text:
Is heritability just slope?
Is broad-sense heritability just the slope of the line that passes through the coordinates:

(1, The phenotypic correlation among monozygotic twins)
(0.5, The phenotypic correlation among dizygotic twins
[Optionally] (0, The phenotypic correlation among unrelated individuals)?

Here, the X axis is the relatedness (0 for unrelated, 0.5 for dizygotic, and 1 for monozygotic) and the Y axis is the correlation coefficient r. Is this the same as twin-based broad-sense heritability?
(This would also mean you can estimate heritability by taking the slope of the line through only dizygotic siblings, as they don't always share 50/50 of their DNA and there will be some spread in the X dimension.)

Context here is important, slope of what? Wht kind of plot are you looking at.

@John Slope of the line which passes through dizygotic twin correlation and monozygotic twin correlation, where the x-axis is relatedness (0 to 1) and the y-axis is correlation (0 to 1).

typo: bounty should not say "twin A," it should just say "A."

In a population without genetic variation, the slope would be 0 while the offsprings are essential clones. Wording a meaningful definition of what it is, that you are calculating is not so easy. Maybe it would be easier the other way round: You start with a definition of what you want to calculate.

The broad-sense heritability is the ratio of total genetic variance to total phenotypic variance. H2 = VG/VP (as defined here), so no, unless in a very limited sense of one trait with binary values for phenotype.

@bob1 the slope from the axes described in the question would correlate with twin-based heritability very well. This makes it seem to me that we can define heritability by modifying the situation I laid out somewhat.

@KaPy3141 By "relatedness," I mean "genetic relatedness," which is similar to the kinship coefficient.

@bob1 it turns out the original post is exactly what the Falconer's formula says heritability (including for continuous values) is. So heritability is just the slope.

I found this paper, where the "heritability value" was taken as the regression coefficient (slope) between offspring height and parental height. https://doi.org/10.1203/00006450-199810000-00016. However, they also express it as fold-SD (standard deviations) further characterize it by stating the the correlation coefficient (Pearson R).

@KaPy3141 Great! This is very interesting. I have seen a similar paper comparing siblings

The original question's guess happened to be exactly how heritability is defined in the Falconer's formula.
Given genetic relatedness (1 for mz identical twin, 0.5 for dz fraternal twin) on the $x$ axis and twin correlation for the phenotype on the $y$ axis, we can define these two points:
$$\begin{align}
(x_1, y_1) &= (0.5, r_{dz})\\
(x_2, y_2) &= (1, r_{mz})
\end{align}
$$
Then, we can write the line between them in the two-point form:
$$(y - y_1) = \frac{y_2 - y_1}{x_2 - x_1}  (x - x_1)$$
$$(y - r_{dz}) = \frac{r_{mz} - r_{dz}}{1 - 0.5} (x - 0.5)$$
Therefore, the slope is $\frac{r_{mz} - r_{dz}}{1 - 0.5} = 2(r_{mz}-r_{dz})$, which is equal to the broad-sense heritability.

See also the pages leading up to page 185 in INTRODUCTION TO QUANTITATIVE GENETICS by D. S. FALCONER, University of Edinburgh. It seems he arrived at this in a similar way (by looking at genetic relatedness), though he maybe didn't make an explicit connection to slope.


text:
If we were to discover an alien ecosystem that has a D-configuration of proteins, how would it react to our L-sided biology?
I'm concepting a hard-sci-fi story where a scientist discovers microorganisms in our solar system with disastrous results. I was thinking about how any cross-contamination with an alien ecosystem would cause the organism to self-destruct like matter, anit-matter. I'm more inspired by science fiction works like War of the Worlds, The Andromeda Strain, Annihilation, etc., but I'm also interested in explaining how alien life could have evolved with novel-yet-similar mechanisms than life on earth.
Leading me to the whole L-sided vs D-sided amino acids and protein synthesis. So how would the organisms interact with each other? I was thinking all the cells would self-destruct leaving behind traces of organic material and a myriad of novel viruses. Any material, references, or input is always appreciated. Thanks

L- and D- are not matter and anti-matter. Racemic mixtures of enantiomers are common in chemistry here on earth, you don't need to imagine some fictional world. You could consider some particular cases of "wrong-handed" molecules, like https://en.wikipedia.org/wiki/L-Glucose You could also consider that in a fictional story you can do whatever you want, that's why it's fiction, and consider that the interesting parts of science fiction are typically the statements and reflection on the condition of humankind. The rest just helps drive the plot.

Welcome to Biology StackExchange. I think your question might be more suitable for the Worldbuilding StackExchange where you can find plenty of similar "hypothetical" questions.

I think it's important for creative writing to be grounded. Not just in realism, but (since poetry is my passion) also with form. This is also my own opinion about the Fermi Paradox, where life in the universe has no interest in looking for new life because of incompatibility with each other. L- and D- are concepts I'd heard about, so I was curious how a D- evolved ecosystem might interact with our L- evolved ecosystem hypothetically.

One of the reasons I love Isaac Asimov's science fiction is the science is accurate, which made the stories more relatable to me (a science-field major), so kudos for your aim. I can't answer your question as it is, because I don't know what kind of interactions you expect might be disastrous. I don't think they would survive on earth because most of our food sources are made with L-matter, just as we could not survive on theirs. But here's an article that might help you: https://www.smithsonianmag.com/space/must-all-molecules-life-be-left-handed-or-right-handed-180959956/

On the other hand, Ray Bradbury didn't let science hold him back from writing incredible, beautiful, dreamy, nightmarish, metaphorical (you pick, he wrote them all) sci-fi. It's not about the science, it's about the story.

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text:
Does Plasmodium affect the female Anopheles mosquito?
I was studying the life cycle of Plasmodium, and I read that the infectious form (sporozoites) is what causes malaria in humans. I also read that this form resides in the salivary glands of the female Anopheles(carrirer of Plasmodium). My question is that if the sporozoites reside in the salivary glands, do they affect the mosquito itself? Or, in general, do the pathogens attack, or affect the disease vectors in any way?

tl;dr yes, Plasmodium does appear to interact with its mosquito vectors — many species of mosquito have reduced fitness when infected with plasmodia due to the cost of mounting an immune response (this implies that they would lose even more fitness if they didn't mount an immune response ...). However, mosquito species that are frequently infected in the wild appear to have evolved tolerance, so they incur less fitness cost (there is even a positive correlation between infection intensity and fitness in some cases (for not-fully-understood reasons).
From Shaw et al 2022:

Numerous studies using rodent model species have detected a fitness cost of infection to mosquito fecundity [26–29], fertility [27,28], and survival [30], most likely due to the considerable investment by the infected female in immune responses (Box 1). When Anopheles stephensi or An. gambiae were infected with Plasmodium yoelii nigeriensis, there was a reduction in fecundity of 21–41% [26–28], but with no significant correlation between egg numbers and oocyst loads [26,28]. The reduction in fecundity was due to apoptosis of follicular epithelium cells, promoting resorption of ovarian follicles in infected females [31,32]. The density independence between
egg and oocyst numbers suggests an all-or-nothing cost to activation of the mosquito immune system preventing significant egg investment [33,34]. An. stephensi also showed reduced survival when infected with a number of rodent malaria parasite species [26,35–37]. Compared with uninfected controls, mortality rates were significantly higher when mosquitoes were infected
with P. berghei or with P. yoelii nigeriensis, while infections with P. chabaudi reduced median survival (with parasite strain- and experiment-dependent effects).

On the other hand, a meta-analysis on 11 published studies found that in infections involving
P. falciparum and its natural mosquito vectors – An. gambiae, Anopheles funestus, and An. stephensi – no costs to survival were detected [38]. Similarly, in recent studies, An. gambiae and An. stephensi females infected with P. falciparum developed the same number of eggs as
their uninfected sisters [39]. In An. gambiae, an unexpected positive correlation existed between paired egg and oocyst numbers from individual infected mosquitoes, with females that invest more in reproduction supporting higher infection intensities [40].  ...

Shaw, W. Robert, Perrine Marcenac, and Flaminia Catteruccia. “Plasmodium Development in Anopheles: A Tale of Shared Resources.” Trends in Parasitology 38, no. 2 (February 2022): 124–35. https://doi.org/10.1016/j.pt.2021.08.009.

It does not because it causes no structural damage to mosquito in either stage i.e while penetrating into endolymph via gut and also while penetrating the salivary gland since there is complimentary protein ligand (on surface of gut and on surface of salivary gland) which facilitates its entry without causing any harm, on the other hand some research even goes to the extent that it's mutually beneficial since it enhances the smelling capacity of mosquito thus their relationship is advantageous hence sustained in nature over the course of evolution.
https://phys.org/news/2021-11-mosquitoes-mutual-symbiotic-relationship-malaria-causing.html
https://www.pnas.org/doi/10.1073/pnas.241491198

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text:
Bite force of seagulls
I'd like to know whether the biggest seagulls are strong enough to bite off a finger?

There's this news report but I have no idea if it's reliable ...

"Bite Force of Seagulls" sounds like next year's Oscar-contender movie title

This reference states the force needed to fracture a finger was 467 N{1}. The Galapagos finch has a strong beak in the bird world, only 70 N{2}. Most animals that will take your limbs will both have sharp objects and are strong enough to hang on to use body weight to take the limbs. So it is unlikely to be able to rip off your finger, but if you have significant disease and are weak, it might be a good idea to hide your chips.
References:

Hohendorff B, Weidermann C, Pollinger P, Burkhart KJ, Müller LP. Jamming of fingers: an experimental study to determine force and deflection in participants and human cadaver specimens for development of a new bionic test device for validation of power-operated motor vehicle side door windows. Biomed Tech (Berl). 2013 Feb;58(1):39-49. doi: https://doi.org/10.1515/bmt-2012-0004. PMID: 23314498. Deutsche Nationalbibliothek full text pdf link here.

Sakamoto, M., Ruta, M., Venditti, C. (2019); ‘Extreme and rapid bursts of functional adaptations shape bite force in amniotes’; Proceedings B; doi: https://doi.org/10.1098/rspb.2018.1932

The large ground finch is a ~40g bird with a bill adapted for crushing, compared to the largest seagulls (the Great Black-Backed Gull) at ~2kg, with sharp hooked bills. Removing a finger is a different biomechanical process to fracturing a finger (fracturing requires breaking bone; removing can be done by cutting between bones, which can be much easier if you have a sharp cutting edge). I don't think this answer provides details that are relevant to the OP's question.

Lowest force in first reference Table 3 is 291 N (specimen 12, MP, little finger) - still way above 70 N though.

The great mcaw has one of the strongest bites of all birds, similar to a finch except 50 times heavier, they can crack walnuts with difficulty, so they could perhaps get though a kid's finger.

A word of warning. Ornithologically, cats and humans kill 1.3 billion wild birds indirectly, and 20 billion poultry. A seagull related heart attack happens every 20 years.
this is a bite on a 1-year-old's finger, but from the news article, you would think she nearly died:

They can slice open a finger using the hook of their bill to snatch, there are 1-2 attacks per year in the UK. They have been know to attack pets.
A seagull attack can cause someone to fall off a pier or jump into the road head-first.
in 2007 a chef contracted cellulitis from a seagull cut, where all his arm was affected.
in 2002, an old man was cleaning the roof of his garage where he disturbed a nest of chicks, and he fell, was mobbed by the birds and suffered a heart attack.
Birds that can crack nuts like toucans and great macaws have a bite force of 10-20kg. https://www.youtube.com/watch?v=-pUvg9Yis4Q
Seagulls don't really crack open snail and clam shells on the beach, to get into them, they must fly up and throw them onto some rocks. https://www.youtube.com/watch?v=EWQqG6cwlBU
To break a finger bone you need 50-100 kg of force.
Seagulls have slender bills for pecking, impaling and hooking fish. Their bite force is unlikely to be above 5 kg, probably 2-3 kg.
A seagull is most dangerous to a human when it scares them from above and they jump into the street and land in an ungainly way, i.e. colliding with a car.
Out of the approximately 11,154 known bird species, 159 (1.4%) have become extinct, 226 (2%) are critically endangered, 461 (4.1%) are endangered, 800 (7.2%) are vulnerable and 1,018 (9.1%) are near threatened.


text:
What species does this tooth belong to and how old could it be?
As far as I can tell, this is a single rooted tooth. I suspect (or hope because it would be very cool) it being pretty old, since it is so dark in colour. It is not very pointy, so it doesn´t look like a carnivore tooth to me.
On the picture I think the sequence of the the positional relationship from front left to bottom right is labial, palatinal, mesial, distal.
I'm leaning towards a mandibular incisor. I'm not sure if this could be a human tooth, but it fits size-wise.
It was found on a glacial freshwater lake in Germany. The right side of the scale is in cm.
I would be grateful if anyone has an idea about the owner of this tooth, or could point me in a good direction on how to further narrow it down.

there's a reddit called what's this bone.

Tooth is a good guess, but it's not a human tooth, that much is certain. The root is curved, which would imply (if it's a mandibular tooth) that the mandible is shorter and more curved than ours. My goats had teeth that looked similar to this, but that's not much help, sorry.


text:
In atherosclerosis, why do apoptosed macrophages stay on the endothelium?
In atherosclerosis, the following process happens:

Lipid deposits of LDL-cholesterol happen on the endothelium
They triggers an inflammatory reaction of the endothelium: macrophages circulating in the bloodstream comes in and assimilates the LDL-cholesterol
The macrophage enters apoptosis when they are full of LDL-cholesterol, and this triggers collagen production which ends in creating a plaque

My question is: in a common inflammatory reaction, the secretion of caspase triggers the apoptosis of the macrophages that have assimilated foreign material. Then the macrophages migrate to lysosomes where they are degraded. Why does this migration not happen in atherosclerosis?
Might be linked with this question: Why oxLDL accumulate to form foam cells?

Why do you write "the macrophages migrate to lysosomes"?

I think you have some problems with your terms - perhaps look up what lysosomes are, and whether this might be something that a macrophage could migrate to? You might also want to look up whether caspases are secreted for initiation of apoptosis.

@bob1 Thanks but could you please be more specific about the interrogation? For caspase for example, I have read an article about a study asking whether caspase triggering apoptosis is a unique or multiple effect of caspase. What is the problem with that?

The term "secrete" means a specific something in biology and I don't think you are using it correctly. Caspases do trigger apoptosis, but is this done by secretion of the caspases or not?

My understanding is that caspase is secreted by cells and that caspase triggers apoptosis by linking to chemical receptors on other cells


text:
50-400 bps consciousness: why do we draw the line there?
I have found studies that suggest the human consciousness can process 50 to 400 bps.  The exact number varies, but it's always quite small.  It is usually associated with some test results, but how do they decide where to draw the line?  How do they argue their test is the right one?  Is there some strong knee in the curve, or maybe a brainwave being detected which we recognize as occuring with conscious thoughts but not unconscious thought?

You'll have to read the individual papers. Personally I find these not to be very useful or meaningful measures. Brains aren't computers, they don't process bits.

Stating generalizations about consciousness is crazy because, while the conscious mind can process a small amount, the brain has like an L2 cache, a secondary level of consciousness that is immediately available if necessary... Consider you senses can record 2-3 megabytes per second of sound, image, and other information. secondary subconcious processes make that data available to the conscious process if necessary, and it's more about what we choose to ignore than what we have the power to focus on. we have a vast amount to data which is nearly in focus and available for deliberate thought.

The brain also has culture, so the 400kb of concious thought is built on a previous library of 10gb of best reactions for a given time, it's like a processor that builds itself, so a guy playing tennis or driving a car, processes huge amounts of previously concious thought automatically.

For the benefit of many if not most readers could you add at least a bit of background of what bps is and how it applies to human consciousness, if not some evidence of prior research beyond the unsupported "I have found studies..." Thanks!


text:
Reproduction number in SAIQR model
$$ \dot S (t)=\Lambda-\beta_1 S(t)A(t)-\beta_2S(t)I(t)-\mu S(t)$$
$$ \dot A (t)= \beta_1 S(t)A(t)+\beta_2S(t)I(t)-(\mu+\alpha) A(t)$$
$$ \dot I (t)=\alpha A(t)-(\mu+\theta)I(t)$$
$$ \dot Q (t)=\theta I(t)-(\mu+\mu_1+\gamma)Q(t)$$
$$\dot R (t)=\gamma Q(t)-\mu R(t)$$
On the above problem, where all parameters$$\Lambda, \beta_1,\beta_2, \mu, \mu_1, \alpha, \theta, \gamma$$ are known, I wanted to calculate the Basic reproduction number of the system of ordinary differential equations using next-generation matrix method(or even any other known method). However, I could not find any inbuilt function for this method. Can somebody point me in the right direction? Or can somebody help me to write MATLAB code for it?
thanks for any help.

The following derivation follows closely Vivas-Barber, A. et al. Dynamics of an "SAIQR" influenza model. 2014. I have used Wolfram Mathematica for calculations as shown below. You should validate yourself that the calculations are correct.
First, we define the state vector $E=(S,A,I,Q,R)$ and the total population size $$N=S+A+I+Q+R.$$ Solving  $\dot{E}=0$ for the trivial, disease-free equilibrium, we obtain:
$$N = \frac{\Lambda -\mu_1 Q}{\mu}.$$
Next, we calculate the Jacobian of the system at $E_0 = \left((\Lambda -\mu_1 Q)/\mu,0,0,0,0\right)$:
$$\left(
\begin{array}{ccccc}
 -\mu  & -\frac{\beta_1 \Lambda }{\mu } & -\frac{\beta_2 \Lambda }{\mu } & 0 & 0 \\
 0 & -\alpha +\frac{\beta_1 \Lambda }{\mu }-\mu  & \frac{\beta_2 \Lambda }{\mu } & 0 & 0 \\
 0 & \alpha  & -\theta -\mu  & 0 & 0 \\
 0 & 0 & \theta  & -\gamma -\mu -\mu_1 & 0 \\
 0 & 0 & 0 & \gamma  & -\mu  \\
\end{array}
\right)$$
and the corresponding eigenvalues:
$$
\begin{array}{l}
\lambda_1 = -\mu,  \\
\lambda_2 = -\mu,  \\
\lambda_3 = -\frac{1}{2 \mu }\left(\sqrt{2 \beta_1 \Lambda  \mu  (\theta -\alpha )+\mu  \left(4 \alpha  \beta_2 \Lambda +\mu  (\alpha -\theta )^2\right)+\beta_1^2 \Lambda ^2}+\mu  (\alpha +\theta +2 \mu )-\beta_1 \Lambda \right), \\
\lambda_4 = \frac{1}{2 \mu }\left(\sqrt{2 \beta_1 \Lambda  \mu  (\theta -\alpha )+\mu  \left(4 \alpha  \beta_2 \Lambda +\mu  (\alpha -\theta )^2\right)+\beta_1^2 \Lambda ^2}-\mu  (\alpha +\theta +2 \mu )+\beta_1 \Lambda \right), \\
\lambda_5 = -\gamma -\mu -\mu_1.
\end{array}$$
Rephrasing the conditions $\lambda_3<0$ and $\lambda_4<0$ as $\mathfrak{R}_0 < 1$ leads to:
$$\mathfrak{R}_0 = \frac{\alpha  \beta_2 \Lambda }{(\theta +\mu ) (\mu  (\alpha +\mu )-\beta_1 \Lambda )},$$
and a necessary condition on the parameters: $\beta_1 < (\alpha +\theta +2 \mu )\mu/\Lambda $.

Clear["Global`*"];

eqs = {
   S'[t] == Λ - β1 S[t] A[t] - β2 S[t] Ι[t] - μ S[t],
   A'[t] == β1 S[t] A[t] + β2 S[t] Ι[t] - (μ + α) A[t],
   Ι'[t] == α A[t] - (μ + θ) Ι[t],
   Q'[t] == θ Ι[t] - (μ + μ1 + γ) Q[t],
   R'[t] == γ Q[t] - μ R[t]
   };
vars = DeleteDuplicates@Cases[eqs, _Symbol[t], All];
params = DeleteDuplicates@Cases[eqs, _Symbol, All];

$Assumptions = Thread[params > 0];

Eliminate[{Total[Last /@ eqs] == 0, Ν == Total[vars]}, {R[t]}];
Ν0 = First@SolveValues[%, Ν];

J = D[Last /@ eqs, {vars}] /. S[t] -> Ν0 /. (vars -> 0 // Thread);
λ = Eigenvalues[J];

FullSimplify[Reduce[λ[[3]] < 0 && λ[[4]] < 0, Reals]]
(* β1 Λ < μ (α + θ + 2 μ) && β2 < ((θ + μ) (-β1 Λ + μ (α + μ)))/(α Λ) *)

Dear @Domen
Thank you very much. This advice and your valuable reply helped me a lot and I am now studying more closely and checking what you have said. If there is a problem, I will definitely take your and other researchers' valuable time again.


text:
Bird in Taipei knocking on the window glass - juvenile hawk? white throat, white beak(?) striped breast, black head(?) brownish body(?), not small
I received these photos from a friend today - a slightly larger than average size bird tapping on the window glass; maybe a brownish body with a white throat and white beak and black head.
The tail is spread in a fairly wide fan, maybe to scare "the other bird" reflected in the window?
There's a front view and one with its head turned, but it's a little tricky to be sure of the colors since the sun is (roughly) behind the bird. I suppose it's possible that the beak may not be white, but just smooth and shiny and reflecting the sunshine.
Taken on a sunny, hot July afternoon in July in Taipei. Coat hangars for scale suggest it's a bit larger than the typical bird.
It reminds us somewhat of a Chinese Bulbul, but those distinct vertical stripes between its throat and breast are very distinctive.
It looks scary/predatory, could it be a juvenile hawk?
Chinese Bulbul photos (mostly from Hong Kong):

https://nhillgarth.com/2013/10/25/more-birds-in-taiwan/
https://cms.hkbws.org.hk/cms/en/hkbws/work/resarch/hk-bird-atlas-2020-en
http://birdingtaiwan.blogspot.com/p/idiots-guide.html

Light-Vented Bulbul (also Hong Kong)

https://theworldsrarestbirds.com/birds/birds-in-hong-kong/

The light-vented bulbul looks quite promising, but I think this bird looks less song-birdy - the size and the large beak makes me think probably not.
I think the Taiwan scimitar-babbler (Pomatorhinus musicus) is the most promising.
you can check out this gallery: https://media.ebird.org/catalog?taxonCode=taiscb1&sort=rating_rank_desc&mediaType=photo
This bird shares the black stripe over the eyes, the thick and slightly curved beak, the breast feathers, the white stripe of feathers just above the eyes, the black feathers on the top of the head, and I think even the orange shoulder feathers if you look closely in the first image.

This seems inescapably correct, WOW! What a perfect fit. Both ebird's taiscb1 and Wikipedia's Taiwan scimitar babbler say that it's "endemic to Taiwan" and the ebird map shows only sightings all over the main Taiwan island - from coastal to mountains, and the island(s) of Penghu - I'm just curious, is it really never, ever sighted outside of Taiwan?

I mean, I wouldn't say its absolutely NEVER seen outside of Taiwan, but when it comes to its natural range, endemic would mean that, yes, it is only found in there. According to https://avibase.bsc-eoc.org/species.jsp?avibaseid=A37AFA6B7625915F , this species used to be considered a subspecies of a related species found elsewhere in Asia and in fact right next to Taiwan in China, the streak-breasted scimitar babbler.

Interesting! As of August 2005, there are at least 13 recognized subspecies of Pomatorhinus ruficollis.  In Taiwan, the song is lower-pitched with 3–4 upturned notes on the same pitch.  P. r. stridulus. which inhabits hill forests of southeast China (Guandong, Fujian and Jiangxi), is the nearest population to Taiwan.


text:
Minimum conditions for human life
I don't know so much about biology, my strengths it is in physical science and mathematics.
Well i like rifle shooting, I don't hunt, i think that is cruelty and coward.
In some conditions of temp,humidity and pressure, you can do a great shot, but i think that the limits or conditions are wrong.
So i would like to know what conditions of humidity, pressure and temp at the same time, it is possible to be a live as human in a fixed position over the ground without moving or doing some excercise.
Looks like a cold weather, but you know better that than me.

No help? The blood freeze at -3 Celsius


text:
Why is there a negative sign before voltage in the gate variable functions of the Hodgkin-Huxley model?
In Hodgkin and Huxley's articles (1952, J. Physiol.; 1990, Bulletin of Mathematical Biology), the gate variables are formulated as

In particular, as $V$ increases, $\alpha_n$ decreases and $\beta_n$ increases, as shown below:

However, in many other textbooks, e.g., Spiking Neuron Models and Fundamentals of Computational Neuroscience, as well as quite a few websites like HHsectionOnly.doc (illinois.edu) and Hodgkin-Huxley Model | SpringerLink, there is always a negative sign before $V$.

I CAN'T UNDERSTAND why there should be a negative sign. If so, the monotonicity of $\alpha_n$ and $\beta_n$ will be inverted, which is not the real case.
What makes me even more confused is, when I remove the negative sign, I cannot obtain valid results through programming.
In a word, I wonder why there should be a negative sign before the voltage. What's its physical interpretation? Thank u in advance!

Voltage is a potential difference. Membrane potential is a difference across a membrane. When you calculate a difference A - B or B - A, you get a number that has the same magnitude but opposite sign. So, if A is inside a cell and B is outside a cell, how do you know if the difference should be noted A - B or B - A? The universe won't tell you, you've got to make a decision. It's helpful if everyone makes the same decision and it becomes a convention.
These sorts of conventions are everywhere in physics: there's no real reason that protons shouldn't be thought of as "negative" and electrons as "positive", for example. All the math works out the same way, but it's helpful if the whole field uses the same convention.
Similarly, the field of neurophysiology has settled on thinking about things from the perspective of the inside of cells. That means, by convention, when we say a membrane has a "negative" voltage, we mean that "inside is negative relative to the outside".
Hodgkin and Huxley initially used the opposite convention in their experiments and papers. There's nothing right or wrong with that, but it means if you are using the typical convention that a "negative membrane voltage" means there is more negativity inside the cell versus outside, you'll need to multiply voltage by -1 when you use the original HH paper equations. See also e.g. http://nelson.beckman.illinois.edu/courses/physl317/part1/Lec3_HHsection.pdf - search for "sign conventions" for the relevant discussion.

Thank you Bryan. You really helped me a lot.


text:
Which was the first restriction endonuclease to be isolated?
I kind of have confusion between the first restriction endonuclease to be isolated and discovered.
In class XII NCERT, it says that,
"In the year 1963, the two enzymes responsible for restricting the growth of bacteriophage in Escherichia coli were discovered. One of these added methyl groups to the DNA, while the other cut DNA. The latter was called restriction endonuclease".
Now, "one of these added methyl groups to the DNA" refers to DNA methylase clearly and "the other cut DNA" must refer to EcoR1, I think?
In the next paragraph it is given that,
"The first restriction endonuclease, Hind II, whose functioning depended on a specific DNA nucleotide sequence was isolated and characterised five years later".
What I understand from this is that,
Hind II was the first restriction endonuclease to be discovered but EcoR1 the first to be isolated?
I went on many sites, but they all use these terms interchangeably.

The restriction endonuclease (RE) isolated from E. coli K strain was a type I restriction endonuclease, identified/characterized by Meselson and Yuan1 in 1968.  Type I REs are site specific, but cleave DNA randomly.
The one isolated from Haemophilus influenzae by Smith and Wilcox2 in 1968 was the first type II RE and is now known by the name HindII - the isolate they had was actually a heterogenous mixture with HindIII, for which there are no sites in the one of the viruses they were digesting, so they were able to work out the specific site of digestion for HindII, but not HindIII. Type II REs are site specific and cleave at specific sites too, which makes them useful in molecular biology, as opposed to type I REs, which aren't so useful.
EcoRI (type II RE) wasn't isolated until 1971, and was done by Yoshimori as his PhD thesis at University of California, San Francisco (see reference 27 in Roberts; ref 3 below).
Roberts (2005) a succinct history of it all3. See sections on Restriction Enzymes and Polyacryamide Gel Electrophoresis for information about the discovery of type I and II REs respectively.
Refs:

Meselson M, Yuan R. DNA restriction enzyme from E. coli. Nature. 1968 Mar 23;217(5134):1110-4. doi: 10.1038/2171110a0. PMID: 4868368.

Smith HO, Wilcox KW. A restriction enzyme from Hemophilus influenzae. I. Purification and general properties. J Mol Biol. 1970 Jul 28;51(2):379-91. doi: 10.1016/0022-2836(70)90149-x. PMID: 5312500.

Roberts RJ. How restriction enzymes became the workhorses of molecular biology. Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):5905-8. doi: 10.1073/pnas.0500923102. Epub 2005 Apr 19. PMID: 15840723; PMCID: PMC1087929.

So, EcoK I (?) is the RE referred to in the first paragraph and not EcoR I. On comparing Hind II and EcoR I, Hind II was the first to be isolated (1968), EcoR I being isolated only in 1971. Am I right? Man, my teacher got me hella confused.

I could be EcoKI, but I don't know if this is actually the case; though a quick scan of the literature shows references to the Meselson paper, but whether this is related to KI itself??? I suggest you look through the literature and try looking up the history of EcoKI.


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Why have mammalian predators been so small compared to their prey compared to theropod dinosaur predators?
So this is different than the question of "why are megafaunal mammals smaller than dinosaurs", which I understand to be a combination of:

live birth limiting size (even sauropods had miniscule egg sizes, on the order of ostrich egg sizes).

Breathing efficiency due to not having to rebreathe the same air breathed out.

Lighter bones

Mesothermy in large bodied animals.

Different life stages filled different niches.

Dinosaur mass estimates have historically been overblown

Dinosaurs weren't that much bigger excluding sauropods (Many members of the paleoloxidon genus were significantly heavier than modern T-rex estimates, and the estimates of most non sauropod dinosaurs, even African Elephants can get 2x the mass of an edmontosaurus and larger than a T-rex, lots of animals and the ranges of megafauna today are also smaller specifically because of human intervention, perverting our perception of animal sizes).

The only thing I can think of is the tendency for mammalian predators to hunt in packs (Even within the same biome, Hyenas, Painted Dogs, Lions, heck even Humans!), replicated in virtually every landscape on every continent except Antarctica and some what to a lesser extent in Australia (cave hyenas, wolves, cave lions plus sabertooth cats, and again, members of the homo genus), and afaik, the evidence for dinosaurs seems to show even those that hunted in groups weren't necessarily doing it to the same extent as mammals are/have been. This still doesn't explain why mammalian predators seem to cap out at around 1000kg -> 1500kg in mass through out virtually all of prehistory, even the "solo" hunters, such as short faced bear, when T rex itself seemed to be similar in mass to much of it's prey, as well as T rex relatives. The largest mammalian land predator (Andrewsarchus) has had it's mass estimate swinging downwards (back towards 1000kg, possibly no longer making it the largest) but even if it had been 2000kg, it still wouldn't be the mass I would be expecting.
So what are the hypothesis on why mammalian predators haven't gotten to the same relative sizes as prey as theropod dinosaurs did, or vice versa why didn't theropod dinosaurs stay smaller relative to their prey?


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An interesting paper on hunter-gatherer social dynamics and cooperation
I've read a paper long ago on the cooperativeness in the hunter-gatherer primitive societies. Their conclusion is that for hunters, cooperation dominates competition; for gatherers, competition dominates cooperation. Some of their arguments are:

Cooperation is necessary in hunting activities, especially in hunting large beasts; cooperation is less necessary in gathering activities.
The location abundant of fruits is static and limited. Gatherers must compete for that location. However, the herds are usually moving and large.
The easy location for gathering is strictly limited, meaning that, if one gatherer collected most of fruits from that location, other gatherers have nothing left. For hunters there is another story. One good hunter may collect one buffalo from the herd, and this does not prevent another hunter to collect anther buffalo from the same herd: the resource is relatively not the limiting factor, the limitation factor is the cooperative-hunting skill

I cannot remember all information precisely as it's been a long time. The problem is that I forgot the exact citation of that paper. What are some related paper in literature?


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Trying to identify a mushroom found in my backyard
I'm new at trying to describe mushrooms though I will try my best.

subtract from growth : grass
color : light grey/brown then a faded orange at the top
gill color is also light brown
ovate shape
believe the gills attachment is adnate
I think that this mushroom could be part of the coprinopsis family and found that the coprinopsis martini is pretty similar
-Also could possibly be a humpback inkcap
location is southern Georgia (USA)
extremely delicate, it ripped very easily

Were they growing in open area or in shade? Where they growing in a circular pattern or randomly? Over a wide area or clustered together?

From my experience, this is definitely a species of Coprinopsis, as you said. However, when it comes to this and related genera I find that the great diversity of species makes it pretty hard to pin down IDs. Coprinopsis martinii/acuminata like you suggested indeed seem pretty promising appearance-wise, but like I said you'll find this to be the case with many species of this genus, and neither seem very biogeographically relevant to Georgia. Try using iNaturalist to search the area for Coprinopsis species and narrow down your search from there.


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I’ve been searching the internet for days and I can’t seem to find out what insect this is, can anyone help?
I saw this tiny insect and I first thought it was an ant because of the body shape. However its legs were really really green, I’m adding photos but it’s hard to see how green they actually were. It also moved like a spider, and not like an ant which I thought was curious. For reference I live in Norway. Sorry about the grainy pics but it’s a screenshot from a film I took. Hope someone can tell me!

First, count the legs. Have you tried looking for spiders?

Certainly looks like a spider.  How big was it roughly and do you have any other photos from other angles?

It was a bit larger than your average ant, not the brown/reddish ones but the black ones. I thought it was an ant first because the body looked too long to be a spider but it moved like one. It definitely had 8 legs, a black body with a few white dots (?) and very green legs. I have a film of it so I can see if I can screenshot other angles but I’m not sure how to post them in comments.. I haven’t used this platform before. Thanks for the reply by the way!

Myrmarachne formicaria does occur in Norway, but the body shape doesn't fit: M. formicaria is much more elongated and has longer legs. Also it is at least partially of brown color.

Counting the legs (4 on each side, so 8 in total), it must be a spider. According to the compact body shape and the relatively large "head" (prosoma), I guess it must be a jumping spider (Salticidae) (at least in Europe). Several jumping spider species are known to mimic ants, what also fits the ant-like moving.
A quick web search brought me to the genus Heliophanus which resembles the specimen on your photo (black body, white spots on the opisthosoma and bright legs), whereof four species occur in Norway according to Fauna Europaea:

H. cupreus
H. dampfi
H. dubius
H. flavipes

According to the description on the Spinnenforum (only in German), all four of them match the given characteristics. So, a determination on the species level would need a microscopical dissection.

H.cupreus matches perfectly with the spider I saw. I’m actually really impressed you found it, I googled in both English and Norwegian but I couldn’t find a site that gave me a full overview of all spiders. I  spent an hour or two trying to figure it out. Thank you, I know you said it was quick but I appreciate the effort regardless!

It was an educated web search -- I identify arthropods since years and so knew what and where to search. You're welcome :)

I found this ant mimicking spider. Could it have been a female? The green legs don´t fit and the 4(?) white dots. I don´t have much experience with spiders, but that might just be variation of their phenotypes.
This genus of spiders lives mostly in the tropics, but a few species occur in temperate regions. I didn´t deep dive into that, but if it is not M.formicaria (De Greer, 1778) there might be another palearctic species that matches your find.

I honestly don’t know if I’m replying to my own question or yours right now so sorry or not sorry. I saw the ant your referred to and it doesn’t fit in color or body type to be honest. The body is slightly too long. The white dots fits but the body was black and it had green legs. It could be a variation I guess but looking up spiders in my country and also other countries has resulted in nothing. I’m actually really puzzled and have gone through what I could find on ants and spider with green legs and still nothing..


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How do the qualitative tests for E.Coli work, which chemicals are used?
There are test kits that to detect E. Coli in water, by mixing a small sample of water with a certain chemical. After a certain time, the sample changes color depending on the presence of E. Voli above a certain treshold.
How do these tests work and what reagents are used?


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How is the fate of endosperm decided?
I was studying about the post-fertilization events in angiosperms and I came to know that in most dicotyledons, the endosperm is completely consumed and in most monocotyledons, the endosperm is not consumed completely. Why does this happen? Does it have anything to do with the suspensor cells? Does it depend on how much the suspensor cells push the developing embryo into the endosperm? Or, does it depend on something else?


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What type of shell is this?(Answered)
This is Calcareus tube worm and Was found and Located on Culebra Island, Puerto Rico
Picture 1: A up close image of the shell
Picture 2: a view of the top part of the shell showing the shells coloring.
Credits for the answer: @Jiminy Cricket
Website Credits:
https://gohiking.ca/animals/fish/marine-worms/calcareous-tube-worm/

given that they are both calcium carbonate, as soon as the coral started growing on it, the fusion process would have started.

perhaps it's a parchment tube or a keel worm. https://www.beachstuff.uk/marine_worms.html

Could you try to make some pictures with a scale? It would be helpful to see a bit more of it. To secure it in place you could place it on some plasticine, than you don´t have to hold it and the hand isn´t the star of the picture.

It's a Tube Worm.

Calcareous Tube Worm, Vancouver Island, BC, Photo By Bud Logan
From Gohiking.ca.
They anchor themselves to rocks, or animal shells, poking out their filter-feeding aparatus which draws small invertebrates and algae into the mouth. As they grow they deposit a calcerous tube around their bodies for shelter from abraisive silt-carrying currents
and protection.
They're seen in a variety of sizes and shapes in marine habitats, from squiggles on rocks to large, straight stands, much like a small forest.
Giant Tube Worms: (Courtessy of Seasky.org)

NOAA, public domain.


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Tardigrade scaling and survival
Tardigrades have attracted the attention of researchers with their amazing endurance. They withstand enormous temperatures, high doses of ionizing radiation, resistant to harsh atmospheric factors and high pressure, used in experiments in outer space and survive in conditions of many years of lack of moisture.
At the same time, they have tiny sizes (the body of tardigrades has a size of 0.1-1.5 mm) and a very slow speed of movement (only 2-3 mm per minute).
Suppose tardigrades would grow to the size of an average cat. Would they have the same survival rate if everything else (conditions and habitat) had not changed? Would size scaling affect their bodily functions in any way?
Partially, this topic answers my question, but I would like to know if tardigrades have any features here too.
What are some examples of scaling laws in biology?


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Question on protonation/deprotonation of amino acid side chains
I understand that actual pKa of amino acid side chains is greatly influenced by the surrounding environment. I am trying to deeply understand the equilibrium between protonated and deprotonated form of amino acid side chain by taking Lys as an example. Lets imagine a protein having solvent exposed Lys residue. At physiological pH, theoretically this Lys residue on every protein is in largely protonated form (ofcourse some are deprotonated). Now say with some reagent I modify few of this particular Lys residue (using NHS ester etc.). Now does the remaining unmodified Lys residues undergo protonation/deprotonation to nullify the effect caused by the chemical modification and maintain the state of such equilibrium? Also, I am curious is it always impossible to achieve 100 % modification of this particular Lys residue due to the existence of equilibrium state?

I want you to imagine the protons pressing on the radicals. When you increase the protons in solution, the pressure becomes greater. Some radicals will pick up protons before others can. Water also comes into play pulling the protons from the radicals so you have this sort of back and forth at the very small scale. Equilibrium is when these effects basically cancel out, the radicals lose some protons to water which they gain back the next moment. The system sensibly tends towards equilibrium if you think about it. Now try thinking about what happens if I decrease the amount of protons.


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Linking models of spreading of infection to type of network describing the relationships of animals of a habitat
I am studying  networks describing the relationships between  animals in a habitat.There are many types of networks studied which are useful and we can approximate a real network to one of the studied networks.Now suppose a disease starts spreading in that habitat.There are state models of the spreading of the disease such as the SI ,SIS and SIR model.Inside these models there are different parameters which define the rate of infection , recovery or immunity.My question is : do these parameters depend on the type of the network which describes the relationship between the population?


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Is it a common behaviour in insects to mate with a dead partner
I have a few specimens of Orgyia antiqua of both sexes, and I've been able to observe a mating behaviour where male and female sit close to each other, their rear ends connected.
Today though I've seen the same, but the female was day-long dead - and that didn't stop the male from the mating attempt.
I do understand that it can be explained with the male just reacting to some pheromones, still present on the female body, but that is a bit weird anyway.
Thus the question. Is it a common or well-known behaviour for an insect male to mate with a dead female?


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How can nerves slide without tearing
While reading about an exercise called nerve glides I learned that nerves are quite inelastic. With all the nerve branches and relatively straight path how do nerves slide back and forth without stretching or snagging? My idea is they have to be located at the neutral axis (imagine your joints as beams) so that they only ever bend and never stretch. But they would have to travel directly through the center of the joint for that to be true which they don’t (except the spine more or less).

Hi and welcome. This site requires evidence of prior research (a source, link and quote). Can you please link to the site where you are getting your information? What support from reasonable sources do you have for your idea? Thanks!

Inelastic compared to what?

Muscles, skin, etc. Am I wrong and they are fairly elastic? I couldn’t find sources that really pinned down just how inelastic nerves are. I would think it would cause issues if it was less elastic then everything surrounding it.

Look at nerve placement in the body, most large nerves are close to or inside the bone thus in locations that don't  stretch much.


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Is this bug a termite?
Noticed this bug on my kitchen floor, and am wondering whether it is a termite:

I have a video of it crawling too, but don't see how to upload video here.
Edit:
Regarding scale: it is small, perhaps 3 mm (~1/8 inch).
Location is northern Arkansas, so is within termite territory.

Could you tell us your approximate location to aid in ID? Nice pictures BTW. but could you add some idea of scale.

Thank you @JiminyCricket. I have edited the question to include that additional info you suggested (~3mm and northern Arkansas).

As someone who is not entomologist, that would not even cross my mind as being a possible termite because the abdomen looks all wrong. It looks like a beetle to me. But as I said, not an entomologist.

This is a beetle rather than a termite:
in comparison to a termite, most beetles have sclerotized forewings (so-called elytra) and from above, you can recognize its head, pronotum and forewings.
Termites, however, have soft bodies and most often are wingless.
From above, you can additionally see their meso- and metanotum and their abdominal tergites (latter are covered by the wings in most beetles).
Commonly, they are unpigmented and thus, pale.
Winged termites have transparent wings that are longer than their bodies.
Beetles are extremely diverse with almost 200 described beetle families with more than 300,000 species, so it's super hard to tell even the family let alone the species from a photo.

Image source (in reading direction): Sanjay Acharya CC-BY-SA-4.0 | Teechippy CC-BY-SA-4.0 | Dulneth Wijewardana CC-BY-SA-4.0


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How to calculate average Corneal Thickness?
I have a question which I may be making out to be a lot more complex than it actually is.
In my department we have a machine which can image the cornea and give values of various parameters (eg curvature, thickness, elevation etc). In particular I am interested in the thickness.
This machine is able to export these values into a .csv file. The data is of all the points of thickness that the machine has measured.
As the cornea is spherical, the data is arranged such that the rows represent radii starting at 0 (the centre) all the way to 6 mm (the periphery) in increments of 0.2 mm. The columns represent meridians of which there are 256, starting from 12 o'clock.
Now the machine spits out data for say the central corneal thickness, but it does not automatically spit out data for the superior, nasal, temporal or inferior peripheral thickness. As such I need to calculate that from the data I have.
I tried to test simply taking all the values for the central 3 mm (ie up to row 1.2 mm) and then dividing them by n (the number of data points) but as expected this did not give me a similar value to the machine calculate central corneal thickness.
I don't have a background in maths or geometry other than A-levels. I am a doctor by training. On doing some quick google searching it appears I need some spaced interpolation method to calculate this but I'm not sure where to begin.
Is anyone able to help me with this or at least point me in the right direction? Is the solution very complex?
Thanks
EDIT
I have attached a diagram with an anterior view, a cross sectional view and an example of how the data is stored in the .csv file
NOTE: the column in the table is meant to represent meridians in degrees, from 0 until 360

I'd recommend starting by sketching out the problem. That is, draw a cross-section of the cornea with how the measurements are arranged and what they physically measure versus what you want to calculate.

Hi thanks. I have drawn out a cross section of the cornea as you say and the method I used initially as described in my question but I am not getting the same answer as what is used by the machine. I suspect this is because I am not taking into account the curvature? I’m not quite sure what other variables I need to take into account to correctly calculate this

Without seeing the drawing or the data or your calculation it's pretty much impossible to figure out where the discrepancy might be.

Hi, I have added a diagram above. I hope this clarifies my question.
Essentially I took data from radii 0 until 1.5mm for all meridians from 0 degrees to 360 degrees to give me the central 3 mm circle of the cornea.
I then summed all of these values together and divided by the number of data points to give me a value for the average thickness.
The value I end up with is between 5 - 20 microns off from what the machine gives me. As such I concluded my method is unreliable.

I don't know what the machine is doing exactly (you could ask the manufacturer perhaps), but you could try weighting the measurements by the circumference at each radius, or the sector area of each radius plus half a step minus the radius minus half a step. The points further from the center effectively cover more area if the spacing is by degree. You could also interpolate a uniform sampling of arbitrary uniform density.

E.g., for points in the 0.4 radius (3rd row), you could consider those to be measurements that correspond to the area between r = 0.3 and r = 0.5. Each measurement in that row then corresponds to area (pi0.5^2/256 - pi0.3^2/256). Measurements in the 4th row would be weighted by (pi0.7^2/256 - pi0.5^2/256), and so on.

Thank you for your help. This was useful.


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Need help identifying insects in home, Morgan Hill CA
The creature in the attached photos just started appearing in small numbers in various locations inside my home. Would like to positively identify.

Yeah, I think you've got it. Lots of farmland around here, and it has been very hot lately (like everywhere else).

This is a true bug (Heteroptera), likely a nymph of the family Rhyparochromidae. Until recently, this family was part of the Lygaeidea ("seed bugs"). As their colloquial name reveals, they (mostly) feed on seeds (one exception would be the predatory Geocoridae).
Distinctive characteristics of (almost) all true bugs which are visible on the photos, are the rostrum and the scent glands (which are located dorsally in nymphs and abdominally in adults). The position of the scent glands, thus, indicates that it must be a larvae. Another indication is that its wings are still in pockets.
Determining true bug larvea to the species level is tricky and rarely done. But with some experience, it is possible to tell the families apart. Lygaeid bugs (and thus, also rhyparochromid bugs) are elongated with compact legs and antennas. Often, they have a pointed nose (a long head) and relatively large eyes. All charactericstics match with the specimen on the photo, which makes me think it must be a rhyparochromid bug.


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What is the best way/kit to extract total proteins from biopsy tissue?
I need to extract total protein from 2mm skin biopsies for western blots.
I was thinking about miRNeasy Micro Kit (50) Cat. #217084 while it's ok for total RNA extraction, I am not sure if it is still fine for proteins. There's a trizol (quiazol) step that provides you with organic fraction that suppose to contain protein fraction, but I am still not sure if it's a best way.
There's also a so-called Urea Sample Buffer (USB), that contains urea, 20% SDS, glycerol, Tris and Pyronin Y - but I am not sure it's a good choice since the percentage of SDS is high and it will be a disaster if I will try to disrupt my tissue.
Or, maybe there's a better solution or kit for that purpose?

This entirely depends on what you want to get out of it. If you need the RNA or DNA, then trizol extraction can work, but no need to buy a special kit for it, just the trizol and chloroform will work too - though for miRNA (as opposed to mRNA), a kit is a good way to go.
If you just want the protein, use a dedicated protein lysis solution for this. Something like RIPA buffer is a good start. make sure you add protease inhibitors and work with cold solutions to prevent proteolysis of the proteins. Depending on what you want to find, you may need to disrupt the biopsies a bit first - chop them into smaller chunks and/or do a collagenase digestion to allow removal of the mass proteins and look at less abundant ones. RIPA buffer is quite strong, so you may want to use a gentler solution without the SDS and/or deoxycholate, but this (again) depends on your final aims.


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Is this plant in my urban garden poison ivy?
Is this plant in my urban garden poison ivy?

Toronto, Ontario area.
July 19, 2023
Full shade
Three leaves; toothed but not serrated.

Possible Answer: (I can’t post an answer due to the question being closed)
I suspect it is Boston Ivy (Parthenocissus tricuspidata).

Eastern Poison Ivy vs Boston Ivy
Boston Ivy: A deciduous woody vine native to east Asia, introduced in North America. Established in numerous scattered locations, mostly around urban areas. It is a close relative of the native Virginia creeper.
Middle leaflet has no stem or a short stem not much longer than that of side leaflets.

Related: Vine has simple and compound leaves

Virginia creeper has leaves in 5s, not leaves in 3s. Definitely not virginia creeper.

Almost certainly Toxicodendron (poison ivy) genus; I think Toxicodendron rydbergii (western poison ivy). Leaves are in threes, with the central one longer than the others. Leaves are variable in toothing and serrations on the same plant. This one will be a shrub rather than a climbing vine.
Incidentally, the other, dark-green leaved, plant in there is common ivy (Hedera helix).


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How to estimate calcium concentration from fluorescence microscopy?
Is there a way to get a rough estimate of a [Ca2+] based on fluorescence microscopy images (obtained using GCaMP for example)? Usually what we get is the ratio f/f0, but is there a way to estimate the absolute value of [Ca2+]?
I found an old paper on this subject, but using their formula, there are still paramewters which I wouldn't know how to access experimentally.


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what are average, median, and minimal dna closeness of stranger peoples, compared to closeness of relatives?
i thought: a parent closeness to a person can be marked as 50%. seems that is 50% of all parts of dna of humans that have variability across all human population. i heard that chimpanzees are 98% close to humans by their dna, so, 100% here may match like absolute 1 or 2 % of dna.
then, if to say only about siblings with both parents same, for simplicity, a sibling also must have 50% closeness in average. then, an uncle has 50% * 50% = 25% . (because he is sibling of a parent). a cousin has 12,5%. (child of uncle). a grandfather is 25%, his sibling is 12,5%, son of his sibling is 6,25%, and grandson is 3,125%, that is, second cousin. third cousin should be 0,78125% .
and here a question appears: so, this number goes very low very quickly, when going to farther relatives. but it should not go to 0, because stranger people also must have some similar genes by chance.
so, i want to ask, what is that average level of the similar genes by chance? what is median level of it? and what is the distance between 2 of the most far persons?
i think, maybe this question is not possible to answer nowadays. because i searched, browsed in wikipedia, and saw that, seems, it is not known, to how many parts chromatids are split in meiosis. so, must be, it is not known, how much is that variability of human dna. i think, maybe this question may stay waiting for future answers.

this seems to give info for that: https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.biorxiv.org%2Fcontent%2F10.1101%2F716662v1.full&psig=AOvVaw0_Jvz-G-KdHgzCPIiTukBP&ust=1689930420026000&source=images&cd=vfe&opi=89978449&ved=0CBEQjRxqFwoTCKjTwsX3nIADFQAAAAAdAAAAABAw  would the fourth image on this page give the information that you wish for? https://www.quora.com/What-two-human-ethnicities-are-the-most-genetically-different

Everyone is related, it just gets harder to know exactly how related you are when you go beyond a handful of generations. When you talk about "shared" DNA with close family members, you're talking about shared variation. When you talk about "shared" DNA between chimps and humans, it's more like you're talking about similarity of the average. These are two very different, not-comparable measures.

The 1-2% difference refers to SNPs in coding regions. There are drastic higher-order differences like chromosome fusion (chromosome 2a/b) and deletion or reversion of long stretches in MB level. What you are calculating is theoretical inheritance of alleles by identity of person from which it comes, which is abstract and has nothing to do with the actual sequences.

I am speaking of chimpanzee vs human.

0.1% and 0.
the average person varies by around 0.1% from another random person, or two random people are 99.9% the same. Humans actually have very low genetic diversity as a species. Total variation is around 0.4% by copy number. Of course the catch is it all depends on how you calculate difference. Different ways of calculating it will give you slightly, but not insignificantly, different answers. For instance you have issues with duplication and deletion, humans can have multiple copies of the X chromosome with little effect, is a translocation one difference or do you count each difference in a 1:1  base pair map, do you count genes if we don't know if they code for anything, ect. There is a whole rabbit hole of competing ways to calculate genetic difference.
the 50% you are referring to for relatives is really 50% of the parts that vary, or 50% of 0.1% thus 0.05%, or you are roughly 99.95% identical to each parent and 99.6% identical to the most unrelated person on the planet, again depending on how you calculate it.
The minimal difference is 0, identical twins who don't know each other exist. Also the cutoff for relative is completely arbitrary, there are humans who don't share 100% of genes within themselves.
Mean in this case does not make a lot of sense, the closest you might get is something like a genetic distance map, because it is not a single variable axis. there is a whole wiki devoted to human genetic variation if you want to dive deeper. https://en.wikipedia.org/wiki/Human_genetic_variation
More sources
More on how relatedness works.


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Can the instantaneous center of rotation of a vertebrae be mathematically determined for flexion of lumbar?
I am starting to learn spinal anatomy and I want to determine the Instantaneous axes of rotation (IAR) of individual vertebrae. I have referred many research papers but haven't come across any useful material.
Let's say I have the center points of superior and inferior plates of L5. Similarly I have the center point of superior plate of S1.
Is there any way to mathematically determine the IAR for L5 for lumbar flexion(say) ?.


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Can anyone identify a fungus with a tiny fruiting body that I found in a plant pot
I recently found what I think are fungi in the growing medium in a 30 cm pot that contains an epiphyllum 'orchid' (cactus). There are several that appear new and more that look old or are decaying.  I've included a picture with the fruiting body on the left - the coin is 1.8 cm in diameter and the small round ball is Osmocote.
The fruiting feels 'woody' when I touch it and is close to or touching the soil surface.  I let the soil get kind of dry between waterings and I'm in Southern California where it is hot.  The soil surface gets no direct sun. I've not repotted the plant but the soil is well draining and appears to have woody material in it.
I realize that it is unlikely that it will be identified to species but I'd like to know a bit about it.

I took a look with a magnifying glass and found the fruiting bodies of 'Bird's Nest Fungi' that eat dead plant material.
So the answer is 'Bird's Nest Fungus'.

Excellent, when patience pays off :)

Cyathus cf.fimicola
Black peridioles not densely packed within basidiocarp
Peridioles shiny; basidiocarp conspicuously shaggy

This answer could be improved if you were to include complete sentences in order to clarify what you mean. Perhaps include a picture (with source properly attributed) to support your conclusion.

As I asked, could you add attribution to the picture ensuring the copyright is respected. As the notice on your post states, also add a reference and an explanation why your answer is correct, using whole sentences.

I have already added attribution in the edit summary

The place to add it would be in the body of the post. You'd need to also cite the licence that entitle you to reproduce the picture here, as it's a requirement of the whole Stackexchange network - and a legal requirement in many jurisdictions. Don't forget to edit the text to explicitly explain why your example answers the question.


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Relation between image on retina and the real one: looking at the two objects that are 45 degrees apart, what's the distance in the actual image?
These are what I understand about the vision.

lights come through the pupil.
an inverted image of the real objects is formed on the retina. which is determined by the angles.
(so (a, d) and (b, c) look the same)
the retinal image is tiny(about 3~5cm?) and inverted.
our vision is somehow flipped and magnified version of the image on retina.

My question is: what's the relation between the actual angle on the objects and the distance appeared in the real vision. As shown above, what's the distance between two objects which are 45 degrees apart? On the retina, we can calculate the distance between the image of the two dots which are 45 degrees apart(for example, the image formed by a and c), but how do we know the distance between two dots on the real vision?
In short: What's the magnification rate? between the two(image on the retina and the actual vision)?

Usually we measure that distance on the retina just in terms of "degrees". For the rest of your question I think you actually just want to read about depth cues, specifically monocular depth cues. There are some existing questions here on that.

On your sketch, draw also the other eye next to the existing one, and repeat the drawing of light rays and image on the retina. This will help you understand how we can reason about depth and distance between objects.


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What can be the issue during the total RNA extraction using QIAGEN kit?
I am trying to isolate total RNA using QIAGEN miRNeasy Mini Kit (50) - Cat #217004 from a 2mm biopsy. While there are only two samples (B4 and DT11) the quality of RNA is bad.
The goal is to use this RNA for RNAseq afterward and qPCR (do the cDNA).
All is done on ice, a centrifuge is cooled down, and no additional DNAse step is added.
What can be the problem?
Is this RNA really bad for the goals indicated above?

What is your problem? Have you measured a A260/280?

In addition - how were the biopsies stored prior to extraction? You are also using a kit aimed for miRNA - is this what you want or do you want total RNA or mRNA?

@bob - we aim at mRNA

@Chris yes, these ratios are 1.97/2.02 correspondingly. The problem is the smear. It is supposed to be 18S + 28S rRNA in general... Or am I wrong?

@bob biopsies were at -80

Ok, the kit should work, though you'll get more of the small RNAs than you might otherwise. What do the RIN show?

@bob1 RINs are 2.40 and 2.20 :(

@Lara unfortunately that is very degraded RNA and you aren’t likely to get any useful RNAseq results. Sorry it sucks, I’ve been there, but there’s not much you can do.

As mentioned in the comments, RIN are about 2.2 - 2.4.
These values are typically too low for RNA-seq, and indicate that the samples are quite highly degraded. One study by Reimann et al1 found that about 35% of the variation in transcript abundance in RNA-seq was caused by RNA degradation. That's not to say you can't sequence these samples, just that you shouldn't rely on the data for transcript abundance measures. The same applies to qPCR - where it is recommended to have RIN above 5.02.
As to what you can do about the RNA being degraded - that all depends on the samples.
It may be that you need to improve storage conditions - store samples (including the biopsies) at or below -80, preferably in the presence of RNase inhibitors. If you can't store the biopsies at -80, put them into and store them in RNA-later or similar as quickly as possible after being taken from the patient.
Extracted RNA should be aliquoted into single-use aliquots, stored at -80, freeze/thawed only once and used in down-stream applications ASAP.
It could also be that you are working in a contaminated environment - you should be using dedicated RNA extraction pipettes, filter tips and good lab practices - certainly don't use pipettes that have been anywhere near PCR products or RNases (cDNA conversion).
Preferably work in a laminar flow cabinet to prevent external contamination of samples and if you can, do RNA work in a room dedicated for that purpose to prevent cross-contamination with DNA from other sources such as PCR products. DNA contamination from PCR is a huge problem - you can get it from aerosols in the air and it WILL show up in your sequencing.
Use tubes from a reliable source that state "RNAse and DNase free" straight out of the bag (for example; don't autoclave the tubes or transfer to another container) and only touch that bag with gloved hands. Wipe work surfaces with RNase-away or similar product before use. Change gloves regularly and make sure you change them if you touch your skin or hair (e.g. you move a strand of hair off your face or scratch an itch - change your gloves!).
It may be that this is just the state of the RNA in these samples. In which case you can only work with what you have. You just need to be very careful about declaring these results when publishing - be very clear on the RIN values and what compensatory analyses you did or didn't do!
Edited to add: if you are new to the field - find some samples you can practise on before working with valuable real samples, which are often a finite resource. This could be cultured cells or samples from a euthanized lab animal (with appropriate ethical approval).
Refs:

Reiman, M., Laan, M., Rull, K. and Sõber, S. (2017), Effects of RNA integrity on transcript quantification by total RNA sequencing of clinically collected human placental samples. The FASEB Journal, 31: 3298-3308. https://doi.org/10.1096/fj.201601031RR

Padhi BK, Singh M, Rosales M, Pelletier G, Cakmak S. A PCR-based quantitative assay for the evaluation of mRNA integrity in rat samples. Biomol Detect Quantif. 2018 Mar 16;15:18-23. doi: 10.1016/j.bdq.2018.02.001. PMID: 29922590; PMCID: PMC6006387.


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What would actually be the ecological impact of deep sea mining?
In the last few months I have read a number of articles with increasing alarm concerning the potential of many countries soon engaging in deep sea mining. The idea is that in order to produce numerous technologies key to moving green, such as batteries, industry needs a good supply of metals that are currently rather rare, such as manganese or cobalt, and there are so-called polymetallic nodules covering various parts of the sea floor (for example the Clarion-Clipperton Zone) believed to be rich in these materials.
As covered in numerous places, for example here, the International Seabed Authority was supposed to draft some kind of agreement on what kind of mining like this is acceptable but the deadline has passed for it to set down laws so currently we're in a kind of "wild west" scenario where many companies can mine down there potentially with little regulation.
My question is: what will be the ecological impact of this kind of mining?
In some sense, there are obvious arguments as to why we shouldn't do something like this. One would be that it is a relatively untouched part of the world (in terms of human influence) and that fact inherently gives the idea of leaving it alone value to me. However, this could be applied to absolutely anywhere and we do probably have to occasionally conduct mining, farming etc. activities somewhere so what makes this different?
Let's imagine two counterfactuals:
One is that instead of deep sea mining, the recent events had concerned mining in the Amazon rainforest or the Great Barrier Reef. I have chosen these places as being ones I know are widely accepted to be extremely biodiverse and home to numerous unique species. Clearly this would be horrific for life on earth and I would hope most people on this site would be against it unless there really was no other option.
Another is that instead of deep sea mining, recent events had concerned mining in the middle of some deserts, say the Gobi. In this case, there is wildlife in the desert which is of intrinsic interest (for example, they give plentiful examples of extremophiles) but broadly speaking there's barely anything there. Arguably it would be difficult to find a better place to conduct mining if you want to minimise ecological impact! Thus I can't imagine many biologists being as concerned beyond the fact that these are again relatively untouched and thus hold intrinsic value.
I am interested in where the deep sea mining lies between these two extremes. My (admittedly fairly lay person) perspective is that on the sea bed it was definitely a surprise by biologists to find complex life but that, broadly speaking, there still isn't much going on. Furthermore, the Clarion-Clipperton Zone (the major area of interest) varies in depth between 4-5.5km deep. If we say it's on average 4.75km deep that's around 11 Empire State Buildings end-to-end stacked on top of each other! The point is that at such a depth, can life down there or activities down there really affect or be affected by things happening above, say at the surface?
As I understand, there is such a separation between life down there and above that creatures share very few similarities at the bottom to surface dwellers (if you need a specific example of how this distance can affect lifeforms, consider deep sea gigantism and we're looking even deeper!). Surely then even major activities down there will have little effect on the rest of the biosphere?

I just want to give a postscript to this question that I do not support mining in untouched areas of the world. This question is not supposed to advocate for deep sea mining but purely to understand better what is currently going on by asking experts.

In 10, or 5, years time we will be able to look back on the evidence.


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Species Identification: Waterborne worm/larva, California, USA (and is it safe)
Can you help ID this species? The photos are low quality, so I'll do my best to describe them.
I found them after I left a cup of dechlorinated, freshwater aquarium water outside with a plant in it, hoping the plant would grow better in sunlight. I do not think they came from the aquarium, but I might as well add it.
I left this cup on my second floor balcony. I don't know if this might narrow down the search, but whatever insect it is is somehow present on my roof (flying or climbing, I don't know).
They have a black head, are visibly segmented inside, but their outside is smooth, with no ridges. They are about 3-5mm long (I think based on age). I put them on a bit of cardboard paper to take the photos, and as the paper dried it appears that they need water or at least a moist surface to survive.


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How does mitochondrial uncoupling enhance performance in muscle cells?
As far aas I understand, in mitochondria, the citric acid cycle breaks down fatty acid or glucose to produce NADH and FADH2, which are then utilized by Complexes I through IV to generate a proton gradient in the intermembrane space. This gradient powers ATP synthase to ultimately generate ATP for the cell.
Uncoupling refers to alternative ways of decreasing the proton gradient without involving ATP synthase, such as through transmembrane fatty acids or Uncoupling Proteins (UCPs).
On the one hand, I recall learning that uncoupling is considered a disease condition since it disrupts the 'pull-effect' where an increased need for ATP essentially drives the entire reaction chain from the back, and because it generally dissipates energy into non-productive work. For instance, a textbook I recently read stated that ketones promote uncoupling in cardiac muscle cells, which is detrimental for obese individuals as the heart's performance capacity is impaired due to efficiency loss.
On the other hand, it is widely accepted nowadays that physical activity leads to significant mitochondrial uncoupling. This is surprising to me since one would assume that during a biologically relevant process, such as the adaptation of a muscle to movement, the adaptation would typically be 'beneficial'. Multiple authors write sentences like 'this optimizes the mitochondria's ability to synthesize ATP.'
It is evident that mitochondria deal better with a high nutrient supply when uncoupled, as fewer superoxides and peroxides are produced. But during physical exertion, an excess supply of nutrients is probably not the main issue?
I'm looking for insights to guide my understanding. How could the uncoupling of the electron transport chain I-IV from ATP synthase potentially enhance the performance capability of mitochondria and by this means the performance capability of skeletal muscle cells?

Skeletal muscles have multiple systems that increase the rate of energy generation in response to faster energy consumption during excercise.

System
Rate
Sustainability

Phosphagen
highest
10-15s

Glycogen-lactic-acid

30-40s

Aerobic
lowest
indefinite

The phosphagen system represents the immediate source of ATP, it is relied on for power surges. ATP itself and phosphocreatine, which can donate its phosphate radical to ADP, form this system.
When muscle activity is prolonged, the other two systems come into play. Which of the two being predominant depends on the intensity of the activity (rate of ATP utilisation).

The glycogen-lactic-acid system is used for strenuous excercise because it generates ATP faster than the aerobic system. It involves glycogenolysis, glycolysis and homolactic fermentation. Glycogenolysis is the breakdown of glycogen to glucose. Glycolysis is glucose oxidation into pyruvic acid by oxidative coenzymes with production of ATP (substrate-level phosphorylation). In homolactic fermentation, which happens under anaerobic conditions (oxygen insufficiency), instead of the reduced coenzymes (byproducts of glycolysis) being oxidised by the ETC in the mitochonderia, pyruvic acid acts as the final hydrogen acceptor to oxidise them so they can be used for another cycle of glycolysis. This produces lactic acid which is a strong acid that causes fatigue as will be explained later. Krebs' cycle is not part of the glycogen-lactic-acid system because there is no pyruvic acid to oxidatively decarboxylate into the acetyl moiety of acetyl-CoA (active acetate).

The aerobic system involves glycogenolysis, glycolysis, Krebs' cycle and the ETC. The Kreb cycle substrate is the active acetate radical that is oxidatively decarboxylated completely by oxidative coenzymes, with substrate-level phosphorylation. The ETC requires oxygen supply since oxygen is the final electron acceptor that drives the movement of hydrogen from the reduced coenzymes and its splitting to electrons and protons. (Oxygen is the second most electronegative element in the periodic table.) The movement of electrons (redox reactions) generates energy that is used to pump protons in the matrix across the inner mitochonderial membrane into the intermembrane space. This pumping continues until a proton back-pressure (proton motive force or proton gradient) is established. Once established, ATP synthase inhibits further proton pumping and stops the activity of the ETC. The pumped protons then diffuse through ATP synthase (chemiosmosis) and the energy that was used to pump them before is now used to phosphorylate ADP to ATP (oxidative phosphorylation). ATP synthase is sometimes also called complex V though it doesn't transport electrons, only facilitates proton diffusion. ATP synthase is activated by high ADP concentration in the matrix which discharges the proton back-pressure and consequently activates the ETC. ADP is produced from ATP hydrolysis and increases at low energy states when energy consumption is faster than energy production. The aerobic system is thus relied on for moderate-intensity prolonged excercise where oxygen consumption by the ETC is balanced by oxygen supply and where the long metabolic pathway still provides ATP at a sufficient rate. The reduction of oxygen by electrons can form either

water if the electrons are sufficient $\ce{O2 + 4e- + 4H+ \to 2H2O}$ (The protons are taken up from the matrix).
superoxide ion if the electrons are insufficient to form water $\ce{O2 + e- \to [O2]-}$.

Superoxide ions form hydrogen peroxide $\ce{2[O2]-  + 2H+ \to H2O2 + O2}$. Hydrogen peroxide, as with all ROS, has a high affinity to electrons and pulls them from other compounds damaging them, to combine with the electrons and with protons forming water $\ce{H2O2 + 2e- + 2H+ \to 2H2O}$. This causes peroxidation (oxidative damage) to lipids, proteins and DNA. Cells therefore have to split hydrogen peroxide to water and oxygen $\ce{2H2O2 \to 2H2O + O2}$ by catalase enzyme. Hydrogen peroxide can also be useful for the same reason. It is used by immunity cells to kill pathogens by damaging their cell membranes, which are made up of phopholipids, causing their lysis.
The muscle burns through the phosphagen system first and then operates through the aerobic system indefinitely, as long as there is sufficient oxygen and glucose supply. Any extra energy needed in a short amount of time is supplied by the glycogen-lactic-acid system. However, the latter limits activity time (causes fatigue) as will be explained later.

Muscles are divided into fascicles which are groups of muscle fibers (cells). Following are the most important organelles in a muscle fiber.

A sarcolemma (plasmalemma)
A sarcoplasm (cytoplasm)
Many mitochonderia
Multiple nuclei
Many sarcoendoplasmic reticula (smooth endoplasmic reticula) that surround the most important organelles, myofibrils
Many myofibrils

Myofibrils are formed of many myofilaments (actin and myosin) organized into contractile (motor) units known as sarcomeres.

Muscles contract when a threshold electrical stimulus depolarises the sarcolemma resulting in an action potential that propagates to T-tubules. At the T-tubules, the reversal of relative charge accross the membrane changes the shape of dihydropyridine receptors so they now allow for the influx of $\ce{Ca^{2+}}$. Consequently, ryanodine receptors on the terminal cisternae of sarcoendoplasmic reticula open and more $\ce{Ca^{2+}}$ diffuse into the sarcoplasm ($\ce{Ca^{2+}}$-induced $\ce{Ca^{2+}}$ release). This increases sarcoplasmic $\ce{Ca^{2+}}$ concentration. $\ce{Ca^{2+}}$ binds to troponin which changes shape. Since troponin is bound to tropomyosin, changing the shape of the former displaces the latter. Tropomyosin consequently exposes myosin-binding sites on actin so myosin can now bind, bend, detach and get back to original conformation to repeat the process (cross-bridge cycling) until $\ce{Ca^{2+}}$ is actively pumped back to where it came from causing tropomyosin to block active sites and relaxation. The magnitude of the response of the muscle to stimulation (whether acetylcholine or depolarisation can elicit an action potential) depends on

strength of the stimulus (amount of acetylcholine or change in membrane potential).
duration of the stimulus (time for which acetylcholine or charge persist).
frequency of stimulation or rise of stimulus intensity (since acetylcholine and charge accumulate).

Muscle fatigue as we know it can be attributed to different mechanisms that happen at different stations.

Neural (central) fatigue
Metabolic (peripheral) fatigue

Neural fatigue happens because the muscle stops listening, specifically because the frequency of electric stimulation is not high enough to maintain contraction. It can happen because of exhaustion of neurotransmitter (acetylcholine) stores for example. That is to say, the rate of release and breakdown of acetylcholine by acetylcholinesterase is greater than the rate of its formation and packaging into vesicles. Neural fatigue is what limits activity time in well-trained athletes. It's not associated with pain. Athletes work on increasing the capacity of their neurons to keep firing at a high frequency by training.
Metabolic fatigue on the other hand happens because the muscle gives up, specifically because of

$\ce{Ca^{2+}}$ not doing its job being too little or ineffective.
substrate shortage.

Lactic acid, being highly acidic, dissociates readily into protons and lactate. The protons, having the same charge as $\ce{Ca^{2+}}$, displace it decreasing the sensitivity of the muscle to $\ce{Ca^{2+}}$. The binding of protons can also deform proteins by breaking the bonds that form their secondary, tertiary and quaternary structures. Amino acid radical groups pick up the surplus of positive charge and the interactions between them change. Thus, lactic acid causes inhibition of active $\ce{Ca^{2+}}$ pumping outside the sarcoplasm by deforming pumps, so high $\ce{Ca^{2+}}$ concentration is maintained allowing for more forceful contraction. However, it's a matter of time until the insensitivity becomes too much. Lactic acid (which would have been an active acetate inside mitochonderia in the aerobic system) also causes hydrolytic damage to myofilaments. Any damage to a muscle is called microtrauma. Repetitive strain on myofilaments, connective tissue, tendons and bones by lengthening (eccentric contraction) can also cause microtrauma. Microtrauma results in inflammation and muscle soreness. Muscle soreness (pain) aims to stop the physical activity which can cause more microtrauma to the muscle. Muscles can adapt to metabolic fatigue and microtrauma by increasing

substrate stores (glycogen)
$\ce{Ca^{2+}}$ stores (sarcoendoplasmic reticula)
number of myofibrils (hypertrophy)
number of connective tissue fibers, to increase stiffness
diameter of nerve fiber, to increase speed of conduction
amount of glycolytic enzymes

as seen in pale (also known as type II or fast-twitch) muscle fibers, to decrease the likelihood of reinjury.

Thus, muscles don't necessarily need the ETC to generate energy and in fact, rely on the fermentation pathway for faster and more forceful activities because of its higher rate of ATP production despite its fatiguing effects which they can adapt to.

Now, we can look at the effects of uncoupling. Uncouplers work on the aerobic pathway by uncoupling oxidation from phosphorylation; they make it possible for oxidation to take place without phosphorylation. They cause proton discharge through the inner mitochonderial membrane before the threshold back-pressure required for protons to flow through ATP synthase is established. As a result, the energy from proton diffusion across the membrane is released as heat instead. This mechanism is utilized for example in brown adipose tissue where thermogenin transmembrane protein (uncoupling protein 1) causes rising of body temperature (to maintain body temperature in cold environments) and fat loss by metabolising fatty acids in stored fat which enter Krebs' cycle as acetyl groups and the resulting reduced coenzymes are oxidised by the ETC, with no oxidative phosphorylation. That's why this type of adipose tissue is more vascular relative to white adipose tissue; to maintain the high rate of oxidation which requires oxygen. The increase in heat can

decrease viscosity of myofilaments so they slide more easily over each other.
increase enzyme activity since more enzyme-substrate complexes form as enzymes and substrates move faster with greater chances to collide which increases the rate of ATP formation and utilisation.
relax blood vessel smooth muscles resulting in vasodilatation and increased blood flow, with consequent increases in oxygen supply and lactic acid removal during excercise. Whether lactic acid causes fatigue depends on the difference between the rate of its production and the rate of its flushing during activity. At rest, the remaining lactic acid is flushed or oxidised locally. We maintain the vasodilatation and high ventillation rate at rest, to oxidise the remaining lactic acid and myoglobin and form ATP by the ETC to rephosphorylate creatine to phosphocreatine (oxygen debt). The flushed lactic acid is mostly reoxidised into pyruvic acid then glucose in the liver by reversal of glycolysis, also known as gluconeogenesis (Cori cycle). The remaining lactic acid is reoxidized locally to pyruvic acid which enters Krebs' cycle instead, but the majority is flushed. The increased blood supply also helps in healing from microtrauma at rest which ultimately stops soreness. Cold, on the other hand, treats soreness directly by decreasing blood flow carrying inflammatory cells that cause pain by secreting cytokines.

Besides increasing temperature, uncoupling causes

faster flow of electrons through the ETC since the sufficient proton back-pressure is never established so ATP synthase doesn't inhibit pumping of protons and electron transfer (electron transfer is continuous). As a result, oxygen is reduced rapidly to water instead of being reduced merely to hydrogen peroxide that can cause damage if catalase is saturated and can't split the excess to water and oxygen.

Wow! What did you do? That's 1/2 a textbook! 1000s kudos! Great job! I really appreciate your effort!

Thank you. I truly appreciate your nice words. It just so happens I am studying biochemistry and physiology. So I thought why not try writing a logical, comprehensive, self-contained answer that makes total sense to make sure I understand what I am learning that can also be my reference since it integrates everything. My former answer also didn't address peroxidation so I had to fix it.


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Were these spiders burried alive by a spider wasp?
I moved a stone plate in the garden in europe, that was stored vertically, leaning against another one.
In the space between the two, I found some soil with small cavities filled with spiders.

Most of the spiders had a (what I think is a) larva attached to their backside. See the white sausage thing in the right half of the image. I noticed that there's what seems to be spider web on the right edge of the cavity.

Some of the spiders showed movement when lightly blowing air onto them. I took some of them out to get more detailed photos. The larva seems to have a white/translucent head attached to the spider body. The internals of the larva appear to be light brown through the translucent body. The larva has a thin white line at the sides of its body.

The least lively of the spiders had a larger larva attached. It has a darker inside and some white dots on its body. It disengaged from its spider and the mouth is visible.

A while ago, I found other spiders in a comparable situation. Having learned that some wasps apparently catch spiders and paralyze them, to be eaten by their larvae, I did some search and found spider wasps
Is the above the work of a spider wasp? I had a look at bugguide - Family Pompilidae - Spider Wasps, but there are no images of their burrows shown.

That's horrific.

Excellent photos. Also look up mud dauber wasp.

I agree, I'd say it is the work of a spider wasp. I'm not familiar with those, so I can't determine what species or genus it might be. But it sure does look similar to some of those stages of the larvae. Very nice pictures! I will try to find out what the white dots on the body of the oldest larva (the last and hungry one) are.

In picture (G) of your link one can see those white dots as well - would be interesting what those are all about - please keep us updated if you find out more.


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What should be considered a GC clamp in a qPCR primer?
Hello there!
After reading different sources regarding designing of qPCR primers, I'm a little confused regarding the concept of GC clamp.
Can you help me by telling which of these cases below is considered a GC clamp:
A) Any single G or C found at the last 5 nucleotides of the 3' end of a primer.
or
B) Any single G or C found at the very last nucleotide of the 3' end of a primer.
or
C) A couple of G or C (GG, GC, CG, or CC) found at the last 5 nucleotides of the 3' end of a primer.
Thank you!

Edit 1 in response to (Maximilian Press)

Here in this book titled "Real Time PCR" Page 131 , based on table
7.1 one would say that option C (couple of G or C) is the correct one
https://www.google.com.eg/books/edition/Real_time_PCR/-v-U-mXWg-gC?hl=en&gbpv=1&dq=gc+clamp+qpcr+primer+design&pg=PA131&printsec=frontcover

And in the source by Steven Bradburn, PhD. which (Maximilian Press) has kindly provided
the author explains that any single G or C base is considered a GC
clamp regardless of its position as long as it is in the last 5
nucleotides of the 3' end
which makes option A the correct one

https://toptipbio.com/gc-clamp-pcr/

Yet again in this conversation the contributor (Somanna Ajjamada) said: "GC clamping at 3', that is having a single G or C at the 3' end or  a couple of G/C within the last 6 bp at 3' end of primer"

Making a (couple of G or C) is considered a clamp and also a single G or C base is a clamp but only if the said single base is at the end of the 3' end and he also states that you should look at the last 6 nucleotides not 5 nucleotides as suggested by Steven Bradburn, PhD
This makes option B correct
https://biology.stackexchange.com/a/80622/76328

Can you clarify which sources you are looking at? It helps us to evaluate. For example this resource explains the idea and gives several examples. See also past questions on the topic: https://biology.stackexchange.com/questions/10843/when-designing-primers-how-important-is-the-gc-clamp

Thank you for response I tried to add resources showing discrepancy based on what I read elsewhere and what you have kindly provided in your response above.
Waiting your opinion!

I have never heard it being called a "GC clamp" but designing primers with GC near the 3' end is a standard way to make the 3' end duplex more stable, allowing for greater efficiency but possibly lower specificity. It is NOT a rule, just something to keep in mind. It seems some people interpret "near the 3' end" as 5 nt and others as 6 nt. I does not matter. What matters is Tm, possible secondary structures, primer dimers, too high AT content near the 3' end lowering the efficiency, too high CG content near the 3' end resulting in non–specific annealing, etc.


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Is it possible for a non-self antigen to NOT be recognized by the body?
The amazing diversity of antigens that the body can recognize (by virtue of T and B cells that express receptors complementary to them) is truly fascinating. The explanation mooted for this is the concept of V(D)J Recombination - somatic recombination creates a massive repertoire of TCRs and antibodies. As a result, any antigen, no matter how "foreign", hooks up with an immune cell triggering an immune response manifesting as a typical "cold".
I want to know if it is possible for this process of recombination to miss a particular antigen. In other words, can there be such an antigen which has no complementary antibody at all toward it?

Welcome to Biology StackExchange! Have you ever heard about antibody (binding) affinity? Namely, the ability to "recognize" an antigen is not all-or-nothing property, but a continuum (which can be quantified via affinity constant).

@Domen I am not sure if I follow, could you explain?
Do you mean to say that an antibody needn't be "perfectly" complementary to an antigen, but can somehow modify itself to better fit in if it's almost complementary?

I just wanted to emphasize that there is a varying degree of antibody affinity, and asking for "no affinity" is slightly ill-defined. Moreover, note that antigen is by definition something that can bind to a specific antibody. So I think your questions is more about whether there exists molecules that are not antigenic, right? In that case, look at haptens.

@Domen I referred the articles you linked, but I am sorry to say that I still do not understand.
For example, there are thousands of molecules in our body which, by virtue of immune tolerance, do not "bind" to antibodies simply because they are tolerated. Thus these are not "antigens". My question is - is it possible for there to be a molecule which is NOT tolerated (and thus SHOULD be "antigenic" in that it should bind to an antibody) because no complimentary antibody to it has been synthesized by somatic recombination?

@A-big-neutron Yes. Just look at vaccines - they stimulate the immune system to recognize antigen(s) that it otherwise isn't recognizing, or isn't responding to quickly enough. As far as tolerance is concerned, human proteins generally aren't bound by naturally-occurring TCRs and antibodies. However, if you were to immunize a rabbit, for example, with that protein and adjuvants, it would create antibodies to it.


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Why do flies and fruit flies exhibit two distinctive (but not exclusive) flying patterns?
I live near a forest with a canal, and often see fruit flies, they also sometimes come in our house and occasionally feed on bits of fruit. Also, sometimes I meet regular house flies here and there, and also in the city I commute to.
I noticed that most fruit flies and alike most often fly in circular shaped trajectories in the air, their curvature of flight contains bends, as if they were riding an invisible rollercoaster all the time. Their flight can be faster or slower, centered around a lamp fixture or near my face eventually, but most importantly, circa 80% of the time I see them flying in this fashion. Also, this is the way I see regular flies flying around, in 99% of cases.
On the other hand, in roughly 20% of cases when I see fruit flies flying, they fly in straight lines, with abrupt and sharp changes in their direction. This is usually (but not necessarily) slower than their rollercoaster way of flying, and it can also be varied regarding how often they change direction abruptly. However, this "sharp" way of flying is extremely rare in case of the house fly, I have only seen it two times actually, so let's say it happens in 1% of house flies.
What are these distinct flying styles? What is their cause?
Are both styles natural and should occur in healthy fruit flies, and house flies as well? Then why is it much rarer in case of house flies? Isn't the "sharp" style a result of some infection around these animals?
Those house flies that I saw flying in the "sharp" pattern were rather slow anyway, and I saw them in/near my home. Does it occur more rarely in cities?
Thank you for any helping answers, I am very curious!