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Confused about the transport of materials across cell membranes
I am very confused about how exactly substances are transported across cells. For example, if a cell is placed in a hypertonic solution, the cell loses water. If the cell is placed in a hypotonic solution, it gains water. This happens due to osmosis.
My confusion is, however, why don't any of the solutes within the cell move in or out of the cell instead of the water, to maintain an equal concentration inside and outside the cell? Why is it always the water in these cases that moves in and out of cells? Is it because the cell allows free movement of water, but it controls the movement of the solutes according to its needs using carrier or channel proteins? How exactly does the cell control what substance will move in and out during diffusion?

What does your source/textbook say about transport of materials across membranes? That's usually where these discussions begin, before getting into osmosis.

Really, basic osmosis is Chemistry, and in my experience always refers to semi-permeable membranes which, by definition allow water but not solutes across. As the most cursory research would make clear — research that we expect from posters to this site — what prevents polar solutes passing across a cell membrane is its non-polar lipid nature, making specific transporters necessary.

Before membranes and membrane transport, there's something called osmosis and diffusion to become familiar with. Because one of the roles of membrane transport of cells is to maintain osmotic pressure :)

A few short inputs:

The membrane is permeable for some molecules but not for others. Small and uncharged molecules can pass easily (such as H2O). Others like Sodium (Na+), Chloride (Cl-) etc. have a harder time doing that, due to electric charge (the membrane is hydrophobic, hence, energetically it doesn't really like to mix with something that is that hydrophilic). However, larger molecules can pass through the membrane, if they are very hydrophobic (think about different steroid hormones).
Furthermore, many ions, such as sodium, are actively transported in a particular direction. Water is usually not.
That is also, why when doing an osmosis experiment in a physics book you have a "semipermeable" membrane which only allows water to move across, but not ions. A cells membrane is basically "semipermeable".

I would suggest to read the chapters about transporters, ion channels etc. in a molecular biology book, such as "Molecular Biology of the Cell" from Alberts.

First you say 1) uncharged molecules can pass easily (such as H2O) but thereafter 2) the membrane is hydrophobic, hence, energetically it doesn't really like to mix with something that is that hydrophilic. These statements bite each other. Water is hydrophylic, since it likes itself :) Hence, it is lipophobic

Well, not necessarily. Water also doesn't mix very easily with membranes (water is still polar, membranes are largely not, at least on the inside). Otherwise they wouldn't be able to exist as stable entities. Think about oil (the membrane) and water. However, water, because it is fairly small and uncharged, can at least pass it regularly. That's why bacteria have things like aquaporins, where lots of water can get through the outer membrane (but not the inner membrane).

That's interesting, I'll read on it a bit :)

Felix, Cell or Berg & Stryer still would be quite up the ladder in my view. Start with AP chemistry and bio would be of some value.

By that comment do you agree that it is difficult for water to diffuse into the membrane and easier to pass through aquaporins? I am quite confused of what you finally have to say.

@Patrick Yes! :)

I would first like to define some terms first based on the permeability.
Impermeable: A membrane that does not allow any substance to pass through it is called an impermeable membrane. e.g. Cuticle layer
Permeable: A membrane that allows the free passage of substances through it is called a permeable membrane. e.g. Primary cell wall
Semi permeable: Semi permeable membranes allow the movement of most substances if they are small enough by osmosis or diffusion. It does not require any energy or in other words uses passive transport. e.g. Egg membrane
Selectively permeable: As the name suggests these membranes are more selective and the substance that can pass through are limited. Substances that cannot pass through by passive transport is transported by active transport through integral proteins embedded in the cell membrane.
Though the cell membrane acts semi-permeable to the small oxygen and carbon dioxide molecules it is best to call the cell membranes as selectively permeable membrane because of the degree of the control they have over on what to allow and not to. Try reading this page for the difference between semi permeable and selectively permeable.
You were right in saying that the cell membrane allows the free movement of water but controls the movement of other solute particles according to its needs. If the molecules are small enough and they are non-polar, they can easily diffuse inside. If they are polar , like water and glucose, it is difficult to push their way through the non-polar tails of the phospholipid bilayer. The channel proteins will aid in the movement of such substances through passive transport. The channel protein that allows the rapid flow of water through is called an aquaporin. If the substances need to move against the concentration gradient, from a lower concentration to a higher concentration, they use energy and pass through the proteins. This is active transport e.g. Sodium potassium pump.
And for the last question, diffusion is the net movement of substance from a region of higher concentration to a region of lower concentration. Note that this happens along the concentration gradient and does not need any energy. The cell cannot exactly "control" that movement. If the particle is small enough and the polarity is right, it can pass along the gradient. Movement of $CO_2$ out of the cell and movement of $O_2$ inside the cell is by diffusion.
Correct me if I went wrong somewhere.

"Water can pass through biological membranes via two pathways: simple diffusion through the lipid bilayer, or water-selective facilitated diffusion through aquaporins (AQPs)" Ibata et al., 2012


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Is there a way to refine a low resolution Cryo-EM structure using high resolution partial crystal structures?
I'm working on running simulations of human topoisomerase IIa. These are best done by starting with high resolution structures to ensure the system is as accurate as possible. However, no crystals exist of the full TOP2A structure (catalytic & DNase domains).
What do exist are high resolution crystals of the separate catalytic and DNase domains and low res complete structures.
Is there a way, through simulations or otherwise, to impose the high resolution structural information onto the lower resolution full protein model?
Low-res full cryo-EM structure (~8 A)

High-res partial crystal structure (~2 A)

Not sure you’ll find an answer here. Quite a high-power question for this very broad group. If not, you might try SE Bioinformatics, although they tend to be more nucleic acid oriented. But you really need to talk to experienced protein structure people. Bite the bullet and email a biggie.

seems related, may be applicable: https://www.pnas.org/doi/10.1073/pnas.1506788112, https://academic.oup.com/bioinformatics/article/23/19/2558/185859, "fragment assembly" here: https://www.nature.com/articles/s41580-019-0163-x

@David I was aware that this isn't the standard type of question asked around here, but I figured I'd give it a shot. Perhaps I'll post this over on the bioinformatics exchange too!

@MaximilianPress Thanks for the articles! I'm actually very familiar with the nature pub you linked and its relevant, but tangentially! I will look into them, but I've found a few potential solutions that fall into the approach of "Hybrid Structure Modelling/Refinement". I'm looking into using a software I'm semi-familiar with, Chimera, that apparently has this capability. I'll report back here if it works out!

@Paul yes please answer your own question if you can! It seems like something that would be of interest to a lot of people.

Don’t cross-post. It’s frowned upon on SE.

You should use the original electron density map, not the atomic coordinates associated with it.
Other than that, what you are describing is fairly routine. Briefly, the high resolution structure is used as the starting point for a simulation, the atoms are moved around using the low-resolution information as a potential energy field, and the motion of the atoms is constrained with a level of granularity chosen by the user. I use the "Real Space Refine" program in the package PHENIX, but if you are familiar with VMD, you might prefer their flexible fitting plugin. Chimera can do "rigid body fitting" well, but that's not ideal unless you're certain the low-resolution and high-resolution structures are both of the exact same molecules.

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how do phagocytes receptors work now and in the past?
As we know, phagocytes have receptors on their cell that are used to detect pathogens which they bind to and engulf them. That seems easy.
Though, I'm trying to wrap my head around the fact how the receptors on phagocytes can detect pathogens ? I get it that they bind to molecules found on the pathogen and if binded successfuly, engulfing begins.
Question: the phagocytes' receptors that are shown in today's human body, were the same receptors present even 2000years ago ? If the answer is yes, how human body was created 2000years ago with those same receptors(as today) that can detect today's world's flue pathogens/bacterias ? If the answer is no, then do these receptors get added in the phagocytes by the vaccine that we create depending on the current virus and we know exact receptor that this virus can be detected by ?

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There are several different kinds of phagocytes in the immune system including macrophages, dendritic cells, neutrophils, and others. All are capable of ingesting viruses, bacteria, some parasites, cell debris, and even intact whole cells. They differ in how those materials are then processed and displayed on the cell's surface, and how the cell responds to the phagocytic event, but that is beyond the scope of this question.
Phagocytes recognize pathogens via pattern recognition receptors (PRRs) for pathogen-associated molecular patterns (PAMPs). These PAMPs are patterns or motifs that are conserved within particular types of microbes. Examples include lipopolysaccharide (LPS) in Gram-negative bacteria such as E. coli, lipoteichoic acid from Gram-positive bacteria, double-stranded RNA (dsRNA) from certain types of viruses, etc.
PRRs exist in many different organisms in different kingdoms, including the fruit fly Drosophila melanogaster and plants like Arabidopsis thaliana, also known as thale cress. They have existed in humans (and many of our ancestors) since we evolved. The exact same PRRs that you and I have in our bodies were in the bodies of humans that lived 2,000, 20,000, and 200,000 years ago. Their genetic sequences may have changed very slightly over that time, but from a functional perspective they are the same. The reason for this is that (pathogenic) microbes have had the same PAMPs for millions and millions of years. PRRs are also not sequence-specific, instead recognizing molecular patterns - the chemical "shape" of a molecule. These patterns are evolutionarily conserved, meaning they are the same in species after species and remain essentially the same over long periods of evolutionary time.
Orthomyxoviruses are a viral family from which originate the viruses that cause influenza in humans and animals. These viruses have several different PAMPs in their structure and genome that allow phagocytes to recognize and destroy free virus particles as well as infected cells. These PAMPs are conserved between the different Influenza A viruses that can cause human pandemics. However, while these PAMPs are recognized by phagocytes (part of the innate immune system), which then go on to activate the rest of the immune system to fight the infection, this activation period can sometimes take up to two weeks or more. Therefore, flu vaccines focus on teaching a different part of the immune system (called the adaptive immune system) to recognize influenza infection via antibodies and patrolling memory cells, which can respond much more quickly than the innate immune system can. The reason you need a flu shot every year is because the exact molecular components of the influenza virus can change quite quickly, meaning you need to develop new antibodies and memory cells to recognize it quickly. The PAMPs do not change from year to year.
In response to comments:
As I mentioned, one of the main viral PAMPs is double-stranded RNA, which is produced (or released) inside the infected cell by most (but not all) viruses. PAMPs are typically vital parts of the organism - LPS in Gram(-) and lipoteichoic acid in Gram(+) bacteria are integral parts of their cell walls, dsRNA is part of the viral replication cycle - and can't just be evolved away. That is likely a reason why PRRs evolved in the first place - PAMPs generally don't change much over time.
I should also clarify: 20,000 years is a very short period in evolutionary time. As an example, the last common ancestor to chimps and humans lived between 4 and 13 million years ago. While new viruses have emerged as human pathogens in the past 20,000 years (heck, the last 3 years), the families they belong to and even some of those viruses themselves are not new, and possess similar PAMPs that have existed for millions of years, which has allowed specific PRRs to evolve and remain relevant today..
Another part of the story, which perhaps isn't clear from my original text, is that phagocytosis doesn't just involve PAMPs. Sometimes the target cell recognizes that it is infected and produces various "kill me!" signals that are expressed at the surface of the cell, targeting the immune system to destroy it. Additionally, if the body has seen that type of pathogen before either from previous infection or immunization (or both), memory cells that produce antibodies will likely be present. These antibodies will bind to their targets and can induce phagocytic cells to engulf them, whether they be free virus particles, other microorganisms, or infected cells. So, in some cases, phagocytosis can occur completely independently of PRRs and PAMPs.
On the subject of malicious bioengineering to remove PAMPs to create "super pathogens" - hopefully you'll see from above that most if not all PAMPs can't just be casually removed from an existing species the way we can cut and paste individual genes from plasmids. So, any potential super-virus will likely still have dsRNA that can be recognized by PRRs. But, because the innate immune system (of which PRRs are a part) takes some time to get the adaptive immune system geared up in the absence of strong pre-existing immunity, viruses can often infect, replicate, and begin spreading before the body can completely eliminate them.

Note: I included Wikipedia links as they are generally accessible to people who are not scientists or area specialists. They contain links to relevant reviews and primary literature.

Thanks so much for this detailed answer  ! Highly appreciated.  Somehow I ended up learning immunology due to the fact that I need to learn immunotherapy. I wonder one thing: You say that PRR's don't change (the same receptors were 20,000years ago in humans as now), but if that's so, how can they still today bind to viruses and cause the special effect(engulfing), I mean, viruses have changed, evolved and how can the same old PRR(from 20,000years ago) still can detect the modern, viruses(PAMPs) ?

If you say microbes/viruses/bacterias have the same parent of PAMP, then, it should be fairly easy to create a artificial virus that don't have the PAMP thing and that's it, would be super easy to be malicious doctor and spread bad virus that wouldn't be detectable by PRR.

@GiorgiLagidze please see my edit that addresses your questions.

Thanks so much.. quick last question. In terms of covid, if it also had double stranded RNA, why couldnt our phagocytes kill it ? What happened in that case ? Also, approving the answer, but would appreciate this last bit of question to close the gap

I think phagocytes would recognize covid virus and kill it(1 cell) but since it would take more than 2 weeks for the adaptive system to kick in. Hence the damage is already done.  This makes me to believe that phagocytes are killing things very slowly and they dont seem to be many, otherwise B cell would not be necessary(if we dont count memory cells and remembering the virus).

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What motivates an organism to reproduce?
What is the biological factor (gene or something else in case of humans) which motivates an organism to reproduce?
By reproducing the evolutionary success of an organism increases. But why would an individual organism care about evolutionary success? Is there something inherent in the body of an organism that motivates the organism to take part in reproduction? From an organisms point of view, it can very well live happily without reproducing, in fact, the act of reproduction might lead to eventually more difficulties (raising the offspring, protecting the offspring etc.).

"But why would an individual organism care about evolutionary success?" - Every organism that didn't died without reproducing; you only see the ones that reproduced.

"you only see the ones that reproduce" - so the evolutionary success is the driving force of reproduction? I don't think a simple life form (let's say a bacteria) can understand evolutionary success, but still it none the less optimises for evolutionary success? What forces it to optimize for it?

Nothing forces anything; organisms with a genetic tendency to reproduce will reproduce and you'll see their offspring in a future generation. Any organism with genes that prevent it from reproducing will not reproduce, and you won't see their offspring in a future generation.

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You are confusing proximate and ultimate causes.
What causes an organism to keep eating, most are not smart enough to know they will die if they don't eat. The ultimate reason may be to keep from starving but that is not the proximate reason.
The proximate reason they eat is because their brains are built to want to eat when their senses detect food. to get hungry and feel pleasure when that hunger is sated.
eating, drinking, scratching, pain, disgust avoidance, vomiting, reproduction, they all come with basic urges, proximate motivations. the brain is built to want to do these things under the proper conditions. Why do songbirds sing, because they want to, they have a desire to and acting on that desire in the correct circumstances gives them pleasure or not acting on it causes discomfort.
Animals have sex because they want to, that is the proximate cause. The ultimate reason they want to is brains with that desire are the brains most likely to pass on their genes to the next generation. Thus genes that make brains that get the animal to reproduce are the genes most likely to make it into the next generation.
To look it another way you are the product of an unbroken line of genes that built brains that reproduced, because genomes that did not don't leave descendants.

+1 for introducing a new idea.

I reached to this independently and I had no idea before just randomly.

Life processes are ways of long term survival of genetic information, being carried by individuals with momentary lives inside their cells.
Since each individual life is momentary, only that genetic information survives for a long time which has developed efficient ways to ensure individuals continue to bud off new ones before they die.
In other words, individuals are only tools in the control of the super-organism of genetic information. And thus, it is not surprising to find only those variations of genetic information continuing to survive around us which have been able to drive their individual buds to continue to replicate. This includes driving the individual to resist death, driving it to seek and gather resources, and driving it to reproduce.
The tree of genetic information continues to find these ways of driving individual buds primarily through chance, enabled by the huge number of tiny variations that it introduces in each individual, and the humongous numbers of individuals; when a branch (or twig) of the genetic tree can no longer ensure it, it dies out.

I always thought sexual urges had something to do with it.

"Individuals are only tools in the control of the super-organism of genetic information." I'll use that line next time someone takes themself too serious if you don't mind.. ;)

-1. Humans aren't forced to reproduce. More and more humans don't reproduce now that 1. children are no longer necessary for labor/elder care and 2. contraception is widely available. Many humans who accidentally may or do conceive prevent or end their pregnancies. If we were forced genetically to reproduce, these choices would not exist.

@anongoodnurse I agree that "driving" could be a better verb than "forcing" here. Thank you so much for pointing it out. I have replaced it. I am sure you know that my usage of "force" wasn't meant to be irresistible; quite difficult to resist but not irresistible.

@iLuvLogix Thank you so much for valuing it, and thank you even more for telling me that you value it. I also find the idea philosophically humbling. I have now emboldened it for cursory readers.

@David Thank you so much for your comment. Sexual urges in individual buds are only a tiny part of how the super-organism of genetic information ensures its survival. If you think about it, all of our living processes are primarily designed around its survival. That is why, I have mentioned "This includes driving the individual to resist death, driving it to seek and gather resources, and driving it to reproduce."


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Chloroquinaldol and fresh peppers tasters and non-tasters?
Chloroquinaldol is an over-the-counter antiseptic drug sold under many names, often in the form of lozenges for mouth infections.
I absolutely hate its taste. The unpleasant sensation is unlike any other bad taste - it feels metallic, "chemical" (like the smell of the storeroom behind the chemistry lab at school) and sends shivers down my spine like bitter taste does - but it is not bitter taste.
To most people Chloroqinaldin is just a sweet lozenge, but I have met a few people who describe the same reaction to the drug.
Interestingly, the same people (me included) also describe a similar reaction to fresh bell peppers, equally puzzling to "non-tasters". Thermal processing as well as pickling removes the awful taste, so this specific aversion is distinct from simply not liking bell peppers in any form. In fact I love grilled stuffed peppers my dad makes, and I would probably be emptying jars of pickled peppers while sleepwalking if I sleepwalked ;)
Is this a known phenomenon? Could it be similar to how PTC can be tasted by most but not all people, except here the tasters seem to be a minority?


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Which organ receives blood from arteries and veins at the same time?
This is a question in my exam paper.  I answered 'the heart' as it receives blood from venae cavae and the coronary arteries.  However the correct answer should be the liver.  How is that so?

The questions is not very good. The lung is another organ which receives blood from arteries and veins at the same time.

The liver gets all the venous return from the GI tract, so it may well be the largest organ getting venous blood. But the question is a bad one, as every organ needs arterial blood and a number of them deal with venous blood as well (liver, spleen, lungs and heart off the top of my head.)


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Roses are red ... and have thorns
Just had an unpleasant encounter with a wild rose. Not her fault, should've kept my distance.
Roses are some of the plants that have anatomical defenses (I'm talking about thorns). Well, what transpired was I walked into it and as I was leaving I felt the tug of the thorns. That is to say their morphology was similar to shark teeth (curved backwards towards the gut to prevent prey from escaping), which at some level means rose thorns are designed for a "similar purpose" (offense in a weird sense because roses are not carnivorous, instead of defense like e.g. cacti thorns).
Any good reason why this is the case?

The offense is to day that they are designed really. You probably meant to say that they evolved this way.

@CaroZ, spot on! Why would rose thorns evolve like shark/python teeth instead of like cacti thorns? Turns out rose barbs are technically prickles. Do you know what the difference is between them?

I think the size of the thorns indicate the type of animal they defend against. Like a lot of plants have fur, which is like insect-sized thorns, but roses don't have fur as far as i know. so the thorns are probably mostly to prevent large herbivore predation.  It doesn't seem to deter the deer in my backyard though, they're always licking the thorns with their tongues to get the juicy leaves.  but probably for animals with weaker tongues, the thorns would be quite painful.

They are considered natural defense and they have evolved like that way only: https://www.birdsandblooms.com/gardening/flower-gardening/why-do-roses-have-thorns/ and yes, thorns and prickles are different: https://huntington.org/verso/2020/07/spines-thorns-and-prickles

@NilayGhosh, interesting

I think a good way to think about this is to analogize it to something closer to home.  Imagine if someone approached you with the following hypothesis:

The tread on my tires is there to make sure the car doesn't slip when
it moves.  The bumps on my shower mat are similar in design and so
must serve the same purpose.  Does that mean that shower mats were
originally designed to be mobile?

The flaw in this logic is clear.  The common selective factor here is grip, not motion.  The car needs grip to facilitate motion.  The shower mat needs grip to hold your feet in place.  They share common features because they are doing similar things but for a very different purpose.
Now think of that in reference to the thorns vs shark teeth question.  The shark has curved back teeth so that its prey will get stuck on them, and they can't get away while the shark is chowing down without tearing themselves up even more.  The rose also has curved back thorns so that they will stick into animal skin, but the rose isn't trying to hold you down.  It just doesn't want you to eat it.  But if it uses the same kinds of thorns then, likewise, an animal that gets caught on them is going to tear itself up getting uncaught, which is going to hurt more than it would if the thorn slid right out, making the animal even more averse to that plant in the future.  Both sharp curvy barbs serve to get stuck in your skin and do damage on the way out, but the shark is trying to prevent you from moving, while the rose just "wants" it to hurt.

Arigato gozaimus for the answer, but it still don't make sense to me.


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How are ray-finned and lobe-finned fish related in terms of their evolutionary history?
I'm trying to trace human evolution back to the first eukaryotic cells (as a tool to research the evolution of various bodily systems), and I understand that lobe-finned fishes are considered a key transitional group between early fishes and the first tetrapods. However, I'm struggling to understand the relationship between ray-finned fishes and lobe-finned fishes and how they fit into the larger picture of evolutionary history. I’ve tried using google, Wikipedia, and YouTube, but I can’t seem to find a straightforward answer.

[should possibly be a comment but can't embed images there]
The rather clear consensus is that tetrapods are a subordinate group within lobe-finned fish, which is a sister group to ray-finned fish. See diagram below from here. This should be apparent from the wiki article on lobe-finned fish.
Just to be clear, yes, we're all fish from a cladistic point of view.
.

What was their common ancestor like?

@SeanHolm https://en.wikipedia.org/wiki/Osteichthyes

i loved those armored fish as a kid!

@shigeta my personal favorite- phenotypic variation of the armor character!


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Dry Bulb Temperature VS Dew Point, which one is most relevant to insects?
I study insects that are leaving freely on my campus. The campus weather station has two different measures of temperature, the Dry Bulb Temperature and the Dew Point Temperature. Which one is the most relevant when studying insects? Are they very different? In other words, can you state the main differences between the two that are relevant when studying insect biology.

Insect development and activity are strongly associated with dry-bulb temperature. Development rate is usually predicted using degree-days (Links here: http://ipm.ucanr.edu/WEATHER/ddconcepts.html and https://entomology.ca.uky.edu/ef123). Basically this takes advantage of the nearly linear relationship between development rate and temperature in almost all insects (in some the type of food available can also be limiting). At temperatures above a certain threshold -- usually around 50 F or 10 C --  the warmer it is, the faster development will take place, up to a certain temperature cut-off above which development is drastically slowed (varies widely from species to species).
Insect activity is also strongly associated with dry-bulb temperature. In general most insects cannot fly at temperatures much below about 50 F or 10 C. They cannot generate energy fast enough at lower temperatures. The species that do fly at lower temps are generally Hymenoptera or Lepidoptera that use group or individual muscle movement to generate heat. Those that do fly in cooler weather or at night are often covered with fur or hair, which allows them to retain more of the heat generated by their flight muscles.
Wet bulb temperature generally relates to relative humidity, which has little to do with insect activity except in extremely hot, dry environments, wherein insects will be much more active during higher relative humidity (as it helps them retain more moisture) times of day such as morning or evening.
I hope this helps.

By wet bulb do you mean dew point? On Wikipedia it is said that those two are different.

Sorry, no. They are different, but they both relate to the same idea, of describing the moisture content of the air. The Dew point temp is always somewhat lower than the wet bulb temp, as wet bulb temp is in dynamic equilibrium between warming from air temperature (measured by dry bulb temp) and adiabatic cooling via evaporation from the wet bulb. Dew point temp is the temperature at which relative humidity is 100%.
Insect activity and metabolism are not strongly affected by humidity (except as  I noted above) so it is the dry bulb temperature that is significant, in any case.

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Viability of Toxoplasmosis oocysts on dry smooth surfaces
This is a weird question. My wife is terrified of contracting toxoplasmosis during pregnancy and I was hoping I could get an expert opinion here to potentially make her feel better.
She recently took the toxoplasmosis test and it came back negative. The next day, we cleaned the house. We have four cats, all indoors, who have intermittently gotten into the trash and licked containers containing raw meat or eaten raw meat that we had bought from the store. We also live in the city, no rats or rodents that they could find and kill. We keep our house fairly clean. There was a smear of dried cat poop hiding under a rug on our tile floor that I cleaned that has to be at least 5-6 months old. I had to really pick at it after spraying it to get it up. She's worried that because she handled the towel I used to clean it up with that she's potentially exposed herself to infection.
How likely is it that old, dried cat poop like that could still harbor viable oocysts? Assuming that it was infected in the first place. Do they dry out and inactivate if they're not exposed to moisture?
Thanks!


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what will be the effect of cockroach bite?
I know the cockroaches are creepy for humans. But I want to know why humans are afraid of cockroaches and what will be the effect of there bite on my body. Can I touch them or if they walk over my foot is safe for me!

Are they toxic like snake or scorpion?
How they bite us?
What will be the effect if more than one cockroaches bite me?
Do I still get any disease if they don't bite me but present in my house?

There is already a question related to cockroaches bite on this form but it's about cockroaches lay eggs or not while biting and it doesn't explain the possible effects of the bite.

hmm... I don't think cockroaches "bite" people. I have heard of having eyelashes nibbled on as you sleep, but not sure if that's real or an urban legend.

I have reared cockroaches by the thousands, for years. Three species, but mainly the infamous Periplaneta americana which I am sure everyone has at least heard about (see picture at the end).
First of all: Cockroaches do bite, and they have powerful mandibles. This is in the paper below:
https://doi.org/10.1371/journal.pone.0141226
Many people think they won't bite because they have never handled cockroaches. In fact, cockroaches are amongst the most common insects scavenging dead bodies, and they'll pester sleeping individuals when they're starving (e.g. in crowded infested buildings or ships).
In the case of large P. americana, males are way more prone to biting than females, especially when they're flying around. I have been bit three times by these cockroaches, and it hurts. Once I was wearing latex gloves and seized a large male, and it bit me through the glove. Because of the pinch, I pulled it off with my other hand, and the glove teared open. Last time, I was bit about 1.5 year ago on the shoulder in my sleep by an adult female P. australasiae. The pinch was enough to wake me up (so I could kill the bloody roach) and left a red mark that lasted for 2 days.
There are numerous reports of cockroach bites going infected, specially around lips. Linked paper is referenced as: http://dx.doi.org/10.1590/S1413-86702006000100006
Finally, they're not poisonous neither venomous insects, as they produce no relevant toxins. However they may carry many pathogenic microbes, so laster effects from contact with cockroaches may develop.

Hope this was clear enough!

Your answer would be much improved if you focused on the Prado paper rather than your personal experience: we don't typically allow appeals to authority here, rather we prefer experts to use that expertise to supply proper citations. Also please add references in text form and preferably with a DOI, the link to a journal page may very likely die sometime in the future.

@BryanKrause There is a DOI paper there. I will try to make it more conspicuous

@Scientist your answer give much info about cockroach bite but there are some technical terms in your answer like pathogenic microbes and lasting effects as I am from the CS field so I had to google them. If you explain these terms then it will be more helpful :)

Millions of people live with cockroaches and there are nearly zero cases of hospitalization, thousands of times more people are admitted for wasp/spider stings, putting marbles in their nose, knife injuries etc.
They may cause damage to food, like rodents, without any serious illnesses unlike rodents.
Here is the only roach attack hospitalization that I can find, versus thousands of bee and wasp incidents, a normal and sober person would sneeze and wake up. Apparently she did not suffer a bite:
https://newsinfo.inquirer.net/868535/doctors-remove-live-cockroach-from-indian-womans-skull


text:
Can Green color give Rest to Eyes?
Is it correct that Green color gives rest to our eyes compare to other colors?

In a quick search I found some blog posts claiming that some scientists believe that green gives rest to the retina, because green is in the mid range of the visual spectrum and therefore "easiest" to detect.. Of course these posts didn't cite any sources for that. So, I couldn't track down the supposed research..

@Rk003 not sure, if you're talking to me, but as I said: I couldn't find a reliable source for that claim and therefore don't believe it.

Similar question and answer is  here

In our eyes, the dioptric difference between the dispersion of red versus blue light is approximately 2D.

Remembering that the human eye's peak spectral sensitivity lies at 550 nm (green), the human retina is deliberately placed such that it is in between the dispersion of white light, i.e., between red and blue. This optimizes the best level of focus specifically for its peak spectral sensitivity. The pupil and the nucleus of the lens also help to minimize chromatic aberration.
In short, the eye is constructed such that it is easiest to focus on green light, which is in the middle of the visible spectrum and has the strongest receptors.


text:
How are ray finned and lobe finned fish are sister clades?
I think my previous questions may have been misinterpreted (I honestly was too tired to formulate what exactly I was confused about), so I’d like to elaborate on my confusion about the phylogeny of Osteichthyes.
Ray finned fish (actinopterygians) and lobe finned fish (sarcoptertgii) are classified by the shape of their fins. Their common ancestor obviously had some type of fins, so either one of the groups is paraphyletic (in the sense that their common ancestor belonged to or evolved from one of the groups), or the common ancestor had fins that didn’t resemble either rays or lobes
Despite my efforts I can’t find a straightforward source saying the latter is true, so how are the 2 groups sister clades?

Or Osteichthyes have intermediate fins with characteristics of both. there are actually quite a variety of fin types in extinct fish. just because their descendants have evolved drastically different fins does not mean the basal forms did. Imagine if the two surviving group of mammals were ungulates and bats and you asked did there ancestor have wings or hooves?

Please re-read the title of your question and remove one of the instances of “are”. Also take out the first paragraph: I have no idea what your previous question was, and it is irrelevant to this question, which should stand by itself. If you need to explain anything of this sort do it in a comment.

The misunderstanding here is the difference between phylogenetic classification and character evolution. Essentially, just because an organism has one certain trait it doesn't automatically belong to some group.
Words like paraphyletic, monophyletic, and clade, are descriptions of groupings by ancestor-descendant relationships. Clade and monophyletic, for example, refer to an ancestor and all of its descendants. Paraphyletic generally refers to an ancestor and most of its descendants, but excluding some portion. Talking about "bony fish" but excluding tetrapods would make bony fish a paraphyletic group.
Character evolution is the study of how characters have evolved among a group of organisms in light of their phylogenetic relationships. Textbooks often talk about clades having synapomorphies, or characters that have evolved in some ancestor and are present in its descendants. Some clades have clear synapomorphies that do indeed strongly match a clade (e.g. all the members of the clade have the character, and other organisms do not). However, it's not uncommon for synapomorphies to only be mostly true. Perhaps some members of the clade lost the new trait, or some species outside the clade independently evolved the same trait. These exceptions, however, don't change the group membership of those organism.
It's not the character that defines a species' clade, but the ancestor-descendant relationships. It's not exactly true that Actinopterygii and Sarcopterygii are "classified by the shape of their fins." It's just that fin shape is a really good synapomorphy for those clades because it's both consistent and probably has important evolutionary consequences. Because of this people adopted the common names ray-finned and lobe-finned fishes, giving the implication that that's what defines those groups.
The misconception is understandable because we use characters (previously morphological characters, recently increasingly genomic characters) to craft our hypotheses about what we think are the true ancestor-descendant relationships.
All that is to say that the most recent common ancestor of Osteichthyes is just that—it is an ancestor of both Actinopterygii and Sarcopterygii, but doesn't belong to either clade, regardless of its fin morphology. Actinopterygii and Sarcopterygii share that common ancestor to the exclusion of other groups, which makes them sister clades.

Here's a pretty nice resource from Berkeley relevant to this topic. I'll also recommend the Understanding Evolution site that it came from.

to be fair those groups are also both clades and taxon, as groups they are robust enough to have survived the transition in methodology. so you also get a confusion of cenvention.


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Can the genetic sequences for CRISPR components be inserted into the host genome so that the cell perpetually produces CRISPR components?

Theoretically speaking, can you insert the gene sequences for cas9, sgRNA, and promoters into the host genome so that the cell perpetually produces CRISPR components?

In this scenario, I'm guessing there would be no way to have the host cell produce DNA templates for HDR?

How long do CRISPR plasmids last in the nucleus and is there any way have them persist for 10+ days?

Quick answers/comments: 1) yes 2) why not? 3) stable transfection/genomic insertion using retro or lentiviruses. If the insertion is stable, it can last the life of the organism.

Comment to 1:
Yes. Many labs have integrated Cas9 stabely into their cell lines. E.g., for CRISPR/Cas9 screens (forward genetic screens). It's very useful, since then you can avoid double transfections (of Cas9 and sgRNA) which lowers the efficiency.


text:
How to figure out growth/culture conditions for a specific strain?
Specifically, I'd like to find out how to grow ME-3 L.Fermentum (DSM 14241) at home without any fancy equipment.
What food does it need? Sugar? Lactose? Something else? At what temperature does it grow? How fast?
How can I generally find answers to these questions? ME-3 is not the only strain I'd like to grow.
I know ME-3 grows in milk, but that doesn't work for me. Can I grow it in vegan milk? In just water with sugar?
I'm even more interested in finding ways to find out the answer to these questions. Where would you look to answer this? I tried to google it but it's hard. Is there not some cool data base that has growth conditions for every known strain?

Why not grow it in milk? Bacteria aren't vegan...

Another thing to consider is that, as an intestinal bacterium, L. fermentum is almost certainly anaerobic, meaning you need to culture it in conditions with little to no oxygen in the atmosphere. While not impossible, this is rather difficult to accomplish at home.

It's not anaerobic. ME-3 may not be vegan, but I am ;-) . That's why animal milk doesn't work for me.

I saw a paper where they were culturing it under anaerobic conditions. that's why I made the comment. Doing more research, I see that it's a facultative anaerobe, not obligate.

If you do not have any experience culturing microbes do not attempt this.
You are very very likely to contaminate your culture with things that could make you very sick or even kill you. Pathogenic microorganisms are part of our natural microflora and are a significant cause of hospitalizations throughout the world as a result of food poisoning. For this to work you would need some skills in both identification of microorganisms (to make sure you have the right one) and in sterile technique. Growing specific microorganisms is NOTHING like making yogurt or beer with high inoculums of culture organism that suppress the growth of contaminants, or even like starting a sourdough starter, where you have a relatively low inoculum but the right  the culture to the right bacteria/yeasts.
This would mean that you need, at a minimum, a microscope (with 40-100x objectives; for identification purposes), slides, a differential bacterial stain (e.g. Gram stain), sterilization equipment (for preparing media; this could be a pressure cooker), media and an incubator with the right conditions.
This organism needs some carbon, nitrogen and a number of elements to grow happily. I don't think you will be able to do this at home easily; it would require quite a bit of experimentation and you are likely to grow something nasty as a contaminant before you get a decent culture of your target organism.
The American Type Culture Collection recommends Medium 416 for growth of Lactobacillus group organisms. This medium is comprised of lactobacillus MRS medium from BD and contains:

Proteose Peptone No. 3 10g/L, Beef extract 10g/L, Yeast extract 5g/L, Dextrose 20g/L, Polysorbate 80 1g/L, Ammonium Citrate 2g/L, Sodium Acetate 5g/L, Magnesium Sulfate 0.1g/L, Manganese Sulfate 0.05g/L, Dipotassium Phosphate 2g/L.

Now this might look like a scary list of things, and fairly unobtainable, but beef extract is essentially beef broth, and yeast extract is hydrolyzed yeast. The Polysorbate is an emulsifier used to help solubilize the ingredients and as a carbon source. I don't know if it is obtainable outside of a laboratory setting. The other chemicals may be hard to find too, though citrate = citric acid (fruit acids, you can buy this in a supermarket), acetate = vinegar/acetic acid. Manganese and Magnesium might be obtainable as health supplement pills, but you would need to work out how much is in a pill and do some calculations to convert. As a bonus, supplement pills often contain calcium phosphate as a bulker/tableting agent. For the peptone you might be able to substitute milk powder or "protein shake" powder. You would need to know a bit of chemistry to for the citrate -> citric acid, acetate -> acetic acid, and etc. conversions.
The last problem is that the ATCC recommends that the organism be grown in 5% CO2 at 37 degrees Celsius (98.6 F). This requires a sealed incubator box, with a means to get the CO2 in there. You might be able to achieve this by chemical means, reacting some chalk (calcium carbonate) with acid, but it would take some experimentation to do so effectively. It should grow at lower temperatures too, but it will grow slowly, if at all. I don't know if the CO2 is a requirement or just something that helps with the growth. This is not an obligate anaerobe as suggested in the comments, but can grow anaerobically too (facultative anaerobe).

I don't know... I've made DIY yoghurt with all sorts of probiotics countless times and never got sick from it. Now I want to do the same with ME-3 yoghurt. It doesn't have to be a 100% only the ME-3 strain, i.e. it doesn't need to be sterile. As to avoid food poisoning, I just add some other standard yoghurt strains to the mix, e.g. L.Bulgaricus (found in most yoghurts) to create a stable environment. I've done this many times with cow milk. But now I want to do it without milk, i.e. vegan yoghurt. That's why I want to know what ME-3 (and other's that I want to grow as well) need to be happy.

The ATCC link leads to a a different L.Fermentum strain. Is this not strain dependent? ME-3 is DSM 14241, but somehow I can't find it in the DSM (why?). HOw would you find out the ATCC number of ME-3 ?

An MRS medium doesn't work for me, since my goal really is to make a vegan yoghurt that I can eat.

Also, I'm particularly interested in a general approach as to how I can answer these questions myself such I don't always have to ask this forum. I struggle with just googling it since I don't know what websites to go to. I take it from your answer that culture collections are the place to look for answers? Here I often struggle to find the type number of that strain. E.g. it took me a lot of googling to find out ME-3 is DSM 14241.  Is there not some great data base that has everything that there is to know about all known strains? What temperature, pH, salt content etc do they tolerate?

@AntonRodenhauser if you have an inoculum (i.e. the strain itself) this makes it a whole lot safer to do. Trying to isolate is a lot harder. If you do inoculate with other bacteria you will likely result in those dominating the culture, especially if they are ones that are already selected for growth in those media. You would have to do some relative growth rate experiments to work out how well it would work.

@AntonRodenhauser Not strain dependent as far as I can tell. Most bacteria of the same species will have no difficulty growing in the same medium.  ATCC may not have ME-3; as they are a public repository where things are "free" (you have to pay for shipping, handling and some recompense for time, reagents etc.) to the scientific community. ME-3 is patented, so can't be handed out for free.

@AntonRodenhauser for vegan substitutes - you would need to work those out for yourself. There is a whole community of scientists out there trying to make non-animal product derived substitutes for common lab reagents. Some have been worked out, but you would need to dig through the literature for that. You might need to look for individual components (e.g. beef broth = gelatin, minerals (particularly Ca I think), salts, collagen etc.).

@AntonRodenhauser Answering them for yourself can be difficult - we (microbiologists) have reference books and the like to work from, as well as received knowledge and the scientific literature. Culture collections are a good place to start. Generally what works for one strain will work for another within the same species, and even within genera, assuming no selective reagents added. Another place to look is pubmed - the scientific literature. Find a free paper (pubmed central...) and look at the materials and methods section. I don't think you'll find a giant tablulated database of any sort

@AntonRodenhauser as to why the DSMZ doesn't have it - probably similar to ATCC; patented so they can't supply it. It is registered with them as a strain though.

Thank you! That is all very helpful! I've marked your answer as "correct"


text:
Do all animals with eyesight get an upside-down image on their retina, or is it right-side up with some?
here's as good an image as any for showing the thing about human vision that I am asking about:
So, our retina gets an upside-down image.
My question is, do all animals' eyes work this way? Or do some have their cells report the image as-is?

How do you know that ours don't? How would you tell if another animal does?

"Or do some have their cells report the image as-is?" You can't objectively make judgements about perception since perception is subjective. You might as well ask what the colour red looks to different animals. Think carefully about what you mean when you say "report image as is". Relative to what? Relative to your inner ear says is down? That's not going to change how you interpret the world because "down" in the image is still going to be perceived as "down" in your ear.

Look at your image (which is not quite right, btw.). Where, exactly, does the angle of light entering your eye change (there are actually three places). Any animal with a cornea and a convex lens will have an inverted image on their retina if their eyeball is deep enough. All you need to do is a search for which animals don't have the above to know if they have an inverted image on their retina or not.

https://www.cell.com/current-biology/pdf/S0960-9822(05)00441-0.pdf

@bob1 - Physics. Plain old physics. This has been studied extensively in almost every animal. Not sure exactly why, but it has, and it's interesting.

@anongoodnurse I was thinking along the lines of insects, crustaceans etc, where there is no lens etc. My point was to get OP to think.

"How would you tell if another animal does?" Ah, I didn't read this carefully enough. Thanks.


text:
Are there foods which not only prevent but help fighting cancer?
I was reading a probably not to serious webpage and I found this quote

" Certain types of vegetables, such as the cruciferous variety, are
  not only nutrient-dense but contain compounds that may fight cancer,
  according to the National Cancer Institute."

Then I looked more information about this, but I can only find references to foods helping prevent cancer but they dont seem to say they help fight cancer when it's already present.
This page says the following foods help prevent cancer, but later make an ambiguos statement that you could think they imply those foods help fighting cancer when it's presented

The following is a list of foods that have been shown to have
  cancer-fighting properties. While some are well-known super foods,
  others may surprise you. You won’t find a burger or fries on this list
  – when it comes to cancer prevention, clean eating prevails:

http://www.cancercenter.com/community/newsletter/article/Foods-that-have-cancer-fighting-properties/
So, my question is, are there foods which not only prevent but help fighting cancer when it already exists?

Short answer: No, for neither of the two questions.

What about this, is not serious or fake? "In conclusion, the results from our laboratory and from others provide ample evidence for the benefit of I3C and DIM for the prevention and the treatment of prostate cancer."  https://www.ncbi.nlm.nih.gov/pubmed/15570059  (sorry for insisting, just looking to understand why there are some aparently real sources which seems to claim so)

It seriously shows that you can put chemicals in a petri dish and kill cells from cell cancer lines.  That is not evidence that the chemical would do the same thing in a person.  The "MAY fight cancer" (emphasis mine) is doing a lot of work there.

Lack of evidence of foods that prevent or fight cancer is not the same as there being no foods that prevent or fight cancer.  There are logistical issues and lack of monetary incentives associated with running clinical trials to test the efficacy of foods in preventing or fighting cancer.

@swbarnes2 so to summarize, it's doubtful.

Lack of evidence when one has looked certainly doesn't make the proposition more likely.  Food companies would LOVE to have evidence that their products inhibit cancer.  Pharma didn't prevent people from testing the heck out of resveratrol;

The short answer is, no.  There really isn't any good evidence that a person can eat enough of any chemical to have a clinically detectable effect on cancer.
Note that any study that shows an effect on cancer cells in a petri dish doesn't count as demonstrating that it would do anything in a person with cancer.  It might be that the chemical would not work the same in the body, or would not work the same on real cancer cells growing in a person (not cells cultivated to grow in a petri dish for 30 years).  And even if they did kill cancers like in a petri dish, that doesn't mean that you can actually eat enough of the chemical to get a high enough concentration to have that effect.
That link is pretty much click-bait, and nothing more.

Cryptotanshinone is a good example. Exhibiting anti-cancer effects against cancerous cell lines such as LOVO cells, the bio-availability through oral administration in rats was found to be less than 10% (ref1, ref2). The oral dose was 100mg/kg of HPLC-purified CT in the rat model. A separate production paper was able to produce 23.2mg of CT per gram of inoculum (Salvia miltiorrhiza root cells) (ref).

And the half-life is ~6.67 hours in the rat model, from the 1st reference. So just imagine: You're 88kg and need to consume 100mg/kg every 12-18 hours. That means eating 0.85lb of root material. Never mind poisoning from accessory compounds in the roots, among a list of other potential problems, such as even lower bioavailability in an impure form.

I've received an email from a cancer researcher from Denmark. I asked her if it was true she stated a chemical component of carrots delay cancer development in rats. She gave me some links and stated yes.

What cancer researcher?  Where are her findings published?  No matter what nonsense you propose, you can find a quack willing to support it.

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


text:
Figure out which is the risk allele from SNP in GWAS article
I do neuroimaging research, and am interested in dabbling in genetics. I am trying to create an anxiety risk profile score from several SNPs shown to correlate with measures of anxiety in past GWAS studies. However, many of the GWAS studies, such as this one (https://www.biorxiv.org/content/10.1101/540245v1) don't seem to explicitly state which allele was the risk allele (i.e. which allele was positively correlated with anxiety). It's likely that in most cases the minor allele is the risk allele, but I don't want to assume this. Am I missing something in the text of the example manuscript, or would I need to contact the author to find this out?

I suggest you contact the authors, because they do not show the direction of effect. They should share this information, otherwise you will never be able to tell which one is the allele that gives risk and which one is protective. And, as you said, it is better if you do not assume that the risk allele is the minor allele. There is no reason to be like this.


text:
(How) do horizontal pupils dialate?
I was looking at mongoose eyes in particular, but my understanding is:

Circular (human-like) pupils simply get larger/smaller depending on light levels, no change in "shape"
Vertical slit (cat-like) eyes get wider or narrower, from "almost a line" to "almost a circle".
Goats, mongooses, etc. have horizontal "bar" pupils — more-or-less straight edged across the top and bottom, with rounded (semicircular?) sides.

Do horizontal bar pupils, like those of a mongoose, change size in varying light levels? If so, how does their shape change? Do they get taller or narrower? Do the top and bottom become convex or concave? Does the radius of the sides increase? Does anyone have good reference pictures or diagrams?


text:
Anybody know of any sources/papers on wild animals identifying birds by their calls/sounds?
I'm doing a literature review about identifying birds, and was hoping to find some examples of animals being able to identify birds by sound (eg a mouse knowing the normal call of a sparrow is not the normal call of a sparrowhawk), but alas when I tried to search google for anything all I got was a bunch of pages showing humans how to identify bird noises, or apps to do the job for you, even making sure the word "animal" was included lead to the same results.
I vaguely remember watching a BBC show that had meerkats using a bird to alert them for dangers, but when I tried to find this online all I found were sources saying how it's actually a bird pretending to be a meerkat to score a free lunch, so if anyone knows any more about this I'd be grateful for any information.


text:
Diffussion coefficient of blood
What it the diffusion coefficient of blood in, e.g. water?
It is needed for microchannel length calculations
I have found a bit different nubmers: 0.94 and 1.66 microns^2/ms, but not sure

Welcome to Biology.SE! Please add references to your question (i.e. where you obtained those numbers). Also, please clarify whether you are asking about human blood. If so, can you specify what population(s) of humans this blood is from. There wont be a single number since blood viscosity (which will affect diffusion) can vary significantly both within and between populations — e.g. people living at high altitudes typically show increased blood viscosity.  You may find this article interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162413/


text:
Why is easy to clone cats but it's hard to clone dogs?
According to this article, Here is why we're not cloning humans
there are species who are easy to clone and other who are hard to clone. Cats and mices would be in the easy to clone set , and dogs and humans would be in the hard/very hard to clone set. Why is this so? Why is easy to clone cats but it's hard to clone dogs?

If you have enough money, you can have your dog cloned.

Out of date. Primates have now been cloned.

But there it doesnt say they havent been cloned. They say it's hard. I have to assume this is confidential information and nobody knows why


text:
is there any theory about why life evolved to have DNA with 4 different bases and not 6 or other number like in organisms created with artificial DNA?
If organisms can carry DNA with 6 bases which supposedly stores increased genetic information, why living organisms evolved to have DNA made of 4 bases and not 6 or other number? is there any theory about this, were the chemical process to reach those 2 additional bases much more complex or something?

There isn't a theory about that particular question as far I know of, but a possible answer is in the issue of complexity optimization in evolution. See, life is like a well-oiled machine-it always chooses the simplest and most reliable solutions to any problem it can face. What is simple in this case-a code of 4, 6, 8 or even more bases? Since it's double pair code the number must be even and 4 is the second even number-e.g. complex enough to provide redundancy but as simple as possible at the same time. The best optimization point possible. I hope this might serve as your answer.


text:
Why are fertilizers with polonium 210 used when growing tobacco?
Why are fertilizers with polonium 210 used when growing tobacco?
I'm thinking of pursuing a science fair in which I create my own fertilizer for tobacco that doesn't contain polonium or lead. However, I need more background research. Does anyone know why these fertilizers are used?

do you have a link to support your claim that fertilizer contains Po-210?

What brings you to the conclusion, that these fertilizers contain bigger amounts of lead and polonium?

Just wait a couple weeks for the Po 210 to turn into stable Pb 206.

According to RADIOACTIVITY IN CHEMICAL FERTILIZERS by Milica M. Rajačić, Nataša B. Sarap, Marija M. Janković, Jelena D. Nikolić, Dragana J. Todorović and Gordana K. Pantelić at the Institute for Nuclear Sciences "Vinča", University of Belgrade, Belgrade, Serbia, and the relatively short half-life of polonium, it appears that primordial metals are the only hazard in fertilizers:

Natural radioactivity results mainly from primordial radionuclides,
  such as 40K and the radionuclides from the 232Th, 238U and 235U series
  and their decay products. Terrestrial radioactivity and exposure due
  to gamma radiation depend primarily on the geological conditions and
  appear in different quantities in the soils of each region in the
  world. 1 [...]
Fertilizers usually employed in the agriculture contain traces of
  heavy metals and relatively high concentrations of naturally occurring
  radionuclides. Phosphate containing fertilizers have been used
  worldwide to increase the quantities of the micronutrients, which are
  being continuously taken off from the soil due to farming activities.
  At the same time, the use of such fertilizers is the main
  anthropogenic source of the uranium input in the environment (about 73
  % of the total input of uranium) 2. [...]
A total of 140 samples of different types of fertilizers were measured
  for their radioactivity content using gamma spectrometry technique in
  order to assess the implications of extended use of fertilizers on the
  concentrations of natural radionuclides in cultivated soil. The
  obtained data show that the activity concentration of naturally
  occurring radionuclides in fertilizer samples were 87 Bq/kg, 4860
  Bq/kg and 220 Bq/kg for 226Ra, 40K and 238U, respectively, which
  exceeds the activity concentration in soil by an order of magnitude.
  As it was shown in the paper, the use of fertilizers has a negligible
  effect on Raeq and D in soil due to dilution of fertilizer used on the
  large amounts of cultivated soil. However, the long term application
  of these fertilizers can have the effect of an accumulation of
  radioactivity in soils that can be harmful for the health of farmers
  and consumers of the products. [...]
1: Akhtar N. Radionuclide pollution due to fertilizer use in some
  saline soils of the Punjab and their potential risk assessment on
  human health. Department of Physics Bahauddin Zakariya University
  Multan, Pakistan, 2006. 2: Stojanović M, Stevanović D, Milojković J,
  Mihajlović M, Lopičić Z, Šoštarić T. Influence of soil type and
  physical–chemical properties on uranium sorption and bioavailability.
  Water Air Soil Pollut 2012;223:135-
  144.

Artificial fertilizer is cheaper than regular fertilizer that also contains long-term nutrients, but also contains Po-210:

Among all carcinogenic substances contained in tobacco smoke, Polonium
  210 (Po-210), with a half-life of 138 days, is one of the most
  dangerous, by exerting a devastating, chronic, slow and progressive
  carcinogenesis activity. The main source of Po-210 in tobacco is
  represented by fertilizers (polyphosphates) containing radium-226
  (Ra-222) which decades to plumb 210 (Pb-210). Through the thricomes
  Pb-210 is concentrated in the tobacco leaves, where it turns to
  Po-210, which at the cigarette combustion temperature (800-900 degrees
  C) reaches the gaseous state and it is absorbed by the micro particles
  released into tobacco smoke. Thus, smoke becomes radioactive in both
  its gaseous and corpuscular components and reaches the airways, where,
  particularly at the branches level and together with other substances,
  it exerts its carcinogenic activity, especially in those subjects with
  impaired respiratory mucosal clearance. The carcinogenic risk/one year
  lifetime of a smoker of 20 cigarettes per day is equivalent to that of
  undertaking 300 chest x-rays. It is calculated that Po-210 may be
  independently responsible of 4 lung cancers every 10,000 smokers.
  During cigarette's combustion, tobacco smoke is also released in the
  air, contributing to serious health risks for those exposed to passive
  smoke.


text:
Which kind of electrical brain activity is associated with consciousness and why?
According to this article The ethical brain
At the end of the week 5 into the 6 (42-43 days) the first electrical brain activity occurs in a pre-born developing human.
And according to the same article

This activity, however, is not coherent activity of the kind that
  underlies human consciousness, or even the coherent activity seen in a
  shrimp's nervous system

My question is, which kind of electrical brain activity is associated with consciouness and why?

Gamma band oscillations (GBO) (Wikipedia) (NCBI)  are 30-90 Hz electrical waves generated by the brain and are thought to possibly be associated with cognition and consciousness (Panagiotaropoulos, 2012). Some evidence for this putative relationship can be seen with experiments such as pre-pulse inhibition (PPI), which can describe how our sensations are interpreted by the brain. Also, PPI may be aberrant in Schizophrenic patients (who have altered cognition). Changes to PPI are associated with aberrant GBO, which could imply an association between GBO and an individual's interpretation of stimuli, their cognition and by extension consciousness.
But of course, the counter-argument is that the intrinsic activity of the brain isn't changed, merely how the brain processes stimuli. However, all forms of measuring cognition that I've studied involve investigating responses to external stimuli, so as far as I know, this is a universal problem. Furthermore, there's a lot we still don't know about consciousness and no model or measurement is perfect. This article gives quite a nice overview on neural correlates of consciousness.

Can you cite some sources on "experiments as pre-pulse inhibition"? For me it should be clear that we dont know a lot of things about consciousness since human features such as intelligence and learning can be partially reproduced in computers, but as far as I know anything about consciouness can be reproduced.

@Pablo I've tried to expand my answer - I've only studied this in relation to changes to cognition in Schizophrenia but I know some people who research changes to attention via EEG and fMRI studies, so I'll ask them and try to add to my answer.


text:
Are there known life expectancy differences in non human mammals by sex?
In humans either for biological or cultural reasons there are life expectancy differences by sex. But how about non human mammals? Are there known life expectancy differences in non human mammals by sex?

Are there known life expectancy differences in non human mammals by sex?

Yes, there are. It is not well studied in general, but for certain species it is. Here is a relevant excerpt (Austad, Fischer, 2016):

Females live longer than males in humans and all Old World monkeys and apes for which we have the best data. . . This appears to be true in both wild and captive populations. . .  Yet whether there is a general mammalian pattern of greater female longevity under protected, captive conditions where intrinsic physiological aging dominates mortality patterns, is not known because so few species have been rigorously investigated. What is known about the best described species indicates that all show a substantially different pattern from humans.

See the linked study for more information. There is a whole section on sex differences in lifespan in mammals.
In general, in any species where males fight fiercely amongst each other for status, I would also consider it likely that males have shorter lifespan on average than females. Although I don't have a good citation for this at the moment.
In a more recent review, Lemaître et al (2020) confirmed the tendency for females to outlive males across many mammalian species:

In human populations, women consistently outlive men, which suggests profound biological foundations for sex differences in survival. Quantifying whether such sex differences are also pervasive in wild mammals is a crucial challenge in both evolutionary biology and biogerontology. Here, we compile demographic data from 134 mammal populations, encompassing 101 species, to show that the female’s median lifespan is on average 18.6% longer than that of conspecific males, whereas in humans the female advantage is on average 7.8%. On the contrary, we do not find any consistent sex differences in aging rates. In addition, sex differences in median adult lifespan and aging rates are both highly variable across species. Our analyses suggest that the magnitude of sex differences in mammalian mortality patterns is likely shaped by local environmental conditions in interaction with the sex-specific costs of sexual selection.


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Is there any known reason why 6 leg mammals are only found in mutations?
Taking a look in internet you can find photos of mutated mammals with 6 legs. Some cows with legs in unnatural positions were shown in website versions of widely known newspapers (you can easily guess here that if the animal gets his additional legs in the back or another unuseful position why a mutation like that wont spread, but the point here it's 2 additional legs in mammals do appear occasionally) . Also there are some dubious photos of sheeps with appparently functional 6 legs, these ones are dubious and hard to confirm if real, some clearly fake but the dubious ones are there and make you wonder. Insects have 6 legs, there are confirmed mutations of mammals with 6 legs, then why did it never appear a mammal species with 6 legs. Is there any known reason why 6 leg mammals are only found in mutations? (how about size and enviroment, is there any reason in those for them not to get 6 legs?)

What make you thing that those cases are caused by mutations (in other words than leg number has a non-zero heritability) rather than some other developmental defect?

If stability is the goal, more legs tend to be better. However, having lots of legs also comes with a cost: they take energy to build and use, have extra weight, etc, and they don't really add any speed.
Insects are incredibly successful and likely evolved from many-legged ancestors, losing legs for efficiency but stopping at six. For small creatures with exoskeletons like insects, having fewer than 6 legs means too much loss of stability, because they rely on a tripod of 3 legs while moving the other three.
However, mammals and the vertebrates in general are larger and don't have exoskeletons and can use balancing and moving strategies that insects cannot. Further, they have evolved with four appendages since before they walked on land.
For a 6-legged vertebrate to evolve, there would need to be a selective advantage for having 6 legs versus 4; since vertebrates get along just fine with 4 legs, adding two more isn't likely.
I would also add that just because you can observe mammals with more than 4 legs does not necessarily mean that is a heritable trait. It could instead be caused by environmentally-induced errors in development. I think for the cases you mention this is probably most likely.

Lanham, U. N. (1951). Why do insects have six legs?. Science, 113(2945), 663-663.

Also worth pointing out that many insects have adhesive feet, and more feet allows for more adhesion. An ant with 6 legs sticks to a wall 50% better than an ant with 4 legs. Water skimming insects, too, spread the hydrophobic force over all their legs, and might fall through the surface of the water with fewer legs.

@NuclearWang Good point. Although larger mammals like OP is thinking of are certainly too large to achieve some of those feats that could benefit from extra limbs, other vertebrates have done so by having longer toes rather than extra appendages (like the Jesus lizard).


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Random X-Inactivation and Duchenne
I'm reading about X-inactivation and I can't reconcile some things with it being truly random. In only a small percentage of female carriers Duchenne's will be expressed. But if this was truly random, wouldn't 50% of female carriers expressing the disease?
As one of the X-chromosomes is silenced at random, this seems sort of contradictory. Then, in females that do express the disease phenotype it's because of non-random X-inactivation. For me, this sounds like it's the other way around, so clearly I'm not up to speed and am in need of a bit of clarification on the subject.

Duchenne muscular dystrophy (DMD) is caused by the body's inability to make the protein dystrophin, which is needed for proper muscle function (1, 2). In an individual carrier, half of the cells that would normally make dystrophin cannot, but the other half still can. This leads to two explanations (AFAIK) for why carriers do not express DMD:

The cells that can make dystrophin make twice as much, so the total amount produced is the same as a normal individual.
Only half as much dystrophin is produced, but that is enough to prevent symptoms from manifesting.

This is actually the stock explanation for why female carriers exist for X-linked recessive diseases. You can substitute 'DND' and 'dystrophin' with another X-linked recessive disease and the associated protien (e.g. 'hemophilia' and 'factor 8 or 9') and it would still be mostly true.
I say mostly true because DMD is actually an unusual. Its carriers do sometimes exhibit symptoms (3, 4). Different studies give different rates for how often this happens, but the NIH says it is about 20%.
EDIT: I am still a little unclear on what your asking, but I think you are confused about why any carriers for Duchenne express the disease. The answer to that is a phenomena called skewed X-inactivation, which is when either the paternal or maternal X chromosome is inactivated and turned into a Barr body more often than the other. This can happen for 2 reasons:

Primary: When Barr bodies are forming, the paternal or maternal chromosome is selected more than 50% of the time.
Secondary: After Barr bodies form, cells with the paternal chromosome active reproduce less than cells with the maternal chromosome active, or vice versa.

Both types of skewing can be happen for genetic causes (e.g. the Xce locus in mice can cause primary inactivation) or stochastic causes (i.e. by pure chance some people will have unlikely things happen to them).
I spent the last few hours reading up on which type happens specifically during Duchenne and I am still not 100% sure. What I am confident about is that carriers for Duchenne can have a translocation, which causes the skewed X-inactivation and therefor symptoms in carriers:

A few cases of translocations involving DMD have been reported22; these translocations will cause DMD in both males and females, the latter owing to non-random X-inactivation of the unaffected X chromosome. In these cases, cells with inactivation of the mutated X chromosome (cells that could, in theory, produce dystrophin) are not viable owing to the inactivation effect of the chromosomal translocation on the autosome. Only the cells where the unaffected X chromosome is inactivated will be viable. However, these will not produce dystrophin owing to the chromosomal translocation affecting DMD. Therefore, females with these translocations are unable to produce any dystrophin.

What I cannot figure out is if the translocation happens on the chromosome with the functioning DMD gene or the chromosome with the defective DMD gene.

Thank you for your answer, my question was more about the seemingly confusion naming of (non) random X inactivation

Would it be helpful if I rephrase to include the relation between X inactivation and dominanc?

Thank you for your elaboration, my question is about naming, I think. I understand the process of (skewed) x-inactivation, in principle, but the thing that's not clear is why it's called random inactivation if only a few % of carriers express the disease phenotype. If it would be truly random, 50% of carriers would express the phenotype, as one chromosome at random gets silenced. This probably has to do with dominance, but I find it a bit counterintuitive and would like to know a bit more about this.

Having read your comment again, I think it brings me closer to an understanding. I'm gonna do some more reading on non-random X inactivation. Thank you!

Random/ stochastic just means that the event is non-deterministic. As long as we are talking about probabilities we are describing a random process. The uniform distribution, where every outcome is equally likely, is not more random. The lottery is random and there are only two outcomes (you win or you lose), but that does not mean you have a 50-50 chance of winning. No matter what the probability of a carrier for Duchenne has for will presenting the disease, that fact we are describing the process with probability means that we are describing a random process.

Thanks for your elaboration!


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Which others human species/subspecies are known to have coexisted in the past with anatomically modern humans?
According to this article,
interbreeding between archaic and modern humans

There is evidence for interbreeding between archaic and modern humans
during the Middle Paleolithic and early Upper Paleolithic. The
interbreeding happened in several independent events that included
Neanderthals and Denisovans, as well as several unidentified hominins.

According to this other article discoveries change picture of human history-evolution,

Now, new research reveals that a third human ancestor was hunting and
gathering in the same landscape. Two studies published Thursday in the
journal Science describe a previously unknown hominin called the
Nesher Ramla homo

And this other article enigmatic human relative outlived neanderthals also mentions,

The provocative find joins a number of recent discoveries that
continue to point to a stunning diversity of hominins in ancient Asia,
including the announcement just yesterday of a new species, Homo
luzonensis, in the Philippines.

So far 4 species Neanderthals, Denisovans,  Nesher Ramla homo and Homo luzonensis are mentioned.
Which others human species/subspecies are known to have coexisted in the past with anatomically modern humans?

This is a difficult question to answer exactly - I think it might be useful to split it up based on the degree of evidence.
Since you asked about Anatomically Modern Human (AMH), it's worth considering their distribution and timing. The oldest and most basal individual which is still considered AMH is Jebel Irhoud, Morocco, which is dated to ~315kya. In Europe, we have the Apidima samples from Greece which date to ~200kya and in Asia we have Misliya1 which is the oldest West Asian sample from slightly earlier 180kya.
Of course, these are the only specimens that have been positively identified as AMH. Therefore, it seems highly likely that there would have been earlier migrations out of Africa that didn't leave fossil remains.
Certain

Neanderthals and Denisovans. There is very solid genetic evidence that humans have lived alongside two archaic species; Neanderthals and Denisovans. There are fairly large, unambiguously archaic chunks of Neanderthal and Denisovan DNA in many present-day non-Africans.

It's likely that there was a single mixture event with between modern humans and Neanderthals.
On the other hand, there was likely several admixture events between Denisovans and modern humans, particularly modern humans in Southeast Asia.
Possible

Nesher Ramla Homo, dated to 140–120kya from a cave in Israel. There is evidence that AMH lived in Western Asia as early as 200kya, so it is possible they may have lived aside one another. However, it's also possible that the AMH lineage present in Misliya may have gone extinct before the Nesher Ramla was present.
Homo naledi lived in South Africa 335–236kya. This appears to be well within the likely dates of AMH occupation of Africa, given the Florisbad skull is AMH and dates to 259kya. It's been proposed that the signals of superarchaic admixture in present-day Africans could be Homo naledi.
Homo heidelbergensis, dates to roughly between 200-600kya and is found at least across parts of Southern Africa and Southern Europe. Given AMH almost certainly existed in Africa at this point, it seems plausible that they may have lived alongside heidelbergensis.

Possible but unlikely.

Homo floresiensis lived on the island of Flores, Indonesia, approximately from 50/60kya - 100kya. Data suggests that modern humans did not inhabit this part of the world further ago than 50kya.
Homo luzonensis lived in Luzon, Philippines and has also been dates to 50kya. Note that humans have existed in this region for almost 1 million years, but these would not be considered anatomically modern humans, who would only have arisen within approximately the last 350ky.
Middle Pleistocene East Asians hominins. There is growing evidence of a clade of modern, but with archaic features, hominins who lived in East Asia (particularly China) ~150kya. It's proposed that these may have been the result of a mixture between an early out of Africa migration and some archaic lineage such as Denisovan. It's highly unlikely there was a major AMH lineage present in East Asia at this point, but they may have interacted with early dispersals out of Africa.

It's also worth considering that we only have snapshots for these samples. It's possible, for example, that the Nesher Ramla Homo lived between 500-100kya, but that we only have samples from 200kya. The same goes for the dates of AMH presence in certain locations; even though we only have samples for AMH in e.g. North Africa at 315kya, it seems plausible the true date is somewhat older.
This probably isn't an exhaustive so happy for others to edit in things where necessary.


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Are these 2 procedures to fight cancer (cancer "vaccine", and cancer drugs which can attack all tumours) related?
Last year appeared the new of a cancer "vaccine" (not a vaccine in the traditional sense) tested in animals for 4 types of cancer and which worked in 97% of the cases to eliminate already existent tumours.
Cancer Vaccine Trial
Now appeared the new of "cancer drugs which can attack all tumours" to be fast-tracked by NHS.
Game changing cancer drugs can attack tumours
I would like to know if both procedures are based in similar ideas (meaning the second one could have a similar effectiveness to the first one) or if they are completely unrelated.

The first source (Science Direct) says that the "vaccine" treatment stimulates T cells to attack cancer. In general, this treatment is intended for all tumors and has been very successful in studies in mice. Cancer.net and Cancerresearchuk describe cancer treatment vaccines in a bit more detail.
The second source (Telegraph.co.uk) mentions “tumor agnostic” or "tissue agnostic" drugs, which target tumors according to their genetic make-up, rather than the tissue from which they arise. This treatment is intended only for specific tumors with known genetic mutations. Examples of tissue-agnostic drugs are pembrolizumab and larotrectinib, which are approved by FDA for treatment of certain metastatic solid tumors.
So, these are two different ideas and most of these drugs are currently in a research phase.

in complement to Jan's answer, the 2 therapies discussed here are unrelated. The first one stimulates T cells locally at/around the tumor site with TLR ligands and is a class of immunotherapy, while the second one aims at shrinking the tumor cells by targeting some genetic alterations. Note that the second one may induce immunogenicity


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Chloroplast arrangement in high and low intensity of light
I have read that there are different alignments of chloroplast according to the intensity of light.
I read that in high intensity the chloroplast align themselves parallel to the incident light (Parastrophe).
While in low intensity they align themselves perpendicular to the incident light(Epistrophe).
But somewhere else I read that they align  perpendicular to the light in high intensity while parallel in low intensity.
So I'm confused which information is true...can u please tell me which one is correct?

Where did you read this?

Well....I read the first one in a book....and the second one on Google....and now I'm confused which fact is true....at high intensity, do chloroplast align themselves parallel or perpendicular to the incident light....and why...and the same for low intensity too.

That's why it would be important to know the sources.

Yes but....can you please tell which one is true then?


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Why does hypercalcemia cause muscle weakness, yet hyperkalemia causes muscle excitation?
The reasoning I've been given is that high extracellular $[K^+]$ increases the $E_v$ of potassium; therefore, membrane potential increases and the threshold for action potentials is more easily reached. Conversely, high extracellular $[Ca^{2+}]$ increases the accumulated positive charge outside the cell membrane and therefore increases the membrane potential.
However, like with $K^+$, wouldn't high ECF $[Ca^{2+}]$ also increase its $E_v$ and therefore membrane potential of the cell? Vice versa, high ECF $[K^+]$ should also increase membrane potential by accumulating charge.
Why are the effects different? A guess I had is that the relatively higher permeability of $K^+$ makes the effect on equilibrium potential larger than the effect of accumulating positive charge.

You're correct about your reasoning for potassium; high extracellular potassium concentration reduces the concentration gradient of potassium across the membrane, pushing the reversal potential for potassium towards neutral and therefore depolarizing cells due to resting potassium conductances.
For calcium it's quite different. Neurons and muscle cells are mostly impermeable to calcium at rest, and calcium is already high outside of cells relative to inside, so changing calcium concentration doesn't have any appreciable impact on resting potentials. From a pure ion-flow perspective, the primary change you'd expect in neurons is an increased action potential amplitude at the very peak: calcium reversal tends to be more positive than sodium reversal, so the very peak of the action potential is the part most influenced by calcium concentrations. This peak amplitude doesn't have much impact on all-or-nothing signaling, though.
You might also expect calcium concentrations to affect release probability of vesicles - that could increase neurotransmission.
However, that's not what's going on with muscle weakness. Instead, this is something special about calcium (well, divalent cations more generally) interacting with voltage gated sodium channels:

High Ca2+ levels (hypercalcemia) can block sodium movement through voltage-gated sodium channels, causing reduced depolarization and impaired action potential generation.

There's no way you can predict this from the principles of ion flow given by concentration gradients and voltages, and these sorts of things are why you have to do biological experiments with biology and not just computers: sometimes it doesn't work how you expect. The mechanism here is physical: calcium ions are big relative to sodium ions, but they have the same sign charge, so if possible, both would flow through a channel from the outside to the relatively negative inside. There's a place in the outer pore of voltage-gated sodium channels where calcium ions get stuck and just physically plug the hole. When a calcium ion is in the way, sodium can't flow (see Yamamoto et al 1984 and Santarelli et al 2007; the former looks at mechanism by altering voltage, the latter looks for specific residues on the channel that mediate calcium binding in the pore).
At typical low extracellular calcium levels, there aren't as many calcium ions around to block channels.

Santarelli, V. P., Eastwood, A. L., Dougherty, D. A., Ahern, C. A., & Horn, R. (2007). Calcium block of single sodium channels: role of a pore-lining aromatic residue. Biophysical journal, 93(7), 2341-2349.
Yamamoto, D., Yeh, J. Z., & Narahashi, T. (1984). Voltage-dependent calcium block of normal and tetramethrin-modified single sodium channels. Biophysical Journal, 45(1), 337-345.


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Chains of ganglia on each side of the nerve cord belongs to the spinal cord
One of my textbook says this: "A double chain of ganglia on each side of the nerve cord belongs to the spinal cord."
But the diagrams I saw on internet depict only one dorsal root ganglion.
I am unclear which is wrong my textbook or the diagram.

There are only single dorsal root ganglia on each side of the spinal cord, within the dorsal (sensory) root of the spinal nerves.  If it is specifically referring to dorsal root spinal ganglia, the textbook is presumably describing the bilateral anatomy as a 'double chain'.
In addition, the dorsal root ganglia develop in the embryo from neural crest cells, as opposed to neural tube cells. Thus, the spinal ganglia can be considered grey matter of the spinal cord that is translocated to the periphery: that is, they 'belong to the spinal cord'.
Alternatively, the textbook may be referring to the Sympathetic Chain of Ganglia, a 'double chain' whose two components lie either side of the vertebral column and spinal cord, and consist of nerve fibres emanating from its ventral roots.  Any decent textbook of Anatomy should be pretty clear about this.
For your interest, 'Wikipedia' describes the latter in part as follows:
Sympathetic Chain Ganglia.
The bilaterally symmetric sympathetic chain ganglia, also called the paravertebral ganglia, are located just ventral and lateral to the spinal cord. The chain extends from the upper neck down to the coccyx, forming the unpaired coccygeal ganglion. Each ganglion within this chain is either cervical, thoracic, lumbar, or sacral. Preganglionic nerves from the spinal cord synapse at one of the chain ganglia, and the postganglionic fiber extends to an effector, a visceral organ in the thoracic cavity, abdominal cavity, or pelvic cavity.
There are usually 22–23 pairs of these ganglia (which is interesting number in view of chromosomal numbers): 3 in the cervical region (cervical ganglia), 11 in the thoracic region (including the stellate cervicothoracic ganglia), 4 in the lumbar region and 4–5 in the sacral region, collectively known as the 'Sympathetic Trunk'.

I hope this helps to clarify things in an area which is clearly problematic to describe without a precise anatomical diagram.

Can someone please explain the down-vote: is the answer incorrect or incomplete?  And voting like that without explanation is akin to assaulting someone on a public street for no apparent reason.  Very cowardly.  State your case sir.