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What are the long term consequences of settling an isolated territory with an extremely limited gene pool?
I remember reading about a discredited theory - I'm afraid that, despite some frantic Googling, I've been unable to track down a link - which stated that Australia was first settled by a woman, pregnant with a son, who washed up on a beach. It struck me as surprising that such a theory was ever proposed; I know very little about genetics, but it seemed implausible that all Aboriginal Australians, who seem about as physically healthy as any other race, are descended from just a mother and her son. But could just one woman be the progenitor of a healthy nation? And, if not, what is the minimum number of distantly-related individuals required?
As was stated in the answers to a related question: the more immediate consequences of inbreeding are a dramatic rise in inherited diseases, as well as, perhaps, some mild intellectual disabilities. But what are the consequences over several generations? The Pitcairn Islands and Easter Island/Rapa Nui spring to mind when thinking of historical examples of isolated territories with limited gene pools: both seem to have been settled by around two dozen individuals. Did either community experience specific problems over the centuries due to a small gene pool?

The above, obviously, is concerned with our own species, but I'd be very interested to hear about this topic with respect to other species too. I seem to remember, in one of his "Dark Horse" podcasts, Bret Weinstein talked about how a particular species of Hawaiian bat colonised those islands by way of a single pregnant female being blown off course and/or washing up on a beach. Again, is such a thing plausible, and, if so, what would be the long term consquences for the colonisers?

I think this is a potentially interesting question that I will have a go at answering, but I think the section about whether or not the 'unsavoury goings on' in the history of those islands are related to inbreeding depression needs to go; fitting culture and history in terms of genetics in this way isn't a good avenue to go down, in my view.

@4galaxy7 I am wholeheartedly on board with the point of view that 'fitting culture and history in terms of genetics... isn't a good avenue to go down', and I'll do my best to amend my question along the lines you suggest. I think the way I phrased the question leant itself to being misunderstood. What I meant was: "Did the Rapa Nui community  experience specific problems over the centuries due to a small gene pool?" And not, "Was [insert racist stereotype here] caused by inbreeding?" As I said, I'll amend the question.

Minimum number of individuals needed to start a population

But could just one woman be the progenitor of a healthy nation? And,
if not, what is the minimum number of distantly-related individuals
required?

Healthy is a pretty subjective term, and it's perhaps easier to think of things in terms of a minimum viable population, which is more about straight survival than population health. However, Marin & Beluffi (2018) performed some simulations of humans in a multi-generational space exploration scenario, using 'healthy population' as a desired outcome and found:

A initial amount of 25 breeding pairs of settlers drives the mission
towards extinction in 50 +/- 15% of cases if we completely forbid
inbreeding. Under the set of parameters described in this publication,
we find that a minimum crew of 98 people is necessary ensure a 100%
success rate for a 6300-year space travel towards the closest telluric
exoplanet known so far.

So according to this simulation, it seems quite unlikely that a single woman could be the progenitor for some kind of colony. However, as I discuss a bit further down, some human populations went through bottlenecks of ~20 individuals and remained viable. They may have incurred some health costs, but they would be able to propagate the population.
Long term consequences of founder effects
There are several different case studies of modern human populations relating to the founder effect.
Achromatopsia Pingelap
The atoll of Pingelap in the Pacific Ocean is extremely remote, and up until the late 18th century had around 500 inhabitants. Around then, it was hit by a devastating typhoon which reduced the population size to around 20 individuals. In following generations, it was estimated by that 10% of the estimated 3,000 Pinglapese had Achromatopsia (Carr et al 1971), an autosomal recessive form of colour blindness that otherwise has an extremely low frequency of about 0.003% in other populations (Thiadens 2011).
Subsequent studies used homozygosity mapping in order to determine the genetic basis of the high levels of Achromatopsia. Sundin et al (2000) demonstrated that Pingelapese achromats are homozygous for a missense mutation (serine to phenylalanine) in a highly conserved membrane-spanning domain. This is quite solid evidence for the deleterious consequences of the founder effect in modern human populations.
Jewish populations
There is also reasonable evidence of a severe bottleneck in the ancestors of the global Ashkenazi Jew population. Carmi et al (2014) estimated that the total population fell as low as 350 individuals:

The AJ population is much larger and/or experienced a more severe
bottleneck than other founder populations, such as Amish, Hutterites
or Icelanders.

Other studies have suggested that the high incidence of particular diseases found in Ashkenazi Jew populations was the result of genetic drift following the bottleneck, rather than subsequent co-sanguinity (Bray et al 2010):

We identified genomic regions under selection that account for lactose
and alcohol tolerance, and although we found evidence for positive
selection at some AJ-prevalent disease loci, the higher incidence of
the majority of these diseases is likely the result of genetic drift
following a bottleneck

Rapa Nui
Since you asked about Rapa Nui. Gonzalez-Martin et al (2006) have this to say:

The population of Easter Island is one of the most interesting extant
human communities due to its unique demographic history, its geographic
isolation, and the development of an incomparable culture
charac-terized by the towering ‘‘Moais’’ and its enigmatic writing.
Following the colonization of its population by Polynesians from the
Mangarevan Islands in the 5th century AD, the island remained isolated
up until the middle ofthe 20th century. Under these conditions, with
endogamy levels ﬂuctuating between 61.04–96.54% and given such a small
population, a high rate of inbreeding, and consequently, an elevated
level of genetic relationships would be expected. Using data from
church and civil records, we calculated the consanguinity of the
population of Rapa Nui. The results of this analysis do not support
the hypothesis of a high level of consanguinity.

That said, I have heard some unverified rumours that there was a high incidence of having 6 toes on Rapa Nui, but I can't find anything solid to back it up with.
Norfolk Island
One last example. I've taken this text from a nice paper by Macgregor et al (2009):

The population of Norfolk Island, located off the eastern coast of
Australia, possesses an unusual and fascinating history. Most
present-day islanders are related to a small number of the ‘Bounty’
mutineer founders. These founders consisted of Caucasian males and
Polynesian females and led to an admixed present-day population. By
examining a single large pedigree of 5742 individuals, spanning >200
years, we analyzed the influence of admixture and founder effect on
various cardiovascular disease (CVD)-related traits.

Further...

Marker-derived homozygosity was computed and agreed with measures of
inbreeding derived from pedigree information. Founder effect
(inbreeding and marker-derived homozygosity) significantly influenced
height

Non-human species
I think the last part of your answer is referring to the Hoary Bat, which colonised Hawaii from mainland USA. It was originally hypothesised that the population was the result of a single founding event, but this has been disputed by mtDNA markers (Russell et al, 2015):

Our results point to the colonization of Hawai'i by hoary bats on two
occasions by lineages that experienced distinct evolutionary
trajectories

There is some evidence of single-individual founder events occurring, however (Clegg et al 2002);

Here we undertake a genetic analysis of a series of historically
documented, natural colonization events by the silvereye
species-complex (Zosterops lateralis), a group used to illustrate the
process of island colonization in the original founder effect model.
Our results indicate that single founder events do not affect levels
of heterozygosity or allelic diversity, nor do they result in
immediate genetic differentiation between populations

Further..

A Bayesian analysis based on computer simulation allows inferences to
be made on the number of effective founders and indicates that founder
effects are weak because island populations are established from
relatively large flocks.

There is a lot of literature on this in wild populations which might be of interest, e.g. https://link.springer.com/content/pdf/10.1007/s10592-010-0049-0.pdf
References
Thiadens, Alberta. "Genetic etiology and clinical consequences of cone disorders." (2011). APA
Carr, Ronald E., Newton E. Morton, and Irwin M. Siegel. "Achromatopsia in Pingelap islanders: study of a genetic isolate." American journal of ophthalmology 72.4 (1971): 746-756.
Sundin, O.H. et al. Genetic basis of total colourblindness among the Pingelapese Islanders. Nature Genet. 25, 289– 293 (2000).
Carmi, Shai, et al. "Sequencing an Ashkenazi reference panel supports population-targeted personal genomics and illuminates Jewish and European origins." Nature communications 5.1 (2014): 1-9.
Bray, Steven M., et al. "Signatures of founder effects, admixture, and selection in the Ashkenazi Jewish population." Proceedings of the National Academy of Sciences 107.37 (2010): 16222-16227.
APA
Marin, Frédéric, and Camille Beluffi. "Computing the minimal crew for a multi-generational space travel towards Proxima Centauri b." arXiv preprint arXiv:1806.03856 (2018).
Russell, Amy L., et al. "Two tickets to paradise: multiple dispersal events in the founding of hoary bat populations in Hawai'i." PLoS One 10.6 (2015): e0127912.
Clegg, Sonya M., et al. "Genetic consequences of sequential founder events by an island-colonizing bird." Proceedings of the National Academy of Sciences 99.12 (2002): 8127-8132.
Macgregor, Stuart, et al. "Legacy of mutiny on the Bounty: founder effect and admixture on Norfolk Island." European Journal of Human Genetics 18.1 (2010): 67-72.

I'm always impressed by the answers I receive on SE for my malformed "shower thoughts". But this one stands head and shoulders above the others in its breadth and rigour. Thank you.


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Why don't hamsters exhibit a fear response when other hamsters nearby are under attack?
There is this live feeding video on youtube that displays 30 live hamsters being eaten by 4 bullfrogs. You can find it here: https://www.youtube.com/watch?v=rz4Or3o-jHA
What struck me as extremely odd was that none of the hamsters exhibited any kind of stress when one of them was being eaten alive.
The first one got eaten head first at 0:28 https://youtu.be/rz4Or3o-jHA?t=208 yet none of the other hamsters tried to run away. Instead, some of them even approached the attacking frog and started sniffing its eyeballs. Then somewhere after 3:25 https://youtu.be/rz4Or3o-jHA?t=206 another hamster is attacked from the side which causes it to scream out in pain. Yet the other hamsters are still unfazed by it. Some are even cleaning their fur as the carnage around them unfolds.
So how does this work. Why do all these hamsters seem so comfortable?
EDIT: At the end a few of the hamsters do seem to freeze a bit, but no real panic. There is another live feeding video that shows a single bullfrog eating a group of mice. You can find it here. https://www.youtube.com/watch?v=9RDwz8mjOIw These mice do exhibit real fear. Since both hamsters and mice are part of the same larger family called Muridae, it's very strange that hamsters react so differently.

This does seem odd indeed. I don't have time to look into and research an answer, but I can't help but notice that "The entire laboratory and pet populations of Syrian hamsters appear to be descendants of a single brother–sister pairing." (Wikipedia) representing one heck of a bottleneck. Inbreeding  may play a part.

Maybe the hamsters are instead pretty clever and realized they're confined in a death trap and have simply accepted their inevitable fate

source: Stack Exchange

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

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What reproductive advantage do superhydrophobic spores bring?
Clubmoss plants produce spores that are superhydrophobic, meaning they will not mix with water. When you drop water on top of a whole bunch of these spores, the water will form tiny water droplets on top of the spore powder instead of being absorbed by it. You can see an example of this in this video. The spore powder is also known as lycopodium powder and is used in fire shows and magic tricks.
To my knowledge clubmoss is the only plantspecies that produces superhydrophobic spores. This made me wonder what the reproductive or evolutionary advantage of a superhydrophobic seed or spore could be.
I personally think the superhydrophobic layer could protect the spores from being digested when the clubmoss plant is eaten by a herbivore. The superhydrophobic layer could also prevent the spores from sinking when they fall into water like a river, instead they would stick to the surface. A river could help disperse the spores accross a larger area pretty easily. Eventually the spores would drift to the shore again where they could settle and become new clubmoss plants.
What do you think the reproductive advantage could be?

Water encourages pathogens and is generally detrimental to long term conservation of seeds, actually, nearly all commercial seeds have a lower shelf life in a humid environment, and are generally packed in wax or foil paper.

This paper seems to agree with you; It says that the spores of the clubmoss plant are likely hydrophobic to spread more easily.

This is also a part of the secret of the well-known Lycopodium powders: the clubmoss-spores (diameter ca 30 μm) are weakly hydrophobic, but as powder, they exhibit remarkable functionalities. Many spores—even of aquatic organisms such as the spores of Isoetes or fungi, or myxomycetes [80] are hydrophobic for dispersal purpose.

[80]
(citation from the paper)
Hoppe T, Schwippert WW. 2014 Hydrophobicity of myxomycete spores: an undescribed aspect of spore ornamentation. Mycosphere 5, 601–606. Crossref, ISI, Google Scholar
Additionally, this article believes spores are hydrophobic to protect against environmental factors.

When spores are carried over a long distance, survival is compromised by exposure to diverse abiotic stressors, such as drought, extreme temperatures, and ultraviolet (UV) radiation [12, 13]. Thus, fitness can be estimated using not only developmental parameters but also spore properties that influence dispersal efficiency in different media and resistance to stressors.

Most filamentous fungi disperse through airborne spores that can be transferred by wind over a long distance [11, 14]. For this reason, fungal spores usually remain dry and hydrophobic [15].

(citations from the article)
[11]
Wyatt TT, Wosten HA, Dijksterhuis J. Fungal spores for dispersion in space and time. Adv Appl Microbiol. 2013;85:43–91.
[12]
Fuller KK, Ringelberg CS, Loros JJ, Dunlap JC. The fungal pathogen Aspergillus fumigatus regulates growth, metabolism, and stress resistance in response to light. mBio. 2013;4.
[13]
Norros V, Karhu E, Norden J, Vahatalo AV, Ovaskainen O. Spore sensitivity to sunlight and freezing can restrict dispersal in wood-decay fungi. Ecol Evol. 2015;5:3312–26.
[14]
Roper M, Seminara A, Bandi MM, Cobb A, Dillard HR, Pringle A. Dispersal of fungal spores on a cooperatively generated wind. Proc Natl Acad Sci USA. 2010;107:17474–9.
[15]
Aimanianda V, Bayry J, Bozza S, Kniemeyer O, Perruccio K, Elluru SR, et al. Surface hydrophobin prevents immune recognition of airborne fungal spores. Nature. 2009;460:1117–21.

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


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How are the muscles of some dead animals still able to function for an extended period of time without oxygen?
I found this video on youtube that features several butchered and sometimes cooked animals that are still able to move despite of this. Some of these animals have been dead for several hours already but they're still able to move, like this frog or this chicken filet. Other animals still display movement after they've been cooked in the oven, like this fish.
These aren't just random movements either. Some of the animals still seem to be able to respond to aversive stimuli as well. An example of this is the decapitated fish at 0:30 that only starts moving when its being sliced by a knife. Another example is this this dried fish at 1:21 that starts moving its mouth when a bit of water is poured
over it.
So how are these dead animals still moving without their muscles receiving any oxygen? I've looked up how long muscles can survive without oxygen. In humans this appears to be 60 to 90 minutes at most. Perhaps the same goes for many other vertibrate species. But the compilation even shows cooked animals still able to move. So how does this work?

Check out muscle metabolism.

@theforestecologist how is this an answer?

It's not. It's a comment. I think you'd benefit from reading about the different pathways/mechanisms of muscle metabolism. You might find particular interest in anaerobic glycolysis

Please take our [tour] and visit our [help] to further understand how the site works. Thanks


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Beetle Identification / able to retract its head

I can't find any identification of this beetle online. The closest guess I got to it is "Hister beetle" but the rough surfaces on its shell make me think otherwise.
The most common behavior is that when feeling threatened, it plays dead for some time. It retract its head, and then covers it with its 2 front limbs, which make it look like a piece of wood or a tree seed.
Here's a video showing its movement
https://www.youtube.com/watch?v=cSjQ_8vbYw4
Philippines, Southeast Asia.
under tropical savanna climate

Welcome to Biology.SE! For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where you observed this creature. The location can be an essential clue for identifications. ——— If possible clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Edit: Based on Arthur J Frost's comment, Trox Beetles more likely resemble it in movement and behavior. So it's probably more like a member of Trogidae beetle family.

Um, no.  I'm not completely sure, but the Scarab family Trogidae (the Skin Beetles) looks more likely to me (see here for photos of some North American species; the family is worldwide).

You're right. I saw some videos about it on youtube which greatly resemble the movement, including the behavior of playing dead, retracting its head(not sure if it's the right term) and covering it with their front limbs. Though this is probably just one of the types under it, since one video shows it's able to produce sound when playing dead, but this one is not.


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What phase of Action Potential (AP) exactly defines the Relative Refractory Period?
I am posting below, word for word, two statements made on Relative Refractory period - the first from the text: Human Physiology for Medical Students by Magdi Sabry, and the second from a web page with the URL:
https://content.byui.edu/file/a236934c-3c60-4fe9-90aa-d343b3e3a640/1/module5/readings/refractory_periods.html.
In addition, I've attached a photo from Google which appears to be in support of the second statement.
But which of these is correct?

"Relative refractory period (RRP)...corresponds to the remaining part of the descending limb of the AP till the start of after-depolarization (i.e. during the later 2/3 of RP)"

2."...there are two types of refractory periods; the absolute refractory period, which corresponds to depolarization and repolarization, and the relative refractory period, which corresponds to hyperpolarization. "

By "AP", I assume you're referring to action potential? (I'm not a neurologist)

Yes, I mean Action potential, and I've edited the post.

Neither is an accurate definition; both are correct and not conflicting if you interpret "corresponding" to mean "typically/approximately corresponding".
The absolute refractory period is any time in which you cannot evoke another action potential no matter the strength of stimulus, due to an action potential in progress/that has just occurred.
The relative refractory period is any time in which you can trigger an action potential but need a stronger stimulus than normal.
Neither of these definitions refers to specific phases of the action potential in terms of voltage or change in voltage. Yes, typically the absolute period includes the ascending and descending phases of the AP, but there's no reason it can't last longer depending on the gating properties of the sodium channels. Similarly, the relative refractory period starts with the end of the absolute refractory period and continues through the hyperpolarization phase, but there is no reason it cannot end sooner or later, again depending on gating properties.


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Why does increasing concentration of extracellular sodium have no effect on electrical gradient of potassium?
I learnt that the permeability of an ion across the membrane contributes to the membrane potential as much as(or even more than) its concentration and electrical gradients. And so far I've made peace with the fact that Sodium, having a very low permeability, doesn't contribute much (through its own movement) to membrane potential despite having a high electrochemical gradient directed towards the cell's interior.
Now, the confusing thing is that, if I imagine dumping some sodium ions (with their positive charge) on the cell's exterior, this would affect the electrical gradient of potassium (and in fact other ions)--because more positivity is recorded externally-- making potassium in particular less "ready" to diffuse out of the cell. The result of which would be a depression (that is a more negative value ) of the resting membrane potential.
If potassium's extracellular concentration were increased instead, a similar effect would be observed.
What exactly is wrong with this reasoning?
I'm putting this forward because my Professor mentioned only extracellular potassium ion as having an effect on membrane's resting potential.

You can't just add a bunch of positively charged ions in a bucket; they always come with a negative counterpart. If you somehow could, you would create lightning. Electricity is pretty powerful stuff.

Are you sure that adding extracellular $Na^+$ would inhibit $K^+$ migration?

I've answered a bunch of very similar questions here and on Psych & Neuro. They all end up being approximately duplicates but the underlying question is really just "how do membrane potentials work" and everyone has a slightly different misunderstanding. Some places to start: https://biology.stackexchange.com/questions/88730/when-is-voltage-generated-across-a-membrane/88777#88777 https://biology.stackexchange.com/questions/64762/cell-biology-resting-membrane-potentials/64773#64773

https://biology.stackexchange.com/questions/76166/ambiguity-about-the-relation-between-membrane-potential-and-concentration-gradie/76167#76167 https://biology.stackexchange.com/questions/52122/why-does-the-side-of-the-mebrane-of-a-neuron-with-a-high-concentration-of-positi/52595#52595 https://biology.stackexchange.com/questions/77919/why-does-resting-potential-not-become-continually-more-negative/77925#77925 https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne/57066#57066

@BryanKrause , thanks for the links. But before I check them out, I'll like to make sure I understand your answer. Since we cannot add positive ions without accompanying negative ions, the change in membrane potential resulting from increase in potassium's extracellular concentration is NOT due to change in its electrical gradient (since just about same amount of negative ions from wherever counteracts that). But what then would be responsible? The change in its concentration gradient?

@Chemo-Mike Yes. If you add extracellular potassium, there is less of a concentration difference between in and out so the net flow of potassium ions from inside to outside is lower at any given voltage. Therefore, the voltage that takes the net to become zero (the "reversal potential for potassium") is less negative. The Nernst equation shows this for potassium considered by itself, and the Goldman equation will tell you what resting potential will be once accounting for other permeable ions.

Ok. Got that!


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Understanding muscle tone
I am relatively new to Physiology, and I've just learnt about muscle tone.
I however find it difficult to understand the electrical changes that initiate (and/or accompany) muscle tone in smooth muscles .
To be specific, I know that action potentials(AP) cause muscle contraction (just like they cause nerve impulse propagation), and I also know that smooth muscle tone is a result of irregular contractions of the muscles at rest.
How then can these muscles contract when no AP is generated at rest?
PS: This question has been edited to achieve more clarity.

Action potentials usually maintain muscle tone in skeletal muscles, but muscle cells are affected by other influences that can affect their contraction and thus the tone of the muscle.
Smooth muscle occurs in the walls of hollow organs, most notably the blood vessels and the GI tract, and in a few other places.  Contraction of smooth muscle is generally involuntary and can be stimulated by the APs from the autonomic nervous system, but often for the slow maintenance of muscle tone contraction is controlled by hormones, other external molecules, or external pressure.  The mechanisms that cause this contraction generally involve the phosphorylation of myosin light chains. (1) (2)

If action potentials can at all maintain muscle tone, why is muscle tone spoken of as passive contraction? (https://en.m.wikipedia.org/wiki/Muscle_tone). As much as I know, passive processes don't involve ionic changes seen in active ones (such as action potentials). If I am wrong about this can you point out the misconception?

Disclaimer: it has passed some time since my studies in muscle physiology.
Muscle have stretch receptors to monitor the change in length. These are connected to the central nervous system, where information is properly processed and the response triggered. This response, as far as I know, propagates through action potential (AP) across neurons, which activate the muscle (transverse tubules, AP, Ca2+). In summary, muscle tone should be regulated by APs and I am not aware of another mechanism of muscle contraction in this case.
Do you have some references where they discuss another mechanism of non-AP muscle tone? I am very curious to know more.
/Emilio

My several days of research on the mechanism has turned out futile. But this is the statement which prompted my question: "...smooth muscles of some visceral organs maintain a state of partial  contraction  called  tonus  or  tone.  It is due  to the tonic contraction  of the muscle  that occurs without any action potential or  any stimulus...". It is from the text: essentials of Medical Physiology by K Sembulingam

@Chemo-Mike Pretty important to indicate you are talking about smooth muscle in your question if that's the case.


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Presynaptic inhibition
For presynaptic inhibition, I am aware of these:

Ca²+ influx (into the presynaptic nerve terminal) is decreased. And this in turn reduces the probability of releasing synaptic vesicles from the presynaptic neuron.

The influx of Ca²+ is under the influence of voltage-gated Ca²+ channels.

My questions:

What inhibitor(s) can be involved in this inhibition?

What is the ionic basis of this inhibition? (By this, I want to know how the movement of ions affects the voltage-gated Ca²+ channels)

Does the reaction cascade intitiated by the inhibitor in any way affect the amplitude of the AP generated upstream when it reaches the presynaptic nerve terminal?


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Do circadian hormones fluctuations follow sleeping patterns or the time of day?
It is said that testosterone and cortisol are at their highest early in the morning, at 8 am, and lowest at night.
What happens, though, if someone regularly goes to sleep at 8 am and wakes up in the afternoon/evening over a long period? What happens if sleep times are inconsistent, sometimes sleeping overnight and sometimes in the morning? Do hormonal fluctuations follow the sleep pattern or do they follow the time of day?

I think your question will be better received without the "I" parts of it, so I've edited it accordingly. Additionally, it's good to provide citations for things you read about, so if you can cite where you read about daily cycles of testosterone and cortisol that would be great.


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Could eidetic memory be related to glial cells?
I am a plasma physicist so I apologize in advance for my biology ignorance.
I recall from a neuropsychology class I took in college (used Lezak, Howieson, and Loring, 4th Edition) that there are several types of glial cells, at least one of which acts to prune neurons in your brain.  I am curious if those with an eidetic memory have fewer or different or altered glial cells?  That is, could the pruning done by some glial cells affect long-term memory or brain function but not be operating (or at least in a diminished capacity) in those with an eidetic memory?
I found a somewhat related question but it's not directly tied to this one: Is an Eidetic Memory (or other unusual forms of memory) less susceptible to anterograde amnesia?
References
Lezak, M.D., D.B. Howieson, and D.W. Loring Neuropsychological Assessment, 4th Edition, Oxford University Press, Inc., New York, New York, 2004.

Usually we talk about pruning synapses rather than neurons, and I don't think that's something that has changed. I think your edits have improved things but I don't think you'll get more than a speculative answer.


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Biological Neural Network Modification to Unlearn Understandings
Lets assume that a person grows up thinking that religion X is true religion. So he builds up a profile in ones head and when notion of religion X appears the neurons that is related are fired, giving sensation of God and related stuff.
Lets us also assume that later in life he learns that religion X was not correct, then does "realization" of this fact happens by modifying old neural networks or a new profile is created for religion X and old profile gets deleted?
In other words do neurons associated with sensation that religion X was true religion "modified" or a new network is created giving a new sensation that religion X was not true religion along!
In my general understanding modification of old network could be challenging assuming that they are surrounded by other neurons associated with other stuff, a certain modification by having more or less neurons would result in borrowing neighboring neurons and wiring them to create a modification or loosing some connections to create a modification, which doesn't seem efficient.

I am not sure how is this question "opinion based"? I have asked a concrete question with a general example.

i'd suggest putting this on psychology and neuroscience instead, I don't know if you're going to get a good answer here: https://psychology.stackexchange.com/

I will, do you think its not related to biology?

Why was this close as opinion-based?

@BiologyEnthusiast Since there is a SE site specifically pointed towards neuroscience and cognition, that is likely a much better place to get informed commentary. Moreover, I personally can't tell if there is enough information to answer the question but I suspect there might not be (for example, there are no linked sources); this suggests to me that an expert would need to look at it to decide whether it can be answered. That expert would be a psychologist or a neuroscientist; and such specialists have their own site.

This has now been cross-posted at Psych&Neuro. I don't necessarily agree that it should have been closed here, but I think now that it's been posted there it shouldn't be reopened here.


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Why does the thickness of the Loop of Henle have to be less than the convoluted proximal tube and the distal convoluted tube?
We are currently being taught "Homeostasis through excretory system" in college. After seeing the structure of a nephron, it is not quite evident as to why should the Loop of Henle be the thinnest.
Only sense that I could make out of it is that- "Thin cross sectional area implies higher fluid velocity". Since, water and ions are majorly reabsorbed in the proximal convoluted tube, the loop of Henle is thin to increase the flow of fluid because there isn't much left to reabsorb and hence it won't require as much reabsorption time as the PCT. This decreases the filtration time and makes the process faster. I am not quite sure if this makes sense.
Can someone help?

there is a bit more to it actually,

The Henle -loop only occurs in birds and mammals, giving them the ability to make the urine hyperosmotic in comparison to their blood, other vertebrates can't do this.

how does the henle loop achieve this further concentration of urea(= more resorption of H2O)?:

-> by using the physical principle of countercurrent exchange
Beware: the explanation follows the opposite direction as the flow of the liquid!

A potential is build up in the bigger upgoing part Pars recta by active Na+& Cl- resoption , the water cant go out because the membrane is impermeable here.

this leads to build up of osmotic pressure (positive osm. potential of 1200 mOsmol/kg)

The Henle -loop  loops back up as a thin part(!) the Pars ascendens

the downgoing part right after the PCT (pars descendens) uses the potential of the corticomedullary osmosis gradient to let water (resorption) out using passive osmosis while taking urea in (no ATP needed).

CONCLUSION: So why is the left and bottom part of this henle loop thinner?!  to resrobe H2O using passive osmosis ! (also, if the lowest bottom part would be thick, it would not loop so nice, therefore hindering the coutercurrence effect)


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Why do people's hands get cold for the first half an hour and then suddenly they are warm when they are doing exercise outdoors in winter?
When people do exercise outdoors in winter at temperatures less than zero degree celsius, their hands are quite cold and hurt for about half an hour. Then, there is a sudden rush of blood into the hands and they are warm afterwards, just as if they are indoors all along. Why does this happen and is there anything one can do to trigger the warmth faster?

Probably because your body is now trying to get rid of heat after 1/2 hr of exercise.

Why is it not a gradual process and happens so suddenly, like a some valve is opened and warm blood flows into my arms?

That valve being opened could be the capilliaries opening, well expanding, allowing more blood flow...

Cold extremeties are a reaction of endotherms where they reduce warm blood circulation to prevent losing core body temperature, otherwise the cold blood in your hands would lower your central blood pressure from 37'C, which makes the body less efficient and at risk of catching colds.

The reaction is called vasoconstriction.
quote:
Active cutaneous vasodilation occurs via cholinergic nerve cotransmission and has been shown to include potential roles for nitric oxide, vasoactive intestinal peptide, prostaglandins, and substance P (and/or neurokinin-1 receptors). It has proven both interesting and challenging that no one substance has been identified as the sole mediator of active cutaneous vasodilation. source
The above research can give you some clues about exercise and cold hands:

When you have exercised for 30 minutes, the above quote applies, and perhaps there is also a hormone contribution from natural opiates, endorphins, and other chemicals like nitric oxide.
quote:
The endomorphin peptides, endogenous ligands for the mu-opioid receptor, and nociceptin (orphanin FQ; OFQ), an endogenous ligand for the ORL1 receptor, have substantial vasodilator activity. source
For some very good reading on the subject, search for "thermoregulation vasodilation", the corresponding pages give advanced general knowledge of the biology.


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Eye Optics/Emmert's law: Where to place scaled copies of an object so they have identical images on the retina?
I read that the center of projection of the human eye is the entrance pupil. So given a light ray which intersects the objects position and the center of the aperture stop, all copies of said object when placed along that line should cover the exact same position/area on the retina (assuming they are scaled according to their distance).
However, doesn't this ignore the effect of accomodation of the human eye: If the original object is quite near, but a scaled copy along the ray is quite distant, the focal length of the lens is changed and thus a different position and area of the retina is covered.
I tried to visualize this by using the ray simulator at https://ricktu288.github.io/ray-optics/simulator/:

Image A:
Lens focussed on distance of Object A which is projected onto A' on the retina. Object copies B and C are placed at fixed distance either along a ray via the aperture stop (B) or via the center of the lens (C).

Image B:
Lens is focussed on distance of Object B/C which are projected onto B* and C* on the retina. Both are in focus (difficult to see in the picture), but B* is further away from A' than C*. Object B would appear larger than Object C.

So I guess this boils down to the question:
Given the position P of an object A and a lens system, what is the point Q which creates a ray PQ so that all scaled copies of A (A', A'', ...) at different distances along that PQ ray appear at the same position and area on the image created via the lens system.
Is there such a point Q? Is it the center of the lens (i.e. is C* == A') or one of its nodal points?
I am thankful for any pointer to help me understand this!

I suppose that you need to use the thin lens equation (https://en.wikipedia.org/wiki/Lens#Imaging_properties), but with different focal distances. Now, the focal distance is not the same as the distance to the object  - so one needs some data on how the focal distance of an eye adjusts to the distance to the object. You may try asking this question in the physics community.


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Is there an example of a new species through mutation breeding?
Is there a demonstrable species that went through mutation breeding and through successive generations it drifted so far away from its initial parent species that it can't breed with them anymore? (I assume it would need to be able to breed with intermediate generations though). Also by "demonstrable" I mean a case where we can directly demonstrate this process by starting from a parent species to a new species and not establish this relationship by looking back (like observing the connection between corn and teosinte through genetic information).
Edit: I'm mainly curious about postmating/post- zygotic reproductive isolation. As I understand, the timescale of us is not enough to observe that kind of speciation (we can either directly observe the start of the isolation or the end of it but not both), that's why I'm curious about whether induced mutation could speed up the process enough to directly demonstrate speciation by the most difficult to achieve definition.
I have checked the thread Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? but it seems to me that those results only shows premating isolation.
I have checked: Sexual and postmating reproductive isolation between allopatric Drosophila montana populations suggest speciation potential article which says, that postmating barriers observed may be due to postcopulatory-prezygotic mechanisms.
Thank you for the corrections, Im reading into Examples of creating a new animal species by humans

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There are also many other related questions on this site this one includes links to extensive documentation of such events.

Definition of species by the criteria of not being able to breed is problematic: e.g., some breeds of dogs cannot breed, due to the differences in their sizes, yet they are the sale species, as could be dhown by artificial fertilization.
Now, if we take any two closely related species and trace their genealogy deep in the past, we run into the same ambiguity: it turns out that at some point they could breed, and their separation into two dustinct species unable to breed was a process that lasted hundreds of thousands ir millions of years.
This brings us to another point: the characteristic evolutionary times for most animals are too long, compared to the existence of our civilization, for dustinc species to appear
This may not be true for faster evolving organisms, such as viruses or bacteria - e.g., HIV had diverged from SIV about hundred years ago. However we cannot define them as different species, except by saying that the dissimilarity if their genetic sequences exceeds certain threshold.


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What plants are these

These are aquatic plants. Anyone knows the name please? Well. For a week more and most of them stems rotted. So, wondering if its planted by submerged in the soil or what.

I notice you've neon tetras indicating a tropical temperature, are the plants especially meant for that or just any random plants?

i have no idea either since the seller just gave random plants different than what I ordered. I wanna know how to care for these.

Take these with a grain of salt, as it is quite difficult to tell from a single, far-away, picture, and I am no expert on aquaria or aquarium plants.
The narrow-leaved (lanceolate) one appears to be Pogostemon, possibly the species * stellatus*, though I think this should (under optimal conditions) have red stems and upper leaves. This seems to have strict requirements for growth of added CO2 and intense light.
I found a site Tropica.com (I have no affiliation with, nor is this an endorsement of, the company) that sells a lot of aquarium plants and has good listings of the conditions needed for growth, along with pictures and descriptions, so it might be worth a browse through there to see if something fits better.
The second, broad-leaved with toothed margins, plant might be Erythranthe guttata (Monkey Musk), which is a common (sometimes invasive) plant of stream margins, but I don't know how well it will grow fully submerged. It will certainly tolerate short submergings (a few days), but as an aquarium plant??


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Is it incorrect to assume alveoli as spherical and distinct, especially when analysing lung inflation/deflation?
I have recently read the paper "Laplace’s Law and the Alveolus: A Misconception of Anatomy and a Misapplication of Physics". To summarise it, here is a section from its abstract:

The typical representation of the acinus as a “bunch of grapes”
bears no resemblance to its real anatomy; the alveoli are not independent little
balloons. Because of the prevalence of this misconception, Laplace’s law, as it
applies to spheres, has been invoked as a mechanical model for the forces of
alveolar inflation and as an explanation for the necessity of pulmonary surfactant
in the alveolus. . . . Alveoli do not readily
collapse into one another because they are suspended in a matrix of connective
tissue “cables” and share common, often perforated walls, so there can be no
pressure differential across them. Surfactant has important functions along planar
surfaces of the alveolar wall and in mitigating the forces that tend to close the
small airways. Laplace’s law as it applies to cylinders is an important feature of the
mechanics of airway collapse, but the law as it applies to spheres is not relevant
to the individual alveolus.

This paper made many claims that I want to investigate. I have tried reading other papers to make sense of them and it appears fully understanding the lung is still a difficult problem in physiology.
Please could you help me verify if any of the statements put forwards by the paper and listed below are true:

The lung's acini should not be thought of as "bunches of grapes". They are instead much more polyhedral. The interalveolar septa contain numerous interalveolar pores that, although some may contain fluid, can equalize the pressures in the lung and allow ventilation of alveoli with blocked airways. So it is more accurate to think of the lung alveoli as a foam or sponge.

The application of Laplace's law is then flawed in the traditional analysis of a smaller alveoli connected to a larger alveoli (see the image below for the traditional analysis). The alveoli are not spherical nor can they ever attain unequal pressures due to their interalveolar pores. It is instead the tensile properties of the lung parenchyma that keeps alveoli from collapsing, instead of the variable surface tension generated by surfactant.

These 2 points the author makes seem to be very fundamental, yet overlooked in the usual teaching of lung physiology, which is why I want to verify whether they are true or not. Additionally I have read a paper that states "In a healthy lung macro- and micromechanical properties
are dominated by surface tension at the alveolar air–liquid interface at low lung volumes while at larger lung volumes extracellular matrix components become stress bearing and define lung structure and mechanics (Bachofen et al. 1987; Wilson and Bachofen 1982; Bachofen and Schürch 2001)". This seems to state that surface tension of alveoli is in fact more important than lung parenchyma when considering lung collapse, contrary to the paper above.

Not quite getting your point. Applying  Laplace's law, the effect of surfactant should be relevant much more in smallest alveoli than in larger ones or "tubes"? Then, your question asks if alveoli are  interconnected - hence share same pressure, hence same effect of surfactant -  or,  are you assuming this to be a proven fact? If it'd be true ("to think of"...) - the role of surfactant seems over- or underestimated (that''s what your queston is "up to"  that kind of result would interest me.)?

The paper refutes the traditional idea of surfactant playing the major role in preventing alveoli collapse due to points 1 and 2 I mentioned in my post. I want to know whether points 1 and 2 are actually valid, as this conflicts with what I've been taught about lung physiology. Point 3 is just the author's explanation of what actually happens during lung collapse, and how it is only here the author thinks Laplace's law should be used. In hindsight, I should not have mentioned point 3 in my post as it only adds confusion - I will edit it out.

Is the following correct understanding? a. interconnecting alveoli lessens - does not heighten -  air pressure thus enforcing surface tension leading to "collapsing" i.e. tightening of alveoli? Hence, according to the paper, surface tension  is less relevant in spite of "bigger impact in smaller spheres.  What is confusing with point 3 and "hindsight", you say?`To me, biggest caveat, paradox is "drum role" of surfactant. If surface tension is heightend by "spooness", then surfactant becomes more, not less, important, correct?

It appears we are not doing a very good job of understanding each other - I apologise if I have been unclear. I am not putting forth any new ideas, I am just summarising what is in the paper. If you cannot understand my summary of the paper, please read the paper instead. If you do fully comprehend the paper and can comment on the paper's validity, then that is great - I would be very happy if you could post an answer explaining whether you think the paper is valid or not.

I read the paper, and "all this" I hereby  recommend to anyone into biology of the  lung.Your very question  reflects the gist of the paper: alveoli being interconnected contrary to common textbooks. Do I think if the paper is "valid"? No empirical knowledge - contrary to the author who apparently "on his own" has done autopsies and thought about it.If the answer is "no" to your question I'd find that valid! However, if you'd extend your question into the messing and mixing up in conclusions to be drawn from the empirical findings of the author that would make me want to answer.

I'm a newbie myself. Guess you should add some reference for the standard knowlege (alveoli are spheres) the author citicizes, and, second, add some searches you have done on any other authors confirming the .author's findings. P.S. You are right about you not having brought  up new ideas. Me neither, just conclusions right or wrong.


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Why are adenoviral vector vaccines safe in terms of insertion mutagenesis due to genome integration and E4 region's proteins effects?
Disclaimer: I'm neither a genetics professional nor an anti-vax fanatic, I just tried to compare COVID-19 vaccine types currently available on the market and got some questions that I'd like to answer rationally.
Some of the vaccines that are being actively used now are based on adenoviral vectors, such as ChAdOx1, Ad26, or Ad5. These vectors are replication-defective, usually due to removed E1/E3 regions.
I looked for existing information about adenoviral vectors and found some facts that may relate to safety, but I can't conclude if they are rational or not for vaccine applications, since most studies are made for gene therapy or animal models.
Proteins activity
Wild-type adenoviruses are considered to be able to lead to tumors in rodents (Wiki: DNA oncoviruses), mostly due to E1 region activity, but E4 also adds to its oncogenic effect
(Cell transformation by the adenovirus oncogenes E1 and E4), and may affect DSB repair (Expression of the adenovirus E4 34k oncoprotein inhibits repair of double-strand breaks). That may be related to the “hit-and-run” mutagenesis theory.
For Ad9, E4 alone can show that effect, E1 is dispensable (Adenovirus type 9 E4 open reading frame 1 encodes a transforming protein required for the production of mammary tumors in rats)
Genome integration
It's thought that adenoviruses do not integrate into the host genome, since they don't have a tool for that, but occasionally it happens with low probability (10^-3 .. 10^-7 per cell), particularly in cells where the virus can't replicate and lysis doesn't happen, which is always the case for replication-defective vectors (Chromosomal Integration of Adenoviral Vector DNA In Vivo, Frequency and Stability of Chromosomal Integration of Adenovirus Vectors, Insertion vectors for gene therapy, Illegitimate DNA integration in mammalian cells, Viral Vectors: The Road to Reducing Genotoxicity, Viral Epigenetics).
That raises questions about the possibility of insertional mutagenesis. As I see, such questions are often discussed in the context of DNA vaccines, but extremely rarely for adenoviral vectors which also deliver DNA into cells.
Finally, the question itself:
Should risks of insertional mutagenesis due to viral genome integration and E4 region's proteins activity be considered and discussed or they are not important / do not exists at all for adenoviral vector vaccines? Have I missed any studies about these topics?
Can these risks be estimated in numbers and compared with similar natural events?

This question envisages putative harmful changes arising in host tissue cells infected with the replication-defective virus of a 'vectored' vaccine.
The scenarios of the question leave out of account a significant factor that opposes such putative harms. That is, one of the main purposes and effects of such vectored virus vaccines, which is to produce an adaptive cytotoxic T-cell immune response, targeted on (cell-surface-displayable fragments of) the viral gene-products (i.e. proteins) foreign to the tissues of the vaccinated host.
The aim of stimulating cytotoxic T-cell responses from vaccination is especially important against pathogens such as viruses (or intracellular parasites such as malaria) that disappear into the interior of cells of the host, and thereby become 'invisible' to circulating antibodies of the host immune system. This makes the antibody part of the response less useful against such pathogens.
Once such cytotoxic T-cells have been developed, they circulate and can detect and kill host tissue cells displaying fragments of those 'foreign' proteins on which the T-cells are targeted.
All of the host tissue cells infected by the vaccine virus are in this targeted category, and the consequence is that those infected host tissue cells have only a short life. They also are generally somatic cells with little cell-division, e.g. where the vaccine is given intramuscularly. Also, the replication-defect of the vaccine virus means that the vaccine-virus-infected cells are number-limited by the number of infectious units in the vaccine dose, there is no production of fresh generations of virus particles.
These factors and the processes of the cytotoxic immune response altogether oppose any likelihood of the putative harms envisaged by the question.  The cited prototypes of those harms appear not to be reported in respect of situations that arise after vaccination with vectored virus vaccines.
(Supporting background can be found described and explained in the various editions of Janeway's 'Immunobiology'.  The original author died in 2003, but the later editions have been retitled "Janeway's Immunobiology", in memoriam, to mark his founding contributions, e.g. the 9th edition (2017) is from authors/editors K Murphy & C Weaver.)

Do you know of any - other -  empirical studies trying to find DNA integrated into cell genome?

@Peter Bernhard - not sure what you're seeking here. The cells infected with the vaccine DNA/RNA (depending on the type of the vaccine) express a foreign antigen, evoking a cell-mediated immune response  that among other effects targets them for cell killing. Not clear where you think a search for something could be directed.


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Question about : RNA interference - small-interference RNA AND about Rab-protein in vesicles
First Question :
RNA interference - small-interference RNA
in the textbook -Essential cell biology By Bruce Alberts, Dennis Bray, Karen Hopkin
this Figure is Shown

my question is : if the foreign RNA is double stranded and the Dicer Cleaves it so it is still double stranded and Risc Forming with single stranded RNA ,i feel there is step missing here ? and how siRNA is finding those complementary RNA when they are in the cell in double-strand ? steps are missing or it is not essential or i myself miss somthing ?
Thank You

Welcome to SE Biology. Please finish reading the [Tour]. Note that you should only ask one question at a time. This is two quite distinct questions and needs to be split in half, deleted, and reposted. The second thing is that questions should be about specific problems in biology, rather than a help service for interpreting textbook diagrams. So you need to focus on the point at issue — Where does GTP hydrolysis take place in  *nameofprocess" — and then show that you have checked another text (NCBI Bookshelf has the other Cell Biology book — Lodish) to try to solve the problem.

@cisco_guy if you are still looking for resources, Wikipedia has a similar diagram outlining the formation of the RISC complex, with a step showing the degrading of the passenger strand. I recommend you read the rest of the Wiki and its references


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How do gene locations change during crossing over events?
Suppose you have two variants from the same species, which have slightly different chromosomes I's to each other. Genes may be in slightly different positions on the chromosome, and the lengths of the chromosomes might be somewhat different. Suppose these are crossed to produce offspring. If a crossing over event occurs in the offspring during meiosis, what happens to the positions of the genes?
A concrete example of what I'm asking is the following. Suppose that in the above scenario, the first chromatid is 1Mb long and the second is 1.05Mb long. "Gene A" occurs between 6kb-8kb on the first chromatid and 10kb-12kb on the second. If the crossing over occurs and replaces the first 9kb on the first chromatid, what happens to gene A there? Does it cease to exist? Or does the crossing-over process somehow know to grab DNA from above 12kb from the second chromatid?

Are we talking purely about the natural process here, or also about the artificial? In the latter, making cuts and realignments is possible.

Jabath, can you please add some reference?
(Interesting subject, I thought horse and donkey wouldn't have any off spring "any way".)

It depends on the regions of sequence homology between the two chromosomes. Crossing over occurs through pairing of homologous regions. If there's a substantial stretch of chromosome without a matching homologous region on its pair, that non-homologous region should loop out and not be involved in crossing over. Crossovers will occur only in paired homologous regions.
For example, if you have a chromosome I and I' as follows:
I   ABCDEFG
I'  ACDEHFGM
They should pair as:

A-(A)
B
C-(C)
D-(D)
E-(E)
(H)
F-(F)
G-(G)
(M)

Crossovers should not happen in the B, H, or M regions lacking homology with the other chromsome. Crossovers in a homologous region will just result in a new chromosome containing the left end of one crossover partner and the right end of the other.
Using I and I' above, a crossover in region E would produce either:
ABCDEHFGM or ACDEFG
Now, if you have repeated regions of homology in one or both chromosomes, or regions inverted on one chromosome vs. the other, pairing possibilities expand rapidly and all kinds of weird things can happen (and do in real life).

Please add some basic reference.
For instance, Wikipedia, Crossing-over, would not do.
"I'd go ahead" as form of addressing made me delete my comment above

"Molecular Biology of the Cell" by Alberts etc is a classic. I'm not sure of the best free/online into, maybe Khan Academy? That's why I suggest that you post a new question asking for the type of introduction you are looking for (with the usual evidence that you have done some searching on your own first).

Just to let you know, what I found was "As in mitosis, the sister chromatids in each pair are tightly connected along their entire lengths, as well as at their centromeres, by proteins called cohesins." Any pairing seems to lead to one single exchange, no more.

If a crossing over event occurs in the offspring during meiosis, what
happens to the positions of the genes?

Most of the time, things do not line up right, so the gametes do not contain the full information needed to make a complete organism, which is why when species are able to cross breed, usually the hybrids are sterile.

I've made a small edit to my post, but I actually meant to write that the variants are from the same species. In that case, is there a mechanism to make things line up?

Can you elaborate on "line up". Is there some adherence without exchange of DNS. Do homologous positions serve as point of adherence in any way (cp. answer by Armand: there is looping out). See also:    "Does crossing over happen in mitosis? It was a surprise for geneticists to discover that crossing-over can also occur at mitosis. Presumably it must take place when homologous chromosomal segments are accidentally paired in asexual cells such as body cells." (source: shortinformer, Emma Jonson). Maybe this is some other form of the foregoing comment.


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Do some vascular tissue cells have chloroplast?
Vascular tissue includes xylem, phloem, parenchyma, and cambium cells. Does photosynthesis occur in some vascular tissue cells? Do some of them have chloroplast?
Vascular tissues are made up of xylem and phloem, each of which are complex tissues (having more than one cell type). So some of their parenchyma cells may have chloroplasts.
The bundle-sheath cells are the photosynthetic cells arranged into a tightly packed sheath around the vein of a leaf. It forms a protective covering on leaf vein, and consist of one or more cell layers, usually parenchyma.
I am not sure whether these two "parenchyma"s are the same or not.
Are the bundle sheath cells vascular tissue cells?

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

@MattDMo ok, I added something :)


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Is this some form of cabbage?
I would appreciate if someone could identify this plant. It's tall, but not very difficult to pull from the ground, and it has yellow flowers in large groups. I was told it's not mustard. Is it wild cabbage, and if so, what variety?
Location: western Illinois, in a garden.
Season: it's late April, and their roots are now rotting.
Height: I think they were around 3 feet.

More pictures:

Welcome to Biology.SE! Please [edit] in size information (e.g. how tall) and if possible add closeup pictures of flowers from both the front, top, and side. It would be great if you could also include pictures of dissected flowers — i.e. cut up using a razor blade and spread out on a dark background. Without being able to see details of the flower structure I wouldn't try to narrow this down to a family let alone a species! However, it does look like it could be in the mustard family ...

@tyersome Hi, thank you! I will update it soon

The Brassicaceae family (of which cabbage and mustard are members) has a characteristic pattern of flowers - each flower has four equal sized petals, arranged in a cross-shape hence their other name - crucifers.

[h/t wikimedia commons]

It's not easy to see from your photos whether this is true, but I'm going to say, yes, it does look like a member of the Brassicaceae family. The cross-shape of the petals would confirm this.
I don't think these plants are native to Illinois, and it also does look somewhat like a crop plant, rather than a weed, so maybe it is an escape from a farm/garden. It could be canola, possibly.
Wild cabbages are native to the Mediterranean and Atlantic coasts of Europe , so it is probably not a wild cabbage, unless someone planted it in Illinois.

Thank you! This is helpful. The flowers are definitely cross shaped. I'm wondering what to call this plant. Is it canola? And yes I found it in a garden, in an urban area.

@JonathanMoore is correct, this is indeed a Brassica species. The brassica family (Brassicaceae) is a quite diverse family with something like 370 genera and 4000 species. They are found world-wide (apart from Antarctica, although Tryggve Gran tried mostly unsuccessfully to grow Sea Kale during the Terra Nova Expedition to the South Pole). You likely walk past several different types of Brassicaceae every day without knowing that they are there as they are common weeds of untended areas and will take advantage of small cracks in footpaths/pavement to grow.
There are a number of species that are common garden weeds throughout the world. They include many varieties of the Brassica rapa species (known for bok choi, Napa cabbage, choi sum and turnips amongst others, and is known for the oil "canola/colza").
In particular there is one variety called field mustard (Brassica rapa var. rapa, AKA common mustard, wild mustard, wild rutabaga, rape mustard) that is very commonly spread among gardens by its abundant seeding.
It has the long narrow leaves and the clusters of bright yellow flowers characteristic of the Brassica rapa group. However, the Brassica species commonly cross-pollinate and produce mixed varieties, so it is quite difficult to pin down exactly which one you have.


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Is sonic hedgehog a gene or a protein or both?
Is sonic hedgehog a gene or a protein or both?
I think sonic hedgehog is okay as a name for a chemical.
Having said that, I am a little bit concerned about the way sonic hedgehog seems to mean the protein and the gene that codes for it, which is likely to cause confusion.
"Sonic hedgehog is a protein encoded for by the SHH gene." says en.wikipedia.org/wiki/… which later says: "Two of these genes—i.e., desert hedgehog and Indian hedgehog—were named for species of hedgehogs, while sonic hedgehog was named after Sonic the Hedgehog, the protagonist character of the eponymous video game franchise. The gene was named as such by Robert Riddle, who was a postdoctoral fellow at the Tabin Lab, after his wife Betsy Wilder came home with a gaming magazine containing an advert for the Sonic the Hedgehog video game"
The New York Times: "A Gene Named Sonic". The New York Times. 1994-01-11.

SHH gene stands for Sonic Hedgehog Signaling Molecule. This gene "codes" for the protein Sonic hedgehog protein. Normally genes and the proteins they code for have similar names. It can be confusing if you only use the abbreviation.
https://www.genecards.org/cgi-bin/carddisp.pl?gene=SHH#:~:text=SHH%20(Sonic%20Hedgehog%20Signaling%20Molecule,Solitary%20Median%20Maxillary%20Central%20Incisor.
BTW: I am unsure why people downvote your question. It's totally valid. Don't get demotivated because some people think they are too smart.

Your confusion is warranted! The formatting rules for gene and protein nomenclature differ between model organisms. Even within a species, naming conventions may be inconsistently applied across the literature.
In Homo sapiens, the sonic hedgehog gene SHH (note italicization) encodes the sonic hedgehog protein SHH (or Shh protein, as on Uniprot). Human gene nomenclature is standardized by the HGNC.
As in humans, Drosophila gene and protein names are distinguished by different italicization; per FlyBase:

Protein product names and symbols should not be italicized in printed text. Where feasible, proteins that are named for the gene should be further distinguished by capitalizing the initial letter of the gene symbol or name. For example, the protein product(s) of the hh (hedgehog) gene could be correctly denoted as Hh or Hedgehog; the protein product(s) of the RpL38 (Ribosomal protein L38) gene could be correctly denoted as RpL38 or Ribosomal protein L38; and the the protein product(s) of the AGO1 (Argonaute-1) gene could be correctly denoted as AGO1 or Argonaute-1.

I’m partial to the naming conventions in Saccharomyces, where gene encodes PROTEIN (e.g. mpk1 and MPK1).
For both eukaryotic and prokaryotic microorganisms, the ASM Molecular and Cellular Biology submission guide for authors is a good resource for genetic nomenclature conventions.

Thanks for saying my confusion is warranted. But your answer doesn't mention 'sonic hedgehog'.

I've updated my answer to clarify that the human sonic hedgehog gene symbol is SHH, and the human sonic hedgehog protein symbol is SHH. Indeed, both the gene and the protein are named "sonic hedgehog".

So a hedgehog is a gene and a Hedgehog is a protein?

The first line on Wikipedia states "Sonic hedgehog is a protein encoded for by the SHH gene." Which part of it do you have trouble with? I'm genuinely curious.

@SPr The trouble is that this is only one opinion, that is contradicted by the NYT. Also, why is it 'hedgehog' and not 'Hedgehog' as stated by FlyBase?


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How fast is dopamine released in the brain?
Dopamine is released when one anticipates a pleasurable event says https://www.psywww.com/intropsych/ch09-motivation/pleasure-and-pain.html.
"People with more sensitivity to ritalin rated higher on Depue's positive emotionality index. "When our dopamine system is activated, we are more positive, excited and eager to go after goals or rewards, such as food, sex, money, education or professional achievements," according to Depue (Lang, 1996)/
Dopamine is associated with anticipation of sex, drugs, drinking, getting money, winning competitions, and religious worship. Religious worship? Yes, Previc (2006) summarizes the relevant research showing "dopaminergic activation as the leading neurochemical feature associated with religious activity." Dopamine is apparently a marker for the purusit [sic] of enjoyment of any type."
Is it released instantly like adrenaline, or more slowly?

Dopamine is a neurotransmitter and released from synaptic ends via transporters. Such a release happens within milliseconds; the time present Dopamin needs to move some tens of nanometers.
Adrenalin is a hormone produced by the adrenal gland, which needs to distribute through your body. This is several orders of magnitudes slower.

Within milliseconds of what exactly. I was thinking of the start time being the time a person decides to go to a bar and drink some alcohol, or to be more objective, the time someone hears a friend says, "What about going to bar now?". Also, does dopamine come with a recognizable sensation, like adrenaline or endorphin?

I am referring to the speed of release: The time the neural end needs to release Dopamine after receiving the electric signal. It seems you are interested in control of Dopamine synthesis/degradation. Unfortunately, I can't confidently answer such a question. Maybe edit your question and someone will answer it in this regard.

"control of dopamine synthesis and degradation" seems like a promising search string for me. Is it that a certain type on neural end (which I take to mean the first half of a synapse) always uses dopamine as a neurotransmitter to trigger the second half, and then the residue of dopamine then drifts around the brain modifying how other synapses behave in such a way that the brain becomes more pleasure seeking? Or does work some other way? Or has this not yet been worked out by science?


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Why do animals with more mass tend to have brains with so much more mass when it seems like a similar mass brain should be able to do the job?
Why does a wolf have a brain so much bigger than that of a poodle, when a poodle's brain is big enough to do the job, I would have thought. Likewise, if tigers are not smarter than house cats, why do they have brains that are so much bigger? Brain tissue is metabolically expensive, and so you'd think there would be a strong selection pressure to have the smallest brain that could do the job.
I'm familiar with the idea that a large body needs a large brain to control it, but I've never understood why that should be the case. And since poodles are modified wolves, it should be easy for wolves to quickly evolve poodle brains in nature. Has anyone tried to create a large breed of dog with a small brain, to see whether it's possible, and what problems if any the animal has in controlling it's body, for example?
So my question is: Why do animals with more mass tend to have brains with so much more mass when it seems like a similar mass brain should be able to do the job?

"Why are animal brains so often so big and therefore metabolically expensive?" I don't think you have the best wording here. I think what you are asking is why do animals with more mass tend to have brains with more mass when it seems like a smaller brain should be able to do the job. Because typically when people say "large brains" they are referring to brain-body mass ratio and in this sense, animal brains are often not very big.

@DKNguyen I agree with your comment and have edited the question accordingly. Thanks.

I have to challenge you here on size of wolf and poodle brains. How well do you think a pack of poodles would do at hunting and tracking elk? Communication (social skills), working together, solving puzzles, self-sacrifice (a wolf female will nurse an alpha female's pups when the alpha needs to hunt - like during very lean times - to the point of her own starvation), these survival-of-the-pack tasks require brainpower! Poodles are smart, but they need people to solve their problems. That, and doggie eyebrows so they can beg effectively.

@anongoodnurse: But this raises a question.  Is the OP comparing wolf brains to toy poodle brains, or to standard poodle brains?  Per Google, a grey wolf brain weighs about 119.5 g, that of a standard poodle 92.5, and a toy poodle 59.1 g.  So there's a greater percentage difference between the two poodles, than between the standard poodle and the wolf.  The wolf typically weighs a good bit more than the standard poodle, too, so the ratio of brain mass to body mass is about the same, or maybe ever higher, for the standard poodle.

@jamesqf - Those are good questions, but the OP doesn't really elaborate. I'm only pointing out that you can't expect a wolf to operate with the brain of a poodle; they are not equal in nature. My guess would be that brain tissue samples of wolves and poodles would show some interesting differences.

The search term for these studies is "brain body size scaling" if you type in "brain body size" you end up with ratio studies. https://pubmed.ncbi.nlm.nih.gov/14673198/ https://www.frontiersin.org/articles/10.3389/fnana.2014.00077/full#B23

@DKNguyen The pubmed article you linked to makes sense to me. Just because energy is plentiful, that doesn't mean you should waste it. There's less selection pressure for a small brain that can do the same job just as well, but there is still pressure. Depressing that it says, "Brain size scales with body size across large groups of animals, but exactly why this should be the case has not been resolved." It's amazing the things that are still mysterious in biology. I think both sexual reproduction and sleep are still unexplained. Also homosexuality in humans.

@anongoodnurse Do you have any evidence that wolves are smarter than poodles?

Poodles are smart animals; so are wolves. They are different, and you seem to think that a poodle's brain is adequate for a wolf. It's not. Surviving in the wild takes a certain kind of intelligence that domesticated dogs don't possess; they lost it through domestication (and picked up eyebrows, curly tails, floppy ears, etc.) The majority of dogs on their own die quickly (yes, some wild dog packs do well for a while.) Release 20 poodles into the wild; they will not hunt and bring down an elk.

@anongoodnurse Is that a fair comparison though? What if the poodles were raised by wolves? Poodles were bred as hunting dogs after all.

@DKNguyen - I don't know that anyone has been unkind enough to try that. First, the wolves would eat the dogs. Second, domestication for over 30K years has taken the aggression needed to hunt out of dogs, and given them appealing eyes and eyebrows so they can enchant us. Third, poodles' jaws can't crack bones as well as wolves' jaws. Fourth, if poodle pups were substituted for wolf pups and accepted by a female grieving the loss of her pups, wolf cubs mature more quickly, which matters for survival. Etc., etc. Personally, I believe they could not learn to be wolf-like.

I think that you can find a good answer to your question in a more careful evaluation of the hypothetical that you pose:

since poodles are modified wolves, it should be easy for wolves to quickly evolve poodle brains in nature.

How easy is it, actually, for a wolf to evolve into a poodle vs. evolving only the wolf's brain into a poodle's brain?
The answer can be found in the science of evolutionary developmental biology (evo-devo), a good popular introduction to which can be found in the book Endless Forms Most Beautiful.
In general, evolution of scale and morphology operates by controlling the differentiation of tissues in the early development of a body-plan via Hox genes and other related regulatory elements. When understanding their effects on an organism as a whole, in many cases, each such gene can be thought of as a variable that shifts or distorts a body coordinate system. The more fundamental such a gene is to the body plan, the more widespread its effects will be and with a greater degree of side effects. This means that sometimes it's actually much easier to select for a large complex of linked changes than for a single specific change.
In fact, it turns out that for many animals the overall scale is one of the easiest variables to control! Consider, after all, how much you yourself changed in scale during your own growth from birth to adulthood, while maintaining viability and system integration the whole time. Many animals can thus readily become bigger by running the growth program more or smaller by running it less, and these scale changes are often also associated with neoteny. It is, in fact, pretty easy to turn a wolf into a chihuahua, and a chihuahua is pretty close to a wolf pup.
To change only the brain of the mature animal, however, is actually harder, requiring a more specific selection signal. Brains appear to have gotten bigger with respect to body under selection pressure that led to novel architectural features giving specific highly-competitive capabilities. Selection pressure for a small brain, however, would likely be about metabolic burden instead, and there are a lot of potential strategies for reducing metabolic burden, at the same time that many of the variables affecting brain size are likely to be entangled with other critical features as well, such as the jaw.
Bottom line: it's evolutionarily a lot harder to shrink just the brain than to shrink the whole animal.

'Evolutionarily harder' would be an explanation if small-bodied-small-brained wolves had the same ecologic niche as big-bodied-small-brained wolves. Then the 'hardness' would come into play. But that is not the case

@bukwyrm The point is about the ability to follow moving constraints with regards to a niche.

https://www.frontiersin.org/articles/10.3389/fnana.2014.00077/full#B23

@bukwyrm: While I don't know their brain sizes, coyotes are basically smaller wolves - close enough that they interbreed to create the coywolf.  Then there's the even smaller fox.

@DKNguyen Was that link posted in support or in opposition to my answer? From my read, it is consistent.

@jakebeal Indeed.

@DKNguyen That paper  you linked to ( https://www.frontiersin.org/articles/10.3389/fnana.2014.00077/full#B23 ) seems to use way more jargon than necessary. I find it very hard to understand, not because the concepts are hard, but just because of the way it is written. Even with instant look up of words with Google, I can't read it, which I suspect the authors are glad about.

@MatthewChristopherBartsh Yeah, I did a lot of filtering when reading it.

What is it that this paper says, that you think supports your evo-devo-inspired answer? They go into the nitty gritty of neurons/g in different clades of mammal, but it is neurons/g brain matter (of different locations in the brain) not /g animal mass. Additionally they explicitly say that there is much more going on than simple whole-brain scaling - so what gives?

@bukwyrm I do not claim it as a direct support (note that it is not in my citatations), only that its findings (high consistency across scale within a clade, differences linked to anatomical differences between clades) are consistent with the same evo-devo model that leads to my answer.

Well, it's worth noting that the number of neurons doesn't scale linearly with the brain size; in particular for two dogs analyzed by Herculano-Houzel et al. (2017), the number of neurons in the cortex scaled the least:

Both dog individuals examined (a 7.45 kg mixed-breed and a 32 kg golden retriever) had larger brains than the cat (brain mass in dogs, 58.4 and 114.5 g, respectively; cat, 34.8 g), and also more brain neurons than the cat (dogs, 1.8 and 2.6 billion neurons, respectively; cat, 1.2 billion neurons). The same applies to the cerebral cortex of the dogs, at 46.2 g with 429 million neurons and 84.8 g with 623 million neurons, against 24.2 g with 250 million neurons in the cat. Strikingly, although the cerebral cortex of the golden retriever was almost twice as large as the cortex of the smaller dog, it only had 46% more neurons than the smaller dog cortex (as expected from the non-linear scaling of cortical mass with number of cortical neurons [of carnivora in general]);

And the authors of this paper also write that this unsurprising because cortex neurons are apparently the most expensive to scale up in numbers:

We have previously shown that the metabolic cost of the brain is proportional to its number of neurons, regardless of brain size, and that neurons in the cerebral cortex cost on average 10 times as much energy as neurons in the cerebellum (Herculano-Houzel, 2011). Thus, cerebral cortical neurons are expected to be both more vulnerable to caloric shortage than other brain neurons, and to also contribute more to decreasing total metabolic cost when their numbers are reduced than the loss of other neuronal populations would.

And seemingly being a bigger carnivore with somewhat more cortex neurons might actually make one a little bit smarter. The paper notes in support of that that:

Cognitive performance in carnivorans was recently addressed specifically by Benson-Amram et al. (2015). Across these species, even though brain size relative to body mass is a significant predictor of success in opening a puzzle box, species with larger absolute brain volumes also tended to be better than others at opening the puzzle box (Benson-Amram et al., 2015).

(This paper might have been somewhat sensitive to the method used for testing, like the scaling of the box. It actually found that [unsurprisingly to me] bears were champions at opening boxes... but Herculano-Houzel's paper actually found that bears don't have that many cortex neurons... "the brown bear has [...] 251 million [cortex] neurons, which is only about as many as the house cat, even though the brown bear cortex had a nearly 10-fold larger mass". So something doesn't quite click here.)
Anyway, your hypothesis that a cat and a lion (or actually a bear) have the exact same cognitive abilities might not be correct, when generalized. (Lions have as many cortex neurons as dogs, on average, 500 million, according to Herculano-Houzel.)
There is also a 2019 paper by Horschler et al. on dogs specifically that finds something similar based on more data on dogs:

Using citizen science data on more than 7000 purebred dogs from 74 breeds, and controlling for genetic relatedness between breeds, we identify strong relationships between estimated absolute brain weight and breed differences in cognition. Specifically, larger-brained breeds performed significantly better on measures of short-term memory and self-control. However, the relationships between estimated brain weight and other cognitive measures varied widely, supporting domain-specific accounts of cognitive evolution.

I haven't looked at their methods section yet.

"We have previously shown that the metabolic cost of the brain is proportional to its number of neurons, regardless of brain size" - That is a salient first half of an answer- it is not about size, it is about number of neurons, - but the other half, showing why big dogs need so many more neurons (even if it does not scale liearly with mass), is missing


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How much extracellular matrix is there in the human body?
I just found out that there is an extracellular matrix. I had imagined that the tissues, organs, and the whole body was a bone skeleton with cells attached to the bones and to each other. I imagined the cells to be joined directly to each other like atoms in a crystal.
In fact, most of the cells are not adjacent to each other. Rather the cells (except blood cells) sit in a solid matrix that is a mixture of proteins, especially collagen, which is like a plastic or hardened glue or rubber. The matrix is secreted by the cells, and holds them in place and connects them to each other, and separates them from each other. In bone, the extracellular matrix is strong, rigid and hard, while in cartilage it is strong but flexible like some types of rubber or plastic. In the brain it is very soft. The differences in rigidity, strength and hardness come from different mixes and densities of proteins, except in the case of bone which has a lot of calcium compounds (minerals) in the extracellular matrix (as an aside, for the sake of completeness, I'll just mention that some say the blood is a connective tissue, and that blood plasma is the extracellular matrix of the blood).
Finding out (so recently) about the existence of the extracellular matrix, for me has been absolutely amazing, and it has changed how I look at my own body.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995612/ (which has a lot of information about the extracellular matrix including a colorful and impressively detailed giant poster that you can magnify repeatedly) says, "Collagen is the most abundant fibrous protein within the interstitial ECM and constitutes up to 30% of the total protein mass of a multicellular animal. Collagens, which constitute the main structural element of the ECM, provide tensile strength, regulate cell adhesion, support chemotaxis and migration, and direct tissue development (Rozario and DeSimone, 2010)." but doesn't say how humans compare to the multicellular animal with 30% of the total protein mass being collagen, nor what the total mass of that collagen would be.
https://biology-pages.info/E/ECM.html contains the closest to an answer that I've found, though it speaks of 'bulk' and not mass and some multicellular organisms and not humans :"While it is true that all living things are made of cells, that is only part of the story. Most of the cells in multicellular organisms are surrounded by a complex mixture of nonliving material that makes up the extracellular matrix (ECM). In some cases, the ECM accounts for more of the organism's bulk than its cells."
So my question is: How much extracellular matrix is there in the human body? I leave it to you to decide whether blood plasma is extracellular matrix and similar issues. Also it's up to you how you want to quantify the amount, whether by mass (my preference), volume, or some other measure. Also, it's up to you how precise and quantitative (my preference) or approximate or qualitative (that could also be good) your answer is. My aim is to see, in my mind's eye, the human body as it really is.

Here's a rough estimate based on data found in this Nature scientific report :

Muscles (around 40% of our mass) contain around 11% of extracellular matrix proteins in mass.
Connective tissues (around 45% of our mass) contain a variety of values of ECM protein content :
31% (cartilage),
20% (tendon),
30% (bone)
(this is not exhaustive)

So combining these values we could estimate that around 17% of our mass is proteins in extracellular matrix.
If you're not just interested in proteins but anything that isn't cells, so including minerals in bones (85% of 14% of our mass), plasma in blood (45% of 7%), and fat in adipose tissue (90% of 20%) then around 38% of our mass is non-cell stuff.
Note that my values are not precise at all. The studies are based on values in dry tissue, but they took water into account to estimate the percentages for normal tissue. And then I took those numbers to estimate an average on the whole body, but obviously body composition, especially fat, can vary a lot. I also ignored nervous and epithelium tissues because I assumed they didn't influence the results much (and I couldn't decide whether dead cells in skin should be considered as cells or matrix)
Funnily enough, after calculating this I just found a wikipedia article that sums up what I said with a value of 34.3% "extracellular mass" shown in an image. Sadly the cited article does not contain that value, or at least I couldn't find it. It seems unnecessarily precise, but at least that indicates that we're in a reasonable range with 38%.
I hope that gives you the representation you were looking for about what our body "is", at least I came here hoping to find that kind of estimate and since there was no answer yet I tried my best.


text:
Any databases with AAMI ECG and ECHO?
There is no AAMI 12-lead ECG databases available online.
All of them have problems.
I and my friends finally finalised our tests with St Petersburg.
It is not AAMI.
So the next step is to search any ECG databases with some leads (at least lead 2) with ECHO data.
Is there any AAMI standarded ECG databases with ECHO data?
This data need to be from the same patient.

One possibility is PTB Diagnostic ECG database here.
However, its AAMI verification is still under process here.
Some ECHO findings also there.

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Any tips to reduce cell death (from thawed fibroblast cell cultures)?
I have been doing cell culture for about a year now. When I thawed my fibroblast cell line, everything went to plan. When I checked them a day later, they were all dead (<3-5% confluent). I'm not sure what happened since the media is fine, the incubator is fine and I didn't change anything in the protocol. I have used this protocol dozens of times before. Any tips or ideas of what could have happened?
The only things I can think of are a mistake that I didn't realize or an error in the freezing process...
EDIT:
My thaw protocol is the following: add warmed growth media and incubate until cells are thawed. Then transfer into 15mL conical tube followed by 3mL warmed media (used to wash out cryo vial). Centrifuge to pellet cells. Remove supernatant and resuspend pellet in fresh (warm) media. Place in a T25 flask and incubate.
This is all that I have done to the cells.

If you post you thaw protocol and how you treat the cells further, we can possibly help you.


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How can I be more accurate in my cell counting?
For some reason, when I use my hemocytometer, my counts and calculations always come out really small. My equation is: (cell count / # of boxes) * dilution factor * 10,000 = cells/ml. (I usually only count the four corner boxes for my fibroblast cultures).
My calculations usually are less than half of what I expect them to be from the microscope estimations and confluency. I have tried various dilutions and have even vortexed the cell mixtures to ensure even distribution. Are there any suggestions as to what I'm possibly doing wrong?
EDIT: I usually use a dilution factor of 10 and then multiply the end number by the original number of mLs that the sample was taken from.

What do you put into your dilution factor? Diluting the cells from the original culture to get something you can count?

Ok: So you take a sample from your cells, dilute it 1:10 and then add some Trypan Blue?

Without further information it is quite hard to say. However, there are a few things that might be playing into this.

Statistics - For your counts you need to be counting a decent number of cells on each side (and each square) of the hemocytometer. Counting 4 squares is fine, however you need to be counting at least 100 cells over that space (see step 3 in link from Bitesize Bio). This doesn't mean stop counting if you reach 100, finish the square you are in at least and it means 20+ cells per large square. If you are counting fewer cells, your counts will be inaccurate.

Statistics - hemocytometers have about an error of about +/-15% in the hands of an experienced user.

Statistics - Low cell density; this plays into the one above. If you resuspend your cells in too large a volume, it is much harder to take a representative sample of your cells, this means you can't rely on the sample to accurately represent your cell population. This also goes for your subsample and dilution - there's no reason you can't do a 1:1 dilution with trypan blue rather than a 1 in 10.

Settling - cells settle quite fast in all the tubes you use. You must resuspend the cells immediately prior to sampling and immediately prior to loading the hemocytometer. I've documented an example of how fast they settle in my own counting (out of interest, decided to see if there was an effect): If I take up 100 ul of cells in a micropipette (say P-200) and load both sides of a hemocytometer from that same volume (takes me less than 20 s for both sides), there is a consistent ~20% difference between the sides due to settling of the cells in the tip. If I take separate samples, that error goes away.

Cell type - Fibroblasts are large. This means you don't get as many per area as you might see in examples of cell density (e.g. Invitrogen's guide to Useful Numbers for Cell Culture), which plays into 1 and 3 above.

Cell type - Fibroblasts attach quite firmly. This means you need to visually inspect the cells to ensure detachment and look to see that you have successfully harvested the majority (there are always a few left behind). Don't use too large a volume for this as it plays into 1 and 3 again.

Cell handling - if you over detached your cells (i.e trypsin for too long) or scraped your cells off instead of using trypsin (or similar), then the cells will clump. It is very hard to count clumps of cells accurately and even harder to sample them accurately - they settle much faster than single cells.

Cell handling - Making a single cell suspension. You successfully detached your cells, but they have clumped and you didn't make a single cell suspension. As in 7 above, these are very hard to count. You must ensure that the majority of the cells you count are single; you should have <5% clumps.

Incorrect usage - you are counting using the large squares right? That's the ones sub-divided into 16 or 25 smaller squares (see red squares in image by step 3 in Bitesize Bio link) and often surrounded by 2-3 lines (Neubauer hemocytometer). If you were using the small subdivisions, you will be out by a factor of 16, but sampling errors will play a big role in how accurate the counts are.

Part of my work in Molecular Biology was with human fibroblasts. This is a very helpful answer indeed.

Thank you! I think 1-5 are the most likely to be my issue. Would it cause an issue if the cell concentration is "too high"? I was counting FB cells that should have been around 2.1M/mL (which is why I diluted 1:10).

Too high is also possible - more than about 200/large square is getting hard to keep track of in terms of which ones you have counted (that's what the small subdivisions are for), so then you should dilute your cells and reload. However, you can do this quicker and easier than it is for too low and account for it. Lower numbers are more of a problem for accuracy.


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Which three functional groups are found in the general structure of amino acids?
Yes, I know, not two, but THREE.
EDIT: Yes, sorry but I did quite a bit of research, searching my notes and textbook for the answer, but all I could find was TWO functional groups as a opposed to the three my guide said there should be. Trust me, I looked quite a bit and there were many conflicting sources with different answers.

Your original statement of the question is a little bit lazy and lacking in background info. Please reword your question a little bit, and explain more of the background context and your own thinking on the matter, and then I'll update my answer, including the version of it that your professor was probably looking for in the first place.

Amine, alkyl, and carboxylate.

I'd guess the part that you're having trouble on is that the alpha carbon in the center of the generic AA structure is part of an alkyl functional group
Edit
The original answer that I gave might have been too clever for its own good. Depending on how one looks at the question, the third functional group could instead be the functional group of the particular side chain, i.e. for Alanine it would be a methyl group, for Tryptophan it would be an indole group, etc.

Please read our homework policy before answering questions such as this. We should not be giving out free answers to students who have not even done the most rudimentary thinking about their problem. This doesn't help them learn at all. Instead, I would recommend that you leave a comment asking for which groups they've already come up with, wait for an answer, and then ask them to think about the central carbon, and see if they can come up with the answer themselves. Spoon-feeding direct answers is not terribly helpful.

Homework question or no, it seemed interesting enough to merit an answer on this site. Also, having had a couple of hours to think about it the answer I gave is probably wrong, but out of deference to your concerns I won't correct it.

as long as the answer is here, you may as well correct it. I also agree that the question is interesting, all I was trying to say is that ideally, you want to get the OP to think about their problem a little bit. Suggest that they edit their question to describe what they've already tried. Some people are genuinly stuck, and it's fine to help them, but it's best to try and get some more info out of them first.

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