Herd immunity without vaccines? (corona question)

This is not just a corona related question, this is true for each disease which is can be transmitted easily and which builds up a lasting immunity.

Herd immunity per se means that a large proportion of a given population is immune to a given disease, either because of vaccination or because the population went through the disease, survived it and built up lasting immunity. This means that even when this disease comes around again, it will only infect few people who have no immunity, but will not spread through the population. This can be seen in the figure below (from here), which implies vaccination, but works as well with getting the disease.

The first case is what happens right now with SARS-CoV-2, it is a new disease to which no one has immunity, so everybody who gets in contact will get the disease (either more or less severe).

If no vaccine would be available, this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread (go to the third part of the figure). At this point a big pandemie would stop.

However, this strategy has one problem: People who are coming into the population (newborns for example) who have no immunity are susceptible for the disease. This ensures low level infection rates and will make sure that the disease will stay in the population, but mostly not noticable. Over time the number of not immune people will rise until there are enough of them to feed another big breakout.

As @bryankrause pointed out, in the past getting to the point to reach herd immunity (at least partly) for diseases like smallpox or measles and to maintain it, cost a lot of lifes.

This is exactly what can be seen in the number of measles cases before the introduction of the vaccine in 1967. Before vaccination every 18 - 24 months enough people without immunity where present, causing another wave of cases. After introducing the vaccination this pattern changes and case numbers went down drastically. See the figure (from reference 1) for illustration. This figure uses data from the US, but you see similar pattern in the rest of the world.

For some more information have a look at reference 2.

Reference:

Evolution of measles elimination strategies in the United States.
Vaccination and herd immunity: what more do we know?


If DNA has a half life of about 500 years, how can old seeds be planted?

That half-life was for temperatures of 13.1ºC. In more ideal conditions, such as for temperature of −5 ºC or drier conditions, the half-life would be longer. The Wikpedia article in fact states that the seeds that were 31,000 years old were frozen under permafrost.

The original article estimates that the half-life at −5 ºC (for a 30 bp fragment of mtDNA from bone) would be 158,000 years. I'm not sure how well this data can be extrapolated to seeds.


What happens when cells in your body run out of telomeres?

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.
So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.


Why do the host cells containing iC3b fragment not undergo phagocytosis?

There's a relatively new concept of self-associated molecular patterns (SAMPs), which much like DAMPs and PAMPs, help immune cells make a decision in a slurry of signals. There's at least a fair article on SAMPs here, and to go even further, the suggestion that tumor-associated SAMPs can dampen immune clearance of cancer cells.

In my head a few things are going on:

(1) The opsonins are potentially binding to everything. Of course, there are surfaces like ECM that don't have any receptors or patterns that you don't want getting damaged, and there's at least some evidence that complement clearance by factors I and H (paywall) may contribute to ablating that effect.

(2) The actual targets for the immune system are expressing patterns that specialized pattern recognition receptors on your phagocytes and so forth can recognize.

(3) Self cells are expressing receptors and patterns that tell the very same cells there's no threat, either through direct inhibition or degradation of kill signals.

Remember that when self cells are damaged, the expression of DAMPs help macrophages and the like come clear them away, so there's obviously a way for self cells to control that effect.


Anomalous base pairing of nucleotide tautomers

The tautomers are rare but they can form and it is suggested that tautomerization can lead to mutations because of non-cognate base pairing.

Khuu & Ho (2009), have inferred the presence of adenine and thymine tautomers from the crystal structure of an in-vitro assembled holliday junction. They infer that imino-Adenine base pairs with amino-cytosine (normal form) and enol-thymine base pairs with keto-guanine (normal form).

  Reproduced from: Khuu & Ho (2009)

Khuu, P., & Ho, P. S. (2009). A rare nucleotide base tautomer in the structure of an asymmetric DNA junction. Biochemistry, 48(33), 7824-7832.


Endogenous retroviral insertions as evidence for evolutionary relationships among primates

The Yohn et. al. (2005) paper (from Evan Eichler's lab) is describing a single type of endogenous retroviral element (loosely think of it as a 'species'), called PTERV1. They show that there were multiple independent infection events that resulted in permanent integrations in the ancestors of modern species (~3-4 MYA in the ancestors of gorillas and chimps, ~1.5 MYA in the ancestors of baboons and macaques). This in no way contradicts the notion of common ancestors among the apes/monkeys; indeed, they state this as a given in their analysis (emphasis mine):

  A total of 275 of the insertion sites mapped unambiguously to
  non-orthologous locations (Table 2), indicating that the vast majority
  of elements were lineage-specific (i.e., they emerged after the
  divergence of gorilla/chimpanzee and macaque/baboon from their common
  ancestor).

The presence of an ERV (or intron, or any general genomic synteny), can be used as evidence to support a particular model of common decent. Changes in genomic architecture are stochastic processes, and the work you cite by Li et. al. (Lynch lab) is showing us that ERV placement can occur at a similar, or nearly identical, location at a much higher rate than previously thought. We therefore need to take this into account then calculating how strongly a shared ERV increases our confidence in a given phylogenetic model.

The video you linked to uses a completely random (i.e., very simple) model of ERV integration, setting the chance of an insertion at a given location at 3.3e-10. The findings by Li tell us that this is incorrect. In daphnia, at least, ‘hotspots’ may account for nearly 25% of new intron gain. The video also failed to include all of the instances of ERVs that are not shared between humans and chimp (back-of-napkin, this could account for differences of ~0.3% between their genomes, see Mun et al. 2014). This will increase the probability of an exact match occurring by chance (e.g., put two people in a room, what’s the chance of them having the same birthday? Put 100 people in a room, what’s the chance of any of them having the same birthday?).

So, let’s be extremely conservative and say that the chance of the same insertion at a given location in both chimps and humans is one in one thousand (1e-3, seven orders of magnitude more probable than in the original model). Sixteen shared ERVs are identified in the video; if each is considered an independent event because of no shared decent, we are still looking at odds around 1e-48 (1e-3 ^ 16). An alternative could be that they are derived from insertions that predate the split from a common ancestor. Given Li et. al., maybe each event should be given a probability of only 0.75 instead of 1.0 (as per the video) because up to 25% of them could be from hotspots. In this scenario, the probability is 0.01 (0.75 ^ 16). Therefore, the second hypothesis is 46 orders of magnitude more probable than the first. In my mind, this is extremely compelling evidence that humans and chimps share a common ancestor, using only ERV data.

I want to be clear, I am fudging these numbers extensively towards not supporting common descent. The real odds will be much higher in favour of common descent.

For further reading, Welkin Johnson wrote a comprehensive review on ERVs in 2015 (paywalled, so you may need to search for Alexandra Elbakyan's scientific literature retrieval method if you don't have institutional access).

References

Johnson WE. (2015). Endogenous Retroviruses in the Genomics Era. Ann. Rev. Virology. doi: 10.1146/annurev-virology-100114-054945

Li W. et al. (2009) Extensive, Recent Intron Gains in Daphnia Populations. Science. doi: 10.1126/science.1179302

Mun S. et at. (2014) Chimpanzee-Specific Endogenous Retrovirus Generates Genomic Variations in the Chimpanzee Genome. PLoS One. doi:  10.1371/journal.pone.0101195

Yohn et. al. (2005). Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans. PLoS Biol. doi: 10.1371/journal.pbio.0030110


It looks like it's the other way around to me. More likely a member of Auchenorrhyncha, which includes cicadas and leafhoppers. I say this judging from the leg structure, abdomen shape, and the eyes. It is however missing wings... perhaps they were removed by another organism?

It somewhat looks like Philaenus spumarius, the "meadow froghopper" which is found in Germany. As for the green tail bit, I am not all that sure.


Confirmation of organoid's character with the respective organ

Verification of organoids is done by detecting the cellular proteins for particular tissue type using Immunofluorescence.

For verifying intestinal organoid, apical membrane markers  (villin or alkaline phosphatase) and basolateral markers (E-cadhehrin) are detected by immunofluorescence. Transporters present in intestinal membranes are also displayed on organoids.  The peptide transporter PEPT1 and the glucose transporter SGLT1 are located on apical membrane, and the glucose transporter GLUT2 is present on basolateral membrane. So, these proteins can also be used as markers for verifying intestinal cells.

Via:

https://www.nature.com/articles/srep16831
https://www.ncbi.nlm.nih.gov/pubmed/19329995


Are pheromones capable of activating changes to the Phenotype of a complex organism?

Pheromones are means of communication between individual within a species, not between species.

  [A]re [pheromones] capable of changing the phenotype of an organism[?]

Yes! It actually necessarily does, by definition. If a chemical produced by an individual does not affect the phenotype any individual of the same species, then it is not a pheromone! You will note that behaviour is part of an organism phenotype.

Pheromones can have drastic impact on an organism phenotype. Most notable examples are from social insects, such as caste differentiation in termites (Matsuura et al. 2010).


Does severing the Corpus callosum, effect the brain's communicating ability?

Yes, it does; the corpus callosum is a major communication pathway between the hemispheres. Severing the corpus callosum is only done when seizures are severe enough to warrant it, and other options are ruled out for various reasons.

The condition of having a severed corpus callosum is often referred to as being a split-brain patient. There are some individual differences between patients, but hopefully searches using the keyword "split-brain" can help you find tons more information (summarizing it all here would give much too long of an answer).

One thing that is important to keep in mind is that although the corpus callosum is a very substantial connecting pathway between the hemispheres, it is not the only one, so the hemispheres are not completely severed. The cortex also communicates substantially with other brain structures that are not directly impacted by severing the corpus callosum.


I now found this Wikipedia article on biological immortality. It's pretty much what I was looking for.

Wikipedia describes the phenomenon as follows:

  Biological immortality refers to a stable or decreasing rate of
  mortality from cellular senescence as a function of chronological age.
  Various unicellular and multicellular species may achieve this state
  either throughout their existence or after living long enough. A
  biologically immortal living thing can still die from means other than
  senescence, such as through injury or disease.

It has a list of such organisms as well, consisting of

tardigrades
hydras
turritopsis nutricula, some sort of jellyfish
lobsters*
planarian flatworms

Addendum: This blog post takes a good look into the myth of lobster immortality. It seems to be as much a myth as the result of any substantial observation.


What percent of the population has some form of synesthesia?

The phenomenon

Synesthesia is a neurological phenomenon in which a stimulus in one sensory or cognitive pathway triggers an experience in another.  Some hallmarks:1

It tends to be developmental, arising early in childhood.
It is involuntary.
It is stable over time (i.e. the same stimulus leads to the same sensory experience).

Epidemiology

The best paper I found on the issue is by Simner et al, 2006.2 The authors first review prior literature on the topic and then describe their own methodology and study addressing the question of prevalence. Regarding prior research:

  Estimates of the prevalence of synesthesia have diverged widely....estimates range from 1 in 4.....to 1 in 25000 - 100 000.

Not so helpful.

They point out some problems with prior studies: one group of surveys relied on self-referral and made the (conservative) assumption that all non-responders to an invitation to participate were non-synesthetes. Another set of studies avoided this problem by questioning every member of a participant pool but established the prevalence only “subjectively” (their wording, although I note that this is an inherently subjective phenomenon!).

Simner's own group used a validated survey questionnaire about specific synesthetic experiences (the specificity and prior validation of this overcoming the  "subjective" aspect in their view). They found an overall prevalence of 4.4% for any type of synesthesia. Importantly, the male: female ratio was not significantly different from 1 in this group, in contrast to many prior studies which have found a marked female predominance, ranging from 2:1 to 5:1 (references in Simner's paper for those interested).

Modalities of experience

To address your question about the types of sensory experience involved, I turn to a more recent review article1 that compiled results from multiple studies. In this report, grapheme-color type synesthesia was most common (86%). These participants see a number or letter and experience a particular color in association. This was followed by followed by time-space type (62%), a group who associates units of time with a particular space relative to their body.  The third most common was music-color type (41%), which is fairly straightforward. The majority experienced more than one type (clearly, given the percentages).

Here is a graph showing the percentage of the cohort who reported particular synesthetic experiences, grouped according to the category of inducer:

Note that the most common type mentioned above, grapheme-color, includes all three of the first categories - "digits," "letters," and  "words" on this graph. Although only the inducers are listed here, the most common associated perceptions were indeed color (97%), followed by spatial configurations (62%). In most cases the color was static (73%) but in some people it moved in a specific direction (16%).

Niccolai V1, Jennes J, Stoerig P, Van Leeuwen TM. Modality and variability of synesthetic experience. Am J Psychol. 2012 Spring;125(1):81-94.
Simner J1, Mulvenna C, Sagiv N, Tsakanikos E, Witherby SA, Fraser C, Scott K, Ward J. Synaesthesia: the prevalence of atypical cross-modal experiences. Perception. 2006;35(8):1024-33.


This looks like an immature passionvine hopper (Scolypopa australis).  They are informally known as fluffy bums.

Source: http://ketenewplymouth.peoplesnetworknz.info/friends_of_te_henui/images/show/1486-nymphs-fluffy-bums-scolypopa-australis

This is am image of the adult stage from the Encyclopedia of Life site:

More information can be found at the Encyclopedia of Life link above.  It appears that their distribution may be only in Australia and New Zealand and I'm not sure where this photo was taken so take this information into consideration.


The following answer only deals with theorical feasability

Can a species populated solely by males be saved from extinction?

Short answer : No, not with certainty
Nuanced : yes, in some species, it could be possible
It varies in function of how you determinate the sex of your species.
Sex determination is a wide topic, see the appropriate wikipedia page
Some reptilian species are not sexually determined by chromosomes but by temperature. An example is the painted turtle, of which thermal sex determination has been studied by Carrie Lynne Morjan in an article titled Temperature-dependent sex determination and the
evolutionary potential for sex ratio in the painted
turtle, Chrysemys picta
Thermal sex determination allows you to get 2 different sexes from the "same" genome, as temperature will be the driver of the hormonal differentiation.
Cross-species cloning: influence of cytoplasmic factors on development, by Sun and Zhu states that cross species cloning has been successfully made with fishes and mammals.

Nevertheless, cross-species NT has succeeded in cloning some endangered mammals, such as the gaur
In fish, a type of relatively primitive vertebrate, cross-species NT [nuclear transfer] could be achieved in quite a few genetically distant species

It means we are able to use as a mother and egg-layer a different, albeit related, species.
We can, with a massive grain of salt, hypothesize that we could, in a specie solely constituted of sperm producing male, use the oocyte of another specie to clone it, then use the thermal differentiation to make a female out of our clone.
However, I am not aware of any information about how much genome and spermatozoids genetic payload is modified by the sex differentiation. Therefore, it is possible that sex-determined genes cannot produce a sexually naive clone.
For more information, and if you want to research more about it, I recommend you to see the current state-of the art in de-differenciation technics and DNA-demethylation for cloning.
I hope I provided a sufficient answer for you.


Is there a difference between splice-site mutations, and non-stop mutations

No, those kinds of mutations are quite distinct.  Also, you misstate the nature of a nonstop mutation; the change of a stop codon affects termination of translation, not transcription.  This is quite different from a splice-site mutation, which affects splicing, a form of mRNA processing that occurs between transcription and translation.


What is the identity of this flower found in Mavericks Beach in Half Moon Bay, California, USA?

Based on the habitat, color, and size that lupine looks like Coastal bush lupine (Lupinus arboreus).

Please note that Coastal bush lupine can be invasive, so be responsible about where you plant it!

You can also learn more about this plant and its growth requirements from the California Native Plant Society

Images for comparison:


Online toolkit that provides functional similarity scores (in the form of a matrix) between two functional gene sets in the context of gene ontology

I think that you could try a similar approach to GSFS:

use transduction in proteins (if you don't know star code, then you must use 3 strings for each gene)
use a basic tool (a stand alone like UNIPROT tools) to identify the proteic domain type (chain alpha, ..)
divide the genes by proteic domain type (pdt): which contains which pdt and the pdt order frequencies

Now, you could use DAVID or similar (try wconsensus: it's old, basic but very custom) to compare similar sequence and obtain your scores.


Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?

Rice and Salt$^1$ bred fruit flies for 35 generations and from one line of flies created two groups that were isolated from each other reproductively. They could not interbreed because they no longer bred in the same environment. Depending on one's definition of 'species' this could be a case of artificial speciation.

$^1$Rice WR, Salt GW (1988), Speciation via disruptive selection on habitat preference: experimental evidence". The American Naturalist 131 (6): 911–917.


Do serotonergic (5-HT2A-mediated) psychedelics elicit stimulant effects?

I think you'll like this article. It's on monoamine release / reuptake inhibition for a host of different psychedelic and empathogenic drugs.

This wakefulness inducing effect you describe for LSD is widely reported for all common 5-HT2 mediated psychedelics.


Why is fructose not glucose the main energy source of sperm?

I have been searching this for a while and I got something of an answer, which I am posting below.

There are primarily two advantages of using the polyol pathway and aldose reductase to produce fructose from glucose via sorbitol:-

1) Quoting the book here,

  Seminal fluid contains up to 11 mmol/L (200 mg/dl) of free fructose.
  It is the major energy source for the sperm cells in their
  all-important race for the ovum. The advantage of fructose over
  glucose may be that many bacteria, which compete with the sperm cells
  for the available nutrient, prefer glucose to other energy sources.

Thus, to avoid other competitive bacteria and cells from utilising the energy source of sperm, fructose is used as the energy source since the bacteria prefer glucose.

2)Another reason is that the metabolism of sorbitol into fructose is energetically efficient way (no ATP required) as compared to glycolytic conversion of glucose into fructose(G$\rightarrow$G6P$\rightarrow$F6P$\rightarrow$F). Tapping the polyol pathway is energetically preferred to metabolizing fructose produced during glycolysis.This is only to show the possible evolution of the polyol pathway once the advantage of using fructose as the energy source was established. It does not explain why the fructose was advantageuos but just that if it was advantageous, the semen-producers would develop the currently existing machinery to produce fructose as the exclusive source of energy.

Hence, sperms (seminal secretion) contains fructose as the primary energy source and not glucose.


Mycorrhizal fungi are often used in small-scale agriculture for just that reason.  If you search mycorrhizae on amazon they sell it by the tub.  I think its especially used in organic gardening for just what you said, the slightly less-processed organic fertilizers are harder to take up by plants without their mycorrhizae partners.

I'm not sure about how widespread the practice of applying mycorrhizae is in large-scale non-organic farming.  Judging by how big of a problem fertilizer runoff is, my guess is that a lot of companies have decided that their bottom line is best served by just swamping everything with artificial fertilizers.  I'm not sure how mycorrhizae is produced either, it might really be prohibitively expensive to scale production of it up that much.


It might be useful to look at how 23andme works, to see how this analysis product is generated, in general:

  The 23andMe genotyping platform detects single nucleotide polymorphisms (SNPs). A SNP is a DNA location, or "marker," in the genome that has been shown to vary among people in terms of the DNA base or bases. There are four DNA bases: adenine (A), thymine (T), guanine (G), and cytosine (C). So, for example, at the same genomic location, you might have a C and someone else might have a T. These DNA base differences are known as "variants."

These SNPs can differ by population types. Some subsets of a population type might suffer a disease and appear to have SNPs that others do not. So-called GWAS studies (discussed below) work at associating SNP distributions with diseases or other phenotypic traits.

You send some spit to 23andme, they tell you who you are likely related to and what diseases or other physical attributes you may have, based on patterns of these SNPs.

23andme uses Illumina chips for figuring out what genotypic variants you have in the spit sample you send to them. Illumina is a company that manufactures "chips" that react to the presence or absence of markers in the DNA sample you send to 23andme. Each chip in this platform calls different sets of markers.

These markers often have identifiers associated with them, each called an rsID.

  The rsID number is a unique label ("rs" followed by a number) used by researchers and databases to identify a specific SNP (Single Nucleotide Polymorphism). It stands for Reference SNP cluster ID and is the naming convention used for most SNPs.

They also map variants that do not use rsIDs, and instead use some other internal identifier.

Whatever the identifier, GWAS — Genome-Wide Association Studies — are research projects that analyze populations of people in different ethnicities or other cohorts, looking for over- or under-presence of various markers, compared with the larger human population.

For instance, here is such a GWAS study that is used by 23andme to indicate risk factors for Parkinson's disease, in sample donors who have these variants. There are other such studies for schizophrenia, for autoimmune diseases, and so on.

The power of these studies to make a positive, correct association depends on various factors, but the product 23andme sells is ultimately a packaged summary of a lot of work by researchers around the world.


Do mucous membranes surround visceral organs?

You are correct.

"Serous membrane" might be what the Wikipedia editor was thinking of, for example the pleura of the lungs; other examples include the pericardium and peritoneum.


This paper suggests that bats have a comparatively high depth of focus.

It's believed that butterflies (depending on species) have the widest visual spectrum.


Why denatured proteins can't fold back in their native form

In short: the unfolded state is a high-energy state of the protein, which will move towards lower-energy states. Some of these states are the folded protein, while others states are denatured protein (forming "wrong" interactions with itself or other proteins). Energy barriers between these states keep the protein in the denatured state even though the folded state might me more favorable.

Or in other words: it's trapped in the denatured state because of kinetics, even though thermodynamics would favor the folded state.

A nice figure to illustrate this: http://www.ghrnet.org/index.php/jbmbr/article/viewFile/1027/1397/6798

If you go into a little bit more detail, you will find that a lot of proteins (especially larger ones) are usually folded by chaperones. These helper proteins will bind to the emerging protein chain to prevent it from aggregating. In a sense they guide the protein to a folded state. In a similar way, chaperones can help proteins overcome the energy bariers that normally prevent it from going from an aggregated state to a folded state.

This review in Science  is very complete, but also contains some nice figures that give you an idea of what happens:
http://science.sciencemag.org/content/353/6294/aac4354.long /

If you're a pirate: http://science.sciencemag.org.sci-hub.bz/content/353/6294/aac4354.long


Why is Electrical Cardioversion contraindicated in AF and Digitalis Poisoning?

The mechanism of action of digitalis-like preparations based on inhibition of myocardial NA+/K+-ATPase as well as of cardiac conducting tissue. The inhibition of latter (conducting) is 2.5 greater than those of former (myocardial). This is why the main feature of digitalis intoxication are arrhythmias due to ectopic electric impulses and spontaneous depolarization (there is overloading of conducting system by Calcium as well as excess amounts of Noradrenaline released from sympathetic endings).

These metabolic changes in a case of digitalis intoxication could lead to irreversible ventricular arrhythmias after cardioversion - there are sporadic reports about this phenomenon. Based on these reports, it was thought that the use of digitalis during electrical cardioversion would provoke ventricular arrhythmias in patient even with clinically desirable concentration of digitalis.

In a study in patients with therapeutic nontoxic digitalis levels determined that these patients may safely undergo electrical cardioversion without reducing or withholding the dose of digitalis. Thus, the cardioversion is not contraindicated in a patient without signs of digitalis toxicity.

Although, the exact mechanism of the ventricular arrhythmias after cardioversion is not well understood, it is clear that mentioned above changes in electrolytes concentrations with electrical stimulation lead to premature beats overtaking restored sinoatrial pace. The rate of ventricular arrhythmias is in direct correlation with the level of the energy used for the cardioversion (this is why there is "pre-cardioversion" with low-energy pulses). Until these metabolic changes are not corrected, the resulting ventricular arrhythmias can be irreversible. This is why, digitalis intoxication is relative contraindication to electric cardioversion of atrial fibrillation/flatter.

Excerpt from the article mentioned:


Single stranded DNA in gel electrophoresis

As already mentioned formamide can be used. However formamide has to be incubated with the nucleic acid sample and heated. Urea can be included in the gel (8%). DNA can also be denatured using NaOH. NaOH, however, cannot be used for RNA because it will cause alkaline hydrolysis.
I don't much agree on this point. Though dsDNA can produce diverse structures, as buzrw mentioned, so can ssDNA (in fact more diverse). Moreover, linearization solves the issue of supercoiling. We never compare circular plasmids with each other on the gel. Long linear dsDNAs can form structures but then in such cases gel electrophoresis is not a very suitable method for comparison. PFGE might be a better option in such cases.


How do ascending neural pathways filter unimportant information?

A neuron cannot know the importance of a signal in any applied sense, that is, it can't know the difference between one triggered by a feather or one by a hammer... on an individual basis.

A single neuron can however accumulate information in a number of ways, either by requiring multiple incoming triggers (filtering out localised signals, i.e. from a single connected neuron) or they can require repeated triggers (filtering out weak/freak/accidental signals from a connected neurons). This is called summation:

These filtering events occur at the synapses, so how would a neuron filter a signal as it was passing through it? As far as I know, it doesn't!

NOTE:
As noted by @WSYWYG, LTP and LTD are also important, they stand for Long Term Potentiation and Depression. These are names given to the long term increase or decrease in sensitivity of a synapse, that is a neuron can become more or less likely to pass on a signal over long periods of time due to the pattern or frequency of signals it receives. Googling the terms will lead you to a wealth of vastly more detailed information on these topics.

EDIT:
As an addendum, your body can inhibit neurons selectively, so as a wild stab in the dark, it may be interesting to see if ignoring a sensation from part of your body is the direct result of of external inhibiting (filtering) of signals incoming from ascending neural pathways... but don't trust me on that!


It's best to leave the bird alone. The parents are likely still in the area and tending to the young, including feeding and chasing away would-be predators. You're better off staying away so as to not intimidate or upset the parents. If you have outdoor pets, relocate them indoors or to an enclosed area for a few days.

Failing this, the advice given in comments to call your local animal rescue is best.


What are the principles of stem cell engineering?

The roles of the reprogramming factors Oct4, Sox2 and Klf4 in resetting the somatic cell epigenome during induced pluripotent stem cell generation

  Current reprogramming technology, pioneered by Takahashi and Yamanaka
  1, was built on several seminal advances in the field of
  developmental biology. First, nuclear transfer experiments
  demonstrated that a somatic cell nucleus could be epigenetically reset
  to an early developmental state [2]. Second, cell culture conditions
  were developed that allowed for the isolation and culture of
  pluripotent cells, termed embryonic stem (ES) cells, from the inner
  cell mass of the human and mouse blastocyst [3,4]. Finally, study of
  these cells and of early embryonic development led to the
  identification of factors that were ultimately able to reprogram mouse
  embryonic fibroblasts (MEFs) to the iPS cell state when ectopically
  expressed, albeit at low frequency.

  Reprogramming of somatic cells is a multistep process that culminates
  in the expression of pluripotency genes such as Nanog. Although
  morphological changes occur at early and intermediate stages of
  reprogramming, pluripotency gene expression is only induced during the
  late stage and indicates faithful reprogramming.

  The core reprogramming cocktail, consisting of the transcription
  factors Oct4, Sox2 and Klf4 can be augmented by the
  addition of factors that enhance the efficiency of iPS cell
  generation

Its a multistep process in which much research is still needed,

  The frequency with which somatic cells convert to iPS cells is
  typically below 1%. Therefore, much effort has gone into improving
  reprogramming.

specially to increase efficiency of iPS cell generation

  The ability of cells to pass through the cell cycle has also been
  shown to be an important determinant of reprogramming efficiency.
  Knockdown or gene deletion of p53, p21 or proteins expressed from the
  Ink4/Arf locus allows cells undergoing reprogramming to avoid the
  activation of cell cycle checkpoints and cellular senescence, leading
  to greater iPS cell formation [21],24-27].

Gene expression changes during reprogramming


What is the biological age of grafted plants?

In my experience (in common with the experience of everyone I've talked to who could be considered an expert on the subject), taking old wood and using that as a scion when grafting new trees rejuvenates them, and they grow as new trees.

I'll take apple trees as an example. As you can see from the table here, there is a distinct age after which the tree begins to decline. Now, that's not concrete (I've seen some apple trees last over 100 years (didn't plant those myself btw)), but generally, an apple tree will lose vigor and productivity before it reaches 50 years of age. This tree's 'immune system' also goes down, and it becomes susceptible to many diseases. You'll rarely see such a tree, as orchardists generally replace them rather fast.

But to the point of your question. When you will graft an apple tree, you will generally bud graft it, as described here. That article (which is spot-on) says:

  Select a healthy branch of this year's growth from your desired variety of tree. Look for a plump leaf bud about halfway down the branch. Leaf buds are close to the branch where fruiting buds tend to stand out more.

Note that it says nothing about the tree's age, simply stating that the wood must be healthy. That's because old wood/young wood produce the same result in the new trees. I was using a 40 year old razor russet to graft onto all the Malling V rootstocks I had for that variety. And of course they grew as expected, as a young sapling should. I've heard of a nearby nursery taking budwood from a 100 year old tree that still looked good.

Additionally, you can use a rootstock taken from an old plant, and also a scion from an old plant, and the new plant created will grow as a young sapling. Here's how the rootstocks I use are created: You cut down a tree at ground level, and it sends out a lot of shoots. You pile soil over it, but allow the ends of the shoots to stick through. These shoots will root into the soil, and can be cut at the base, and planted out for grafting later. This way, you can have 1000's of identical (cloned) rootstocks. You can also get rootstocks from old trees. Here's a diagram of the process.

About herbaceous perennials, I've found (to some people's surprise) the same thing. The scion grows as a young plant again once grafted. I found this out because I graft heirloom tomatoes onto hybrid tomato rootstocks (the latter are seedlings). Usually, the scions will be from seedlings, but at times I take the scions from a large mature plant.

Just so you know, an indeterminate tomato plant will, once mature, flower and fruit until frost. A determinate tomato variety will produce a large crop all at once, and then die back (this is the kind preferred by owners of mechanised (machine harvested) fields).

In my tests, you could take the scion from an old determinate plant that was through fruiting, right before it started dying back, and successfully use that for grafting the new plants. These new plants' growth was identical to the growth of grafted plants whose scions came from seedlings, and they began to flower and produce fruit at the same time. Of course, actual seedlings did not have the vigor of the grafted plants, and were behind in growth.

Off-topic for your question, but possibly still of interest, I've found that cuttings and layers (not scions) taken from old plants (both woody and herbaceous), and rooted, would grow as young plants again.


How to retrieve logical expression (KO based) for reactions from KEGG?

To rephrase what you already mentioned in your question: For a KEGG Module to be completed (so that an organism can perform a certain function) you need a certain set of functional units or enzymes. So to evaluate the abilities of an organism you would check its genome for the gene sequences related to the module by performing the logical operation you mentioned above.

A Module is composed of chemicals (C) and reactions (R), as you can see in your given example. To explain the differences between modules and reactions best have a look at the last reaction, Isocitrate to 2-Oxoglutarate. There are three boxed reactions (one of them is a combination of two) that all lead to Oxoglutarate. When you look at the Orthology (the enzymes involved) for the reactions in the first box (R01899+R00268) and the second box (R00267) you will see, that it's the same enzyme (K0030) performing different reactions. The third box now contains a reaction (R00709) performed by a second enzyme (K0031), that leads the same way (it differs in using NAD+ instead of NADP+ as electron acceptor). So for the module to be completed you could use either of the two (that’s the reason for the OR-operator in the logical operation).

If you now want to evaluate if a certain type of reaction occurs in a given organism it is sufficient to have one of the possible enzymes catalysing this reaction. So:

K01648 OR K15230 OR K15231


Photosynthesis and thermosynthesis(?) in plants/organism

Theoretically it should be possible for an organism to use hat to produce a chemical that it can then use to make useable energy however at present we know of none that do this. If it is possible though it would allow for life in the warm, dark oceans of Europa and if life is not there already it would make it pretty easy to introduce life permanently to a planet like the moon Europa. However in deep sea vents types of anaerobic respiration are most effective and on the surface light is and so if any organisms ever did use thermosynthesis on earth they were probably outcompete do by other forms of energy production and forced to extinction.


How long can Legionella survive at 60°C?

Usually cell death would follow first order kinetics.

$$X=X_0e^{-kt}$$

where $X$ is the number of cells at time $t$, $X_0$ is the initial number of cells and $k$ is the death rate constant. You can get the constant by solving for 90% reduction in 2 minutes. Then just substitute and get the time required for 99.99999% reduction — 10 minutes.

For your follow up questions, see the same wikipedia article.

  Moist heat sterilization (superheating to 140 °F (60 °C) and flushing)
  is a nonchemical treatment that typically must be repeated every 3–5
  weeks.

It also depends on how much is the bacterial load in the input.

Other sources (Farhat et al. 2012; Whiley et al., 2017) suggest 70°C treatment for 30 minutes.

However, Legionella has been shown to survive heat treatment of 70°C/30min (reviewed by Whiley et al., 2017). Legionella can also be "protected" by other micro-organisms such as certain types of Amoeba, in the water.

So, probably multiple levels of disinfection is needed.


How many cyclic and non-cyclic photo-phosphorylation is required to produce one molecule of glucose?

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.
Source: Cyclic, pseudocyclic and noncyclic photophosphorylation: New links in
the chain. John F. Allen. TRENDS in Plant Science Vol.8 No.1 January 2003.
Cyclic photophosporylation, does not occur under normal conditions in higher plants. It is believed to occur only when either light intensity is low (lower frequency so as only PS1 can function) or when carbon fixation is not at par with light irradiance (i.e, too much light).
And hence it is not advisable to come to this generalization "Six Turns of non cyclic photophosphorylation will produce 12 NADPH2 and six ATP molecule"


How to determine the height/bits in a sequence logo?

Wikipedia has a page on sequence logo which discusses the calculation briefly.

The "bits" here are related to those used in Shannon entropy. This is an information-theoretic equivalent to the Boltzmann entropy from thermodynamics. This is a measure of how "disordered" the position is, or more precisely how specific the distribution is.

The general formula for the total entropy (expressed based on probabilities/fractions) is

$$ S = -k \sum_i p_i \cdot log( p_i ) $$

where $i$ ranges across all the various states (e.g. each nucleotide).

The difference between Shannon entropy and Boltzmann entropy (aside from the contexts where it's used) is the value of the constant (one for Shannon, Boltzmann's constant for Boltzmann entropy) and which logarithm used (the natural logarithm for Boltzmann entropy, and typically base-2 for Shannon entropy.) As it uses base-2 logarithms, the Shannon entropy is typically measured in units named "bits".

The wrinkle is that the entropy of a distribution isn't really what you want to display in a sequence logo. Instead, you want something that gets larger (not zero) when the sequence becomes more defined. As such, the values displayed are not the entropy itself, but the "entropy loss" from a completely random (maximal entropy) distribution.

That's how you get the total number of bits at a position (the total height). The height of the individual letters comes by taking the total height and multiplying it by the probability of each state. This might not have rigid theoretical justification (you can't attribute the entropy loss to individual nucleotides like that), but it fulfills the display purposes of making the more prevalent nucleotide identities larger in display size.

For example, if you have a position with 70% G and 30% C, then you have
$$ (4 \cdot -0.25 \cdot log_2(0.25)) - (-0.7 \cdot log_2( 0.7 ) + -0.3 \cdot log_2( 0.3 )) = 1.12$$ bits of total height. G gets a height of $1.12 *0.7 = 0.78$ bits, whereas C gets $1.12 *0.3 = 0.34$ bits.


Can you design a bacteriophage that attacks the part of the bacteria that makes them antibiotics resistant?

Check out phage therapy. For more details check out the reviews by Levin & Bull (2004) and Skurnik & Strauch (2006). The idea was around for quite some time and there is active ongoing research in this field.

However, this idea just involves killing the bacteria using bacteriophages and not reducing their resistance to antibiotics. The bacteria that are immune to antibiotics can be killed by viruses (and vice versa). If you use them in combination then possibly there can be synergistic effects under a certain regime.

  Another clinical trial was conducted to evaluate a combination of the
  antibiotic enrofloxacin and intramuscularly administered bacteriophage
  (Huff et al., 2004). Both treatments individually provided effective
  treatments of the E. coli infection, but the synergy between the two
  treatments led to a total protection of the birds, thus suggesting a
  significant value of the combined treatment.

  Skurnik & Strauch (2006)

The combined treatment may not always be synergistic; they could also be antagonistic and therefore a good therapeutic strategy should be applied (Chaudhry et al., 2017).

  As suggested above for tobramycin, antibiotics can be antagonistic to
  phage because they reduce the density of the bacteria and thus the
  capacity of these viruses to replicate [43]. Worse, antibiotics may
  even interfere with phage replication within the cell, thereby causing
  a reduction in phage numbers [41, 44, 45]. One way to test the effects
  of this possible antagonism is to treat with phage first and
  subsequently treat with the antibiotic, comparing the outcome with the
  case of simultaneous treatment. Here, we used delays of 4 and 24
  hours. Results show substantial effects of delayed treatment with
  phage for some antibiotics but no effect for others (Fig 4). The only
  statistically significant effects of delay are for the 24 hours delay
  using gentamicin and tobramycin, but the magnitude of the effect is
  profound. These are two of the three drugs for which simultaneous
  treatment suppressed phage replication (Fig 4B). The third such drug
  that suppressed phage replication with simultaneous treatment
  (ciprofloxacin) also exhibited greater kill with phage-first
  treatment, but the statistics fail to reject the null hypothesis of no
  effect of delay. This case warrants further investigation.

Unfortunately, bacteriophages are very host-specific and are hence not as broad spectrum as antibiotics. They are just like viruses of animals: the virus that infects a cat would most likely not infect humans. Very few viruses have a broad range of hosts.

For your query:

  if you can construct a drug that somehow can attack the bacteria because of the specific genetic code that gives the bacteria the ability to produce beta-lactamase then you might be able to attack all bacteria that shares the same genetic code that gives them that ability and the bacteria can not mutate to escape without losing their resistance to penicillin.

the answer is that it is possible in principle. There are ways to knock out certain genes (CRISPR-Cas is one of the ways). However, the problem is the delivery of these molecules that mediate these knockout, to the bacterial cells. For that, you again have to rely on virus like particles for the delivery which gets us back to square one: how to make delivery machines/viruses that target all pathogenic bacteria. Moreover, the mechanisms of antibiotic resistance are diverse. Considering several other factors (that I am not going to list here), it is very difficult to make an efficient system for targeting antibiotic resistance genes in different bacteria.


Most likely it is Polymopheus moth caterpillar, known as Antheraea polyphemus  from the giant moth family.

yellow-green, and the setae become relatively less prominent with each molt. The translucent yellowish-green to green, full-grown (fifth instar) caterpillars are 60 to 75 mm in length. They have yellow mid-segmental lines that run from the sub-dorsal scoli (setae-bearing, wart-like bumps) touching the spiracles and to the lateral scoli on abdominal segments 2 to 7.

Reference

The species is widespread in continental North America, with local populations found throughout subarctic Canada and the United States. The caterpillar can eat 86,000 times its weight at emergence in a little less than two months.

Reference

The adult wingspan is 10 to 15 cm (approximately 4 to 6 inches). The upper surface of the wings is various shades of reddish brown, gray, light brown or yellow-brown with transparent eyespots.

Reference

Adult male moth

Adult female moth


First you should decide whether you want to design an shRNA or use siRNAs.

If you want to use shRNA you should look at the rules that "Mad Scientist" mentioned. You can insert mismatches but make sure not to disrupt the secondary structure. You can use RNAFold to verify.

shRNA always has issues and you have to optimize your design, test it by realtime PCR or Northern blot etc to confirm the production and the concentration.

You can design siRNAs and there are online algorithms to help you design one.
You have to choose a sequence which is specific to your gene. This step is important for both shRNA and siRNAs in order to minimize/avoid off-targeting.

A common practice is to use a pool of siRNAs for a single gene. Pooled siRNAs are commercially available for many genes.

For the experimental controls you would need to do two experiments:

mock siRNA treated; which wont affect any gene
Your siRNA treated

then test for a reference gene such as GAPDH and your gene. A good reference gene should be the one which is not expected to change expression. GAPDH may not be a good reference always (for example in cases where metabolism is affected). The choice of reference gene is intuitive and depends on your prior knowledge of the system. Instead of GAPDH you can also transfect GFP and quantitate that as a control (spike in).


How can I find the mRNA sequence for a specific prokaryotic gene?

mRNA specific queries

Add this to your NCBI query: AND mrna[filter]

If it's not available in major databases it may not be known.

However mRNA data can be obscure to find even in those major databases but it should be there. I would be surprised if that is the case, however since you're not working with model organisms there may well be nothing available.

When looking for a transcript gene, NCBI have some tips that you can see here for searching their database. #8 might be relevant to you as it's a way of filtering exclusively mRNA records.

  If there is no UniGene cluster for this gene and organism, perform a
  search in the Nucleotide database with the gene name, product name, or
  symbol. Include the organism in the search to find the most relevant
  results and filter for transcript sequences, for example: Cytochrome c
  AND bullfrog[orgn] AND mrna[filter].

Predicting mRNA

Basic: ExPasy DNA translation tool

Advanced: regrna 2

Assuming that advanced querying doesn't reveal what you need you might be able to make some useful predictions before taking it to the lab. There are a handful of other predictive tools that can maybe help you out if that's the only option available. I can't get my head around exactly what information you have as an input. Assuming you have the DNA sequence, I would start with the obvious choice: the ExPasy DNA translation tool.

I would then say that regrna 2 might be able to steer you in the right direction regarding more subtle translational elements.


Identification of an insect from Florida

It's a cockroach nymph. Unfortunately it's barely visible given the angle of the photo, but it looks like the pronotum (head shield) has a pale margin - which, coupled with the pale markings at the sides of the tergites, makes me think this is a late-instar nymph of the Australian cockroach (Periplaneta australasiae). This looks very similar to the American cockroach apart from the pale markings, and is found in the southern US as well as many greenhouses. Within the US, it is most abundant in Florida and the coastal southern states. It is found primarily outdoors, where it prefers to live under tree bark, in piles of firewood and other locations that are moist and sheltered, but it can also be found indoors (source). It is the most prevalent cockroach outdoors in south Florida.

It mostly eats vegetable matter but when it enters homes it may eat holes in clothing and feed upon book covers (source).

(image copyright J L Castner; source: University of Minnesota).


Can bacteria or other microorganisms be killed by applying pressure?

Yes, you can kill bacteria using pressure. The devised used is called a French press

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

http://www.glenmills.com/cell-disruption/high-pressure-homogenizer/french-press-gm/

However the pressure use is about 40k psi.... which is a lot higher pressure than anything a human body can generate.

Other methods to kill bacteria include,
heat, gamma radiation, oxidative chemicals, antibiotics, dehydration, salt, oxygen exclusion, freezing.

However bacteria are a very diverse group, so it might take one or more methods in combination to kill all bacteria (and their spores) in a sample.


Why magnesium ion is needed for activity of G-proteins?

Ion can change secondary structure of an enzyme. Magnesium ion is coordinated within certain domains (for example, EF-hand motif) and makes them more ordered. Usually it happens via hydrophilic shell of residues embedded into a hydrophobic one (https://www.pnas.org/content/87/15/5648).

You can reverse it by adding a chelator (EDTA, for example) and protein is more disordered which can affect it's activity.


Impact of Natural Selection on Population Size

This is pretty basic, should have learned it in year one bud, but, here... everyone should be able to decipher this.

You can also use Calculus to solve this.

Edit: The dip was most likely because natural selection often has a bit of a delay until it becomes advantageous to the population. Otherwise, the increase should continue if you go on to further generations.


Metapopulation structure - book recommendations

Probably the best source to start would be Ilkka Hanksi's work, you can find a full list here: http://www.helsinki.fi/science/metapop/People/IlkkaPub2.htm.  The seminal work would be "Ecology, Genetics and Evolution of Metapopulations"  It gives a strong mathematical treatment


Which bird species/families worm-dance and is this learned behaviour?

Short answer
Sea gulls indeed tap the ground to surface earth worms, which is known as worm charming. Traditional human societies have practiced a similar technique known as worm grunting, involving vibrating the ground. Worm grunting is obviously a learned behavior passed down for generations in Florida. In other animals, such as gulls, I wasn't able to find evidence whether it is learned or innate behavior.

Background
From wikipedia:

  Worm charming is especially [observed] among birds. The methods used vary; however, tapping earth
  with feet to generate vibrations is widespread. One common example is
  the "Seagull dance". The wood turtle also seems to be adapted for worm
  charming, as it is known to stamp its feet – a behavior that attracts
  worms to the surface and allows the turtle to prey on them.

It is popular belief says that the charming mimics the drumming vibrations made by rain and that worms are attracted by it. However, studies have indicated that the charm vibrations sound similar to those made by burrowing moles, a voracious worm predator and that the charming behavior of worms surfacing reflects an escape behavior of worms, namely the abandoning of their safe burrows to expose themselves to the real danger once surfaced (Catania, 2008).

The authors investigated the charming reaction of the worms by studying human-indiced charming, a technique used by fishermen. For generations, many families in and around Florida's Apalachicola National Forest have supported themselves by collecting the large endemic earthworms (Diplocardia mississippiensis). This is accomplished by vibrating a wooden stake driven into the soil, a practice called “worm grunting”. This worm grunting is obviously learned behavior.

However, I couldn't find evidence whether the worm charming in birds and turtles is learned yes or no.

Reference
- Catania, PLoS ONE 3(10): e3472


Can animals, like monkeys, be homosexual?

Cases of homosexuality have been described in numerous species, including primates, and the wikipedia link posted by @shigeta lists and describes some of them.

It could be difficult to untangle the difference between an animal not being able to identify sexes very well, or, deliberately mating to anyone and those actively making a choice to engage in intercourse with a same sex individual.

I there are some species where sexes are very difficult to tell apart so they may just go around having sex with anything that looks like the right species because the mating is relatively low cost so doesn't matter if the partner was male or female. This is one such example in sea snails:

  "In a laboratory mate-choice experiment, male N. radiata preferred to
  mate with females, indicating precopulatory sex identification. They
  copulated with males, however, at the frequency of 37%, perhaps
  because of sex misidentification."

Other likely candidates are those with little sexual dimorphism and those with sneaker males that mimic females.

I have also heard theoretical discussions (oh the joys of lunchtime in an evolutionary biology department!) which suggest it may be a way of individuals (particularly males) practising or keeping up fitness relating to sex or stimulating better sperm production etc.

Once you decide what constitutes "a homosexual animal" then it is perhaps easier to examine. I would say a homosexual animal is one that mates exclusively (or highly preferentially) with same sex individuals when given the choice.

Models of genetic and epigenetic inheritance have been used to suggest just how homosexuality could evolve and you can read more about it in this Biology.Stackexchange post.

So it seems that monkeys, and other animals, have been documented to exhibit homosexuality, reasons for them to do so could exist, and it could be a heritable trait which persists despite seemingly strong negative selection.


Why Is Most Life Symmetrical Externally But Not Internally?

First, I think it worthwhile considering 'Why would internal symmetry be beneficial?' Developmental simplicity jumps to mind immediately. You can also consider relationship to external organs; the stomach and esophagus are lined up with the mouth which is symmetrical about the sagittal plane. Or maybe even balance; the lungs are large organs and if put to one side would likely cause locomotive issues. (Perhaps this is even an interesting topic for another question.)

That said, I feel, at it's core the evolutionary advantage which led to the lack of ubiquitous internal symmetry is space. Simply put, there is only so much room inside an organism and every little counts. Thus, if there isn't a need for a particular organ to be mirrored about a plane then there is a benefit in putting elsewhere: utilization of space.

I think a fantastic example of this is the human digestive tract. The key factor in the shape of the intestines is utilization of space, which directly affects the point at which is connects to the stomach, itself contributing to the asymmetrical shape of the stomach. One could envision other configurations, sure, and nature has. However, this configuration works quite well and the extraordinary use of limited space seems to outweigh all benefits of symmetry.

To directly respond to your questions above:

Question: Why do we not have an even number of each organ so it can be placed symmetrically?
Response: Each organ addresses (or addressed) a need of the organism. Addressing that need with multiple organs working in concert has benefits and consequences, as does addressing the need with a single organ alone. These benefits and consequences are balanced throughout the evolution of an organism.
Question: If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?
Response: I feel space. Again, there are benefits to symmetry but there are many other factors at play. Some of which, it seems, are more important than symmetry at times.
Question: Is there some evolutionary advantage that led to this setup?
Response: I hope this has been addressed - I don't claim to have 'answered' anything, this is a question for discussion.

Other fuel for discussion:

In thinking through this question I found myself able to rationalize why internal symmetry isn't necessary. However, I'd be interested in seeing opinions on why, then, external symmetry is so prevalent.


why is LPL (lipoprotein-lipase) down-regulated during fasting?

LPL is largely expressed on tissues that metabolize or store a lot of fat, including muscle and adipose tissue, and it's regulated by a number of factors (1). This includes diet, hormones and other protein regulators. The current literature on LPL has shown that regulation of LPL is tissue-specific. The activity of LPL, like other proteins, may be controlled at the transcriptional or the post-transcriptional level. A review by Goldberg et al (2009) notes that the activity of LPL in adipose tissue during fasting is low, but high in skeletal and cardiac muscle. They also note that insulin increases transcription of LPL in adipose. So why the down-regulation? One of the proposed mechanisms for LPL down-regulation in adipose tissue is rapid inactivation by a protein inhibitor known as ANGPTL-4 (2)

ANGPTL-4 (also known as a fasting-induced adipose factor), is up-regulated in adipose tissue two to four-fold in response to glucocorticoid stimulation (3). It's commonly known that you have a cortisol spike within a few hours of fasting, which is intended to try and increase glucose availability, for example.

The idea is that ANGPTL-4 attempts to control the distribution of fatty acids (4). In a mouse study, Cushing et al. demonstrated that ANGPTL-4 in fact diverts uptake of fatty acids and triglycerides away from adipose tissues (5). And this study was published in August 2017, so the phenomenon is still under investigation. It makes sense though, right? Why does the adipose tissue need to continue to receive fats during fasting? They can be better served elsewhere like muscle, the brain or the liver. Not only so, but Catoire et al. also demonstrated in 2014 how the interplay between ANGPTL-4 and LPL between non-exercising and active skeletal muscle during exercise allows for fine-tuning of fatty acid delivery to sites that need it most (6). So the regulation extends to both inter- and intra-tissue needs.

In closing, LPL is regulated during fasting in a targeted manner, but it is not generally down-regulated. Regulation is controlled in a manner that allows the demands of tissues to be reactive to their environment.


Original paper about the all or none law for neurons

This probably goes back to Lucas (1909), Adrian (1912), and Bernstein (1912). But the idea might have started from Helmholtz (1850).

Lucas, K (1909). The ``all or none'' contraction of the amphibian skeletal muscle fibre. Journal of Physiology; 38: 113--133.
Adrian, ED (1912). On the conduction of subnormal disturbances in normal nerve. Journal of Physiology; 45: 389--412
Bernstein, J (1912). Electrobiologie. Braunschweig: Vieweg.

See also: Galvani's Spark: The Story of the Nerve Impulse and The great Era of English Electrophysiology:
from Francis Gotch to Hodgkin and Huxley


What is the evolutionary reason behind the fragility of teeth?

The evolutionary biologist in me would argue that, on average, teeth are exactly as strong as they need to be. In other words, the fitness cost of producing and maintaining teeth is balanced with the the fitness benefits of having teeth.

To address your questions from an evolutionary lens:

Why haven't humans evolved in the past tens of thousands of years to the point where repairing or regrowing teeth by natural means is feasible? Simply put, why don't teeth grow back contrary to hair, nails or skin?

The short answer is that we have evolved the ability to regrow teeth. That's why you lost your baby teeth and a new set grew in their place. And why most folks have wisdom teeth that grow in later in life.
Essentially, we only need enough functional teeth to get us to the point of reproduction. After that, the effects of selection for stronger, more, better teeth wanes.

You may find this review article1 helpful wherein the authors explore the evolution of teeth, and specifically health issues related to teeth from an evolutionary perspective.

[1] Koussoulakou et al. (2009) A curriculum vitae of teeth: evolution, generation, regeneration. Int J Biol Sci; 5(3): 266-243.


How does the placement of it's motor domain affect the directionality of a motor protein?

No. DNA, and RNA have a polarity in the orientation of their sugar-phosphate backbones, based on the numbering of the carbon atoms in the sugar rings. So, for example, we say that the sequence of this RNA is being read from the 5' to the 3' end, which indicates that the first nucleotide is exposing the hydroxyl at the 5’ carbon on its sugar ring.  At the other end of the linear polynucleotide the sugar is exposing the hydroxyl on its 3’ carbon of the sugar ring.

All mRNAs are translated in the 5’ to 3’ direction and all proteins are synthesized from the amino terminus to the carboxylate terminus, because the peptide bonds in the protein also have a directional polarity.

You appear to have mislabeled the N and C termini of Dynein in your diagram. Perhaps the  lecture was about the domain structure of these two motor proteins? And the point might have been that they each have three equivalent domains but in one case the part we call the head is synthesized first and in the other case the tail is synthesized first(?).


Which requirements are needed for 2 different species to be able to have offsprings?

Lets break this down like a logical problem. In reality, it involves the correct gene expressions at the correct time, place, etc. But that would be a book.

Prezygotic reproductive isolating mechanisms

Environment

A bull and a whale can't mate; they don't live in the same environment. Lions and tigers similarly do not mate in the wild due to lack of overlap in the environment. In captivity, yes.

Delivery of gametes

Sperm must be able to be delivered to the ovum for fertilization to occur. Some species just can't get this part right. Your house cat would not be a suitable donor for an elephant.* In closer species, say a chicken and a peacock, the rooster's courtship display (which is nowhere near as spectacular at the peacock's) will not be accepted by the female; no opportunity for delivery of gametes.

Some gametes can be delivered but not ova (the female isn't "in season".) Zero there as well.

Unity of gametes

If the gametes are both delivered at the correct time, can the sperm bind to the egg? Successful binding requires a receptor-ligand interaction which actually has a high degree of species specificity. So binding requires that the sperm and the egg can, say, "communicate" successfully. Dog sperm doesn't "speak" cat ovum.

If they do "speak the same language", can the sperm penetrate the ovum's protective coating (the zona pellucida)? Assuming sperm capacitation (a big hurdle right there), the sperm may not have the correct enzymes in it's 'head' to penetrate zona pellucida. Not all enzymes carry out the same function on all molecules, and if the correct enzymes are present to digest/break through the zona pellucida, is there enough? Is the sperm active enough? I'll liken this kind of communication to 'pillow talk'. We're getting much closer. Let's say the sperm has his pillow talk down, and can penetrate the layer.

Postzygotic isolating mechanisms

Viability

The hybrid embryo must be able to develop into a zygote. Hybrid inviability means there wasn't enough similarity to proceed to a blastocyst and the hybrid dies.

Say viability is achievable. The blastocyst/blastomere must "communicate" with the mother so that attachment is not only possible but can be sustained. In effect, it must "shout" to the mom, "I'm here! Pay attention to me!" (In humans, this involves secretion of large quantities of a hormone called chorionic gonadotropin, which stimulates continued secretion of progesterone, thus no shedding of the uterine lining. Not all mammalian blastocysts communicate the same way. If what we have here is a failure to communicate... as with Cool Hand Luke, the result is not good.

Hybrid sterility

The species were close enough for the conceptus to be heard by the mom. The right chromosomes with the right gene expression results in a live birth.

Success!

If the hybrid is fertile, it is by one definition not a different species. (There is much debate as to what exactly defines a species. See the references.)

If you are still left saying, "But why?", then it must be explained on a genetic/molecular level, with sentences like,

  The zona pellucida of mammalian eggs is composed mainly of three glycoproteins, all of which are produced exclusively by the growing oocyte. Two of them, ZP2 and ZP3, assemble into long filaments, while the other, ZP1, cross-links the filaments into a three-dimensional network. The protein ZP3 is crucial: female mice with an inactivated ZP3 gene produce eggs lacking a zona and are infertile.

If this is the level of explanation you seek, there's a book for you: Molecular Biology of the Cell. Alberts B, Johnson A, Lewis J, et al.

Fertilization
The Process of Speciation
Fertilization

*Note here I'm referring to morphological differences, one way used to define species.


what is the modern, molecular explanation of independent assortment of alleles?

Parts of your general idea are correct, others need some refinement. To skip ahead to the conclusion: I'm going to recommend that you read up about linkage disequilibrium. Everything else is background information that will hopefully help you understand why linkage disequilibrium is what I think you're looking for.

Background: Meiosis Basics

Firstly, in the bare principle, meiosis is quite simple. Let's consider meiosis in a human cell, i.e. the division of a primary spermatocyte (the only other example is division of primary oocytes). That's this one we're talking about: http://en.wikipedia.org/wiki/File:Figure_28_01_04.jpg In simple terms, the ready-to-develop primary spermatocyte contains 46 chromosomes, two (2n) each of chromosomes 1-22, an X and a Y chromosome. Two chromosomes of the same type (e.g. "chromosome 4") are called homologues. Homologues contain different versions (= alleles) of the same genes. During Meiosis I, homologues align in pairs, recombine, and then separate into two new cells (which are now 1n). The following Meiosis II is basically a mitosis, meaning that the two (identical apart from previous recombinations) chromatids of the chromosomes are separated and packaged into separate cells.

Recombination and Interstices

During the alignment of homologues in Meiosis I, the attraction between the two chromosomes depends on their homology - i.e. similarities in DNA sequences that end up being close to each other in this setting. This attraction is on the molecular level, so the tightly-condensed neighbouring DNA double-helices actually physically stick to each other because the polarities/charges across relatively large stretches of the molecules complement each other. I don't think how this exactly works is well understood yet, but what is clear is that homologues attract each other at this point because they contain mostly the same DNA sequence, apart from small differences (which make the different alleles).

How exactly recombination occurs at this point isn't entirely clear either on the molecular level (http://en.wikipedia.org/wiki/Homologous_recombination#In_eukaryotes). Just to get an idea of how it could work: while the two chromosomes are aligned, it's not difficult for them to actually tangle up and break, leaving the repair machinery with the potential to fuse the wrong chromosome ends together. The breaking and exchange might also be a programmed process with dedicated cell machinery (quite probably so I think personally).

In any case, not all locations are equally likely to recombine. It depends on levels of homology (i.e. "stickiness") between individual stretches of DNA and other unknown factors. Just in the same way, the number of break points in each chromosome isn't pre-determined.

Mendelian Inheritance

First of all, the concept of loci is arbitrary and has no molecular basis. A locus is simply "a place on a chromosome" and could refer to an individual base(-pair) or a whole stretch of DNA. The concept is however useful when talking about inheritance, as it illustrates the principle of linkage, or rather linkage disequlibrium.

As far as I am aware, it comes from a time before we began thinking in chromosomes. One could study whether there was linkage between two traits (or more generally loci), i.e. a higher-than-random chance to inherit the two together. We now know that linkage simply means that the two loci are on the same chromosome (for example, chromosome 6). Thus, if no linkage exists, the chance to inherit both loci together is no larger than expected by random Mendelian inheritance (which makes sense as there is no molecular mechanism that makes offspring e.g. more likely than 50/50 to inherit chromosome 6 and 19 together from the same parent). If linkage exists , the loci are on the same chromosome, and any case where the two are not inherited together must be caused by recombination.

The idea of linkage disequlibrium is that loci that are close to each other on a chromosome are more likely to remain together (and be inherited together) than far-apart loci. This is obviously due to the increased chance of a recombination event occurring between them with increased distance. This actually seems to be what you are looking for as a pointer for where to go next, so I recommend using your preferred internet search engine to learn more about that :)


Why doesn't chloride cause high blood pressure?

Osmotic pressure is not the main mechanism of sodium-induced high blood pressure.

  high dietary salt raises cerebrospinal fluid [Na(+)]. This leads, via the Na(+)-sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction

How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.


What is the dependent variable of a relative fluorescence graph?

When a variable is independent, it's not affected by any other variable. Relative fluorescence obviously depends on the time parameter in this case. If you stopped at 30 minutes and took readings ever 3 minutes, your data would look very different.

Without more information about the experiment, however, it's hard to tell if there are additional variables.


Using punnett squares to express sex/gene linkage and recombination frequency

The Punnett squares are a general way to visualize the product of any two polynomials; for example, you know that the result of (a + b)(c + d) is the sum of the four terms ab, ac, bc, bd. You may put it this way:
  | a   b
----------
c | ac  bc
d | ad  bd

Suppose that the female sex gametes are of two types, X1 and X2, which are transmitted with probabilities 0.9 and 0.1; suppose that males form three types of gametes, X1, X2, and Y, with probabilities 0.45, 0.05 and 0.5. Then, you may visualize the outcome of a general population mating this way:
    |Fem   X1   X2
    |      .9  .1
--------------------
Male|
X1  |     X1X1  X1X2
.45 |     .405  .045
    |
X2  |     X1X2  X2X2
.05 |     .045  .005
    |
Y   |     X1 Y  X2 Y
.5  |     .45   .05

(You may note that this situation roughly depicts the population genetics of color blindness)


Alan is right to call this a Cichorium. It is  Cichorium endivia, Endive. It is a tropical plant that is widely cultivated for its edible leaves. However, when it flowers the leaves die, so you don't recognize the plant as Endive. The dying leaves can be seen on the picture below, from the Dutch wikipedia page.

https://nl.m.wikipedia.org/wiki/Andijvie


What Animal is This Skin From? A Wooly Mammoth?

Yes, this is the remains of a wooly mammoth. Many mammoths have been found frozen and well preserved in Siberia.


Is poison venomous and is venom poisonous?

I think you are both confused about terminology, and asking a very broad question. An organism that produces venom is venomous. Poison is not venomous, the black mamba is venomous. Venom is not venomous.

According to the Wikipedia article on venom,

  Venom is a form of toxin secreted by an animal for the purpose of causing harm to another.

A toxin is a poisonous substance produced by a living organism. The article goes on:

  Venom is injected into victims by means of a bite, sting or other sharp body feature, which differentiates it from poison (that is absorbed, consumed or inhaled).

However, a toxin is a poison, and poisons are defined (by wiki) as

  substances which cause disturbances to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism. (emphasis mine)

So, the definitions are kind of circular.

From what I understand of your question, you are wondering whether a venom would still be dangerous if it were, for example, ingested rather than injected, as well as whether a poison would still be dangerous if injected rather than ingested (or inhaled, or whatever), and this is where the "Too Broad" category gets applied. There are thousands if not millions of different types of toxins in the world, ranging from full proteins to peptide-based to small organic molecules to completely different structures, such as lipopolysaccharide (LPS, the component of Gram-negative bacteria that causes septic shock). Some may not survive the digestive tract, others might. Some can act through the skin, others can't be absorbed. Inhalation is the next best thing to injection, but probably not for every single one of them, so it's impossible to make broad statements about their efficacy and median lethal dose via different routes of exposure. The exact same thing applies to the "poisons" category - while something that is damaging when absorbed cutaneously, such as methyl mercury, is probably just as damaging directly injected into the bloodstream, it's impossible to say that with certainty about all poisons.


What is the actual speed of nerve impulses in humans?

Short answer
A conduction velocity of 440 km/h is possible in thick, myelinated fibers. However, this number is probably more representative of the upper range of conduction velocities, rather than a conservative average.

Background
First off, there are a heap of variables that affect neural conduction velocities (in myelinated fibers) in complex ways (Waxman, 1980), including but not limited to:

axon diameter;
myelin thickness;
internode distance;
temperature;
axonal milieu;
age of the subject.

Having said that, in humans myelinated, thin A-delta fibers the average conduction speed was established at 19 m/s (Gyberls et al, 1983), or 68 km/h. A range of pain-conducting fibers exist, with different diameters. As a result, they range in their conduction velocities from 0.5 m/s (2 km/h for thin C-type fibers) to 120 m/s (432 km/h for thick A-alpha type fibers).

Hence, the 440 km/h is certainly possible in thick myelinated fibers. Note I just highlighted pain-conducting fibers here as an example, and other classes of neurons may feature even faster conduction in their axons.

References
- Gybels et al., J Neurophysiol (1983); 49(1): 111-22
- Waxman, Muscle & Nerve (1980); 3(2): 141–50


What is the fundamental reason for death from too high or low internal temperature?

As mentioned in the comments, half of your question is answered elsewhere. Generally you are right, different processes change at different rates. Blood viscosity changes. Some complex systems, such as the heart, may completely fail to function. The other half of your question has a simpler answer. As heat increases, yes in theory so should enzyme performance. However enzymes have a tendency to denature if they get too hot. When heat is excessive, heat shock proteins are released which are naturally stable in hot conditions and which attempt to stabilize other proteins. This is only possible up to a limited extent, and sufficient heat will cause proteins to become entirely non-functional.


Although I found this study, where mean and 95% CIs of median time to
eclosion (h) are provided for some strains of D.m. (with a resolution of 12 h) (in table 3), the moment of eclosion seems to be under circadian control: "in Drosophila melanogaster, the emergence of adults from their pupal cases (eclosion) is gated by the circadian clock such that it occurs during a window of approximately 8-10 h starting 1-2 h before lights-on in 12-h light:12-h dark cycles (LD)". In that particular study Canton-S flies eclosed within 4-5 days after pupation (LD 12:12, 25°C) with the following distribution over day (digitized from Fig. 1A [numbers are approximate, percents don't sum up to 100]):

Hours   % eclosed
Dark
12-14   0.5
14-16   0.4
16-18   0.6
18-20   1.1
20-22   1.4
22-24   5.6

Light
0-1     20.4
1-2     9.3
2-3     13.7
3-4     12.0
4-5     10.3
5-6     11.3
6-7     6.6
7-8     4.9
8-9     2.1
9-10    0.8
10-11   0.8
11-12   0.4


Where can I find SSR and/or SNPs that locate RC1 genes in Soybean?

SoyBase has Illumina SoySNP50K iSelect BeadChip and they've identified soy SNVs. You could find them in dbSNP - identifiers starts with 'ss'.


Recap of the question:

Looking at a single locus trait ($A$) controlled by two alleles, $A_1$ and $A_2$, the phenotypic mean is only affected by inbreeding depression, $f$ (Wright's inbreeding coefficient), if there is some degree of dominance, $d$. Why?

Answer:

If we take inbreeding as a higher than expected frequency of homozygotes, such that if the frequencies of alleles $A_1$ and $A_2$ are $p = q = 0.5$ the expected frequencies of the genotypes in an outbred population, $P_{outbred}$, would be $p^2 = 0.25$, $2pq = 0.50$, and $q^2 = 0.25$.

Each genotype has the following phenotypic result on a trait $A_1A_1 = 5$, $A_1A_2 = 7.5$, $A_2A_2 = 10$... this is an additive trait with allele $A_1$ having an additive effect of 2.5, and $A_2$ an additive effect of 5.

We can then compare an inbred population of 100 individuals, $P_{inbred}$ where the frequency of $A_1A_1 = 0.5$, $A_1A_2 = 0$, $A2_A2 = 0.5$, to $P_{outbred}$ , where I use $\bar{X}$ to symbolise trait means.

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 7.5) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 7.5) + (25 \cdot 10)}{100} = 7.5$

So when the trait is additive the population means are equal. It is onlt when we add dominance to the situation that the population means will differ as a result of inbreeding. Continuing from the above example, the populations are the same size and structure, but $A_2$ is now completely dominant to $A_1$ such that $A_1A_2$ individuals now have a trait value of 10. Now

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 10) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 10) + (25 \cdot 10)}{100} = 8.75$

Thus inbreeding has affected the population mean in a trait which has dominance, it is basically because the heterozygotes are less common in an inbreeding population and this is where dominance effects are seen.

  "there is a linear decline in the mean of a trait with increasing f... with overdominance (di > ai)"

This is because in the case of overdominance, the outbred population mean becomes even more elevated - if we say now the $A_1A2$ trait is a phenotype of 15 the means become

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 15) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 15) + (25 \cdot 10)}{100} = 11.25$

  " there is a linear decline in the mean of a trait with increasing f... if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0)"

The mean will increase if the dominant allele produces a smaller phenotype. Here we say $A_1$ is now completely dominant,

$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 5) + (50 \cdot 10)}{100} = 7.5$

$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 5) + (25 \cdot 10)}{100} = 6.25$

I hope that answers the question, I tried to answer last night but was too tired to think - this is just what I came up with on the walk to work today so I haven't had the time to check it/overthink it


unknown bird in Long Lake Michigan......chocolate brown head and neck, charcoal body and tail, ivory wings, top and bottom

That's a very interesting set of colors.  Unfortunately nothing springs out at me, although I can think of a couple of birds that might sort of (maybe) match.
First, common pigeons come in all sorts of colors and patterns, and it's possible that yours is one.  On the other hand, common pigeons tend to be very familiar to most of us, so I don't think you'd be asking about that.
Second, there is a tern that is moving through the area about this time of year, that might fit:  Black Terns can have a lighter wing.
Here's a link and a representative photo:
 https://www.allaboutbirds.org/guide/Black_Tern/overview

There is another, even better possibility, if your bird is ternish:
The White-winged Tern (formerly White-winged Black Tern) is an uncommon late-summer wanderer through much of the region.  Here is a link and a representative photo:
https://avibirds.com/white-winged-tern/


The genetic and physiological origins of laughter?

I recommend this article: The Evolution and Functions of Laughter and Humor: A Synthetic Approach by M Gervais and DS Wilson, 2005, University of Chicago Press.

For your question about the origin, firstly they explain that all laughter is induced by stimuli which are unexpected or unpredictable, experienced in a non-serious (unthreatening, safe) context. Given examples include peek-a-boo, which can make a child laugh but also cry if the child is not perceiving the situation as safe. Also that we can't tickle ourselves and tickling is induced by stimulating vulnerable body areas. Similarily, apparently in apes laughter is mainly induced by "tickling in conjunction with mock aggression and chasing".

They explain the function of (Duchenne, that is stimulus-driven "honest" as opposed to voluntary) laughter to be propagation of "positive affect" in a group, as it utilises the chameleon effect (it is contagious) which apparently has been shown to exist for its "cooperative value". Other studies seem to have shown that a) we are thirty times more likely to laugh in a social context than by ourselves and b) the contagiousness of laughter response increases with group size, making it an efficient tool for coordinating a group and getting everyone into the same emotional state.

As for other animals, the article doesn't address that. It does seem like a different question to me so I would consider separating that into a second one.


What is the evolutionary purpose of white spots in nails and how can they be characterised due to Leukonychia?

This is a common misunderstanding from newcomers in evolutionary biology. Not every trait is the result of an adaptation. Evolution is way more than just natural selection and is not as deterministic as you may think. There is stochasticity inherent to mutational processes and there is stochasticity in reproductive success (called genetic drift). This seemingly totally unrelated post may help you getting a quick grasp of what are the stochastic processes in evolution.

The white spots you observe very likely do not result from an adaptive process but it just happen to be the way it is. For the physiology part (but this would be the subject of another question) I have no idea what drives these white spots.


I am not too sure but this looks like Polycelis sierrensis.

Though it is apparent that the worm in your pictures is a tricladid planarian, I was not too sure about the species and the geographical distribution.

However, from the Smithsonian list of freshwater planarians in North America, I deduced that this should be Polycelis sierrensis which is found in California and Nevada (Kenk ,1973).

The EOL page on this species also concurs with the geographical distribution. Moreover, the shape and dimensions of the worm, as described in EOL, matches with that of the ones you have got.

I could not find a picture of P. sierrensis but this is how a general Polycelis looks like:


Are there known 3- or 4-nucleotide RNA linkers with no RE sites?

I don't know the answer, but you could simply brute force the answer by generating all possible combinations of 3- or 4-nt length sequences, and comparing against the restriction enzyme database (REbase).

It would not take long to do. There are $ 3^4 $ and $ 4^4 $ combinations, respectively. Depending on your purpose, it might be possible when not considering engineered restriction enzymes (which are not likely to have recognition sequences found in nature).


What is this tree that displays sycamore like characteristics but appears to be too small?

This is very likely a London planetree (Platanus × acerifolia), a hybrid species of Platanus often planted in cities.

 Source: Cuyamaca College

 Source: Wikimedia

The tree is a hybrid between Platanus orientalis and Platanus occidentalis (the sycamore tree), and has characteristics intermediate between the two species.

Smaller (heights of only 20-30 m vs 30-40+ m for parent species).
More deeply lobed leaf than P. occidentalis but less so than P. orientalis
Seed balls typically two per stem (one in P. occidentalis, 3-6 in P. orientalis)

Note: seed "balls" = aggregate of many small seed-like fruits called achenes

VERY OFTEN PLANTED IN URBAN AREAS

Because it's very tolerant of atmospheric pollution and root compaction

Description:

Leaves: alternate, simple, 3-5 lobes, maple-shaped, 10–20 cm long, 12–25 cm wide
Bark: pale grey-green (or brown), smooth and peeling (sometimes not peeling)


What could make a person get ill from not eating often enough?

This could be a symptom of hypogylcemia.

Hypoglycemia causes symptoms such as:

hunger
shakiness
nervousness
sweating
dizziness or light-headedness
sleepiness
confusion
difficulty speaking
anxiety
weakness


That’s maybe an oriental spiny orbweaver (Gasteracantha geminata), according to its appearance and location. You can find many more observations of such spiders on iNaturalist: https://www.inaturalist.org/taxa/207992-Gasteracantha-geminata?locale=en-GB
However, I don’t know what advantage there is to the “spines”. They are not the only species. There’s a whole genus of them with at least 70 known species, according to Wikipedia: https://en.m.wikipedia.org/wiki/Spiny_orb-weaver


RNeasy Mini Kit low 260/230 ratio -- can I purify this RNA for further use?

RNAeasy kit will not usually give phenolic contamination. Your poor 260/230 is perhaps because of low yield; check the absolute absorbance values. Low 260/230 (and low yield) also happens because of improper lysis. I would advise that you do the cell lysis using more effective methods. I would not advise another phenol-chloroform or alcohol precipitation step- you will lose your RNA. With what you have now, run a little bit on the gel to see the integrity. Also try heating the dissolved RNA at 65-70deg for 10-15min and measure OD again (use nanodrop or a similar device)


Identity and similarity for Multiple Sequence Alignment (MSA) of proteins

I've never used T-Coffee but it looks like the web-server version gives you a total score as well as a score for each individual sequence; do you know if those numbers are related to the numerical descriptors you need?
A good place to start would be to read the documentation. Another good place to look would be the Google Groups page for T-Coffee.


What is the real meaning of the statement "*ontogeny recapitulates phylogeny*"?

Actually, the statement "ontogeny recapitulates phylogeny" has been largely discredited in modern biology.  The stages of embryonic development were thought by Ernst Haeckel to resemble ancestral species in evolution.  That is, early embryos appeared to have tails and gills and resembled fish, later embryos resembled quadrupeds, and so on.

However, embryos do NOT actually resemble adults of ANY species.  More accurately, one could say that early embryos of different species resemble early embryos of other species, and later stages differ more and more as specialized traits of different species become more obvious.  On the early extreme, one fertilized ovum shows very little difference in gross appearance from any other fertilized ovum, and the blastula of different species look very much alike, but as different organs and limbs become better developed, those of different species begin to look more and more different.

This actually only describes SOME of the changes that occur in embryonic development.  Other changes are not so simple.  One very good book that discusses the strengths and weaknesses in this area is the book "Ontogeny and Phylogeny" by Stephen Jay Gould.


Why is the spirit bear/Kermode bear a subspecies of the American black bear Ursus americanus?

It is because somebody wrote a paper that described it as such, and the paper was published. I don't mean to be flip. Its just that taxonomy is done through publication, not committees (although the peer reviewers could be considered a kind of committee). Subspecies are less stringently regulated than species, and this subspecies does have a particular unique set of gene frequencies that occasionally (as you mentioned) show up in the phenotype. The fact that it has been culturally recognized as special may also have something to do with its subspecies status. A subspecies need not be reproductively isolated from its parent species, and need not have any fixed characters.


Is spiders building webs on plants an example of mutualism or commensalism?

You're thinking too broadly and rigidly about these concepts -- both commensalism and mutualism are types of interspecific interactions.

Commensalism is when one species in a given interaction is benefited while the other is neither benefited nor harmed. In a mutualistic interaction, both species benefit from their interaction with each other.

Like any interaction between two organisms, these interactions can vary between individuals. Although some species pairs will consistently undergo the same type of interaction (e.g., shark and prey -- predation), some groups of species may vary in their paired interactions. This variation may result from two different scenarios:

Variation in interaction type between different species within a taxonomic group

E.g., one type of spider catches insects that don't harm the plant -- commensalism -- while another spider species catches insects that would harm the plant -- mutualism. In other words, not all spider-plant interactions are the same, and the interaction type may be dependent on the species involved.

Variation even from the same individual in different circumstances.

E.g., A spider catches an insect that doesn't eat the plant it's growing on (commensalism) but at another time it catches an herbivorous insect that does eat the plant the spider has built its web on (a mutualistic behavior). In this scenario, the interaction type between the same two species (even the same individuals) can vary based on circumstances.

Put differently, commensalism, mutualism, etc. are not behavioral traits, but interactions, and so are dependent on not only the species involved but the circumstances as well.

Note: To further complicate things, each given interaction can be qualified in various ways. For example, from Wiley ELS:

  Positive interactions can be trophic and nontrophic, can act directly or indirectly (mediated by a third species) and can be symmetric (species have equal effects) or asymmetric (species have unequal effects).


Why do I feel my schoolbag to be heavier after meals?

Could certainly be physiological. After eating more blood is diverted towards the smooth muscles around organs for digestion. This will mean your skeletel muscles have decreased blood flow so less nutrients such as Glucose available to make contractions. As you have less energy available to contract the skeletal mucles you're more than likely to feel slightly weaker.

On the contrary it may he purely psychological! :) Good question though!