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A tree that's making quiet "creaking" sounds, and stops when I tap it...insects?
So I have a very dead tree (not a biologist, so this just means "no leaves when the trees around it do have leaves"), and I noticed when I stand close to it I can actually hear a "creaking" sound - I recorded a video:
https://www.dropbox.com/s/a3ojwzje1ui6phh/PXL_20230514_235204506.mp4?dl=0
It's a little hard to hear, but I think it's distinct enough. Regular, consistent. And....when I tap the tree, it stops for a moment! (I do this at about 0:16 in the video.) And, if you wait long enough, it starts again! (This is around 1:13 in the video.)
I tried to shoot various parts of the tree - there is damage that I think is Woodpecker, and also some damage that looks like insects....could this be insects? I've read that dry conditions can cause a tree to creak, but not only is it not that dry here, but the tree is very dead!
Anyone have any idea what this sound is?

When our southern pines die; borers get into them quickly and are relatively loud  ( in a quiet forest). .Tapping the tree will stop them briefly.

@blacksmith37, ah and https://entomology.ca.uky.edu/ef437 says "the most obvious symptoms [...] These include [...] holes in the bark that exude sawdust or pitch", that might actually be what you see in the video.


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Is there a cellular mechanism that detects Ribosomal damage?
What kinds of options, if any, do cells (Eukary and Prokary) have for detecting, and repairing damage in Ribosomes (of all types)? I am curious as to
what happens when a cell sustains damage of some form, such as radiation, and the Ribosomes are damaged.

I think you should check rRNA synthesis regulation: http://www.nature.com/cdd/journal/v20/n11/images/cdd2013107f1.jpg . So it seems to be regulated by sensing stress and not the ribosome damage directly. Another possible mechanism to measure the mRNA synthesis rate and if it is too high, then build a new ribosome. Maybe there is something like that too in the background, I don't know, interesting question.

I'm unaware of any repair mechanisms. Damaged proteins and RNA are usually dealt with by degradation.

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What is this dried animal for sale?
I found this image on the Internet, which features an African youngster holding up an animal for sale to a potential customer sitting inside a car. It appears to be some sort of dried and disemboweled animal.

What is the identity of the animal?

Looks like bat !

I'd guess it's a primate, or a big rodent.

@Dexter Definitely not a bat. It may be cane rat but I am not sure.

The boy is holding a couple of smoked/barbecued cane rats, also known as "grasscutters".  These are commonly hunted as bushmeat in West and Central Africa and have recently been farmed as well.
You can see some similar photos here:

http://members.virtualtourist.com/m/p/m/178963/
http://westafricaadventure.blogspot.com/2011_04_03_archive.html
http://www.fionaleonard.net/2012/04/rodents-of-unusual-size.html
http://2summers.net/2015/01/23/pop-up-travel-cane-rats-in-ghana/

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Was this snake behaving abnormally?
This morning, I walked out front of my house to find a medium-sized snake balled up on my driveway beneath my motorcycle. I spotted it from my porch so I didn't walk any closer. I believe it was a Texas rat snake.
I've seen a few snakes in my area but none really up close, so I watched it curiously for a few minutes. It seemed to be acting oddly - its head was tightly bent sideways at its "neck," and it was slowly coiling and writhing while opening and closing its mouth. It didn't seem very alert.
Then, a friendly neighborhood cat began batting at the snake's head, and while the snake was not acting aggressively, it did haphazardly snap back in self-defense a couple of times.
I (subjectively) assumed that the snake was injured or otherwise "done for," so I ended up moving it into the street with a long pole and crushing its head with a large rock. I had taken its lack of objection to agitation with the pole as another sign of distress.
I really don't like killing other creatures. In retrospect, maybe I could have handled the situation differently, maybe by capturing the snake and releasing it somewhere else. At the time, for whatever reason it seemed like it was suffering and I felt like I was doing it a favor, as well as potentially saving some local pets from injury.
Moral questions aside, does it sound like this snake was in fact behaving abnormally? Are the actions I described typical of a distressed snake (at least of this species), are there other plausible explanations, or is it unclear? I can elaborate if there are any specific questions.

You shouldn't have killed it. From my point of view, never kill a critter unless it is 100% obvious it is going to die. I killed a pigeon once after it crash-landed into our window. It was crippled and didn't move for a day. We had a cat too and I decided to kill it. In your case it wasn't obvious why the snake behaved the way it did and I would have let it live and relocate it. Others may disagree with me. I vote to close because it is opinion based and an ethical question. +1 because I admire your thoughtfulness.

Thanks @AliceD - I appreciate your point of view. I was hoping to frame the question in a more objective way, so maybe I should downplay the moral uncertainty and update it to something more answerable like "what kind of behavior was this snake exhibiting?"

That sounds like a great edit. if you do so, please ping me @AliceD and I'll remove the vote. Thanks and good luck! Would've loved to see that snake :)

Thanks @AliceD - question updated. Yeah, I really feel bad about it now. It was a beautiful snake. That may be the only non-insect creature I've ever killed, at least intentionally. At least I know to stop and think harder about alternatives next time.

No worries, I slightly edited and formatted the question to make it more information dense.

Not an answer because I can't be sure, but I've seen this behaviour in snakes that have taken a hit from a car etc. It usually means the backbone is injured/broken. I suspect you did the snake a favour.


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Is it biologically possible for an adult's eye color to change?
Can it be that the adult eye can change color? Specifically my question is about a unilateral color change, such that the color of one eye remains constant, while the other changes color over time. Can this happen? Or can it be related to light-scattering, or an illusion of some sort?

At any rate, personal medical questions are off-topic on Biology.SE. Please consult a medical professional for your particular situation.

Short answer: The genes that encode eye color do not change, but the pigments in the eye can change due to external factors like diseases of medication.
Long answer: Yes, it is possible that the eye color of adults can change, and it can also only happen to one eye. It is then called Heterochromia. There are two possibilities for different colored eyes, either congenitial (genetic) or acquired. Since you ask only for eye color changes in adults, we can skip here the genetic reasons, as these show up in kids already. If you are interested in them, have a look into the Wikipedia article on Heterochromia.
The basis for our eye color is genetically determined, changes can later occur due to diseases (so if one experiences a change in eye color, it is always a good idea to consult a doctor) and also due to medications.
The eye undergoing a change in pigmentation can either lighten up or darken.
Fuchs’ Heterochromic iridocyclitis: (also known as Fuchs’ Heterochromic uveitis) The change is caused by an eye infection with different microorganisms like Toxoplasma gondii, Herpes simplex virus or Rubella (an probably others) but it can also have an autoimmune pathology. See reference 1 and 2 for more details.
Horner's Syndrome: This is a syndrome which mostly occurs in kids after damages to some nerves. This can lead to insufficient signals towards the pigment production and heterochromia. Rarely this can occur also in adults, where this is called acquired Horner's syndrome, see reference 3 for details.
Pigmentary Glaucoma: In this disease (also known as Pigment dispersion syndrome) pigment cells from the back of the iris float are seperated from the original place and float through the aqueous humor of the eye where they can produce pigment which over time changes the appearance of the eye. See reference 4 for more details.
Medications: Some of the medications against glaucoma (the prostaglandins latanoprost and bimatoprost) can cause a deeper pigmentation which will not always diminish after the end of the treatment. See reference 5 for more details.
Cancers: Some cancers as melanoma can also cause heterochromia, either when they are darker pigmented that the eye or when they are not pigmented. In both cases they influence the eye color. See reference 6 for more details.
References:

Fuchs' heterochromic cyclitis: review of the literature on the
pathogenetic mechanisms.
Associations of Fuchs heterochromic iridocyclitis in a South Indian
patient population
Acquired Heterochromia with Horner's Syndrome in Two Adults
Pigment dispersion syndrome and pigmentary glaucoma – a major review
Incidence of iris colour change in latanoprost treated eyes
Diffuse iris melanoma: Report of a case with review of the
literature

tl;dr The genes that encode eye color cannot change, but the pigments can change due to environmental factors like medicines or disease.

Short answer: Yes. :-)

you think my summary is worth editing to the top of your answer? I don't have the rep for that

I can do that, probably not a bad idea.

It should be noted that the opposite can also occur in an acquired manner: one iris can become paler.

To add what the previous answer did not: not only medicines and disease change the color of your eyes. Aging does that too in most (if not all!) people. Pigmentation is usually lightest in utero and right after birth. Melanin accumulates over time and makes the hair and eyes darker.
This is why many people are born blond (or green/blue-eyed) and become brunette (or brown-eyed) over a period in their lives. It can take days - usually as a baby - or decades, depending on the individual. The rate is determined genetically, i.e. it does not, for instance, depend on how much exposure to the sun you get. Melanin in the skin can do that.

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Does pupil size affect image focus in persons with no lens?
If an individual has no lens like Claude Monet (who had them removed).
They should be able to still focus the images they see in a well light area if they shrink their pupils to a very small size like the Moken people right?
But they won't be able to see well at all in dim light, as focusing would require them to dilate their pupils which would make everything  very blurred.
Is this right?

This is right. People with slightly defective eyesight (like me) often don't need glasses or lenses under very bright conditions, but vision blurs when it gets darker. Chris' answer nicely explains why this is the case.

PS: A nice analogy comes from photography: With a high f-stop (= small pupil size) the photo will have a high depth of field, i.e. you don't need to focus a lot, whereas a photo at low f-stops (= wide open pupil) requires careful focussing to display an object sharply.

Very nice question! You are right, in that small pupils will help to reduce the blurriness of vision caused by refractive errors.
Removal of the lens (aphakia) results in farsightedness. It is caused by a focus point that falls behind the retina as the absence of the lens prevents focusing of the image, causing a blurred image. The amount of blur is proportional to the pupil size (Colichia et al., 2008). See their figure 2 below:.
In the upper part you see a hyperopic eye, which has a lens that cannot accommodate sufficiently, comparable to an aphakic eye. the bottom part shows the result of when a pinhole is applied, namely a reduction of the blurred circle and improvement of the focus. This could also be achieved by having very small pupils such as when ambient light is very bright (and a characteristic of the Moken peoples when diving (Gislén et al., 2003). And indeed, under conditions of low lighting the pupil size will increase and hence blurring will be worse.


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What exactly is the neural receptive field?
Neural receptive fields map the spatial or temporal distribution of the data to individual neuron excitation, if I understand correctly, but I do not understand if receptive fields (especially in the higher cognitive areas such as the various layers of the visual cortex, etc.) are:

Actual structural distributions of neurons that help map specific spatial or temporal properties of stimuli (such as concentric arrangement for contrast detection, rectangular arrangement for orientation detection, or movement detection, etc.), or,
Merely a mapping of the structure of the stimuli that can excite specific neurons.

If it's the latter, isn't it basically as simple as a pattern/feature/vector that individual neurons are sensitive to?

No, it is not 1. the structural distribution of the neurons themselves.  If by mapping you mean a kind of function that maps real space to cognitive space (or such) then it is not that either (at least, not explicitly/directly).
The receptive field is the region of 3D space in which sensory neurons can make their relevant detection.  It's not a pattern/feature/vector, just the coordinates defining some spatial region itself.
For example, take the neurons making up your audio sensory system.  If an object is making noise and you can hear it, then that object is within the receptive field of the hair cells responsible for the audible frequencies.  That is, the object's physical location is within the spatial coordinates that define your audio system's perceptive field.
Fun fact: for two sounds of the same amplitude, lower frequency detecting hair cells tend to have a larger receptive field since lower frequency signals travel farther.  In other words, the receptive field is somewhat dependent on the quality of the source of perception, not just the sensory neurons.
It's strange terminology coming from physics, because we generally define "fields" by sources, not by receivers.  An audio source has an unambiguous "field" of acoustic radiation.  A receiver does not generate a field but is sensitive to a certain threshold of field quantity.  So to define the field as something coming from the receivers (the sensory neurons) is an unintuitive idea.

I think I'm understanding this, but just to make sure I grasp the implications. There are studies that map specific shapes and orientation of receptive fields to excitation/inhibition of specific neurons. Does this mean there's a running thery that specific neuronal clusters are "programmed" (or have evolved) to detect stimuli from specific receptive fields within the field of view (in case of vision) of an organism? For example, upper, lower hemisphere. Rectangle oriented at 30 degrees, etc. Reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1987328/#!po=14.0000

I think that's kind of a philosophical question. "Evolved to" and "programmed" have a really goal-directed connotation to them.  Maybe you mean "selected for".  I don't know the evolutionary evidence for selective pressures on receptive fields.  Intuitively, you'd think that the strategies animals adopt using their available hardware is somehow selected for, but in some cases it could just be consequence of another adaptation that happens to be useful, couldn't it?  I think this is a new question you should submit formally and allow evolutionary scientists to answer.

I think is closer to 2. It is the subset of sensory space that elicits a reaction in a given neural population.
So you should:

Pick your neural population. Usually it is a single neuron (but can be easily extrapolated to bigger populations). It may be a sensory neuron, or a neuron in a higher processing region.
Determine your sensory space. That is, you should decide the kind of stimuli you'll be dealing with. For example, not only "visual stimuli", but you should identify the parameters, or independent variables, you will vary in your experiment.
Define a criterion to discriminate between reaction and non-reaction. This implies to choose what is the dependent variable in your study (for example neuron firing rate). Then you could define what features in the relation $\frac{dependent\:variables}{independent\:variables}$ you will search for. That is the tuning curve (which well may be a high dimensional curve).
Perform your experiment and analyze your curve. The region of parameters (independent variables) whose reaction goes above threshold according to your criterion is the receptive field. Sometimes is not trivial to define such a criterion (see: http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0040092)

A good general reference is the article in Scholarpedia: http://www.scholarpedia.org/article/Receptive_field
This type of analysis is very useful for position coding, that is, when you expect that the activation of a specific region in the brain correlates to stimuli in a region of sensory space. But sometimes things are more complicated (e.g Olfactory coding http://www.jneurosci.org/content/30/27/9017.full).

Stick a probe in your neuron-of-interest. Now stimulate the organisms in some way.
All the stimuli that make your neuron fire are the neuron's receptive field.
Example 1:
You probe a neuron in the primary sensory cortex of a human subject. Next, you stimulate the patient with light touch to their skin. Let's say you find that the neuron only fires when you stimulate the right thumb. Thus, light touch to the right thumb is that neuron's receptive field. The neuron doesn't fire to light touch to any other part of the body.
Example 2:
You probe a neuron in the primary auditory ganglion. Next you stimulate the patient with different sound frequencies. The neuron only fires at only a narrow band of sound frequencies. The receptive field of that neuron is that specific band of sound frequencies.


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Agglutination test using antibodies

Agglutination test
Latex agglutination using bound antigens : by coating soluble (non - particulate ) antigens on to microscopic latex spheres, their reaction with a particular antibody can be visualized.
Haemagglutination : red blood cells can be used as agglutinating particles.

What are non-particulate antigens ? Why are they used instead of particulate ones ?
How are red blood cells used as agglutinating particles ?

If you have an antibody that is directed against, for example, a bacterial surface protein, then by mixing the bacterial cells with the antibody at a suitable stoichiometry you could observe clumping of the cells as the antibody molecules essentially cross link the cells together. This would be an example of using an agglutination (clumping) assay with a particulate antigen. You can also probably see why it is important that each cell (particle) carries many copies of the antigen for cross linking to take place effectively.
If, however, the antibody of interest is directed against a soluble protein, then mixtures of antigen and antibody are less likely to form cross-linked complexes, although it can happen and can be used for example in the Ouchterlony technique. If you want to use an agglutination test (i.e clumping of particles) with a soluble antigen then you can achieve this by attaching multiple copies of the antigen to macroscopic particles. This is what is being described in the definition of Latex agglutination in your question.
I imagine that there are ways of attaching a soluble antigen to red blood cells (e.g. by chemical cross-linking to the red blood cell surface) in which case you could observe clumping of the red blood cells when you added your antibody.

From your answer,I infer that particulate antigens are those that are attached to a particle.

A particulate antigen is any antigen that is associated with a macroscopic entity (cell, synthetic particle) when it is encountered by an element of the immune system.


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What determines the size and shape of a cell?
What determines the size and shape of a cell? They differ at different tissues / organs/ species

Can you add some specifics to your question? Have you done any previous research, and are you particularly interested in a certain type of cells (eg bacteria, plant, animal tissue etc)?

Can confirm, this is the exact question that motivates my research interests, and I can tell you that even now this is far from a settled question, in pretty much any organism.

This is quite a hard to answer question.
There are different cell cycle molecules that, if mutated or knocked out, have shown to cause the cell to have a different shape or "overgrow" in size or not grow at all...
You might find some insight here.
There are lots of factors that influence cell size and shape, thus it is a very complex system to study. For example, cell shape is influenced by the cytoskeleton but also other factors.


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Mechanism behind negative conductance of ion channels
I am struggling to understand negative conductance shown on I-V curves on ion channels. Mechanistically, negative conductance means that inward (or outward) current increases when voltage across membrane decreases. I-V curves of such a channel have both positive and negative slopes. How it is achieved by ion-channels?
For example, this is in addition to the example posted in the answer by aandreev.

Thanks for the question. I am afraid I do not entirely get your question. How is what achieved? Or specifically, where does "it" refer to in your concluding sentence?

@AliceD. Sorry for the confusion. I've made some edits. A figure added to question shows one mechanism by which negative conductance is obtained.

With this figure you cannot really say with surety that slope reverses direction.  More replicates and data points are required to prove that.

This is the figure OP talks about:

Negative Conductance Caused by Entry of Sodium and Cesium Ions into the Potassium Channels of Squid Axons, Francisco Bezanill, Clay M. Armstrong (1972).
Short answer is that in non-linear mode of ion channel operation other ions start passing through it (channel loses specificity). Cumulative effect (because of different concentrations of different ions) is negative total conductance, if you don't measure currents of specific ions.

The experiment described in the linked article Bazanilla & Armstrong (1972) is about a voltage clamp experiment in squid axon. Voltage clamping basically means that the potential difference across the axonal membrane can be set at will by an external artificial electronic power source.
NMDA receptors are channels that conduct positively charged ions (mainly Na+). If the voltage is clamped at negative potentials under physiological conditions, positive current will be drawn inward. This is generally plotted as a negative current, as shown in your picture in your post. If, however, the voltage is made more positive, current will reverse at a certain point, and positive currents will be measured by the electrodes. This positive current is characterized by an outward flow of positive ions through the NMDA receptor.
The sign of the current is arbitrary, but the most important point to make is that most channels allow current to pass both ways. There are rectifier channels, however, that will only allow one-way traffic. Rectifiers are more exceptions than the rule.
Linked reference
- Bazanilla & Armstrong, J Gen Physiol (1972); 60: 588-608


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Dopamine paradox in schizophrenia
If there is more dopamine action in the mesocortical pathway in schizophrenia, then schizophrenics should always be in euphoric state. Instead, schizophrenics often lack motivation and do not experience pleasure. Why?

Can you provide a reference?

I'm no expert, which is why this isn't an answer, but it may have to do with receptor down-regulation, or an altering of receptor signaling.

Short answer
The dopamine (DA) hypothesis suggests that excessive DA transmission in the mesolimbic pathway in schizophrenia leads to hallucinations and other positive symptoms. It explains the negative symptoms of schizophrenia (flattened affect, reduced motivation) by reduced DA activity in the mesocortical pathway affecting the frontal cortical regions.
Background
You are referring to the dopamine hypothesis of schizophrenia.
The initial dopamine (DA) hypothesis focused primarily on the positive symptoms of schizophrenia, namely the active psychoses, which includes periods of hallucinations and delusions. These effects can be attributed to hyperactivity in subcortical dopaminergic pathways. Specifically, excessive subcortical release of dopamine is thought to increase D2 receptor activation, disturbing the cortical pathway through the nucleus accumbens (Brisch et al., 2014), called the mesolimbic pathway (Fig. 1). These positive effects can be treated quite effectively with the classical, first-generation anti-dopaminergic antipsychotics such as haloperidol and chlorpromazine.
However, there is another important aspect on schizophrenia, which are the negative symptoms. While the full-blown psychoses occur in waves, these negative symptoms are a more continuous and persistent phenomenon. The symptoms include a flattened affect and dysphoria (reduced pleasure in life). These symptoms are thought to occur due to altered prefrontal cortex (PFC) functioning. Specifically, they are thought to be induced by hypoactivity in dopaminergic D1 transmission (Brisch et al., 2014) in the mesocortical pathway (Fig. 1).

Fig. 1. The dopamine pathways in the brain, including the mesolimbic and mesocortical pathway, implicated in the positive and negative symptoms of schizophrenia, respectively. source: Wikipedia.
These two sides of schizophrenia point to an imbalance in DA activity in the brain, namely hyperactive subcortical mesolimbic D2 activity leading to positive symptoms, and hypoactive mesocortical D1 activity in the PFC resulting in negative symptoms. This imbalance hypothesis is the revised DA hypothesis and it is still an accepted working model (Brisch et al., 2014).
However, as noted by others, schizophrenia is a complex disease and it is thought that besides DA, also serotonin, glutamate and GABA play a role (Olijslagers et al., 2006). The current first line of treatment of schizophrenia are atypical neuroleptics, such as Clozapine. Clozapine is a selective monoaminergic antagonist with high affinity for the serotonin Type 2 (5HT2), dopamine Type 2 (D2), 1 and 2 adrenergic, and H1 histaminergic receptors. Clozapine acts as an antagonist at other receptors, but with lower potency. The broad effects of Clozapine are thought to underlie its potent antipsychotic therapeutic effect. It is believed it mainly works through a combination of antagonistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex. D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms.
References
- Brisch et al., Front Psychiatry (2014); 5: 47
- Olijslagers et al., Curr Neuropharmacol (2006); 4(1): 59–68


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Persistency of botulinum toxin in environment
There is information about decontamination times here on pages 6 and 7. My specific question is how persistent botulinum toxin is in a natural environment, or alternatively, what is the half life of this toxin?

I think you shoudld narrow down the scope by asking about specific biotoxins or groups of toxins. From what I know, persistency can vary dramatically between groups and types of toxins.


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How do diving marine mammals avoid decompression sickness?
How do marine mammals, whose very survival depends on regular diving, manage to avoid decompression sickness or "the bends?" Do they, indeed, avoid it?

I think I got the answer....

The primary anatomical adaptations for pressure of a deep-diving mammal such as the sperm whale center on air-containing spaces and the prevention of tissue barotrauma. Air cavities, when present, are lined with venous plexuses, which are thought to fill at depth, obliterate the air space, and prevent "the squeeze." The lungs collapse, which prevents lung rupture and (important with regard to physiology) blocks gas exchange in the lung. Lack of nitrogen absorption at depth prevents the development of nitrogen narcosis and decompression sickness.

Source: Scientific American

Could you please add some references to your answer?

@MattDMo , of course....just check out this article to get an idea..        http://www.scientificamerican.com/article/how-do-deep-diving-sea-cr/                                                                               & for detailed study go through this...                    http://rspb.royalsocietypublishing.org/content/early/2011/12/15/rspb.2011.2088.full

I concur with @souvik.bhattacharya but I wish to elaborate on it. The lung collapse indeed stops gas exchange in marine mammals by keeping the air away from the lung tissue that normally exchanges O2, CO2 and N2. Build up of N2 results in the bends after the pressure drops when re-surfacing (McDonald & Ponganis, 2012). However, a study by Hooker et al. (2012) showed that beached whales, dolphins and seals did show signs of bubble formation in the internal organs, which was linked to exposure to noise and sonar, or other factors such as cold water that may disrupt the functionality of preventive measures such as the lung collapse. So to get back to your question - Yes they avoid it by lung collapse, but under certain conditions this mechanism may fail.


text:
How to determine externally that a whale is a mammal?
Mammals have external qualifying characteristics like body hair, ear pinna, etc. But a whale has none of that. So, can it be identified as a mammal just by external observations?

Whales and dolphins have a few hairs on their snout that they usually shed just after birth, in addition to the warm-blooded thing and the live birth and the milk.

@JeremyKemball Only milk and hairs make them mammals. Warm-blooded and live birth are present outside of mammals.

Whales dont have gills.

@biogirl , I said 'external characteristics"...

Gills can easily be seen in a fish

A whale has a horizontal tail fin which is a typical feature of mammalian marine animals see link. Mammalian sea animals typically have a vertical movement of the tail fin for swimming. Fishes like sharks have a vertically oriented tail fin and move it side-ways for locomotion.

This is the answer. +1

Identification of an organism to a taxonomic rank (Class Mammalia) is not based only on morphological characteristics. It is a function of all characteristics that members of that rank share to the exclusion of others. Mammals have multiple features that have been mentioned before (the obvious ones are milk and hair) that they all share that are not present in other taxa. If you only based identification on external morphology you would risk grouping organisms based on convergent evolution (e.g., bats and birds would be in the same taxa).


text:
What are the mechanistics of stinging nettles?
There is a lot of research on why nettle extracts causes skin irritation and a stinging sensation. However, I cannot find information on how the extract is injected in human skin. Similarly, I haven't been able to find information on  how the pressure is built up in the trichome, nor how the silica tip is inserted in the skin.
Suggestions for articles or books on this topic are welcomed.

Does this answer your question, or is it too unspecific: Wikipedia: Stinging plant?

sorry..but it's too unspecific....but thnx...neways...

The stinging hairs (trichomes) of the common North American nettle (Urtica dioica) are sharp, pointed cells. These nucleated cells are embedded in a base of smaller epidermal cells. The shaft of the trichome is composed of silica. Upon touch, the tip breaks off, leaving a sharp tip similar to a hypodermic needle. The hollow trichome penetrates the skin, and toxin from the base is injected into the skin tissue. The stinging toxin includes a mixture of histamine, acetylcholine and 5-hydroxytryptamine (Online Textbook of Natural History).

Left: schematic of a stinging cell, or trichome of a nettle. Right: trichomes on the stem of Hesperocnide tenella. Source: Online Textbook of Natural History
I couldn't find any info on trichome pressure. It may be that the toxins are released passively. Otherwise, high concentrations of dissolved matter may attract water in the base, increasing the pressure (much like turgor present in many plant cells).

thanx...but this I'm afraid is really a general statement....are there any scientifc studies or experiment demonstrating this??...upvoting the ans...because of the pic & for your effort...but the answer is ...I am sorry to say...incomplete...

@souvikbhattacharya - The information comes from an online Textbook, but I haven't found specific primary research on it. My answer is the best I could do.

no no....I understand....there really is no study from this mechanistic angle....I was just double checking...neway you provided a crucial detail....so thanks again for that...


text:
A question on glycolysis

In the first step of glycolysis, the glucose ring is phosphorylated.
  Phosphorylation is the process of adding a phosphate group to a molecule derived from ATP. As a result, at this point in glycolysis,
  1 molecule of ATP has been consumed.

Is it the phosphate group, or the molecule, that is derived from ATP ?
http://www.sparknotes.com/biology/cellrespiration/glycolysis/section1.rhtml

Welcome to Biology! What is the molecule in your concluding question Is it the phosphate group, or the molecule, that is derived from ATP ??

This is an issue of grammar; clauses should be used properly :P The sentence should be  "Phosphorylation is the process of adding a phosphate group derived from ATP, to a molecule."

@WYSIWYG - absolutely positively agreed - it wasn't critique, just a request to clarify the question. The answer below is great and I retracted my close vote.

See this post too an addition to Koustav's answer, which pretty much summarizes the phenomenon.

The question is a bit unclear, it should be reframed as suggested by AliceD. To simply answer the question,
Glucose is the substrate, and in the first step it is converted to Glucose-6-phosphate.
Only the Phosphate group is added which originates from ATP, your notes also are a bit misleading because it tends to suggest that Hydrogen is released, which is not the case, the phostphate group in ATP loses an OH and Glucose loses an H in an SN2 reaction giving rise to Water in the process.
Always remember that ATP is categorized as an energy donor which drives chemical reactions in your body by breaking chemical bonds. ATP or Adenosine Triphosphate has three phosphate groups. The last Phosphate in ATP produces the highest amount of energy in any given chemical reaction where ATP is involved.
This is an ATP molecule.

The first P that you see is the Phosphate which gets released, and the ring that you see is a five member ring called a ribose sugar, while glucose is a six member ring.

"Is it the phosphate group, or the molecule, that is derived from ATP ?"
The Phosphate group is derived from the ATP molecule (thus why Adenosine triphosphate) NOT from the molecule it would be attaching the phosphate group to.
Phosphorylation - The process of taking this phosphate group and adding it to another molecule in the energy chain.
I hope this clears things up.


text:
What is the second phase of photosynthesis?
I really want to know what the second phase of photosynthesis (in the dark) is. I have a fair understanding of the first cycle where molecular oxygen is generated under the influence of light, but I don't understand the second cycle which can take place in the dark. It would greatly help to have a graphic of the second phase of photosynthesis.
Note: it is not for my homework, but for my own understanding. My textbook doesn't explain things very well.

I believe you are going to have to either elaborate on your question greatly and put forth some effort in specifics of what you are asking

photosynthesis has 2 phases.the first one is made in light,were oxygen is produced(i know this phase cause is easier and my teacher has it very good explained).The second phase is made in dark,were dioxide carbon is produced,but i don't know why and how.that's why i asked...

There are more than enough resources you can seek online to find the answer. Google the calvin cycle

actually i have,and i have found a lot of answers.but i posted here too,because i wanted even more answers. but thanks for your answer :)

I've voted to close because it seems like a homework question. What specifically is unclear to you about the second phase? Why does it confuse you more than the other phases?

well it is not for my homework,but it is for my school.I didn't know the calvin cycle,cause my book is a sh** book and doesn't explain it very well.and that's why i asked...

@user16901 What exactly do you want to know about Calvin cycle. Even after the edit the question is a little broad?

Here's an overview of both the Light and Dark cycles of photosynthesis, which looked particularly useful to me as it shows that the energy-carriers ATP and NADPH2 generated through solar energy are used in the dark cycle to generate sugars.
.
Here is another one that shows more details on the precursors involved in the Calvin cycle:

As commented by others, googling 'dark cycle' or its synonyms will give thousands of optional images to choose from if these don't suffice. The first one is taken from tutorvista.com the second one from users.rcn.com.

The dark reactions don't necessarily need to be in the dark; they're called that because they don't require light.

yes you are right


text:
Protocol for checking pipette calibrations using absorbance readings of a dye in solution?
I've been looking around the net looking for a nice protocol to validate micropipette calibrations using absorbance readings of a dye in solution. Does anyone have one they can share? I'd highly appreciate it!

you mean absorbance?

I just weigh water on an analytical balance and then compare the measured mass to what the mass should have been given the density of water. You should check the temperature of your water to be sure you have the right density.

^ I second this. I don't see why you would calibrate a micropipette using a spectro over gravimetric analysis.

I've never done it, but it seems to me like all you'd need to know is the concentration and extinction coefficient (at whatever wavelength) of the dye.

Thanks for the feedback. We are just trying to come up with the fastest way possible of validating the accuracy of a robot that dispenses into 96 well plates within a given run as well as to check for variations from one run to another over the course of time. We are tight on time and do not have enough trained hands on deck for the gravinometric procedure.  @Chris Stronks, I've edited accordingly.

does the manufacturer of the robot perhaps supply overall error rates and variability measures?

@Yaritza weigh the plate! If you are looking for variations within a plate I would suggest you use 12 or 8 sample strips. good luck, sounds like cool #$%^ your doing.

@Yaritza. Usual spectrometers keep the path length fixed and illumination is done horizontally (to measure conc.). Therefore the differences in volume don't matter as long as the light path is through the analyte. For your experiment you would have to fix a concentration and would need a vertical illumination so that you can measure the level by absorbance (varying path length); you would have to design such a setup and have it built AFAIK there is no setup like that.

To measure dispensed volume you'd have to dispense a small amount of dye into a known-volume container and measure the concentration of dye or something. I'm not sure which technique is better, but you don't have to rebuild your spectrometer. If you're dispensing very small volumes perhaps dye would be better than weight?

I see what you are getting at however this would be a very WRONG way of calibrating such an instrument. If dyes varied among trials it would throw off your calibration. Also, you would need to generate some sort of standard curve to equate absorbance to weight, since true calibration of these instruments is done by weighing the volumes they dispense (1g = 1ml water). The weight of water and the weight of your dye solution will not increase the same in terms of moles/g. Also a scale is far easier to calibrate that the detector in any spectrophotometer. Calibrate pipettes by weighing the volume of water they dispense. It should be done in a chamber that inhibits evaporation and you need a precision scale.
Here's a reliable guide for pipette calibration
enter link description here

A regular 5 place balance with doors and some wet sponges on the edges should help minimize evaporation while you try to take measurements.

I found an article published by Beckman Coulter for measuring the accuracy of their liquid handling automation platforms. It could be used for hand-help pipettes as well

Link-only answers are generally frowned upon on Stack Exchange sites. In time it is possible for links to atrophy (as your's has) and become unavailable, meaning that your answer is useless to users in the future. It would be best if you could provide the general details of your answer in your actual post, citing your link as a reference.


text:
Sensory adaptation regarding smell and hearing
Imagine the scenario. My friend and I are playing a game of chess near a highway. Initially, I notice the sound of the highway. While I'm playing chess, however, I do not notice it. After the game my friend asks me if I can hear the highway, and I regain my ability to notice it. This seems to be different for smells.
If we were playing chess in a room filled with garbage, the smell would gradually fade away. If my friend asked me if I could smell the garbage, I would not be able to smell the garbage as severely. What is the cause of this difference?
It seems that visual and touch follows the same pattern as hearing. What makes smell unique?

Adaptation occurs in every sensory system. For example in vision there is the motion after effect that occurs through adaptation of visual neurons in the cortex. Also, the visual system strongly adapts to low and high lighting conditions through light and dark adaptation. The tactile system also shows substantial adaptation, as touch receptors in the skin fail to convey information after prolonged stimulation (you won't feel a watch/ring/band aid etc after wearing it for a while). For example, mechanoreceptors in the skin such as the Pacinian corpuscles fail to transmit tactile stimuli when activated for a prolonged time. The auditory system also adapts to loud sounds by cortical mechanisms as well as  peripheral mechanisms through the middle ear muscles. Lastly, as you correctly identified, the olfactory system adapts to stimulation as well through metabolic mechanisms that decrease the responsiveness of chemical receptors. The list of adaptational mechanisms provided is not comprehensive, but I just used some obvious examples to show that adaptation occurs in all the senses in a variety of ways. In fact, one of the hallmarks of any physiological intact sensory system is the capability to operate over a wide range of stimulus levels. For example, vision operates over a range of intensities differing 8 orders of magnitude, while hearing operates in an intensity range of 1013. To maintain such an impressive range of input intensities sensory systems have to adapt at various levels. As an analogy, the same applies to your photo camera in which the exposure time has to be regulated in order to take pictures under different lighting conditions.
So to come back to your suggestion that smell cannot be revived after continued stimulation while it can be revived with other senses is not true I think. The attentional revival you are talking about is not so much adaptation but has more to do with the attentional shift, which may occur with any sensory modality.

I do believe that it is true that you cannot revive the smell to a certain degree. For example, when my toilet was broken and it got very smelly, while I was cleaning up in there, it smell was more bearable than initially. I would try to detect the smell again, but it did not seem too bad, and it was bad initially.

@CognisMantis - I agree with you. You need to step outside and 'clear the smell from your nose' to smell it as well again. It's not so much a central effect as a peripheral exhaustion.

To revive the tactile sense you also have to 'reset' it. That's adaptation. It may well be that continued acoustic stimulation results in less pronounced adaptation. Good point


text:
Chemical reactions at the synapse
For my course project, I am thinking of listing out major chemical reactions that occur at synapses, along with their temporal characteristics.
I could not find any textbooks to use as a starting point, and Google did not help me either. I was hoping to receive help in finding a review paper or textbook about chemical computations at the synapse.

Acetylcholinesterase is just one very important example of an enzyme in the synapse. Inhibiting this enzyme is how nerve gases and pesticides work.

If you are interested it from the point of view of "chemical computations", you probably want literature which looks at signal transduction in detail. I would suggest Marks' et al textbook on signal transduction. I have not yet read it through (it is on my list), but I liked the clear writing style of the introduction, and, as you can see from the table of contents, it does have chapters which address synapses and their neurotransmitters specifically.
I doubt that it will contain a complete list (there are several hundreds of compounds which can be considered to be neurotransmitters), but as an introductory textbook, it is likely to contain the major ones.


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Normal death experience
Consider a natural cause of death (no car accidents etc) -
Is it true that death is generally preceded by suffering? In other words, are we destined to experience the most severe suffering we could not ever imagine, that will ultimately end with death?
If this is true, is it true for all living things?

I'm voting to close this question as off-topic because it about philosophical musings on death and not biology.

@terdon in my mind this question fits perfectly, since it is asking about workings of the body and its lifecycle. There are similar questions already, like: http://biology.stackexchange.com/questions/14873/death-by-exsanguination-not-painful which is accepted ok.

That is a very different question. It asks whether a specific cause of death is painful, citing a scientific paper that claims it is not. You are asking whether we can say that in general, death is preceded by suffering. That is really not a good question for the site as it has nothing to do with biology. There are several hundred thousand ways to die. Obviously some will be painful and some will not. I don't see what we can add to that.

just a point, I'm going to suggest that "death with a severe blood-loss" is quite painful, no matter how quickly it occurs (given realistic possible bounds of rate of blood loss).

I edited the question by stripping it from its fluff. It seems more like a thought, not a biological question.

@AliceD thank you! :) I really like your edit, you just cut it to the point, this is much better!

No worries, my pleasure :) In this form it may fuel the discussion better as folks are more likely to read a short question than a long one.

No and no.
I'm not sure what is a "natural cause" in this context, but if it's cardiac arrest caused by age-related dystrophy of the cardiac muscles, then no, there is no suffering, at least not universally: Since age-related dystrophy hits all parts of the body, it's likely preceded by increasing amounts of bed rest, leading to quietly drifting off into the great sleep.
Of course, if you add on other natural causes like age-related diseases or being eaten by predators, the suffering can be great indeed, or not: A tiger will sneak up on you and crush your skull without you ever knowing what happened.
Adding on further causes still, like dehydration or hunger, and the suffering is back.
But is suffering a universal fixture of death? Emphatically no.
As for the "all living things" part of the question, the answer isn't just "no"; it's "that's nonsensical".
By individual count, practically no life is complex enough for suffering to be a relevant concept.
I don't have an exact number for you, because how would I get one, but at a rough estimate, bacteria, algae and archea constitute 100% of all individual life forms by count, and suffering is not a concept that makes sense for them.
If we ignore simple life, even among complex life there is so much variety of capabilities that basically nothing universal exists.

I think this answer is low quality as it stands so -1, it is just opinions. It would be very useful to get some science in to it.


text:
Are antihistamines considered to be psychoactive substances?
I have heard many times that the widely used antihistamines are not considered to be psychoactive drugs. Yet their impact on ones cognitive functions can be substantial. According to some sources, sedatives are also attributed being psychoactive, but not antihistamines. What is the difference?
UPDATE
Some links for the "cognitive effects" that I am referring to include hallucinations as well as drowsiness, anxiousness and irritability.
Besides that, it is well known that antihistamines cause drowsiness and sleepiness which are artificially altered states of mind because they are 1) not naturally-occuring, 2) have different mechanics and flow than their natural counterparts.
from experience I know these effects can be very strong, up to the state when one sees dreams while being awake. I can't find any scientific papers on that, but I have found many reports on the web and among people I've talked to.

When you say "their impact on ones psyche functions", what effect(s) are you talking about?

@naught101 please see the update

Your links list kind of broke. format them like [link name](http://...). Can you actually mention the effect in the question  as well, so people know what you're talking about without going digging?

@naught101 that's strange, on my side the links are working. I don't know what else can I do with them. Also, please read the update, I have been more specific on the effect in there.

I fixed the two references, and removed the dictionary and yahoo answers link, because they didn't relate to antihistamines.

@naught101 Thank you for the improvement! Yes, I guess words would be better than numbers for the link names :) As for the link to yahoo and the dictionary - I can explain - I was referring to the definition of "psychoactive" because it plays a role here too.. However, the links seem to be intact, so it is ok.

Short answer
First-generation anti-histamines are psychoactive, second-generation equivalents may not be*.
Background
According to WHO, psychoactive substances are:

[...] substances that, when taken in or administered into one's system, affect mental processes, e.g. cognition or affect. This term and its equivalent, psychotropic drug, are the most neutral and descriptive term for the whole class of substances, licit and illicit, of interest to drug policy. ‘Psychoactive’ does not necessarily imply dependence-producing, and in common parlance, the term is often left unstated, as in ‘drug use’ or ‘substance abuse’.

Antihistamines are used to treat allergies. First-generation antihistamines readily cross the blood-brain-barrier and have been associated with performance deficits on tests of attention, working memory, vigilance, and speed. By contrast, second-generation antihistamines that do not readily reach the brain do not have these side-effects (Kay, 2000).
Since attention, working memory and vigilance are mental cognitive processes, first-generation antihistamines fall into the classification of WHO as being psychoactive.
Reference
- Kay, J Allergy Clin Immunol (2000); 105(6-2): S622–7
Note
*I am not an MD and data on 2nd generation drugs are based on a single study with a limited number of tests. Consult a medical professional for prescription of the appropriate treatment.

Yes, I follow the medical advice of doctors - having seasonal hay fever since I was a child. But they don't say anything except "take this". So, from the answer, at least, it is clear that AHs do fall under the category officially, although somehow nobody mentions it for some reason. Gen-I force people sleep and forget (too strong). Gen-II surely have psychoactive effects too and allow to stay sober enough to experience it. The prolonged use seems to change personality, giving access to moods and thoughts not availbale without them. It's just that I am so surprised there's so little research.

@noncom - my apologies for the note, but self-help questions are explicitly off-topic here. It's a miracle you question survived in the first place :)

Yes, I know, it looks like the question managed to be as impersonal as it could :) medical topics are very different in that from the technical ones... As for the matter - I see, really there's not much else to say, since nobody really went into researching this. Even MAPS does not pay any attention to it. But I believe AHs (and I mean gen-II too, azelastine, cetirizine) can influence people strongly, especially in long-term use, especially children and people with unusual mental conditions..  Well, maybe some time in the future someone will do more research..


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Linkage distance calculation

What is the map unit distance between L and S allele ?

My working : If we take the normal ratio :9:3:3:1 , first one should be 9/16 = 0.5625
and then subtract 0.51 from it, we get 0.0525, similarly working we get 0.0525 difference for all 4 and so the distance is 0.0525 X 4 X 100 = 21
Is my working correct ?

I did not get your working and the logic behind it.Can you explain it a bit? But I got exact $20%$ as the answer.

I found out the difference between expected and observed and then added them. Could you tell me what you did ?

With the heterozygous genotype $LlSs$, there are two kinds of linkages possible.
1. Cis=$LS.ls$
2. Trans=$Ls.lS$
All the possible gametes ($LS,lS,Ls,ls$) in both cases are same, but their frequency differs based on the strength of linkage and hence, the distance on the chromosome map. In either case, the frequency of $LS$ and $ls$ will be same, and $Ls$ and $lS$ will be same. This is because, in the Cis linkage, the former pair will constitute the parental linkage and the latter will be the recombinants, but both the gametes within the pair are equally likely to be formed. The same is the case for Trans linkage where the former pair acts as the recombinants.
According to the given table, frequency of $llss$ is $0.01$. $llss$ can only be formed by the combination of two $ls$ gametes. Therefore the probability of an $ls$ gamete will be $\sqrt{(0.01)}=0.1$.
The probability of getting an $ls$ gamete is $0.1$. Therefore, the probability of $LS$ is $0.1$, $lS$ is $0.4$ and $Ls$ is $0.4$.
As $Ls$ and $lS$ are more probable, they are more likely to be linked, and hence the genotype will be in Trans linkage. Then the frequency of recombinants($LS,ls$) is $0.2$. The chromosomal distance is $20 \text{ cM}$ or $20\text{ map units}$.
I am not sure whether my line of arguments are true. If you do find any flaw, please let me know.

Yes, 20 is right. (My instructor gave us the answer today.)


text:
What is this image?

What I understand is- I think this is picture of DNA. But why is it in this conformation ? What types of cells have this type of DNA ?

It is called a Holliday junction. It forms during recombination.

Well, I am curoius - how did you find this out ?!

Just guessed it.. It resembled the textbook diagram of Holliday junction. :)

This is a pretty well known image and you definitely come across it, when you study in this direction.


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Removing a restriction site and introducing other at its place

What would you do if you want to remove an EcoRI restriction site
  and introduce BamHI restriction site at apprx. the same location ?

One of the answers in my textbook was : To construct a DNA fragment with the structure:
5'AATTGGATCC3'
    3'CCTAGGTTAA5'

I understand that this would ligate efficiently to the sticky ends generated by EcoRI cleavage and would introduce a BamHI site but I don't understand how this will remove/not regenerate the EcoRI site.

The recognition site for EcoRI is GAATTC, and the enzyme cuts after the first base. See this picture from NEB:

The overhang is: AATT, which is supplied by your oligo and fits into the overhang. If the next nucleotide whould be a C than the site would be recreated, since its a G its not. The new sequence of the old EcoRI site is GGATTG which is not recognized by EcoRI.
One technical note: To avoid religation of the digested DNA which carries this site, I would treat it with alkaline phosphatase to remove the phosphate end at the 5' end of the DNA.

I am still not able to understand how it destroys the EcoRI site. Sorry for being so slow !

Look at the sequences: EcoRI needs GAATTC to recognize and cut DNA. After the ligation with your BamHI oligo the sequence of the site is GAATTG so it cannot recognize the site anymore.

I get it now. I also understood why I couldn't figure it out at first - because I thought the RE just cares about G and A not any further sequence but now I understand that the whole sequence is important. THANKS A TON !

Just in case you are having difficulty visualising what happens in the answer from @Chris, here are the steps with the linker shown in lower case
...NNNNNGAATTCNNNNN...           ds DNA
...NNNNNCTTAAGNNNNN...

          |
          V

...NNNNG          AATTCNNNNN...  after EcoRI digestion
...NNNNCTTAA          GNNNNN...

          |
          V

...NNNNG      aattggatcc        AATTCNNNNN...   incoming linker
...NNNNCTTAA      cctaggttaa        GNNNNN...

          |
          V

...NNNNGaattggatccAATTCNNNNN...    after ligation
...NNNNCTTAAcctaggttaaGNNNNN...

The left hand "EcoRI" is now GAATTG and the right hand "EcoRI" is CAATTC.

I was wrong reading the sequence. Removed that part.


text:
Reduction of size in diatoms due to asexual reproduction
From this we can see that diatoms reduce their size after asexual reproduction.
This would ultimately lead to nonviable small size. Is there any mechanism to avoid this ?

Oh at last... someone used the "answer your own question" option! Anyway, a related This,this and this one are related articles.

The ability to reproduce sexually is closely associated with cell size
  of the diatom. It is the most prevalent method of restoring cell size,
  and it is often triggered when the size of a cell is less than a
  critical level (usually smaller than half of the original size for
  most species).

Source : Sexual reproduction in diatoms


text:
Correlating Ki values of pesticides to bacterial growth

Four pesticides P1 to P4 are reversible inhibitors of an enzyme E that
  is essential for the growth of a bacterium B. Their Ki values are
  given in the table below. Each of these four pesticides is used in
  four geographically different regions R1 to R4. The residual
  concentrations of these four pesticides in the respective regions are
  also shown in the table below:

Which pesticides will be able to inhibit bacteria ?

My question : I know that Ki shows the binding affinity. So, how is that related to residual concentration ? How can I deduce whether it will kill the bacteria or not ?
Unrelated question : Is it acceptable to use the word pesticide here ?!

Ki is the equilibration dissociation constant. The smaller this constant is, the stronger (more specific) is the binding between the inhibitor and the enzyme.
If the residual concentration is now higher than the Ki, for each molecule from the inhibitor which dissociates from the enzyme a new will bind (simply because of the concentration). If the concentration is lower (or much lower), this will not be sufficient to inhibit the enzyme. This assumes that the relation between enzyme, inhibitor and substrate are linear (and we are not getting some kind of saturation here).
Under the conditions mentioned above, P1 and P4 will inhibit the enzyme. For P2 and P3 the concentration is to low.


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Functioning of EDTA
I know that EDTA chelates metal ions. It weakens bacterial cell wall and inactivates the DNases.
What is the reason why it can do so ? I guess it can inactivate DNases by altering the microenvironment. What exactly happens ?

The lipopolysaccharide layer of the Gram-negative bacterial cell wall is stabilised by divalent cations. Most recipes for disrupting E. coli cells include Tris-EDTA for this reason. I seem to just know this, so no reference at the moment.
All nucleases require Mg2+, which is why there is EDTA in the stop buffer added to restriction digests. Carry-over of EDTA in DNA pellets can sometimes inhibit digests.

A lot of enzymes need metal ion in their active center (it is actually the metal ion which is taking part in the catalyzed reaction). These are manganese, magnesium, copper and so on. For DNAses the metal in the active center is magnesium and EDTA simply chelates this ions, making them unavailable for the enzyme and thus hinders the enzyme from working.
Chelation is the process in which metal ions are coordinated in molecules and form coordinate bonds to the chelating agent. EDTA looks like this:

The 3d structure while chelating a metal ions like this:

You can see, that the metal ion is nicely located between the negatively charged oxygen atoms and the nitrogen atoms. These complexes are fairly stable and the metal ions do not escape.

Could you also tell me why it will disrupt bacterial cell wall ?

Who claims that, do you have a protocol for that (so I can have a look)? All buffers I know for this purpose also contain detergents which actually break up cell wall and membranes. EDTA has the function of inhibiting enzymes.

I read it in my textbook.

one might add that 'chelation' means: EDTA has two amines and four carbocylic acids which form a compact shell around metal ions, they bind so tightly that they cannot bind anywhere else.

Good point, i added this to the answer.


text:
Long-term effects of antihistamines on mind and CNS
Can maybe someone share knowledge or guesses on the following questions:

Does the prolonged use of antihistamines cause long-term effects on mind or CNS?
Are there any known evidences of their influence of formation of CNS or personality when taken at a young age?
Generation-II antihistamines are said to be next to devoid of sedative effects since they selectively block just the H1-receptors. However, they are reportedly potentially mind-altering. How is this possible?

This question appears to be off-topic because it is not really a biology question

@GriffinEvo: can you suggest a more suitable stack exchange site? I have not found a site on biochemistry or anything more suitable...?

Not really - it's medical and there's no stack exchange site for that. I know it's not personal medical advice,  but it's not really a question of biology either

@GriffinEvo: yes, well, I agree.. sad but discussion on "medical" SE site has faded out: http://meta.stackexchange.com/questions/229495/stack-exchange-website-for-medical-questions ... well, maybe it is possible to move this question to http://cogsci.stackexchange.com/ ? does it seem more appropriate?

I think a medical SE is untenable because it generates a lot of risks - the people answering questions and offering medical advice aren't necessarily medical professionals, there's a lot of people out there looking to take advantage of those in need and a lot of people offering incorrect advice (with good intention) which might prevent someone from getting the correct treatment.

@GriffinEvo: what do you think about moving this question to cogsci SE site? If you think this could be done, then how can I do this?

I think the Mods have to do migrations - @kmm ?

@GriffinEvo: also, maybe you could propose a more appropriate site (not an SE site) to ask this? I am not into biosciences myself, so I do not know that segment of internet very well, but maybe you have some clue... I would really appreciate an advice since the question is important to me and is persisting in me for several years already.

These questions are ok for me but cannot answer them at the moment. Voted to reopen. However, very big chunk here and too much side tracked. You could reformulate your questions since the pharmacological sides of antihistamines are well known. All antihistamines pass BBB (1st gen most, 2nd gen less while 3rd gen very very little because antimetabolite of 2nd gen). These are Pharmacodynamic! Histamine can be released from all tissues ("hist"). So the drug primarily affects in all your tissues. Long-term effects have not been studied in no standardised situation. Immunosuppressed case neither.

I think you should split this question to many separate questions and then provide links between them: Ph.dyn antihistamines, their penetration of BBB and Pharmacology; long-term study about Ph.dyn antihistamine (take 2nd gen etc cetirizine) and Epidemiology in some standardised setting; same long-term study with some immunosuppressed patients; effect of 2nd gen antihistamines on cognition ... (think some parameter); etc. Personal medical advices are not provided in this site, since there are so many factors which we cannot consider publicly here and many other reasons too.

@GriffinEvo cogsci says it's off topic there too because of the personal medical orientation. I think it would be fine here or there (1) as separate questions and (2) as more general scientific questions as opposed to personal experience.

I edited and removed any personal info and basically stripped it down to a few sentences. The questions, however, are very broad and it may now be nominated for re-closure, if re-opened, but I think it deserves a chance.

And actually, the nature of the question may make it suitable for Cognitive Sciences SE. Specifically, question 2 could be deleted here and re-posted on Cognitive Sciences SE? This would kind of narrow down the question here as well.

Good edits so far, some comments though: The third questions suits Skeptics SE better (and if you insist on posting it here I want a source for "However, they are reportedly potentially mind-altering." and it should be a second separate post). The first and second are ok questions for here but may be better served by splitting in to two separate posts.


text:
By what method do ants dissect and hold soil
Not sure if this is the correct stackexchange site - please migrate/advise as you see fit.
I'm interested in the method by which ants "break off" a small amount of soil and then hold it in their jaws (?).
To clarify I know ants break off soil in small quantities, so that a single ant carries very little soil; I'm interested to understand what exactly how this happens. For example does the ant literally pick the soil directly, or does it brush it loose first etc. Further to this I'd like to know how the ant holds the soil. Is it akin to the soil being atop a palm, or more like being held between two hands?
Broader context: I'm looking into making a model of this type of soil movement and I wanted a more detailed understanding.

This is definitely on-topic here @FraserOfSmeg

Short answer
Ants use specialized facial structures called mandibles to cut, shape and carry soil and other matter.
Background
you say "I know ants break off soil in small quantities, so that a single ant carries very little soil...". On the contrary I would say - Ants can carry relatively a lot of soil, as they can lift up to about 100 times their own body weight. In absolute terms, however, the weight carried is about 500 mg (Spectrum).

Source: The World's Best Photos
The structure that ants use to break off and carry soil are their mandibles:

Source: Tree of Life Web Project
Mandibles are specialized bodily structures typical for insects, and I quote from the University of Sydney website:

The mandibles are the first pair of jaws in insects, moving laterally (i.e. from side to side) when in use. Mandible shape is strongly influenced by function and is therefore highly variable. For example a chewing insect will have strong tooth-shaped mandibles while in a sucking insect they will be thin and needle-shaped. Mandibles are used to cut, chew and tear food as well as to carry objects, fight and mould materials such as wax or soil.

thanks for the thorough answer. Could you help me understand how the ants don't squash (and then drop) or knock soil lose? In every video I've seen they seem to have almost unbelievable precision!


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How can human infants express chymosin with only a pseudogene at their disposal?
I read on the Wikipedia article about Chymosin http://en.m.wikipedia.org/wiki/Chymosin
It stated that chymosin is produced by gastric chief cell in human infants.
But it also stated that human only has a pseudogene for chymosin that does not actually encode the enzyme. On the other hand, another article show that gastric chief cell only secret chymosin in ruminant http://en.m.wikipedia.org/wiki/Gastric_chief_cell
How can infants express chymosin without a functional gene?

TL;DR: Chymosin is similar to pepsin and I couldn't find any evidence of functional/expressed chymosin gene in human genome.
It seems like a common misconception that chymosin is functional in humans. Already in 1940s it has been shown that rennin (aka chymosin) is absent from "gastric juice" in adult humans.
Genetically there is only pseudo-gene for chymosin, as wiki and other sources state. At the same link that leads to chymosin gene page you can find some literature on cloning and structural analysis of chymosin pseudo-gene.
If you use BLAST for finding homologous proteins to chymosin from, say Bos  mutus (aka yak), you can find that in humans closes sequence can be attributed to pepsinogen and similar proteins. Which very much might mean that what is called chymosin in other animals is pepsin in humans, or there is some convergence/divergence which eliminated chymosin in humans. But this is only a speculation.
You can try to scan Google scholar for more sources.
NB link to BLAST search will expire in ~24 hrs.


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Why is succinate dehydrogenase attached to the inner mitochondrial membrane?
Succinate dehydrogenase is attached to the inner mitochondrial membrane. All the other enzymes of the Krebs cycle are located within the matrix of mitochondria, though.
In biological systems, there is often a relation between structural properties and function. For example, two enzymes that function sequentially in a metabolic pathway are sometimes held in close proximity to one another by a scaffold  (e.g., in fatty acid synthesis). Is there a similar biochemical reason why succinate dehydrogenase is attached to the inner mitochondrial membrane, as opposed to being dissolved in the mitochondrial space?

The reason behind this lies in the properties of FAD+. Unlike NAD+, FAD+ is not free to diffuse within the mitochondrion, it is an integral part of the inner mitochondrial membrane. Its reduced form FADH2 contributes electrons directly to ETC.

Succinate dehydrogenase is also known as Complex II in the electron transport chain.
Although textbooks often show Complex II as taking FADH2 as a substrate, this is a little bit misleading. Succinate is the substrate, the oxidation of which facilitates the reduction of an FAD cofactor, which is already bound to Complex II. The resulting FADH2 is then oxidized in order to reduce ubiquinone, and feed electrons to Complex III.
This is a pretty good image explaining the electron transport chain.

A note on the ETC image I just realized - succinate is oxidized to fumarate, not "funarate" as the image mistakenly says.


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How is pain induced by blunt and sharp objects?
Normally, when something touch you, you won't feel pain. With a great force "touching" you, you will feel pain. However, if something that is spiky makes contact with you, you will feel pain. So, how much force should be exerted by a smooth/blunt object to make you feel pain? When and how does a spiky object make you feel pain?

It is a simple matter of biology and physics actually:
Firstly, pain is caused by the simulation of cutaneous nociceptors in the body, beneath the skin and are activated when the sensation crosses a threshold.

Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system,[1] and, therefore, the ability of a body to sense potential harm. It is the afferent activity in the peripheral and central nervous systems produced by stimulation of specialized free nerve endings called nociceptors or "pain receptors" that only respond to tissue damage caused by intense chemical (e.g., chilli powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat and cold) stimulation.[2][3] Once stimulated, a nociceptor sends a signal along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of autonomic responses and may also result in a subjective experience of pain in sentient beings.[3] Nociceptive neurons generate trains of action potentials in response to intense stimuli, and the frequency of firing determines the intensity of the pain.[4]

From the wiki: https://en.wikipedia.org/wiki/Nociception
Now when you consider a knife, the surface area of the knife is small enough that it can cause damage. It's akin to holding a plastic sheet stretched tight and then piercing the sheet with the point of a knife. That is because the force is being transferred on a small point and hence easily extends the pain threshold.
However, when you consider a hammer, when the hammer touches you (lightly) you don't feel the pain because the force is spread over the larger surface area of the hammer and hence doesn't meet the threshold. However, if you hammer your finger in with force, the force being transferred is enough to shatter your bones, and in that case not only the cutaneous pain receptors activate, but the somatic receptors also activate, causing the feeling of pain.
TLDR: Knife has short surface area, and hence force transfer is over a small area, subsequently causing hurt. A hammer has a larger surface area, and hence unless more force is applied, the pain receptor threshold is not met and hence no pain.


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Can sugar be absorbed orally within seconds?
Whenever I feel a little light headed or tired, it helps to eat something sweet.
Specifically, simply chewing or sucking on a sweet seems to aleviate the symptoms within a matter of seconds and then the sugar seems to kick in. So I was wondering whether it is just a psychological effect, or whether sugars are absorbed in our mouth and reach the brain (or wherever the sugars exert their effects?) within seconds. Or is perhaps the taste of sugar sufficient to signal the body that it can safely release some extra energy as resupply is imminent?

Welcome to Biology.SE! You can make the experience yourself. Put a piece of bread in your mouth for several minutes. Don't chew (would be cheating) and see how the bread starts to degrade.

@RoryM - is this a duplicate? I think OP is basically asking whether the sugar can kick in within seconds. Although this is addressed in the linked question, it is not answered there as such. I vote to re-open after edits in this question.

@user3461075 - could you verify that it is a few seconds?

@AliceD Thank you. You did point out the essential question of this matter. The effect really occurs within seconds.

@AliceD Speed is answered in the first answer as far as I can tell?

@RoryM - I searched for a reference to 'time taken' several times in the linked question - it's not there afaik

Yes we do. The first part of digestion starts in mouth. Digestion begins in the mouth, where chemical and mechanical digestion occurs. Saliva  produced by the salivary glands (located under the tongue and near the lower jaw), is released into the mouth. Saliva begins to break down the food, moistening it and making it easier to swallow. A digestive enzyme (amylase) in the saliva begins to break down the carbohydrates (starches and sugars).


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Where do the H+ ions come from in light reactions?
In the light-dependent reactions of photosynthesis, H+ ions pass to the thylakoid space. Where do these protons come from?

Photolysis of water. It is the first step of the light reactions. BTW, H⁺ is ubiquitous.

And the electrons go to PhotoSystem II?

Is this a homework question? It really looks much like it. Additionally: Please have a look at the reaction chart on the Wikipedia page on photosynthesis which explains both questions.

No, I have a biology course in Univeristy, and I just want to be sure I know it before the exam.

@Benjli Read our homework policy. If you have not put an effort in answering a basic question then we consider it as homework. Can you add some points on how you analysed this problem?

All right, I will keep the homework policy in mind. But again: that question was not a part of any homework. I had tried to search it in my biology book. It was written in it that electrons come from water to Photosystem II only when there are no electrons left in it, but H+ ions are being passed into the thyalkoid space even when there are enough electrons left in the photosystem! So I tried to solve the contradiction.

@WYSIWYG I think you meant H+ (not H-) is ubiquitous. H+ is everywhere in the aqueous system. H- is pretty rare and unstable in aqueous/biological systems, that's why there's NADPH.

The photolysis of water is coupled to the reduction of plastaquinone (Q) in photosystem II (PSII) as summarized in this diagram, adapted from Berg et al.:

The overall reaction (which balances) is:
2 H2O + 2 Q + 4 H+ = O2 + 2 QH2 + 4 H+
But the 4 H+ on both sides of the equation are not the same. The generation of the hydrogen ions in the thylakoid lumen is coupled to the uptake of hydrogen ions from the stroma as the plastoquinone is reduced. This is made possible because of the membrane disposition of the components of photosystem II. Hence an electochemical gradient is established that can be used for generating the ATP needed for photosynthesis.


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How much does hearing deteriorate with age?

For the average person, what is the lowest volume of a pure tone at each frequency they can hear as a function of age?
I know some people lose hearing faster than other people, because they are exposed to loud sounds. So I am also interested in hearing loss induced by loud sounds as a function of frequency.
The brain can adapt to the hearing loss, thereby creating the illusion that a sound is just as loud as if nothing happened to their hearing. For that reason, I also wish to know what volume the ear transmits to the brain as a function of frequency and age.

Hearing sensitivity deteriorates with age, which is called age-related hearing loss, or presbyacusis. Presbyacusis is characterized by elevated hearing thresholds. Especially the high frequencies are affected by age, but eventually even the low frequencies may deteriorate substantially. Hearing sensitivity is typically expressed in an audiogram, which depicts the hearing threshold as a function of acoustic frequency. To express hearing loss as a function of age, however, it is more convenient to plot the threshold at various frequencies as a function of age (Fig. 1).

Fig. 1. Hearing thresholds at various frequencies plotted as a function of age. source: Handbook For Acoustic Ecology.

Exposure to loud sounds may be detrimental to hearing, referred to as noise-induced hearing loss. Typically this results in a loss of sensitivity at the moderate frequencies (3k to 4k); a mid-frequency dip (Fig. 2). Old age will add a high-frequency hearing loss on top of that.

Fig. 2. Typical audiogram associated with noise-induced hearing loss. source: American Hearing Research Foundation

The brain will not adapt to elevated thresholds. A threshold represents the minimal intensity level a sensory system can detect. Elevated hearing thresholds due to old age and noise-induced hearing loss are caused by sensori-neural hearing loss, meaning the hair cells in the inner ear (the cochlea) are dying. The brain can never detect a signal that is not transmitted via the auditory nerve and can hence never compensate for elevated thresholds. In turn, when thresholds are elevated substantially, a person suffering from such a hearing impairment may ask you several times kindly to repeat what you were saying, but a little louder. Then, when you start screaming after the third time, the hearing-impaired person returns the dreaded "You don't have to scream at me!". That is because the brain does not adapt to the elevated thresholds; once the sound is transmitted by the degenerated cochlea, it is transmitted at that loudness and perceived at that loudness by the brain. Moreover, a process of recruitment can occur in the hearing impaired, where the perceived loudness is exaggerated. Recruitment may occur at the hair cell level, but it is a not well characterized phenomenon.


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How was gene therapy able to cure diseases through the transformation of actively dividing cells?
I thought that gene therapy, when performed on target cells that regenerate themselves constantly, can be effective for a limited time only. I.e., the effect gradually wears off after a while, depending on how fast the target cells renew themselves. In other words, the patient needs to continue receiving gene therapy every so often to keep getting desired effect.
On the other hand, when targeting cells that do not divide/renew, such as an eye, gene therapy can and actually did cure blindness once and for all, and the patient no longer needs gene therapy injections.
So what about the other diseases that gene therapy allegedly cured? I think they include blood disorders like hemophilia and some serious immune system disorders? I thought they mainly involved cells that do regenerate, like bone marrow and liver?

Short answer
Both dividing and non-dividing cells can permanently be modified with gene therapy by using vectors that incorporate their payload in the host's chromosomal DNA
Background
Vector-based gene therapy can be applied by using vectors, such as modified retroviruses or adenoviruses, that incorporate their payload in the host's chromosome.
Whether the transformed cells are replicating yes or no, the parent as well as any possible daughter cells will carry the new DNA. For example, immunodeficiency has been treated successfully with gene therapy, but the first trials resulted in blood-bone cancers, because the stem cells started to proliferate uncontrollably, hence dividing cells definitely can be permanently transformed. In fact, when germ line cells are transformed in this way, even the offspring of the host will inherit it.
Sources
- American Medical Association
- Learn Genetics
- Utah University

I would also add that "gene therapy" is an increasingly broad term. Viral vectors are one way of altering patient cells, but there are other ways, depending on the cell type. Current gene therapies to treat soft tissue tumors like leukemia include removing patient stem cells, altering them and finally re-inserting them. So far, no cancers have resulted from that cure. Here's a description of the technique: http://www.discoverymedicine.com/Runzhe-Chen/2015/10/cd19-chimeric-antigen-receptor-t-cell-therapy-for-the-treatment-of-b-cell-lineage-acute-lymphoblastic-leukemia-3/

@Forest - the means to obtain the target cells differ, the final method to get the DNA into them is based on vectors afaik

Ah, I see now. Good point.


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Is HSV-vector-mediated miRNA expression in dorsal root ganglia stable?
My question is on the following article:
"Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy"
My question is, do you think the rats continued to have decreased levels of voltage-gated Na+ channels after this experiment, or did they likely gain them back up eventually, because dorsal root ganglion neurons regenerate themselves? I couldn't find this info in the article.

The vector used in this study is based on the herpes simplex virus genome (HSV).
Wildtype HSV mainly infects sensory neurons. After infection, it resides in a latent state in the nervous systems of the host for a lifetime. The viral genome persists in the cell, without integrating into the host genome (Marconi et al., 2000).
The article cited is devoid of background on the vector and its characteristics and I understand your issues. I think that the expression of the RNAi is quite stable in your linked article, because the authors infected neurons in the dorsal root ganglia. The dorsal root ganglia contains sensory neurons. It is an immuno-privileged region, because the blood-brain-barrier (BBB) limits the access of immune cells. Indeed, protein expression through HSV-transfection in the brain is stable, at least up to a year (Suzuki et al., 2008) and possibly longer. Peripherally, outside the BBB, the expression of HSV-plasmids may be compromised within weeks through cellular immunological responses targeting the expressing cells (Suzuki et al., 2008).
Regarding regeneration - The DRG contain mature neurons and is part of the peripheral nervous system. These neurons are known to regenerate readily after injuries, but these injuries are mostly investigated through physical damage (Muratori et al., 2015). Latent HSV infection does not kill neurons, and even an active infection seems to leave neurons relatively unscathed (Rautema, 2002).
References
- Marconi et al., In: Madame Curie Bioscience Database. Austin (TX): Landes Bioscience (2000)
- Muratori et al., (2015); 2015, 860546
- Rautemaa et al., Immunology (2002); 106(3): 404–11
- Suzuki et al., Molecular Therapy (2008); 16(10): 1727–36)


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How can we differentiate between respiration and breathing?
I am a student of 10th grade, and I eagerly want to learn biology. What is the difference between respiration and breathing?

Think of respiration as ‘cellular respiration,’ which is the process by which the body extracts energy from glucose molecules. Breathing is the mechanism of the lungs that brings oxygen into the body and expels carbon dioxide.

It is good that you are eager but you should make an attempt to look for an answer before asking here. I did not vote to close this question because I know that there are certain misconceptions related to some subtle aspects of this topic, even amongst researchers. However you should at least do a google search and ask a specific question. Also, making a habit of putting in your maximum effort before asking for help would be good for you in the long run.

@WYSIWYG i appreciate your suggestions and in future i will try to follow your suggested way.

There are two uses of the term respiration: physiological respiration and cellular respiration
Physiological respiration involves the intake of outside oxygen and its distribution to the tissues of the body. Breathing is a part of physiological respiration and functions to bring oxygen into the lungs and expel carbon dioxide.
Cellular respiration is a chemical process by which energy is obtained within individual cells from biomolecules like glucose. In aerobic respiration, oxygen is used. Cells can also use fermentation and, for some, anaerobic respiration to obtain energy.

I think this is the most interesting example of anaerob respiration: http://www.nature.com/nature/journal/v467/n7314/abs/nature09415.html

@inf3rno Just skimmed the abstract; it is amazing.

I found the full text with google: http://rothlab.ucdavis.edu/publications/huseby_2010.pdf . Btw. this is not a unique ability, B. anthracis (anthrax) uses the same method: http://www.sciencedirect.com/science/article/pii/S1089860314000561 gasotransmitters like H2S, NO, CO promote inflammation in a large quantity.

Breathing is a part of respiration but respiration is not a part of breathing.
Breathing is a process through which oxygen is taken into the body for use in respiration. This involves physical movement to take oxygen (into the lungs) and also chemical action (haemoglobin-carries oxygen from lungs to blood and carbon dioxide from blood to lungs).
But respiration is a chemical process that involves the break down of the glucose that was formed during digestion to form energy (chemically, energy is Adenosine Triphosphate) for our everyday or metabolic processes.

thank you for your response . Your answer helped me a lot.

Your points and claims seems fine, but you can enrich your answer by adding references to it.

Cellular respiration does not actually include breakdown of glucose

@WYSIWYG  You write "Cellular respiration does not actually include breakdown of glucose –" <-- How can you say that , please give a source, particularly when  Googling cellular respiration glucose, and tons of links come up saying it is involved. Google says straight away "Cellular respiration is the enzymatic breakdown of glucose"

@anuragak breathing is not necessarily a part of respiration, as some respiration doesn't require oxygen.. but besides.. who is to say that getting the oxygen that aerobic respiration requires,  needs to be considered part of the definition of respiration? i.e. aerobic respiration could just be the chemical reaction that happens after the oxygen is in.

An addition to previous answers plus some clarification
The term respiration originally meant breathing i.e inhaling and exhaling (See here). It was believed that it is the oxygen and in turn the act of breathing is what lets an organism survive.
After substantial research it had been found that, in individual cells it is the ATP production by mitochondria that requires oxygen (as a terminal electron acceptor) and therefore for a cell, respiration is basically the electron transport chain (ETC).
Note that glucose or any other food molecule or its breakdown has got nothing to do with respiration. The process of glucose breakdown i.e glycolysis is not a part of respiration. TCA cycle is however considered a part of respiration because it is coupled with the ETC.
Later it had been found out that molecules/ions other than oxygen such as Fe3+, Fumarate etc, can also serve as the terminal electron acceptor. So cellular respiration expanded to include these cases as well;  these fall in the subcategory of anaerobic respiration.
Note that fermentation also is a pathway that generates energy in the absence of oxygen but it is not considered respiration. It was previously classified as anaerobic respiration (if I am not wrong) but not any more.
So you can see that respiration which was originally synonymous with breathing now denotes a very specialized process. However, respiration is still used to mean breathing and distribution of oxygen in the body when cellular physiology is not in discussion.

who is to say whether glykosis is considered to be part of respiration or not?  many links describe it to be the first step of respiration e.g.  http://www.rsc.org/Education/Teachers/Resources/cfb/respiration.htm

can you define respiration?  of course, breathing is not synonymous with respiration, as anaerobic respiration (what i've read fermentation to be!), doesn't require oxygen so doesn't require breathing.

furthermore, this article http://study.com/academy/lesson/anaerobic-respiration-lactic-acid-alcoholic-fermentation.html   is an article that carefully describes aerobic respiration, and anaerobic respiration, and the place of fermentation..

@barlop  re my second comment asking difference between fermentation and anaerobic respiration..  I've found the answer.. it's the same difference as between fermentation and any cellular respiration. Cellular respiration (aerobic or anaerobic), involves the ETC, which are a bunch of things in the inner membrane of mitochondria and are involved in a stage of respiration..

To my limited knowledge, I believe respiration is the chemical process of the body converting glucose and oxygen into energy, whereas breathing is the physical process of inhaling oxygen and exhaling carbon dioxide. Breathing is somewhat like an "external" respiration.

Thanks for your quick response. Is there any other difference?

@NigHterz  I guess this answerer has just defined each, and the definitions are different, and that's all the difference there can be.


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What are those visual and auditory reflex controlled by the midbrain?
The midbrain is a centre for certain visual and auditory reflexes. But what are those reflexes exactly? My study book says that these reflexes are, e.g., responsible for moving the eyes to view something as the head turns. But I don't quite get it. What is the difference between those reflexes controlled by the midbrain and those mediated by the spinal cord?

You probably reading about Vestibulo–ocular reflex. This is one that allows your eyes to follow object of interest even though your head rotates.  I see difference as that spinal cord controls motor neurons of limbs, not controlling muscles of the eye.

Where are you after exactly? Are you after the different types of auditory/visual reflexes mediated by the midbrain? Are you after startle responses? Or after eye movements? I think you need to add a little bit more detail, as I don't quite get "it" is quite vague. Also, the concluding sentence does not really match your question title. Are you interested in the difference between spinal-chord-mediated reflexes in particular? That is again quite broad, as the spinal chord covers the entire body including many receptors (pain, heat...)