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What drives max heart rate on beta blockers?
In a healthy human being, the increase in heart rate from rest to around 100 to 110 beats per minute at low intensity exercise is due to withdrawal of the parasympathetic nervous system's influence. If exercise intensity increases beyond that point, the matching increases in heart rate above 100 to 110 beats per minute are due to sympathetic nervous system influence.
There is a transition range around 100 to 110 beats per minute where the intrinsic rate of the heart beat is determined by the body's metabolic activity.
However, when a person takes a beta blocker, the sympathetic influence on the heart rate is attenuated, so that the person's max heart rate is lowered to around 110 beats per minute.
What is driving the heart rate at high intensity exercise in patients who take beta blockers?  Is the heart rate around 110 beats per minute in patients on beta blockers driven primarily by the metabolic influences in the blood? What other factors are influencing heart rate around 110 beats per minute in patients who take beta blockers?


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How do B and T cells work incorrectly in a person with Systemic Lupus Erythematosus?
Systemic lupus erythematosus is an autoimmune disease in which the body's immune system attacks healthy cells. How exactly do B and T cells attack these cells they mistake for pathogens?

The initial trigger for the disease is unknown and can be different from person to person. However, we do know that there can be environmental or infectious triggers that are further potentiated by genetic and hormonal factors.
The pathology of SLE is associated with the development of "auto-antibodies" or "anti-nuclear antibodies," so saying that B cells and T cells attack healthy cells is not exactly correct - More accurately they produce antibodies against proteins on healthy cells, which form immune complexes, activate complement and induce apoptosis.  To produce auto-antibodies, events occur as follows:

The trigger causes macrophages or antigen-presenting cells (APCs) to display self- or auto-antigens
APCs recruit B cells to start producing antibodies against the antigen
APCs activate T helper cells, which stimulate inflammation and perpetually activate the B cells to produce auto-antibodies

The following immune abnormalities are associated with SLE (particular focus on B cells and T cells)

High levels of circulating B cells
Decreased levels of T suppressor cells, which would otherwise regulate the immune system and auto-antibody production
Abnormal B cell signalling and persistent activation of B cells (IL-6, IL-10)
Prolonged life span of B cells, possibly due to poor immunoregulation (#2)

Reference:
Schur PH, Hahn BH, Pisetsky DS, Ramirez Curtis M. Epidemiology and pathogenesis of systemic lupus erythematosus. Up to date. Topic last updated: Feb 5 2016. Subscription access only.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Multiple fission and spore formation

I came across this question today. In the B diagram, zoospores of chlamydomonas is given. Now my doubt is, are the zoospores formed by multiple fission or spore formation? If it is by spore formation, isn't spore formation and multiple fission the same thing when it comes to unicellular organism i.e chlamydomonas? If it is the same thing, why isn't option c correct in the question I attached?

I will answer later, so I can provide a good ref. The issue is whether this shows the result after fission (asexual)  or meiosis (sexual). Showing 9 daughter cells is a bit unfair..2,4,8,16 would be better. After meiosis the 4 daughter cells can also continue to divide by mitosis before release.

But zoospores are produced asexually, so meiosis isn't possible. Also is multiple fission produced by mitosis or amitosis?

All the organisms shown in the figure reproduce asexually. (A) is Penicillium in which non-motile conidia are produced singly or in chains. Organism (B) is Chlamydomonas in which reproduction occurs by zoospores. In Hydra (C) and yeast (D), asexual reproduction takes place by budding.
Mutliple fission and Spore Formation are two distinct processes where in:

Multiple fission can be explained with the following diagram:

Multiple fission is a process of asexual reproduction in which a single organism splits up into multiple organisms or daughter cells of similar type under favourable conditions like availibity of food and suitable environmental conditions.

Spore formation can be explained with the following diagram:

Spores are tiny microscopic hard unicellular sexual bodies which are always suspended in air. Under suitable environmental conditions they settle down and grow into new plants. Above given is a structure of rhizopus(bread mould) reproducing through the process of spore formation. Each rhizopus consists of a globular structure at the top known as the sporangium which consists of spores. When the favourable conditions arrive then the sporangium bursts and the spores get suspended in the air. Soon they settle on the moist bread particles, leading to the formation of new rhizopus plants.

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


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What terrestrial Gastropod (specifically snails) has the fastest reproductive rate?
I am looking to do a series of experiments to test the adaptation of snails to different environments (Controlled environments in a lab setting. No organisms would be released into the wild under any circumstances.), and to also test the potential rates of specialization to an environment or food source, and speciation in a snail species (obviously more experiments would have to be done with many species before the results could be generalized). To do this, I need a snail species that has a very short time between the oviposition and sexual maturity of the species, and that are not extremely difficult to raise or breed in a lab. Any help or leads would be appreciated!

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Why do humans have digestive system present at front and kidneys back?
Outlet of digestive system is present at back of the body but its digestive system at front.
Outlet of urinary system is present at front of the body but its system present at back.
Why do humans have digestive system present at front and kidneys back?

Rather, I'd think of both the digestive and urinary systems as occurring top-down and inward-out, because gravity helps.

Teleologically, one can say the kidneys are fragile and need to be protected from trauma, which does actually occut in the relative safety of the lower ribs and spinat support structure. The GI tract, on the other hand, would be too restricted in the retroperitoneum; it needs to be able to expand (food, gasses, etc.) Realistically, because it evolved that way; all vertebrates have the same basic anatomy (basic, not specific.)

I don't claim to have the full answer to why these organs are located in the way they are, but I think these factors have an influence on the anatomy:
1- The urinary system's link with the reproductive system in male mammals: The male reproductive system outlet needs to be located as far to the front as possible in a 4 legged mammal to facilitate sexual function, forcing the urinary system to follow
2- The kidneys are very fragile and need to be protected by the thick back muscles and partly under the rib cage. They would be too vulnerable at the front
3- The urinary system is generally sterile of bacteria, and so is the reproductive system in males, and partially in females. The digestive system isn't sterile in both. The outlet of the digestive system can't be in the front of the genitals in a male as this will increase the risk of urinary infections overall and also genital infections after mating. It can't be in between the urinary and reproductive outlets for the same reason, so it has to be located behind both to cause the least interference with their functions

Please provide support for your answer.


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How does an isotonic environment affect fish?
Fish receive oxygen needed from water that passes through their gills. If fish were isotonic to their watery environment, what problems would this pose to them?

This sounds like it might be a homework question. We try not to answer homework questions here (we use the term broadly to include any sort of coursework, as well as under researched questions where supporting information is very easily accessible), because figuring out those answers independently is an important part of the learning process. However, if you can show how you are thinking about the question and what work you have already done, then we can help out.

dependson the fish and what kind of environment they are adapted to. Some fish woun't notice others will die within minutes.

Some fish are isotonic to their environment (I read that in some book and they had examples but Google is failing me. Here is a paper instead talking about fish doing well in an isotonic environment). It isn't an issue for getting oxygen; I assume you think that because you think fish get oxygen via osmotic pressure, but "isotonic" (and "hypotonic" and "hypertonic") refer to the transfer of water via osmosis. A fish that's isotonic with its environment doesn't need to take special measures to avoid its cells swelling or shrinking as water floods in or out of them; it doesn't say anything about which specific solutes are in that water to make it isotonic.
As far as oxygen goes, oxygen is constantly being consumed by the fish's tissues so the diffusion is always going to go in the right direction (unless the water doesn't contain enough oxygen in the first place, in which case fish won't survive). In addition I imagine fish blood contains many molecules that preferentially bind to oxygen in ways that make this process even more efficient.

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Why do Petri dish lids not fit?
I understand that they are generally "vented", but why such a poor fit? For the batch I bought, the lid and container don't even recognizably go together (like 1/2" difference in diameter). The wind from a box fan could blow the lid off. Even "non-vented" designs appear to have no positive connection between the dish and lid.
Then it looks like the people that do need a positive connection or a seal have to go through a lot of work with tape or wax to seal them.
Seems like a petri dish lid that has a snap, thread, bayonet, or even just friction fit, would be superior. The manufacturing cost differences would be negligible. What am I missing? Thanks!

I would dislike friction fit because I would likely need two hands to open it, whereas now I can just take the dish in one movement, have my tool in the other hand, do the thing, then put it back and pick up the next one. But for storage I often tape them together by 5 for ease of handling, and that prevents accidental opening. Not too much work IMO.

"Seems like a petri dish lid that has a snap, thread, bayonet, or even just friction fit, would be superior" – Petri dishes work by creating a sigmoid path that any particle would have to travel in order to get inside, which is why you don't need a tight lock. From a practical point of view you are supposed to handle (open) Petri dishes in a controlled environment with a rising air flow (preferably in a box or within a small radius of a burning flame) and you should be able to do it with a single hand, because your other hand would be holding something else in the process.

@EliKorvigo, Now I'm curious. Do bio labs really use rising air? I know clean rooms for semiconductors use downward air to help sweep heavier than air particles and bacteria out of the environment. https://en.wikipedia.org/wiki/Cleanroom#Air_flow_principles

Not entire labs, of course. The laminar boxes generate a laminar airflow  directed toward the operator, i.e. a rising airflow. As I've mentioned before, in the old days people used to work within a very small radius from alcohol burners for the same reason (rising airflow). Additionally, old-school microbiologists never fully remove the lid: they use the same hand to rotate the plate and hold the lid above the plate, so that there is only a narrow opening between the lid and the plate during plating.


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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.

I'm voting to close this question as off-topic because are OP doesn't show attempt at an answer.

Did you try finding an answer? ' Provide details. Share your research. '

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.


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LAMP (isothermal amplification), hydroxy naphtol blue , disodium salt" or just hydroxy naphtol blue?
I am reproducing this work on LAMP (isothermal amplification)
Article A new visually improved and sensitive loop mediated isotherm...
,
but I am a bit confused  about the difference between "hydroxy naphtol blue", and "hydroxy naphtol blue , disodium salt". They hav a very huge difference in price. One is 470 USD and 40 USD for the same aliquote.  Or for LAMP there is no difference?
E.g. Price for HNB
https://www.sigmaaldrich.com/catalog/product/mm/104593?lang=de&region=CH&gclid=CjwKCAjw4rf6BRAvEiwAn2Q76quMK0jzJnsEL5Dsjh_rwYhGCz_Foj5ybiH4o8vNCZQ8S53qkaiA9RoCisIQAvD_BwE
and HNB disodium salt
https://www.sigmaaldrich.com/catalog/product/sial/219916?lang=de&region=CH

The sodium salt is the conjugate base of the raw compound, likely formed by reacting it with a strong base like Sodium Hydroxide. I'm curious what function it serves in the LAMP protocol. Can you cite the protocol? They might be capable of serving similar functions in solution, but they are not interchangeable in a reaction recipe, as one will lower the pH of an aqueous mixture more than the other. Probably a better question for https://chemistry.stackexchange.com

I just found a LAMP protocol which provided a CAS number corresponding to the Hydroxynaphtol Blue, not the sodium salt. Make sure to cross-check the methods section of the work you are trying to reproduce though.


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Can I use dATP instead of ATP (vice versa) for in vitro assay?
For example, polynucleotide synthesis reaction requires dATP which gives H on 3'end and synthesizes polynucleotide. For this reaction can I use ATP because I knew that ddNTPs are used so that ATP cannot be worked but I searched about it and found this,

"The unfavorable thermodynamics of the hypothetical dehydration reaction shown in Figure 4.6 leads us to ask: If polynucleotides cannot be synthesized in vivo by the direct elimination of water, how are they actually made? The answer is that their synthesis involves the energy-rich nucleoside or deoxynucleoside triphosphates. Although the process as it occurs in cells is quite complex, the basic reaction is simple. Instead of the dehydration reaction of Figure 4.6, what happens in living cells is the reaction shown in Figure 4.7. The nucleoside monophosphate being added to the growing chain is presented as a nucleoside triphosphate, like ATP or deoxy ATP (dATP), and pyrophosphate is released in the reaction. We can calculate the free energy change for this reaction by noting that it can be considered the sum of two reactions—hydrolysis of a nucleoside triphosphate and formation of a phosphodiester link by the elimination of water...
The coupled reaction is favorable because the net delta G is negative. The reaction is further favored because the hydrolysis of the pyrophosphate product to orthophosphate, or inorganic phosphate, has a delta G = -19kJ>mol. Thus, the pyrophosphate is readily removed, driving the synthesis reaction even further to the right and yielding an overall Delta G of -25 kJ>mol. Polynucleotide synthesis is an example of a principle we emphasized in Chapter 3—the use of favorable reactions to drive thermodynamically unfavorable ones."[1]

So can nucleotide synthesize can be done with ATP in vitro? If yes, how? Also what kind of ATP required reactions can be replaced with dATP?
REFERENCE:
1)[Christopher K. Mathews, Kensal E. van Holde, Dean R. Appling, Spencer J. Anthony-Cahill - Biochemistry (2012, Pearson)]

It's not clear what you are asking about. ATP is already a nucleotide. I would advise you to read the chapter in your text on enzymes and substrate specificity to discover why what you seem to be suggesting is nonsense.

@user1136 — All very interesting (although I don’t subscribe to the “great men of history” idea, especially in its “great women” revival) but we are dealing here with a chemist, who understands Gibbs Free Energy changes, but apparently has forgotten about activation energy of reactions, and hasn’t yet encountered enzymes.


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Addax in the Land of Israel
The Addax (Addax nasomaculatus) is critically endangered species of a desert anetelope with impressive long horns. Today there are small populations in the Sahara desert and the Arabian desert (Saudi Arabia). The addax is mentioned in the bible ("Dishon"), though the identification is not uninomous. Today in Israel there are breeding centers for the addax, one in Hai-Bar Yotvata (near Eilat, the rift valley, bay of the Red Sea) and the other in the Zoological Center at Ramat Gan ("The Safari"), but as far as I know, there are no plans to release addax in the wild in Israel (although I think it can survive and flourish there).
The question is: was the addax native to the Land of Israel (before it was eradicated from it by overhunting)? Do the conservation organizations support reintroduce it to the wild in Israel (in addition to the Sahara and the Arabian desert) addax herds from the breeding centers? The reintroduction of Oryx to the wild in Israel was pretty successful.

According to Yossef Braslevi, "HaYadata Et HaHaretz - Yam HaMelach Saviv Saviv" ("And you shall know the land - The Dead Sea and its Surroundings", 1956, Vol. C, page 199 -- the answer is positive. There were native addaxes in the Land of Israel.


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Size of Mamenchisaurus sinocanadorum
In most books the size of long-necked sauropod Mamenchisaurus is stated as about 26 meters. Recently, a huge specimen of Mamenchisaurus sinocanadorum was discovered.
However, Gregory S. Paul estimates its size in length of 35 meters and weight of more than 65,000 kg, rivaling Argentinosaurus and Patagotitan, the largest known dinosaurs. However, many doubt these estimates and say they are exaggerated. What are the current and most reliable esimates of the size of Mamenchisaurus sinocanadorum?

The holotype specimen originally discovered in 1993 is described as being 26m in length:

An articulated neck of a large, mature sauropod, with enormously elongated cervical ribs, was discovered in strata of Late Jurassic age in the eastern Junggar Basin, Xinjiang, People's Republic of China. The animal is estimated to have originally measured 26 m in length, but was lightly proportioned relative to Brachiosaurus and Apatosaurus.
...
In the present specimen, one rib from the midregion of the neck was seen to be at least 3540 mm long in the field, and after preparation measures 4100 mm in length.

"A large mamenchisaurid from the Junggar Basin, Xinjiang, People Republic of China", Russell, D.A., Zheng, Z. (1993) Canadian Journal of Earth Sciences

The larger measurements come from additional remains attributed to this species, but not yet formally described. Here is the relevant section from Paul's book:

The Princeton Field Guide to Dinosaurs, Paul, G.S. (2010), Princeton University Press.

Paul's figures are echoed in the following papers:

2006 年，中科院古脊椎所在新疆昌吉奇台（原中加马门溪龙标本发现地附近）发
  掘出一具巨型蜥脚类恐龙，经初步鉴定应归入马门溪龙。从发现的部分颈椎长度推测，
  这具马门溪龙长度可达 35 m 以上，成为了中国乃至亚洲目前发现的个体最大的恐龙。

[Google Translate]
In the year, the ancient spine of the Chinese Academy of Sciences was located in Changjiqitai, Xinjiang (near the original site of the discovery of the Jiamamen brook specimen).
A giant sauropod dinosaur was excavated and the initial identification should be attributed to Mamenchisaurus. From the length of the cervical spine found,
    This [Mamenchisaurid] can reach a length of more than 35 m, becoming the largest individual dinosaur ever discovered in China and Asia.

马门溪龙化石研究综述, (2008)

Mamenchisaurus sinocanadorum (体长26~35 m)

Advances in research on dinosaur gigantism, X XU, Q ZHAO (2016)

Though the first paper does not cite a source, and the second paper cites only Russel and Zheng's original paper describing the 26m specimen.

This is known. The question is if there is other estimation other than Paul's who is known to be unorthodox in dinosaurs taxonomy and size estimations?

@Dr.Evenor As I said, the specimen is "not yet formally described", so as of yet there are no other figures to compare with. Nonetheless I've found another couple of papers which quote the same figure as Paul, but haven't been able to locate the source of this "35m".


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Impact of latitude on agriculture?
I live in southern California, where the difference between seasons is mild, and the dominant limitation on agriculture is the lack of water. (Spring is whenever it rains, not a place on the calendar.)
In my early education, as is usual, I learned the growing season is shorter in more northern latitudes. The natural deduction is to expect less effective agriculture, further north.
Recently, I spent a week in early April in Vancouver (Canada). The weather was very (very!) nice, much warmer than I expected, and the hours of daylight longer. On reflection, all this was obvious ... but I was surprised at the time.
Northern latitudes may have shorter growing seasons, but the hours of daylight during that season are much(!) longer. What is the potential agricultural productivity of more northern latitudes?
Much of the past century of agricultural research was centered on the American mid-west. How much is possible if we further optimize agriculture for more northern latitudes, and higher levels of technology?
As the Earth warms, large expenses of Russia and Canada will thaw. Seedlings started early in artificially warmed and lit greenhouses could jump-start crops. (Or transported from more southern latitudes.) If we took full advantage of the longer hours of daylight in northern growing seasons ... what is the limit to agriculture?
With global warming, could Canada and Russia become the bread-basket of the world? Can agriculture as a technology be adapted to more northern latitudes, and take best advantage of a shorter season with longer daylight?
(In imagination, I see seedlings started in greenhouses, and robot-planters placing seedlings in just-warm fields, to capture every hour and day of longer sunlight.)
Do we know how to best take advantage of long northern days for agriculture?

The days may be longer but the light is much less intense, hence why it is colder.

Is it really much less intense? What does the longer hours of daylight do to plant growth? Are plants only responsive to total cumulative energy from the sun? Vancouver in early April was not colder than southern California ... so, what is the sum?

I know this response is coming a bit late but in case you're still curious I have a response!
I'm a M.Sc. student working in Agricultural entomology in Northern Canada (between 55 and 59 degrees North). You are correct, up at more Northern latitudes our short growing season mainly limits what crops we can grow, but less so our yield. We are also restricted in where we can farm by soil conditions as the further north you go the more you are on the Canadian Shield - so less fertile. If you look at growing regions in Northern Alberta, North West territories, etc. you'll see that they tend to stick fairly close to rivers. Further south in Canada, moisture conditions play a much bigger role in determining yield. Mainly we stick to crop species and cultivars that can produce a good yield in a short time - canola, wheat, barley, peas (although corn and soybeans have some large acreages in the Eastern prairies and Ontario).
Climate wise, the comment about light intensity is not really accurate in the summer. The longer daylength definitely compensates for any differences in light intensity. Even at 59 degrees latitude it can get well into the 30's (Celcius) in the summer.
Canada already produces a large amount of wheat and canola, we are the 6th largest exporter of wheat according to a quick google search. So I would argue that while Canada may not be the bread basket of the world it is pretty close already.
It's tough to say how climate change will affect agriculture, because it's really tough to determine how climate change will affect local climate. The changes to weather patterns (changes in amount and timing of rain and moisture, changes in spring or fall frost timing) will have a large impact on agricultural outputs.

Ag Canada actually has a nice little description of ways that climate change is predicted to affect Canadian agriculture! http://www.agr.gc.ca/eng/science-and-innovation/agricultural-practices/agriculture-and-climate/future-outlook/impact-of-climate-change-on-canadian-agriculture/?id=1329321987305

Understand you are more focused on insects, but still curious about specialization of plants (crops) to the shorter growing season. The varieties developed for more southern (central US) latitudes are probably not optimal.
Also, increasing automation (smarter/cheaper machines) means crops could be jump-started in greenhouses (or warmer latitudes) and placed in northern fields when temperatures permit.
Curious about the state of research for the above. :)


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Chromosome related problems.
1.) How many versions (alleles) of a gene can we carry if every chromosome is in pair?
2) What happens during the gamete formation (meiosis) ? Do the gene pairs stay together?
3) What happens then to the paternal and maternal sets of genes that we inherited ?
My attempts
1) I think that it could be any number, but confused with 2 as an answer.
2) Gene pairs must refer to homologous chromosome pairs which remain together in meiosis-I and get separated in meiosis-II. So in net process, it get separated.
3) It is used for producing proteins essential for body functioning by the process of transcription and translation. These genes with some changes (due to crossover) will also be transferred to second generation.

How many versions (alleles) of a gene can we carry if every chromosome is in pair?

The phrasing "if every chromosome is in pair" sounds a little bit funny. But it probably mean "or a diploid individual".
If an individual is diploid, then it has two copies of any given locus. If the term is new to you, a locus is a position in the genome (it may correspond to a gene or not). With two copies an individual can carry maximum two different copies, that is two alleles. The answer is two.

What happens during the gamete formation (meiosis) ? Do the gene pairs stay together?

You nailed it!

What happens then to the paternal and maternal sets of genes that we inherited ?

This is a slightly vague question IMO but I would suppose the main point that is being expected is a description of segregation and recombination (cross-over). You answer was good but I would suggest.
"The maternally and paternally inherited haplotype will recombine (cross-over) during meiosis so that a gamete resulting from meiosis will contain a single haplotype which is a 'mixture' of the maternally inherited and paternally inherited haplotypes."


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Size of Purussaurus, a giant Miocene crocodylian (2022)
What is the currently accepted size estimates (length and mass) of Purussurus barsiliensis? I quote the relevant part in Wikipedia.
From Wikipedia: https://en.wikipedia.org/wiki/Purussaurus

The skull length of the largest known individual of the type species, P. brasiliensis is 1,453 millimetres (57.2 in).[2] It has been estimated that P. brasiliensis reached about 10.3 metres (34 ft) in length, weighing about 5.16 metric tons (5.69 short tons).[2] Another estimate gave a larger size of 12.5 metres (41 ft) in length, ranging from 9.8–15.7 metres (32–52 ft), and 8 metric tons (8.8 short tons) in weight, ranging from 5.6–12.6 metric tons (6.2–13.9 short tons), with a mean daily food intake of 40.6 kilograms (90 lb).[3] It is also likely that Purussaurus reached only 10.9 metres (36 ft) long and 5.6 metric tons (6.2 short tons).[3] A 2022 study estimated a length of 7.6–9.2 metres (25–30 ft) and a mass of 2–6.2 metric tons (2.2–6.8 short tons) using a phylogenetic approach; and a length of 9.2–10 metres (30–33 ft) and mass of 3.9–4.9 metric tons (4.3–5.4 short tons) using a non-phylogenetic approach.[4]

Old estimates were up to 13 meters but more recent ones decreased it to 10.9 and the newest one from 2022 decreased even further:

A 2022 study estimated a length of 7.6–9.2 metres (25–30 ft) and a mass of 2–6.2 metric tons (2.2–6.8 short tons) using a phylogenetic approach; and a length of 9.2–10 metres (30–33 ft) and mass of 3.9–4.9 metric tons (4.3–5.4 short tons) using a non-phylogenetic approach.[4]

Reference to [4]: Paiva, Ana Laura S.; Godoy, Pedro L.; Souza, Ray B. B.; Klein, Wilfried; Hsiou, Annie S. (2022-08-13). "Body size estimation of Caimaninae specimens from the miocene of South America". Journal of South American Earth Sciences. 118: 103970. Bibcode:2022JSAES.11803970P. doi:10.1016/j.jsames.2022.103970. ISSN 0895-9811. S2CID 251560425.
https://www.sciencedirect.com/science/article/abs/pii/S0895981122002589
Since I don't have access to this paper I ask here few questions:

How did they estimate Purussaurus size?
What is a phylogenetic approach in the context of size estimates? I know phylogenetics is the study of evolutionary "family" trees and cladograms but how it affects size estimates?
What is a non-phylogenetic approach in the context of size estimates?
Why the two approaches yielded different estimations for Purussaurus?
Why the 2022 yielded a lower size estimate? Is it based on new fossils?
What are the scientifically accepted on Purussaurus size, considering the latest studies?

You are asking a lot of questions in one post, on a site that works better if you limit your question to one question - many of the answers to each of these questions will be full essay style answers in themselves. You will probably be better to break it up into several separate questions.

The estimates are based on 4 fossil skulls. As far as I can tell these are not new finds, the wiki link says the largest known skull as 1453 mm, and the largest of the 4 in the JSAES article is 1406 mm. This is probably the same skull measured with two slightly different techniques.
Animals don't just scale up linearly as they get bigger, even in the same species. Younger animals have different proportions from old ones, and different species have different proportions, of course. In particular, the ratio of body length / skull width is different. The 'phylogenetic approach' used in the article in question developed a statistical model for how this ratio varies in the family tree, then estimated the specific ratio for  Purussaurus. The details for this approach are given in another recent article, in case you're able to access that one.
The non-phylogenetic approach estimated the ratio with a linear regression of the full dataset, not weighting for relatedness.
As far as I can tell, the main reason the 2022 study gives smaller estimates of size is their exclusion of data from juveniles from the dataset used to estimate size from skull dimensions. I would have expected juveniles to have a larger head size relative to the rest of their body, but apparently that's not the case.


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Why swordfish aren't put in the same family as Marlins?
Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?
Both has long bill or a sword in the upper jaw, both has (at least in some stage of life) a long sail along the back, both are predators and fast swimmers and both are of similar overall shape and size.

Moreover, as cladistics is prevailing over Linnean taxonomy, the ranks of family or superfamily are not essentially different, can we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae?

Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?

The decision about what we call an order vs a family is very subjective. Someone decided that Istiophoriformes was an order containing the families Xiphiidae and Istiophoridae but someone else could have decided to call Istiophoriformes a family (although the name would have ended in -idae, then) and Xiphiidae and Istiophoridae subfamilies.

[C]an we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae[?]

Yes, you can. This clade is the order of Istiophoriformes. You can hence say that swordfish and marlins are both Istiophoriformes. Or if you prefer, you can say that swordfish and marlins both belong to the order of Istiophoriformes.


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Are Triceratops and Eotriceratops similar enough to be considered as the same genus?
Everybody knows Triceratops, the horned dinosaur from Late Cretaceous North America, who lived 68-66 MYA.
In 2007, Eotriceratops xerinsularis was named and described (Wikipedia). It lived in (what is now) Canada about 68 MYA. It is a little bigger than Triceratops but in many aspect very similar, e.g. they both have long horns and solid frill, and postcranial skeleton. Gregory S. Paul, in his Princton Field Guide to Dinosaurs 2016, suggested putting Eotriceratops xerinsularis in the same genus as Triceratops, renaming it to Triceratops xerinsularis. I find this suggestion appealing, but I know Paul's taxonomy is unorthodox and not mainstream (e.g. I do not agree with the thesis that Torosaurus is merely a full adult Triceratops).
So the question is: can Eotriceratops xerinsularis be put in the same genus as Triceratops and is this suggestion is plausiable enough?

Taxonomists have wide leeway over assigning higher taxa. The publication process in which Eotriceratops was described as a new genus made it a new genus. However, given a different set of reviewers, they may have rejected the new generic description, and suggested that the author put it into Triceratops. The process is somewhat arbitrary, and there are some random elements to higher taxon assignment. But it is the system we use. If somebody were to write a paper to synonomize Eotriceratops with Triceratops, and that paper were accepted, then Eotriceratops would cease to be a valid name. Its all about publication precedence. Gregory  Paul may have good reason for his suggestion, but it must be published before a change is made.

Not sure if relevant to this exact species but a VERY good talk about how & why we have so many different potentially worng) dinosaur species: https://www.ted.com/talks/jack_horner_shape_shifting_dinosaurs

Can you add references?

Eotriceratops was a larger species of triceratops so they both were similar in name but different in size
Well eotriceratops was a larger ceratopsid but both of them had different predators for example the triceratops horridus was hunted by the T-Rex but for the eotriceratops I don't what predators it had

Welcome. We expect answers to be clear and complete, without personal opinions. Importantly we ask answers to be supported by citations, preferably journal papers.


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Heart rate vs body size
It is known that large animals have lower heart rates (beats per minute) than small animals. Is it the same situation in humans?
That is: if we have a group women, about the same age and fitness, and if we record for each women her body size (relevant indicators of body size are height, weight, BMI, body surface area) and her heart rate, will we see a trend that the heart rate decreases as size increases?
References to paper and studies about this issue are also welcomed.

See this paper which briefly states that it found no correlation but said it is not conclusive and should be further examined and studied.

The paper you link finds that there is not a significant correlation between body mass and resting heart rate in humans. While there is a well known negative correlation across mammals:

This is the ever-popular mouse-to-elephant curve that is found in one form or another for lots of physiological measurements.
I'll suggest, but have no evidence, that the lack of a significant correlation in humans is simply a result of there not being enough range in body mass among humans to allow finding a significant result. When the range of one variable is small, the association between that and another variable necessarily lessens. For example:

Although the linear relationship between the two variables is largely similar, when the range of x is truncated, the coefficient of determination, $R^2$, decreases. The correlation goes from 0.97 to 0.7. In this case, that might still be "significant", but I suspect that in humans that variation is much greater in resting heart rate.
It would have been nice if that paper included the actual data on HR, but they act like it doesn't exist just because it was not significant.


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Bruhathkayosaurus matleyi current status and size estimates
https://www.youtube.com/watch?v=BqVqW9A-6eo
I watched this YouTube video about Bruhathkayosaurus matleyi and he basically makes three interesting assertions:

The illium used to define Bruhathkayosaurus matleyi was not of a sauropod but of a 9 meters abeliosaurid.
The huge femur (incorrectly) assigned to Bruhathkayosaurus matleyi is indeed a huge sauropod but needs to be defined as a new genus (the author suggests "Fangorn").
The size estimations coming from the huge femur now lost are valid and suggest a 110-170 metric tonnes animal of length 38-48 meters.

The video is based on a 2023 paper by Gregory S. Paul, a free-lance paleontologist and paleoartist whose hypotheses are often disputed (especially in taxonomy) and are not mainstream.
I ask if these three assertions are accepted by the scientific community? what is the status of the giant sauropod formerly referred to Bruhathkayosaurus matleyi and whether is it a valid species? And I ask if the size estimates are widely accepted, making it the largest dinosaur?


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Why can't we grow more teeth?
A similar question but about teeth healing themselves is Do teeth have the capacity to heal?.

So I understand that teeth have the capacity to heal themselves to a certain degree. It appears to be that part of the reason they can't heal all of themselves is that they are not surrounded by cells. In that case why can't we grow teeth back?
If a tooth is grown in the gum, or somewhere else, it would be surrounded by cells and so should be able to grow back right?
It appears that sharks can grow their teeth back:

New teeth are continually grown in a groove in the shark’s mouth and the skin acts as a “conveyor belt” to move the teeth forward into new positions.

Why can't we do this?

Short answer: Teeth are formed prenatally in tissue destined to become bone (the mandibles), that is, in the embryo. Once they have formed, they can grow and develop, but new teeth do not form after mid-gestation. Shorter answer: that's how the genes for tooth formation expression are regulated. It's like asking why we don't grow a new leg if our leg is amputated.

@anongoodnurse why not put that as an answer?

@another'Homosapien' - I don't know;  "because" is not much of an answer.

@anongoodnurse it would be enough for an answer. I might edit that up too :)

Possible duplicate of Why do some bad traits evolve, and good ones don't?

Note everything but mammals continue to grow new teeth, sharks are not the weird ones, mammals are weird for not doing it

Unfortunately, the answer to your question isn't as well researched as other areas, I believe...let's add some complexity into this.
You're correct, teeth does "grow" in the gums. And it does start off surrounded by cells (look up: tooth bud, cap, bell stage)!
The tooth originates from an interaction between the ectomesenchyme (likely originating from the neural crest cells) and the epithelium of the mouth when it is forming while you're still an embryo in your momma's tummy.
Unlike sharks, which are homodonts (meaning, their tooth are all of one morphology), we are heterodonts (e.g. we have different shaped teeth - e.g. molars, canines, incisors, premolars). There are a couple of theories to why this occurs (look up: clone model, field model, odontogenic homeobox code - a combination of all these theories). Basically, a bunch of genes transcribe for proteins and signalling factors that create the complexity of your tooth shape and position in the mouth.
Basically, this means, our teeth are going to take longer and require more energy and effort to carve into (yes carve! lot's of the tooth shape is create by apoptosis of the regions around the "cusp" area when it is developing).
When your primary/baby teeth pop out, they serve functions such as developing speech, allowing you to eat, strengthening your jaw muscles (which in turn helps to develop your mandible and shape of the face), all this so you can have a great bite when you get older!
Luckily, sharks don't speak much underwater, so they probably don't give a poop about having properly lined up teeth. Their teeth grows everywhere. Proper bite for eating various nuts, fruits, meats and vegetables? NAH. WE JUST CHEW OFF LEGS. WE CAN ONLY SHRED STUFF. Sharks need strong ankylosed teeth (ankylosed = like an anchor? teeth are anchored into the mandible of the shark).
In contrast, humans have teeth in gomphosis (sockets), which gives our teeth some cushioning and sense of proprioception (the sense knowing how hard you're biting) when we bite on something extremely hard, to prevent us breaking our teeth - thus helping us preserve our teeth. Sharks don't have that, they just break their teeth.
Humans do finally replace their teeth, after our jaw grows enough for us to accommodate them at a genetically planned stage. This happens by tooth germs (cells) being bud off (like a flower yes :D) from the baby teeth. Note though, your 1st adult/permanent molars are already beginning to form when you're still in your momma's tummy.
I believe that the continuous creation of teeth requires more energy, but takes less time (sharks). For humans, one time creation of teeth requires less energy, but takes wayyyyy more time (and also has to be timed correctly with all our other growing bits).
TL;DR Evolutionary reasons and different functional uses of teeth between sharks and humans probably determine why we only have two sets of teeth (diphyodonts). That being said, it would be cool if we were like rats (have molars/incisors) though, which replace their teeth anytime its lost. Maybe one day we can evolve into it? Yay!

Some interesting points: You mentioned teeth "healing".
Your teeth is made up of enamel on the outside, which is NEVER replaced. It "heals" by remineralisation which is not exactly the same as growing new crystals on top of it. Kinda complex, won't go into it.
However, your teeth is always forming new dentine, which is below the enamel. In a way, your tooth really is growing back all the time. Because a new layer of dentine is deposited everyday (like...4 micrometers). This is because the dentine producing cells, called odontoblasts, are still around. In contrast, the enamel producing cells, called ameloblasts, are removed when your tooth has developed. I THINK, the reason is to make space in your enamel so it can be fully mineralised and completely filled up by hydroxyapatite. (Too much fluoride when young can block this removal of ameloblasts and its proteins like amelogenin and enamelin = forming holes, which cavitate resulting in fluorosis).
Hopefully all that answered your question. But, it was fun for me to rant anyway. Cheers.

Nice effort on this answer! However, please provide some resources or citations to back-up your claims. We want all of our users to feel confident that the information they read on Bio.SE is well-researched and reflects scientific understanding and not simply opinion. Thanks!

Actually it is quite well researched, Mammals are the only group of animals that grow only a limited number of teeth but socketed teeth and heterodont teeth are not limited to mammals.

Also rats do not replace lost teeth, they have incisors which never stop growing, those are very different things.

Because mammals had to be different, and spent way too much of their evolutionary history being tiny short lived creatures.
No seriously, mammals are outliers in this. Growing endless numbers of teeth (Polyphyodont) is the normal aka basal condition in vertebrates. Every other group of animals with teeth just keep replacing them forever. Mammals uniquely have lost this ability.
All mammals grow a fixed number of teeth, most are diphyodont growing their teeth in two distinct sets, a few mammals (elephants and kangaroo) spread their number of teeth into multiple series but the total number of teeth they produce is still fixed, they are sort of pseudo-polydont. Some whales produce a much larger number of teeth but the total number of teeth is still fixed.
Why are mammals weird, because the ancestors of all extant mammals were small short lived insectivores. If you are short lived insectivores wear is insignifiant on teeth and dislodging them is a minimal risk. Multiple sets of teeth is not a significant advantage. What is a significant advantage is tightly occluding teeth, that is teeth that fit together very tightly with multiple cusps, this shape is perfect for processing insects into digestible pieces,  but it does not work well when teeth are replaced. The current thought is that mammals repurposed or lost the genes that allowed for new tooth bud formation. Many believe the genes were repurposed possibly into some of the genes that control tooth shape allowing the complex tooth structure mammals have. This is difficult to test but is supported by the fact the groups of mammals to increase the number of teeth, whales, armadillo, and some seals, also have extremely simply tooth structures and high numbers of anomalous teeth, that is teeth with seemingly no controls on their shape. Although I should note extra erroneous teeth occasionally occur in  nearly every mammal line.
The exact changes have not yet been discovered and is an are with much interest. We know why pretty well even if we don't know how. Although there is some fascinating work being done by studying how reptiles continue to replace teeth throughout life. Certain basal cell lines persist in reptiles but completely differentiate in mammals during early development. Whales get around this by making a lot of new buds early on and holding on to them, but they still can't make new ones past a certain point.
Also related, why mammals have bigger nerves in their teeth.


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Why are some bird species placed as family Incertae sedis while some families are simply monotypic?
The Bananaquit and Western Spindalis are passerines of Incerta sedis. But species such as the Osprey, Limpkin and Olive Warbler belong to their own, monotypic, family.
Why aren't Bananaquit and Western Spindalis simply assigned to a new family?


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Which Geologic time scale is the most accurate?
I kindly ask to show me some pictures that is a generally accurate geologic time scale.
In google, a lot of geo time scales are different.
On what i have searched there are 2 major eons which are
I.Precambrian eon
 1. Archean eon
 2. Hadean eon
 3. Proterozoic eon
II.Phanerozoic eon

Palezoic
Mesozoic

3.Cenozoic
But along with it Precrambiann is further divided to proterozoic eon, archaaen eon and hadeon eon are ERAS of but it clearly says its an EON.
And how about in Phanerozoic eon?
Kindly please clarify the following. Thank you!!

I don;t quite understand your question. The only question mark in your post is "And how about in Phanerozoic eon?" which question is rather vague. Are you asking for the subdivision of the Phanerozoic eon? It would not match with the title. Are you asking "What is the difference between an eon and an era?"?

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".
The ICS International Chronostratigraphic Chart, ambiguously, puts "Eonothem/Eon" over both the "Precambrian" column and the "Hadean - Archean - Proterozoic" column, with the next column over being "Erathem/Era", which corresponds to what's in the other periods.
It seems clear that 1) the Hadean, Archean and Proterozoic are considered "Eons" like the Phanerozoic is (with their sub-divisions all being called "Eras"), 2) the Precambrian is a larger period of time that encompasses the Hadea, Archean and Proterozoic, and 3) there might be some disagreement as to how to name the period of time the Precambrian is; Wikipedia says "Supereon", which makes sense, but the ICS chart doesn't include that word and seems happy to have it share the name "Eon" with its immediate subdivisions. But the name is just a name, the more important things are how the different periods relate to each other, which is covered by 1) and 2).


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How do Addax defend itself from predators?
The addax (Addax nasomaculatus) is a critically endangered antelope adapted to live in extreme desert conditions. It has long impressive horns that can potentially serve as a weapon because they are sharp. Does addax use its horn to fend off predators?
I read somewhere that addax is not a fast animal so trying to escape by running does not seem like a good option for defense.

Picture of Addax and its horns, taken from Wikipedia, photographer: Zachi Evenor
https://commons.wikimedia.org/wiki/File:Addax-Jerusalem-Biblical-Zoo-IZE-611.jpg


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Did the Broadbill Swordfish population fully recovered?
Regarding the Broadbill Swordfish Xiphias gladius:
I read Richard Ellis "Swordfish: A Biography of the Ocean Gladiator", Chicago University Press, 2013. The chapter about industrial-strength fishing described that up to the late 20th century, swordfish population was decimated due to overfishing. In chapter 11 he discusses whether the swordfish is endangered and describe the late 1990's conservation efforts. It says that there is a rise in swordfish population in the North Atlantic (but say we don't know if the population fully recovered to its heydays) and say there is little information for the Pacific and Mediterranean populations.
I found some info in https://www.fishwatch.gov for the North Atlantic and North Pacific population, saying that north Atlantic and western north Pacific are not overfished and not subject to overfishing (I think this is good), while the eastern north Pacific is not overfished but subject to overfishing. The ICCAT published a report Atlantic, ICCAT 2017 which is hard to read. What I understood the north Atlantic is not overfished while the south Atlantic population is overfished and in danger.
For the Pacific, see Pacific, ICCAT 2018, which says that the north central and western Pacific are not overfished:

Overall, the base case model indicated that the WCNPO swordfish stock is not
  likely overfished and is not likely experiencing overfishing relative to MSY-based
  or 20% of unfished spawning biomass-based reference points.

These reports are hard to read for non-expert, so I ask here few questions about the populations of swordfish:

Is the swordfish endangered species?
Is the swordfish population sustainable?
Per population P = { North Atlantic, South Atlantic, North Pacific, South Pacific, Indian, Mediterranean }:
3.1 Is the population P endangered?
3.2 Is the population is safe (non-threatened) or least concern?
3.3 Did the population fully recovered and reach a healthy size?


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How can you gain 1 lb of bodyweight from eating less than 1 lb of food surplus?
A commonly referenced "fact" is that a caloric surplus of 3500 kcal is equivalent to a 1 lb gain in bodyweight. But I'm confused. If you get 3500 kcal worth of, say, fatty acids, which are 9 kcal per gram, then that's about 390 g, which is just under 0.86 lb. How can you gain 1 lb of bodyweight from eating a surplus of less than 1 lb? Am I missing something?

Probably water.

Also, although there are problems with the 3500kcal equals 1 pound rule, even when it works, the point isn't that eating 3500kcal adds a pound of bodyfat: rather, catabolizing 1lb of body fat equals about 3500kcal of energy.

agree with @BryanKrause above concerning water... however, the way you have phrased the "fact" mentioned above is not entirely correct, which is a common misconception - it costs some energy to store energy in the body. In other words, even though 3500 kcal is ~1 pound thermodynamically, that does not translate into exactly one pound of body weight gain. To store energy as lipid, the body "spends" some of the energy to package and store it as lipid. Thus, if you gain a pound, you've actually eaten more than 3500 calories. (Note: the 3500=1 pound is hotly debated, etc)

@VanceLAlbaugh Thanks, you explained a bit more thoroughly than I did. Also: proof that it is easier to lose a pound than to gain one! Call the daytime TV 'doctors'! (all a joke, of course...)


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How did a plant evolve to know there were animals alive that would eat it's fruit when it decided to produce this fruit?
How did plants come to "know" there were animals alive that would eat it's fruit when it first produced this fruit?

How did a plant know there were animals to have have spines, prickling hairs, acidic leaves, soapy sap, stings, wooden seed protection, poisons, and fruit? Same theory.
A fruit is only plant flesh with water and citric acid and sugar in it.
Beetles and lizards also eat seeds and leaves. Even since the first mosses and ferns colonized the planet, the most abundant food was normally forest leaves. So plants "knew" they were being eaten since the times of the first animals because when you get eaten into oblivion, you dont know anything any more:(
All plants contain lots of sugar C6H12O6 in their sap, sugar is very easy thing for the plant to produce. Putting sugar into the seed pod is a easy for a plant as growing hairs from leaf cellulose, growing spines and making stings.
So, plants already had seedpod protection containing acids, poisons, soaps, wood protection like pine cones, and the only necessary change is to go from acid or cellulose, for example citric acid, to sugar, which is chemically an easy thing to do in evolution.
If a mutant tree one day makes a seed pod than some animals like so much, that they don't even break the seeds, then the tree's babies can travel many kilometers and be reborn into an animal nitrate dropping.
Fruit developed independently in yew trees, strawberries, figs, very simply by changing acid or poisonous seed pods into sugar ones that get transported for kilometers in every direction. If a fruit is not sugary, then it has some poisons like chilli peppers, spines like chestnuts, and other seed protection devices.

The plant does not "know" there are animals. It is just that plants, that accidentally evolved (due to mutations) a fruit that attracts animals (which can spread its seeds etc.) had an advantage over plants that did not have them. The disadvantaged plants just became extinct after a while. And you must be aware that the first fruits were rather "pre-fruits", but already a selective advantage to their bearers.


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What is cognate miRNA?
I understand what miRNA are, but I'm unsure of what cognate means. Looking at this post, it seems that a cognate miRNA is a known miRNA vs. a recently discovered/possible miRNA. Is this thinking on the right track?

The use of the word cognate in molecular biology reflects adjectival definition 2 from Lexico:
2 formal Related; connected.
‘cognate subjects such as physics and chemistry’
The example given shows that this can be used in the most general sense of related, so that there is no requirement for some common antecedent as a surrogate for a human mother or ancestor.
Specifically there is no implication of the involvement of a common DNA sequence, as in the answer from @Dirigible, nor that of a common origin as invoked in an earlier answer on this topic.
This is quite clear if one considers the much earlier usage of cognate in molecular biology in relation to an mRNA codon and the tRNA anticodons that can recognize it, or a tRNA and an aminoacyl tRNA synthetase that can aminoacylate it.
As far as the usage with microRNAs is concerned, a cognate mRNA is one with which the miRNA can interact by base-pairing — no more, no less.


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Collagen, are fibrils arranged in overlapping fashion too just like tropocollagen?
Collagen molecules (tropocollagen) are interlinked into fibrils, with a banded structure showing the spaces ("lacunae") between the molecules. Do fibrils in turn also interlink in a similar way, or, do fibrils run from end to end in the fibers?


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ID: Ant or ant-like insect in North Central FL (velvet ant?)
I heard my cats messing with something in my apartment, and when I went to check on them, I found them playing with this insect:

It's roughly a centimeter long. I am located in North Central Florida. I'm leaning toward a female velvet ant. When I showed up, a cat ran away from it and was licking his paw pretty intently, so I want to be sure of what it is in case it stung or bit him (he seems completely fine now, so it might just have been a sensory response from touching it).

You nailed it; that's a female velvet ant, a member of the Mutillidae wasp family.
Only the (flightless) females sting, and their sting is reportedly very painful. However, they're not aggressive, and sting only defensively.

Velvet ants are not ants at all; they are wasps in the family Mutillidae. Although more common in the southwestern U.S., they can be found throughout the Southeast.

From the second link:

They are known for their extremely painful stings, (the sting of the species Dasymutilla klugii rated a 3 on the Schmidt pain index and lasts up to 30 minutes[1]), and has resulted in the common name "cow killer" or "cow ant" being applied to the species Dasymutilla occidentalis.[2] However, mutillids are not aggressive and sting only in defense.


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Identification of Ulva lactuca
I am trying to find an ID guide that I can use to identify macroalgae. I specifically want to differentiate between Ulva species.


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What is the use of having 3 antipodal cells and 2 synergids?
The embryo sac which is developed from functional megaspore contains 8 nuclei.2 polar nuclei and egg fuses with sperms.3 antipodal cells and 2 synergids degenerate after fertilization.Then what is the use of having 3 antipodal cells and 2 synergids?


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How exactly does chemotherapy cause anemia?
I’ve been trying to figure this out for the past few hours but I still can’t find something as in depth as I’m looking for. So far all I’ve found is that chemo drugs kill bone marrow cells and some other drugs can damage the kidney which decreases red blood cell production, but I’m looking for something a bit more in depth.
From my understanding, there are multiple “groups” of chemo drugs (such as alkylating agents, antimetabolites, etc), so I assume there isn’t one answer which covers every group (unless, hopefully, I am wrong). I’ve read explicitly that some groups, like alkylating agents, are known to cause death in bone marrow cells. This also made me question if anemia/bone marrow cell death is a side effect from every chemo drug. If not, is it known which groups of chemo drugs are most likely to cause anemia and how exactly they do cause anemia (as in anything more in depth than “they kill red bone marrow cells”)? I’ve also read that some chemo drugs containing platinum can damage the kidney, but I wasn’t able to find how exactly it damages the kidney in a way that red blood cell production is decreased. I’m assuming this is due to a decrease in EPO production/secretion? If anyone has any relevant information/sources I would greatly appreciate it! Sorry if this is really specific and if this happens to be the wrong place to post such a question.

https://medicalsciences.stackexchange.com/questions/tagged/chemotherapy


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Does mushroom likes low air pressure room?
I know that mushroom likes high humidity and low temperature, but want to know that Does mushroom likes low air pressure room ? because of at low air pressure high humidity and low temperature can be achieved easily.


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Crispr/CAS9 genome editing is actually processed at which phase of Cell cycle?
all,
Is it only happens in certain phases, like S, G1,...or it can happen any time....or maybe, it has some perferences.
Put it in another word, does it going to processe edit if the cell is not growing ?
Thanks for any helps or comments.
Best
Bill Zhang


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Are “Rings” in fish like rings in a tree?
A lot of fish have structures like the rings in a tree. Is the number of “rings” an indicator of age, as in a tree, or is it fixed?

Can you please clarify about what structure you are talking about. You could for example upload a picture with a clear red arrow pointing to the structure of interest. In any case, the answer will probably be "no, it does not indicate age".

I am VTC as unclear as the OP has not clarified what structure she is referring to.

It depends which structures you're talking about. However, several body parts of bony fish such as the scales and otoliths (earbones) generally contain a record of seasonal growth patterns. So in that sense yes, the process of ageing fish is similar to finding the age of a tree by counting rings in the wood. For different species of fish, different structures are used to determine ages.
https://www.nefsc.noaa.gov/fbp/basics.htm


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Any volumetric data for areas of the brain?
I was trying to write an overview of AI and wanted to quantify some numerical data about the brain.  It is easy to find many sources quoting 100 billion neurons.  However, I would like to get the number of neurons (obviously approximate) in each area.  Also, while I can find the average number of synapses to neuron, it would be nice to know if there are higher numbers is certain areas of the brain.
This is not my field, it would simply be instructive to generate a table of data.
Is there any source, even approximate volume for different areas of the brain?

Not volume, but number of neurons in distinct coarse areas: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776484/#B46

For the number of neurons, assuming you are referring to the human brain: https://biology.stackexchange.com/questions/53587


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How does the body differentiate between sources of good and bad cholesterol?
I keep hearing "good cholesterol, bad cholesterol" everywhere, and how certain food sources of cholesterol raise LDL and certain other raise HDL.
I don't understand how any food can increase specifically HDL or LDL. I just don't understand the mechanism. Cholesterol is cholesterol, regardless of whether it ends up in LDL or HDL, or whether it came from eggs or or dairy. Somebody please explain to me how specific sources of cholesterol raise HDL and why others raise LDL; how does the body differentiate between the source.
As far as I know, all cholesterol and fat digested from the intestines, regardless of the source, are packaged in chylomicrons as 1) phospholipids, 2) triglycerides, 3) cholesteryl esters, and enter circulation from the lymphatic vessels, then deposited as a chylomicron remnant (CR) in the liver.
How does the liver know whether the 3 particles in the CR came from a good source or bad source? And how does this trigger HDL vs LDL synthesis?
[Btw, if im not mistaken, the liver only makes HDL and VLDL, not LDL]
I'm looking for the biochemical pathways behind these claims. I just cannot picture the mechanism.

The body doesn't differentiate between types of cholesterol. It simply does what it does. Cholesterol is cholesterol, that's a fact. You need to read about the difference in HDL and LDL, with emphasis on the "L" (lipoprotein). That's what matters, not the cholesterol. You might want to edit your question.

I know the difference. I'm asking the mechanism behind claims such as: "olive oil raises HDL, butter raises LDL" etc.


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Why doesn't the rate of photosynthesis increase with increasing light energy (frequency)?
Why doesn't the rate of photosynthesis increase with increasing light energy (frequency)? I know that green light is not absorbed by chlorophyll, yet I am confused as to why this certain "frequency" is not absorbed. Intuitively, it makes sense that increasing frequency would make the rate faster.

I don't think this question is sufficiently different from other well-answered questions about the wavelengths of light used by plants for photosynthesis: (1) What types of light can't a plant photosynthesize in?, (2) Does the light color spectrum and frequency matter for photosynthesis?

To understand why the wavelength doesn't change the rate of photosynthis you have to look at the chemical processes. I won't name the molecules and all the stuff but I'll try to paraphrase it in generic terms.
Photosynthesis means that in the end a carbohydrate has been assembled where you had only water and carbon dioxide when you started. The assembly of carbohydrates can be broken down in very clear steps. The power needed for this assembly comes in well defined quantities. These quantities are fixed by the amount of energy needed to activate a certain center (in fact two different ones) inside the chlorophyll. It is clear, that any surplus energy doesn't change the modification of the molecule (electron transport), because when the needed energy is delivered, the reaction takes place. The surplus energy is lost and dissipates in different ways (photons, phonons etc.), because there is no other place where it can foster a reaction.
The other fact related is: Light also comes in portions and not as a continuum. Single light quantums accidentally hit the centers where they can deliver the energy for a single reaction. So the energy from a light quantum can start the reaction if it contains enough energy but only one. Neither it can't be spread over more reaction centres nor can the surplus energy transferred as "change" to another reaction. Even if possible, the arrival of the surplus energy of photon A used in reaction 1 must be rather synchronous to the arrival of photon B at reaction 2. This is very unlikely.
That's why lamp manufacturers declare the usable power of their grow lights with μmol/s and not in Watts or lumens. Only the number of photons counts. More energetic photons (having a shorter wavelength) can't start more than one reaction per photon.

There are 2 frequencies/wavelengths absorbed and used by green chlorophyll  ( forgot the numbers). To increase photosynthesis rate you need to increase the amount of light ( lumens) at those frequencies. Not provide different frequencies .

side note: It is unlucky to use lumens in this context. Because depending on wavelength there's a very different power and also a very different photon count for one lumen. I recommend referring to the particle flux (μmol/s) when talking about light for photosynthesis.


text:
Why there are two types of medium (YPGlu and YPGal) in the *K. lactis* Protein Expression Kit?
I am planning to use the K. lactis Protein Expression Kit from NEB for the expression of certain protein. I am not experienced with working with yeast. I started by reading the manual for this kit and I am a bit confused with the fact that there are two types of medium: YPGlucose and YPGalactose. Do I understand correctly that YPGlucose medium should be used for cell propagation while YPGalactose should be used for protein expression and if so, why is that?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, it isn't reasonable to expect users of this site to find and read this manual for you! At a minimum you should make sure you've read all the entire material and then provide quotes and links for the relevant sections that you are having trouble with. ——— The answer is probably in there (in particular pay attention to the promoter on the expression vector that drives expression of the transgene). Thanks!

NEB also has very good customer support, you can always call or email them to get in contact with the people that actually design and produce the kits.


text:
What is the expected result when using Sanger Sequencing for Bisulfite analysis on an unmethylated CpG?
Hello fellow molecular biologists!
I'm currently starting out doing a lot of Bisulfite Sequencing and as COBRA is not sufficiently working on my sequence, I do Sanger Sequencing instead, as suggested by my PI.
The problem is I was told a single peak of "T" means the Cytosine is methylated, in a CpG context. However, thinking about it, I have trouble explaining how you would get to this conclusion.
My though was:
Imagine you have:
5' CpG 3'
3' GpC 5'
Now if both are unmethylated you get:
5' TpG 3'
3' GpT 5'
If you now do a PCR, they give rise to two types of DNA molecules (TG/AC) and (CA/GT).
If you perform Sanger Sequencing just with the forward primer, this would mean you get 50% "T" and 50% "C" at the original position.
In other words, the reverse strand (3'-GC-5') should always restore the "C" at the original position, when I perfom a PCR.
So who is wrong?
Should I expect 100% "T" or 50% "T" and "C" for a completely unmethylated CpG?
By the way, I asked ChatGPT. Initially he told me 100% "T" would be correct. As I explained my thought process, he agreed with me, but then cited imaginary papers with links that do not exist. :D
Thanks in advance!
Best regards, Felix

I would not go to ChatGPT for trusted scientific advice, it has a tendency to make stuff up, as you have discovered. I would suggest going back and interrogating further what "single peak of T" means. It is not easy to tell what it is supposed to mean from your question. Notably: does 50% T count as a peak? I would say so, if I was expecting C. If it's not the CpG context that's methylated but rather just that Cs are methylated, you would instead expect 2 peaks of 50%, right? Possibly misunderstanding.

"single peak of T" should mean that the sequencing result really just shows a clean "T", without any major peak for "C", "G" or "A" (hence the C being unmethylated).
To maybe elucidate that a little bit more: I'm really just aiming at analysing CpGs (not just Cs) and I try to conceptually get an understanding for what my result should be for a fully methylated CpG dyad, hemimethylated dyad (on one of the two strands) and fully unmethylated.
So the question is very straightforward. What would the Sanger Sequencing result look like, if the CpG dyad is fully methylated? And why?

Well, have you looked at the literature or wikipedia?

With all due respect, if your contribution is "read more" and have you looked on  Wikipedia, then I seriously question the motif behind you answering this question. It's really not that trivial if you think about it - and yes, I have read some papers about data interpretation of BS-Seq data and of course Wikipedia as well. So far I do not have found a comprehensive answer to what the expectation would look like (some just take the relative difference between C and T at the "C" position of a CpG) and to me the answer seems to be more complicated.

I am not trying to answer your question, or I would not have written in the comment field. I am trying to help you improve your question such that someone else can answer it (there are many people who are experts in this field but I'm not one of them). I'm sorry if this seems disrespectful. When someone feels prepared to answer your question, they will answer it in the "answer" field below. It is standard for people asking questions to directly cite the sources that they have already consulted and explain why they haven't answered the question; I am trying to help you to do that.

Thank you for the clarification. I wasn't aware of that.


text:
Theoretical question: Would immune cells that produce blue light be an effective and better alternative to inflammation?
It's well known that blue light is effective against a wide range of bacteria (type "antibacterial blue light" into Google for starters). This article (https://www.ncbi.nlm.nih.gov/pubmed/23009190) claims that blue light also works on some fungi.
With that in mind, would it be advantageous to have immune cells that produce localized blue light when they detect a bacterial infection? In particular, instead of producing inflammatory chemicals, reprogram white blood cells to produce bioluminescent compounds rigged in the 400-470 nm range when they detect bacteria.

The difference in light intensity between known bioluminescent samples and the blue light used as an antibacterial is huge. There is simply no known biological mechanism that would produce the intensity of light required.
If you could somehow make an immune cell produce high intensity blue light to damage bacteria, you would find that it would also damage surrounding cells - the chemical products released to destroy bacteria are much more short-ranged.


text:
Are the foramina of Magendie and Luschka genuine defects of the ependymal epithelium?
Question:
Are the foramen Magendie (or the median aperture) and the two foramina Luschka (or the lateral apertures) genuine defects of the ependymal epithelium? So the ventricular lumen truly communicates with the subarachnoid space? If so, how is the defect maintained? Also, what do the boundaries of the defects even look like?
Context:
The fact that there can be non-pathological defects in an epithelium is jarring for me, because I have always been taught that an epithelium consists of an uninterrupted layer of cells juxtaposed against each other, limited by a basement membrane on one side and encasing a lumen or facing the exterior on the other side.
So really there are no 'holes' in an epithelium, and even structures that might look like a hole, such as ducts for a gland, are in fact just invaginations of the epithelium.
I've been able to apply this concept to understanding other anatomical structures with no difficulty. If the foramina of the 4th ventricle are really epithelial 'holes' then this is a major anomaly. In fact, I cannot think of a single example other than this one in which a normally developed, intact epithelium (and a basement membrane) has a 'hole' in it.
Also if this is the case, how is the defect maintained? As far as I know, epithelia, when penetrated by trauma, promptly close the gap and re-epithelialize. I believe a persistent epithelial defect must have some kind of supporting mechanism that forces tolerance to such defects.
Lastly, I know almost nothing about cell polarity, but I've learned that that the surface of epithelial cells which faces the lumen is apically polarized, the surface facing neighbor cells is laterally, and the surface in contact with the basement membrane is basally polarized. Would cells at the boundary of the defects have their apical and basal surfaces directly in continuation with each other without an intervening lateral surface, having no neighbor cells to contact?
I've been searching the literature for quite a while, but nobody seems to be really bothered like me by the implications of holes being present in a normal epithelium. Perhaps I'm taking it too seriously and all that 'epithelia are uninterrupted layers of cells' talk is just a rule of thumb, a crude generalization meant to serve only pedagogical purposes. But these foramina of Magendie and Luschka are the only counterexamples to this maxim I could come up with so far. I believe that a rule this widely applicable must have some physiological basis, and therefore that deviations from it demand explanation.

I assume the opening would be contiguous with the arachnoid but I have failed to find any histological images or descriptions that demonstrate this.


text:
Treatment of bicarbonate versus fixed acids in acid-base regulation by the kidney
My question concerns the differential treatment of bicarbonate versus other buffer anions in human acid-base physiology. In Guyton (2021)'s physiology textbook, we see the following argument:

Because $\ce{HCO3−}$ must react with a secreted $\ce{H+}$ to form $\ce{H2CO3}$ before it can be reabsorbed, 4320 mEq of $\ce{H+}$ must be secreted each day just to reabsorb the filtered $\ce{HCO3−}$. Then, an additional 80 mEq of $\ce{H+}$ must be secreted to rid the body of the nonvolatile acids produced each day for a total of 4400 mEq of $\ce{H+}$ secreted into the tubular fluid each day. (p. 410)

Similar passages can be found in Boron (2017)'s textbook:

(...) $\ce{HCO3−}$ reabsorption does not represent net $\ce{H+}$ excretion into the urine. It merely prevents the loss of the filtered alkali. (p. 823)

In our example, the kidneys secrete 4390 mmol/day of $\ce{H+}$ into the tubule lumen. The kidneys use most of this secreted acid—4320 mmol/day or ~98% of the total—to reclaim filtered $\ce{HCO3−}$. The balance of the total secreted $\ce{H+}$, 70 mmol/day, the kidneys use to generate new $\ce{HCO3−}$. (p. 825)

On the other hand, as tubule cells excrete $\ce{H+}$ into the lumen, some titrate $\ce{HPO4^2-}$ to form $\ce{H2PO4-}$. This is viewed as net acid excretion, instead of reclamation of filtered $\ce{HPO4^2-}$.
Mathematically, the form of the net acid excretion formula expresses this differential treatment:
$\rm NAE = TA + [NH_4^+] - [HCO_3^-]$
Whereas any amount of filtered $\ce{HCO3−}$ contributes negatively to NAE, since TA is defined to be the amount of base necessary to titrate urine back to pH 7.4, the amount of $\ce{HPO4^2-}$ and $\ce{H2PO4-}$ in the initial filtrate do not affect NAE (assuming that pH of the initial filtrate is 7.4). What matters is the additional amount of titration done.
Why the difference? Any amount of $\ce{HPO4^2-}$ filtered would also mean a loss of buffering capacity of blood. Therefore, shouldn't the formula instead be $\rm NAE = [NH_4^+] - [HCO3^-] - [HPO_4^{2-}]$?
One could argue that since urine contains $\ce{H2PO4-}$ as well as $\ce{HPO4^2-}$, and since $\ce{H2PO4-}$ is a Bronsted-Lowry acid, we must account for the effects of both ions. When the two effects precisely neutralize each other, pH should equal 7.4. Acid is excreted only if phosphate is protonated more than the degree of protonation at pH 7.4. Therefore, instead of subtracting $\rm[HPO_4^{2-}]$, we subtract the difference $\rm[HPO_4^{2-}] - [HPO_4^{2-}]_{pH=7.4}$, which equals -TA by definition.
But then why can't this argument be applied to bicarbonate? Shouldn't we subtract the difference $\rm[HCO_3^-] - [HCO_3^-]_{pH=7.4} = [HCO_3^-] - 24$?

Deliberation on this problem over the past few months has led me into a Stewartian rabbit hole. I now think I have an answer, though I can't cite any sources for this specific issue. I will nevertheless try to share my thoughts just in case anybody is still interested.
Short answer
I think Sabyasachi Pramanik has a point. To state it in other words, the key difference is that bicarbonate ion is the conjugate base of a volatile acid, whereas other buffer ions are conjugate bases of nonvolatile acids.
My initial argument went like this: say there is a buffer ion $\ce{A-}$, which is part of a buffer system characterized by the reaction $\ce{HA} \leftrightharpoons \ce{H+} + \ce{A-}$. Titratable acidity reflects not simply $[\ce{A-}]$, but only the difference $-\mathit{\Delta}[\ce{A-}] = -([\ce{A-}] - [\ce{A-}]_{\rm{pH} = 7.4})$. To justify this, one may think of $\ce{HA}$ as an acid and $\ce{A-}$ as a base. Since plasma and urine contain both ions, we should account for the acid-base effects of both ions. When the effects precisely cancel each other out (in physiological terms), pH should equal 7.4. Titratable acidity measures the discrepancy from that base state. From here, I proceeded to object that the same logic could also be applied to bicarbonate.
However, whereas the conjugate acid of $\ce{A-}$, namely $\ce{HA}$, is 'contained' in the solution, the conjugate acid of bicarbonate, namely $\ce{H2CO3}$, cannot be said to be 'contained' in the same way. The species itself exists in minute quantities; the majority degasifies into CO2. So there is no 'acid effect' to counterbalance the 'alkali effect' of bicarbonate. At all pH levels, even at pH 7.4, bicarbonate is exerting a net 'alkali effect' on plasma. This is why we don't subtract $[\ce{HCO3-}]_{\rm{pH}=7.4}$ when calculating NAE.
Stewartian answer
The above discussion is very informal and nonconventional. I did have those ideas vaguely in mind when I first posted the question, but I was having trouble phrasing them in the language of traditional theory. The Stewart view of acid-base physiology helped me see things more clearly.
In Stewart's view, there are three major independent variables that determine the acid-base status of bodily fluids: $P_{\ce{CO2}}$, SID, and ATOT. If some simplifications are made, it can be said that $[\ce{HCO3-}]$ is determined by the balance of $P_{\ce{CO2}}$ and SID, and $[\ce{A-}]$ by SID and ATOT. The difference lies in the fact that whereas SID and ATOT depend on the composition of the solution, $P_{\ce{CO2}}$ does not; its value is given by the composition of atmospheric air and the rate of ventilation.
Although excretion of buffer ions through urine is usually viewed as simply one component of 'acid excretion', from the perspective of Stewart theory it affects both SID and ATOT. Effects on the two variables might as well cancel each other out. However, renal bicarbonate excretion can only affect SID. This is why Stewart argues that sodium bicarbonate is equivalent to NaOH in terms of long-term acid-base balance. The only reason bicarbonate might be preferred is to avoid the immediate effects of high alkalinity. If equilibrium is allowed to be achieved, the two compounds will produce identical effects on acid-base homeostasis. Building upon Stewart's idea, we can predict that any amount of bicarbonate lost through urine is equivalent to a loss of same amounts of NaOH.
To see this, consider a solution containing sodium and a buffer system characterized by the reaction $\ce{HA} \leftrightharpoons \ce{H+} + \ce{A-}$. Suppose it is isolated from the surrounding atmosphere so that bicarbonate and CO2 are absent. Then the pH of this solution will be determined by the Henderson-Hasselbalch equation for the $\ce{HA}$-$\ce{A-}$ buffer system:
$$\textrm{pH} = \textrm{p} K_a + \log_{10} \frac{[\ce{A-}]}{[\ce{HA}]} \ .$$
What would happen if we took out half of all the solutes from the solution? Probably $[\ce{A-}]$ and $[\ce{HA}]$ would both be reduced by half, so their ratio would remain constant. Therefore, pH of the solution would also remain the same.
To analyze this example using Stewart theory, first observe that electroneutrality demands that $[\ce{A-}]$ equals $[\ce{Na+}]$ (ignoring small terms such as H+ or OH-). This is the value of SID in this case. Also, mass conservation dictates that the total mass of $\ce{HA}$ and $\ce{A-}$ remains constant if there is no input or output of materials. This is the value of ATOT in this case. To summarize,
$$[\ce{A-}] = \textrm{SID}, \ [\ce{HA}] = \textrm{A}_{\textrm{TOT}} - \textrm{SID} \ .$$
Consequently, the values of SID and ATOT completely determine the acid-base status of the solution. Informally speaking, SID exerts an alkalinizing influence, since it opens up a charge gap waiting to be filled by anions including OH-. Alternatively, a positive SID can be understood as the 'footprint' of strong alkalis (e. g. Na+ indicates that NaOH has been added). ATOT indicates the presence of weak acids. In this example, taking out half of all the solutes has removed both acid (ATOT) and alkali (SID, as the footprint of NaOH). The two effects have canceled each other out.
On the other hand, consider a sodium bicarbonate solution in equilibrium with a fixed partial pressure of CO2. The pH is given by the Henderson-Hasselbalch equation:
$$\textrm{pH} = \textrm{p} K + \log_{10} \frac{[\ce{HCO3-}]}{s \cdot P_{\ce{CO2}}} \ .$$
Again, electroneutrality demands that $[\ce{HCO3-}] = [\ce{Na+}] = \textrm{SID}$. If SID is halved, $[\ce{HCO3-}]$ would also be halved. However, $P_{\ce{CO2}}$ would remain constant. According to the equation, pH would fall. In this example, taking out half of all the solutes has removed alkali (SID, as the footprint of NaOH) but not acid. Therefore the solution acidifies.
Deriving the NAE equation (without ammonium) from Stewart theory
Armed with this conceptual machinery, let us see if the NAE equation actually makes sense. Ammonium secretion will not be considered, since it seems to involve other issues unrelated to the question at hand.
The hypothetical solutions in the previous section stood for plasma, since the aim was to study how plasma acid-base status changes as a result of urine excretion. Now the focus is on urine, so we shall consider a hypothetical solution that stands for urine. Solutes will be added to, rather than removed from, the solution, in order to represent H+ secretion into the tubule lumen.
Suppose a solution containing strong ions and the $\ce{HA}$-$\ce{A-}$ buffer system is in equilibrium with CO2 gas. Assume that the pH of the solution is 7.4 initially. According to the Henderson-Hasselbalch equation for the $\ce{HA}$-$\ce{A-}$ buffer system,
$$7.4 = \textrm{p} K_a + \log_{10} \frac{[\ce{A-}]_{\textrm{pH} = 7.4}}{\textrm{A}_{\textrm{TOT}} - [\ce{A-}]_{\textrm{pH} = 7.4}} \ .$$
If CO2 were removed and the value of SID were adjusted to $[\ce{A-}]_{\textrm{pH} = 7.4}$, every term of the equation would remain the same. Therefore, the pH of the soultion would again be 7.4. This thought experiment suggests that the size of acidifying effect of the weak acids in the solution can be represented by the quantity $[\ce{A-}]_{\textrm{pH} = 7.4}$, since it is precisely canceled out by an SID of $[\ce{A-}]_{\textrm{pH} = 7.4}$.
Now, suppose that strong acid is added to the solution, as a model of urine acidification. By excreting this solution from the body, we remove alkali by an amount identical to the final SID of the solution. Along with this, we also remove some amount of weak acid. But this quantity has no reason to change compared to the initial state, since only strong acid has been added. Therefore, the amount of acid excreted is $[\ce{A-}]_{\textrm{pH} = 7.4}$, and net acid excretion can be calculated as $[\ce{A-}]_{\textrm{pH} = 7.4} - \textrm{SID}$.
Electroneutrality demands that the following equation approximately holds:
$$\textrm{SID} = [\ce{HCO3-}] + [\ce{A-}] \ .$$
Substituting, we obtain
$$\textrm{NAE} = [\ce{A-}]_{\textrm{pH} = 7.4} - \textrm{SID} = [\ce{A-}]_{\textrm{pH} = 7.4} - [\ce{A-}] - [\ce{HCO3-}] \ .$$
Titratable acidity is defined as $\textrm{TA} = [\ce{A-}]_{\textrm{pH} = 7.4} - [\ce{A-}]$. In conclusion,
$$\textrm{NAE} = \textrm{TA} - [\ce{HCO3-}] \ .$$
(One article has attempted a similar derivation based on Stewart theory, but I think it contains an error. The authors assert that NAE can be understood as equivalent to $\textrm{SID}_{\textrm{pH} = 7.4} - \textrm{SID}$, but according to the calculations presented above, NAE as defined by the authors would differ from the true value by $[\ce{HCO3-}]_{\textrm{pH} = 7.4}$.)


text:
Is there a favoured mathematical model of bacterial growth?
One of the most regularly measured phenotypes in bacterial synthetic biology is growth. Anyone who does wet lab microbiology or synthetic biology will have performed a growth curve measurement. However, it is quite rare in synthetic biology papers for growth to be characterised using a mathematical model - even though growth curves are regularly shown in supplementary materials.
There are a plethora of growth models around - from basic logistic growth to the more biologically grounded Monod growth. I recently discovered the Richard's model which seems to be a more general form encompassing logistic, Gompertz etc. Is there a favoured model for the microbiology and/or synthetic biology community? Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

A few rather general remarks: Models are usually designed to describe specific situations using the minimal number of parameters. So the models that you listed are not necessarily mutually exclusive. One could design a more general model, but it would necessarily have more parameters and less statistical power. From statistics point of view it is also necessary to keep in mind that all these are parametric models, which can only approximate the growth curve.

Some clarifications:
Commonly used models for bacterial isothermal growth curves (which represent the growth curve directly) are for example:

Exponential

Logistic

Generalized logistic

The Monod equation expresses how the growth rate changes with the availability of substrate see a related question here.
The Monod equation can be incorporated into an exponential growth model (differential equation) like this:
$$
\frac{dX}{dt}=\mu X
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X$ is the biomass concentration and $[S]$ is the substrate concentration. Or into a logistic growth model:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X_{max}$ is the carrying capacity.
Other growth-substrate relations like Haldane which takes into account growth inhibition by the substrate can be used instead of Monod one.
Regarding this:

Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

It depends on what branch of synthetic biology you are looking into. Model-based design engineering biology interpretation of synthetic biology goes around the DBTL cycle. In the DBTL cycle, there are always (at least) models of both growth and gene expression.

the more biologically grounded Monod growth

Why is the Monod model more biologically grounded? It is empiric and NOT based on biological considerations! I only know this equation from enzyme kinetics, not for cell-growth, where the identical Michaelis–Menten equation assumes a random collusion model. So according to this model, your cells would grow more, the more substrate (glucose?) collides against the walls!
It seems quite logical to model enzyme-kinetics or chemical reactions with random collusion models. However, the only relevant biological facts I see are the following:

Cells divide, which naturally suggest exponential growth.
Cell-cycles and circadian cycles exist, which naturally suggests a
constant generation time. (within the limits that everyone knows)

So, if everyone learns about growth curves and logistic fits in their wet-lab courses, where logistic fits work perfectly fine to predict growth within the log-phase, then why would there be a need to use other - more complicated - models, while the logistic model is conceptually indicated? (Also note that the Monod model still fails to predict the lag phase and death phase.)
This leads to the final answer to the question:

Is there something holding the synthetic biology community back from
regularly reporting growth characteristics of their cells?

Practical use!

In daily routine, the typical wet-lab scientist is merely
interested in knowing the expected time until a certain optical
density (OD) of the cell-culture is reached. Practically, this is
done with as few measurements as possible, based on experience and a guess of a generic generation-time.
Exact predictions are needed in large-scale biotechnological
production. In such a context all parameters must be accurately predicted and validated. Given your exact microorganisms and your production plan, small-batch trails will be performed and up-scaled. Everything must be known and planned in detail and quite often, the whole production facility is designed and built to achieve a single task! Everything, including the generated heat, O2, CO2, Glucose, (end-) concentration of the yield.. is monitored and legally binding deviation-limits must be set before-hand and met at all times. Small deviations can cause losses of millions of dollars and companies don't rely on simple models like "Monod", but stress-test every aspect and monitor and react in automated systems. There is vast knowledge regarding growth-curves and models, just you are not aware of it, as it is kept company-internal, or written in expensive bioprocess-technology books.

Yes, that is true! Good addition!

I've been appreciating your answers, and I think you'd be a good contributor to the more interdisciplinary SynBio StackExchange we're trying to launch. Want to support the proposal? https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MzNjZmVjYzI0NDg3NzNmMmI1Y2YzZTlmNDk3ZGIyOWU1ZWZmNGQ0YTBjZmFhODA2ZWQ4OWJkOTgwN2M3YTM0NPwIycDDlI9PcBruZ0as_SrnCeYJMauTp-s2V857fCra0


text:
excitatory-inhibitory synapse ratio
For each inhibitory synapse, how many excitatory synapses are in the brain?
It is the same ratio along the animal kingdom or nervous system areas?

E/I synapse ratio probably isn't the most informative measure, because you leave out the release probability of synapses, the postsynaptic efficacy of a synapse, the level of presynaptic activity, the spatiotemporal correlation of inhibition and excitation, the meanings of excitation and inhibition in different parts of the animal kingdom, the temporal features of rapid neurotransmitters vs slower neuromodulators, etc etc.

I'm aware that at a dynamical level E/I balance could be very different than E/I balance at the anatomical level. For my purposes, I want to have an estimation of the E/I ratio in terms of connectivity alone.


text:
Is there any correlation between animal diet and blood pH?
The alkaline diet claim that as we humans have a slightly basic pH we shouldn't eat acidic food like meat (I think they claim that meat ashes are acid).
I was wondering that if carnivores animals share similar blood pH to humans and herbivores, that argument falls.
I did a google search, but I couldn't find the answer, even though it seems like basic data for a physiology textbook.
Similar questions have been posted here but without satisfactory answers.

The alkaline/acidic diet bit is all pseudoscience junk. You'll find related questions at Skeptics.SE. There are also a couple of diet pH questions here already if you search.

I know that it's pseudoscience. The question that I post is a scientific one that is meant to refute a pseudoscientific claim. I don't think the question to this specific question could be found in Skeptic.SE

Note that pH would not be the only factor to determine how much a type of food could influence the body pH. It would also be important to know the buffer capabilities of that food.


text:
Can I use multiple bicistronic RBS sequences in a synthetic biological circuit?
The bicistroninc RBS sequences (BCDs) developed by Mutalik et al. [1] aim to remove context sensitivity from translation and therefore ensure more predictable gene expression. However, I have been told that having multiple transcriptional units, each using BCDs, can make cells sick. The explanation that I was given was that the toxicity is from small peptides that are produced from transcription from the first RBS sequence.
Has anyone demonstrated toxicity from multiple BCDs or is it apocryphal? If it has been demonstrated, is the mechanism of toxicity known and is there a way to use multiple BCDs while maintaining healthy cells?
[1] V. K. Mutalik et al., “Precise and reliable gene expression via standard transcription and translation initiation elements,” Nat. Methods, vol. 10, no. 4, pp. 354–360, Apr. 2013.

That’s a great question and has lot of opportunities to explore. I am not sure anyone has followed up on this original BCD work systematically. We did try cloning these elements on a medium copy plasmids, in an operon design, driving multiple genes, and now I think about it, that was not a smart thing to do. Cloning was very challenging, probably due to toxicity you mention. Didn’t have time to investigate this in depth (that it self is a cool project), but I think the toxicity is due to too much resources (ribosomes?) titrated out on these units. But that’s a hand-wavy explanation. Need mechanistic study to investigate. I think Tom Ellis’s group and others have done some beautiful work on toxicity associated with protein expression. Personally I think the toxicity is not related to the inert peptide (1st gene in a BCD operon) that’s produced. Another story we tried was to replace this first gene with something functional but not published.
Coming back to using BCDs for driving multiple genes, I would say if you clone these directly on genomes they should work like charm. We did try this and works good. Not published much (oh god, that’s so much work unpublished!) Bacterial operons have these junctions and elements of different strengths. Happy to discuss more if you have a follow up question!!
Thanks for your interest in this work. Really proud of our work on this system. Of course happy that we did this work as there were so many early effort on these BCD type elements. And love this open discussion SE platform! Don’t know how synbio survived without this system of sharing knowledge and experiences. Best wishes
Vivek Mutalik

In the documentation for this recent cloning method from Richard Murray's group at Caltech (,https://doi.org/10.1021/acssynbio.8b00060)  they include a parts library with various BCDs. I haven't tested this directly myself, but the warning they note for multiple BCDs is not that they are toxic, but that because they have long homologous regions that they are prone to recombination. This makes sense since the dummy peptide region is I think around 50bp and shared across all the BCDs. You could imagine making variants in this region to combat recombination issues, but who knows if that would affect the robustness of the BCD expression.