Interaction of charged triphosphates with the ATP binding region in proteins

Summary
Many proteins that bind the nucleotide triphosphates ATP and GTP have an evolutionary conserved motif — the P-loop — that binds the phosphate portion of the molecule. This has the sequence, GXXXXGKS/T. Although the conserved basic lysine (K) is interacts with two of the positively charged phosphate moieties, other interactions involve Mg2+ ions (with which NTPs are always complexed) and polar, rather than charged, amino acid residues and the polypeptide backbone.
Detailed Illustration
Although the question asks about ATP, I have chosen the GTP-binding protein H-ras p21 as an illustration because the paper by Pai et al. describing it gives full details of the interactions of the phosphates, which are essentially the same for ATP and GTP. (Many other papers tend to show only ribbon diagrams of the protein.) Note also that the crystal structure was, of necessity, of a complex with the GTP analogue, GppNp. (GppNp is not rapidly hydrolysed, unlike GTP itself.)
In this case the evolutionary conserved P-loop that binds the phosphate has the sequence:
Gly Ala Gly Gly Val Gly Lys Ser

 10  11  12  13  14  15  16  17

A three-dimensional representation of the phosphate-binding region is shown below. The left-hand frame shows the P-loop and residues Thr35 and Asp57 without the nucleotide. The right-hand frame is the same but with GppNp and a magnesium ion included, and only the conserved residues of the P-loop labelled.

[Own work based on Fig.6 of the paper by Pai et al. using Jmol software and Protein Data Bank file 5p21.pdb.]
A two-dimensional schematic of the interactions is shown below. The side-chain interactions (and those from the magnesium ion) are shown as red dotted lines, whereas those from the backbone are shown in black. The conserved residues of the P-loop are indicated by blue text.

[Simplified redrawing of part of Fig.5 of the paper by Pai et al., excluding water interactions and interatomic distances.]
Reflections
Although positively-charged basic amino acid side-chains are involved in neutralizing the negative charges of nucleic acids and nucleotide phosphates, they are not the sole means of doing so, and in the case of the NTPs they are not the main means. Magnesium ions and polar residues (including the protein backbone δ+ve NH groups) can play an important role. To my mind this reflects two things. First, that life is dynamic; so weaker interactions are often favoured in enzymes because they can be easily broken as well as made. (NDP must be released from the enzyme after hydrolysis.) Second, and more speculative, the P-loop is thought to be very ancient as it is found in a wide variety of conserved NTP-binding proteins. A specific backbone conformation has been identified that facilitates this interaction. It could have arisen before all 20(ish) proteins specified by the genetic code had arisen, when the protein backbone could have played a greater role in interacting with small molecules. (This has also been suggested for backbone NH groups binding δ+ve sulphur in iron–sulphur clusters.)


Definition of life

The definition of what is alive and what is not is not a matter of biology but a matter of philosophy. Most definitions are based on:

Physiology

Existence of a metabolism

Evolution

Ability to reproduce and have heritable traits

Ecology

Ability to respond to the environment

There are plenty of possible definitions of "life". Note also that behind the complexity of defining what is alive there is the issue of defining the unit (the individuality if you want) on which the concept of life applies.

Your definition of life

You suggest a quick and simple definition so let's consider it.

  to be considered life, it must be able to reproduce

If you talk about the watermelon tree

If this is your definition, then Citrullus lanatus is definitely alive as it is able to reproduce (otherwise we would not be able to cultivate them).

If you talk about the watermelon fruit

Now you may ask is the fruit itself alive. Then, using your definition again, I suppose the answer is no because a given seedless watermelon will not be able to give birth to other seedless watermelons (even via the make-up of a watermelon tree).

Note that following the same logic one could argue that one's head is not alive either as one's head does not reproduce. Only your gonads do. Your dog might not be considered alive either. A castrato (singer) would not be alive either. A woman, after menopause, cannot reproduce either! Arguably, a cloud replicates or a fire replicates and could eventually be considered alive following your definition. So really, as you can see your simple definition hardly fit your intuition of what should be called alive.

My opinion on your definition

Personally, I am not a big fan of your definition but again it is nothing but a matter of preferences. I don't like that your definition is unclear because there are plenty of limit cases and because there are plenty of cases we would want to call alive that we can't anymore (like a woman after menopause for example!) Every definition of life would eave limit cases but with your definition, it really easy to find these limit cases.

Is this question about Biology?

No, it is not. It is a question of philosophy.

Other interesting post on Biology.Stack

You might want to have a look at why isn't a virus alive.


Is there an instinct-driven body language for birds?

In general, animal communication contains both "cultural" aspects and genetic components.

As you suggest, the cultural aspects vary more across geographies and times. The genetic components might vary as well, with genetic differences among different populations, but you'd expect them to be more conservative than the cultural aspects. To make the matter even more complex, if the communication behaviors affect mating; they could in turn have an effect on the genetic components!

This article describes birds raised in captivity that had "maladjusted" songs (which would support both genetic and cultural components), and North Carolina cowbirds raised by Texas parents who grew up with a Texas birdsong dialect (evidence for cultural components). Although the piece is mostly focused on song, I imagine the mechanisms would be similar for body language.


Role of isopropanol in plasmid isolation

In a standard DNA preparatory procedure, isopropanol is used to precipitate the DNA. Nucleic acids are insoluble in alcohols, and bulk or stick together. This sticking together can be further enhanced by increasing the ionic strength such as through addition of sodium acetate.

alcohols in fact don't really denature the DNA.


Are these birds in video real? What are they called?

Yes, they are real, that's not a CGI. That footage belongs to The Cornell Lab of Ornithology, and those are birds-of-paradise.

The first one is a Wilson's Bird of Paradise (Diphyllodes respublica). Here is an image of it:

The second one, showing a courtship display, is a Superb Bird of Paradise (Lophorina superba). Here is an image of it:

And the courtship display:

The third one is a King Bird of Paradise (Cicinnurus regius). Here is an image of it:

The next one is the Wahnes's parotia (Parotia wahnesi). Here is a picture of it:

The last one is a King of Saxony Bird of Paradise (Pteridophora alberti). Here is its picture:

Finally, here is the only correct way (just kidding) to watch any video with birds of paradise: narrated by David Attenborough! Have a look:

https://www.youtube.com/watch?v=nWfyw51DQfU


What do the qualifiers used in botanical species names mean?

agg. means aggregate and is used when species have been grouped together.

s.s. stands for sensu stricto and is used for a strict or narrow usage of definition.

s.l. stands for sensu lato and is used for a wide or broad usage of definition. these two pop up a lot in paleontology since species definition can be vague.

cf. stands for "conferre" and is used for provisional names when an organism is not completely known, such as when a variant is found and they are not sure which species to place it in.

cv. stands for cultivar and is usually followed by the unitalicized name of the cultivar.

auct. means "of author" and means the name is used in a different way than it is currently or in a different way than the paper using it does, such as quoting a incorrect name from another author or a debate between two possible usages. (used a lot with overturned or contested names) it is often followed by a qualifier giving more information about usage.

ined. means undescribed, and is used for a new proposed species before it has been formally described (common in paleontology when many papers about the same new specimen may be released at the same conference or where a specimen might not be identified yet still yield useful information in other ways.)

if you put the exact form of the epithet (include the period) followed by the word "species" in google it will usually return the usage, failing that you can search this site.


Can Thraustochytrids such as Schizochytrium do photosynthesis?

I think not.

from Kingdoms and Domains: An Illustrated Guide to the Phyla of Life on Earth By Lynn Margulis, Michael J Chapman. as found on google books

You will see there are no chloroplasts depicted.  These are eukaryotes and so to do photosynthesis they would need chloroplasts which should be evident.


In 2014, a review article was pushlished by the Department of Food Science and Nutrition at the University of Minnesota-Twin Cities, one that outlines  studies that (collectively) target the top 14 food-borne pathogens in attempts to identifying any potential antimicrobial properties of chili peppers, given that chili peppers can contain high amounts of capsaicin.

From the abstract of the article:

  Chili peppers are used worldwide in foods for their pungent flavor, aroma, and to prolong food spoilage. With capsaicin contents ranging from zero to millions of Scoville heat units, the different varieties offer a wide range of options for people all over the world. In addition to their use in cuisines, chili peppers have been explored for their antimicrobial and antifungal properties.

..

  This review goes over some relevant research that has already been done in this area. In addition it lays the ground for the new research that is emerging testing new varieties of chili peppers for nutrient content, flavor profiles, and for antimicrobial activities against numerous human pathogens.

The fourteen pathogens that were targeted and tested against were chosen due to their high risk of harm to the general public, most especially pregnant women (according to the FDA). To name a few that are well known, there's: Clostridium botulinum; Escherichia coli; Salmonella (enteritidis and typhimurium); Staphylococcus aureus; and Listeria monocytogenes.

After reading the conclusions of several studies that were provided by the review article (as well as the conclusion of the review article itself), it would seem that the current (as of 2014) consensus is that the efficacy of capsaicin (in chili peppers) as an antimicrobial agent is still to be determined. Of the (multiple) studies that were considered, collectively they produced quite mixed results. The reason for this is because each study has their own method for testing the antimicrobial activities of capsaicin, which makes the comparison of results between tests difficult to perform with confidence.

  There are a variety of methods for testing the antimicrobial activities of chili peppers. These methods strongly affect the observed levels of inhibition. Various reasons may contribute in the differences between results, including inconsistency between analyzed plant materials.

..

  In these experiments, crude extracts of chili peppers were used; no
  separation of pepper components was done. Based on the data, it seems that capsaicin had a lesser antimicrobial effect compared to other components of chili pepper extracts. Therefore, future studies should try to determine what compounds in the chili pepper gives the spice its antimicrobial properties, and to do so purification of the extracts is necessary. Capsaicin gives chili peppers the ‘hot’ sensation, which some people might not like. It would, therefore, be beneficial if there is another substance in the pepper that could be used in the food industry as a preservative without the pungent taste and hotness.

So, it would seem that, since the idea of using capsaicin as an antimicrobial agent is (fairly) new, there hasn't been a defined method for testing, and because of that, definitive conclusions aren't able to be made yet.


There exists a bunch of population genetics forward and backward (coalescence) simulation platforms. Here is a non-exhaustive list. They all differ and you'll have to go through their manual to see what is more adapted to your needs.

List of softwares

Here is a long list of such platforms. The list might arguably be a little bit outdated today though and many of these softwares might be slow or abandoned by their authors.

Most common softwares to my experience

Some are more known than others. Personally, I already saw uses of the following platforms in publication: SimCoal, Nemo, Slim and SFS_Code.

SimBit

Of course, I must indicate my own simulation platform SimBit. To my experience, SimBit is typically faster than Nemo. It is slower than SFS_Code and SLim for very small simulations but become much much faster than SFS_Code and SLim when you need simulations with a descent amount of genetic diversity.

Most important point about these softwares

You should compare softwares based on

Availability of the author to advice and bring new features

I won't talk about my personal experience here by respect for the authors!

Speed / RAM usage

I think SimBit is typically faster (and use less RAM) than Nemo. SFS_code and SLim are very fast for simulations with low genetic diversity but very slow for simulations with high genetic diversity.

Flexibility

Nemo, SLim and SimBit are very flexible (but they do different things) but SFS_code is not really.

User interface

I find Nemo error report pretty poor. I like SimBit error report. SLim interface is very nice (using eidos) and it even comes with a GUI (I have never used the GUI myself).

Free of Bugs

Several people have found important bugs in SFS_code (personal communication and experience).

Slightly more detailed comparison between Nemo, SLim, SFS_code and SimBit

I have personally used NEMO, SFS_CODE and SLim in the past (I now use SimBit only). So I can only talk about these 4 below.

All four models are well updated and maintained by their authors and of course everyone has a access to the source code.

SFS_code and SLim are very fast for small simulations. The issue of SFS_code and SLim is that the RAM usage and run time are exponential function of the genetic diversity. This means that some simulations can quickly become totally unmanageable. But it is a great tool if you expect little genetic diversity.

SimBit is typically faster than Nemo, at least for large genomes. This difference becomes particularly obvious for large genomes. One might think "Oh I am fine to wait a few extra days to get my results" but the difference in speed between two softwares can also be a difference in whether you have to wait a week or 20 years to get your results, so do not neglect the importance of running time and RAM usage without estimating your needs.

Nemo is very flexible when it comes to the order of life-cycle events (is migration before or after selection for example) and the newest version allows for simulating age structured population. SimBit is very flexible, very fast and allow for simulating multi-species and their ecological interactions. SFS_code is less flexible.

  My only concerns about NEMO are that each individual dies after reproduction and that there can't be more than 256 alleles at the same time.

SFS_code limits the number of alleles to 4. Nemo limits the number of alleles to 256 (but you can also use phenotype and have a float number at each locus). SimBit uses either bi-allelic loci, a block in which the number of mutations are counted (max: 256 mutations; this is different than 256 alleles per say) or continuous float number at each locus for the phenotype. Do you really need more alleles? Why can't you just use several loci to represent a sequence with multiple alleles? Real biology can only have 4 alleles in its smallest locus! SimBit uses a bit-per-bit system. If you need, say 50,000 alleles, then you just need to ask for a sequence of 16 bits (2 bytes) and you can get $2^{16} = 65,536$ alleles.

If you need more alleles in a single block (which is a little surprising to me a priori), you can probably just ask the author and he might accept to helping you if you convince him it is of interest to add this feature (he might also be more willing to help in exchange of authorship if you need more support).

Hope that helps. Good luck!


What's the evolutionary reason behind decussation?

I don't think it is a clever thing to group all types of decussation and look for a general explanations. I would tend to think that different decussation have different explanations. It is like asking what are the hypothesis to explain evolution of body size. There is no general answer to that but only a list of case specific impact of different factors on body size (see this post). Consider the two case-studies 1) "why does left brain controls the right part of the body" and 2) "Torsion in gastropoda" as examples of how different explanation applies to different decussation.
why does left brain controls the right part of the body?
See @shigeta's answer to this post. It is very interesting.
Torsion in Gastropoda
Torsion in Gastropoda is an interesting case. In this lineage individuals undergo some torsion during their development. This wikipedia articles say:

Snails are distinguished by an anatomical process known as torsion, where the visceral mass of the animal rotates 180° to one side during development, such that the anus is situated more or less above the head. This process is unrelated to the coiling of the shell, which is a separate phenomenon. Torsion is present in all gastropods, but the opisthobranch gastropods are secondarily detorted to various degrees.[13][14]
Torsion occurs in two mechanistic stages. The first is muscular and the second is mutagenetic. The effects of torsion are primarily physiological - the organism develops an asymmetrical nature with the majority of growth occurring on the left side. This leads to the loss of right-paired appendages (e.g., ctenidia (comb-like respiratory apparatus), gonads, nephridia, etc.). Furthermore, the anus becomes redirected to the same space as the head. This is speculated to have some evolutionary function, as prior to torsion, when retracting into the shell, first the posterior end would get pulled in, and then the anterior. Now, the front can be retracted more easily, perhaps suggesting a defensive purpose.
However, this "rotation hypothesis" is being challenged by the "asymmetry hypothesis" in which the gastropod mantle cavity originated from one side only of a bilateral set of mantle cavities.[15]
Gastropods typically have a well-defined head with two or four sensory tentacles with eyes, and a ventral foot, which gives them their name (Greek gaster, stomach, and poda, feet). The foremost division of the foot is called the propodium. Its function is to push away sediment as the snail crawls. The larval shell of a gastropod is called a protoconch.

You can find more information there


How to watch a Zebrafish embryo in detail?

From personal experience, it should be sufficient to observe zebrafish at 10-20x magnification for broad structural changes during development.  If your microscope has a 10x eyepiece, then that would be 1-2x zoom. If you are observing sub-cellular changes, you would benefit from higher magnification.


Think of what happens when you don't wash your hair for days. It gets oily and greasy. This oil-like substance on your hair is called sebum and mainly works as a lubricant . The Sebaceous glands responsible for excreting sebum don't stop working when the hair follicles attached to them do. The result is a "shiny" head.


This is likely a honeycomb created by some species of honey bee.

A beekeeper (Jessie Brown) from New Mexico shared to her blog the following photos of a "free form" bee hive some of her bees created:

 Photo credit: Nina Dubois

In that instance (as well as the one mentioned here and pictured below), the beekeeper moved some "burr comb" to a new location and the bees used that moved remnant piece to build a mound-like comb.

 Photo credit: Phillip Cairns


Can two different species in the same genus generally succeed in the same habitat?

It is not correct to say that genera are based on genetic similarity. Different lineages diverge genetically at highly variable rates, and there is no set cut-off for what defines a genus. Instead, genera are based on publications, which could be over 100 years old. Genera are not a biologically real category the way species are, so one genus may hold hundreds of species, while another, only one. Most of these genera were defined before molecular data was possible. There are no set phenotypic criteria for the definition of a genus, except that a well-described genus should have at least one fixed character that defines it. So in answer to your question, yes, two species in the same genus (congeners) will often exist in the same habitat. There would be selective pressures to separate them in terms of the niche that they occupy. The publication you referred to is simply a best guess: if you don't have information on the habitat requirements of a species, it would most likely share many similarities with its close relatives. Phylogeny is predictive, but different species in the same genus need not be identical in terms of their ecological requirements.


Why are cancer rates low in large animals?

Short answer
Large animals do get cancer. They may contract cancer with an incidence less than that estimated by absolute cell numbers, but there seems to be a lack of data on cancer rates in large animals to support this hypothesis conclusively.

Background
Whales contract cancer (Martineau et al, 2002). There does, however, seem to be a lack of correlation between body mass and cancer risk, which is counterintuitive since larger animals have more cells. This is known as Peto’s paradox (Caulin & Maley, 2011), after epidemiologist Richard Peto of Oxford University in the UK, who noted it in the 1970s. He reasoned that larger organisms have more potentially carcinogenic cells, tend to live longer and require more ontogenic cell divisions. Therefore, statistically, cancer incidence should scale with body size (Nagi et al., 2007).

It is thought that larger animals use protective mechanisms that many smaller animals do not. For example, blue whales have 1000 times more cells than us, if they would contract cancer at rates 1,000 times higher than humans, they would die before they were able to reproduce and the species would quickly go extinct. However, the paradox itself has been scrutinized, because there may simply be a lack of data on cancer rates in large animals (Source: Nature News, 2013). In addition, it is thought that malignant tumors are disadvantaged in larger hosts. In larger organisms, tumors may need more time to reach lethal size, so tumors have more time to evolve without becoming lethal. Hence, in large organisms, cancer may in fact be more common, but less lethal (Nagi et al., 2007).

The persistent myth that sharks don't get cancer seems to stem from clinical evidence that cartilage has antiangiogenic properties, i.e., it inhibits the development of blood vessels, which are crucial to the growth of many cancerous tumors. Since shark skeletons are made of cartilage, it was thought that they can't get cancer. Recent studies have found that while the incidence of cancer in sharks and related fishes such as rays does seem to be low, cancerous tumors, including chondromas (cancers of the cartilage), have in fact been found in sharks. The reasons for the apparently low incidence are not necessarily related to their high cartilage content, but may simply be a matter of lack of directed research on cancer in sharks and related fishes (Source: American Museum of Natural History). Indeed, tumors have been found in 23 species of sharks, measuring up to 30 cm in a Great White (Source: Scientific American, 2013).

References
- Caulin & Maley, Trends Ecol Evol (2011); 26(4): 175–82
- Martineau et al., Environ Health Perspect (2002); 110(3): 285–92
- Nagi et al., Integr Comp Biol (2007); 47(2): 317-28

P.S. All animals, including whales, age and die, otherwise the oceans would've been pretty crowded, at least before whaling started.


What in neurons and their connections changes during the process of learning?

What changes in the process of learning:

The connections (the way one neuron is connected to another). New synapses can form or dissolve in the process of learning. The glial cells such as astrocytes and microglia can facilitate this process.
Strength of connections: Existing connections can be made weaker or stronger in the process of triggering the same circuit. This happens by up/down regulation of the ion channels at the synaptic junctions.

This process is not fully understood and is an active area of research. You can find some mathematical models too for learning processes such as Long Term Potentiation etc.


Transport of newly synthesized proteins to cellular organelles

Mature RNA is translated into proteins by the ribosomes.  Ribosomes bound to the ER (endoplasmic reticulum) translate proteins that are bound for export from the cell.  Free ribosomes, which are found in the cytosol, are used for structures within the the cell (http://www.brighthub.com/science/medical/articles/110037.aspx)

Proteins made on the ER are sent to the Golgi apparatus, and are packaged there for transport out of the cell. (http://www.ncbi.nlm.nih.gov/books/NBK9838/)

As far as I know, the proteins made by free ribosomes remain in the cytosol and are incorperated into certain organelles or pathways upon contact with specific other proteins or signalling molecules.


Where can I find the pMON7124 plasmid sequence?

It seems that no good map of this plasmid is around. Life technology uses it in some of its bacterial strains, the quote:

  E. coli also contain the helper plasmid, pMON7124 (13.2 kb), which
  encodes the transposase and confers resistance to tetracycline. The
  helper plasmid provides the Tn7 transposition function in trans.

They link to the original publication, but the image quality in there is pretty bad:

They give some information in the text, so I would recommend reading the paper (if you have no access, let me know, I can help here):

A broad-host-range shuttle system for gene insertion into the
chromosomes of gram-negative bacteria.

If this is not enough, you could still try to get a better version from the author Gerard F. Berry (you can find his Monsanto email adress by googling for it).


Inflammation includes accumulation of inflammatory cells, such as neutrophils or macrophags, in a tissue. The typical four local signs of inflammation include redness (Latin rubor), heat (calor), swelling (tumor), and pain (dolor) (Britannica).

Fever is a symptom, which may or may not be present in a certain inflammatory condition. For example, lung inflammation in pneumonia is usually accompanied with fever, while joint inflammation in rheumatoid arthritis is not.


Are there examples of encryption in nature?

One example is in the development of the immune system. V(D)J recombination, antibody production, and T-cell receptor production generates a specific "key" that, in most cases, can only be bypassed by that individual's molecular inventory.

In that sense, parasites, mutualists, and commensalists could be viewed as black, white, and grey hat hackers, respectively.

Another example is the organism-specific tRNA synthase inventory and the matching tRNAs.


There are a few important things to consider as you interpret these data.
Here potency means Chlorpromazine equivalents
When your linked review refers to potency, it is likely referring to the old concept of chlorpromazine equivalents. The table in the article cites Jibson and Tandon in a review in CNS news special report from 2001. This is not a standard peer reviewed article, and I can't access it, but it lists relative potency in mg, with chlorpromazine set at 100mg and haloperidol at 2mg:

This is almost certainly chlorpromazine equivalents. You can read a discussion of the limitations of this understanding of antipsychotic potency here, but these numbers are not based on a mathematically rigorous pharmacodynamic analysis. They are not consistent, especially for atypical antipsychotics, and are estimated based on clinical data of the minimum effective dose among other methods.
So, where the affinity in this article, $\frac{1}{K_D}$, has a rigorous pharmacodynamic definition, potency does not. Here it is, effectively, shorthand for how much of a drug you have to administer in order to get a therapeutic effect.
Antipsychotic drugs act at many CNS receptors
To understand exactly what Miller means when he says:

For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone.

You need to understand that $H_1$ receptors do not mediate the primary clinical target. So the lower potency of quetiapine means you have to give more of it to have a clinical effect. Because of the higher typical dose of quetiapine, even though the affinity for $H_1$ receptors is relatively low, you're going to get more binding to $H_1$ than with, e.g., risperidone, which requires a lower dose.
Take a look at the chart in the Richelson and Souder article Miller cites to see the different receptor targets for these antipsychotic drugs.

The primary therapeutic targets (used to characterize the general clinical potency) are (probably) the $D_2$, $5HT_{1A}$, and $5HT_{2A}$ receptors. The action at the $H_1$ receptor is primarily an adverse effect. Miller is trying to say that the sedation effect does depend on affinity at $H_1$, but you also have to consider the dose required to get an effect at $D_2$ and the relevant $5HT$ receptors.
A rigorous definition of potency involves simplification
There is a rigorous definition of potency for an agonist (and also of inhibition for an antagonist, and antipsychotic drugs are antagonists). Potency is both distinct from and dependent on affinity.  I'd recommend Goodman and Gillman Chapter 3, if you'd like to learn more. It's not particularly relevant to understanding this article, in part because Miller doesn't use this definition of potency, and in part because the model involves a single ligand-receptor interaction that directly mediates a desired effect. It's based on the following equation, where $LR^*$ is an activated ligand-receptor: $L + R \rightleftharpoons LR \rightleftharpoons LR^*$.  Because both desired and adverse effects of antipsychotics involve actions at many different receptors even beyond those in Richelson and Souder, the simple model falls short.


How does the microbial environment in your gut initiate?

The initiation of gut flora come from maternal cervical and vaginal flora (Bezirtzoglou, 1997)1. These predominantly include facultative anaerobes (e.g., Staphylococcus, Enterobacteriaceae and Streptococcus). Birth by caesarean section can cause problems because these bacteria are not passed on in the  usual manner.

Vael et al. (2011)2 found an association between early gut flora and obesity later in life

  High intestinal Bacteroides fragilis and low Staphylococcus
  concentrations in infants between the age of 3 weeks and 1 year were
  associated with a higher risk of obesity later in life.

suggesting that monitoring or alterations of gut flora might be effective in reducing rates of obesity.

Bezirtzoglou E. 1997. The intestinal microflora during the first weeks of life. Anaerobe 3:173-177.

Vael, C., Verhulst, S.L., Nelen, V., Goossens, H., Desager, K.N. 2011. Intestinal microflora and body mass index during the first three years of life: an observational study. Gut Pathog 3: 8.


what is the effect of soda water on digestion?

Soda, anything carbonated causes bloating, which stretches the stomach. Mechanoreceptors in stomach detect the stretching resulting in parasympathetic innervation to GI smooth muscle. This causes an increase in GI motility.


The answer depends which species (melanogaster, simulans, yakuba etc.), strain/population (e.g. Canton S, DGRP), mutant line (e.g. eb, CiD), food substance, larval density, and incubator settings (temperature, humidity etc.).

The rough answer is no, but if you clear the already hatched flies from the vial in the morning (~1 hour before lights on) and collect flies within a few of hours they should be virgin. Day 12 will likely be too late to collect many as most will have hatched at 25 degrees, at 18 degrees this may slow development but you should be certain that it will not affect your experiment, and report it properly in the methods. You could also collect and store them for a few days in single sex vials (all males or all females), then check the food that you store them in for larvae before using them, this helps to ensure virgins are actually virgins. If you find lots of eggs or even a single little larvae then throw the vial away. This also allows the females to mature properly, allowing them to eat some yeast and they will be more willing to mate when needed.

An experienced fly handler should be able to sort consistently enough to have just a few back up vials. If it is a beginner then make many vials with few flies in, this reduces the damage if a male slips through, it's much nicer to throw away a vial of 10 females than a vial of 100!

(Answer based on >7 years practical experience with D. simulans and D. melanogaster, collecting tens to hundreds of thousands of virgin flies in that time).


Is there a biological reason for spreading food intake into breakfast-lunch-dinner?

The three meals a day seems to be a cultural trait. Then what is the optimal number of meals a day? It is not known. Here are the results of some studies:

Reduced meal frequency:

It was found that the body can adapt to a single meal a day by modifying circulating hormone levels and glucose tolerance [1]. However it does not modify lipogenesis rates [2]. It may support cardiovascular disease risk factors [8].

Increased meal frequency:

Although there are studies that claim 5-6 meals a day help in maintenance of weight loss [3], others claim this habit increases hunger and the desire to eat and has no significant effect on fat oxidation [4]. A higher number of daily meals is recommended to the elderly suffering from cardiovascular diseases [5] because less but square meals lead to a redistribution of blood to the gastro-intestinal tract to increase absorption, which causes reduction of blood pressure [6].

Conclusion:

Energy balance is more important than meal frequency. As this study says [7]:

  ... there is no evidence that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of meal pattern on the regulation of body weight are likely to be mediated through effects on the food intake side of the energy balance equation.

References:

Carlson O, Martin B, Stote KS, Golden E, Maudsley S, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Rumpler WV, Baer DJ, Egan J, Mattson MP. Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women. Metab. Clin. Exp. 2007 Dec;56(12):1729-34. doi: 10.1016/j.metabol.2007.07.018. PubMed PMID: 17998028.
Jones PJ, Namchuk GL, Pederson RA. Meal frequency influences circulating hormone levels but not lipogenesis rates in humans. Metab. Clin. Exp. 1995 Feb;44(2):218-23. PubMed PMID: 7869919.
Bachman JL, Phelan S, Wing RR, Raynor HA. Eating frequency is higher in weight loss maintainers and normal-weight individuals than in overweight individuals. J Am Diet Assoc. 2011 Nov;111(11):1730-4. doi: 10.1016/j.jada.2011.08.006. PubMed PMID: 22027056.
Ohkawara K, Cornier MA, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity (Silver Spring). 2013 Feb;21(2):336-43. doi: 10.1002/oby.20032. PubMed PMID: 23404961.
Ortega RM, Redondo MR, Zamora MJ, López-Sobaler AM, Quintas ME, Andrés P, Gaspar MJ, Requejo AM. [Relationship between the number of daily meals and the energy and nutrient intake in the elderly. Effect on various cardiovascular risk factors]. Nutr Hosp. 1998;13(4):186-92. PubMed PMID: 9780751.
Westenend M, Lenders JW, Thien T. The course of blood pressure after a meal: a difference between young and elderly subjects. J Hypertens Suppl. 1985 Dec;3(3):S417-9. PubMed PMID: 2856754.
Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br. J. Nutr. 1997 Apr;77 Suppl 1:S57-70. PubMed PMID: 9155494.
Stote KS, Baer DJ, Spears K, Paul DR, Harris GK, Rumpler WV, Strycula P, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Mattson MP. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am. J. Clin. Nutr. 2007 Apr;85(4):981-8. PubMed PMID: 17413096.


What's this black, white and orange beetle?

Yes this is an adult carpet beetle.

Specifically,  this is a Common carpet beetle (Anthrenus scrophulariae)

See here for more info.

2.5 to 3.8 mm in length.
Black head (mostly hidden by the prothorax) + black  thorax and elytra with distinct scale patterns.

The thorax is covered with white scales except for a large midline.
The elytra have orange to red scales down the midline with variable patches of white scales.

Note: in older individuals, some or all of the scales may be lost and the color pattern may look different.

This species is found worldwide.

Unlike the larvae,  the adults are primarily pollen grazers.


How to reduce the number of sequences in a Multiple Sequence Alignment?

The bioconductor package "ShortRead"  might be what you are after.
It has a function "clean" to remove sequences with ambiguous bases. It also can remove duplicates if you need to.


What plant is this? (Found in Southwest Germany in June)

I am almost sure this is Sedum reflexum (aka S. rupestre), in English prickmadam or crooked yellow stonecrop and in German Felsen-Mauerpfeffer. It usually grows at rocky or stony ground, not full of grass.

Distinctive features are the pointed leaves, which are not as round as in S. album and also the bended stem (flower stalks are always bend, hence the name reflexum). Its' flowers should be yellow.

These features can be seen well at the botanical drawing below (from wikipedia commons).

The reason I'm not completely sure is that in garden (and on roofs) exotic sedums are often planted.


Why do we go blind for a few seconds after switching off the light?

Short answer
The eyes need to adapt to the low lighting condition after you switch off the lights, a process called dark adaptation.

Background
The process behind the reduced visual function when going from bright ambient light to low-lighting conditions is caused by a process called dark adaptation. The visual system works on a huge intensity scale. The only way to do that is by adapting to ambient lighting intensity.

The sensitivity of our eye can be measured by determining the absolute intensity threshold, i.e., the minimum luminance of a stimulus to produce a visual sensation. This can be measured by placing a subject in a dark room, and increasing the luminance of the test spot until the subject reports its presence.

Dark adaptation refers to how the eye recovers its sensitivity in the dark following exposure to bright light. The sensitivity of the visual system increases approximately 35 times after dark adaptation.

Dark adaptation forms the basis of the Duplicity Theory which states that above a certain luminance level (about 0.03 cd/m2), the cone mechanism is involved in mediating vision, called photopic vision. Below this level, the rod mechanism comes into play providing scotopic (night) vision. The range where two mechanisms are working together is called the mesopic range, as there is not an abrupt transition between the two mechanism.

The dark adaptation curve shown below (Fig. 1) depicts this duplex nature of our visual system. The sensitivity of the rod pathway improves considerably after 5-10 minutes in the dark. Because after you switch off the light the rod system is still inactive, you are unable to perceive much. The reason why rods are inactive is because they are said to be photo bleached. Photo bleaching refers to the visual pigments in the rods and cones to become used up because of the high light intensities when the light was still on. The pigment needs to be regenerated and that takes time.

Fig. 1. Dark adaptation curves of rods and cones. Source: Webvision

Reference
- Kolb et al (eds). Webvision. The organization of the retina and the visual system (2012)


How does 2-mercaptoethanol lead to shift of the band to a higher molecular weight?

2-mercaptoethanol (2ME) reduces the disulphide bonds in proteins. If disulphide bonds are connecting two polypeptide chains ("intermolecular") then 2ME would cause them to separate and therefore instead of a higher molecular weight (MW) band you would get one or more lower MW bands.

However, if there are disulphide bonds in the same polypeptide chain, they may cause the chain to fold up. This results in the polypeptide chain to effectively have a smaller hydrodynamic radius compared to the fully denatured chain. In such cases reducing the disulphide bonds using 2ME would cause the band to shift to a higher MW.

  What is the easiest and lowest cost method to separate closely related proteins

This is a different question altogether and there are several techniques depending on how "dissimilar" or "similar" the closely related proteins are. 2D PAGE (with isoelectric focussing) is one technique that can offer higher resolution compared to a normal SDS-PAGE. There are many other chromatographic methods.


What information does the nociceptor relay to the brain about stimuli below threshold?

Short answer
D.

Background
Nociceptors are free nerve endings, and usually consist of bundles of unmyelinated fibers (Messlinger, 1997).

So nociceptors are basically axonal fibers. Below threshold, activation of these fibers do not cause action potentials to occur. Since action potentials are, basically, all-or-nothing events no signals will be sent to the brain. Hence, the brain will not receive information on either duration (A), or location (B) of the pain stimulus. The membrane potential (C) is a non-sense answer. Membrane potential, although it may affect receptor response properties, is never the primary message of a receptor signal. It is about the sensation of physical stimuli (in this case painful mechanical, heat or chemical stimuli).

So the answer is -D- as we have disputed A, B and C.

Note
When receptors convey graded potentials, the term 'below-threshold' doesn't really apply anymore. Graded potentials can, in principle, convey the smallest stimulus difference as they operate on an analogue scale. Therefore, this question targets your understanding of the binary nature of action potentials and their threshold, and what that means for the detection of below-threshold stimuli.

Reference
- Messlinger, Anaesthesist (1997); 46(2): 142-53


Do RuBisCo and Haemoglobin have any similarity?

Try reading about these proteins. Apart from wikipedia, you can check out pfam which classifies proteins into families. Globins and RuBisCO are very different protein families. Perhaps the only similarity is that both these are made up of amino acids!


When are population dynamics models useful?

Population dynamics occupies a whole subset of mathematical biology. Perhaps the most pragmatic uses for modelling population dynamics come from the fields of epidemiology for modelling disease infection and transmission through a population (one such article), or ecology modelling things like forestation, fishing dynamics, predator-prey relationships (an example). Then there are more abstract uses, when you cannot measure a population to test a hypothesis because the labour is too intensive, or it's too costly, or no such surveillance mechanism exists. Theoretical models of population dynamics are built to gain an understanding of what the system as a whole may do under certain conditions. In this sense, population models are more of a theoretical exercise or a thought experiment.


How many coronavirus particles are in the body at the peak?

This measure changes dramatically between viruses and infected individual but there are some estimates that have been done.

Bar-On, Flamholz, Phillips & Milo, Apr 2020, eLife
From MERS and SARS (similiar to the current coronavirus) we know that from each infected cell emerge around 10^3 virions and it takes them 10 hours from the infection of the cell. We cannot deduce that every 10 hours the magnitude of virions in the body increases by 3 because:

Not all virions infect a new cell
Some virions infect the same cell and the burst size depends greatly on the cell
Not all virions are viable or able to infect

Another paper from Sender et al. (Nov, 2020) that is still in preprint (this is a long time for Coronavirus related articles) estimates the number of virions in peak infection at 10e9-10e11.
This estimate was done by analyzing data from Rhesus macaques (a monkey).
Concentration of virions per tissue weight was multiplied by the tissue weight to get total amount of virions.
On the relevance of Coronavirus information
Since our knowledge of Coronavirus advances and changes all the time it is important to note the date and source of information. Also, to advance science many papers published preprint articles regarding Coronavirus. This articles are published before peer-review and should be taken with a grain of salt as every peer-reviewd paper gets many revisions before published to the public.


How much fat can the body absorb? Implications for daily fat distribution

Indeed, lipid fecal loss remains below 5% (w/w) even in situation of
  high fat supply in healthy humans, [30].

All about those guts and bowls folks!

Niot, I., Poirier, H., Tran, T. T. T., & Besnard, P. (2009). Intestinal absorption of long-chain fatty acids: Evidence and uncertainties. Progress in Lipid Research, 48(2), 101–115. doi:10.1016/j.plipres.2009.01.001

https://sci-hub.tw/10.1016/j.plipres.2009.01.001

[30] Ross AC. Overview of retinoid metabolism. J Nutr 1993;123:346–50

The issue remaining is how Ross' work doesn't seem to say anything about lipids. Yet, it appears from the mice studies nearly all fat is absorbed (except for ones with special conditions).

Ross, A. C. (1993). Overview of Retinoid Metabolism. The Journal of Nutrition, 123(suppl_2), 346–350. doi:10.1093/jn/123.suppl_2.346

https://sci-hub.tw/https://doi.org/10.1093/jn/123.suppl_2.346


Do trees really get a large share of their mass from the carbon in the air?

The vast majority of a tree's carbon comes from the air, which averages 0.03-0.04% by volume (300-400 ppmv) CO2.  This is fixed through photosynthesis and eventually stored as glucose which the plant can then use for its metabolism.

Doing some quick math, this means that in order to produce 1 kilogram of carbohydrates (e.g. cellulose) a plant needs to process on the order of 2000-3000 cubic meters of air (and ≈550 g or mL of H2O), which would fill a cube measuring 13-14 meters on a side.  Note this is an ideal figure; a plant's fixing efficiency will likely fall as it depletes the air of CO2.

Plants do take a great deal from the ground, namely water, fixed nitrogen (for proteins),  phosphorous (for nucleic acids), and several ions (sodium, potassium, calcium, among others)


To which ungulate species does this tooth remainder belong?

Its definitely not a marine mammal, just based on size and general configuration.
those convoluted ever growing teeth are pretty diagnostic of non-cetacean ungulates.
Just based on the pattern I would say bovidae, but that does not narrow it down much in turkey, the H shaped central portion is fairly diagnostic of bovidae. However you have several antelope species not to mention domesticated animals that each would fit that category.
I suggest changing the title to ask for ungulate tooth identification. You need someone specialized in mammalian teeth to narrow it down to species. if you can add more shots of the tooth crown (the complex ends like those below) that is the part most useful for identification. See the examples below. The more you have the better.

Source


What is the purpose of getting a rabies vaccine after exposure?

Rabies virus enters the body, typically from a bite, and then enters nerves which it follows up to the brain. An immune response to a first exposure of a pathogen generally takes many days, perhaps weeks, to develop to the point where it's protective. This is often even slower when the pathogen is in nerves, which are relatively sheltered from the immune system, and when there's only a small amount of virus present.

After rabies exposure, people are given two treatments: They're given  rabies immune globulin, which contains pre-formed antibodies against rabies, and they're also given the vaccine.

The rabies immune globulin is the most important of these. It provides immediate protection, beginning within minutes of injection. If the virus has not yet entered the nerve cell (which often takes quite a while) then this globulin will bind to and inactivate all, or almost all, of the virus.

Giving the vaccine as well is an added precaution. It will give a faster, probably much faster, response than would the natural virus. There may be only a few rabies viruses present -- it only takes one! -- and of course the natural virus is doing everything in its power to avoid making a strong immune response, whereas the vaccine is the opposite. It has large amounts of antigen, and it's optimized for making a strong immune response. (Rabies vaccine post-exposure is boosted on days 3, 7, and 14 after the first dose. That's an extremely aggressive vaccination procedure that you don't see with any routine treatments.) The vaccine might drive a protective immune response within a few days, while the natural virus might take a month, or never.

If the rabies immune globulin doesn't catch all the virus, or if it temporarily blocks it but then some escapes -- then the vaccine-induced immune response might protect them.

CDC page on post-exposure vaccination
CDC page on post-exposure globulin


Do dead cells always contain no nucleus?

If you're looking at cause of death by standard apoptosis, to initiate the process, cytochrome c will be released from the mitochondria, bind with apaf-1, and undergo a structural change resulting in what looks like a biochemical ninja star (figure 4). This will activate caspase-9 which will activate other executor caspases, eventually creating an avalanche of protein-degrading enzymes that will leave the structure and organelles of the cell looking like paper mache. Regarding the nucleus, the complexes of enzymes meant to maintain dna integrity and structure will be degraded, the DNA's network influence on the cell will become largely inert, and the dna will be condensed and broken apart by nucleases. The membrane of the nucleus is full of proteins and ribosomes, and these will be degraded too. If you are looking to simply identify an inert nucleus by its skeleton, you may not have much success either - here are a few good images from a nice study showing the progressive destruction of a nuclear structure.


What is the difference between sequence, reads, and contigs of genetic material?

My understanding of those three words as follows:

sequence is a generic name describing order of biological letters (DNA/RNA or amino acids). Both contigs and reads are DNA/RNA or aa sequences
reads are just a short hand for sequenced reads. Usually sequenced reads refer to somewhat digital information obtained from the sequencing machine (for example Illumina MySeq) and stored in the fastq file with quality scores per base. Reads are usually short. However "short" changes rapidly. Right now MySeq produces reads anywhere between 50-150 base pairs long (bp). From a single run (it will really depends on the run) you can get millions of reads, where each read will be set bp size e.g 100bp long. All reads are stored in a single fastq file per replicate, where all reads in that file are usually of uniform size e.g all 5 million reads are 100bp long.

As a bioinformatician your first job is to identify where about those reads come from. Depending on the experimental goal and on what sort of sequencing you were doing e.g DNA-seq or RNA-seq you may or may not encounter contigs.

contigs are simply reads that have been assembled together. For example if you are doing de novo transcriptomics. Then you would:

purify your transcript from a tissue and send it off for sequencing
get your fastq files with sequenced reads, that are all short reads
(e.g 100 bp)
assemble those 100bp reads into a longer contig that hopefully will resemble your individual transcript


Are there animal species that sense infrared light with their eyes?

Short answer
As far as I can see, there are no animalia with high-sensitivity infrared photoreceptors in their retinae. Instead, infrared is detected at low thresholds with a dedicated sensory system in some species - the pit organ. This organ is separate from the retinae and its output does not merge with the retinal image. However, red cones, and even green cones for that matter, have low sensitivity to infrared light and when intense enough, infrared stimuli may be detected by the eye, as was shown in a small study in ferrets.

Background
Infrared (IR) light is classified as light at wavelengths of 700 nm and up. In Fig.1 is depicted the light sensitivity of man under scotopic (dark-adapted) and photopic (light-adapted) conditions. It is readily apparent why we cannot perceive IR.

Species that can detect IR use it in general to detect heat. Notable examples are the blood sucking species, including mosquitoes, bed bugs and vampire bats as well as nocturnal predators including species of snake (source: National Geographic). Although this heat detection can be classified as IR vision, IR is not detected by their eyes. Instead, all of these species use specialized IR-sensing organs called pit organs to detect IR. Basically, these are heat detectors (source: NSF). While snakes are able to construct heat-maps, the IR image and visual images as detected by the retinae are not combined into a single image. As far as I understand, the visual image and IR images co-exist in snakes and are not fused (or 'overlaid') (Campbell, 2002).

So the most notable of IR detecting species have IR vision, but these heat maps are sensed by dedicated pit organs separate from the retinae and as far as I can see the images are not combined.

However, last but not least - IR cameras are often used to study nocturnal critters as it is assumed they cannot detect the IR. Interestingly, a study on a small population of 5 ferrets showed that 3 of them responded at above-chance level to light stimuli well into the IR (870 nm) (Newbold, 2007). It should be noted that sensing of stimuli is all about thresholds. The Fig. 1 shows a nearly zero-response in humans at 700 nm, but when we would make the stimuli strong enough, we may elicit a small response nonetheless. Fig. 2 shows the absorption spectra of red and green cones. As becomes apparent here, red cones and even green cones have spectral sensitivity in the IR domain. Then it might become a question not whether we can sense IR, but at what level we can detect it. Under normal everyday lighting conditions, we obviously can't, but that does not exclude the possibility we may perceive it at extreme light intensities.

Fig. 1. Human spectral sensitivity. source: Webvision

Fig. 2. Spectral sensitivities of red and green cones. source: Dowling, 1987)

References
- Newbold, Master's thesis. University of Waikato, NZ
- Kalloniates & Luu. In: Kolb et al (eds). Webvision. The Organization of the Retina and Visual System
- Schnapf et al, Nature (1987); 325: 439-41


Why do two different E. coli reference genomes have different lengths?

U00096.2 is an updated version of U00096.1; you should preferably use the former for your analysis. In fact, even U00096.2 has been updated. The latest version is U00096.3. In general, the number after the dot (period) in NCBI accession numbers, denotes the version.

From NCBI:

  VERSION is made of the accession number of the database record
  followed by a dot and a version number (and is therefore sometimes
  referred to as the "accession.version")


Energy transfer from P680 to oxygen-evolving complex

You have to think the other way around: don't pay attention to where the electron from P680 is going.

Instead of that, pay attention to this fact: after PSII absorbs a photon and triggers the loss of an electron from a P680 chlorophyll a molecule, this P680 has now an electron deficit. That is, this P680 has lost one electron.

This P680 without one electron is now called P680+. And here comes the important information, which answers your question: According to Lodish (2002),

  P680+, the photochemically oxidized reaction-center chlorophyll of PSII, is the strongest biological oxidant known. (emphasis mine)

And that explains what (thermodynamically) drives O2-evolving complex (still according to Lodish, 2002):

  The reduction potential of P680+ is more positive than that of water, and thus it can oxidize water to give O2 and H+ ions. (emphasis mine)

I hope those terms are simple enough for you. Finally, for better understanding all this, have a look at the concept of reduction potential (which, as a college student, I believe you have to study).

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman.


If they are "pure-breeding", that means that they are homozygous.  If they were heterozygous, the offspring would not all have the same color as the parents.  But tree-breeding" means they all do.


There has been a lot of research in this field which asserts that mangroves desalinate sea water.
Scholander (1968) concludes that this process in mangroves use an ultrafiltration mechanism in the roots of the plant where membranes extract freshwater which is taken up the plant.

 Scholander, P.F., 1968. How mangroves desalinate seawater. Physiologia plantarum, 21(1), pp.251-261.


Can anyone identify this mystery caterpillar?

Best assumption, Gulf Fritillary Caterpillar (Agraulis vanillae). I could be wrong though.

  The larva is a caterpillar which grows to approximately 4 cm (1.6 in) in length. It is bright orange in color and covered in rows of black spines. The spines are soft to the touch and do not sting, but the larva is poisonous if eaten. Source: Wikipedia.


Understanding the brain: how are neurotransmitters released in the brain?

The release of neurotransmitters is a very specific type of SNARE mediated exocytosis. The action potential from the influx of sodium propagates along the axon and reaches the axon terminal, containing the calcium channels. This causes the calcium cations (ions) to travel down the electrochemical gradient. The Ca2+ then binds to a protein. The vesicles containing the neurotransmitter called synaptotagmin (Ca sensors), would cause conformational changes leading to the formation of a SNARE complex. Some good animations can be seen here and here.

Regarding whether there is an energy threshold: there is a threshold on the amount of Calcium needed to cause the activation of synaptotagmin, as with all types of SNAREs.

See this article: http://www.pnas.org/content/93/23/13327.full.pdf

Past a certain calcium threshold, all the neurotransmitter should in theory be released, but whether they cause a response would depend on the receptor and on the postsynaptic membrane, as each synapse is specific in the neurotransmitters and receptors it expresses.


What actually happens when my leg 'falls asleep'?

The feeling you describe is called "paresthesia," and according to the NINDS info page, it happens "when sustained pressure is placed on a nerve."


Is it possible for any animals today to have more than one brain?

To some degree the answer depends on your definition of what counts as a brain.

Bilaterally symmetrical organisms tend to have some level of cephalization, which involves the concentration of sensory and inter-neurons at one end of the organism (the head).

This aggregation of neurons at the head is typically more complex than aggregations of neurons elsewhere in the body and so it gets designated as a brain whereas the others are designated as ganglia (if they are outside the central nervous system or nuclei if they are within the central nervous system).

In vertebrates, cephalization is very well developed so the brain is typically much more complex than the ganglia (although the enteric nervous system is pretty awesome, its not the brain). However in many invertebrates, the ganglia at the head of the organism (its brain) is not much more complex than the other ganglia around the body.

For this reason, many invertebrates can survive decapitation (at least for a while) and some like the flat worm, can famously survive and regenerate their head after decapitation.


You are probably right that it is a Gymnopus, It's difficult to know which one. There's also Gymnopus Fusipes. For a difficult ID, it's best to have a cross section, a description of the scent, compare the color under the youngest specimens, as the gills often change from very light to very dark with age.


Ex vivo simply means "outside the normal, living organism", whereas in vitro means "within glass", usually in a cultured system.  They are not exactly same as there is no need for the work to be done in a culture system, although both are not in vivo.  Harvested tissue could be examined ex vivo without being in a test tube, or surgical systems could be tested ex vivo on artificial organ models.  In vivo requires the natural, living organism, although it depends on just how much you are perturbing the natural.

To answer your scenarios,

in vivo
ex vivo, as it is not within the normal organism, although I could understand someone taking issue with that; definitely not in vivo, which is usually for normal conditions only, even including temperature.
ex vivo
If you mean the artificially oxygenated environment of a tissue culture system, then in vitro; if you mean the artificially oxygenated environment of a lab bench with an open $O_2$ valve, then ex vivo would suffice.


Homologous chromosomes refers to the "twin" chromosomes in your cells (one from your mother and one from your father). Each somatic cell has at least one nucleus containing all your chromosomes*2. Having two sets of all chromosomes is referred to as diploid. On a chromosome, genes are encoded through different nucleotide sequences in DNA, and thus have a specific spot on the chromosome. The spot where a gene is located is called the locus, and because you have two chromosomes in your cells that contain the same genes (though maybe different alleles!), the genes will be in the same locus (same spot) on the both of the chromosomes.

The alleles do not actually combine to form a gene. An allele is simply one variant of a gene, and there can be many alleles for one gene. If a person has the same allele on both chromosomes they are considered homozygous for that allele and if they have different alleles they are considered heterozygous for it. Genes can also be considered either dominant or recessive. If they are dominant, they can be expressed with just one copy in the cell, but if they are recessive the same allele must be present on each chromosome. The alleles do not "combine to form a gene", they are simply separate copies of the same gene with possible variations on them. Homologous chromosome simply means the other copy (e.g. a gene on the 3rd chromosome of your mother will be present on the 3rd chromosome from your father although it could be a different allele due to a variation in nucleotide sequence). I hope this helps, although I would suggest doing some more research on your own, perhaps through https://www.khanacademy.org/science/biology. Their videos tend to be very descriptive.


When we eat the architecture makes sure most if not all the food ends up in our foodpipe rather than our windpipe. This is aided by a structure called the epiglottis.

However frequently foods may be inhaled, for example if a drink is sucked through a straw more if it gets into the lungs compared to if we drink it. Occasionally we will inhale a peanut or something else which typically occurs due to abnormal relaxation or muscular problems in the structures involved. This may be due to a neurological disease (e.g. myasthenia gravis) or because simply drinking too much and inhaling peanuts or vomit (aspiration).

If the inhaled substance is small and lipid soluble e.g. alcohol, it can pass through the alveoli at the end of the lung to the rich blood supply. If it doesn't we rely on macrophages to digest the food. They aren't frequent enough to digest anything substantial. Bacteria however are great at munching this up and increase substantially in number. Typically your lowest airways are sterile but food can interfere with clearance mechanisms and provide a home. The part of the lung blocked (distal to the foreign object) can collapse and frequently does. In the long run this may cause bronchiectasis, where an infection recurrently affects the area due to permanent damage done during the initial event resulting in widened airways and an ongoing inflammatory response. The inflammatory response reveals even more receptors for bacteria to latch on to.


Renin angiotensin is for regaining homeostasis. If you have lost salts, blood pressure and blood volume will decrease due to loss of fluids. But the renin angiotensin mechanism will try to undo this by stimulating uptake of Na+ and water. But still, they can not fully compensate for loss of Na+, INTAKE of Na+ is NECESSARY.

By the way, the main stimulus for triggering renin angiotensin is Blood volume and pressure rather than Osmolarity of blood. In conditions like hemorrhage where blood loss occurs but there is no change in osmolarity, Renin-Angiotensin will still respond (but ADH(vasopressin) will not as ADH responds only to change in osmolarity.)     —  biogirl


How does the body detect irreversible binding to receptors?

The process of downregulating a receptor by internalizing and degrading it in response to (sometimes prolonged) activation or (sometimes prolonged) failure to activate is what pharmacologists call desensitization (in either context). You can read about this generally in Goodman and Gilman's Pharmacological Basis of Therapeutics, Chapter 3, under the subsection "Receptor Desensitization and Regulation of Receptors". There are a number of mechanisms, not all well understood, but the basic idea is that when a signal is constant (either always on or always off), it no longer has any value as a way of providing information. Receptor regulation, or desensitization, is a mechanism for, effectively, resetting the cell or tissue. Removal of the receptor can be followed by recycling, or protein synthesis and return of new receptor to the site.

One well studied mechanism for desensitization is seen in G protein coupled receptors (GPCRs), such as some Dopamine receptors. It is well reviewed here.

To answer your specific question, binding that leads to desensitization is detected the same way any other binding is detected. A receptor produces a signal on binding (or stops producing a signal). The downstream effect of that signal includes a process that involves internalization of the receptor from a location where it can receive signal.

Here that process is mediated by phosphorylation by GRKs (GPCR kinases), which allows for binding of arrestin, and so on...


Why does NaCl react differently with a boiled potato and with a raw one

Maybe this passage is referring to this experiment?

The key missing from your description is that each potato is placed in water. When the cells are intact (unboiled), this causes water to flow into and out of the cells via osmosis: into the cells from the tray of water, and out from the cells into the salt. Once the cells are destroyed via boiling, there are no intact membranes to cross to osmosis does not occur and the salt remains undisturbed.


What is the biological mechanism linking temperature and probability to be infected with a virus?

It is common knowledge that when you're cold you could get a cold.

This may be a nice illustration why we need to be wary of “common knowledge”.

  What is the mechanism linking temperature and viral infection?

This isn’t clear. There are a few proposed mechanisms but a likely explanation is: “there is no mechanism” – and the assumed correlation between cold temperature and catching a cold might be nothing more than an illusion – a form of confirmation bias.

In fact, we don’t even know for sure that the cold season coincides with cold temperatures.

On the other hand, a 2007 review [1] found that

  … most of the available evidence from laboratory and clinical studies suggests that inhaled cold air, cooling of the body surface and cold stress induced by lowering the core body temperature cause pathophysiological responses such as vasoconstriction in the respiratory tract mucosa and suppression of immune responses, which are responsible for increased susceptibility to infections.
   [emphasis mine]

So according to their results, potential mechanisms which link temperatures and viral infection are indirect:

The lowered core body temperature would imply, in my interpretation, that the body has to expend more energy to maintain its temperature, and hence less energy to power its immune system (which is expensive).
Lack of respiratory tract mucosa removes an important physical barrier between the environment and the body, and allows pathogens to enter the body with much less resistance.

[1] Mourtzoukou & Falagas: Exposure to Cold and respiratory tract infections, in Int J Tuberc Lung Dis. (2007), pp 938–943


Transmission of HIV from Mother-to-Child Through Breastfeeding

In short, yes. Breast milk can contain virions which can be transferred from Mother-to-Child.

These are the guidelines from the National Institute of Health in the United States regarding the Prevention for Mother-to-Child Transmission of HIV and how the prevent Mother-to-Child Transmission of HIV After Birth

While the guidelines in the US are geared towards the fact that we have alternatives to breast milk, the World Health Organization has compiled evidence that suggests that Antiretroviral therapies along with exclusive breastfeeding may provide the most benefit for the health of the infant. This likely has to do with the access to suitable nutritional alternatives, clean water, and vaccines in developing countries, and in fact, it appears that mothers in wealthy countries that have HIV are advised not to breastfeed at all. This site outlines the different guidelines in place. The choice between breastfeeding and not in lesser developed countries has to do with the fact that the risk from waterborne illnesses and their impact on infant mortality rates is likely far greater than the risk of HIV transmission from mother to child through breastfeeding while both are on Antiretroviral therapy. The reason that exclusive breastfeeding is recommended is that it keeps the viral concentration in breast milk lower than if the baby was suckling only part of the time.

Italics in previous paragraph indicate an edit to the answer in order to clarify the reason why breastfeeding is recommended in lesser developed countries, even though it poses a risk for HIV transmission

Please note that these guidelines are in flux and as more evidence is obtained and as the virus mutates, things may change. It is always best to consult with a physician on the most current recommendations in the care of your infant if you are HIV+.


What is the evolutionary advantage of regret?

Very interesting question.

First I'd like to highlight that this question relates to a very hypothetical field of evolutionary biology which is evolutionary psychology. This wikipedia article on evolutionary approaches to depression might be of interest as well. One sentence says: "Feelings of regret associated with depression also cause individuals to reflect and analyze past events in order to determine why they happened and how they could have been prevented". It basically says the same thing than you said in your question.

What other advantages might "regrets" have? Before trying to answer it, I'd like to ask : is it necessary that it has advantages? A behavior or a feeling might as well be a by-product of selection for big brains. It might therefore not be selected for but it exists only because there is not much selection against this by-product trait.

Our brain are often considered to have evolved for social purposes. I would hypothesize that if someone express "regrets", he might benefit from other's care and pity. And the best way to express "regrets" is to feel the "regrets". Robert Trivers would maybe say that in order to fool someone else (make someone else think we regret) the best thing to do is to fool ourself (make ourself feel "regrets"). See his book, the folly of fools.


I think that Fair meiosis (I assume that you are referring to that chromosomes have an equal chance of transmission) can be seen as a byproduct of recombination at meiosis, which makes every chromosome a mosaic of maternal and paternal chromosomes. Therefore, selection does not act on chromosomes as a single unit, and "unfair" meiosis becomes meaningless. The "value" of "fair meiosis" most likely lies in the adaptive value of recombination.

Addition: To expand on the value of recombination, it has been suggested that the specific value of recombination is to break up linkages and thereby prevent meiotic drive (Haig & Grafen 1991, also see Okasha 2006). Haig & Grafen 1991 also specifically discuss selection for recombination. For an interesting analogy between economy and fair meiosis (veil-of-ignorance vs fair meiosis) see Okasha. 2012. Okasha notes that:

  In both, randomization is used to deprive self-interested agents (genes and individuals) of information about their identity, forcing them to adopt an impartial perspective.

In summary he also writes that:

  A gene that distorts segregation in its favour can spread despite reducing its host’s
  fitness. This harms genes at unlinked loci, who are thus under selection to
  restore fair meiosis if they can. One effect of fair meiosis is to equalize the
  interests of all the genes, thus ensuring they work for the common good.
  One way of achieving this is to destroy linkage, given that segregation
  distortion typically involves linked genes working in concert.

Okasha's paper also has a nice and accessible description of the biological process, and of the selective forces that are operating to counterbalance meiotic drive/segregation disorders.


How to get rid of mosquitoes in a small lake

There are a number of environmentally destructive methods that would be effective, including draining the lake, covering the surface with a continuous layer of oil, or adding toxins to the water, but I'm assuming you're looking for a method that will have the minimum possible off-target effect.

Different mosquito species breed in different habitats and are thus susceptible to different control strategies, so good photos of some adults might help, but I'm assuming here that you've correctly identified the lake as the breeding site. If there are any other possible breeding sites in the area please add them to your question.

If the assumptions above are correct then, broadly speaking, your best options are habitat modification or biological control. I'm not going to go into chemical control here since as stated above I assume you want low environmental and financial cost; if this is incorrect let me know.

Habitat modification: regularly removing
plant growth within the lake and trimming vegetation overhanging the edges will limit the ability of mosquito larvae to escape predators and may have some effect. However, the recent management you describe has
probably gone some way towards this (did you
notice whether the mosquito problem got any better after the plants
were removed?)
Biological control: introduce predators or parasites into the environment. Plenty of species eat adult mosquitoes but there aren't really any that primarily feed on them (unless they're the only food source available) and many adult mosquitoes will have laid eggs already - the most effective strategy will be to target the immature population. Larvivorous fish have been shown to be effective in many parts of the world, for example fish in the genus Gambusia ('mosquito fish'). I don't know of any that have been shown to be effective and can thrive as far north as Scandinavia, but if you stock the lake with fish (combined with managing vegetation as above) I'd be surprised if you don't see some improvement.
Biological control, part 2: Use Bti (Bacillus thuringiensis var. israelensis). This is a bacterium that produces toxins which are highly specific to dipterans and don't really affect anything else. You can buy the bacterium in various formulations including sprays, tablets etc. I'm mainly familar with its use for controlling container-breeding mosquitoes, but this paper describes its use in large lakes so should give you some idea of dose required, optimal application method and time to reapplication.

Without knowing more about your budget, available time/manpower etc I can't really help you choose between these but I suspect #3 is your best bet.


NADP and NADPH in in vitro metabolisme test

Are you sure your question is accurate?

NADP in solution does not exist... it can either be NADPH which is the reduced form (has gained an electron in the form of a H atom and now has the potential to give that electron to another molecule in the solution) or NADP+ which is the oxidised form (has lost an electron in the form of H atom and now has the potential to gain an electron from the solution).

In your experiment, Fiprinol to Fiprinol Sulfone is an oxidation reaction, so the enzyme catalyses the removal of an electron from Fipronol, and it does that with the help of NADP+, which is missing an electron itself and therefore takes it from Fiprinol (oxidises it) to give a high Fiprinol Sulfone yield.


Kinetic binding / unbinding constants of protein + mRNA ⇌ mRNP

Ridgeway and coworkers designed a really neat microfluidic device for making these kinds of kinetic binding measurements on RNA and protein (Ridgeway et al. 2009). Their device works sort of like a stop-flow, and they used a FRET based scheme to detect binding and unbinding events. They took measurements for one particular rRNA/ribosomal protein pair and got (6 ± 0.4) × 105 M-1s-1 for the bimolecular on-rate kon and  (5 ± 0.9) × 10-3 s-1 for the unimolecular off-rate koff.

Ridgeway cites references 23,24,26, and 33 when talking about experiments with "similar constructs and buffer conditions", so those would probably be a good place to start looking if you want to assemble a diverse set of kon  and koff  values.


A source for leaf architecture of different plant species/genus?

Quantitative descriptions of leaf shape used as diagnostics are hard to come by. There are numerous qualitative descriptions (lyrate, cordate, acicular, etc.), and I think this fits within the example you give that "the laminar shape for this species is mainly ovate." But actual quantitative ranges as you mention (e.g., that the L:W ratio of Acer lies within a certain range) are much more difficult to come by. Also, there are ways of quantifying leaves using all the shape variance present in their outlines, and I describe some of these methods below. By using quantitative methods such as these, you can avoid the trap of a subjective criteria that arbitrarily distinguishes leaf morphs by a particular feature. Plus, you won't be biased by using a particular shape attribute, as you will be measuring the entirety of shape. Use of these various methods though depends on the species you are studying.

Oreotrephes I think is on track saying that, if possible, you should build your own diagnostic criteria for whatever system you are working in. You mentioned certain "ranges" that can diagnose a species ... this is a critical question. Measuring intra-genotype/individual variance in shape for your system is critical. Which leaf to measure for a species? ... i.e., shoot position, developmental age of the leaf, if working with compound leaves, the placement of the leaflet along the proximal distal axis of the leaf, what about heteroblasty (changes in leaf form at different nodes), leaves from lateral vs. main branches, environmental effects on leaves (e.g. sun vs. shade leaves)?

For tomato, I measure shape quantitatively using Elliptical Fourier Descriptors, which reduces the shape of an object to a series approximation and explains variance with a Principal Component Analysis. I use the resulting Principal Component values of leaves as a trait and explain shape quantitatively that way. A very useful program to perform Elliptical Fourier Descriptors is described in Iwata & Ukai 2002 and can be downloaded here. In Chitwood et al 2012, I describe how to perform shape analysis on tomato leaves, separating components of shape based on genotype (e.g., by species), by position in the leaf series (heteroblasty), the ontogentic age of the leaf, and placement of leaflets along the proximal-distal axis.

Other easy ways to measure shape: Circularity, solidity, L:W ratio (or aspect ratio) as you mentioned. All very easy to measure in ImageJ!

You mentioned Acer leaves, which piqued my interest because I study differences in the shape of grape leaves. But like grape, many Acer leaves are palmately lobed. If every one of your samples has certain features (e.g. 5 lobes and 5 sinuses as in Acer, including petiolar sinus) then you can perform a landmark analysis using a Generalized Procrustes Analysis (The "Shapes" package in R is useful for this analysis).

Using global methods to describe shape, that is, methods to quantify the totality of shape variance, are critical to distinguish leaves. It may very well be that two leaves are so similar from different species that they are not statistically separable by shape! Be creative in the ways you measure shape, and if need be, create your own system for doing so!

 Chitwood DHD, Headland LRL, Kumar RR, Peng JJ, Maloof JNJ, Sinha NRN. 2012. The developmental trajectory of leaflet morphology in wild tomato species. Annu Rev Plant Physiol 158: 1230–1240.
 Iwata H, Ukai Y. 2002. SHAPE: a computer program package for quantitative evaluation of biological shapes based on elliptic Fourier descriptors. Journal of Heredity 93: 384–385.


On stochastic Lotka-Volterra predator-prey model

To interpret $a$ and $c$ as a birth and mortality rates is somewhat inaccurate, as $a$ and $c$, as written are density-independent rates that grow or shrink populations exponentially. If $a$ were negative, the prey population would shrink and most people would find a problem like that unexciting unless it was, say, a sink population maintained by immigration from another population. This is true of $c$ being negative, where the predator population would grow independent of the prey population. More accurately, $a$ can be interpreted as the difference between birth, $b$, and deaths, $\delta$; i.e., $a = b - \delta$. In this case, depending on the kinds of stochasticity being added to the model, negative $a$ is not just normal, but expected. The same is true for $c$. Ultimately, a perturbations like the white noise in this equation is simultaneously perturbing the difference between birth and death rates, which explains the negative difference.
The value of the rates seem to have the same interpretation if they are constant or are perturbed to an arbitrary magnitude.

I hope this helps!


4DGenome or another comprehensive database of chromatin interactions

This problem has been finally solved with help from prof. Kai Tan.
It occurred that his lab has been moved from University of Iowa to Children's Hopspital of Philadelphia, so has been this service.
Now, the working link is:
http://4dgenome.research.chop.edu


The relationship between the shape of the bacterial DNA and the blocking of replication machinery

This has been covered elsewhere (I highly recommend this page ) but it basically has to do with the priming of the strands and the fact that all polymerases work from the 5' prime to the the 3'. I made a quick schematic to illustrate (the explanation is below):

The priming is done with RNA during DNA replication in the cell, unlike PCR where you use DNA oligo's to prime. This RNA-DNA is called the Ozakazi fragments. After replication RNAse H will remove these primers leaving only DNA's and gaps. In the middle of the sequence the gaps can be filled in by the normal repair machinery but at the ends there is no 3' terminus to fill in the gaps. That is where the telomerase comes in and fill these gaps with a fixed sequence (also based on an RNA template but that is going into details).
If you have a circular chromosome there is always a 3' to complete the gap.


Short answer
Neurons, and in fact all cells in the body, utilize water-dissolved oxygen to fuel their energy metabolism.

Background
The brain, and tissues in general, obtain their oxygen through passive diffusion (Fig. 1). Water, carbon dioxide, and oxygen are among the few simple molecules that can cross the cell membrane by passive diffusion,  or osmosis (source: Estrella Mountain Community College).

The body uses hemoglobin to transport oxygen (Fig. 1), because passive diffusion would take too long, especially in oxygen-hungry warm-blooded animals like humans.

Gaseous exchange in fluid medium is mediated by hemoglobin. source: Kokyo


Evolution is a change in allele frequency through time. Alleles underlying moth melanism are changing through time in response to environment change, so indeed moths are evolving.

The environmental change is induced by human activities indeed. But the question of what is the cause of the environmental change causing the selection pressure is totally irrelevant to the question of whether there is such selection pressure.

Artificial selection is in essence the exact same thing than natural selection except that there is a goal (increasing milk production or making smaller dogs for example) that is decided by humans. In the moth example, the environmental changed is caused by human activities, but it has never been a goal for human to put selection pressure on moths to force them to change color. As a consequence, change in color melanism is an evolutionary process that is induced by natural selection, selection toward a new environment.

Evolution is not just the same thing as natural selection. The reason is that other mechanism than natural selection yield to change in allele frequency. One of them is genetic drift. You can have a look to this post to have a better understanding of what genetic drift is.

Hope that helps.


Why are X-linked illnesses less common in females if females have X-chromosome inactivation anyway?

Barr bodies (X-chromosome inactivation) don't form in the initial fertilized embryo — it's not that one X-chromosome is inactivated, and then that same inactivation is passed down to daughter cells. Rather, X-chromosome inactivation occurs on a cell-by-cell basis in differentiated cells.  Note how the accepted answer to the question you linked mentions that different cell lineages will have different X-chromosome inactivation patterns — in other words, inactivation occurs later in the differentiation and proliferation processes than I think you might be assuming.

To use your example: the liver cells do not all derive from a pluripotent (undifferentiated) cell with one inactivated X-chromosome, but instead derive from said pluripotent cell, and then undergo X-chromosome inactivation.

Although the jury is out, scientifically speaking, on the mechanisms of selection of the X-chromosome to be inactivated, it's been postulated that some sort of decision-making may occur on this cellular level, resulting in a higher likelihood of inactivating the damaged or deleterious chromosome, if one is present.

Regardless, as the accepted answer to the question you linked mentions, the 50% of functional cells that would result from chance or random X-chromosome inactivation tends to be sufficient for the body's needs.


Why do red muscle fibres have more mitochondria than white muscle fibre but less ATP than White muscle fibres?

This is because of the difference in mitochondrial protein expression of red and white muscle fibres. There is difference in posttranslational modification, which leads to functional difference as red muscle contraction is slow, and white muscle contraction is rapid.

Metabolic control in mitochondria contributes in speed of activity and cellular energy production. So, these differences effect the cellular energy levels in both white and red muscle fibres.

Following factors also contribute to the ATP production:
White muscle mitochondria have higher proton leak.
Red muscle contain high palmitic acid and oleic acid, but white muscle possess more phosphate ions.
Collagen and elastic fibers are largely distributed in red muscle mitochondria, whereas high titin levels and densely packed sarcomeres are present in white muscles. Whereas high levels of long sarcomeres are present in red muscles.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118618/

https://www.hindawi.com/journals/bmri/2018/5816875/


Why can't we defibrillate the heart within 1 minute after ventricular fibrillation by electroshock?

To say that there is a cutoff of one minute at which time shocking becomes ineffective is incorrect. The best way to defibrillate a heart within one minute of VFib onset is with electric shock. In fact, short of certain drugs in certain instances, it's the only way to defibrillate Vfib, regardless of the amount of time that has passed.

If the one minute cut-off were true, survival rates of out-of-hospital arrests would be more dismal than they are. Even with the availability of automated external defibrillators (AEDs) to treat out-of-hospital arrest, the collapse to response time is well over a minute. Someone has to notice a collapse, feel for a pulse, and call for a defibrillator (or get it themselves), expose the chest, apply the paddles, wait for the monitor to display the rhythm, clear the area and shock. If you were told that this usually occurs in under a minute, you were misinformed.

Seattle is the best city in the US (probably the world) in which to have a heart attack.[1] The population has a high rate of training in CPR, a highly trained corps of paramedics and EMTs, and a quick response time. So it's logical to do studies about factors affecting survival of out-of-hospital arrests in Seattle.
A study published in 1999 found that CPR did not have any effect on outcomes of out-of-hospital arrests unless the interval time (from arrest to defibrillation) was greater than 4 minutes.[2] (In other words, shocking without CPR was no different in outcome than shocking preceded by CPR; both resulted in cardioversion to a stable rhythm and a return of of spontaneous circulation in the same percentage of patients.)

However, that is not to say that CPR (chest compressions +/- respirations) are unimportant. A 2003 study found an unacceptable level of CPR was performed when AED paddles were connected (i.e. there was an over-reliance on shocking).[3]

The new Advanced Cardiac Life Support guidelines call for CPR to be initiated immediately, regardless of witnessed or unwitnessed arrest (i.e. down time).[4] It needs to be noted, though, that this recommendation does not rest on defibrillation with the aim of return of spontaneous circulation(ROSC), but on improved neurological outcomes.[5] This, not ROSC, is what the new ACLS recommendations are based on, because ACLS is not considered highly successful if the patient leaves the hospital only to be hospitalized elsewhere in a persistent vegetative state.

[1] King County may be the best place to have a heart attack
[2] Influence of Cardiopulmonary Resuscitation Prior to Defibrillation in Patients With Out-of-Hospital Ventricular Fibrillation
[3] Interruption of cardiopulmonary resuscitation with the use of the automated external defibrillator in out-of-hospital cardiac arrest
[4] VF/Pulseless VT
[5] Delaying Defibrillation to Give Basic Cardiopulmonary Resuscitation to Patients With Out-of-Hospital Ventricular Fibrillation A Randomized Trial


Should corn be considered an invasive species in the Midwest?

I agree with commenter Bryan Krause in that this question requires opinion -- but I think it only requires opinion as to the definition of what we consider "invasive".

The concept of an "invasive" species is highly contested among biologists. It is often used interchangeably with the terms non-native, non-indigenous, and alien.

Some people think we should consider a species as 'invasive' even if it is native to the region but is causing "economic or environmental harm or harm to human health". For example, the USDA considers Juniperus virginia a native species, despite its spread from plantings and its economic and ecological impacts in 'invaded' regions.


What is the name of this black-ochre striped snake?

Great find!  Based on the picture and location, I believe this is the Corsican grass snake (Natrix natrix corsa).  It is a pretty rare subspecies, and is listed on Annex IV of the European Union Habitat and Species Directive.  Worth mentioning that it's nonvenomous.

Photo cred to Frank Deschandol/Philippe Sabine

Unfortunately, I was not able to find too much more info on this subspecies.  I know Natrix natrix are pretty widespread throughout Eurasia, but this subspecies is much more restricted.


Does arterial blood always flow away from the heart?

Simple answer, yes.

It really is a matter of how technical you wish to be. By defintion, all arterial flow conveys blood away from the heart. The largest arteries exhibit the Windkessel effect which allows for the compression-based effects that bobthejoe inferred. Explicity, as blood is pumped out of the left ventricle, it stretches te aorta, and this tension in turn causes compression on the artery and pushes blood forward. On the flip side, venous vessels (except the pulmonary vein) return blood to the heart, but here you are likely to encounter local areas of reverse flow. This is counteracted to a degree by one-way valves present in the large veins to keep the net movement of blood in the body always toward the heart.


Dried grains are very mostly viable means they are in a dormant state until and unless suitable condition are provided. More dried it will be viable for longer.
In fact there are seeds found in Siberia which are ~32,000 years and still viable.

Courtesy: National Geographic
Source:
US Emergency Supply: Introduction to Seed Viability


Do restriction enzymes on read 3' to 5'?

Whatever sequence (plus direction) is target, so enzyme will cut. In your example "correct" and "antiparallel" sequences are two different sites.

Actually, your example of 5'-CTTAAG-3' is cut by AflII enzyme.


Is using Hidden Markov Models to find homologues sensible in abstract, short sequences?

TMHMM is a very good standard on predicting the TMHs in the first place, so it stands to reason that predicting homologues using this approach is completely viable.


We can look at the list of amino acids on wikipedia for a start. And we can look at this L-alanine:

What makes your image confusing is that it's a Fischer Projection, and I hate those because you have to remember what way the stereochemistry goes. In Fischer Projections, vertical lines face away from you, while horizontal lines face towards you. So if we convert the L-alanine I provided to a Fischer Projection, first we have to rotate the alpha carbon to put the methyl side chain in line with the rest of the carbon backbone. Now we look at the alpha carbon with the NH2 and H looking at us to create the Fischer projection. Here, the amine is on the left, not the right. You drew the amine on the right, which would give you the opposite orientation. If your professor had the amine on the right, I think he was wrong.

Additionally, the D vs L nomenclature is confusing. I prefer the S vs R nomenclature because that's what I was taught for molecules in general. Most amino acids fall into the S configuration, but cysteine is an R, because the sulfur atom has higher priority. However, cysteine is still an L, and the amine would still appear on the left in the Fischer Projection. This is why biologists stick to D and L for amino acids.