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Why draw blood from veins rather than arteries?
Why draw blood from veins rather than arteries? Is it more convenient or safer?

Veins have several advantages over arteries. From a purely practical standpoint, veins are easier to access due to their superficial location compared to the arteries which are located deeper under the skin. They have thinner walls (much less smooth muscle surrounding them) than arteries, and have less innervation, so piercing them with a needle requires less force and doesn't hurt as much. Venous pressure is also lower than arterial pressure, so there is less of a chance of blood seeping back out through the puncture point before it heals. Because of their thinner walls, veins tend to be larger than the corresponding artery in the area, so they hold more blood, making collection easier and faster.
Finally, it is somewhat safer if a small embolism (bubble in the blood) is introduced into a vein rather than an artery. Blood flow in veins always goes to larger and larger vessels, so there is very little chance of a vessel being blocked by the embolism before the bubble reaches the heart/lungs and is hopefully destroyed. Blood flow in an artery, on the other hand, always moves into smaller and smaller vessels, eventually ending in capilllaries, and there is a chance that a bubble introduced by a blood draw (generally rare) or more commonly an intravenous line (IV) could block a small blood vessel, potentially leading to hypoxia in the affected tissues.

+1 - all good points. The main risk, though, is bleeding. Puncturing an artery can cause it to bleed until it tamponades, causing a hematoma which can  cause ischemia downstream and might compress/damage the nerve in that neurovascular bundle. Because of that, pressure must be applied for a while (longer for larger arteries). Before doing a radial artery stick (common for blood gasses), one should do an Allen's test for collateral circulation. The risks are acceptable for blood gases or monitoring but not for blood collection.

(Oh, btw, the paper deals with cannulation, not just puncture, but the principles are the same.)

Yes, arteries are punctured when arterial blood gas readings are required. Patients then wear compression bandages for days.

Right of the bat, veins are superficial so it is much easier to hit a vein than an artery. Arterial sticks are very difficult if you are not practiced at them while veins are much much easier. Also arterial sticks have a very specific purpose usually for example arterial blood gas. Also veins are low pressure compared to the higher pressure of arteries so less chance of bleeding.

Blood is not always drawn from the veins depending on the medical need and situation. For example critically ill ICU patients will often have an arterial catheter placed to provide an accurate measure of blood pressure. Blood is sometimes sampled from this line to provide a more accurate measure of blood gases and cardiac performance.
But the risks of dealing with arterial blood are greater as others have mentioned.


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What is the mechanism by which lamins regulate gene expression?
The heterochromatin is generally localized at the nuclear periphery (also near nuclear lamina), whereas active genes are preferentially found in the nuclear interior.
Children with Hutchinson-Gilford syndrome have a mutation in a LMNA gene, which codes lamin A and C, therefore, mutation in a LMNA gene causes overexpression of genes near nuclear lamina, this shows that nuclear lamina has something to do with gene expression regulation.
What is the mechanism by which lamins regulate gene expression?

Based only on your description, it would seem that lamins repress expression. Thus it would make sense that they're associated with hetero- as opposed to euchromatin.

@canadianer: Yes, they repress expression, if there's no mutation in LMNA gene and nuclear lamina is located near heterochromatin, I just don't know why.

Euchromatin is actively transcribed. It wouldn't make sense to localise it near something that presumably represses transcription.

@canadianer: But how does nuclear lamina repress gene expression?

So you want to know the mechanism by which lamins regulate gene expression?

@canadianer: Yes, that's what I want to know.

If someone wants to build an answer here, this article listed is where it's at. The fact is, we're at the frontier of understanding this, and so it's not a comprehensive mechanism, yet.
/e I'd also look here, the article is 2013, where the above is 2015, however:

So my answer was deleted because it "didn't answer your question."  Except that it did.  The article linked here, Gene expression, chromosome position and lamin A/C mutations, is an entire paper devoted to what we knew as of 2011 about lamins and gene expression, with references.  Your question was not a simple question, and article details how lamins are involved in gene expression.
I shall quote it here in order to "answer your question", and perhaps the moderators will see fit to not delete the post this time.  If said moderators think I should write a review of a review to facilitate your understanding, then I obviously have not understood the meaning for this board.
I don't have enough rep to leave a comment on anything other than my own answer, which seems to have been the appropriate way to link to the paper.  I figured an answer to your question would still be useful.
I would recommend reading the entire article as it is very useful in understanding additional indirect hypotheses for lamins controlling gene expression.

The Lamina as a Regulator of Gene Expression
In most cells, a dense heterochromatin network is visualized as electron dense material adjacent to the inner nuclear membrane and the nuclear lamina. The dense network is typically considered to reflect the association of transcriptionally inactive genes with the nuclear lamina. Specifically, this heterochromatin is thought to reflect a repressed gene state and suggests that the nuclear membrane and lamina may play an active role in gene repression.5 Lamin A/C and its binding partners can interact with DNA, histones, transcription factors and chromatin.6 Lamin-associated domains (LADs) are cis-acting sequences thought to range in size from ∼0.1–10 Mb, and these domains are thought to regulate the interaction of chromatin with the nuclear lamina; generally LADs are considered to be transcriptionally repressive.7 The precise sequences that define LADs have been elusive but nonetheless the LAD concept implies that the lamina and the genome interact in a specific manner. Therefore, it follows that one mechanism by which LMNA mutations may confer pathology is by altering the interaction between the lamina and chromatin. Consistent with this, LMNA mutant cells have altered chromosome territories.4 Meaburn and colleagues first examined chromosome localization in proliferating LMNA mutant fibroblasts and found that it resembled the chromosome organization associated with quiescent or senescent fibroblasts. They suggested that mutations in LMNA produced structural disruption to the lamina inducing a chromatin organization that may resemble an inappropriate cell cycle state. The presence of LADs and the fact that mutations in LMNA associate with altered nuclear architecture suggest that the nuclear lamina plays a vital role in both scaffolding chromatin and regulating chromatin organization. In this model, it is possible that distinct LMNA mutations may alter distinct regions of the genome leading to mutation specific profiles of altered gene expression.

An answer usually and preferably contains an answer that specifically targets the question. This question is really quite broad, and I understand it's hard to write a concise answer. However, it's best not to just link an article, or paste an entire abstract. You might want to get rid of the fluff and answer the question and only the question.

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how do macrophages have the capacity to digest pathogen in opsonization
how do macrophages  have the capacity to digest pathogen in opsonization but not in the            first time when the pathogen is new  and they play the role of antigen presenting cells(APCs) first they digest polypeptide of antigen and then let the plasma cells first secrete an antibody and after that they can destroy antigens?

There are multiple mechanisms to induce phagocytosis by macrophages. One includes B-cell antibodies (specifically the Fc region) and another includes chemokines emitted by local cells that can also induce phagocytosis. I do not have my material with me at the moment, but the short answer is: Macrophages can do both. They can eat pathogens without antibody stimulation, but antibodies can also stimulate them into action.

It's a simple matter of ionic charge
Opsonization works because it is masking negative charge with positive charge. Phagocytosis works on positively charged things.
Your right though, the sequence seems odd.

First something is phagocytosed (by a macrophage or another monocyte-derivative, these are the APCs... but neutrophils, which are not APCs or monocyte-derivates also perform phagocytosis but they dot not have the MHC-II to be described)
then digested in endosome/lysosomal,
then presented on the MHC class II,
recognized by TCR on T-cell,
then much more complicated stuff to get to B cells to convert to plasma cells
plasma cells secrete the antibody, in order for opsonization of the pathogen to be phagocytosis more easily.

Yet it was the initial phagocytosis that led to this. A bit of a circle.
Here are three answers:

one is cytokines
another one is about how the TLR receptor mediates phagocytosis
a third is how complements act as opsonins

local presence of cytokines (ex. interleukins, interferon, TNF) from either innate or adaptive "immune system" (by "immune system" I mean immune cells other than macrophage, but also epithelium which secretes types of interferons) that lead to "signal transduction" ("signal transduction" is the intracellular chain reaction in response to the activation of the cytokine (or other ligand) binding to the receptor, too complicated for me to explain) that alters the behavior of macrophage to enhance phagocytosis.

On the other hand, PAMPs activate the TLR which could permit phagocytosis without prior activation from sources "other" than the thing being phagocytosis.
By "other" things I mean opsonins and cytokines.
PAMPs (pathogen associated molecular pattern) are things on the pathogen that are distinctively foreign to the host, like flagella or LPS [which is the outer membrane from gram (-) bacteria]
TLR is the receptor on the macrophage that recognizes PAMPs. I think that TLR simply enhances phagocytosis via signal transduction much like cytokines. As an interesting side note, the TLR is quite ancient in kingdom animalia, having it's origin in sponges  as close to the beginning as you get). Other aspects of the immune system evolved later on specifically in vertebrate. In fact the lymphocytes is unique to jawed vertebrate (aka absent in agnathans and invertebrate) and i don't know much about antibody production in non-mammals. Also in lower vertebrate and invertebrate, phagocytosis is done by hemocytes. In other words, the TLR is pretty fundamental as far as immune stuff goes, more so than cell types doing their things (ex. plasma cell making antibodies, macrophages doing phagocytosis).

But there is also complement mediated opsonization, primarily C3b but other complement proteins as well. Finally there are yet more (less important) opsonins, Mannose-binding lectin and C-reactive protein (CRP). all of these things are "Acute phase reactants" that are secreted by the liver under inflammatory conditions, mediated by cytokines. Complement is not always activated by the immunoglobulins.
Complement is activated by

classical pathway, again Fc region of antibody (IgG/IgM), just like antibody mediated opsonization. In addition, classical pathway can be activated by CRP binding to microbial polysaccharides

alternative pathway, which is the spontaneous hydrolysis of C3. Under normal (non-infected) circumstances, this is normally prevented by a variety of mechanisms.
activation by mannose binding lectin. MVL recognizes certain sugars that are found in certain positions that are unique to bacteria, fungi, viruses.

I'm saying all these things as explanations of human immune system. It's probably different in different animals, the more different the further away from human. The complement system has been discovered in primitive vertebrate (agnathans) and invertebrate (specifically in deuterostomes like protocordates and echinoderms) but there are variations.

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Multi-modal distribution for gene expression data
Why would some genes have more than two modes in their expression distribution? What external factors would cause this anomaly?
I'm referring to the expression distribution of a gene across different tissue samples. For example, if one was to download a bunch of data from NCBI GEO, and pinpoint one gene and plot the expression level versus the frequency for that gene across all those data sets, some genes would have more than 2 modes (2 expression levels with very high frequency). This is the only case I'm interested in: more than 2 modes - not bimodal. So what would cause more than two modes?

Could you expand please? Expression distribution over what? The same tissue? Same cell over time? Different tissues?

@nico's point is spot on, we can't answer until we know more. Also, should I intepret your question to mean you are not interested in bimodal (i.e exactly 2 modes) distributions? Those are usually easier to explain, have more concrete examples, and should generalize to a multimodal case. But if you are not interested in bimodality please make that clear.

My original question was a bit vague - here are some clarifications. I'm referring to the expression distribution of a gene across different tissue samples. For example, if one were to download a bunch of data from NCBI GEO, and pinpoint one gene and plot the expression level versus the frequency for that gene across all those data sets, some genes would have more than 2 modes (2 expression levels with very high frequency). As I alluded to in my post, this is the only case I'm interested in: more than 2 modes - not bimodal. So what would cause more than two modes?

@newintern Edit your question instead of clarifying in the comments.

One trivial situation in which this can happen is when the tissue used for expression studies is heterogeneous. Different cells express different levels of the gene.
Bimodality can be observed when the system can actually occupy two stable states; i.e. a gene can either have a high expression or a low expression. When you sample the population you would get two peaks. Bistablity (two stable steady states) is a common phenomenon in biological systems and positive feedbacks generally exhibit such behavior. In bistable systems there is also an unstable steady state which lies "between" the two stable states (like a mountain separating two valleys). If the system is in the unstable state, it can fall to either of the two stable states. (See this article for an example). This concept can be extended to multistable systems but they are a little more complex than the simple feedbacks. However they can theoretically exist (I don't know of a biological example yet).
Bimodality/multimodality can be also observed in the absence of a deterministic bistability in the system. This happens because of the expression noise due to stochasticity and is observed in case of transcription bursts (See here).

Sure - different cells can express different levels of the gene, but the frequencies will be relatively smaller, won't they?

@newintern Depends on the parameters. They can be comparable as well.

Just saw your edit. If this raw expression data were clustered or smoothed to eliminate noise would transcription bursts still be significant enough to be considered another major peak?

@newintern This is true biological noise not a technical noise because of the experiment. By removing it you are dismissing a natural phenomenon. And yes the bursts can give rise to significant effects. See the linked paper.

Alright I understand now. This will help me explicate my data. Thanks!


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Why is water a polar molecule?
Also, what is the definition of polar in this case? (9th Grade)
Does it have to do with the bonds it makes?

I recommend posting this on Chemistry. Here on Biology it is just a bit out of place and that's why we put it on hold. It's an interesting question for sure. Good luck! And a pretty darn smart question for a 14-year-old. At your age, I was pondering other questions - like, what star wars figurine to buy next and stuff :)

Thank you for your advice! Haha, and of course a 14 yr old wouldn't be a 14 yr old without games right? I'm a gamer lol.

Polar means there's a higher density of electron on the oxygen and a lower density of electrons on the hydrogens. This has to do with the electronegativity of the elements in question. Hydrogen is in group 1 which likes to lose it's electron and oxygen in group 16 which likes to get two electrons (in this case one from each hydrogen) in order to complete the octet in it's valence shell.
Also it has to do with the shape, water molecules are not linear, but rather bent in a 'v' shape. the two sides are positively charged and the middle is negatively charged. if it were linear then the middle wouldn't matter, but because it is bent, on side has a negative charge and the other side has positive charge. It's not an negative/positive change the way it is in an ion, just a slight negative/positive charge.

Basically this means it has a hydogen bond?

hydrogen bonds are intermolecular, as in they occur between different water molecules that are interacting. the bond between hydrogen and oxygen is covalent.

not all molecules that are polar and have dipoles are examples of hydrogen bonds... hydrogen bonds are a special case... hydrogen bond is when Hydrogen is covalently bonded to nitrogen, oxygen or fluorine, and this slightly positively charged hydrogen comes in contact with a negative dipole on some adjacent (neighboring) molecule...

@JasandPruski A molecule is polar when there is a net non-zero dipole moment. So asymmetric charge density though a factor, is not sufficient. You have alluded to this point when you mention linear molecule but note that canceling of dipole moments doesn't require the molecule to be linear; for e.g. CCl₄. DM is a vector and it follows the principles of vector addition.

yes of coarse, I merely narrowed it down to linearity on the case of the water molecule, because the molecular formula could indicate linearity if you didn't know the actual shape of the water molecule...

Polar simply means the electron density is not distributed evenly across a molecule. In water this is caused by the comparatively higher electronegativity of the Oxygen (you can think of this like Oxygen wants the electrons it shares in the covalent bond a lot more than the Hydrogen does so it keeps them closer but this is an oversimplification). This translates to the Oxygen having a partial negative charge (higher electron density) and the Hydrogen being slightly positive (lower electron density). The individual water molecules will form Hydrogen bonds between each other, with the positive Hydrogen of one molecule forming a weak bond with the negative Oxygen of another molecule. A molecule being polar has an effect on many of physical and chemical properties of the molecule.
http://en.wikipedia.org/wiki/Electronegativity
http://en.wikipedia.org/wiki/Hydrogen_bond

Polar simply means the electron density is not distributed evenly across a molecule... Not completely correct. Polar means when there is a net non-zero dipole moment.


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Why do adults lose hearing at high frequencies?
Children and teens can hear high pitched sounds that adults can't hear anymore. Why do adults lose high-frequency hearing?

Hearing declines with age and, typically, high frequencies are affected first. Age-related hearing loss (or presbyacusis (Kujawa & Liberman, 2006)) is progressive and starts at the highest frequencies and as a person ages the lower frequencies are affected. The reduction in hearing sensitivity is caused by the loss of hair cells. Hair cells are sensory cells in the inner ear that convert acoustic vibrations into electrical signals. These signals are transmitted to the brain via the auditory nerve.
Because of the tonotopic organization of the inner ear (the cochlea) one can conclude that presbyacusis develops from the basal to apical region. The following schematic of the cochlea from Encyclopædia Britannica, Inc. nicely shows the cochlear tonotopy (i.e., high frequencies in the base, low frequencies in the apex);

As to your question why the basal region is more sensitive to aging - that is a very good and interesting question that has not been answered, as far as I am aware. What is known, however, is that the basal regions of the cochlea are also more sensitive to the damaging effects of ototoxic antibiotics such as kanamycin (Stronks et al., 2011) and other aminoglycosides, and some chemotherapeutics such as cisplatin (Schacht et al., 2012). In low doses these compounds specifically target the basal regions over the apical ones (at high doses the whole cochlea is affected).
Perhaps the specific anatomy and circulation causes the basal region to be affected more by these chemicals. For example, blood flow may be enhanced basally whereby environmental and food-based chemicals may enter the basal region more readily (educated guesses, I can dig up references of authors posing these possibilities if necessary). This scenario may also contribute to presbyacusis, since it is quite imaginable that years of exposure to various substances may cause accumulation damage specifically to the basal parts of the cochlea.
In addition, since high frequencies are coded in the basal region, and given that sound enters the cochlea in the basal region (see picture below), all sounds, including damaging loud low-frequency stimuli first travel to the base on their way to their point of processing.

Because sound is analyzed as a travelling wave, sound travel stops at that point where the frequency matches the cochlear characteristic frequency. There the wave quickly dies out due to cochlear filtering (Mather, 2006); see the first picture above. In effect, more apical parts of the cochlea are exposed less frequently to (damaging) sound stimuli, while the base of the cochlea is exposed to all sounds entering the inner ear.
Hence, chemical exposure and acoustic wear and tear may be more prominent in the cochlear base, which can explain why presbyacusis starts at the very high frequencies and progresses to low frequencies (upward in the cochlea) from there.
References
- Encyclopedia Brittanica* The-analysis-of-sound-frequencies-by-the-basilar-membrane
- Kujawa & Liberman, J Neurosci 2006; 26:2115-23
- Mather, Foundations of Perception, 2009
- Schacht et al, Anat Rec Hoboken 2013; 295:1837-50
- Stronks et al, Hear Res 2011; 272:95-107

Well researched! Great answer!

@CRags - Thanks! The topic is closely related to my Phd :)

Love this answer, "whereby environmental and food-based chemicals may enter the basal region more readily."  It appears you are suggesting there is a relationship between premature loss of hearing and toxin intake.  I have long been an advocate of healthy, toxin-free living.  Thanks for sharing.

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Known ways to modify the genetic structure of the 13 loci used in CODIS
After reading the answer to Does our DNA change during our lives?, I was wondering if and how it would be possible to change the structure of the 13 loci that are used in the CODIS database, in such a way that forensic biometrics would not be able to identify/verify you anymore.
I have read about DNA chimeras, and cases exist where a bone marrow transplantation altered the DNA, depending on the sample that was taken. However, are there any other known ways to alter DNA, such as cancer, radiation, etc?

What do you think will happen, when you alter you DNA in this way? Short: No, it's not possible.

Well the nuclear plant example is of course ridiculous, but I'm wondering if cancer or aging may have an effect which is of high enough significance to circumvent DNA tests.

To cause enough mutations to make the DNA a mismatch would assuredly result in the death of the person long before the sample were obtained. The answer is still no with cancer.

@Chris I disagree that it is necessarily impossible. New techniques such as CRISPR-Cas allows for directed mutagenesis of specific loci, and if you can predict in advance the tissue they are obtaining the DNA from, it is not implausible for a modification to be carried out (for example using retroviral-induced modification).

@MarchHo In all cells of the body so that forensic biology cannot identify you? That'S impossible.

@Chris / March Ho: Any pointers to research papers about this, or do you know this from own experience?

@Michael Forensic biology works with a number of different markers which are located throughout the genome. If you want to change your genetic fingerprint, you need to change all these regions in all your cells. Otherwise you will leave a trace which makes you identifiable.

@Chris , yes I agree, so my question is if it is possible to change these (13) markers.

@Michael Depending on the source you look at, you body has something like 3,4 x 10^13 cells (or 34 trillion). See here for example. How do you want to change all these cells? No, that impossible.

@Chris, I edited my question. I understand that it is impossible to change them all, but cases are known where a bone marrow transplantation caused certain samples to have a different DNA than other samples, of the same body. I'm looking for other ways to accomplish that, maybe more creative, but scientifically proven.

This is important when you look at blood. A lot of forensic biology is done on lost hairs, dendruff...

So for blood it is possible, but for hairs, dendruff, saliva, etc, there are no known (proven) cases?

I have edited my question to be less opinion-based. I'm looking for scientific sources where it has been proven that it is possible to alter DNA structure of the 13 loci used in CODIS. Bone marrow transplantations are known to alter the DNA structure of the blood significantly. Blood transfusions as well, but here, the impact is temporary. In case you still feel it is too much opinion-based, I'm open for suggestions.


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In a typical model ecosystem, what might the percentage of plants be to top predators and everything inbetween?
I'm not sure if this will be a simple question that is almost a natural law for an ecologist, or a complex serious of assumptions.
I vaguely remember from school that only 10% of the energy is converted to biomass at each 'level up' however I have never seen any academic support of this. Lets say we have a fairly representative model ecosystem. In a pyramid of biomass, what percentage of biomass would I expect to see at each level (top predator, primary predator, herbivores, plant mass)?
An additional part I would like to know is does this ever correlate to the ecosystem of any given tier. i.e typically 5 predators will be found in the same area as 20 herbivores rather than 10% of predator biomass for 100% of prey.
There are plenty of diagrams available on google, but I have yet to see anything that looks credible. Any citations to academic sources would be greatly appreciated.

The percentage of biomass at each stage will vary tremendously, based on the following factors:
1: Relative turnover rate of the biomass. When biomass turnover is very high (for example in plankton and whales), it is possible for whale biomass to exceed that of the plankton, even through the whales feed on plankton. Therefore, it is better to use a pyramid of energy, where the total energy flux through a specific trophic level is used. See the article here for more detail.

Just as with the inverted pyramid of numbers, in some rare exceptions, there could be an inverted pyramid of biomass, where the biomass of the lower trophic level is less than the biomass of the next higher trophic level. The oceans are such an exception because at any point in time the total amount of biomass in microscopic algae is small. Thus a pyramid of biomass for the oceans can appear inverted (see image part b). You should now ask "how can that be?" If the amount of energy in biomass at one level sets the limit of energy in biomass at the next level, as was the case with the hares and foxes, how can you have less energy at the lower trophic level? This is a good question, and can be answered by considering, as we discussed in the last lecture, the all important aspect of "time". Even though the biomass may be small, the RATE at which new biomass is produced may be very large. Thus over time it is the amount of new biomass that is produced, from whatever the standing stock of biomass might be, that is important for the next trophic level.

2: Biomass conversation rate in each trophic stage. For example, the article on entomophagy cites a number of papers that insects convert vegetation to biomass approximately 10 times more efficiently than cattle. A population of humans that fed on cattle would have a different biomass (and energy) pyramid than a population of humans that fed on locusts, for example.


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Parallels between pixelized image and the human retina
On Wikipedia it is explained that the human eye has a certain 'resolution'. Does this mean that the retinal image consists of pixels? If yes, what shape would these pixels have?

Are you asking about the shape of the actual physical representation (rods/cones) or the subjective visual  impression?

I can't imagine this meaning anything other than physical representation, since we do not actually perceive pixels at all.

What shape are stars? Presumably a point light source would illuminate precisely one 'pixel' and you would perceive the shape of that pixel only. In terms of the actual cells, they're roughly round when looked at from 'above'. They're round tubes. Like straws.

Related: What's the smallest size a human eye can see?

You need to realize that the human eye doesn't in any way work as a camera. Only a small area of our eye can see sharp images at high resolution, and resolution and sharpness also differs over the rest of the retina as well. So the resolution varies over the retina. The image we actually see is also a continiously interpreted and updated, and the brain is very creative in this process by basically "filling in the blanks". We therefore don't see in pixels.

I have edited the question in the hopes of saving it from going on-hold. Parallels between cameras and eyes are often made and these parallels are often pretty handy for teachers. However, they lead to confusion in many students when the limitations of the analogy are not properly clarified.

The key to your answer lies in the fact that the brain interprets what we see. What we see is not what we perceive. We see as pixels (logical), which get interpreted as a seemless (unpixellated) image in brain through neural processing.

The pixels of the visual system are represented by the photoreceptors. Their shape is the following (adapted from "The Brain from Top to Bottom, MgGill University"):

There are about a 180 photoreceptors packed on 288 microns on the retina (see "What's the smallest size a human eye can see?") so about 1 pixel per 2 microns. The rods and cones are packed closely together on the retina, referred to as the retinal mosaic. This retinal mosaic is not unlike a photosensitive chip, as can be seen on the folllowing image (Developmetal Neurobiology lab, UCLA, Santa Barbara):

We do not visually perceive this mosaic, as the optics of the eye (e.g., light diffraction by the cornea and the lens, and distortions due to the relatively large pupil size) prevents optimal use of the photoreceptor density (the maximal resolution). Furthermore, especially outside the field of view (the foveal region), the output of many photoreceptors are funneled onto one single optic nerve fiber, thereby fusing the output of many photoreceptors (See the question "Why can we not see around our point of focus of our eyes?"). Lastly, the brain actively 'glues' any gaps in the visual field together. Most strikingly, the blind spot, which is the place where the optic nerve exits the eye is fairly large, is normally not visible to us: see the following picture (PNAS online content):

Hence, any gaps in the retinal image are in fact actively smoothened out by the brain.

Interesting answer. In the field of view do the photoreceptors each connect to a single nerve? Roughly speaking how many photoreceptors may channel into a single nerve fiber, on average (unless there are actual values for different areas of the eye!)? This would ultimately be the smallest "resolution" or "pixel size" then, rather than the size of the photoreceptor itself. Thanks again

Thanks. Good question :) As to neural retinal connectivity see: "Why can we not see around our point of focus of our eyes?" You can click the link in the answer above.

If you by pixels are referring to the photoreceptors (rods & cones), their density differs over the retina, and we can only see sharp images at high resolution in a small region of our eye (fovea). So the resolution varies over the retina. The image we actually see is also a continiously interpreted and updated, and the brain is very creative in this process by basically "filling in the blanks". We therefore don't see in pixels, and our resolution is influenced by (at least) light conditions, contrast, photoreceptor density, signal merging and interpretation of the visual signals by the visual cortex in the brain. However, our eye is also constantly scanning the visual field (see saccade), so even if the "static" visual resolution (when we focus constantly on a single point) is drastically different over the visual field, this does not match our visual perception. As a sidenote, saccades are possibly the fastest human motions, and can reach speeds well above 400°/s (Boghen et al, 1975) - wikipedia reports 900°/s but without a clear reference - and takes place several times per second.
If we focus at the resolution in terms of photoreceptor density (densities of rods/cones), this is drastically different over regions of the retina. For instance, Jonas et al. (1992) reports ~150,000 cones/mm2 close to the center of the fovea to 2500-6000 cones/mm2 towards the periphery. The approximate density of rods goes from 150,000 rods/mm2 to 30,000 in the periphery. Cone & rod diameter also differs over the retina, with larger diameters towards the retinal periphery, which relates to light sensitivity.
A nice summary of the flexibility and limitations of human vision can be seen in this xkcd comic (click for larger version):

(from "xkcd: Our central visual field" at http://xkcd.com/1080/)


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Why is ATP the main nucleoside triphosphate used to exchange energy?
Out of all of the nucleoside triphosphates what makes ATP the most used? Is it its structure? The amount of energy it contains? Why is GTP not used as much? What is the deal with the other nucleoside triphosphates (dATP, dGTP, dTTP, dCTP, UTP, CTP)? Are there any artificial NTPs that can substitute for ATP? (like something that could cure Cyanide poisoning or a disease/illness that somehow de-functionalizes the Electron Transport Chain)

This was a question I too asked, during intro biochem. I still don't know the answer. I'm not sure if there's a satisfactory one beyond "evolutionary contingency".

I know GTP is often involved in signaling pathways such as in G Proteins.

@tel do you think there is a way to find this out? an expirement or something?

Apparently some GTP is involved in energy transfer. Following those references might be helpful.

@user137 Yes, so maybe the best version of the question is "Why ATP and not GTP?", since the two molecules are so similar in terms of their chemistry and biological role.

In terms of experiments, you could find an organism (probably some extremophile archaea or something) that produces mostly GTP during glycolysis in place of ATP. Alternatively, you could synthetically alter one of the ATP producing enzymes so that they instead produce GTP. Either one would provide strong evidence that the preference for using ATP in metabolism is mostly a matter of coincidence.

I think that it would be more questionable if every nucleotide was used equally.

It would require multiple and/or multispecific enzymes.

I believe the purines are more reactive, and ATP has a number of factors that make it's hydrolysis much quicker than GTP. Lots of GTP-mediated mechanisms seem to be time-dependent. The hydrolysis energies should be equal.

Cyanide poisoning is because of inhibition of Cyt-c oxidase. Nothing to actually do with ATP. Other complexes are not affected.

@tel that's a great idea. I am only a high school student, and I do not know much about running my own experiments. So, any suggestions on where to get materials for it? and by the way what equipment do I need? I need to know, because the high school doesn't have a lot of equipment

@WYSIWYG I thought cyanide disabled the electron transport chain. Am I wrong?

@Kendall Where did you find out this piece of information? can you point me in a direction that would allow me to learn more?

@AlexStacks it does; but at a particular step. There are some electron transport chains that are insensitive to cyanide


text:
Which came first in hominid evolution: language or bipedalism?
I suspect both language-use and upright-posture have anatomical consequences. So does the fossil record show which came first?
NOTE: To the folks who marked this question "homework": This is certainly not an actual homework question. I have been an accomplished biologist for over 30 years and I am genuinely interested in the evidence for the timing of these critical human attributes. If you feel that the answer is so trivially obvious, that I should have been able to find out with only modest research, could you please leave a comment explaining, as if to a child, exactly how it is so obvious?

Question, although short, is in my opinion valid.

@Christopher Bruns - "homework" is defined here as a question with no research effort made to find an answer. If you hover on the downvote button, a message comes up: This question does not show any research effort. The homework close reason is explained: unless you have shown your attempt at an answer. That's all we're asking. As to defending it by claiming your accomplishments, this is the internet, remember. I can claim to be a Nobel Prize winner. If I post a question that is one sentence, without any explanation or support, it's still a poorly researched question.

@Christopher Bruns- I suggest you modify your question by editing in some useful information, and nominate it for reopening, or post a reopen request in meta

Thank you @anongoodnurse for your thoughtful and helpful comments. I think I will allow this question to fall into closed status and die, then later reask it, next time demonstrating more evidence of research.

Homework question doesn't mean the question is homework. They key statement to that closed reason is unless you have shown your attempt at an answer. I think the close reason shouldn't say homework at all but just say you need to show work so it dosnt cause people to debate that a problem isn't actually homework.

This article by Philip Lieberman On the subcortical bases of the evolution of language, page 22, he asserts the neurons associated with language may have developed based on the demands of bipedal posture. While there's no concrete data to support when we see the first languages, here we see evidence of arches (and presumably bipedal posture) in Australopithecus afarensis. So there are still some dots that need connecting.

OK, so if that one A. afarensis toe bone is convincing, then bipedalism is at least 2.5 million years old. Aren't there also skeletal changes in the skull and neck to allow our modified larynx position, so we could bracket the timing of spoken language development too?


text:
Glycerol 3-phosphate nomenclature
Why is Glycerol 3-phosphate named in such way? Shouldn't it be named as Glycerol 1-phosphate by proper IUPAC- nomenclature?

You're right, according to standard rules of nomenclature it would be called glycerol 1-phosphate. It comes back to the outdated D/L configuration nomenclature. A more thorough explanation is quoted below.

When the R/S system (sequence rule) is applied, substitution of one of the primary hydroxyl groups often leads to changes in the configurational prefix, thus obscuring chemical and biogenetical relationships; it is generally inapplicable to the steric description of such mixtures as occur in triacy1glycerols isolated from natural sources. The stereospecific numbering of glycerol and its derivatives as proposed by Hirschmann [9], described above and in 1, avoids these difficulties; it has proved useful and is widely accepted.

Source.


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Why is DNA antiparallel? Can it be parallel?
My biology textbook mentions that DNA is antiparallel and it got me wondering - can DNA be parallel? What would happen if it was parallel? Could DNA still replicate correctly?

Interestingly the answer is yes. The problem with parallel strands is that the DNA is not pairing in the known way it does when it is combined anti-parallel (or Watson-Crick-pairs).
I have found different images illustrating the problems:

Both images are from this blog post (originally from a publication cited there which is not available online). Both pictures show a distorted DNA structure.
This article ("NMR structure of a parallel-stranded DNA duplex at atomic resolution") shows a more schematic solution of this problem by showing the single pairings. C and G cannot build up 3 hydrogen bonds as they do this in the Watson-Crick-pairing.

Subfigure A and C show the Watson-Crick-pairs, the others come from parallel bindings.
This changes in structure disrupts the function of the DNA (which for example depends on the reverse strand for proof reading). Enzymes which replicate, transcribe, repair etc. DNA will not work on this changed structure, as their function depends on the structural features of the DNA.

here is an interesting paper about parallel double stranded RNA with A-A base pairing. This requires ammonium chloride though.

Wow. Thank you. that was more than I was hoping for. Thank you for adding all of the details.

I think one interesting possibility is that using PARALLEL construction it's very hard to make 'interesting' structures. This isn't important for DNA itself, but is critical for RNA molecules now... and even more so historically in the 'RNA world'. Consider: if making a structure using ANTIPARALLEL pairing, all the nucleic acid needs to do is 'turn around' 180 degrees (known as a 'hairpin' turn) before being able to pair with itself (i.e. form starting structure). This is well illustrated by tRNA
http://www.wiley.com/legacy/college/boyer/0470003790/structure/tRNA/trna_intro.htm
Now--try to draw a tRNA-like structure using PARALLEL pairing--a strand must go through a FULL 360-degree turn before being able to self-pair. This is wasteful and perhaps even impossible without lots of added sequence. Since most folks accept that the beginnings of life were RNA or RNA-like molecules that were both functional (which requires meaningful shapes) as well as 'coding' (DNA or RNA sequence), if shapes were overly convoluted or could not form, life cannot start.
This would be an evolutionary, as opposed to structural, argument against parallel structures.

Seems like an interesting hypothesis. Can you add references for the second part of your answer?

There is another issue here which is more biological.  In general, the enzymes that replicate and "read" DNA run in one direction along the single strand of DNA that they are operating on.  The fact that the other strand of DNA is running in the opposite direction makes it impossible for these enzymes to jump from one strand to the other and ensures that they are operating on the proper information to do their job.  If the DNA strands were parallel, the enzymes would be likely to attach at a locus and then randomly read information from either strand, and the information produced would be gobbldygook.  So while it is chemically possible to have parallel DNA, a biological system that was based on parallel DNA would be at a big competitive disadvantage and so if they ever arose, they were probably driven extinct by the systems we now see that use anti-parallel DNA.

welcome to bio. Could you add your sources?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What are the advantages of blood's redness?
Although this page (http://evolution.berkeley.edu/evosite/evo101/IIIE5aNotadaptation.shtml) denounces the idea that blood's redness is not an adaptation, I remain inquisitive on the matter since no scientific research has been performed in studying its possible advantages.
Does anyone have any ideas on the advantages of having red blood?
Thank you for your time and effort

I don't think there is an advantage in blood being red. It is a byproduct of the heme being coordinated in the middle of the heme as the active center. Hemolymph has a copper atom there and is more blue/green due to this fact.

I think your article explained it quite well. Blood is an adaptation. The color of blood is not; it's a coincidence.

@Chris Thank you for your detailed reply, your chemical background has proved useful here.

@anongoodnurse So what should I do with this question? Delete it?

Totally up to you. If you want a better answer, you can leave it and see what comes up?

I can make this into an answer if you want. It would be a rather short one, though.

@Chris I would be extremely grateful if you could do so please.

The reason why blood is red is rather simple: It is the iron atom in the middle of the heme, which plays the central part in binding oxygen. Depending on the oxidation state the blood looks either dark or light red. The structure is the following (taken from here):

That the color only depends on the coordinated metal atom is shown by another related molecule, the hemocyanin, which is the oxygen carrying molecule in the hemolymph of insects. It contains copper which is colorless in one oxidation state and blue-green in the other. The function is the same, the color is different.

Thank you for your answer but I'm a little confused - weren't there four Fe molecules?

This is true for the hemoglobin. This consists of four subunits. Each of these carries one heme with one iron atom. Together you have four hemes in the hemoglobin molecule.

Ah, I see - so your picture shows one heme and one iron atom

Yes, this is clearer this way.

@Chris did you mean blood is red rather than heart is red? I am changing it. Please revert if you feel it is wrong.

@CRags You are absolutely right. Thanks for finding this error.


text:
Cell evolution: immortality vs reproduction
Many sci fi movies produce interesting ideas and technologies that we seem to be able to realize in real life at some point. "Lucy" was not one of those movies.
But Morgan Freeman's speech in the movie on cell evolution did interest me.
The speech claimed that cells in harsher environments evolve towards immortality, while cells in favorable environments evolve toward reproduction.
Is this idea accurate?

Just for the pleasure to hear Morgan Freeman's arguments, can you please link the video of his speech?

How would you compare survival to immortality? There are many examples of adaptation for survival, but immortality is a stretch.

@Remi.b I would like to; I welcome someone to find this clip - It doesn't seem to live on Youtube yet.

@anongoodnurse I think "immortality" isn't meant literally. It's a dramatization for increasing lifespan.

You may want to read a bit about the evolution of ageing. This post for example is very interesting (it won't necessarily answer your question though).

In Nick Lane's book Life Ascending he talks about caloric restriction resulting in more mitochondria in cells and less mitochondria leak. This is a stress response that may inhibit cell degradation (death). I'm sorry I don't remember who the researchers were who discovered this or theorized on it, but I thought it might be germane to this question.

It wouldn't be good to replace reproduction with immortality even if it were possible. Let's assume some animal was immortal, could not die of old age or disease. There would still be accidents, injuries, starvation, or predators to worry about, so they would still have to reproduce to keep the species going.

"All the cells that make up the worm or human has only two options ...
Immortality ...
Or reproduction.
If its habitat is not quite favorable ...
The cell chooses immortality ...
That is to say, self-sufficiency, self ...
But if the habitat is favorable ...
This is the reproduction is selected.
And when they die the essential data is passed to the following cells ...
Who in turn pass on these cells ...
The knowledge, knowledge is devised through time."
http://www.springfieldspringfield.co.uk/movie_script.php?movie=lucy  I found the script, no video though.

It's absolutely true what Morgan Freeman said in Lucy........
....immortality is possible in organisms. The organism which might interest you is:
Turritopsis dohrnii - a jelly fish Harsh environmental conditions favour TRANSDIFFERENCIATION....a special type of METAPLASIA.

You'll see that in many cases, when any sort of cell enters a zone of intolerance or zone of physical stress, the replication machinery gets put on the backburner (and thus replication). Expression of stress-response proteins like heat shock proteins is increased as a result (1). If a cell isn't within acceptable parameter to undergo division at G1 or G2 (anoxic environment, etc.), you'll find mechanisms like G0 phase or sporulation are preferred until the environment returns to something less stressful (2). I wouldn't say cells would rather be immortal, per se, but longevity or even apoptosis/entosis/etc. would be preferable to replication if nothing is going right (3, 4).
To be clear, when we're talking about evolution that's a tough one. Sure, some sort of stress-response transient signal could induce some lasting cell memory selecting toward a specific function. I simply don't have the data to quote you in that aspect, however.

Biology of the heat shock response and protein chaperones: budding yeast (Saccharomyces cerevisiae) as a model system.
Slonczewski, J., & Foster, J. (2011). Microbiology: An evolving science (2nd ed., p. 143). New York: W.W. Norton.
DNA damage-induced apoptosis
Cellular Stress Responses: Cell Survival and Cell Death

As a footnote, while replication does occur in sporulation, the replicated chromosome is destroyed in the process of forming the actual spore.


text:
If we change our breathing rate so easily, then what is the point of measuring it?
When we are self-conscious of our own breathing, its rate changes very easily. Therefore, if it changes so easily, what is the point in measuring it?
Thank you for your time and effort

We may be able to voluntarily control our respiratory rate, but only for a short while. The buildup or depletion of CO2 will force us, against our will, to either speed up our respiration or slow it down. So, you can't effectively "fake" your respiratory rate for long, nor, to an astute observer, convincingly.
Normal breathing patterns are "normal" for a reason. Aberrations from normal do occur in pathological states, but they are compensatory mechanisms driven by a number of factors your blood chemistries: the pH and the intimately linked CO2/H-CO3 concentrations, etc. You can pretend any way you like: you won't be able to keep it up comfortably. Also, normal breathing isn't simply "breathe in/breathe out". It is a more complex thing characterized by an inspiratory phase of certain duration, an expiratory phase of a different relative duration, and a normal, periodic deeper breath (close to a sigh), all done physiologically and unconsciously.
With certain illnesses come certain breathing patterns. You might be able to fool one person's quick assessment, but not more than that. If the faked breathing pattern (largely unsustainable anyway) doesn't appear physiological, you will be quickly found out.
For that reason, a sustained increased or decrease in respiratory rate is indicative of particular pathologies, whereas a normal respiratory rate is a helpful sign.

Thank you. Excellent and fast answer. This is what Stackexchange truly is.

But what about doing slightly deeper or shallower breaths instead?

@imallett - See the edit.


text:
What shows how healthy someone is by their heart rate?
What shows how healthy someone is by their heart rate - how low it is at resting pulse or how low it is during exercise or how large the difference is between the resting rate and rate with load? Any ideas?
Clarification:
Essentially, how does the heart rate reflect healthiness and in which ways (is it the resting pulse, pulse during exercise, differences, etc.)
Thank you for your time and effort

As an additional note, Chris from the chat room says that "the time you need after an exercise to get to the complete resting pulse is a good indicator."

"Which questions are off-topic?: personal medical questions and health advice."

@fileunderwater I don't quite think that my question is off-topic since it is not listed under:
-> personal medical questions and health advice
-> philosophical or ethical questions related to biology
If you read the question carefully, this question is the relationship between heart rate and health, not "I go to the gym every week, what else should I do?"

In general, these types of health related questions are closed at BioSE, since they could 1) be a reformulated question on personal health advice or 2) be used to evaluate individual health. Both are off-topic for the site. Your Q is also not framed in terms of biological processes, but only asks about evaluation of health.

@fileunderwater "personal health advice" "individual health" - This is an entire field in biology on the research of fitness where graphs of heart rates (bpm) and breathing rates (metres cubed per hour) are used on a regular basis. User Chris has done some training in this field too. This question stems from research, not individual health interests and actually results from a team practical.

I'm simply stating my view and how I interpret the off-topic guidelines. See these three meta posts for earlier discussions: http://meta.biology.stackexchange.com/questions/556/policy-on-health-questions , http://meta.biology.stackexchange.com/q/139/3624 and http://meta.biology.stackexchange.com/questions/597/clarifying-our-scope-with-regards-to-medical-questions

@fileunderwater Don't worry, I don't mind a grudge here or there ;) It's part of life.
Anyway, in reference to your first link, [quote from answer:]
"As you say, questions that ask for mechanisms on e.g. how something will affect the body would still be on topic, if correctly phrased."
All I am asking for is how do scientists determine the healthiness (if that word exists) of a person from the heart rate and how reliable is it.

I can see myself the misreadings of the questions so I will hasten to edit it.

@fileunderwater For heaven's sake, my question has got NOTHING to do with personal health!

And now a whole load of closers have piled in

@TimTimmy Can you please leave out other persons from your questions/replies?

@TimTimmy I voted to close when I left my earlier comments, which should make my reasoning clear. BioSE is in general very restrictive towards medicine/health, especially if questions aren't phrased in terms of biological processes. You only mention 'health/healthiness', without any definition of what you mean with this, and do not include any reasoning on e.g. how different aspects of heart rate is related to oxygen uptake, immune response or other aspects of "health". I therefore find it off-topic, but others might see it differently.

@Mad Scientist I don't see any purpose to this question anymore due to the wide miscomprehension of it and it will just clutter the community. Could it please be possible if it could be deleted? Thank you

@fileunderwater I see what you mean, but I have to note that the purpose of this question will help me to write key points for a book on GCSE Biology. Truthfully, I don't see much of a point any more in arguing. Hopefully the moderator will delete the question

A healthy heart and cardiovascular system distributes oxygenated blood more efficiently than a less healthy one. Therefore, for a given level of exertion, a healthy heart will need to pump fewer times than a less healthy one to provide the same quantity of oxygenated blood to the rest of the body.
It's pretty much that simple.
However, the whole patient has to be considered. A low heart rate in and of itself doesn't mean someone is fit since there are many drugs and medical conditions that can create a low heart rate. Person A sitting in front of you appears fit and healthy, is on no relevant medications, and has a heart rate of 50? Fitness almost certainly explains it. Person B sitting in front of you is overweight, on several meds and not very fit? Fitness almost certainly doesn't explain it.

Is there also a relationship with the difference between the heart rate during excise and during rest?
e.g. I did a team experiment and Will had a lower heart rate than Harry. However, when it came two exercise, the difference between the exercise heart rate and normal heart rate was larger than Harry's. Is this an error, mere coincidence or something that can tell us more about his health?

@TimTimmy Not an error unless the measurements were in error, but I don't know how to interpret the results you pose. Someone who is more fit should start with a lower heart rate and end up with a lower heart rate for the same level of exertion than someone who is less fit. But that's a huge generalization. Individuals respond very differently to the same levels of exertion.


text:
Death Psychology

Why do we sympathize in general when we see something or someone dying even if we personally don't know it/them?
Is there any species which sympathize with the death of its own species?
Is there any species which sympathize with the death of other species?

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

This question seems to be off-topic in biology unless more technical details are included. I think CogSci.SE would be suitable for this question.

Thanks for pointing out. I have submitted a migration request

@CRags - migration is often performed only with rockstar questions. As you haven't had any upvotes whatsoever I suggest cross posting.

@ChrisStronks do I close the question here?

@CRags - nope, just leave it as is, or close it if you wish of course


text:
Factors for sensitivity to electric shock
I'm frequently getting electric shocks in my office when touching things. I basically know why this happens and how to avoid it.
Still I started to wonder what would be the best way to touch something if you knew you will be shocked. I know that fingertips have more nerve endings but I guess they also have more callus. What are factors for sensitivity to electric shock and what part of the hand is therefore the least unpleasant to be shocked?

Practical advice: Take a metal thing (pen, key, etc.) in your hand and ground yourself over it. Then the current will flow through the metal and not hurt you.

I've built a lot of electric fence in my youth. If you MUST touch an electric fence, use the back of your hand, so if you get shocked you'll pull away instead of grab on. Also, a leather wallet makes a decent insulator to push down on a wire so you can step over. To this day I can't touch a wire without testing it first even if I know it's cold. Don't know if these tips apply to your job, I haven't seen an office building with electric fence.

@user137 the problem is static charge. Maybe it's the carpet or something. So it has nothing to do with touching things that actually carry an electric current.

@AndréStannek Can you put a humidifier in your office? The humidity will help dissipate static charges.

@user137 it's in the office of a customer so no big influence on anything there. To avoid long discussions in the comments I'd like to point out that this is not what my question is about. Of course I still appreciate your concern and help :-)

The dorsum of your hand is less sensitive than the palmar surface. It's hard to touch or pick up things with the dorsum of your hand, though.

I synced the title and body and made some additional changes to make the question more clear. Please feel free to roll back if it is not to your liking.

Inspired by this study on bee sting pain, you could do your own study involving electric shock. This piezo electric lighter claims to deliver 10,000V shocks at safe currents, and if you do the experiments on just yourself you usually don't need approval for human subjects.

@ChrisStronks I changed the title again because that's the part of the question I'd like to emphasize. Otherwise your edit is fine, thanks!

@user137 that would answer the second part of my question. Still I'd like to know the reasons. Does it only rely on the number of nerves or are there other factors? See my last comment for the emphases of my question.

@AndréStannek This may be a nobody knows (for now) question. I would certainly be curious if there is research on this and more so why said research was carried out! Who would fund this? The only electric-pain experiment that springs to mind is the (in)famous Milgram experiment. This still doesn't even begin to answer your question.


text:
What were the first neural systems like?
I'm curious about the origin of the neural network.
I'm thinking perhaps once life evolved beyond the single cell organism, it needed a simple neural network to coordinate those cells, and cell functions.
What were the first neural systems like?
More specifically: What kind of cell did the first neurons evolve from and how did they work at first? (assuming there were few, if any, neural connections in the first organisms to develop neurons of some sort)
From what I understand about a neural system, it needs a few neurons linked together to keep firing.
Perhaps the first neurons had triggers other than dendrite connections?

I think this is too broad, since you are basically asking about the evolution of nervous systems (in any type of organism?), and there are multiple questions rolled into one. Also, why do you think that single neurons would be useless? They could still transfer information between cells (e.g. sensory/environmental input to motor action). Wikipedia: Evolution of nervous systems will also answer/hint at some of your questions.

@file I'll focus the question.

I think this question is unanswerable as neural tissue is not preserved in fossils. Looking at relatively 'simple' organisms may help to get an idea. For example the neural system in cephalopoda (various ganglions throughout the body each driving one tentacle etc) or in insects.

@ChrisStronks We know tons about evolution that isn't preserved at all in the fossil record. For instance, we can study evolutionary model organisms and do comparative genomics. In fact, fossils play a fairly minor role in the modern study of evolution.

@KonradRudolph : sure, that's what I say, perhaps use insects or other organisms. And if there's tons of info on the first neural systems I am curious to your answer!

In hydra it is like a net— no central organization. Developmentally neurons arise from the ectoderm (from where skin also arises). This may perhaps be a recapitulation of the evolutionary trajectory

This question can be answered by taking a look back evolutionary and see how other organisms have utilized neurology. The prime example, because it was one of the first real models of the neurological system, is the squid. It has neurons with singularly long axons to send electrical pulses long distance. This method of electric pulse transfer has been evolutionary updated, essentially, but we can get an idea of how these cells came to be. If we look back at squid predecessors, like the jellyfish, we see that it also developed electrical impulse cells to aide in defense and movement. Back further, we see the sponge has no neurons, but has something similar. This gives us potential insight into the development of the cell. It has protein clusters that act similar to post-synaptic signaling. So it is likely the electrical impulses were developed based on the function of these protein clusters, and bam! Electrical pulses became a must faster way to communicate to different regions of a system than simply trying to protein signal across cells.
Of course, looking at this question evolutionary is tricky since the question of divergent evolution comes into play, and we can't know if the sponge protein clusters offer a potential answer to neuronal development. But, is interesting evidence and makes an interesting debate!
Source= Sakarya O, Armstrong KA, Adamska M; et al. (2007). Vosshall, Leslie, ed. "A post-synaptic scaffold at the origin of the animal kingdom". PLoS ONE

I would really emphasize how limited our conclusion can be through looking at current organisms.
Yes we can say one organism may be "higher level" than the other, but knowing exactly what the primitive state was? That is most likely something we will never truly know.
Perhaps when we can finely simulate evolution through computers. An interesting new advancement has been the creation of circuit boards using algorithms for evolution. Essentially the circuits that are less efficient die out.

I agree!  New networking algorithms offer interesting new insight to these types of questions (and many others!). I actually am currently working on developing such algorithms for alternative toxicity testing methods! It's crazy the diversity of uses of different tools, right?

@FrankyG this ironic thing is, the use of algorithmic evolution of a brain was my purpose for asking this question to begin with. I've been experimenting with throwing out random configurations of tens of thousands of neurons of virtual neurons, which behave in a similar way to actual neurons, and let the ones die which arent capable of overcoming a pre-defined environment. This is a vague experiment at this point, and it hasnt gotten anywhere, because I think I need to start smaller, simulating an extremely primitive small group of neurons accomplishing a simple task.

But the issue with that is, our modern day neurons seem to be fairly useless in small groups. Theoretically, being able to figure out how the most primitive group of neurons worked would allow a good starting point for the evolutionary model.

I think starting smaller would be a good idea and then expanding off of that to see how evolutionary the different ways neuronal networking could have occurred. You could even throw in probability curves to estimate likelihood of evolutionary occurrence, but that would have to considered unknown environmental factors. Anyway, if you think the question is answered well don't forget to mark it as answered so other people can reference it!

The problem is that in smaller groups there isn't much pressure for neuron selection. What I suggest you do is simulate having many smaller groups of neurons all with connections to one another and allow it to start choosing the most effective way to send signals between the groups. We know primitive neurons worked much in the same way our own do using either chemical or electrical signaling. The problem isn't how they send signal but how they choose which signal pathway is the proper one to enhance and strengthen.

So if you create your simulation with small groups of neurons (say 100 per group, mess with the size) and have an algorithim that strengthens connections to groups around it based on what information needs to be sent and where. You can probably simulate it to have groups of neurons that do a particular mathmatical operation and give it (lets call it a "brain") problem sets to solve that require it to use either all/some/few of the small groups. Of course I have no clue where to start from a theoretical standpoint it sounds feasible.

You can further add variation to this by having the type of connections created be varied. You'll have to do some more research on specific neurology though as there are several different types of connections neurons can make to one another and it affects not only the speed of the signal but the strength when it arrives and how that signal propagates, reaches threshold, etc etc.


text:
How does vasoconstriction/vasodilation change blood pressure?
Background: I am coming at this question from an electrical engineering background, and I feel like I am missing certain assumptions that are going into the statement found in my physiology textbook, "vasoconstriction increases blood pressure"."
Consider a simple series circuit and a parallel circuit run by a battery/heart [you will find the parallel and series circuit in any physiology book description of the vasculature, yet I can't find any exploration of the assumptions made when applying these circuit models]:

In the series circuit, if I have an increase in resistance across
one of my resistors, this will basically redistribute the pressure
drops across the resistors, but it will not alter the total pressure
drop across all the resistors [fixed by the heart].
In the parallel circuit, if I have an increase in resistance across
    one of my resistors, this will redistribute the flow to different
    branches, but the pressure drop will not change as again this is
    fixed by the heart.

This analysis seems to suggest that if the resistance across an organ [branch of parallel circuit] changes, the flow changes, not the pressure. The heart, I would assume, then responds by increasing the pressure to increase flow ie actually injecting energy into the system.
Here is the problem with the circuit model though:

it assumes that the battery/heart is the only source of energy in
the system, and the resistors are passive re distributors of that
energy.
the controllers of vascular resistance are smooth muscle which must actively put energy into the system to vasoconstrict. This could be
a source of pressure increase as the smooth muscle would be actively
constricting against an incompressible fluid, but I am really not
sure.
it does not account for the compliance of the vasculature.

-the tubing the heart is hooked up to modifies the blood pressure the heart has to generate to inject fluid into that tube. If the tubing was stiff, the heart would have to generate very high systolic pressures that would then rapidly decrease during the diastolic phase. The more compliant the tubing, the less pressure the heart has to generate to inject fluid into the tube. Intuitively though, there would seem to some relationship between the ability of a fluid to flow and vessel compliance. A highly compliant vessel with a fluid injection will simply expand and hold the fluid while a less compliant vessel will maintain a pressure necessary to push the fluid along.
Sparknotes in the form of questions:

Is the only source of energy in the cardiac circuit the heart? Or
does artiole smooth muscle actually inject energy into the system,
        and result in systemic increases in the pressure available in the
        closed circuit.
I don't think vascular compliance ie expansion of the artery walls
due to volume filling results in any active injections of
        energy into the system..it should simply transfer the energy
        available to push fluid to elastic energy in the connective tissue
        of the artery walls. Is this correct?
Does vessel compliance partly determine the pressure the heart has to inject into the system?
What is the relationship between compliance and flow if there is one?

How do say pressure drop is fixed by heart?

Its  engineering lingo..I apologize. It essentially means that the only energy in the system is provided by the heart.

I mean, if you increase a single resistance in a series circuit, will there be no change in the potential drop across the entire circuit?

correct by conservation of energy

The circulatory system is a dynamic system which cannot be adequately explained by your example (at least not by me). You need to understand it, not seek to make it fit your (especially) electrical circuits with resistors. Blood isn't electricity. At least try a fluid dynamics model.
Let's take this very simple model: Blow up a balloon four-fifths of the way, and put a wide inflatable cuff around its middle. Inflate the cuff so that the balloon bulges just a tiny bit at the ends, then stuff it all into a plexiglass box so that the balloon has no room to expand. The plexiglass box represents our body. Lets call the pressure inside the balloon now normal blood pressure. The air in the balloon represents your total blood volume. It can't change from moment to moment; it's fixed. The box can't change it's volume moment to moment either. It's fixed.
The cuff represents arterial smooth muscle. Vasoconstriction can be represented by inflating the cuff further. Constriction (inflation of the cuff) will increase the pressure throughout inside the balloon, because the same amount of gas now has to exist in a smaller space. Vasodilation (deflating the cuff) decreases the pressure inside the balloon, because the gas can now inhabit a larger amount of space.
That's it, really. If the same volume must inhabit a smaller, constricted space, the pressure exerted by blood in that space will be higher. If the blood vessles dilate, the pressure in the blood vessels falls.
Now add about 20 layers of complexity to that simple model, and you have a working model of the circulatory system.
Sparknote answers:

Arterial and arteriolar smooth muscle "injects energy into the system", resulting in systemic increases in the pressure existing in the vascular "circuit" (meaning somewhat elastic tubing) if resistance requires energy. (So I have misunderstood: see @Raoul's answer.)
Sorry, I didn't read this properly the first time around. Yes, the heart supplies the energy. The contribution of the elastic walls of the arteries is not active, but passive.
Absolutely. The more elastic/compliant the arteries are, the less work the heart must exert to pump the blood through the circuits. The stiffer and narrower the arteries are, the harder the heart must work to pump blood through the circuits. The result of that increased work is a thickening of the muscular walls of the heart, called ventricular hypertrophy, which is a sign of elevated pressure in the system.
I'm not sure I want to commit here to your lingo, but the answer should be inferable from numbers 1-3. Elastic vessels help (by rebound compression) to propel the blood through the circuits. Stiff vessels hinder it, making the heart do more of the work.

I am not an engineer, so I may be misusing some of the terms.
Edited to add: Please see @Raoul's answer for a better explanation.

I just want to add a few points to the above answer:
Heart is not the only organ which helps blood flow. The following structures also help:

The action of muscles on deep veins acts as a pump - Soleus is called peripheral heart for that matter
The compliance itself adds to the flow - Infact the compliance of the blood vessels is what makes the blood flow continuous instead of pulsatile like a system with stiff tubes would be expected to act when the pump is pulsatile in nature

Some Critical Points to keep in mind:

The circulatory system is made in such a way that the total sum of cross sections of all the vessels at a particular level is as follows:

The sumtotal of cross-sections of all capillaries is the largest cross section ~ 11308 cm2, (approximately only 1/4 are open under normal pressure, so effective cross section is ~ 2827 cm2)
The sumtotal of cross-sections of venules followed by arterioles (~141 cm2) (venules more than arterioles as arterioles normally are under a tonal contraction)
Sumtotal of cross-sections of veins followed by arteries (~63 cm2)
Cross-section of Vena Cava ~ 1.38 cm2 followed by Aorta ~ 1.13 cm2

So if the cross sections are added up: Capillaries > Venules > Arterioles > Veins > Arteries

The Pressure Blood Pressure we measure is not exactly the flow pressure aka the pressure gradient. We measure the radial pressure not the pressure gradient. Special equipment is needed to measure pressure gradient.
The volume of fluid inside a parallel circuit (artery to capillary to vein) is not constant as plasma diffuses out at the small arterioles and capillary levels and diffuses back in at the venous side.
The pressure flow curve is not linear due to the compliance of the blood vessels.
The heart contributes very little to the blood flow in the veins. (To re emphasize that heart is not the only organ driving circulation). It is mainly through postural drainage and muscle action.

Coming to your question I like to point out one thing:
If there is a need to increase perfusion, the vasoconstriction occurs at the venular side. The capillary pressure is responsible for perfusion.

$$P_c = \frac{(R_{post}/R_{pre}).P_a + P_v}{1 + (R_{post}/R_{pre})}$$
  Where P - pressure and the characters a, v and c denotes artery, vein and capillary
  resistance
Rpost - Post-capillary resistance
Rpre - Pre-capillary resistance

The equation and picture are taken from Boron and Boulpaep textbook of Medical Physiology, 2nd Edition, Chapter 19: Arteries and Viens.

When there is a need to increase the perfusion to an organ the post capillary pressure is raised by venoconstiction (or in the case of glomeruli of kidney constriction of efferent arterioles). As you can see from the above equation, such a rise will cause rise in the capillary pressure and increase the perfusion.
Otherwise vasoconstriction occurs to do exactly what you assumed would happen: to redirect blood flow. In fact this happens at several levels:

Vasoconstriction of periphery (limbs) occur in cold conditions which causes cyanosis (meaning the flow is so reduced that most oxygen is used up)
Vasoconstriction of Splanchnic vessels occur when muscles need more blood (during exercise, flight, fight, etc...)

If you can read this chapter you will understand the equation much better. This book explains the physics behind physiology in a beautiful manner.

I'll try a brief answer myself.

No, the heart is not the only energy provider, as others have stated above. Does vasoconstriction inject energy into the system? Not really. Arteriolar constriction will increase the resistance of the system. Therefore, more energy will be required to keep flow at a constant level when vasocontriction occurs. Arteriolar vasoconstriction forces the system to function at a higher energy level, yet it does not inject energy targeted at facilitating flow.
Yes, your assumption is correct.
@anongoodnurse answered correctly.
There is no direct relationship between compliance and flow. They are independent factors. The important point is the following: during diastole, the heart is isolated from the vessels. The higher the vessel compliance is, the more potential elastic energy will be transferred from the heart to the vessels during systole, to then ensure good flow during diastole. In elderly persons for example, arteries are usually stiff, systolic pressure is high, and diastolic pressure is low (as is flow).

To conclude, I would say that the most important lesson that is to be learned here is that although a higher blood pressure means a higher energy state and more work for the heart, it is incorrect to assume that blood flow is physiologically adequate because pressure is high! This is a common mistake made in the emergency room.

+1 - glad to read your answer. You understand fluid dynamics better than I do. Because of your different answer, I had to rethink my own, and see my errors. I do find myself sometimes wishing you were around more. Care to weigh in on the cardiac output question? ')

@anongoodnurse Thanks! I'll have a look at that one. I spend a lot of time on stackoverflow, but I like it here as well. I'll definitely stick around. BTW, your answers are usually very good!


text:
Why don't stem cell therapies use viruses?
Why don't stem cell therapies use a virus to deliver gene editing sequences to stem cells instead of the harvesting-transformation-transplant route.
I thought it might be because of a lack of specificity on the part of the viruses, but then I saw phage display techniques that would seem to make that a non-issue.
I thought it might be trans-cytosis or getting the phages out of the blood-stream and into contact with the stem cells. I haven't found an easy solution to this hurdle, but it doesn't seem to be insurmountable.
I think the main issue is regulatory? Perhaps a lack of precedents in this area. What do you think of my analysis? Is this idea even feasible?

There is active research in this area using animal models, which bypasses many ethical hurdles (I assume that's what you mean by regulatory). The immune system is a significant hurdle.

Phage display isn't that good at making structures that actually work in vivo. I'm not saying there are no successes, but the rate is pretty low. And any time you're delivering viruses into a patient you're likely to develop antibodies against that virus, making repeated doses harder. That's how vaccines work.

Any idea how far along the animal model viruses are?

Interesting read relating the subject.

Stem cell therapies do in fact utilise viruses. In the examples cited, the stem cells were infected by viruses in vitro, genetically modified, and then reintroduced into the target as autologous transplants. The main issue at hand is that live viruses introduced directly would be targeted and destroyed by the immune system, which greatly reduces their efficacy in causing transformation of cells.
In a recent Nature paper, zinc finger nucleases were used to target and disrupt the CCR5 or CXCR4 gene, which greatly reduces the efficiency of HIV binding to CD4+ T cells. The zinc finger nucleases were introduced into the cells using an adenovirus vector.

Generation of cxcr4 ZFN adenovirus and CGW-siX4s lentiviral vectors. The CXCR4 targeting locations of siX4s and ZFN are shown in Supplementary Figure S1.

This technique was then used in a number of clinical trials to modify hematopoietic stem cells using zinc finger nucleases, as summarised in this review paper. The recent advent of CRISPR-Cas systems will probably lead to an increase in similar techniques, due to the higher specificity and ease of engineering of Cas9-based nucleases.

This is an exciting field. I am very interested in the potential to avoid the immune system.

Thanks to you guys I googled, "stem cell virus animals" and found some promising links! I appreciate you guys emphasizing immunological response. I was hoping that the virus would be effective enough to work on the first shot and thereby avoid most of the immunological complications. However it seems that the second generation of adenovirus vectors in animal models was abandoned for just that reason: source - NCBI.
Here is a nice excerpt regarding animal models:

“third-generation adenovirus vectors”: This research focuses on the development of improved production systems for gutless adenovirus vectors and their use for the efficient introduction of large or multiple transgenes into human progenitor and stem cells with minimal vector-related toxicity. In addition to the use of regular third-generation adenovirus vectors for the transient genetic modification of target cells, we have embarked on the generation of new vector types for stable transgene expression in transduced target cells using locus/site-specific transgene integration or homologous recombination. For example, we have generated new adenovirus/adeno-associated virus vectors. These vectors stably integrate into a specific locus on human chromosome 19 and are capable of genetically complementing dystrophin-deficient human myoblasts.
-Leeds Universitair (NZ)


text:
How to prevent e coli from clumping (for FACS)?
I'm performing FACS on e coli, but the cells are clumping together so each event is multiple cells.
I ran a control where I had one flask of e coli expressing GFP, and one flask expressing RFP. Run separately, I got a clean population of either high-GFP fluorescent events, or high RFP fluorescent events. If I mix 10uL of each population into 200uL TE buffer and immediately run that sample, all the events have high RFP AND high GFP fluorescence, indicating the cells are sticking together immediately upon mixing.
Cell line: ER2566 (NEB)
F- λ- fhuA2 [lon] ompT lacZ::T7 gene 1 gal sulA11 Δ(mcrC-mrr)114::IS10 R(mcr-73::miniTn10-TetS)2 R(zgb-210::Tn10)(TetS) endA1 [dcm]
Host strain for the expression of a target gene cloned in the pTYB vectors.
Carry a chromosomal copy of the T7 RNA polymerase gene inserted into lacZ gene and thus under the control of the lac promoter. In the absence of IPTG induction expression of T7 RNA polymerase is suppressed by the binding of lac I repressor to the lac promoter.
Deficient in both lon and ompT proteases.
Growth media: M9 minimal media
FACS running media: TE
I know there are anti-clumping agents for yeast and mammalian cells, but I haven't come across one for bacteria.
Can anyone recommend:

an e coli protein expression strain that is known to not clump
an anti-clumping agent for bacteria
any other possible solutions
?

Thank you!

Check out the (many) strains and methods in this paper: http://www.ncbi.nlm.nih.gov/pubmed/18926860

If you don't have access to that journal, I put a copy of the PDF in my Dropbox here.


text:
What is the biological basis for tiredness after eating?
I can sometimes feel quite drowsy after some "meals" (e.g. a cold cut & cheese sandwich with juice on the side) and less drowsy (or maybe less often) after others (such as a salad).
This drowsiness sometimes affects my work at the office, so I wanted to ask these questions:

What biological factors lead to the body getting tired after eating?
Are there any strategies that can be used to minimize this effect?

Eating shunts blood to the intestines and puts the body in the state of regeneration instead of mental and physical performance. To prevent it, eat light stuff (bread instead of hot foods, carbohydrates instead of proteins/fat), and limit quantity.

High carbohydrate meals will undoubtedly increase the relative levels of insulin, increase the shuttling of glucose from the blood to the cells, and leave you fatigued in wake of that. See reactive hypoglycemia. Reducing carbohydrate consumption should, to some level, reduce this effect. Caffeine should just as likely increase blood glucose levels by increasing glycogenolysis through PKA activation.
As Chris Stronks pointed out, eating can cause low blood pressure via redistribution of blood.

I think it has a lot more to do with redistribution of blood to the intestines (depleting the brain from it)


text:
Pituitary giants - is the fusing of growth plates dependent on amount of growth hormone in blood?
I wanted to ask a couple questions related to pituitary giants (people who are giants because of some anomaly, such as a tumor, in their pituitary gland).
Some of these giants seem to keep growing and growing until the tumor (or the gland) is removed. Is this because the fusing of the growth plates is controlled by the amount of growth hormone in blood?
The reason for this question is that many of the giants have been described to grow past when the growth plates should probably have fused. For example (all heights in meter, m):

Bernard Coyne This giant is described as having been 2.36m at the age of 20, but 2.54m at the time of his death at the age of 23.
Edouard Beaupré At the age of 17, this giant was measured as 2.16m tall and at the age of 21, he was measured at 2.50m tall. At the time of his death, at the age of 23, he was listed (in his death certificate) as having been 2.51m tall and "still growing".
Väinö Myllyrinne This giant was 2.22m at the age of 21 but is described as having "experienced a second phase of growth in his late thirties", attaining a height of 2.51m by the time of his death at 54.
Adam Rainer This giant was, unusually enough, a "dwarf" at the age of 18, reaching a height of 1.22m. However he had a growth spurt afterwards, reaching a height of 2.18m at the age of 30 and 2.34m by the time of his death at age 49.

Also, in some cases the giant individuals facial (bone) structure changes as he/she ages. Considering that the human skull does not have any growth plates, or anything that would (as far as I know) put a stop to the skull bones response to growth hormone, can changes in face structure also happen to "regular" people who take growth hormones?

The hormone controlling growth plate fusion is normally testosterone.

Gigantism is caused by too much growth hormone (GH) and causes increased growth in kids (healthline website). After adulthood, increased GH leads to acromegaly which leads to continuing growth of fingers, feet, forehead, jaw, nose, and lips (UCLA Health website). Note that structures like the nose and ears also keep on growing in healthy folks.
Hence, GH does not prevent closure of the growth plates, which happens normally as far as I am aware.
Taking GH during childhood will likely lead to gigantism, and to acromegaly in healthy individuals.
EDIT: In answer to the QUESTION EDIT: the comment by @Raoul is interesting here, as the first guy Bernard Coyne was an eunich. Perhaps that was why his plates never fused as he will have had no testosterone production. I couldn't find specifics in the other 3 cases, but my guess is they are also exceptional cases (otherwise they wouldn't have made it in the record books). As to the question title I dare say that GH is not involved in plate fusion.

Thank you for your answer, Chris Stronks. I have edited my question with details of some giants who kept growing taller when they were older. If GH does not prevent the closure if the growth plates, is the lengthening of the legs in these types of giants then a form of acromegaly (distortion)?


text:
How to determine if this blood disorder is recessive or dominant?
This question is from "Concepts of Genetics," Klug & Cummings, 10e.
"Thalassemia is an inherited anemic disorder in humans. Affected
individuals exhibit either a minor anemia or a major anemia.
Assuming that only a single gene pair and two alleles are
involved in the inheritance of these conditions, is thalassemia a
dominant or recessive disorder?"
I know from a quick Google search that the disorder is recessive, but how would I come to this conclusion based on the question alone?
Edit: I've spoken to my professor, and he shared his opinion that is essentially the same as canadiener's answer. Thanks to everyone that replied!

I would say neither, as ">either a minor anemia or a major anemia" implies two phenotypes. This is co-dominance if I am not mistaken. Dominant would mean always major anemic (either homo or heterozygous) when affected, recessive would mean only major anemic (homozygotic). Perhaps the geneticists among us can look into this?

I was under the same impression about codominance, but the text splits up inheritance patterns by the usual dominant/recessive in one chapter and all the modified patterns in another. This question is listed in the first of these two, so I assume I'm given enough info in this chapter to be able to answer, but I just don't see the reasoning.

no answers in the back o/t book? ;)

Not for this one, unfortunately. Only evens get answers >_<. I'll consult the professor when I can.

don't forget to answer your own question then :)

I think in general, we prefer to use "incomplete dominance" when the heterogeneous phenotype is in between the two homozygous conditions, and "co-dominant" when the het show both distinct phenotypes.  If a red and white flower cross yields pink flowers, that would be incomplete dominance.  A and B blood types having an AB child is co-dominance.  But these terms don't really tell you much about the underlying molecular genetics

Given that this is a text book question about classical genetics, you can safely disregard any reality about the disorder.
I'd argue that the two alleles show incomplete dominance. The mild anemia, which is intermediate between healthy individuals and those with severe anemia, can be attributed to heterozygous individuals. In this case, the expression of the functional allele is not enough to compensate for the nonfunctional allele, producing the mutant phenotype.


text:
How do we look inside the cell?
My sister is in 9th grade biology and her teacher avoided answering the question of how we actually study the inside of a cell. I haven't taken biology in a while but I'd like to give her an answer.
Can someone roughly summarize how we actually learn about what goes on inside a cell? Just mentioning a few of the most common or used techniques would be fine.
Note: I hope this isn't a bad question. It's a bit vague. But I didn't want to leave her without a decent answer.

Techniques to look at whole cells are: Light microscopy (cells, large organelles), electron microscopy (detailed analysis of subcellular structures and even proteins) and confocal fluorescence miscroscopy (look at particular cellular planes, reconstruct 3D images).
And of course you can analyze the insides by Biochemistry by breaking the cell membranes and look at individual proteins and DNA/RNA by extraction and electrophoresis followed by Western / Northern / Southern blotting, or isolate organelles by centrifugation.
It is a broad question, and I just gave the most obvious examples of techniques (not anywhere near exhaustive). By googling the bold-out terms you may provide some details to your sis.

Beyond the conventional methods listed by Chris Stronks, Berkley Labs have far advanced the state of the art in probing the internal structures of cells using x-ray tomography. See:
http://ncxt.lbl.gov/ . The images obtained are absolutely incredible and allow researchers to probe the cell layer by layer and visually contrast specific organelles for study much in the same manner that organisms are examined using CT scanners.

That was fantastic. Nothing can replace seeing it for yourself!

One technique that I like is Immunofluorescence. You get images like this:

The staining are caused by applying antibodies with an flourescent probe. The antibody 'sticks' to certain parts of the cell, & the probe produces the light patterns you see.