text:
How much energy does a small spider expend per day just waiting for its web to vibrate?
Roughly speaking, a small, complex electronic circuit or IC might sit in "sleep mode" using a current of roughly 1 µA (e.g. 1, 2), thereby using roughly $3\times 10^{-6}$ Watts, and that converts to roundly $2.5\times 10^{-6}$ kcal/hour or $62\times 10^{-6}$ kcal/day.
I suppose you could call that 62 micro-kcal/day or 62 milliCalories/day.
One day I noticed a small spider in my home, sitting in its small web, and kept an eye on it. After several weeks of watching I hadn't seen it catch anything. I slightly perturbed the web and it reacted. It was still alive.
Question: I'm curious to know roughly how much energy a small spider needs to sit and wait. Might this be termed roughly the spiders Basal metabolic rate? It could be for any small spider that spends much of its time waiting for prey. As long as an approximate size or mass is available then it could be expressed as kcal/day/kg or some similar unit.
I have read about Kleiber's law in this answer, but I don't think it is meant to extend down to small spiders.
note: I'm just asking for the energy expended during resting periods. Of course during a day the spider may do web maintenance, catch or eat prey, but it's the resting rate of energy consumption, on a daily basis, that I'm asking about.

Short answer
Approximately 240 J on a daily basis.
Background
Ballesteros et al. (2018) modeled basal metabolic rates of insects. They reckoned that endotherms, like insects, basically use energy directly correlated to the number of cells, which is linearly correlated to their body mass. They checked their model with experimental data from Chown et al. (2007) (Fig. 1).
Acknowledging that arachnids aren't insects, but that both are arthropods, let's take an average-sized web making spider, like the black widow, weighing in at 1 g. This yields a basal metabolic rate of 10 J/h, or 240 J/day. However, and given the linear correlation between energy expenditure and mass, a dwarf spider weighing in at 1 mg expends 1000 times less, and a Goliath bird eater approaching 200 g will expend 200 times more.
To convert the unit for the Black widow to a Watt scale, we get 1 J/s that corresponds to 1 W, so 1 J/h corresponds to about 0.3 mW.

Fig. 1. Base metabolic rate for insects. Data from more than 300 species were extracted from Chown et al. (2007). source: Ballesteros et al (2007)
References
- Ballesteros et al., Sci Rep (2018)
- Chown et al., BES (2007); 21(2): 282-90

Wow, all kinds of goodies here; thank you for the well-sourced answer!

@uhoh - thanks! You may wish to check the math, however, where needed - I'm just a Biologist and your post seems to radiate quite some proficiency in math :) I added my sources, so that should work out. Cheers.

A bee perhaps consumes 100 times more than a spider on a busy day, so some added graphs would be helpful. Also consider that a spider at 12'C consumes way less than at 25'C... Essentially you can weigh their energy demands from the mass of their diet, by counting their midden. they can stay alive on about 5-10 times their body mass every year, depending on the species, and they generally get a catch ever few days, so they can go into low wattage mode or high wattage mode, where high wattage mode produces lots of web reserves and broods.

@com.prehensible - the answer pertains to basal metabolic rates only, per the question, and as mentioned in the answer's body text.

basal metabolic rates depend on temperature and food input, i.e. a pregnant woman will spend a lot more energy when pregnant and spiders have dozens of babies... So basal metabolic rate of an idle spider can be equivalent to 5 times it's body mass in lymph per year.

@com.prehensible, yes the paper models energy expenditure for a certain temperature range. And of course there are more exceptions to the rule. Obviously it is the basal rate, no extreme temperatures, no babies, no running, no weaving, no nothing.

@AliceD so, using your numbers, the basal energy consumption of the small IC would be about equal to that of the dwarf spider?

@mpprogram6771, well, yeah, perhaps in the same ball park, but yet a few orders of magnitude larger than uhoh's calculation.

For the black widow, you said it would be 10 J/h, and that 1 J/h = 0.3 mW, so black widow would be 3 mW, which is 1000 times larger than the microprocessor from uhoh's calculation. you also said that the dwarf spider would be about 1000 times less based on mass, which brings it to 3 micro watts, or 3*10^-6 W, which was the measurement that uhoh got for his IC. Is my math right?

@mpprogram6771 - ah yeah, my bad.

This all works out very nicely and indeed at 1 mg spider would seem to be of the order of 3 uW just like a low power IC in idle mode. Cool result, thanks!

@uhoh - thanks a lot for confirming the math here :) My pleasure!

A 400 pound human can survive a year without food, and an arachnid can manage the same, 3000-7000 hours if it consumes it's body mass equivalent.
A spider consumes about 110  to  1933 μW per gram of body mass, standard metabolic rate at 20'C.
By measuring spider oxygen consumption, scientists have found a range of 21–356 μl O2/g per hr.
Its good efficiency compared to other poikilotherms of same size.
A human an adult at rest consumes about 16 liters of oxygen per hour. This gives a nominal basal metabolic rate of 75 kcal/hr which translates to 87 watts(=1.2 milliwats per gram).
1 liter of oxygen gives 5.43 watts per liter... 1 microliter = 5.43 microwatts.
21-456 *5.43 = 110 to 1933 microwatts per gram.
Big garden spiders from temperate regions are about 1g, so a big spider from the garden can use 0.1 - 2 milliwatts at 20'C.
1 gram of fat is about 7kcal, that's 8 Watts. So, if a 1gram spider has a 0.5 gram meal, they can keep going for about 10,000 hours, perhaps 3000-7000 hours at 30/70% efficiency.
https://jeb.biologists.org/content/214/13/2175

Interesting answer. But... How can a 1-gram spider eat half of its body weight? And, probably related, if it can survive 10,000 hours, i.e., more than a year, with a single meal, why would it even bother catching pray at all? And, related, a 'meal' is hardly pure fat, instead, it will mostly be chitin and other proteins. Importantly, why is exotherm data included in this answer? If that human hourly O2 data is used for the later calculus, it is likely inaccurate, as exotherms use a lot more base-energy than endotherms.

Lastly, it's best practice to write the references out in full (J. Doe, Journal of something (2020) etc), as web links may grow cold over time. In fact, they quite frequently do.

Are you saying that respiration and the use of ATP in arthropods and humans generates a different amount of energy? It's the same respiration conversion of oxygen to carbon dioxide, at 20 vs 37 degrees, correct me if I am wrong, it's basic biochemistry with 02 in and C02 out, so the energy maths are the same. Also correct the maths if you see a specific error. If you scale up the black widow to 65 kg and 37 degrees, it consumes almost exactly 1W/gram. Silicon wafers are 50 micrometers, though, so the  IC silicon using a 1x1x0.01mm wafer weighs about 0.00023 grams.

It wasn't clear to me why the human data was in there. Your train of thought slipped me, as it's just respiration Biochemistry you were needing the human data for, it was quite confusing. Thanks for clearing that issue up.


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What is the difference between monoecious and homothallic?
In my plant reproduction book there are two distinct definitions for these two terms, but when I read them I found out that they are very much alike that I was confused and couldn't catch the difference between them. I searched on Google and found this on wikidiff:

As adjectives the difference between homothallic and monoecious is
  that homothallic is (of some algae and fungi) producing male and
  female reproductive structures in the same plant while monoecious is
  (botany) that has male and female reproductive organs on the same
  individual plant (rather than on separate individuals).

But, still, isn't this the same sentence using another words?
Thanks for answering.

Hi @Anonymous I rolled back your last edit because the text you edited is taken directly from Wikidiff and so should, I think, be left as is even though it could be better phrased.

The difference is that they come from different scientific traditions and describe the same idea for different kinds of organisms. Homothallic is applied to fungi and algae, whilst monoecious is applied to plants (and sometimes invertebrates). This use of different words to describe the same phenomena in different types of organisms is unfortunately quite common. You could also had hermaphrodite as another example for organisms with both male and female reproductive parts. One can point to crude phenotypic differences to justify the distinction in terms but the underlying concepts are the same.
I note as well that the separation into different types of organism used is usually based on older classification systems rather than reflecting any biological reality.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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Identify this avian courtship ritual
The female drops a twig from high up on a tree and the males have to catch it midair. The female is checking if the males can catch things midair because this species nests on cliffs, and the chicks may fall to their deaths while learning to fly. Apparently, skilled males can catch the chicks midair.
Which species is it?

Where did you hear about it?  Do you know anything else about the bird?  It sounds a lot like an eagel, but it's hard to validate that it's the only bird that exhibits those patterns.

So eagles actually do that? Do you have a source? My friend says this happened in a documentary we watched together, but I have no recollection of ever seeing such a thing.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Is there a word for the length of time an animal stays with parents before going off on their own?
Gestation is a word describing the pregnancy for animals, and you can use 'gestation period' to describe how long a pregnancy generally takes for a species. I'd like to know if there's a corollary word for the time an animal stays with its parents before leaving.
For example, after birds are hatched, they stay in the nest for a while, but they eventually leave the nest. Is there a single word or phrase that is used to describe the time between hatching and leaving the nest? I imagine different bird species have different periods, and other animals (that don't stay within families their whole life) can also be describe in a similar matter. Perhaps 'puberty', though I'm guessing there's a more specific word.

As you talk about bird, most of the terminology I am suggesting below comes from the ornithology literature.
Fledging period
Defined on wikipedia:

Fledging is the stage in a volant animal's life between hatching or parturition and flight.

Nestling period
Defined in Kouba et al. (2015):

In altricial birds, the nestling period is an important part of the breeding phase because the juveniles may spend quite a long time in the nest, with associated high energy costs for the parents.

Rearing period
See its usage in for examples Yuan et al. (1994) and Brickell et al. (2009)
Juvenile
While the term juvenile does not refer to a period of time, you can refer to this concept as the period while children are still juvenile. From dictionary.com

a young bird in the stage when it has fledged, if altricial, or has replaced down of hatching, if precocial.


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How does a decrease in free Ca2+ result in nerve/muscle overexcitability?
I have in my notes that a decrease in free Ca2+ increases membrane permeability to Na+ so that it is brought closer to threshold, but no further details. So how does this work?

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


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What Type of fly is this? its huge
I found this stunningly beautiful Fly in a graveyard in Point Lonsdale Australia.  Can someone tell my what type it is Please.
It was wide as my thumbnail about 3cm long.

Could be a blue rutila fly (Family Tachinidae) http://www.brisbaneinsects.com/brisbane_tachinids/BlueRutiliaFly.html. Or the green rutila fly, which is similar.
Or the golden head rutila:

I believe that you have the correct family; I'm less certain the species is right.

Why down vote my post? My answer provides new information that is useful because it identifies the family of the insect, which is more than the OP had to begin with.

I am not familiar with the site,  I didn't vote you down or if I did I didn't mean to.  Picture by Perfectionist has more similar features.  Thankyou for responding.  They are quite stunning and detailed.


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Neurons and nerves
What is a nerve compared to a neuron? Is it a collection of axons alone or does it include cell body too? I'm pretty confused of what actually the "nerve" is composed of. I had imagined that the nerve is actually having a no of neurons synapsing together but I guess it's not so.. Pls do make a clear demarcation between a neuron, nerve,  nerve fibre, ganglia, nuclei

@novo  I vote to close the question too

This is a rather broad question, but the categorization is as follows:

A neuron is a cell of the nervous system, its role is the transmission of electric signals.
A nerve is a bundle of axons, meaning that it contains neurons but only part of them.
A nerve fiber is another (and in my experience rarely used) term for an axon.
A ganglion is an aggregation of neuron cell bodies in the peripheral (i.e. autonomous and sensory) nervous systems.
A nucleus is an aggregation of neuron cell bodies in the central nervous system.

As you can deduce from the info above, a nerve is distinct from a neuron and does not include its cell body.


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Surviving only on another's exhales?
While reading this - Surviving under water in air bubble - this question came to me:
How long can an adult person survive on breathing in only exhales of another adult person? Can this be even calculated by not relying on rough approximations or there are too many variables?
In order CPR (mouth to mouth breathing part) to be effective, logic says that exhaled "air" is not poisonous to bring a fatal blow, but for how long?

Ok, I'll bite. Now, I'm going to assume that in this scenario, Alice and Bob are stuck underwater. Alice has a SCUBA tank filled with compressed air (not pure O2) and though she won't share it with Bob, she magnanimously agrees to share her exhaled breaths with him.
Exhaled air contains 13.6–16.0% oxygen and 4.0–5.3% carbon dioxide in addition to other gasses which we'll ignore here. The real question here is: can you survive on that?

13.6–16.0% oxygen is 66%-80% of the amount of oxygen in normal air (which is ~20.1% O2). If we assume that the air pressure of the exhalation is the same as the air pressure at sea level, then the amount of oxygen available to Bob is roughly equivalent to being at an altitude of 2000 - 3500 meters above sea level, which is certainly survivable.
The CO2 is likely to be a bigger problem. CO2 is toxic and, in sufficient quantities, can case asphyxiation even in the presence of sufficient O2. Amounts above 1% can cause drowsiness, headaches, and mild narcosis while higher levels lead to dizziness, confusion, and unconsciousness.
It looks like you need amounts around 7%-10% for death, so Bob will probably survive in the short term, he definitely won't be happy and he won't be doing much. According to wikipedia's page on Hypercapnia, the time one can expect to perform useful activity varies greatly based on the exact amount of CO2:

1 week at 4%,
8 hours at 4.5%,
4 hours at 5%, and
1 hour at 5.5%

If Alice and Bob are just relaxing and waiting for rescue, it's likely that the CO2 in her exhalations will be on the low end of that range and Bob will likely be able to survive (albeit in great distress) for a significant period. If they were exerting themselves, however, Bob wouldn't do well at all.

so is it safe to assume that ~ after 30min Bob would feel really bad due to CO2 levels and ~ after 3+ hours he would have huge difficulties to survive coz he could forget how to breathe?

I think that would be a reasonable assumption, though keep in mind that I'm making a lot of assumptions here and you should not use this advice to make any medical (or SCUBA diving) decisions. Also, it's not that Bob would forget how to breathe, though, just that as CO2 toxicity gets worse he will become more and more impaired

Alice could probably keep Bob alive for longer by increasing her dead space ventilation.


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Infecting yeast with viruses
Is there any virus, either natural or engineered, known to infect yeast through mechanisms similar to phages/human viruses, that is, by horizontal contamination mediated by extracellular viral particles?
I have found examples of eukaryotic viruses replicating in yeast (Zhao, Microb Cell, 2017 - link) but it seems that natural yeast viruses only transmit through mating or vertical transmission, without extracellular steps (Luque, Viruses, 2018 - link).
Has anybody ever reported, say, non-specific mechanisms like VSV-G mediated fusion, to fuse virions with yeasts?


text:
What is this strange flower which I found on an upheaval in Rhodes (Greece) in July?
It looks like it carries berries instead of blossoms. Is it actually a flower or rather a baby tree? I found it in a Google image search (see here: https://goo.gl/images/vfBDSP), but there was no description with the picture.

Looks like the berries of an arum.  Search for "arum berry image" and you'll see what I mean.

I agree, it looks like Arum creticum from the picture.  It is a kind of lily, and these fruits form after the plant has finished flowering.


text:
Would Ants and Termites be considered r or K strategists?
My initial assumption is that most swarm species would fall under r strategists due to their prodigious number of offspring, but it also occurred to me that since worker types are non-propagating we would only consider the queen/drones which would be K. So which viewpoint is correct?

Its not an either or question, r and K are directions on a line scale.

@John I know, I just had some trouble phrasing the question. My question is more would the non-propagating workers affect the conclusion, or are only viable offspring factored into r/K?

What are r or K strategists? Your question is unclear to me.


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How to derive the deactivation time constant in this model of Acetylcholine Receptor state kinetics?
I came across this simple analytical expression of time constant of deactivation in Elenes et al., 2006. How does one derive this expression
$$\displaystyle\tau_\text{deactivation}\approx\frac{1}{D_+ + 2j_- + \frac{\alpha_2 2k_-}{\beta_2+2k_-}}$$
for the model given below.

 An allosteric reaction mechanism for the muscle AChR. C, O, and D denote the closed, open, and desensitized conformations of the channel, whereas A denotes a molecule of ACh. For simplicity, only one of the (probably several) desensitized conformations is included in the model. Also, the two neurotransmitter binding sites are assumed to be functionally equivalent and independent and, therefore, the two possible monoliganded configurations are considered to be functionally indistinguishable. These simplifications have no consequences on the interpretation of our data. The red arrows indicate the rate constants that, according to Eq. 1, determine the kinetics of the macroscopic current decay upon stepping the concentration of ACh from saturating to zero (i.e., during channel deactivation).

The material is esoteric, but I am hoping someone will be able to answer. The same paper also mentions that deactivation time constant is the reciprocal of
$\frac{\alpha_2 2k_-}{\beta_2+2k_-}$
and references Colquhoun and Hawkes, 1982. This reference will take quite a while to grasp completely.

I just checked the linked paper and the paper that it refers to. Both of them do not explain how the expression was derived. No supplementary methods also. You may find the derivation (not the final one, still) in the 1981 paper but you need to spend some time on it and perhaps read a bit about continuous time Markov chains. This is certainly beyond my scope and if we don't get a reasonable answer from anyone else then we may migrate it to [math.se] or [physics.se] and try our luck there.

I'm trying to solve the system, but I'm having some troubles with the mathematics. On the meantime I recommend reading the chapters of Colquhoun and Hawkes in the book Single Channel Recording specially the Q matrix cookbook. These are a digest of their papers.


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Why do some animals have beards?
Why do some animals such as some Goats, Ibex, Orangutan etc, have long well-shaped beard like men?

Probably for the same reason men have beard.

Apparently, the "sexiness" of beards is conserved in the animal kingdom.

@Frieke Some biologists argue that beards have less to do with female choice per se, but more to with intrasexual competition and status hierarchies. So a male beard may have more to do with intidimating other males than females finding them sexy. I'm not saying that this is true necessarily; I just wanted to note  that I have seen it been argued.

@Eff: yes indeed. Growing a long beard is costly (concerning resources but also potential handicap). Being able to afford a nice beard is showing dominance among males and attractiveness for females. Maybe I should just put this into an answer.. ;)

In humans and animals beard growth is usually restricted to males, since it's dependent on hormones (testosterone or, specifically, according to wikipedia it's dihydrotestosterone). By no surprise it starts growing during puberty.
But why?
Growing a long beard is costly concerning the necessary resources but also because of a potential handicap. Being able to afford a nice beard is showing dominance among males and attractiveness for females. It could be seen as a direct display of high testosterone levels. This is comparable to peacock feathers. They are very impractical, but have great value for showing dominance and attracting females.
I think, there are many psychological theories around to explain the attractiveness of beards. Some might also be meaningful in animals. Apart from cultural, religious or hipster beard trends, we generally consider old men with long beards as wise and knowledgeable. In animals the beard might also signal social status in groups, additionally to male dominance and sexual attraction.
Further reading:

Importance of hair in humans and hormones involved
Sexual attraction of beards in humans
Trustworthiness of bearded men
Intrasexual competition influencing sexual dimorphism (here: size)
Sexual selection
Costs and benefits of male hair (lion mane)

The research of animal beards is pretty sparse, but hair at the chin is just one of many "appearance traits". So, I provided some studies about various aspects of sexual selection and human psychology that give explanations.

Further reading: https://en.wikipedia.org/wiki/Handicap_principle


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Why does a cell need siRNA?
My question is about small non-coding RNAs. miRNA and siRNA are both known for mRNA regulation. miRNA can both transcriptionally inhibit and degrade mRNA by cutting it. For inhibition just a small fragment (seed) of miRNA is complementary to the mRNA while for degradation miRNA and mRNA must reach 100% match.
siRNA is almost the same molecule and its only function is to 100% match mRNA and degrade it.
So if siRNA appears to be just a subtype of miRNA, can we confirm that? Or are there any other differences that make these two molecules different kinds of small non-coding RNAs?

So if siRNA appears to be just a subtype of miRNA, can we confirm
  that? Or are there any other differences that make these two molecules
  different kinds of small non-coding RNAs?

siRNA and miRNA are not identical, but similar. It's not incorrect to consider them similar phenomena in biology, but history places them apart and there exist small differences. Both are processed inside the cell by the enzyme Dicer and incorporated into the RISC complex where their target is degraded ("RNA interference"). However, there are important differences, in case you want to be absolutely correct.
siRNA is typically exogenous (introduced from outside by viruses or by engineering). It typically has 100% complimentary to its target mRNA, because we want to reduce off-target binding. If designed well, they target only the intended target and are checked to be incompatible with any other potential mRNA targets, i.e. are designed to be specific.
miRNA is endogenous (occurs naturally within cells) and is single stranded in vivo. Its complimentary is not always 100% perfect, and often has multiple targets. This is the major difference between the two. It pairs with its target mRNA imperfectly; it simply inhibits translation (protein production from the mRNA). In rare cases where it's a perfect match, it causes the cleavage and destruction of the target mRNA just like siRNA. If I remember correctly, plants miRNAs, in contrast to animal miRNAs, usually have perfect complementarity with their targets. miRNAs are also derived from shorter stemloop RNA products than siRNA.
As you probably know, both are non-coding RNAs and do not enter ribosomes for translation. They have similar effects on gene expression. If you are interested in the very first reports of either kinds of RNA, here goes:
miRNAs discovered in 1993 in worms.
siRNAs discovered in 1999 in plants.
Notice the phrase antisense RNA in both titles. Interesting!
Further reading, in case you are interested.

Why does a cell need siRNA?

This is a very different question. Why? Probably to fine-tune the expression of its genes. Small RNA species can accumulate, aggregate, and regulate mRNA levels in ways that are probably not possible inside the nucleus at the DNA transcription level. Small RNAs are also understood to be epigenetic and function in the cytoplasm and endoplasmic reticulum!

Perhaps you would want to add a note on endogenous siRNAs and shRNAs. Also, siRNA, as we know it in the context of RNAi, was discovered in C.elegans (1998) (Fire & Mello got Nobel for it). It doesn't matter much anyway and I don't want to debate on who did it first :P


text:
Why more than one chromosome in an organism?
Why not one chromosome to house genome in organisms but multiple?
Is it for epigenomic purposes?

Are you asking about ploidy number or chromosome number? Do you have any reason for expecting every organism ro only have a single chromosome? Why did you suggest epigenetics? What are your thoughts?

I am asking about the chromosome number. I ask this because the chromosome numbers are not the same across different organism and I feel there could be a reason for this. I suggest epigenetics because of the need for histones to interact with genomic sequence for modulation of genes.

The problem here is in attributing purpose to evolution, when it's a series of accidents, some of which survived.  There are a number of things that can cause chromosomes to be duplicated. (Colchicine is commonly used in modern plant breeding.)  If an organsm has its single chromosome accidentally duplicated, and the offspring survive, that change gets propagated to ensuing generations...

@jamesqf Then why do we have different genes on different chromosomes and not duplicates?

@Atajera If a chromosome were duplicated, for it to stay a duplicate and not diverge, every change would have to happen at the same time to every chromosome. That's not really feasible.

@BryanKrause That explains the duplicity, how about the change to different but essential genes. Why not essential genes only on the parent chromosome if the theory is true?

@Atajera What mechanism do you propose that would cause genes to only change on one chromosome once there is more than one?

I seem to remember a related question in relation to maximum chromosome size. Those interested might do worse than look for it.

@Atajera: Understand that I am only guessing/making logical deductions here, but once you have two chromosomes, each will undergo random mutations, some of which will prove beneficial.  Carry that process on long enough, and the organism now has two different chromosomes, potentially carrying twice as much information.  (It also seems as though copying one long chromosome would be less efficient and more error-prone than  several short ones.)

@jamesqf: I agree with your theory

@BryanKrause: None but what I meant was that the change occurs in both but results in two different essential gene but not two variants of the same gene.


text:
Is there an adjective I can use to describe body parts like hands, feet, eyes, and ears that exist on both sides of the body's sagittal plane?
Body parts like human hands, feet, ears, eyes, etc. exist on either side of the human body's sagittal plane and can therefore be specified with the adjectives left and right. Is there a special adjective I can use to describe body parts like this that a creature has a left and a right one of? Sentence with desired usage: Hands, feet, eyes, and ears are all ____ body parts.
I need this adjective to not apply to body parts like noses, stomachs, lips, lymph nodes, etc. that a creature either has one of, has more than two of, or has precisely two of but it wouldn't make sense to call one the left and the other the right (e.g. lips).
I'm specifically looking for an adjective to describe body parts that I could say "this creature has a left ___ and a right ___" for.

I think you are describing bilateral symmetry, structures with two copies, one on the right and one on the left. So to directly answer your question: Hands, feet, eyes, and ears are all bilaterally symmetric body parts.
Noses are a little tricky, because there is only one on the midline, but the nostrils are bilaterally symmetric.
Generally, if you can draw a line in the mid-sagittal plane and there is a copy of each structure on the right and left, it's bilaterally symmetric.

The exception for the nose is a dealbreaker for what I'm working on unfortunately. I'm specifically looking for an adjective to describe body parts that I could say "this creature has a left ___ and a right ___" for.

The nose is midline, but its parts aren't (left nostril, right nostril). I don't see a problem there. It's not clear what you are looking for, I guess (or why).

I guess isobilateral can also be used synonymously with bilaterally symmetric.

@kmm The problem there is the body part "nose" can't be used in the sentence I specified in my comment: "this creature has a left nose and a right nose". I don't know how to be clearer about what I'm looking for than the information I've already given. I'm architecting some software relating to the human body that could benefit from an interface that describes an object as being able to have a left or right modifier applied to it.

A structure can be unpaired but have, within it, left and right parts (nose, heart, etc.). Why do you need this rigid, one size fits all definition?

@WYSIWYG neither of those terms properly exclude the body parts I want to exclude. Please re-read the question.

@kmm "A structure can be unpaired but have, within it, left and right parts." Of course it can, but as I've said those body parts need to be excluded from the set of objects that the adjective can be applied to. Also I've explained my use case: I want to be able to call something (e.g. a shoe, hand, earmuff, etc.) a human's left or right version of that thing. A human does not have a left and a right nose, therefore I can't use the term bilaterally symmetric to describe objects in my set since it also applies to objects outside of my set. Trust me that my software needs to be this rigid.


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Is there a practical upper limit to ploidy?
In my AP Biology class, we were discussing polyploidy, specifically, its deleterious nature in mammals and its prevalence in plants.  We also learned that commercial crops, especially fruit, are often selectively bred for high magnitudes of ploidy.
Fascinated, I googled the subject and ended up reviewing the Wikipedia article to get a little more background info, where I read this:

Polytene chromosomes of plants and fruit flies can be 1024-ploid.[44][45] Ploidy of systems such as the salivary gland, elaiosome, endosperm, and trophoblast can exceed this, up to 1048576-ploid in the silk glands of the commercial silkworm Bombyx mori.[20]

From this, I have three questions. The first is, is there an upper limit to ploidy that can occur in nature? I understand that polyploids can "lose" ploidy by haploidisation, but is this as common as increases in ploidy? I believe that the answer to this would imply the answer to my first question, however, I could not find much literature in the way of this area.
My second question is, is there an upper limit to synthetically induced polyploidy? Is the Bombyx mori's ploidy arbitrary, or is it at the max that technology can produce? Can it's ploidy be expanded further?
Lastly, does arbitrarily high ploidy serve any purpose in agriculture or science? Is there a threshold where utility is no longer maximized?
Thank you in advance.

Note that it is customary to restrict posts to a single question, which is easier to answer for these complex topics. I'll do what I can here. I'm going to deal with everything at once and then reference pieces in direct reference to your 3 questions.
MECHANISMS OF CONSTRAINTS ON PLOIDY
I think that it's worth separating out some of the different mechanistic ways in which a practical limit can be set for how many chromosome copies you could have.
Another point is that the examples you give in flies and silkworms are organs with high ploidy, rather than whole organisms. It's a lot easier for an organism to have a few weird snippets of tissue with weird ploidy than to maintain that ploidy in the germ line.
Ciliates are weird and instructive:
As another totally insane example of how some organisms have evolved to reconcile this somatic desirability of lots of DNA with a stable germ line, you should look into the nuclear organization of the ciliates, which have a germ-line micronucleus (which is just passed on to future generations) and a somatic macronucleus (which is generated by amplification of the micronucleus and does all the cellular work of DNA). The macronucleus is of extremely high "ploidy" (it's more complicated than that but that's close enough), but the germ line is of a more sensible ploidy.
Some constraints I could think of:
Physical limits:
DNAs are basically huge polymers. Packing polymers into a cell imposes a physical constraint, in the sense that you need to 1) fit all that polymer into the cell/nucleus, and 2) need to still be able to use the DNA for all of the necessary cellular processes. These constraints will vary vastly from organism to organism, based on cell volume, plasticity, morphology, etc.
Metabolic limits:
DNA is expensive to make, energetically and physiologically. It ties up a lot of sugar and nitrogen that you could use to do other more interesting things, like the rest of cellular metabolism. Silkworm silk glands are obviously eye-popping, but I assume that there is some theoretical limit above that million-ploid amount (for silkworms) that would be too much DNA to support. For a little more information see this Mike Lynch paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697398/
Chromosome segregation limits:
Moving homologous chromosomes to daughter cells is not a perfect process; cells mess it up frequently, leading to aneuploidies and cancers. Some ploidies such as triploid, and presumably higher numbers with 3 as a smallest common denominator, are particularly unstable in meiosis. However, any high ploidy leads to errors at a higher rate than lower ploidies. Look at the ciliate example also. This is I believe the main reason for the "collapse of high ploidies into lower ploidies that you mention.
UPPER LIMIT TO PLOIDY IN NATURE
See all above answers.
UPPER LIMIT TO SYNTHETIC PLOIDY
See all above answers. Synthetic increases should behave the same as natural ones, as we are honestly much worse at getting making things happen than nature itself. Nature will have gotten higher already than we ever will, in all probability.
PURPOSE OF HIGH PLOIDY
See the cost/benefit of ploidy article from above.


text:
How do DNA, enzymes, hormones etc. reach their proper cellular locations?
I was trying to understand DNA transcription from this chapter, and there seems to be no explanation on how exactly the proteins, enzymes and other molecules manage to find each other inside the cell. How do they get attracted to each other in order to start reactions or transcriptions?
Same way, when the body secretes a Follicle Stimulating Hormone, how does it reach the follicle instead of losing its way in the bloodstream and ending up in a woman's feet or getting excreted out of the body? In minute 20 of this video, the person speaks of how medicines are first "sent" to the liver, but this MIT article says that medicines go all over the body.
At least for a wound it's an understandable process. An artery of vein is severed and any blood that was supposed to flow through it now can't, so there's an accumulation of white blood cells and antibodies there which can disable any intruders (though I'm sure they wouldn't be able to see an intruder and move toward it, but rather just probabilistically bump onto the intruder), and if the intruder enters the bloodstream it would probabilistically bump into other WBC's or antibodies and get killed. Else there's always fever to kill them.
Similarly, one study says sperm use heat sensors to find the egg. Another assumes it's a chemical signal.
I went through the information about cell signalling, signal transduction and allosteric regulation, but although they speak about receptors, they don't explain how the chemicals manage to find those receptors. It's like saying that I entered a huge college campus and found the secret place where my friends were meeting and they receive me when I met them, but there's no explanation on how I knew which way to travel in that huge campus to reach my friends. Given how accurately DNA transcription happens and how viruses know to shed their shell on entering a cell and make use of the cell's transcription mechanism, I believe there has to be a specific process through which these molecules "know" how to find these receptors. Is there any research that could throw light on it?

Just as I have removed "know" from your title, you should remove all anthropormorphic references from the interpretation of the sources you read — if you read popular science you will unfortunately find non-scientific expressions. So replace "finds" by "reaches", "is sent" by "is released". For the rest, the answers discuss whether after release a molecule reaches its target by diffusion or specific transport etc. But you need to trim your question which is far too widely drawn, accept your ignorance and see what answers you get before deciding that it's magic.

The answer given by Sadegh gives a general correct broad view. But one part of the puzzle is missing, which is molecular recognition.
Molecules bind to each other via physical/chemical interaction like forming hydrogen bonds, electrostatic interactions and other mechanisms. The sum of all interaction defines the strength of the binding. If molecules have enough interactions, they stick together otherwise not.
Mind that all these interactions have a range of action (a field). Like with magnets, two opposite magnetic poles attract each other at a distance, before they get in contact. Imagine a small molecule getting close to a receptor, if they are "magnetically" compatible they will be attracted toward each other.
Indeed, molecules in the bloodstream (like the Follicle Stimulating Hormone) flow all around the body. However, not all the molecules end up in all the cells. That is because cells have specific receptors on the surface that bind selectively their target. In the case of the Follicle Stimulating Hormone, some cells, like the Sertoli cells or the granulosa cells have the right receptor able to bind that specific hormone.
In the case of a drug targeting the liver, the drug gets assimilated or injected into the bloodstream, it travels all around the body but it is retained by specific molecular interactions only (mostly) in the liver. It is not that the drug knows where the liver is, it is just forced to pass through it and then it is retained by it. The drug passes also through the lungs, but it has no affinity for them so it doesn't get retained.
Inside the cells, it occurs the same. Molecules pass all around, but they do not stick to anything unless a specific protein/receptor/enzyme is found.
There is an intricate network of interactions both inside and outside the cells, molecules randomly flow throughout this network bouncing on each other until they find the binding partner and they stick to it.
Randomness is not the only factor. Brownian motion occurs, but molecules are also actively moved by different chemo/physical stimuli causing the network of interactions to be in fact extensively regulated.
For example, during the cell cycle, the cytoskeleton is actively remodeled to favor the flow of certain molecules in determinate directions (look metaphase). The cell can also alter its own permeability, actively influencing the influx/efflux of a variety of molecules.
At the body level, the circulatory system itself forces the flow in a specific direction (from the stomach to the liver for example).
The fact is, that there are mechanisms to selectively control the flow of the molecules at any level in the body, from organs to tissues, to single cells and inside subcompartments of the cells. The topic is complex but very well understood.
I suggest a big dive into this book if you really want to get a grasp on how biological systems work.
UPDATE: As suggested by @WYSIWYG, the picture would be more complete adding a very short note (the topic is way to broad to be extensively discussed here) on chemokines which are a perfect example on how cells can respond to concentration gradients. Chemokines act as a chemoattractant to guide the migration of cells. Cells can sense the concentrations of chemokines in the surrounding environment and, usually, move toward the source of the signal following the increasing concentrations of the signal molecule. In general, it cannot be overstated the importance of chemical gradients during embryogenesis, inflammation and countless other events. Gradients effectively indicate to cells the path to follow.

Perhaps you can also add a note on chemokines.

Yes, good point. I should add something about concentration and diffusion as well. I will add it as soon I have time.

It's both simple and complex. The simple answer is Brownian motion. All the particles in the cell do have mobility which is related to their mass. A small particle like a soluble enzyme undergoes random walks through the cytoplasm or nucleoplasm. Thus by having a grand number of a certain molecule you can be sure that at some point it interacts with the right target. Besides that, cells have solutions for increasing the chances of interactions by creating local concentrations of the factors in metabolic or signal transduction pathways. Look at this.
Larger Particles like vesicles are transported through cytoskeleton and motor proteins. The main reason that prokaryotes have had limitations in growing their size is lacking such a system and depending on diffusion and Brownian motion to relocate molecules.
About the complex side of the story! One might ask how some random and stochastic behaviors of molecules lead to these definitive and precise actions in the cell. You can Google up "Stochastic in cell biology" or look at this book.

Hmm...I'd take stochasticity as a theory, but maintain that there should be an alternate theory too. When I learnt of Prions, I felt there has to be another explanation to how decisions were taken to create scaffolding proteins, cytoskeleton etc. There seems to be an intelligence to it. Couldn't just be randomness.

This is definitely part of it, and indeed, I think it's an underappreciated part from the perspective of a novice, but there are also molecules that are trafficked on the cytoskeleton, which is especially important in cells like neurons that can have extremely long processes relative to the rate of diffusion.

Shortly, understanding a process called molecular recognition (as stated by @alec_djinn) under crude biological environment would answer all your questions.
Before explaining answers for your questions, to understand biochemical aspects of Transcription better, I would highly recommend to read a textbook written by Lubert Stryer.

Proteins including enzymes basically work by very specific non-covalent interactions.They do so because these interactions are reversible.(For example,  after one transcription cycle is over, same guy can work again and again). The inside situation at transcription site is complex as many biomolecules work in a complex coordinated manner and follow the rules of thermodynamics.The proteins have a 3 dimensional structure whose active site channel can only accomodate specific substrate molecule say DNA. (Think about a lock and key).This complementarity in-turn is achieved by complementarity in Shape, number/type of non-covalent interactions it can have, free energy considerations etc.
Indeed, the drug goes all over the body. However, the specific drugs contain a chemical motif which gets only recognized by specific receptors through molecular recognition.The new drug delivery systems also make use of a phenomenon called EPR effect (enhanced permeability and retention effect).The drug which is more specific towards the target and which has more retention time in the blood is more effectively acts upon the target and others eventually excreted out through renal system.

So coming back to molecular recognition, let's take the same example you have given. Think when you entered your huge college campus you specifically get attracted towards certain girls (Imagining you are a boy) but not for all. Because those girls are in a way as your mind likes. This can be compared with large class of enzymes like peptidase which break peptide bonds.Some may break between Alanine and Glycine and some may not (as you like girls).Some other may like to break between Tyrosine and Proline.That is because those enzymes have evolved in such a way that they perfectly fit in there.Continuing, now you want to find your girlfriend. This case is more specific.Its not bunch of girls. Its only one.What will you do? You will send a message/call out loud!.Similarly, biomolecules send a message through chemical signals/secretions etc.
About sperms and eggs I know they attract through chemical signals and thermal gradient.I cannot comment much about it.
Ofcourse, all these mechanisms have been proved by researches either by direct or indirect method.Modern techniques such as Fluorescence microscopy has tremendously helped us to understand the finest things of life in its native conditions.Because seeing is believing!

Thanks. This is a nice answer, but it'd have helped more if there was a mention of how these molecules learnt to locate and move toward each other. Other answers say it's just randomness (and it probably is), but when I go to a restaurant when hungry, it's not because I'm attracted to it and the restaurant has doors (receptors). It's because I know that I can get food at the restaurant. How do these molecules "know"? How do the organs that secrete these molecules "know" that the molecule could eventually reach it's target? There seems to be some kind of actual research these cells do.


text:
Would prehistoric humans have been considered negroid or australoid by modern standards?
What are your thoughts about this?
For myself I think that the subject statement is rather obvious isn’t it, since Africans, & especially Australian Aboriginals, have the most archaic features & share the most traits with prehistoric humans & other primates within modern humanity? Africans have neotenized greatly, culminating with the khoisan people, whereas australoids don’t have any neotenous traits which the other races have been developing & don’t lack archaic traits which the other races have devolved.
Which of the great races, the highest general division of humanity, mongoloid, caucasoid, negroid, australoid, etc. would prehistoric humans have been considered both by layman’s perceptions, & classified as more scientifically, by contemporary standards, if the choice had to be made, or at least considered closest to or most resembling?
What we’re probably thinking of then are remains going really far back enough to not be of obvious contemporary racial categories aren’t we?
Since prehistoric humans are said to not resemble any modern race, this question may end up being more about opinions rather than hard answers, might it?
Please explain & fill in details regarding your opinion & knowledge. But please do answer the main question first before adding in more details, even if to explain how this subject statement has no merit!
Not sure how much merit this book holds, but do have a look at the tables in ‘Section II: Traits of Living Populations’ for a nice summary:
https://analyseeconomique.files.wordpress.com/2012/12/richard-d-fuerle-erectus-walks-amongst-us.pdf
Here’s the tables themselves. The site’s in French but you can translate it in google. You can also click on the images & save them:
https://analyseeconomique.wordpress.com/2011/11/20/erectus-walks-amongst-us-richard-d-fuerle-section-2/amp/

Which prehistoric humans? The ones giving rise to modern day Native Australian, Congolese, Han Chinese, ... ?

Your right, I should have been more specific, since the term prehistoric really means anytime before history. In human evolution terms, that would mean the whole time ranging from when our ancestors split from chimps’ some 6 to 10 million years ago to the eve of civilization some 6,000 years ago, & the current races already seem to have long evolved by then. Let’s take it gradually then, step by step.

I was really being generic & referring to all prehistoric remains not identifiable with modern human races. Let’s discuss gradually, starting from our earliest ancestors, then move on to the earliest identifiable human beings, being Homo Habilis & Erectus, then to our most recent genus cousins like Neanderthals & Florensis, then to the earliest identifiable anatomically modern human remains, currently being Jebel Irhoud, & the earliest outside Africa currently being the Skhul & Qafzeh hominins, then moving to other remains around the world.

The first question to answer might be: Has phenotypic diversity in humans increased or decreased since prehistory?  It might be the case that prehistoric humans were as diverse as modern humans, or more so, since there have been a number of diversity-reducing bottlenecks in our evolution.

https://australianmuseum.net.au/learn/science/human-evolution/how-have-we-changed-since-our-species-first-appeared/ This article might answer your question partly. Nice concise article overall. I thought it was interesting to read them explain in the 6th section that modern humans’ diversity is enormous compared to early Homo Sapiens, who they seem to suggest were all much more similar to each other in physical characteristics?

Still, I’m pretty sure that there would have been fair amounts of variation for most of our’s as well as our genus cousins’ histories, just as there is variation among just about all isolated organisms. Even far traveling bird populations have their physical & genetic isolations & variations within genera & species, so how could one expect terrestrial beings like us to be able to avoid that? You have a good point on how our species has had some bottlenecks. The only studies & information there seems to be available for that is genetics, & not so much about phenotypes.

We don't really know yet what archetypes were like in the paleolithic.
this is your reference: "L’incapacité des noirs à différer la gratification les conduit à louer au lieu d’épargner, à voler au lieu de travailler et d’attendre, et à violer au lieu de courtiser et de séduire. " blacks worship/rent not save, steal not work, rape not seduce? is that your best research? there are many africans with an IQ of 140 and europeans with an IQ of 60, sometimes entier villages of europeans. So he generalizes foolishly.
There probably never was an archetype from any age, there were instead dozens of geographically isolated populations at all times, and the variety of tribes and ethnicities in history is beyond what can be visualized, understood and imagined.
40,000 years ago, there were already chinese looking people, caucasian looking people, african looking people, you would be comparing thousands of different groups at any single time in the paleolithic, and we don't have that information.
The mesolithic, neolithic, bronze and iron ages, are all prehistoric times.
Your timeline is 300,000 years, and your reference compares negro's anthropometrics to orang-utans and gorillas and caucasians. It's a silly old racially biased pseudoscience document. Real science using DNA classes Africans into a dozen ethnicities as different amongst one another as europeans, chinese and australians.
This is a list of human fossils with images: https://en.wikipedia.org/wiki/List_of_human_evolution_fossils#Middle_Paleolithic:300,000%E2%80%93_50,000_years_old
Australians are geographically isolated people so they don't represent an archetype. They are an ethnic group amongst thousands that would have existed prior to boats and horses (3500 years ago), rather than an archetype.
There were probably many dozens of groups of peoples as exotic looking as Australians which have become mixed into todays spectrum of facial types. Nearly all the faces that existed 50,000 and 100,000 years ago have contemporary examples. https://www.bbc.com/news/av/world-14929644/beast-from-the-east-nikolai-valuev-seeks-siberian-yeti

Yes I am aware that the provided article seems to have racist agendas. I haven’t actually read the book & don’t know much about it yet. The agendas are not what I’m interested in however. All I’m interested in the book is the summary tables on the physical characteristics of the races. It’s nice & concise & seems to be accurate for the most part even if only brief & summarized. The tables were probably composed by the author himself, can’t seem to find such summary tables on the races elsewhere, especially considering how this kind of subject is considered politically incorrect in this era

https://www.diffen.com/difference/Ethnicity_vs_Race As quoted from these articles, race should not be equated with ethnicity, which has a sociological meaning. Ethnicity is a self-described category that has three components-ancestry, language, and culture that all have affinities to certain ancestral groups. Race refers to a person's physical characteristics such as bone structure and skin, hair, or eye color. Ethnicity, however, refers to cultural factors, including nationality, regional culture, ancestry, and language. http://www.biologyreference.com/Ar-Bi/Biology-of-Race.html#ixzz5e0Udb5cb

By ‘archetype’ I imagine you mean race by that term? I would agree that is a good way to describe the concept of the major races of humanity. I just hope you understand where the concept of race comes from, that all of human variation can be summed up into 3 or 4 broad but distinct categories phenotypically, & that it’s shown now that these categories don’t overlap with genetics. 40,000 years ago seems to be as far back to when we can trace current races, caucasoid & australoid to be specific, negroid & mongoloid is far newer, so what I’m interested in are the mysterious remains before that.


text:
How many nucleotides in the DNA molecule?
Suppose I cut a human DNA molecule that was 6800Å long into 5 equal sized pieces using molecular scissors, how can I find out number of nucleotides in each of the cut pieces? Please give a bit detailed solution. I'm kinda new to these kind of questions.

This is a homework question. Such questions are considered on-topic only if a significant effort has been made by the asker towards finding out the answer. Moreover, if we do your homework for you then what will you learn?

What kind of efforts do you expect? Moreover, I am in my 10th grade and have very little knowledge on this topic. (And this is not a HOMEWORK question. I found these sort of questions in bunch of question papers).That was why I mentioned that I was new to these questions and I needed a bit of explanation
.SideNote: This is not even in my School Textbooks and I am asking this out of my own interest. I failed to find a concrete answer to this question online (if there exists one, please post it.)

At least in Math, I can tell people what formulae or theorems I`ve used. What do you exactly mean by efforts here? (Please tell, I am new.)

@WYSIWYG is a moderator on this SE Group (you can tell by the diamond). He is explaining to you as a new user how the site works. The answer to your question "What kind of efforts do you expect?" is given in the Help on asking questions which we expect you to make the effort to read. The fact that you are still at school is really irrelevant. If you read the tour you will see that "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students". If you don't fit, don't post.

Angstroms are a measure of distance. 1 angstrom is a tenth of a nanometer, i.e. 10 nanometers make 1 angstrom.
Your DNA molecule: 6800 A
Cut into 5 equal pieces: 6800/5 = 1360
Each cut DNA piece is 1360 A long.
A DNA helix has the following properties: 10 base pairs extend 34 A.
1360/34 = 40 = how many '10 base pairs' of length you have in each cut DNA piece.
If a cut piece has forty 10 base pairs of length, the full length has 40 * 10 bp.
40 * 10 = 400 bp.
Each cut piece is 400 bp long. The original DNA piece, uncut, is five times the size of its cut. In other words, the original DNA piece is (400 * 5) 2000 bp long.


text:
How can I extract DNA from horse hair?
For my project I have to find an inexpensive, quick and simple-to-use method to extract DNA from horse hair. The sample does not have to be purified because the sample will be used for LAMP and not PCR.
I will do my internship at a university so most kinds of equipment and materials are available to me. I also have a budget for my project. I searched online for DNA extraction kits but didn't have much luck because many kits were for human hair and horse hair is a little bit thicker.
Does anyone have experience with a method that would work for my case as well and can advise me?

What kind of equipment and materials do you have access to?

i will do my internship to the Wageningen university so most kind of equipment and materials are available for me, i also have a budget in terms for helping my project. i did search online to find DNA extraction kits but not that much luck because many kits where for human hair and horse hair is a little bit thicker. Do you know a method that kan help me with this, or perhaps a link where the method is explained ?


text:
What happens to drug metabolism when CYP450 enzymes are presented with two substrates
What happens when two substances, both substrates for Cytochrome P450 metabolism, are both present in the bloodstream?
For example, with sertraline and cannabidiol (CBD), if someone took a sertraline tablet and later used CBD, how does the presence of two CYP substrates affect drug metabolism? Does one drug inhibit the metabolism of the other? What happens to blood levels of the drugs? Does the order of administration matter?

If you want to ask the question about two specific substances and one specific enzyme, you should edit the title of your question to make that clear. If you are asking about the broader biochemical principle then you should edit the body of your question to make that clear.

Welcome to SE Biology. As a new user you should take the tour and read the help on asking good questions, where you will see that you are expected to demonstrate that you have researched a question before posting. This question can be answered by an understanding of the basic principles of enzyme action. Read, for example, this section of Berg et al. online, paying particular attention to the meaning of Km. Oh, and what is CBD? Don't tell me, edit your question.

@David Km? I think you're overly simplifying this question, as if you are pointing someone asking about events at relativistic speeds towards Newton's laws. The whole point is that this is a case where MM kinetics don't necessarily apply (I don't know about the specific example OP references, but I am thinking of liver enzymes like this one ).

@BryanKrause  The etermal question — what does the poster already know? I would assume from the terminology of "take priority" and "take over" in a question written in reasonable English that the poster is unaware that different substrates for an enzyme can have different affinities. Likewise his reference to x mg of one substrate but an unspecified amount of the second suggests he is unaware of the effect of concentration (and relative concentration of substrate). But I may be wrong.  Let him tell us.

@David I agree that the language is a bit sloppy, but it seems like OP is coming at this with some knowledge of medical implications of pharmacology rather than biochemistry and I think this question is better researched than you are giving credit for.

@BryanKrause and David honestly, this sounds very much to me like someone who is asking "Can I take my antidepressant and cannabidol together, and if so, how?"

I edited to, I think, maintain the kernel of the on topic question. It seems to be about CYP activity specifically (vs. other classes of enzymes). I kept the CBD/Sertraline example because it limits the teaching points (from my perspective), mainly, to: there are many CYP enzymes, they are promiscuous, and this isn't the only thing to consider when evaluating drug-drug interactions.

I think the OP is asking the following:

If an enzyme is not specific one substrate, but is simultaneously presented with a pair of substrates, which one 'wins' and how do we decide?

For example, if an enzyme is presented with a racemate such that the D-form has a 10-fold lower $K_m$ than the L-form, but the L-form has a 5-fold higher $k_{cat}$, which one is preferentially metabolized, and how do we decide?
It was Fersht who first provided the definitive answer, at least for single-substrate enzymes (Fersht, Enzyme Structure and Mechanism, 1977; see also here)

The kinetic parameter determining the specificity for competing substrates is neither $K_m$ nor $k_{cat}$, but the (so-called) specificity constant: $$\frac{k_{cat}}{K_m}$$

If it assumed that both substrates, considered in isolation, obey the Michaelis-Menten kinetics, then it is very easy to derive (starting with the ratio of the respective Michaelis-Menten equations) the following expression for the initial velocities when both substrates are present simultaneously.
$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{cat}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{k_{cat}^2}}} \ \ \ \ \ (1)$$
(The equation is derived by, among others, Cornish-Bowden (2004, pp 36-39):
If $V_{max}$ is preferred to $k_{cat}$:
 $$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{V_{max}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{V_{max}^2}}} \ \ \ \ \ (2)$$
${{k_{cat}}}\over{K_m}$ has units of a second-order rate constant and, giving it a symbol (${k_{1}^{\prime}}$ for $S_1$ and ${k_{2}^{\prime}}$ for $S_2$) to reflect its status as a fundamental kinetic constant and not just a ratio, allows the following equation to be written:
$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{1}^{\prime}}}\over[S_1]}}  \times{{{[S_2]}\over{k_{2}^{\prime}}}} \ \ \ \ \ (3)$$
This equation provides the answer to the OP question. For the racemate described above, we need only calculate the ratio of the specificity constants to get the answer:
$${
    {
     {
      {v_{i}^{D_{form}}
     }
     }\over{
             v_{i}^{L_{form}}}
            }
    }   =
{
    {
     {
      {k_{D_{form}}^{\prime}\times{[D_{form}]}
     }
     }\over{
             k_{L_{form}}^{\prime}}\times{[L_{form}]}
            }
    } = {
    {
     {
      {k_{D_{form}}^{\prime}
     }
     }\over{
             k_{L_{form}}^{\prime}}
            }
    } =  2 \ \ \ \ \ (4)$$
Much could be written about the specificity constant (diffusion control, enzyme 'perfection', Haldane relationships), but I'll make just one. Considering the single-substrate Michaelis-Menten enzyme, the following holds AT ALL SUBSTRATE CONCENTRATIONS
$$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}][E]}   \ \ \ \ \ (5)$$
When $S_o$ is very low, $[E]$ = $e_o$ (approx) and the following may be written (where,unlike $[E]$, $e_o$ is usually known or may be determined)
 $$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}]e_o}   \ \ \ \ \ (6)$$

But it is Eqn (5) that is the important one: $k^{\prime}$ (the so-called specificity constant) may be thought of as the second-order rate constant governing the combination of ('free') enzyme with substrate at all substrate concentrations, not just when $S_o$ << $K_m$

Much could be written about this as well
Definitions
I think it is reasonably obvious what everything means. Nevertheless, here is a list:

$K_{m}^1$  is the Michaelis Constant for substrate 1
$K_{m}^2$  is the Michaelis Constant for substrate 2
$k_{cat}^1 $ is catalytic constant for substrate 1
$k_{cat}^2 $ is the catalytic for substrate 2
$V_{max}^1 $ is the maximum velocity for substrate 1
$V_{max}^2 $ is the maximum velocity for substrate 2
$k_{1}^{\prime} $ is the specificity constant for substrate 1
$k_{2}^{\prime} $ is the specificity constant for substrate 2
$v_{i}^{1} $ is the initial velocity due to substrate 1
$v_{i}^{2} $ is the initial velocity due to substrate 2

Reference

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press (London)

You really think? If only questions on SE Biology were at that level. To avoid your answer going to waste I’d edit the question drastically so there is no doubt your answer fits. If the poster doesn’t like it he can always revert, but his lack of response to comments suggests this unlikely.

I enjoyed this answer. I'd be curious to see your thoughts about how well this applies to drug metabolizing CYPs in vivo, given their particular properties.

FYI I've edited the question to, I think, let the useful pharmacology question be more clear. Along with @David, I'd encourage you to edit the question as well, since you saw a useful biochemistry question in it.

What are CYPs? How are they different from other enzymes?
Cytochrome P450 enzymes (CYPs) are a large family of enzymes involved in the metabolism of many endogenous and exogenous compounds (including typical dietary substances and pharmaceuticals). There are many different CYPs, each individual CYP form can metabolize many different compounds, and a single compound is typically metabolized by more than one CYP, sometimes at the same site, sometimes at multiple sites, sometimes in an ordered sequence, and sometimes not. This promiscuity in substrate/enzyme interaction is in contrast to most human enzymes, which are highly specific. Its cost, though, is efficiency.
CYPs and drug-drug interactions
CYP effects are an important subset of drug-drug interactions, but this is typically not described in terms of race conditions. Perhaps this is because of the particular relationship between enzyme and substrate. In addition to being metabolized by CYPs, many drugs and dietary substances can inhibit some CYP forms and induce others (including forms that do not metabolize the substance itself).
To answer the particular question about whether the order of administration matters, while inhibition is typically at the level of protein interaction, induction involves gene interactions. Because induction involves gene interactions, induction results in interactions that do not depend on both drugs being available to CYP at the same time. This means that (for induction effects) neither changing the order of administration or staggering doses will prevent the interaction. Generally, those examples of drug-drug interaction that are readily prevented by dose order involve pharmacodynamic interactions, i.e., interactions at the drug's intended molecular target.
Is this all you have to consider when evaluating for a potential drug-drug interaction?
For emphasis, I'll say it again: CYP effects are an important subset of drug-drug interactions. There are many things to consider when evaluating the effect of polypharmacy.
Further reading
You can read about this in Goodman & Gilman, the Pharmacological Basis of Therapeutics. Ch 6 has a good subsection about CYP metabolism in general, with specific discussion about the metabolism of different compounds in other chapters. Most good basic pharmacology textbooks will cover this, but I think G&G does a particularly good job. Full prescribers information on any drug will include information on CYP450 metabolism, inhibition, and induction.  You can look at wikipedia, but this is not the best wikipedia article I've read.
So what about sertraline and CBD?
I am not going to make a statement about whether a particular combination of drugs does or doesn't interact, if only to encourage anyone with a drug-drug interaction question TALK TO THEIR DOCTOR, or whoever prescribed your medication. Different jurisdictions have different laws about CBD, but doctors are not law enforcement officials. You can and should tell him/her about everything you take.

If you think that this is a personal medical question (that hadn’t occurred to me), surely you should vote to close.

@David as, alas, we often see, it seems to me like there is one  question in the text of the OP/post (not personal medical) and another question in the mind of the OP/poster, but the OP/poster hasn't engaged with the comments. I tried to answer the text of the question, and only because there was excellent information in another answer.


text:
Why is cartilage replaced by bones in a vertebrate adult?
Why is cartilage present in a vertebrate embryo replaced by bones in an vertebrate adult even though cartilage can also provide me the structural framework like as in Chondrichthyes and they seem to do well with it as Sharks are members of Chondrichthyes which are some of the most fearsome creatures of the world.

Bones are complex organs, made of more than just a structural element. Cartilage is just a tissue, usually devoid of nerves and blood vessels.
Chondrichythes live in water (ἰχθύς ichthys is Greek for 'fish'); the difference in specific gravity and buoyancy is considerable, and cartilage is not robust enough to mechanically support your body out of the water.
Vertebrates have evolved to have a bone marrow, which is part of the bone. If the structural element of the bone (the dense mineral matrix) was replaced by cartilage only, then the hollow structure would make things even worse.
Additionally, cartilage has about the same density as water (Pan et al, 2016) whereas dense bone is 60-90% more dense, which means extra weight pulling aquatic animals down.

Bones evolved in fish that lived in the same water as sharks, so the mechanical argument doesn't hold. Maybe land vertebrates would be hindered (but there are plenty of insects, etc. that do just fine).

@kmm The mechanical argument only means that "if you live on land and have a significant mass, then you need bones", it does not mean that "if you have bones, you cannot live in the water". There is no contradiction here :)

Then I don't understand the point you are making in the 2nd paragraph with respect to the poster's question.

It's an example of why in certain contexts, vertebrates (like you and I) have a biological advantage because they have bones instead of cartilage. Which contributes to explaining why the presence of bones has been maintained in aerial vertebrate lineages. It does not explain everything but it explains why vertebrates are ecologically successful on land (which is where the majority of described vertebrates species live) so that helps answer the question

bone marrow is unrelated to bone, marrow actually evolved before bone. https://www.ncbi.nlm.nih.gov/pubmed/3636583

Short answer, cartilage can't provide the same support as a bone,  bone is stronger and stiffer.
Sharks may be big but they have pathetically weak bites for their size and that even when they partially ossify their jaws. They just can't fully ossify the tissue. The main swimming action of "fish" works even with flexible connections because each muscle is linking to the next linearly, the cartilage and collagen is mostly subjected to tension. But things like jaws and limbs need to withstand shear forces and withstand flexion, which cartilage sucks at, but bone is quite good at. It is not coincidence that the first bones evolved in jaw.


text:
Can I change the genetics of a group of plants naturally?
I have been thinking about introducing all sorts of types to certain environments where the plants will have to adjust to survive.
For example having a dark area with one light source right next to the plants so they all want to grow towards the light.. however this could be made more difficult by either introducing slight angle adjustments or artificial wind (custom controlled fans).
Would it be possible to start slowly introducing such challenges to change the plants? for example strengthen their stems to be able to fight the gravity or wind?

Of course, you can place a population of anything (incl. a population of plants) into a specific environment and you could expect this population to slowly adapt to it.
Most plants don't have a particularly fast generation time and therefore, the evolutionary experiment might take longer than your lifetime. The experiment would be much faster if you choose some unicellular algae such as Chlamydomonas reinhardtii for example.

Related: https://biology.stackexchange.com/a/59670/27148

Can I change the genetics of a group of plants naturally?

Of course.  Start with a mix of plants with a mix of traits.  Kill off all plants which lack the traits you want.  You now have a group with different genetics than you started with.

For example having a dark area with one light source right next to the
  plants so they all want to grow towards the light

Plants already have the genetics to grow towards the direction of light.  Making them all grow sideways would not be a genetic change.

Would it be possible to start slowly introducing such challenges to
  change the plants? for example strengthen their stems to be able to
  fight the gravity or wind?

Do you understand that you cannot change the genetics of individual organisms?
But sure, kill all the plants that don't have the trait you want.  Let the survivors breed.  The offspring will be genetically different, due either to recombination or mutation.  Keep culling the ones you don't want, and the population will have different genetics than the original population.

I meant to slowly introduce these over multiple generations.


text:
Were there any terrestrial species in the ancestry of all crustaceans?
To the exception of woodlice, Crustaceans live in aquatic (marine or freshwater) environments. Crustaceans are arthropods which is an immensely diverse taxon. Many arthropods live in terrestrial environments and many live in aquatic environments.
Pisani et al (2004) report evidence of fossil of terrestrial arthropods as old as ~450 million years ago. According to Wikipedia > Arthropoda citing Lin et al. (2007) (the paper is behind a paywall, I could not read it myself) report evidence of fossil of arthropods as old as ~550 million years ago.
Were there any terrestrial species in the ancestry of all crustaceans?

Are you asking if all extant crustaceans descend from a terrestrial species?

Yes. Whether the MRCA of all crustaceans (or another organism in that lineage before that) was terrestrial.

There is free pdf from researchgate (link).


text:
Where does Darwin state his "principle of multiple utility"?
I have never heard of Darwin's 'principle of multiple utility', but several papers refer to it. For example, from Darwin at the molecular scale: selection and variance in electron tunnelling proteins including cytochrome c oxidase

Such a high degree of conservation is probably the consequence of many parallel and concurrent aspects allied to the construction, manifold functions and demolition of cytochrome c oxidase as illustrated in the molecular scale view of Darwin's principle of multiple utility (Darwin 1872) shown in figure 7.

Also, from the pape, Engineering enzymes.

Another source of biological complexity arises from Darwin’s principle of multiple utility. The principle originally applied to organisms recognizes that any one trait in an organism is subject to be selected by multiple forces.

The citation to "On the Origin of Species" in these paper provides no page numbers. Neither do any of the other papers that mention the principle. I searched the sixth edition of "On the Origin of Species" for terms such as utility, multiple, roles, etc., but found nothing that sounds like such a principle.
It seems to me that anything described as a Darwinian principle would be extensively discussed in the literature. That does not seem to be the case with this so-called 'principle of multiple utility'.

I also can't find anything specific from Darwin himself. The phrase is used in a number of places, but almost always by the same two authors (Dutton and Moser), who invariably refer unhelpfully to (Darwin, 1872). A couple of other papers use the phrase and cite Dutton and Moser. I believe that this is a paraphrase that D&M came up with, not an actual principle that Darwin spelled out.

I agree with @iayork, and the earliest reference I found was in 1991 with no citation to anything. Origin does talk about biological complexity, and specifically has explanations for why we should not expect all life to be "complex" (according to a particular definition of complexity), but if Darwin talks about the multiple utilities of a particular trait that must be in later work, not in Origin.

I agree with both of you, @iayork and Bryan Krause, that Dutton appears to have coined the term 'principle of multiple utility'. Accordingly, I emailed him to ask for a more precise citation to Origin of Species.

@Nick Gall It would be great if, once you receive Dutton's answer to your email, you could report his answer here! Thanks

@Remi.b Absolutely, with his permission of course.

I heard back from Prof. Dutton and Prof. Moser, who referenced the principle in their joint paper. Here is the gist of their response. Basically, they claim to have gotten the principle George McLendon.

I wrote to Prof. McLendon. This is the gist of my question to him. Basically, I think Wallace's "principle of utility" mutated into the "principle of multiple utility".

I just checked my copy of The Origin of Species and it's been released in 1859. The book Darwin released in 1872 was The Expression of Emotions in Man and Animals, so I would assume that's the book they refer to - maybe they mixed up the reference. Unfortunately, I have not read it, but that might be worth to check out.

The 6th edition was published in 1872 as The Origin of Species.


text:
What's the difference between the neuroendocrine system vs endocrine system?
This is what I have understood so far:
Neuroendocrine system involved neuroendocrine cells (also known as neurosecretory cells) that receive nerve impulses by a sensory neuron to release neurohormones into the blood stream. The endocrine system releases hormones by endocrine cells into the blood stream when a receptor protein senses a stimulus.
Here are my questions:

When it comes to the brain, are the neurosecretory cells located in
the hypothalamus or the posterior pituitary gland or both?
Is the hypothalamus and the posterior pituitary gland classified as
    neuroendocrine glands and is the anterior pituitary classified as an
    endocrine gland?
If the posterior pituitary gland is indeed a neuroendocrine gland,
    is ADH and Oxytocin, which are both released by the posterior
    pituitary gland, classified as "neurohormones", not just the classic
    hormones?

I'm pretty sure not all ('neuro')hormones released by neuroendocrine cells actually enter the bloodstream. Some of them are only released inside the brain.

Neuroendocrine systems can be defined as the sets of neurons, glands and non-endocrine tissues, and the neurochemicals, hormones, and humoral signals they produce and receive, that function in an integrated manner to collectively regulate a physiological or behavioral state.
The neuroendocrine system is the mechanism by which the hypothalamus maintains homeostasis, regulating reproduction, metabolism, eating and drinking behaviour, energy utilization, osmolarity and blood pressure. (Source)

The central neuroendocrine systems serve as an interface between the brain and many of the peripheral endocrine systems. This chapter discusses the hypothalamic control of anterior pituitary systems regulating stress, basal metabolism, growth, reproduction, and lactation. Each of these systems involves one or more hypothalamic releasing or inhibiting hormones, released from hypothalamic neurons that terminate in the portal capillary vasculature that projects from the median eminence at the base of the hypothalamus to the anterior pituitary gland. There, the hypothalamic hormones act upon subsets of anterior pituitary cells to regulate pituitary hormone release and downstream physiological functions. Other hypothalamic neuroendocrine cells control water/salt balance, and lactation/parturition, through the release of vasopressin and oxytocin from nerve terminals that arise in hypothalamus and project to the posterior pituitary gland. Together, these hypothalamic neuroendocrine functions enable the central nervous system to respond rapidly to internal or external environmental change, and to maintain a response through endocrine hormonal transducers. (Gore, 2013).

The endocrine system is a group of glands and other structures that release internal secretions called hormones into the circulatory system.

Endocrine organs are richly vascularized ductless organs that produce hormones. The epithelial cells of the organ secrete their hormone product directly into the bloodstream where, upon binding with specific receptors in target organs, cellular functions are affected. The endocrine systemincludes not only the endocrine glands (pineal, pituitary, thyroid, parathyroid, and adrenal) but also single cells and small clusters of cells in the thorax and abdomen known as paraganglia. This chapter addresses the thyroid, parathyroid, adrenal, pituitary and pineal glands, and paraganglia. In addition to size differences, several features of endocrine tissues differ between rodents and humans, and often between rodents. (La Perle & Dintzis, 2018).

Question 1

When it comes to the brain, are the neurosecretory cells located in the hypothalamus or the posterior pituitary gland or both?

Neurosecretory cells are found in the hypothalamus. (Source)

There are two types of neurosecretory cells: magnocellular cells and parvocellular cells. Magnocellular cellsare large cells, having long axons that terminate in the neurohypophysis (also known as the posterior pituitary). Magnocellular cells release the hormones vasopressin and oxytocin to the general circulation; we will talk about the physiology of these hormones in Conjoint 403.  The parvocellular cells are small cells, with shorter axons that terminate at a capillary-rich bulge at the base of the hypothalamus known as the median eminence.

Question 2

Is the hypothalamus and the posterior pituitary gland classified as neuroendocrine glands...

No

...and is the anterior pituitary classified as an endocrine gland?

Yes.
The following is from: https://courses.lumenlearning.com/boundless-ap/chapter/the-pituitary-gland
(emphasis mine)

The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system. Despite its name, the posterior pituitary gland is not a true gland; rather, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland.

The pituitary gland is an endocrine gland, about the size of a pea, that sits in a small, bony cavity at the base of the brain whose secretions control the other endocrine glands and influence growth, metabolism, and maturation.
While the pituitary gland is known as the master endocrine gland, both of its lobes are under the control of the hypothalamus: the anterior pituitary receives its signals from the parvocellular neurons, and the posterior pituitary receives its signals from the magnocellular neurons.
The anterior pituitary, also called the adenohypophysis, is a major organ of the endocrine system, and is the glandular, anterior lobe of the pituitary gland.
The anterior pituitary gland secretes 7 hormones: follicle stimulating hormone, luteinizing horomone, adrenocorticotropic horomone, thyroid stimulating horomone, prolactin, endorphins, and growth hormone.
The posterior pituitary gland does not synthesize any hormones.  Hormones known as posterior pituitary hormones are synthesized by the hypothalamus, and include oxytocin and antidiuretic hormone (ADH), also called arginine vasopressin or vasopressin (Liu, 2007). The hormones are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the bloodstream.
With regard to neurohormones mentioned in question 3, neurohormones are hormones that are produced by neurosecretory cells and released by nerve impulses (e.g., norepinephrine, oxytocin, vasopressin).
This is the part which can be confusing. Whilst ADH and oxytocin are released from the posterior pituitary gland, which is an endocrine gland, the hormones are produced by neurosecretory cells within the hypothalamus and they are stored in and released from neurosecretory vesicles within the posterior pituitary gland. Therefore they are classed as neurohormones.
References
Gore, A. C. (2013). Neuroendocrine systems. In Fundamental Neuroscience (Fourth Edition) (pp. 799-817). doi: 10.1016/B978-0-12-385870-2.00038-X
La Perle, K. M. D., & Dintzis, S. M. (2018). Endocrine system. In Comparative Anatomy and Histology (pp. 251-273). Academic Press. doi: 10.1016/B978-0-12-415759-0.00058-3
Liu, K. D. (2007). Hyponatremia and Hypernatremia. In Critical Care Secrets (Fourth Edition) (pp. 285-290). doi: 10.1016/B978-1-4160-3206-9.10044-8

Not all hormones enter the blood - just as a quick addendum to the thorough reply above, and as per a comment above stating not all hormones from neuroendocrine cells go into circulation - seems to be true: many of the neuroendocrine cells release hormones directly into the organ where those cells appear - as per the gut, heart, lungs - here's a nice visual overview
https://byjus.com/biology/hormones-heart-kidney-git/


text:
What are haplotype blocks and what is the effect of hybridization on these?
In this PDF, there is a quick definition of haplotype blocks.

A haplotype block is a set of closely linked alleles/markers on a
  chromosome that, over evolutionary time, tend to be inherited
  together.

Also look at this definition:

We defined a haplotype block as a region over which a very small
  proportion (<5%) of comparisons among informative SNP pairs show
  strong evidence of historical recombination. [We allow for 5% because
  many forces other than recombination (both biological and artifactual)
  can disrupt haplotype patterns, such as recurrent mutation, gene
  conversion, or errors of genome assembly or genotyping.]

Although in the abstract they say:

haplotype blocks: sizable regions over which there is little evidence
  for historical recombination and within which only a few common
  haplotypes are observed.

But the first definition confuses me because it really looks like the definition of linkage disequilibrium:

linkage disequilibrium is the non-random association of alleles at
  different loci in a given population.

Which means that they are inherited together (non-randomly inherited).
The other definitions don't seem to agree in the same paper...
Just as a reminder a haplotype is: "The set of alleles found on a single sequence is referred to as a haplotype."
(Hahn, M. W. 2018. Molecular Population Genetics. Sinauer Associates, Incorporated, Sunderland, Massachusetts.)
So:

What are haplotypes blocks precisely and compared to LD? How to estimate haplotypes blocks?
Why is this an important concept (what is it informing us, why would want to study that specifically)?
What influences haplotypes blocks and how is it useful to get some information when doing genomic analysis (can we account for that)?

Here are 2 relevant resources on the subject:

Daly, M. J., J. D. Rioux, S. F. Schaffner, T. J. Hudson, and E. S.
Lander. 2001. High-resolution haplotype structure in the human
genome. Nature Genetics 29:229–232.
Patil, N., A. J. Berno, D. A.
Hinds, W. A. Barrett, J. M. Doshi, C. R. Hacker, C. R. Kautzer, D. H.
Lee, C. Marjoribanks, D. P. McDonough, B. T. N. Nguyen, M. C. Norris,
J. B. Sheehan, N. Shen, D. Stern, R. P. Stokowski, D. J. Thomas, M.
O. Trulson, K. R. Vyas, K. A. Frazer, S. P. A. Fodor, and D. R. Cox.   2001. Blocks of limited haplotype diversity revealed by high-resolution scanning of human chromosome 21. Science
294:1719–1723.