Is consuming proteins different vs. consuming amino-acids and how? Yesterday I had a discussion with a friend. He said that consuming proteins and amino-acids is different. He said that those who grow muscles would agree on that. I wanted to argue against that statement, but I lacked arguments... As far as I know, amino-acids are part of proteins. So, when proteins go to our body with food, we digest it and make amino-acids. Then they can form any kind of proteins we need. The same would happen when consuming amino-acids directly, not in protein form. Maybe then the process would be faster. But from my point of view, there is no much of a difference. Could anyone please give me a more sound opinion on why is consuming proteins and amino-acids different, if it is?

To put it shortly:

Proteins have properties that individual amino acids that make up the protein does not have.
Similarly the individual amino acids have properties that the protein does not have.

This is analogous to elements vs compounds.

The site referenced below quotes 3 experiments done to examine this phenomena.

All experiments compared effectiveness of whey protein with that of essential amino acid (EAA) supplements. Experiments 1 and 2 involved old people while experiment 3 involved young people.

Conclusion of experiments is as follows:

Both EAA and whey protein (15 g of EAA and 15 g whey was taken by the respective groups) induced muscle growth, however EAA had better anabolic effect as compared to whey.
In this 3 groups were compared. 15 g of whey vs 6.72 g of EAA vs. 7.57 g of non-essential amino acids. Whey had higher anabolic effect as compared to EAA while the third group showed no improvement. This additional anabolic effect is attributed to unknown mechanisms. The anabolic effect was measured using a different method add compared to the first experiment. So results may not be comparable.
In this 3 groups of young men were compared. The first group was given carbohydrate (30 g) and EAA (15 g) drink, the second group liquid meal containing same quantity of EAA and total 850 calories while the third group was given both. The conclusion:

The third group, as expected had the highest anabolic rate
The first group (protein and carbohydrate drink) had better anabolic rate when compared with the liquid meal group though they both took the same amount of EAA. The difference was in carbohydrate content. The liquid meal had higher carbohydrates content when compared with the first group.

Whey has insulinogenic effect invitro. Whey also has the same effect whether taken before or after exercise while the protein drink has better effect when taken before exercise.

Among amino acids leucine, when taken alone has anabolic effect comparable to a mixture of EAA.

In conclusion:

  However, whey contains various bioactive peptides that act to enhance recovery and potentially in other ways that positively effect the adaptive process to exercise (12). These bioactive peptides are not found in EAA, BCAA, or Leucine, and appear to be a unique quality to dairy proteins. So what we can't say is that these aminos are the deciding factor in whey's effects...or that we can use one in place of the other (interchangeably) in all cases.

http://www.vpxsports.com/article-detail/supplements/whey-protein-versus-amino-acids-whats-the-difference

Please read the article which has more details and graphs and references for further study.


What is overdiagnosis? What is overdiagnosis ?

I have searched this Wiki result but didn't understood at all.

Can you please explain the first two line of Wikipedia :

  Overdiagnosis is the diagnosis of "disease" that will never cause symptoms or death during a patient's lifetime. Overdiagnosis is a side effect of screening for early forms of disease.

Also

What is over treatment ?
Are overdiagnosis and over treatment same or different ?

Overdiagnosis and overtreatment are intertwined. There is debate about how to best describe the problem, but narrowly defined, overdiagnosis occurs when increasingly sensitive tests - or changing definitions - identify abnormalities that are minor, non-progressive, or likely to resolve on their own, and that, if left untreated, will not cause symptoms or shorten an individual's life. Having a diagnosis makes well-persons think they're ill (overdiagnosis). If they are then treated for this diagnosis, they are overtreated.

An example involving changing definitions pertains to diabetes. When the official definition of diabetes changed from having a fasting blood sugar (FBS) of "X" or greater to an FBS of "X-y" or greater, 1.6 million new diabetics were instantly diagnosed, some of whom are not likely to develop symptoms and complications and are not likely to benefit from treatment. This is overdiagnosis.

If one goes on to put such a patient (let's say, on the lower end, "X-y+1" on a blood sugar (BS) lowering agent, and they pass out because their BS drops too low, then they are overtreated. If they happened to be driving when they pass out, and get into a fatal accident, they literally die from overtreatment, if it can't be shown that they would have suffered from a marginally elevated FBS. (If it can be shown to be dangerous to have an FBS of X-y+1, then this is a risk of treatment, not overtreatment.)

For an example of increased sensitivity of tests, say a new test is available, a blood test called a "D-dimer", which will reveal with 100% accuracy the presence of a dangerous pulmonary embolism (it's very sensitive). However, it is also known to be positive when there is no pulmonary embolism as well, but it's not known how often (so it's not specific). But it's an exciting new test!

A patient goes into the Emergency room for one of the following: atypical chest pain, dizziness, shortness of breath, leg pain consistent with a blood clot in the calf, or loss of consciousness. In addition to an EKG, chest x-ray (CXR) and a few other tests, a D-dimer is ordered. The EKG, CXR and other tests are negative, but the D-Dimer is positive. The tentative diagnosis is pulmonary embolism (PE).

Because the D-dimer indicates that a dangerous condition may be present, a spiral CAT Scan with contrast is ordered on all those people. Some will have a life-threatening PE (appropriately diagnosed*). A large number will have a negative CAT Scan. (diagnosis excluded) But a significant number will have a very small PE. Because this is relatively new and surprising, and it's not known whether they should be treated (maybe nothing will happen if they don't treat? Maybe this happens in normal people and we just never knew it?), the doctors, who are accustomed to treating all PE's will put the patients on blood thinners. This is overdiagnosis of PE, and treating it is overtreatment, because some treated people will have "bleeds" - a stroke, GI bleeding, other. It is now known that these tiny PE's are often seen in patients who suffer no harm at all from them, therefore in order to stem overdiagnosis (and subsequent overtreatment), the D-dimer test is ordered less frequently.

  ...[We] are in the midst of an epidemic of diagnosis. Conventional wisdom tells us that finding problems early saves lives because we have the opportunity to fix the problems early. [Conventional wisdom tells us that} There is no risk in finding things early. The truth is that early diagnosis is a double-edged sword; while it has the potential to help some, it has a potential to harm us. Such overdiagnosis leads to overtreatment when these “pseudo-diseases” are conventionally managed and treated as if they were real abnormalities; because these findings have a benign prognosis, treatment can only do harm.

Overdiagnosed: Making People Sick in the Pursuit of Health
Overdiagnosis
Using Evidence to Combat Overdiagnosis and Overtreatment: Evaluating Treatments, Tests, and Disease Definitions in the Time of Too Much


Real time PCR standard curve As blunt as possible: when performing real time PCR it is a routine step to run one PCR in order to plot a "standard curve" with several decreasing dilution ratios from your sample. what is the real purpose of this?
how should results be used/interpreted?

You can use 3 or 4 dilutions- 1:1, 1:5, 1:25, 1:125

Purpose of doing this is to calculate the primer efficiency. Ideally primer efficiency should be 2 i.e. two molecules of DNA are formed in a round of PCR. So after n-rounds of PCR there should be $2^n$ DNA. However, this may not be the case always. You calculate primer efficiency like this:

Plot $Ct$ vs $log_2(Conc)$
Get the trendline (in excel) or use a linear regression command for other applications
Get the slope ($s$) of the trendline
Efficiency in this case would be $2^{-s}$.

Some people use base of 10 in the log instead of 2 (for which you have to do $10^{-s}$ instead.

This, you can directly use to find out how many copies are produced after n cycles i.e instead of $2^n$ it will be $x^n$  where $x$ is the calculated efficiency. This is particularly useful when you are calculating the fold changes using the comparative Ct method. For details see this article.


What do cells do when they aren't creating proteins? I've always thought that the majority of the "work" in a cell is protein production, until I read the following.

The Wikipedia article on the central dogma of molecular biology states this:

  80% of the human genome is transcribed even though only 1% codes for
  proteins.

and this:

  Current research focuses on investigating the function of non-coding
  RNA, that is, RNA that does not follow the dogma trend and does not
  code for polypeptides.

If 99% of what's transcribed isn't used for creating proteins, what is it used for?  If it's not known - are there any hypotheses?

As indicated in the comments there are several non-coding (untranslated) RNAs, that the cell produces. Most of these perform gene regulatory functions.
However, widespread transcription is known to take place throughout the genome (pervasive transcription), but the functions of these RNAs are not clearly understood. It has been suggested that in certain cases the event of transcription, rather than its product, is responsible for chromatin regulation.


Does this procedure for extracting DNA from strawberries work? I wanted to try out this experiment for extracting DNA from strawberries that can be done at home:

https://www.stevespanglerscience.com/lab/experiments/strawberry-dna/

However, while doing a bit of reading, I came across this article:

http://www.ncbe.reading.ac.uk/PRACTICALS/PDF/DNA_isolation.pdf

It states that, "Although these fruits [kiwi fruit, bananas and strawberries] seem to yield copious amounts of DNA, the substance produced is in fact little more than pectin."

Are they right? How could you tell that what you've extracted is actually DNA?

The extraction protocol described in the first article is a standard DNA extraction protocol. I've used variations on this method in the lab (with some refinements) on other types of cells at least hundreds, if not thousands, of times. The "strawberry" experiment is very popular for classroom demonstrations, especially at the middle-school and high-school levels, because it's visually interesting and uses commonly available reagents. While these reagents aren't laboratory-grade, they're more than sufficient for a basic extraction of DNA.

I can't think of a scientific basis for why the author in the second article would claim that the extracted substance is "little more than pectin". Since he didn't provide data, or a reference to any data, it's hard to know what he's basing his conclusion on.

It's definitely possible that the DNA is pulling down a certain amount of cellular proteins during the alcohol precipitation step (the final step). This is why in a lab setting you typically perform a few more steps to "clean up" the DNA and remove any co-precipitating proteins. This would be essential if you plan to do further analysis of the DNA, because protein contaminants can interfere with subsequent analyses, making the data unreliable. One exception would be if you're studying protein-DNA interactions, but that's a separate type of experiment.

I'm assuming this experiment will be done for/by beginner level students, as opposed to a college or graduate level class? If so, then for the purposes of a classroom demonstration, those extra purification steps aren't warranted. It's time-consuming, and it would be very boring to watch... As is the case with most labwork. :-) Even if you perform those additional steps, the purified DNA is often precipitated with alcohol again, and it's visually similar to what you saw in the first alcohol precipitation, just a bit less opaque. Probably not something most students would notice or find interesting.

Either way, it's entirely acurate to say that the strawberry experiment is extracting DNA. You could always explain that the DNA might have cellular proteins binding (or "sticking") to it, and that a few other steps would have to be performed if you wanted to analyze the DNA in a lab setting, because the proteins would interfere with DNA analysis. This would also give beginner-level students an introduction to the fact that DNA and proteins interact with each other.

Hope that helps!


Is the nuclear envelope present in G1 of interphase? Is the nuclear envelope present in G1 of interphase of eukaryotic cell? If so how does a method like Calcium mediated transfection get DNA past the nuclear envelope?

To answer the question about nuclear envelope in G1 phase, yes it exists. The nuclear envelope is reformed at the end of Telophase after the 2 copies of the DNA are pulled apart, but before the two daughter cells are separated by cytokinesis. We can see the new nuclear envelope in these images:

Image from here

Nuclei visible near end of cytokinesis, centrosome still visible. Image from here.

As for how DNA gets into the nucleus without cellular division I don't have a good answer and I'm not sure anyone does right now. The nuclear envelope is a major barrier for non-viral gene delivery.


How does isopropyl alcohol disinfect less in higher concentration? Isopropyl alcohol (2-propanol) can be used as disinfectant.

For increasing concentration of it in water, the effect as disinfectant increases, and then decreases again.

Typical concentrations for use as disinfectant seem to be 60-75% isopropyl alcohol in water.

Wikipedia: Isopropyl alcohol - Medical mentions membrane pores of bacteria that will not open without water.

That does not feel like the full explanation to me; I expect there are bacteria with membrane pores of diverse kind.
Does 100% isopropyl alcohol not disinfect at all - or just more slowly? What abour the effect on other pathogens?

The main reason why alcohols (isopropanol and ethanol mostly) can be used as disinfectants is that they denature (bacterial) proteins. This is also the reason why they work on such a broad spectrum of microorganisms (bacteria, fungi, viruses), but not on spores, as these are better protected.

The higher the concentration of the alcohol is, the faster this denaturation is happening. And this can cause problems: When you denature the proteins of the bacterial cell wall, they will form some kind of protective layer around some of the cells which allows their survival. Diluting the alcohols makes the disinfection happening slower and thus gives the alcohols more time to get into the cell.

For more information about concentrations and also for a ton of references, have a look into the CDC's disinfection guidelines in the subchapter on alcohols.
More details can be found in this review:

Antiseptics and Disinfectants: Activity, Action, and Resistance


How do trees communicate in the "Wood Wide Web"? I read on The New Yorker - The Secrets of the Wood Wide Web that trees communicate with each other through electrical impulses sent through their roots. Through these impulses they can ask other trees for some nutrient if they are getting it in insufficient amount or warn the other trees about an upcoming pest attack. This phenomenon is termed as the Wood Wide Web.

So how do trees distinguish in different types of impulses that they receive if they don't even have a brain? And does this process show any resemblance to nervous system in animals?

Additional YouTube video: Trees can talk to each other, but how?

I have to say: when you claim that "trees communicate with each other through electrical impulses sent through their roots", you're thinking about Avatar.

Joking apart, what you call wood wide web is the mycorrhizal network.

Mycorrhizal fungi are well known to botanists and ecologists. They are the fungal partner in the mycorrhiza, which is a symbiotic association between a fungus and a plant.

Mycorrhizal hyphae (white) in a root

The novelty about this mycorrhizal network is that, as it was demonstrated, plants can use it to exchange some chemical substances. And, in certain cases, this exchange can be used to improve disease resistance.

However, there is no electrical impulse in this process.

According to Song et al. (2010):

  In theory, plants can also communicate with each other through underground common mycorrhizal networks (CMNs) that interconnect roots of multiple plants. However, until now research focused on plant-to-plant carbon nutrient movement and there is no evidence that defense signals can be exchanged through such mycorrhizal hyphal networks. Here, we show that CMNs mediate plant-plant communication between healthy plants and pathogen-infected tomato plants (Lycopersicon esculentum Mill.). After establishment of CMNs with the arbuscular mycorrhizal fungus Glomus mosseae between tomato plants, inoculation of ‘donor’ plants with the pathogen Alternaria solani led to increases in disease resistance.

This other research demonstrate that the mycorrhizal network can be used to warn neighbouring plants of aphid attacks (Babikova et al., 2013):

  Here, we show that mycorrhizal mycelia can also act as a conduit for signalling between plants, acting as an early warning system for herbivore attack. Insect herbivory causes systemic changes in the production of plant volatiles, particularly methyl salicylate, making bean plants, Vicia faba, repellent to aphids but attractive to aphid enemies such as parasitoids. We demonstrate that these effects can also occur in aphid-free plants but only when they are connected to aphid-infested plants via a common mycorrhizal mycelial network. This underground messaging system allows neighbouring plants to invoke herbivore defences before attack.

In both cases the mycorrhizal networks play an important role in exchanging chemical substances among the plants.

The network has a dark side too: it can be used to deliver allelochemicals from one plant to another, greatly increasing allelopathy. According to Barto et al. (2011):

  Common mycorrhizal networks (CMNs) form belowground networks that interconnect multiple plant species; yet these networks are typically ignored in studies of allelopathy. We tested the hypothesis that CMNs facilitate transport of allelochemicals from supplier to target plants, thereby affecting allelopathic interactions.

Finally: don't rely on media to get scientific information, specially in these times of alternative facts. Sometimes you can get good information in the media, but good and accurate information is way harder to find (an example is this BBC page about the mycorrhizal network). However, in defense of that page in The New Yorker, there is no mention to electrical impulses.

Sources:

Song, Y., Zeng, R., Xu, J., Li, J., Shen, X. and Yihdego, W. (2010). Interplant Communication of Tomato Plants through Underground Common Mycorrhizal Networks. PLoS ONE, 5(10), p.e13324.
Babikova, Z., Gilbert, L., Bruce, T., Birkett, M., Caulfield, J., Woodcock, C., Pickett, J. and Johnson, D. (2013). Underground signals carried through common mycelial networks warn neighbouring plants of aphid attack. Ecology Letters, 16(7), pp.835-843.
Barto, E., Hilker, M., Müller, F., Mohney, B., Weidenhamer, J. and Rillig, M. (2011). The Fungal Fast Lane: Common Mycorrhizal Networks Extend Bioactive Zones of Allelochemicals in Soils. PLoS ONE, 6(11), p.e27195.


How can succinylcholine cause myorelaxation? I first thought that this is because of prolonged depolarisations.
However, I am not sure anymore, because after reading PubChem, the only possible pathways are are Choline agonist.
So I would say that succinylcholine cause myorelaxation by some cholino-receptor agonists.
I do not think it is about depolarisation and how long it is.

How can succinylcholine cause myorelaxation?

Succinycholine, as its name might suggest, is a cholinergic agonist indeed. It acts on the neural plate of skeletal muscles, where it activates the muscle cholinergic receptors.

Phase 1 block due to succinylcholine thus occurs by activating so many receptors at once, that the whole muscle gets desensitized and therefore paralyzed. A corollary of that is that muscle will twitch during activation, thus accounting for the reason why people twitch shortly before becoming paralyzed after a succinycholine iv injection. This phase 1 block will resolve in 2-5 minutes.

Now an interesting phenomenon is that if you go on stimulating the muscle with more cholinergic agonists (for example, a second iv dose of succinylcholine), you may end up provoking endocytosis and degradation of the cholinergic receptors. This is called phase 2 block, and in contrast to phase 1, it will take at least several hours to resolve. This is why we never use a second dose in the clinics, except in very special cases.
You can also read about it all on wikipedia


Why is the opposite of plantar flexion called "dorsiflexion"? Why is the action of flexing the foot so that the toes move anteriorly/superiorly (i.e. in the direction opposite that which they move during plantar flexion) described as "dorsiflexion?" In the same vein, why is the top surface of the foot called the "dorsal surface?"

If anything, the action opposite to plantar flexion moves the foot in the ventral direction, doesn't it? And surely if you've ever seen a human in the anatomical position, you can see that there's nothing dorsal about the top surface of the foot - it's superior, perhaps, but by no means dorsal.

Anatomical terms must be able to fit a wide variety of organisms, from insects to fish, dogs, horses, chimpanzees to humans. That's why the terms are sometimes confusing to people who are thinking only of bipedal humans.

In anatomy, the dorsum is the upper side of animals that typically run fly, swim or crawl in a horizontal position. In vertebrates the dorsum contains the backbone. In such an animal the "ground side" is the ventrum.

Due to varied orientation on quadrupedal mammals (where the term is more appropriately used) the "back"-side of the hand, the "top"-side of the foot and the upper surface of the tongue are referred to by the term dorsum.

Does this picture help? Note the dorsal surfaces of the body, muzzle, feet.

In anatomy, the sole of the foot is called the plantar surface. The top of the foot is called the dorsum of the foot. (Imagine us walking on all fours like apes.) Therefore when you extend your foot, it's called plantar flexion; when you flex your foot upwards towards your head, it's called dorsiflexion.

Similarly, the arteries feeding the bottom of your foot form the plantar arch. Those feeding the top are the dorsal artery (or the dorsalis pedis).

Because anatomy must describe other animals than ourselves with other orientations, it must be consistent. In a quadruped, the dorsum of the tongue and the feet do actually point to it's "back" surface. See the picture below:

Lynxes have big paws, so it's more obvious that the surface facing the backbone is appropriately called the dorsum of the paw/foot. This picture is particularly interesting because it shows three degrees of dorsiflexion and one paw in full plantar flexion.

In humans, the "back" is actually the posterior surface, because we are not primarily in a horizontal orientation. The ventral surface is called "anterior". Thus we speak of the anterior chest wall and the posterior chest wall, not the dorsal and ventral surfaces, although those designations would still be entirely correct.


Difficulties understanding a pathway I am not a biologist and I would love to understand what is going on with this pathway.
I went to the description but it's still complicated, and I couldn't follow. Can someone please help me with it? Is this a comprehensive pathway or is it based on specific details? How do i read this pathway?

So if you're reading the flowchart, understanding the notation of the arrows is important:

We have rectangles around the gene products
There's a circle, denoted by DNA, noting that the proteins are expressing the product that follows through interaction with DNA
The solid line with an arrowhead means there's some sort of interaction
The solid line with the blunted or T head means this pathway or interaction has been abrogated somehow
The solid line with the slash through it means there's some missing interaction that we don't see
The +p means phosphorylation
The double solid line to the left is the plasma membrane, whereas the dotted line central to the figure is the nuclear envelope
The dotted line means an indirect effect

Source: http://www.genome.jp/kegg/document/help_pathway.html

The pathway is kind of broad but it provides some mechanisms for tumorigenesis from two standpoints: chromosomal instability, and microsatellite instability. The pathways we're seeing promotes the tumor development by upregulating proliferation signals, and downregulating apoptosis pathways. There's bound to be more to it, especially since we see other players involved when we get into cases like metastasis like snail1/2, Met, Src, etc. Below is a survey of apoptotic pathways from Nature, with pro-apoptotic in red, and pro-survival in green:

Source: http://www.nature.com/reviews/poster/apoptosis/index.html

Ignoring the therapeutic targeting jargon, you can see that when growth factors bind, the cell generally pushes towards a survival state. When death factors bind or something goes wrong, the cell pushes toward an apoptotic state. Cancers, however, are intrinsically disregulated:

They have methods of overstepping their boundaries as cells, which is what makes them problematic. The general conclusion I'd draw from that KEGG pathway, though, is that many pathways need to be disregulated to end up with colorectal tumors, and the method of disregulation is (a) downmodulated mismatch repair, and (b) chromosomal aberrations due to duplication, etc. Andkeeping in mind the box of oncogenes vs tumor suppressors in the corner: "An important difference between oncogenes and tumor suppressor genes is that oncogenes result
from the activation (turning on) of proto-oncogenes, but tumor suppressor genes cause cancer when they are inactivated (turned off)"


What happens when too much sodium flows in the cell due to a faulty voltage-gated sensor? What about too little? The activation gate opens, signaling depolarization. Eventually, the inactivation gate closes, ending depolarization and beginning repolarization.

What is the physiological impact of the inactivation gate remaining open too long, letting in too much sodium into the cell than a normal action potential? This would raise the magnitude of the action potential.

What would be the impact if it remained open for too short a time?

To answer the OP directly: You may be interested in looking at diseases that abnormally increase or decrease the activity of sodium channel proteins, changing the degree to which sodium ions cross the cell membrane. Some diseases are genetic in basis, which means they are inherited. This lends them to characterization and study.

This review paper by George summarizes some of the genetic diseases associated with sodium channel mutations, which might give you some direction for further research:

Muscle sodium channelopathies (SCN4A)

Hyperkalemic periodic paralysis
Paramyotonia congenita
Potassium-aggravated myotonia
Painful congenital myotonia
Myasthenic syndrome
Hypokalemic periodic paralysis type 2
Malignant hyperthermia susceptibility

Cardiac sodium channelopathies (SCN5A)

Congenital long QT syndrome (Romano-Ward)
Idiopathic ventricular fibrillation (Brugada syndrome)
Isolated cardiac conduction system disease
Atrial standstill
Congenital sick sinus syndrome
Sudden infant death syndrome
Dilated cardiomyopathy, conduction disorder, arrythmia

Brain sodium channelopathies (SCN1A, SCN2A, SCN1B)

Generalized epilepsy with febrile seizures plus
Severe myoclonic epilepsy of infancy (Dravet syndrome)
Intractable childhood epilepsy with frequent generalized tonic-clonic seizures
Benign familial neonatal-infantile seizures

Peripheral nerve sodium channelopathies (SCN9A)

Familial primary erythermalgia

Generally, you might search on the term "sodium channel mutant" or "mutations" to see what kinds of health problems are caused by under- or over-activity of these proteins.


Exploring speed of ants I'm working on developing a model of ant foraging. To do this, I have simulated food morsels distributed randomly within an area, with the minimum distance between morsels being variable. I'm trying to get a good idea of the scale at which I should define the distances. This has to depend on ant walking speed and their usual foraging distance.
I'm not very species-specific in my approach. One study (1) shows a survey of foraging distance for different species. They found that most of the species had a maximal foraging distance of less than 1m. Some species did go upwards of 10m. I presume this distance would increase with the presence of trails, but to only focus on finding food by exploring, I can keep the distance between food morsels to be 2m-3m.
Now, I also want to figure out the time that it would take an ant to start from the nest and reach the food given its distance. This is where I'm stuck. I wasn't able to find any survey or study on walking speeds of different ant species. I need an approximate 'exploring speed' of ants, which is just time taken to reach a morsel after leaving the nest. Are there any references I could use to estimate this value for my model?
References:

Eguchi, K., Bui, T. V., & Yamane, S. (2004). A preliminary study on foraging distance and nesting sites of ants in Indo-Chinese lowland vegetation. Sociobiology, 43(3), 445-457.

I don't think it's reasonable to try to do this in a species-independent manner, since there is so much difference between ant species. Leaf-cutter ants, for example, will build trails to forage 200 meters away from their nests. Likewise, ants vary by two orders of magnitude in size and the walking speed of an ant will vary accordingly as well. Finally, I don't think that you can reasonably exclude trail-building from your simulation, since that's a key ingredient of foraging.
Bottom line: pick a species to model and look for information on its specific mobility.


Frog in Akaka / Loango Région Gabon I was recently in Gabon, and I did some long and serious treks with Pygmées into some forest mostly to see Chimps and Gorilla around the Akaka area in Loango national park.
During a trek in forest I took a picture of this frog, it's been a little while now I can't find the exact species of it.

Any ideas guys ?

https://ibb.co/eU4ROk Full sized picture here

I'm not completely sure as it's very difficult to determine frog species with just one picture taken from the side.
Morphology-wise it looks like this is a Afrixalis dorsalis, although it's colour doesn't comply with the most comomon pattern. You can find pictures of this species with specimen looking exactly the same or very similar.
Colour deviations occur in several frog species...

interesting article about frog species in Gabon
AmphibiaWeb Afrixalis dorsalis (this also mentions differences in patterns and light coloured populations)

Source: Wikimedia Commons

Source: http://calphotos.berkeley.edu

Common colours and pattern
Source: http://calphotos.berkeley.edu


Is there any strong factor against human edible plants being widespread and easy to gather? While many habitats have plants, fruits, nuts and berries available for consumption by humans walking by, most places (if any?) seem to require significantly more effort than simply picking our food from trees and bushes in order to survive.

Borrowing @BryanKrause's words in a comment below:

"Why don't you find enough things like broccoli, green peppers, almonds, and wheat to support a human population when you are walking in the woods/natural fields?"

Define "easily available to human", lots of fruit are perfectly edible to humans. Human have only become widespread in the last few million years so there is not enough time to see things specialized in humans via natural selection. Especially since we  are both generalists and for most of the world completely new factors in the environment.

But there are plants that have evolved to be eaten by humans. Wheat, rice, and, maize have done amazingly well by having the right factors to be useful to humans, they are also some of the most common plants on earth now thanks to us.
Artificial selection is still evolution, it's just not natural selection. Humans are generalists and its hard for natural selection to push things to specialize in edible symbiosis with a generalist, especially in as short a time as humans have been around, but artificial selection can do it just fine becasue it is faster, provided the plant in question survives us long enough.

Being useful to humans is also a bit of a mixed bag sometimes it means we spread you over the whole world, such as wheat and dogs, but sometime is means harvesting to extinction like Silphium. Then you have things like avocado which almost went extinct becasue humans killed off their parter animals and almost nothing else could eat them, then we invented farming and decided we liked them and brought them back from the brink. Human intelligence and cultural information sharing means capabilities and technology change so much faster than the speeds natural selection tends to work at, most things just have not had the time to really adapt to how fast we changed the world,  unless we take an interest in forcing them to.


Why HIV need integrase enzyme to integrate their DNA into host cell? In gene transfer by microinjection, the gene of interest is injected into the nucleus of host cell without using integrase enzyme. So why does HIV need that enzyme? Why they not just place their DNA into the nucleus and let it stay there?

During gene transfer by microinjection the DNA has at least some fragments of identical DNA sequence to the host genome. Usually DNA that is used for microinjection will have flanks on either side identical in sequence to two nearly situated, sometimes adjacent blocks of DNA sequence. This allows homologous recombination to occur which engages proteins already present in the host cell: https://en.wikipedia.org/wiki/Homologous_recombination

In case of HIV, there are no fragments of identical sequence flanking the genome of the virus, so no homologous recombination can occur, therefore integrase is necessary. Furthermore, integrase inserts viral genome into random parts of the host genome unlike homologous recombination, which would always localize that viral genome into the same spot each time.

Now, this is my wild guess, as I couldn't really find any evidence in the literature but I'd say it gives the virus certain advantage. Site-specific insertion could be easily inhibited in the course of evolution by mutations within the host genome and eventually the virus would be eliminated. This is not the case with random allocation, as no mutations in the host genome will ever substantially change the probability of integration.

Here is a good review on the process of DNA integration regarding HIV: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385939/

Let me know if this helps, confront your opinions with what I think.

Cheers,

Krzysztof


Why do we need to replicate incomplete DNA fragments by PCR from a crime scene? If the DNA from a crime scene is damaged, why would it be helpful to replicate it by PCR (polymerase  chain reaction)? Even if we get billions of those copies, it is still incomplete, isn't it? How can the PCR make the forensic process easier?

This process helps with the signal to noise ratio.  In theory, you could use the fingerprinting techniques to dice up the few billion copies of the DNA and carefully measure them.  However, it is far easier to replicate the DNA to increase the number of molecules of DNA available to the process.

Remember, fingerprinting for crime investigations doesn't involve reading the DNA, but merely uniquely identifying it.


Don't understand how multiple replication bubbles work I'm not exactly sure how multiple replication bubbles work, assuming were working with a linear, eukaryotic chromosome.

This is a diagram for reference:

It appears that the DNA is being synthesized "towards" the centre. What I mean is that in one replication bubble, the top strand is being replicated from left to right, whereas for the other replication bubble, the top strand is being replicated from right to left.

I don't understand why this is. Aren't the directions reversed? Isn't synthesis always supposed to be from 5' to 3'?

Thanks!

You mistake replication direction with polymerase synthesis direction. Indeed, the polymerase synthesizes new strands 5' -> 3' but if the replication of each strand was continuous, there would be  no such structure as a replication bubble whatsoever. Take a good look at the drawings:

The thing is the direction of replication is consistent with the direction of leading strand synthesis, so the bubbles will "spread" outwards. Lagging strand is synthesized in the form of fragments 5' -> 3'. If you look closely fragments that are closest to the center of the replication bubble are synthesized first, then polymerase detaches and works on the next fragment which is actually closer to the 3' end of the lagging strand.
Here's an article on Wikipedia about those fragments: https://en.wikipedia.org/wiki/Okazaki_fragments

Hope this makes things clear.

Cheers and happy learning,

Krzysztof


How do DNA viruses keep themselves in the nucleus without inserting themselves into genome? If I'm not mistaken only RNA viruses insert themselves into the host genome. As an example of DNA viruses, herpes viruses for example do not insert themselves in the host genome.

Then how do DNA viruses keep themselves inside the nucleus? Do they just float around without their capsid? And if the cell duplicates, would the DNA of a DNA virus also be duplicated even though it isn't inserted in the host's genome?

Herpesviruses maintain themselves during the latent state as "episomes", circular DNA elements, with no capsid, that are in the nucleus but that are not integrated into the host genome. Host enzymes replicate these episomes, and different viruses have evolved different strategies for ensuring that the episomes are passed on to newly-divided cells.

  After they first infect cells, many herpesviruses establish a latent lifecycle with the viral genome existing as circular genetic elements called episomes inside the host cell’s nucleus that are closely associated with, but not integrated into, the host DNA. During latent infection, episomes are replicated during S phase, but new viral particles are not produced and the infected cell survives. The maintenance of herpesvirus genomes as episomes contrasts significantly with retroviruses, which insert their genome within the host cell genome to ensure their replication and inheritance by daughter cells and establish long-term infection. ... EBV uses a mechanism to tether the EBV genome to host DNA, facilitating the equal distribution of episomes in daughter cells with a larger number of cells having at least one EBV genome. In contrast, KSHV uses a clustering strategy that promotes a higher number of episomes per cell, but at the expense of not passing on the episome to some daughter cells

--How herpesviruses pass on their genomes

Another mechanism many herpesviruses use is to establish their latent infection in non-dividing cells, especially neurons, so that there's no concern about daughter cells.


What's the difference between Ki and IC50? I have just read this post at researchgate: "How to calculate experimental binding free energy from the IC50 value"

I am not be very sure about what the difference is between Ki and IC50. Could anybody explain?

In biochemistry the Ki is the dissociation constant of a complex and molecules bound to it. It is a measure for the  functional strength of the inhibitor. This can for example be an enzyme and its substrate, the Ki defines the stability of the complex.

The IC50 on the other hand is the halfmaximal inhibitory concentration of a substance on a biochemical process. This can be an inhibitor of an enzyme.
See this figure (from the Wikipedia article on the IC50):

The Ki plays an important role in the calculation of the IC50, as it defines the strength of the enzyme-inhibitor complex.


What do the column labels in this table mean? This table shows the effect of sound (song and tones) on female birds. However, I'm not sure what the labels (F1 22, P and η2) mean. I've seen the labels on other tables too.

(from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508516/)

If anyone could help I'd be very grateful :)

thanks!

F(1,22) is the result of an F-test with degrees of freedom 1 and 22, in this context most likely this is an F-test in the context of ANOVA; for the meaning of those degrees of freedom I would suggest further reading on ANOVA. Specifically, in this table it looks like we have a 2x2 ANOVA: with stimulus songs or tones and treatment E2 or none, and the interaction between them.

P is the P-value associated with that F-test; it is the probability of observing a result as extreme or more extreme than the F-test gave in this circumstance, given the null hypothesis was true (typically the null hypothesis is something like "the groups don't differ"), and assuming all of the assumptions of the statistical test hold true.

η2 is read as "eta-squared" - it is a measure of effect size, meaning it describes the magnitude of an effect controlled for some other characteristics of the measure, typically the variance. Many statisticians prefer presentation of effect sizes rather than p-values. A large value of η2 means that lots of variance in the outcome variable is explained by the parameter of interest.


Are some non-coding RNA spliced? Are some non-coding RNA spliced like mRNA? I tried to find some information but I don't find anything...

You should check out Howald C, et al[1].  This is one of the many recent papers tied to the ENCODE data. They've used RT-PCR to amplify exon-exon junctions and then sequenced the results. Supplemental table 2 shows 3076 validated exon-exon junctions in putative processed transcripts which, in the main body of the paper may be sub-classified as:

  Non-coding, 3prime_overlapping_ncrna, Ambiguous_orf, Antisense,
  LincRNA, ncRNA_host, Retained_intron, Sense_intronic,
  Sense_overlapping, Processed transcript.

Howald C, Tanzer A, Chrast J, Kokocinski F, Derrien T, Walters N, Gonzalez JM, Frankish A, Aken BL, Hourlier T, Vogel JH, White S, Searle S, Harrow J, Hubbard TJ, Guigó R, Reymond A. 2012. Combining RT-PCR-seq and RNA-seq to catalog all genic elements encoded in the human genome. Genome Research, 22: 1698–1710, doi:10.1101/gr.134478.111.


RFLP Pedigree question A relatively frequent, completely penetrant recessive disease variety of mutations in the gene. The gene has been recently cloned. Analysis of the region flanking the gene reveals that the population has at three (3) RFLP (this is a type of DNA marker; they are not SNPs so have much larger sizes) alleles in this region. The sizes of the RFLP alleles are 7, 10 or 13 kb in length. Shown here are two small pedigrees of families in which affected individuals are shaded in black. The size of the RFLP alleles each individual carries is shown below the pedigree. enter image description here

Question: If the male child from the left pedigree marries the female child from the right pedigree, What is the probability their child will be a carrier?

I said that there isn't enough information to tell since the parents genotypes are unknown.

I said that there isn't enough information to tell since the parents genotypes are unknown.

It seems like you are misreading the diagrams since you say the parent's genotypes are unknown.  All 8 individuals in the two pedigrees have the same information given for each, appearing in the eight columns directly beneath the eight individual's symbols.


Terminology question: the scope of an allele in an organism Let us consider a gene FOO with novel type foo.

If I were discussing an organism that has inherited foo in every cell during classical zygote formation, then I would ordinarily just say that the organism has foo.

If I were discussing a SNP of FOO that gives rise to foo in a tumor cell of an organism, I wouldn't say that the organism has foo, but I might say that the tumor has it.

If I were discussing a chimeric or mosaic organism in which some fraction of the chimera had foo and the other fraction had FOO, I would have to say something like "in foo-containing cells ..."

But what if I wanted to particularly draw attention to the scope of applicability of the allele in question? That is, I want to talk about the scope explicitly, rather than implicitly. How could I directly refer to the scope of applicability of an allele? Is there a single adjective that captures the concept of "This organism has foo in every cell except in rare ones where a point mutation may have occurred; it's probably been inherited during normal meiosis" and is there a contrasting term for "The organism only has foo in a particular subset of its cells and there is some other genetic process necessary to explain that."?

If I were discussing a SNP of FOO that gives rise to foo in a tumor
  cell of an organism, I wouldn't say that the organism has foo, but I
  might say that the tumor has it.

You can call it a somatic mutation. See this paper. They report such mutations in cancer.

You can use the term like this:

  Carcinoma tissue had a somatic mutation in XYZ oncogene, thereby making it constitutively active.

  If I were discussing a chimeric or mosaic organism in which some
  fraction of the chimera had foo and the other fraction had FOO

In this case you can say:

  The organism is chimeric for gene-X, expressing variants X1 and X2

From this article:

  Effects of AngII-Infusion Into LDL Receptor−/− Mice That Were Chimeric
  for AT1a Receptors


Do some colors trigger more neural activity in human brain? On this webpage I found this:

  The study found that “globs” in the brains of monkeys reacted differently to colored
  stimuli, and reacted based on color. The brain was most triggered by specific colors
  (red, then green, then blue) and colors with the most saturation. What this tells us is
  that these colors immediately impact a user and draw attention.

Question: Do humans show similar increased neural activity to some colors?

Then I found a perception curve in this webpage

While this curve tells that yellow and green are seen before other hues while red and violet are difficult to perceive; I am not sure if yellow and green elicit more neural activity in the brain.

Anything to say on this matter?

The paper from Stoughton & Conways (2008), where the linked Design Shack webpage refers to, explains that in the visual nucleus in the brainstem (LGN) as well as in the primary visual cortex, most of the color-selective neurons are selectively responsive to colors in the red-cyan axis (Fig. 1).

Fig. 1. RGB color space. source: Commodore 128 forum

This indeed means that these colors evoke more brain activity in these regions of the brain.

Note that a perception curve mentioned on the linked D'Source webpage is nonsense terminology


Why are certain baby (water)fowl yellow? Why are e.g. ducklings, goslings, turkey and chicken chicks (partly) yellow?

What is the chemistry background to this? What compounds from the egg cause this to happen?

What is the evolutionary background to this? How could it help the bird to survive?

While domestication has led to selection of all-white adult birds and thus more common all-yellow babies, why does an all-yellow baby become an all-white adult, in terms of biochemistry?

Wild ducklings, like these baby Mallard ducks, are in fact typically only partly yellow:

Photo by TheBrockenInaGlory via Wikimedia Commons, used under the CC-By-SA 3.0 license.

While I'm no expert, I would guess that the mottled yellow-brown coloring of the juveniles is, at least partially, protective coloration, just like the somewhat similar pattern on the adult female's feathers.  While it may appear conspicuous on open water, ducks in their natural habitat will often seek shelter among reeds and other vegetation, where the irregular pattern of light and shadow would create a very effective camouflage for the ducklings.

As for the all-yellow ducklings of domestic ducks, these presumably arose via elimination of the darker parts of the coloring as a result of selective breeding, perhaps as a side effect of artificial selection for the white adult plumage found in many domestic ducks today.

Specifically, according to a recent study of domestic duck genetics, it appears that the all-white plumage of domestic Pekin ducks is caused by a single recessive mutation to the MITF gene, which regulates melanin production.  The mutation, when homozygous, causes the normal melanin production pathway in the skin to be almost entirely shut off, so that the adult plumage is pure white regardless of what other plumage color genes the bird may be carrying (a fact apparently known for a long time from cross-breeding experiments, even though the specific mutation behind this effect was not determined until recently).

Apparently, however, the yellow base pigmentation in young ducklings is not affected by the MITF mutation, and thus appears even in individuals homozygous for it.  Presumably this is because the yellow color is produced via some other pathway, which is active in young ducks but gets shut off as they develop their adult plumage.  The brown pigmentation pattern overlaid on top of it in wild-type ducklings, however, is controlled by MITF, and thus fails to appear in ducklings with two copies of the mutated version of the gene, leaving their juvenile plumage pure yellow.

As far as I can tell, the specific reason why the yellow pigmentation in ducklings is not controlled by the MITF gene still remains unknown.  Or, if it is known, my Google search skills were not good enough to find it.


How does the Cuttlefish camouflage itself accurately despite being color-blind? I have seen/read that the Cuttlefish is able to camouflage itself extremely accurately. I have also seen/read that they are completely color-blind, though see with very high contrast. How does the Cuttlefish manage to blend itself so well to its changing surroundings if it is not able to perceive the colors it is changing itself to?

The reason why the cuttlefish is colour blind is because

  it just has one type of cone cell. Humans have three different types,
  each sensitive to a different color of light. With only one cone type,
  you couldn’t differentiate between different colors (reference).

A study was conducted in the lab of Dr Lydia M. Mäthger where two different checkerboards were used to test their colorblindness.

  1) Gray – Green. One green shade, matched to the maximum absorption
  wavelength of cuttlefish, was combined with 16 different shades of
  gray. As supposed some shades of gray couldn’t be distinguished from
  the green by the cuttlefish, which didn’t adapt the body pattern.
  Experiment one was successful.

  2) Blue – Yellow. A checkerboard of blue and yellow matching in
  intensity was used for the second experiment. The skin color of the
  test species didn’t change either and therefore experiment two was
  also successful (reference).

These experiments concluded that it was indeed colourblind.

To confirm the effectiveness of the camouflage, HyperSpectral Imaging (HSI) was used to measure the colour match between the cuttlefish and its background. Using this technology it was perceived as to how a predator would view a camouflaged cuttlefish. It was found that

  Cuttlefish can produce color-coordinated camouflage on natural
  substrates despite lacking color vision, and that the color aspect of
  cuttlefish camouflage is highly effective against fish predators. Much
  of the contrast information (which allows a predator to "pick out" a
  cuttlefish from the background environment) resides in the brightness
  (luminance) rather than in the color (chromatic) aspect of the
  reflected light. What this means is that cuttlefish camouflage
  strategies take away a tool from predators in their ability to pick
  out their prey from the background and instead leave them with only
  brightness as a method for prey identification (reference 1 and reference 2).

And now we get to the main question as to how they do it. Cuttlefish are apparently able to detect the intensity of light reflected from objects in its surroundings. It is able to perceive even a 15% change in contrast. In an experiment, it was found that

  The animals did not respond to the checkerboard pattern when placed on
  substrates whose color intensities were matched to the Sepia visual
  system, suggesting that these checkerboards appeared to their eyes as
  uniform backgrounds (reference).

In another bit of interesting research done on the ability to copy the patterns on checkerboards (reference), three inferences were drawn

  The first find was that the range (relative to the size of the
  cuttlefish ‘white square’) for the animal to exhibit disruptive skin
  patterning had to be withing a certain  narrow range. Secondly, given
  the appropriate size of checker, cuttlefish regulated their disruptive
  skin patterns according to the contrast between white and black
  squares. Third, by manipulating the number of white squares on a board to just  4
  among 316 black squares (or 1.25 %) produced disruptive patterning,
  yet increasing the number of white squares to 20, 40 or 80 did not
  increase the frequency of appearance of the cuttlefish ‘white square’,
  but only its clarity of expression.

This study shows that the number of white objects in the background significantly influence cuttlefish skin patterns further putting stress on its ability to view the polarization of light (reference).

Some cuttlefish camouflage examples


Why can't NMR be used on large RNA molecules? While reading my Molecular Bio textbook, I came across a sentence that stated that NMR cannot be used on large RNA molecules to determine their structure. Why is this? Is it because RNA is single stranded?

RNA usually has pretty complex structures. What causes the problem with NMR however is that large RNAs, such as mRNAs, don't have 1 structure, they have a population of possible secondary structures, and even if small parts of the RNA always have the same local structure, the overall molecule will occupy a variety of forms. The NMR will see a population of structures and won't be able to get good signal. DNA and RNA seem like tempting targets for NMR because the phosphorus in the backbone is NMR active, potentially allowing for backbone structure determination, but this only works on short pieces of RNA that adopts a single conformation.

Unfortunately I don't have sources to cite, only a couple semesters of NMR courses and a year of in vitro transcription of mRNA.


Will a vasectomy prevent genetic engineering of a child? Making the assumption:

  Within 10 years, an adult will be able to genetically engineer (modify, enhance, clean, etc.) a child from their own DNA (and the DNA of a non-related partner).

then would getting a vasectomy today preclude this?

From the wording of your question the 'genetic engineering' that you are envisaging will involve sperm. So the question is really, does vasectomy affect sperm production?

The answer is that it does, but it doesn't abolish it. For example:

  McVicar et al. (2005) Effects of vasectomy on spermatogenesis and fertility outcome after testicular sperm extraction combined with ICSI. Human Reproduction 20: 2795-2800

These authors found that sperm yield fell to about 35% > 5 years post-vasectomy.


What spider is that? It was scared because my cat was playing with it. I saw it tonight (22 October) in Slobozia, Romania. I never saw something like it. The back is white with no points or marks or lines.

It's pretty clearly an Araneid of some kind, based on the large, globular abdomen, the eye arrangement at the front of the 'head', and the characteristic defensive posture when out of the orbweb.  All known orbweavers are completely harmless to both cats and humans, so nothing to worry about!
Unfortunately, I'm not familiar enough with central European spiders to tell you exactly what it might be, but I can assure you that it is not the only problem biter in your area - one of the Black Widows.  I include a photo I found of a common orbweaver in Europe (the Cross Spider) which was also caught out of its web, and in a similar position (although clearly not having been attacked by a cat..).  Whether yours is normally a plain white species, or yours is a leucistic (all-white or partially-white) variation of a normally darker and patterned species, I have no idea.  As I say, I'm not familiar enough with European spiders to be confident about something like that.


Biological Neural Network Training for Babies I am concerned by the fact that babies cant walk because the muscles in their limbs arent developed and tuned to give directional control, it takes years before babies gain mobility and dexterity. So technically the neural nets in the motor cortex requires years of training before that capability is achieved.
However, when the babies are born they dont need training for ocular muscles for directional control of their eyeballs (which is quite computationally challenging problem due to high degree of freedom compared to hinge movement) . Do biological neural network for occular muscles come pre-trained while the neural network for limb muscles come untrained by birth?

Biological neurons function in a very different way, as compared to the simplistic artificial neural networks of machine learning. For example, see how real neurons work and how they connect with each other. The types of neurons themselves are very varied:  "...neurons to take specialized forms such as unipolar,bipolar,  multipolar,  anaxonic,  pseudounipolar,  basket  cells, purkinje cells, Lugaro cells, spindle cells and more.".
As for the eyes, light passes through a large network of neurons before hitting the rod and cone cells. It's the opposite for the octopus retina. Animal babies are able to learn to walk much quicker than human babies. Also, have a look at videos of how blind children learn to walk.
So essentially, there's a lot lot lot more going on in the creation and working of the human body than just "neural network training". A really nice paper titled "facts and anomalies" gives perspective into this complexity.
Nobody fully understands how the system of cells and the equilibrium works. It's extremely complex and multi-dimensional. When you look at the complexity inside a single cell and the electron transport chain, you'll notice that there's a heck of a lot of things that are already pre-programmed and designed to make use of the molecular properties of nature to create structures and motors using the equilibrium of chemical properties. When such an equilibrium is created, evolution and adaptation can happen, but only in a very controlled manner. So I do not believe a baby's neural network is getting trained to walk or see. It's pre-trained from millions of years of evolution. The reason it may be taking some time to mature, is probably because the corresponding neurons in the brain are taking some time to get created, grow and find their way in the brain to form the right synapses.


Why do mitochondria have a phospholipid bilayer? So, a thought came up and I couldn't find all that much info online, so I thought I'd ask some professionals here!
The endosymbiont theory states that: mitochondria came to be ingested by bigger prokaryotic cells about 1.8 bYa, and by chance of luck came to a mutualistic relationship.
Now, mitochondria are said to have been archaea, right? But the mitochondria in our cells have phospholipid bilayers, with ester bonds in them, like all eukaryotes, but when you look at archaea, you see that they have monolayers because of their ether bonds, with rings and all sorts of branching, which is what gives them that extremophile-acclaimed resistance.
Question is if the endosymbiont theory is so widely accepted and mitochondria are meant to be archeae, why do they not present a monolayer with ether bonds?
Thanks for your time!

I think the question is based on a false premise:

  Poster: Now, mitochondria are said to have been archaea, right?

  Me: Wrong, I’m afraid.

The closest bacterial relation of mitochondria is  Rickettsia, an alpha-Proteobacterium (see Lang et al. for a review). Rickettsia is a eubacterium, not an archaebacterium.

The confusion is probably due to misreading one of the two alternative theories of the origin of mitochondria. This is the theory that the host for the original mitochondrion was an archaebacterium (rather than a primitive nucleated eukaryote). In both theories this host aquired a eubacterium related to Rickettsia, which gave rise to the mitochondrion.


RE: Fasting gastric pH vs Normal gastric pH If fasting gastric pH values are more acidic then why is it recommended to eat no more than three hours before bed time to prevent reflux. It seems at some point during sleep the stomach would become more acidic therefore make reflux worse.

Food only partially buffers the pH of stomach contents and acid is not the only esophageal irritant present in the stomach.

The goal, therefore, is to have as little as possible present in the stomach when lying down (supine) to reduce risk of gastro-esophageal reflux (GER) through the lower esophageal sphincter (LES) into the esophagus. Avoiding meals just before bed, especially fatty meals (which delay gastric emptying), may help in this regard perhaps by avoiding supine position while there is a low pH layer, formed in response to the meal, lying atop the stomach contents.

Weight loss and smoking cessation are frequently recommended to reduce GER symptoms, with some evidence to support this advice. Use of tobacco or alcohol may relax the LES and tends to be associated with GER symptoms, though trials of counseling to reduce their impact have not significantly reduced those symptoms (and another study).


Gibbs free energy and its change for the hydrolysis of ATP So in my book I have the reaction

$$ATP \rightarrow ADP +P_i$$

and hence $$\Delta G^0 = G^0_{ADP} + G^0_{P_i} - G^0_{ATP}$$

This is easily understood, but I have not been given any actual concentrations of values to use to calculate the result, which is given as

$$\Delta G^0 = -31.0kJ\text{mol}^{-1}$$

  Where do I find the values of $G^0_{ADP}, G^0_{P_i} \text{ and } G^0_{ATP}$?

I have the formula $$\Delta G = \Delta G^0 + RT\ln \bigg( \frac{AB}{CD} \bigg)$$

where $A,B$ are the concentrations of the products and $CD$ are the concentrations of the reactants.

You can use tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$ , such as those found in Table 1 of the following reference, to calculate apparent equilibrium constants of biochemical reactions, and to calculate standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$ (at pH 7), which I think is exactly what you require.

Calculating apparent equilibrium constants of enzyme-catalyzed
reactions at pH 7 (by R. A. Alberty)

The first thing to say it that you need to include water as a reactant.

$$\ce{ATP + H2O = ADP + P_i}\tag{1}$$

Secondly, the reaction shown in Eqn(1) is used as an example by Alberty in the paper cited above, where he calculates both $\ce{\Delta _rG^{'o}}$ (at pH 7) and the apparent equilibrium constant (at pH 7).

The following values were taken from Table 1 of the Alberty reference cited above.  They refer to pH 7, 25oC, and an ionic strength of 0.1.

              $\ce{\Delta _fG^{'o}/{kJ mol^{-1}}}$

ATP             -2276.43

ADP             -1409.95

Pi              -1059.17

H2O              -156.05

Knowing these values, it is now very easy to calculate the standard transformed Gibbs energies of formation, $\ce{\Delta _rG^{'o}}$, for the reaction shown in Eqn (1) (it is merely a case of 'pluggin in' the values).

$$\Delta _rG^{\ce{'o}} = \sum v_i^{'} \Delta_f G_i{^o} = (2276.43 + 156.05 - 1409.95 - 1059.17)\tag{2}$$

$$\ce{\Delta _rG^{'o} = -36.68 kJ mol^{-1}\tag{3}}$$

In Eqn (2), $v_i^{'}$ is the stoichiometric number (positive for reactants
and negative for products)

The criterion which determines whether a reaction will 'go' in the forward direction or the reverse direction is the transformed Gibbs energy of reaction, $\Delta_rG^{'}$, (not $\Delta_rG^{'o}$).

  If  $\Delta_rG^{'}$ is negative, the reaction goes in the forward direction.

We can say that under standard conditions, Eqn (1) goes to the right, and as $\Delta_rG^{'o}$ (not $\Delta_rG^{'}$) is directly related to the apparent equilibrium constant (Eqn 4), we can say that the equilibrium constant for the rection of Eqn (1) is very much to the right.

$$\Delta _rG^{\ce{'o}} = \ce{-RT ln K^{'}}\tag{4}$$

We can go a step further (Alberty,2000) and calculate the apparent equilibrium constant, $K^{'}$, for the reaction shown in Eqn (1).

$$K^{'} = e^{\frac{-\Delta _rG^{'o}}{RT}}=e^{36680/(8.3145 \times 298.15)}\tag{5}$$

$$K^{'}  = 2.67 \times 10^6\tag{6}$$

The great value of tables of $\ce{\Delta _fG^{'o}}$ it that they allow $\Delta _rG^{\ce{'o}}$ and $K^{'}$ to be calculated for many reactions, even those for which there is no known enzyme, or where the equilibrium constant has not been determined.

Notes

In Eqn (5) above, $R$ is the gas constant ($\ce{8.3145 J K^{-1} mol^{-1}}$
) and $T$ is the temperature (in Kelvin)

IMO, the Alberty reference cited above is a model of clarity that makes these type of calculations very easy. It is also an 'easy read' with many great examples.

Two other good refs, if you are 'into' such things, are

Biochemical thermodynamics (by R.A. Alberty)
Recommendations for nomenclature and tables in biochemical thermodynamics (by R.A. Alberty)

Other  tables of standard transformed Gibbs energies of formation, $\ce{\Delta _fG^{'o}}$, may be found in

Calculation of Standard Transformed Gibbs Energies and Standard Transformed Enthalpies of Biochemical Reactants  (by R.A. Alberty)
Calculation  of Standard Transformed Formation Properties of Biochemical Reactants and Standard Apparent Reduction Potentials of Half Reactions (by R.A. Alberty)


Is it better to take a half dose of paracetamol and a half dose of ibuprofen together rather than a full dose of either? Recently, I heard on this health-related radio programme that it was better to take a half dose of paracetamol and a half dose of ibuprofen together, rather than the full dose of either one, for acute pain. Could anyone explain the reasons for this ? Could it be something along the lines of there being diminishing returns to higher doses, so you get more bang for the buck, as it were, for the first half of a dose than the second, but due to possible toxicity or drug interactions, two full doses are not recommended ?

In the same radio programme it was stated that caffeine also helps. Can anyone explain that ?

There are many different reasons for an acute pain and inflammation (both directly via pain receptors, and indirectly via swelling etc.) plays not the least role in this phenomenon. Therefore the combination of a classic analgesic without anti-inflammatory activity (as paracetamol) with a strong anti-inflammatory agent (as ibuprofen) is a reasonable one and potentially alleviates the pain manifestations in more cases than a single administration of every agent.

You are right with you suggestion that the doubled dose could be dangerous: even though the complications of Paracetamol administrations are not often, they are very dramatic (acute liver failure) with rather pessimistic prognosis. This is why one generally tries to half the doses if combined with other similar-acting agents (historically paracetamol was for the long time a member of the non-steroid anti-inflammatory agents).

Caffeine is generally believed to be a pain reliever, especially as concerns the pains with migraine background (source). One review, however, points out that there are still not enough data to support this belief (source).


When contracting a muscle will the muscle spindle stretch or contract? When you contract your muscle, will your muscle spindle stretch or contract? And why? I was always under the impression that it was contracting your muscle spindle, but now I am not sure.

The muscle spindle normally stretches/contracts in concert with the muscle fibres in order to maintain detection of changes in length.

This image should demonstrate it clearly:

  When the muscle spindle is stretched and excited it sends impulses to the spinal cord more rapidly (increased frequency). The sensory neurons synapse with alpha motor neurons in the spinal cord, which stimulate the extrafusal muscle fibers of the stretched muscle to contract and resist further stretching.
  Contraction of the muscle (extrafusal fibers) would cause the muscle spindle to become slack and stop transmitting impulses, however descending fibers of motor pathways synapse with both alpha and gamma motor neurons (alpha - gamma coactivation) so the ends of the intrafusal fibers contract and maintain muscle spindle sensitivity when the muscle contracts.

Further reading: here.


What were the first neural systems like? I'm curious about the origin of the neural network.

I'm thinking perhaps once life evolved beyond the single cell organism, it needed a simple neural network to coordinate those cells, and cell functions.

What were the first neural systems like?

More specifically: What kind of cell did the first neurons evolve from and how did they work at first? (assuming there were few, if any, neural connections in the first organisms to develop neurons of some sort)

From what I understand about a neural system, it needs a few neurons linked together to keep firing.

Perhaps the first neurons had triggers other than dendrite connections?

This question can be answered by taking a look back evolutionary and see how other organisms have utilized neurology. The prime example, because it was one of the first real models of the neurological system, is the squid. It has neurons with singularly long axons to send electrical pulses long distance. This method of electric pulse transfer has been evolutionary updated, essentially, but we can get an idea of how these cells came to be. If we look back at squid predecessors, like the jellyfish, we see that it also developed electrical impulse cells to aide in defense and movement. Back further, we see the sponge has no neurons, but has something similar. This gives us potential insight into the development of the cell. It has protein clusters that act similar to post-synaptic signaling. So it is likely the electrical impulses were developed based on the function of these protein clusters, and bam! Electrical pulses became a must faster way to communicate to different regions of a system than simply trying to protein signal across cells.

Of course, looking at this question evolutionary is tricky since the question of divergent evolution comes into play, and we can't know if the sponge protein clusters offer a potential answer to neuronal development. But, is interesting evidence and makes an interesting debate!

Source= Sakarya O, Armstrong KA, Adamska M; et al. (2007). Vosshall, Leslie, ed. "A post-synaptic scaffold at the origin of the animal kingdom". PLoS ONE


What's the current conclusion about humans being omnivores vs herbivores? What's the current conclusion about humans being omnivores vs herbivores?

And particularly, how is this relative to time? That is, is possible herbivoreness a "strictly" modern phase in human evolution? Or has it even occured yet?

Humans are omnivores as they can eat and digest meat. Early humans were hunters and gatherers and meat was a part of the menu from time immemorial. I don't know the exact technic term but some of our teeth were designed to handle meat (canines?). Sure, people can willfully limit their diet to plants only but from the biological point of view humans are omnivores.


Where can I find comprehensive data on animal distribution? I'm looking for vertical distribution or tidal height of several intertidal species, specifically from the Pacific Northwest.

I considered looking for published research for each species however, my search likely would not be comprehensive and perhaps be biased in site-specific differences.

Is there some kind of open database where I can find this information?

I've found that EOL draws some data from the Ocean Biogeographic Information System, but when I go to the site directly, I can't find the tidal height data. I've also looked through suggestions in response to this question but none are applicable.

Any help with these databases or suggestions on other relevant databases would answer my question.

I like your question a lot! I think what you're trying to achieve is the best way of solving your problem. Unfortunately, although I do have a few links for you that might get you a little bit further, a perfect solution is, I fear, not available. Tides are extremely complicated and depend on many factors. Some of these are large scale effects such as the relative positions of earth, sun and moon, but others are more local, such as ocean currents or the shape of the coast. Especially the latter can make a surprisingly large difference on a relative small spatial scale. Luckily, it is possible to come a long way and have very decent approximations.

The best option, as far as I'm aware, is to use XTide, a software program that can calculate tides at thousands of locations worldwide, making use of actual measurements as well as mathematical models. This will give you by far the largest amount of information, and the most detailed information. better still, it's open source software and completely free. The drawback is that it is complicated to use. Also, if you are a windows user, it is even more tricky as this is an X-windows program, developed for UNIX and UNIX-like operating systems (it should run fine on linux and macos). It is definitely possible to run it on windows, but I wouldn't recommend it for the faint of heart.

My second option would normally be to use rtide, an add-on package for the statistical program R, though in your specific case it's probably not good enough. The rtide package is fairly easy to use if you're familiar with R, and runs equally easily on all operating systems supported by R. The drawback is that it doesn't give as much detail as XTide, and it is based on data from a mere 637 stations, all of which are in the USA, so it's only of limited use for the Pacific Northwest. In addition, it takes more work to calculate certain variables such as the tidal range than to do the same calculations in XTide

A third option would be to use a website like https://www.tide-forecast.com/ where you can click your way to the relevant data. The number of stations they cover is even smaller than those offered by rtide, but they do cover the entire world. If you do not want to go the XTide way, then combining rtide with https://www.tide-forecast.com/ would probably be the best way to go: the former gives you a large number of stations in the Pacific US, while the latter will add some stations in the rest of the Pacific Northwest.

I hope this helps!


Can 'hardware' thermalization explain memory decay? Often we are able to memorize very precise bits of information (exact addresses, birthdays of inlaws, number of dirty socks under the bed), but over time our recollection tends to become fuzzy. We no longer recall the day and month a certain president was killed, only the year, or maybe the decade (despite being straight A students in junior high). Like the smoothing out of a delta function under the heat equation, instead of a pin-sharp value we're left with a range of values where the correct one is likely situated. However, most of the time we are perfectly satisfied with such approximate information and can work with them just fine (except in some extreme cases of function impairment, such as Alzheimer's or the aftermath of binge drinking).

Discrete data must be stored in low entropy structures in the brain that over time spontaneously shift to a higher entropy state. Meanwhile, our biology tries incessantly to slow down the decay by expending energy (with the frequently utilized neural pathways being better maintained than the abandoned ones). Even processes analogous to error correction take place, e.g. when we arrive at a certain lost piece of information by lateral thinking and piecing together available data.

My question is whether the fading of memory exactitude can be explained in terms of the thermalization of the digital-like structures where discrete information is stored, and if anyone can point me to studies in this direction.

Interesting point, but I think there is a simpler and possibly more widespread reason for the decay of memories. Namely, as new memories need to be stored in the same neural networks, the weights, timings and other properties of the network links are constantly changed. In other words, there is competition for the limited amount of memory. This re-use of the same networks for multiple functions and memories is the same reason we have redundancy in our brain - it's also largely why they are as fuzzy in remembering as they are. And since memories are recalled associatively, the more connected two networks that encode different memories, the more likely it is that activations of one will activate the other. But that also blurs the boundaries between specific bits of information stored. It's a trade-off between fidelity of the memory stored and recalled and generality of the recall and associations possible.


When was it discovered XY chromosomes decide the sex of a child in humans? Several stories are told from before-genetic-age (books and movies are my reference, the one present in my mind is Marie-Antoinette by Copola) in which we can always see that women are blamed for giving birth to a girl - when it was a boy which was "required".

How did mankind's (man) society took the discovery of the fact that the sex of a human baby is decided by the Y or X chromosome carried in the masculin genes within the sperm fertilizing the female's egg. (at least this is what I learned in school decades ago).

When was this fact discovered and by whom?

(The occasion for this question is Nettie Stevens 155th birthday today)

The discovery of genetic sex determination, and determination of sex via male gametes (in XY species, female in ZW), occurred over some time in the late 1800's and early 1900's. Advances were made with methods to stain chromosomes and, in 1891, Henking noted that wasps produced sperm with a varying number of chromosomes. However, he was unable to gather evidence that the "x-element" was determining sex. Nettie Stevens, in 1905, then used beetles and noted an odd set of chromosomes in sperm, which later became known as the sex chromosomes. This was the discovery of sex determination through male gametes.

  "In 1905, while studying the gametes of the beetle Tenebrio molitor, Stevens noted an unusual-looking pair of chromosomes that separated to form sperm cells in the male beetles. Based on her comparisons of chromosome appearance in cells from male and female beetles, Stevens proposed that these accessory chromosomes were related to the inheritance of sex." - Link

In 1905, Beecher-Williams also made the same discovery, so they are both credited with discovering sex determination by the sex chromosomes. However, Clarence Erwing McClung also contributed to theory that Henkings X-elements may determine sex in 1901.

Thomas Hunt Morgan also contributed some major work on heredity and sex chromosomes, having been initially sceptical of Stevens' discovery. He found that eye mutations in Drosophila appeared to be sex linked, and concluded that the mutations were likely carried on the sex chromosomes.

There is a paper from 1910 where Michael Guyer concludes that accessory chromosomes (the sex chromosomes) likely determined sex in humans.

  "It is probable that in man and certain other vertebrates, as in the insects, myriapods and arachnids, the accessory chromosomes are in some way associated with the determination of sex."

However, Theophilus Painter, in 1921, concluded for the first time that human sex determination was by the presence of X or Y in the sperm; Guyer had gone for an XO system. While Painter got the chromosome count wrong, being hampered by the techniques of the day (an issue that wasn't resolved until the 1950's), he got the sex determination system right.


Protein tertiary Structure formation As we know that coils and loops are evolutionary variable regions where mutations,deletions, and insertions frequently occur. So does it mean that they don't have much role in the structure of protein? If it so then what are the factors for the protein core structure formation?

Firstly, is important to remember that protein structures are dynamic due to the torsion angles between the N-terminal and C-terminal bonds. There are different conformations to expose different sequences to the outside of the protein to react/catalyze. So there is no one perfect conformation for a protein in a biological system.

The best models we have are taken through x-ray crystallography of the crystalized protein structure. This static portrayal of the protein may be inaccurate, because the biological system will expose the protein to different hydrophobic/hydrophilic interactions than the affect of the protein to itself.

Anfinsen's experiments were able to definitively prove the a proteins structure is coded by its amino acid sequence. To answer your question, this sequence is primarily responsible for a protein's core structure formation.

It is still incredibly difficult to predict the structure of a protein using its amino acid sequence. The tertiary structure is a product of salt bridges, hydrogen bonds, hydrophobic forces  and polar attractive forces within the molecule  (disregarding a proteins possible quaternary structure ). Scientists  (from what I believe is Yale, but I may be incorrect), have been trying to find a pattern using computing software for years. As of right now, we cannot purely use amino acid sequence to determine a protein's dynamic structure.

Loops and coils on the outside of proteins because they tend to compose of polar or charged amino acids. Hydrophobic amino acids tend to get pushed towards the center of the protein structure. This occurs because polar residues do not affect affect the entropy of water molecules as much as the nonpolar residues (in the system).

Many deletions/insertions occur during specific transition states that the protein is in. Enzymes actually target specific conformations of a protein that best produces the P product. See image:


What happens to the nitrogen when an oxygen machine delivers only oxygen? My father recently began using an oxygen machine. He would like to know where the nitrogen goes when the machine takes in air and puts out only oxygen.

The nitrogen is returned to the air around the machine.  See Wikipedia's article on the oxygen concentrator for details about how the machine separates the nitrogen and oxygen.


Why does a wound itch while it's healing? During healing of wound (almost in final stage) it begins to itch a lot around wound.

I wondering what the reason for this is?

While healing your wound the cells in and around it are enhancing their communication via messenger substances to quicken and coordinate the healing process. These messengers irritate the sore nerves which we feel as itching.

Skin tension is another factor to itching.

Scratching is bad for the healing process in any way.


what species of ant is this? I found this queen ant on the pavement (in Adelaide) its about 1 cm long and I am not sure what species it is, is someone able to help me?

Probably a Ponerinae.
(Wikipedia, AntWiki)

It's not the easiest picture to work with, but here's what I did.
Going by the location we have the following distribution of ant species in South Australia (see below, or here).
A critical identification point is the petiole, bumpy segments on the thin part of the back of the ant. Your specimen appears to have none or one.
This excludes Dolichoderinae and Mymicinae, who both have two clearly distinguishable petioles (or rather, a petiole and a post-petiole).
Myrmeciinae have different colours and/or mandibles, leaving the following three likely candidates:

Formicinae
Ectatomminae
Ponerinae

Ponerinae are distinguishable by a constricted gaster, so an impression in the posterior section, which is quite clearly visible in the picture.
(This is technically only an identification to subfamily level, if anybody wants to take a shot at species, feel free)


What causes fruit taste enhancement? I'm not sure if this is a biology or chemistry question, maybe both? Some fruits, such as quince and quondong, taste of nothing when raw but have an extremely strong flavour when cooked. Why?

I am a little confused that does the word "cooked" means ripe？If yes, then the question will be easy to answer. Fruit has a kind of ripener, ethlyene. Ethlyene will help fructose break down and make up more glucose. That is why you may taste a strong flavour when fruit is cooked.


Are all non-breeding naked mole rats the same sex? In many eusocial species, all the non-breeding members are the same sex.  Honeybees are a good example, with only female workers.

Are naked mole rats that do not breed also all either male or female, or are they mixed?

Naked mole rat colonies contain individuals of both sexes, with one breeding female and one to three breeding males, and the rest non-breeding individuals of both sexes.

The other individuals in the colony have an additional caste system that seems to depend on size but not sex (i.e., there does not seem to be a hierarchical relationship between non-breeding males and females).

Non-breeding females, but not males, have suppressed reproductive tracts. In the absence of a queen, some non-breeding females' reproductive systems will begin to activate, until one becomes dominant and the others return to being non-breeders.

References

Clarke, F. M., & Faulkes, C. G. (1997). Dominance and queen succession in captive colonies of the eusocial naked mole–rat, Heterocephalus glaber. Proceedings of the Royal Society of London B: Biological Sciences, 264(1384), 993-1000.

Jarvis, J. U. (1981). Eusociality in a mammal: cooperative breeding in naked mole-rat colonies. Science, 212(4494), 571-573.


How to maximize lung oxygen intake? What method of breathing provides a sudden surge of oxygen into the lungs filling it as full as possible in volume and density. Deep breaths? Shallow breaths? Breaths taken while bent over? Deep inhales followed by further inhales. Breaths held? Movement while breaths are held?

You cannot change the oxygen concentration of inhaled air in the absence of an external source of oxygen. However, you can use your lungs at their maximum capacity doing this:

breathe deeply: =increase tidal volume. Your muscles will inflate your lungs as much as they are able to, inflating parts of the lungs that were not fully inflated (atelectases) in the process. This also allows you to inhale a volume much greater than your physiologic dead space (volume of inhalation that does not participate in gas exchanges)
breathe to high enough frequency: the faster you will want to expel $CO_2$ and replace it with room air, the higher frequency you will need to adopt.

Frequency and tidal volume are the two components of minute ventilation (= (frequency/minute) X tidal volume), which is the physiologic value you are working to increase.

Position: The upright position is best suited, since the weight of the lung tissue pulling downwards will facilitate inflation

WARNING: using those techniques unsupervised can cause acute respiratory alkalosis, which is unhealthy and puts you in immediate danger.


What is the correct model for enzyme-substrate complementarity? This Wikibook shows both proposed models of enzyme-substrate complementarity, the Lock and Key model and the Induced Fit model. I've always been taught that the Induced Fit model is  the proper one. However, my biochemistry professor mentioned that often times, enzymes behave as lock and key. I also noticed that the Wikibook doesn't mention which model is in fact true.

The Lock and Key Model

The Induced Fit Model

Is there currently one accepted model? Which is it, and why?

This is true of all protein binding as well as the special case of enzyme-substrate interaction:

Various proteins are more dynamic than others: some have only one or two overall conformations and are relatively implastic otherwise. An example would be a receptor tyrosine kinase like Kit (or CD117, or Mast Stem Cell Growth Factor Receptor, whatever you want to call it), which has a very stable structure and binds its substrates in a lock and key manner.

Others, for example p53 (not an enzyme), have much more structural placiticity - even to the point of being mostly disordered when not bound. They tend to be induced fit binders (of other proteins, not catalytic substrates) and often exploit that to bind a broader range of possible targets than lock and key proteins.

The point is, it is a continuum between lock and key <-----> induced fit rather than discrete classes you can sort proteins into.


Why is DNA replication so much faster in prokaryotes than eukaryotes? There are many statements to be found on the internet of the sort:

“DNA replication occurs at elongation rates of about 500 nucleotides
per second in bacteria and about 50 nucleotides per second in
vertebrates.”

However none that I have read attempt to explain this order-of-magnitude difference. Is it known why?

The difference in DNA replication rate between prokaryotes and eukaryotes is still under current research, but the basics are understood. It is very much a matter of complexity, as eukaryotes are more complex in many different ways. I found a very useful reference for this and other kinds of related questions. Briefly, some possible reasons:

[...] in eukaryotes, the DNA template is compacted by the way it winds
around proteins called histones. [...]

The DNA-sequence is not as easily accessible in eukaryotes, the unwrapping and re-wrapping of the DNA takes some time.

[...] The coordination of the protein complexes required for the steps of
replication and the speed at which replication must occur in order for
cells to divide are impressive, especially considering that enzymes
are also proofreading, which leaves very few errors behind. [...]

This underlines another rather important factor. The speed of the polymerases replicating DNA is very much related to their accuracy.

[...] This proofreading capability comes with some trade-offs: using an
error-correcting/more accurate polymerase requires time (the trade-off
is speed of replication) [...]

And just for completeness, here is a compete overview of DNA replication in the three big systems.


Vaccination and population dynamics of an epidemic I'm trying to figure out how should a vaccination model be built to correlate with population density, and I'm having problems to understand meanings of the results I receive when I apply theory on specific data I'm provided with.

Theory(i):

The initial phase of an outburst of a disease can be described by an exponential growth
model. The relevant equation is:

$(1)\frac{dI}{dt}=\beta n(1-q)I-\mu I$ where:

$n$ = the population density. Let us measure it in units of $km^{-2}$.

$I$ = the density of already infected individuals in the population; measured in the
same units as $n$.

$q$ = the fraction of the population that is immune to the disease, either naturally of
due to vaccination. Consequently, $1-q$ is the fraction of the population that is
susceptible, i.e., at risk of getting infected. $q$ is a pure number between $0$ and $1$,
and has no units.

$\beta$ = is the transmission rate of the disease. It measures how easily and quickly
the disease can be transmitted from an infected individual to an non-infected
susceptible individual. $\beta$ includes within it both the rate at which encounter
between infected and non-infected individuals occur, and the probability that
such an encounter would result in actual transmission of the disease. $\beta$ has
dimensions of $\frac{1}{time\times density^{2}}$, so let us measure it in units of $week^{-1}km^{4}$.

$\mu$ = the rate at which infected individuals are eliminated from the group of
infected individual, either because they recover, or because they die. $\frac{1}{\mu}$ is the average duration of the infection, i.e., the average time that an individual remains
infected before it either recovers or dies. Let us measure $\mu$ in units of $week^{-1}$.

This equation derives from the differential equation $(2) \frac{dN}{dt}=rN$ where $r$ is called instantaneous rate of increase. It is easy to see that $I$ from equation $(1)$ is equivalent to $N$ from equation $(2)$ and therefore, $r$ for equation $(1)$ will be $(3) r=\beta n(1-q)-\mu$. When we look at equation $(3)$, we see two factors:

$\beta n(1-q)$ - A positive factor(ii)
$\mu$ - A negative factor

Minding the above, when $r=0$, there is no increase in population(iii). From this, we can compute $q_{0}$ which is the minimum fraction of vaccinated/immune individuals in the population that is required in order to prevent the disease from spreading. From equation $(3)$ we can figure out that $q_{0}=1-\frac{\mu}{\beta n}$. Just as $q$, $q_{0}$ is a pure number between $0$ and $1$.

Welcome to the desert of the real (my question):

Suppose we compare two countries with the following data:

Israel: $n=347km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$
Finland: $n=16km^{-2}$, $\beta=0.0015week^{-1}km^{4}$, $\mu=0.25week^{-1}$

When we look for $q_{0}$ for Israel we see that $q_{0}(Israel)=1-\frac{0.25}{0.0015\times347}=0.52=52$% while for Finland we see that $q_{0}(Finland)=1-\frac{0.25}{0.0015\times16}=-9.42=-942$%. Assuming that we've got correct data in the first place, $q_{0}$ is a negative pure numbers which is not between $0$ and $1$.

Do such, and similar results make any sense at all? Especially when they are not between the defined boundaries of the variable.
If they do make sense, what does it mean getting a negative results? How should it affect my vaccination policy?

Footnotes:

(i) Taken from my Populations Ecology lecture slides

(ii) Positive when looking at it from the epidemic point of view

(iii) Of infected individuals

I think it does make sense - with a population density for finland that is so low, the disease with such a low beta cannot communicate to enough people to propagate.

The number of people who have this disease will be fewer each week.  I think this makes sense because at 16 / km^2, you can expect that practically nobody will ever see each other.

This is a flawed model though because it assumes that the mean density is uniform.  In a city like Helsinki (2,800 / km^2) you would expect the disease to get caught by nearly everyone in just a week.

Helsinki: n = 94.5%

In Lapland (which has a population density of less than 2/km^2) , the transmission rate (beta) of 0.0015 translates to 0.003 incidents per week.  This is not a terribly catchy disease, you probably have to kiss someone, wear their clothes, or eat off their plate to get it. With only 2 people per km^2 the chances of this happening appear to be poor, though even here families tend to get the disease and the model breaks down.

So to sum up, the model is consistent within itself, BUT it is a baby model and makes some broad assumptions that do not help it describe the dynamics of the disease in a national scope or in a highly detailed scope.  It probably describes the chances balls will collide in a box as well as disease spreading.