text:
Do animals get sick from eating dirty food or eating off the floor?
Humans have very strict tradition of hygiene, such as washing hands before eating, using utensils, and in general keeping as much distance between food and dirt as possible.
At the same time, most animals would eat off the floor or eat food with foreign particles stuck to it ( after being dropped on the floor). Many animals, like cats groom themselves, practically licking off (and swallowing?) dirt off their coats.
Do animals suffer adverse effects, such as indigestion or disease from consuming food that is dirty by human standards?
Or is it something about the human digestive system that cannot handle the same kinds of dirt that animals can?

Hygiene is very much cultural, compare fastidious Americans that use Clorox wipes on everything to indigenous cultures that have very few taboos against dirt.

There's a parallel to be drawn here with carnivorous animals eating raw meat, too. I naively expect that they just get more parasites (ie. that our admittedly cultural components of cooking do in fact also help protect against infection), but I'd be interested to hear if there's more to the answer.

I'm sure it varies wildly based on the animal and what they're eating.  In general, if in the course of an animal's natural feeding process it picks up a little dirt, it has evolved to cope with that.  Animal's behaviors and guts have evolved to fit their food source and lifestyle.  For a behavioral example, seals will eat rough rocks to help breakdown bones (and barf them up when they get too smooth).  Guts have evolved symbiotic relationships with microbes that are specifically adapted to the food source, termites have microbes to help them break down wood, whereas we don't have the microbe population to pull that off.  Interesting side note: it was found that one of the gut microbes in some Japanese people has gotten a horizontally transferred gene from a bacteria that lives on seaweed, probably helping them break down seaweed.
There could be a problem when the body is challenged with dirt that contains uncommon substances that the body isn't adapted to.  I'm sure if a cat rolled around in soil contaminated with a lot of arsenic it probably wouldn't be doing very well after licking off all the dirt.
This does bring up an interesting current medical hypothesis called the Hygiene Hypothesis.  Basically, these things you are talking about, utensils, antibacterial soap, etc. are all very very recent developments in human evolution.  As a result, proponents of this hypothesis think that our bodies are adapted to challenges by microbes and parasites, and depriving our bodies of that exposure when we are young totally screws up the development of our immune systems.  This would explain why we see a huge increase in allergies and autoimmune diseases in the developed world, our immune systems are totally miscalibrated, and freak out over harmless things like pollen (allergies), or worse, attack self-antigens (anti-insulin antibodies in type I diabetes).  Human children are animals, and baby animals should play in the dirt!

Horizontally transferred seaweed-eating gene? Wow!

One of my all-time favorites :)

Animals certainly occasionally get sick from eating contaminated food, just as humans used to before our standards of sanitation improved.  There are various adaptations/considerations for this. Apologies for not being able to find scholarly references. Here are some anecdotes, some of which are speculation/urban legend:

Predators eat fresh meat, which is less likely to be spoiled
Vultures lack feathers on their heads and bathe frequently to minimize exposure
Dogs supposedly eat grass to induce vomiting when they've eating something bad (fairly disputed)
Rats and other scavengers have excellent senses of smell, and can likely detect common contamination or over-spoilage
Some scavengers may have more aggressive digestive systems to reduce infections

Only 100 years ago, humans weren't so well off ourselves. While food hygiene is only part of it, our increased sanitation has reduced mortality from infectious diseases substantially.  From the CDC:

In 1900, the three leading causes of death were pneumonia,
  tuberculosis (TB), and diarrhea and enteritis, which (together with
  diphtheria) caused one third of all deaths (Figure 2). Of these
  deaths, 40% were among children aged less than 5 years (1). In 1997,
  heart disease and cancers accounted for 54.7% of all deaths, with 4.5%
  attributable to pneumonia, influenza, and human immunodeficiency virus
  (HIV) infection (2).

It would be interesting to find a break down of the improvement from agriculture/cooking, water/sewage, medicine, etc.


text:
Why do people sleep with their eyes open?
It's a fact that some people sleep with their eyes open, but why does that happen? Is it normal behavior, not a symptom of any sort of disorder? Are there any (dis)advantages to sleeping with eyes open?

Do you have any evidence to support your statements ?

@biogirl I once saw someone do that ;)

Something new for me !I have heard about it only in dolphins:)

I've met a few different people that do this. The most common complaint I heard was dry eyes. I suppose over a lifetime it probably damages the eyes faster, but I don't have any source to back that up, and I have no idea why it happens in the first place.

The medical term is "lagophthalmos" if the person is unable to close their eyes at night.
There are several factors involved, and unless it's due to physical obstruction, lid archetecture (such as short lid length (due to surgery etc)), or facial nerve (CN VII) problems, it's not well understood.
I have seen numerous people with varying degrees of this over the years.  For most of those people, it's an intermittent thing.
Tears are essential for eye tissue health, including cleaning and avoiding infection. People complain of dry or irritated eyes mostly.  But in more extensive cases, keratitis and ulcers can occur, which are bad.  If it's frequent, tell the person to make sure they tell their eye doctor (or if they don't have one, get it checked out sometime) so that the health of their eye tissue can be evaluated.
Another possibility is Grave's disease - in that condition, the entire eyeball protrudes and sometimes the eyelids aren't long enough to cover them adequately.  But what you're describing is probably not Grave's disease.
Wikipedia
American Academy of Ophthalmology

source: Stack Exchange

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

sort: votes


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Can plants survive indefinitely without external supply of gases at compensation point?
During photosynthesis, there is a point at which the light intensity is such that the rate of photosynthesis exactly matches the rate of respiration called the compensation point. What this means is that the plant can essentially utilize the $\ce{CO_2}$ produced during respiration for photosynthesis and the $\ce{O_2}$ produced during photosynthesis for respiration. But, does this mean, that a plant which has been given an initial supply of $\ce{CO_2}$ and $\ce{O_2}$ and then subsequently put into another gas (still in compensation point light intensity), say nitrogen, can survive indefinitely? (or as long as it's life span).

If the plant is growing the system will fall out of equilibrium due to more carbon going into biomass than oxygen.

Another concern might be that depending on how much neutral nitrogen there is, the oxygen/CO2 might diffuse into the nitrogen, lowering the available amount.

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


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Reason for seeing grid-like patterns when strobing a solid black-white image?
I was trying to do some stimulation for SSVEPs by strobing a solid black square and a solid white square. Weird thing was, I ended up seeing weird grid like patterns that looked like this, always of the inverted color.
  _        _
 / \      / \
 | |      | |
 \ / _--_ \ / _--_
  O |    | O |    |
 / \ ---- / \ ----
 | |      | |
 \_/ _--_ \_/ _--_
  O |    | O |    |
     ----     ----

And that sort of pattern repeats itself around the strobing area (where the convex areas are always of opposite color than the current color on the screen).
I'm inclined to think about light and dark adaptation, but it still seems weird that it'd be shaped like that in particular. So... What's going on?
EDIT: Additional info that I should've realized was necessary >_<:

Strobe area: ~14x10.5 cm
Strobe frequency: 2 frames/half-cycle @ Laptop Vsync (~60 Hz) ~ 15 Hz
Viewing distance: ~55-60 cm and shorter.

Screen is backlit. Not sure about brightness metrics.
The pattern isn't offset to one corner like I've drawn, it's more evenly spaced. Horizontal bars are more accentuated than vertical ones (and the dark-on-light phenomenon is more visible for me than the light-on-dark). Moving in closer increases the visibility of the effect (I guess that was to be expected), and changes the number of times the pattern repeats across the screen (but it's hard to count them). The larger the area in my visual field the more times the pattern repeats. I'd say that at about 60 cm it's just one box, but with my nose a handful of cm away from the screen (it's hard to measure by myself >_<), there are maybe three in the horizontal direction... Or at least tens of them (increasingly large as it gets toward the center in both dimensions), depending on how focused in on the screen I am.
It's really really hard to count them.
I haven't had the chance to check with other people yet, but I'll try some time (this is just something I saw while working on a personal project).

Do other people see the same pattern as well? How big was the square and how fast was it presented? What's the spatial scale of the pattern?

@Memming Info added. This is just a personal project, so all info I have is just from myself at the moment. -.-' It's really hard to count these things without getting a bit dizzy.

@Memming Other people see the patterns as well, although not necessarily the same patterns I'm seeing.

interesting. let me put a bounty on this question.

It just occurred to me that cogsci.SE might have more psychophysics people.

I have actually experienced something similar before.  What are you using to make the strobe?  You can run into interesting patterns when you start strobing near the frequencies of your monitor (flashing refresh down as it's drawing).  I'd also make sure it's not a programming effect.  What is the difference between what you see and what other's see?

Are you strobing LCD or with LCD?? I bet you could not see that while strobing solid material with strobe light. You might see wiring of your LCD...

@Atash Any update?  Again you are likely seeing the pattern because of the way monitor is strobing, not because of any artifacts in your eye.

@AtlLED Oh, sorry - I can assure you that the screen is solid black and solid white (no vsync issues), and can additionally reference you to the underlying low-level code (SDL2's vsync-waiting update and GTK's GdkFrameClock for two different programs). Others have reported seeing the phenomenon, albeit with different patterns (they aren't necessarily consistent between people looking at the same screen; I have a really small sample size, though).

Seeing in animals is at some level using Gabor wavelets (Marčelja 1980 and later authors). Your images reminds of a combination of two low frequency Gabor basis vectors. Apparently the nervous system does not have time to model the incoming image into Gabor components of other frequencies.
Here is a picture of two low frequency Gabor basis vectors added. (In this image rotated 45 degrees compared to your image.)
http://medicalxpress.com/news/2013-01-feature-combination-perceptual-identification.html
This is a signal processing or a linear algebra question as much as a biology question.
One could argue that even lower frequency Gabor vectors would model the original images even better.

Hi David. Your information is certainly useful. Would it be possible for you to link the original research. This site seems professional enough but I know of many science blogs that exaggerate a lot.


text:
Why are dreams sometimes remembered and sometimes forgotten?
Why is it that sometimes, when we wake up, we are able to remember what we were just dreaming, but sometimes we don't remember any of it?

This kind of question are usually accepted on this site but I always think that the OPs would make a better fit and get better answers if they'd ask on CognitiveScience.SE.

@Remi.b true, i always get confused about partner sites. U r free to migrate it to CognitiveScience if needed.

Scientists say that people can have multiple dreams every night and the ones that are not very significant are easily forgotten. Only those experiences that elicit an emotional response (happy, frightened) seem to stick in memory. Suggestions have also been made that being anxious or depressed makes our dreams stick to memory too (reference). A study suggests that people woken up during REM sleep seem to recall their dreams more often (reference). Here is a link to some common questions about dreams.


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Honeybee decision process: new food, new home, new threat
I have heard that honeybees send out scouts, then based on the scout reports more bees go then come back and report and so they are supposed to be efficient decision makers.
Can you give as complete as possible of a description of how honeybee decision making works with regard to:

finding new food/water sources for the hive
deciding where to place a new colony
how they determine if a big enough predator is around to merit a swarm

If you could point to published material that would also be appreciated.
Some links:

http://link.springer.com/article/10.1007%2Fs00265-011-1298-8?LI=true#page-1
http://cis.uws.ac.uk/research/journal/V9/V9N3/bees.pdf
http://www.igi-global.com/article/honey-bee-swarm-cognition/44981

There's also this: http://rstb.royalsocietypublishing.org/content/364/1518/755.

But, realistically, it seems like this, while interesting, is probably too broad of a question and doesn't have a defined answer. In one sense "as complete as possible of a description" is a model; and as in any model building you're going to have to make a lot of subjective choices about which parameters to include, and then a lot of subjective choices to estimate those parameters based on a fairly broad literature.

FWIW the query (bee AND (learn* OR decision OR communicat* OR swarm* OR forag*) AND (model* OR experiment* OR field)) in scopus returns 3000+ hits.

I was looking for something to the effect of the link you provided.  Will try and figure out what SCOPUS is.  http://rstb.royalsocietypublishing.org/content/364/1518/755.full

Scopus is one of the big academic papers repositories – you could use google scholar for similar purposes. When I get time, I'll post links to a few more published papers.


text:
What are common causes of unexpected ligation products?
I digested two plasmids, one with EcoRI and AgeI and the other with EcoRI and XmaI. Digests looked as expected, so I purified the respective fragments and set up the T4 DNA ligation (AgeI and XmaI sites are compatible).
After E.coli transformation, culture and miniprep from 12 of the resulting cultures, I digested the isolate from the minipreps with BclI to confirm I had the correct product (because there was one BclI site in the insert and another one in 1.4kb away in the backbone). The results of this digest clearly show that there are two different ligation products: four lanes share one banding pattern and the other eight share a pattern which is different from it.
I checked both plasmids for other restriction sites of the enzymes used which I overlooked before, but found none. Because EcoRI and XmaI/AgeI sites are radically different (AATT vs. CCGG), I would exclude the possibility of the insert being ligated in reverse orientation.
Are there any common causes of unexpected ligation variants besides unnoticed restriction sites and reverse ligation?

A second investigation has suggested that the ligation product in question was indeed the vector, without ligated insert!
The vector also contained a BamHI site close to the XmaI site, so in a subsequent digest with EcoRI and BamHI, I was expecting to see the same band sizes that I ligated together in the first place.
All colonies contained plasmids that produced the long (vector) band, and the same eight as before produced the shorter (insert) band as well. However, those four which were aberrant in the previous experiment were this time lacking the shorter band.
This means the eight colonies with two bands contained the desired ligation product, while the other four contained a plasmid which was restricted at a single site (undigested it would have produced three bands like the control).
As the BamHI site was in the vector and untouched throughout the whole process, I conclude that those four were missing the EcoRI site, which should have been regenerated during the ligation, and hence indeed the EcoRI site and the XmaI site must have been ligated without insert somehow.
Long story short
This means that either

An exonuclease digested the sticky ends of the vector away, or
The sticky ends simply degraded by chance

resulting in a blunt-ended re-ligation of the vector without insert and consequently loss of the EcoRI site.
I believe these to be quite important things to consider in cloning - in subsequent experiments I have had several colonies growing on negative control plates (i.e. colonies transformed with a control ligation that contained no insert), all of which were probably due to loss of sticky ends and blunt ligations, resulting in functional plasmids that conferred ampicillin resistance despite containing an undesired plasmid.

Could be insert polymerization.  If you have your stretch of DNA like this:
 (5')-AATTagctagcatcgtgatcgacg-(3')
          ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')

And you take that, flip it around, it will ligate onto itself, like this:
 (5')-AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacgatcacgatgctagct-(3')
          ||||||||||||||||||||              ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')(3')-gctgctagtgctacgatcgaTTAA-(5')

This is easy enough to check for.  Just calculate the size fragments you'd expect from a vector with two inserts (there'd be an extra BcII cutsite now, and the extra fragment would probably be the size of the insert).  If this is just out of curiosity, and one of your things is the correct size, I'd ignore the ones that didn't work and go ahead with your ones that did.
If you do have a problem with it, or you are getting all your clones polymerizing, you can treat your insert with an alkaline phosphatase.  This will eat off the (5') phosphate that the ligase needs to stick the on to the (3') hydroxyl.  The result is that an insert cant bind to another insert, but once it finds a vector it will be able to ligate:
 insert to insert:    AATTagctagcatcgtgatcgacg-(3') :( CCGGcgacgatcacgatgctagct-(3')
                         ||||||||||||||||||||              ||||||||||||||||||||
                    (3')-tcgatcgtagcactagcagcGGCC  :( (3')-gctgctagtgctacgatcgaTTAA

 insert to vector:    ....ctagct-(3')     AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacg....
                      ||||||||||              ||||||||||||||||||||              |||||||||
                      ....gatcgaTTAA-(5')(3')-tcgatcgtagcactagcagcGGCC     (3')-gctgc....

There will be nicks on the top left, and bottom right, but the bug you put it into should clean those up for you.  You can get alkaline phosphatase for fairly cheap from lots of places, NEB is always a safe bet.


text:
Is there a database of pollen-seed distances across plant species?
I was enjoying Richard Smith's excellent answer to this question, and wondered:
If you consider the pollen/seed distribution range to be plant locomotion, is there a database that compares these distances across plant taxa, or perhaps a paper that treats these distances as a trait (in a phylogenetic context, for example)? One might assume that in the transition from wind-pollination to animal pollination (or from wind seed dispersal to animal seed dispersal) there is a sacrifice of decreased distance for increased "accuracy", but maybe this isn't the case.
It seems like this information should be around somewhere – it has relevance to evolution, speciation, climate change adaptation, etc.

In my searching I didn't find a comprehensive database of this information. There are biologists interested in analyzing seed dispersal distance as a trait however.
Vittoz and Enger (2007) used plants with known seed dispersal along with characteristics about these species to predict dispersal distances for other species.
There is another study here that examines the relationship of plant height and seed dispersal. They provide interesting background information as well on the trade-offs associated with a particular dispersal mode. For example,
"It is often assumed that there is a trade-off between maternal provisioning and dispersal capacity, leading small-seeded species to disperse further than large-seeded species."
It is certainly an area of research actively being pursued but there doesn't seem to be a list or database of these dispersal traits by species. There is information on dispersal distance by mode in the appendix of the second link I've provided.


text:
What is the standard deviation of adult human heights for males and females?
The wikipedia article on human height reports mean height for many different countries by sex but it does not report standard deviations.
What is the standard deviation of adult human heights within sexes?
Obviously the size of the standard deviation would vary across countries and by other factors.  That said, I think good data on a few representative countries would be sufficient to get a reasonable sense of what it typically is and the extent to which the standard deviation varies.

It's probably around 7 cm for men and 6 cm for women.
The Evolution of Adult Height in Europe, which is a source for some of the statistics reported on that Wikipedia page, gives averages, standard deviations, and sample sizes for both sexes across 10 european countries (and across a number of different age cohorts).
Taking their numbers for men and women born between 1966 and 1978, the average male standard deviation of height across all ten countries is 7 cm (range 6.7-7.3) and female 6.1 (range 5.6-6.4).
For a more global context, Subramanian et al. give heights with standard deviations for a much wider selection of countries, mostly "developing countries". Unfortunately for your question, they only report numbers for women. However, these  look pretty similar to the Europe numbers: the across-country average SD for women is 6.3. (with all these countries, the range is greater at 5.4-8.1, but 32 out of the 54 countries have SDs within the Europe range for women, i.e. 5.6-6.4)
Note: for this estimate I just ran averages across years/countries, I didn't weight the averages by sample size.

 Subramanian SVS, Özaltin EE, Finlay JEJ. 2010. Height of nations: a socioeconomic analysis of cohort differences and patterns among women in 54 low- to middle-income countries. PLoS ONE 6: e18962–e18962.

The first link is broken now, btw


text:
Do hormones make men think of sex?
I remember hearing a saying that goes like "men think of sex every 7 minutes (or seconds?)". I take this saying to mean that men have sex related thoughts more often than women.
I'm interested if these thoughts are related to hormone expression within the male body. particularly, I'm interested in the very few seconds before a sexual thought emerges - one moment a man is thinking about daily stuff, next moment his thinking has sexual content. What is responsible for this shift in thinking?
I've read that oxytocin is responsible for men feeling romantic attachment to a partner, but is there a hormone that initiates sexual thoughts or fantasy? For example, would a burst of testosterone increase the likelihood of a man thinking of sex?

Interestingly it does seem as if this is at least in part the case.
Testosterone levels are tied to sexual impulses, but also risky behavior and aggression.  Its responsible for sexual drive in women as well.  Low testosterone can cause depression and loss of the ability to make decisions.
You'll note that the work cited is done on criminals, patients and rats.  Remember that is not medically or scientifically ethical to change the androgen levels of a functioning human being.  Testosterone supplements might increase the chances of prostate cancer.
While its not scientific, there's a fascinating set of interviews about how testosterone affects human thinking at this transcript of American life, Act 2 :

After testosterone, there was no narrative. There was no language
  whatsoever. It was just, I would see a woman who was attractive or not
  attractive. She might have an attractive quality, nice ankles or
  something, and the rest of her would be fairly unappealing to me.
But that was enough to basically just flood my mind with aggressive,
  pornographic images, just one after another. It was like being in a
  pornographic movie house in my mind. And I couldn't turn it off. I
  could not turn it off. Everything I looked at, everything I touched,
  turned to sex.

thanks for putting in the quote @AlexStone!  Well done!  This is all anecdotal, but a lot of men seem to find it a reasonable reaction to a flood of testosterone in their brain.

"Low testosterone can cause depression and ability to make decisions" ?? Does low testosterone give the ability to make decisions, or is this a typo?

its not a typo.  the hormone doesn't do anything though.  For humans it is interpreted by our brains and other tissue to all these effects.  It could easily not mean these things if the selection pressure of human evolution had been different.  I have no doubt that some individuals have very low testosterone and do not have these problems, but its a common problem in testosterone inhibition therapy for instance.

Yes, I understand that. In that case I believe there is a grammatical error in that sentence, as it doesn't really make sense.


text:
Are there any scientifically based predictions or theories of future human evolution?
Reading this question of the stack exchange got me thinking. I believe human evolution is an ongoing process and will not stop. Are there any predictions/theories about the phenotypes and genotypes of humans in the future? and how they may differ in a few thousand years compared to present day?
I remember watching a youtube video and in the video the user predicts that there will be two branches of human species; a short dwarf like species and a much taller species. I'm still skeptical about this claim. Is there any evidence to back it up?
One could argue that modern medicine is preventing natural selection. How will this effect human evolution?

Its pretty much impossible to predict what will happen in the evolution of species.  Evolution is a parallel search with millions (or in the case of humans 8+ billion) of threads.  Our adaptive capacities have never been fully understood and will always surprise us I think.
Of course that doesn't stop people from trying!  The prediction you mention is based on one man's ideas of dominant selection pressures on humanity now... for a men's TV show.  In Dr Curry's scenario, technology users, and economic disparity, producing Eloi and Morlock like dimorphism as in the HGWells book "Time Machine". This seems like hogwash to me.  All socioeconomic classes try to find high quality partners and height and attractiveness will be hard to stamp out in a large segment of humanity.
Economic elites breed slowly and even if they will try to skim the evolutionary cream of humanity off the top, there will be plenty of beautiful, tall and smart people who will lack economic opportunity in my opinion.
There have been more serious, IMHO, questions about whether medical technology, which lets the sick recover and may even compensate for genetically problematic traits.  There are no inoffensive examples I can think of so I'll take male pattern hair loss - apologies.  If medicine allows all men (and women) to grow a thick shock of hair regardless of our genes then the baldness traits might spread through the species.  Sure it could happen, but then most bald and balding people end up having children now anyway.
In fact since civilization has started feeding the hungry, making the hunting of wild beasts less important, causing the shrinkage of the male physique (we used to be much more muscular), inventing medicine and schools where smarts can be selected for, and giving us all more choice when it comes to mates, evolution has accelerated for human beings. The authors specifically cite social factors as being more important in our evolution now.

Do you have a reference for "..causing the shrinkage of the male physique (we used to be much more muscular)"? Considering that e.g. body size has increased due to better nutrition (at least in more recent times) it seems unlikely that overall physique has deteriorated. Also, even if we have become less muscular, this could simply be a phenotypic change due to how we live our lives (less fighting with wild animals) without an adaptive genetic change.

heres one - only a book review.  you'd want to look at the book   http://www.theregister.co.uk/2009/10/19/wuss_men/

Interesting, although some parts sounds like hyperbole. However, here is another popular account by the author of the book that goes further into the specific cases: http://www.huffingtonpost.com/peter-mcallister/pre-modern-man_b_836265.html. It also mentions that reasons (at least in more modern comparisons) are likely to be due to lifestyle. Comparisons with H. erectus and Neanderthals are more problematic since they represent different species, and it will be harder to infer that the changes are due to modern civilization.

There's a general thread on this in the literature - this requires at least a question on its own, but you have to remember that for their size, humans are just about the weakest primates around.  Even chimps which are much smaller can throw around hundreds of pounds easily.  There's a thread in the literature that in order to gain fine manipulation skills and dexterity we had to group muscles into smaller fibers with more nuanced innervation, resulting in lower strength.

Predicting future evolution is always extremely difficult (or impossible), and this is especially true for long-lived organisms such as humans. Therefore, your question is basically impossible to answer objectively. However, the question made me wonder about what research there is on the topic, and if there are any hypotheses or attempts to measure current selective pressures. A quick litterature search yielded a couple of interesting papers that you might be interested to look more closely at (along with hidden "gems" like "Do Women Prefer More Complex Music around Ovulation?"). They all touch on aspects of ongoing evolution or selection in humans.
Reed & Aquaro. 2006. Mutation, selection and the future of human evolution

Finally, it is frequently speculated that both positive and negative selection acting in modern humans is slowing down or coming to a halt because of our increasing insulation from the demands of the environment by the use of technology. The lessons being learned from studies in humans and other species, in fact, suggest that we will continue to be under certain forms of strong selection well into the distant future.

and

In summary, the maintenance of our genomes against deleterious mutations could have been a major selective component in shaping levels of human genetic variation. In addition to the probable role of rank-order selection (Box 1), the purging of deleterious alleles in gametogenesis might be a particularly efficient way to achieve this.

and

Furthermore, although selection against mildly deleterious alleles might be relaxed in modern humans, selection for the fixation of new alleles could be intensifying (and these could be detected with genome-wide data and statistical approaches; cf. Ref. [45]). This suggests a shift from the maintenance of our genomes against new mutations towards accelerated genetic change for a subset of new mutations (and possibly an associated shift from genetic drift to genetic draft dynamics [55]) as a theme for the future of human evolution.

Powell. 2012. The Future of Human Evolution

Abstract
  There is a tendency in both scientific and humanistic disciplines to think of biological evolution in humans as significantly impeded if not completely overwhelmed by the robust cultural and technological capabilities of the species. The aim of this article is to make sense of and evaluate this claim. In Section 2, I flesh out the argument that humans are ‘insulated’ from ordinary evolutionary mechanisms in terms of our contemporary biological understandings of phenotypic plasticity, niche construction, and cultural transmission. In Section 3, I consider two obvious objections to the above argument based on the growing literatures related to gene-culture coevolution and recent positive selection on the human genome, as well as a pair of less common objections relating to the connection between plasticity, population size and evolvability. In Section 4, I argue that both the ‘human evolutionary stasis argument’ and its various detractor theories are premised on a fundamental conceptual flaw: they take evolutionary stasis for granted, since they fail to conceive of stabilizing selection as a type of evolution and drift as a universal tendency that dominates in the absence of selection. Without the continued operation of natural selection, the very properties that are purported to reduce the evolutionary response to selection in humans would themselves drift into non-functionality. I conclude that properly conceived, biological evolution is a permanent and ineradicable fixture of any species, including Homo sapiens.

Keightley. 2012. Rates and Fitness Consequences of New Mutations in Humans

The human mutation rate per nucleotide site per generation (mu) can be estimated from data on mutation rates at loci causing Mendelian genetic disease, by comparing putatively neutrally evolving nucleotide sequences between humans and chimpanzees and by comparing the genome sequences of relatives.
  ...
  A genome-wide deleterious mutation rate of 2.2 seems higher than humans could tolerate if natural selection is "hard," but could be tolerated if selection acts on relative fitness differences between individuals or if there is synergistic epistasis. I argue that in the foreseeable future, an accumulation of new deleterious mutations is unlikely to lead to a detectable decline in fitness of human populations.

Nettle & Pollet. 2008. Natural Selection on Male Wealth in Humans

Abstract:
  Although genomic studies suggest that natural selection in humans is ongoing, the strength of selection acting on particular characteristics in human populations has rarely been measured. Positive selection on male wealth appears to be a recurrent feature of human agrarian and pastoralist societies, and there is some evidence of it in industrial populations, too. Here we investigate the strength of selection on male wealth, first in contemporary Britain using data from the National Child Development Study and then across seven other varied human societies. The British data show positive selection on male income driven by increased childlessness among low‐income men but a negative association between personal income and reproductive success for women. Across cultures, selection gradients for male wealth are weakest in industrial countries and strongest in subsistence societies with extensive polygyny. Even the weakest selection gradients observed for male wealth in humans are as strong as or stronger than selection gradients reported from field studies of other species. Thus, selection on male wealth in contemporary humans appears to be ubiquitous and substantial in strength.

You can't predict the evolution of anything because evolution is driven solely by the environment. It is the environment that squeezes species into to specific forms. We have has a much say in our shape and form as a whirlpool does and for the same reasons, both humans and whirlpools result form powerful outside forces.
In order to have shot at even making a credible guess about future evolution, you'd have to know what the environment around humans will be over the next 100,000 years at a minimum. About all you can say is the likelihood of this or that modification, based on existing physiology. The more that has to change to evolve a new structure, the less likely it will, even given strong selection pressure. We won't evolve wings or eyes in the back of head but we could get taller, shorter, hairier, larger brained, etc.
The idea that evolution is the result of some innate guiding or shaping natural force arose shortly after Darwin advanced the theory of transmutation of the species by natural selection. The scientific community got on board with whole transmutation of one species into another, but they view natural selection as to happenstance and taking to long to be the primary mechanism. Instead they came to believe that some force was driving organisms to become more complex, in a particular pattern, over relatively short periods of time 1,000 of years.
That is why, we call the concept "evolution" in the first place. It was not a word Darwin used or liked because it had existed since the 16th century. Literally, it meant "to unroll" like a scroll and implied a preset motion or sequence. Seeds were said to "evolve" into plants. Sailors and soldiers practicing repetitive drills, practiced their "evolutions". The word meant the unfolding of predetermined pattern, the exact opposite of natural selection.
Unfortunately, this erroneous mechanism would dominate evolutionary theory for 80 years until the development of synthetic theory in 1947. But by then, the idea of evolution being predetermined, fixed, with "levels", "stages", "higher", "lower" and generally progress, had been fixed in the public mind.
So you still see a lot of nonsense about the "next stage of human evolution" when under natural selection such a concept is simple gibberish. We will be what ever the environment shapes us to be.

It is an interesting question, and I definitely agree with shigeta's question about medical technologies enabling the transmission of certain negative traits that would probably otherwise be less frequent.
Remember, evolution is really just a numbers game of whose genes get passed on the most.  In general this was very strongly correlated with the fitness of that individual at being the best at getting food, attracting mates, and not getting dead.  At this point we've got a fast food joint on every corner, and most people in the developed world live to be able to reproduce as many times as they see fit regardless of any reasonable form of fitness.  Most people find a partner if they want one, and the incredibly fit do not procreate en masse like male leaders of packs of animals since polygamy is not an acceptable practice in many societies (notable human exceptions are cases like Genghis Khan who is thought to have fathered a ridiculous number of children [albeit this is not a great example of selection for a very nice trait]).
Just think about traits that people have who reproduce less, and traits people have who reproduce more, and we're evolving towards the latter.  There is an absolutely hilarious (and depressing) intro to a movie based on taking these sorts of arguments to one extreme.. but I'm not sure this is the right venue to post it :)

If you can reproduce, you are fit. Period. The idea that the "wrong" people reproduce is simply elitism and various bigotries dressed up in the scientific guise of eugenics. Historically, it's always been the case that the wealthy reproduce at higher rates than the poor. It is still the case, though the gap as narrowed in the industrial age. Nevertheless, the idea that the "wrong" people are reproducing is not only completely unscientific but the basis of some of the worst evils ever. Yet still it's a very common idea, usually in the social/political classes you'd least expect it to be.

What if life was simply testing all possible genomes. The viables survive while the worst die. Thus it should have begun with small genomes and becoming always longer, like a brute force process acting since billions of years. This but would mean that it is not evolved but simply tested DNA, also genetical modern technologies could use this way ?


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Plant identification?
Can anyone identify the plant below? It's in a backyard in Pennsylvania, and the photo was taken today.

It would help if you provided more photos, such as a detail of the flower (where petals and other structural elements can be counted), the stem, the leaves, etc.

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange. This topic is not found in the following appropriate topics listing in the Help center: 1) General questions about biological concepts 2) Questions about the biological mechanisms behind medical conditions 3) Questions about techniques in a biological or biochemical laboratory

Gardening and Landscaping only? what about the wild plants?

And when asker don't know whether it is cultivated or wild?

Those flowers don't come from the same plant as that big leaf in the front do they?  Cant help you with the leaves, but the flower looks like a daylily. source: I know nothing about plants, but happen to have a mom who got a degree in horticulture :)

And the big leaf could come from some kind of zucchini. Source: grandmas garden.

The flower is a Hemerocallis fulva (Hemerocallidaceae).
The leaf seems to be a Cucurbitaceae, as said above, the same family as the zucchini


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Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?
It is difficult to assume that the massive number of co-ordinated developmental sequences in a developing embryo is controlled by molecular signalling alone. Is anyone aware of a molecular or developmental clock within the genome which control the on off states of the genes concerned with developmental sequences? If it has not been reported is it likely to exist? (This is not about the molecular clock in evolution.)
Assuming there is a molecular clock, is it possible that the clock is switched on at the time of fertilization, and the zygote transfers the elapsed time to the progressive generations of the cells?

You think it is difficult to believe that development is only timed by molecular events, but you are asking whether there is a molecular clock? Seems a bit contradicting... Anyway it has been shown that disruption of clock genes leads to developmental defects: for instance (these are just two random papers I found, but there is surely more) http://www.ncbi.nlm.nih.gov/pubmed/22884368 http://www.ncbi.nlm.nih.gov/pubmed/17963275

Thanks for the comments Nico, I did not say events, i said molecular signalling and molecular clock. by molecular clock I meant something like a run time clock or a timer for that matter for referance.The circardian rhythm is too slow for temporal refernce control of the fast paced developmental process in an embryo.

Ok, now I understand what you mean. In general when speaking about "molecular clock" one refers to a set of genes and their derived proteins that govern circadian rhythms and that indeed act as a "24h timer". See also my explanation here: http://biology.stackexchange.com/questions/2299/how-is-human-biological-clock-modelled-in-modern-science/2856#2856 . Now, although these genes are involved in circadian (~24h) rhythms, they possibly also have a role in shorter (<24h, ultradian) and longer (>24h infradian) rhythms, although this is still very much an unresolved question.

I think that the "molecular clock" that you refer to and the "molecular signaling" that you are skeptical of are one and the same thing.
In the 1960s, nuclear transplant experiments established that molecular signals in the cytoplasm can dedifferentiate terminally differentiated nuclei, "resetting" your molecular clock, or in the more common terminology "rerunning" the "developmental program" to yield viable animals.
This "developmental program" metaphor has been frequently used to describe this process, seeing development as a series of gene regulatory cascades; they called it a program because they were thinking of procedural computer programs. It isn't really a clock so much as a complex process by which different sets of genes are turned on and off in a concerted fashion, where one step depends on what happens in the previous step. An undergrad course discussing some of the mechanisms of this is posted here.
We've known for many decades that interrupting cellular processes such as transcription, translation, and DNA replication tend to arrest development at different points (for one early example see here).
A good example of a step/series of steps in the developmental program is the maternal-to-zygotic transition in metazoans, where embryos transition from using maternally deposited mRNAs as molecular raw material to de novo transcription of their own mRNAs.
From the linked review:

As development proceeds, two processes are triggered that together form the maternal-to-zygotic transition (MZT): first, a subset of the maternal mRNAs is eliminated; second, the transcription of the zygotic genome begins. Initially, the destruction of maternal mRNAs is accomplished by maternally encoded products. However, zygotic transcription leads to the production of proteins and microRNAs (miRNAs) that provide feedback to enhance the efficiency of maternal mRNA degradation. In addition, among the earliest mRNAs synthesized de novo in the embryo are transcriptional activators that enhance the efficiency of zygotic transcription. The net result is that the control of development is transferred from the maternal to the zygotic genome.

Figure 1. A comparative overview of the maternal-to-zygotic transition (MZT) in several model organisms. Key embryonic stages for each model organism are depicted schematically above the corresponding cleavage cycle and time after fertilization. The red curves represent the degradation profiles of destabilized maternal transcripts in each species. The light and dark blue curves illustrate the minor and major waves, respectively, of zygotic genome activation. The last embryonic stage presented for each organism is the developmental point at which there is a major requirement for zygotic transcripts.

This transition requires that the developmental steps based on maternally-deposited mRNAs have completed successfully before de novo transcription of embryonic RNAs can begin.

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


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Neuromediator, Neuromodulator, Neurotransmitter?
Of these three words, perhaps Neurotransmitter is the most obvious. I took a look at Wikipedia page for Neuromodulation and found that this is pretty similar to Neurotransmitter too. I guess Neuromediator is somewhat more broad. Could someone clarify these nomenclature for me?

Neurotransmitters were classically the most specific in terms of demands on experimental demonstration (thus, the so-called "classical neurotransmitter") but the chief role of neurotransmitter is direct neuron-to-neuron communication via the synaptic cleft in which the post-synaptic neuron has channels that readily engage the neurotransmitter.  Classical neurotransmitters also require inactivation and are stored in vesicles in the presynaptic terminal (while under the modern definition, these last two requirements aren't as strict, allowing peptides and gasses like NO to be considered a neurotransmitter).
Neuromodulators, are more of an extra-synaptic application... a bath in the extracellular medium that modulates the excitability of a population of cells.  In this regard,neurotransmitters can be considered neuromodulators when their action is on channels outside of the synaptic cleft.
I have never heard the term neuromediator before, but looking at the results on Google suggest that it is the result of translation from Easterm European languages (Polish and Romanian) and seems to be synonymous with neurotransmitter.


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How do lilies sense day and night and open and close their flowers?
We have lots of lily flowers inside our garden. Their flowers are open in day and closed in night. How do lilies sense day and night and open and close their flowers?

The three main cues for flower opening/closing used by plants are temperature, light and humidity (van Doorn & van Meteren 2003, freely available pdf), with the first two being most common. Plants with daily opening and closing of flowers can be divided into nocturnal (open at night) and diurnal (open at day). There exists several different mechanisms for how flowers open and close, and these include e.g. reversible expansion and contraction of cells by changes in water balance and differential growth of cells due to temperature (in either the petals themselves or cells at the base of flowers). See the previously referred paper for examples.
The evolutionary advantages and molecular mechanisms (along with the circadian clock of plants) behind opening and closing of flowers are open research fields. Several evolutionary hypothesis exists for explaining different flowering strategies, and these often deal with efficient pollination (close when good pollinators are absent), protection against frost, conservation of resources (e.g. water) or predator/pathogen defence.
I do not know what the specific mechanism in lilies is, and it can possibly/probably differ between different species.


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Why isn't there a standard unit of promoter strength?
Sometimes in synthetic biology, we need to know rates of transcription of one promoter in relation to others (particularly inducible vs constitutive) in order to perform tasks like balancing transcription products and ensuring an excess of one product over another. As far as I know, there is no standard method of characterizing promoter strengths in relation to one another. However, a logical unit for transcription rate made (by organism or in vitro) could look something like:
Promoter Strength = number of transcript made / (concentration of RNA polymerase) (length of transcript) (unit of time).
Why hasn't this been done yet? What other factors could contribute to rate of expression in a particular organism? Is there another system for comparing promoter strengths?
Note: a similar system could be used for strength of repression.

What if there are multiple regulatory elements acting on a given locus?

I think the quantity you suggest is suitable only if the relations between the different factors is linear. Is there any proof of that?

@Amory, this is exactly why a characterized number would be useful to define promoter strength. You would be able to quantify a particular promoter's strength with or without activators/repressors, as well as in relation to other promoters with their respective regulatory elements.

The destruction ratio of the mRNA also varies, for example. Also, different mRNAs may have different affinity to the ribosomes (for instance, differences in Shine-Dalgarno sequence in prokaryots). Finally, unless you're using retrotranscriptase RT-qPCR, you shoudn't have a fiable method to quantify gene expression.

I think this paper defines a standard unit: https://jbioleng.biomedcentral.com/articles/10.1186/1754-1611-3-4

Transcription rates are very context dependent. This shouldn't surprise you, since the same genes aren't expressed in your lungs and your eyes. They're also very environment dependent, this shouldn't surprise you either, since it's pretty obvious every organism is going to respond to temperature, their current nutritional state and so on.
So, in order to define promoter strength, you'd first need to define the exact conditions under which you're measuring it, including the exact strain you're measuring it in. Because if you get any of those even slightly different you're going to get a different answer. Doing this might get you a consistent number but you're abstracting away the most important parts of differences in transcription anyway: how it varies between cells and contexts.
Moreover, even if got past these hurdles you'd not have a particularly useful answer anyway since the rate of transcription is only a small part of the whole process. Why not consider mRNA durability, or rates of translation, or protein durability? What matters very much depends on what you're considering.

I do realize that transcription is very context-dependent, but disagree about its importance. Even if strictly used in characterized in vitro systems, a number associated with a promoter is very useful, and can be extrapolated to its general abilities for transcription in vivo.

No, it can't. Consider DUO1 in Arabidopsis: it's a gene that expresses strongly in the germline but is entirely unexpressed in somatic tissue (and, in fact, is detrimental if it is). How will expression in vitro be extrapolated then? If your in vitro model is similar to the germline you'll get results irrelevant to any other cell; if your results are relevant to the somatic tissue you'll fail to understand key processes in the germline. The major issue in gene expression is its variation.

Not all genes need to be expressed in their "proper" context. Think of the Tet and lambda pR promoters being expressed in E coli (or really synthetic biology as a whole). If the purpose is exploiting or engineering and not discovering novel protein functions at a particular developmental stage, these promoters strengths are extremely relevent.

the measurement - counting # of mRNA from a specific cell state over a period of time would be difficult to do.  a single cell measurement where you are simultaneously monitoring the promotion state of the gene.  Sounds like quite a bit of work!

@LanceLafontaine: Extremely relevant for a particular purpose carried out in a particular way. That doesn't call for a standard measure; instead if you want to compare the effectiveness of two promoters you can simply compare them by Western Blotting or qPCR and see what you find. If you are desperate for a number, this will quantify the difference.

It's true that the expression of a promoter is context-dependent, i.e. depends on the overall status of the cell, but some work has been made to boil down such context-dependency into some measurable parameter. For example, for constitutive promoters such a parameter seems to be the growth rate. You could characterize promoters by that:
Gerosa, L. et al. Dissecting specific and global transcriptional regulation of bacterial gene expression. Mol. Syst. Biol. 9, 658 (2013)

I realize this is an old question, but in Synthetic Biology, we nowadays use the Relative Promoter Units (RPU)1. This is a standardized measurement of promoter strength to circumvent inter-wet-lab variability.
Reference:
1: Kelly, J. R., Rubin, A. J., Davis, J. H., Ajo-Franklin, C. M., Cumbers, J., Czar, M. J., ... & Endy, D. (2009). Measuring the activity of BioBrick promoters using an in vivo reference standard. Journal of biological engineering, 3(1), 4.

Welcome to Biology.SE! This looks like a reasonable answer, but I think it would be helpful if you could add more detail and if possible at least one more supporting reference. In the future, please also include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. ...

... You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

Years of discussion about this:
"Polymerases Per Second.
A standard unit to measure the inputs and outputs of a BioBrick Device.
PoPS have yet to be directly measured in vivo."
http://openwetware.org/wiki/PoPS
*understanding this would be a great feat and it would get us one step closer to measuring complex systems.


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Steroid Hormone Signalling
Can the lipid-soluble hormones (like steroid hormones) go inside every cell, as their particular receptors are located in the cytoplasm or nucleus of the target cells? Is there anything special on the membrane of the target cells which enables the steroid hormone to know that it has to enter that particular type of cells and avoid others?
(Peptide hormones function through cognate receptors located on the cell membrane of the target cell.)

Hi @biogirl - I edited the last sentence of your post to word it in a more scientific way. Water soluble hormones are really peptide hormones, to distinguish them from steroid hormones.

Note: Since my area of expertise is with peptide hormones, I will offer a partial answer.
Steroid hormones are carried through the circulation by binding to globular proteins. When these hormones are released from binding proteins, the classical route of action is by free diffusion through the cell membrane. This diffusion is due to their aromatic structure. You rightly point out that the classical receptors of these hormones are found in the cytoplasm or nucleus. For example, estrogen signalling as a classic signalling template which has genomic (DNA) and non-genomic (protein) targets to exert its effects.
Non-canonical signalling can occur through at least one G-protein coupled receptor (GPCR). Unlike most GPCR's which are localized to the cell membrane, GPR30 appears to be localized to the endoplasmic reticulum, which means steroid signalling still occurs through canonical means and also this newer pathway.
Then again, there are also steroid effects that modulate ion channels, for example GABA receptors. These are not specific receptors where only a steroid hormone can have an effect, yet they can activate or inhibit the effects (along with other drugs).


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Origin of human intelligence and thought
I've been debating this topic with a friend of mine and we can't get to a common answer. She argues that we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have. I am arguing that a high protein diet allowed the first humans to have the possibility to develop a higher memory, intelligence and other mental procedures.
But after all, what would be the real origin of the intelligence? And if animals do have intelligence too, why isn't theirs as advanced as us.

Read https://en.wikipedia.org/wiki/Evolution_of_humans.  We did not evolve directly from chimpanzees or orangutans, but rather humans and chimps share a common ancestor more recently than most other species.

Ok, but what about cognitive thinking?

Could you make it clearer as to how these arguments can't coexist? It seems to me that (hypothetically) we could or could not have a common ancestor with chimpanzees and have become more intelligent thanks to a higher protein diet.

You're right. The main debate here is the origin of the thought. She replies that thinking is a faculty of the soul, and not a matter of biological evolution. My question would be, When does in the line of evolution humans/primates started to actually think. And why ?

I feel that a tighter set of definitions could help the discussion. What do you mean with thinking, cognitive thinking and intelligence? Intelligence/thinking is also not (in my mind) an on/off thing, and there is a continuum between 'pure' instinct behaviour and behaviour based on intelligent thought. Also, if your friend has the starting point of a mind(soul)/matter separation (dualism), where evolution cannot affect the mind, you will probably have a hard time convincing her.

I use them without difference, it's just for the matter of this. I know that they are completely different, but just for this discussion, I'm using them as the same besize they are completely different. The term that I should be using is Reason. The fact of recognizing myself as a human being.

I recommend watching the PBS documentary [The Human Spark] (http://www.pbs.org/wnet/humanspark/episodes/program-one-becoming-us/video-full-episode/395/ ) for a thorough look on this particular question, including this evolutionary approach to it comparing with chimpanzees and other primates. PS: I am not aware if everything is available for free, it will take maybe a little bit of browsing to find them, but I know I managed to.

How is

"we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have"

not equivalent to

"We are not related to the chimpanzee or orangutan because, if we did, they would also have [the same amount of body hair]/[the same sized mouths]/[the same muscular strength] that we have"

?
Any related species are going to differ in some respects (otherwise they would not be different species, after all), and it is plain to see that intelligence is one of the ways in which species can differ.
Regardless of that (if your friend thinks intelligence is special in a way that hairiness is not), you can make your argument even while sticking to talking about intelligence, and there is no need to go into the reasons for changes (increases) in intelligence to see that.
To make the point with your friend, it might be best to point to two different animals that

she recognizes as related, and that
she also recognizes as having different levels of "cognitive thinking ability".

In light of such an example, her argument falls flat (unless she further considers only human thinking ability special, in which case you will have a harder time!)

Actually yes, she does think that human race is the only one to think, being this good a faculty from the soul(again, which only humans have). I certainly don't agree with her, but with evolutionary theory. But, in which point do humans differentiated from the rest of the animals, (that means, stopped being like the rest of the animals by having cognitive thinking and self recognition as a being) and why?

All the evidence suggests that we aren't qualitatively different from other animals - most of our cognitive traits are present to some extent in other animals. For example, birds, primates and cetaceans can all solve abstract puzzles, and some aniamls apparently recognise themselves in a mirror.

Regarding self-recognition: https://en.wikipedia.org/wiki/Mirror_test#Animal_species_capable_of_passing ...in fact, according to the same wiki article, humans aren't capable of recognising their own reflection until around 18 months. By your friend's logic, do babies therefore have no soul?

@atrichornis Nice.  I was going to link to exactly that article.  +1  (at)Eric Frick, the fact that the list of animals who recognize themselves in the mirror is non-zero should be enough, but let's also consider that self-awareness can be present without understanding of the specific concept of image reflection, so the list is longer still.  Also, people who have their sight restored after being blind from birth can fail the mirror test, so your friend can't dismiss atrichornis' baby argument purely on the basis of babies not having all of their cognitive faculties yet.

@EricFrick The second part of my answer, which admittedly will probably not move your friend, is that the onus is on her to prove the existence of the soul, or that human thinking means a soul is there.  On that second part, if she does not want to end up concluding that some humans don't have souls, she will have trouble defining thinking that is present in all humans (including those with severe disabilities) but no animals (including the clearly intelligent ones).

Indeed. It seems the soul must be a temporary gift. It is given to toddlers who then become self-aware, and then taken away from a proportion of the elderly population who then sink into dementia and lose most of their higher cognitive function. Makes perfect sense!

One thing we haven't discussed much is emotion. While the science is somewhat anecdotal here, there is good reason to believe that emotions aren't unique to humans. Alex the African grey parrot, apart from having a better grasp of language than a human toddler, also seemed to have comparable emotions to a toddler (for example, he was prone to sulking and acts of kindness). http://en.wikipedia.org/wiki/Alex_(parrot)

@atrichornis I doubt you will find anyone who is not a crackpot who claims that animals do not have emotions. Try wetting a cat and telling me she is not pissed off.

Certainly, but @EricFrick's friend sounds like she might be a crackpot!


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Do the phage repressors CI and Mnt exhibit crosstalk?
I am interested in using the CI and Mnt proteins as well as their respective promoters (pR and Pmnt) within the same synthetic system, but am concerned as to their similarity and potential crosstalk. A quick search of the literature yielded no results and a Multalin did show some significant sequence homology (although Mnt forms a homodimer while CI does not).

Sequences: CI and pR, Mnt repressor and Mnt promoter
Has it ever been reported that the CI or Mnt repressor exhibit crosstalk on the pR and Pmnt promoters?

There are no reports for it yet. I don't think just because they show overall homology, they would exhibit crosstalk. Just see the alignment of the DNA binding domains of these proteins first ~70 residues from N-terminal. Moreover their DBDs belong to different PFAM families.
Similarly with the promoter sequences.
As reported in iGEM website:

Mnt promoter: tagatctcctatagtgagtcgtattaattt
cI promoter: gtgttgactattttacctctggcggtgata

They are quite different.
Moreover, if iGEM has a reported standard part such as a bistable system component: Mnt/cI promoter (BBa_K228003) then it would have been pretty much standardized. iGEM parts are usually reliable.


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The role of antibodies interacting with cancer
I'm learning about antibodies. As I understand it, antibodies detect stranger cells/bacterial/viruses by the molecules present in their membranes. In cancer cells, the cancer cell have produce some unknown protein, so why antibody cannot detect that molecule and kill them?
Is it that the cancer cell is surrounded by a normal cell?
Or is the protein it produces is not obvious in the cell membrane?
Or that the protein can bypass antibody? if so, why?

This article on the University of Kentucky website is pretty good, it seems the cancer cells hide because they do not express CD80, a co-stimulating molecule. Co-stimulating molecules are often necessary for an effective immune response.
This is a big part of the article and I think they do a good job of explaining it so I'll just quote:

"People once thought that cancer occurred because of a weakness in the
  body's immune system," says Yannelli, "but we have known for years
  that overall that is not the case. The immune system in cancer
  patients actually works quite well. Otherwise, they could not survive
  the disease for long periods of time nor could they fight off other
  viruses, which they routinely do. The problem is not that the immune
  system doesn't work; it is that the immune system doesn't recognize
  the tumor."
According to Yannelli, for the body's defense system to work properly,
  key antigens must be presented in a specific way to lymphocytes, the
  cellular mediators of the immune system, which then kill the cancerous
  cells. Normally, antigens are tipped off by co-stimulating molecules.
  When the co-stimulating molecules are not present, the immune system
  does not "see" the cancer cell, and therefore does not act to destroy
  it.
Scientists have discovered that lymphocytes have very narrow job
  descriptions, each one designed to attack only a specific molecule.
  The researchers have also discovered a wide range of co-stimulating
  molecules. A critical co-simulating molecule is CD80. Because cancer
  cells do not express CD80, they are invisible to the lymphocytes
  responsible for destroying them.

This paper has more on the function and mechanism of CD80.
Thanks to @Nico for pointing out that not all cancers are the same so the generalization discussed in this answer may not be true of all cancers.

We also need to specify that "cancer" is not ONE illness but a series of very different pathologies with very different etiology and development. What is true for one cancer may not be true for another one, so it is always difficult to generalise.

In general the immune system sees the world in very simplistic terms: Self vs Non-Self. Ideally, threats to the health of the animal are all non-self and can be attacked strongly. Whereas self cells and proteins are tolerated - effectively invisible to the immune system. Cancer is a particularly insidious disease because it arises, not from the outside world, but from subtle changes within the host's own cells. Therefore, cancer cells are starting as 100% self, but can adopt changes that make them more different over time.
A good review of this interaction between cancer cells and the immune system can be found here.
A second aspect of your question that is important is how antibodies are made and what they are capable of 'seeing'. I wrote a short essay about B cells, the cells that produce antibodies, and how they are activated on my blog. That might be a good resource to check for you - I also link to one or two other articles there. Briefly, B cells can only 'see' cellular antigens that are either expressed on the cell surface or secreted. Although some cancer cells alter these types of molecules, many more are part of the internal workings of the cell and therefore invisible to antibodies. For this reason, many oncologists focus on T cell responses, which are capable of detecting non-native internal antigens.


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Population genetics and the fitness probability distribution. Why is the arithmetic mean all we need?
When recording change in allele frequency in diploid, bi-allelic, infinite and panmixic population we usually use this kind of equation:
$\delta_p = \frac{p * q *( p (w11 - w12) + q * (w12 - w22))}{\bar{w}}$
$\bar{w} = p^2 * w11 + 2*p*q*w12+q^2*w22$
$\delta_p$ = change of $p$ (frequency of one of the allele) from one time step to another
$w11$ is the mean fitness of individuals of genotype 11. $p$ and $q$ are the allele frequencies.
The only indicators for the fitness distribution is the arithmetic mean. Why don't we include other indicator of the probability distribution of fitness? The skew, the sd, the median for examples. Could you argue why we don't need to care about the probability distribution of fitness of individuals with genotypes 11 (for example)? In other words, why is the mean fitness (=w11) a sufficient statistics?
I wouldn't be able to answer if one asks me:

Why don't you take the median instead of the arithmetic mean?"
Why don't you care about the variance, the skew (or any other moment) of your distribution?
What if the traits were not countinuous but discrete (sex is a discrete trait for example)?

Could you point us to where you have seen the statement "we don't care about the prob... the mean fitness is a sufficient statistic"

@GriffinEvo I am stating that we don't care about the probability distribution, distribution skew, etc... as only the mean fitness per genotype and overall mean fitness (pondered by their frequency) appear in the equation.

Thanks kmm. I didn't Mathjax. Can we make the overline over w for mean.w ?

@GriffinEvo To add to my last comment. Does it make sense? Do you know any mathematical formulation that take into account other indications (sd, normal/poisson, skew, etc...) of the probability distribution of fitness when describing a change in allele frequency over time due to natural selection?

I doubt it is going to be the case where evaluating the mean is going to be adequate for describing the population fitness.  Its just a common compromise in experimental and mathematical fitness... this would presuppose that the distribution of fitness is gaussian, extrapolating to a large population.  even then you'd need to have an estimate of standard deviation.

@shigeta so you think our models depend on this very strong assumptions that fitness is normally distributed with a given sd (maybe 1). Isn't it weird that we never tell this assumption when talking about this formula although we talk quite a lot of the assumptions of panmixia in introductory class of evolution?

Wonder if studies often don't have a large enough sampling to justify an SD calculation.  For such studies posting a mean value might be all you can do.  Also the stats training of the authors is not great in many cases.  more recent studies have been larger scale and more rigorous and take years and whole crews of biologists.  If you were to post some paper links i'd try to turn this into a response.

It's simplest to think about a haploid population with size $N$. Say there are two alleles, $A$ and $a$, with $A$ having frequency $p$ in this generation. Each $A$ individual will have some realized fitness (i.e., number of offspring) in this generation; let's call this number $w_A^{(i)}$ for the $i^\text{th}$ individual. The total number of $A$ individuals in the next generation is then $\sum_{i=1}^{Np}w_A^{(i)}=Npw_A$, where $w_A$ is the arithmetic mean of the fitness distribution, $w_A\equiv\sum_{i=1}^{Np}w_A^{(i)}/(Np)$. So regardless of how weird the distribution of the $w_A^{(i)}$ was, all that matters (in the large-$N$ limit) is the arithmetic mean.


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Collective term for both exons and introns
Is there a term I can use to refer collectively to both exons and introns? By collectively, I don't mean ligated as with an unprocessed transcription product. I'm just writing about exons and introns and getting frustrated that I keep on having to write "exons and introns", wishing there was a more concise term I can use in the place of that phrase.
For example, the term I am looking for would fill in the following blank perfectly.

The gene has 5 exons and 4 introns, so it has 9 _____.

uh...a sequence!? a gene sequence? a sequence that get transcribed. I personnaly don't know any other word for that.

Could you clarify the context?  If on single RNA molecule you could say pre-mRNA or hnRNA, or in general "the transcript."

You should be aware that if you refer to "splicing fragments" with no explanation, I doubt you will be understood. With no context, I would assume you were talking about excised introns.

sorry for the late comment.. Instead of this you can say that the gene has 8 splice junctions- I guess it is more precise.

How about "splicing fragments"? It might be easier to refer to them according to the mechanism of production.

What of single exon genes with no introns and, therefore, no splicing?

Are they really exons with no introns? If there are no introns at all, it's just a transcript, or a coding sequence.

There are certainly single exon genes, yes. I am not 100% sure that they also have no introns but I would imagine so since splicing always joins two ends of a sequence excising what is in between.

There are definitely no-intron genes, that's usually one of the hallmarks of a former virus that was integrated into the genome.

This is a good answer - there is no explicit word to answer to this question I think.

I mean, there are lots of genes with no introns. Are they really exons if there aren't introns to compare against? Maybe that is semantic trickery.

Yes, they are exons because they are translated into amino acids. Given that the species in question has splicing, anything that is translated is an exon by definition. In species that lack splicing, all genes are single exon genes and you could call them exons but that might be semantic trickery indeed. In species with splicing however, things are quite clear cut, translated? therefore exon.

I think your best bet would be transcript. Gene is actually quite close but most of the current definitions include the promoter sequence in the gene so that is not restricted to introns and exons.
Transcripts, on the other hand, are all of a gene's sequence that is transcribed and consist exclusively of introns and exons (UTRs are also exons and are actually spliced in some cases). Note that I am using transcript and not mRNA since mature mRNAs do not of course contain introns. Immature ones do and transcript can apply.

This isn't the word I'm looking for. The word I'm looking for will fill in the following blank: "The gene has 5 exons and 4 introns, so it has 9 ____". Splicing fragments is the best answer so far, I was just hoping there was a more concise term for it.


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Why don't antibiotics affect mitochondria?
Given that mitochondria are evolutionarily closely related to bacteria, and antibiotics kill bacteria, why don't antibiotics also kill mitochondria?

Just found this interesting information from the wikipedia article about ribosomes: "Even though mitochondria possess ribosomes similar to the bacterial ones, mitochondria are not affected by these antibiotics because they are surrounded by a double membrane that does not easily admit these antibiotics into the organelle"

And so how do they get into bacteria?

I think many bacteria only have one membrane instead of the two on mitochondria.

Gram-positive bacteria have no outer membrane, but gram-negative bacteria (from which mitochondria are thought to derive) have a double-memberane. Gram-negative bacteria are susceptible to aminoglycosides, so I am afraid that your explanation (and the first statement in the accepted answer) is inadequate.

I think this answer by David should provide further insight. Macrolides do have an effect on protozoan plastids. http://biology.stackexchange.com/a/48004/20449

The short answer is, as you found, that mitochondria are wrapped in a double membrane and are thus harder to penetrate with antibiotics.
The long answer is some of them do.  Good antibiotics target structures widely found on and conserved in bacteria that are not found in human bodies.  Some antibiotics are a little less specific and can indeed interact with other molecules.  The allergy to penicillin, for example, is caused by the immune system reacting to a "novel" protein formed when penicillin binds to the surface of red blood cells.  Some antibiotics can indeed harm mitochondria, but we tend not to use those and in fact wouldn't even call most of them antibiotics since we wouldn't use them because of their harmful effects.  Here is a very recent report looking at some of the anti-mitochondrial effects of some antibiotics.  To quote from the abstract:

We show that clinically relevant doses of bactericidal antibiotics—quinolones, aminoglycosides, and β-lactams—cause mitochondrial dysfunction and ROS [reactive oxygen species] overproduction in mammalian cells. We demonstrate that these bactericidal antibiotic–induced effects lead to oxidative damage to DNA, proteins, and membrane lipids.

Absolutely fascinating stuff. Thanks for sharing the article.

Also note the fluoroquinolone group of antibiotics (Cipro, Levo, etc) are very good at damaging mitochondrial DNA, causing long term, sometimes permanent, debilitating effects. https://www.ncbi.nlm.nih.gov/pubmed/8913349


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Is there a difference between pig and cow anatomy that makes religious slaughter of the latter less painful?
This question is not for the squeamish. I was told that non-Kosher animals like pigs have a different anatomy in their neck compared to kosher animals like cows such that the Shechita method of religious slaughter (a very sharp knife held on the neck only by the weight of gravity rapidly going back and forth in a single cut that drains blood and results in an "instant" drop in blood pressure in the brain), while causing pain in the non-Kosher animals, doesn't cause pain in the Kosher animals. Is there such an anatomical difference and thus difference in pain?
(If this would be more on-topic at Skeptics.SE, let me know.)

This could be extended as well to other religions, such as Islamic dhabīḥah

@nico Possibly. That's how I had an earlier version of this question before I edited it. But the original claim was in context of Kosher/shechita and I'm not familiar enough to know if there's a practical difference with the Islamic method.

Difference between kosher and non-kosher animals
Rabbi Zamir Cohen, in his book The Coming Revolution - Science Discovers the Truths of the Bible, quotes modern day scientists that have made an incredible discovery of a major difference in the way the blood flows in the species that are kosher and those that are not. In non-kosher mammals, the vertebral arteries flow directly to the brain through the rete mirabile. However, in cloven-hoofed, cud-chewing mammals and permitted foul, the vertebral arteries drain into the carotid artery and do not have any direct flow to the brain. There will therefore be an immediate drop in blood pressure at the time of shechita that causes the animal to lose consciousness, thus feeling no pain.

It was my understanding that the vertebral arteries bring blood to the brain even in cattle, and are not severed, and keep them conscious far longer than any kosher bird. Do you have a source other than a rabbi?

The technical details on this are a bit muddled. The wording "drains into" doesn't seem to fit with what an artery does. Could we get a more biologically precise description of what is alleged to be happening here?


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Goats are so fearless but sheep are not. Is there any genetic difference responsible?

As you see in the picture goats (not only wild goats) are so fearless, but I never saw any sheep do this. What is the source of this difference in behavior?

How is this getting so many up-votes?  No offense to the OP but do we really feel that this question shows research effort?

Perspective update: Are they fearless, though? Or just desperate to escape from a predator (i.e. fearful)? Perhaps they are not so brave as they are naive; having never experienced, or witnessed, the perils of a fall? Perhaps they are just following the brave/naive "leader goat" (to the right). I would be cautious in using the word "fearless"... some background reading, as recommended by @KennyPeanuts, would be nice.

Obviously there are genetic differences. What other possible explanation could there be? If you're asking what genes are involved in the differences, no one has any idea which thousand of the tens of thousands of genetic differences are responsible for this complex behavior.

But there must be some previous scientific attempts to answer this or part of this question

1. Sheep are fearless

2. English common names are misleading when it comes to the genetic differences between goats and sheep
You posted a picture of Mountain Goats (Oreamnos americanus), which are a different genus than Domestic Goats (Capra aegagrus). Both Capra and Oreamnos are members of the Subfamily Caprinae, as are Domestic Sheep (Ovis aries).
Within Caprinae, Capra and Ovis are actually more related to each other than either one is to Oreamnos, despite the confusing way that we parcel out English common names. Oreamnos is, in fact, more closely related to the Musk Ox! (Here's the Tree of Life page that shows the phylogeny of Caprinae).
The Domestic Sheep genus Ovis also includes mountain species such as the Bighorn Sheep Ovis canadensis, which is plenty fearless. See the Bighorn Sheep above, and in this incredible photo. For what it's worth, the Domestic Goat genus Capra also includes cool mountain species, such as the Ibex.
Edit: the differences in behaviour between the domestic goat and sheep would be a combination of the initial differences between wild Ovis and Capra and the coevolutionary process of domestication; where humans shape niches to fit animals and animals to fit niches. It's possible that there has been more neotenization in the domestication of sheep, in which individuals who show immature characteristics are successfully selected for. See also this other question on apple and pear domestication.

(Bighorn Sheep photo by TwelveX, used under CC BY-NC-SA license.)

@MySky the fearless and awesome Urial Sheep (Ovis orientalis vignei) should be near you! At least, Wikipedia says it lives in the mountains of NE Iran.

Beautiful answer.

You are right. what about differences between domestic goat and sheep. Which genetic difference leads to difference in behaviors (not abilities).

@MySky I've added a paragraph about the differences between domestic goats and sheep.

You should also bear in mind that the fact that they are great climbers does not make them fearless. For example, if I were to find myself floating 500 meters above the ground, I would be terrified. The fact that birds do not appear to be scared in the same situation does not make them fearless, it just makes them fliers.
Similarly, I am sure a fish would be terrified if forced to spend half an hour in a beach bar. I, on the other hand, would find it enjoyable and not scary at all. It does not mean I am fearless or brave. You can only be brave when you ignore your fears not when you have none. Since mountain goats are exquisitely suited to jumping around on sheer mountain cliffs, it probably causes them no more fear than visiting a beach bar would cause me.


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What biological processes cause leaves to change colours in Autumn?
I am curious to learn what are the biological mechanisms that cause leaves of deciduous plants to change colour? What happens to the chlorophyll?
What environmental phenomena (temperature/air pressure/length of sunlight) are they responding to?

While we're waiting for an answer, I'll point out this page from the University of Illinois, which has a superb and comprehensive explanation. Essentially, it's a combination of pigments being revealed as the chlorophyll is broken down and pigments being produced for a variety of reasons.

@Oreotrephes thank you for that, it is indeed these mechanisms and the triggers that I am interested in.

Here is a quite nice Chemistry of Autumn Leaf Color. And here is a less chemical, but more detailed explanation regarding the triggering of colour change, which is quite similar to the one from the University of Illinois that @Oreotrephes already gave.
As I understand it, during sunny days a lot of chlorophyll is broken down, but also built up. When after the summer the days get cold and dark, chlorophyll is built up slower (or not any more at some point) and you start to see the colour from the carotenoids and anthocyanins. A harsh change from sunny to cold and dark is supposedly bringing up the brightest colours. At some point, also the carotenoids break down and leaves get brown. The faster the change to cold and dark the larger is the frame between having all chlorophyll broken down and having the other colouring molecules broken down (-> bright colours).
But that's the amateurs explanation.


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Raphide toxicity in Pothos plant
Recently I found out that the common houseplant Pothos (Epipremnum aureum) is toxic to cats and dogs due to the presence of "insoluble raphides." I have a lot of these plants around my house and my cat drinks water from the vase that they are in (I put drinking water into the vase that he always drinks from). He doesn't chew the Pothos leaves, he only drinks the water, is it still dangerous? I tried several times to give him water in an ordinary bowl, but he prefers the water that's associated with the Pothos plant, so I thought that maybe the roots of the plant excrete something nutritious (but I guess that's not the case, apparently...).
Is it harmful for an animal (cat) to drink water that has a Pothos plant immersed in it?
Also, my other cat does chew on the Pothos leaves (he goes crazy for them). Is it possible to have immunity and not be affected by the toxic chemicals? I read that chewing is supposed to provoke stomach irritation, but I would think that if the cat that chews the leaves suffered from irritation he wouldn't keep getting excited about chewing the leaves...
So what is going on? Many thanks!

Perhaps someone else can answer this with more certainty, but I'd guess that because raphides are essentially sharp crystals that cause irritation-related symptoms, rather than toxic chemicals in the way one might usually think of them, that drinking the water wouldn't pose a problem (actually, I suppose the word "insoluble" might be a clue here). Raphides are defence against herbivory, and chewing raphide-containing leaves is what you want not to do (or not let your pets do).
Veterinary Toxicology p. 889 has more info.

"insoluble" is a big clue, I'm dense today. Thanks for the input and link.

I wasn't being sarcastic! I'm still trying to work out the whole soluble/insoluble fiber thing, myself.


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molecular indicators of apoptosis: clarification needed
I understand that DNA fragmentation is a molecular indicator of apoptosis. What distinguishes this as a hallmark of programmed cell death, versus one of necrosis?

Although both involve DNA fragmentation, the pattern produced is very different.  During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern.  Necrosis, on the other hand, is a more stochastic process, and will produce a smear.  This details the difference rather nicely, including different ways to assay for either one in table 18.3.1 such as morphological staining or flow cytometry.
Here's a nifty image from the link.  Figure 18.3.2.  M is the marker, and in panel A, a conventional gel, lane 1 is apoptotic DNA, lane 2 is unprocessed DNA, and lane 3 is necrotic DNA.  In panel B, a pulsed-field gel, lanes 1 2 and 3 are untreated, apoptotic, and necrotic, respectively.

I understand that DNA fragmentation appears as a regular pattern on a conventional gel. However, I wonder how can the experimenter distinguish apoptosis from necrosis on a typical FACS experiment using propidium iodine DNA staining?


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What is a good source for info on disease frequency distribution among age groups?
I need information on the disease frequency distribution among age groups for an Android app I'm building... Hopefully I've come to the right place. Is there a good data source for this? Like a bioinformatics database?

related http://biology.stackexchange.com/questions/2009/downloadable-worldwide-database-of-disease-statistics?rq=1  and http://biology.stackexchange.com/questions/2016/human-disease-and-associated-phenotype-database?rq=1

I'd say this is also a bit vague in its current format, could you expand on what sort of information you are looking for.

As the title says, I'm looking for the frequency distribution among age groups...Something like what percentage of type II diabetes patients are among age 40-50. And it's not just the distribution of one specific disease, but all kinds of diseases.

You may need to study each disease individually or do a literature review.  The Online Mendelian Inheritance in Man website may be a good starting point http://www.omim.org/
The Centers for Disease Control and Prevention lists several diseases with a variety of different statistics here:  http://www.cdc.gov/DiseasesConditions/

I've been to the CDC site. I guess I can use the statistics there, but what makes it less ideal is that ages <18 are not included. I am currently working on other stuff, so please feel free to improve your answer in the next few days :) I'll accept your answer if no other better ones pop up.