Can neurons be inhibited with electric current?

Yes, but maybe not how you think.

It is important to recognize that voltages refer to potential differences. When we say the "a cell is at -65mV" for example, we mean "The potential difference across the cell's membrane to the extracellular space is -65mV." When you stimulate electrically, you create a transient electric field, whereby the extracellular space is no longer effectively isopotential.

Let's imagine for the sake of some neuron that this field strength is on the order of 40 mV across the membrane. If this electric field is perpendicular to some neuronal process, the voltage across the membrane will be about -105mV on one side, and -25mV on the other side. The -25mV side is now depolarized enough to open voltage gated sodium channels, and some current is flowing into the cell. Once the shock has passed, positive current will continue to flow through those open channels and open more channels. It doesn't matter much that the other side is transiently at -105mV, all that matters is that you opened a bunch of voltage gated sodium channels which starts a positive feedback loop.

Therefore, transient electrical simulation will almost always be excitatory. There are two exceptions:

1) Neurochemical inhibition. If you excite a particular brain region that is specifically inhabited by inhibitory projection neurons, you will primarily excite those inhibitory cells and therefore cause excitation elsewhere. Of course, in this case, the electrical stimulation itself is still directly exciting cells, they just happen to have inhibitory effects elsewhere.

2) Depolarization block. If you continually stimulate the same population of neurons with a high-frequency stimulation, you can put neurons in a state called "depolarization block." Voltage-gated sodium channels have a chance to inactivate whenever they are activated. If you inactivate enough channels, there aren't enough available to produce an action potential. Therefore, if you can keep a cell pretty much constantly depolarized by continually stimulating, you can prevent action potential propagation because too many of the voltage gated channels in the axon initial segment are inactivated.


Who were "Dawson and Wilson" (mentioned as authors of an embryonic postmortem examination method)?

This article (A Note on the Staining of the Skeleton of Cleared Specimens with Alizarin Red S) looks to be the one by Dawson.

Update: I think the Wilson your text is referring to is James G. Wilson, an important researcher on terathology. I can't find any reference to a single article, though.


Do we see protocells forming in nature today?

we don't think so, some parts are easy. liposomes form all the time, and can be created in lab quite easily. They quite readily encapsulate any material present when they form, including DNA. So once you have the right stuff (likely RNA) it is very easy to enclose it in a lipid bilayer.

RNA has been formed from scratch in a lab it is even easier than we thought it would be. It may form in nature today but is unlikely , the current atmosphere is very oxygen rich and bacteria are not just willing to eat RNA but also basically all the chemical building blocks as well so it is difficult to build up a concentration of the precursors in nature today.

Worse evidence of it forming today would be ridiculously difficult to demonstrate because there is a constant contamination of biologically produced RNA from decaying organisms. There is basically no place on earth today with liquid water that does not have life in it.

Here and here is a review of our current models for the origin of life, Be warned the first link is a file.There are many steps involved to get a cell but it all starts with the first molecule capable of making copies of itself.

Forming self catalysis strands in a lab would be the best evidence but has one major problems, Money. Earth had an ocean sized laboratory and millions of years to stumble one of the strands with one of the right codes through random chance (remember a self-replicating code only has to happen once) which likely could only be duplicated by doing millions or even billions of identical laboratory experiments.

Finally while the Urey-miller experiment was historically important it is by no means the best nor most modern experiment you can find much more information about the variety of experiments at this question.


Is hands-only CPR as effective as traditional CPR?

The wikipedia page for CPR actually goes into some detail on this, going to block quote the section here for ease of access,

Compression-only (hands-only or cardiocerebral resuscitation) CPR is a technique that involves chest compressions without artificial respiration. It is recommended as the method of choice for the untrained rescuer or those who are not proficient because it is easier to perform and instructions are easier to give over a phone. In adults with out-of-hospital cardiac arrest, compression-only CPR by the lay public has a higher success rate than standard CPR. The exceptions are cases of drownings, drug overdose and arrest in children. Children who receive compression-only CPR have the same outcomes as those having received no CPR. The method of delivering chest compressions remains the same, as does the rate (at least 100 per minute). It is hoped that the use of compression-only delivery will increase the chances of the lay public delivering CPR. As per the American Heart Association, the beat of the Bee Gees song "Stayin' Alive" provides an ideal rhythm in terms of beats per minute to use for hands-only CPR. One can also hum Queen's "Another One Bites The Dust", which is exactly 100 beats-per-minute and contains a memorable repeating drum pattern. For those with non cardiac arrest and people less than 20 years of age, standard CPR is superior to compression-only CPR.

The American Heart Association has assembled some efficacy testing studies in the following review article, Hands-Only (Compression-Only) Cardiopulmonary Resuscitation: A Call to Action for Bystander Response to Adults Who Experience Out-of-Hospital Sudden Cardiac Arrest. Importantly, the human clinical studies reported no significant difference between those who received conventional cpr and those who received compression-only CPR. Some animal efficacy studies are noted, and with respect conventional CPR, the animals that didn't receive "rescue breaths" experienced a lower survival rate. In the end they note some limitations to hands-only CPR:

"...raised concerns about the possibility that recommending hands-only CPR for witnessed sudden cardiac arrest will, in fact, increase the complexity of decision-making for bystanders or that unresponsive victims of noncardiac medical emergencies (eg, drowning, drug overdose) will not receive rescue breathing."
"There may be situations in which ventilation alone could be life-saving but is not provided. There may be an interval after cardiac arrest when ventilations become absolutely critical for survival."

And as to the content in the second paragraph of the original post,

"It is important to acknowledge that during cardiac arrest without lung inflation and ventilation, there is a continuous decrement of blood oxygen saturation. At some point in time, the possible hemodynamic advantage conferred by continuous chest compressions (without ventilations) will be offset by this reduction in oxygen saturation, and the ultimate result will be a compromise in oxygen delivery. One porcine cardiac arrest study (3 minutes of untreated ventricular fibrillation, then 12 minutes of CPR) suggests that after 4 minutes of continuous chest compressions without rescue breathing, the delivery of 2 rescue breaths every 100 compressions provides a survival advantage over chest compressions alone."

The paradigm, again, is that hand-only CPR provides opportunity to get some help, other than no help at all, but the review also notes that more clinical data is needed on all fronts.


Mitogen-activated protein kinase (MAPK) is a generic name for a family of different but related enzymes involved in this specific signalling cascade. RAF is a MAPKKK, MEK is a MAPKK and ERK is a MAPK. This is evident in the Nature article from which your image is apparently adapted:

  Activated RAS triggers the activation of the MAPKKK RAF. Activated RAF then phosphorylates the MAPKK MEK (MAPK and ERK kinase) on serine residues leading to its activation. Subsequently, activated MEK catalyses the dual phosphorylation of the MAPK ERK.


What effect do oligosaccharides, like those found in legumes, have on the composition of intestinal flora in humans and if so how so?

The answer to this is fairly complex, and it depends on whether you are talking about short-term or long-term changes to the microbiota.

When talking about short-term changes, the answer is almost certainly a resounding yes. Any ingested nutrient will lead to an increase in the growth rates of bacteria capable of metabolising that nutrient, and will therefore lead to a change in the composition of the intestinal microbiota.

This is, unfortunately, difficult to observe, as most studies of the intestinal microbiota use fecal samples to look at intestinal microbial composition. Since stool represents an average of what happens between two bowel movements, it is difficult to draw inferences about short-term changes in the microbial composition of the bowel. However, there is evidence from Pythons that suggests extensive remodelling of the microbial composition does indeed occur, at least in animals with less regular feeding schedules.

In the case of long-term changes, there is strong evidence that specific oligosaccharides contained in human milk specifically select for certain strains of Bifidobacterium and Lactobacillus. Apart from this very specific set of oligosaccharides however, there is a paucity of studies dealing with the effects of diet on the gut microbiota, and even fewer looking at specific nutrients.

The premise that long-term changes to the gut microbiota can be made with diets is the foundation on which the entire prebiotics industry is built. The most popular prebiotics are fructo-oligosaccharide, inulin, galacto-oligosaccharide and lactulose. These are said to encourage the growth of beneficial strains of Bifidobacterium and Lactobacillus. However, there is currently no consensus on the long-term effects of these oligosaccharides on the microbiota.


How can a homozygous mutation, considered pathogenic, occur on a gene such as HFE without the disease developing?

What happens when you have a homozygous mutation on a gene (eg. a swapped base), that is considered pathogenic, but without developing the disease?

It may be an example of incomplete penetrance of variable expressivity. Simply, you are probably dealing with a complex trait in which either more than one gene is involved, or there is interaction between genetics and envronmental factors.

  Also, what happens when heterozygous mutations develop the disease? In these cases why does the healthy version of the gene goes "quiet"?

I assume you are still talking about a putatively recessive disease. One possible explanation is haploinsufficiency, i.e. the WT allele alone doesn't produce enough transcript and the heterozygous individuals has "problems"

  One example is HH caused by HFE gene mutation (mostly C282Y and H63D), and not everyone develops the disease, doesn't matter if they are heterozygous or homozygous.

And indeed HH is an excellent example of complex disease, in which genetics is involved, but the inheritance is not purely Mendelian.


The IHH gene encodes the Indian hedgehog homolog protein, a member of the family of hedgehog proteins that  regulates bone formation. The ihh-/- notation represents an animal which is homozygous for a null mutation in the gene (i.e. the animal has no functional IHH gene).


Can light function as a neurotransmitter?

I don't think there is a theoretical reason why this wouldn't be possible.  However, I think there might be some practical problems with a system that relied upon light signaling.

1) It would be susceptible to interference.  Many bio-luminescent organisms are transparent, so other sources of light could depolarize a post-synaptic cell.  Light also penetrates tissue in organisms that are not transparent.  Blue light can penetrate 2 mm of human tissue and higher wavelengths like red can more than double that.  I could see light acting to replace signal molecules in quorum sensing though.

2) Neurotransmitters aren't really much of a limiting factor in nervous system speed. A monosynaptic reflex travelling a short distance might take 30 milliseconds, but neurotransmitter transmission is only 1 of those milliseconds.  In more complicated neural pathways, the speed of neurotransmitters might only account for 1/100th of the time.  So, if we're just imagining time-saving nervous system improvement, fiber optic neurons are the way to go.


Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage?

https://en.wikipedia.org/wiki/Concussion#Mechanism

We did not evolve in order to become knocked out. See the wikipedia link. The "water" in the head is designed to not make us get knocked out that easily. However each dampening system has a limit.


What are the function(s) of Alu elements in the cell?

Alu elements are a type of transposable element. They possess the means for their own duplication and movement.  Alu is a SINE-like element that is transcribed by RNA Pol III, and so a single DNA copy can make multiple RNA copies, each capable of inserting into DNA, so it's no wonder they have a very high copy number.  Here is a picture of one means of insertion http://www.nature.com/nrg/journal/v3/n5/box/nrg798_BX1.html, although there are likely others.

They do not have "a function" per se, in that they are not selected for, they are just rarely selected against and there are so many of them.  They do not add functionality, but rather are one half of the "war" between transposable elements and viruses versus the genome's evolution to mitigate the damage they cause.  They are, of course, commonly used as sources of new DNA for sequence evolution, or can be used to create transpositions or other chromosome rearrangements, but mostly they just fail to cause too much damage and so tend to accumulate in the genome.


How do the homologous chromosomes pair up and position themselves along the center of the cell?

There are many things involved in the pairing of homologue chromosomes.

Before mitosis can occur an important prerequisite must happen: the division of centrosome. This small complex is the principal microtubule-organizing center in the (animal and therefore human) cells. During interphase the microtubules originating from the centrosome, project to the cell perimiter with their + ends (this where they grow). At the beginning of mitosis the duplicated centrosomes separate and migrate to oppsite sites of the nucleus to form the poles of the mitotic spindle. As the nuclear envelope disintegrates the spindle captures the chromosomes at the cetromeres. Since the microtubules are growing from the centrosomes this capture eventually pushes the choromosomes to center. Source: The Molecular Biology of the cell. Fourth Edition. ISBN: 0-8153-3218-1 (hardbound) 0-8153-4072-9 - (pbk).
A searchable online version: http://www.ncbi.nlm.nih.gov/books/NBK21054/

I've found a few good articles with many details:

Current Biology, Volume 12, Issue 17, 3 September 2002, Pages 1473–1483
The Dynamics of Homologous Chromosome Pairing during Male Drosophila Meiosis
Julio Vazquez, Andrew S Belmont, John W Sedat

and
Homologous pairing and chromosome dynamics in meiosis and mitosis
Bruce D. McKee

I took a quick glance at the above mentioned articles, and it seems that homologous chromosomes tend to be close together (paired if you wish) during interphase most of the time.


Some spiders are known to eat their own silk when breaking down a web and reconstructing it (https://en.wikipedia.org/wiki/Spider_web#:~:text=It%20is%20common%20for%20spiders) or even stealing the web of other spiders and eating it (https://frank.itlab.us/photo_essays/papers/Argyrodes_kleptoparasite_spider.pdf). It may very well be that some types are able to digest various silks or other fibres. I'm not aware of any studies that test whether a spider could digest - say - wool or other natural fibres.
If your sheets were silk or other natural fibres, it's feasible that their digestive juices were strong enough to break down your fibres. Who knows, maybe their digestive juices are even strong enough to break down synthetic fibres (unlikely, but I don't know any study that has looked at that).


Strategy for tree and shrub identification

Species ID books with pictures, or photos, will generally never be comprehensive enough to include all species, although with some there will be additional information it the text that will give details about other related species, varieties, hybrids or cultivars.

Importantly look for ID books that include an ID key, generally at the start, and learn how to use it. They are usually accompanied with a good explanation of how it works.

The key takes the form of

  Does it have this...?

  If it does go to [3]

  If it doesn't go to [7]

And so on, making successive distinctions until you end up with the species.

They can take some getting the hang of, and you need to know the botanical terms that they refer to.

Also importantly, if you don't already have and use one, you must have a decent hand lense, or magnifying loupe, that you take with you everywhere. Often the deciding features can only be properly be assessed when looking close up, and you need to get to know what the species you are familiar with look like under the lense.

An experienced ecologist friend, an expert in flora and fungi, has a couple of books that have no images in at all, it is just the species ID key, that he takes with him when he is surveying. Granted he already knows his species very well, but you can't remember everything all the time and so you need a book that can tell you the final distinguishing features, even if it is text.

But again a hand lense is a good place to start. My favourite is an Eschenbach 10/40 Pocket hand-held magnifier from Germany http://www.eschenbach.com/cdd40611-ceda-4188-a5c3-882565859296/products-hand-held-magnifiers-pocket-detail.htm

Someone gave this site http://dendro.cnre.vt.edu/dendrology/syllabus/key/key1.cfm?state=&zone= as a good resource for trees in the US


Where does vasoconstriction occur in limbs?

Vasoconstriction is a phenomenon that can be caused by many factors, from mechanical events (such as stretching) to hormones (epinephrin, neurepinephrin, angiotensin ...). But no matter what is the cause, the end-result is an increase in intracellular calcium concentration in smooth muscle cells (which compose the arteries and veins). So it seems that constriction does not happen in specific points but rather all along the limb. Furthermore angiotensin receptors are found in high concentration in smooth muscle cells [1], suggesting that every such cell has the ability to change it's morphology in order to induce vasoconstriction.

As for your second point, I think the response is as much endocrinological as neurological, since it involves both peripheral and central regulations. (Well, as a side note, endocrine systems rarely have no interaction with central ones).

Angiotensin receptors : distribution,
signalling and function


How does a single-stranded RNA bind to a double-stranded DNA to form a "triplex structure"?

DNA-RNA triplex formation is well-documented. It was originally analysed in simple model polynucleotides where the DNA has a polypurine strand and the RNA has a polypyrimidine, e.g.

rCCCCCC
dGGGGGGGGGGGGGG
dCCCCCCCCCCCCCC

rUUUUUU
dAAAAAAAAAAAAA
dTTTTTTTTTTTTT

but it is now known to occur in more complex sequences. One of the best studied examples is in the promoter of the human DHFR gene:

  Gee, J. E. et al.(1992) Triplex formation prevents Sp1 binding to the dihydrofolate reductase promoter. J. Biol. Chem. 267, 11163–11167

In this work the oligonucleotide GR19 was shown to bind in a triple helix to SpI binding site I in the DHFR promoter (CR19 was used as a control). Triplex formation was detected by gel shift, and the specificity was confirmed by DNase I footprinting.

This effect is part  of the regulation of DHFR - the transcript from a minor upstream promoter binds to the major promoter, see:

  Martianov, I. et al. (2007) Repression of the human dihydrofolate reductase gene by a non-coding interfering transcript. Nature 445: 666-670

The structure of these triple helices involves a combination of Watson-Crick base pairing in the DNA duplex together with Hoogsteen base pairing in the RNA-DNA interaction:

Figure taken from:

  Morgan, A. R. & Wells, R. D. (1968) Specificity of the three-stranded complex formation between double-stranded DNA and single-stranded RNA containing repeating nucleotide sequences. J. Mol. Biol. 37, 63–80


What are the physiological effects of retinal exposure to 380–400nm light?

Answering my own question after thorough research:
Definitions
First, I noticed that there is no consensus on where the UV spectrum ends and the blue portion of the visible light spectrum begins.
According to the WHO, as well as to most other sources, the UV spectrum covers the wavelength range 100–400nm (1). However, a few other sources, notably the SCENIHR, define visible light as starting at 380nm (2), hence UV light would be 100–380nm.
Another source, the ICNIRP, directly mentions that the boundary is not clear-cut, “the band 315 to 380–400 nm is designated as UVA” (3) . At least one source refers to the 385–405nm band as the “UV/Visible Radiation Boundary Region” (4).
Tinted Lenses
To address the part about the dark tint of lenses causing pupil dilation, it is first worth noting that not all lenses that filter out UV light have a dark tint.
In fact, clear lenses can actually offer up to UV400 protection (5). There is even some research specifically on UV protection by clear lenses (6).
Back reflection of UV light
UV380 and UV400 are not the only eyeglass specifications relevant to UV protection. There is also eye-sun protection factor (E-SPF®), which was introduced in order to also account for back reflection of UV light from eyeglass lenses to the eyes (7). Therefore, this back reflection should also be taken into account when examining the effects of 380–400nm light exposure on the eye.
The 380–400nm Band
Now let’s get to answering the question.
According to the Texas Technical University Health Sciences Center, 40% of the radiation harmful to our eyes falls within 380–400nm, which they call the “UV protection gap” (8). Another source states that, while 100–380nm light is “very harmful”, 400–460nm blue light can still cause retinal damage and macular degeneration (9). The American Optometric Association also states that blue light, which they define as the range 380–500nm, may cause eye damage (10).
An article by ZEISS Vision Care explains that the UV380 standard was a “pragmatic choice” by the ophthalmic industry, and does not reflect “biomedical realities” (11). The article refers to the 380–400nm spectrum as the “most intense portion of solar UVR on Earth”. I assume the author is referring to the physical definition of intensity of radiant energy, which is the power transferred per unit area, however I am not 100% sure that this is the intended meaning of “most intense”.
I also found an article claiming that the WHO recommends UV protection up to 400nm (12), which again implies that 380–400nm does cause significant retinal damage. However, I couldn’t find the actual WHO publication stating the recommendation.


Which monkey species features two distinct male phenotypes?

Patas monkeys exhibit "sneak mating" where a male other than the resident male sires offspring. Resident males do sire more offspring than sneaker males, but both strategies do co-occur. I'm pretty sure there are other species that have a similar mating strategy as well.


Has an ectopic pregnancy's blastocyst ever been made to implant?

Not in an independently confirmed case.

A paper was once published claiming this was performed successfully:

Pearce JM, Manyonda IT, Chamberlain GV. Term delivery after intrauterine relocation of an ectopic pregancy. Br J Obs Gynaecol. 1994; 101:716–7.

This article and several others by the same author Malcolm Pearce were found to be fraudulent and were retracted:

Lock S. Lessons from the Pearce affair: handling scientific fraud. BMJ. 1995; 310(6994):1547-8.


What biological process was taking place?

As outlined in my comment, I hypothesise it must have been the growth of exothermic bacteria. As the name suggests, these produce heat. An especially interesting phenomenon concerns the danger of fire erupting from moist hay, as the bacteria feed from it and dry it simultaneously! This is outlined here. A memorable quote from that article:

  Dry hay (stored at 15 percent moisture or less) is safe for long-term storage. However, if the hay has become wet the quality has been permanently changed and the potential fire hazard from spontaneous combustion increased.

The same principle underlies the heating of compost, about which you can read in greater detail here.

Most astounding I found the post dealing with the possible contribution of exothermic gut bacteria to our thermoregulation.

As of now, I don't know about the basic mechanisms by which these bacteria generate heat, but the abstract of this article implies that heat absorbing bacterial growth is extraordinary.

I myself have forgotten everything about chemistry, but from the comments below I gathered that what happens is similar to the oxidations of sugar. You can read examples here, which demonstrate that these are exothermic.


How does laser surgery correct accommodation problems?

Overview

Laser eye surgery works by altering the shape of the cornea.  The cornea works together with the lens to focus rays of light onto the retina.  The cornea accounts for two-thirds of the optical power of the eye (1) (i.e. the eyes capability to focus light), however unlike the lens is of fixed power. It is the lens that changes is shape by the action of suspensory ligaments and ciliary muscles in order to focus light by the correct amount depending on how far away the light originated from (and consequently the angle of incidence with the cornea).  I'm sure that you are aware of all this, however for the benefit of future readers this is fully explained diagrammatically on this webpage.

Specific Conditions

Three forms of accommodation problems can be treated by laser surgery:

Hypermetropia (long-sight) is where light focusses behind the retina:

Laser treatment is used to make the cornea thicker, resulting in a greater degree of refraction of light and correction of the focus.

Myopia (short-sight) is where light focusses before the retina:

Laser treatment is used to make the cornea thinner, resulting in a reduced degree of refraction of light and correction of the focus.

Astigmatism is where the cornea is not the correct shape - it is closer to a rugby ball rather than the sweeping curve demonstrated in the first diagram.  This results in multiple focal points therefore a blurred image.

Laser eye surgery is used to alter the shape of the cornea until it is more normal.

Presbyopia is an age related condition where the lens becomes more rigid and is less able to change its shape to accommodate the light.

As this is a problem with the lens rather than the cornea, it can not be treated with laser eye surgery.  It must be corrected with glasses, as shown in the above diagram.

(1) Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.


Could we detect GMO foods if there were no samples to compare with?

[G]iven two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

No, you can't distinguish them without knowing a priori the DNA sequence of the wildtype and of the GMO. There is no other mark left within a GMO in the general sense.

Of course, one particular GMO is created with one particular goal in mind. One particular phenotypic effect. If you detect the phenotype of a GMO, then you can recognize it. For example, if you make a GMO tomato that produces a new type of pigment, you can, of course, recognize it by the presence of this pigment! However, there is no general attribute of being GMO that you can recognize. You need to look for something specific that you know about a specific GMO (or specific wildtype).

There are also phenotypic traits that you find (quasi) exclusively in GMO such as Cytoplasmic Male Sterility (CMS) for example. If you find CMS in a plant, then you can be pretty sure it is a GMO. But if you can't find CMS though, you can't be sure it is not a GMO.


(Bioinformatics) Protein-Protein Software Prediction

This review about protein docking will hopefully get you started.

Xue, L. C., Dobbs, D., Bonvin, A. M., & Honavar, V. (2015). Computational prediction of protein interfaces: A review of data driven methods. FEBS letters, 589(23), 3516-3526.

There is a page where they provide a short description about the different algorithms used, as well as links to the web servers. I also believe that most of these website should have a downloadable source code that you could compile and use on your own computer/cloud.

Here is a brief summary of the main methods highlighted by the paper:

Homology-based methods. In this approach, biological properties of a query protein are inferred from its homologs. The assumption here is that homologs share significant similarity in their sequence, structure and functional sites. Therefore, this approach performs best when close homologs are available.

Template-free machine learning methods. In this approach, machine learning algorithms are used to classify a target residue as either interfacial or non-interfacial, based on properties of both the target residue and the neighbouring residues. This approach is best used if there is limited availability of homologs, or when templates are not available or of poor quality.

Conclusion: If you have the sequence data available, then the 2nd approach seems most appropriate. You could also apply both methods and see the extent of agreement/disagreement between the methods, i.e, you could use the machine learning approach to detect the interfaces, and subsequently validate your docking predictions based on sequence data, if close-enough homologs are available.


Saccus simply means sac or bag and is is closed cavity. The lymph nodes develop from the structures, see this image:

Superior cardinal vein (jugular vein)
Jugular lymphatic sacs
Right subclavian vein
Axillary lymphatic sacs
Left brachiocephalic vein
Thoracic duct (bilateral)
Lumbar lymphatic sacs
Iliac lymphatic sacs

The image is taken from this webpage, which should be interesting for you.


Why does cold kill humans but not bacteria?

Let's look at what happens when a single cell within a cell wall freezes. We end up with a little drop of ice, within which are encased all the cellular structures. Thaw this ice, and all is well - provided neither freezing nor thawing happen too rapidly.
Now take what happens in a human being.
First, the blood in the extremities gets colder, and cools the interior somewhat. But we have mechanisms to conserve heat in the core, at least for a little while. This doesn't help the extremities much. If the blood freezes there, we get frostbite - the tissues die for lack of blood supply. Fingers and toes and the end of the nose, and other extremities, are compromised.
Now let the core temperature drop. Below a certain temperature, conduction in the heart slows and eventually stops. This is fatal.
There are many other effects, all of them related to the relative vulnerability of different tissues to cold. Freezing is generally bad for animal cells, which will rupture because of the mechanical effects of the expansion of water as it forms ice. Frozen body fluids can't do their jobs. Frozen nerves can't conduct impulses, so muscles won't contract once their temperature drops below the shivering point. And so on.


Prevalent large (>=90kDa) maintenance protein/loading control

Vinculin!  I love our grad-students, I can't believe I didn't think of it last night.

Also, awesome chart, even if it's from a company.


It depends upon exactly what you have done.

The standard way of using a yeast intergrating plasmid (YIp) is for it to integrate into the genome by recombination between a piece of yeast DNA that the YIp carries and the same DNA in the genome. This is often, but not necessarily, the selectable marker. So for example a YIp carrying the URA3 gene as its only yeast DNA will integrate at the URA3 locus (probably mutant to allow selection for Ura+, so more correctly ura3).

If the YIp is linearised by cutting at a site within the URA3 marker this will direct insertion and will increase the transformation efficiency.

Once insertion has taken place, the configuration at the integration site is:

chromosome...URA3...other YIp sequences...ura3...chromosome

This is inherently unstable because a looping-out event can take place via recombination between the URA3/ura3 regions. So removing selection means that you run the risk of losing the insert. Furthermore, it is possible for looping out to occur leaving the URA3 allele behind instead of the ura3 allele. So you can lose the vector even when selection is maintained (but this will depend on the exact nature of the mutation).

More complex configurations are possible where the targetting sequence is separate from the selectable marker, and where digestion removes a whole chunk of the targetting sequence before transformation. So for example if the TRP1 gene was used for targetting a plasmid with the URA3 marker in a TRP1 ura3 strain you would get:

chromosome...TRP1 fragment A...URA3+other YIp sequences...TRP1 fragment B...chromosome

the resulting transformant is now Ura+ because of the integrated URA3 plasmid, but some TRP1 DNA is now missing (the DNA that was excised when the plasmid was digested) so the strain is trp1. The appearance of this Trp- phenotype indicates that the transformation has probably occurred by the pathway described.

In this case the inserted plasmid is much more stable because those two remaining fragments of TRP1 DNA are not identical, so there is no possibility of looping out.

In summary, if your transformant has the insert carrying the "new gene" flanked by a repeating sequence then it is unstable, otherwise it is ok to remove selection. In the first case, if the new gene is at all deleterious then there will be a strong selective pressure in favour of cells which have lost the insert.

Addendum

You can avoid using YIp plasmids altogether by integrating your new gene at any locus using long targetting primers, as shown in the Figure below.

Design primers to amplify your gene as usual, but synthesise them with 40 bp 5' extensions corresponding to two sequences at the extreme ends of the integration site (URA3 used here for illustration purposes). The resulting fragment can then be used in a transformation and will integrate at the URA3 site by homologous recombination, replacing the resident DNA. The advantage of using URA3 for this is that you can select for integrants as Ura- cells by resistance to fluoorotic acid (FOA). Although you can probably select directly for this, I have always co-transformed the fragment together with another selectable plasmid (LEU2, TRP1 etc., but not a CEN plasmid) Then your e.g. Leu+ transformants can be screened for those that have also become FOAR. This co-transformation happens at quite high frequency because the cells that do take up DNA take up a lot of it. Once you remove selection for the co-transforming plasmid it will soon get lost, leaving you with a clean non-reverting integrant.

It's been a while since I did this sort of thing - probably there are even smarter methods around now.


What's keeping living species from rotting?

One can calculate that there are more non-human cells (mainly bacteria) inside human body than there are actual human cells. Why those bacteria don't eat us from within? Epithelium is pretty good barrier between outer world and internal systems. It is essentially one-cell thick layer that protects internal organs and infrastructure. In cases when epithelium breaks, bacteria can get into blood stream and start very bad infection, which can cause necrosis (effectively, rotting, tissue decay). Natural cell death is fought by natural cell proliferation so that there are no gaps in defense layers.

Also one should not forget about immune system that is looking for invaders or anything that should be where it is. In healthy person immune response will close gaps in epithelium and kill bacterial infections pretty quick.

Dead people, as well as dead plants, have their skin and epithelium, immune system destroyed by cell death or infection. Then bugs start to eat vessels, tasty nerve tissues, muscle and cartilages, blood cells filled with proteins and everything eatable.


Can anyone identify this grey spotted insect -- is it a tree bug species?

This is one of the last instars of a bug nymph from the genus Erthesina (Family : Pentatomidae). There are two common species, but according to David Rider, the only species in India is  Erthesina acuminata (Source here, also for the image).

You can recognize it from other bug nymphs by its grayish colour and the distinctive orange patterns on its back. Also, the base of the last antennal segment (where it turns from grey to black) should be orange, but we cannot see it on the picture.

These bugs are phytophagous, and quite generalist. They are phloem-feeding insects that feed from leaves, stems and fruits of various species of trees.

Fore more proper classification and identification of Indian bugs, you can look at:

Ahmad, I., Memon, N., & Kamaluddin, S. (2004). A Revision of Hayline Stink Bug Genus Erthesina Spinola (Hemiptera: Pentatomidae: Pentatominae) and Their Clasdistics. Pak. J. Zool, 36, 285Ğ293.
Salini, S., & Viraktamath, C. A. (2015). Genera of Pentatomidae (Hemiptera: Pentatomoidea) from south India—an illustrated key to genera and checklist of species. Zootaxa, 3924(1), 1-76.


Presence of Aromatase enzyme in males : Result of Natural Selection

Estrogen has other functions in males; it is very misleading to attribute the ability in males to synthesize estrogen to effects on heart attack chances. The relationship between estrogen and cardiovascular disease risk is also very complicated, and current guidelines do not suggest estrogen replacement as a preventative treatment for heart disease.

A better explanation for increased male risk of heart attack might be the increased levels of testosterone, but the data on that are mixed as well.


Which fruit compounds affect the speed of fructose absorption?

Yes they do. The answer is glucose.

Let's begin at the beginning: you eat a piece of fruit. The fruit contains many different kinds of sugars, including fructose and glucose. One of the immediate effects your digestion of this fruit has is to raise the levels in your blood of every type of sugar that was present, and the blood levels of many other types of nutrients as well. This has nothing to do with how well your body does/doesn't absorb fructose, it is simply a normal step in digestion.

Next, GLUT2 transporters in the insulin producing cells in your pancreas import glucose. This acts as a signal that tells those cells to start producing insulin. Insulin then diffuses around the body and produces myriad effects, including upregulation of GLUT4  activity across the body. These GLUT4 transporters are present on cells in many parts of your body and are what are responsible for taking up most of the glucose from your blood.

Now on to fructose. GLUT5 is the main fructose transporter. Just like GLUT4, GLUT5 activity is also regulated by insulin, but in a less quick and dramatic fashion than with GLUT4. Although there's a large body of work showing that GLUT5 does not respond quickly to insulin, recent work has shown that, for example, high levels of insulin lead to increased GLUT5 activity in skeletal muscle over a period of 24 hours.

So if what your trying to get at is some reason why eating an apple is better for you than chugging an equivalent volume of Auntie Jemimah's pure corn syrup, it's always going to be some reason like this where you have co-metabolism of several nutrients that tend to show up together in "natural" food. It is unlikely that there are any complex plant substances that would be primarily responsible for the health benefit of fresh fruit in general.


too low extention time for Taq polymerase PCR

To get amplification of a DNA fragment you need primers to anneal first so that you can extend from. The extension time is designed so that DNA is synthesized from one priming site to the other. Therefore if you have a lower extension time you will make a product that is missing the other priming site. This means that all new template strands can be amplified from one end only and you get linear amplification, not exponential. Therefore there will be too little DNA to visualize on a gel.


Ethanol is not a problem, we use it without any further precautions and it seems to be RNAse free. You should take the usual precautions you should take with all chemicals when you work with RNA, never use a spatula or spoon to get anything out of the bottle (unless you want to bake your spatulas all the time), always pour them to avoid any contamination.

We autoclave the Eppis once, this might be an unnecessary precaution. I think you can also buy them certified RNAse free, but I'm not sure if they are actually treated any different or simply more expensive.


How is the type of genetic manipulation determined in CRISPR-Cas9?

But how do you get from double-strand breaks to editing genes in
  incredibly specific ways?

You should read the wikipedia page on CRISPR-Cas system. The target specificity is provided by the tracrRNA.

  How do you specify which kind of repair mechanism is invoked?

The repair can be done either by Non Homologous End Joining (NHEJ) or Homologous Recombination (HR). If you provide excessive DNA template by transfection then it is likely to increase the chance of HR and this can be used for trangenesis.

When no template is provided then DNA can be repaired by HR with sister chromatin or NHEJ. Depending on the stage of the cell cycle one of these mechanisms is preferred over the other. HR is shown to be the most active in S-phase and starts declining in G2-phase.

So when you want to make transgenics or specific edits then co-transfect CRISPR-Cas with transgene DNA (with flanks homologous to target DNA sequence) or a homologous DNA with point mutation(s), preferably in cells at S-phase. It is possible to synchronize the cells using nocodazole or other molecules that arrest cell cycle.


Why is Bcl2 a good target for cancer therapy?

Bcl2 is an anti-apoptosis protein, meaning that by inhibiting Bcl2 you will inhibit its anti-apoptotic effects. In other words, by inhibiting Bcl2 you actually induce apoptosis in cancer cells. This is one of those concepts in biology that can be hard to follow... that is, "by inhibiting an inhibitor you cause activation".

Cancer cells in particular seem to be resistant to the endogenous pathways in the cell leading to apoptosis, and the reasons for this phenomena are an area of active research. There are two major pathways of apoptosis within the cell, the extrinsic pathway the involves caspase proteins and the intrinsic pathway that involves Bcl2 and a number of other proteins associated with the mitochondria.

Bcl2 is part of a family of proteins that are involved in the intrinsic pathway of apoptosis - for a great and recent review see this recent review... or search on PubMed for a number of recent review articles.

Interestingly, cancer cells have a particular type of mitochondrial dysfunction that may be related to Bcl2, which is still incompletely understood. Cancer cells somehow inhibit the intrinsic apoptotic pathway, which involves the mitochondria. Additionally, cancer cells decrease aerobic metabolism by the mitochondria and preferentially use anaerobic metabolic processes instead - called the "Warburg Effect" by individuals in the metabolism and cancer fields. This was originally described by Otto Warburg almost 100 years ago - i.e. that cancer cells preferentially use anaerobic metabolism - but why this occurs is still unknown to present day.


Why is it called "Ebola virus disease", not just "Ebola" or "Ebola disease"?

This is now how new viral diseases are being named, possibly because one can have/carry a virus without having a disease (e.g. HIV, herpes simplex, etc.). It is not as uncommon as you think.

A bit of googling will turn up reputable sites which discuss the epidemiology of Hantavirus disease, Hendra Virus Disease, Powassan Virus Disease, Lake Victoria Marburgvirus disease, Lujo virus disease, Ross River virus disease, Nipah virus disease, respiratory syncytial virus disease, Kunjin virus disease, Chikungunya Virus Disease, Heartland virus disease, St. Louis encephalitis virus disease, West Nile virus disease, Eastern equine encephalitis virus disease, Western equine encephalitis virus disease, and California serogroup virus disease (includes infections with the following viruses: La Crosse, Jamestown Canyon, snowshoe hare, trivittatus, Keystone, and California encephalitis viruses) and others, but I'm stopping here.

Bacteria cause diseases, but many already had/have names: Typhus (Rickettsia typhi or Rickettsia prowazekii), Rocky Mountain Spotted Fever (Rickettsia rickettsii), Diptheria (Corynebacterium diphtheriae), Lyme disease (at least three species of bacteria belonging to the genus Borrelia), Pertussis/Whooping Cough (Bordetella pertussis), Tetanus (Clostridium tetani), etc.

Interestingly, I have started to see scholarly articles for Clostridium Difficile Disease, which was an entirely new name for what we used to call Antibiotic-Associated Diarrhea. So maybe there will be a shift in that direction as well; time will tell.

How diseases are named is another whole thing.


Nutrient agar as the medium for antibiotic susceptibility testing

The standard breakpoints used in clinical susceptibility testing (Kirby-Bauer/disc diffusion assay) are considered reliable when every part of the testing method is standardized. If you change any part of that standardized method without properly validating those changes, it may or may not affect the outcomes and there would be no way of knowing without some sort of comparison study for validation.
Difficulty obtaining the proper media would seem common enough that this exact problem has been studied. This study did a head-to-head comparison of nutrient agar (NA) and Mueller-Hinton agar (MHA) for susceptibility testing on 149 clinical isolates along with a few QC reference strains. They found that NA agar did not produce acceptable results for the QC strains according to the relevant Clinical & Laboratory Standards Institute (CLSI) guidelines. Use of NA also resulted in many errant determinations among their clinical isolates (including many isolates of Staphylococcus aureus).
Given the error rates in this study, I would say that you should not rely on susceptibility testing results using nutrient agar in any sort of clinical context.
Reference:
Nassar, M.S.M., Hazzah, W.A. & Bakr, W.M.K. Evaluation of antibiotic susceptibility test results: how guilty a laboratory could be?. J. Egypt. Public. Health. Assoc. 94, 4 (2019). https://doi.org/10.1186/s42506-018-0006-1


Visual and clear example of the idea that "animal doesn't need to understand the evolutionary function of its actions"

Use human behavior, they're human, do they understand why they like salty foods or why thiols smell bad to them. These behaviors still work even when you have no idea why you are doing them.

Using humans circumvents the problem of them not understanding animal behavior, which they already have to do to grasp your explanation for animal behavior. Using any other animal requires them to understand that animals mind which an entry level student will not, however as humans they can assess their own knowledge directly.


It looks like a passerine bird, but I can't really tell the species without seeing the whole body. As for what to do with it, your best course of action is to leave it alone. Trust me. Once placed tissue paper over a pigeon's eggs to keep them warm, and the mother crushed them when she landed on the nest because she didn't see the eggs.

If there are eggs in the nest, try noting down what color they are. Passerines have colored eggs.


Does the red blood cell in frogs undergo amitosis?

Unlike mammalian blood cells, blood cells in Amphibia are nucleated (as the paper in your link explains) and can perform cell division (here is an old paper from Acta Haematologica, 1954: https://www.karger.com/Article/Pdf/204534).

Your question is: is this division a regular mitosis or the so called amitosis? According to Barni et al., 1995, amphibian blood cells can perform amitotic cell division:

  The proliferation of haemopoietic cells, detected by the anti-BrdU labelling index, was accompanied by absence of mitotic cell division and the appearance of cells showing features of amitosis (e.g. nuclear constrictions with bundles of electron-dense chromatin)

Source: Barni, S., Fraschini, A., Prosperi, E., Vaccaronel, R. and Bernini, F. (1995) ‘Possible occurrence of amitotic cell division during haemopoiesis in the Urodeles’, Comparative Haematology International, 5(3), pp. 183–188. doi: 10.1007/bf00368042.


I think the definition in Wikipedia is simply bad because it depends on another debatable definition.

I prefer something which follows from an observation made by Ricard Dawkins in The Extended Phenotype (the following is my definition, but I think Dawkins had something similar in mind):

An organism is any system of components which depend on each other for survival and cooperate in proliferating potentially unboundedly.

A single-celled organism is by this definition an organism since it proliferates by coordination of its components.

A single-celled organism with organelles deriving from endosymbiosis (think mitochondria) is an organism: even though mitochondria do proliferate on their own inside the cell, they don’t do so outside of the cell, hence have a bounded proliferation only; and they depend on the cell as a host. On the other hand, they cooperate with the cell division.

Endosymbionts, on the other hand, are organisms because even though they depend on a host (and the host on them), they may theoretically switch host or even survive a limited time without a host.

Similarly, the cells in a multi-cellular organism can sometimes divide independently (in organs) but they cannot survive without the rest of the organism, and the unbounded reproduction of any organ in fact requires going via the germ line of said organism.

A virus which depends on a host to proliferate does not form an organism with the host since it doesn’t use the host’s germ line; if, on the other hand, it does use the host’s germ line (consider virally derived pseudo-genes on our DNA) then, yes, it forms a common organism with its host.

  Is (mother + her unborn child) an organism?

I wouldn’t say so, since the child is only temporally part of the host.

  Is an apple that's just fallen off a tree an organism?

Interesting; I’d say yes, as long as it retains the potential ability to proliferate (it’s a separate organism from the tree though).

  Is (human + their microbiome) an organism?

No. Humans can survive (albeit only shortly) without a microbiome; in the same vein, the bacteria of the microbiome can change their host.

Unfortunately, this definition also has a drawback: there are organisms which cannot reproduce because they are sterile, yet they are clearly still organisms.

Note that other definitions (e.g. “an organism is a collection of components sharing common genetic material”) also don’t work universally since they also break down – the example of genetic commonality would preclude mosaicism and organelles derived from endosymbiosis.


Doesn't osmosis violate the law of conservation of energy?

I'm no thermodynamics expert, but Ill have a go at this.

The energy comes from the original set up, in which you have created a low entropy state. As the diffusion of water molecules equalises their concentration across the membrane so the entropy of the system will increase. This translates to a negative free energy change. That manifests as potential energy stored in the hydrostatic pressure resulting from the changes in volume, which in turn is available to turn the turbine.

So in the case of an experiment of the type described, the energy is derived from the experimenter who sets up the experimental situation in the first place.


If life is discovered on another planet, will it likely be classified using the current domain/kingdom/phylum system?

Background

There are basically three highest taxonomic levels: bacteria, archaea and eukaryotes. Many sources distinguish only prokaryotes and eukaryotes, subdividing prokaryotes into bacteria and archaea. Other sources posit archaea as a third domain on the highest level. That's a long debate though and fortunately not the topic here.

By appearance, the dual-domain system makes more sense because archaea and bacteria look very much alike under a microscope, and can both be clearly distinguished from eukaryotes (which have membrane bound nuclei). At the same time, comparing genetic structure and the protein machinery that interacts with DNA, eukaryotes and archaea are very similar and bacteria are clearly different from both of them. This demonstrates how appearance and molecular organisation have been typical criteria for distinction between branches of the evolutionary tree.

There are, however, many features that even those three most basic branches of life share, and they are in no way simple or few in number. For example, all extant life uses DNA to store genetic information and proteins for almost all processes governing the various reactions going on at any time in a cell. However, RNA for example is able to perform both the information storing function of DNA as well as the catalytic functions of protein. This just shows how the principles behind life are not unique to the molecules in use now, and extraterrestrial "life" may work by the same principles on an entirely different molecular basis.

Extraterrestrial life

If you want to know whether life found on another planet could be fit into our current classification system, the answer would be: No, most likely it will not be classified using the current domain/kingdom/phylum system. This is because our system describes evolutionary descendency, so unless this newly found life shares some common ancestor with an organism on earth, it would have to be classified in an entirely new system. (Of course this is subjective as you may find it more likely that it does share a common ancestor [Panspermia], while I personally find it more likely that life would have evolved entirely separated on this other planet seeing as we haven't heard of any life within reasonable distance.)

However, it is possible that this new life will follow the same evolutionary rules such as natural selection, and similar evolutionary pressures may drive to evolve similar properties. It may then be possible to draw parallels to characteristics of the current classification system, especially based on molecular function, and possibly appearance (micro- and macroscopically).


One of the most common toxins in mouldy food/bread is aflatoxin.

The exposure to high amount of aflatoxin can lead to acute aflatoxicosis with fulminant hepatic failure and even death.

While mild exposure to aflatoxin could be asymptomatic, it is better not to take a chance considering possible complications (citation from the link above):

  Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the
  liver in a number of animal species; no animal species is resistant to
  the acute toxic effects of aflatoxins; hence it is logical to assume
  that humans may be similarly affected. A wide variation in LD50 values
  has been obtained in animal species tested with single doses of
  aflatoxins. For most species, the LD50 value ranges from 0.5 to 10
  mg/kg body weight. Animal species respond differently in their
  susceptibility to the chronic and acute toxicity of aflatoxins. The
  toxicity can be influenced by environmental factors, exposure level,
  and duration of exposure, age, health, and nutritional status of diet.
  Aflatoxin B1 is a very potent carcinogen in many species, including
  nonhuman primates, birds, fish, and rodents. In each species, the
  liver is the primary target organ of acute injury. Metabolism plays a
  major role in determining the toxicity of aflatoxin B1; studies show
  that this aflatoxion requires metabolic activation to exert its
  carcinogenic effect, and these effects can be modified by induction or
  inhibition of the mixed function oxidase system.


A mechanistic study aims to uncover a mechanism. It can be a mechanism of the disease (exactly how does the disease do damage to the body), or a mechanism of a drug (exactly how does the drug prevent or repair the damage) that is being investigated.

Understanding mechanism, be it mechanism of disease or mechanism of the drug, is very important toward targeted improvements of treatments, as opposed to trying lots and lots of compounds, hoping that someday we'll find one that's better.

Non-mechanistic studies involving drugs aim to show that the drug provides a clinically relevant health benefit over competing treatments, or to determine the safe dosage of a drug. At that point, the mechanism of action of a drug is known to a reasonably large extent.

In short, there are many different things that need to be known for drugs to reach the market. Mechanism is one of them.


There are fundamental problems with defining what it means for an animal to feel pain, especially when the animal is a life form as different from us as an oyster.

I wasn't able to find any specific info online about oysters, but there is quite a bit of information that allows us to reason by analogy with related species.

Oysters are molluscs, and molluscs do have brains and sensory systems, but their level of sophistication varies a lot. Cephalopod molluscs, such as squid, octopuses, and cuttlefish, have extremely sophisticated nervous systems, and it has been argued (Peter Godfrey-Smith, Other minds, 2016), that we should think of intelligence as having arisen twice on earth through parallel evolution: once in vertebrates and once in the cephalopods. Cephalopods have sophisticated communication systems, and they can use tools and solve problems. There has been extensive research on pain in cephalopods.

So it's inherently pretty plausible that cephalopods can (in some difficult to define sense) suffer and feel pain, and by extension that their less advanced cousins the oysters can as well. However, the nervous system of an oyster is much more rudimentary than that of a cephalopod. A better analogy might be with snails, and there is some research on snails. They avoid damaging stimuli, have opioid systems, and respond to morphine and naloxone analogously to humans (e.g., showing less aversion to a hot plate when they've been dosed with morphine). So it seems likely to me that oysters can feel pain (for some reasonable definition of the word), but this whole area is one where people don't really know the answers to the questions or how to construct the philosophical foundations.


This is rather easy to do if you synthesize oligonucleotides chemically and not enzymatically. This is typically done using phosphoramidite chemistry, and it allows for the synthesis of chimeric RNA/DNA oligos. You can even incorporate modified nucleosides like 2'-O-Me or LNA.

This is typically done if you want to change the properties of an oligo, e.g. if you want to make it resistant to degradation by enzymes.


The concepts of relatedness - Hamilton's rule and kin selection

Is that really trying to imply that there are significantly different definitions?  It seems to me the intent was just to put it in terms of an equation with more useful numbers.  This terrifying paper from 1964 gives some of the follow-up works, in particular works from Cockerham in 1954 and a number of papers by Kempthorne, in particular this from 1955 and this from 1963.  There is also Malecot's method of coancestry from 1948. (WorldCat.org link)  The idea was mainly to look relatedness outside of the specific limitations present in Wright's work.  Some of the math in those are more accessible than others...


I think it really depends on the level of detail and accuracy needed.

Giving a quick look on Google Scholar, it appears that indeed there is (or at least was) a belief that hippocampal networks could be reasonably modelled by Hopfield networks (e.g. see Neuromodulatory control of hippocampal
function: towards a model of Alzheimer’s disease by Menschik and Finkel, and its references). However, many of these papers are somewhat old (though this certainly does not invalidate them!) and computational neuroscience moves fairly fast.
So yes, to a certain extent, after reading some papers that corroborate it, it might appear that some macroscopic behaviour of CA3 neurons can be reproduced by Hopfield networks.

That being said, in more recent works, I have personally never seen anyone model biological neurons with such simple neurons, when cellular level accuracy is required (often it isn't). At least stochastic Hodgkin-Huxley or integrate-and-fire, for instance, are used, even if as point processes (so that it is a system of ODEs/SDEs, not PDEs/SPDEs). Even the neurons used in today's deep neural networks (which make no effort towards biophysical plausibility) are (or at least can be) more complex than sigmoiding a linear combination of inputs!
Also, for slightly larger scales, as you note, the connectivity structure is extremely unrealistic. (Just look at the histology!)

So anyway, it depends on the goal. For simple macroscopic, qualitative similarities it may suffice. But if the goal is biophysical accuracy of simulation then I would look at newer papers and see what they do.
Check out Synaptic mechanisms of pattern completion in the hippocampal CA3 network by Guzman et al.

As for your second question, just searching for papers on Hopfield networks finds a number of them. However, they appear to be largely computational or mathematical, rather than neuroscientific modelling papers.
Maybe others can find better ones though!

Disclaimer:
I am not in the field of hippocampal modelling nor have I worked much with Hopfield networks, so take my thoughts with a grain of salt.
My suggestion is to do an extensive literature search, and post what you find as an answer here :)


The main reason for phenol being antiseptic is it's effect on proteins which it denaturates. It also causes leakage of cellular membranes. See the paper in reference 1 for some details and a load of references. They say in the section on phenol:

  Phenolic-type antimicrobial agents have long been used for their
  antiseptic, disinfectant, or preservative properties, depending on the
  compound. It has been known for many years (215) that, although they
  have often been referred to as “general protoplasmic poisons,” they
  have membrane-active properties which also contribute to their overall
  activity (120) (Table (Table22).

  Phenol induces progressive leakage of intracellular constituents,
  including the release of K+, the first index of membrane damage (273),
  and of radioactivity from 14C-labeled E. coli (242, 265). Pulvertaft
  and Lumb (386) demonstrated that low concentrations of phenols
  (0.032%, 320 μg/ml) and other (nonphenolic) agents lysed rapidly
  growing cultures of E. coli, staphylococci, and streptococci and
  concluded that autolytic enzymes were not involved.

Reference:

Antiseptics and Disinfectants: Activity, Action, and Resistance


Is it possible to be allergic to the yolk of an egg but not the egg white?

The protein composition of the egg white and egg yolk differ appreciably. Hence, it is plausible for one to countenance symptoms of indigestion when consuming the egg yolk as opposed to the albumen, egg whites. It is important to stress that your friend may only an indigestion towards egg yolks as opposed to an immune response to an antigen.

If we consider the protein family, the egg yolk comprises a family of phosvitins, a group of highly phosphorylated proteins capable of mustering iron and calcium metal cations - serving a role in embryo development.

These are primarily absent from the albumen which comprises (with an unexpected name!) a highest percentage of suspended ovalbumin, ovotransferrin and ovomucoid. As demonstrated by the American College of Allergy, Asthma & Immunology, it is feasible to suffer an intolerance towards the egg yolk and yet suffer no gastro-enteric indigestion to the egg whites.
More information regarding the American College is available from: https://acaai.org/allergies/types/food-allergies/types-food-allergy/egg-allergy

Your friend evidently does not suffer a severe anaphylactic shock after consumption of the egg yolks otherwise he/she may be adverse to both the egg whites and egg yolk. In conclusion, it is possible that he/she may simply have a mild intolerance towards certain proteins in the egg yolks.


Is there a biological explanation for a 0.5 difference in allele size with PCR product?

In my experience, working with a similar approach in Campylobacter jejuni, the base pair measurements from these techniques are imprecise and need to be carefully calibrated. I am unsurprised to see 0.5 base pair differences, this can be seen been runs and even, in the worse case situation, between even and odd wells in the same plate(!).

I would use Sanger sequencing to determine the sequence you are getting in one of your isolates, and then use this as a calibration control included in every run.


Identify a lone bone (jaw including teeth) found on a beach at Trouville-sur-Mer (France) in 2018

It would be great to have a scale bar in the photo, so that the size would be easier to determine. However, by the shape of the teeth, I will propose that it is the back half of the jaw of a pig. Here is an image from the National Maritime Museum:

This one is from Vanuatu and has a rather elaborate mesial portion of the jaw, but the teeth look very similar. It's virtually impossible to know the bone's age or species, however.


Why doesn't the polar side of the plasma membrane block nonpolar diffusion?

Polar and nonpolar molecules don't actually "repel", it's that polar molecules attract each other much more than nonpolar molecules attract anything. Therefore, to take a polar molecule from the (polar) water on one side of the membrane and bury it in the nonpolar region in the middle of the membrane is difficult because it means breaking its relatively strong interactions with the polar water molecules without forming new strong interactions to compensate.
In the case of a nonpolar molecule passing through the membrane, it is already in water when it approaches the membrane, and transferring it past the polar head groups isn't much "worse" (there's likely a slight effect of the often charged head groups attracting ions that bridge them to one another, but this would be small). The large effect of it being nonpolar, however, is to make it less unfavorable to move it into the middle layer of the membrane where there aren't polar groups for it to interact with.


Is there a way to measure the amount of bytes that are possible to encode in a DNA molecule?

Unfortunately the answer is highly dependent on what you mean. In the simplest terms, comparing it directly to how we measure data storage in digital media, the number of different states of a DNA string of length $n$ can have is simply $4^n$. A byte holds $2^8$ different states so the number of bytes in a DNA string of length $n$ is $\frac{n}{4}$. Of course, actually accessing this information would be more difficult than simply having it in a strand of DNA.

DNA in real organisms is not random, however, so sequences are not randomly distributed meaning that you could compress that information down into less bits than that, Shannon information style.

However, you can decently argue that this doesn't really tell us how much information is in real DNA because real DNA has structure that matters. It has exons and introns and promoter regions and so on. Meanwhile, the sequences in protein coding regions are a lot more important than sequences in non-coding regions for the most part. Large parts of the genome are functionally irrelevant but because of this they tend to be more random and thus have higher Shannon information.


Transcription when Chromosomes are Condensed

The compaction of DNA into chromatin is a very complex process that involves not only DNA, but on the histone code. Some may say that the histone code plays more of a role in chromatin state To develop a screen you would have understand the act of methylation, acetylation, ubiquitination, and phosphorylation of all modifiable histone residues. The modification of histone residues determine if the chromatin is in a heterochromatin or euchromatin state and even in which sections of DNA are accessible and transcriptionally active.

It is also important to note that the same modification of any of the 8 histone proteins in any nucleosome (the fundamental unit of chromatin) may not produce the same result.

For example: The methylation of H2 histone in the first nucleosome of a chromatin "string" may cause silencing while the methylation of H2 histone further down the chromatin "string" may cause activation.

It's alot of information but maybe one day you will be the one who solves the pattern! It sure is fascinating.


What is the mechanism by which quitting smoking causes increased appetite?

Research has generally focused on weight gain, rather than increased appetite, since it's a more objective outcome.

Smoking cessation has been clearly and consistently shown to be associated with weight gain, in both retrospective and prospective studies, and nicotine replacement seems to reduce some, but not all of the effect, at least while it's used.

There is an excellent, though now aging review of both the effect and potential mechanisms behind a paywall by Filozof. One of the most cited early articles is free at NEJM.

The mechanism of this weight gain is an active area of research, and, as discussed in Filozof, includes increased appetite with associated increase in calorie intake, decreased resting metabolic rate, and decreased physical activity.

Leptin, a hormone that increases both satiety and energy expenditure, is actually increased in people who stop smoking at the same time they are gaining weight. This finding has been convincingly demonstrated and replicated. Leptin insensitivity is a strong candidate for the primary driver of the increase in appetite (and weight gain) after smoking cessation.

Of course, since cigarette smoking causes profound changes in gene regulation, smoking cessation likely does as well. The full answer is almost certainly multifactorial.


See these two papers:

Early Loss of Xist RNA Expression and Inactive X Chromosome Associated Chromatin Modification in Developing Primordial Germ Cells
X Chromosome Reactivation Initiates in Nascent Primordial Germ Cells in Mice

Basically it happens just before the meiosis.


The difference between RNA and DNA is rather small, and both can form a double-helix structure. So if you had two sequences of RNA complementary to each other they would basepair and form a helix.

There were also some ideas to use this for therapeutic purposes, antisense RNA, an RNA oligo complementary to a messenger RNA, can theoretically be used to silence gene expression by base-pairing to the mRNA.


This kind of thing is normally calculated using the $K_{a}/K_{s}$ ratio, the ratio of synonymous to non-synonymous substitutions. It is not enough to count mutations for coding sequences, you should also take into account whether or not that mutation will actually change the resulting product.

There are various online tools that can help you do this, for example Phylemon:

http://phylemon.bioinfo.cipf.es/evolutionary.html


The two I know of off the top of my head are

OMIM : Online Mendelian Inheritance in Man. This is very good and very well organized but only deals with inheritable diseases, no infections etc.

Human disease ontology. From their webpage:

The Disease Ontology has been developed as a standardized ontology for human disease with the purpose of providing the biomedical community with consistent, reusable and sustainable descriptions of human disease terms, phenotype characteristics and related medical vocabulary disease concepts through collaborative efforts of researchers at Northwestern University, Center for Genetic Medicine and the University of Maryland School of Medicine, Institute for Genome Sciences.

The DO is probably perfect for your needs.


Lab experiment: Enumeration of Leukocytes

First I'd make sure all the RBC were gone just by visually inspecting. What should remain are your WBC and platelets at this point, and platelets are tiny so you can probably count anything between 5µm and 25µm. So for me that would include basically everything I can see minus background or debris.

So the problem now is with quantifying your count. You should know what the volume of your blood is, and here's why: What you're doing with a hemocytometer is counting #cells in a given volume, but you also diluted your whole blood with 150µL before you counted. So for example if a drop is ~60µL, and you diluted it with 150µL your dilution factor is 3.5, and it's important because your cell density equation is

For reference, you typically end up with 4-10 million leukocytes per mL of blood, however.


What is the mechanism behind sympathic effusion of serous cavities due to nearby abscess?

The left perinephric space is adjacent to the left subpleural space so inflammation can spread from the former to the latter.

Diaphragmatic inflammation then results in a left exudative sterile pleural effusion. It's called sympathetic since it's not infective.

https://radiopaedia.org/articles/perirenal-space

https://emedicine.medscape.com/article/1979032-clinical#b4


Question regarding Rate of Photosynthesis AP Biology Lab

Your task is to determine how light intensity and wavelength affect ATP production. Therefore, we know for sure that your dependent variable (or response variable) should be ATP production. It is customary to depict the response variable on the vertical axis (Y-axis), so let's trying doing this.

Now we need to sort the other two variables. I suggest that you make one variable a control variable -- a variable that you don't change and keep constant, and the other then will be an independent variable (or explanatory variable). Then you swap them around, producing at least two plots.

In a nutshell:

You pick one value of wavelength and don't change it. Then you change the light intensity and record ATP with constant wavelength. You plot ATP (vertical axis) vs the light intensity (horizontal axis).
You pick one value of light intensity and don't change it. Then you change the wavelength and record ATP with constant light intensity. You plot ATP (vertical axis) vs the wavelength (horizontal axis).

Make sure to generate enough data points in order to be able to fit a smooth curve.

Another option would be to make a 3-D graph, with 3 axes: Y for ATP, X for wavelength and Z for light intensity. Initially, this might seem like a better approach, however 3-D graphs are not very common in science, and maybe there is a reason for it. Your goal is to make your data intuitive, easy to read and straight to the point. Science can be rather complex even without additional effort to complicate it with confusing graphs.

I would try it out as well, and see which one of two approaches shows you the trend more clearly. If I had to pick one straightaway -- I would probably go with the previous option that included a control variable.


That looks like a live oak covered with oak galls


Will bark-beetles infest the Methow Valley?

I had trouble finding any academic or governmental references for rates of spread of Scolytids (bark beetles) in your region, but the answer to this would require speculation (i.e. prediction). Many factors, including the 'health' of the trees surrounding your home, and the connectivity of your trees to invaded areas, would aid in bark predicting whether these beetles will eventually make their way onto your property.

If your property is large, consider cost-share programs for management/prevention in your area.

See the bottom of this .gov webpage for more references. Good luck.


How can insects survive without an adaptive immune system?

There is not really a definitive explanation for why, although it's important to note that many mammalian pathogens are not adapted to insects and vice-versa. Insects need to survive insect pathogens, and they have a number of defenses for this purpose. Animals and their pathogens co-evolve and exert selection pressures on each other.

Killing the host (or killing the host quickly) is often not in the pathogen's best interest. Pathogens evolve towards their own successful reproduction as much as animals do. Success may ultimately mean evolving towards a less pathogenic state that improves a pathogen's chances of being transmitted.

As animals develop new defenses, they gain an advantage (relative to others of their own species) in surviving various pathogens. Pathogens evolve to escape these defenses, and a new equilibrium is established. An animal lacking this defenses is likely to be more susceptible to dying of infection, as the new equilibrium is dependent on them having these protections.

Here is an interesting paper on this view: http://hedricklab.ucsd.edu/PDF/HEDRICKImmunity113.pdf


Excitability has definitely been tested and measured, but I'm not sure about your exact definition (sort of hard to prove a negative).

For differences in "excitability" across neuron types, I can think of two general approaches.

1) You could simply consider the firing rate and define cells as more "excitable" simply if they fire more or have a lower current threshold (though one must be careful in interpreting the actual "mV" value of threshold, because resting potential and input resistance are crucial and thresholds are dynamic).

These parameters have nothing to do with the number of synapses on them or the number of synapses it takes to fire; if you focus too much on these parameters you risk making a comparison that isn't all that helpful (see the analogy below). This approach is most suited to comparisons across cell types.

2) The second type of excitability concerns the intrinsic properties of a cell: what is it's input resistance, spike threshold, how much current do you need to inject at the soma to evoke a spike, etc. These properties can indeed vary across cell types, but you really have to think about it in the context of (1) to avoid the same problems with the analogy below. A cell might be near threshold but receives very small inputs; should that cell be considered more excitable than another?

Instead, it makes more sense to think about changes of excitability: "how does Manipulation X affect the excitability of Cell K?" If it changes the amount of current you need to inject to the soma to evoke a spike by depolarizing the cell or increasing the input resistance, you would say it increases excitability. This is, in my experience, by far the primary way in which "excitability" is discussed in neuroscience, rather than as a factor that varies across neurons. I did a search on Google Scholar for "neuron excitability": every one of the first 20 results was using it in the context of a change in excitability from one condition or manipulation to another.

A tangential analogy (the problem with your proposed definition of excitability):

Your proposed definition of excitability is a bit like measuring income based on paycheck frequency or number of digits on the check. You could certainly do comparisons between jobs on those merits, and in some cases they might be valid for what you'd normally think of as "income", but as soon as you move between countries (i.e., brain regions or cell types) currency changes, and suddenly the number of digits doesn't help because you don't know if you are talking about British pounds, US dollars, or Brazilian real. And even within a population, if the paychecks come weekly rather than monthly, the same face value of a check means a totally different annual income (i.e., if a cell has synapses that are rarely active, they contribute less to depolarizing it than synapses that are active all the time).

Contributions to excitability

Your question proposes that morphology is a defining characteristic of excitability. In a previous question you asked, I directed you to a review by Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature reviews. Neuroscience, 1(3), 181. - this review is applicable here, too. Active conductances in the dendrites and variation of synaptic properties with distance from the soma (larger, faster EPSPs the further from the soma you go) act to regularize the influence of EPSPs with distance, so you cannot rely only on passive properties. That also means you can't simply assume that a cell with lots of synapses far from the soma is not excitable.

However, there are definitely differences in firing rates and firing thresholds across neuronal subtypes, and you can take these to mean differences in excitability. There are many papers that talk about the diversity of intrinsic properties or firing rates of cells. I'll list a couple here for further reading:

Llinás, R. R. (1988). The intrinsic electrophysiological properties of mammalian neurons: insights into central nervous system function. Science, 242(4886), 1654-1664.

Izhikevich, E. M., & Edelman, G. M. (2008). Large-scale model of mammalian thalamocortical systems. Proceedings of the national academy of sciences, 105(9), 3593-3598.

It's also important to recognize that excitability is dynamic and cells that are highly excitable in one state may not be as excitable in another state, even though their morphology does not change.


Generating custom human DNA sequences based on traits such as eye colour?

A major limiting factor in such an exercise is the complexity of the biological process under question (eye colour etc.,) and thus, our nascent understanding of these. What I mean is that there is not a single gene that determines a given characteristic, rather it is the complex interaction of a set of genes in different conditions responding to environmental cues and such. We are barely at the level of scratching the surface when it comes to understanding the mechanisms that underlie such outputs. And so, we are long ways off (maybe hundreds of years?) before we can even start thinking about coming up with feasible approaches to such objectives.


In genome research, what is the problem in Mapping that may be caused by reads being too short?

Being a bioinformatician as well, I am not really what you asked for, but I work with plant genetics so I'll try and answer anyway.

What you are mapping is RNA. So, as you already figured out, splicing events will be a problem for end-to-end mapping of the reads. There are tools managing that, though, so let's assume you used one of them and still a lot of your reads do not map. To put in WYSIWIG's good point: Another event that can mess up with your alignments is RNA editing, although this is not too likely to cause a high proportion of reads to not align at all.

Some aligners might filter out "too short" queries, so make sure you are not using one of them.

Then, have you preprocessed your reads? If you have not, there might be adaptor sequences left. Or may reads have very poor quality, thus are also aligned with poor quality, thus might be counted as unaligned.

And then check what you are aligning to. Many published plant genomes are also of minor quality, including lots of unassigned bases. So, there could be large proportions of your reference genome that count in the genome length, but are only Ns and nothing will align there.

Last but not least, your thought about a virus could also be right. Depending on the experiment, there might be pathogenic RNA in your sample, so check against a suitable database.

If the problem is only that the reads are "too short" for whatever reason, try doing transcriptome assembly before comparing to your reference.


Authority on Microbiological Definitions

So in a very broad definition, yes, chromatin encompasses DNA, RNA and protein. The primary function of chromatin is to provide a method to effectively package all the DNA in a cell. This packaging is dynamic, and it's constantly regulated in a cell type-specific manner. We can see the broad interactions of protein and DNA in this cartoon representation from wikipedia:

Combined with histone-modifying complexes, and chromatin remodeling complexes, we obtain the aforementioned mode of regulation. Histone protein can be modified (acetylation, methylation, glycosylation, phosphorylation, etc.), they can also be moved, substituted in their subunits for specific pruposes (think H3.3 or H2A.X). We can also end up with varying regions of dsDNA, 10nm or 30nm fiber.

The RNA comes in as a structural and functional components of the chromatin, participating in many controls as noncoding RNAs.

I believe most of the method in defining chromatin comes in very much as the amassed literature on the subject to-date. You'd even consider it "common knowledge" entering the field (i.e. a quick google search can return you the right definition).

  "only during the mitotic interphase can it transcribe to produce RNA and protein."

Transcription halts entering M phase or mitosis, transcription may occur during G1, S, G2, or "interphase."


How can fresh cavities form at the margins of sliver amalgam fillings on teeth?

Amalgam fillings are made from an alloy. The properties of the chemical elements bound into an alloy are different than the properties of those elements in different forms. The fillings do not release any biologically significant form or biologically significant amount of either silver or mercury. They are essentially inert.

Plus silver antibacterial effects are quite modest. The existence of fine cracks and gaps between amalgam and tooth provide wonderful hiding places for bacteria - and that shelter is probably more important to the bacteria than any negative effects of the silver.


Is a Linker sequence mandatory in primers for PCR Cloning?

This is the website you need, and yes, most of the time it's better to have several extra bases at the start of your primer.

https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments


Why is the swelling of bread when placed in water not considered to be caused by osmosis?

The phenomena that you are describing, where bread, which is a porous material, similar to a sponge, absorbs water, is the absorption of water by capillary action.

As @Joel mentioned, osmosis is specifically the flow of a fluid across a semipermeable membrane, such as the plasma membrane of a cell or dialysis tubing, that occurs in such a way as to cause a flow from an area of low concentration to an area of high concentration. This flow eventually leads to a state of equilibrium when the concentration on both sides of the membrane is the same.

The wikipedia article on Osmosis gives this definition:

  Osmosis is the spontaneous net movement of solvent molecules through a semi-permeable membrane into a region of higher solute concentration, in the direction that tends to equalize the solute concentrations on the two sides. It may also be used to describe a physical process in which any solvent moves across a semipermeable membrane (permeable to the solvent, but not the solute) separating two solutions of different concentrations. Osmosis can be made to do work.
  - Wikipedia: Osmosis

- By OpenStax College [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

The bread is not selectively permeable, and it will continue to absorb liquid until it is fully saturated. This isn't actually an equilibrium, because additional water would do nothing to change the concentration on one side of the bread or the other. If you added more water to one side of a semipermeable membrane in equilibrium, by Le Chatelier's principle, you are will force the reaction (in this case, you change the concentration) to one side, then the liquid would again flow from the area of low concentration to the area of high concentration.

Capillary action is the result of water flowing into the small spaces, such as the air bubble that form in bread when it bakes, in the absence of a force "pushing" it into those spaces, or against the force of gravity. The liquid accomplishes this through intermolecular forces that cause adhesion of the molecule to the surface of the material that is absorbing it and cohesion of the molecules in the liquid keep them associated to one another, and as the liquid moves into the spaces, it is able to pull the other liquid molecules along into the space.


The role of duration of infectiousness in SIR models

My question concerns the way that $d$ enters the SIR model, because I
  find it not so plausible:

  to consider all persons that are infected today and take a fraction $ν$ of them that will have recovered tomorrow.

Well, it is in fact not very 'realistic' as you point out, but in the assumptions of the model, we see that the population has no structure (it is well-mixed, constant) and there are no birth-death events. So, in this case, it is not so problematic to take $v$ as a constant across the entire simulation, because what you are trying to calculate is the rate at which the three sub-fractions of $N$ ($s$, $i$, and $r$) change, not really which individuals are moving from one class to another (which you cannot really know anyways, if you talk about fractions of $N$).

  Wouldn't it be much more plausible

  to consider all persons that became infected $d$ days ago and let    these be recovered tomorrow?

So, considering my previous comment, it would not make much sense really to take a time-delay form on $d$, because you cannot really know which individuals got infected at any given point, you can only talk about fractions of $N$ (there is no population structure, as they say in the model formulation). So, the fact that your formulation seems to have a slower dynamics might not be very informative, because what you did is simply applying $d$ to a fraction-of-the-fraction of the population classes, so it makes sense mathematically that it runs slower, but as per the model formulation it does not make much sense, unless you have population structure defined from the beginning (which in this case is not), and unless you can explicitely know individual-per individual class transitions. In fact, I believe that taking the fraction-of-the-fraction would lead to an artifactual 'undercounting' of these individuals that actually needed to be in the $i$ class (and overcounting of the other classes).


Can parts of a human brain be asleep independently of each other, or vary in the times required for them to fall asleep?

Have you ever tried to read a complicated book after several hours of hard work that required a high concentration? Imagine that you have forced a particular area of your brain. After a hard work, the areas of the brain that we used to finish a work seem don't respond to any stimulation and make us feeling tired and as we can't understand what we are doing anymore. This happens because we have forced that particular area of the brain and it needs to reinforce the connections it made and to do this, it has to sleep, such as we do during the conscious (you know you are going to sleep) sleeping. Eventually we can say that some particular areas of our brain must sleep if forced to a hard work and they do it when you feel like you can't get something which you know you can. A recent study has demonstrated this by understanding physiological functions of sleeping.

Nature article of Vyazovsky V. et al. Vol. 472, pages 443-447, April 2011 (I am not copying the link anyway, have to search it by yourself). Or to Science of Bushey D. et al. Vol. 332, pages 1576-1581, June 2011. And on Nature Review Neuroscience of Diekelmann S. And Born J. Vol 11 number 2, pages 114-126, February 2010.


What is the name of this plant with small, 5-leaved divided pink blooms?

It looks like a Red Campion, which is native to northern and central Europe.

It would be nice to see a close-up of the calyx (which is usually striped) and the leaves to be sure; it may be a cross between a White and Red Campion.

There are many members of the genus, and many look alike. Your close-up is of a male flower (anthers only). The plants are male or female.


Can a brain process auditory signals at 18 weeks of human development?

According to a concise review by Graven & Brown (2008) the development of the auditory system (Fig. 1) in the human is as follows:

15 weeks gestational age*: structural parts of the cochlea and the middle ear are well formed;
20 weeks: middle ear and cochlea are anatomically functional;
Around 25 - 29 weeks: auditory system as a whole becomes functional, as the spiral ganglion cells in the cochlea connect inner hair cells to the brain stem
and temporal lobe of the cortex. In other words, only at this point, the peripheral end organ becomes connected to the central nervous system. At 25 to
26 weeks' gestation, a loud noise in utero will produce detectable changes in autonomic function.
28 - 30 weeks: neural connections to the temporal lobe of the cortex are functional. The development of tonotopic columns in the auditory cortex commences. They are needed to receive, recognize, and react to language, music, and meaningful environmental sounds.

* Gestational age is a measure of the age of a pregnancy which is taken from the beginning of the woman's last menstrual period (LMP), or the corresponding age of the gestation as estimated by a more accurate method if available. Gestational age can be obtained by adding 14 days to the point of fertilization.

Fig. 1. The adult auditory system. source: Graven & Brown, 2007

Reference
- Graven & Brown, Newborn Infant Nurs Rev (2007); 8(4): 187-93


Do all human cells have all the same organelles?

I believe that yes.

Here is more to read about:
https://bscb.org/learning-resources/softcell-e-learning/golgi-apparatus/
"is found in all plant and animal cells"

and explanation why so
https://sciencing.com/would-did-not-golgi-bodies-8657737.html

I am no expert in this but I was looking for it as well, I believe it is right.


How does the nucleophilic attack in DNA replication occur?

Polymerases uses a two-metal ion mechanism to carry out the addition of a new NTP to a growing RNA strand. Two Mg2+ ions are used in this process; metal ion A is involved in the formation of the nucleophile (O-) for the SN2 reaction to occur and metal ion B is involved in the stabilization of the transition state in the reaction. For the addition of a NTP to a RNA strand to occur, an activated 3’ hydroxyl group (O-) acts a nucleophile and attacks the alpha phosphate of the incoming NTP. The reaction is initiated by a deprotonation event. Metal ion A aids with this deprotonation as it reduces the pKa of the hydroxyl (so it is more acidic), making it easier to deprotonate and form the nucleophile, the proton is accepted by a nearby aspartate residue (not water) - doi: 10.1021/ja403842j. After the hydroxyl attack, the mechanism proceeds through a pentacovalent transition state like in a standard Sn2 reaction and the pyrophosphate group (PPi) is kicked out. The image is not mine but comes from this paper: https://doi.org/10.1038/34542, which is quite good, as is this paper: doi: 10.1074/jbc.274.25.17395 and this one https://doi.org/10.1016/j.molcel.2006.03.013


This is a white morph red fox, not an arctic fox.

As noted in the question, this fox has larger, more pointy ears than an arctic fox, and the second picture shows it to have a longer muzzle as well.

Another clue is that these pictures were taken in the springtime or early summer (which you can tell from the new growth on the plants in the picture), and that arctic foxes are only completely white during the winter. During the spring, an arctic fox should look like this:

You can also easily tell that the fox in the picture is not an albino, because of the dark pigment in the nose and eyes.

The red fox has quite a few different color morphs, and this fox looks to be a white color morph.

In that diagram, this fox would be labelled as leucistic (white).

Here are some other white morph red foxes: