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Can an amoeba go through states that would be analogous to pain?
Amoeba can move freely.  Would I be correct in assuming that this movement is not completely random?  Would it be correct to assume that an amoeba can seek out food and can attempt to avoid danger?
If this assumption is correct, would it be reasonable to assume that the amoeba has states which are roughly equivalent to being in pain? If this is not the case, what is it that motivates the amoeba to pursue food and avoid danger?  Or is it believed to be instinctual -- that is, fully scripted without a need to presuppose a pain state?

Update from a search on the web:
I did find this article which suggests to me that amoebas might also show avoidance behavior.

This question is about perception which can't be answered because perception is subjective.

I was thinking solely about behavior.  Does an amoeba ever move in a way that would indicate "avoidance" or in another way that indicates "targeting"?  I was thinking that the state that precedes avoidance or the state the precedes targeting might be analogous to a "pain" or "pleasure" state.  I agree that we can never know if a subjective state exists for an amoeba.

The second paragraph is not too different from asking whether free will exists, albeit at the level of an amoeba. "Pain" is a subjective state, if you take the subjective state out of pain you don't have anything at all. A chemical motivation to perform some behavior is, at a cellular level, no different than what happens in our own nervous systems.

See also https://biology.stackexchange.com/questions/36401/can-plants-feel-pain https://biology.stackexchange.com/questions/19446/can-insects-feel-pain https://biology.stackexchange.com/questions/60949/do-lobsters-possess-a-nervous-system-to-feel-pain https://biology.stackexchange.com/questions/60337/at-what-stage-is-the-nervous-system-developed-enough-to-interpret-neuronal-signa

@BryanKrause, I am unclear on your first comment.  Why does pain behavior presuppose a subjective state?  If an amoeba shows avoidance behavior, then there is a biochemical state that precedes it.  That's what I am interested in.  I call this "pain" only so much as :"avoidance" would suggest that state. If there is no such behavioral state of pain, what is motivating the avoidance?

@LarryFreeman I mean that pain is a label for a subjective experience. If you call anything else "pain", you should know that you are no longer using "pain" in the way it is used in the fields of psychology/neuroscience/biology. Avoidance doesn't require pain, nor does it require any preceding state: common avoidance and approach behaviors in single-celled organisms are directly chemically mediated. "Motivation" is similarly a fraught term.

@LarryFreeman Well, they do respond to stimuli in the environment if that's what you mean.


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Confusion regarding the role of the capacitor in the electrical equivalent of a membrane
I am having trouble understanding the electrical equivalent of a cell mebrane as it is shown in this picture taken from Kandel:

What I cannot understand is the capacitor in the specific image. Why is it set parallel to the resistances and what does it symbolize? Does it symbolize all the charges that are accumulated in the cell border? What does the derivative of its charge $\frac{dq}{dt}$ that is shown in the relation $C=\frac{q}{V}$ mean? From my point of view the capacitor symbolizes the two sides of the membrane and so the derivative mentioned above should be equal to the total current through the membrane. However this is my personal opinion that I have not confirmed and which contradicts the electrical equivalent given above. Can someone give me some help?

Please ask one question at a time. Right now the answer to your question would be a chapter in a neurophysiology textbook (seems like you should have one in Kandel). What does it teach you?

@BryanKrause I have the  Jessell, Thomas M.; Schwartz, James H Principles of Neural Science. My problem is not related to what the book sais but to the physical  interpretation of all these membrane properties.

Okay; I think if I am understanding your questions correctly the first and last have already been answered here, and your middle question isn't really about biology but just physics and what capacitance means. Have you searched for these answers? If you can't find one, then still please ask individual questions supported by what you know about each.

@BryanKrause I edited my question in order to refer to a single topic. I cannot understand however what do you mean that the first and last questions have been answered. I don't see any answers.

Did you use the search to look for existing posts on the site? That's where you would find answers.

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Can a pathogen be totally resistant to the human immune system?
Can a pathogenic organism be totally resistant to the human immune system? For the purpose of this question, the organism in question must cause a disease.
Examples of organisms that would qualify as totally resistant:
Pathogenic organisms that are completely undetected by the immune system while the disease that they cause runs its course.
Pathogenic organisms that, even if detected, are completely invulnerable to the immune system. For instance, macrophages and other immune cells would not be able to destroy even one cell of such an organism.
Is it possible for such a pathogen to exist? Are there any such pathogens?
(For the purpose of this question, the HIV and diseases that only manifest in immuno-compromised individuals do not count)

The problem is  much of the immune system is passive, that is it resists everything equally.

???? The HIV attacks the immune system. The infection is obviously easier in already immuno-compromised individuals...

I can't think of any pathogenic organisms that are completely resistant to the immune system. Some bacteria that cause chronic diseases (e.g. tuberculosis) are relatively resistant, and a handful of viruses (e.g. spumaviruses) are relatively invisible, but the nature of pathogen transmission would mean that completely resistant organisms would spread through a population pretty fast and we'd know about it.
Pathogenic prion agents, like scrapie and Creutzfeld-Jacob disease, are essentially invisible to the immune system, and can be transmitted; but they aren't pathogenic organisms. They might be the closest to your description though.

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Does loss of dopaminergic neurons totally eliminate voluntary muscular control?
Breathing is a function that is not only autonomic, but can also be temporarily overridden and placed under voluntary control. In fact, you are now breathing manually. Now, suppose that someone has completely lost the ability to voluntarily control his/her muscles due to destruction of the brain's dopaminergic neurons in the substania nigra (such as due to Parkinson's Disease or MPTP poisoning). This would normally result in total paralysis of voluntary muscles and inability to move. Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically? What about defecation (Which requires one to voluntarily relax the anal sphincter)? What about rolling the eyes?

"Otherwise the person is totally fine" is very inaccurate and does not describe Parkinson's. I do think there is an interesting question here but it would be better separated from this bizarre scenario.

No it would eliminate only fine motor control; Patients with parkinsonism are not paralysed as much as loss of fine movement they have spastic movement...

Suppose that someone has completely lost the ability to voluntarily control his/her muscles due to the destruction of the brain's dopaminergic neurons in the substania nigra
This is not correct. The substantia nigra plays an important role in both reward and movement. The degeneration of dopaminergic neurons in the substantia in Parkinson’s disease leads to loss of fine motor movement (leading to limited movement and tremors) and some loss of non-motor skills (loss of smell).
What locations control breathing?
The autonomous regulation of breathing is controlled by bundles of neurons called the dorsal respiratory groups (DRG) and ventral respiratory group (VRG) that together make up the medullary respiratory center. Source.

Though the exact mechanism of how we control our voluntary breathing is still a debated. We have a general idea:

Voluntary control of breathing is mediated primarily via the
  corticospinal and corticobulbar tracts and is important in activities
  such as speech, singing, and voluntary breath-holding. Disorders
  involving this mechanism occur mainly in bilateral pontine infarctions
  and lesions involving the pontine tegmentum that interrupt the
  descending motor pathways. - Neurology and Clinical Neuroscience, 2007

Would that person be able to breathe manually if he/she so wished, or would he/she only ever breathe autonomically?
Although the exact mechanism for voluntary breathing is not fully understood, the voluntary process is controlled by a series of nerve bundles. If the nerve bundles were severed, there would be decreased voluntary control over the breathing process. Losing the ability to manually breath could be bad for overall health. One study has found that a lack of the ability to manually breath can lead to poor spinal stabilization and posture.
What if you lost autonomous control?
There is a rare disorder known as central hypoventilation syndrome (CHS) that results in respiratory arrest during sleep (also known as Ondine's Curse). This disorder is caused by a lack of development of the neural tube (aka Medulla and the VRG/DRG) during birth or some type of traumatic brain injury. Treatment for this disorder is a lifetime of mechanical ventilation.


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How do anticholinesterase pesticides kill nematodes?
Compounds that inhibit the enzyme acetylcholinesterase are commonly used as pesticides. In animals with centralized respiratory systems controlled by the nervous system, poisoning with an anticholinesterase would lead to death due to respiratory arrest. I presume that, in insects, the inhibition of AChE would lead to closing of the spiracles necessary for respiration
However, nematodes and other worms rely on diffusion of gasses for respiration and do not have respiratory systems controlled by a nervous system, so how would inhibition of AChE by agents such as aldicarb kill them, especially if the pesticide in question happens to be a reversible inhibitor?

Cholinesterase inhibitors and plant-pathogenic nematodes
While it is true that cholinesterase inhibition does not affect gas exchange in nematodes, it does produce other effects by paralysing motor activity:

Inhibition of larval hatching

Reduced movement to new roots

Impairment of root invasion and feeding

Impairment of copulation

Acetylcholine also has a role in sensory neurotransmission in nematodes, which could further contribute to the toxic effects.
Thus cholinesterase inhibitors do not directly kill nematodes, but only slow down their growth and reproduction. This is why some prefer to use the term 'nematostatic' over 'nematicidal' for these compounds.
Effects on vertebrate pathogens
Pyrantel is a cholinesterase inhibitor used to treat intestinal nematode infections in man and other mammals. Little is known about how exactly it works, except that it causes spastic paralysis of the worms. Possibly, it impairs feeding and reproduction (like its counterparts in plant pathogenic nematodes).

References and further reading:

Wright DJ. Nematicides: modes of action and new approaches to chemical control. In Zuckerman BM, Rohde RA, editors. Plant parasitic nematodes. Vol. 3. New York: Academic Press; 1981. p. 421-449. Link to publisher site.
Martin RJ, Robertson AP. Mode of action of levamisole and pyrantel, anthelmintic resistance, E153 and Q57. Parasitology. 2007 Aug 1;134(8):1093–1104. https://doi.org/10.1017/S0031182007000029

In nematodes, Acetylcholine is the main excitatory neurotransmitter at neuromuscular junctions. Large amount of nervous system cells in Caenorhabditis elegans secrete acetylcholine for Cholinergic neuromuscular transmission.
Cholinergic transmission is involved in various physiological processes in many C. elegans, such as locomotion, egg laying, feeding, and male mating.
So acetylcholinesterase which is an enzyme responsible for hydrolysis and inactivation of acetylcholine plays an essential role in regulation of cholinergic transmission.  Thus inhibitors of this enzyme can act as nematocide.
Reference:
http://www.wormbook.org/chapters/www_acetylcholine/acetylcholine.html#:~:text=Acetylcholine%20is%20the%20major%20excitatory,elegans%20nervous%20system%20release%20acetylcholine.
https://pubmed.ncbi.nlm.nih.gov/16569291/#:~:text=Acetylcholine%20is%20the%20major%20excitatory,for%20regulation%20of%20cholinergic%20transmission.


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What happens when too much sodium flows in the cell due to a faulty voltage-gated sensor? What about too little?
The activation gate opens, signaling depolarization. Eventually, the inactivation gate closes, ending depolarization and beginning repolarization.

What is the physiological impact of the inactivation gate remaining open too long, letting in too much sodium into the cell than a normal action potential? This would raise the magnitude of the action potential.
What would be the impact if it remained open for too short a time?

Is this a homework question or related to studying for a course/class?

No, I'm just curious as to what happens and trying to understand the concept. If it helps I'm studying for a 'standardized test.'

To answer the OP directly: You may be interested in looking at diseases that abnormally increase or decrease the activity of sodium channel proteins, changing the degree to which sodium ions cross the cell membrane. Some diseases are genetic in basis, which means they are inherited. This lends them to characterization and study.
This review paper by George summarizes some of the genetic diseases associated with sodium channel mutations, which might give you some direction for further research:

Muscle sodium channelopathies (SCN4A)

Hyperkalemic periodic paralysis
Paramyotonia congenita
Potassium-aggravated myotonia
Painful congenital myotonia
Myasthenic syndrome
Hypokalemic periodic paralysis type 2
Malignant hyperthermia susceptibility

Cardiac sodium channelopathies (SCN5A)

Congenital long QT syndrome (Romano-Ward)
Idiopathic ventricular fibrillation (Brugada syndrome)
Isolated cardiac conduction system disease
Atrial standstill
Congenital sick sinus syndrome
Sudden infant death syndrome
Dilated cardiomyopathy, conduction disorder, arrythmia

Brain sodium channelopathies (SCN1A, SCN2A, SCN1B)

Generalized epilepsy with febrile seizures plus
Severe myoclonic epilepsy of infancy (Dravet syndrome)
Intractable childhood epilepsy with frequent generalized tonic-clonic seizures
Benign familial neonatal-infantile seizures

Peripheral nerve sodium channelopathies (SCN9A)

Familial primary erythermalgia

Generally, you might search on the term "sodium channel mutant" or "mutations" to see what kinds of health problems are caused by under- or over-activity of these proteins.

This answer provides some good information about channelopathies but doesn't address the misconceptions in the OP or answer the 'what happens' question directly.

Thank you for the links... as for the misconceptions... that's why I'm here!


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What is the difference between protein translated by a free ribosome and protien translated by a ribosome attached to endoplasmic reticulem?
There are protiens translated by free ribosomes and proteins translated by attached ribosomes.  But how do these two types of protein differ from each other? I am just talking about a eukaryotic cell. I know that proteins made by free ribosomes do not have a covering but proteins made by attached ribosome gradully have a vesicle around them but I am not able to understand what difference in use does the vesicle make? (I am new here so pls forgive if there are mistakes in my question)

As a newcomer to Stack Exchange Biology, you may not realize that your question has a couple of problems that may result in it being ruled off-topic. The first is that it looks rather like a homework question, for which there are specific rules you can find in the Help. One of these — which also applies generally — is that you should show that you have made an attempt to answer this question yourself. This means doing some research. Try Wikipedia on free and membrane-bound ribosomes.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


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Can foxes move their ears independently?
I've read that dogs can do move their ears independently, i.e., point one ear in the direction of a sound without having to point the other one at the same time. Is this a common trait with other canids, such as foxes? Can most eared mammals do this, with humans being an exception (except for a few exceptional humans)?

Yes, they can. Here are a couple pics I found of foxes moving their ears independently:

This is something all canids can do (1)(2) Btw, I can move my ears independantly. It's all in the finding the right muscles.

How can you tell from a still photo that only one ear is moving?

@daniel Easy - because it is swiveled from it's natural position. Red foxes will point both ears at one thing if paying it full attention. The foxes pictured were pointing both ears in different directions, because apparently two things were catching it's attention.

Not easy for me. Your reference (1) does not support your point directly and  reference (2) is to a book with no page number. Can you please find a reference that directly supports the point?

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Lost Ability to Regenerate Body Parts during the Transition from Amphibians to Mammals
Why have higher-order animals lost the ability to regenerate body parts during evolution? Wouldn't it be better for survival? What is the evolutionary theory behind it?

the liver regenerates.. The regenerative ability of which animal are you talking about?

My question is about Limbs and other body parts. Like lizards can regenerate a whole limb but crocodile can't(just an example).

How do you deduce that higher animals lost the ability to regenerate during evolution? Can you please give me an example of such an animal which lost its ability to regenerate?

Like I said in my last comment, Limbs of Lizard and Crocodile.

Rephrase your question to "lost the ability to regenerate body parts during the transition from reptiles to mammals."

Sounds Better!!

You might want to rephrase your question just a little more and add some background. First, there was never a transition from reptiles to mammals. They share a common ancestor but evolved within their own clades. And do you know if the common ancestor of mammals and reptiles is believed to have limb regeneration? In other words, are the examples of regeneration in nature mostly conserved or have they evolved independently? Why do you think they were lost instead of never evolved?

I changed Reptiles to Amphibians in the title, because there is no reptile to mammal transition.

Regeneration of limbs in amphibians is an adaptation where new limbs are generated by dedifferentiated cells. This process is tightly linked to the embryonic program which, in most animal cells, is a difficult program to access once terminal differentiation has occurred (but it's possible, e.g. induced pluripotent stem cells).
Of note, amphibians have a unique life cycle that includes metamorphosis. It is thought that organisms with more diverse stages in their development may have increased potential for regeneration. Mammals, after birth, do pass through multiple stages of development, but these stages are largely continuous.
So the quick answer is: mammalian limbs are made up of terminally differentiated cells (and specialized stem cells) with high barriers of reprogramming. They're difficult to reprogram because there hasn't been strong selective pressure to do so. Limb regeneration might seem like a great adaptation, but it doesn't seem to be that important for the success of mammals. Additionally, selection for "maintaining a full set of functional limbs" could evolve many different ways. For example, primates may have evolved behaviors or reinforced anatomy that reduces their risk of injuring a limb. Also, larger animals are probably less likely to have limbs removed just given their size. And if they do, it may have little effect on their reproductive fitness. A legless amphibian probably finds few, if any, mates.
Yun Gates, and Brock. Regulation of p53 is critical for vertebrate limb regeneration, PNAS 2013

Wow, great answer. Can you add some references?

Thanks! I've added a reference. The introduction and citations in the linked paper include the relevant information.

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Why does cracking a joint make noise?
What causes the noise when you crack a joint? Is joint cracking harmful?

The exact mechanism is unclear. Here are some possible causes:

rapid collapsing of cavities inside the joint [1];
rapid ligament stretching [1];
breaking of intra-articular adhesions [1];
escaping gases from synovial fluid [2];
movements of joints, tendons and ligaments [2];
mechanic interaction between rough surfaces [2], mostly in pathological situations like arthritis (and it is called crepitus [3]).

There are no known bad effects of joint cracking [1, 4].

There are no long term sequelae of these noises, and they do not lead to future problems. There is no basis for the admonition to not crack your knuckles because it can lead to arthritis. There are no supplements or exercises to prevent these noises [4].

And no good effects either:

Knuckle "cracking" has not been shown to be harmful or beneficial. More specifically, knuckle cracking does not cause arthritis [5].

References:

Wikipedia contributors, "Cracking joints," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Cracking_joints&oldid=617403659 (accessed July 22, 2014).
The Library of Congress. Everyday Mysteries. What causes the noise when you crack a joint? Available from http://www.loc.gov/rr/scitech/mysteries/joint.html (accessed 22.07.2014)
Wikipedia contributors, "Crepitus," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Crepitus&oldid=615557134 (accessed July 22, 2014).
Johns Hopkins Sports Medicine Patient Guide to Joint Cracking & Popping. Available from http://www.hopkinsortho.org/joint_cracking.html (accessed 22.07.2014)
WebMD, LLC. Will Joint Cracking Cause Osteoarthritis? Available from http://www.webmd.com/osteoarthritis/guide/joint-cracking-osteoarthritis (accessed 22.07.2014)

It might cause your significant other or roommates to go crazy and bop you on the head, though.

I don't really see how anyone can say that there is no benefit.    Only based on my experience, there is a reason for cracking a joint.   Before cracking it, it "feels odd".  Afterwards that feeling is relieved.   Just because we don't know why that is, doesn't mean it's not beneficial.   At the very least, subjectively it was beneficial, immediately.

I believe I read that cracking your fingers causes reduced grip strength for some period of time. I cant recall the duration. I suppose that could be a slight negative but it eventually the grip strength is returned to normal.

I can crack joins all day, so how's this so hard to figure out for scientists? It's not something you need years to wait for, it happens all the time...

I used to crack my fingerjoints a lot, and noticed that my fingers had become a lot weaker. Not sure if actually weaker, but playing piano had become a lot harder. Some anecdotal information if anyone's interested.

Is joint-cracking harmful?  No.  Donald Unger was told by his mother that he'd get arthritis if he cracked his knuckles so he cracked his left knuckles every day for 60 years but never his right knuckles. He had no arthritis or any other problems in either hand and got a publication (D. L. Unger, "Does knuckle cracking lead to arthritis of the fingers?", Arthritis and Rheumatism 41(5):949–950, 1998 – online version for those with appropriate access) and an Ig Nobel Prize (2009) for his troubles.
OK, so one guy's knuckles prove nothing but who can resist the opportunity to cite an Ig Nobel winner?

A paper was just published that explains this phenomenon in PLOS One, found here. It looks like the sound is caused by the formation of a gas cavity in synovial fluid of the joints. They do mention that contrary to what is stated in the most upvoted answer here, the sound does not come from the collapse of the bubble, but rather its formation.
And in response to the comments, as mentioned in the paper, this does not seem to cause any harm to the meniscus or surrounding tissue.


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To what extent is it possible to understand if a bacteria can produce a protein? (in silico only!)
I have to answer a question about a sub-task of my thesis: Can the bacteria X produce the protein Y?
I searched of course Google and BLAST. There is no data supporting that this specific bacteria ever produced this protein sequence.
However, my thesis supervisor wants me to go deeper[1], but I don't know how to do it in silico in a way to offer a proper answer.
What I'm thinking of doing with the data at hand is to create a DB on localhost with all the versions of the protein listed in BLAST (I'm using ruby, not sure how can I fetch all this data in FASTA format yet, but I'll figure it out), and all the strains of the bacteria listed in BLAST and perform a fuzzy string matching.
That's like brute-forcing. After I have a possible score I can get the closest score of them all, study it a bit and then submit my answer.
Is there any other way to attack this problem in order to submit a proper, at least partially polished answer?
NOTE: I don't have access to any lab, any experiment must be performed in silico.
[1] My supervisor believes that IF this bacteria needed this protein it WOULD be able to to produce it at will without undergoing mutations. And since his level of dedication and knowledge revolving molecular biology is scary, it's kind of hard to believe that he is wrong.

I am coming from the wet lab - and my experience is that you can clone practically every gene into a fitting vector and express is in bacteria. You need the right regulatory sequences (promotors and so on), but it is possible. The question, if this protein is produced in big amount and if it soluble is something different. Also many proteins are modified posttranslationally which is something bacteria cannot do.

Hello Chris. I'm not interested in to cloning anything but thanks for the info.

I understood that. I simply wanted to add some comment on the practical side of this problem, this might help you as well?

Of course @Chris, I will mention to my paper that it's possible to achieve the wanted result with cloning. Without your comment I wouldn't had that extra paragraph, which will make my paper better anyway :-) ... So thank you again!

To be clear: You want an algorithm to match if the given fasta can be produced by the bacteria genome?

@DevashishDas No, I already have a gem with a list of fuzzy matching algorithms. I'd like to know if there's any other approach worth pursuing except that. NOTE: Any comment on the algorithms would be good also: Hamming, Jaro, JaroWinkler, Levenshtein, LongestSubsequence, LongestSubstring, PairDistance, Sellers. These are the ones supported by the library I'm going to use.

Are you talking about whether the Bacterium naturally produces a protein or whether it could express a particular protein?

@JackAidley Whether if needed it could express a particular protein (at any quantity).

you can predict an ORF from DNA/RNA sequence but you cannot be sure if the protein is produced. You can either do LC-MS to see if signature peptides are produced or use molecular bio experiments as Chris suggested. You can also tag your sequence with GFP and see if it expresses.

you can download proteomics data (if available) for your bacteria and search for the signature peptides that your protein-x is likely to produce.

If you're just looking at whether a protein can be expressed, you might be misunderstanding your supervisor. The set of proteins needed by a given bacteria is a tiny, tiny subset of the set of proteins that bacteria is capable of producing, provided the gene coding for the protein is provided to the bacteria. If instead you're curious about whether a bacteria can express a given protein without any changes to its genome, there are plenty of proteins that are coded for in the genome but only expressed under specific circumstances. I'd look into promoters if I were you for more info on that

Your problem will finally boil down to searching your sequence in the Blast databases. Performing Blast seems to be probably the best way to find out if your bacteria has that specific protein expressed or not. If you could not find it in the nearest species using Blast, then try running PSI-BLAST, which would return you distant homologs, by which you can see if your protein is expressed in the other bacterial species.

I'm on to something using blast (I dropped out the idea of writing my own script to do this as soon as I played around with BLAST). I know that E. Coli can produce my protein (it's documented) at protein level. I couldn't find a perfect match thought, I've found a 74% positive match. Then searched about Desulfovibrio and found a 75% positive match (for a specific strain). I think it's enough, I can't take the risk to answer the question in a definitive way but, it's enough data to give some food for thought and possible direction. Comments are more than welcomed! Ty!


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My understanding of chromosomes and the processes related to them is lacking
I'm sorry for the incredibly simple question, I just can't seem to find any answers elsewhere online.
I am a high school student currently studying for the upcoming AP biology exam, and recently I have realised that I do not quite understand chromosomes. To be specific, I understand what they are (the condensed form of chromatin that one sees when viewing a dividing cell), but my understanding is still lacking when it comes to:

Ploidy, specifically when it changes.
Alleles and how they move/interact during meiosis.
How homologous chromosomes work: When do they occur? Is each chromatid pair identical, or is one chromatid in each pair from each parent?

I made a diagram that details my current understanding, because it can be a bit difficult to describe what I don't understand, but I can try to elaborate more if necessary.

If this is the wrong sort of place to ask this question, some advice on a better place to ask would be greatly appreciated.
Thanks.


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What is the actual mechanism of the birth control pill?
I've been trying to figure out through online sources (I don't own any medical textbooks) what the exact mechanism behind the birth control pill (henceforth "the pill") is, and I am often finding contradicting information. This surprises me, since so many women take hormonal birth control that what it does should be known and accessible to everyone.
The following is gathered from PBS and Harvard. As I understand it, the female menstrual cycle is controlled by several organs working in feedback loops: after menstruation, there is a low concentration of estrogen and progesterone in the bloodstream, impelling the hypothalamus-hypofysis to secrete FSH and LH. This stimulates the maturation of a single follicle in the ovaries. This follicle secretes estrogen, signalling to the hypothalamus-hypofysis duo to stop producing FSH and LH. With enough estrogen, a sudden burst of FSH and LH is secreted, causing ovulation. The rest of the cycle is high in progesterone, and by lack of implantation, progesterone production slows and we are back at menstruation.
The goal of the pill is to prevent ovulation (rather than prevent implantation) by playing into these feedback loops.

A first confusion is as follows: I know the pill contains estrogen, yet (as both sources attest to) it is supposedly the high levels of estrogen that induce the FSH/LH spike that triggers ovulation. So then, why wouldn't taking exogenous estrogen cause ovulation rather than preventing it? You are essentially replacing the follicle by a blister pack.

A second confusion is that FSH and LH are so often mentioned in the same breath (i.e., you'll see "FSH" and "LH" less than "FSH and LH") that it is unclear to me what their separate role is. On this ScienceDirect page, in the only exercept that mentions "CHC", it is mentioned that we should consider FSH and estrogen as one loop, and LH and progesterone. The former causes maturation of follicles, the latter causes ovulation (maturation of lutheal cells). This is the only place I have found this distinction, and I'm unsure if it is true; in any case, the above point of contention still applies, because as the pill also contains progesterone, taking exogenous progesterone would cause ovulation.
Besides, I am aware that there exist progesterone-only pills. I'm not sure if they use the same mechanism (this thread is too unclear), because if they do, I don't see the point of having the combined pill contain estrogen.

According to Healthy Women, it is actually the change in estrogen rather than a stable level which causes ovulation. (Rephrasing this as an engineer, the hypothalamus-hypofysis duo detects a high derivative rather than a high baseline in order to trigger the FSH/LH spike.) This seems to be confirmed by Cleveland Clinic in saying

"Chronic (long-term) estrogen exposure inhibits FSH release, whereas rising estrogen levels, which normally occur before ovulation, trigger your pituitary gland to increase levels of gonadotropins (FSH and LH)."

On the other hand, the Crash Course Biology video at 6:02 says in a pop-up that FSH and LH are inhibited by low estrogen but boosted by high estrogen. So, we have a third confusion: does the pill mechanism play on the hormone level, or its rate of change?

So far, I've hypothesised two possible pill mechanisms:

Pill keeps estrogen constant, which means the derivative is 0, so the FSH/LH spike isn't triggered (and their initial boost after menstruation is triggered due to GnRH from the hypothalamus which is secreted due to the drop in estrogen due to placebo pills, mimicking menstruation).
Placebo pills during menstruation cause very low estrogen. This causes GnRH, which causes FSH. Then the pill saturates the body with estrogen to make it seem like a follicle is growing (above a lower threshold), causing FSH to stop, yet a real follicle would keep increasing estrogen (above a higher threshold) to trigger the spike during ovulation.

I don't like either explanation. There should be a clear mechanism that disambiguates all of the above confusions and comports with all sourced cited above (assuming they're all correct), and comports with all the styles of pill (combined vs. progesterone-only).

+1 for the effort you've put into this post. Please understand there are more than two kinds of HBC; you can't make blanket statements/assumptions unless you specify exactly the pill you are referring to. Please edit your post to include the pill, by name at least, if that's all you have. Two additional nit-picky things: placebo cannot by definition have an active physiological effect - psychological, yes, and mind-body counts - and how the pill works is known and accessible, but requires some  preexisting understanding of endocrinology to really understand (as you've discovered.)

@anongoodnurse Glad to hear the mechanism is known. W.r.t. placebo pills, I guess I should have said "placebo pills give way to" rather than "cause", but indeed it is nuance that I'll gloss over. From your question, can I assume that there are multiple pill mechanisms? Note that I am not talking about HBC in general (e.g. progesterone-excreting IUDs), because that obviously involves multiple mechanisms. I am specifically talking about the pill. I have no knowledge of pill brands; AFAIK, there are two types (combined and progesterone-only). That's as far as I can specify. Does that work?

@Mew There is more variety than that; different doses of the progesterone-only pills work differently, and all of them have multiple mechanisms of action, not just one. It's a complex hormonal dance with multiple phases and interactions and delays and feedback, not something simple like antagonist drugs that primarily block a single receptor protein.

@BryanKrause Consider writing an answer sharing your knowledge, in that case.

The point is that without knowing to which pill you're referring, the "answer" will be w a a a a a a a a a a a a a a a a a a a a y too long, equivalent to a book on Reproductive Endocrinology. Edit to specify a specific pill or you'll not get an answer. Thanks.

@anongoodnurse I'm confused. Given that I don't know more than I have written, how would I have practical knowledge about pill brands? If you intended to ask me about the distinction made on this page (monophasic, biphasic, triphasic COC, and POP) then as my question already says, I am interested in knowing the difference between all those mechanisms. Sample your favourite brand from that page; presumably all monophasic COCs (e.g.) work the same at the level of analysis in my question.

Sorry, but anyone can google birth control pills and pick one. But as I said, I think you're expecting a course on reproductive endocrinology. That is not the role of any SE site.

The question appears to be over complicating what is a fairly straightforward mechanism of negative feedback characteristic of most endocrine function in the body, in this case, the effect that oestrogen in the usual or predominant form of oestradiol inhibits the release of FSH from the anterior pituitary required for follicle development and consequently ovulation.   By far the dominant effect of both exogenous oestrogens and progestogens -- the respective dosages of which are merely variations on the same general mechanism -- is this negative feedback on the release of gonadotropins from the anterior pituitary, thereby circumventing the natural interaction between the pituitary and its target organ.
To quote from 'Wikipedia' which is usually a good place to start such an inquiry;

Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding), but was also found to inhibit follicular development and help prevent ovulation. Estrogen negative feedback on the anterior pituitary greatly decreases the secretion of FSH, which inhibits follicular development and helps prevent ovulation.

That should resolve the 'first confusion'satisfactorily: that is, the follicular development induced by FSH has been inhibited by exogenous oestrogen, and ovulation cannot therefore occur.

Under normal circumstances, luteinizing hormone (LH) stimulates the theca cells of the ovarian follicle to produce androstenedione. The granulosa cells of the ovarian follicle then convert this androstenedione to estradiol. This conversion process is catalyzed by aromatase, an enzyme produced as a result of follicle-stimulating hormone (FSH) stimulation.

Progestogen negative feedback and the lack of estrogen positive feedback on LH secretion prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of an LH surge prevent ovulation.

That should address the 'second confusion' and its proliferation into the 'third confusion' regarding the peculiarities of feedback, notwithstanding the anomaly that oestrogen positively feeds back on LH secretion.
The rest of that section of the article deals further with the influence of progestogens (progesterone) on cervical mucus and so on.
The relevant references cited are as usual noted at the end of the article.

Oh my, I missed the notification for this answer. I do follow the first quotation, which essentially matches my second hypothesised mechanism (it's the level of estrogen, not the rate of change, that inhibits FSH in the hypofysis; correct?). However, it doesn't answer the "first confusion", i.e. why the exogenous estrogen itself doesn't cause the FSH/LH spike. The second quotation essentially says that LH causes (is metabolised into?) estrogen catalysed by FSH, but nothing is said about LH's secretion nor about progesterone, so this doesn't really answer the "second confusion" either.

@mew.  You should read your question and my answer very carefully once again, and understand that the primary mechanism of effect is a NEGATIVE FEEDBACK on FSH/LH secretion by oestrogen, endogenous or exogenous, preventing follicle development in the ovary, and therefore making ovulation impossible, regardless of what happens in the mid-cycle: i.e. the effect you mention, that oestrogen also appears briefly to stimulate the release of those gonadotropins (in a mechanism about which I am ill-informed). It's all a lot simpler than you think, and more a medical question than biological.

Okay, let me give it a shot: you are saying that taking exogenous estrogen takes over for the follicle's estrogen production, hence shrinking the supply of LSH and LH faster than usual, keeping the follicle underdeveloped and hence even if the "surge" mechanism were to occur at a certain level of estrogen, no mature follicle would exist to be released. Is that what you are conveying? If yes, I still need an explanation on where progesterone comes in and how it is possible that progesterone-only pills exist if estrogen is what we intercept in the feedback loop.

@mew.  Correct. 'Negative feedback'.  Progesterone only pills function in essentially the same way, through this same typical negative feedback on the HT-Pituitary, to suppress the release of gonadotropins FSH and LH, both of which are necessary for follicular development and thus ovulation. The mid-cycle surge in LH said to trigger ovulation either doesn't occur or is ineffective in most cases. The follicle simply cannot mature. Progesterone also has other contraceptive effects on cervical mucus etc., but is usually prescribed in cases in which oestrogen is problematic.  FSH, LH: read wiki.


text:
Are there any "good" gases which "accidentally" diffuse into the lungs and get exhaled?
The purpose of breathing is to bring oxygen into the body and to rid the body of waste gases such as carbon dioxide and excess water vapor. This is done by diffusion with the blood. I am wondering whether the respiratory system also "accidentally" removes good gases from the body via diffusion and exhalation. (These good gases do not include oxygen, since it doesn't diffuse from the blood into the lungs.) This might be useful if a person has low amounts of a good gas and breathing too much, such as doing too much exercise, is the culprit.
Such good gases could come from food. Just like alcohol vapor is exhaled, maybe these gases might be exhaled too. Good gases could also come from a specific metabolic process.

Related:  https://biology.stackexchange.com/questions/111813/besides-carbon-dioxide-and-water-vapor-what-waste-gases-are-removed-through-the

Your question might get more attention (i.e. additional suggestions) if the title were changed on the lines I suggested, e.g. "Are there any important gaseous metabolites or signalling molecules in humans that may be lost through exhalation?".

Biological scientists do not usually ascribe moral attributes to metabolites, despite the use of the term ‘good’ in reference to lipids by those who communicate with the public. So I think it better to rephrase the question more precisely, as something like:

“Are there any important gaseous metabolites or signalling molecules in humans?”

One gas that comes to mind is nitric oxide, which is a natural signalling molecule that causes vasodilation of smooth muscle. The production of this is stimulated by the erectile-disfunction drug, sildenafil (marketed under the trade name, viagra).
Thus, nitric oxide fits the bill (and, in so far as a penile erection is considered a ”good thing” — most men will be of that opinion, nitric oxide can even be considered a ”good gas”).
Nitric oxide has certainly been detected in the exhaled breath of normal individuals, but the majority is excreted in the urine as nitrite or nitrate.
So I would look for causes other than heavy breathing to explain the decline in its tissue concentration, and any unwelcome effects that this might have for the individual.

Is nitric oxide actually exhaled?

@mathlander — NO is exhaled, as can be found from the paper you linked to. I have modified my answer providing information on the metabolism of NO from this and another paper.


text:
Why is it that I can only detect smells if I breathe, and not when I hold my breath?
At school we're told that the receptors for smell (olfactory receptors) are present in the Schneiderian membrane. But I've noticed that I'm only able to detect smells only while I breathe and not when I hold my breath.
I even tried an experiment to confirm my observations and the results were positive. I placed an open bottle of really strong perfume fairly close to my nose, and lightly inhaled. I could easily detect the smell. But as soon as I hold my breath I'm not able to smell it anymore, even though I placed the bottle right under my nose I wasn't able to smell anything. Immediately I moved the bottle away, walked into another room and took a breath, and the smell of perfume was so strong it made me choke.
I guess this 'experiment' of mine contradicts what we've been taught. That Olfactory receptors present in the nasal passage simply pick up traces of molecules (in this case, perfume) and this is perceived as smell, since by keeping the bottle right under my nose the perfume would've already diffused into the air in large quantities and would've already entered the nasal passage, yet I was unable to detect it.
So my question stands, 'Why is it that I can only detect smells if I breathe, and not when I hold my breath?'

if you are breathing it is actively moving the air, containing the scent, in to your nose, otherwise you have to rely on diffusion which doesn't work well with such a narrow passage

@rg255 I suppose you can make an answer out of your comment

The olfactory epithelium is located in the highest part of the nasal cavities, overlying the cribriform plate of the ethmoid bone.  In order for you to smell something, the odoriferous molecules have to travel the length of the nostrils (which are a pair of very narrow passages which also happen to be filled with hair) and up though the full height of the nasal cavities, having to pass three sets of baffles (known as the nasal conchae) on the way.
When you take a breath, your lungs and inspiratory muscles form a suction pump which pulls air through the nostrils up into the nasal cavities; some of this air, along with any odoriferous substances contained therein, is swirled up to the top of the nasal cavities, where the olfactory epithelium is located.
In contrast, when you're holding your breath, there is no significant air movement through the nasal cavities, and even airflow contained entirely within the nasal cavities is considerably obstructed (thanx to the aforementioned hairs and baffles); therefore, for any odoriferous substance (such as the perfume you're probably sick of smelling by now) to reach the olfactory epithelium, it has to diffuse all the way from the tips of the nostrils to the top of the nasal cavities on its own.  This is a much slower process, and, therefore, it takes rather a while to notice anything smelly when you're holding your breath - even if it's, literally, right under your nose.


text:
What is this spider hunting in the tree in the night?
I took the following picture of this spider in northern Switzerland (alt: ~700m) with macro flash/lense.

The picture was taken during the night in a cedar tree (Thuja occidentalis).

Nice picture :)

That is a really well taken picture.

Thanks for the comments, it was taken without tripod, then I was a bit lucky to got it in the focus range.

It's look like Sac Spider (Clubiona lutescens) to me.

Source: http://ednieuw.home.xs4all.nl/Spiders/Clubionidae/Clubionidae.htm

Nice catch, I am wondering how you could find this. I tried to browse many spider database but did'nt find anything.


text:
How big can cold-blooded animals get?
It seems impossible to have reptiles the size of dinosaurs, just because they are really big! Did they have different systems of maintaining body temperature or maybe they weren't the exact type of animals that we today call reptiles?

Wikipedia http://en.wikipedia.org/wiki/Physiology_of_dinosaurs#Metabolism looks like a good place to start.

You should have a look to the correct vocabulary and concepts in order to describe organism intern temperature. This post will help you

It seems that giant turtles are not so cold as we used to think. They are too big to quickly lose the warm from metabolism, so they may be thought of somewhat homeotermic. Perhaps that's what happened to dinosaurs.

Answer is quite simple as from @Alan Boyd link. They are cold blooded and thus, can go out for hunt in cold, they need to stay put till they get some prey.
So, it mainly depend on the temperature of the outside, I found this interesting paper on relation of body sizes and latitude.

Body sizes of poikilotherm vertebrates at different latitudes
Maximum sizes of 12,503 species of poikilotherm vertebrates were
  analyzed for latitudinal trends, using published data from 75 faunal
  studies. A general trend appears which may be summarized by the rule
  "among fish and amphibian faunas the proportion of species with large
  adult size tends to increase from the equator towards the poles". The
  rule holds for freshwater fish, deepsea fish, anurans, urodeles, and
  marine neritic fish arranged roughly in order of decreasing clarity of
  the trend). In general the rule applies not only within these groups
  of families but also within single families. In reptile groups, the
  rule holds weakly among snakes and not at all among lizards or
  non-marine turtles. Possible explanations include an association
  between small size and greater specialization in the tropics; the
  possibility in poikilo-therms of heat conservation or of some other
  physiological process related to surface/volume ratio; selection for
  larger size in regions subject to winter food shortages; and an
  association between large adult size and high reproductive potential
  in cold regions. Other suggestions can be advanced, but all are
  conjectural and few are subject to test. Global size - latitude trends
  should be looked for in other living groups.
Cite: Lindsey, C. C., 1966: Body sizes of poikilotherm vertebrates at
  different latitudes. Evolution: 456-465

Now lets compare some of the largest cold blooded Animals:

Reptiles
Amphibians
Fishes (Pisces)

Reptiles:
The smaller size of Reptiles give them more agility to hunt andsave them predators but some times when they are top of food chain they can grow as giants.
Anacondas (Eunectes), gigantic snakes from South America, are undoubtedly the largest living snakes.
The largest species, the green anaconda (E. murinus), likely only rarely exceeds 9 metres (30 feet) in length; nonetheless,
persistent but unsubstantiated reports have been made of anacondas that are 12 metres (40 feet) long.
The reticulated python (P. reticulatus) of Southeast Asia and the East Indies has been recorded at 10.1 metres (33.3 feet).
Others:

King Cobra(Ophiophagus hannah) 5.5 meters (18 feet)
Keeled rat snake (Ptyas carinatus), at about 3.7 metres (12 feet).
Nile crocodiles (Crocodylus niloticus) 6 metres (20 feet)
American crocodile (C.acutus) 4–5 metres (12–15 feet).
Marine leatherback sea turtle (D.coriacea) 2.7 metres (9 feet)
Galápagos tortoise (Geochelone nigra) 255 kg (560 pounds).
Komodo dragon (Varanus komodoensis) 3 metres (10 feet)
Green iguana (I. iguana) 2 metres (7 feet)

Green Anaconda http://www.wallshq.com/wp-content/uploads/main/2013_01/green_anaconda-wide.jpg
Green Anaconda

Amphibians:
According to Wikipedia:

"The Chinese giant salamander (Andrias davidianus) is the largest
  salamander and largest amphibian in the world, reaching a length of
  180 cm (5.9 ft), although it rarely—if ever—reaches that size today"

Others:

West African goliath frog, 30 cm (12 inches) 3.3 kg (7.3 pounds)
Caecilia thompsoni 1.5 metres (5 feet)
Axolotl(Ambystoma mexicanum) 30 cm (12 in)

Chinese giant salamander

African goliath frog

Axolotl (Small 12 inch)
Fish:

West Indian Ocean coelacanth, (Latimeria chalumnae), is 80 kg (176 lb), and they can reach up to 2 m (6.5 ft)
African lungfish (Protopterus aethiopicus), 2 m (6.6 ft) and may weigh as much as 50 kg (110 lb)
Ray-finned bony fish (Actinopterygii)
Ocean sunfish (Mola mola) 4.3 m (14 ft) from fin-to-fin, 3.1 m (10 ft) in length
and weighed about 2,300 kg (5,100 lb)
King of herrings or oarfish (Regalecus glesne) 6 m (20 ft)( The longest
known king of herrings, which was hit by a steamship, was measured as 13.7 m (45 ft) long)
Bowfin (Amia calva)  109 centimetres (43 in) in length, and weigh 9.75 kilograms (21.5 lb).
European conger (Conger conger) 3 m (10 ft) and a mass of 110 kg (240 lb)
Lancetfish (Alepisaurus ferox) 2.1 m (7 ft) long and can weigh up to 11 kg (24 lb)
Houndfish (Tylosurus crocodilus) 1.5 m (5 ft) and a weight of 6.35 kg (14.0 lb)
Giant Tigerfish (Hydrocynus goliath) 1.5 m (5 ft) and 50 kg (110 lb)
Golden Dorado (Salminus brasiliensis) 1 m (3.3 ft) in length and weigh 31.4 kg (69 lb)
Tambaqui (Colossoma macropomum) 1 m (3.3 ft) and 32.4 kg (71 lb)
Giant barb (Catlocarpio siamensis) 3 m (10 ft) and a weight of as much as 300 kg (660 lb)
Muskellunge (Esox masquinongy)  1.8 m (6.0 ft) and 45.4 kg (100 lb)
Atlantic tarpon (Megalops atlanticus) 161 kg (350 lb) and length is up to 2.5 m (8.2 ft).
The Atlantic cod (Gadus morhua) grows to 2 m (6.7 ft) long and 96 kg (212 lb)
milkfish (Chanos chanos) 22.7 kg (50 lb) and 1.84 m (6.1 ft) long
Electric eel (Electrophorus electricus) 2 m (6 ft 7 in) in length, and 20 kg (44 lb)
Opah (Lampris guttatus) 2 m (6.6 ft) in length and weigh up to 270 kg (600 lb)

Source: http://en.wikipedia.org/wiki/List_of_largest_fish
Source: Britannica.com

Mola mola

Oarfish

West Indian Ocean coelacanth

Bowfin

wow great answer bro really elaborate , to the point and deep answer

@Nick_Tsaftaridis: Can you mark as answer if it is correct?


text:
What is the name of this flower? The photo was taken in the Okanagan Valley, British Columbia
This little flower was growing on dry ranchland in Kelowna, it flowered in April:

Looks a lot like Claytonia lanceolata

Yes it is.rundown


text:
How does a metronome help in controlling breathing rate?
I'm new to the Bio/Medical field so kindly bear with me. I am doing studies on volunteers to formulate algorithms for evaluating Respiration rate from ECG and accelerometer data. I learned about this device when I read this paper. I'd like to know how exactly the metronome device helps in controlling the breathing rate, how is it to be used and precautions to be taken?

The paper in question used metronome to aid test subjects control their breathing rate. This seems like a good approach, much better, than asking "please, breath with 0.1Hz frequency".

The subjects were asked to remain at rest in a supine position for 10 min, and then to control their respiratory rate with the help of a metronome at different breathing rates: 6 (near 0.10 Hz), 10 (near 0.16 Hz) and 16 (near 0.27 Hz) breaths/min.

Metronome is a device that produces any perceivable ticks (sound clicks or, maybe, light flashes can be used) with given and constant frequency. So patients were asked to synchronize their breathing with metronome clicks.
Only precaution in mentioned experiment is that high frequency of breathing can cause voluntary hyperventilation. Or if preset frequency is low and patient is trying to follow it, hypoventilation might occur. Fainting seems among the worst of consequences in both conditions (if person is relatively healthy).


text:
What is the average speed of human sneeze?
I sneeze a lot, at various times and various "volumes", and often wonder about the speed of the sneeze itself, i.e. the speed of the air coming out of the nose while sneezing.
What is the average speed of that, in humans? Are there any records for such a thing?

About 35-40mph
According to the Mythbursters who subjected this to their tests showed that their own sneezes went around 35 to 40mph. This is anecdotal since it only has a sample size of two persons, but it at least gives an indication about the speed of a sneeze.

@Charles depends how the measure the speed, which we don't really know

@Charles sure, but wait a minute, "velocity" is not always "speed". Maybe with such velocity, it reach a final speed of 35-40 mph. Sure they mean actual speed in that article?

It also depends what exactly has been measured. The air moves fastest, the smallest aerosol particulates are a bit slower and larger liquid particulates move slower again.

@Charles not native English speaker, for some reason I confused velocity with acceleration. All clear now, thanks and sorry!

@Charles Fair enough, I upvoted your answer anyways, it provides a much better source than mine.

Yup, the "common belief" vs. "scientific research". Both have value.

@Charles: While I agree with your point regarding the accuracy of Mythbusters' experiments, I feel obliged to add this xkcd link: https://www.xkcd.com/397/

@tonysdg Sometimes it's a shame I'm restrained to only one upvote per post. Yours is one of those occasions.

Results seem to vary wildly depending on the methodology. Charles' article on plos.org seems to be serious, and is very complete. Still, looking at an earlier study of Penn State University published by LiveScience, they measured speeds of up to 200 miles per hour.
See it here: https://www.livescience.com/3686-gross-science-cough-sneeze.html
As mentioned in the article:

"The smaller and lighter particles are less affected by gravity and
  can stay airborne almost indefinitely as they are caught up in and
  dispersed by the room's airflow. [...] Some of [these particles]
  rocket out at speeds greater than 200 miles per hour."

It does not go into details of how the Penn State University experiment was measured, but it clearly shows that you would have to agree on a methodology and which particles' top speed to use to get some consistent results.


text:
How did the cardiovascular system evolve?
How has evolution created our blood, lungs and the heart?
We can't exist without blood, which transports the oxygen to all areas of our body. However, the blood needs a lung, which gives it the oxygen to transport. The blood also needs something which lets it flow through the whole body, which are our veins. And in order to allow the blood to flow through our veins, an organ is needed to pump the blood, which is our heart. We also need a brain which controls all that, and the brain in turn needs the blood in order to function right.
Evolution makes very slow steps....."it just doesn't jump". So, How did evolution manage to create all that?

The systems you mention, the blood, heart, vessels, and lungs exist in partial forms in other organisms. For example, insects have open circulatory systems with primitive blood vessels and a simple heart. Instead of lungs, air is moved through a system of tubes. Earthworms are even simpler, they get their oxygen by diffusion across their skin, but they still have a simple heart and blood vessels. The systems did not simply appear fully formed, but evolved one piece at a time over many millions of years.

But even for those little creatures, with less organs and simpler structure, applies the same thing.
For example the earthworms: in order to allow blood flowing, a heart  and a oxygen input (by diffusion across their skin) is needed. But how did that evolve by one piece after another, when no piece can exist without the other.

this is a complex/broad question... basically asking how did evolution lead to the body as well know it... do you think you could narrow down your question a bit?

Of course: There had to be a jump in the evolution, because, as written above, there are many functions, which can't exist without other functions. So, evolution is taught, that this isn't possible, because the steps are made very slowly.
So my question: how is this possible, or is it even possible if laws or rules of the evolution are considered?

In case of interest: Understanding Evolution by UC Berkeley is a short and free online very introductory course to evolutionary biology.

Aspagus, you contradict yourself: you say that all these systems are interdependent, then you gloss over the fact that worms don't have lungs, and continue to claim that all these systems are interdependent and can't exist without each other. The fact that worms don't have lungs is evidence that the circulatory system does not exhibit irreducible complexity.

user151841, concerning lungs you are right, but I didn't just mean the organ, but the process or the function, which makes all that interdependent.
Because, the system of the earthform still can't be without getting oxygen through the skin.
So, the earthworm can only live, when the blood is flowing.
In order to allow bloodflowing, there have to be a heart, vessels, and, to let the blood carry the oxygen, a function of getting in oxygen.
But now I know a little bit about how this has happened, and that this is clearly possible.

So: All that didn't come at once, there just have been other organs or other "ways in order to bring the body to life" which replaced these functions.
For example: There wasn't always blood which was transported through the body, but other ways in order to maintain the body, which didn't need organs we have today.
I really don't understand everything about it, but all answers gave me "a picture" of it.

@asparagus A good course in comparative anatomy will show you all the intermediate forms you are looking for. Try Kardong's Vertebrates.

@asparagus A closed circuit (blood vessels) is not essential to a circulatory system (see open circulatory systems). Nor does a pump require a circulatory system to work effectively (see flatworms), but it does need one to work efficiently. The circulatory system isn't even IC...its just that each part works so much more efficiently with the other parts...

Makes me want to create a breadboard-type kit that allows for incrementally adding, and later obsoleting, components so that there is continually increasing complexity and capability. It could help illustrate things in a very testable, repeatable manner. New components would have only incremental improvements.

@asparagus "Because, the system of the earthform still can't be without getting oxygen through the skin." The key to a surprising amount of what our bodies do is diffusion. I.e. molecules just... moving around like they do. That's how oxygen gets through the earthworm's skin, and it's also how oxygen gets from our lungs into our blood. Most of our super-complex organs are, when all is said and done, about making diffusion more efficient. Understand that it's all diffusion and you go a ways to understanding how the cardiovascular and digestive systems could have evolved.

While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics.
Have a look at the heart (or more accurately, the hearts) of the earthworm:
They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.
Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.
So, the worm has a simpler system (no chambered heart, no lungs) that works.
All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart:
which is a more sophisticated pumping vessel with two chambers.
Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:

So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems.

the evolution of the human heart from simpler, working system How did this simpler system appeared? the information is readily out there Can you please share some links to that pages?

@A.L Sure! Here is a graphic of the evolution of lungs: http://images.slideplayer.com/13/4156687/slides/slide_2.jpg To get this, I just did a google image search for "evolution of the lungs".  For the evolution of actual bloodtubes from non-tube systems, it's a little more tricky. You could start at this page: https://en.wikipedia.org/wiki/Flatworm#Distinguishing_features see the "more advanced bilaterans" column

This kind of question was raised in a book called "Darwin's Black Box" by Michael Behe, who is a biochemistry professor in the U.S. - he calls this 'irreducible complexity' (IC). For example, the blood clotting cascade system where you have a large number of components that are all apparently essential for the process.
Now I have to say I find the idea that this is a problem very unconvincing, to say the least. However, it's a reasonable question to ask; how does a system of interdependent elements evolve, if we assume that no part can change gradually without the whole system breaking?
There are - at least - two major problems with this. Firstly, the assumption that you can't change any part of such a system has mostly turned out to be false. Secondly, systems would obviously evolve from other, simpler systems which are just as effective.
Say I start out with three elements in my system (three proteins, for example). They are all essential as each requires the other to function properly. Now I introduce another protein to the system and make it dependent on only one of the existing proteins. Is this system IC? No, we can remove the new protein and the whole thing still works. Gradually, we make the other parts of the system dependent on the new protein and suddenly we have an 'IC' system.
In other words, the 'problem' lies in imagining that you have to go from nothing to a complete working mousetrap. What seems more likely is that elements of a system are changed one by one, and that the system evolves through a series of states where you could point to some element and claim that it is essential.
One final point to note is that no multicellular organism is born whole in one step. The processes that an embryo goes through are conceptually similar (though not exactly ) to evolution in that you can have different organs developing at different times, or simpler versions of them that can work together as a simpler system.

To make this a little less abstract, consider the earthworm example given in the top answer. It has just a simple heart(s) and blood vessels - it doesn't seem that difficult, therefore to add in some lungs. Here's a trivial diagram:

The lines here are interactions between the organs - the heart pumps blood through the vessels, and the lungs (if any) oxygenate the blood. We evolve from the simpler system (1) to the more complex system (2) just by adding another element.
However, the difficulty with some systems is that the interactions between the parts are dependencies. A very simple example could be proteins that activate/deactivate other proteins (by phosphorylation, say). Then we could theoretically get a situation like this:

Here, the final system (4) looks like it is 'irreducibly' complex because you can't remove any of (A, B, C, D) without breaking the cycle. However, at each step, we only added or removed one dependency. This also shows the importance of redundancy in biological systems. If you knock out either C or D from system (3) then it still works.

This nearly makes the point of the most convincing argument I've ever heard for evolution. That is, the intermediate steps for the "mousetrap" were simply to make a better paperweight, and the resulting random configuration accidentally worked as a mousetrap. But it still ignores the "required functionality" aspect of the original question. Each of the functions in an IC system is separately required, but each structure is collectively interdependent.

@JedSchaaf Yeah, the mousetrap is a pretty standard metaphor. It may even have been used in Behe's book. I think the key idea is that elements of the system and dependencies within the system can be introduced independently. I see it like a network or graph, where elements are vertices (eg: proteins) and dependencies are edges. I can add a new vertex, then add a new edge, then another edge, and suddenly I have an 'irreducible' system where I can't delete that vertex! Perhaps I should add this to the answer...

If we have a system where A depends on B and C, B depends on A and C, and C depends on A and B, then we could add D that depends on A, but we cannot then make A also depend on D. A might incorporate D into its functionality, but it doesn't depend on it. D could be removed and A would still work.

@JedSchaaf Hmmm. Unfortunately my model is too simple to say what 'depend' really means. I just have some association between two elements (say protein-protein binding) like an undirected edge.

This doesn't answer the question except in the most general, abstracted sense. To someone who doesn't "get it", a mousetrap probably doesn't seem all that complex, compared to the vertebrate cardiovascular system.

@user151841 Fair enough. That's why your answer is much the better one. I still think it is worth addressing the general, abstract sense if only because it's a problem that potentially affects biology at all levels of organisation - including organs. I was going to add a diagram, but maybe I'll save it for when (if) there is the more general question.

This is a good question, but it has a vast scope, as you're talking about the progression of millions of different living animals over hundreds of millions of years, none of which are still alive, so we have to make inferences based on what we observe in their surviving offspring.
That means if you want to learn how 'intermediate' (say, not-quite-lungs, not-quite-heart, not-quite-brain) body systems could function, you'd first need to learn about the biology of lots of other animals.  Not all animals have lungs or hearts or nervous systems.  Not all animals have blood.
More to the point, though, the key factor is that several hundred million years is a really, really, really long time.  It's such a long time that it's well outside any typical human scale of comprehension.  Consider the entirety of your life experience thus far and everything you've seen change.  In comparison to how long the evolutionary process has been operating, your life's span has been on the order of a millisecond out of a day.

Thank you for your great answer!
What I don't understand is, how the evolution managed it to create that all.
Because, the evolution makes very slow steps, so "it just doesn't jump".

The amount of time is irrelevant if there is no method that can show how the changes would have occurred. The fact that other organisms exist with structures that could be called 'intermediate' is also irrelevant for the same reason. Remember, these other organisms also need to have evolved through other 'pre-intermediate' "stages".

I would argue that this is a poor answer for someone who lacks a fundamental understanding of biology and evolution. Truthfully, one can talk about how the cardiovascular system at a simplified, generalized level without learning the biology of lots of other animals.

Simpler forms developed to handle simpler requirements. Take planarians, for instance, which are thin and small enough that they can receive their oxygen supply by diffusion straight through their surface. Now imagine a slightly bigger animal that needs a slightly more sophisticated system to oxygenate their internal regions well. A muscle with an aberrant, autonomous twitch would be enough to stir/circulate more oxygenated fluids through the body. Past that, any little accident that facilitates this (e.g. some cells bind to oxygen a little better, the muscle twitches a little stronger or more regularly, etc.) is another form closer to what we see today.

A good question, indeed, and not easy to answer (or grasp). I'll give a very simplified answer. Bear in mind that the processess I'll describe are REALLY complex.
You have to think way before blood, brains, etc. Billions of years ago, organic molecules were formed in the planet. These organic molecules started to """join""". Millions of years latter, simple cells which didn't even have a nucleus were formed. Some millions of years latter, cells with nucleus started to form. Latter, these cells started to agreggate, turning into colonies of unicellular individuals. In time, these colonies turned into multicellular individuals, but with all cells being equal to one another. After that, cells in one organism started to differentiate into some functions (digestive and neural, for example). Slowly, more complex organisms were formed, as the cells which formed these organisms started to differentiate and form various kinds of tissues, which, through millions of years, developed into more and more complex organisms. Think of Cnidarians, for example. They are very "simple" (I use "simple" as a proxy for "not complex") beings. They have no circulatory system. A circulatory system developed in latter groups: the first, "simple" circulatory system appeared in Nematodeans (if I'm not mistaken). But it was really "simple". With time, other, more complex, circulatory systems started to originate due to various evolutionary pressures. The same applies to every type of cell, tissue or organ you can think about in any organism: complex organisms are the result of millions of years of simpler organisms which generated more complex organisms, by really little steps.
I hope you get the idea of what I'm trying to say. For really grasping all this, you have to study a lot of evolution, because it is a hard concept for us to deeply understand.

you have to study a lot of evolution That's a strange answer, like this is a secret kept by biologists. Can someone that studied evolution write explanations of this concept for everyone?

Well, I didn't express myself correctly. When I said "a lot" I didn't mean that one must have a major in biology. What I think is something like this: suppose one has a class about this topic ("How does evolution creates complexity"). When the class is finished, one might think "Ok, I get the idea", and maybe that person gets the idea, but to really grasp the concept of how evolution creates complexity from simplicity is harder to understand than just by watching a couple of classes. It takes reading and critically thinking. I just wanted to emphasize that.


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Is unihibited exhalation beneficial for someone with a contagious respiratory disease?
If someone has a contagious respiratory disease (I'll refer to as CRD - eg. COVID, FLU, etc.) I'm wondering if the process of exhaling could be beneficial for them.
My first thought is that exhaling would be beneficial because expelling the virus from the lungs (which is the same process that makes it contagious) could lower the viral load in the lungs.  Instead of those virii replicating in their own lungs it would be expelled.  It would seem that wearing a mask in a case where a person has a CRD would be detrimental because the virus would be caught by the mask when they breathe out (which is why masks protect other people) but then could be re-inhaled when they breathe in.)
On the other hand, it could be that for someone to be contagious they would have such a viral excess that the amount they would re-inhale would not be significant.
It is clear that if someone might have a virus and be might be contagious should wear a mask around other people.  The question is, would such a person benefit from not wearing a mask when they are not around other people (in a closed room or car or outside away from people) or would it not make a difference?  For example, I've often seen people driving around in a car by themselves while wearing a mask.  It's not clear to me if this is a harmless practice or is detrimental to them.

Short answer
No, there isn't going to be any benefit to an infected person by allowing them to breathe out virus particles freely. The number of viral particles breathed out is tiny relative to the number captured in a diagnostic swab, which itself is tiny relative to the virus contained in the entire rest of the respiratory tract. Simple exhalation is just not an effective manner of removing virus.
Longer answer
Fabian et al 2008 measured exhaled virus from subjects with influenza.

Concentrations in exhaled breath samples ranged from <48 to 300 influenza virus RNA copies per filter on the positive samples, corresponding to exhaled breath generation rates ranging from <3.2 to 20 influenza virus RNA copies per minute.

Granados et al 2017 estimated viral loads of influenza on the order of 10^5 to 10^8 copies per milliliter, median around 10^6.6 (from 200 microliter extracts of clinical samples).
There are 1440 minutes in a day, if we go from the top end that's 20*1440 = 28800 exhaled particles over an entire day, easily an order of magnitude less than would be picked up by a diagnostic swab and likely a fraction of a percent. That doesn't even account for the fact that a diagnostic swab is itself not taking any sizable fraction of the infected particles in that individual, nor that new particles are being generated throughout the day.
Wanting to confirm a bit, I went to another source. Milton et al 2013 collected particles of two sizes from breath exhalations, as well as swabs from the same subjects. Median swab concentrations were around 10^5 to 10^6 on different days, similar to those from Granados. Virus particles from the coarse and fine exhaled particles were much lower; the peak was in fine particles on the first day with a median over 30 minutes of 610 particles (plus another 23 in the coarse particles), the same as the high end of Fabian.
It is not feasible that these tiny numbers would have any influence on the severity of the infected individual's illness. If it were, you'd be much better off just getting a bunch of respiratory swabs (no, this won't actually work)! It is feasible, however, that these particles go on to infect others, and that's what mask-wearing is trying to avoid.
As far as people alone in cars, likely the main benefit to them is that by keeping their masks on rather than removing them repeatedly, they're avoiding contact between their hands and anything that's ended up on the mask, and avoiding bringing the mask that they'll breathe through into contact with whatever has ended up on their hands.

Fabian, P., McDevitt, J. J., DeHaan, W. H., Fung, R. O., Cowling, B. J., Chan, K. H., ... & Milton, D. K. (2008). Influenza virus in human exhaled breath: an observational study. PloS one, 3(7), e2691.
Granados, A., Peci, A., McGeer, A., & Gubbay, J. B. (2017). Influenza and rhinovirus viral load and disease severity in upper respiratory tract infections. Journal of Clinical Virology, 86, 14-19.
Milton, D. K., Fabian, M. P., Cowling, B. J., Grantham, M. L., & McDevitt, J. J. (2013). Influenza virus aerosols in human exhaled breath: particle size, culturability, and effect of surgical masks. PLoS pathogens, 9(3), e1003205.

Thanks for the great answer.

Based on what you're saying, it seems a comparable analogy would be that when a fire spews out burning ashes, it can start other fires.  But keeping the sparks contained in the original fire is not going to make it burn any stronger.

While I don't doubt your short answer, I'm not sure I follow the long one, either.

@anongoodnurse The short form of the long answer is that the number of viral particles breathed out is tiny relative to the number captured in a simple swab, which itself is tiny relative to the virus contained in the entire rest of the respiratory tract. Simple exhalation is just not an effective manner of removing virus.

Ah, thank you! Senior moment... no, several minutes, there. :-/


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What causes morning wood?
Sometimes men wake up with an erection in the morning. Why does this happen?

Sometimes men wake up with an erection in the morning. Why does this happen?
Shortly speaking: REM (Rapid Eye Movement) is one phase of sleep. During this phase, we dream and some of our neurotransmitters are shut off. This include norepinephrine, which is involved in controlling erections. Norepinephrine prevents blood from entering the penis (preventing the erection). In absence of norepinephrine—during REM phase norepinephrine is absent—blood enters the penis, leading to an erection. This phenomenon is called nocturnal penile tumescence. Such erections typically occur 3 to 5 times a night. A related question concerning similar erections in women can be found here.
High pressure in the bladder may also lead to a "reflex erection". This erection allows for preventing uncontrolled urination. The drawback is that when in the morning one has an erection and can't wait to pee it might get hard to accurately target the toilets!
This video is also a nice and easy source of information on the subject.
Is it bad?
(Reading my "note" below, you have edited your post to get rid of this question, thank you)
It is perfectly healthy you don't have to worry about that. These erections are even thought of as contributing to penile health. At the opposite end of the spectrum, the absence of erections during the nights are an index of Erectile Dysfunction (E.D.).
Note
Be aware that medical questions are often considered off-topic on this site. Asking "is it bad?" turns your question into a medical one. Health-related questions (but not personal health) should be asked on health.SE


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Can oncogenesis happen without apoptosis pathway being affected?
Has there ever been incidences of one or more cancerous cells having all it's cell-death pathways and apoptosis mechanisms intact and functional?

Are any apoptosis mechanisms in a cell that are not functioning or suppressed or damaged a typical sign of a cancerous cell?

Could something be used to cause a mutation in a cancer cell that is 'noticeable' to the immune system?

Usually the cell death mechanisms are overridden and therefore oncogenesis. The pathway components themselves are not mutated. One classical case I can cite is that of Ras-oncogene. See this article for details. Usually the survival/growth signals (MAP-kinase) are activated with simultaneous inactivation of apoptotic regulators (Akt-pathway). A mutation of MAP-kinase component ERK can also cause cancer but apoptosis is nonetheless supressed because of the interconnections of these tow pathways in the gene regulatory network.
Whereas in the case of tumor suppressors, the cause of cancer is genomic instability and failure to initiate apoptosis.

This is pretty unlikely, since one of the most important steps for cancer cells is to shut off apoptosis and proteins which control it (like p53, BCL2 and so on). Cancer cells (especially when they are genetically unstable) acquire so much mutations and misregulations, that these would otherwise trigger apoptosis which would result in the removal of the cell.
This can look like the following (figure taken from here), when you compare normal and cancer cell:

quite a complete figure.. i like it..

Thanks. It is a slightly different perspective to your figure.

Does a pre-cancerous cell shut off apoptosis and the proteins that control it before it becomes a cancer cell or is it the case a cancer cell shuts off apoptosis mechanisms after it is already cancerous?

Usually apoptosis is affected in a later stage of oncogenesis. However, in case of DNA damage induced oncogenesis, there is a failure to initiate apoptosis when the DNA is damaged and not repaired. In this case the signal has not yet reached the apoptotic pathway. This ensues genomic instability which may further lead to uncontrolled growth i.e cancer (as you can imagine, to grow and multiply maximally is the first instinct of any lifeform)

Is there some way to detect if a cells apoptosis mechanisms have been shut down or made to malfunction? If so could this be a way to detect if a cell is cancerous?

@user128932 You could do a genome analysis and search for inactivating mutations. Since there is more than one way to activated apoptosis, this usually happens only in cells which have already gone down the cancer path.

Is there a less involved method then genome analysis to see if a cell has had its apoptosis mechanisms 'turned off'? If cancer cells are immortal-like can they withstand many types of viruses or harmful bacteria or phagocytes?

If a cell sample has only cells with no apoptosis mechanisms but it has not been determined if they are cancerous ; if some process can induce cellular growth that would not occur if the cells were not cancerous would this show this cell culture has no apoptosis mechanisms?

Can a cell with no apoptosis mechanism spontaneously reproduce in conditions it shouldn't be able?

@user128932 Sorry, but I don't understand your last question. You want to know if cells without apoptosis can divide?

My question on Nov 2 at 3:48 ; yes , can a cell without any apoptosis mechanisms divide , given it is in a 'situation'(possibly artificially induced) were it shouldn't be able to divide?

Again, cancer cells are an example. Disabled apoptosis is not uncommon, this mechanism is used to evade apoptosis.

If a cell has a lot of mutations yet it can still function would this make any apoptosis mechanism not 'work'?

This depends on the specific mutation itself.

So some types of mutated cells can still have all its apoptosis mechanisms working? What kind of mutation can cause an apoptosis mechanism to malfunction?

@201044 Can you please stop asking questions in the comments and open a new question instead?

@201044 First: Perpetual questions in the comments are not liked. Then: You ask questions, so you need to decide if you want to know more or not. I am not going to open a question for this.

I don't repeat the same question over and over again; that would be a perpetual question. Why argue about 'meta-biology' stack exchange issues  or other syntax or 'administrative' issues when I have asked relevant questions even in the comments. If this bother's you people just ignore it. Don't make a separate issue out of it.

The original question was ; have there been  any examples of active cancer cells with an apoptosis mechanism that is functioning?


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Where is ATP used in Phosphorylation?
In the section describing the Calvin Cycle, under the subheading "Reduction",  my textbook states that:

The steps involve utilisation of 2 molecules of ATP for Phosphorylation...

I could not get where is ATP used in Phosphorylation (ATP synthesis by cells)? Please help me to understand.

This is a homework question. Even though you got your answer, please put in some effort on your part before asking a question. It is a good practice for everyone.

In biology phosphorylation marks the addition of inorganic phosphate groups to proteins or other organic molecules. The phospho-group usually comes from ATP which is converted into ADP in this process.
In the context of the Calvin Cycle there are two positions where molecules get phosphorylated. The first is the phosphorylation of 3-phosphogylcerate to 1,3-bisphosphoglyerate, the other is the phosphorylation of Ribulose 5-phosphate to Ribulose 1,5-bisphosphate.
See the image (from here):

Thanks for the help! so is it incorrect to say that phosphorylation is synthesis of ATP (since you said that the ATP is converted into ADP in this process)?

Yes, this is incorrect. Synthesis of ATP is usually referred to as "ATP synthesis".

@Abdullah, perhaps your confusion about the meaning of 'phosphorylation' in relation to ATP synthesis is because you may have previously learned of a process called 'oxidative phosphorylation' (sometimes abbreviated to OxPhos, or similar) that occurs downstream of the Kreb's Cycle--and is a mechanism cells use to synthesize ATP? Just a thought. The typical and predominant usage in lectures, textbooks, and papers is in Chris's answer that you accepted. The acid anhydride ATP donates its gamma phosphate to some other molecule in a reaction catalyzed by an enzyme.

Also substrate level phosphorylation…


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Can you please identify these yellow dot parasites which grow on non-living surface?
Little yellow dot parasites have screwed me for years and I still don't know how to fight back as I don't know what they are. I just know that they are living beings because they grow in number.
Images:

(Click the images to enlarge)
Location: North India
Size: Visible to naked eyes (one dot is approx 0.25 mm in diameter; their colony is upto 5 mm in length or diameter; their colonies aren't perfect circles as seen in the images)
Behavior: They grow on any plastic, metal and glass surfaces (but not on clothes, walls or wood) if they are stored in open (the surface is in contact with oxygen)
Can you please identify it?

' I just know that they are living beings because they grow in number' How do they react when exposed to a biozide (Triclosan, Zink-Pyrithion etc..)?

@iLuvLogix Never tried.

This looks like the work of an insect, perhaps a fly.
You can check by experimentation.
Try covering part of one surface with a fly-proof covering.
Take photos at weekly intervals of exactly the same area, compare images.
black-and-white images below from
Forensic Science International 137 (2003) 152–159
"Distinction of bloodstain patterns from fly artifacts"
Mark Beneckea, Larry Barksdale
DOI: 10.1016/j.forsciint.2003.07.012
Bar on images is 1cm

Can you expand on the reasoning behind your conclusion?