text:
Why does inert gas asphyxiation trigger unconsciousness almost immediately?
According to an official safety bulletin from the U.S. Chemical Safety and Hazard Investigation Board:

"Breathing an oxygen deficient atmosphere can have serious and immediate effects, including unconsciousness after only one or two breaths."

Most people can hold their breath for at least 30 seconds and sometimes up to several minutes; clearly, breathing an oxygen-deficient inert gas will affect a person far sooner than simply holding one's breath.
An inert gas like nitrogen is not inherently toxic, so why does breathing a concentrated inert gas cause unconsciousness almost immediately? Does it replace the oxygen that would otherwise remain in the body while holding one's breath?

Truth: it doesn't. That's why Wikipedia is a terrible source for scientific information.

@anongoodnurse The Wikipedia article is merely quoting an official safety bulletin from the U.S. Chemical Safety and Hazard Investigation Board, which is why you should actually check the citations in an article. I even included their citation in my question.

I did check Wikipedia, and the article (it's curious why people assume commenters don't read the citations.) They do not cite a study to support the statement (not rodent studies or other; not even solid observations.) I've been reading scientific literature all of my adult life; I'm also a physician. That statement is flat out incorrect. There are substances/gasses that can kill in a few breaths, but inert gasses in normal circumstances are not as dangerous as the statement makes them appear. If they were, people would die from recreational helium use (they don't.)

One reason you can hold your breath for 30 or more seconds is that you are not denying your body oxygen during that time.  Wikipedia says:

After exhaling, adult human lungs still contain 2.5–3 L of air, their functional residual capacity or FRC. On inhalation, only about 350 mL of new, warm, moistened atmospheric air is brought in and is well mixed with the FRC. Consequently, the gas composition of the FRC changes very little during the breathing cycle.

Hence you are refreshing your lungs' air with only 10-15% fresh air with  each breath.  Furthermore, normal exhaled air has reduced the oxygen to about 16% from the 21% of fresh air.  So there is a significant amount of oxygen remaining in the lungs at the end of a normal breath.  When holding your breath, much of this remaining oxygen can also be used, albeit at a declining rate due to the reduced amount of oxygen.  Note also that when trying to hold one's breath it is typical to fill the lung with more air than usual, thus providing a greater amount of oxygen.
When breathing an inert gas instead of air, the situation is radically different. There is no period where you are receiving any level of replacement oxygen. Normally your blood has some oxygen in it at all times, even when returning through the veins to pick up more oxygen from the lungs.  However if the lungs have only inert gases in them, the remaining oxygen in the blood will be diffusing out of the blood and into inert gas in the lungs, making the lack of oxygen more severe.  This means that highly-deoxygenated blood will flow out to the body's tissues, where if there is any oxygen present it will diffuse out of the tissues into the blood.  This will quickly impact the tissues, and brain tissue has one of the highest requirements for oxygen.
The problem is not that the inert gas replaces the oxygen in the blood as such, it's just that the oxygen isn't available.  All gases diffuse between the blood and the gas in the lungs.  The inert gas nitrogen (79% of air) normally diffuses this way and is in balance between the blood and the atmosphere. Oxygen and carbon dioxide diffuse too, of course, but they are also helped along by the hemoglobin in red blood cells.  The hemoglobin grabs either carbon dioxide or oxygen, preferring the latter.  The gas molecules so grabbed had already diffused into the blood.  The lack of oxygen in the inert gases in the lungs means carbon dioxide will build up, which is a negative thing but minor compared to the lack of new oxygen for the tissues.

Great answer, thanks!

This answer is wrong.  Lung/plasma O2 % cannot be diluted to ~0% in one or two breaths (look at helium). The quote is an oft repeated one which has no scientific source (google it in quotes. You'll see it stated on a number of websites without one study to back it up.) Also, CO is not an inert gas, it is preferred by Hgb, yet death does not follow one or two breaths. Even cutting off all O2 to the brain (e.g. effective manual strangulation) is not immediate. The quote is nonsensical BS, which you've treated as fact. Note that there's no source on Wikipedia, which is always a bad sign.

As an example of inert gas inhalation, take helium. Someone on a talk show has a helium balloon. They exhale and take a breath (#1) and talk in a high voice. When done, they take a second breath (#2) and squeek on. Have you ever seen them suddenly keel over dead? No. Because it isn't true. The physics/physiology of breathing is much more complex.

@anongoodnurse The Wikipedia article does have a citation for the quote, it's currently citation #3 (which appears a few sentences later in the paragraph). The quote comes from an official safety bulletin from the U.S. Chemical Safety and Hazard Investigation Board, a federal agency.

No, the Wiki citation is for accidental deaths from nitrogen inhalation over a period of decades, not specifying "number of breaths" (i.e. it does not have a source for that statement.) Wikipedia editors often misinterpret scientific literature, which is why I think it's a terrible source for scientific information. Writers of publications sometimes make inaccurate statements, which make it into the lay press. This is one of them. For whatever reason, there's a lot of BS floating around as "facts".

@anongoodnurse You are mistaken. The quote which I used is a direct quote from an official safety bulletin from the U.S. Chemical Safety and Hazard Investigation Board, a federal agency. This is cited in the Wikipedia article and I included the citation in my question. If the quote is wrong, that's the USCSHIB's fault, not Wikipedia's fault. See page 2 of the bulletin.

@anongoodnurse And of course if an article on Wikipedia is factually incorrect, you should edit the article to correct the mistake.

@user45623 - I'm not a Wiki editor, and I don't make a habit of going around correcting all the mistakes on the internet. I don't know why you're so defensive of this incorrect statement; it's not directed against you personally. I'm an ER doc, and I have seen plenty of death, but not even one from an inert gas, which makes sense as there were only ~80 deaths from Nitrogen inhalation in the decade covered by the CSHIB. (That makes the likelihood of my seeing one pretty damn low.)

@user45623 - I am not mistaken; I know how to read. Most inert gasses aren't widely available, but Helium, Nitrogen and CO2 are, and recreational helium use is quite common. Have you ever seen a death from recreational helium use? Neither have I. Do you not think you would have heard of at least a few if the statement were true? As an ED doc, I certainly should have seen one or two in my career if the statement were true. However, it is not. You don't need to take it personally unless you made the statement yourself.

@anongoodnurse My apologies; I was not questioning your knowledge or credentials. It sounded like you were saying Wikipedia had no citation for the quote, and I was saying "yes, they have a citation, it's in that safety bulletin". As far as the accuracy of the safety bulletin, I have no opinion on the subject. My question was originally prompted by a recent news article about 6 workers dying from nitrogen exposure in a poultry facility; one source said they died instantly, but specifics are light. If you'd like to share your knowledge as an answer, please do so.

@user45623 - The way your question is framed, "It's not true" is not an acceptable answer, only why it's true. As to the citation, see the above comment to this user. I don't mind people questioning my knowledge or credentials; anyone can claim to be a physician. Common sense is my defense: the rarity of deaths attributed to "one or two breaths" of an inert gas compared to the common use of helium and nitrogen should be telling in and of itself.

@anongoodnurse When a question is framed incorrectly, just acknowledge this in your answer. If I wrote a question with some ridiculous premise like, "How come humans are immune to harmful effects of radiation?", it would be perfectly valid for you to post an answer explaining that humans are not immune to radiation but rather are vulnerable to radiation sickness, cancer, and other effects.

@user45623 - I appreciate your encouragement, but SE doesn't work that way. You answer the question asked, or you skip it. Comments are used for disagreement.

"Your question contains a flawed premise; here's why" is answering the question that was asked. It's a valid type of answer; I've seen it used by others and have used it myself.


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How much oxygen is released by Hemoglobin per 100ml blood
Question

Red blood cells carry oxygen from lungs to the whole body. The percent saturation of hemoglobin
with oxygen depends on the partial pressure of oxygen. Higher partial pressure of oxygen means more
hemoglobin can carry more oxygen, while lower partial pressure of oxygen means hemoglobin releases
oxygen. The relationship is shown in the graph.
Partial pressure of oxygen
In lungs = $\ce{11 kPa}$, in muscles = $\ce{2 kPa}$
100% oxygen saturated hemoglobin carries:
$\ce{20 mL oxygen/100 mL blood}$.
While going to muscles from lungs, what is the amount of oxygen (in mL) released by hemoglobin per
$\pu{100 mL}$ blood? Write it as an integer.

My progress
So, it seemed like too easy question to me.
As the graph says, Saturation of Hemoglobin with Oxygen is 100% when partial pressure of oxygen is $\pu{14 kPa}$ So, at $\pu{14 kPa}$ it carries $\ce{20 mL oxygen/100 mL blood}$
With this information, it can be said that at $\pu{11 kPa}$ and $\pu{2 kPa}$ it will carry $\pu{15.71 ml}$ and $\pu{2.85 ml}$ respectively.
Which are actually the amount of oxygen carried in lungs and muscles. So, while going to muscles from lungs, it should release
$\ce{15.71 - 2.85 = 12.86 ≈ 13 ml}$
So, $\pu{13 ml/ 100ml of blood}$
But I have confusion if this is correct reading this part

Higher partial pressure of oxygen means more
hemoglobin can carry more oxygen, while lower partial pressure of oxygen means hemoglobin releases
oxygen.

I am confused, if the way I found the difference is proper
So, I am not sure if that was the correct way. Is it the correct procedure ?

If you can solve this problem, why are you posting here? Don't you have an instructor to mark your work? This is a biology question and answer site, not a homework checking site.

I’m voting to close this question because the question appears to be an attempt to use the site as a homework checking service.

I don't have any tutor to check and I am practicing a olympiad questions which answers are never given. People here ask for efforts to add so I added how I progressed. But when I have done this, people are closing it. How funny

Your calculations are wrong and you don't seem to be using the values from the graph. For example, the graph does not show the hemoglobin 100% saturated at 14 kPa.

I think this question demonstrates the sort of effort required under our homework policy; they've shown their work towards an answer. I am also, however, a bit concerned with this site being used as an "answer checker" service when answers are not provided, even if work is shown. Questions should be asked in ways that are useful to others.

@Armand, I noticed it just now. But all I am concerned about is the process. Thanks though

I'd solve differently, in a way that removes some imprecision in your estimates and incorrect assumptions.
We care about two points on the graph: saturation at 11 and 2 kPa. At 11 it reads approximately 96% saturated; at 2 it reads about 22% saturated. So we can say the difference from 11 kPa to 2 kPa is 74% of the total capacity of hemoglobin.
If we know the total capacity is 20 mL/100 mL; then 74% of 20 mL is 14.8 mL. As an integer approximation I'd write 15 mL.
You shouldn't be caring or using the 14 kPa number at all, it's completely irrelevant. As Armand points out, hemoglobin is not 100% saturated at 14 kPa. More importantly, the graph shows that the relationship between pressure and oxygen saturation is not linear. It seems like you've done your math by assuming 14 kPa is maximal and then there is a linear relationship so that at 7 kPa it is 7/14=half, at 2 kPa it's 2/14, etc. You could plot these assumptions out on the graph and you'll find it doesn't look like what is shown at all. It turns out to be not a completely terrible approximation, since your answer of 13 mL is fairly close to 15 mL, but it's not precise enough to get to the nearest integer.

Thanks for pointing out my problems. I never noticed those errors in my assumption. Thanks a lot

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Pathogens vs Microbes and the Immune System
I hope my question isn't too basic or silly. I am currently learning about infectious diseases in Year 11 Biology right now, and I'm stuck at the concept of pathogens and micro-organisms. Whenever I search online, I get the definition for a pathogen as "a micro-organism that causes disease" but I also see other definitions that say it is just an "organism that causes disease." I asked my teacher and she said that it is an organism that causes disease, but especially a micro-organism.
Assuming that my teacher's definition is correct, why are most pathogens micro-organisms? I was also wondering, in regards to the immune system's three lines of defence, does it also apply to pathogens that are not micro-organisms, like tapeworms?

Not all microorganisms are pathogens
Firstly, not all microorganisms are pathogens - some can be harmless and some can be even essential for the host organism functioning (e.g., many microorganisms that are a part of our microbiote).
Many pathogens are not microorganisms
Here one have to mention viruses and subviral entities (prions, viroids) which are not technically organisms, although they fall itno the category micro-.
Then one has to mention pathogens other than bacteria: funghi, parasitic worms, various kinds of larvae, parasitic plants feeding on their host, etc. There are many interactions between two organisms that can be characterized as parasitism, i.e., they benefit one organism but detrimental to the other.
Disease is an ambiguous term as well
Now, even when we talk about multicellular parasites, they are usually smaller than their host. It has to do with what we call disease - indeed, this term focuses on the condition of the host organism which may or may not be due to a pathogen. In addition, a pathogen is usually understood to be in a parasitic relationship with its host, that is - it takes advantage of the host without killing the latter. This again implies smaller energy consumption which typically means smaller size. If a "pathogen" killed a host and consumed it as a whole (or most of it), we would not be calling it a disease/parasitism, but rather a predator-pray interaction.

Just a note that plenty of pathogens are deadly (ebola and rabies spring to mind) even if they don't consume the whole organism.

Most diseases that cause death don't do it by consuming the host, but by causing gradual decline in their metabolic functions or damage to crucial organs.

@Armand This is a good point. But their energy needs are still much smaller than those of the host, which is related to their size - the reason why they are deadly is because they locally disrupt vital functions in teh host, as Barmar has pointed above.

@Barmar Thanks for this precision. See my comment above.

Terminology in biology often gets a little fuzzy around the edges, sometimes as a result of overlapping definitions, or the desire to avoid overlap. For whatever reason, many eukaryotic pathogens are more commonly referred to as parasites. This seems to be more common with (though not exclusive to) multicellular parasites, like tapeworms, possibly leading to some definitions which exclude them as pathogens (even though they are clearly causing infectious disease). A more generalized technical term for pathogens, often used in biosafety protocols and research regulations is 'infectious agent.' This covers the whole gamut of infectious parasites, protozoa, fungi, bacteria, viruses, and non-living agents (like prions) with less potential for ambiguity.
But, the hard truth is that many biological terms lack a rigid and universally agreed upon definition. Conflicting or even ambiguous definitions can persist because such definitions aren't always necessary for biologists to perform productive research. I don't need to know if guinea worms are technically considered parasites or pathogens or both in order to study their transmission and pathology. I don't need to know if prions are living or not to study the infectious diseases they cause. What's more important is to have working definitions that don't cause confusion when used consistently in a given context (in your case, that context is learning year 11 biology).
In response to your second question:

Assuming that my teacher's definition is correct, why are most pathogens micro-organisms?

This answer is a bit of speculation, but, the vast majority of biological diversity on Earth is microscopic. Given how outmatched we multicellular organisms are, both in numbers and diversity, it's a wonder of nature that we persist at all. Eukaryotes are a small branch on the tree of life, and multicellular organisms are only a small minority of that branch. Plus, the most abundant and diverse biological entities on the planet, viruses, don't even have a permanent home on that tree.

I love this idea: "Given how outmatched we multicellular organisms are, both in numbers and diversity, it's a wonder of nature that we persist at all."

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Do TADs derive from operons?
TADs (Topologically associated domains) are DNA sequences in the eukaryotes genome (except plants) that are between two sequences named "Insulator". The genes in TAD just are affected by enhancers and suppressors that are in the same TAD.
This structure can be seen in operons that exist in bacteria. Is there evidence to say that TADs derived from operons?

The short answer is "no".
Operons have very closely coupled regulation, even in eukaryotes. The classic operons are polycistronic, meaning that transcription of adjoining genes occurs as part of the same process.
TADs on the other hand are merely (not always very well defined) regions in between insulators, as you say. They probably have some common regulatory context, but it is nothing like the direct coupling observed in operons.


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Tiny deep red flower shrub species ID
I found this plant with maple like leaves blooming after rains this july.I am in Bhubaneswar,India.

It's Jatropha gossypiifolia, a medium-sized (maximum 15m) shrub.The leaves are similar to the leaves of a cotton plant (Gossypium). Often categorized as an agricultural weed. Poisonous for mammals also. Commonly used for the production of Biodiesel.
As per wikipedia-

There are many common names for Jatropha gossypiifolia including bellyache-bush, black physicnut, and cotton-leaf physicnut in English; pinon negro, pinon colorado, and tua-tua in Spanish; medicinier noir and medicinier rouge in French; mamoninha and peao-roxo in Brazil; jarak merah and sibidigua in India.[4]

NCBI Taxonomy ID: 454931


text:
What does it mean to quantitatively describe a cell?
To begin this question, I will quote Molecular Biology of the Cell (page 38):

... Biological systems are, ..., full of feedback loops, and the behavior of even the simplest of systems with feedback is remarkably difficult to predict by intuition
alone; small changes in parameters can cause radical changes in outcome. To go from a circuit diagram to a prediction of the behavior of the system, we need detailed quantitative information, and to draw deductions from that information we need mathematics and computers.
... You might think that, knowing how each protein influences each other protein,
and how the expression of each gene is regulated by the products of others, we should soon be able to calculate how the cell as a whole will behave, just as an astronomer can calculate the orbits of the planets, or a chemical engineer can calculate the flows through a chemical plant. But any attempt to perform this feat for anything close to an entire living cell rapidly reveals the limits of our present knowledge. The information we have, plentiful as it is, is full of gaps and uncertainties. Moreover, it is largely qualitative rather than quantitative.
(Johnson, A. D., Roberts, K., Lewis, J., Morgan, D., Raff, M. C., Walter, P., Alberts, B. (2015). Molecular Biology of the Cell. United States: Garland Science, Taylor and Francis Group.)

Thus comes a fundamental question: what does it mean when cell biologists want to quantitatively describe a cell?
In my understanding, a cell is a complex system, and a quantitative description of it invokes treatment of the cell as a mechanistic, mathematically determinate system. For example, a projectile in the context of Newtonian physics is a product of such treatment. Physicists use a series of equations to represent motion of the projectile. They also plug in initial values such as velocities and positions to supplement the equations.

As an analogy, quantifying a cell might mean finding a series of mathematical expressions for every chemical reaction or every biochemical inside a cell, and using a set of initial conditions to calculate the overall state of the cell at its very beginning. In this way, cell biologists can theoretically calculate figures of interest for whatever chemical reaction at any point during the cell's life. Of course, such an effort would be astronomically large and complex, and not feasible at present.
However, if this is what quantification of a cell means, why do Bruce Alberts and other authors cite feedback loops as a hurdle that stands in the way of quantifying a cell? How do feedback loops affect quantification of a cell?

I don’t think cell biologists have or ever had any interest in “quantifying“ cells, whatever that may mean — and it will certainly mean little to people describing themselves as cell biologists. By definition and the origin of the term, these are people whose interest lies not at the molecular or chemical level, but in the behaviour of those components visible through a microscope. The book section quoted is at best an apologia for the non-molecular or numerical nature of the discipline. It worst it is pretentious nonsense and in any case it is best ignored.

The 2017 article "The quantified cell" ( https://www.molbiolcell.org/doi/full/10.1091/mbc.e14-09-1347 ) seems appropriate to cite here

Quantitative in the context of biology is similar to chemistry, and means "how much of something there is" - for example, how much of a particular protein is produced under what conditions.
Now, you might think this is a simple problem, just measure the protein/RNA/DNA and find out. However, it isn't quite as simple as that. Even if the best methods we have were truly quantitative (e.g. see Western blot quantitation for measurement of protein changes), which a lot of them aren't, the changes you see in one cell type might be different in another cell type (or even between cell lines of the same type of cell) and certainly between species.
You then have to consider - how well does a lab strain of something (say a bacterium like Escherichia coli or a cell line or cultured virus) differ from those found in the wild, and how does that vary geographically.
Life consists of huge numbers of feedback loops - stimulus results in action, which removes stimulus, which returns to baseline, allowing stimulus to function again. You experience this all day, every day of your life. It is how things like nerves function for example. In almost all situations it is not a single input results in a single action, rather that multiple inputs result in multiple outcomes, meaning an interconnected web of feedback loops. Have a look at this figure for a well known pathway and well studied, Caspase 3 signalling, from this article (I have no affiliation to the study):

This is one of the simple ones, which results in just one form of cell death - notice how many inputs there are and all the players. In general we can model 2-3 part systems fairly easily, so to work this out, each individual part of it needed to be studied and worked out empirically, determining which parts interact with which and why they do that under what stimuli.
Go and have a play at string.db with something like the well known and heavily studied tumour suppressor p53 (hit search, type in p53, choose human (Homo sapiens), then hit continue). Keep clicking the "more" button on the results page, and it will give you some idea of just how complex this is. Similarly, have a look at a metabolic pathways chart - this happens in every single cell.
We cannot currently reduce life to equations.

Even more fun: many of the feedback loops share the same intermediate signals so that when one loop is running, it implicitly modifies the behavior of the other loop.  The biggest difference between biological and engineered systems is that biological systems have absolute no design constraint for comprehensibility.  Evolution can and will build ridiculously complex systems that stretch belief as to how they can possibly work, yet somehow they do or they wouldn't have been selected for.

Quantitative vs. qualitative
Quantitative description usually implies numbers, rather than just saying which response follows which stimulus. For example, describing a chain of biochemical transformations is qualitative description - we know what processes happen, in which order, etc. Quantifying how many of the molecules would actually undergo this transformation up to a certain step (or to the very end) would be an example of a quantitative description.
Types of quantitative description
Quantitative description usually implies doing some math to relate the input and the output parameters, although the origin of the equations can be different. One typically distinguishes:

first principles description - when the model is based on the fundamental laws of chemistry and physics;
phenomenological description - when one uses the laws attested experimentally.

Examples of quantitative description of a cell
One should not really be looking for one fits all sizes mathematical model. Rather, the mathematical/quantitative description is usually tailored to a problem in hand. I give below a few examples, but this list is by no means exhaustive:

elastic properties - one can use elasticity theory to describe the deformations of a cellular membrane in response to pressure, attempts to pierce it, etc. In the former case one may be able to provide the mathematical expressions for the shape of the cell in response to specific level of pressure, in the latter one aims at determining the breakdown point
transport of chemicals/molecules - most of molecules absorbed by a cell or produced in it, travel to their destinbation via diffusion or with convection flows. Such flows can be modeled using diffusion equation and hydrodynamics equations respectively. Alternatively, if we are dealing with more directed transport chains, various random walk models become of great use. This allows to extimate the efficiency and the speed with which chemicals are transported to their destination.
transcription/translation are routinely described quantitatively, e.g., using rate equations models for the transcript/protein molecular growth.
Protein and RNA folding are a domain where thermodynamically motivated energy minimization has been of use for many decades.
Cellular dynamics is often modeled using non-linear dynamics, e.g., an HIV infection goes through a few phases: early on the auxhiliary proteins for reaction catalysis and interfering with the cellular machinery are produced, which is followed by synthesis of the essential proteins and then the new viral genomes. The transition between different stages is triggered by concentration of earlier synthesized proteins, and is nicely modeled by non-linear equations similar to Lottka-Volterra type. The feedback loops mentioned in the OP are often studied using non-linear dynamics.

One could go on further, to propose quantitative models for describing optical, thermal, chemical, replication, growth, and other processes - whatever is of interest. I suggest consulting the books I cite below for information on more specific topics.

References

Phillips et al., Physical biology of a cell
Keener and Sneyd, Methematical Physiology: I Cellular physiology

Let’s start by considering a very simple feedback loop, namely a system with just two genes A and B which repress each other.
Such a system can be in two possible states (it is bistable):

A is expressed and thus suppresses B, which is not or hardly expressed.
B is expressed and thus suppresses A, which is not or hardly expressed.

We may perfectly understand this system on the biochemical and genetic level, which allows us to quantify the two above states.
However, without further information about the system’s history (initial state), we cannot say in which state the system will be at a given time.
Moreover depending on the strength of the expression it may be that the system occasionally switches between the two states just due to noise.
(Note that for the above bistability, a second ingredient is needed, namely non-linearity, but we get that from the thermodynamics of chemical reactions and genetic expression anyway.)
Now, in a cell you have a myriad of such feedback loops intertwined, which grants you a bazillion potential states to consider through combinatorial explosion.
The challenge is now to figure out which of these states are generally and historically plausible.
This is horribly difficult even when you perfectly understand all the individual molecular processes.
Note that through the complexity you have more than just binary on and off states like in my introductory example, but a fine spectrum of potential states which gets fully continuous through molecular noise – thus affecting quantification.
A helpful analogy might be a modern computer running several interacting programs compiled with a highly efficient compiler.
You can perfectly understand single operations on the level of a transistor and similar fundamental components, but this doesn’t get you very far with understanding the programs that are running.
Also, to even remotely predict the computer’s behaviour, you need its history, i.e., what is currently stored in memory.


text:
Help identifying this Queen Ant
Could someone please help us identify this queen ant ?  We live in the North Island of New Zealand. So far our google image searches haven’t found a match. Any help would be appreciated.

Any chance of more photos? if you can, to count the teeth in the jaws at the front, number of segments in antennae, segments on abdomen etc. from above also.


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Difference between live and dead body from atomic perspective?
Sorry if this is a dumb question, recently I have been interested in the question of how "life" should be defined and got a specific question:
If we compare a live body of a person and a dead body of someone who just died, what is the difference in term of their molecule? Say for example, when the heart stops beating, the blood won't cycle through the body, but if we focus on individual cells, say the blood cell, which has hemoglobin molecules, it stops carrying oxygen when the person dies, but if we dig further, the hemoglobin molecule is defined as:

A hemoglobin molecule is made up of four polypeptide chains, two alpha chains of 141 amino acid residues each and two beta chains of 146 amino acid residues each.

A bit more further we would reach the microscopic world, where there are atoms, protons, electrons, etc, AFAIK, these things would still obey the rule of thermal motion, although the motion may be less active due to the reduced temperature of the dead body.
So from the atom's perspective, what is the difference between a live person and a dead body?
Thanks and sorry again for this dumb question!

From atoms prospective there is no difference. It is like a car that has crashed: from the atomic (and even material) perspective it is still a pile of metal, glass, and plastic... but the shape of the parts and their position in respect to each other are such that it cannot function anymore as a car. One could say that being a car is more than just being a collection of atoms - it is an emergent property. You can search this site for emergence.

Thanks @RogerVadim to me the car example feels a bit different, a dead body can be lifeless without any damage or deformation, yet there is no life in it, the atoms, molecules, organs, skins, etc, are still in good shape, it's more like a machine that runs our of power and no power can be provided to it for some reason, and comparing such a machine with a running machine that does have power supply, there's no difference even between parts / components.

@hzhu What you say is correct. The difference is that car materials are stable, soone can restart it long time after it stopped, whereas the molecules in an organism start to degrade. If new molecules are not synthesized, this degradation becomes irreversible. In other words, there is damage, even though it is not immediately visible. Although forensic scientists are trained to see even insignificant markers.

None.
Say you were to take a skin sample from a living individual, and a skin sample from a deceased person. If you were then to somehow extract and isolate a single atom from each sample, they would be indistinguishable. In other words, if you were to mix up the two atoms, there would be no way if telling which came from the deceased individual.

From an atomic level which I believe you are after, the difference is quite simply, the living body has electricity running through it.  Without electricity the atoms in your body could not be manipulated by cells to become more negatively and positively charged leading to a voltage and ultimately a current the central nervous system takes as a signal for your heart to beat, for an arm to move, to breath.  So atomically the living and the dead are the same.  But the living person through the process of the nerves and other cells create electricity through a process of letting in sodium or potassium.  Obviously food is where we get the atoms to not only build tissue but the energy to make our own electricity.


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Why did Rivers replace Koch's postulates?
In 1937, Rivers introduced a new set of postulates that were meant to replace those formulated by Koch.
However, I couldn't find an article (or other scientific literature) that describes why Koch's postulates weren't valid anymore.
Is there literature that explains why the old postulates were not valid anymore?

What's wrong with the reasons Rivers gives?

If you read his 1937 article, Rivers himself makes a case for why Koch's postulates are too restrictive and that all the postulates need not be satisfied to confidently associate a pathogen with a disease. Here, I've highlighted excerpts and added my own emphasis.

[Koch's] dictum has had a profound influence on workers investigating infectious maladies and for many years an infectious agent was not accepted as the cause of
a disease unless the postulates had been satisfied. With the development of the science of immunology, however, immunological reactions added much to the knowledge of the specific relation of microbes to disease, and now it is possible to bring excellent evidence that an organism is the cause of a malady without the complete satisfaction of the postulates.
...
At the time when they were formulated Koch's postulates were essential for the progress of knowledge of infectious diseases; but progress having left behind old rules requires new ones which some day without doubt will also be declared obsolete. Thus, in regard to certain diseases, particularly those caused by viruses, the blind adherence to Koch's postulates may act as a hindrance instead of an aid.

Koch's postulates were published in 1890, but the first virus wasn't isolated until 1892 (at the earliest), so the postulates cannot be readily applied to diseases resulting from viral infections. That is not to say Koch's postulates were wrong, just that their blind application to all diseases may prevent the identification of novel etiological agents due to the requirement for isolation in pure culture. Rivers addresses this, and supplies less restrictive postulates for the characterization of viral infections.

It is obvious that Koch's postulates have not been satisfied in viral diseases. Moreover, it is equally evident that proof of the etiological significance of viruses has been obtained without their satisfaction. Such a statement, however, does not imply that certain conditons do not have to be met before the specific
relation of a virus to a disease is established. The conditions are: (a) A specific virus must be found associated with a disease with a degree of regularity. (b) The virus must be shown to occur in the sick individual not as an incidental or accidental finding but as the cause of the disease under investigation.


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Can chain-linked genetic segment data be used to reliably assign unknown relatives to either the donor's mother or father?
I am analyzing DNA matching segment data, and I am trying to broadly group all DNA matches by my donor's parents.
Based on documented evidence, I can confidently identify "Person 'B'" as a familial match to my donor "Person 'A'" via a particular parent.
Is it probable that extrapolating the assignment of family members to each of the donor's parents by 2nd and 3rd step matching will yield accurate results?  I will explain my question more clearly below.
In my graphic below, persons 'A' and 'B' are known relatives via paper trail documentation.  "Person 'C'" shares common DNA segments with both 'A' and 'B', so I want to know if it is safe to accept "Person 'C'" as being related via the same parent as "Person 'B'" is to the donor without a supporting paper trail.
Furthermore, if it is indeed acceptable to identify person 'C' as being related via the donor's same parent, would it be safe to also assume that "Person 'D'", who does not match "Person 'A'" (aka the donor) or 'B'(the paper-trail linked relative to the donor) on the same segment as "Person 'C'" but matches the donor and person 'C' each on unrelated segments, is a genetic match via the donor's same parent?
Here's a graphic to illustrate my scenario described:

If, in the illustration, person 'B' was known to be related to 'A' via the donor's father's side, is it highly probable that person 'D' would also be related via his father's side as opposed to his mother's side?
For the purpose of this question, assume any direct descendants of the donor are excluded from the analysis, only ancestors and branching descendants (parents, uncles, cousins etc.) are included .

Much depends on how unique your "matches" are. If they are short matches of low-polymorphism stretches of DNA, they are not worth much.  I'm a bit confused about what you mean by "related via ... side" in your examples. Posting one or more possible or putative family trees would help clarify things.

I'm finding that the answer is no. At least without considering polymorphisms. I did this across the donors father's matches, and the result is that about 84% of the donor's DNA would have come from his father. So that's definitely not right.


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The very first living organism model
Can you advice me where I can find explanation, what was the very first living organism on Earth? I am looking for nicely explained material, preferably with some 3d models and animation, showing how it could work. Maybe a computer emulation?
The sources I was able to find so far were very theoretical and dry, they didn't allow me to get a good grasp on the concept. Basically I am looking for the simplest living organism possible in order to get a good grasp on the mechanics of life.
From the sources I studied so far I understood that it was just a molecule of RNA, which could copy itself, right? But I didn't find exact description how it could look like..

Not the first living organism, but Julia Child on how to make primordial soup: video

Nobody knows for sure -- there are many theories, tending to be quite general. "RNA world" is indeed one theory, but there are others. You will become quite celebrated and famous if you end up providing an answer for your question.

Does this answer your question? Thermodynamically, how did the first cell arise?

@Armand Haha, yes! After asking the question I found out that nobody got an idea what was the earliest self-replicating structure in the first place. And I wanted to see a nice simple model of it!

@Luigi Not quite, but it is an interesting information. I wanted a visual easy to understand model of the first structure that could replicate itself. But it seems that it is yet unknown.

Fundamemtal basis of establishing something as living is the capability of replication and producing copies of forms similar to itself. Therefore, something which has two properties  i.e to act as enzyme and information carrier at the same time can perform that function and qualify to be called as first living *(but we will call it first living system or molecule not first living organism some say so, there are many arguments, depending upon how they look upon something to be called as living, it is itself a big question but it seems strongly persuasive that something like RNA world model is surely first form of life) This system is self perpetuating(heredity is basis of evolution and this is basically  heredity). If you want the story behind how it was done and quench your thirst (its short read) I'm giving the link below
https://www.sciencedaily.com/releases/2009/01/090109173205.htm
After you'll read that It was not easy to make this cross replicating system. And get that result to establish grounds of RNA world.


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Identification of a plant
Please help me to identify this plant

The plants can be found on italian balconies and I would like to buy one, but I do not know what I should look for.
The habit of the plant is trailing.

Can you give us more information please? - what is the habit of the plant - trailing? Upright? If you have any photos of flowers that will definitely help with identification.

Yes, the habit of the plant is trailing. I will try to make more photos, but I do not think I have seen some plants with flowers...

This looks to me like it may be a type of Jade plant, genus Crassula.  Probably many cultivars out there.  Alternatively, may also be a Sedum.

This is likely to be a stone plant (Aizoaceae), depending on habit, it could well be the ice plant (Carpobrotus edulis). Stone plants are a quite diverse family of succulents from southern Africa, but are widespread throughout the western world as stabilizers of sand-dunes and in gardens as they are very tolerant of lack of watering and high salinity.
Ice plants are very common in the Mediterranean region, having become an invasive pest on much of the coastline.
If it is ice plant, then you can sub-cultivate it by taking a small part of the plant, usually leaves with a bit of stem, but even a leaf by itself may work, and placing it in water or on sandy soil. With regular watering, it should grow roots and then be plantable.
Apparently the leaves of ice plant are edible (hence the edulis part of the name), similar to Aloe I suspect.


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Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C? (but not much higher)
Background
Discussions below several recent posts in Space SE (links below) indicate that bacterial spores are a serious problem when considering how to prevent a future spacecraft mission to subsurface ocean worlds like Europa or Enceladus, ice-crusted moons of Jupiter and Saturn believed to have substantial liquid water oceans below.

Is there any demonstrated or even proposed technology that can sterilize a spacecraft with 100% certainty and yet leave it electronically functional? The answers posted are essentially "No"
Who decided that a <1 in 10,000 probability of contaminating the europan ocean by a viable Earth microorganism was legally and ethically sufficient? The answer seems to be "nobody" and the value comes from a temporary guideline from the early 1960's. "Legally and ethically" comes from a block quote from a 2016 document.
This answer to Why are we trying to prevent life from spreading via landers rather than actively encouraging it?
This answer to Why aren't there any robotic missions on Europa or Enceladus? where item #5 and exchanges in comments lead to a meta post. That absolute sterilization is considered currently unachievable for a working spacecraft poses the challenge of deciding what is sufficient and acceptable. It's a head-scratcher of a quandary.
Are any space agencies working on a 100% reliable sterilization technique for spacecraft bound for subsurface ocean worlds?

The 2018 Extremophiles paper:
All that discussion of bacterial spores lead me to Beladjal, L., Gheysens, T., Clegg, J.S. et al. Life from the ashes: survival of dry bacterial spores after very high temperature exposure. Extremophiles 22, 751–759 (2018). https://doi.org/10.1007/s00792-018-1035-6 (also downloadable from researchgate).

Abstract
We found that spores of Bacillus amyloliquefaciens rank amongst the most resistant to high temperatures with a maximum dry heat tolerance determined at 420 °C. We found that this extreme heat resistance was also maintained after several generations suggesting that the DNA was able to replicate after exposure to these temperatures. Nonetheless, amplifying the bacterial DNA using BOXA1R and (GTG)5 primers was unsuccessful immediately after extreme heating, but was successful after incubation of the heated then cooled spores. Moreover, enzymes such as amylases and proteases were active directly after heating and spore regeneration, indicating that DNA coding for these enzymes were not degraded at these temperatures. Our results suggest that extensive DNA damage may occur in spores of B. amyloliquefaciens directly after an extreme heat shock. However, the successful germination of spores after inoculation and incubation indicates that these spores could have a very effective DNA repair mechanism, most likely protein-based, able to function after exposure to temperatures up to 420 °C. Therefore, we propose that B. amyloliquefaciens is one of the most heat resistant life forms known to science and can be used as a model organism for studying heat resistance and DNA repair. Furthermore, the extremely high temperature resistivity of these spores has exceptional consequences for general methodology, such as the use of dry heat sterilization and, therefore, virtually all studies in the broad area of high temperature biology.

Here are two separate excerpts from the Results and discussion section that seem germane to my question:

These observations showed that extensive DNA damage occurred in the spores during exposure to extreme heat. While no germination of inoculated spore ashes occurred immediately after heating, continued incubation did indeed result in germination and vegetative cell growth (Fig. 1c). That result, together with the fact that DNA was present in the spores, suggests that spores of B. amyloliquefaciens contain a very versatile and efficient DNA repair mechanism able to “reverse” the heat-induced damage, resulting in spore germination and the production of vegetative cells.

Remarkably, activity was found for these two enzymes immediately after heating, showing clearly that these proteins survived extreme temperatures within the spores of B. amyloliquefaciens. Moreover, we also found that both enzymatic activities were preserved at the same levels, over two generations (Fig. 5). We assume it is very likely that spore proteins are responsible for the repair of damaged DNA after extreme temperature exposures.

My current understanding is that it is proposed that the spores contain proteins that are ready to repair the substantial DNA damage caused at 420 °C as soon as the spores are incubated.
Question
Is it known how some heat-resistance Bacillus spores repair their DNA after having been heating to 420 °C? Do spores so treated then incubated first absorb enough water to provide mobility for these proteins to start moving around and repairing the DNA? Do they require energy to do this? If so, is the energy source stored in the spore or absorbed from the incubation medium?

Fig. 2 Quantitative survival of dried spores after heating at different temperatures

Here's a good place to start:  doi: 10.1128/MMBR.05020-11 https://dx.doi.org/10.1128%2FMMBR.05020-11
DNA Repair and Genome Maintenance in Bacillus subtilis


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delta coronavirus: Why isn't similar viral load in vaccinated people causing as severe adverse effects as in unvaccinated people?
In latest news, it is reported that:

if vaccinated people get infected anyway, they have as much virus in their bodies as unvaccinated people. That means they're as likely to infect someone else as unvaccinated people who get infected.

But vaccinated people are safer, the document indicates. "Vaccines prevent more than 90% of severe disease"

I've understood in general viral load is related to severity of the sickness. Do we know why would it not be in this case?

I believe the news report you cited is not accurate in its reporting.  Of course, it's not actual science, and we will wait for the release of the actual science, but here's my understanding (which may end up being wrong):

if vaccinated people get infected anyway, they have as much virus in
their bodies as unvaccinated people.

This seems to be incorrect. My understanding is that the CDC info looks at vaccinated people who were infected AND developed COVID symptoms, not all vaccinated and infected people. Also, the tests did not look at the virus levels in the whole body, just in the nose and throat. Obviously, the nose and throat release virus into breath which is exhaled, so that directly impacts how contagious a person might be.  However, what should be important for the person's own level of illness is the amount of virus in the lungs and other internal systems, not the nose and throat.
This mis-reporting would seem to account for the apparent discrepancy you noted.

I'd say this is consistent with my understanding, too: there's a sampling bias here. I think the reporter misunderstood and should have written "if vaccinated people get infected anyway and are symptomatic, they can have as much virus in their bodies as some infected unvaccinated people". Those nuances don't always make it to the news articles.

I now found these links from CDC: 1 and 2, which claim "Real-time RT-PCR Ct values in specimens from 127 fully vaccinated patients (median = 22.77) were similar to those among 84 patients who were unvaccinated, not fully vaccinated, or whose vaccination status was unknown (median = 21.54)." - so not sure if discrepancy is fault of the news report.

@eis The data in your MMWR link seems consistent with my and Bryan's description. In particular, the MMWR did not discuss "if vaccinated people get infected anyway", but rather (mostly) symptomatic people who were then discovered to have been vaccinated. That is, the group studied was selected from among those who were already known to be sick, not a random sample from among vaccinated individuals in general.

@Armand however, I think "some" are not consistent - it would seem from the data that pretty much all examined people did have roughly as much virus (in their throats and noses). Of course, the amount of people involved in this study is small and there is selection bias, but at least in this study the levels seemed to be similar in all samples they had, if I'm reading this correctly.

@eis You may have misinterpreted the whisker plots in Fig. 2 from CDC. The larger an RT-PCR Ct value, the less target was present. Normally, Ct values as small as 38-40 are considered very weak/negative results. The plot shows that some of the vaccinated infected had Ct values this small, while none of the unvaccinated group did.

First of all there is one error in the article: Vaccinated people do not get infected anyways. Vaccination prevents somewhere between 80-90% of infections (see reference 1). There is no perfect protection against infection, but in the symptomatic cases the viral load goes down much faster in the vaccinated people than in the unvaccinated (reference 2):

The figure show the Ct-values of the PCR from infected patients (figure 1 from reference 2). The lower the Ct value, the higher the viral load. However, this is only a test for the presence of viral RNA, it does not state how infectious these patients are. There are good indications (see reference 3) that vaccinated patients are not as infectious as unvaccinated patients.
And this might be the reason why vaccinated people have less severe disease when they get infected. Lower viral loads (or a faster reduction), less infectious virus which both means less cells in the body can be infected and affected. To sum up: Yes, vaccinations are highly recommendable as well are boosters.
References

Impact and effectiveness of mRNA BNT162b2 vaccine against SARS-CoV-2
infections and COVID-19 cases, hospitalisations, and deaths
following a nationwide vaccination campaign in Israel: an
observational study using national surveillance data
Virological and serological kinetics of SARS-CoV-2 Delta variant
vaccine-breakthrough infections: a multi-center cohort study
Longitudinal analysis of SARS-CoV-2 vaccine breakthrough infections
reveal limited infectious virus shedding and restricted tissue
distribution


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How RGB cones see other frequencies?
Orange,violet and yellow have different frequencies.
How can we see them, as we have only three receptors rgb?
Merely combining those frequencies cannot generate a new one.

This question has rather detailed answers in the physics community. In a nutshell - they don't see other frequencies, but rather the color is determined by our brain by the relative excitation of different cones.

How does your compute display create all sorts of colors when it has only 3 colors of pixels?


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What's the process for determining whether a GC -> AT conversion in bisulfite sequencing is due to degradation?
I'm working on an ancient DNA project (humans) examining the methylation patterns for a single nuclear gene on chromosome 5. I understand the protocols of bisulfite sequencing, and in general how the methylation is identified from the sequence results, but due the degradation in ancient DNA, some methylated cytosines may become deaminated to thymines, creating a GC->AT conversion. Since bisulfite sequencing allows for all retained C's to be classified as methylated in the original sequence, I'll be underestimating methylation depending on how degraded the samples are. Is there a way to address this?


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Does mixing alcohol types result in faster intoxication or worse hangover?
There is a widespread belief that mixing (drink one, then the other) alcoholic beverage types results in faster intoxication and/or worse hangover. E.g. beer, wine, vodka etc. The claim is that sticking to one type is better. Even drinking different brands of e.g. beer is sometimes claimed to cause the same effect.
Is there any truth? Compared to simply computing volume * % alcohol = drunk amount. Assume time to drink that amount is constant e.g. 4 hours.

EDIT:
Thanks guys for the comments and especially @MikeyC's answer! Despite the poorly worded question.
This is a hot topic among youngsters (which I am unfortunately not anymore) but Skeptics.SE (as I flagged my question to possibly be moved to) would have been a poorer fit there as here are all the experts.
Peace.

How can one objectively measure a hangover?  Also, the title is confusing: when you say types of alcohol, I'd expect questions about how for instance methyl & isopropyl compare to ethyl alcohol.

@jamesqf I know nothing of biology. I have flagged the question for moderation attention. But in the meanwhile - edit away, or even recommend me to delete it. By 'alcohol' I mean conventional ethanol.

I think that the belief arise because mixing alcohol types correlated to drinking a lot (and some of bad quality among them) and that correlates to worse hangover. I don't see any chemical base for the belief.

Skeptics.SE requires a "notable claim"; basically, you have to reference something specific making the claim rather than a vague "widespread belief". That said, we don't typically migrate questions that have been answered.

@Vorac: But all varieties of alcoholic drinks have the same type of alcohol: ethanol.   Other common alcohols are toxic, for instance the occasional batch of bad moonshine that containa methanol.  The difference is the other components.  I've seen claims that hangovers are mostly due to the other stuff, not the alcohol.   I don't know if they're more than anecdotal, though, and have insufficient personal experience to judge.

I did a quick literature search for clinical studies, not expecting to find much, but I actually found a published study partially investigating this question using a pretty robust study design. In short, mixing beer and wine didn't seem to impact hangover severity. Since it only covers beer and wine, you'll have to set up your own clinical trial to see how liquor plays with others.
They set out to test whether drinking beer before wine (or vice versa) contributed to greater hangover symptoms, with control groups drinking beer or wine alone. They found no difference in hangover severity between those who mixed beer and wine (regardless of the order in which they were consumed) and those who had only beer or wine. Perceived drunkenness and the occurrence of vomiting were the best predictors of hangover severity. Interestingly, the most objective measure of drunkenness used, peak breath alcohol concentration, was a poor predictor of hangover severity.

Reference:
Köchling J, Geis B, Wirth S, Hensel KO. Grape or grain but never the twain? A randomized controlled multiarm matched-triplet crossover trial of beer and wine. Am J Clin Nutr. 2019 Feb 1;109(2):345-352. doi: 10.1093/ajcn/nqy309. PMID: 30753321; PMCID: PMC6410559.
Full Text Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6410559/


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What is the structure of PduK in the Pdu BMC?
My lab is creating 1,2-propanediol utilization bacterial microcompartments (Pdu BMCs) with an operon containing genes for PduA, PduB, PduJ, PduK, PduN, PduU, and PduT. According to Mayer et al., all of these Pdu proteins form homohexamers, except for PduN, which forms homopentamers. Additionally, all of these Pdu proteins, except for PduK, can be found in the Protein Data Bank. Where can I find information on the structure of PduK in the Pdu BMC? Is there a reason for this apparent lack of PduK crystallography data online?

If the structures of all the other Pdu gene products are in PDB, then presumably the structure of PduK has not been determined for Lactobacillus reuteri. Why this is so is anyone’s guess. May be difficult to crystallize, group run out of money, in progress etc.  Best to email the lead author, Yeates, and enquire. (And thanks to @acvill for pointing out  that I'd got  the genes confused in my answer, now deleted.)


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I saw these strange bee in my garden, and they drag little insect and/or caterpillar to their nest

I saw these strange bee in my garden, and they drag little insect and/or caterpillar to their nest. What are they?
When I catch them by gloves, their body is extremely hard. I notice since a few of my normal honey bee are found dead on the ground. I am in tropical region, is this a type of Asia Hornet? I haven't seen US hornet, so I can't compare, but I felt like these bee are much smaller than the American Hornet for some reason. These bee are either smaller or same size as our Asia honey bee.
Is there anyway I can find the nest? I saw a bunch of small insect near where I saw 1 Asian giant hornet (I am assuming this is a hornet, I will exterminate them regardless, just want to verify if this is indeed Asia Giant Hornet - though this is quite small to be call giant). Is it plausible that where they gather the insect is where their nest is?

Welcome to Biology.SE. Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this essential information — also try searching online for "Asian Giant Hornet". ——— Finally, please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

In addition, your question isn't really clear — I'm assuming that what you really want to know is the identity of this insect. If so, please remove the irrelevant parts of your post. Note that "is this dangerous" isn't a good question for this site — it depends on many factors. Is the question: Is this dangerous to humans or some other organism(s)? If to humans, we don't answer personal medical questions and what constitutes "danger"? Anything with mouthparts can bite and that type of insect could be able to sting. Does the person in question have an allergy?

if you don't have another photo take another picture of that plate with a ruler paid across it, preferably from a similar angle. but yes location will be important.  I also suggest googling "parasitic wasp". behavior wise it seems like a fit.

where are you located?


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What is this super-fly?
This fly repeatedly buzzed in my girlfriend’s ear. Eventually got it from it being caught in her hair. I clapped it between my hands. It fell on the floor and twitched a bit as flies sometimes do. It started walking away again. I hit it hard with the side of my fist against the carpet. Still going. I hit it multiple times and it left a blood mark. I went to get some paper to collect it. And it’s walking away again! I pinched it in the paper. Still moving about. It’s now in a jar. I suspect it is actually a forward member of some kind of nation-state engineered nano invasion force.
I have a lot of experience with fly disposal but this thing is actually scarily hard! Also the fact it was ear-buzzing seems very mosquito-like behaviour. But it clearly isn’t a mozzie.
If you are a fly researcher and want the next breakthrough in self-healing psycho DNA give me a shout.
But what is it?
Location Yorkshire UK. Size about 6mm head to tail?

Please leave a comment if downvoting (snooze). This is my first question on this site so apologies for my layman’s effort.

@user338907 Haha no, we have a 2 year old so it’s kind of past that stage.

Welcome to the site. Links, particularly for images, within a question can age and rot, leaving the question unanswerable and not useful for anyone reading the post. Please make your question self-contained.


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can a cell evolve into a different species in the lab?
A friend of mine does not believe in evolution. He claimed that we can not as humans observe a single cell evolving into a different cell. Is that possible to be observed in the lab?
Thanks in advance.

First it is worth noting individuals don't evolve, populations evolve.
We can observe cells giving rise to different cells, the long term E.coli experiment is a famous and ongoing example, not only can evolution be observed but because sample cells from the population are taken and frozen periodically, it can be repeated! that is you can observe a change then set up the same line of cells under the same or under different conditions to see if the changes are different. In some cases even the exact same mutations can be observed.
https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment
http://myxo.css.msu.edu/ecoli/
https://www.pnas.org/content/105/23/7899

+1 Moreover, building devices to observe evolutionary changes has become nearly "popular mechanics" level activity: morbidostat


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Which processes in the human body depend on natural selection among cells?
Are there processes in the human body which occur via natural selection among cells? Could anyone provide examples?
E.g. when tissues are conditioned to be stronger, such as a rock climber's skin getting thicker, would that be natural selection at work? What about muscle conditioning via lifting weights?

Please read about natural selection; the process requires reproduction of the organism. For that reason, it's not possible among an individual's cells. Cells have distinct purposes. They don't compete.

Cancerous tumors...

@anongoodnurse Whether we call it natural selection or not, I see no reason why cells can't compete for survival under some contexts, and become enriched in a population in virtue of particular genes. I can also imagine this process happening in the absence of higher-level regulatory / tissue-level processes, but I was just wondering if people had examples. I think Roger's example of cancerous tumours will sometimes be one such case.

Normally cells work together for the good of the whole. Cancerous cells certainly compete/outcompete, but that's not normal.

@anongoodnurse — My understanding is that natural selection can operate at multiple levels including at the cellular level. That previous source specifically mentions cancer, so I don't think the distinction you are making reflects current usage in evolutionary biology.

Yes, I thought my use of language was in line with the language of modern evolutionary biologists (as @tyersome says) and modern philosophers of biology / theoretical biologists (I'm thinking of Jablonka & Lamb's Evolution in Four Dimensions and similar work).

Arguably T cell maturation in the thymus is such a process.

That's an interesting example. +1 I'm not sure, though, that a normal process of elimination or enhancement qualifies it as natural selection. Maybe it does, but it would raise a lot of questions about what, exactly, the definition is. Are younger RBCs selected for O2 carrying because older RBCs are being picked off by the spleen?  Etc.

T cell maturation involves generating an enormous surplus of immature T cells with recombination and enhanced mutation in the receptor genes. Among those the body retains only those with binding affinity to certain molecules within a given range, killing off the majority that have too high or too low binding affinity. Thus, cells divide to form a large initial population, which is then severely winnowed by selection to produce the final population that emerges into the body. Some cells then undergo further clonal selection upon immune challenge. This seems like natural selection to me.

I understand the process. My comment stands.


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Can one mouse gene have multiple human orthologs?
I was trying to map a mouse gene: Arfgap1 to it's human ortholog. Uniprot shows there are two human orthologs of this gene:
https://www.uniprot.org/uniprot/?query=yourlist:M2021081292C7BAECDB1C5C413EE0E0348724B68210A46CH&sort=yourlist:M2021081292C7BAECDB1C5C413EE0E0348724B68210A46CH&columns=yourlist(M2021081292C7BAECDB1C5C413EE0E0348724B68210A46CH),id,entry%20name,protein%20names,genes,organism,length,reviewed
The two human genes are: ARFGAP1 and ARFGAP3 (it says ARFGAP3 is a synonym of ARFGAP1)
When I tried to find the human homolog in the Mouse Genome Informatics (MGI) database: http://www.informatics.jax.org/downloads/reports/index.html#homology
I found that mouse gene, Arfgap1 only maps to human gene ARFGAP1. What could be a possible explanation for this? Is it possible for a mouse gene to have multiple human orthologs?
Edit: This is just one example. I have encountered mouse genes that have four human orthologs.

ARFGAP1 and ARFGAP3 are distinct proteins.  I think the "synonym" deal is that the two proteins were both referred to as ARFGAP1 in early literature, and one had to be renamed.  So, if you're searching for ARFGAP3 literature and want early literature, you may also need to search for the term 'ARFGAP1'.

Yes.
If duplication of the human gene happened after the speciation event, we have multiple orthologues. This is shown in the following diagram from Ensembl as one-to-many orthologue (ortholog_one2many). In the example from the figure, one human gene has two mouse orthologues, but it could be vice-versa as in your case.

This is an answer to your general question about orthologues. I haven't looked into details about your particular gene (ARFGAP1).


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Why is it easier to spin in one direction than in the other?
When I use a rotating floor disk to spin fast (while standing), I notice that I can keep balance much easier and rotate much faster in clockwise direction rather than in counterclockwise direction. I can even spin while standing on one leg clockwise, but not counterclockwise.
How this asymmetry can be explained? Does it happen for all humans? If yes, is clockwise spinning direction is always simpler or sometimes it is vice versa (like left-handedness)?

Welcome to Bio.SE! This seems like personal experience that isn't a universal phenomenon. Have you looked into its generality at all? We ask that posters try to research their own question and explicitly indicate what research they've already done, what they learned, and what is still unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Good old-fashioned learned behaviour, just like crawling, but I have no proof.

You are right handed, no? Handedness extends to many, many other factors, including vision. Visual connections to parts of the brain are stronger form the dominant eye. This is probably the reason, but I'm happy to be wrong if you're left handed.

@bob1 - Don't just take a guess... Physiology is complex.

@anongoodnurse, I am indeed right handed.

@Anonymous - If you are right-eye dominant (which is likely), your visual "skills" (such as spacial orientation, etc.) are better for the right side of your upper body. It makes sense that you would commence practicing a skill demanding good spacial orientation in the direction in which you are most confident. And that doesn't even take into account footedness)

I’m voting to close this question because it is unsuitable for the following reasons: 1) idiosyncratic and therefore not of general interest; 2) a personal medical question; and 3) multiple questions (i.e. unfocused) — there is also no evidence that any prior research was attempted.

It is just idiosyncrasy of practice and learned behavior, and it almost certainly has little-or-nothing to do with some genetically-determined asymmetry within one's vestibular system. Humans of the same handedness prefer to spin one way, or the other, and footedness and handedness are often not shared on the same side. It's like preference for holding the phone with one hand, or turning in one direction during a startle reflex, or using a tool such as a hammer with a preferred hand. All these are reversible with training and the less dominant side is eminently trainable, even beyond the comfort level of the dominant side. To my knowledge there are no studies that would indicate otherwise (hence the "lack of sources" mentioned in the comments). I think the reason that we have sidedness, or handedness for instance, is because of small initial preferences being reinforced, conditioning, and habit. These of course can present as differences in relative nerve or muscle or tendon sizes - however, I stress that these are very individual-specific and subject to change throughout life, i.e. idiosyncratic and plastic.
Here is a review from 2019 from Marcori et al. which goes into some of the underlying neurological phenomena, which tries to detail exactly how dynamically handedness can change. It is only a primer and does not delve into the sidedness that you specifically ask about (spinning) nor the vast majority of sidednesses that you may allude to.
Everyone has some deep, personal experience with their vestibular experiences, be it during exercise, sport or movement, so I feel a comparison of a few anecdotes can do this topic justice, for the sake of understanding the variety of experiences humans have.
If I may: I have a natural preference for keeping balance in counterclockwise spinning, unlike you. Though like you, I am right handed, right footed, and with board sports I ride goofy stance, which is less common than regular stance. With practice you can very obviously and overtly build comfort for the 'lesser preference'. Time spent playing team sports has resulted in a high degree of ambidexterity (confidence, or comfort) in both arms and legs, but with skateboarding, a newer hobby (which incidentally require a considerable degree of 'detaching yourself from the ground', as well as lateral motion, both being new and unfamiliar sensations), I find myself far from able to comfortably ride fakie or in switch stances (with weak foot toward direction of motion, for goofy riders). They are very alien feelings, just as kicking or throwing a ball used to be with my less dominant limbs. There are right-handed musicians that play left-handed instruments (e.g. guitars) and vice versa. The same goes for archers, martial arts, the list is surely endless. There are myriad examples that disprove your suggestion, so I hope that you now better understand that there is no universality, and that the extent of your suggestion was limited in the first place.
However, to elaborate on the biology of things... Certainly at the neural (circuitry) level, and perhaps even within the vestibular system, there are - and must be - differences that cause you to have a preference. Preferences are ultimately physiological, and the fact that you turn this way or that to cover your face from incoming objects is not completely random or indeterministic. But there is no universality that you suggest for a certain direction among humans, especially for spinning or correcting for experienced centrifugal force. Even handedness, which to us may seem fixed, is not fixed; in many parts of the world, left-handed writing was frowned upon and children were forced to write with their right hands, and became right-hand dominant. Certainly some folks from the older generations have experienced this first hand and can attest to how plastic handedness can be.

Re the plasticity of handedness, that's not entirely true, at least in my experience.  You can certainly train yourself to do things with your off hand, but unless you are naturally fairly ambidexterous (or in my case, ambi-clumsy :-)). you'll never do them as well.

So many...incorrect statements, and all without sources! And some bolded no less!!!

"[T]he "lack of sources" mentioned in the comments" is not because this is unstudied, because it has been studied enough to easily find multiple sources with a quick google search. Otherwise I could not say that "Visual connections to parts of the brain are stronger form (sic) the dominant eye." Which is the tip of the iceberg in eye sidedness. Heck, it's even been studied in flounders (which, given, is kinda unique.) And the edit? If I could downvote again, I would. So many incorrect statements...

Sorry to disappoint. As a more informed person on the matter, you should feel encouraged to write a better answer to help OP out. If this has not already resolved the relatively simple question posed, I made a deeper search and found a few that truly do not seem an ideal fit, but perhaps to others. I add them here for posterity: somewhat of a tangential review of recent findings, vestibular processing in rats and handedness-depedence to vestibular function.


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Searching for a vaccine vs searching for poor genes in the covid-19 pandemic
I have only basic knowledge about biology. I have some propositions (may be wrong) and a question about the covid-19 pandemic.
In 1918, the world had a similar pandemic, the Spanish Flu. Millions of people died because of natural selection. Poor genes on flu were eliminated and strong genes survived. Nowadays flu is just an ordinary disease for people because we are the generation of strong genes and our genes are also strong for flu.
Similarly, for the Covid-19 pandemic, poor genes are getting eliminated unfortunately. (I think Covid-19 disease will be just as ordinary as flu in 5-10 years.) For almost 2 years, people have worked for vaccines and we learned that the mortality ratio of Covid-19 is nearly %3 by statistical data.
My question is, instead of quarantining all people for almost 2 years, trying to find a vaccine for almost 2 years and trying to vaccinate all people (only %3 of people are under a death risk), couldn't we just had searched for a pattern for poor genes? So that we might have to quarantine only those with poor genes and might have searched for a cure or vaccine for them?
Is anyone working on something like this, or am I thinking too simply for such a complex problem?

Wow, just wow...

The immune response in those that are going to die isn't trackable to a few genes but the interacting expression of hundreds of genes - so not predictable.

Unfortunately your assumptions are almost completely incorrect.
The reasons some get sick and die and others don't are multi(multi)factorial. There will be some genetic component, but also things like prior exposure to similar disease(s),socio-economic status, health status, age (this is a big one for COVID-19), all play into it.
The 1918 H1N1 influenza outbreak had a large number of confounding factors - it was in the middle of a global war, with large numbers of people (especially troops) crowding together (e.g. transport boats, barracks), often in terrible conditions (trenches), large portions of the world (esp. western Europe, China, Korea, parts of Africa)  being refugees with poor nutrition, stress etc.
In addition it was at the very beginnings of modern medicine - there were no antibiotics to take care of the following bacterial infections, no supportive medicine, no respirators etc. The people largely killed by the 1918 H1N1 were young men in their prime (20-40 y), who succumbed to something known as a cytokine storm, where their immune response was actually super strong (too strong) and they died from the resulting inflammation. There is a fairly large school of thought that says that the same is happening with COVID-19. It is thought that the cytokine storm against H1N1 is actually a heightened immune response because of prior exposure to another influenza virus. So, these people actually have "good" immune genes, but were the ones killed off by the virus.
Secondly - "just search for poor genes" - you are advocating for something that a) we don't yet know all the genes involved in immune responses, and b) segregation of the population based on genetic characteristics (now where have I heard of that happening before...here, here, here); might have some sort of impingement on things like human rights, especially when you consider that age is one of the largest factors for COVID-19 death.
Now those 3 comparisons above are a lot shitty, because those were horrific things done with no just cause, and you could make an argument that those more at risk of COVID-19 should take more precautions (as many do) - but how do you enact that into law? How do you enforce it? Can you tell if someone walking down the street has diabetes or asthma and are thus more at risk?

thanks for the answer.as you suggest maybe it would be better to inform someone whether he/she is in more danger. and i think its just same as to inform a diabetes patient to not eat sugary foods. i think law and human rights for this case are another topic of argument

@M.SEL that's exactly what happened in countries with good health care systems (and almost all other countries), public health advisories were made for those more at risk, efforts were made to protect the elderly and unwell by prioritising them for vaccines, isolating aged care facilities, mandating masks (which is about protecting not just yourself but others too) and social distancing, shutdowns/lockdowns - these are all effective public health measures that worked in many places. That some people chose to ignore advice from experts does not reflect on advice given, but on the individual.


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Is there any alternative to peptone and beef or yeast extract?
I am trying to start a small microbiology project and I need a growth culture for bacteria. I do not want to use the costly nutrient agars you can buy online. I would like to create my own nutrient agar using the recipe below, but I do not have peptone. I found a paper that seems to be using extruded beans instead of peptone and beef or yeast extract.
Is possible to edit the recipe below and use extruded beans instead of peptone and beef or yeast extract?
This is the article about beans:
Batista, K. A., Bataus, L. A. M., Campos, I. T., & Fernandes, K. F. (2013). Development of culture medium using extruded bean as a nitrogen source for yeast growth. Journal of microbiological methods, 92(3), 310-315.
The exact recipe I would like to edit.

Welcome to Biology.SE. Please take the [tour] and consult the [help] pages for additional advice on [ask] effectively on this site. I've edited your post for clarity, please check to make sure I've preserved your intent. In addition, please add in a summary of the 'recipe' since questions are expected to be self-contained (and thus should not require other users to follow links to external sites). ——— Since you now seem to be posting using two separate accounts, you may find this information on merging accounts to be of interest ...

There is an article about using cheap substitutes for peptone, one of the main ingredients of culture medium as a nitrogen-source. The authors used coconut cake (meal), ground-nut or gingelly cake which worked just as fine as the peptone.
The article is: An indigenous substitute for peptone as the
ingredient of culture media. by Raghavendra Rao et al. 2020 (ISSN: 2456-1045).


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Identification of a spider — South India
I found this spider jumping around in my garden , to describe it is blue and black . I noticed that it has strong front legs and a pointed posterior , it has blue designs on a black body . I live in South India ,ie , a tropical region . It is approximately 1cm in length .

was that two-three mm?

This looks to me like Thiania bhamoensis (Metallic Blue Jumper), whose species distribution includes India. It has a notably pointy abdomen, as you noted, and the listed size range appears to be consistent as well.
I do not believe this is Phidippus audax due to the colour inconsistency (only the chelicerae are blue) as well as the fact that the known species distribution lies entirely within North and South America.

Yes , seems like a female since , it's greenish .The body design patterns and habitat all checks out .

This is Phidippus audax commonly known as Jumping spider or Daring Jumping spider.

Idk anything about spiders but isn't the colours different .

-1. Phidippus audax is an American species; the OP is in India. Also, answers should be detailed and explain why an answer is correct. Please update accordingly or consider removing.


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How many cells are there in C. elegans in each hour of its life?
I'm a high school student planning to write a math essay to model changes in the number of cells in a living organism over time. C. elegans is the only organism that I know with a known number and lineage of cells. I found the full lineage of cells in C. elegans here, which is plotted in respect of time. However, counting the number of cells in those diagrams is impractical. So, is there a summarized database for the number of cells in each hour in the life of C. elegans?

Could you clarify " write a math essay to model changes in the number of cells in a living organism over time" -- what kind of essay or model?

The lineages provided at WormAtlas include references to the original publications. Concerning the embryonic lineage at the top of the page, the corresponding paper was published in 1983.1 Looking at that publication, we see that the authors provide a summary figure depicting nuclei counts over the course of 800 minutes, from the first embryonic cleavage until hatching:

FIG. 4. Marker events and count of living nuclei during embryogenesis. Fertilisation is normally at -50 min. Note that the comma stage is defined in a precise way, as the moment at which the ventral surface of the tail lies perpendicular to the long axis of the egg.

Post-embryonic nuclei counts for young worms and adults are given in Tables 2 and 3 of a 1977 publication by the same first author.2 I can find no data on hour-by-hour cell counts over the interval of an adult worm's lifetime, though such a dataset might be out there.

References

Sulston JE, Schierenberg E, White JG, Thomson JN. The embryonic cell lineage of the nematode Caenorhabditis elegans. Dev Biol. 1983 Nov;100(1):64-119.
Sulston JE, Horvitz HR. Post-embryonic cell lineages of the nematode, Caenorhabditis elegans. Dev Biol. 1977 Mar;56(1):110-56.


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What animal is this track from?
Last week I noticed this odd track made of "squiggly triangle footprints" on the outside surface of a dirty skylight in my home in the northern Netherlands, and I found it odd that I can't imagine what kind of animal this track would have come from. I assume it's animal since the movement seems very intentional and the triangle shapes are periodic, rather than being a continuous smudge that might be caused by a tiny leaf blown in the wind for example. Each tiny triangular "footprint" is around 3mm wide. Any pointers on how to identify what caused this track?

My guess is a rocking and rolling pinecone.

any kind of close up would be a huge help, I can't see any detail.

Yeah I thought of a pinecone-like object being blown around, but note that it appears to all be a single track which moves up and down and around in a very consistent pattern, no skips. Also note that this is a pretty steep skylight; I wouldn't expect even a very fortuitous wind to keep a roundish object in place long enough to do such an intricate pattern. @John sorry that's the only image I grabbed before I washed the offending window :-) but a reasonable amount of detail is visible if you zoom in.

@TopherHunt Is there a coniferous plant above the window? Have you tried taking one of the cones and reproducing the pattern? Perhaps if the cone is not roundish, but more cylindrical or cone-like shaped, this could explain the left-to-right wiggly pattern of its descent ...

Snail feeding.
It is really obvious if you have seen it before. It is the track left by a feeding snail.
Here is the grazing pattern of the common snail.

https://commons.wikimedia.org/wiki/File:Land_Snail_radula_tracks.jpg
https://alexhyde.photoshelter.com/image/I0000oboo93ZzSEI

YES thank you. And that fits because Friesland is teeming with snails and slugs. Allegedly they don't have many predators here.


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Is there any way siblings could be related more than 3/4th siblings, but less than full siblings?
I couldn’t find anything on Wikipedia. 3/4th siblings are 37.5% related while full siblings are 50% related. Is there anything in between?

You may be confusing averages with the actual (genomic) relatedness of two given siblings. Two given siblings can in theory be anywhere from 0% to 100% related, but on average will be 50% related.

The International Society of Genetic Genealogy Wiki provides the following situations for which siblings may be considered $3/4$ siblings (a coefficient of relationship of 37.5):

a man has children with each of two sisters (the children are related    as half-siblings and first cousins)
a woman has children by each of    two brothers (the children are related as half-siblings and first    cousins)
a woman has children with both a man and his father (the    children are related as half-siblings and half-aunt or half-uncle and
half-niece or half-nephew)
a man has children with both a woman and    her daughter (the children are related as half-siblings and half-aunt    or half-uncle
and half-niece or half-nephew)

Note that the above situations assume that all grandparents are unrelated. If you consider a situation where either or both sets of grandparents are full siblings, then you have a coefficient of relationship in the sibling grandchildren that is intermediate between 37.5 and 50.

I edited my question, what I wrote was not what I meant.

I've extended my answer