How can an animal live without a head / brain? The human body is unable to do anything if it loses its head - as the brain is separated from the body, the body immediately dies.

But why does the same not happen to other species or animals? (As they are somehow similar organisms/living things, like humans). However, when the head is cut off from a chicken, snake ( also insects, but it's different system, answered here... I mainly interested in bigger animals) ... the body continues to move. Why and how does this occur? Who manages the functionality of body, if there is no manager (brain)?

In general, and this is somehow speculative, the animals that you mention have more autonomy in their extremities and less control from a head, muscles have evolved autonomous responses perhaps as an evolutionary advantage, ( i.e. having a brain be in charge of reactions can add precious milliseconds ), there also seems to be a relationship in between brain size ( specific motor control areas) and this autonomy, which introduces a metabolic cost (i.e. our big heads need a lot of energy)  Further, there are other biological considerations for providing extremities with their own resources and thus to a degree be more independent, perhaps another evolutionary strategy. At the other end of this control-autonomy relationship, the head takes control of the extremities most of the time and their interdependance is greater, so if you cut it no movement will happen, although we still possess a few hard coded reflexes that work for a while provided they have enough energy left or a blood source.

To give you an example: a cat ( somewhere in the middle ) can still walk when you cut the connections from the brain /head  to the legs due to reflex actions ( the cat has to be on a treadmill though).


Why do men have nipples? I'd be tempted to call nipples in men vestigial, but that suggests they have no modern function. They do have a function, of course, but only in women. So why do men (and all male mammals) have them?

I believe it is for this reason: the female body plan is the default one. Males are a variation upon that, in humans at least. Nipples are part of the basic body plan. For a man to not have them, he would need to actively evolve something that would prevent nipples from developing. There is no selective pressure for the development of such a thing, so it hasn't happened. Keep in mind that the code for the general body plan is shared between males and females. The Y chromosome modifies the development of that body plan so the person becomes male.


Identification of small creature this is my first message here. Let me tell you why I came to this stackexchange:

A couple of years ago, I took an empty transparent jar (5 liters) and put in it some water (taken from a pond), some dirt and some randomly chosen acquarium-plant. And waited. It was (still is) an amazing experience! The jar went through a number of phases but is still alive, very green, surviving well without any maintainance for more than 2 years (maybe I have added 1-2 liters during this period of time, due to some very low evaporation).

Recently, a friend gave me as a gift a small 15liter acquarium and I decided to do another experiment of this kind. The larger acquarium (compared to the 5L jar) will also give me the possibility to observe better the environment and it's evolution.

Now 2-3 months have passed. The water is still quite yellow-ish, but from previous experience with the jar this has to be expected for the first year or so. [the jar became transparent/green from yellow all of a sudden after about 1 year of life]

However the jar is full of life, the plants are doing fine and there are a lot of little creatures.

QUESTION: could you help me identify one of these creatures? It is a very very small one and I'd like to know more about it.
In this video you can see a number of them going around a small piece of cotton that fall down in the acquarium yesterday.

LINK: https://www.dropbox.com/s/jrkoa5kswghiizm/Video%2011-01-2018%2012%2037%2055.mov?dl=0

thanks for any suggestion!

The creatures in the video do indeed show the shape, size, coloration, and typical behavior of ostracods ("seed shrimp"), a type of freshwater crustacean (class Ostracoda) that is distributed worldwide (Martens et al. 2008). They lay eggs either on plants or directly in the water as plankton. Some researchers consider them to be potentially useful as bioindicators (e.g. Ruiz et al 2013), or even keystone species (Lawrence 2002). You can find many photos of ostracods on the Internet.

Lawrence, J. et al. 2002. Microb. Ecol. 44: 199
Ruiz, F. et al. 2013. Int. J. Environ. Sci. Technol. 10: 1115
Martens et al. 2008. Hydrobiologia 95:185


What happens to the mold spores we inhale? What happens to the mold spores we inhale?

I'm guessing when we exhale, many of them are expelled back out to the environment.

But given that disease can be caused by mold exposure, I'm also guessing that we do not immediately expel a percentage of them.

Molds can colonize in the lungs, causing detrimental effects.  Can they colonize elsewhere in the body?

For mold spores that do not colonize inside the body, what happens to them?  Are they expelled?  If so, by what mechanisms?  Are they alive or dead when they are expelled?

Mold spores are capable of landing and becoming dormant. Unless conditions are severe enough, mold spores will not just simply die off; they will essentially wait for conditions to improve and once those conditions do improve, they will take root and grow. When it comes to the human body, it all depends on the type of mold and the overall health of the host. The body is designed with natural defense mechanisms - mucous, enzymes, beneficial bacteria, filaments, etc. - against airborne particles and microorganisms. Basically, you'll never know if a sneeze or cough - other forms of defense - saved you from a miserable existence as a mold host.

As for whether or not mold spores are expelled from the body, that is not so easily answered. Mold spores can sometimes teem in the millions, especially around a dense infestation (such as grain silos or a house that has structural mold rot). Research has concluded that farmers (who make up 30% of victims who suffer respiratory illness in the U.S. alone), for example, inhale up to 750,000 mold spores per minute. The odds aren't exactly in their favor when it comes to expelling mold spores simply by exhaling.

(I write for MoldBlogger, by the way. If you have anymore questions or are curious about other mold-related scenarios, feel free to check it out.)

Edit:

Here are some of the sources where a lot of this information can be read about.

National Institute for Occupational Safety and Health. Agricultural Safety. Centers for Disease Control and Prevention website. https://www.cdc.gov/niosh/topics/aginjury/. Published June 19, 2014. Updated December 15, 2014. Accessed February 1, 2017.

Glen H. Hetzel, et al. Farmer’s Lung: Causes and Symptoms  of Mold and Dust Induced  Respiratory Illness. National Agriculture Safety Database website. http://nasdonline.org/1853/d001796/farmer-039-s-lung-causes-and-symptoms-of.html. Published 2005. Accessed February 1, 2017.

Dennis J. Murphy. Agricultural Safety and Health: Farm Respiratory Hazards. PennState Extension website. http://extension.psu.edu/business/ag-safety/health/e26. Published 2017. Accessed February 1, 2017

Also, please feel free to check out a simple post that summarizes this type  of information: Occupational Respiratory Diseases: The Farmer, His Lungs, and Mold


Blood Group Notation In a textbook, I encountered a notation used when writing blood groups down, which was "I" with the blood group type as a superscript. I was curious as to why the letter "I" is used in this notation and what it means. E.g. Iᴬ and Iᴮ.

Thanks.

Those are names of alleles involved in the ABO blood group system. The “I” stands for isoagglutinogen which is an antigen that causes agglutination of blood cells when reacting with a specific antibody (an isoagglutinin).


EC number classification of synthase? It is quoted in wikipedia that:

  Following the EC number classification, they belong to the group of ligases , with lyases catalysing the reverse reaction.

And we all know that enzymes are biocatalysts which catalyses reaction in both forward and backward directions.

So my question is that how can the reaction in one direction catalysed by one enzyme and in reverse direction catalysed by other enzyme? If we assume that they are telling that one direction synthase acts as ligase and in other direction it acts as lyase then how can lyases have more than one substrate for reaction? Because products(more than one) of ligase acts substrate for reverse
reaction.(taking for example a ligase, glutamine synthetase as synthase)

It is also quoted from wikipedia

  Lyases differ from other enzymes in that they require only one substrate for the reaction in one direction, but two substrates for the reverse reaction.

A reasonable question, but it contains a fallacy. This is because what are referred to as the forward and reverse reactions being catalysed by different enzymes are generally not, in fact, the same overall reaction.

Consider the relationship between DNA and its constituents (or RNA or Protein or fatty acid). You may be thinking of this as:

  DNA ⇌ DNA constituents

But in fact, because hydrolysis (actually a hydrolase reaction) is thermodynamically favoured, synthesis of DNA (a ligase reaction) needs to be coupled to the hydrolysis of ‘high group-transfer’ deoxynucleotide triphosphates in order to shift the equilibrium in its direction. So the two reactions are (somewhat simplistically):

  DNA → n dNMP (catalysed by DNases)

and

  n dNTP → DNA + n pyrophosphate (catalysed by DNA polymerases)

Although in certain circumstances you can force reactions of this sort into reverse, in the cell they tend to be unidirectional, and are classified accordingly.

(In this sort of ligase reaction in the cell there is a further factor affecting the observed direction. That is the presence of pyrophosphatases that catalyse the thermodynamically favourable hydrolysis of pyrophosphate to orthophosphate, removing the former.)

Coda: Is the reaction in the reverse direction from a ligase necessarily catalysed by a lyase?

Although not affecting the principle expressed in my answer, I think that the latter part of the statement quoted from the Wikipedia page that “(synthases)...belong to the group of ligases, with lyases catalysing the reverse reaction” is not generally true. As mentioned above, the enzymes catalysing the reactions in the reverse direction from ligases involved in ‘polymerization’ are generally hydrolases (EC 3.1...), not lyases (EC 4...). I couldn’t immediately find an example of a lyase that fitted this description. You can peruse the links on this authoritative page if you wish to follow this up.


Can Serous inflammation on pleura pulmonalis cause dry cough and runny nouse? I am interested in the mechanism between the dry cough and runny nose (serous inflammation) here.
I started to think how Acute respiratory viral infection is causing the dry cough.

The serous membrane, pleura pulmonalis, connects diaphragma to pars basalis pulmonalis.
It can be the source of the serous inflammatory response spreading to the nose probably.
There must be some source of inflammatory responses such that reflex arches can use them fast, thinking physically.

Assume medication Montelukast (stop asthmatic symptoms), codeine (to stop irritated dry cough) Flixotide (with Montelukast).
Assume that there is a diaphragm press on pars basalis pulmonalis.
Assume you breath mostly by abdomen 15 minutes in the supine position.
Assume opposite-astonic person in thorax.
You then feel that you exhale too much - the serous membrane pushing on pars basalis pulmonalis - serous inflammatory response in pleura pulmanalis.
The breathing process moves thoracic muscles and thoracic cavity gets shortly extended only little.
Negative tensor on lungs i.e. the volume of the lungs is getting smaller.
Consequently, a cough reflex arch and sympaticus start a deep dry cough to protect lungs.

Characteristics of the pathway against Acute respiratory viral infection

serous inflammation on pleura pulmonalis
serous membrane pleura pulmonalis presses on pars basalis pulmonalis
negative tensor on lungs
cough reflex arch and sympaticus
dry cough
positive gradient on the pleura spreads inflammatory response through the surrounding lymphatic system is sensed as dry in larynx
negative gradient is sensed on the nasal mucosa membranes as serous inflammation (runny nose)

Can the serous inflammation of plera pulmonalis cause a deep dry cough and runny nose?
The cause of this inflammatory response can then be Acute viral respiratory infection in some part of the lungs.

If serous inflammation produces a large amount of serous fluid this leads to lung compression and limitation of respiratory movement. This, as you said produces dry cough by means of reflex arch.

However lung compression leads to alveolar collapse or atelectasis through pleural effusion. After atelectasis, pneumonia can develop quickly as a complication.

And nasal congestion is a symptom of pneumonia. Also if pneumonia develops, the cough, initially dry and reflex, will turn to cough with mucus expectoration.

Cough stimulates nasal congestion when it brings up mucus from the lungs and extends the alveolar inflammation up to the nose by taking and concentrating all the bacteria in the upper airway (pharynx and larynx bacteria gets in the nasal sinuses) - and in case of bacterial pneumonia mucus also contains the etiologic agent of that pneumonia (so not only from the upper airway).


How do Sertoli cells protect sperms? I was reading Developmental biology by Gilbert and stumbled upon a fact that Sertoli cells provide protection to the developing sperms with no futher explanation.

I googled it and found a few books mentioning that it protects sperms from cell mediated immunity and antisperm antibodies. Yet I found a website called fertilitypedia that said:

  Sertoli cells do not only control the process of spermatogenesis, but they are also responsible for creating so called immunologically privileged area in the testicles. It means, that Sertoli cell manage to keep blood separated from seminiferous tubules through the connection between them, called tight junction. Tight junction keeps bloodborne substances from reaching germ cells, so all stages of germ cells are protected from the body immunity. Tight junction also keeps surface antigens found on developing germ cells from eluding into the bloodstream so no autoimmune reaction could happen. Since Sertoli cells form the block between the blood and lumen of seminiferous epithelium, they are also in control of the entry and exit of nutrients, hormones and other chemicals into the tubules of the testis.

I'm unable to verify this explanation from the cited sources as none contain the mentioned information.

So my question, how does it actually protect the sperms?

The Wikipedia pages on Blood-testis barrier and Sertoli cells have some information relevant to your question, with some academic references included.

You could also search for reviews on Sertoli cells on Google Scholar - several of the first returned results seem relevant, if you are able to access them.


Why are melodies/harmonies perceived as pleasurable by humans? Is there any evolutionary advantage to finding melodies or harmonies pleasurable? Does the ear pick up these particular oscillating waves differently from other sounds, and if so, how does that affect our perception of pleasure? I'm looking for some sort of signalling pathway (most likely involving neurotransmitters I realize).

There are strong connections between the auditory cortex and the limbic system, which includes such structures as the hippocampus and the amygdala.

A recent paper [1] builds on earlier notions of emotional "significance" of music without any lyrics.  It adds in lyrics, so giving a perspective of which portions of the brain are reacting to which component of the music.

  Additionally, contrasts between sad music with versus without lyrics recruited the parahippocampal gyrus, the amygdala, the claustrum, the putamen, the precentral gyrus, the medial and inferior frontal gyri (including Broca’s area), and the auditory cortex, while the reverse contrast produced no activations. Happy music without lyrics activated structures of the limbic system and the right pars opercularis of the inferior frontal gyrus, whereas auditory regions alone responded to happy music with lyrics.

One of the limitations of this particular study is that the subjects self-selected their own pieces, which may limit the reliability of the results.  Of course, defining "happy" or "sad" for every individual is slightly subjective and difficult.  They cited an earlier "pioneering" study which standardized the musical selection between subjects.  Without consideration of the lyrics:

  The first pioneer study using functional magnetic resonance imaging (fMRI) by Khalfa et al. (2005) chose a controlled manipulation of two musical features (tempo and mode) to vary the happy or sad emotional connotations of 34 instrumental pieces of classical music, lasting 10s each. Sad pieces in minor-mode contrasted with happy pieces in major mode produced activations in the left medial frontal gyrus (BA 10) and the adjacent superior frontal gyrus (BA 9). These regions have been associated with emotional experiences, introspection, and self-referential evaluation (Jacobsen et al., 2006; Kornysheva et al., 2010).

As an aside to answer your final thought, in cases like this I think trying to jam everything under an umbrella of one "neurotransmitter system" or another can make things overly simplistic to the point where you lose focus of the diversity of receptors expressed.  You can say a system is driven by Dopamine, but D1 and D2 receptors have exactly the opposite effects on the neuron.

  [1] Brattico, E., Alluri, V., et al (2011) A functional MRI study of happy and sad emotions in music with and without lyrics.  Frontiers in Psychology, 2: 308.  doi: 10.3389/fpsyg.2011.00308 (free pdf)

(see also, http://www.sciencedirect.com/science/article/pii/S0028393206003083 and related)


What are "primary amino acids and secondary amino acids"? Context: analysis of amino acid content using reversed-phase HPLC In a Russian document I'm translating, an HPLC system is used to analyse the amino acid content of a substance.

The detector wavelength is set at 262 nm for "secondary amino acids" and 338 nm for "primary amino acids". But what are those?

I googled and found a lot of mentions with exactly these wavelengths being used, but I haven't been able to quickly understand how a "primary" amino acid differs from a "secondary" one. Is it that the secondary amino acids are the products of the destruction of the primary amino acids (those that initially existed in the substance)?

What is the difference between a "primary amino acid" and a "secondary amino acid"?

I would guess that 'secondary' refers to amino acids that have been derivatized in some way, possibly by reacting with o-phthalaldehyde. (To measure the fluorescence of an OPA-derivatized amino acid, you excite at 340 nm, so I presume the derivative will absorb at this wavelength?).


Speciation by polyploidy Speciation can occur by polyploidy. My understanding of the process is as follows:

'polyploidy is when the number of chromosomes in an organism's cell doubles. This means that the organism has more chromosomes than other individuals of the same species, meaning it cannot mate with other individuals. The polyploidy organism then evolves, eventually leading to it becoming a separate species'.

I realise this may not be exactly correct. Is someone able to provide a better description of speciation by polyploidy?

By definition, polyploidy just means that a cell or organism contains more than 2 pairs of homologous chromosomes (or is more than 2n). This is more common in plants than it is in animals. The plant, as shown below, undergoes failed meiosis, which means that the diploid (2n) cells never become haploid (n). As a result, a plant ends up with more than 2n when it self-polinates. The shown result is tetraploidy (4n), but there are other possible results (3n, 5n, etc).

Multiple plants within a population can end up with the same polyploidy number. They can then reproduce with each other but not with the original plants or any other plants. As a result, they become biologically isolated from the original group of plants and are considered a different species. It is a type of sympatric speciation, which means that it occurs without geographic isolation.


Is the Klein's bottle a good analogy to the relation between T-tubule and sarcolemma? I am not quite seeing how the T-tubule and sarcolemma is connected. It says that the T-tubule is an "invagination" of the sarcolemma, which is sarcolemma folded from the inside to form a T-tubule

Can someone verify whether the following picture is a good presentation of this relationship?

If we're looking at diagrams for the t-tubule with respect to the sarcolemma, we see the two are actually fused:

The function therein is to allow depolarization to penetrate the interior of the cell quickly. The surface isn't transected anywhere, it simply folds inward. You can visualize this by sort of pushing a hole through some putty with a finger, and making a hole to the other side. Really no need to upvote me here, just easier to paste images in answers.


A question on exclusion of study participants for an Exome genotyping array I'm reading a paper that used whole exome sequencing on an African
 American and European populations to discover novel low frequency and
rare variants associated with lipid levels & the risk of coronary
heart disease.

They used the Illumina Human exome genotyping array that was designed
based on coding variants discovered from sequencing the exomes of
12,000 individuals. Therefore, they selected their participants from a
study who were not among the 12,000 individuals utilized to design the
array .

My question is: Why would they select individuals who were not among
the 12,000 used to design the array? (I'm thinking because maybe it
could produce false positives associations? bias?)

When you design the arrays, you need to have probes on the surface complementary to the sequence you want to detect. Depending on what you want to detect, you need to design these probes with known sequence on a known position.
If you want to detect single nucleotide polymorphisms (SNP), then you need a library of known SNPs on your ChIP, which are basically the position of the SNP and the surrounding sequence.

SNPs can be roughly grouped into two subgroups, common (I call them like this) and rare (frequency in the population lower than 0.1%). The problem with this ChIP based method is that it can only detect SNPs which are already known (or at least are located close to known SNPs with which they in linkage disequilibrium). So if you want to detect rare SNPs in your population sample, you need a big group of people from which you take the SNPs into you ChIP design. If you look at the numbers, one rare variant will only be present in about 12 of the 12.000 persons used in the design.

Your study group is then different from the group of people, which where used to make the ChIP design. Here you take people with a certain background (high lipid levels for example) and then compare, if people which had coronary heart problems have SNPs in common which might be connected to this disease. This can help to identify a mutation in a protein which is the risk factor.


Do mosquitos vary in toxicity? I already had a question about dealing with mosquitos: Really virulent mosquitos - dealing with them and their bites

But this question is about whether they really do vary in virulence and toxicity. A few people in the other question suggested I am naturally a target and react badly to bites. However:

I haven't in other locations had such big reactions, I get nasty lumps but not swellings several centimetres across
My wife gets even worse reactions, e.g. her whole calf went red and swollen from a single bite - and I currently can't clench my fist because one bite made it swell up!
several other people, including a gardener and a tree surgeon who both deal with such things all the time, have commented they react particularly badly when working in our garden

Interestingly this summer I am reacting differently than this time last year - bigger swellings but less itchy and no weeping wounds. This may be due to the difference between midges and mosquitos.

So - are there a large number of sub-species prevalent in the UK (NE UK specifically) or can a given population become more nasty for some reason?

This is more a biological (immunology, serology) question, than one about gardening. It is possible that mosquitoes vary in 'toxicity', however I think the greatest part of the reaction is caused by yourself (no offense, I am prone to allergic reactions to mosquito bites too). So the chemicals that enter your body can vary per mosquito species (or even individual), which can trigger a milder or worst reaction. Just like different pathogens (bacteria, viruses) can also trigger different reactions (influenza can be innocent or deadly). But it is more likely that your own immunological 'state' is causing a worst reaction. For instance if you also have hay fever, levels of immunological molecules (etc. cytokines, chemokines) are already high in your blood and cause a larger or more intense reaction than in periods when less of these molecules are present in your blood.


Ammonia smell after physical exercise? What is the explanation? After exercising vigorously one can sometimes smell ammonia and it feels like it's coming from within the nose actually. There is no indication that others can smell it when I do (i.e. seems to be internal rather than external). I know I'm not the only one experiencing this, but I was wondering what the physiological processes are that are responsible for that?

Also: is this merely a perceived smell or is there actually ammonia in/on my body after the exercise.

There are two explanations which come to mind answering your question:

I asked if you eat a lot of protein, because the amount of protein which some body builders consume leads to renal failure. And one sign of renal failure is the smell of ammonia. It's a quite common problem. But I don't think this applies to you. Your protein intake shouldn't exceed 2g per kg of body weight per day, some body builder eat up 4g per kg.

Ammonia is normally linked to your protein metabolism, which is higher during and after sport. The smell of Ammonia can occur when your carbohydrate reservoir is depleted and the body is mainly using protein as fuel. This effect also occurs when fasting or in patients with diabetes.

Try to keep your blood sugar level raised during exercise by eating something, like a banana, powerbars (also known as high energy bar) or directly dextrose. Or eat more long-chain carbohydrates. And this always depending the form of sport you are practicing. Just like the pasta party prior to marathons.


Why can't we move our toes and some fingers separately? In our feet, other than the large toe, the other toes cannot be moved separately. If we try to move them, then all the four toes move together. We cannot move each toe by itself.

Same thing occurs in the hands of some of us, where we cannot move the little finger by itself. While folding the little finger, the ring finger before that also has to be folded to some extent, and vice-versa.

An explanation to the problem with the ring finger and the little finger can be found here.

The phalanges make the toes. Are the phalanges of the small toes connected, such that we cannot move them separately?

A relatively new area of the brain's cerebral cortex evolved to enable humans and other primates the necessary small motor skills to pick up small objects and deftly use tools, scientists now say. https://www.youtube.com/watch?v=zyl6eoU-3Rg

Primates can move their ears too, here's a theory of it. Other motor skills that are not often developed are individual eyebrow movement, pectoral flexing, ability to sneeze with your eyes open.

Hand movement is new and developing compared to chimps.

Toe movement is latent and receding.

The human hand is built up onto a squirrel/clawed paw, If you take a while to rotate your forearm and the flexors of the fingers, you will see that it's a mutated simple flexing mitt thing with with a new fine motor dexterity that you use all day, added on top of the vestigial clawing and grasping hand.

https://www.youtube.com/watch?v=vlwAoKpSI7s

This page says:
Signals generated in the primary motor cortex travel down the corticospinal tract  through the spinal white matter to synapse on interneurons and motor neurons in the spinal cords ventral horn. Ventral horn neurons in turn send their axons  out through the ventral roots to innervate individual muscle fibers.

The motor cortex is subject to plasticity and remapping. To know this question is beyond my field of knowledge, someone else can go on from here :) you'd have to learn about the motor cortex, plasticity, vestigial nerves, nerve mappings, it's a fantastically complex topic.

What's interesting is the variety and quantity of different muscular abilities that are inherited by a population, it reflects an optimized level of evolutionary plasticity and specific types of variety of useful traits like muscle and joint proportions to ensure fast and flexible species development.


Zygosity and Strands I am not a biology expert but I have done some homework on understanding alleles, chromosomes, dna in the human genome. Still baffled by a question though:

As I understand it at a particular locus for e.g. if a human has a A on one chromosome and a G on another that individual is considered Heterozygous at that locus because of the difference in the nucleotides (A/G in this case).

However, my question is. What about an individual that has an A on the 3' -> 5' strand (and hence a complement T on the 5'-> 3' strand) on one chromosome but T on the 3'-> 5' (and its complement on the other strand) on the other chromosome. Is this individual considered heterozygos or homozygous?

Basically my question boils down to does the "directionality" of the A-T pairing matter on both chromosomes?

I was thinking it should as only one strand can code for genes which the other doesn't so it should matter whether the A is on the (3'-5') or on the other strand..

Any advice would be great!

The directionality of the strands matters, because genes can be encoded on both strands of a chromosome (each strand can be read in 3'-5' direction by RNA polymerase). Therefore someone with the A-T case you described is also heterozygous.


Height and natural selection in humans? I watched the documentary "Evolve" recently and in the segment on "size" Scott V. Edwards, Harvard evolutionary biologist mentioned the idea that humans might evolve to be 7' tall in 'hundreds of years'. (I think this may have been taken out of context... I have emailed him to find out, but do not expect a response from someone so busy)

The reasoning goes that the trend in the past 100 years has been greater height, and women show a strong preference for men who are taller than they are. (Though a large share perhaps all of this difference has been due to diets higher in protein at an early age)

I wonder, though, if this is only part of the story. The preference women have is not just for tall men, but for a man who is taller than she is. Likewise, men seem to prefer woman who are shorter than they are. There is even cultural pressure: the classic western image of a couple on wedding cake always shows a man who is about 4" (to scale) taller than the bride.

Thus, women who are short have an advantage as they have a greater pool of men to choose from. (Colloquially, simply ask any 6' tall woman if she feels her height helps her find dates.)

Let's say that men seek women who are shorter than they are, but no more than 8" shorter. Women seek men who are taller than they are but no more than 8" taller. Given that the current average height for men is 5'8" and for women it is 5'4" (and distributed normally SD 2.8") will we have selective pressure that leads to greater or lesser height? (This is, obviously, oversimplified, but it is a starting point.)

@kate has what is probably the more correct answer for the observed pattern.

But as an experiment, I set up a basic simulation to approximate the conditions that you lay out:

Starting mean heights of 5'8" (172.72 cm) and 5'4" (162.56 cm) with standard deviations of 2.8" (7.112 cm). I used cm, because it's easier than dealing with inches.
Males will not mate with females that are taller than themselves.
Females will not mate with males more than 8" taller.
Males will not mate with females more then 8" shorter (follows from #3 above).

The problem that I quickly ran into was that, by truncating part of the normal distribution, the variance in height at each generation gradually decreased. After about 20 generations, the means weren't evolving because there was so little variation in height.

Human height is one of the most studied quantitative traits, going back over 100 years to some of the very first statisticians (Fisher, Galton). Height is a polygenic trait with very high heritability (h2 = 0.8)1. Genome-wide association studies have reported 54 genes involved in determination of human height2.

Imagine that each of these 54 genes has just two alleles: a and b. a gives a +1 to height. b gives a -1 to height. So aa would be +2, ab or ba 0, and bb -2. The sum of all those alleles is correlated to height. So if all 54 were aa, then the height would be +108.

The problem comes in when people only mate with taller people. Over time, the proportion of b's will decrease, and the proportion of a's will increase, but only to a point. Once all the alleles are fixed at a, there won't be any room left. The genetic variation will be exhausted. Without the input of new alleles, height will cease to evolve.

1 Lettre, G. 2011. Recent progress in the study of the genetics of height. Hum Genet 129:465–472.

2 Visscher, PM. 2008. Sizing up human height variation. Nat Genet 40(5):489-90.


From 46 human chromosomes, is each one from a single parent? Humans have 23 pairs of chromosomes. Each chromosome in pair is homologous to another one in pair.

Does this imply, that the entire chromosome in any cell is obtained from only one parent? I mean entire single chromosome from one parent, and entire homologous one -- from another parent?

This is obviously true for sex chromosomes, especially in boys. They get Y from father and X from mother.

Is similar true for any other pair of chromosomes?

Or they are exchanging genes during mitosis too?

I.e. parents data is distributed grouped by chromosome or by gene?

Yes, each single chromosome came from one parent.  However, it is not true that each chromosome came from one grandparent.  Due to crossing over in meiosis, the copy of Chr 1 that you got from your father is partially from his father, and partially from his mother.  And the same for all the rest of your chromosomes.  You will not pass on a whole chromosome as you inherited it onto your children, crossing over will happen in your gametes, so that your kid will get whole chromosomes that are part from your mother, and part from your father.  The sex chromosomes are exceptions, because in men, they can't do crossing over, since men have a mismatched pair.  (At least in biologically "normal" men.)


Changing the definition of life? Viruses at this period of time do not fit the current definition of life.

Much of the reasoning behind this is that we currently believe that all life must be made up of cells.

Also, many biologist/scientists say that viruses are not living because all they are is just chemicals carrying out their predefined chemistry.

Has anyone every considered the fact that cells, the supposed building blocks of life, themselves simply only carry out predefined chemical actions? All actions cells carry out are chemically driven, not consciously or spiritually driven. Cells do not make choices, they follow chemical directions present in their DNA and RNA. Viruses act very similarly, following the action transcribed in their DNA or RNA.

How can we really even draw a defined line of what life is?

How can really even draw a defined line of what life is?

It's easy, really: just make one.  In the answer I linked to I go into the reasons why viruses aren't alive (spoiler alert: no ribosomes) and what our current definition is, but the bigger question is why does it matter?  We can draw the line wherever we want to, but it's still an arbitrary construct placed onto the universe by humans so we can sleep at night.  It's similar to intelligence.  We draw arbitrary lines around primates and dolphins and elephants and pigs and what have you, because they're the smartest and most thinking, but that's only for our own (legal) convenience.  Intelligence and awareness is a spectrum, there needn't be a point beyond which you "count."  There's no reason life can't be the same way.

Edit 1.5 years later to add a short, somewhat fanciful video I just watched, it goes into some of the complexity and difficulty with defining life; viruses show up about half way through.  It waxes philosophical toward the end, but that's sort of my point.  Arbitrary delineations are just that.


Purpose of intensive protein synthesis in G1 phase of mitosis What is the purpose of intensive protein synthesis in G1 phase of mitosis, and what purposes do these synthesized proteins serve? Why are lipids and carbohydrates not synthesized intensively as well?

The G1 phase of eukaryotic cell cycle is part of interphase, which is when the cell is replicating its DNA ready for division. To understand the need for intense protein synthesis, we first need to understand how DNA is organised during mitosis.

Before DNA is condensed into chromosomes ready for nuclear division it is in the form of chromatin, a long fiber-like structure inside the nucleus. In order to condense into chromosomes, this chromatin must undergo a process of coiling and folding in order to create the chromosome 'X' structure we are familiar with.
A major part of this DNA 'miniaturization' is the folding of the double helix around proteins called Histones - this creates new structures called nucleosomes.

In order to fully condense the roughly 3 meters of DNA in the average human cell down to a singular chromosome, millions upon millions of these Histone proteins are required.

And that answers your question; intense protein synthesis during the G1 phase is required in order to produce the extremely large amount of Histone proteins that are needed for packaging DNA into chromosomes ready for cellular division.

As for carbohydrates, these are constantly being processed by the body in order for the production of ATP for use as energy. The use of said energy for mitosis is a just another constantly required use of ATP within the body. Therefore there isn't any noticeable increase in carbohydrate processing/production, as it is happening regardless of the cell's stage in its cycle.

-See the image below (from shmoop.com) that explains the process of getting DNA into a chromosome.


How does an axon "know" it's not connecting to its own neuron? I recently read about an experiment where they removed the dendrites and axons from rat neurons and placed them on a grid. After a while they started reconnecting and were able to learn things.

Since I'm trying to create a model simulating this, I'd like to know (as much as is needed to make it look at least a little bit realistic) how they reconnected. As far as I know some molecules are secreted attracting or repelling axon growth cones.

I think I can model that part, but the problem is that the axons can easily grow back to where they came from, so how do the axons in a brain 'know' they are not growing back to the neuron they originated from.

I think I can partially answer you question. As far as I'm aware, there are many surface receptor molecules such as ephrins that are responsible for axonal guidance and dendritic repulsion in developing organisms such as flies (Drosophila). As you can tell this is extremely crucial since its important for neurons to spread their dendrites and axons as far as possible, evenly spaced out with axons bifurcating (separating) correctly and not sticking together. This is for example important in the Drosophila brain for axonal projections into different lobes.

One such surface receptor, which helps achieving the above is Dscam (Down syndrome cell adhesion molecule) (schmucker et al 2000 Cell). Dscam gene is expressed in over 38000 isoforms (through complex alternative splicing of Dscam mRNA) in flies. It is the homophilic binding and subsequent repulsion of Dscam protein isoforms that enables an intrinsic self-recognition for repulsion of same-cell axon. As far as I understand it, if a number of similar Dscam isoforms are present on axons or dendrites of a neuron, this is self recognised and the dendrites and axons get repelled from one another. This is the molecular pathway that ensures sister dendrites are not adhered together or become concentrated in one area.

In the absence of Dscam or when Dscam protein isoform diversity is removed flies die during larval stages and the early embryonic axonal patterning of the fly nervous system is clearly disrupted. In the absence of Dscam protein, Bolwig's axons exhibit frequent axon pathfinding errors at a specific intermediate target. Most of these processes are conserved in mammals.

For further information please look at Schmucker & chen, 2009 Genes and Dev


How can there not be purpose movement in the fetus until week 18, when a fetus can open its mouth and suck its fingers at week 11? According to Fetal Movement

  According to an overview produced by the Royal College of Physicians
  of Edinburgh, purposive movement begins at about 18 weeks, gradually
  replacing reflex movements

but in the same article says

  At week 11, the fetus can open its mouth and suck its fingers; at week
  12, it begins to swallow amniotic fluid.

I highly doubt that open a mouth and suck its fingers can be classified as "reflex movements", then how it is asserted that there is not purpose movement in the fetus until week 18 when a fetus can open its mouth and suck its fingers at week 11?

Swallowing (Nishino, 2013) and sucking (rooting reflex) are reflexes. The fingers may just happen to be in the vicinity of its oral region (they often are; Fig. 1.), and oh boy are babies keen to grab a nipple when it's close! Mouth openings can henceforth be also reflexive, being part of the rooting reflex.

Fig. 1. Fetal hands in facial area. sourceL: ABC News

Reference
- Nishino, Front Physiol (2012); 3: 4892013


Why are sponges sometimes not considered multicellular? I read somewhere (I can't find where) that there is no scientific consensus whether sponges should be considered multicellular organisms.

It seems I don't understand where is the line between unicellular and multicellular life.

I am not able to find a more elaborate explanation of that doubt. What are the reasons for it?

Sponges are generally considered as colonial organisms because there is little cell specialization and little separation of function/role. All cells do pretty much the same thing; it looks more like a pile of individual cells than an actual multicellular organism. In reality it is a little bit in between.

In any case, what one wants to call multicellular or unicellular is a matter of definition and preferences. You cannot find the line between unicellular and multicellular because there is no such line that would not be very arbitrary and filled with special cases.

You can study a little more the physiology of sponges and then decide for yourself if it looks sufficiently like a multicellular organism or more like a colony of cells (a colonial organism).


Can anyone Id this flower? Small pink flower, started out as tiny buds, leaves look almost like Maple leaves..

It's a mallow.

The leaves - they look like maple leaves - and the flower are identical.

Mallows are from the family Malvaceae, which includes food plants (okra, cocoa beans, kola nut), economic plants (cotton), and ornamentals (e.g. hibiscus) One species of this family (Althaea officinalis) is actually the original ingredient to make marshmallows.

I'm not sure which mallow it is (there are 243 genera with 4225+ species), but it's a common weed wildflower all over the world.


Is there sufficient evidence that human cells are not intelligent? Being structurally composed of one or more cells, which are the basic units of life.
Yet within a cell, there seems to be the same behaviors that define life:

Regulation of the internal environment to maintain a constant state;
Organization: Don't most cells have organs?
Metabolism.
Growth ~ not sure about this one.
Adaption ~ Think this is accurate, but I'm not well versed in cellular biology at all.
Response to stimuli. Cells interact with external whatnots.
Reproduction - Cells do this, at least many of them.

Most of what lead me to this question came from chapter 5 of Spontaneous Healing by Andrew Weil, M.D.. I'll type the parts relevant to the discussion below - in case he's wrong and I'm basing my thoughts on wrong information. bold sections indicate my interjection

DNA takes the same form in all organisms, from human beings to viruses - an enormous molecule with a double-helix structure made up of two chains of sugar molecules, with "rungs" linking the two chains. The rungs form between complementary pairs of nitrogen-containing subunits 'nucelotides', whose specific sequences differentiate the DNA of one organism from that of another. Only four different nucelotides occur in DNA; they are the "letters" of a genetic code spelling out "words" of information that direct the construction and operation of all forms of life. The so-called Central Dogma of modern molecular biology states that DNA replicates itself in order to pass its genetic information on from one cell to another and from one generation to the next reproduction; DNA also transcribes its information into another macromelecule, RNA, that can travel out of the cell  nucleus; RNA, in turn, transslates this information into the manufacture of specific proteins that determine the structure and function of organisms. regulation? These three processes - the replication, transcription, and translation of genetic information - are the most basic processes of life. They are also amazingly intricate and risky, because there are so many points at which things can go wrong.

Snipped for relevance.

Therefore, sophisticated mechanisms have evolved for the repair of this molecule in order to assure nearly error-free transmission of genetic information from one generation to the next, even in the simplest forms of life. organization, regulation, reproduction - evidence of response to stimuli?
All of the mechanics of replication, transcription, and translation are directed by a special class of proteins called enzymes. A great deal of the genetic code specifies the manufacture of enzyme molecules, which, in turn, oversee the chemical reactions that develop the genetic code into biological reality. evidence of intelligence?

much snipping.

In practical terms, they (enzymes) function as ingenious machines that alter the substrate molecules: cutting them apart, putting them back together, snipping particular pieces off them, adding others back, all with astonishing precision and speed.

more snippage

Therefore, polymerase I actually proofreads its own work, editing mistakes as it directs the synthesis of new copies of DNA.

He goes on to talk about plasma membranes, which seem to be how cells interact with the "outside" world..

You seem to be asking if single mammalian cells are capable of intelligence. Yet, in your introduction, you mention that within a cell there are these seven characteristics that are fundamental in defining life. Then, you target more of your supporting quotations and interjections toward the definition of life. Of course cells are alive. You are alive, and so are the bacteria on your skin. Your title question is:

  Is there sufficient evidence that human cells are not intelligent?

You have strayed from your question in your line of reasoning. Let's get back to answering the title question.

Is there sufficient evidence that human cells are not intelligent? The definition of "intelligence" is controversial, but let's look at Wikipedia:

  Intelligence has been defined in many different ways including, but not limited to, abstract thought, understanding, self-awareness, communication, reasoning, learning, having emotional knowledge, retaining, planning, and problem solving.

Human (or any mammalian, fungal or bacterial) cells are able to communicate, and solve problems, but most likely lack abstract thought, understanding, self-awareness, reasoning,  and emotion. Retaining and planning are somewhat more difficult.  Cells are able to retain information about a state of "being" and transmit that to progeny, a recent phenomenon known as epigenetics. Does this qualify as retaining and planning? I don't know. Cells also change based on environmental pressures through stochastic processes (a process known as evolution). Does this qualify as learning? Probably not, since the changes are usually pre-existing. The human equivalent would be finding out that you can swim by falling into water and not drowning. Did the person "learn" how to swim, or did they already possess an aptitude for it?


RF Cautery DNA damage? I'm concerned about the safety and mechanism of RF cautery. The frequency of the radio waves used is 4Mhz so normally there should not be any DNA damage BUT the thing you read everywhere is that only UV, X-rays and Gamma rays have enough energy to pop an electron from the orbit. Can't the same energy be reached with radio waves (higher amplitude instead of higher frequency). After all the RF cautery evaporates the cells why wouldn't it damage the DNA of the remaining cells?

The thing about DNA is that it's very durable, compared to the rest of the cell. It's not too difficult to extract DNA from cooked and processed food, even though the definition of "cooked" is "denatured and broken many of the proteins in the cell". The long DNA strands may be broken into long pieces, but overall the DNA holds up very well to heat. There's no risk of DNA damage to neighboring regions with RF radiation because the primary way RF energy destroys DNA is through heating, and at the temperatures where DNA starts to accumulate damage the cell around it is cooked/destroyed.

The quantum explanation for why ionizing radiation can destroy DNA is that high-frequency radiation is powerful enough to zip through the surrounding tissue and break/damage individual DNA molecules. Individual radio photons can't "gang up" on a DNA strand to do the same thing because of how quantum mechanics works, so you won't be able to break the strand or damage the bases without high-energy ionizing radiation.

Metaphorically speaking it's like trying to get at a peach pit. Ionizing radiation is like a knife, it zips through the flesh and can get at a peach pit without damaging the peach much. RF radiation is like a belt sander. You can definitely get at the peach pit, but you'll cause a lot of collateral damage doing it.

Mutations or DNA damage that might cause cancer can only happen to cells that are alive that receive DNA damage. If the DNA is damaged by heat, the cell around it is dead, and that DNA damage doesn't really matter.

I encourage you to read about ionizing radiation and the photoelectric effect.


Negative feedback loop and oscillations According to the textbook Alberts Molecular Biology of the Cell (5th ed., p. 902), negative feedback loops cause oscillations when they are long delayed. I just can't figure out why.

Except for that, in case of short delayed feedback, the inhibition doesn't seem to be full and to go down only mid-way, according to the attached plot. Why?

For that you would need to understand the dynamical systems theory behind the loop. The point at which the oscillation starts is called the Hopf-bifurcation. I shall explain this in simple intuitive terms. Lets assume that Protein-X activates the production of Protein-Y which in-turn causes inhibition of Protein-X production. This is a negative feedback loop.

X → Y
Y ⊣ X

Situation-1: No/little delay

You switch on the production of X. This leads to rapid production of Y which will in-turn quickly repress the formation of X. This would happen so quickly and all that would be observed is a reduction in the steady-state level of X (compared to an unregulated system). Mathematically, the eigenvalues of the system (jacobian matrix- denotes the slope of the function) evaluated at the steady state would be negative and real.

Situation-2: Some delay

In this case, it will take some time for Y to accumulate. This will cause X to shoot up above its final steady state level. This, in-turn, will cause higher production of Y. Because of higher production of Y, X will start getting repressed strongly when Y gets accumulated and starts acting. This will cause X to shoot down below the steady-state but the magnitude of this shoot-"down", will be less than the first shoot-"up". Finally, the system will settle to the steady state. This phenomenon is called damped oscillation. In this case, the eigenvalues of the jacobian are complex with negative real parts.

Situation 3: long delay

In this case the delay between production of Y and its action is so high that the system does not damp but sustains its oscillations. The eigenvalues of the jacobian are imaginary. These kind of oscillations are generally sensitive to different factors.

More robust forms of oscillations exist, called limit cycles. The network structures responsible for this are more complex than a delayed negative feedback loop. Typically it has a coupled positive and negative feedback. Understanding limit cycles is little bit more complicated and I shall not discuss them here.

Also, check out these reviews:

Tyson, John J., and Béla Novák. "Functional motifs in biochemical reaction networks." Annual Review of Physical Chemistry 61 (2010): 219.

Tyson, John J., Katherine C. Chen, and Béla Novák. "Sniffers, buzzers, toggles and blinkers: dynamics of regulatory and signaling pathways in the cell." Current Opinion in Cell Biology 15.2 (2003): 221-231.

and this book:

Alon, Uri. An introduction to systems biology: design principles of biological circuits. CRC press, 2006. ISBN 9781584886426


Do all Gram negative bacteria cause septic shock? Do all Gram negative bacteria cause septic shock? If they don't could they if you attacked them with an antibiotic that could lyse the cell? For example any antibiotic that attacks the cell wall, although I suppose that could be difficult with the gram negative wall, not to many gram negatives are susceptible to a wall attack.

all Gram negative bacteria can potentially cause septic shock, but septic shock is not limited to Gram negative cell wall lipopolysaccharides. Any infectious agent can cause septic shock, including gram positive and gram negative bacteria, fungi and even viruses (this is quite evident in the recent Ebola outbreak).[1]

The causative agents for sepsis/septic shock have evolved. Originally strongly considered to be related to Gram-negative bacteria, that is no longer the case. About 25 years ago, sepsis was considered to be a response to endotoxin thought to be relatively specific for Gram-negative bacteria. That Gram-negative bacteria were the most common causes of sepsis[2] resulted in trials that focused on  specific therapies for G negative endotoxins.

It is now recognized that sepsis may occur from bacterial, fungal and viral organisms. More recent epidemiology studies reveal that Gram-positive bacteria have become the most common cause of sepsis in the past 25 years. According to the most recent estimates in sepsis, there are approximately 200,000 cases of Gram-positive sepsis each year, compared with approximately 150,000 cases of Gram-negative sepsis.[3]

Fungal causes of sepsis have also grown at a rapid pace. Why this occurs may be two-fold: a general increase in nosocomial (hospital acquired) cases of sepsis, and more effective treatment of bacterial infections, thus promoting fungal infections to a more leading role. The increase of fungal nosocomial infections has also shifted away from the common Candida albicans organism to the more recalcitrant torulopsis, glabrata and krusei subspecies.[4]

So while the Gram negative Lipopolysaccharide or “endotoxin” is unique to Gram negative bacteria, cell components of Gram positive bacteria have been identified that appear to be biologically equivalent to endotoxin in stimulating the inflammatory response associated with sepsis and septic shock. These include a peptidoglycan layer outside the cell membrane of Gram positive bacteria as well as non-peptidoglycan polymers (such as the teichoic acids). They have been shown to stimulate the release of cytokines, specifically tumor necrosis factor and interleukin-1.[5]

[1] How Ebola Kills You: It's Not The Virus
[2] Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy
[3] The epidemiology of sepsis in the United States from 1979 through 2000.
[4] Nosocomial bloodstream infections. Secular trends in rates, mortality, and contribution to total hospital deaths.
[5] Sepsis and Septic Shock
Sepsis, severe sepsis and septic shock: changes in incidence, pathogens and outcomes


Nonlinear (Quadratic) selection gradients formula Under scenarios of stabilizing or disruptive selection, we can add a quadratic component to our model of phenotype and fitness like so.

Specifically, I am not clear on where the 1/2 comes from nor do I understand the derivation of gamma, which is equal to as follows:

x is the phenotype of interest, w(x) is the fitness of said phenotypic value. uBS is the mean phenotype before selection. Any help would be greatly appreciated.

Coefficient $1/2$ is a matter of definition/convenience. One could have written $\beta x_i + \gamma x_i^2+\bar{w}$, but then a factor of $2$ would surface in the other forumals.
The other two equations are adapted to one-dimensional case (one trait) from the Lande and Arnold's paper The measurement fo selection on correlated characters. In particular, the equation with covariance is their equation (13a), which follows from their more general equation (4) for quadratic selection. The last equation is the restatement of their (14b).
Update
Here I retake the notation of the above-mentioned article by Lande, but adopt it to the case of a single trait. Then the variance matrix $P$ is just a number (variance). Equations (14a) and (13b) define
$$\gamma=\frac{1}{P^2}C, (A)\\
C=Cov\left[w, (z-\bar{z})^2\right],
$$
which is the definition of $\gamma$ in the OP. It is essential here to use the correct expression for the covariance:
$$
Cov\left[f(z), g(z)\right] = \int \left[f(z)-\bar{f}\right]\left[g(z)-\bar{g}\right]p(z)dz=
\int f(z)g(z)p(z)dz -\bar{f}\bar{g}
$$
In our case we thus have:
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - \bar{w}\overline{(z-\bar{z})^2},
$$
where $\bar{w}=1$ by definition, whereas $\overline{(z-\bar{z})^2}=P$ is the variance of the trait. We thus have
$$
C = \int w(z)(z-\bar{z})^2p(z)dz - P, (B)
$$
where
$$
p(z)=\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}.
$$
Let us now consider the integral
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} - \int \frac{\partial w(z)}{\partial z }\frac{\partial p(z)}{\partial z }dz=\\
\frac{\partial w(z)}{\partial z}p(z)|_{-\infty}^{+\infty} -
w(z)\frac{\partial p(z)}{\partial z }|_{-\infty}^{+\infty}+
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz
$$
The first two terms vanish, since $w(z)$ is bounded, whereas $p(z)\rightarrow 0$ as $z\rightarrow \pm \infty$.
We thus have
$$
\int \frac{\partial^2w(z)}{\partial z^2}p(z)dz=
\int w(z)\frac{\partial^2 p(z)}{\partial z^2 }dz=
\int w(z)\frac{\partial^2 }{\partial z^2 }\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=\\
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]\frac{1}{\sqrt{2\pi P}}e^{-\frac{(z-\bar{z})^2}{2P}}dz=
\int w(z)\left[\frac{(z-\bar{z})^2}{P^2}-\frac{1}{P}\right]p(z)dz=\\
\frac{1}{P^2}\int w(z)(z-\bar{z})^2p(z)dz - \frac{\bar{w}}{P}=\\
\frac{1}{P^2}\left[\int w(z)(z-\bar{z})^2p(z)dz - P\right]=\frac{C}{P^2}=\gamma,
$$
where we used $\bar{w}=1$, and equations (A) and (B) above.


Are there baby drinks closer to breast-milk? Many women cannot or will not feed their children with breast-milk. It is my understanding breast-milk has many advantages over formula. Some psychological like oxytocin and some physiological like advanced antibodies. Have there been any attempts to create a formula with better psychological and physiological properties? Is it even possible to include antibodies in formula or milk?

It is definitely possible to include antibodies and other biological molecules in formula to better approximate that of its mother's milk.  However, there's no way you could mass-produce this. Every mother has unique antibodies, even horomones that are the same in different people are present at different concentrations. The current "formula" on the market is good for as many people as possible.

Isolating antibodies from a mother to include in formula milk would be insanely, insanely expensive. Think thousands of dollars for a carton of formula. Not to mention the hassle of frequent blood and serum draws from the mother for antibody isolation.

So, yes, this is possible (and I wouldn't be surprised if someone with a lot of money to burn has tried it). It's not remotely cost-effective or feasible, though.


Can a chicken really be hatched outside of the egg? This YouTube video (screenshots attached) claims to show Japanese schoolchildren breaking an egg into a kind of clingfilm "hammock in a cup", and then growing and hatching a chick from it in an incubator.

Is this really real?

My first immediate thought is, "If this can happen, why don't the eggs in my cupboard at home sometimes hatch? Why do I never see an embryo in my frying pan?"

Obviously the egg has to be fertilised, but depending upon where you get your eggs (like an "organic home farm" or something) this might happen.

If it's more a matter of temperature, how warm do the eggs have to be? For how long? (ie, Could a warm kitchen cupboard in a hot summer do it?)

What other biological requirements are there to make this work?

Yes it is real, in the sense that this protocol has been through a peer reviewed journal.

Note that the embryo is developing outside the shell, not outside the egg. It is the fertilized egg that develops into the embryo. The shell only provides protection and allows exchange of gases. You can replace the shell with any other material that does the same job. Embryos of non-placental animals can grow in a petridish as well. Someone seems to have done this back in the 1980s (Scadding, 1981).

You can see a video along with the detailed protocol of this process in this article published in the Journal of Visual Experimentation.

  Why do I never see an embryo in my frying pan?

Because it has probably become an omelette.

  how warm do the eggs have to be?

37-39oC is the ideal temperature and usually hen eggs hatch in 21 days (common poultry facts). However, the incubation time can depend on other factors (including temperature) such as humidity and air composition.


Why is it that heterozygous loci appear as two separate bands during gel electrophoresis while homozygous loci appear as one band? Is it because heterozygotes have a greater base pair length? (And if they do, why is that?) Or is it because recessive alleles are moving slower than the dominant alleles in the gel?

A heterozygous locus has two different alleles and therefore it is possible that their DNA sequence lengths are different. However, it is unlikely that they are so different so as to be clearly resolved in a gel electrophoresis. Agarose gels can at best resolve 20bp; polyacrylamide gels can resolve smaller differences but it is only done for small DNA fragments.

I think upto 50bp difference is possible between alleles. But such huge insertions/deletions are rare and the difference between the alleles is usually a point mutation or small insertions/deletions(indels). Big indels are possible when a transgene is inserted specifically in one chromosome; these cases are mostly experimental.

If you consider paralogs as alleles then they can be of different lengths and can be resolved in agarose gels— usually the difference is in the untranslated regions. If you are doing Southern blot and using a probe that can bind to both paralogs then you will end up getting two bands.

Having said that, it is possible to see a difference in gel bands even if there is no size difference. This is possible by a technique called RFLP. In this technique the DNA is digested using a restriction enzyme which basically cuts the DNA at a specific sequence (usually a hexamer). If a point mutation abolishes or creates a restriction site then the fragment length would be different between the alleles. This is detectable on the gel.

A similar technique is AFLP.


Obtaining protein atomic co-ordinates from dihedral angles https://en.wikipedia.org/wiki/Dihedral_angle#/media/File:Protein_backbone_PhiPsiOmega_drawing.svg

I've been reading on Protein Amino Acid Sequences and their 3D structure. It seems that the 3D structure is encoded by the three torsion angles as shown above. My professor said there is a 1-1 encoding between 3d cartesian coordinates and the torsion angles, but I cannot find any way to do this either in pyrosetta or biopython. Is there any formulas/packages that would be of use for this conversion?

As I indicated in my comment:

You need the amino acid sequence and values for bond lengths before you could determine the atomic co-ordinates from the dihedral angles.
Originally the dihedral angles are calculated from the experimentally atomic co-ordinates (with the help of the sequence), so that what you propose is in its nature an academic exercise.

There is, however, a situation in which I have — in effect — done that, in exploring the structures that would be produced if the dihedral angles were varied. Rather than a command-line tool, there is a graphical tool that allows you to vary the angles interactively and see the results. This is the excellent Ramachandran Plot Explorer (Rama) by Bosco Ho. And yes, it can also generate the co-ordinates — you can save the results in PDB format to reopen or to visualize with other protein graphic software, such as JSmol.

The only problem is that the last version of this software was released in 2006, and is not 64-bit, so it will not run on the next version of Mac OS X (no idea about Windows). Bosco’s blog is still active, so perhaps he could be persuaded…


Why and how is DNA synthesis so much faster then RNA synthesis in bacteria? DNA synthesis in E. coli is 20x faster than RNA synthesis at 1000nt/s vs 50nt/s. (Mirkin'05)

I find that perplexing since DNA polymerization has better proofreading than the RNA variety, which requires extra time as you need to backtrack, excise, and replace. Also, in bacteria there's almost no splicing, so that doesn't slow you down. And the 1000nt/s is a single replication fork. We are not talking about several replisomes together clocking 1knt per second.

Is there an explanation of this or, in the absence of evidence, hypotheses?

I wouldn't call them hypotheses, but the question is intriguing, and, as it seems to be ignored in the literature, I'll make a couple of suggestions.

Perhaps it has something to do with recognition of termination signals in relation to selective pressure for speed in the two processes.

Perhaps if elongation of the RNA chain were any faster it wouldn't be able to respond to the rho-independent termination signals which are thought to be specific stem–loops in the DNA that cause the RNA polymerase to pause and fall off the DNA. The speeding RNA polymerase might disrupt the loops instead. The termination system for DNA replication may have evolved to be much more robust so as to be able to bring faster elongation to a stop. (Note: my suggestion of different ‘robustness’ in termination is not based on any data, it's pure speculation.)

If this were true, it would beg the question of why transcription hasn't evolved a more efficient termination system in concert with the a evolution of a smarter RNA polymerase. Perhaps the answer here is that there is no selective pressure for faster transcription — the rate is clearly sufficient to supply the needs of the cell — whereas the rate of DNA replication determines the time between cell divisions and thus the rate of growth, which is subject to selective pressure.

Perhaps it has something to do with error frequency in relation to selective pressure for speed in the two processes.

First I'll make it clear that I think the proofreading argument in the question is a bit of a red herring. If the rate replication is 20x as fast as transcription, the occasional backtracking will not have much effect on the overall difference. However errors and proofreading could be involved in a different explanation.

RNA transcription does not have proof-reading. The length of RNA transcripts is such that the cell can tolerate the errors that occur. However if the speed transcription were increased it is reasonable to expect an increase in error frequency, which might be detrimental. The current rate of transcription may be a trade-off between efficiency and accuracy. Of course one can imagine a proof-reading system for transcription evolving if it were necessary, but, as discussed above, if the rate of transcription is adequate there would seem to be no selective pressure to produce.


What is the meaning of the word 'bin' in the context of RNA-Seq? I have a question from a book about RNA-Seq. I would like to know the meaning of the word "bin" in the below cited paragraph:

  RseQC has several nice features not found in the other programs: (a)
  When calculating read distribution between different genomic features,
  it reports also several bins upstream and downstream of transcripts.

It's talking about things like "TSS_up_1kb", which is a "bin" of 1kb upstream of the gene. A bin is a somewhat generic term that in this context means "a region of some given size". Another example where you might see the term is with histograms. There, values are grouped into bins, with each bin then being represented by a separate bar in the graph.


Measuring tumor heterogeneity I would like to ask if there's any method (established or not) in order to quantify heterogeneity found in mutations occuring in primary neoplasms and metastatic lesions (either common or private) and potentially correlate this number to standard clinicopathologic traits.

The methods that come immediately to mind are mostly related to next-generation sequencing. You can do deep sequencing on your sample, which is just increasing the coverage as much as possible to find rare events. You can do RNA-seq to look at the transcriptome, ChIP-seq to look at chromatin modifications, and single-cell sequencing (a form of deep sequencing operating on individual cells) to get truly cell-by-cell data, either from the genome (DNA) or transcriptome (RNA).

If you are purely looking at phenotypes, flow cytometry is quite useful for analyzing relative expression levels of proteins, using both extracellular and intracellular markers and stains. FACS is an extension of flow cytometry that allows for the sorting of various cell populations into separate containers. These "purified" samples can then be used in any of the methods listed above.


Why does uterus have to be prepared every month for fertilization? I'm just curious why it has to happen every month when the uterus could have been prepared from the beginning and kept that way throughout life or till a certain point. But why make and break it every month? (The breaking of this preparation is the cause of menstrual pain, which is what I'm worried about).

A quick search through the Internet, as well as any textbook, will reveal that the lining of the uterus (endometrium) created thickened during every menstruation cycle is rich in nutrients, and requires a constant blood supply, in order to accommodate a fetus.

Therefore, maintaining the lining would be more costly to the body than rebuilding it every month; in fact, as part of the lining is reabsorbed, rather than destroyed and expelled, thus conserving energy and nutrients. The reason a part of the endometrium is not reabsorbed is its thickness, which prevents its total reabsorption.

Also, the menstrual pain is, in fact, caused by the breaking down of the endometrium, although not directly, but by muscular contractions (cramps) and the contraction of blood vessels, which happen to prevent blood loss and help with the expelling of the endometrium.


position of cell penetrating peptide I'd like to add a cell penetrating peptide to my custom peptide (30aa). Can I just add it to the end of the peptide sequence or does it have to be positioned on an outward facing external chain?

This papers tables shows that cell penetrating peptides are placed before their cargo peptide and do not need to be on a side chain.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576229/table/tbl1/


Differences between Heracleum mantegazzianum and H. sphondylium I have heard about the hazards associated with Giant Hogweed and the trouble is when trying to identify it, it is very similar by the looks to normal hogweed.

When fully grown, there is a big difference in height with Giant Hogweed (hence the name Giant Hogweed, but when it is small, how can you tell the difference?

Giant hogweed (Heracleum mantegazzianum)

Image from WikiMedia

Hogweed (Heracleum sphondylium)

Image from WikiMedia

Yes, the species can be identified by the shape of the leaves. The leaves of H. sphondylium are more or less flat (in one plane); the leaves of H. manteggazianum are more crisped and much more pointed.

Here are two pictures from the Dutch wikipedia (h. sphondylium last):


DNA replication during Mitosis I am a bit confused.
During Meiosis, DNA is replicated to form a cell with half the DNA and likely to have variations.
But since the replication process of meiosis and mitosis are the same, why do DNA in different cells of an individual organism not have variations? Or do they have variations that are just not expressed?

In meiosis crossing over takes place which leads to variations
 in chromosomes while in mitosis no crossing over takes place


Are male and female brains physically different from birth? Male and female brains are wired differently according to this article:

  Maps of neural circuitry showed that on average women's brains were highly connected across the left and right hemispheres, in contrast to men's brains, where the connections were typically stronger between the front and back regions.

But since learning in the brain is associated with changes of connection
strengths between neurons, this could be or not the result of learning.
What about physical differences from birth? Are there differences in size, regions, chemical composition, etc. from birth?

Short answer
Yes, men and women's brains are different before birth.

Background
First off, learning effects versus genetic differences is the familiar nature versus nurture issue. Several genes on the Y-chromosome, unique to males, are expressed in the pre-natal brain. In fact, about a third of the genes on the Y-chromosome are expressed in the male prenatal brain (Reinius & Jazin, 2009). Hence, there are substantial genetic differences between male and female brains.

Importantly, the male testes start producing testosterone in the developing fetus. The female hormones have opposing effects on the brain as testosterone. In neural regions with appropriate receptors, testosterone influences patterns of cell death and survival, neural connectivity and neurochemical composition. In turn, while recognizing post-natal behavior is subject to parenting influences and others, prenatal testosterone may affect play behaviors between males and females, whereas influences on sexual orientation appear to be less dramatic (Hines, 2006).

The question is quite broad and I would start with the cited review articles below, or if need be, the wikipedia page on the Neuroscience of sex differences.

References
- Hines, Eur J Endocrinol (2006); 155: S115-21
- Reinius & Jazin, Molecular Psychiatry (2009); 14: 988–9


Are there any animals that celebrate communally? Are there any animals that are known to celebrate events? For example, we humans might celebrate a birthday or passing an important test. An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

To clarify, I am more interested in positive celebrations. I know a number of animals having mourning behaviors (which absolutely count as a response to external events, no denying); I'm just more interested in celebrations in a positive sense.

I'd like to take this one step further.

Are there any cases proven or postulated of animals celebrating. I don't necessarily need something firm and proven, could be a theory.

An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

Celebrations usually mean large group activity but a play can be considered an event which is simply by joy and not any sort of survival instinct, and hence would fit your question. One can easily spot their pet playing around with objects when they are sitting around, busy in something 'boring' for the pets, like - reading a newspaper. But here it can be argued that pets have learned to do this to get the attention of the owner, and hence associated benefits.

Well, plays of pure enjoyment have been documented in wild animals too.

  I once observed a young elk in Rocky Mountain National Park, Colorado, running across a snow field, jumping in the air and twisting his body while in flight, stopping, catching his breath and doing it again and again. There was plenty of grassy terrain around but he chose the snow field. Buffaloes will also follow one another and playfully run onto and slide across ice, excitedly bellowing “Gwaaa” as they do so (Canfield et al. 1998).

Certainly, there was no motive here apart from having fun.

I would encourage you to go through this article - Bekoff, M. (2000). Animal Emotions: Exploring Passionate NaturesCurrent interdisciplinary research provides compelling evidence that many animals experience such emotions as joy, fear, love, despair, and grief—we are not alone. BioScience, 50(10), 861-870.

Speaking of the celebration, such as - birthday, or the largest homo sapiens gathering Kumbh Mela, I would also be interested to know of some group of animals doing it periodically.

Reference:

Canﬁeld, J., Hansen, M. V., Becker, M., & Kline, C. (1998). Chicken Soup for the Pet Lover’s Soul. Deerﬁeld Beach, FL: Health.


What are the differences in the two possible methods to calculate the Hardy-Weinberg Equation? I am more than flabbergasted by calculations of Hardy-Weinberg equilibria. The formula's theory assumes a binomal distribution of allele frequencies in a population, and hence allows the comparison of observed phenotype frequencies to an ideal model distribution.

$$
p^2 + 2pq + q^2 = 1
$$

with

$p^2$ = Frequency of homozygous phenotype PP

$2pq$ = Frequency of heterozygous phenotype PQ

$q^2$ = Frequency of homozygous phenotype QQ

There are two different methods of working with the HW equation that I have come across, and they do not seem to be compatible; used on the same data sets they yield wildly different results. I feel like I'm not seeing the forest for the trees, to be honest.

Is either of these methods (technically) wrong? How do I decide which one to use for each data set (i.e. is it valid to use method #1 on 3-allele-data sets)? Or do I just use whatever method is easiest? Doesn't this lead to discrepancies in the results? This seems like a big thing, especially when comparing real-world observation data to assumed HW distributions.

Example data set (EST/California) and results of HW calculations. I'm using observed phenotype in the place of the original data's observed genotype.

Phenotype     n  |   HW1   HW2p   HW2q
PP           37  |  33.9   37.1   28.8
PQ           20  |  25.0   23.0   28.2
QQ            7  |   4.5    3.8    7.0

Calculation method #1

As suggested by above-linked data set source and Beebee/Rowe's Introduction to Molecular Ecology, alleles are simply added up to get values for p and q respectively:

Phenotype    n  |   P    Q
PP          37  |  74    0   (37 * PP = 74 P)
PQ          20  |  20   20   (20 * PQ = 20 P + 20 Q)
QQ          7   |   0   14   ( 7 * QQ = 14 Q)
Sums        64  |  94   34

From this we can directly infer p/q: $p = 94/(94+34) =0.73$ and $q = 34/(94+34) = 0.27$; with the condition $p + q = 1$ remaining true.

Using these values for p and q in the HW equation yields:
$$
p^2 + 2pq + q^2 = 1
\\
(0.73)^2 + 2(0.73)(0.27) + (0.27)^2 = 1
$$
And a population-wide phenotype distribution of

Phenotype      n
PP         33.92    p^2 * 64
PQ         24.96    2pq * 64
QQ          4.48    q^2 * 64

Calculation method #2

The second method of utilising the HW equation is a lot more direct, and just about every text book I could find uses this method to solve 3+ allele problems (as, for example, blood types); Wikipedia commends its usefulness in calculating heterozygote frequencies of genetic diseases in large populations.
In this calculation frequencies are directly inferred as per the definition of the HW equation. This means $p^2$ is equal to the frequency of the phenotype PP (see above).
$$
p^2 = \frac{37}{64} \\
p = {\sqrt 0.578} \\
p \approx 0.76
$$
$$
q = 1 - p = 0.24
$$
Leading to a HW distribution of
$$
(0.76)^2 + 2(0.76)(0.24) + (0.24)^2 = 1
$$

With a new ideal phenotype distribution:

Phenotype      n
PP          37.1    p^2 * 64
PQ          23.0    2pq * 64
QQ           3.8    q^2 * 64

Inverting the calculation by starting with $q^2 = 7/64$ leads to even more diverging results:

Phenotype      n
PP          28.8    p^2 * 64
PQ          28.2    2pq * 64
QQ           7.0    q^2 * 64

Using both $p^2$ and $q^2$ inevitably violates the condition $(p+q)^2 = 1$.

Okay, so the Hardy-Weinberg Equilibrium is just that: an equilbrium.

In physics, a system (some object) is at equilibrium when no net energy crosses its boundary with the surroundings.

no energy change means no change in motion (the state of the object) due to outside influence on the system.

In chemistry, a system (the beaker/reaction container/cytosol) is at equilibrium when no change in the concentration of the chemical species inside of it occurs over time

no chemical makeup change means the (molecular) state of the atoms in the system is free of energetic influence from the outside world.

In the H-W Equilibrium, a system (the gene pool) is at rest when no change in the frequency(concentration) of its alleles occurs over time.

no change in the frequency of alleles means that there is no outside influence on the state of the gene pool.

Just like in basic physics, we have to define our system. If our system is the gene pool, then even the behaviors of the organisms in whose cells those alleles are found are outside of the system. The system is only the alleles aka gene pool.

The most important part about understanding the H-W Equilibrium is that it only applies when those conditions of the gene pool being free from outside influence hold. In fact, in the link you gave, the introduction has it in the second sentence (don't feel bad, I missed it the first few times, too—too focused on applying the algebra to understand what it was really saying):

  The model has five basic assumptions:

  1) the population is large (i.e., there is no genetic drift)

  2) there is no gene flow between populations, from migration or transfer of gametes

  3) mutations are negligible

  4) individuals are mating randomly

  5) natural selection is not operating on the population.

Let's break them down/group them:

2: Obvious in terms of equilibrium == system is in isolation from surroundings
4 & 5: Selection pressure (4: sexual selection, or 5: natural selection) is not pushing on the system.
1 & 3: Random effects are not pushing on the system (1 = statistical sampling error that can push small populations, and 3 = mutation that pushes the system like adding a new chemical species to a system at rest.)

With that solid grounding in the theory, let's move on to your questions about the algebra. Remember, the equilibrium only applies when the gene pool is not being pushed around by external factors. Which means that the physical copies of alleles (gametes) should pair randomly with the possible gametes at every mating. If those assumptions didn't hold true, then the math of the equilibrium wouldn't hold up. If you run the numbers on a system at equilbrium, barring small amounts of sampling error (reducible with a bigger n), the H-W Model's predictions will be accurate. All the methods will yield similar results.

However, if the predicted values don't match the actual with one method, you can assume that other methods will also yield inaccurate predictions, and that the two different calculation methods' predictions will vary widely from each other, largely because of the assumptions you are making (Method 2: 1 = p+q), or aren't making (Method 2).


How to tell petiole apart from stem? How to tell petiole apart from stem? Is it by the rule that there is usually a pair of stipules at the base of a petiole?

Petioles typically have the presence of one or more of the following:

Stipule at base of the stalk
Axillary bud between the stalk base and attached stem
Leaf scar when removed

Source: Miami University

Source: Wikipedia
None of these characteristics would be present if the stalk you were looking at is a stem.

However, they are not always each visible on every species...
From: Oregon State University Dept of Horticulture:

It is not always easy to find the bud at the base of a petiole, it may not be visible early in the growing seaon and sometimes a mature bud is “hidden”, such as being enclosed by the petiole base.

From Wikipedia:

although in many species the stipules are inconspicuous or entirely absent (and the leaf is then termed exstipulate)

Leaves are usually borne from petioles and rarely from the stem itself -- so presence of a leaf (or compound leaf parts) is usually indicative of a petiole as well. However, sometimes plant leaves lack a petiole altogether, as in the case of sessile leaves.
In other instances, specifically those of compound leaves, the stalk of compound leaves (i.e., the rachis) will lack the properties previously described for a petiole, but following the compound leaf to the nearest stem typically will result in locating the petiole with one or more of the above mentioned characteristics at its base connecting the compound leaf to the stem.


Can you answer Ray Comfort's question on Biological Evolution? https://www.youtube.com/watch?v=U0u3-2CGOMQ

There's this video on Youtube about biological Evolution that has gone viral. I'll paste it above for your convenience.

To cut to the chase, Ray Comfort asks this question repeatedly to various people, and I guess he never got an answer or a good answer. The question is:

Can you think of any observable evidence for Darwinian Evolution where there is a change of kind?

By change of kind, I assume Comfort wants observable evidence of one species/kind morphing into a new or different kind/species.

How would you answer this challenge?

The question is really not well defined for two reasons:

What would you accept to consider being an observation? It seems to me that many creationist would accept to consider something to be an observation only if it is extremely simple to understand it. The methodology of observation in evolutionary biology (just like in most science field) are not always very simple to understand for non biologists.
The word "kind" is not define in the sentence "what is a change of kind?".

Because the question is poorly defined, it makes it impossible to answer. And that is the common problem with creationist arguments. Their arguments are not scientific and therefore cannot really been argued for or against. Just want to say also that evolutionary biologist do not need non-scientist to fight against their work. Scientists create their own criticism. Scientists do not form a political party that fight for one point of view just for the purpose of defending it. They think neutrally and objectively (as much as a human can).

Change of kind

If change of kind = change in DNA sequence

Let's assume change of kind means change in the DNA sequence. Change of kinds have been observed in real time in almost all lineages we looked at (including humans). These changes are not only observable at the genetic level but also at the so-called phenotypic (loosely speaking the phenotype is way the organism looks like) level. We can for example think of disease in humans that are due to de novo mutations.

If change of kind = a population/species adapt to a new environment

If by change of kind, one mean "adaptation", then adaptation to new environment have been observed in tons of lineages again. In a lab it can be observed in bacteria within the course of a month. It has been observed in many mammals, birds, plants and unicellular eukaryotes.

If change of kind = one lineage splits and there is reproductive isolation

If by change of kind, one mean "reproductive isolation", then reproductive isolation has also been observed in real time and many times in nature and in labs (see this post for example)

If change of kind = something else

Just tell me what is this something else and we'll let you know if it has ever been observed. We can also let you know if this something is a prediction from the theory of evolution or not.

Observation

If you accept observation based on slightly more complex method such as molecular clocks and comparative genomics, then you'll find thousands of example of "change of kind", again in roughly speaking all lineages of the tree of life.

Very recently I worked on the speciation of clownfishes. This speciation was dated and we observed morphological and genetic adaptation to specific environments.

P.s. I haven't looked at the video completely but only some randomly selected part for a total duration of about 30 seconds! At first sight I'd like to say: Please don't fall into the trap of the media. One making interviews of people that are sometimes identified and sometimes not and that select for some part of their answer and that ask poorly defined question can really easily say anything from his records.

I welcome editing and I welcome anybody wanting to add references. One can find tons of them!


Does genetic morbid obesity exist? With the acceptance of being a little overweight

I hear of people saying they were born morbidly obese and it was genetically passed on. I'm aware being so obese leads to countless health issues, yet we have people defending fat shaming and the likes. Is the excuse of having 'obese' genetics scientifically justified? Do people have genetics that make them ridiculously fat? Alongside, would this simply be down to the diet of the person from a young age?

Thanks.

It is certainly a very difficult question to answer.

There are some genetic disorders that can predispose individuals for becoming obese: https://www.ncbi.nlm.nih.gov/pubmed/18230893

There are also evidence of epigenetic influences on obesity: http://www.nature.com/nrendo/journal/v12/n3/full/nrendo.2016.18.html

Typically each case of obesity is caused a combination of both genetics, epigenetics and lifestyle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873060/

However also keep in mind that obesity is a fairly recent problem and as such the genetic changes are likely minimal between the 1980 and 2008 populations sampled by WHO: http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
A doubling in the prevalence of obesity in the two populations are most likely caused by changes in lifestyle and the availability of food, rather than genetic changes as the time frame is so short.

So to sum up: Morbid obesity caused by currently unfavorable genetics exists but is very rare. People can be genetically and epigenetically predisposed for developing obesity, which when combined with certain lifestyles can further increase the risk of becoming obese.


Why are the results of local BLAST and miRbase BLAST different? I am trying to reproduce locally on my computer what I get running mirbase on their website using BLAST. The search sequences is: mature miRNAs which I had downloaded on my computer and make it as a BLAST database with command:

./makeblastdb -in /home/marianoavino/Downloads/mature.fa -dbtype 'nucl' -out /home/marianoavino/Downloads/mature

then on mirbase I see they use an e-value of 10, which I leave locally.
On mirbase at the end of the analysis they give you these parameter setting:

Search parameters

Search algorithm:
    BLASTN
Sequence database:
    mature
Evalue cutoff:
    10
Max alignments:
    100
Word size:
    4
Match score:
    +5
Mismatch penalty:
    -4

and this is the command line I use on my computer for BLAST

./blastn -db /home/marianoavino/Downloads/mature -evalue 10 -word_size 4 -query /home/marianoavino/Downloads/testinputblast.fasta -task "blastn" -out /home/marianoavino/Downloads/testBLast.out

The results of the two analysis are different, with mirbase finding much more stuff than local BLAST.

Do you have any idea on which parameters I should use on local blast command line to match those listed mirbase parameters in order to get the same answer?

The main problem I could identify is that your scoring matrix is not the same; as you said miRbase uses match score of +5 and mismatch penalty of -4.

The BLASTN defaults can be found here. However, I ran the local BLAST using the exact command that you mentioned and the default values that it used were:
reward = +1
penalty = -2

Matrix: blastn matrix 1 -2
Gap Penalties: Existence: 0, Extension: 2.5

The other reasons could be the difference in the database itself (the sequences used) or the version of BLAST used in the two cases.


Proteins that are strongly overproduced in E. coli and S. cerevisiae? I'm looking for some pointers to proteins that produce at really gigantic levels in E. coli and yeast (S. cerevisiae).  Can anyone point to some champion proteins?

Even in inclusion bodies and non functional, just cases where the yield is very high - how much of a given protein can a liter of E. coli or S. cerevisiae make?

I've seen bands on gels like this, but I've probably not seen the champions:

It would be great if you could cite and discuss the plasmid/promoter used and whether codon optimization or other such tricks made a difference.

Heat shock proteins - HSP70 and HSP30.

You may also have ribosomal subunits as well.


What is this ornamental, yellow flower that looks like a smooth pineapple skin? My mom got this in her Mother's Day arrangement and we have no idea what it is.

This is a beehive ginger, Zingiber spectabile.

Its inflorescence will become a bit different sometime soon:

I believe the one in your image is not yet fully developed, like this one here:

Source of the images:

http://www.geneticjungle.com/2008/08/deceptive-petals-7-orchid-mimics.html
http://specialflowersintheworld.blogspot.com.au/2015/04/zingiber-spectabile-flower.html