which kill fast dividing or growing cells preferentially, leaving the slower growing tissues relatively viable.   Still its quite toxic and disruptive to the patient.


Why would evolution favor blue as a color in bugs?

Similarly, you could ask

Why are bees yellow?
Why are some frogs so colourful?
Why widowbirds have such long tails?
Why do peacocks have such a tail?

There are a number of reasons why such traits could evolve. The main reasons are:

Sexual selection (esp. intra-sexual selection when it comes to colors)
Mimicry (esp. batesian mimicry)
Aposematism

I let you investigate further by yourself through reading the linked wikipedia articles.

For the specific beetle, you have seen, it will be impossible to address the question unless we know the species.


It is great bowerbird (Chlamydera nuchalis). It is much bigger than the mentioned flycatcher. I have seen both species and there is no room for confusion. Most of the pictures online are birds perched on the ground next to their "buildings", but I found a picture that should convince you.

Notice:

-Stout bill

-Patterned wing coverts

-Marks on the undertail coverts


This paper describes dewaxing of sunflower seeds using various solvents. As you have already shown for yourself, using hydrophilic substances such as bleach and acids do not work well in removing the waxes.

Waxes are highly hydrophobic substances, and must be removed with either hydrophobic solvents (much like washing away acids with water at the emergency eye-shower) or detergents and water. The hydrophobic solvent mixtures used for lipid extractions recommended in WYSIWYG's link will likely work as well.


Which process is needed to complete male reproductive development?

Regarding option C:

Although it is correct that testosterone is converted into DHT, it is the former, not the latter, which is responsible for differentiation of the mesonephric (a.k.a. Wolffian) ducts:

  Between 8 and 12 weeks, the initial secretion of testosterone stimulates mesonephric ducts to transform into a system of organs—the epididymis, vas deferens, and seminal vesicle—that connect the testes with the urethra.*

DHT (dihydrotestosterone) is produced in the Leydig cells by the 5α-Reductase enzyme. It is required for induction of the external male genitalia (urethra, penis, and scrotum) and prostate from the embryonic ureteral groove, and for testicular descent into scrotum.

Regarding option D:

Sertoli cells secrete Anti Müllerian Hormone (AMH), which causes degeneration of the müllerian (a.k.a. paramesonephric) ducts between weeks 8 and 10.  It is normal to speak about degeneration of the müllerian ducts as a defining aspect of male embryology, and thus I believe answer D is correct. Your point is taken, however:

  Nevertheless, small müllerian duct remnants can be detected in the adult male, including a small cap of tissue associated with the testis, called the appendix testis, and an expansion of the prostatic urethra, called the prostatic utricle.*

*Larsen's Human Embryology , Fourth Edition. Chapter 15: Development of the Urogenital System. pp 479-541.
Copyright © 2009 by Churchill Livingstone, an imprint of Elsevier Inc.


What technique biologists use in order to determine the function of organs?

A very common way of getting information on the function of an organ, part of an organ (such as a region of the brain) or a protein is to look at the outcome (symptoms or phenotype) in cases where it is not functional. E.g., a lot has been understood about brain function for speech production by studying aphasia in stroke patients (see wikipedia) and linking the symptoms with the brain region that is damaged.

This is still the way we mostly study living cells or organisms: mutants defective for such or such protein, or in which external disruption (such as ablation) is used and the resulting phenotype or symptoms are studied.

This is indeed very different from what can be done for research in physics e.g., where reduced systems with simpler functions can be studied. The approach in biology is much closer to reverse engineering, where a given system has to be studied as a whole but a rational approach on some subpart allows to build an understanding of that subpart.


Breathing with Clogged Nose during Sleep

Most people with colds/allergies/stuffy noses don't die in the middle of the night. Why?
Prevention of oxygen deprivation is powerfully regulated. If insufficient air intake is possible through the nose, the mouth opens automatically (regulated by the autonomic nervous system. If you exercise, at some point, nasal breathing isn't enough, and you start mouth breathing. It's not conscious.

The autonomic nervous system (ANS)... is a division of the peripheral nervous system that supplies smooth muscle and glands, and thus influences the function of internal organs. The autonomic nervous system is a control system that acts largely unconsciously and regulates bodily functions such as the heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. This system is the primary mechanism in control of the fight-or-flight response.
Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting. Those are then subdivided into other areas and are also linked to ANS subsystems and nervous systems external to the brain. The hypothalamus, just above the brain stem, acts as an integrator for autonomic functions, receiving ANS regulatory input from the limbic system to do so. (emphasis mine)

The answer is a complex interaction between blood pH and oxygen/CO2 receptors and the autonomic nevous system.


What are the differences between insects and spiders?

Spiders and Insects have been separate independent linages of animals for 500 million years. Spiders have two body parts (cephalothorax and abdomen), while insects have 3 (head, thorax and abdomen). Besides the differences in number of legs, spiders and insects have different forms of respiration, different mouthparts, and different exoskeletons. Insects have antennae, while spiders don't. In short, spiders and insects are more different from one another than mice are from sharks.


By just looking at an unlabeled picture, how do you know it is a protein?

Shapes
This is a common way of illustrating a protein and is often called a "protein cartoon". There are other common ways of illustrating proteins.
This cartoon shows you where α helices are (spirals) and where β sheets are (arrows) which are important structural elements. The strings connecting those structural elements are flexible "loop" regions.
If you want to query this against other structures and see which protein it is, check out PhyreStorm. You'll need the PDB file, not just an image.
Colour
The colouring is also common. The N-terminus (the first amino acid) is coloured blue, and the colours go through the rainbow to red, the C-terminus (the last amino acid in the polypeptide chain).


Petioles typically have the presence of one or more of the following:

Stipule at base of the stalk
Axillary bud between the stalk base and attached stem
Leaf scar when removed

Source: Miami University

Source: Wikipedia
None of these characteristics would be present if the stalk you were looking at is a stem.

However, they are not always each visible on every species...
From: Oregon State University Dept of Horticulture:

It is not always easy to find the bud at the base of a petiole, it may not be visible early in the growing seaon and sometimes a mature bud is “hidden”, such as being enclosed by the petiole base.

From Wikipedia:

although in many species the stipules are inconspicuous or entirely absent (and the leaf is then termed exstipulate)

Leaves are usually borne from petioles and rarely from the stem itself -- so presence of a leaf (or compound leaf parts) is usually indicative of a petiole as well. However, sometimes plant leaves lack a petiole altogether, as in the case of sessile leaves.
In other instances, specifically those of compound leaves, the stalk of compound leaves (i.e., the rachis) will lack the properties previously described for a petiole, but following the compound leaf to the nearest stem typically will result in locating the petiole with one or more of the above mentioned characteristics at its base connecting the compound leaf to the stem.


Are the irises an exact match in a human's set of eyes?

Short answer
No. Not two irises are alike, including the irises of identical twins and even the two irises of one and the same person. This uniqueness of the human iris is used in iris scans. The variety of the iris is caused by its complex structure and coloring pattern.

Source: Jean-François Mainguet

Background
The iris is explained on Biometric Technology's website, and I quote:

  The iris [...] is a thin, circular structure in the eye, responsible for controlling the diameter [...] of the pupil [...]. “Eye color” is the color of the iris, which can be green, blue, or brown. In some cases it can be hazel (a combination of light brown, green and gold), grey, violet, or even pink. In response to the amount of light entering the eye, muscles attached to the iris expand or contract the aperture at the center of the iris, known as the pupil.

A striking example of the dissimilarity of the iris in one person are people with heterochromia. Heterochromia can result in both eyes having a different color. Examples are given in the figure below: On the left is Demi Moore (if you look closely her right eye is hazel, while her left eye is green). On the right-hand side a more striking example is shown (taken from the Kliproject):

Heterochromia iridium (differing iris colors) and heterochromia iridis (a variety of color within a single iris) are relatively rare in humans and result from increased or decreased pigmentation of the iris. Most cases are the result of an alteration in the expression of the EYCL3 gene (which codes for brown/blue eye color) and EYCL1 (which codes for green/blue eye color), among other genes within the cells of the entire iris or even a particular section. Other potential causes include trauma around the time of birth or later in life, congenital pigmented nevi or even medications such as those used in the treatment of glaucoma.

Fun fact
David Bowie's eyes are in fact of the same color - his pupils are of a different size:

Reference
Scientific American (November issue, 2001).


Can predator-prey relationship be an example of negative feedback?

From my experience, "negative feedback" is more often used in the context of processes in the body which attenuate themselves or in the context of stimuli and sensors. However predator-prey dynamics could fit the general definition of the term. In general, negative feedback is just when a process or output of a system leads back into the system to attenuate itself.

  Negative Feedback:

  "A feedback in which the system responds in an opposite direction to the perturbation. "

  Source: biology-online.org, access date: 2018-04-06.

In a general case of a closed-loop (feedback) control system, you've got a stimulus that gets sensed by a sensor, which sends a signal to a controller. The signal is then passed on to an effector, which can change the original stimulus. In the case of negative feedback, the stimulus is attenuated. In positive feedback, it is potentiated.

$$\begin{array}{ccc}
\fbox{Stimulus}&\rightarrow&\fbox{Sensor}
\\
\uparrow&&\downarrow
\\
\fbox{Effector}&\leftarrow&\fbox{Controller}
\end{array}$$

A common example of this would be high body temperature being detected by neurons, which send a signal to the brain to cause the body to sweat more. In this case, the sweat glands are the effectors and can lower the body temperature.

$$\begin{array}{ccc}
\fbox{Change in body temp.}&\rightarrow&\fbox{Neurons}
\\
\uparrow&&\downarrow
\\
\fbox{Sweat Glands}&\leftarrow&\fbox{Brain}
\end{array}$$

In your case, I think you could describe it with an increase of prey population being the stimulus, which is detected by the predators as they see more prey. The predators would then choose to eat the prey (I suppose this could be the controller) and then act as the effector by eating the prey (and thus, reducing the prey population). Though I'm a little iffy on this since you'd have the predator acting as both the sensor, controller and the effector. Conversely, if the prey population were lowered, the opposite would be true.

$$\begin{array}{ccc}
\fbox{Change in prey pop.}&\rightarrow&\fbox{Predators sense prey}
\\
\uparrow&&\downarrow
\\
\fbox{Predators eat prey}&\leftarrow&\fbox{Predators choose to eat prey}
\end{array}$$


help identifying marine item found on beach

You've found a swim bladder. Swim bladders are largely made from collagen, so when they're dried out on beaches they feel tough and rigid.

Swim bladders differ in shape between species. As an example, the swim bladders of oyster toadfish are similarly-shaped to the one you have found, but that general shape isn't uncommon, so it could have come from many other species.


Using perceptual adaptation for enhancing realism of VR/other entertainment

Adaptation to altered vision is probably most well-investigated using prism-glasses. Prism glasses can shift the visual horizontally, for example by 20 degrees (Redding et al., 2005):

The use of horizontal shifting goggles has been investigated intensively to treat the symptoms of attentional neglect. Neglect occurs due to unilateral parietal brain lesions. For example, a lesion in the right hemisphere may induce left-sided neglect, where the left part of the visual field is seen, but simply not processed and neglected (Rosetti et al., 1998). Wearing prism goggles for approximately 6.5 hours/day, over the course of 2 weeks has been shown to reduce the symptoms of neglect significantly by as long as 17 weeks(!) after treatment (Frasinetti et al., 2002).

For the treatment of a neurological disorder such as neglect adaptation to prism glasses is great. However, treating healthy controls with comparable methods may induce unwanted side effects. 15 min of prism exposure has been shown to lead to several degrees of error in pointing tasks, for up to two weeks after the adaptation in normally sighted controls (Klapp et al., 1974).

To mention some studies closer to your question: in a virtual reality experiment subjects wore a head-mounted display that shifted the virtual position of their eyes. Their performance on a hand-eye coordination task first decreased by ~40% and then increased again with ~30% after adapting to the display. After taking the display off, there were transient after-effects, that impacted eye-hand performance (Rolland et al, 1995; Biocca & Rolland, 1998). In other studies wearing a head-mounted display longer lasting discomfort was reported in 5% of the subjects (Cobb et al., 1999) as well as binocular stress after removal of the display (Mark Mon-Williams et al., 1993).

Although the latter studies did not report serious after-effects, the more rigorously performed studies with the prism glasses have shown long-standing effects after visual adaptation. Hence, although the performance with virtual-reality head-mounted displays and comparable devices will undoubtedly increase after adapting to them, visual functions in everyday life may correspondingly be compromised.

So although this answer may not be addressing all your practical questions, I would say it is not advisable to let one actively adapt to head-mounted displays, or other wearable virtual-reality glasses that change visual function in the first place.

References
Biocca & Rolland, Presence 1998; 7:262-77
Cobb et al., Presence 1999; 8:169-86
Frasinetti et al., Brain 2002; 125:608-23
Klapp et al., Perception & psychophysics 1974; 15: 399-400
Redding et al. Neurosci Biobehav Rev 2005; 29:3, 431-44
Rolland et al., IEEE Proceedings of VRAIS 1995
Rosetti et al. Nature 1999; 365:166*9


Under the right conditions, emulsions of lipids (fatty compounds) and water can cross cell membranes. If the emulsion is prepared correctly, a structure known as a liposome forms, which is essentially a "bubble" with a layer of fatty molecules on the outside and water at the center. This has been studied intensely in biotechnology, because such liposomes can be used to carry DNA inside (DNA is water-soluble) and then be used to deliver DNA to cells, as in gene therapy.

Typically, oil, which contains triglycerides, is not used for this though, but another compound known as a phospholipid. This is also a "fatty" substance, but unlike triglycerides, one end of the molecule is polar, which helps it interface with water. Phospholipids are the main ingredient in cell membranes, and therefore liposomes made of this stuff can interact with cell membranes. Essentially, the liposome can "merge" with the cell membrane in such a way that the water inside it (and any other contents) ends up inside the cell. For an example of how this technique is used, see this article.

As for the cooking-related question, I would say oil-water emulsions found in foodstuffs are unlikely to cross cell membranes. They contain mostly triglycerides which are not so effective at this, and they are probably not prepared in the right conditions (oil/water concentrations, etc) for liposomes to form.

Also, even if there would be liposomes in some foods that could cross cell membranes, foodstuffs do not actually get into contact with cell membranes in the digestive system, until they are broken down into smaller (harmless) molecules. In the mouth, esophagus, stomach, etc, tissues that come into contact with foods are heavily protected by layers of mucus to prevent cells getting "attacked" by all the weird biomolecules (and organisms) that we eat.

Finally, various molecules from food don't actually enter the cells of taste buds; instead, they are sensed by taste receptors present on the outside of the cells. (Well, the sour taste sensor involves transport of small ions, but not larger molecules.) So you should probably revise you answer on Cooking SE.


Swelling is one of the signs of inflammation. Inflammation involves release of histamine by mast cells present in the tissues. Histamine causes vasodilation and leads to leakage of fluid from the blood, along with which neutrophils and other WBCs also enter the area. They phagocytose microbes that might have entered with the injury.

Applying ice would cause vasoconstriction* (i.e. narrowing of blood vessels.) which would reduce the leakage of tissue fluid and hence swelling.

*If you wonder why ice(or any cool thing) causes vasoconstriction think why you turn pale in winter ? Vasoconstriction reduces blood flow to the particular area and hence the exchange of heat is reduced which conserves body heat in cold environments.


Why would a 2019-nCoV protein sequence in the NCBI database match a protein submitted in 2018?

2019-nCoV is a virus that originated from the bat (at least this is the current hypothesis). It shows 96% squence similarity to the BatCoV RaTG13 sequence (see reference 1), showing its origin.

It still is 87,99% identical to the "Bat SARS-like coronavirus", which explains the hit you found and is not unexpected, as these viruses are very closely related (see reference 2).

These viruses are closely related, so I wouldn't expect too many differences at all. Then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. Additionally, due to the redundancy caused by the codon degeneracy, not every mutation in the genomic material translates into changes in the protein.

References:

Full-genome evolutionary analysis of the novel corona virus
(2019-nCoV) rejects the hypothesis of emergence as a result of a
recent recombination event
Genomic characterisation and epidemiology of 2019 novel coronavirus:
implications for virus origins and receptor binding


The concept of backpropagation in neural networks actually occurs in the brain?

I recommend Yoshua Bengio's recent works. E.g.: https://arxiv.org/abs/1502.04156 and his slides from the NIPS 2016 Brains and Bits workshop.

Also, Timothy Lillicrap's work: http://www.nature.com/articles/ncomms13276

This is still a big open question. In short, we (the neuroscience community) have little idea on how the brain learns at a circuit/systems level in general. We know a thing or two about how individual synapse changes under specific experimental protocols, but those are phenomenological models (e.g. STDP; there has been many many normative models of learning that concludes their learning rule is STDP-like). (Some systems such as cerebellum, we know relatively more, but the learning seems to be more specific to motor timing.)

The main technique we use in machine learning and artificial neural network are mostly gradient descent (or some sort of stochastic optimization algorithm), and people have been trying to find if the biological neural network learns in a similar way. There are several issues:

There's no error gradient being propagating according to chain rule. Information gets mushed together within a neuron, so there's no plausible way to trace exactly the forward-path during an backpropagation.
There's a lot of recurrent connections but they are not symmetrical.
Temporally, it is implausible that there's a clocked signal to backpropagate after a each forward path. Neuronal network doesn't seem to operate with clocks (some thing there are precise clocks, but I think there's little evidence).

Recent efforts have made some progress with random backprojection, decoupled updates using synthetic gradients, target prop, autoencoder, weight/signal quantization, deep belief networks, etc. But there seems to be several more jumps needed to make it biologically plausible such that it agrees with the neural architecture and information flow. Even then, there's no guarantee that neocortex is learning with a similar principle.


Function and Characterization of poly(T) and (AT)

Poly(T) is an oligonucleotide with only repeating thymine residues. These are generally used as primers in Reverse Transcription PCR, as mature eukaryotic mRNAs have a Poly(A) [adenosine] tail added to them as a post transcriptional modification in order to protect against mRNA degradation. You would also sometimes see this referred to as an oligo dT. It could also be the primer for some paired end adapters used in next-generation sequencing (NGS)

The 45 generally would indicate the number of residues in the oligonucleotide.

Poly(A) could be a primer for a paired end adapter for NGS, however I would need to see the context of where you saw the terms to be sure.

d = Deoxyribonucleotide, in other words you are dealing with a DNA oligonucleotide (though Thymine is also an indication). Technically the d refers to the 2' Carbon on ribose having a hydrogen instead of a hydroxyl attached to it making it deoxyribose.

Without the d it is a Ribonucleotide, indicating that you are looking at an RNA molecule and that the 2' Carbon on ribose has a hydroxyl group.

You will sometimes also see ddN (N for any base). This indicates a chain terminating dideoxynucleotide which has a hydrogen on both the 2' and 3' Carbon instead of hydroxyl groups. The reason this molecule is chain terminating is because you need the 3' hydroxyl in order to link to a 5' phosphate group to form a phosphodiester bond, which is needed to continue the elongation of the nucleic acid molecule.

As for the ss(AT)15, I think you are correct in saying that this is a 15 pair repeat of AT so a 30 nucleotide oligonucleotide. Though it didn't say dAdT, you are likely correct that they are deoxyribonucleotides as they use thymine instead of uracil as the base.

Just in case, the ss stands for single-stranded, which is often the case for oligonucleotide primers for PCR reactions.


What causes a 'stuffy' or 'runny' nose when you have a cold?

It's mainly caused by swelling of large veins and by an increase in vascular permeability that leads to an accumulation of fluids in the nasal mucosa. These effects are mediated, at least in part, by bradykinin and histamine, and can be counteracted by epinephrine. These mediators are part of the immune response to the viral particles.

You can read more about it here:

http://www.cardiff.ac.uk/biosi/subsites/cold/commoncold.html
Chernick-Mellins basic mechanisms of pediatric respiratory disease
By Gabriel G. Haddad, Steven H. Abman, Victor Chernick (page 520)


Lysozyme amino acid sequence: N-terminal extension

If you scroll down through the uniprot entry you will come to a section with the heading PTM/Processing.

From this you can see that the first 18 amino acids are a signal peptide.

You can learn more about signal peptides from any good introductory textbook covering cell-biology — alternatively Khan Academy is a good source for learning the basics.


Can prawns and lobsters live out of water for more than six hours?

TL;DR version is they are gill breathers and need to be in a humid and moist environment to have a considerable longer life span outside sea water.

Dr. Cowan's on being asked the same question about lobster said:

  “Gills work best in seawater, but if lobsters are kept in containers of seawater with no aeration, they quickly use up the oxygen and suffocate,” she said. “That it why it is imperative to transport lobsters in containers with no standing water.” - New York Times

Many lobsters, shrimps and even crayfish & crabs are transported in boxes with a small amount of water in the bottom and they survive for several days like that. However the long term side effects of this are still to be discovered as most crustaceans transported this way get cooked.


It means the following:

$$\log P = \log(P) = \log_{10}(P) = \log_{10} \left(\frac{C_{\mathrm{octanol}}}{C_{\mathrm{water}}} \right) $$

With $C_{\mathrm{octanol}}$ being the concentration of the solute in 1-octanol and $C_{\mathrm{water}}$ the concentration of the solute in water.


How is insulin transported in vivo in mammals?

The process is described here. This is my summary, plus a few extra details:

The primary gene product of the INS gene is preproinsulin. As the N-terminal signal sequence (pre-) emerges from the ribosome during polypeptide elongation the signal sequence binds to a signal recognition particle which arrests elongation until the nascent chain has engaged with the translocation apparatus in the membrane of the endoplasmic reticulum (ER). The preproinsulin polypeptide is translocated across the ER membrane in a cotranslational process, and the signal sequence is cleaved off by signal peptidase.

The proinsulin molecule folds in the ER lumen, assisted by various chaperones and, in particular, by protein disulphide isomerase, which ensures that the correct disulphide bonds form. The correctly-folded proinsulin polypeptide is exported from the ER in COPII-coated vesicles which deliver it to the Golgi. At this stage the proinsulin is cleaved by furin-type proteases (pro-hormone convertases; cleave at pairs of basic residues), removing the internal C-peptide (pro-) and after a little C-terminal trimming, leaving the insulin A and B peptides covalently attached via disulphides. This is mature insulin.

The mature insulin leaves the Golgi in secretory vesicles. Since insulin secretion is regulated, these vesicles do not fuse with the cell membrane constitutively, they are stimulated to fuse by a Ca2+-dependent signalling pathway. Vesicle-membrane fusion is mediated by SNARE proteins. At this stage the insulin has been released from the pancreatic β cell. Notice, however, that the insulin has been extracytoplasmic since it was translocated into the ER: all other steps in the transport process are achieved by rounds of vesicle formation and fusion.


Are any biology research journals free to publish in?

Many biology journals are free to publish in. As a rule of thumb:

Most journals from for-profit publishers such as Elsevier, Wiley, etc. charge nothing to the author (but of course bill the libraries handsomely).
Many but by no means all society journals charge page charges even if they are not open access.
Most but not all open access journals charge substantial publication fees. You could try this website to search for open access journals that do not charge publication fees.


What does the "*" in haplogroup I2A1* mean?

From the 23andMe website:

  Sometimes there are a few lineages that don't fit into any subgroup of a haplogroup. Since there isn't a mutation that links these lineages, they don't get their own subgroup. Instead, these lineages are given the main haplogroup label plus a star (*) to indicate that they are part of the main haplogroup but don't fit into any of the known subgroups

So there are defined subgroups for I2A1 (I2A1A and I2A1B) for which more information is available, but you dont fit into any of them.

What "doesn't move down stream" means, I have no idea.


Your question' better suited to Gardening SE where members can identify plants. As it is, I'm an active member there and the identity of these flowers are straightforward. They're all different cultivars of the daylily (plants in the Hemerocallis genus). If you use Google image search, you'll see photos of various cultivars. Basic structure:

Notice the flowers on a branched (or unbranched) scape (tall stem); leaves arise from the base of the plant. Flowers can be single or double (sometimes more); single flowers (as in your lower left photo) have six petals.

While Asian and Oriental lilies are toxic to pets (even the pollen is toxic to cats if they lick it off their fur), daylilies aren't. They're easy to tell apart as the daylily has long narrow strap-like leaves with flowers on stems with no leaves. Asian and Oriental lily have small leaves continue up the length of the stem like this -

This includes Easter lilies.

Daylilies are named for the reason individual flowers lasts only one day. But each stem has many buds on it that continue to mature over a few weeks so will produce flowers for about a month (as some stems don't have open flowers yet when the first stems start flowering).


Compatibility between spytag/spycatcher versions

I am currently working with these tags, so going off experience here. The binding efficiency is not 100% even when the correct versions are mixed e.g. version 2 spytag and version 2 spycatcher. I believe this is the original paper (https://pubs.acs.org/doi/pdf/10.1021/ja910795a) it reported 60 % binding efficiency after an hour (I presume for version 1) and this paper (https://www.pnas.org/content/pnas/109/12/E690.full.pdf) revealed 40 % binding efficiency in the first minute (unclear whether version 1 or 2 but I presume 1).  In terms of between versions I can only speak to a mistake I made once by accidentally mixing version 1 spycatcher with version 2 spytag. There was visible binding that could been seen by SDS-PAGE however, it was very faint and required significant amounts of protein to view (~10 mg/ml). I never did any sort of quantitative measurements on binding efficiency as it was a mistake. But from subsequent correctly run experiments, I could see it was significantly lower so I would always use version 2 with 2 and version 3 with 3 etc as they were designed to have maximum binding efficiencies.


Alternatives to fittest-win and Moran processes as simple mathematical models of selection

I may suggest to give a look to game theory based model and their generalization from homogenous spatial diatribution to network like model. An easy review can be found in Martin A. Nowak's Evolutionary Dynamics (Harvard press 2006).

In particular you can see the classical Moran process as an evolutionary graph game going on a complete graph with identical weights. Changing the topology of the graph can give different results, though it is not necessary (and there're results showing in which case a graph behave just as a Moran process).

Graph related behaviour are, i.e., suppressing or amplifier of selection...


Addiction specialists and others who study human behavior often catageorize addiction into the two broad categories of physical dependence and psycological dependence. They are not always mutually exclusive, and they can both manifest in serious or mild cases of addiction depending on the person and a number of other factors.

What differentiates them is how they affect your physiology. A person severly addicted to alcohol or opioids can become extremely ill or even die from the withdrawl of those substances, due to the strong physical dependence their body has developed. To my knowledge, people do not experience a physical withdrawl after cessation of compulsive pain seeking behaviors. Since they didn't cite any source, we can only guess as to the intended meaning of your second source, but it's probably related to this lack of withdrawl. A quick search on PubMed shows publications referring to certain endorphins as mediating this type of addiction. Meaning that the endorphin is not addictive per se, but a compulsive or addictive behavior can be communicated to the brain in terms of a native neurochemical pathway which is otherwise a normal part of a healthy brain.

I think the lesson here is to be somewhat skeptical of online sources that don't link to peer-reviewed science. Attempts to simplify a topic for the purposes of communicating with a lay audience often result in more confusion than clarity. And if you search something on PubMed or google scholar, you'll probably find an answer in the same amount of time it took you to post your question here.


Glucose Carrier Proteins in Cell Membranes

First thing's first: there are many different kinds of glucose transporters (genes), even within the same organism. These genes share partial sequence identity in mammals, and are part of the SLC2A, or "GLUT" gene family. In yeast, there exist glucose- and galactose-specific transporters.

Often, not always, a glucose transporter type may be tissue specific. GLUT3 is expressed in neurons, in the placenta, and elsewhere. Compare this to the expression of GLUT1, found in red blood cells, and GLUT4, found in adipose and skeletal muscle tissue.

Each kind of transporter has various affinities for glucose (or other sugars for that matter), and various levels of permeability for similar molecules. This is what is called the specificity of the transporter. The rate at which sugars can pass through the pore of the transporter is called the frequency. Together, these properties define the function of a hexose transporter, and hence why there are different kinds with site-specific expression across the body.

In terms of regulation: GLUT1 is dynamically regulated based on available glucose (up-regulated during shortage and down-regulated during excess). This is not the case with GLUT4; instead, GLUT4 is insulin-regulated, so that muscles and fat tissues can uptake glucose for storage, which is a hormone-controlled process.

Here is a great webpage to help you understand the characteristics of hexose transporters, especially with regard to galactose, fructose and glucose.


How to interpret a phenotypic frequency density plot

Judging from the first section of the Results part of the paper, it looks like the x-axis represents a continuum between two divergent phenotypes.  At one end is parental learning, and at the other end is social learning.  The density (y axis) represents the proportion of the population that displays a given balance between the two extremes.

Generally, density plots are a normalised way of presenting observations, such that the overall area underneath each density plot is equal, regardless of the number of actual observations making up any given plot.


"Biomass is defined as live material, necromass as dead, attached material.
Biomass + necromass form the "standing crop" or phytomass." (from https://link.springer.com/chapter/10.1007%2F978-3-642-68786-0_22)

But even if we were only talking about biomass, there is only a loose correlation between that and photosynthetic activity -  think about single-celled algae, where 'every' cell is photosynthesizing, versus trees, where most cells are non-photosynthesizing, and there may even be times where none are (in trees that loose their foliage in winter).


I think its important to mention that the particulars of memory storage in the brain are still being worked out.  I think what we do know about it is that memory storage depends a lot on the physical configuration of the neurons in the brain.  They move about and make new connections as they process information (and probably also when they are not processing information!).  Different regions of the brain store short vs long term memory and different sorts of memories.  They neurons themselves have a lot of internal cell physiology that can change as well - there are many different neuroreceptors that constitute the synaptic junctions.

All these things may not be a comprehensive list.  But at the basis of all these processes, the cell expresses new proteins in mRNA and these proteins are doing all this work.  beta-actin and histone de-acetylase, as mentioned in your link, are responsible for the cell rearranging itself in the cell shape and in terms of its internal transport processes and in the nucleus respectively.

I'm pretty sure that exactly what is happening here is not really well understood.  monitoring the interior of the cell is difficult.  The work where histone deacetylase is inhibited is a fresh new thought, showing that the arrangement of the chromosomes in the nucleus is involved in hiding memories.  Its still the equivalent to getting a stopped watch to start again by shaking it - there are parts there that fell into place and started ticking again, but we don't really know what the parts are doing in any detail yet.

This hints that if you were to disrupt the cells in some ways you might be able to free up memory, but its a long way from guaranteeing that any given approach will work.  I'd be surprised even if Dr Tsai's cell treatment worked even 70% of the time in her experiment.  Hypnosis or a focused meditation session might still be just as effective.  I think that its a bit too much to expect that Alzheimer's memories are completely preserved and recoverable.  In some cases probably, but categorical statements rarely hold in bioscience.

Like a lot of neuroscience, this work is suggestive, but still just progress towards a clearer understanding of these processes.