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Does the recent concern over several papers about Aβ*56 call into question the association of Alzheimers Disease with any amyloyd beta oligomer forms?
The news item by Charles Piller just published in Science BLOTS ON A FIELD? A neuroscience image sleuth finds signs of fabrication in scores of Alzheimer’s articles, threatening a reigning theory of the disease highlights the recent news and activity around a series of papers discussion Aβ*56, a specific, proposed type of toxic oligomer of amyloid beta or Aβ.
There are questions of image altering and of the veracity of Aβ*56 isolation and measurements, and expressions of concern have been recently added to online versions of a numnber of papers referring to it going back to the 2006 Nature paper A specific amyloid-β protein assembly in the brain impairs memory.
Several drugs developed for treatment of Alzheimers Disease have targeted Aβ.
I'm having difficulty understanding how far the implications of the recent concern reaches. Is it simply the correlation with the particular form Aβ*56 associating with Alzheimers, or is it the connection between any oligomer of Aβ? Does the recent concern over several papers about it call into question the association of Alzheimers Disease with any Amyloyd beta oligomer forms?

Does the recent concern over several papers about Aβ*56 call into question the association of Alzheimers Disease with any amyloyd beta oligomer forms?

From my understanding, no.  alzforum.org has many great comments on it, e.g. from David Brody:

In my own group, we tried replicating the Aβ *56 western blots for about a year, without success. We then moved on to other things.
Our later work on soluble Aβ aggregates/oligomers from human brain tissue indicated that they are considerably larger than Aβ *56 (Esparza et al., 2013; Esparza et al., 2016).
I think these larger soluble Aβ aggregates/oligomers may still be important potential therapeutic targets, but not Aβ *56.
The strongest evidence comes from the labs of Dennis Selkoe and Dominic Walsh.
References:

Esparza TJ, Zhao H, Cirrito JR, Cairns NJ, Bateman RJ, Holtzman DM, Brody DL. Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls. Ann Neurol. 2013 Jan;73(1):104-19. PubMed.
Esparza TJ, Wildburger NC, Jiang H, Gangolli M, Cairns NJ, Bateman RJ, Brody DL. Soluble Amyloid-beta Aggregates from Human Alzheimer's Disease Brains. Sci Rep. 2016 Dec 5;6:38187. PubMed.

or from Thomas Bayer:

In my view, Aβ-amyloid oligomers are valuable and realistic drug targets. However, not all Aβ oligomers described in in vivo or in vitro model systems do exist in human brain. Besides full-length Aβ, N-truncated Aβ peptides, pyroglutamate Aβ 3-42 and Aβ 4-42 represent a dominant fraction in the brains of patients with Alzheimer’s disease. Both N-truncated peptides show a high aggregation propensity to form stable aggregates as observed by NMR spectroscopy, for example (Bouter et al., 2013).
References:

Antonios G, Borgers H, Richard BC, Brauß A, Meißner J, Weggen S, Pena V, Pillot T, Davies SL, Bakrania P, Matthews D, Brownlees J, Bouter Y, Bayer TA. Alzheimer therapy with an antibody against N-terminal Abeta 4-X and pyroglutamate Abeta 3-X. Sci Rep. 2015 Dec 2;5:17338. PubMed.

Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, Bayer TA. N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody. Acta Neuropathol Commun. 2013 Sep 6;1(1):56. PubMed.

Bakrania P, Hall G, Bouter Y, Bouter C, Beindorff N, Cowan R, Davies S, Price J, Mpamhanga C, Love E, Matthews D, Carr MD, Bayer TA. Discovery of a novel pseudo β-hairpin structure of N-truncated amyloid-β for use as a vaccine against Alzheimer's disease. Mol Psychiatry. 2022 Feb;27(2):840-848. Epub 2021 Nov 15 PubMed.

Bayer TA. N-Truncated Aβ Starting at Position Four-Biochemical Features, Preclinical Models, and Potential as Drug Target in Alzheimer's Disease. Front Aging Neurosci. 2021;13:710579. Epub 2021 Aug 20 PubMed.

Bayer TA. Pyroglutamate Aβ cascade as drug target in Alzheimer's disease. Mol Psychiatry. 2022 Apr;27(4):1880-1885. Epub 2021 Dec 8 PubMed.

Bouter Y, Dietrich K, Wittnam JL, Rezaei-Ghaleh N, Pillot T, Papot-Couturier S, Lefebvre T, Sprenger F, Wirths O, Zweckstetter M, Bayer TA. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathol. 2013 Aug;126(2):189-205. PubMed.

Bouter Y, Liekefeld H, Pichlo S, Westhoff AC, Fenn L, Bakrania P, Bayer TA. Donanemab detects a minor fraction of amyloid-β plaques in post-mortem brain tissue of patients with Alzheimer's disease and Down syndrome. Acta Neuropathol. 2022 May;143(5):601-603. Epub 2022 Apr 16 PubMed.

Thanks for the link - some very interesting comments on the blog post. One takeaway message from some of the comments is that the Science article contains some misguided views, so they are definitely worth reading to get a more well rounded picture of what happened;


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Examples of seeking behavior by brainless animals
Are there any examples of brainless animals (e.g. jellyfish) exhibiting seeking behavior, such as following smell or light gradients towards food, or following hormones towards mates?

Yes, there are plenty of examples! We refer to this seeking behaviour as taxis.
Taxis
There are many types of taxis such as chemotaxis (attracted to chemical stimulus) or phototaxis (attracted to light). A complete list of taxis can be found on wikipedia > taxis.
For the purpose of this answer I will restrict to chemotaxis only

Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.

Chemotaxis in Bacteria
Chemotaxis is very common in bacteria such as E. coli for example (Macnab and Koshland 1972, Wadhams and Armitag 2004).
Chemotaxis in Plants
Chemotaxis is also observed in plants such as rhibozium spp (Currier and Strobel 1976) for example
Chemotaxis in eukaryotes
Chemotaxis is also found in eukaryotes such as in Amoeba or Tetrahymena (Köhidai 1999,Bagorda and Parent 2008) for examples.
Chemotaxis in animals that have "primitive" brains
Nematodes (Ward 1973) and plathelminthes (Bone 2012) for example show chemotaxis.
Chemotaxis in "brainless" animals
Evidence of chemotaxis also come from Echinodermata (sea stars, sea urchins and others) (Miller 1985).
Echinodermata have quite definitely no brain!

source: Stack Exchange

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A website for identifying birds
I am not sure if this is the right place to ask this question, but I guess that ornithology enthusiasts (or ornithologists) will have the best knowledge about it.
I am wondering if there is a website which would identify birds by their looks. For example, I would specify that the bird is similar to a sparrow in size (just a little bigger), it has a gray back and yellow-ish-orange-ish belly and it would tell me the exact species.
Does such a website exist?

There are actually a few, the problem with these websites is that they usually cover only a part of all birds on this planet. I use:

Bird identifier: Usefull website for a lot of European birds.
Backyard Bird Identifier: Useful for some European birds but
mostly for North American and Canadian birds.
All about Birds: Useful, but needs more knowledge for the identification

What I also do is using Google with a description of the bird, which sometimes works surprisingly well.

I've ran into problems today while trying to identify a bird provided as an example in the question on google. Turns out it was a nuthatch - the first website you provided gave me that answer. Thanks!

If you're looking at birds in Britain the RSPB's bird identification web pages have worked well for me and it works in a way described in the question.

If you are on the go, the Merlin app for your smart phone is great. Especially if you are in North America!
Merlin is a smartphone app that you can download via your preferred app provider (apple, google, etc.). It is maintained by the Cornell Lab of Ornithology, and is related to the All About Birds online archive.
The app does exactly what you are looking for, where you specify the approximate size, up to three colors, where the bird was seen (in water, at a feeder, in trees or bushes, etc) and where and when you saw it and it can provide a list of suggested birds. The suggestions have information on identifying the bird species, maps of the species distribution, and example sounds that each species makes.
If you are an avid birder that records your sightings in eBird (also created and maintained by the Cornell Lab of Ornithology) there is an option to add the bird to your "Life List" from within the Merlin app.

Please add a bit more context to your answer. If your link dies, then we are left with basically no information here. A summary, screengrab, highlights, etc all could be useful. (FYI: don't use the 7 year old other answer as a guide -- our standards have increased since the very early years of the site)

I didn't think that was necessary because it a smartphone app, but more background has been provided.

There is a proposed edit from "selene" — are you posting using more than one account? If so, you may find this information on merging accounts to be of interest ...

I don't think so? I think it is just one one account. I only see one, and keep track of points in one.

So, is the currently pending edit on your answer something you wrote or not? If it is yours, then you are definitely posting using two different accounts (possibly from different devices) and you should merge those accounts. If it isn't, then you should either approve, edit, or reject the pending edit.

I added the edit with more info about how Merlin works.

I see now. Great edit, @selene!

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

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What is this tiny lizard?
This tiny guy stumbled into our house in the suburbs of Sydney. What species is it?
It's dark and has two yellow stripes going along the length of its body. They start on its head and go right above its eyes.

This looks like a Common Garden Skink (Lampropholis guichenoti)
Further information can be found here and here
The description is a quote from the first source:

The colour of the skin of a common garden skink is mostly a brown-grey colour, and it usually has a black or dark coloured stripe down either side of its body and a copper coloured head. The diet of common garden skinks generally consists of insects and vegetation, and can include caterpillars, spiders, slugs, cockroaches, crickets, worms and ants, and fruit and vegetables. Small and enclosed spaces, such as rocks or trees, are the sought after home for common garden skinks, and they are commonly found in urban gardens, hiding in among plants or leaves. Common garden skinks generally grow to a length of 9 centimetres (3.5 inches), and they have five toes on each of their four legs, as well as a long tail. Common garden skinks can release their tails when caught by predators, such as birds, cats and larger reptiles like snakes.

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Tumour resistance: single-cell or population effect?
Drug resistance can arise through a number of mechanisms. For instance, EGFR mutation when treating with EGFR inhibitors, or compensatory activation of alternative survival pathways. But does it occur at the level of a single cell, or would it be a population effect? In other words, would cells exposed to e.g. targeted kinase inhibitors slowly compensate with other pathways (and that would happen in every such cell) or would there be a sub-population of cells that is sensitive to inhibitors and another subpopulation inherently resistant and predisposed towards amplifying other pathways.

I don't know if this can help. There's something called the Allee effect. http://www.nature.com/nrc/journal/v14/n5/full/nrc3712.html

Both can happen.

And much more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488437/

http://www.rjme.ro/RJME/resources/files/510210259264.pdf

There certainly can be co-operation or competition among cancer cells within a tumor that can provide some types of population-based influences on cancer-cell survival. Present evidence, however, suggests that resistance to therapy is almost always due to resistant sub-populations of cancer cells within the tumor. In many cases, such as after treatment with EGFR inhibitors, the resistance mutations have been identified. Sometimes these mutations are in such a small fraction of the cancer cells that they can't be detected in the original tumor before treatment, but in most cases they probably were already present before therapy, caused by the mutations that are inevitable during tumor growth. This review on intra-tumor heterogeneity is a good place to start learning about this topic.


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Importance of Double Helix DNA Structure
Gene expression involves transcribing only one strand of DNA molecule. So i was wondering what are some biological advantages of the double stranded DNA?

It maintains a certain structure - and it also holds a second copy of a strand (though reverse complement). This can be used to repair damages.

@Chris — Please make the point about DNA repair into an answer.

The structure allows for the DNA to be tightly packed into chromosomes. It also provides an extremely stable backbone with the negatively charged phosphates pointing to the outside of the molecule. This charge aids in the attachment of other molecules to the strand of DNA.
DNA double helix allows it to be stable and it won't easily destroyed.

Unconvincing answer lacking critical comparison to support your points. You don't explain how dsDNA can be packed more tightly than ssDNA or how it is "more stable".

The most important role of this peculiar double helix structure of DNA is to facilitate replication....in preparation of cell division each of the 2 strands acts as a template thus facilitating precise copying of genes....in the Nature(1953), Watson & Crick also suggested that " It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material"...
Also, the extremely stable structure doesn't allow DNA to mutate rapidly, unlike RNA...thus converting it into an "efficient information storage structure"....
& lastly this double helix structure is also resistive against extreme physical changes...as is evident from Griffith's experiment, where the heat-killed bacteria had their DNA intact...
Also try this link- "Genetic Implications of the Structure of Deoxyribonucleic Acid"- Watson & Crick....as it always helps to learn from the very masters of DNA structure;)

Your first point is valid, but only to a point. It is necessary that a dsDNA is formed at some point as the replicative form, but ssDNA viruses show that there is no need for a dsDNA genome for replication. Your second point is nonsense. It is the phosphodiester bond between the deoxyriboses that is more stable than that between ribososes and the lack of proof-reading that is the difference in mutability. And the third point likewise is nonsense. You don't show the heat resistance is due to the double strandedness. And your final reference is dead.


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Why do I hear beatings with stereo headphones?
When I play a sine wave together with another pitch shifted sine wave I hear the beating very clearly. This is the expected physical phenomenon.
When I use headphones to play the lower frequency sine wave in my left ear and the slightly higher frequency sine wave in my right (or vice versa), there should be no way for them to physically interfere with each other? But I still hear the beatings, just less strongly.
I tested it with a few different people and how strongly one perceives the beatings varies between people, but many do still hear it. Why?

Short answer
Dependent on the auditory stimuli used, it sounds like binaural beats to me.
Background
Binaural beats are the resultant perception evoked by the interaction of two auditory tones with different frequencies when presented to both ears (Lane et al., 1998). The presented tones should be below 1000 to 1500 Hz and differ in frequency between 1 and 30 Hz. For example, if a pure tone of 400 Hz is presented to one ear and a 410 Hz tone in the other, an amplitude modulated standing wave with a frequency equal to the frequency difference (10 Hz in this case) is perceived. Note that these 1-30 Hz beat frequencies are below the dynamic range of acoustic hearing. Hence, the beatings are the result of neurophysiological interactions in the brain, and not the result of physical interactions of the auditory stimuli impinging on the inner ear. From an experimental point of view, limiting the sound levels to 60 to 70 dB should prevent gross cross-over stimulation to the other ear.
Binaural beats are thought to be elicited in the auditory brainstem, and specifically in the the superior olivary nuclei, when the two wave forms mesh in and out of phase within the brainstem.
Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52
Source
- Web US
Related post
- How can binaural beats change mental state?

Thanks for your answer. However when playing a pure tone of 400Hz and a pure tone of 410Hz I hear the beating (meaning periodic varation in volume). I do not hear the frequency that is equal to the frequency difference.

No. I perceive periodic varations in volume (aka beating) as you would perceive if you play the two pure tones on one channel, due to physical interference of the waves.

Interesting. Although I would not rule out bone conduction, because bone conduction sounds very reasonable too. I will have to test with studio headphones and the little earplug headphones (since the little ones would have far less bone conduction hopefully?). I will also test with frequencies above 1000 Hz. (For example with 2000Hz and 2010Hz, since that would rule out binaural beats) From the papers presented it seems you can only perceive binaural beats with auditory stimuluses below 1000 Hz.

The ear phones versus ear buds shouldn't make any difference. Make sure to limit the sound level to say 60 to 70 dB to prevent cross over between the ears. Let me know how you go. Try 8000 - 8020 Hz too, as an extreme example (exceeding the carrier frequency by a few octaves). And try 1000 and 1100 too (to exceed the difference limit). I'd love to hear more on your experiments.

I used studio headphones at pretty low volume. I didn't find any absolute threshold frequency where I don't hear the beating anymore. It was progressively (though not totally uniform) harder to hear at higher frequencies. At about 150-1500Hz it was pretty easy to hear. Then at 2500Hz I could hear it too though weaker, and very very weakly (very hard to tell) at 5000Hz and above that I can't hear it. When you increase the difference between the frequencies you hear a faster beating (as expected) until you hear two separate tones, as you would if you played it on only one channel.

It could as well be both bone conduction (since low frequencies travel further) and binaural beats. I didn't find much research on this topic online. I don't see any argument to rule out bone conduction completely, since the beatings I hear are very weak (But they are still there!) compared to the beatings when I play the two frequencies on the same channel.

@macco -   What was the sound level?

Sound level on headphones is hard to measure exactly. I listened less loud than the human voice while speaking normally, so around ~60dB. I didn't test with other people except myself this time.

Given the observations I'd say binaural beats, otherwise you should keep on hearing it when the difference is higher than 100 Hz or so and base frequency shouldn't matter too much

Actually there is a way for waves to interact with each other. Our bones conduct vibrations very well: bone conduction. Some of hearing aids are based on this effect.
I can think about another example: the Weber test. It is a quick test for hearing.

In the Weber test a vibrating tuning fork (Typically 256 Hz ...) is placed in the middle of the forehead, above the upper lip under the nose over the teeth, or on top of the head equi-distant from the patient's ears on top of thin skin in contact with the bone. The patient is asked to report in which ear the sound is heard louder. A normal weber test has a patient reporting the sound heard equally in both sides.

So the explanation could be the bone conduction of vibrations.

Yes, I think that is what must happen. If someone knows could you please specify where exactly it cancels out physically (I think it is somewhere in the ear before it reaches the brain) and how exactly the signals get there. Maybe I will have to ask in Physics stackexchange...

What do you mean by "cancels out physically"?

Sorry, cancels out is an inaccurate word. The two soud waves have to interfere with each other which causes the beating. (See wiki page I linked in question if you dont understand)

Bones vibrations affect middle ear (mostly). In normal situation sound waves (in air) conduct into osculation of middle ear bones (incus, malleus, stapes) through the ear drum. In case of bones conduction waves conduct to middle ear directly (without ear drum vibrations). Therefore, i think, waves interference occurs in middle ear.

Bone conduction might well be the answer, but I'm quite interested in whether something neurological might also play a role. Perhaps there is interference within the neural pathway combining left and right sound input?

If it transmits to the middle ear directly through bone conduction it will physically interfere in the middle ear. I would still like if the answer were updated with these details (and maybe some more?). Right now the answer only says: bone conduction. If there is already physical interference it will make it impossible to find out if something weird is going on in the neural pathways or not. That would probably need a seperate question.

Bone conduction has nothing to do with the question. Using normal head phones the contribution of bone conduction is negligible. That is in fact the very basis of discerning middle ear problems from inner ear problems; a difference in hearing sensitivity measured with bone conduction and head phones is a strong indicator of conductive hearing loss. In these tests head phones and a bone conductor are used, respectively. The contribution of bone conduction at moderate loudness can be disregarded using head phones.

I used studio headphones, so there is a considerable area of your head that is exposed to the sound. One could test with earplug headphones to see if one still perceives the same effect.

@macco - to prevent cross-over from the contralateral ear prevent high loudness levels. That should minimize any bone conduction involved.


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Philosophy of Science question permitted here?
Clarified my question re vernacular - science codependency, shortly after it was put on hold. Also, 'Philosophy of Science' IS a topic in biology stack exchange  Please explain why my post's still on hold?

Questions about what is and is not on-topic are off-topic on Biology.SE! There is meta.Biology.SE for that! I am voting to close.

From wikipedia: Philosophy of science is a sub-field of philosophy concerned with the foundations, methods, and implications of science. There are 150 questions tagged "philosophy of science" on Philosophy.SE. There are only 6 open questions tagged "philosophy of science" on Biology.SE and they really are not about philosophy of science!

Note however, that I doubt Philosophy.SE will accept your question in its current form as it feels quite unclear to me (as I explained on your other post). You should probably try to add links for every concept you refer to and make sure to define the words you're using. Good luck!

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

Did you consider posting the original question on Linguistics.SE?


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Do babies conceived naturally or artificially have any differences in long-term health?
Are there any long-term differences in children conceived via artificial insemination or sexual intercourse, pending that the mother successfully delivers the child?

A review paper on children born by the advent of assisted reproductive technologies (ART) and frozen sperm (Lansac & Royere, 2001) concludes that ART children, as compared to the general population:

Have normal weight;
Do not suffer increased occurrence of premature births;
Do not have increased rates in stillbirths;
Have equivalent sex ratios;
Show no increased occurence of birth defects and no chromosomal abnormalities;
Have normal overall health.
Have normal psychosocial development, at least up to 8-9 years of age, but the available data is scant in this area.
However, the rate of multiple pregnancies was higher in the ART group. This may be caused by excessive hormonal treatments during artificial insemination therapy, or by ovulation induction treatments and embryo transfer policies (multiple embryos implanted) that may increase the rate of multiple pregnancies.

The authors do conclude that larger and longer studies are needed to support these findings more conclusively, given that their review paper was based on just two studies. It deserves note, however, that both of these studies were prospective in design and included a large population of subjects.
Reference
- Lansac & Royere, Hum Reprod Update (2001); 7(1): 33-7

In addition to Christiaan's answer I'll cite an article by Bonduelle et al. (1999) that reports a seven-year follow up study of children born via an assisted reproduction technology known as intracytoplasmic sperm injection (ICSI), in which the sperm is injected inside the ovum via a micropipette.
Bonduelle et al. report that there were no higher number of malformations in the ICSI children compared to the control group.


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Why does excess dopamine activity in the pleasure centers results in less pleasure in schizophrenics?
According to the dopamine hypothesis of schizophrenia, there is an excess of dopamine in the mesolimbic pathway (nucleus accumbens), and this contributes to the positive symptoms of schizophrenia.
I am not sure what the cause of anhedonia (reduced interest), one of the negative symptom of schizophrenia. If nucleus accumbens plays a role in the reward system and there is an excess of dopamine, isn't it the case that there should be an increase in interest, that is, no anhedonia?

Welcome. Nice question! I edited the title to make a question out of it. Feel free to roll that edit back.

Hi @AliceD, thanks for the reply and great reference on Milan et al (2014). Sure, I am okay with the new title. Just to double check if I understand it correctly: it seems to be the case that we can not look at it only from nucleus accumbens point of view (as the author of the paper states, "amotivation and anticipatory anhedonia of NS ... in terms of defective cortico-striatal integrated processes indispensable for reward acquisition and anticipatory pleasure").

Yes, it's a lot more complex than DA + n.accumbens alone

Short answer
The dopamine hypothesis includes brain regions with reduced dopamine transmission as well. The prefrontal cortex in specific has reduced dopaminergic activity and is implicated in anhedonia. It affects pleasure seeking behavior through interactions with the nucleus accumbens.
Background
The negative symptoms of schizophrenia are less well understood as the positive counterparts. One thing is for sure, the dopamine hypothesis cannot explain everything. It is a very useful working hypothesis, but primarily based on the first generation antipsychotics such as haloperidol with mainly dopaminergic mechanisms of action. In turn, these drugs mainly and effectively target the positive symptomatology (excessive dopaminergic transmission).
Second-generation antipsychotics are more effective in treating the negative symptoms and are thought to actually increase cortical dopamine, as well as and acetylcholine release, as well as have a variety of effects on the glutamatergic system not shared by the typical agents first-generation antipsychotics (Meltzer, 2004).
In fact, the dopamine hypothesis has been improved and adjusted during decades of intensive research. One of the important things that has come out of this is that dopamine neurotransmission is regionally affected, with a prefrontal hypodopaminergia (prefrontal cortex, or PFC and a subcortical hyperdopaminergia (e.g. in the pleasure centers). An excellent review of the historic developments in the dopamine hypothesis was published by Howes & Kapur (2009)
Now on to anhedonia. Pleasure perception per se seems largely unaffected in schizophrenic people, it is the anticipation of pleasure that seems negatively affected. This is accompanied by reduced motivation and goal-directed actions to seek pleasure. Anhedonia is primarily attributed to disturbed interactions between the ventral (nucleus accumbens) and dorsal striatum (mainly the caudate) and the PFC and not so much in the experience of pleasure per se. In addition, insular cortex, amgydala and hippocampus may be involved. A dysfunctional coupling between the anterior cingulate and the insular cortex (the “salience network”) has also been linked to the failure to appropriately process reward in schizophrenia. Lastly, goal-directed actions needed to obtain the reward and dependent on the PFC is dependent on not only dopaminergic, but also adrenergic and other mechanisms. This is all nutshelled information and I would encourage you to read Milan et al. (2014), who have written an extensive and excellent review focusing on anhedonia in specific as a negative symptom. Fig. 1 is obtained from that paper and shows the complexity of anhedonia.

Fig. 1.  Cerebral circuits involved in negative symptoms, with a focus on deficits in anticipatory reward. source: Milan et al. (2014)
Reference
- Hows & Kapur, Schizophr Bull (2009); 35(3): 549–62
- Meltzer, Curr Opin Pharmacol (2004); 4(1): 53-7
- Milan et al., Eur Neuropsychopharmacol (2014)24(5): 645-92


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what is the word origin of myelo- as in myelofibrosis or myeloma?
what is the word origin of myelo- as in myelofibrosis or myeloma? I know that these are plasma cancers originating in the bone marrow.

I'm voting to close this question as off-topic because it is about the etymology of words and not biology.

myelo- is from Greek related to the word for 'marrow'.
See also: http://www.dictionary.com/browse/myelo-
Most cancers are named in a similar matter, with the tissue of origin followed by the suffix "-oma": glioma from glial cells, sarcoma from the connective tissues/"flesh",

medical terms are mainly based on Greek and Latin words, myel(myelo) is a root which means bone marrow and it also can mean spinal cord , it depends on the word. in myeloma , myelo means bone marrow and oma is a suffix which means tumor just like lymphom( cancer of lymphatic system ).
ex: meylitis: inflammation of spinal cord , but , myeloma : cancer of the bone marrow

Read the comments of a respected user — comments that have been upvoted — and follow the injunction in the Help section on answering questions: Answer well-asked questions.


text:
Is vermiform appendix no more a vestigial organ?
The appendix has a role in the immune response.
So is it therefore recently removed from the list of vestigial organs?

Short Answer: No, the appendix is still considered a vestigial organ.
Long Answer: The idea that that vermiform appendix is vestigial originated when Kumar et al (1989) removed it from the body, but failed to find any side-effects. From then on, it got widely established that vermiform appendix is a vestigial organ and has lost all its functions during the course of evolution. The reason behind appendix becoming vestigial was given by Darwin himself in The Descent of Man, and Selection in Relation to Sex where he stated that appendix was used by early primates to digest leaves, and slowly became vestigial as ancient humans shifted towards foods like cereals and meat. This theory was also supported by presence of very long cecum in herbivores like koala and horse.
The only problem with this idea was that the role of appendix in only digestion was being considered. As appendix was connected to large intestine, so early scientists (kinda) presumed that it should be related to only digestion.
This theory got its first challenge when Parker et al (2007) suggested the appendix to be a safe-house of healthy bacteria when illness (such as diarrhea) flushes them out of the GI tract. It was based on the understanding, which came in 2000s by Sonnenburg et al (2004) and Everett et al (2004), about how the immune system supports the growth of beneficial intestinal bacteria. This was experimentally established when Dunn et al found that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile colitis.
After this, more functions of appendix were discovered, especially those related to immune system. It is because of the efforts of Zahid et al (2004) (the one you cite) and Rankin et al (2016) that appendix is now identified to be more related to immune system than digestive system in humans.
Also, research by Laurin et al (2011) and Smith et al (2013) concluded that during the evolutionary course, appendix has evolved about 38 times and lost as many as 6 times, suggesting that the cecal appendix has a selective advantage in many situations and argues strongly against its vestigial nature.
Conclusion:

Vermiform appendix is identified as Gut Associated Lymphoid Tissue (GALT) and important component in mammalian mucosal immune function, B-cell mediated immune response and extrathymically derived T-cells.
This structure helps in the proper movement and removal of waste matter in the digestive system, contains lymphatic vessels that regulate pathogens, and lastly, might even produce early defences that prevent deadly diseases.
It is thought that appendix may provide more immune defences from invading pathogens and getting the lymphatic system's B and T cells to fight the viruses and bacteria that infect that portion of the bowel and training them, so that immune responses are targeted and more able to reliably and less dangerously fight off pathogens.

Discussion: The problem is in the definition itself of vestigial organs. The point is that being vestigial is not equal to being useless. See this definition by Wikipedia (emphasis mine):

In the context of human evolution, human vestigiality involves those traits (such as organs or behaviors) occurring in humans that have lost all or most of their original function through evolution. Although structures called vestigial often appear functionless, a vestigial structure may retain lesser functions or develop minor new ones. In some cases, structures once identified as vestigial simply had an unrecognized function.

Now, since vermiform appendix does not perform its (suggested) original function of digesting cellulose and other indigestible materials, and performs much less of its (possible) function in immune system, it is still officially considered as vestigial organ.
References:
• Vermiform Appendix - Wikipedia
• Human Vestigiality - Wikipedia
• Kumar, Vinay; Robbins, Stanley L.; Cotran, Ramzi S. (1989). Robbins' pathologic basis of disease (4th ed.)
• Darwin, Charles (1871) "Jim's Jesus". The Descent of Man, and Selection in Relation to Sex
• Bollinger, R.R.; Barbas, A.S.; Bush, E.L.; Lin, S.S.; Parker, W. (21 December 2007). "Biofilms in the large bowel suggest an apparent function of the human vermiform appendix"
• Sonnenburg J.L.; Angenent L.T.; Gordon J.I. (June 2004). "Getting a grip on things: how do communities of bacterial symbionts become established in our intestine?"
• Everett M.L.; Palestrant D.; Miller S.E.; Bollinger R.R.; Parker W. (2004). "Immune exclusion and immune inclusion: a new model of host-bacterial interactions in the gut"
• Dunn, Rob. "Your Appendix Could Save Your Life"
• Zahid, Aliya (2004-04-01). "The vermiform appendix: not a useless organ"
• Rankin, Lucille C.; Girard-Madoux, Mathilde J. H.; Seillet, Cyril; Mielke, Lisa A.; Kerdiles, Yann; Fenis, Aurore; Wieduwild, Elisabeth; Putoczki, Tracy; Mondot, Stanislas (2016-02-01). "Complementarity and redundancy of IL-22-producing innate lymphoid cells"
• Laurin M.; Everett, M.L.; Parker W. (2011). "The cecal appendix: one more immune component with a function disturbed by post-industrial culture"
• Smith H. F.; Parker W.; Kotzé, S. H.; Laurin, M. (2013). "Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors"

How is it concluded that vermiform appendix had original function of digestion?

@jm97 I ain't sure about this...I suppose Darwin's theory?

@JM97 many herbivores have a large appendix that functions as a sort of protected space for their gut bacteria, so a single bad food or illness cannot deplete their gut bacteria.

Short answer
The appendix is a vestigial organ.
Background
According to the Oxford Dictionaries vestigial means:

Degenerate, rudimentary, or atrophied, having become function-less in the course of evolution.

This doesn't mean that a vestigial organ necessarily has to have no function at all, as in the case of the vestigial wings in mutant fruit flies for example that serve no purpose whatsoever.
The appendix has lost all of its original food digestive functions, and therefore it is,  per definition,  a vestigial  organ.  However,  it still has a role in immune responses.

It turns out that the vermiform appendix is NOT a vestigial organ based on Darwin's definition.
Without rehashing what the appendix actually does, I'll quickly address the faulty arguments that it is a vestige.
Point 1: Darwin called the appendix a vestige because it was a remnant of a larger cecum used for digestion:
RESPONSE to Point 1: In most cases of evolution of the appendix (as we assessed with our collaborators in France and Arizona), the appendix is actually getting larger (or appearing) as the cecum gets larger. The appearance of the appendix in the anthropoid apes is an exception. So the appendix, in general, cannot be characterized as the remains of a cecum in the ancestral state.
We covered this in a paper published about 5 years back: World J Gastroenterol
2013; 19(34): 5607-5614.
Point 2: Related to point 1, the idea is that the appendix still has some function, but has lost it's digestive function.
RESPONSE to Point 2: Based on what we know about its function, the vermiform appendix has ENHANCED functions in terms of maintaining beneficial bacteria compared to a cecum without an appendix. In other words, in some regards, it has more function, not less function, than the ancestral state. (Thus explaining the tendency of it to occur repeatedly in evolution more than it is lost.)
Discussion: The human arm is probably akin to our appendix in many ways. We would never think of our arms as a vestige even though we do not use our arms for locomotion as did our ancestors. But we still use them, in some ways probably more than our ancestors, and we still need them.
The definition of a vestige in biology does cause confusion. In my lab, we prefer to think of a vestige as a structure that is best understood based on a function that has been lost rather than on a current function. Darwin meant it to be descriptive, not to cause confusion. In English (non-biology), a vestige means simply a remainder of something that is gone or disappearing. (e.g., the vestiges of colonial rule) It is best to think of the odd wiring of facial nerves, the wings of flightless birds, or the hip bones in certain legless animals as vestiges. These are much more clear-cut cases, where the current structure is best understood when one understands both the structure and the function in the ancestral state.  This does not apply to the human arm or to the vermiform appendix, of course.


text:
Are these fruit flies really coming back to life after being frozen?
I've found this video on Reddit where they pretend these are frozen fruit flies coming back to life... I didn't find any publication related to this specific experiment. Is this just a fake video?

! froze grasshoppers in a jar for a few weeks ( home freezer 10 F +/-) .When slowly warmed to room temperature , they began moving.

Short answer
Short-term freezing kills fruit flies. Long-term cryo-preservation of D. melanogaster is also not possible.
Background
Per a publication of Koštál et al. (2016), long term preservation of insects is only possible for embryos, or larvae in diapause. Indeed, freezing is an effective way to kill adult fruit flies (source: Phys.org)
However, D. melanogaster adults show very weak capacity to enter reproductive diapause, and larvae possess absolutely no capacity for diapause Koštál et al., 2016).
Reference
Koštál et al., Scientific Reports (2026); 6: 32346

When I worked in agrocery store I was in charge of taking down the salad bar. Regularly, fruit flies would land on stick to the cold/frozen metal. When the salad bar was turned off, they would fly away.


text:
Why are fearful stimuli more powerful at night?
For example, horror movies appear to be scarier when viewed at night than during broad day light.
Does light have any role in this phenomenon?
Are there changes in hormones at night versus during the day that makes fear stronger?

I think this is a really awesome question, I might try to edit it a bit if you don't mind, I'll try not to change the meaning. I might also write up a quick answer based on rodents, though something you may or may not realize is that "fear of the dark" is certainly not universal - if you were a mouse asking the question, you might wonder why the daytime is so scary.

I don't have time right now for a full response, but I'll just dump a couple starters out there. The hormonal side I'll have to do a little research on, there are certainly hormones that change throughout the day but I don't have detailed knowledge of this specific effect. There is also a direct projection from certain cells of the retina directly to the amygdala, an important brain structure in fear. The topic is actually of high interest because similar circuitry is implicated in anxiety disorders and PTSD and belongs in the broader category of "what makes 'normally' not-scary things scary."

@Bryan Krause: Indeed, fear of the dark is not universal even among humans.  I've always liked the night myself, and can't really understand why people use nightlights & such.  Nor have I ever noticed any change in intensity of 'fearful' stimuli that wouldn't be explained by not being able to clearly see the source.  E.g. that growl might be a bear, or your neighbor's friendly dog.  In the day, you would know (unless it's in the bushes) and react accordingly.  In the night, you assume the worst case and prepare.

I think it would be necessary to report references that this is actually the case (fear response is activated more easily at night), otherwise it is just an opinion.

here:  http://cogsci.stackexchange.com/questions/16751/why-do-we-fear-more-in-the-night

I suspect that it's a combination of uncertainty and expectation, and there might some related neuromodulatory effect, but I don't know any relevant literature.

Maybe it is psychosomatic; we as children grew up fearing the dark. We are let to believe that ghosts haunt at night. It can be considered similar to Triskaidekaphobia (fear of 13) or Hexakosioihexekontahexaphobia (fear of 666).

Short answer
The increased fear responses during the night are believed to be mediated by elevated corticotropin-releasing hormone (CRH) levels in the brain that drive the fear responses in the amygdala.
Background
Fear responses can be experimentally assessed by recording the startle reflex. For example, loud noises can evoke gross startle responses in rodents (whole-body startles) and more subtle responses in humans (eye blinks).
In nocturnal animals, it has been shown that startles are facilitated by bright light. In contrast, fear responses in humans, a diurnal species, have been shown to be stronger in the dark (Grillon et al., 2007).
In the rat, the light-enhanced startle has been associated with the hypothalamic–pituitary–adrenal axis (Fig. 1). Specifically, light exposure has been shown fear mediated by corticotropin-releasing hormone (CRH) (Grillon et al., 2007).

Fig. 1. HPA axis. source: Wikipedia
The HPA-axis is affected by the circadian clock and therefore exhibits a pronounced daily rhythmicity. The HPA axis is activated by hypothalamic release of CRH, which stimulates the secretion of adrenocorticotropic hormone (ACH) from the anterior pituitary. ACH triggers the production of cortisol by the adrenal glands. Cortisol, in turn, provides negative feedback and shuts down HPA-axis activity by binding to corticosteroid receptors in various HPA-axis structures, e.g.the hypothalamus (Fig. 1). As a result, cortisol levels show a robust diurnal rhythm that runs in opposite phase with CRH. Cortisol in humans peaks at the time of awakening and drops to its lowest levels around bedtime, whereas the opposite is true for CRH (Miller & Gronfier, 2001).
The startle reflex shows a diurnal variation roughly opposite to the rhythm of corticosterone and in phase with CRH. Specifically, startle responses in nocturnal animals such as rats are highest during daytime (their passive phase) when CRH is peaking, and corticosterone is at its lowest. Conversely, startles are lowest during the night (their active phase) when CRH levels are lowest, and corticosterone levels are high. In man, a diurnal species, exactly the opposite pattern is observed. Hence, startle responses are thought to be endogenously modulated by the circadian system, most likely via effectors of the central pacemaker such as the HPA-axis (Miller & Gronfier, 2001).
In rats, administration of exogenous CRH enhances the startle reflex and blocking of the glucocorticoid receptors which produces a blockade of negative feedback, also increases startles. Conversely, blocking CRH receptors decreases the startle response, as does corticosterone administration (Miller & Gronfier, 2001).
CRH receptors are expressed at various brain centers, including the amygdala. The amygdala is a key structure in the limbic system, the emotional control center of the brain. The amygdala is specifically associated with anxiety and fear responses. Indeed, it is thought that CRH receptors in the amygdala are responsible for the fear-promoting actions of CRH (Grillon et al., 2015).
Hence, it is not darkness or light per se that mediate fear responses. Instead, it is the circadian control of the HPA axis that controls the daily variations in fear responses.
References
- Grillon et al., Biol Psych (2007); 62(10): 1183–6
- Grillon et al., Neuropsychopharmacol (2015); 40: 1064–71
- Miller & Gronfier, Psychophysiol (2006); 43(3): 297–301

@Mesentery - no rush :-) Apologies for the delay, but complex questions like this one need some careful preparation :-) It took me a while to gather the appropriate references and get the story right. Especially because most research has been done in nocturnal species the subject is quite complex

Great answer. Of course this is almost certainly only part of the story - I would expect there could also be learned and instinctual associative learning related to darkness and fear - the strength of which no doubt displays a lot of situational and inter-individual variability. And great find on that Grillon paper - I was searching for something similar when I initially commented and wasn't immediately successful, finding mostly the rodent work in the light instead.


text:
How are colors outside the standard RGB color scheme perceived?

I found this image in a German book about biology. It's called DIN 5033 and represents the RGB color scheme.
What colors are outside the RGB scheme, i.e., in the black areas of the picture?

DIN 5033 covers wavelengths 380nm to 780nm along its edges. Everything in that space not on the edge varies only in spectral purity. Anything outside those wavelengths would be not covered by this color space (e.g. ultraviolet). Anything in the black area makes no sense (light consisting of nothing but precisely X nm light can't be any more "pure"). Human visual range varies but roughly covers that same spectrum. Outside the range is more towards infrared (higher wavelength) or ultraviolet (lower).

Note also that the bottom right edge (magenta) isn't on the visible spectrum, it's a blend of red and blue. Also the black area isn't light outside the 380-780 range, it simply isn't defined, just as (x,y)=(1,1) isn't a possible solution for x^2+y^2=1. If you wanted to modify that colorspace to add infrared/ultraviolet, you would simply increase its perimeter, inserting ultraviolet in the bottom left, infrared on the right, thus shifting magenta more towards the center and the bottom edge becomes a gradient of ir/uv mixes.

If you mean "perceived" by something other than human eyes/brains, I would also love to know if cameras/devices that are sensitive to the full spectrum of light have been used to map "invisible" chromatic territory (i.e. by having a machine that can measure frequency)

This question is both biology and physics I think (I guess it's biophysics! :) so I feel it's worth answering here.
First, we must recognize the difference between wavelength, which is just a physical property of light, and color, which is by definition a human visual perception. The color "red", for example, is a particular visual sensation humans have when encountering light of certain wavelengths. A color cannot be described by a single wavelength number, because the light we see in nature is never monochromatic; it's a complex mix of photons of all sorts of wavelengths.
As John's answer also pointed out, the human eye has three types of cone cells which responds to wavelenghts differently, determined by their absorption spectra (see picture below; R represents the rod cells, which I ignore here). Human color perception can be described as a mix of signals from the L (long wavelength, red), M (medium wavelength, green) and S (short wavelength, blue) cone cells. Mathematically, this is a linear combination $l \cdot f_L + m \cdot f_M + s \cdot f_S$ of the three spectra $f_L$, $f_M$ and $f_S$. The coordinates $(l,m,s)$ generate the LMS color space, which by definition contains all colors humans can perceive.

Now for your question: what colors are outside the RGB scheme?
This depends on precisely what you mean by "the RGB scheme" and "color". The picture you posted is actually not an RGB scheme but a two-parameter color model known as CIE 1931, which is roughly the same as the LMS color space, minus a light intensity parameter. If by "color" you mean the human visual perception, then by definition there are no colors outside the LMS space.
On the other hand, there are many kinds of light that humans cannot perceive correctly: you can imagine from the figure above that there any many cases where two different wavelength mixtures give the same response. For example, a mix of "red" and "green" light may result in the same $(l,m,s)$ values as "yellow" light, even though this is physically different. And of course, some wavelengths our eyes don't register at all, but we usually don't consider such wavelengths as "colors".
Finally, if by "RGB model" you mean the types of light that RGB devices like your computer screen can produce, then the answer is that there are many colors outside RGB. This because RGB devices use light sources for R, G and B with different wavelength profiles than those of the cone cells. Therefore, a typical RGB device generates only some subset of the LSM space. For example, in the figure below, the triangle represents the colors generated by mixing three monochromatic R, G and B light sources in the CIE RGB space, one of many possible RGB spaces.

the colors we humans with our trichromatic eyes cannot see.

.Color for us is produced by a combination and comparison of cell activation. We can see every wavelength between about 4-700nm, we can't differentiate well near the ends or at all for that matter compared to non-mammals. for most of the RGB  one wavelength activates more than one cell the comparison of activation creates a color, by activating more than one type of cone cell by different amounts. example activate both red and green but red more than green and you see orange, activate both the same and see yellow.
The deep purples or magentas however are weird and can be activated in two ways. Our red cones actually also pick up light in the 400nm range. so light  close to 400nm activates both blue and red but not green (if our red cones did not have this bleed over it would normally be impossible to active red an blue but not green), but you can also trick the eye by using both red and blue light together which produces the same result of activation. that's why you have that purple smear across the bottom of the color chart.

But there are also wavelengths below 400 and above 700, Other animals can see part of these wavelengths as colors. There are animals that see colors in what we see as white light. Animals with more than three types of cones or with cones that are activated by different areas of the spectrum see different colors.

Well ...  The RGB model is certainly designed to create colors that we humans can see, but it's not the same color space, since the R,G and B primary colors of RGB devices have different frequency envelopes than our cone cells.

if you look at the OP's graph you can see the same plot our eyes are stuck with, a smooth spectrum from blue to red and purple is when the ends of the spectrum are active without the middle. past that you get into the infrared and ultraviolet.

I think you need to distinguish between color and wavelength. Colors are properties of human biology; wavelengths are just physics.

If you look at the OP's chart it is graded by wavelength, Color for us is produced by wavelength or a combination of wavelengths. we can see every wavelength between about 4-700nm, we can't differentiate well near the ends or at all for that matter compared to non-mammals. But there are also wavelengths below 400 and above 700, Other animals can see part of these wavelengths as colors. There are animals that see colors in what we see as white light.

This answer is incorrect. The black area does not contain "colors we cannot see". The black area is undefined because it would represent signals with more than 100% spectral purity (if a signal is already precisely 750nm wavelength with no other components, it can't be more pure than that). IR and UV, if you wanted to add them to that space, would go on the right and bottom left corners respectively, expanding the perimeter of the space and shifting magenta towards the center and making the bottom right edge a gradient of IR/UV blends.

In other words, you are correct in your notice of the wavelength gradations on the edges, but light outside those wavelengths is not what the black area represents. The black area is undefined in the same way that (x,y)=(1,1) is not a solution to x^2+y^2=1. The black area doesn't have anything to do with human perception either, only math. The only part of this colorspace related to human perception is the choice of wavelength range it represents, which was chosen to roughly match the visible spectrum. That choice, even though it makes sense, is essentially arbitrary.


text:
How do S and L cone cells sense colors like deep blue and red beyond their peak?
So I found this diagram of retinal cone cells:

It looks like the S, M, and L cones peak at blue, chartreuse and orange, respectively. If so, how do we see colors past 575 nm and before 445 nm? If the cones really respond to purple, green, and red, (as I previously thought) why do they peak at colors closer to green, as shown in the image?

The answer is actually present in your chart: color perception depends on the ratios of activations of different photoreceptors. For example, as you go "more red" from 575, the responses of the Green photoreceptors are falling off more quickly than the Red ones. The same is true for any colors in between, and on the other end, where 400nm light would activate only the blue receptors, whereas at 445nm there would be some mix of activation of the green.
From the context of Fisher information it is actually interesting that photoreceptors don't actually provide much color discriminability at their peaks.
For example, around 575 nm, the "red" photoreceptors actually don't provide very good color discrimination: the response to 565 or 585 is going to be almost identical, for example. The way you can perceive a difference, though, is that the response from the green photoreceptors will be very different at those two wavelengths (just consult your chart!). In vision, as in all the other senses, the information is really held in the slopes!

The cones responsive to long wave lengths (L cones) are simplistically called 'red cones', those sensitive to intermediate wave lengths (M-cones) are often called 'green cones', and those sensitive to short wavelengths (S cones) are often referred to as 'blue cones'. Red, green and blue cones are hence terms reflecting simply their peak absorbance.  However, as your plot shows, there is a great amount of overlap in the absorption spectra of the red, green and blue pigments in the cones in the retina.
To your question: How can we perceive see light with wavelengths larger than 575 nm, and shorter than 445 nm
This is because the cones are sensitive to a whole range of wavelengths outside of their characteristic peak absorbance in the visual spectrum. However, the sensitivity does drop beyond the peak, so red light with wavelengths >445 nm will be perceived less and less clearly, up until the point it becomes undetectable (infrared). Likewise, shorter wavelengths than 445 will loose intensity and eventually become invisible (ultraviolet).
The green and red opsins are basically the same proteins with only a slightly shifted absorption spectrum - indeed, these opsins split late in evolution due to a tandem repeat and small point mutations.
Color vision is nonetheless very specific and millions of colors can be discerned by someone with normal trichromatic vision.
This is accomplished by color opponency:
The opponent color system has 2 channels, namely a red versus green and a blue versus yellow system. The input are the photoreceptors in the retina: red, green and blue cones. A third achromatic channel is used to code visual brightness (Fig.1.). The neurophysiological machinery is located in the retina and higher visual structures such as the lateral geniculate nucleus.

Fig. 1. Color opponency
This model is referred to as Hering's opponent color theory (Gouras, 2012). It states that the blue channel suppresses yellow (and vice versa) and red suppresses green (and vice versa). The advantage of this system sharpens color contrasts between opponent colors (Hurvich and Jameson, 1957). In other words, the broad flanks of the absorption spectra of the opsins are sharpened at their edges by opponent colors. This mechanism causes the fact that we cannot see yellowish blues or reddish greens etc. Instead we can only see mixed colors between channels, e.g., yellowish greens or reddish blues (purples).
References
- Gouras, Color Vision. In: Kolb et al., Webvision. The Organization of the retina and visual system, Utah University
- Hurvich & Jameson, Psychol Rev (1957); 64(6): 384-404


text:
Determining whether X chromosome from sperm or egg
Is there any way of determining which X chromosome a female inherited from her father and which from her mom ?

You could try to follow this up by sequencing the X chromosome from the father and try to find unique polymorphisms which are not present in the X chromosome of the mother. You can than try to find them in the childs "X". This makes not much sense though, since one of the X chromosomes is ramdomly inactivated.

@Chris So, we could use RFLP for this ? Could we also use FISH ?

RFLP could work, I am not sure if the resolution of fish is good enough.

@Chris Thanks! I don't know much about FISH, so what exactly do you mean when you say that resolution won't be good ?

For FISH you need a probe that binds to the chromosome. If the difference you want to see is so small (a SNP for example), that the probe will bind anyway, than the resolution of the method is too small to detect the difference. Insertions or deletions are bigger an can be detected.

yes it is possible... in placenta (trophectoderm) the paternal X is epigenetically silenced [ref].
That is if you do the test in the pre/neo-natal stage. Otherwise, at later stages, you have to check by DNA fingerprinting + karyotyping/FISH as Chris suggested.


text:
Vesicular and non vesicular transport

I have to classify them either as transported in vesicles or without vesicles.
What I think -

Non-vesicular

2.vesicular
3.vesicular
4.vesicular
5.non-vesicular
6.vesicular
7.vesicular
8.vesicular
9.vesicular
Am I right ? Is it true that a  protein transported by vesicles is made on ER ribosomes ?
How are proteins transported non-vesicular transport ?

Any protein which enters the secretory pathway will proceed via vesicular transport to some point on that pathway. That includes lysosomal proteins, integral plasma membrane proteins and secreted proteins (also, not on your list, resident proteins of the ER, Golgi proteins, some endosomal proteins).
Cytoskeletal proteins are cytoplasmic: I suppose you could argue they are 'transported' sometimes, e.g. tubulin treadmilling, motors etc., but no vesicles are involved. Nuclear proteins enter the nucleus from the cytoplasm through nuclear pores. They have nuclear localisation signals; vesicles aren't involved. Mitochondria, chloroplasts and peroxisomes all have their own protein import systems with associated unique signals; again no vesicles are involved.


text:
Are fatty acids and glycerol lipids?
As far as I know, lipids are defined as biomolecules which are hydrophobic.
Triglycerides are composed of fatty acids and glycerol and are considered lipids but, are fatty acids alone or glycerol alone considered as lipids ?

From IUPAC Goldbook:

A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

That means that lipid does not mean any hydrophobic molecule.
Lipids can be amphipathic as you already know about fatty acids.
Glycerol is not a lipid; neither is it hydrophobic. Glycerol, if to be classified into one of biomolecular classes, it would be that of monosaccharides (in the form of sugar alcohol like sorbitol and xylitol).

I would rather classify glycerol as an alcohol, but this can be debated.

I dropped my answer and fully support this one. The wiki page on glycerol says it is a poly-alcohol and thus a sugar.

@Chris. Yes it is alcohol no doubt. I was talking about a biochemical class and it is one of the simplest sugar alcohol (like sorbitol, xylitol etc).

Instead of calling glycerol a monosachharide, shouldn't it be called derivative of a monosachharide as it doesn't have a ketone / aldehyde grp ?

@biogirl I didn't call it a monosaccharide. I said if at all it is to be grouped somewhere it would be in that of monosaccharides. And yes it is a reduced form of glyceraldehyde and dihydroxy acetone (which are the simplest aldose and ketose resp.). It would be called a sugar-alcohol (so yes it is a derivative).

Okay. Makes sense.

Glycerol is not lipid (short chain polyol, so it is polar and water soluble), but fatty acids (amphiphilic) and triglycerides (hydrophobic) are.

Lipids may be broadly defined as hydrophobic or amphiphilic small
  molecules; the amphiphilic nature of some lipids allows them to form
  structures such as vesicles, multilamellar/unilamellar liposomes, or
  membranes in an aqueous environment.

wikipedia - lipid


text:
Allergic rhinitis vaccine
Note : Any answer to this question will not be (and should not be) taken as medical advice.
One of my friends has allergic rhinitis and has been prescribed an oral vaccine. He is allergic to 3 different classes of substances and so, has been given 3 different types of vaccines. He has to place them below his tongue.
I am curious about some of the procedures he has to follow.
1.How does a vaccine of this type work ?
2 He has been given 2 vials for each type of vaccine. First one is labeled SRS and other one as I understand is - it's allergen. So, What is SRS ? What's the requirement of it ?
3 It is written in the instructions that he should not eat anything one hour before and one hour after taking the vaccine. Why ?

SRS-A stands for slow-reacting substance of anaphylaxis. It is a leukotriene which causes eosinophil chemotaxis and thereby causes allergic reactions in rhinitis.
The described technique is called sublingual immunotherapy. I am not sure how it works (Cant find any article on that. Most articles are from medical journals which don't emphasize on mechanism). I shall find out and get back.

Rhinitis is irritation and inflammation of the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic rhinitis, which is usually triggered by airborne allergens such as pollen and dander [1].
Many questions regarding sublingual immunization still remain to be addressed, including the use of proper adjuvant and the optimization of vaccine formulation to further enhance the vaccine efficacy [2].
Sublingual immunization can induce both systemic and mucosal immune responses against a variety of antigens, including soluble proteins, inter particulate antigens, and live-attenuated viruses [2].
Sublingual immunization has been shown to be safe and highly effective in generating robust immune responses against the administered antigen. Moreover, it has been shown to confer protective immunity by simultaneously eliciting systemic IgG and mucosal IgA antibodies as well as cytotoxic T lymphocyte responses in the peripheral lymphoid organs and mucosal tissues. Studies also suggest that sublingual immunization could be a better alternative to the traditional parental route of vaccine delivery against both genital and respiratory pathogens [2].
Although the s.l. mucosa does not allow passage of macromolecules into blood, s.l. immunization with ovalbumin, a model soluble protein antigen, administered
alone or together with cholera toxin adjuvant, induces mucosal antibody responses as well as systemic immune responses in mice. The magnitude of serum antibody responses induced by s.l. immunization was in fact comparable to that seen after intranasal (i.n.) immunization and far superior to that after o.g. (oro-gastric) immunization [3].
Upon stimulation of mucosal surfaces by foreign antigens, dendritic cells among the antigen presenting cells are immediately processed and transport antigen via afferent lymph to draining lymph node for presentation to T cells. Subsequently they induce secretory IgA antibodies. This suggestive link between trafic pattern of dendritic cells and their functions led to the investigation of the chemokine responsiveness of dendritic cells during their development and maturation. It has been observed that type II mucosa tissues (e.g., skin, vaginal, and buccal), which are covered with stratiﬁed epithelia and devoid of
mucosa-associated lymphoid tissues, mainly express CCL20, CCL19/CCL21, or CCL27/CCL28 individually [4].
CCR7 (chemokine receptor) expressed CD8α-CD11c+ cells ferry antigens in the sublingual mucosa, migrate into the cervical lymph nodes, and share the antigen with resident CD8α+CD11c+ cells for the initiation of antigen-specific T and B cell responses following sublingual challenge. The sublingual mucosa is one of the effective mucosal inductive sites regulated by the CCR7-CCL19/CCL21 pathway [4].

References:

Wikipedia, Rhinitis
Byoung-Shik Shim, Youngjoo Choi, In Su Cheon, and Man Ki Song. Sublingual Delivery of Vaccines for the Induction of Mucosal Immunity.
Cecil Czerkinsky, Nicolas Çuburu, Mi-Na Kweon, Fabienne Anjuere and Jan Holmgren. Sublingual vaccination.
Joo-Hye Song, Jung-Im Kim, Hyung-Joon Kwon, Doo-Hee Shim, Nirmala Parajuli, Nicolas Cuburu, Cecil Czerkinsky and Mi-Na Kweon. CCR7-CCL19/CCL21-Regulated Dendritic Cells Are Responsible for Effectiveness of Sublingual Vaccination.


text:
Trimming of tRNA precursors
From Molecular Biology of the Cell (4th edition) by Bruce Alberts et al. (Chp 6, Pg 338) :

Both bacterial and eucaryotic tRNAs are typically synthesized as
  larger precursor tRNAs, and these are then trimmed to produce the
  mature tRNA. In addition, some tRNA precursors (from both bacteria and
  eucaryotes) contain introns that must be spliced out.

What's the difference between the two statements (and between trimming and splicing) ?

Trimming = removing RNA sequences from one end.

Splicing = removing introns and joining exons back together.


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Erythroblastosis Foetalis
If Rh- mother has Rh+ baby, the mother can become sensitized during first pregnancy and then if subsequent fetuses are also Rh+, there can be eryhtroblastosis foetalis.
I read that if mother is O- and baby is any +ve blood group other than O+ , then mother will not become sensitized during first pregnancy because a and b antibodies present in her blood will attack the antigen present on the fetus RBC and there will be no time for the mother to synthesize antibodies against Rh.
My Question : Can't the same logic be applied to all other blood groups? For example : A- mother and B+ baby.

if mother is O-

That means:

group O in ABO system: anti-A and anti-B antibodies
group Rh- in Rh system: no D antigen and no ant-D antibodies unless previously senzitized

baby is any +ve blood group other than O+

ABO system: A, B or both antigens present
Rh system: D antigen present

So, the mother has anti-A and anti-B antibodies and her immune response will be directed towards the fetal RBCs containing A, B and D antigens. But, in theory, the immune system should also produce anti-D antibodies because of antigen presenting cells which will expose D antigens to T lymphocytes.
What is known is that if the mother already has anti-D antibodies, no other are secreted from fetal D antigens. This is how passive immunization vaccines work:

This is done so that the fetal Rhesus D positive erythrocytes are destroyed before her immune system can discover them. This is passive immunity and the effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies gradually decline to zero in the maternal blood [1].

But the mechanism is not clearly understood:

The most fascinating aspect of the story scientifically is that we still do not have a complete, mechanistic understanding of how this therapy works. The original hypothesis that Rh-immune globulin functions by clearing fetal Rh(D)-positive red blood cells from the maternal circulation, thereby hiding this foreign antigen from the maternal immune system, is inconsistent with the fact that passive immunization with Rh-immune globulin guides the fetal red blood cells directly to antigen presenting cells, the same cells responsible for initiating an immune response to foreign antigens [2].

References:

Wikipedia contributors, "Rh disease," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Rh_disease&oldid=615938189 (accessed July 28, 2014).
Eldad Hod. A Treatment for RH Disease. Available from http://pathology.columbia.edu/rh_disease.html (accessed 28.07.2014)

I read about this in nelson pediatrics. Will add that information whenever possible. ..


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If mammals evolved to be nocturnal, then how did we get so staunchly diurnal in such short time?
Much of human health revolves around sleeping well through the night.  We know about circadian and body temperature rhythms which make us sleepy at night, peak melatonin production in the middle of the night, deep sleep phases, sleep disruption from light at night, and high cancer rates among people who work the night shift.
Clearly, we are built to sleep at night.  You would suppose, then, that we must have evolved to be diurnal long ago and descend from a long line of diurnal animals.
Yet, the evolutionary legacy of mammals is predominantly nocturnal.  Mammals started out as nocturnal (to avoid the reptiles) and most mammals today are still nocturnal.
How did we get so staunchly diurnal so quickly?

You think 65 million years is a short period of time?  Part of the answer is that the extinction of the dinosaurs left a lot of daytime ecological niches for previously-nocturnal mammals to fill.

jindeed, a short enough time to turn an pig into a blue whale isn't a short time.

The Nocturnal bottleneck for mammals as it's called was assumed 'til recently to have only ended at the Cretaceous–Paleogene extinction event 66 million years ago.

At the basis of the nocturnal bottleneck hypothesis lies the idea that
Mesozoic ectothermic reptiles (including dinosaurs) would be
restricted to daytime activity at times when the sun can help to heat
up their body to operating temperatures.......

The arguments against:

include:

(i) presence of insulating proto-feathers,

(ii) fossils of breeding dinosaurs in cold regions

(iii) raised body posture

(iv) fibrolamellar bone structures

(v) presence of nasal turbulate bone structures

(vi) stable growth rate (isotope deposits in bones and teeth)

(vii) possible ‘mass homeothermia’ or ‘inert homeothermia’ in large dinosaurs

(viii) the occurrence of small dinosaurs in cold regions

(ix) the existence of potential external thermoregulatory structures in some dinosaur species (e.g. dorsal boney plates in Stegosauria).

Recent molecular analyses have added to the doubt of the original theory:

saurischians are now generally believed to have had partial
endothermia, allowing them to incubate their eggs and inhabit colder
regions......
Independently, parallel evolution in Synapsida led to partial
endothermia in therapsid reptiles (250 Ma, Late Permian) and full
endothermia in mammals

Nespolo RF, Bacigalupe LD, Figueroa CC, Koteja P, Opazo JC. 2011. Using new tools to solve an old problem: the evolution of endothermy in vertebrates. Trends Ecol. Evol. 26, 414–423
The implication being that the pure nocturnal adaptation in mammals would not be a completley effective strategy for predator evasion.

In a large comparative study [Roll], divided 700 species into classes of
dominant temporal activity niche: nocturnal, diurnal or both (mostly
crepuscular). They used an existing phylogenetic construction to
reconstruct the evolution of diurnality in rodents, which are thought
to have diversified after the K/T boundary. The reconstruction of
temporal niche usage within rodents led to the conclusion that rodents
shared a nocturnal ancestor that existed before the K/T boundary.
Subsequently, diurnality evolved through secondary evolution at least
seven times independently in Rodentia.
Using the molecular phylogenetic construction of [Huchon et al],
we constructed the temporal niche phylogeny within the full therian
subclass using the nocturnal, diurnal and
crepuscular/arrhythmic classification of [Roll et al.]. The most
parsimonious interpretation leads to a minimum of 16 changes of
dominant temporal niche.

Bolding mine.

Most subdivisions of Theria are indeed nocturnal, but many changes and reversions occurred, and different interpretations may be
possible, especially when higher-quality data on activity patterns in
more species become available.

Conclusion.
It apears that mamals may have been chased by the saurischians throughout the day, night and twilight hours and that many adaptations and reversions may have occured over a period (possibly) much longer than the 66 million years previously thought. Research is ongoing.
Bolded references:
Roll U, Dayan T, Kronfeld-Schor N. 2006. On the role of phylogeny in determining activity patterns of rodents. Evol. Ecol. 20, 479–490
Huchon D, Madsen O, Sibbald MJ, Ament K, Stanhope MJ, Catzeflis F, de Jong WW, Douzery EJ. 2002. Rodent phylogeny and a timescale for the evolution of Glires: evidence from an extensive taxon sampling using three nuclear genes. Mol. Biol. Evol. 19, 1053–1065

Another point against strictly diurnal dinosaurs is that birds evolved from their dinosaur ancestors long before the K-T extinction event.  While most modern birds are diurnal, there are exceptions, notably the owls.  Although owl fossils only date back 30-40 million years, there doesn't seem to be any obvious reason why earlier birds, or their dinosaur ancestors, couldn't have evolved a similar lifestyle.

@jamesqf 250Ma ago, in fact.There was a bit about sexual selection and owls in the study (I linked to under the word "argument") that you might find interesting: "highly enhanced scotopic vision (e.g. owls), or other senses (e.g. echolocation in bats), may negate such disadvantages. In this respect, it may be hypothesized that the complex sexual selection mechanisms that have arisen through diverse and vivid feather coloration may be the main drive for a diurnal lifestyle where an acute colour visual sensory system would be an advantage."

Interesting, yet I wonder if predator evasion is a really a satisfying explanation.  After all, many small mammals today are preyed on by birds (among other creatures): hawks in the daytime, owls at night, yet don't seem to be in danger of extinction.  (At least from non-human causes.)  And many small mammals are burrowers, which means they'd encounter low/no light conditions in daytime.


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Do lower animals have instinctive behaviors?
Can an organism such as C. elegans, with only 302 neurons, exhibit "instinctive or innate behavior"? If not, then at what basic minimal structure is instinct manifest?

Pretty much anything that such a simple organisms would do with its neurones would be called instinct behaviour, wouldn't it?

Short answer
'Lower' organisms like C. elegans exhibit innate behaviors. In fact, unicellular organisms [without any nerve cells at all] can exhibit instinctive behaviors.

Background
Let's start by defining the central terms here, namely Behavior and Instinct:
Merriam-Webster has a general definition of Behavior:

[A]nything that an organism does involving action and response to stimulation

And according to the Cambridge dictionary, Instinct is:

[T]he way people or animals naturally react or behave, without having to think or learn about it.

And Merriam-Webster defines Instinct more elaborately:

Largely inheritable and unalterable tendency of an organism to make a complex and specific response to environmental stimuli without involving reason
Behavior that is mediated by reactions below the conscious level

Hence, C. elegans' actions are indeed instinctive behaviors.
An interesting distinction here is whether behaviors in simple organisms should be indeed called behavior, or rather be classified as [lower-order] reflexes.
According to Merriam-Webster, a Reflex is:

[A]n automatic, often inborn response to a stimulus that typically involves a nerve impulse passing inward from a receptor to the spinal cord and then passing outward from the spinal cord to an effector (such as a muscle or gland) without reaching the level of consciousness and often without passing to the brain, such as the pain-withdrawal reflex, or the knee-jerk reflex.

This is a typical schoolbook approach-based definition of a reflex. Strictly spoken C. elegans' behaviors would not classify as reflexes according to this definition, because invertebrates do not have a spinal cord.
Nonetheless, sea anemones show protective withdrawal responses by retracting their tentacles and oral disc. Some may even detach from the substrate in response to a variety of aversive mechanical, electrical, or chemical stimuli. And earthworms show rapid withdrawal responses mediated by giant nerve fibers when subjected to unfavorable stimuli, that are in fact classified as reflexes (Smith, 1991).
Indeed, Wikipedia defines a Reflex as

...[A]n involuntary and
  nearly instantaneous movement in response to a stimulus. Scientific
  use of the term "reflex" refers to a behavior that is mediated via the
  reflex arc.

Thus the question then becomes what is a reflex arc? The Medical dictionary defines a Reflex arc as:

Route followed by nerve impulses in production of a reflex act, from peripheral receptor organ through afferent nerve to central nervous system synapse and then through efferent nerve to effector organ.

Hence, in all, instinctive behavior is appropriate general terminology. When in simple organisms the behavior can be directly linked to a responseive action to a sensory stimulus, the term reflexive behavior may be a more appropriate term than instinctive behavior as far as I can see.
To push the definition of instinctive behavior even further, we can conclude from all this that single-celled organism exhibit it too, as they can show simple instinctive behaviors, such as phototaxis and chemotaxis, where they change their direction of movement in response to light and chemicals, respectively (source: Khan Academy).
Reference
- Smith, ILAR J (1991); 33(1-2): 25-31

I would like to poke at this a bit more. I believe instinct does require a nervous system, and in fact requires a higher CNS organ or brain.  I agree it does not require learning, but would preclude simple reflexes. I think instinct also involves memory, and an inheritable, yet "conscious  behavior". Reflex action can be studied in the unconscious or even transected CNS. But instinctive behavior I think requires a conscious, awake animal with a fully intact brain.   I realized these statements are at a minimum debatable, and possibly just incorrect, but might keep the topic alive.

I just surveyed eight definitions of instinct, some of them "biological". None of them indicate a nervous system is necessary. For example: "a largely inheritable and unalterable tendency of an organism to make a complex and specific response to environmental stimuli without involving reason" https://www.merriam-webster.com/dictionary/instinct#medicalDictionary
The protist Euglena gracilis, for one "lower animal" example, shows an innate photatatic response to light. http://www.nature.com/nature/journal/v216/n5119/abs/2161042a0.html Euglena's response to light includes the "complexity" that some definitions include.


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What is the death mechanism of an electrocuted Mosquito?
While using the Electric bat, does the mosquito get killed by primary electrocution, or it secondarily by burning?


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Perception of white in the absence of rods
If the retina would not have any cones, one would be color blind. If white is the presence of all colors (in the matter of color mixture, not addition), then what would white look like without rods?

Short answer
Cones mediate the perception of white in photopic conditions. Rods mediate the perception of white in scotopic conditions. The rod system is not needed for cones to mediate white perception and vice versa.
Background
Cones code for red, green and blue. The remaining colors, as you rightfully state in the question, can be generated by mixing these three colors, as shown in Fig. 1.

Fig. 1. Color mixtures. Source: Davidson College
The millions of different color hues that we can perceive are generated by the retina and the brain by mixing colors and adding the weight that each cone class adds to the color percept (Fig. 2).

Fig. 2. Color Triangle. Source: Wikipedia
As you can see in Fig. 2, when all three basic colors are present in equal amount, perceptually a white color is perceived (the middle point of the color triangle). That is, the combination of co-activation of each cone class yields the perception of white, i.e., without the need for rod activation. Rods are not needed for color vision, including the perception of white or black. In fact, under photopic (well-lit) conditions the rods are adapted to high light levels and are less responsive; their photopigments are said to be bleached and the rods become unresponsive to light. Hence, under photopic conditions the contribution of rod-mediated vision is low (Ambler, 1974).
Rods mediate vision in low-lighting conditions (scotopic vision), as opposed to photopic vision where sufficient amount of light is present to feed the photon-hungry cones. While rod-mediated vision operates at much lower lighting conditions than cone-vision, it only mediates the perception of low-resolution gray-scale images.
References
- Ambler, Perception & Psychophysics (1974); 15(3): 586-90
- Gouras, Color Vision. In: Kolb et al. (eds). Webvision. The Organization of the Retina and Visual System. Utah (2012)

So I person who has trouble seeing at night to drive may have low rod count?

@Jen - May be, for example in retinitis pigmentosa sufferers the outer retina degenerates and with it the rods. Among the first signs is indeed night blindness.  I'll edit my answer to include this when I find the time - good point.

A person with an absents of cones and more rods are more color blind. but may be able to see great at night.

Some animals like dogs may only have rods.

@Jen - Like cats do, yes


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Is ATP Synthase a channel or an enzymatic protein?
Today in a biology lecture about plasma membranes and functions of proteins, we learned about channel and enzymatic proteins along other kinds of proteins. ATP synthase is considered an enzyme that synthesizes ATP, but it also creates a channel for H+ ions to pass through into a lower concentration area.

My question is could ATP synthase be considered a channel protein as well as enzymatic protein? Or no since the ion channeling is part of the enzymatic reaction? Also are there more examples were some proteins could have more than one kind of protein to them?

ATP synthase is an enzyme, a molecular motor, and an ion channel all wrapped together in one structure (Fig. 1). It is an enzyme, because it generates ATP. It is a molecular motor, because the central rotor part turns about 150 times every second during ATP synthesis (Source: MRC mitochondrial Biology Unit). It is an ion channel, because it funnels protons into the mitochondrion during ATP generation (Source: Davidson College).

ATP synthase. Source: Ace Biochemistry
ATP synthase is composed of two subunits, F0 and F1. The 0 subunit is embedded in the inner membrane, and the other, containing the catalytic parts, protrudes into the matrix.
F0 contains the proton channel and is connected to F1 with a stalk.
F1 consists of five polypeptide chains, alpha (a), beta (b), gamma (g), delta (d), and epsilon (e). The alpha and beta chains make up the bulk of F1 and are arranged in a hexameric ring. Both chains bind nucleotides, but only beta participates in catalysis (Source: ACE Biochemistry).
Another example of complex proteins are G-protein coupled receptors, for example those linked to ion channels (Fig. 2).

G protein coupled receptors. Image source: Wikipedia
Here, a receptor is bound to a G-protein, that becomes activated after receptor binding. The G protein then leaves the receptor and travels to an ion channel and activates it (or inhibits it).

You explained how ATP Synthase works, but could it be considered both an enzymatic protein as well as a channel protein?

@JovanyMerham - First sentences of the answer! Because it is ultimately ATP that is the final product of the protein, ATP synthase is what it is called, as a functional reference.

So the idea is a protein is considered to be one type or another is by the major function of the protein, am I on the right track?

@JovanyMerham - nomenclature is often murky and there are no strict rules. If the H+ gradient reverses it may even become a H+ pump that hydrolyses ATP, making it a a H+-ATPase instead of a synthase. The important thing is that everyone calls it ATP synthase, which is its physiological function.


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In which direction does ATP synthase rotate?
I heard about the rotation of ATP synthase in a biochemistry course. The professor said it will rotate counterclockwise. Is that true? If so, what mechanism defines its direction?

Short answer
The direction of rotation depends on the viewing point of the observer and the reaction catalyzed by the ATP synthase. When synthesizing ATP, and viewed 'from the bottom' (observer faces the intermembrane space looking into the mitochondrial matrix) it rotates clockwise.
Background
ATP synthase is a membrane bound enzyme with two large subunits; F0 and F1. F0 is inserted in the membrane and funnels H+ ions from the intermembrane space into the mitochondrial interior (Fig. 1). The stalk region connection F0 and F1 contains the γ subunit, which basically forms a rotating shaft powered by the flow of H+. This causes the entire F1 unit to rotate during ATP synthesis.
Now importantly to know before continuing; enzymes basically work two ways, as they merely establish equilibrium. As such, any ATP synthase is also an ATP hydrolase. When it synthesizes ATP, the γ subunit runs in clockwise direction when observed from the “bottom” (the side closest to the F0 and the membrane, see Fig. 2). When it hydrolyzes ATP (e.g., under non-physiological laboratory conditions) it runs counter-clockwise as the reaction, as well as the movement of the γ subunit reverses (Nakamoto, 2008).
The direction in which the rotation takes place is dependent on the steps involved (Fig. 3). In this figure, ATP hydrolysis is shown and that can be compared to burning fuel in a combustion engine. Now the direction of H+ reverses, against its concentration gradient and needing energy (the road speeding below a car if you like). Because ATP binding, hydrolysis and release of waste (ADP + Pi) each cause a 120o turn of the rotor, the F1 subunit rotates one full turn in each cycle (Yoshida, 2001). During ATP synthesis the opposite direction is established, as waste (ADP + Pi) is taken in and phosphorylated to ATP, during which the flow of H+ reverses (akin to a car going downhill, only combustion engines cannot generate gas from carbon dioxide and water, unfortunately).

Fig. 1. ATP synthase subunits. source: Penn State University

Fig. 2. ATP synthase. source: Noji, 2004

Fig. 3. ATP synthase compared to a combustion engine. A combustion engine converts fuel energy into rotation of a rotor. It can drive the intake of the fuel gas, compression, ignition and exhaust sequentially just by a simple rotation of the central rotor (right panel). The F1 gamma-subunit has and three reaction chambers (the catalytic beta-subunits (left panels). The three reaction sites each go through three cyclic steps in a 120° phase difference to cause rotary motion, very similar to a combustion engine. source: Yoshida, 2001
References
- Nakamoto, Arch Biochem Biophys (2008); 476(1): 43–50
- Noji, Biohistory journal (Winter, 2004)
- Yoshida, Nature Rev Mol Cell Biol (2001); 2: 669-77

It should be F_o instead of F_0

Why does it rotate in that direction?

@latra figure three shows why.

I have read the caption of figure 3 and the third paragraph, but it only says ATP synthase is similar to a combustion engine.  It did not tell me why that direction.

@latra I can't explain it in more detail. Why does the crankshaft of an engine rotates left or right; because it is structurally engineered to do so.

@latra it's all about conformational changes in the protein


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What is the function of the human eye white?
If you have a look at the eyes of most animals, you never see the white part unless the eyes are averted. In contrast, humans always have the whites visible because the iris is quite small. The only explanation I found so far is that the evolution made it this way because we are very social animals and we express a lot by eyes movements. I wonder if there is any other explanation?

Short answer
The relative large surface area of the white sclera in humans has been linked to an enhanced ability to detect eye gaze.
Background
The white of the eye is caused by the sclera. Human eyes indeed have the highest relative amount of visibly exposed white sclera. The amount of visible sclera provides information about the orientation of the eyeball. Specifically, the iris-to-sclera ratio is an important cue for eye gaze perception (Schulze et al., 2013).
Eye gaze is important. Most mammals generally interpret direct gaze as threatening, or as a sign of dominance. Humans, in contrast, tend to associate mutual gaze with positive interest, love and attraction. A preference for direct gaze seems to be present at a very early age. Infants as young as 2 days old prefer to look at faces that gazed directly at them, than to faces with averted gaze. Yet, humans sometimes find eye contact uncomfortable, for example if a stranger keeps staring at them (Schulze et al., 2013).
The ability to detect gaze has been established in many primate species, other than humans. Gaze detection may have evolved because direct gaze can signal that a predator is attending, making its detection an important tool for survival. Many animal species respond to the presence of staring eyes with displays of fear and submission, indicating that such stimuli act as warning signal. In humans, prolonged eye contact can also be perceived as an aggressive approach signal, as it leads to increases in galvanic skin response (Frischen et al., 2007).
The cooperative eye hypothesis assumes that the large scleral surface in humans developed especially for gaze detection (Tomasello et al., 2007). The authors base this conclusion on the fact that human infants mainly followed gaze, while several species of great apes (including gorillas and bonobos, but not macaques) mainly followed head movements.
However, from my humble opinion, concluding that humans developed a large relative surface of white sclera for communication purposes is kind of far-stretched. For one thing, macaques also have quite a large white scleral surface (Fig. 1.) and macaques share a dedicated neural circuit with humans that involves the superior temporal sulcus (STS). The STS is thought to process biological motion, including gaze. The STS projects to the amygdala, a structure of the limbic system that implicated in the processing of the emotional content of stimuli, including facial expressions and gaze detection. It links this information to emotional responses in the observer. There are also connections between STS and the intraparietal sulcus, an area that is associated with spatial processing and shifts of attention. Via these connections, information about eye-gaze direction could project to spatial attention systems to initiate orienting of attention in the corresponding direction, as in joint attention. Indeed, passive viewing of a face with averted gaze elicits a stronger response in the IPS than viewing a face with direct gaze (Frischen et al., 2007).

Fig. 1. Macaque. Source: Fine Art America
Personally, from these data I think the brain in humans and primates like the macaques adapted to process the information available from the eyes. It can be true, however, that brain circuits and eye structures developed/evolved in parallel to ultimately result in a large white scleral surface and a dedicated neural circuit to process its information.
References
- Frischen et al., Psychol Bull (2007); 133(4): 694–724
- Schulze et al., Front Hum Neurosci (2013); 7: 872
- Tomasello et al., J Human Evol (2007); 52 314-20
Further reading
- Frans de Waal

Wow! Thank you so much! It is indeed a very detailed and informative answer.  Im very grateful!

For further reading I've added a link to Frans de Waal's FB page. I have searched through online material but couldn't find a better source than that :) He's awesome and I own a book from him, but currently it's heading back home across the Pacific. When I get my hands on it again I can add a reference. That may take a few months - it's sent by sea mail :-)

Oh, you are so kind! I will follow all the links you gave. I find it very interesting :)

Awesome answer. I have to agree with you that it is less likely that the brain function driving the physiology and more the physiology driving brain function, given that there is much more plasticity in neural networks... I was wondering if the enlarged brain case "pushing" the orbital bones further forward causes more of the Human sclera to show.