text:
Which immunosuppression caused by long-term usage of these antibiotics in untreated celiac disease?
These antibiotics include

amoxicillin + acidum clavulanicum (beta-lactam, inhibit cell wall synthesis, broad specturm, 3rd gen aminopenicillin) / last part preventing the resistance
ceftriaxone (3rd gen cephalosporine, inhibit cell wall synthesis, broad spectrum)
clarithromycin (macrolide, inhibit protein synthesis by binding to ribosomal subunit S50)

used regularly for cyclic middle ear infections for years during the childhood - ages 2-10 for a patient with untreated celiac disease.
I am thinking what kind of immunosuppression can this lead to.
I think it mostly conquered by suppression of adaptive immune system.
Little lowered innate immunity lowered too.
I am especially interested in the antigen-presenting cells (mostly dendritic cells) and their function in an immunosuppressed patients of the antibiotics.
There may be other factors which I have not mentioned related to this kind of immunosuppression.
Feel, free to propose.
How can dendritic cells work in an immunosuppressed patients?
You can assume any combination of cases for the three antibiotics: 8 possible cases.
For instance,

(1) and (2) high antibiotic resistance, and only susceptible to (3)
High antibiotic resistance to (1)-(3)
...

Possible cases which reminds

this immunosuppression can remind this one: immune reconstitution syndrome like in HIV but milder

Amoxicillin is often combined with a beta-lactamase inhibitor like clavulanic acid. This oversomes the problems with the resistance, but can cause problems in patients which are sensitive to this additive. It can cause vomitting.

@Chris Thank you for your comment! Yes, indeed - Acidum clavulanicum added next to Amocillinum.

I am a bit confused by your question. So you want to know if and how immunosuppression by antibiotics work and how APC are involved or affected?

One further question: What are your references for these antibiotics beeing immunosuppressive? There are some, which have this effect, but these are not widely used to fight infections.

@Chris. Yes to first question. Please, open me on this topic. There may be other antibiotics in the case. There may also be cases that such antibiotics cause immunosuppression in some patients - this is what I am studying now. I am just not understanding the mechanism.

Off the top of my head, chloramphenicol is the only antibiotic I know of that causes immunosuppression (by causing aplastic anemia).

I don't think these antibiotics has immunosuppressive effects. There are immunosuppressants which are completely different drugs... Antibiotics simply kill pathogens, or stop/slow down their growth and multiplication. I think you should clarify your question, at least I don't understand how using antibiotics can lead to immunosuppression...

I added the case to be with a patient with untreated celiac disease during that time.

Thanks. Interesting question, I'll check it when I have a little free time...

One possibility is that these antibiotics could disrupt your normal gut bacteria. Given that your gut has the surface area of a tennis court and is typically coated with symbiotic microbes, antimicrobial therapies could dramatically change the population dynamics of your gut ecosystem. One might imagine that the immune system of the gut is in homeostasis with these gut microbes, and if they all die off all at once because you're taking some sort of 'cillin, your immune system might suffer for lack of stimulation. Fewer immune cytokines released by your intestinal immune cells into your blood => systemic reduction in immune function.
Other possibilities could include: the drug just randomly fits into a bad spot on some important immune protein; the drug targets bacterial-related genes in the mitochondrial genome and disrupts the metabolism of the immune cells; the drug disrupts your ability to absorb nutrients required for immune function...the list of potential mechanisms is undoubtedly long.

Thank you for your answer! I added untreated celiac disease to the description which disrupts the normal gut bacteria.


text:
How are chickens affected by light?
When I was young, I was told never to put a fluorescent light in a hen house because it continuously turns on and off. Extra lighting is used, as far as I know, to 'extend' a chicken's day. Human eyes don't have the refresh frequency to notice that, but there are animals who have a frame-rate of up to 200 Hz (so they actually see the lights turn off and back on again). I was told chickens are among those animals and that they'd stop laying eggs when continuously exposed to interrupted lighting.
However, my neighbour has fluorescent lighting in his hen house. So either the above is bogus, or I have my facts mixed up. So, how (if at all) are chickens affected by light?

Haha, nice question. They hear between 0-200 Hz, but it is hard to find anything about how they see...

http://ps.oxfordjournals.org/content/77/11/1695.short

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=621444&fileId=S004393399800004X

It seems like they are not affected by fluorescent light frequency. I did not find anything about their visual sampling rate. Their hearing is between 0-200Hz with an average of 86Hz so I guess the visual sampling rate is under this, but that's just a guess.

We conclude that at the illumination levels used in this experiment,
  the hens did not perceive the flicker of low-frequency light or they
  perceived it but did not find it aversive. Low-frequency fluorescent
  light does not appear to adversely affect the welfare of hens.

1996 - Laying hens do not have a preference for high-frequency versus low-frequency compact fluorescent light sources

It concludes that there is no evidence that fluorescent or high
  pressure sodium lighting, irrespective of intensity or spectral
  distribution, has any consistent detrimental effect on growth, food
  utilization, reproductive performance, mortality, behaviour or live
  bird quality in either domestic fowl or turkeys, nor in the egg
  production of geese.

1998 - Responses of domestic poultry to various light sources
A monochromatic (LED) light can be more beneficial according to this:

A significant reduction in egg production was observed in all 880nm
  groups; no differences in egg production and quality were found in the
  other groups. Feed consumption was significantly lower by 7% in all
  0.01 W/m2 groups. We suggest that an important reduction in rearing costs of laying hens may be obtained by using this system.

1998 - New monochromatic light source for laying hens

source: Stack Exchange

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

sort: votes


text:
How does non-homologous end joining (NHEJ) work?
I was reading about non-homologous end joining (NHEJ) in my molecular biology of the gene textbook but the explanation provided in the text was rather vague to me, and I was not able to understand it completely. I understood that NHEJ can be used as a repair mechanism when double-strand breaks in DNA occur. The two broken ends are then joined together. What I didn't understand is how this is done. The two broken ends won't always have complementary bases so, won't this lead to mismatched bases? How is this problem fixed? I really need a detailed explanation of how NHEJ occurs please.

Non-homologous end joining indeed induces errors in the affected sequence. But you have to keep in mind, that NHEJ is an emergency repair mechanism which involves a "repair or die" chance. If the chromosomal break is not repaired it is not unlikely that the cell will get into apoptosis, or, even worse, develops into a cancer cell. Introducing small errors is a relatively small price compared to this, although this can still disrupt genes or regulatory sequences. For the mechanism have a look onto the figure (from the first reference):

For further reading have a look onto the Wikipedia article on NHEJ and/or the following references:

The mechanism of human nonhomologous DNA end joining.
The mechanism of double-strand DNA break repair by the nonhomologous
DNA end-joining pathway.

NHEJ is indeed error prone. It is called "non-homologous" because it does not use a "homologous" template from another sequence-matching piece of DNA to guide the repair. Homologous repairs avoid causing mutations because the similar string of DNA  acts as a template so that the cell knows what letters to put into the gap. When there's no template, there's no way for the repair machinery to know what specific letters to use...hence the mutations in NHEJ.
Interestingly, this NHEJ phenomenon is used to drive the current state-of-the-art in genetic engineering: CRISPR/Cas9 RNA-guided endonucleases. If you cause a double-strand DNA break near the beginning of the protein-coding sequence of a gene, this break will be repaired with NHEJ, causing an "indel" (insertion or deletion) mutation to occur. Inserting or deleting letters into the coding sequence of a gene will cause a "frame shift" where the 3-letter codons which tell the cell which amino acids to use get all jumbled up because the normal 3-3-3-3-3-3-3 pattern is disturbed. In this way, we can turn off genes that we want to target: just cause a frameshift in that gene with CRISPR.
If we want to INSERT something using genome editing, we need "homology directed repair" -- we'll give the CRISPR alongside another string of nucleotides which matches the strings that flank the place we are cutting, with a new sequence in the middle. So when CRISPR makes the cut, our homologous template will stick to the sides of the cut and the center piece will provide the cell with a blueprint for the insertion or edit we want to make.
So, you'll see as you think about it that the "homology" which is missing from NHEJ is the strand used as a repair template, and by manipulating these natural DNA repair processes which may or may not use homologous templates, we have a possible method to turn on, turn off, edit or insert genes. This means NHEJ isn't just a biological process anymore: it is an engineering technique.

authors: Денис Крамаренко

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


text:
What is the difference between the basal membrane and the basal lamina?
I'm researching about the basal lamina in lung tissue and I'm not sure if the basal membrane is the same.
What is the difference between them?

The basal lamina is a specialised type of extracellular matrix. It is found on the basal side of all epithelial tissue but can also surround other cell types like myocytes and adipocytes. It is also called the basement membrane, although it is not the traditional plasma membrane that we have come to know and love. Rather, it is composed of proteins (often glycosylated) and polysaccharides.
The basal membrane is the actual plasma membrane on the basal side of an epithelial cell (adjacent to the basal lamina/basement membrane).


text:
What is the difference between rheobase and threshold?
Neuronal tissues can be excited by electrical stimulation. Two commonly encountered characteristics for electrically stimulating nerve cells is the threshold and the rheobase. My question is what the difference is between rheobase and threshold? In the definitions I've read it's described as almost the same thing. The threshold, or minimal stimulus, is defined as "the electrical stimulus whose strength (or voltage) is sufficient to excite the tissue. Rheobase is defined as "the minimum strength (voltage) of stimulus which  can  excite  the  tissue". What is the difference?

You need to clarify your question with a short background. 'Threshold' is a general term, not only dealing with membrane potential (which I assume is what you're after).

by threshold i mean that strength (voltage) that can cause action potential

Add this to your question, along with the confusing/unclear definitions that you've read.

Excellent question! The difference is the fact that the rheobase is an example of a threshold measure. The threshold, as you correctly suggest, is the minimal energy (typically current level and not voltage as you suggest) to excite neural tissue. The threshold applies only under the specific experimental parameter settings used. These parameters include the type of electric stimulus (for example, a biphasic current pulse), the electrode configuration (for example, bipolar stimulation) and the stimulus duration (for example 200 microseconds).
The rheobase is the minimal current level needed to excite a tissue when an infinitely long stimulus would be applied. The rheobase is typically found by plotting the threshold level (as defined above) as a function of stimulus duration. The reason for developing this measure is the fact that excitable membranes integrate the injected current, so charge builds up in the tissue. In other words, increasing the pulse duration decreases the threshold current level needed. Hence, the rheobase is a convenient threshold measure because it incorporates the duration parameter of the stimulus. It will still depend on things like electrode configuration and stimulus shape.
The function of the strength-duration relationship can be fitted with a decaying exponential:
I = Ith / ( 1-e(-t/Tsd) )
where I= Threshold current level;
Irh = rheobase
t = stimulus duration
Tsd = Tau = exponential
Here is a picture of a theoretical strength-duration curve copied from the wiki page on rheobase. [NB: I find the wiki page needlessly complicated].

The rheobase is the horizontal asymptote. An often used parameter to characterize the function is chronaxie, which is the pulse duration equivalent to two times the rheobase.
The explanation given here was adapted from the book "Cochlear Implants", chapter 5 "Biophysics and Physiology" by Abbas and Miller, two veterans in cochlear implant electrophysiology. Unfortunately I cannot give you a link to the pdf as I own the work in hard copy.

PS: If you want access to the chapter your library will be able to get a hold on a copy of Cochlear Implants (Zeng & Popper, Eds.) I'm sure.


text:
What kind of fly is this?
I found this dude hanging out in my sink, but he didn't fly away when I put a dish in the sink. Turned out it was dead. The front part looks exactly like a housefly. But, I've never seen the back end (abdomen) look like this. Any ideas?

This is probably a fly killed by the fungi Entomophthora muscae (or closely related) or maybe a Cordyceps fungus. These kinds of fungi mainly attacks insects, and you sometimes see attacks as white, swollen abdomens in flies.

(Picture of common infection, from bugguide.net)
These fungi are also known to change the behaviour of infected individuals, so that they e.g. climb up tall plants to die (sometimes called "zombie-insects"), to allow for better dispersal and transmission of the fungal spores. Lots of information about the behavioural modifications of hosts by fungi can be found in Roy et al. (2006), but they can involve both climbing to exposed locations and special mechanisms for host attachement at death:

In many cases the final interactions, or endgames, between a host and pathogen involve complex behavioral modifications such as the infected insect seeking an elevated position where wind currents can effectively disseminate conidia. Elevation seeking by insects at late stages of infection is a common phenomenon that was recognized by early insect pathologists who noted that diseased lepidopteran larvae, such as Lymantria monacha (the nun moth), infected with baculoviruses migrated to the tops of trees where they died (94). This host-altered behavior was named “Wipfelkrankheit” or “Wipfelsucht” (meaning tree top disease in German) for viral diseases (41) and “summit disease” for fungal diseases (24, 57, 106).

and

Some fungi do not produce rhizoids, but the host is held in situ by host structures alone, namely the legs or mouthparts (mandibles or stylets). The pose of the dead insect is generally characteristic of the pathogen species involved. For instance, E. grylli-infected grasshoppers (Figure 3a) and E. scatophagae–infected yellow dung flies (Figure 3b) seek elevated positions on grasses or other vegetation and cling tightly (death grip) with their legs (96). Tipulids infected with fungal species from the genera Eryniopsis and Entomophaga also attach to grasses with their long legs, often overhanging water (Figures 5b,c).

If you do google image searches on "Entomophthora fly abdomen" or "fly Cordyceps" you can see some examples of infections. I don't know about the fly species, but Musca domestica is probably likely.
For some more examples and information on Entomophthora muscae and related fungi see:

Roy et al. 2006. Bizzare Interactions and Endgames: Entomopathogenic Fungi and Their Arthropod Hosts. Annual Review of Entomology 51(1) (pdf)
Biological Control: Entomophthora muscae, webpage from Cornell Uni.
Harmon. 2012. Fungus that controls zombie-ants has own fungal stalker. Nature
Mind-controlling fungus turns insects into zombies (blog post)

Cordyceps-like fungi (there are several genera from two families) have very prominent fruiting bodies, I think this alternative can be ruled out.

authors: Ντίνος Τσακαλάκης


text:
How can I compare the STRIDE and DSSP output files of a particular pdb file?
I have the pdb file of H-ras protein 5P21.pdb. I am supposed to compare the output of DSSP and STRIDE files after feeding this pdb file to respective servers. My question is how to make a quick comparison between these two results?

Here a solution that does not require you to upload the files to the servers: You can graphically visualize DSSP and Stride at the Sequence Page at RCSB PDB:
http://www.rcsb.org/pdb/explore/remediatedSequence.do?structureId=5P21&bionumber=1
"add annotation" -> Stride and look at the graphical comparison between DSSP and Stride.


text:
Why is the vermis of the cerebellum associated with speech?
I've found multiple sources claiming that damage or impairment as a result of alcohol to the vermis of the cerebellum results in speech impairment. I find this a bit surprising, since the only areas I know that are used for speech production are Broca's area. Additionally, I don't know of any way that the vermis influences this area or any other facial nerve that may need co-ordination to produce speech.
So why does damage/impairment of the vermis result in dysarthria?

Although speech production is in generally executed in the cerebral domain, the dysarthria resulting from damage of the vermous is a symptom of the resulting general muscle weakness. So yes, you get slurred speech because your muscles are weak, but the weak muscles certainly aren't ever isolated to speech production.


text:
What is the name of the critter depicted in the attached image?
I found a critter on my bathroom towel. It's really tiny. Maybe 2 milimetres? I placed it on an envelope for the photograph.
Can someone identify what it is?

Possible duplicate of Bug Identification: Is this small tubular, black bug a bed bug?

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insect specimens..., Varied Carpet Beetle Larvae, What small insect is this?, What bug is this...

That is the larva of a carpet beetle.

Larvae feed on natural fibers and can damage carpets, furniture, clothing and insect collections.

"Anthrenus verbasci - larva side (aka)" by André Karwath aka Aka on Wikimedia
Related question: What kind of caterpillar is this?, though I think that the larva photographed in that example is either of a different species or at a different time period within the larval stage.


text:
Hill's function for translational regulation
Transcriptional regulation is generally modeled as a Hill's function (similar to Michaelis-Menten Kinetics):
$$\frac{dm_X}{dt}=\alpha _{m_X}.\frac{R}{K+R} -\beta _{m_X}.m_X$$
Where $m_X$ is the mRNA for some gene-$X$, $R$ is a Regulator $\alpha$ and $\beta$ are formation and degradation rate constants respectively. This equation denotes a saturation kinetics; increasing activator wont cause indefinite increase in transcription. Sounds logical because all promoter sites will be occupied at some point.
In case of a repression the equation looks like:
$$\frac{dm_X}{dt}=\alpha _{m_X}.\frac{K}{K+R} -\beta _{m_X}.m_X$$
I want to model repression of translation using a similar equation. However, the issue is that even though a single mRNA can be saturated by a regulator, increasing mRNA will require more regulators. So effectively the regulator available for a single mRNA molecule will be total regulator ÷ total mRNA.
My question is that whether in such a case the following equation is logical:
$$\frac{dX}{dt}=\alpha _{X}.m_X.\frac{K}{K+R/m_X} -\beta _{X}.X$$
Where $X$ is the protein.
Which means we are taking into consideration the effective concentration of a regulator per mRNA. In other words the Hill's constant $K'$ should scale with mRNA concentration. ($K'=K\times m_X$)
Assumptions:

Well mixed system
System at thermodynamic limit
Amino-acid pool infinite
Ribosomes infinite

I am confused are we talking about regulating translation or transcription? By translation for example there can be competitive inhibition caused by RNA intereference afaik, so it does not depend only the amount of mRNA... And ofc there is a max speed which depends on ribosome count.

Oh no no.. No complications involved. This is just some regulator (mechanism unknown). Ribosomes are plenty (they are not considered variables). I mentioned transcription so that those who have seen that equation for transcription regulation can draw parallels with the equation that I mentioned.

Ohh okay. So ribosome count can be considered infinite in this case, and only mRNA count and the regulator affects the speed of the translation. Am I right? If yes, then please edit your question with these details!

Does X mean the amount of proteins in your equation?

See the edit. "Speed of translation" is not affected; just the rate of protein formation.

Yepp you are right they are different things. :-)

For me it makes sense if we are not talking about ribosome count, and we assume that the regulator instantly finds free mRNAs (and if R regulates the translation in your equation). Now I think these constraints taking us far from reality, but who knows...

It can be assumed that ribosomes are not limiting. If they were then protein synthesis would be globally affected which doesn't generally happen during the usual gene regulation (happens under drastic conditions such as UPR and stress). Regulator may not instantly find mRNA. We can adjust the rate constants accordingly. My doubt was mainly regarding normalizing regulator concentration with total mRNA for the hill's equation

I checked some articles, and almost all of them use f(r), r = (mx, X) to describe regulation and they are talking about regulatory networks. So you'll probably need Fourier transformation and such nice mathematical tools to understand them.

Articles about regulatory models of transcription and translation - http://arxiv.org/ftp/arxiv/papers/1204/1204.5941.pdf - http://arbor.ee.ntu.edu.tw/~brdai/papercollection/Bioinfo/chenmg99.pdf - http://bioinformatics.oxfordjournals.org/content/22/14/e489.full.pdf+html - http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.100.9757&rep=rep1&type=pdf - http://psb.stanford.edu/psb-online/proceedings/psb03/dehoon.pdf - http://www.uv.es/gfl/documentos/TIG.pdf - http://www.ihes.fr/~zinovyev/papers/MorozovaRNA2012.pdf - as far as I understand none of them used your approach by translation...

It looks right to me. I don't have references at hand right now, but iirc even Hill functions in the context of deterministic models assume the ratio of TF concentration to the number of TF binding sites to be large; otherwise, you would have to consider binding ratios even at the level of transcription modeling, similarly as to what you are doing now for translation. E.g. consider a hypothetical situation where 10 TF molecules would compete for binding to 5 different promoter regions, each having 10 binding site repeats. (cont.)

Similarly, in your specific case, introducing the ratio of regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway. If this assumption cannot be made, then your reasoning makes sense. One thing you could consider doing is establishing system reactions, then deriving Hill-free ODE equations according to the law of mass action; you could then compare this model to the one you propose. Furthermore, performing a stochastic simulation might make sense (I can recommend tools if desired). Let me know if you need help with any of this.

@w128 Thanks for the answer. I have also been discussing this issue with my PI and he also said that adding scaling in the equation is not necessary if the dynamics are not very different from unscaled one. I would do stochastic simulations later. Thinking of using fortran for implementing Gillespie's algorithm. Can you post this as an answer because this seems logical. You can add some logical/mathematical explanation. I don't need references (I don't think anyone has modeled translational regulation as saturation kinetics). PS: If you do it in 24h you will get the bounty :)

@w128 "Similarly, in your specific case, introducing the ratio of regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway".. I agree but unlike promoter sites the mRNA concentration is not static and so the number of mRNA-sites will keep changing with change in mRNA levels. That's why I thought scaling should be important. Otherwise the model would mean that the regulator is just repressing the ribosome allocated to this mRNA.

Your logic looks correct to me. Essentially, what you are doing is uniformly distributing the regulator among the available mRNA.
Note that even when using Hill functions to model transcription, the ratio of transcription factor (TF) concentration to the number of TF binding sites must be large - otherwise, you would have to consider binding ratios even at the level of transcription modeling, similarly to what you are doing now for translation. E.g. consider a hypothetical situation where 10 TF molecules compete for binding to 5 different promoter regions, each having 10 binding site repeats - you need to somehow distribute the available 10 TF molecules among 50 target binding sites. Clearly, this is not something accounted for by the standard Hill equation, which would in such case wrongly assume that 10 TF molecules are regulating each construct.
In your specific case, introducing the ratio of the regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway. Note that the maximum level that $m_x$ can reach (at steady state) is equal to $max(m_X) = \frac{\alpha_{mX}}{\beta_{mX}}$. If you can ensure this value to be much smaller than your translational regulator concentration, you will get similar results even if you use simply $\frac{K}{K+R}$ for translation modeling.
If the latter assumption cannot be made, then your reasoning makes sense. For each individual mRNA molecule:
$$\text{X produced per mRNA} = \alpha_{X} .\frac{K}{K+R'}$$
where $R'$ is the amount of mRNA bound to this molecule. If $R$ is the total available regulator concentration and uniform binding affinity is assumed, this means that $R'=\frac{R}{m_X}$. Summing this over a total of $m_X$ mRNA and considering degradation yields exactly your final ODE.
Note that another important assumption you are making is that regulator binding/unbinding to/from mRNA is fast compared to translation, and that no cooperative interactions are present.
If you want to verify things further, you could establish system reactions, then derive Hill-free ODE equations according to the law of mass action. You could then compare this model to the one you propose. Furthermore, performing a stochastic simulation might make sense. If you want to go down this road but don't want to implement Gillespie's algorithm on your own, you can use e.g. SGNSim or COPASI.

Thanks for the answer. This was helpful. I understand that there are many considerations to be made to make the right model. I had to simulate different kinds of regulatory motifs so I wanted to keep the equations simple while at the same time allowing saturation.


text:
Which organs in the body are responsible for measuring temperature?
As an instrumentation engineer, I have designed temperature control systems
capable of measuring and controlling temperature with a precision of 0.001K over a
wide temperature range.  I have always wondered how the human body maintains its
temperature within a fraction of a degree; specifically, where and how is the
temperature measurement done?

https://en.wikipedia.org/wiki/Thermoregulation#In_humans

http://en.wikipedia.org/wiki/Thermoreceptor

As @inf3rno said there are thermoreceptors (TRPV ion channels) that are responsive to temperature. They are involved in temperature sensation of the environment as well as the body itself. I am not fully sure if they are the sole temperature sensors of the body. Have a look at these articles: [1], [2] and [3]

Human thermo detection comes from a protein, expressed in high levels in the nervous system.
As per comments, there are a group of transmembrane proteins called transient receptor potential cation channel subfamily V (TRPV) ion channels that can detect temperature changes. Although the exact mechanism of the protein remains unclear, a study published in Nature 2010 showed that a protein called TRPV1 opens and closes to allow increased or decreased sensitivity to temperature change.
There is no specific organ that is responsible for temperature detection, however TRPV1 is expressed in high levels in the nervous system.


text:
Help me understand my membrane potential assignment
Epithelial with the ability to transport NaCl is bathed in an isotonic salt solution with these values (in mM): 136 Na, 6 K, 140 Cl.
The intracellular concentrations are: 45 Na, 100 K, 13 Cl.
The cell's resting potential is -63 mV and the temperature is 37 Celcius.
Which ions will passively diffuse over the membrane?
My attempt: I calculate the nernst potential of each ion and taking the first ion (Na) as an example I get that it's equilibrium is at 29 mV. So as there are more of these cations outside the cell and the membrane potential is negative, the ions will want to "reach" 29 mV by flowing INSIDE the cell (to increase the membrane potential). I think they will do this by diffusing into the cell? I'm not sure if I am attacking the problem correctly or if it's rather lunging at my abilities in transporters. The NaK transporter is active transport so maybe the do not diffuse at all?? However there are Na channels that can open...Which is passive diffusion..
Calculate the cation permeability Pna/Pk
I have no idea how to do this. I still need more constants in the Goldman equation (Pcl for example) before I could isolate even one of these.
Thanks!

You can find the relative permeabilities here: http://nernstgoldman.physiology.arizona.edu/using/

Btw. if this is a homework you probably don't have to use the Goldman equation to solve it. At least my experience is that they usually give you all the variables you need.

You think I should just use the average P values like on the link? This is not really "homework", it's an assignment for next class where it will be discussed and solved in front of everyone. It's best that I try to solve it before class.

If there is passive transport for each ion, then every ion will diffuse over the membrane until the concentrations will be the same, and the membrane potential will be zero. So there is active transport in the cell, which maintains the resting potential which is -63mV.
So with the current concentrations the membrane potential will differ from this -63mV, and so the cell will change the ion levels to change the current potential to be equal to the resting potential.
I think you should try to simply summarize the Nernst potentials. It won't be so accurate as the Goldman equation, but you don't have the relative permeabilities of this cell type, so the questioner probably does not wait the Goldman equation from you.
I would solve it this way:
Em = RT/zF * ln(out/in)

R = 8,314 J/molK
T = 37 + 273 = 310K
F = 96485 J/molV

RT/F = 26,712mV

ENa = 26,712mV*ln(136/45) = +29,543mV
EK = 26,712mV*ln(6/100) = -75,152mV
ECl = -26,712mV*ln(140/13) = -63,486mV
Em = ENa + EK + ECl = -109,95mV

Emr = -63mV
Emr - Em = -63mV + 110mV = +47mV

So we have to increase the membrane potential. Decreasing intracellular K+, Cl- concentration and increasing intracellular Na+ concentration can do that.
Concentrations: extracellular 136 Na, 6 K, 140 Cl, intracellular 45 Na, 100 K, 13 Cl. So possible passive transports are increase Na+, decrease K+, increase Cl-.
Conclusion the passive transports will be increasing Na+, decreasing K+ the active transport will be decreasing Cl-.
Note that I haven't used these terms for 5 years, so if you can consult with somebody else about this, then ask him/her whether this is correct.


text:
Is there a maximum size for an insect?
I have read in biology text-books that one of the most important constraints on the size of an insect happens to be the importance of the surface-volume ratio. It simply states that
if we assume constant oxygen levels and increase the size of an insect there would be a point where the insect's exoskeleton would no longer be able to support its weight.
Some textbooks go on to say that this is why we don't have insects the size of elephants. But, if this is true...is there a least upper-bound on the maximal body mass of an insect?

Also relevant are http://biology.stackexchange.com/q/13444/107 and  http://biology.stackexchange.com/a/20677/107

Also see http://biology.stackexchange.com/questions/17488/will-the-increase-in-atmospheric-carbon-dioxide-lead-to-larger-insects

I assume there must be a maximum size for insects, and I atmospheric oxygen probably has something to do with it. Insects do not breath like vertebrates, they have a series of tubes call trachea that run through their bodies and open to the surface at spiracles. Air passes through these tubes and oxygen and CO2 passively diffuse through the tissues. Insects can force air through the trachea to increase the diffusion rate, but they just aren't as efficient as vertebrates with lungs and hemoglobin to carry oxygen around the body.
In the past, oxygen levels were much higher. Higher amounts of oxygen could allow for larger invertebrates, and there were 6 foot long millipedes and giant dragonflies. Their size probably was not entirely caused by the extra oxygen, this was before they faced competition from vertebrates, so increased competition probably had more to do with their size reduction than loss of oxygen.
I don't know what the maximum size for an insect is at modern oxygen levels, but you'd have to eliminate the other selective pressures such as competition and limits on food before an insect could reach that size.

Good point. But, in that case I wonder why text books sometimes deduce with confidence that insects can't be as large as elephants? Unless a biologist has approximated the maximal size of a terrestrial insect...

Another limit on size is strength. An insect can't be directly scaled up to large sizes because an object's weight scales with the volume, but strength tends to scale with cross-sectional area. Since volume is cubic and area is squared, weight can overcome strength unless the legs are made thicker relative to the rest of the body. Additionally, insects have less efficient circulatory systems, where hemolymph escapes from the vessels and passes directly over the tissues, being collected at the other end of the vessels and passed back through the heart.


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Is the activity of enzymes in the human body affected by the outer temperature?
I have to do a research about the enzymes in the human body and the things that affect them. I know that the body temperature affects the activity of enzyemes but I'd like to know if the outer temperature of the air affects them, too?
When the temperature goes to 47°C or more we get tired and exhausted. Is this because the activity of enzymes decrease or is something else?!

Is this a homework question? What are your ideas for solving the question?

@Chris no i do a research and this's a part on it but i can't find the answer

Enzymes usualy have a relative narrow temperature optimum, for those of our body this is usually around 37°C. It is around 37,2°C in the morning and goes slightly up to 37,7°C in the evening (see reference 1 for details). The temparature optimum for most enzymes looks somewhat like displayed in the figure (from here, interesting to read):

Enzymes are relatively tolerant to lower temperatures (although their reaction rate is much lower), but generally they work. If you go too high with the temperature, the activity will soon be reduced to zero, as the enzymes are denaturated and are not able to catalyze any reaction.
The human body does quite a lot to control its temperature and to keep it within a pretty small limit. It does either excessive sweating (when it's hot) or shivering (when it's cold) to maintain its temperature within or at least near the optimum. For further details on the themorgulation have a look on the Wikipedia article on this topic or reference 2 and 3.
Although our enzymes work at slightly lower reaction rates when the body temperature is higher (think of fever), this is not a major issue. Slightly higher temperatures can thus be tolerated, although you don't feel very nice.
The effect of to hot temperatures is different, though. It is mostly due to not consuming enough water, so that the body has not the possibility to control its temperature via sweating. This condition will ultmatively lead to a heatstroke, see here for more details. Before you reach the temperature in which your enzymes reaction rate will go down drastically, you have long collapsed.

References:

A critical appraisal of 98.6 degrees F, the upper limit of the
normal body temperature, and other legacies of Carl Reinhold August
Wunderlich.
Skin blood flow in adult human thermoregulation: how it works, when
it does not, and why.
Thermoregulation: some concepts have changed. Functional
architecture of the thermoregulatory system

"Although our enzymes work at slightly lower reaction rates when the body temperature is higher (think of fever)..." I'm very puzzled by this statement. Do you have support for it? Without reading, I would posit that the body is metabolizing more quickly, thus generating additional heat.

He is doing more metabolism, not necessarily faster.

Sorry to repeat the request, but do you have support for that?

@anongoodnurse Have a look at this and this articles. They both show the activity of enzymes depending on the temperature. And both show a sharp decline in activity above 37°C. The first is acid phosphatase, the second pancreatic lipase.

Good grief! The first reference is about two enzymes, one from Pseudomonas and one from wheat! Since neither of these organisms are thermoregulatory, they do not even apply to warm blooded animals.


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Burning fat transferred from one part of the body to another
While doing some research on cosmetic surgery, I discovered that there are several ways of doing breast enhancements, one of which was using body fat. While I haven't researched this method, I assume they transfer the patients body fat from one part of the body to another.
Would the body use this transferred fat for as energy, or would it ignore it as it wasn't stored there in the first place? Does the body differentiate fat cells stored in different parts of the body?

It is hard to answer the question whether after transplantation the breast size will reduce or not. I think it will, but without experiments this is just a hypothesis...

Would the body use this transferred fat for as energy, or would it
  ignore it as it wasn't stored there in the first place?

It would use it as energy source, there is no such thing as "ignored tissue". Fatty acid mobilization is regulated by epinephrine and insulin. These are hormones which are ofc. carried by blood, so every white adipose (fat) tissue is affected by them.

Figure 1 - FFA and glycerol mobilization - source
2003 - Fatty acid mobilization from adipose
tissue during exercise

Does the body differentiate fat cells stored in different parts of the body?

This is obvious, just check breasts and butts of girls. ;-) (Those are subcutaneous fat depos. They size is probably regulated by estrogen.)
There are other things involved here, we can talk about subcutaneous (fat below the skin), intramuscular (fat in the muscles) and visceral (abdominal fat) white adipose tissue (there are white, brown and beige adipose tissues). The visceral fat is associated with metabolic diseases, obesity etc...

1995 - Pathophysiology and Pathogenesis of Visceral Fat Obesity
2012 - Lower Thigh Subcutaneous and Higher Visceral Abdominal Adipose Tissue Content Both Contribute to Insulin Resistance
2013 - Genomic and epigenomic regulation of adipose tissue inflammation in obesity

The regulation of body fat distribution and amount is complicated and regulated differently by subcutaneous, intramuscular and visceral fat.

The total transmissible variance ranged from about 40 percent for the
  amount of subcutaneous fat to 60 percent for the pattern of
  subcutaneous fat distribution. Biological inheritance accounted for
  only 5 percent of the variance for subcutaneous fat and the body mass
  index, but 20 to 30 percent for the percentage of body fat, fat mass,
  fat-free mass, and fat distribution. These data suggest that the
  amount of internal fat is influenced by heredity more than the amount
  of subcutaneous fat. Furthermore, we consistently found that
  nongenetic influences are quite important in determining the amount
  and distribution of body fat in the population.

1988 - Inheritance of the amount and distribution of human body fat

These data suggest that adiponectin concentrations are determined by
  intra-abdominal fat mass, with additional independent effects of age
  and sex. Adiponectin could link intra-abdominal fat with insulin
  resistance and an atherogenic lipoprotein profile.

2003 - Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex

The FFA storage pathway, which had remained undetected in
  postabsorptive humans until recently, can have considerable,
  long-term, and sex-specific effects on body fat distribution. It can
  also offer a way of protecting the body from excessive circulating FFA
  in obesity.

2011 - Storage of Circulating Free Fatty Acid in Adipose Tissue of Postabsorptive Humans
Quantitative Measures and Implications for Body Fat Distribution

Different colors (white, brows, beige) and orgin (subcutaneous, intramuscular, visceral) originate from different progenitor cells.

These results reveal a major ontogenetic difference between visceral
  and subcutaneous WAT, and pinpoint the lateral plate mesoderm as a
  major source of visceral WAT. They also support the notion that
  visceral WAT progenitors are heterogeneous, and suggest that
  mesothelium is a source of adipocytes.

2013 - Visceral and subcutaneous fat have different origins and evidence supports a mesothelial source

Brown and white adipocytes have been shown to derive from different
  progenitors. In this study we sought to clarify the molecular
  differences between human brown and white adipocyte progenitors cells.

2014 - Comparative gene array analysis of progenitor cells from human paired deep neck and subcutaneous adipose tissue

The regulation of fat distribution is under research, and not fully understood yet.

Fat distribution differs in men and women, but in both sexes, a
  predominantly gluteal-femoral compared with abdominal (central) fat
  distribution is associated with lower metabolic risk. Differences in
  cellular characteristics and metabolic functions of these depots have
  been described, but the molecular mechanisms involved are not
  understood.

2012 - Distinct Developmental Signatures of Human Abdominal and Gluteal Subcutaneous Adipose Tissue Depots

It would be great if you used some references to support your response! As it stands this is more like a comment!

@Bez Okay, I'll edit soon.

Very complete answer.

@pbond Not really, they needed some references, so I gave them.

You are correct - we suction out subcutaneous fat (fat in-between the skin and muscle layers) which is commonly referred to as "liposuction". Then we make a "slurry" type of solution with the fat and saline-like solution. Then using long needles we inject this 'transplanted' fat into another area. Many times if a woman has a breast reconstructive procedure and needs some contouring done around an implant (i.e. to smooth the surface under the skin where the breast implant and surrounding tissue meet) this can be done. Not all the transplanted fat will grow enough blood vessels in this new area and some of the fat tissue will die. This dying process is called "necrosis" and the body will reabsorb the dead cells and their contents. It works very well overall.

This was informative. Can you also add a note on OP's this question: "Does the body differentiate fat cells stored in different parts of the body?"


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How do kidney cells excrete their own wastes?
The kidney is composed of tissues, and those tissues are made up of numerous cells - so how do these cells excrete their wastes?
Lastly, are there any wastes in the venous blood (renal vein), what makes the renal artery and vein different? - what substances do they each carry?

Then there should be some selective resorption of water compared to urea somewhere along the Loop of Henle. That's how the kidney does all the amazing stuff it does. Read about the Loop of Henle and you'll have your answer to this and other great functions of the kidney, the autoregulatory functions, etc. It's amazing!

I checked my anatomy notes and online figures about the kidney. There is no mention about dedicated arteries for feeding kidney cells. So it does not work the same way as the heart does, where there is a dedicated coronary artery. The kidneys use the same blood vessels for filtering and for nutrition/waste transport purposes too.

Figure 1 - kidney anatomy - source

Figure 2 - nephron anatomy - source

The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH-.

The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.
In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3- by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3- per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.
Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine:

Figure 3 - nephron with material transports - urea resorption at the end of the urine creation process - source

About 40% of the urea filtered is normally found in the final
  urine, since there is more reabsorption than secretion along the
  nephron.

wikipedia - Renal urea handling:
2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

The kidney secretes the urea to the urine, but it absorbs more by the reabsorption than it secreted.

The kidney freely filters urea at the glomerulus, and then it both
  reabsorbs and secretes it. Because the tubules reabsorb more urea than
  they secrete, the amount of urea excreted in the urine is less than
  the quantity filtered. In the example shown in Figure 36-1A (i.e.,
  average urine flow), the kidneys excrete ∼40% of the filtered urea.
  The primary sites for urea reabsorption are the proximal tubule and
  the medullary collecting duct, whereas the primary sites for secretion
  are the thin limbs of the loop of Henle.

Medical Physiology by Walter F. Boron and Emile L.

So if we are talking about urea, then it is secreted to the urine. If we are talking about other waste products, then e.g. CO2 is certainly handled by the veins.

The kidneys keep the composition, or makeup, of the blood stable, which lets the body function.
Each kidney is made up of about a million filtering units called nephrons. The nephron includes a filter, called the glomerulus, and a tubule.
The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes.

Could you describe "if you talking about the areas were the actual waste is dumped" a bit more precisely.  This is quite unclear as to what you mean.

This is not an answer to the question


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Dead skin cell decomposition
What would be the resultant by-products of a completely decomposed dead skin cell?
What would be the size of each of the by-products of a decomposed dead skin cell? How long would it take for a dead skin cell to begin to decompose?
I am curious because anything below the 10 micron range can enter the alveoli of the lungs and cause emphysema. I have had eczema since early childhood, and therefore have breathed in more dead skin cells and by-products of dead skin cells than those without eczema, principally during sleep.
The epidermis, the outermost layer of the skin, sheds corneocytes. Corneocytes are 30-50 micrometers in diameter. http://www.nanoscience.de/richter.old/corn.html

I don't think this is "Personal medication/health advice" question. But I suggest to the OP that they modify the question a little bit so that it sounds more general

I think your risk would be higher with psoriasis than with eczema.


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Why do I feel funny in my tummy when riding a virtual roller coaster?
I've ridden a virtual roller coaster on an Oculus Rift. I felt tension as I went up to the top, but more interestingly I actually felt my stomach drop when I went down the steep drop on the other side. Why can I feel this, when no forces are actually being applied to my stomach?
A bonus question: If you took someone that had never ridden a roller coaster, or even been exposed to rapid acceleration, and had them try a virtual one - would they feel the same stomach lurch as I did?

Why can I feel this, when no forces are actually being applied to my
stomach?

Acceleration sensors are in the ears and are part of the vestibular system. The vestibular nuclei in the brain uses acceleration- and visual signals to decide what happens to your body. It can be fooled by visual signals without the presence of acceleration signals. The role of the vestibulo-autonomic reflex - you feel in your stomach - is probably to protect your inner organs from the damage they can possibly suffer by acceleration.
The same can happen by watching films with fast camera movements on a monoscopic display (e.g. normal films in the cinema or video games on an average LCD monitor, etc...), however not so often than by stereoscopic displays (e.g. 3d films in the cinema, stereoscopic video games on a head-mounted display like Oculus Rift, etc...). This is because stereoscopic displays create the perfect illusion of depth (e.g. they can even be used by a therapy to overcome acrophobia), while monoscopic displays don't. So your vestibular nuclei is fooled much easier by stereoscopic displays.
References:

These data show that a subset of PBN/KF neurons, whose activity is
altered by a nauseogenic stimulus also respond to body motion and that
irritation of the stomach lining can either cause an amplification or
reduction in the sensitivity of the units to vestibular inputs. The
findings imply that nausea and affective responses to vestibular
stimuli may be modified by the presence of emetic signals from the GI
system.

2011 - Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes

1995 - Study on vomiting related to the vestibulo-autonomic reflex.

This study describes the relation between the vection produced by
optical flow and that created by galvanic vestibular stimulation.
Vection is the illusion of self motion and is most often experienced
when an observer views a large screen display containing a translating
pattern. This illusion has only limited fidelity and duration unless
it is reinforced by confirming vestibular information. Galvanic
vestibular stimulation (GVS) can directly produce the sensation of
vection.

2005 - Virtual acceleration with galvanic vestibular stimulation in a virtual reality environment

Neurons in the vestibular nuclei are not only activated by vestibular
signals, but also by visual information. Consequently, the sensations
of body motion derived from visual and vestibular signals are
indistinguishable.
Sensations of body movement can also be generated by visual signals
arriving at the vestibular nuclei. During unnatural movements of the
body, conflict between visual and vestibular information leads to
disorientation and nausea, as in the oculogyral illusion, the Coriolis
effect, and vection.

Foundations of Perception - The body senses - The vestibular system

Three-dimensional movies presented via stereoscopic displays have
become more popular in recent years aiming at a more engaging viewing
experience. However, neurocognitive processes associated with the
perception of stereoscopic depth in complex and dynamic visual stimuli
remain understudied. Here, we investigate the influence of
stereoscopic depth on both neurophysiology and subjective experience.
Using multivariate statistical learning methods, we compare the brain
activity of subjects when freely watching the same movies in 2D and in
3D. Subjective reports indicate that 3D movies are more strongly
experienced than 2D movies. On the neural level, we observe
significantly higher intersubject correlations of cortical networks
when subjects are watching 3D movies relative to the same movies in
2D. We demonstrate that increases in intersubject correlations of
brain networks can serve as neurophysiological marker for stereoscopic
depth and for the strength of the viewing experience.

2014 - Stereoscopic depth increases intersubject correlations of brain networks

Statistical differences in theta activity showed that the real and 3D
environments caused similar cognitive processes, while the 2D caused
an increase of anxiety indicating that perhaps participants were
looking for the third dimension. Beta and gamma activity showed that
participants perceived the third dimension of the stereoscopic
environment as in the real one, something that did not happen in the
2D environment. Our findings indicate that stereoscopic 3D virtual
environments seem to approximate the real ones as far as it regards
the cognitive processes they cause. Three dimensional stereoscopic
environments increase users’ attention over the 2D and cause less
mental effort.

2013 - Stereoscopic perception of women in real and virtual environments: A study towards educational neuroscience

2001 - Human Cortical Activity Correlates With Stereoscopic Depth Perception

In this study the effects of virtual reality exposure therapy (VRET)
were investigated in patients with acrophobia. Feelings of presence in
VRET were systematically varied by using either a head-mounted display
(HMD) (low presence) or a computer automatic virtual environment
(CAVE) (high presence). VRET in general was found to be more effective
than no treatment. No differences were found in effectiveness between
VRET using an HMD or CAVE. Results were maintained at 6 months
follow-up. Results of VRET were comparable with those of exposure in
vivo (Cyberpsychology and Behavior 4 (2001) 335). In treatment
completers no relationship was found between presence and anxiety.
Early drop-outs experienced less acrophobic complaints and
psychopathology in general at pre-test. They also experienced less
presence and anxiety in the virtual environment used in session one as
compared to patients that completed VRET.

2004 - Treatment of acrophobia in virtual reality: The role of immersion and presence

Despite the increasing use of virtual reality, the impact on cerebral
representation of topographical knowledge of learning by virtual
reality rather than by actual locomotion has never been investigated.
To tackle this challenging issue, we conducted an experiment wherein
participants learned an immersive virtual environment using a
joystick. The following day, participants' brain activity was
monitored by functional magnetic resonance imaging while they mentally
estimated distances in this environment. Results were compared with
that of participants performing the same task but having learned the
real version of the environment by actual walking. We detected a large
set of areas shared by both groups including the parieto-frontal areas
and the parahippocampal gyrus. More importantly, although participants
of both groups performed the same mental task and exhibited similar
behavioral performances, they differed at the brain activity level.
Unlike real learners, virtual learners activated a left-lateralized
network associated with tool manipulation and action semantics. This
demonstrated that a neural fingerprint distinguishing virtual from
real learning persists when subjects use a mental representation of
the learnt environment with equivalent performances.

2009 - Impact of the virtual reality on the neural representation of an environment

Our main results are (1) stereoscopy in games increased experienced
immersion, spatial presence, and simulator sickness; (2) the eff ects
strongly differed across the three games and for both ge nders,
indicating more affect on male users and with games involving depth
animations; (3) results related to attention and cognitive involvement
indicate more direct and less thoughtful interactions with
stereoscopic games, pointing towards a more natural experience through
stereoscopy.

2012 - Understanding User Experience in Stereoscopic 3D Games

The results indicate that in a 2D movie viewers tended to look at the
actors, as most of the eye movements were clustered there. The
significance of the actors started at the beginning of a shot, as the
eyes of the viewer focused almost immediately to them. In S3D movie
the eye movement patterns were more widely distributed to other
targets. For example, complex stereoscopic structures and objects
nearer than the actor captured the interest and eye movements of the
participants. Also, the tendency to first look at the actors was
diminished in the S3D shots.

2014 - What do people look at when they watch stereoscopic movies?

For the correlation between anxiety and presence, the results show
very low correlation between anxiety and presence.

2009 - Using augmented and virtual reality for the development of acrophobic scenarios. Comparison of the levels of presence and anxiety

Stereoscopic visualization in cinematography and VR creates an
illusion of depth by means of two bidimensional images corresponding
to different views of a scene. This perceptual “trick” is used to
enhance the emotional response and the sense of presence and
immersivity of the observers. An interesting question is if and how is
possible to measure and analyze the level of emotional involvment of
the observers during a stereoscopic visualization of a movie or of a
virtual environment. The final goal of this research is a challenge,
due to the large number of sensorial, physiological and cognitive
stimuli involved. In this paper we begin this research by analyzing
eventual differences in the brain activity of subjects during the
observation of monoscopic or stereoscopic contents. To this aim, we
have performed some experiments collecting EEG data using a
Brain-Computer Interface device from two groups of users, during the
observation of stereoscopic and monoscopic short movies inside the
Virtual Theater of the University of Milan. From the analysis of the
collected data, it seems that interesting differences are present in
the average brain activity among the observers in the two groups, with
a significative effect of stereoscopic visualization.

2012 - Analysis of brain activity and response during monoscopic and stereoscopic visualization

If you took someone that had never ridden a roller coaster, or even been exposed to rapid acceleration, and had them try a virtual one - would they feel the same stomach lurch as I did?

Probably not. A congenitally blind person, who can distinguish between a globe and a cube by her touch, is not able to tell which one is which (without touching) when given sight. For details see the article "The newly sighted fail to match seen with felt" from Nature: http://www.nature.com/neuro/journal/v14/n5/abs/nn.2795.html.

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


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Forum on synthetic biology and hypothetical biology?
I am interested in synthetic biology, but not a scientist, and would like some advice on where to look for an online forum on synthetic biology and creating fictional species and animals or if someone could suggest the best website to set such a forum up on.
The current research into synthetic biology with biobricks and all the complicated discussion of biochemistry and genetics is too advanced for myself and not what I am interested in. I have fictional ideas of how to create new organisms and symbiotic organisms that are designed and grown for humans to wear and utilise and would like to bounce ideas off other people who may be in to the same area - the potential application of synthetic biology in the far future.
Thank you for any suggestions.

what you ask for is not synthetic biology but science fiction. SF&F-SE would be a suitable forum for this kind of discussion.

Synthetic biology is currently at the level of constructing genetic circuits and modifying bacteria. We still don't fully understand all the details of how single-cell organisms work, so creating new types of animals is pretty far away.

What you want is not a forum on synthetic biology, rather a science fiction site. I recommend visiting the sister website found in https://worldbuilding.stackexchange.com which is a "is a question and answer site for writers, artists and others using science, geography and culture to construct imaginary worlds and settings." I am positive that you will find intriguing discussions on synthetic biology there.

I'm voting to close this question as off-topic because it is not about biology.

Your best bet might be the sub forum on reddit specialized in synthetic biology. Have a look here
Happy science!


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Is there any research paper which identifies left and right brained behavior?
There are many web puzzle to identify, but does it really have any scientific proof?
something like - http://braintest.sommer-sommer.com/en/
any logic behind it?

could you give an example of these so we can get a better insight in to your question

Even if there was some scientific foundation those very short tests can't be reliable. I did one (think it was the same) months ago and got approx. 50%/50%. This time was 70%/30%. Too much variation!

In general I'd say "left and right brained behaviour" is total nonsense. I guess the origin of this kind of claim is a bad press release or something.
Let's start with something simple. Say hearing. When you hear a sound to your left ear, it is projected strongly to the contra-lateral side (right hemisphere), and weakly to the ipsi-lateral (left hemisphere) of your brain. So the brain response to a sound presented to the left ear is lateralized. Typically, this means that the other hemisphere is "more" responsible for processing the input. Similar thing happens for the other senses too.
So what is interesting about lateralized brain responses? Well, it would be very interesting to know for example are memories lateralized. It would tell something about the system: is it a kind of distributed system, where parts of a memory are scattered here and there, according to some logic, or is a single memory stored on a small area (and maybe only on the other side of the brain), etc. The distributed hypothesis seems more plausible according to recent research.
Let's talk about handedness next. Are you right handed? Or left handed? Or ... something between? Actually, even something like handedness is not a binary thing. It is more like a value on a range from 0 ("very left handed") to 100 ("very right handed"). This is taken into account in decent research, where ~1 hr per participant is used to assess that value (if it is relevant to the study).
So we have now talked about lateralization. How about the "left and right brained behaviour" then? In the URL you have provided it is implied that certain behavioural attributes are somehow related to lateralization. Lateralization of what? All the attributes, e.g. "being rational" depend on so many things: seeing, hearing, thinking, retrieving memories, ... that saying such a thing is not plausible.
Anyway, many brain processes are lateralized. That is the word to look up for for more information. But a thing like "behaviour" is too complex to be put to one hemisphere.
Reference: Accumulated wisdom from being a research assistant in a neuroscience project. (so you should trust pubmed.org more than me).

It would be great if you added some references to support your response!

http://en.wikipedia.org/wiki/Doreen_Kimura (who has since passed) had some papers from the 1970s that describe the effect of handedness on audition (so they would cover both of your main points).

@rainy-day-today: thanks for such valuable info. Actually I wanted to develop mobile app which does some mind related stunts like what I asked..But with science as a base. I appreciate if give any guidance for the same


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Alkaline Phosphatase
What is the predominant purpose of Alkaline Phosphatase in skeletal muscle fibers and liver cells. I know that it is a hydrolase enzyme that speeds up the degredation of proteins, lipids, starch and other biomolecules. But what does it does it specifically do in muscle and liver cells. And why is it in higher concentration in the liver ? Is it because of the livers purpose as an organ (cleanse and detoxification) ? Therefore pino/or endocytosis occur in higher rates ? I appreciate anyone with any intelligent insight.

http://pharmascope.org/ijrps/downloads/Volume%204/Issue%203/08-10265.pdf

It has a very wide role and there are multiple types of alkaline phosphatases...


text:
Are there birds with knees instead of elbows?
Are there any birds whose legs fold the same way human legs do, in a knee, instead of an elbow which is what all the birds I know have?

The joint you are thinking of is not a knee, nor is it an elbow, instead it is an ankle which is bending the same way as us humans. You can see from the below diagram that the knee - the joint between the femur and tibia - is just further up the leg normally hidden by feathers.
Birds have a comparatively elongated metatarsus which gives the impression that the knee bends backwards more like an elbow, but it's just the ankle. (Image from here)

I also liked this diagram from a blogpost on a similar theme...

To follow up there appears to be no animals whose ankles bend the "wrong" way.
http://www.answers.com/Q/Which_animal_has_backward_knees
http://qi.com/infocloud/knees
http://www.ehow.com/info_12317202_birds-knees-backwards.html#page=1
Though these are far from conclusive resources. I'd guess the way knee is defined (it means something to humans but not to nature (a bit like the species being a concept which has weak biological bounds)) has something to do with that

Good point, thank you! It didn't occur to me. However, the joint I'm talking about is between Tibia and Metatarsus (ankle, right)? Are there any birds whose ankles bend backwards?

according to the blogpost mentioned above no, no tetrapods do this

@violetgirraffe edits made

+1 Nice answer. You should add a reference to the first figure thought.

Did you replace the first illustration? You shouldn't have, the other one was much larger and clearer; I can hardly read anything on this one.


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Molecular Cloning- Blunt end restriction endonucleases
I work in a microbiology lab where we do a lot of cloning. I have always used restriction endonucleases to cleave the DNA to have sticky ends and not blunt ends. I currently am working on a project that suggests using a blunt end restriction enzyme, such as EvoRV, and then to perform a T-tailing of the plasmid, pl4440. My question is why do I not treat my pcr'd insert with a restriction digest just like I would the plasmid as the protocol suggests? How do I know the insert has ends that are able to ligate into the plasmid if I don't design the restriction sites into the primers?

If i understand the question correctly, your are asked to make a single EcoRV cut in your backbone plasmid and make blunt ended inserts?

Well, the plasmid has a single cut in the back bone but I'm not sure how the insert will ligate correctly if I do not treat the insert to make blunt ends.

if then you can only use EcoRV and nothing else then you have to use blunt ended inserts but you will have problems with insert orientation and multiple ligations of insert!

I think you can turn sticky ends into blunt ends with klenow enzyme. Been too long to be sure.

@user137, yes thats correct! the OP can use DNA polymerase I, large (Klenow) fragment (from NEB) to blunt end the insert. or alternatively an EcoRV site can be designed into the primers so long as it is not present elsewhere in the insert.

Just remember that in blunt end ligation the insert can go in either direction, so you need some way to differentiate direction, such as sequencing, and that half of your clones that look right on gel will be backwards.

To know if the ends are compatible see compatible cohesive ends (isoschizomers) from NEB website.
If you are unsure then do a blunt end ligation. For blunting a sticky end (From the comments):
Use Klenow or Pfu polymerase (or any proofreading/high fidelity polymerase).
You can use Taq if you intend to to a TA cloning.


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Can "human exclusion zones" in national parks for preserving Wolves and Grizzlies be a good idea?
There are National Preserves in the National Parks where some human activities are permitted. But can it make sense to create "exclusion zones" so no human would be permitted in a certain area, not even scientists or researchers just so Grizzlies and Wolves can have a whole world to themselves ?
I know we won't be able to find out how those species are doing, but would there be any benefit ? Has any country ever tried that ?

Good idea from what perspective/for whom? For species conservation, the ecosystem, the individual animals ("..a whole world to themselves"), humans (having untouched ecosystems), Gaia?

I think it is a neat idea that should be discussed.
Not just for wolves or large predators but for all wildlife situations
There should be small habitats for all wildlife to refuge scattered around. Of course national parks, reserves and refuges are there for this purpose, but humans have become far too abundant on this planet to coexist anymore, and maybe we need to take it a step further? Again, it's something that should be discussed and awareness made of the issue.
And by far the best reason for this if nothing else is to have a scientific "control" spot for environmental research. It is important to have a control in all experiments, and to have a human exclusion zone helps create that control. If we had that, maybe someone could actually prove how much humans really are screwing up the planet, or maybe someone will prove they aren't :D


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Why are the largest land/air animals today smaller than in the Mesozoic?
The largest dinosaurs and pterosaurs seem to have been much larger than the largest animal terrestrial/avian species since. Was the Mesozoic somehow more hospitable to large animal species than today's world? Have subsequent evolutionary innovations shifted the balance towards smaller species?
Interestingly the still-existing blue whale seems to be the largest animal ever.

Closely related/maybe partial duplicate of What are the atmospheric requirements for large dinosaurs? and What was the reason for some plant and animals to become giant in course of evolution?

Although the specified question is not an exact duplicate, this answer pretty much covers my question.


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How reactive are reduced antioxidant molecules?
When antioxidant molecules stabilize free radicals, they themselves become unstable and reactive but to a lesser degree. How reactive are these reduced antioxidant molecules? And what substance stabilizes reduced antioxidants?

How do you measure "reactiveness"?

Shouldn't this be better suited for http://chemistry.stackexchange.com/?


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HIV and effectiveness of inhibitor cocktail over single inhibitor
I'm looking for clarification on the answer to this question. It's in my biochemistry class but I figured this is more Biology than Chemistry, so I'm asking it here.
The question is:

One of the more effective treatments for HIV-positive individuals has been for them to take
  protease inhibitor cocktails. Certain proteases are required for the virus to mature and these inhibitors prevent them from functioning. A cocktail of inhibits means that numerous inhibitors are used at once. Why would a cocktail be more effective than a single inhibitor?

My answer to this is that there could be more than one mutation of the virus, and with each mutation a variation in specific protease. So, the protease cocktail would defend against a wider range of the mutated virus.
Is this correct? Is there an answer that might involve describing epitopes?

Your answer is correct. HIV-1 encodes a single homodimeric aspartic protease, with each monomer containing the classic Asp-Thr-Gly motif, and the dimer's active site being formed with the two monomeric active sites creating a cleft where the proteolysis takes place. In it, water acts as a nucleophile in conjunction with the aspartic acid residue to hydrolyze the peptide bond in the protein's target.

WikiMedia: Aspartyl protease mechanism.png
A number of HIV-1 proteins are synthesized as polyproteins, and protease is required to cleave them in the appropriate spot(s) so they can assume their mature forms. This is a very big deal, because without these cleavage events HIV-1 cannot complete its replication cycle, and so becomes non-infectious.

WikiMedia: HIV-replication-cycle.svg
Protease inhibitors act by "sticking" in the binding cleft, obscuring the aspartate and preventing binding of the target proteins. However, these small-molecule inhibitors are very specific to HIV-1 and the amino acid residues that compose the binding cleft, otherwise they could potentially inhibit one or more of the many aspartyl proteases our body makes naturally. While it is not very likely that a destructive mutation in the Asp-Thr-Gly motif would result in a replication-competent virus, other more conservative mutations may occur in the binding cleft that still allow the target to bind and be cleaved. However, depending on the exact protease inhibitor being used, a single mutation, even if it's conservative, may still be enough to dramatically decrease the inhibitor's binding efficiency and allow protease to maintain some or all of its functional capacity. This is why cocktails of inhibitors are used: they each depend on different amino acids for their binding, so if mutations arise at some point that do affect the activity of one inhibitor, others may still be unaffected. Evolutionarily-speaking, the inhibitors put a tremendous selection pressure on the virus, which combined with HIV-1's naturally "sloppy" replication process, leads to mutants appearing in relatively short periods of time.
There are two kinds of epitopes in the adaptive immune system: those recognized by antibodies and B cells, and those recognized by T cells when presented in the context of MHC. Antibody epitopes are generally found on the surface of a pathogen or a pathogen-infected cell (when speaking in the context of infectious diseases), as proteins or other compounds capable of raising an immune response that are only located completely inside of the pathogen or infected cell are not available for binding. T cell epitopes, on the other hand, are linear peptide fragments (and sometimes other molecules, like glycolipids) generated by internal processing in the antigen-presenting cell, and are usually pretty representative of the complete contents of the cell, native and foreign. Native epitopes generally don't produce immune responses - when they do, autoimmunity occurs. Foreign epitopes are recognized by circulating T cells, and help prime an immune response against the infected cells. (As a side note, since HIV-1 infects a subset of T cells, it is a way for them to escape immune detection). Mutations in the protease protein may affect some of the epitopes it produces, but those mutations are just as likely to increase visibility to the immune system as decrease it, so overall there's no net gain or loss.

According to wikipedia:

HIV protease inhibitors are peptide-like chemicals that competitively
  inhibit the action of the virus aspartyl protease. These drugs prevent
  proteolytic cleavage of HIV Gag and Pol polyproteins that include
  essential structural and enzymatic components of the virus. This
  prevents the conversion of HIV particles into their mature infectious
  form.

Competitive inhibition means that it just slows down the conversion, but it does not stop it. In the case of building a virus we are talking about a multi step process. By using multiple inhibitors we slow down multiple steps in this process. So it is much more effective than just using a single inhibitor for slowing down only a single step in the process...


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What is the difference between eugenics and evolution by natural selection?
So with the working definition of Eugenics: "the aim to improve the human gene pool". What are key features that distinguish Eugenics from evolution by natural selection?  I mean, besides that natural selection occurs naturally.

With that definition, the major difference is that eugenics is artificial. Additionally, natural selection has no aim.

Natural selection is a descriptive theory that aims to explain the diversity of life. Eugenics was a political/ideological project for "improving the human gene pool." Obviously, these are completely different.

Eugenics is selective breeding to artificially promote certain 'desirable' genetic traits. Natural selection occurs without human interference and is due solely to the challenges of nature.

Selection is a mechanism of evolution which favours specific forms of traits over others, this can cause the spread of beneficial mutations through a population.
Natural selection is the spread of beneficial traits/genes through populations as a result of the natural variance in their effect on reproductive output (a function of life history traits like lifespan aging and reproductive rates). A classic example is that of Darwin's finches, where different variants of bill length and shape have evolved in populations based on what food resources (types of seed) are available to them and their ability to utilise those resources.
Artificial selection is selection imposed on a population by humans to deliberately affect specific traits. Examples of this would be milk yield in cattle (we want more efficient production and better quality milk), dog breeds (selection on a whole host of traits like colour, beardedness, height, length) and crops like wheat and barley (selected for higher efficiency and  quality output).
Eugenics, coming from the greek for "well-born" or "good" race, is the application of artificial selection principles to humans. Just as with cattle or crops, there is an aim, it may be to increase height, remove genetic diseases, or promote a certain set of traits like blonde hair and blue eyes. Historically we can associate with a number of radical political ideologies, such as Nazism. Even here in Sweden (people tend to think of it as a very progressive and equality driven country) there was a program of eugenics until very recently, achieved by forcibly sterilising or coercing people in to it, for various reasons (racial purity, health, and antisocial behaviour). Here's an interesting example of a girl designated as being genetically inferior because her family had a history of alcoholism (that page gives a good history of eugenics too). The social and ethical problems of eugenics are obvious.
Under normal conditions a persons reproductive output is largely determined by their own choices and actions whereas under eugenics that choice is taken away and made by someone else and specifically with the aim of "improving" the quality of the population.
So in summary:

natural selection is the result of natural variance in fitness linked to traits
artificial selection leads to a change in traits, in a specifically targeted direction, decided and imposed by another organism (usually humans, I know of no other species which does this)
eugenics is practice of artificial selection on humans enacted by humans with the specific aim of improving quality: often for social, economic, or political reasons and is generally accepted as being against human rights these days.

First, you need to recognise the difference between Natural selection and Artificial selection. As a basic definition, you can say that in natural selection, selection is done on fitness (overall, long-term success of reproduction) and is determined by the complete living environment of the species. In artificial selection, selection is done by humans on a plant or animal species for specific attributes that are desired (see any Evolutionary textbook for more on the difference). So the two processes generally try to optimize completely different things, and artificial selection has a goal which is not the case for natural selection.
Generally, Eugenics can be likened to artificial selection, done by humans on humans. The methods used (selective breeding, culling, trunkated selection, sterilization etc.) are potentially the same. The difference between eugenics and articifial selection on plants and animals other than humans is purely moral and political (and therefore off-topic for Bio-SE).
However, eugenics has also often been misguided in practice (if you ignore for a moment the usually horrible morals behind it). First, it relies on desired and undesired genotypes and phenotypes. Most people would not regard these as valid concepts, and even so, what will be desired/undesired will clearly differ between societies and over time. Second, eugenics does not appreciate the value of genetic diversity for the long-term success of a population (it will rather result in lower diversity). Third, eugenics is usually aimed for obvious physical traits and diseases, without much regard for their genetic background (e.g. heterozygious recessive carriers of disease). Fourth, eugenics usually devolve into a hunt for "weaker" groups of people, even if this has nothing to do with the gene pool of the population (for instance, many birth defects and the prevalence of Down's syndrome has almost nothing to do with the genetics of the population).
I guess you could argue that ongoing selection in humans is a form of eugenics since it is to a large extent determined by human interactions and choices (see e.g. Courtiol et al 2012 & Geary et al. 2004). However, this is definitely not a standard definition, and big difference compared to "normal" eugenics is that it is not guided by a common and explicit goal. I also know that some people label the collective outcome of individual decisions as a form of eugenics, which might be relevant for how you view Preimplantation genetic diagnosis (PGD) and prenatal screening.

In principle, eugenics is just like selective breeding of animals and plants. For example, dogs have been bred for a variety of traits to fit into several niches, and corn has been bred to produce large yields in several climates. Eugenics would attempt to do the same for humans. However, no one agrees on how to "improve" the human gene pool, and far too often eugenecists have sought to remove criminals, the disabled, the jews, or whoever they feel is inferior. And the methods used to bring about their genetic utopia include forced sterilization and/or death camps. There is no moral way to implement eugenics, and I don't think humans should be in the business of deciding which people are superior or inferior and who is allowed to reproduce, it's always dangerous.

what about PGD and using it to prevent the birth of a child who would otherwise lead a life of suffering? or inevitable death?

@user125535 Preimplantation genetic diagnosis (PGD) is not done with the purpose to improve the human gene pool (which is the case for Eugenics), so I think there is a big difference. As you say, they are done with the purpose to relieve potential suffering or for the sake of the parents. However, the same methods could theoretically be used by an eugenics programme.

authors: ميخائيل مينا


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What are the sources of energy that alcohol provides?
Milk contains sugar and proteins which give energy. What compounds in alcoholic beverages (edited) give energy? Are they more likely to turn into fat (as in beer belly) than blood glucose?

alcohol is not a mixture, it is one defined molecule, ethanol (assuming the colloquial definition of alcohol, it can also mean a class of molecules).

@MadScientist My bad, I meant alcoholic beverages like beer, wine, rum and whiskey.

Ethanol is converted into AcKoA, which can be "burned" in the Krebs cycle or can be used to build fatty acids.

By chronic alcohol consumption there is another pathway involving MEOS which converts ethanol to AcKoA as well.

Are they more likely to turn into fat (as in beer belly) than blood
  glucose?

It won't turn into glucose, just into fat.
Note:
It is suspected that in extreme cases, like low glucose diets and starvation there is an AcKoA -> glucose pathway.

2011 - In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans

So in theory it is possible to convert ethanol to glucose, but there is not enough evidence of that yet. Normally this conversion (if it exists) does not happen, or it has a very low rate...

What compounds in alcoholic beverages (edited) give energy?

Mostly ethanol and sugar. E.g. sweet wine contains a lot of sugar, not just ethanol...

Is AcKoA more likely to be deposited as under-skin fat, like the myth of beer makes your belly especially fatter? Sorry I was vague about "turn into fat"

Liver does not produce fat normally, it just mediates the fat transport after eating by creating lipoproteins. I don't know the details of the process, but alcohol can cause fatty liver, so I think the fat is more likely deposited in the liver and in visceral fat depos, than by eating fatty foods. So the myth can be true, but you need more googling to find evidence. http://scholar.google.com

Regarding energy:
Going off the assumption that you are using 'alcohol' in the sense of 'alcoholic beverage', it really depends on what kind of beverage we're talking about, but all that information is on the label of the bottle, can or box.
As for ethanol itself, some energy is freed by the metabolising of ethanol into ethanal and further into ethanoic acid, before finally being decomposed to carbon dioxide and water.
Finally, energy is energy: The source of the energy doesn't really affect where the energy ends up, that depends mostly on external factors.

Regarding beer:
Ethanol gives roughly 7 kcal/g, compared to carbohydrates which give roughly 4 kcal/g.
100 ml of beer contains (about) 4 grams of ethanol, beyond which the carbohydrate content varies according to the beer in question, but usually hovers around 3 g.
At a rough estimate the caloric contribution from ethanol is about 0.28 kcal/ml, and carbohydrates about 0.12 kcal/ml. When accounting for the traces of proteins, this gives roughly 0.4 kcal/ml, roughly the same as your common or garden variety soda.

So what compound provides most of the energy in, say a beer?

@aitchnyu: Updating answer with this information now.

Right, ethanol can be oxidized.

Carbohydrates, as in leftover fruit sugars from the source?

@aitchnyu: In addition to additives and adulterants, yes.


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How prominent is the gene-centric view of evolution among professional researchers?
Richard Dawkins famously advocated a gene-centric (as opposed to organism-centric) viewpoint on natural selection, most notably in The Extended Phenotype. However, I have also heard "on the grapevine" that most professionals in biology and related areas do not take the gene-centric viewpoint altogether seriously.
My question is simple: how prominent is the gene-centric view of evolution among professional researchers in biology and related fields?

Okasha's levels of selection might be interesting here

What do you mean by gene-centric view of evolution
I am not totally sure you know what really means the gene centric view of evolution. Everybody agrees that selection (also) acts on genes and that selfish genetic elements exist. I think that what one calls the gene centric view of evolution is nothing but the modern synthesis of evolution (following the work of Ronald Fisher, Sewall Wright and some others such as Motoo Kimura).
Or maybe by gene centric view you refer to the concept of level of selection.
Some people however argue that because of the gene centric view of evolution, we tend to underestimate the importance of some parameters in evolution and some are willing to rename the evolution theory into Extended Evolution Theory according to new insights about how parameters such as developmental bias for example influence the evolution of populations.
Modern snythesis of evolution theory
You will find more information in this recent article that you may appreciate reading if it is not too complicated. I personally endorse the "No, all is well" opinion. It is important to understand that those who criticize the gene centric view in this article are NOT saying that selection do not act on genes neither that selfish genetic elements do not exist (thinks that R. Dawkins talk about in his books). They totally agree with those things. They just argue that the fisherian view of evolution in not enough and that according to recent findings we may want to rename our theory. The "no, all is well" opinion totally agrees with the importance of these new insights that do not come from what one may call the gene-centric view of evolution but they just don't think it is worth renaming the theory for that because our knowledge in evolution is just growing as it has always been growing and it doesn't seem that we are currently living a revolution in our understanding of evolution. I think that the main revolutions that happen to occur in evolution these days mostly have to do with the methodology of testing rather than with the theory itself. These revolutions have to do with increased computer power, better statistical methods and faster and cheaper sequencing.
Level of selection
Now, by gene-centric view of evolution you may refer to the concept of level of selection. To my knowledge everybody agree that selection occurs at different levels. Again, NOT everybody agree on the relative importance of selection acting at different level. The vast majority of research focus at evolution at the gene level, sometimes implicitly only.
To conclude, we all agree on the theoretical principles (I think) but not everybody agree on the relative importance of the different mechanisms. In saying this, I don't mean that everybody agree with everything that is written in R. Dawkins books!


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Difference between medicinal caffeine and regular caffeine
There are some OTC paracetamol tablets, some with caffeine. Is this caffeine the same as the regular caffeine (found in a coffee)? Does it perform better than it in any way?

From a pharmacology point of view, there is no difference between caffeine in caffeine pills and in a cup of coffee. It doesn't matter, how a chemical substance (in this case caffeine) is made, the effect of the substance is the same. What can make a difference is the presence of secondary plant ingredients.
For pure caffeine there are two possible sources: By chemical synthesis ("A Novel Method of Caffeine Synthesis from Uracil") and as a byproduct of the decaffeination process when producing decaffeinated coffee.
What is also different is the amount of caffeine. While pills contain standardized amounts of caffeine, the amount for caffeine in brewed coffee varies between different kinds of coffee beans as well as for different brewing methods. See this figure (from here):


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Do you produce more sperm after 1 week of abstinence vs 1 year of abstinence
Question: I was wondering if the amount of sperm increase with the amount of abstinence?
Side questions:

Is their a max amount of sperm?
What happens with the excess amount?

Wet dreams happen, of course.

Orgasm does not necessary involve ejaculation in those wet dreams.

I have read after 8 days of abstinence an significant increase is noticed in the amount of sperm and the amount of little soldiers.

Excess/old sperm is broken down (by phages?) and is re absorbed in the body

There is an increase by abstinence.

The within-subject variability of the semen sperm count (n), volume
  (v) and the total number of spermatozoa (N) was studied on 220
  ejaculates from 36 normal subjects after an abstinence of 7 days or
  less.
The three semen characteristics for a given subject were highly
  correlated with the length of abstinence: for an increase in
  abstinence of 1 day there were mean increments of 13 × 106/ml for n,
  0·4 ml for v, and 87 × 106 for N.

1979 - Within-subject variability of human semen in regard to sperm count, volume, total number of spermatozoa and length of abstinence

Semen analysis was performed on six men after various sexual
  abstinence periods (from 2 to 18 days). The variations in semen
  parameters were analyzed statistically as a function of the duration
  of abstinence.
Lengthy sexual abstinence was found to affect all semen
  characteristics. Semen volume and concentration and total sperm count
  showed significant increases, whereas motility and normal morphology
  decreased significantly with duration of abstinence. Significant
  changes in the percentage of normal sperm forms were observed after
  more than seven days' abstinence.
The study indicates that the influence of long sexual abstinence on
  semen quality varies with the variable considered. With regard to
  fertility, a long abstinence period might induce senescence of
  spermatozoa.

1994 - Effect of long abstinence periods on human sperm quality.

Sperms can die of "old age", as the previous quotes mentioned long abstinence period induces senescence. It is hard to find anything about their lifetime, it is at least 7 days I think.

For humans, entire process of spermatogenesis takes 74 days. Including
  the transport on ductal system, it takes 3 months. Testes produce 200
  to 300 million spermatozoa daily.

according to wikipedia

So there is a constant rate of sperm production.
I think the following differential equation can describe the change of the sperm count:
$$ \dot{x} = μ - Dx $$
where

x is the sperm count
μ is the production rate regulated by testosteron (about 250 million per day)
D is the death rate which depends on the age of the population (depends on the lifetime, production rate, elapsed time)

So there will be a maximum amount by abstinence. By that amount
$$ μ = Dx $$
so
$$ x_{max} = μ /D $$


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What is this beetle? Found in heather in snowdonia
We were walking in the hills of snowdonia the other day and my girlfriend found this in the heather:

I've never seen anything like it. Can anyone identify it? It was the biggest beetle I've ever seen.

Ah, the rare Dimentium stupidus. It's legs contain a special chemical that makes you impotent and turns your mind to mush. They're harmless otherwise, just don't let one crawl on your bare skin.

That's fine, it was my girlfriends hand! @OlinLathrop ha ha

I believe it's the Violet Ground Beetle -
Carabus violaceus. This is a close relative to the Carabus coriaceus posted by Jon.
The purple colour is a give away, but as in many insect groups there are often very similar species. As pointed out in the comments to this anwer, this is the case for C. violaceus and C. problematicus (differences)
There are websites  like observado.org where sightings can be added as a species or for instance "unknown beetle", where they are reviewed (depending on the availability of the volunteering experts) or identified.

Great answer! Yes I think your correct. Something about the other option didn't quite add up. The violet was very prominent.

In the key I use for the Netherlands, I remember there is a very similar species to the Carabus violaceus, I think it is Carabus problematicus. but I can not find my key now so I can not tell you the differences.

ah of course there is a internet page about the differences: http://www.thewcg.org.uk/idaids/cproblematicusviolaceus.htm, based on your picture I think I see the longitudinal granulations, so I tend towards C. problematicus...

I would say that it is a Carabus coriaceus. It might have a size of 30 to 40mm and is very common around Europe.

Unfortunately the English wikipedia article is rather tiny: https://en.wikipedia.org/wiki/Carabus_coriaceus