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Osmolarity vs. Tonicity
We're learning about osmoregulation in AP Biology and the terms Tonicity and Osmolarity are really confusing me. I watched this video on Khanacademy to try to understand what the difference is, and from my understanding Tonicity refers to strictly two solutions (ex: you can't take a cup with water and salt in it and claim it's hyper, hypo, or iso- tonic because there's nothing to compare it to), whereas Osmolarity refers to the composition of the single solution itself.
But then my Campbell's biology textbook completely confuses me. It has the following picture and text:

...osmosis, a special case of diffusion, is the movement of water across a selectively permeable membrane. It occurs whenever two solutions separated by the membrane differ in osmotic pressure, or osmolarity (total solute concentration expressed as molarity, that is, moles of solute per liter of solution).....If two solutions separated by a selectively permeable membrane have the same osmolarity, they are said to be isoosmatic. Water molecules continually cross the membrane, but under these conditions they do so at equal rates in both directions....

And then as if to clarify, they claim that tonicity refers to "solutions of known solute concentrations"...but how does this differ from osmolarity?

You're correct that tonicity needs two solutions to define.
Osmolarity (or osmotic concentration) is the measure of solute concentration, defined as the number of osmoles of solute per litre (L) of solution (Osm/L).
Tonicity, on the other hand, refers to the relative concentration of two solutions separated by a semipermeable membrane.
The difference is based what is considered for osmosis and tonicity. In case of osmosis, it is the water (or solvent) which moves across the membrane, while tonicity depends on the solutes which cannot move across the membrane. From Wikipedia:

... osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of only non-penetrating solutes.


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Entropy and Open Systems - AP Biology
I had the following question on an exam of mine and I got the points for the question, but I am wondering if someone could please explain why it is correct, or rather, if it is correct at all:

As living organisms grow, they increase in complexity and decrease in entropy. How does this relate to the second law of thermodynamics?
(A) Living organisms, like everything else in the universe, spontaneously decrease in entropy over time.
(B) The increase in entropy of the universe exactly balances out the decrease in entropy as the organism grows.
(C) Energy cannot be created or destroyed, so the energy used for growth is later used to increase entropy.
(D) The resulting increase in entropy of the universe is greater than the decrease in entropy associated with the growth.

I answered D, as it seemed like the most likely answer out of all of them, and I got the points.
According to the 2nd Law of Thermodynamics, the entropy of the universe will increase with time.
Please correct me if I am wrong, but from my understanding this only applies to closed systems--so how exactly would it apply to organisms (which are open systems)? Is it because organisms release heat through chemical reactions and thus add to the entropy of the universe while decreasing their own entropy?
Thank you!
-Aleksandr

If you mean "von Neumann entropy", (B) seems correct. However, if "thermodynamics entropy" is meant, the correct answer would be  (D).

You are correct. Anything within the universe is part of the closed system of the universe. Therefore, they must also increase the entropy of the universe. You are correct, they do release a lot of heat. Plus, while making ATP, the major source of cellular energy, they convert a complex molecule, glucose, to simpler molecules, H2O and CO2, increasing entropy as they release these chemicals.
Also, the key fact is that to lower entropy in their body, organisms must use up energy. Energy is required to avoid the entropy from increasing (which actually means they actually expend energy to prevent equilibrium; high entropy means reaching equilibrium). So they would follow the 2nd law of thermodynamics. Which reminds me of a joke!
Old chenists never die, they just reach equilibrium!

I would say D.) too.

The resulting increase in entropy of the universe is greater than the
  decrease in entropy associated with the growth.

We can argue that the cells and the universe together are a closed system and entropy increases in a closed system by time. So the sum of their entropy changes must be always positive.

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Is the increased/decreased enzyme activity (tyrosinase) caused by an environmental factor (UV radiation) considered to be gene expression?
My AP Bio assignment asks that I research the effects of UV radiation on melanin production, but the directions and questions suggest that UV radiation influences gene expression. From what I could find, such as on this university site or this abstract on NCBI, it seems that UV-B radiation directly affects the enzyme tyrosinase, which is responsible for producing melanin from tyrosine. So here is what I'm wondering: is our lesson wrong in stating that UV radiation affects gene expression, since it seems that it actually affects enzyme activity?

Since @anongoodnurse already nicely covery the effects of UV radiation on the cellular level, I will only have a look on the molecular level.
UV radiation of the skin causes increased DNA damage and thus activity of p53 in the keratinocytes of the skin. This causes (amongst others) the production of Kitl (Kit ligand, binds to the Kit receptor) and POMC (Proopiomelanocortin) which is later processed to ACTH (Adrenocorticotropic hormone) and the different MSH-forms (Melanocyte-stimulating hormone). These act on the MC1R (Melanocortin 1 receptor) on the surface of the melanocytes and induce pigmentation. See the figure below from reference 1 as illustration:

In the melanocytes the binding of these ligands activates different signal transduction pathways which all finally lead to the activation of the transcription factor MITF (Microphtalmia-associated transcription factor) which then upregulates the transcription of tyrosinase.
See the figure from reference 1 as an illustration about what goes on in the cell:

So the activity of the sun directly influences the signal transduction and later on the gene expression of Tyrosinase by a specific transcription factor. This translates a external stimulus (as UV light) down to the gene expression level. The stimulus does not affect the activity of the enzyme, only the amount available.
This upregulation stops when there is no further signalling down from the keratinocytes and eventually the Tyrosinase will be degraded due to normal turnover of the enzyme. Since no or only little is made without the right stimulus, this causes a stop or reduction in the pigment production. This happens when you get less UV light on your skin which happens for example in the winter time in Europe. Shedding of the upper layers of the epidermis then leads to the loss of the pigmented keratinocytes which makes persons lighter.
References:

The melanoma revolution: From UV carcinogenesis to a new era in
therapeutics
The roles of microphthalmia-associated transcription factor and
pigmentation in melanoma.

Awesome, this is exactly what I needed. If only I could select two answers. By the way, I'm a visual learner, so those diagrams really helped. Thank you, Chris!

@AleksandrH - Please feel free to accept Chris's answer. It directly answers your question, and is frankly a lot better than my answer. +1. This kind of answer makes me appreciate how much I've lost touch with molecular biology.

@anongoodnurse Alright, thanks to both of you for your thorough answers & the references :)

Unless there's a feedback mechanism shutting off gene expression (which controls the proteins made by a cell), activation or deactivation of an enzyme is not in itself a matter of gene expression, it's a matter of external factors controlling the enzyme's activity. You need to decide on what exactly causes skin pigmentation: the enzyme or cell proliferation, and what is under the control of gene expression and what isn't.
Most of what you find on ultraviolet light and melanin will be somehow related to melanomas, the formation of which does involve gene expression, so it's important to keep the two separated.
Ultraviolet light does cause proliferation of melanocytes, which cause the skin to darken. Melanocytes impart melanin to keratinocytes; these cells then are what give you a tan. The keratinocytes undergo constant turnover, so are eventually shed, and in the absence of continued exposure to UV radiation, there is no need to keep producing melanin-heavy keratinocytes.

The keratins and proteins within the stratum corneum act mainly by scattering and absorbing the UV. UV-R sets in action an integrated mechanism for the formation and delivery of melanin within melanosomes from melanocytes to keratinocytes. This mechanism is probably triggered by keratinocytes, which respond to UV-R with bursts of mitoses and with increased production of ET-1 and POMC, thus creating a new demand for melanosomes. The mitotic rate of basal keratinocytes increases a day after UV exposure, reaches a maximum 2 days later, and maintains this level for ∼1 wk. It then declines, and the skin regains its original thickness after 1–2 months if there has been no subsequent exposure.

Continued exposure to UV light stimulates the melanocytes to grow. This increases the chance of the development of melanomas. Since skin cells containing melanin are shed (there's no getting around that), in light-skinned individuals, keeping a tan is to keep injuring the skin and risking carcinogenesis.
Melanin Pigmentation in Mammalian Skin and Its Hormonal Regulation
Human skin pigmentation: melanocytes modulate skin color in response to stress
Mechanism of UV-related carcinogenesis and its contribution to nevi/melanoma

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Ischemia-induced deploarization in excitable cells
I have read in many sources that ischemia-induced depolarization is due to the opening of ATP-sensitive potassium channels and inactivation of Na/K exchangers [1,2]. However, K-atp channels are inward-rectifiers and their extensive opening should cause extracellular hypokalemia besides the fact that in low [ATP]i during ischemia, Mg++ ions are free (not complexed with ATP), and magnesium ions are outward potassium current blockers (i,e, they increase the rectifying power of k-atp, Kir, K-Ach channels)[3,4]. this would cause extracellular hypokalemic depolarization. What is the source of hyperkalemia then?

Inward-rectifying means positive current passes more easily in the inward direction, however it won't flow differently than the membrane voltage and reversal potential dictate. See for example https://en.m.wikipedia.org/wiki/Inward-rectifier_potassium_channel
The only time you'll have potassium flowing in to a cell, rather than out, is if the cell is very hyperpolarized, beyond the reversal potential for potassium, which is more negative than the resting potential.
Open potassium channels will almost always reduce intracellular potassium concentration as potassium flows out of the cell. Without ATP to fuel the sodium-potassium pump, there's no way to restore the lost potassium.
The existence of a negative resting membrane potential is due to relative concentrations of potassium (high inside cells) and the existence of primarily potassium conductance in the membrane, which means a few positive ions leak out to make the inside negative. If you don't maintain that concentration gradient, the cell is going to depolarize.

I'd also suggest an honorable mention of the chloride anions that stayed within the membrane in the last graph.

i will try to explain what i understood. So, when the K+ channels open during repolarization the permeability is so high that according to goldmann's equation the resting membrane potential (RMP) is closer to K+ reversal potential(hyperpolarization) But as repolarization ends the fast and slow rectifyer channels close so the RMP shifts to a more positive voltage and then K-leak channels and K1 (inward rectifyer) channels open and since they are not as abunduntly opened as the channels during repolarization.........

..... the RMP is still more positive than it was at end of repolarization. this causes the correction of RMP to the pre-depolarization state. So the main function of K1 is to allow rapid influx of k+ ions to correct hyperpolarization as fast as possible and thne k+ leak channels maintain their efflux. Am I right?

@kljiuklk1 Unless the membrane voltage is more negative than the potassium reversal potential (which can never happen by potassium flowing alone, no matter what channels are open), potassium net flow is always out of the cell. There's no "rapid influx of potassium ions". Leak channels are always open. Recovery from hyperpolarization happens because other ions (mostly sodium) are leaking in faster than potassium is leaking out.

@BryanKrause, but if that is the case then why the correction of hyperpolarization is attributed to K1 channels. And why would there be an inward rectifyer if potassium is always flowing out even at hyperpolarized state?

@kljiuklk1 Mostly those channels can be thought of to be somewhat self-closing when cells depolarize, which allows for cells to both have more "leak-like" current at rest, making them less susceptible to "accidental"/random depolarizing events, yet not interfere with the depolarizing current which is metabolically costly if you have lots of sodium and potassium flowing against each other.

It's somewhat random luck that at severely hyperpolarized potentials those channels are even more conductive, but those conditions only occur artificially.

Note also that "inward-rectifying" is just the direction of the rectification... The function continues in that direction within the physiological range where potassium is always flowing out, it's just that there is a higher conductance when closer to rest and lower conductance when further depolarized.

I cannot think of a non-artificial circumstance in which a typical neuron or muscle cell would have a potential more negative than potassium reversal. Im not sure where you've gotten the idea that they are responsible for "correction of hyperpolarization" outside of artificial circumstances.

so if i understand correctly inward-rectifier is another way of saying weak (semi-closed on efflux) K+ channels (i,e, it allows the membrane to reach the point of RMP according to goldmann equation but at less permeabilty and slow rate (slow K+ efflux) ). If we were to remove the rectifier function of these channels, the RMP will decrease because non-rectifier channel is more permeable to K+efflux .right?

@kljiuklk1 I wouldn't think of them as weak, either, actually I don't know what their overall single channel conductance is, but it need not related to the presence of rectification. Rectifying is a relative thing. It's mainly that they are just most permeable closer to resting potential, so they help maintain resting potential without interfering with spikes as much.

So, inward rectification is just an identification property rather than a functional property (at normal physiological level) and if inward-rectification of a channel increases this means in the other way around that outward-rectification K+ effllux decreased and thus its conductance decreases. as inward rectification can be increased by increasing [Mg]i which according to some research blocks the outward-rectifier portion of the gate and thus the cell will b emore depolarized.

@kljiuklk1 No. I'm sorry, my patience for this has run out. Read to what I am writing, read about these channels in more than one reputable source, and don't keep trying to add on your own meaning to things or inventing terms like "outward rectification decreased". Channels are what channels are. If you lose potassium channels, of any type that have any open probability at rest, the resting potential will be less negative. You can test this out using the Goldman equation.

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What is an intuitive explanation of linkage disequilibrium?
Is it possible to give a simple and intuitive explanation of the concept of linkage disequilibrium? You know, so I can sort of sound like I know what I'm talking about. Everything I read about it has me lost.
I am a writer and specifically I write lyrics and raps and I love this phrase "Linkage Disequilibrium". I would love to put it in a rap I'm writing about a friend of mine.

What have you read so far and what is your current understanding? Where specifically are you needing help with understanding?

non-random assortment, torment / the haters who wanna split us, we don't even see 'em / wouldn't want to be 'em / me 'n my homie tight like alleles in linkage disequilibrium / we're correlated, ya see / you n' me, tied up in LD

love to see spontaneous collaboration @acvill

I'd recommend looking at some learning resources (links). If you don't understand what you read, you are welcome to bring your thoughts here and ask for help with what doesn't make sense. https://biology.stackexchange.com/questions/31618/what-is-linkage-disequilibrium-supposed-to-measure, https://www.discovermagazine.com/the-sciences/basic-concepts-linkage-disequilibrium, https://faculty.washington.edu/tathornt/sisg2013/Kerr/3LD_Kerr.pdf

Just channeling my inner Aesop Rock, @MaximilianPress

Intuitively, Linkage Disequilibrium, suggests a problematic sexual relationship. Biology, yes, explanation of the term, no.

Thanks so much everyone. It's just a couple lines in a song to make people have to think a little bit in order to understand what I'm saying, and I believe I already have enough to make that happen. In other words I'm totally gonna use a little bit of that from @acvill. With your permission of course

Be my guest, @JasonScaff

I’m voting to close this question because if it were intuitive, the poster wouldn’t have needed an explanation. This leaves the question of whether the purpose of this site is to explain concepts for which good accounts can be found elsewhere. The answer is no.

During sexual reproduction, the process of crossing-over means that parts of the maternal and paternal chromosomes become shuffled up with one another into chromosome 'chunks', as shown by the red and blue colours here:

We can tell by looking at this that if you had two genetic markers right next to each other on a chromosome that they very likely to be inherited together on the same chromosomal chunk. Similarly, if they are on opposite ends of the chromosome, they are much less likely to be inherited on the same chunk.
All other things being equal, we say that the markers close to each other are in high linkage disequilibrium (LD) with one another and markers further apart with be in lower LD with one another. In other words, the probability of recombination occurring between two markers, driven by physical distance and variable recombination rates is what causes differences in LD.
If we want to get a bit more in depth, then the recombination rate (i.e. the probability of a recombination event occurring between any two markers) varies across the genome. Something like a gene fusion event may totally impede recombination, meaning that region is always inherited as a single 'LD block'. This can result in things like supergenes in eusocial insects. Conversely, there are regions of very high recombination which reduce the amount of LD between markers.

This is not an intuitive answer or indeed a simple answer for a non-specialist. I am not a geneticist and was not familiar with this term, but I am an educator, so I would expect a good answer to start with a single sentence summary and then go on to explain any technical terms. For example if I do a web search I find statements like "Linkage disequilibrium is the non-random association of alleles of different loci." Now to explain it I would have to find a replacement for the word "allele" and clarify "loci" as the positions of genes, and then explain what is meant by association.

@David feel free to write your own answer then if you think you have a better way of explaining it

No. I am not the student, not the teacher, but am explaining what is lacking in your explanation and suggesting how you might improve it. But it is not easy.


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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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Polyandry in birds
The Wikipedia article on Bateman's principle states:

Until recently, most bird species were believed to be sexually
monogamous. DNA paternity testing, however, has shown that in nearly
90% of bird species, females copulate with multiple males during each
breeding season

citing two articles. But the Polyandry in nature article says:

Polyandry… occurs in … around 1% of all bird species, such as jacanas
and dunnocks.

(No cites provided.)
Am I correct that the second article should be updated?

"no citation provided" would be the relevant information.

I did work on the Louisiana waterthrush 15 years ago and found some instances of polyandry. Wasn't previously recorded in that species to my knowledge

I think you're confused about the definition of polyandry. Firstly, polyandry normally refers to sustained relationships, not simply mating. In birds this means nest biulding, incubating eggs, and feeding young. If a pair of birds raise chicks in one nest, and neither interacts with another nest of chicks, then they are a monogamous pair - it doesn't matter if there are other chicks with their genetic material.
Also, polyandry normally refers to females taking more than one male partner, while males stick with that single female. The article states that most females "cheat" on their partners but a similar percentage of males do the same.
The dunnocks given as an example often form trios where 2 males and a female collectively raise chicks, with the young having a mixture of paternities. The jacanas have a system where males build nests and females claim up to 4 males, and defends all her nests while the males raise the young. These are very different to the standard bird system, where a female bird may have many sexual partners, but only cares for one set of young.

Do you have a cite for “polyandry normally refers to sustained relationships, not simply mating”? Both https://en.m.wikibooks.org/wiki/Animal_Behavior/Polyandry#Polyandry and
https://en.wikipedia.org/wiki/Polyandry_in_nature start w defn in terms only of mating. Perhaps in parallel with ‘social monogamy’, (see https://en.wikipedia.org/wiki/Social_monogamy_in_mammalian_species#Monogamy_in_mammals),
nest building, etc., could be termed ‘social polyandry’?

It also varies among species. A study by the local college ( Sam Houston , Huntsville TX) found Carolina Wrens were almost monogamous; different from other birds studied . It was years ago and I do not recall what species were in the study.


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Blood pH at Higher Altitudes
My Campbell's Biology Textbook says the following:

"For example, when an elk or other mammal moves up into the mountains from sea level, physiological changes that occur over several days facilitate activity at the higher elevations. The lower oxygen concentration in the air stimulates the animal to breathe more rapidly and deeply. It therefore loses more CO2 through exhalation, raising blood pH above its set point.

I was wondering if anyone could explain why blood pH increases as your altitude increases? I know that an increase in pH is a sign of less H+ ions in the blood, but what exactly causes you to lose the ions when you're exhaling CO2?
Thanks!

The following chemical equation explains why pH decreases with increased $CO_2$:
$CO_2 + H_2O \rightleftharpoons   H^+ + HCO^{-3}$
pH changes are the reason why oxygen binds to hemoglobin in you lungs and then dissociates from hemoglobin at other parts in your body where the oxygen is low because cellular respiration turned the oxygen into carbon dioxide. The binding of oxygen to hemoglobin is in turn explained by the Bohr effect.


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Thermoregulation Question
I had the following question on an exam of mine and I got it wrong, so I was wondering if someone could help explain the reasoning to me. Below I list my explanation.

An overheated and sick dog in a hot environment will have an impaired thermoregulatory response when its
(A) evaporative heat loss increases
(B) metabolic heat production decreases
(C) body temperature increases to match the environmental temperature
(D) blood vessels near its skin increase vasoconstriction

So here's how I approached this: A and B are clearly incorrect, as they aid the thermoregulatory response of the animal by allowing it to lose excess heat.
Thus, it comes down to C and D. I chose D because I thought that since vasoconstriction traps more of the heat inside the body, it would be counterproductive to what the dog actually needs (vasodilation). I'm assuming that the correct answer choice is C, but could someone please explain it to me?
Thanks in advance to all who reply :)

You're right, A and B both are normal thermoregulatory responses, so those can't be the right answer.
I'm guessing the rationale for C is that, if the dog's body temperature is increasing to match that of the hot environment, it must mean the dog has an impaired thermoregulatory response. It's kind of tautological.
But D also seems correct to me. If a dog is in a hot environment, and its blood vessels near the skin are constricting (say, because it's sick), that's counterproductive to the normal thermoregulatory response. If the dog isn't dilating its blood vessels near the skin, that's an impairment to the normal thermoregulatory response.
Perhaps the question is written wrong? Maybe D was supposed to say "vasodilation" instead of "vasoconstriction"? If this is a question written by a teacher I'd say you have a case for arguing it.

This is a question from Ch40 of Campbell's Biology, they seem to be getting at the fact that C is right because the dog is endothermic and only operates properly within a certain range of temperatures. For D, the argument is that since the environment is already hot, vasoconstriction to decrease heat interface is beneficial.

@Kendall - Such a helpful comment! Might you want to turn it into an answer?

Thank you everyone. I asked my teacher (since she's technically not the one who designs these questions) and she said that D is correct, so she rewarded me the points.

Heyy
Like you said, A and B are actually not the answers. However, C could be in this case the answer. The dog is already overheated meaning the core temperature is very high. The environment stated also has a very high temperature. The body is not supposed to match the environments temperature, instead, its (hypothalamus) supposed to set a lower temperature to be matched. Therefore, the dog body matching the environments temperature indicates an impairment in thermoregulatory response. In addition, since the dog is already overheated and trying to match the high temperature of the environment, it can lead to tissue deterioration or damage which is a huge problem


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Help identifying a bug which looks like a housefly and mosquito hybrid
I'm from Kochi, India (southern part of India). I found this bug inside my house , it was about a centimeter long . But how can such an hybrid be possible. (It was raining before I found it).
1: https://i.sstatic.net/Dlyio.jpg

Welcome to Biology.SE! Do you have some reason to assume this is a hybrid? If not, that is an extremely naïve assumption to make and I encourage you to remove it from your question. Please also [edit] additional information such as local ecological factors including the dominant types of plants and if possible clear close-up pictures from multiple angles. This may enable someone to narrow down the identification of this insect.  ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

This is a long-legged fly (Condylostylus spp).  Unfortunately your image is not sharp enough to give a specific species.  See this post of another Indian fly that is virtually identical to yours:
https://www.jungledragon.com/image/13762/long-legged_fly_-_condylostylus_spp.html

Thanks for your answer. However, Your post does not provide enough evidence /support for you to definitively claim the genus of the OP's specimen. Please consider explaining why you think this is the correct genus.

The OP and many other visitors will likely see your post and consider it fact. This is insincere given that it appears (based on what evidence you provide here) that you simply did a Google image search. The picture you link to is from a photography website with no evidence of taxonomic expertise. (It seems to just be amateur photographers tagging their own photos). Much more convincing and reputable sources exist and should be used as support if you truly feel confident in your answer. Again, please consider updating to strengthen your answer. Thank you


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Some related questions about DNA differences in a single organism

If you took a DNA sample from someone's brain and that same persons liver at more or less the same time, would that DNA - all else being equal (e.g. no mutations from radiation) - be exactly the same?

If you took a DNA sample from an embryo, and then that embryo went on to be born, live a long life for 80 years and become an old man/woman; if you were to then take another DNA sample of this person, would that sample be exactly the same as the one which you took when he/she was in the womb? (again, all things being equal - so dismissing mutations due to radiation for example).

I don't have much of a scientific background, and am seeking your expertise so that I can consider it's relevance for both the buddhist doctrine of impermanence and christian convictions about souls, personhood, abortion etc.

What do you mean by 'exactly the same'? You should be more specific. You could be talking about the same genes, the same variants, the same heterochromatin configuration, 3-d structure, number of repeats, duplications ....

In addition to the above, what do you mean by "no mutations from radiation etc"? Do you understand that mutations accumulate due to errors in DNA replication?

No. even if you exclude the changes in DNA sequences that originate from mismatch errors in DNA replication, mutation etc.
Because
1.As a person gets old , the short repeat sequences in the telomere of a chromosome  in each cell may be lost or be reduced in amounts leading to a sequence difference.Moreover this changes in telomere sequences may cause cancer/cell apoptosis .
Telomere
2.Do not forget transposons (consisted of DNA transposons and retrotransposons). They change their position in genome and multiply their DNA over time.So they also lead to sequence differences in a person(comparing his/her younger and older DNA)
Transposons
These were the answers to question 2 .You can also think that there might be a slight difference in DNA of two different tissue of the same individual (because of the tolemere and transposons)
As a zygote starts to multiply itself ,slight changes of sequence will happen to the offspring cells .After a dozens of cell division you may encounter a little deviation compared to the original zygote sequence.

+1, but it might help to cite the mutation rate, or at the very least something else.  An overall sense of the scale of the mutation variation within an organism would improve this answer

shorter telomeres is one reason dolly died so young, she was cloned from differentiated somatic cells, so she started with shorter telomeres.


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What can you learn about someone's mother and father by examining their DNA?
Disclaimer: I ask this question from the position of having paid absolutely no attention throughout school/highschool science classes. I am incredibly ignorant, but I don't know how to find the answer to this question using google, and would rather consult actual live minds via this stackexchange.
My question is (I think) fairly straightforward: By examining someone's DNA, how much can you learn about their mother and father? Is it perhaps possible to analyse the DNA and do the equivalent of a "fast fourier transform" to extract and reconstruct the respective DNAs of their mother and father?

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

In principle, you can reconstruct 1/2 the genome of each parent.
Each of these halves is still a "complete" genome, in the sense that it (usually) contains 23 full chromosomes (there are 23 human chromosomes). Every person has two copies of their genome, one of which is inherited from each parent. I strongly recommend reading about meiosis to learn more about this.
Each of these single genome copies is called a haplotype, and is an outcome of recombination between their own two genome copies. So neither copy looks exactly like a parent, but is rather a mixed-up version of that parent's genome.
There are a lot of genomic methods out there that try do exactly this task (reconstructing parental haplotypes) by various means. It is somewhat complicated and expensive, but possible in principle:

One method is trio-binning, which involves also collecting data from the parents, but focusing most effort on the child. This is not very convenient of course if you don't have samples from the parents.

Other methods use only information from the child, but rely on various genome technologies to reconstruct haplotypes inherited from each parent. Here is an early example, and here is a very recent example. These methods however do this mostly on a chromosome-by-chromosome basis, so it is not always obvious how to group the 46 total chromosomes into 2 parental haplotypes of 23 each.

This is a very active area of methods development, so we can expect these references to be quickly outdated.
I do not think that any method will be able to use only the DNA of the child to reconstruct the full genomes of the parents. Maybe if you have a large database of other genomes you can do some imputation of the missing haplotypes, but I doubt that that would work very well.


text:
Why are only 6 water molecules formed in the aerobic degradation of glucose?
I am studying the aerobic degradation of glucose and it seems that for every glucose molecule we should obtain $\ce{10H2O}$ molecules. However, it is known that we only obtain 6.
$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$
(I am not going to focus in all products and reactants, but just in the important ones for the formation of water molecules)
First, in the glycolysis, for each molecule of glucose we obtain two water molecules, $\ce{2NADH+}$ and 2 pyruvate molecules. By the oxidation of two pyruvate molecules we obtain $\ce{2NADH+}$ and 2 acetyl Co-A molecules. So we are going to pass twice through the Krebs cycle, obtaining $\ce{6NADH+}$ and $\ce{2FADH2}$, and requiring 4 water molecules.
So, when we arrive to the electron transport chain, we have a negative balance of 2 water molecules, and we have $\ce{10NADH+}$ and $\ce{2FADH2}$. We have been told that for every of these molecules 2 electrons go to the electron transport chain, that means that a total of 24 electrons go to the system. The problem comes here:
$\ce{4e- + 4H+ + O2 = 2H2O}$
So, bearing in mind that we have $24e^-$, 12 water molecules should be formed, so at the end, we have gained 10 water molecules, but we know that the number of water molecules formed should be 6. So, clearly there is something wrong in my explanation. I would be very pleased if you could tell me what is wrong.

Your confusion comes entirely from this equation:
$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$
This reaction is the combustion of glucose. This is not how glucose is oxidized in cells! Why so many biology texts and courses present this equation when introducing metabolism is beyond me.
Indeed, your tracking of water molecules is correct: starting with one glucose molecule, 2 waters are produced in glycolysis, 4 are consumed in the tricarboxylic acid cycle and 12 are produced during oxidation of NADH/QH2 (ie FADH2). This gives a net total of 10 produced.
Why is this different from the combustion of glucose? The answer lies in the oxygens introduced by inorganic phosphate during substrate level phosphorylation. Consider the balanced net reaction for the biological oxidation of glucose (simplified by ignoring ATP produced by oxidative phosphorylation and substituting ADP/ATP for GDP/GTP):
$\ce{C6H12O6 + 6O2 + 4ADP + 4P_i + 4H+ -> 6CO2 + 4ATP + 10H2O}$
In particular, consider the formation of ATP from ADP and Pi (HPO42-). In both substrate level phosphorylation reactions (catalyzed by GADPH/PGK in glycolysis and succinate-CoA ligase in the tricarboxylic acid cycle), inorganic phosphate nucleophilically attacks the activated carbonyl (thioester) of the substrate and is then transferred to ADP (to form ATP):

The oxygens of the original inorganic phosphate are coloured red. The key point is that an oxygen atom from HPO42- is transferred to the substrate. This oxygen is later removed in the form of carbon dioxide, via oxidative decarboxylation, during the conversion of pyruvate to acetyl-CoA and in the tricarboxylic acid cycle. This occurs four times for each glucose molecule entering glycolysis and is accompanied by the reduction of NAD+ to NADH. Given that NADH is used to reduce molecular oxygen during the electron transport chain:
$\ce{NADH + H+ + 1/2O2 -> NAD+ + H2O}$
...this explains where the four, apparently extra, water molecules come from when comparing the combustion of glucose with its biological oxidation.

Good answer, but I would contest that the plain combustion reaction is actually very useful, even if it does not reflect the mechanism that cells use. The reason is that, if you balance your reaction involving substrate-level phosphorylation with ATP hydrolysis -- which always occurs alongside ATP synthesis in cells -- then you will get back the simple combustion equation exactly. And this must always be the case. So comparison with simple combustion helps us verify that we understand biochemistry correctly.

@Roland Thanks! And good point. I find that it often causes a lot of confusion, but that may be more from poor explanation or comprehension.

@Roland, I am a high school student, I also had the same confusion, that why do so many textbooks compares combustion with respiration? in respiration 10 H20 are released, and I look upto the answer, but it seems like, i don't have enough knowledge to grasp it, can you explain it to me in simple terms? should I say that the other 4 H2O molecules are used somewhere else?

@ArunBhardwaj, This is an old post, but as I mentioned in other comments, it's important to distinguish between (1) H2O derived from glucose oxidation and (2) H2O from ATP synthesis (respiration). Glucose oxidation in cells is always coupled with ATP hydrolysis to provide energy (for example, in muscle contraction). The ATP hydrolysis reaction is ATP + H2O --> ADP + H+ + Pi. So if you balance the the first reaction equation in this answer with 4 x ATP hydrolysis, the extra 4 ATP will cancel out and you get back the basic glucose oxidation reaction. So this is where the extra 4 ATP are used.

@ArunBhardwaj, (continued)  The H2O formed during respiration is very different. Respiration is not even a pure chemical reaction, it's a physical process -- ATP synthase is actually more like a turbine!  In respiration, the number of ATP formed by respiration is not fixed, but varies depending on conditions. It's usually somewhere between 2--3 ATP per NADH, but there are exceptions: some cells don't produce any ATP at all, but instead use all the energy in NADH to produce heat.  So there is no single, exact chemical reaction formula for respiration.

@Roland,I am a high school student, and only knows the various steps involved in respiration, I was confused that if the combustion reaction and respiration gives the same results then why do we have 10 h20 formed in respiration as OP have calculated, but it seems like you are cancelling out ATP to form 6H20 ,,,i.e if we consider ideal cases for calculating each thing formed, we will see that 38 ATP/36 ATP are getting formed in respiration,,but it seems like you have hydrolysed 4 ATP from them just to make 6 H20 molecules? correct me if I am worng.,,and I don't know why u have said extra 4 ATP

In total there are 38 ATP formed by biological oxidation of 1 glucose, 4 from substrate level phosphorylation and 34 By oxidative phosphorylation,,what do you mean by extra 4ATP hydrolysis?

@ArunBhardwaj, sorry, I meant to say "extra 4 H2O" in the comment above. I was trying to address your question of where "the other 4 H2O molecules" go, and the answer is that they are accounted for when the ATP formed is hydrolyzes (used for energy). Respiration is a separate problem, and again, there is no exact number for how many ATP values are formed from respiration (the textbook value 34 is just one possibel scenario). But I think this is too much to deal with in the comment field -- we should probably move this discussion to chat.

how to continue in chat? and again I know that there is no exact no. of ATP formed, but if we consider ideal scenerio than 38 ATP are formed not 34 , it seems like you are hydrolysing 4 ATP just to form 6  water molecules?

I think you are misconceiving the intent assumed within the statement "6 H20 generated from glycolysis". The number 6 is simply in relation to the number of carbons oxidized to CO2 within the TCA..which generates an electron at each oxidative occurance, in which the 6 electrons are then shuttled to OXPHOS requiring 3 O2 to form 6 H20. ... In short: Whenever they say 6 H20 are produced "aerobically"  they are specifically referencing the simplified OXPHOS component (or simply: C6H12O6 + 6 O2 → 6 CO2 + 6 H2O).
Of note:

Stoichometry is relatively useless in real research. Don't overthink it. Metabolism is incredibly dynamic.
Real life H20 involvement within complete glucose oxidation is much more complex: Two turns of the TCA cycle generate: 4 CO2 from 2 acetyl CoA which requires 4+ H20 in total, but only has a net H20 loss of 4. Citrate synthase and fumerase both consume 2 H20 apiece to allow production of 4 CO2. The remaining H20 is used at aconitase, but no loss nor gain of H20 occurs in this reaction. Pyruvate dehydrogenase produces the other 2 CO2's making 6 CO2 in total, but does not require H20 at this step.   ... OXPHOS activity: (following 2 turns of TCA) results in 48 total H20 produced between ATP synthase, cytochrome oxidase, and enolase - and being that 4H20 are consumed in the TCA, the net H20 production per glucose is actually 44 H20.

Don't understand the comment that "Stoichometry is relatively useless in real research". I find it incredibly useful, and I like to think of myself as a real researcher. Admittedly, I've never had to carefully balance waters, but if you do it right, it works out.

This doesn't answer the question. The H2O produced in ATP synthesis is not relevant here, since those H2O molecules originate from the phosphate groups and are recovered during ATP hydrolysis. Also, ATP synthesis is not stoichiometrically fixed to glucose oxidation since chemiosmosis is a stochastic process, so it is not even possible to give an integer coefficient for H2O if you would involve ATP synthase.

@VictorChubukov my apologies, my intention of saying "real" was not to contrast paid vs non-paid research, I meant it only as when looking at real-life biological systems, in vivo. Regarding the stoichometry, I was trying to imply that there can be multiple different reactions in the same place at the same time, that all produce the same product; and trying to break down those dynamics into an equation is impossible as of this moment; I guess I should of clarified what I meant as 'systems stoichometry'. Equation stoichometry itself is very usefull. Cheers.

Two waters come in at each turn of the TCA cycle, one at citrate synthase and one at fumarase. Additionally, I don't think it's right to say that you get a net water from glycolysis (in fact if you look at what you wrote, the oxygens don't balance). I think what you're missing is you also get an ATP, and the water you do get at the 2PG->PEP step is really part of the net reaction ADP + phosphate -> ATP + water.
To really balance the waters you have to consider all the substrates and byproducts of glucose oxidation, including the ATP/GTP.

Thank you very much. However, this only works if the ATP produced in the ATP-synthase does not need water to be formed. Why by this way (with ATP-synthase) the formation of ATP doesn't need water, but if is done in any other way, water is required?

Could it be that the formation of ATP by the ATP-synthase uses PO3 instead of HPO4 + H+?

Every phosphate fixation reaction will release a water molecule and every atp hydrolysis reaction will use a water molecule. That includes ATP synthase.

But then we have 40 water molecules, since in the electron transport chain 34 ATP are formed.

Sure. But then you have to write the equation as 1 glucose + 6 O2 + 34 PO4 + 34 ADP -> 6 CO2 + 34 ATP + 40 H2O. I think that balances.

It should be 38, since 4 ATP are produced before the electron transport chain, but that is not important at all. The problem is that as you pointed out, 6 extra water molecules are formed (40-34), so those 6 waters do not come from ATP formation, at least that is what I understand. My question is were those waters come from.

So talking about water molecules that don't have anything to do with ATP formation we only have: in the glycolysis two Phosphoglycerate are transformed to Phosphoenolpyruvate, producing 2 water molecules in total. In the TCA cycle 2 hydrogenations take place, as it is done twice we have a loss of 4 water molecules. At the moment we have just lost 2 water molecules. Finally at the electron transport chain, oxygen is used as an electron captor, producing 12 water molecules. So at the end we have gained 10 water molecules, but it should be 6. What happens with those 4 water molecules?

Try writing down the entire mass balance equation, not just the reactions that you think are important. Water is a tough one to track because it's used in so many processes (balancing carbons is a lot easier). I think you'll find that the glycolysis water works the way I described, and your other missing water might have to do with a similar thing happening at the succinyl-coa step (fixing phosphate into GTP).


text:
Can phylocode classify viruses?
Can phylocode classify viruses? Based on what I found this system began in 2019, so there is not much information about it.
I know that the Linnaean classification system cannot classify viruses, but what about this new classification system (phylocode)?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, please add links and references about "phylocode" and why you think it might be useful compared to existing viral classifications. Thanks!

PhyloCode is not a new system but it isn't popular yet and actually quite opposed by some.
It overlaps with the ranked based systems but does not nullify them, meaning that even if PhyloCode becomas popular the ranked systems will still be needed.
One might understand from your question that virus have no classification system, but they have. The common one is called ICTV.
PhyloCode can classify virus and there is already a classification for virus (ICTV)


text:
Why do we have to move in the cold for higher chance of survival?
To survive in the cold temperatures, a person should move as much as possible so that they do not freeze to death. But constantly moving also leads to the body becoming more and more exhausted.
Why doesn't the human body "know" that it is better to invest energy directly in heat rather than in movement and the resulting heat?
After all, the body already optimizes blood circulation, protecting the inner organs better than limbs like hands and feet.

Asking "why" about anything to do with evolution is tricky, because the only real answer is "they managed to survive and reproduce".  One might suggest that it has something to do with humans and their ancestors having lived mostly in tropical climates, so there was no great evolutionary pressure to develop adaptions to cold.  Peoples whose ancestors inhabited cold climates for many generations, like the Inuit or Tierra del Fuegans, DO have adaptations for cold tolerance.

It seems to me ironic that you talked about the body “knowing” (commendably in italics), when, in fact, the problem is solved by the fact that we do know — no italics, because it involves our brain. Shades of wanting Nature to reinvent the wheel, but make it square. I think she knows better.

Also note that the body DOES have a way to produce heat (within limits) without movement.  It's the shivering reflex: https://en.wikipedia.org/wiki/Shivering

Don't get me wrong. I believe that the human body and nature in general is a miracle and I admire it. I just ask to learn more about it.

@Dani: If you believe the human body is a miracle, you should migrate the question to the (religion of your choice) site.

As with any evolutionary "why" question, most any answer will likely involve some speculation. But we can still think about what we do know in relation to the question.
First, lets think about thermogenesis in humans. As your questions mentions, humans move to stay warm. This is because the conversion of chemical energy (in the form of ATP) into kinetic energy in our muscles is inefficient, resulting in some of the kinetic energy dissipating in the form of heat (instead of moving your body). Shivering is actually a cold-induced reflex that helps our body maximize the amount of chemical energy converted into heat through skeletal muscle contraction. So, in a sense, you body does "know" how to invest in generating heat without moving (without moving as much at least).
A different mode of non-shivering thermogenesis in mammals is mediated by a specialized type of fat called brown adipose tissue or brown fat. This brown fat is used by some animals to generate heat during periods of hibernation. However, adult humans tend to have very little of it. Human infants on the other hand, carry can carry quite a bit (up to 5% of total body weight). This could relate to a number of factors that make infants more sensitive to cold than adults, including having less developed skeletal muscles that are unable to generate much heat though movement or shivering.
It seems like one reason we can't generate heat very well without moving is that we don't carry much of this brown fat around. So, why don't we then? It could be that it's just energetically expensive, and those resources can be better spent elsewhere. Or maybe there could have been some negative health effect associated with carrying excess brown fat in adults. Whatever the reason, it comes down to a lack of selective pressure to maintain this extra tissue into adulthood.
But there's one other, more behavioral solution that might be worth consideration (although it's purely speculation at this point). In most naturally occurring scenarios where the body would be approaching a state of hypothermia, simply staying put and waiting for the temperature to change will seldom be your best chance for survival, even if you are doing burpees to stay warm. In order to ensure continued survival, one may need to actively change their condition of being in an environment that's too cold to maintain sufficient body heat. Humans are pretty good at changing their immediate circumstances. It might involve getting up and finding/building shelter, gathering fuel to make a fire, or migrating to someplace warmer. But in any case, it would require some amount movement accompanied by a cognitive motivation to move. Feeling less cold seems like a powerful motivator to me. If we had more robust means stationary thermogenesis, it's possible that we'd be able to survive a longer spell out in the cold just by conserving our energy a bit better, but that might not be the most effective survival strategy given the situation. Calories and liquid water can be hard to come by in extremely cold environments, and waiting for some other physiological need to motivate action might be less advantageous than proactively moving around to alter one's state of being too cold. Just a thought.

Actually, the body is able to warm itself by using uncouping protein 1 (UP1) and other physiological methods
The coupling in uncoupling is referred to the relation between the protein gradient and the synthesis of ATP (biological energy currency). UCP1 creates an alternative channel for the protons to pass. This protons have energy that, when not used to create ATP, will dissipate as heat
But every process has it's limitations. By moving you are forcing your body, in addition, to transform chemical energy to kinetic energy and that kinetic energy will transform to heat
Speculation
The movement will pump blood to the limbs and transfer the heat created by UCP1 from the inner cells to the outer cells, heating you up and allowing more UCP1 to be created in the inner cells and to use more energy for heating up.
This is a speculation because:

I don't know and didn't found an article examining what regulates the levels of transcription and translation of UCP1
I don't know if UCP1 are created in all cells or only in the outer ones


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What is the methodogy used to determine the exact genetic flow from one area to another and the times in which it flowed?
For example, I take the instance of Central Asian migration into India.
Say geneticists studied a) ancient bones in CA b) ancient bones in India c) living people in Central Asia d) living people in India.
Case 1: -
Say they found a particular haplogroup (A) which is present only in Central Asians, and another one B, which is present in Indians (both living people, aka options c and d). Then they also found another haplogroup C, which is present in both individuals.
Question 1: - How do they then determine that it was the Central Asians who migrated and not Indians? Is it due to coupling this evidence with other sorts of evidence like general climate/vegetation? Or is it due to the fact that progressively, unique genes found in Central Asians decline in quantity when moving north to south, and the unique Indian genes aren't found outside India at all (Indus Valley genes)? And if I am not wrong, Indus Valley civilization people were descended from Africans who migrated via Yemen/Oman and the historical Elamites were their cousins, so even the so-called unique Indian gene can be found outside India...how do they then describe the direction of the gene flow?
Case 2:- Say the ancient bones of Central Asia (dated to 3000 BC) showed some genes which were common between ancient bones found in India (dated to 1500 BC).
Question 2: - Does this lead to the conclusion that the migration was from CA to India, latest by 1600-1500 BC? Is there any other technique to find the timing of the gene flow?
Question 3: - Modern ancestry tests have several obscure ancient groups like Neolithic Iranian farmers, Oriental Hunter-Gatherers, BMAC etc. Are all of these from bones taken in specific areas like Zagros Mountains (for iranic hg), Central Asia and Bactria (Afghanistan)? And these bones were dated to the specific time periods when these proposed civilizations were also historically dated?
Overall, I want to understand the nuance of the genetic tests which offhandedly say, that xyz group migrated to pqr location at abc era without giving the details.

I would love to answer this question since it's what I study - but I will encourage you to try and trim it down to a single question, since we expect posts to only contain one question.

In any case, this article should give you an idea of the complexity of the subject: "Ancient genomes reveal complex patterns of population movement, interaction, and replacement in sub-Saharan Africa" Science Advances  12 Jun 2020: Vol. 6, no. 24,  eaaz0183 DOI: 10.1126/sciadv.aaz0183

thanks guys! both user438383 and Armand


text:
Is it possible to make a vaccine against cancer?
If we can make RNA vaccines against COVID-19 and we know which errors in our DNA leads to different kinds of cancer, can we make a vaccine that will teach our immune system to detect and destroy cancer cells?

The question is akin to "is it possible to make vaccine against viruses?" - for some viruses the answer is yes, for others no.

@RogerVadim Currently the vaccines agains HIV and Hepatite are testing. That vaccines bring to your body the constant parts of viruses that are not mutate

what I am saying is that there are throusands of kinds of cancer, just as there are thousands (or millions) of viruses... in fact, many of them we don't even know yet. A claim that all viruses/cancers can be cured  is impossible to prove, but easy to disprove. See also Faulty generalization.

This is not a direct answer to your question, but perhaps an interesting comment: Cancer has many different underlying causes. One of those are viral infections, such as certain types of HPV (human papillomavirus), which are known to induce several different types of cancer (cervical, anal, vaginal ...). HPV vaccine already exists, and it does indeed provide protection against HPV-induced cancer. Therefore, this is – as your title asks – a type of vaccine against cancer :-)

@RogerVadim It is not only true for the cancer caused by viruses, it is also true for the treatment of other cancers. I will expand my answer tomorrow.

@Chris I did not mean specifically the cancers caused by viruses, but I see now how my phrasing could be confusing.

@RogerVadim Ok, but I didn't include these and at least mentioning them is probably a good idea.

Like vaccines for viruses, wouldn't vaccines need to be targeted to each type of cancerous cell? Also for a number of cancers, there is a vaccine-ish solution. Want to lower your risk of lung cancer, then don't smoke or work with dust without a respirator. Want to lower your risk of melanoma, wear a hat and sunscreen.

@DWGKNZ "then don't smoke" - if technology gives us ability to smoke without hurt, why not?

@Robotex Your reference to faulty generalization is itself an example of faulty generalization. You have reached your conclusion that "a claim that all viruses/cancers can be cured is impossible to prove" by implied reference to proof by example but that is just one type of proof. It is not impossible to prove the claim (albeit very difficult) using proof by exhaustion. One can, in principle, examine every inch of the earth and gather every known virus and test them all.

It is not only possible, these vaccines are in active development. Biontech (the company which developed the Comirnaty Corona vaccine) was founded to develop vaccines against cancer, Moderna is developing similar approaches. It was the research on the cancer vaccines and the development of the mRNA vaccine approach in general made the fast vaccine development for the SARS-CoV-2 vaccine possible.
Biontech has published results of a mRNA based cancer vaccine against melanomna in the summer of 2020 (reference 1) which shows promising results, Moderna has shown data from a phase I study on head and neck squamous cell carcinoma (reference 2). See references 3 and 4 for an overview over the topic.
References:

An RNA vaccine drives immunity in checkpoint-inhibitor-treated
melanoma
Moderna Announces Clinical Updates on Personalized Cancer Vaccine
Program
mRNA vaccine for cancer immunotherapy
mRNA vaccines — a new era in vaccinology

Might not be the answer you're looking for, but there's already a vaccine for one particular type of cancer - cervical cancer. Cervical cancer is largely caused by a virus though (HPV, Human papillomavirus). See Wiki.

Three HPV vaccines (Gardasil, Gardasil 9, and Cervarix) reduce the risk of cancerous or precancerous changes of the cervix and perineum by about 93% and 62%, respectively. The vaccines are between 92% and 100% effective against HPV 16 and 18 up to at least 8 years.

Note that, if I understand correctly, this is not a vaccine against cancer. It is a vaccine against a virus that can cause cancer but not against the cancer itself.

@terdon, one of the users argued the same in his (now deleted) answer. However, would you then by the same arguing say that "COVID-19 vaccine" is not a vaccine against COVID-19 because it is a vaccine against the virus SARS-CoV-2 that causes COVID-19?

@Domen The question specifically asks "can we make a vaccine that will teach our immune system to detect and destroy cancer cells?". If these HPV vaccines attack the virus, rather than the cells, then this is not what the OP wanted to know. Which is why this answer starts with "Might not be the answer you're looking for", I guess. It's still a useful answer, but the distinction that terdon pointed out is important.

@Domen: COVID-19 is a syndrome that's a direct result of infection with SARS-CoV-2. You don't get COVID-19 without SARS-CoV-2 infection, and if you have SARS-CoV-2 infection, you have COVID-19; the distinction is semantic hairsplitting. HPV causes genital warts (sometimes), but it's lingering damage from HPV that sometimes leads to cancer (of various forms) down the line (years after you've cleared the HPV itself in many cases); you can still get those cancers without HPV, and you can get HPV without getting those cancers. The vaccine stops HPV, it only indirectly protects against cancer.

@domen that is a false analogy. Cancer is not caused by pathogens per-se, it is caused by aberrations in the cell's DNA sequence. The link between a virus and the disease it causes is far more direct and the vaccine that targets the virus is actively targetting that virus and, by extension, the associated disease. However, the HPV vaccine will have absolutely no protective effect from developing cervical cancer through random mutation (as is usually the case with cancers) and not as a result of HPV infection. [cont...]

[...cont] So this is a vaccine against HPV, and by protecting you from HPV infection it can protect from HPV-induced cancer but it will not have any effect on non-HPC induced cancer and HPV is not the only way of developing cervical cancer. You can still develop the cancer if you are unlucky enough to develop the same mutation through other means.


text:
Why do catabolic reactions release heat despite that breaking bonds absorbs heat?
According to Campbell, the definition of a catabolic reaction is:

Some metabolic pathways release energy by breaking down complex
molecules to simpler compounds. these degradative processes are called
catabolic pathways, or breakdown pathways. ... Energy released from
downhill reactions of catabolic pathways can be stored and then used
to drive uphill reactions of anabolic pathways.

The book also mentions that:

It is important to realize that the breaking of bonds does not release
energy; on the contrary, as you will soon see, it requires energy. The
phrase "energy stored in bonds" is short-hand for the potential energy
that can be released when new bonds are formed after the original
bonds breaking, as long as the products are of lower free energy than
the reactants.

Can someone help me link these two ideas considering the apparent "contradiction"? How is it that catabolic pathways, which release energy, work on breaking bonds, which require energy? Are catabolic pathways energy-releasing because of the "net" energy difference because the heat required to break bonds exceeds the energy required to break them? And how are those bonds broken? I think the book was attempting to answer my question in that second excerpt, but I could not fully grasp it from their wording. Thank you!

What do you mean by "breaking bonds absorbs heat"?

I mean that energy is required to break bonds, so how is it that catabolic reactions release energy?

Please define “catabolic reaction”. As far as I am aware the term “catabolic” only applies to metabolic pathways, not individual reactions. And if you read something please quote it verbatim and provide a source.

If it takes energy to push a boulder off a cliff, does the boulder have more or less potential energy at the bottom of the cliff than when it started?

I completely understand your confusion, because this is – in my opinion – a concept in biology/biochemistry that is often not well communicated, and explained without properly involving chemistry. It is true that breaking a bond is always an endothermic reaction, and creating a bond is exothermic. But be careful, this is true for all types of bonds! See, when ATP is hydrolyzed, this is not simply "breaking one bond in ATP", because there is also formation of new bonds between $\ce{P_i}$ and water. This "energy" is also called hydration energy/enthalpy. So, why is ATP hydrolysis ...

... exothermic? Because formation of bonds between $\ce{P_i}$ and water releases more energy than it is required to break the bond in ATP, therefore the net enthalpy change is negative. (Actually, you can make this story more precise: Two covalent bonds are broken ($\ce{O-P}$ and $\ce{O-H}$), one covalent is formed ($\ce{O-H}$), and bonds between water and $\ce{P_i}$ are formed ... But the main idea is the same: Bond formation releases more energy than bond breaking spends.)

You can read more about this concept here.

I see now, thank you so much for your explanation!

Once again you ignore my point about the term catabolic being applied to pathways. Your quotation from Campbell purporting to define "catabolic reaction" does no such thing. It refers to "catabolic pathways". A pathway is a series of reactions. The two statements refer to different processes — in the first to pathways, in the second to individual reactions. Therefore your question is invalid as it stands and should be closed. Please pay attention.

I had simply forgotten to rename the title of my question... I was not aware of the difference between catabolic reaction and pathway in the beginning. I didn't notice the usage of different terms and just put everything collectively as "some catabolic stuff" in my thought process.

The book is right, but you are missing quite a big chunk of information inbetween. In a sentence, catabolism is fairly complex and it cannot be seen reaction by reaction but as whole. Because, in order to produce ATP from glucose so that it can be used to drive reactions in anabolic processes, the metabolism of glucose undergoes multiple processes (or phases) with distinct goals: glycolysis, krebs cycle and oxidative phosphorylation (OP).

Glycolysis, or the lysis (as in breaking down) of glucose is a preparation phase. In this phase, glucose is metabolized in a way of preparing it to eventually generate energy. This phase barely generates any energy (net +2 ATP per glucose molecule), but the initial molecule (glucose) undergoes quite a transformation before being converted into pyruvate.

Krebs cycle is a continuation of the preparation phase where, essentially, carbon is converted into electrons. In other words, one full cycle in the Krebs cycle entails Acetyl-CoA (2 carbons) entering the cycle and the full oxidation of 2 carbons into CO2. With this cycle, several molecules of FAD and NAD+ are reduced into FADH2 and NADH, respectively, using the electrons of the oxidative reactions. Per glucose molecule, only 2 GTP molecules are produced as well.

OP is where energy is effectively generated. O2 is reduced into H2O, NADH/FADH2 are oxidized into NAD+/FAD and ADP is converted into ATP by harnessing energy from a proton gradient inside the mitochondria. Per molecule of glucose, and depending on efficiency, 30-36 molecules of ATP are produced in this phase.

Of course, multiple reactions in these processes release energy (-ΔG'o), while others actually take energy (+ΔG'o). The only way the cells can make up for this is by adjusting the concentrations of products and reagents to drive the reactions in the direct reaction and not the other way around by resulting in a negative ΔG, according to the following equation:
ΔG = ΔG’o + RT * ln([products]/[reagents])
By doing this, metabolic reactions flow in a way that the overall process of glucose metabolism will ultimately result in energy generation, despite some of the reactions barely generating any energy, while some others actually take up energy.


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Why does biomagnification of mercury occur more in large fish?
I love tuna so this question has been bugging me senselessly.
I am aware that larger fish tend to have more mercury concentration in their flesh than their prey, however, I don't understand how this can be possible.
I understand that there will be more mercury in the large fish than the small fish as it collects in the large fish over time, but why isn't it distributed across a much greater volume of animal tissue, therefore keeping the overall concentration the same?
The only thing I can think is that the larger fish have some reduced capability for excreting mercury. Whatever the reason, why don't we hear about it? Why is it always "bioaccumulation" this or "biomagnification" that?

Bioaccumulation occurs when organisms aren't able to excrete/eliminate/metabolize something as fast as they take it in. The specific circumstance of predators higher on the food chain accumulating even more is called biomagnification.
Every organism needs to eat more than it weighs to grow, as a simple consequence of conservation of energy. If you have a predator fish that eats smaller fish, it will have eaten far more than 10 kg worth of smaller fish by the time it grows to 10 kg in size. If it ate 100 kg worth of prey fish that each had 1 unit/kg of mercury and it can't excrete mercury effectively, it would now have 10 units/kg of mercury. The biggest fish eat prey that already experience the biomagnification effect in their own diets, taking the overall effect even further.

You hit the nail on the head! It didn't occur to me that the fish would have to eat substantially more than their body weight to grow (duh).

@JordanRegan This is also the same reason you get more food by eating the vegetables that an animal would otherwise eat than eating the animal itself.

[+1] Now I learnt the difference between "bioaccumulation" and "biomagnification".


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Can features of modified plasmids be divided into prokaryotic features and eukaryotic features?
Here's what I understand and please correct me if I am wrong:
Plasmids modified for gene therapy or genetic engineering should contain factors for certain functions in prokaryotic cells. For example, it should contain an origin of replication for amplification in prokaryotic cell as bacteria.
In the same time, if it's being made to alter a mammalian cell, which is an eukaryotic cell, it should contain features that helps in expression of a certain gene as Kozak sequence
So is it right to say that we can divide features in the architecture of plasmids into features that serve prokaryotic functions and others that serve eukaryotic functions?
are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?

Plasmids are prokaryotic. If used as vectors for cloning they are still prokaryotic as regards their replication transcription and translation. The inserts in the vectors have the characteristics of the organism from which they originated. If the purpose is to introduce the insert into a eukaryote and hope to have it expressed then it will obviously require the transcriptional and translational signals to allow this occur, and these differ from prokaryotes to eukaryotes. You seem to understand this, so I don't quite see what your question is.

Not to be nitpicking, but while I agree that for cloning purposes plasmids are to be considered prokaryotic, eukaryotic plasmids do exist. The yeast 2-micron plasmid is one example (PMC213983).

@david i want to know if my reading is correct and also i want more specificty:
are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?

Unfortunately I don’t think you have a specific biological question in the terms of this list.

are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?
Probably. We still use bacteria to make large quantities of plasmids, so we need to keep the essential prokaryote parts such as origin of replication. Also, we need selection markers markers such as antibiotic resistant gene fro pro and sometimes eukaryotes.

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus inappropriate for this site. This is a good example of how to format references. In addition, it is best to leave poor questions unanswered. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.


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What is the term for the physical and behavioral changes that occur in an adult species due to the change in their hierarchy?
For example, when a chicken becomes a rooster its crest becomes larger and their feathers become more colorful. Dominant male lions get larger and darker manes.
Also, can these changes also occur inversely? If so, what is the term for it?


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Protecting linear ssDNA inside a yeast cell
This is kind of a multi-part question :)
Basically, I want a linear single-stranded polydeoxynucleotide to exist inside an S. cerevisiae cell cytoplasm for a long time without being digested. As far as I understand, the main danger to a linear DNA are 5' and 3' exonucleases (am I right?). So, the first question is:
What particular exonucleases digest ssDNA in yeast? What other enzymes do? Maybe something involved in defence against viruses? Which of them, if any, can be safely knocked out (i.e. are not absolutely crucial to the survival and reproduction of the cells)?
The rest of the question is about protecting the 3' end of the molecule against exonucleases (assuming they aren't knocked out). For the application I have in mind, "unnatural" modifications of DNA (like phosphorothioate bonds or 2' modifications of sugars) are unacceptable. Only 3' modifications of the last nucleoside are possible. In particular, I am considering something like:

Where X = -O-, -S-, -NH- or phosphodiester, and R can anything that's either something small (-H, -alkyl, -acyl, ...) or something big but connected by a long spacer (say, a protein on a PEG tether).
Can an effective 3' end protection be achieved this way?
The problem is, according to this, 3' modifications are generally bad at inhibiting exonuclease activity, but I can either use them or knock out nuclease genes (the latter is less preferred).

Would a locked nucleic acid work?

No. I should have probably defined "unnatural" as modified sugars or phosphodiester bonds. A bridged ribose doesn't work as R, too, because it's bulky.

Can you [edit] in some background about why you want to do this? Is it important the the ssDNA not be digested or that there be a high steady state level of the ssDNA? If the latter, there are alternative strategies that would allow you to achieve your desired ends without extensively modifying the yeast genome or expensively modifying the ssDNA. ——— The problem I see is that yeast also has enzymes with ssDNA endonuclease activity (and 5' exonucleases), so 3' end protection (or complete KO of 3' exonucleases) probably wouldn't be sufficient, again depending on your goals ...


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What does it mean to collapse heterozygous alleles?
I am a bioinformatics rookie. I read a paper, it said:

existing algorithms either collapse heterozygous alleles into one
consensus copy or fail to cleanly separate the haplotypes to produce
high-quality phased assemblies.

So what does it mean to collapse heterozygous alleles?

I suspect this means that either the multiple alleles are represented with an ambiguity code:
Haplotype1:      ATCG
Haplotype2:      ACCG

Consensus:       AYCG

Or, that from a pile up of mapped reads, the "consensus" is simply called as the allele with the majority of reads.
Read1:     ATCG
Read2:     ATCG
Read3:     ATCG
Read4:     ATCG
Read5:     ATCG
Read6:     ACCG
Read7:     ACCG
Read8:     ACCG
Read9:     ACCG

Consensus: ATCG

Without more context, the meaning is unclear.

It would be better to not answer bioinformatics questions with no biological component on this site. It is also best to not answer questions that show no evidence of the expected prior research — this encourages sloppiness on the part of posters and results in an accumulation of poorly formed questions that will be of no use to future users. Note that if you feel compelled to put phrases like "I suspect" into your answer this is a strong indication that the question isn't clear enough — in such cases asking for and awaiting clarification is likely to lead to higher quality posts.

@Darlingtonia - good answer.  Regarding the other comment, it's bad enough to be discouraging to newcomers, but must it now also be discouraged for someone to give a helpful and informative answer?  Based on the logic that helping one curious novice might lead others to come, or that bioinformatics has nothing to do with biology?  It would be much more useful to have a folder or tag system to segregate high- versus low-level questions, as some other forums use.

@tyersome This looks like a typical case where a novice can waste a lot of time trying to find an answer where a more experienced professional can quickly provide a relevant explanation. That said, the original poster could have provided more clues about their previous research efforts. Regarding the absence of biological component in the question, we may add that the question might have been better placed in https://bioinformatics.stackexchange.com/


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Mapping 23andMe data to academic paper
I'm trying to figure out how to map 23andMe genetic data to a paper but having trouble. I'm able to find the gene here (https://www.ncbi.nlm.nih.gov/gene/1813) but the paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128289/) mentions an "A1 Allele" while the 23andMe data says it is "AG".
How can I reconcile this data? Or in other words, how can I see which alleles are present in 23andMe data?

I'd be cautious about overinterpreting your genetic results without consulting an expert in genetic counselling. I'm not sure whether your question should be closed as personal medical advice but I don't think I'd feel good about giving an answer here, I think there can be some risk in giving people some Dunning-Kruger style expertise.

@BryanKrause this is purely for research purposes and would absolutely not constitute medical advice to anybody.

@Bryan whilst this certainly seems like the thing an interested amateur would ask, it's also a totally plausible thing a researcher might do as well.

@user438383 A researcher involved in genetics? I kind of highly doubt it...

@bryan  there’s plenty of non-geneticists who dabble in genetics research to support their (often misguided) e.g. sociological research, and who probably have no idea about what a reference allele is or how to parse a vcf file. But maybe I’m being too generous… (I’m a geneticist btw)

Honestly, I'm just interested if my father (who died from alcoholism) and I have the same genetics related to addiction. I'd like to better understand the causes behind his death and if there's some way that I could help people in the future

Honestly, I would appreciate an answer to this question, otherwise, I'm just going to have to post on other forums/rephrase my question until I get an answer

@Rob That is exactly the sort of thing I was warning about interpreting without expert guidance.

As answered in your other question, you should use the rs ID for the allele. This is a systematic method (rather than the informal "A1" terminology) of being very precise about the variant. This ID will be shared / mappable across a dizzying variety of genetic resources, including 23andme.
For this specific variant, the rs ID is rs1800497.

This is very helpful! Thank you!

@Rob — Please take the time to take the [tour] and then consult the [help] starting with [ask]. You have asked what appears to be essentially the same question twice and are now asking a followup question in the comments. Both of these actions are frowned upon on this site — doing this makes it harder (if not impossible) for other users to find material, which is a primary aim of the site. Please see above links for details. ——— In addition, your posts suggest you have a limited understanding of the basics of molecular genetics. If this is true, you would be best to address that ...

@Rob: I can't evaluate the AG issue since I'm not sure what it's referring to at 23andme. I'll note that AG would be the reverse complement of CT. In other words, there are C and T alleles, which if you turn them around are A and G alleles. Just a guess, not sure.

@tyersome I do think that this and the other question are distinct (and potentially useful to answer independent questions)- obviously or I wouldn't have answered both. This question is more about "how do I figure out what to do with 23andme data" and the other one is more along the lines of "how do I look up stuff about a variant". I agree they're closely related, and the answers happen to converge. But knowing about that convergence is pretty specific domain knowledge about human variant databases (IMO).

Just in case anyone finds this useful:
The data from 23andMe contains information about SNPs (single nucleotide polymorphisms), which are basically single base pairs in your DNA, eg. AT, AG, TT, etc.
However, in many academic papers, the authors usually write about entire genes, which are many SNPs that come together to form a trait. Alleles are simply different configurations of these SNPs for the gene that encodes for something.
Eg.

A gene could be the color of your eyes
Some Alleles for the eye color gene could be ones that encode blue, green, or brown eyes
The SNPs inside each Allele would be different, for example, green eyes could be AA, TT, GG whereas blue eyes could be AG, GG, TT

Therefore, since 23andMe contains information about individual SNPs, there's still work required to understand the SNPs for each Allele. I'm currently trying to figure out where I can find this information.


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Why does human hair grow and behave differently depending on its location?
Why does human hair behave differently depending on its location? For instance, head hair grows to an indefinite length, but eyebrows maintain a particular length and appearance. Head hair and eyebrows may exhibit balding, but not ear, arm, nose, and facial hair (etc). Why is this so?

The answer for why is in this post: basically because of differences in follicle cycling. Are you asking how exactly is this controlled?

Thank you for the link. And, yes, I am asking how this is controlled.


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Why do flagella form a bundle only when they rotate counterclockwise during chemotaxis?
During Chemotaxis in bacteria with flagella, the flagellar rotation dictates how the cell moves. If the flagella rotate counterclockwise, then they form a bundle at one end of the cell (---O) and propel it forward in a coordinated fashion. However, if the flagella rotate clockwise, then each flagella acts independently to push the cell in many different directions.
My question is, why doesn't clockwise flagellar rotation simply cause the bundle to form on the opposite end of the cell? (O---)

In principle this can happen, but you have to read up on flagellar dynamics and polymorphic transitions (Real-Time Imaging of Fluorescent Flagellar Filaments, Turner et al. 2000).
From Howard Bergs lab page:

Runs can occur with filaments of any polymorphic form; although, the normal form predominates. For a cell to tumble, not every filament needs to change its direction of rotation. Different filaments can change directions at different times, or a tumble can result from the change in direction of only one.

If the whole bundle comes apart it can reform on either end of the cell body because E. coli has a random flagellation pattern (peritrichous) and thus no preferred direction of propagation of the cell body.
Also have  look here for some nice movies from the Berg lab.


text:
which specific field to study to know more about genes and genomes
I recently got interested in specific subjects :
1.Evolution
2. DNA, genomes etc and its structure
3. Abiogenesis
I am a software engineer with good fundamental understanding in math & physics and I was thinking to read some biology to get knowledge on it in my free time.
An associate free course or a book which can build my broader understanding in fields of biology would definitely help.
Regards

People who downvoted are seriously useless if they do not consider leaving a comment.

I believe that you're looking for fields with names like "genomics" "genome evolution", "population genetics", "molecular evolution", and possibly "computational biology"/"bioinformatics".
Each of these is a huge field with a large literature. I'll try to recommend some resources but they're not exhaustive.
For a simple mathematical introduction to population genetics and microevolution, I like Joe Felsenstein's book (free online).
Joe furthermore has a lot of slides up along with audio tracks for courses he's taught covering several of these areas. He is coming at it from the perspective of a mathematically-sophisticated computational biologist with an interest in designing software for phylogenetic inference, so it might be a point of view that works for you. I'm sure that there are lots of other similar resources but I'll admit that I'm personally fond of Joe's style.
It does look like there are online courses for genomics intros, I don't know how good they are. The field changes so quickly that it may be hard for them to keep up.
MIT has a computational biology course up- I imagine it's probably pretty good.
Abiogenesis is a bit harder, but you might look into the field of exobiology/astrobiology- here is a list of online courses.

Thanks for replying back with an answer which definitely helps. Can you also point me out some good computational biology courses. Also, books take a lot of time. I may be silly but as a hobby getting a high level knowledge on this will help than to get deeper knowledge.

updated with computational biology info. Understand about high level knowledge. .

This should be good for a start. Will come back again if need be. Thanks :)

My standard recommendation for this is The Cartoon Guide to Genetics. It may sound overly cute, but it's actually reasonably information dense, and pitched at intelligent readers with no background in biology. I covers the basics of both classical genetics and molecular biology.


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How much mass does a person lose in a day through breathing and perspiration?
Water and carbon are lost through perspiration and breathing.
How much mass is lost in this way in a single day for a typical person?

Welcome to the site. It's considered a requisite on biology.se that at least some research is carried out and presented with your question. Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

The simplest route to your answer would be through the kcal consumed/expended equation.
1kg (2.2lbs) of fat has ~7700 kcal of energy. The average person requires roughly 2000kcal per day if they perform mild physical labor throughout their day - 25.9% of the total energy available in 1kg of fat. So you could say that if a person did not eat for a day they would lose ~1/4kg or 1/2lb of fat-mass.
I calculated the above in "fat" because it's the number I knew off-hand, but truth be told the amount of "mass" you'd lose also depends on density. Fat (9kcal/g) is more energy dense than alcohol (7kcal/g), carbohydrates/sugars (4kcal/g), and protein (4kcal/g). For the same energy expenditure of 2000kcal in a single day you would metabolise more than 1/2kg or 1lb of either carbohydrates or proteins.
In reality you will burn roughly equal amounts of fats and carbohydrates (assuming you're not forcing your body into a ketogenic state) at about a 55% fat/45% carbs ratio IIRC.
So, with the assumption that the person isn't on a keto diet, has sufficient fat reserves, and expends 2000kcal of energy in a single day while drinking enough water to replace what is used in the energy metabolism, you will lose ~.14kg of fat and ~.63kg of carbohydrates for a grand total of ~.77kg (~1.69lbs) of mass expended per day.
Since humans vary greatly, however, that is going to vary wildly. Personally speaking, it's easy for me to expend >3000kcal per day with an hour of moderate exercise since I'm simply bigger than the average person and require more energy to do anything. If you're shorter than average, do less work than average (i.e. - are sedentary), or hormonal conditions (which are rare and cannot be self-diagnosed) modify calorie expenditure, your numbers will be different.
Also worth it to note: Ghrelin, a major hunger-regulating hormone, changes its tonic behavior significantly if you go more than 2 days consuming less than 1200kcal. After 2 days fasting it will instigate changes that will result in more fat retained after you resume a regular eating schedule for up to 5 years... So starving yourself for a week to lose 5kg seems great until you realize you'll gain 10kg once you go back to a normal diet.
As always, if you're unsure of any diets please go to a qualified professional for consultation.

I would like to point out that the unit used here in the answer, kcal = 1000 cal = 1 Cal. Note that the unit Cal is also called food calorie and equals 1000 of the calories unit used in chemistry


text:
Species ID: Cape Town mystery insect
This insect bumbled into my bedroom last night - can someone ID it for me? I'm mainly curious because I'd like to know if it poses any danger to my cats (who were very eager to add it to the menu).

It was about an inch and a half to two inches long, and when I picked it up to toss it outside it made a loud squeaking noise. I live just outside of Cape Town, South Africa (but I'm not a native, so I don't know all the species here).

It appears to be a longhorn borer beetle. A more comparable picture is found here. Are there fig trees nearby?

Here you will find numerous images of Longhorn beetles.

Maybe the OP can rent out his cats to the local fig farmers!

@NateEldredge of course then the cats will refuse to hunt since they never do what you want them to when you want them to do it.

Thanks!There are in fact fig trees nearby, one of the family friends brought us a big bowl of figs from her tree a few weeks ago.

It is definitely a longhorn beetle (Cerambycidae), most probably from the subfamily Lamiinae (Flat-Faced Longhorns, > 10000 species worldwide). I'm however mostly familiar with longhorn beetles from northern Europe, and there might be taxa that I'm unaware of. The overall morphology (e.g. downward facing head, robust build, spined pronotum) is however very suggestive of Lamiinae.
The species suggested by @dustin also belongs to this subfamily and is probably correct, especially since it seems to be a common species where you find fig trees. This blog and Biodiversity Explorer - South Africa both label Phryneta spinatorthem as a pest species in Cape town and have nice pictures that are very similar to yours (also pics of larvae and larval galleries).
The sound you heard comes from stridulation of the scutellum against the back edge of the pronotum (similar to the sounds emitted by grasshoppers), and it is common in many longhorn beetles (especially from Lamiinae). It is believed to be a defence mechanism (they stridulate a lot when handled), but might also serve other purposes. Large species of longhorn beetles can have a painful bite, but they are not poisonous (I have at least never heard of a poisonous longhorn beetle) and not dangerous to your cats.