Why are children and adults so different? In many animal species, juveniles aren't just smaller versions of adults. In mammals, the contrast is not as spectacular as in species that undergo metamorphosis, but still quite noticeable.

For example, puppies have shorter limbs and flatter faces than adult dogs. Fawns are coloured differently than adult deer, and males do not start growing antlers until they reach sexual maturity. There are behavioural differences as well: habituation is much stronger and faster in juveniles. In humans, children have different proportions than adults and lack secondary sexual characteristics. But why? Wouldn't it be simpler to form a small version of the adult and grow linearly?

Why delay sexual maturity in the first place?
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
Why the different body proportions?
Why lose play behaviour and learning ability as adults?

I'm interested in mammals in general and humans in particular.

GREAT QUESTIONS!!!
Why delay sexual maturity in the first place?
-I believe it is also related to "the best-used" of resources. Firstly, it is unnecessary and impossible for children to have sex (biologically and evolutionarily), they don't have the physicality to sustain sexual intercourse or the ability to bear a children inside their body. Secondly, it is to focus resources on growth. Children uses lots of energy on growth. Human body does amazing jobs on allocating body resources or material so that we are in the best shape possible. If they don't do sex, they can focus more on growth.

Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
- This one is a hard one. I believe it is just how biologists categorize human growth. We can study how human bodies develop in each stage, which is I believe it's really important on morphology.

Why the different body proportions?
-Evolutionary advantages!!! It is believed that baby has a greater head portion than adult. That's why people say children learn better than adults. Human values their brains more than other organs of the body, developing intellectual capacity as early as possible allows them to win in natural selection.

Why lose play behaviour and learning ability as adults?
If I understand you correctly, you are asking why adults lose their play behaviour and learning ability as they grow up. For learning ability, I believe it is caused by degeneration, just like the other organs of the heart. We have a mortal body and so once the body hits its maximum growth capacity, it will start going downhill unfortunately. For play behaviour, I believe it is a human behavioural changes due to life experience, social expectation and peer interaction. We lose interest of 'games' as we grow up because they are considered to be childish, silly and not useful.


What is protein secondary structure? Could someone please clarify what is protein secondary structure:
https://en.wikipedia.org/wiki/Protein_secondary_structure

I believe I understand the primary structure, I am not sure what's the difference between secondary and tertiary structure. Tertiary structure seems to be 3d structure of a polypeptide but I am not at all clear about the secondary structure.

Proteins are made up of long chains of amino acids covalently joined together. The order of amino acids is the primary structure of a protein. In physiologic conditions, these long chains of amino acids fold into three dimensional shapes. The terms secondary and tertiary structure are used to refer to specific aspects of the three dimensional shape.
tl;dr what's the difference?
Both secondary and tertiary structure refer to the three-dimensional shape of a protein. Secondary structure is the regular repeating patterns, generally stabilized by hydrogen bonds between the NH and CO groups of the peptide backbone. Tertiary structure can be thought of as the way secondary structural elements fold together to create the overall shape of the protein.
Secondary structure
Secondary structure refers to regular repeating patterns stabilized by hydrogen bonding between the NH and CO groups of the peptide bond. Typically textbooks will focus on the $\alpha$-helix and the $\beta$-sheet.
Berg biochemistry has some useful diagrams demonstrating these secondary structures. The first is an $\alpha$-helix. The side-chains are represented by green balls here. Notice the orientation of the NH and CO groups, which stabilize this structure:

The $\beta$-sheet forms a very different secondary structure, but it's also stabilized by hydrogen bonding between NH and CO groups of the peptide bond.

Tertiary structure
Tertiary structure is the larger three-dimensional structure of a protein in its environment. It can be useful to think of tertiary structure as the way different secondary structural elements fold together to form the full, active protein. Notice in this figure, also from Berg, the way the elements of secondary structure (the $\alpha$-helices) fold into an overall three dimensional shape that can nicely cradle the heme group.

Secondary structure proteins are repeating chains of alpha helixes and beta sheets like spider silk.
Tertiary structure proteins are globular proteins, like enzymes.


Sex determination in Drosphila Ive been taught that its based on genic balancing.
But I recently saw this question that has caused me some doubt.

I thought it would be the 1st option but unfortunately they said it to be the 3rd.
But in the answer key, they mention the same line of that of the 1st option.
Ive only been taught genic balance in a general sense .I solved by finding the ratio of no. of X chrom. to no. of autosomes. It would help if someone could give me some clarity.

I think the first possible answer is wrong because maybe by "set" they mean the total number of autosomes. Where as in the figure below it states that the autosome is only responsible for a repressor(Dpn), and that in normal conditions (in pairs i assume) they product equal amounts for females and males.

If the chromosome 2 was not in a proper pair, then I assume the dosage of the Dpn repressor would be off.

The gene dosage is with the activators produced also, sis-a, and sis-b. So I guess in females they produce twice as much activator for the Sxl protein, which later on allows for the repression of male genes and activation of female genes.


How dirty are bugs? And is it okay if they touch food? Sometimes I see people throw out an entire drink or bowl of food because a small bug was in it. Are they justified in doing this? Is there enough bacteria on common species of bugs (like ants, flies, beetles, dragonflies, caterpillars, moths, etc) to warrant any kind of health concern for a larger amount of food than what the bug was in contact with, or at all?

Well, first of all you should consider that insects and generally animals don't have so much hygiene, like us humans. Some of them, let's say the ants, yes some kind of hygiene is present, but not in the human degree. In fact, most insects are responsible for the most dangerous deseases in the world such as malaria , yellow fiver, sleeping sickness (espacially found in Africa because of the tsetse fly) and many kinds of encephalitis. This article claims that most of insects are carriers of deadly deseases. Also, about the second part of your question, you mentioned " If it is okay for bugs to touch food"... Well the answer is ofcourse no, because you don't know:

1. what the insect was touching before it "lands" to your food

2. If it has dropped any fecesto your food

3. And last but not least if the insect layed any kind of eggs to your food.

4. Some insects carry fungi that if a human being consumes them he might have serious problems, because some fungi are responsible for poisoning or infection.

The third one that I mentioned is responsible for the most cases of Tapeworm infection. This means that the eggs and larvae pass straight to your digestive system and create the infection. To sum up, unknown factors (like bugs) must not touch our food, because there is a chance of infection. To help you here's a wikipedia list that shows the most easily transmitted diseases to humans fron insects: List of diseases caused by insects.


Squirrel nest construction I've often wondered how squirrels -- specifically, eastern grey squirrels (Sciurus carolinensis) make their nests. Specifically, I've been curious about how they "weave" everything together to make these so called "dreys" stay together (and stay in the tree).

According to this site:

  [squirrel nests are] constructed from various twigs, leaves, moss and other material. To start, twigs are loosely woven together to make up the floor of the nest. Next, squirrels create more stability by packing damp leaves and moss on top of the twig platform to reinforce the structure. Then a spherical frame is woven around the base, which creates the outer shell. The final touches include stuffing in leaves, moss, twigs and sometimes even paper to build up the outer shell of the new home.

I've tried finding a video (preferably time-lapse) of a squirrel nest being built to better understand/appreciate this animal home. However, I've thus far been unable to find such a video on the internet.

Does anybody have such footage or know where I can find some?

Ideally, close-up and even internal shots would be included.
Additional notes about tree-branch drey construction would be appreciated, too!

Check for:

https://www.youtube.com/watch?v=6uKDpHM-OsI
https://www.youtube.com/watch?v=3jPtZByr740
https://www.youtube.com/watch?v=Kh1HnMFolgw
https://www.youtube.com/watch?v=M5dduAX8iuI

The third one was filmed by BBC. The fourth one is a closer look of the nest complemented with a fairly good analysis.
The first two are reasonably good, but the third one is just awesome for your purpose!

https://www.youtube.com/watch?v=BcTweYHQ-II

It seems like they just pile the leaves on.


How long is DNA stable in a freezer? Inspired by the post about extracting pet DNA, how long would genomic DNA be stable for in a -20°C freezer? It is common practice to store DNA (double-stranded, plasmid) in a -20°C freezer in the lab, but would genomic DNA last longer in a -80°C freezer? With either method, how long would it be stable for?

If the DNA is pure, it should last quite a long time.  If there are enzymes and other biological molecules in there, -80C will work much better.

I think you could keep pure DNA at -20C practically indefinitely.

Purity is the main issue there, also pH stabilized, sealed properly, etc.  That makes all the difference.

You can store your DNA for 1 week at -4C and for one month at -20C but with storing DNA over these period of time there is a deduction of 10-15% of yield from your DNA sample.


Does anyone know if there is a term to describe the following process? I'm actually currently studying physics but this came up in my textbook (taken from Giancoli 7th edition section 16-10):

The random (thermal) velocities of molecules in a cell affect cloning. When a bacterial cell divides, the two new bacteria have nearly identical DNA. Even if the DNA were perfectly identical, the two new bacteria would not end up behaving in exactly the same way. Long protein, DNA, and RNA molecules get bumped into different shapes, and even the expression of genes can thus be different. Loosely held parts of large molecules such as a methyl group can also be knocked off by a strong collision with another molecule. Hence, cloned organisms are not identical, even if their DNA were identical. Indeed, there can not really be genetic determinism.

I'm aware of different biological processes that can affect gene expression but this is random kinetic motion! Would you call this one of the epigenetic mechanisms that can affect gene expression? If so it would underlie ALL epigenetic mechanisms because all molecules have random kinetic motion.

The two terms of main interest to you
Cellular noise

Cellular noise is random variability in quantities arising in cellular biology. For example, cells which are genetically identical, even within the same tissue, are often observed to have different expression levels of proteins, different sizes and structures. These apparently random differences can have important biological and medical consequences
Cellular noise was originally, and is still often, examined in the context of gene expression levels – either the concentration or copy number of the products of genes within and between cells. As gene expression levels are responsible for many fundamental properties in cellular biology, including cells' physical appearance, behaviour in response to stimuli, and ability to process information and control internal processes, the presence of noise in gene expression has profound implications for many processes in cellular biology.

There is also the term developmental noise.

Developmental noise is a concept within developmental biology in which the phenotype varies between individuals even though both the genotypes and the environmental factors are the same for all of them. Contributing factors include stochastic gene expression and other sources of cellular noise.

Developmental noise is often sounds like a synonym of cellular noise, but it is supposed to include more processes that are causing phenotypic variation then cellular noise. For example, it is common to consider "micro-environmental variation" as being part of developmental noise and not of cellular noise.
The way your phrased your question
In your question you describe only sources of cellular noise. However, you end up saying Hence, cloned organisms are not identical, even if their DNA were identical. I just want to highlight that, there are other reasons than cellular noise for which two clones differ. These include micro-environmental variance, physiological noise, epigenetic variance and macro-environmental variance (often just called environmental variance). Note that I had never encountered the term "physiological noise" before, I just made it up but I wanted to highlight that noise also happen in among cells processes, not only within cells processes.
Intro to quantitative genetics
For a short introduction to quantitative genetics and the different sources of phenotypic variance (genetic variance, environmental variance, developmental noise, etc..) and how the concept of heritability fits into this discussion, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Heterogeneous is the term you're looking for I believe.

From Wikipedia,

  A material or image that is homogeneous is uniform in composition or character (i.e. color, shape, size, weight, height, distribution, texture, language, income, disease, temperature, radioactivity, architectural design, etc.); one that is heterogeneous is distinctly nonuniform in one of these qualities.


Frequency of dominant phenotype (Hardy-Weinberg) The question is:

The frequency of a recessive allele a is 0.6. If a population is in Hardy-Weinberg equilibrium, what is the frequency of the dominant phenotype?

This question is a bit confusing to me. I'm not sure how to use my knowledge about Hardy-Weinberg in this problem. I know that when q = 0.6, p = 1 - 0.6 = 0.4. But when they are asking for the dominant phenotype, should it be p^2 or the squareroot of p? I have watched several YT-videos about this, but I still can't get the hang of it. There's not much help in my teacher or books. I would be really grateful if someone could clear up my confusions!

p = p(a) = 0.6

q = p(A) = 0.4

Frequency of homozygous recessive, aa = p2 = 0.36

All other genotypes have dominant phenotype therefore the frequency of the dominant phenotype is 1-0.36 = 0.64

(Frequency of homozygous AA = q2 = 0.16

Frequency of heterozygous Aa = 2pq = 0.48)

And if you want a deeper explanation you really should study this answer by Remi.b

Since the frequency of the dominant allele is 0.4, or 40%, the chance of each allele being the dominant allele is 0.4. Since you are asking what is the probability of BOTH alleles being dominant we use the multiplication rule of probability, 0.4*0.4 = .16.

This is similar to the probability of flipping two coins and having them both be heads. Each coin has a 50% chance, therefore the probability of both being heads is 0.5*0.5 = 0.25.

That is the logic behind the Hardy Weinberg formula, p^2 + 2pq + q^2 = 1.


Can I execute/model a genome? Hi I am wondering if we can execute a genome on the sub-cellular level by running it on the computer. What I mean is using the genome as data to examine by having the cells reproduce and see what happens as they grow.

A simple genome can be modeled, however imperfectly, on a computer, where some have taken experimental genomics data and built simulations from it.
For instance, from the paper A Whole-Cell Computational Model Predicts Phenotype from Genotype:

Understanding how complex phenotypes arise from individual molecules and their interactions is a primary challenge in biology that computational approaches are poised to tackle. We report a whole-cell computational model of the life cycle of the human pathogen Mycoplasma genitalium that includes all of its molecular components and their interactions. An integrative approach to modeling that combines diverse mathematics enabled the simultaneous inclusion of fundamentally different cellular processes and experimental measurements. Our whole-cell model accounts for all annotated gene functions and was validated against a broad range of data. The model provides insights into many previously unobserved cellular behaviors, including in vivo rates of protein-DNA association and an inverse relationship between the durations of DNA replication initiation and replication. In addition, experimental analysis directed by model predictions identified previously undetected kinetic parameters and biological functions. We conclude that comprehensive whole-cell models can be used to facilitate biological discovery...
We have developed a comprehensive whole-cell model that accounts for all of the annotated gene functions identified in M. genitalium and explains a variety of emergent behaviors in terms of molecular interactions. Our model accurately recapitulates a broad set of experimental data, provides insight into several biological processes for which experimental assessment is not readily feasible, and enables the rapid identification of gene functions as well as specific cellular parameters.

(cite)
Also:

Given the vast behavioral repertoire and biological complexity of even the simplest organisms, accurately predicting phenotypes in novel environments and unveiling their biological organization is a challenging endeavor. Here, we present an integrative modeling methodology that unifies under a common framework the various biological processes and their interactions across multiple layers. We trained this methodology on an extensive normalized compendium for the gram-negative bacterium Escherichia coli, which incorporates gene expression data for genetic and environmental perturbations, transcriptional regulation, signal transduction, and metabolic pathways, as well as growth measurements. Comparison with measured growth and high-throughput data demonstrates the enhanced ability of the integrative model to predict phenotypic outcomes in various environmental and genetic conditions, even in cases where their underlying functions are under-represented in the training set. This work paves the way toward integrative techniques that extract knowledge from a variety of biological data to achieve more than the sum of their parts in the context of prediction, analysis, and redesign of biological systems.

(cite)
Gentle advice: Avoid answers from cartoonists, whose domain of knowledge does not include biology.


Is happiness or pleasure an evolutionary programming for survival? I think that whenever we feel some kind of happiness or pleasure it is always related with improving our chances of survival, that might be temporarily or in long term, might be of only of an individual or his/her relatives or all human beings or all living beings as a whole.

I find that a sense happiness or pleasure is linked with the survival (might not be true as it's based on personal observation).
 We crave for things like attention & being cared, beauty & physical health, power (& money). Attaining them gives us a sense of pleasure, and these things improves the chances of our survival. People having power & money dont die out of scarcity. People having beauty & physical health get to pass their genes more often(keeping whole human history in mind). Dogs developed their behaviour around humans so as to get more attention & care thus improving their chances of survival. We also feel happy helping other people, we feel happy making more friends.
  But there is no simple answer to this one as we also have tendencies to hurt ourselves and some people derive pleasure in hurting others.

So is pleasure or happiness evolutionarily programmed into us to better our chances of survival?

Our current understanding is that pleasure is one of the major ways your brain gets "you" to do things, it is the basis of positive reinforcement of behavior and associative learning. It can almost be thought of a a tag for an individual behavior that says "do this again/more". That pleasure alone can motivate animals to do things has been understood since way back in the Skinner box experiments where a wire to the pleasure center was inserted in rats and said rats would keep doing whatever behavior they associated with stimulation via the wire foten to the exclusion of all else. The basis of our learning could be summed up as do things that elicit pleasure, don't do things that elicit pain. tying many complex behavior to a single signal seems to make it easier to control and even prioritize very complex behavior, just do whatever yields the most pleasure, of course humans and many other animals have many more competing emotions and other factors, like metacognition. But for simpler animals it is easy to see how this system is efficient, it is easy to tag new behaviors or experiences into this system, at its simplest form just connect (possibly inhibitory)a few neurons triggered by the behavior or memory of the behavior to the pleasure center.

Of course it is not perfect, few things that evolved are, behaviors that are not beneficial can trigger the system, especially novel or extremely rare behavioral options, especially ones created by technological advancement, drug addiction being a great example. Evolution is very poor at preparing organisms for novel conditions like the modern technological world. And the our brain did not evolve under conditions where cocaine (as an example) existed. Just because something is pleasurable does not mean it is beneficial.  The full range of behaviors that can elicit pleasure would be well beyond the scope of a single question but it is quite clear pleasure itself is an evolutionary advantage, it is one of the major reasons we learn to eat, drink, reproduce, and make social connections.

Happiness, is more difficult, mostly because it is a poorly defined term in biology, it is unclear if it is distinct from simple pleasure.

All features of life have evolved in order to better the chances of reproduction, the feeling of happiness is included.  After all, happiness is just the release of various molecules such as dopamine, oxytocin, and endorphins, that cause the body to more likely produce a certain behavior.

These chemicals can produce advantageous behaviors by promoting deep friendship, mating bonds, and gratitude in an investment paid-off.  However, they can also provide bad behaviors if jealousy or laziness emerges.  All emotions exist in a tug of war in evolution, in fact Darwin wrote a book entitled: "The Expression of the Emotions in Man and Animals".  While I have not read all of it he probably states how fear, jealousy, anger, etc. all can promote both good and bad behaviors.

More recently, scientists have tried to study specifically the evolution of happiness two publication are by Nesse and Buss.  Both are not very sure, but note the evolutionary advantages of evolution.

So the short answer to your question is yes, with the caveat too much, or too easy a sense of happiness has its downsides, and that all other emotions and measures of the body are effected by evolution.


Does human brain store duplicate data? There are several answers and articles about how the brain stores data, but none specifically cover whether a human's brain stores duplicate data.

I was reading in this article that a human brain can have a capacity of 1 terabyte to 2.5 petabytes. But for example, if you read a book a dozen of times, will it be stored as data several times?

Let me put it this way. When we read a book a couple of times, we remember it better. Is that because it's stored in several synapses and then retrieved better while trying to remember, or is it because reading it over and over makes the missing parts be stored?

We do recognize a familiar phrase when reading a book, which means the brain can differentiate the unknown from known. What matters is that does it decide to store it again or not? Just like a computer who refuses to save a file if the file already exists.

The way neuroscientists currently think about storage in the brain, it doesn't make any sense to think about "duplicate" data but rather about the "robustness" of a given memory to interference or confusion, which increases with consolidation and reconsolidation of memories or can degrade over time.

Repeated exposure can contribute to the robustness of a memory, but so can other factors such as the emotional content of a memory (which, depending on the emotional state, can increase or decrease memory robustness, and this can also vary with the "jist" versus "detail" of a memory).

Note that there are also very different types of memory, so that repetition is very important for motor plans and "muscle memory" whereas episodic memory can get lost in the repetition of daily recurrent events, such as parking your car or eating lunch: you might remember where you parked or ate today, but if you have a routine this can blur into all one memory, where you have a notion of eating at a particular restaurant many times, but you would struggle to remember specifically eating there on December 14th, 2011, unless there was some other special event on that day.

In your example of reading a book, there would likely be two types of memory: 1) memory for the episodic event of reading the book, which would be a separate memory because it is a separate event, though it could be confused with other similar episodic events. 2) Semantic memory for the content of the book: this would be a single memory, reinforced with subsequent readings of the book, and supplemented with all your other semantic experience with the content of a book: discussing the characters of a fiction book with your friends, learning about molecular genetics from a textbook and from a lecture course, etc.

Note also that talking about the "data capacity" of a human brain compared to a computer is a bit silly, because data isn't stored in the nervous system in bits, and a "fair" accounting of human memory needs to consider the vastly multidimensional interactions that are easily coded in a nervous system but not at all easily in a binary system. Note that other papers have come up with estimates that diverge greatly from the numbers you cite, for example Wang et al 2003 which gives a value of 108432 bits based on the number of synaptic connections. That number is truly inconceivable to our conscious experience even if it is within the capability of our brain. Clearly there are other limiting factors not involved in a simple binary system, for example confusion with similar memories, and there are types of memory that computers excel at (such as the pixel values of an image) whereas human memory deals in abstractions and hierarchical representations.

References

LaBar, K. S., & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Reviews Neuroscience, 7(1), 54-64.

Walker, M. P., Brakefield, T., Hobson, J. A., & Stickgold, R. (2003). Dissociable stages of human memory consolidation and reconsolidation. Nature, 425(6958), 616-620.

Wang, Y., Liu, D., & Wang, Y. (2003). Discovering the capacity of human memory. Brain and Mind, 4(2), 189-198.

Nature preserves redundancy by duplicating certain parts of living things - two lungs, two kidneys, two testes, two ovaries. I believe that as an instinct of self-preservation the brain does duplicate memory in some form.  Otherwise a caveman who was clubbed on the head or fell and hit his head badly would (if he recovered) be bound to forget how to do some basic task - like remember where his cave is, or how to hunt, or how to eat.
This would explain why most Alzheimer's patients can remember the distant past, at least initially.  It also explains why they have 'good' days (where they seem like their old selves - at least until the ravages of the disease take their toll) and 'bad' days, rather than 'bad' then immediately, 'much worse'.
Another example – you hear an old song from your childhood that's not played on the radio very often. You knew you used to know the title, song, and artist very well – but now you can't remember who the artist is anymore.  You try to resist temptation to look it up immediately on the Internet because you know this can't be good for your memory recall, but curiosity eventually gets the better of you.  When you do finally look it up you say, 'No way - it can't be HIM!".  Reluctantly you accept this new memory but you realise that somewhere in the recesses of your mind this information is already stored (later you remember that you mixed this artist up with another artist at the time and performed some research and found it was this artist after all).
So what have you done?  You have a piece of information already stored in your brain and you've now stored an exact duplicate - and, because of the emotional situation attached to each piece of information, these remain as backups of one another.


Is there any artificial species (in particular, an artificial species of animal)? Dogs were artificially selected from wolves, but a dog and a wolf can produce fertile offspring, and thus are of the same species. I had heard that the aurochs and cattle were different species, but I could not find this information anywhere. I had heard also that some artificially selected flies are considered to be a new species.

Is there any human-made species (especially a species of animal) which is not able to produce fertile offspring witch any other species, in particular with the one from which it evolved?

EDIT: (A similar question in different words.) Is there any human-made animal lineage which was conceived by artificial selection and which is broadly accepted as not being a race or subspecies, but a species on its own.

Artificial selection leading to new species - Domestication

As you talk about dogs in your intro, let's consider them.

You will fail to breed a great dane and chihuahua for obvious mechanical reasons. You will also fail to breed a chihuahua with a wolf. So, yes artificial selection have lead to reproductive isolation.

Artificial selection leading to new species - lab experiment

Artificial selection have also lead to reproductive isolation in non-domesticated species. See for example the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?

Concept of species

As a side note... Above, I consider the so-called 'biological species concept'. For a discussion on the definition of species, please have a look at this post.

There is not clear delineation for speciation, but think more along the line of a spectrum. When I compare the bacteria S. Pyogenes (flesh eating bacteria) and S.Dysgalactiae (commensal pathogen) they are very similar in a lot of their genes but they have also acquired qualities that helps us distinguish these as different species. Still, when found together, they readily undergo bacterial conjugation and exchange genes.
So to comment for the first part of question, the ability to produce fertile offspring does not imply that species are identical...rather compatible.


Can the human brain be reduced to a binary system? Does the brain really function like a computer as in, ultimately every response is related to a binary sequence based on whether particular neurons fire or not?

First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.

That being said, my answer is, some scientists believe so, some don't.

Several things to consider:

Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).
Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)
The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:

Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.

human brain is strictly digital device using defined action potentials (0 volt as logical 0 and specified (fixed) voltage potential as logical 1). these two potentials work same way as complex logic gates systems. brain processes all types of analog-like variations (signal amplitude or response strength) as very short time based sums of logic gates operations. there is no other applicable description of brain functionality


Why doesn't muscle strength depend on its length? In case of tug of war the more people participate the more strength they represent. And in case of muscles - the longer it is, the greater the number of myosin heads bind to actin when muscles contract. So why doesn't length matter?
UPDATE:
Since I've found multiple answers that compare muscles to ropes, let me comment on why those explanations don't work for me. Ropes don't have "muscle" strength, they have tensile strength. So this analogy can only compare tensile muscle strength to tensile rope strength.
In the end I'm pretty sure I'll find out that tensile strength constraints the muscle strength. And that's probably going to be the reason why muscle strength doesn't grow with length - something does not allow it, otherwise it would get damaged.
But I'd like find out what exactly prevents further contraction. Is it mechanical receptors on the muscle cell which block deploarization? Mechanical receptors in tendons which send nervous signals (but then - do tendons get thicker in proportion with the muscle)? Something else?

It's simply that the fibers are arranged end-to-end. If you simplify this down and imagine a single muscle fiber you have actin and myosin like this:
ligament-|actin-myosin-actin-myosin-actin-myosin

If you think of this as a strand of cotton pulling on a weight (ligament). Each group only pulls along the length, so the strength is not multiplied, but rather related to the strength of the individual fibre.
In reality muscles are stacked into bundles, which are much stronger as all the fibers can contract pulling with the strength of the multiple ends. Like this:
         |actin-myosin
         |actin-myosin
ligament-|actin-myosin
         |actin-myosin
         |actin-myosin

This is like the multiple strands of cotton making up a rope, the strength comes from having lots of them distributing the load.
This is something called physiological cross-sectional area, which describes the strength of a muscle by estimating the cross-section of the muscle across its thickest part.

The confusion I had is that I thought that myosin pulls on actin with a force which some how isn't the maximum possible. And if we were to add another sarcomere in a series - each myosin would have to work harder and together with the new sarcomere they would exert a greater force.
But this of course isn't how it works. Myosin doesn't have a notion of a varying strength, it's binary: it either attaches to actin or not. If we were to try to pull apart actin or myosin harder by their "tails" (by a neighbouring sarcomere) - actin would've started to "slip" from myosin. Therefore putting more sarcomeres in series would not make the muscle stronger - we'd simply add more "slipping".
The other possibility in a theoretical world would be to make actin and myosin strands longer and add more myosin heads (we'd have to reinforce lots of structures though). This way we could've made the muscle stronger by making it longer. But that's not how it works: a longer muscle cell merely means more sarcomeres in series.
Thanks @Bryan Krause for nudging me into the right direction in the comments.


Are hens and roosters the same species? I know that one is a female chicken and the other is male chicken. Are the chickens laying eggs considered the same species as those that we use for poultry meat? Or, are they different sub-species, analogous to how there are multiple breeds of dogs?

The main difference between a rooster and a hen is that the former is male and the latter is female. Their appearance differs in several ways [1].

A rooster also known as a cockerel or cock, is a male gallinaceous bird. The term usually refers to a male chicken [2]. The hen or the chicken (Gallus gallus domesticus) is a domesticated fowl, a subspecies of the Red Junglefowl [3].

And yes, the chickens laying eggs could be the same as the chickens that we use for poultry meat.

References:

Anjus Chiedozie. Rooster Vs. Hen on eHow.com
Wikipedia. Rooster
Wikipedia. Chicken

Yes, they are the same species. Meat birds and layers are the same species, they have just been bred differently to produce a certain result. (Along these lines, you may wish to picture a tomato, there are many different shapes and colors. However, they are all the same thing.).
As with humans, certain chickens have certain characteristics. And to an extent "personalities".
It does appear, based on this link, that chickens are a subspecies of Red Junglefowl. However, chickens themselves do not appear to have an subspecies within them. Sorry I had to use Wikipedia.


Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck? Some people who get directly struck by lightning and some more than once (starts at 00:25) survive while others die instantly or later on due to complications/injuries.

Looking at a wiki page for Lightning injuries

  Lightning injuries are injuries caused by lightning strikes.

  They result from three factors:

  electrical damage.
  intense heat.
  the mechanical energy which these generate.

  While sudden death is common because of the huge voltage of a lightning strike, survivors often fare better than victims of other electrical injuries caused by a more prolonged application of lesser voltage.

Lightning can strike or injure humans in four different ways but I'm going to focus on direct strikes.

  Reported mortality rates range from 10–30 percent, depending on the source of data. Most people who are struck by lightning live to tell the story, but many suffer from long term injury or disability.
  Airforce medicine site

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

To be lethal a lighting strike has to do enough damage to a critical organ that the injury is not survivable.  Since electricity can take highly variable paths through a body, the amount of damage inflicted is also highly variable.

For example, current entering on the head and exiting on the foot stands a good chance of passing through both the brain and heart.  This is likely to be a very severe injury.  Conversely, current entering on the left hand and exiting on the left foot does not cross the body and may leave superficial burns but limited internal injuries.

Lightning strikes the ground which then conducts to you.

By keeping minimal contact with the ground, you give the electricity less of a chance to conduct to you. And if your heels touch, this gives the electricity a shorter path to travel.

It is also important to avoid conductors, such as metal items.


Is there a maximum amount of antibodies your body can keep? I am wondering if you were theoretically able to get vaccinations or antibodies for any and every diseases and/or illness, would there be a limit to how many you can get and keep in your body at one time? If so, what is the limiting factor?

What would be the possible effects of this on the body and immune system? Thanks.

Antibodies are simply proteins and like any other protein have a relatively short "life", so after clearing out an infection, they are not retained for long (most of them anyway). What the body keeps is memory cells which can produce a much more rapid response if they come in contact with the same pathogen again.

You could see it as a selective process: the body produces immune cells, one or more specific cells for nearly every potential antigen that might exist in the world (there are more steps involved of course but they are of little relevance here). Only those which are used at some point mature into memory cells.

Unfortunately, I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. One explanation I can think of for why the body produces naive cells first is that either a) their production or b) their maintenance is less costly.

The other explanation I could think of is that even immune cells in the periphery which have undergone the proofing mechanisms of immune cell development already, may not be perfect and target body cells every now and then - in that case it would be devastating if they would go all-out like a memory cell.

From my three explanations, only alternative b) would mean there could be a limitation to how many vaccinations our immune system can bear (if memory cells take more effort to maintain than naive cells, having too many of them may overstrain whatever systems maintain them). Otherwise I don't see any limiting factor for how many memory cells you can retain; except if their numbers become so large that your lymph nodes swell and that causes problems.

Edit note: I'm not aware of any research about that question and couldn't find anything either.

so I work in a B-cell and Antibody Memory lab and the answer to your question is no. First of all, your body does make a B-cell against every possible target conceivable and if they don't bind to their target, they will die within a few weeks. If they do bind to their target however, they turn into long-lived plasma cells, which are stored in the bone marrow and constantly pump out antibodies, and memory cells which are pretty much the same as B-cells except they're way more powerful in their response and they live forever. So, yeah, don't hold back on the vaccines (but careful of any autistic side effects)


Are spinal nerves myelinated and unmyelinated at the same time? I was trying to answer this question when I remembered that the somatic axon is myelinated, while both sympathetic and parasympathetic preganglionic axons are also myelinated. Are they only myelinated or are they both myelinated and unmyelinated? Thanks
Edit:
This is a question from an old lecture quiz (previous year) and unfortunately I do not have the answers for the questions. The wording of the question was

Spinal Nerves are
a.) myelinated
b.) unmyelinated
c.) answers a and b
d) none of the above"

Spinal nerves are mixed nerves containing afferent and efferent neurons of various types. Anatomically, they protrude from the spinal column bilaterally at each vertebral level. They contain both myelinated fibers (e.g., A fibers) and unmyelinated fibers (e.g., C fibers).

The answer is (c): both myelinated and unmyelinated.

Please note that spinal nerves are NOT located in the spinal cord, despite the fact that neurons in each spinal nerve will either originate or terminate there. A spinal nerve is a peripheral structure. It starts at the point where the dorsal and ventral root converge (See April's Clinical Anatomy, Ch. 1). If you have the opportunity to observe back surgery or dissect a human cadaver, you can see and touch a spinal nerve. They are cable like structures containing bundles of many many many axons, but no neuron in its entirety. A nerve is not a neuron. This is a common misconception.

Just to add, the details here may seem like trivia, but they are not. Similar questions (and questions that require you to understand the distinction between a nerve and a neuron) are often asked on US medical licensing exams. This is because they are relevant to understanding and interpreting neurological symptoms and physical exam findings.

Yes, there is grey and white matter in the spinal chord and the parasympathetic nervous system, so they are both myelinated and unmyelinated:

Here is an image of parasympathetic nerves:

Primary afferent fibers of the dorsal roots are either myelinated or unmyelinated. In the rat, cat, and monkey, thin unmyelinated and thick myelinated fibers are located in the lateral and medial parts of the dorsal roots, respectively, in the dorsal root entry zone (Light and Perl, 1979a).


Adult Bugs in Low Humidity House Heated With Wood? I have a home heated with wood. The humidity is currently around 30% but I'm guessing these bugs have reproduced when the humidity was higher. They really have a hard time when I see them in the basement.

I do have some wood that was a little punky. They seem to come out as soon as I start a fire in the stove, probably due to the heat?

Approx 3cm long

Located in the eastern townships of Quebec, Canada. Any suggestion on what this is and how to treat them?

The pictures are not entirely clear, but I’m relatively certain that it is a wood wasp of the genus Xiphydria (family Xiphydriidae). Traits that point to this is e.g. 2 pair of wings (i.e. a wasp and not a fly), narrow slender antenna, elongated body, the shape of the head sitting on a relatively long “neck”, often with light/white markings on the top and or the back of the head (which can be seen on picture 2) and often white markings along the side of the abdomen (which your insect has) The second picture also shows the relatively robust ovipositor (used to inject eggs into wood).

They also lay eggs into dead wood (usually deciduous wood) and are not uncommon to find in houses, hatched from fire wood.

The species is very hard to determine though, but X. mellipes could be one bet. This species also seem to be found in Canada, see zoology.ubc.ca/entomology. It is also similar to Xiphydria camelus which is common here in Sweden, but I’m sure if it is also found in Canada.

(Xiphydria mellipes from wikimedia commons

Pictures of some species can be seen at bugguide.net).

These insects are not dangerous to find inside, and they only attack dead wood in standing or fallen trees, not construction wood. They are not uncommon to find indoors (along with longhorn beetles and other wood insects) if you bring in mixed fire wood, especially if the wood wasn’t processed and dried quickly after felling. An interesting feature of these insects is that many (all?) inoculate the wood with particular fungi spores, and the fungi later function as the food for the larvae.

I think that is a soldier fly.

https://animals.howstuffworks.com/insects/will-black-soldier-fly-maggots-save-humanity.htm

The adults do not eat or sting, only mate, lay eggs and die.  The maggots are very large and awesome devourers of rotten fruit.  They alternate with worms in my worm bin depending on season.

I have no idea what they are doing in your house!


Crow branch pecking behaviour I was walking through a small park when two crows started cawing at me, and followed me, flying from tree-to-tree as I walked. I speculate that this is a territorial or protective behaviour, but what I found different was the crows were violently pecking the branches nearby them. I have no memories coming to mind of seeing this behaviour beforehand. I speculate that this behaviour could be threat displays, but a quick search on Google did not reveal to me any authoritative studies on this phenomenon. I'd appreciate more information and sources.

This is a good question. This type of behavior -- pecking at a branch, wiping the side of the beak on a branch, pulling off twigs and dropping them, or knocking off pieces of bark -- is quite common among many corvid species, particularly when they are interrupted by something or someone that they might consider a threat. This includes not only potential predators but also potentially hostile conspecifics.

It is typically considered to be a form of displacement behavior. The concept of displacement behavior, from classical ethology, posits that when an animal experiences two conflicting drives to do two different things, it doesn't know which to do and does a third thing instead to dissipate the drive or anxiety. For branch-pecking in crows, see E.g Kilham and Waltermire 1990 Ch. 12.

Referece: Kilham, L., & Waltermire, J. (1990). The American crow and the common raven. Texas A&M University Press.

Yes I watch Corvids from my bedroom window as there are two large sycamores outside my house and a large field over behind the two trees ,and regularly find Crows or jackdaws and magpies in the trees displaying beak wiping and doing a sort of Hammer jacking on the boughs with their  beak . I`ve even got to know some of their language now they call . One distinct call I now know is a Danger alert sound they make when a Fox is about.
 The Corvids are without a doubt very intelligent birds. They will even bury any excess of food they find to come back to at a later date..


Why does autosomal trisomy have more adverse effects than sex choromosome monosomy or trisomy? Autosomal trisomy syndromes are usually lethal but sex chromosome number related abnormalities do not lead to that much fatality. why?

It has to do with dosage compensation:

The Y chromosome contains relatively few genes. Interestingly, chromosome 21 and 18, which are over represented in the most common viable trisomies, are also relatively small.
Humans already possess a mechanism to compensate for additional X chromosomes: X-inactivation. Normally this inactivates one of the two X chromosomes in females but can also inactivate two in cases of X trisomy.

  Humans are much more able to tolerate extra sex chromosomes than extra autosomes. … Compared to autosomal trisomies, … sex chromosome trisomies are fairly benign. Affected individuals generally show reduced sexual development and fertility, but they often have normal life spans, and many of their symptoms can be treated by hormone supplementation. The ability of humans to tolerate supernumerary sex chromosomes is quite remarkable, as individuals can survive with as many as four sex chromosomes. This tolerance most likely relates to both X inactivation and to the small number of genes on the Y chromosome. In fact, when cells from individuals with more than one copy of the X chromosome are analyzed under a microscope, all but one of the X chromosomes appear as condensed Barr bodies, the cytological manifestations of X-chromosome inactivation. Supernumerary copies of the Y chromosome may be tolerated because the few gene products of the Y chromosome are not required for survival.

From: Chromosomal Abnormalities: Aneuploidies by Clare O'Connor (emphasis added)

An added bonus (and I feel as though I should actually write something myself), I recently read a paper studying trisomy 21:

Jiang J, Jing Y, Cost GJ, Chiang JC, Kolpa HJ, Cotton AM, Carone DM, Carone BR, Shivak DA, Guschin DY, Pearl JR, Rebar EJ, Byron M, Gregory PD, Brown CJ, Urnov FD, Hall LL, Lawrence JB. 2013. Translating dosage compensation to trisomy 21. Nature 500(7462):296-300.

Using zinc finger nucleases, they inserted a XIST transgene into chromosome 21 of cells derived from Down syndrome patients. XIST is a gene centrally involved in X-inactivation. They found that, by inserting it into chromosome 21, they were able to silence one and revert the trisomic cells to a more normal phenotype.

Assuming you are discussing our species, sex chromossomes abnormalities do not lead to such fatality because of it's purpose, i.e a gene in these chromossomes mainly affects sexual related hormone producing which do not play any role (there are exceptions like steroid hormones) in general metabolism or imune responses so a mutation in those genes or a duplication of chromossomes does not cause the death of the individual and it survives during the embryonic and fetal stages becoming later a healthy individual but with serious sexual problems like infertility and sterility . In the other hand, a mutation or duplication in autosomal chromossomes is likely dangerous to survival of the organism and many times it cannot survive in the early stages. Those who survive many times face serious health problems in their life because unlike sexual activity, autosomal gene functions are necessary for cells to survive. Sexual activity is just a way to pass genes between generations not to survive in one generation !


Do birds grieve and feel emotion? Crows are surprisingly clever with tool making/use and even understanding displacement water over sand! Clearly there's some relatively high level cognitive processes going on up in those avian brains.

When I stumbled across a video of what appears to be a bird grieving over its mate (shown in clip below), I wondered how far animal emotion and psychology goes.

Is that bird in the video grieving? (and shaking because of stress?)
What species of bird is this?

Your "grieving bird" is a video of a peregrine falcon (Falco peregrinus) and its (nearly?) dead chick on a hot summer day in Phoenix, Arizona (USA) in 2016.

 Photo credit: Arizona Game And Fish Department

The video is from a nest camera webcam set up in the Maricopa County building in Phoenix, Arizona by the Arizona Game and Fish Department.(See this video for more information). The camera was active in 2016, but according to here the falcons did not return to the nest in 2017. Your video shows one of the adult birds with the only chick that hatched (out of 4 eggs) in 2016. That chick died from a combination of heat and an 8-story fall in June 2016 [Source]. Your video is an edited and audioless version of a video capture of the live stream that can be seen on Youtube. The information for this video indicates that the adult bird in view is the father.

The adult falcon in the video is not wimpering, crying, or grieving. Instead, the bird is trying to cool down on a hot day. He is displaying a familiar temperature regulatory behavior: panting.

From Bartholomew et al. (1968):

  Most birds pant when subjected to heat stress...

In fact, in the more complete video I link to above (with audio), you can clearly hear the bird making panting sounds while breathing heavily.
The falcon also spreads out its wings to better help cool himself down toward the end of the video as it cares to its injured chick.

You can see another video of a panting falcon in New Hampshire (USA) here, and you can find more information about panting, gular fluttering, and other thermoregulatory behaviors in birds here, here, and here.

There seems to be a long folk tradition that birds do grieve:

“All the birds of the air fell
a-sighing and a-sobbing
when they heard the bell toll
for poor Cock Robin”

See the Wikipedia article on Cock Robin.


Why do the brains of cocaine-users shrink faster than the brains of non-cocaine users? http://news.sciencemag.org/sciencenow/2012/04/cocaine-may-age-the-brain.html?rss=1

  Cocaine-dependent individuals showed a significantly greater-than-normal age-related decline in gray matter in prefrontal and temporal regions compared with healthy controls. By contrast, parts of the striatum appeared resistant to age-related volume decline in the cocaine-using group. Enlarged striatal volume has frequently been reported in stimulant-dependent individuals,5, 6 possibly reflecting a marker of reduced dopamine neurotransmission in this dopamine-rich brain region where drugs like cocaine work. Decline in striatal dopamine receptor density has been associated with normal age-related cognitive decline.7 The relative absence of age-related changes in the striatum of cocaine-dependent people may thus reflect another feature of an abnormal brain ageing process.

Could it be related to possible neurotoxicity, or to the long-term effects of dopamine receptor downregulation? Could the effects also be generalizable to those who take dopamine-based ADD medications?

A link to the Letter to the Editor appeared in Molecular Psychiatry to which the ScienceNow article refers:
Cocaine dependence: a fast-track for brain ageing?

The mechanism of action of cocaine is dependent on pre-existing dopamine production and secretion. Normally, secreted dopamine is cleared from the synapse via the dopamine transporter (DAT) located on presynaptic dopaminergic terminals. Cocaine inhibits
this reuptake of dopamine, increasing it's duration of action on post-synaptic dopamine receptors. Thus, cocaine's effect depends on neuronal dopamine production. Without intrinsic dopamine, cocaine would have no effect. This is actual not exactly true though because cocaine also inhibits serotonin and norepinepherine reuptake transporters as well but the same argument applies to those neurotransmitters as well.

The overall effect of cocaine on the nervous system is extremely complex as it prolongs the action of dopamine, serotonin and norepinephrine wherever those reuptake transporters are present. There is a particularly high density of DAT in the basal ganglia and nucleus accumbens. What these areas of the brain normally do is under intense study and debate. The accumbens may play a role in goal directed behavior and incentive salience, which is the attribution of value to various actions or objects in the environment. This is what naturally guides us to perform one action over another. The simplistic view is that cocaine "highjacks" this system such that cocaine itself acquires greater incentive salience than natural reinforcers such as food, sex, money etc.

Getting back to the original question regarding why cocaine causes brain atrophy. This appears to be a finding quoted from a paper by the original inquirer. It is not obvious to me what the mechanism of this atrophy would be. I suggest you look at the discussion section of the paper from which that abstract was quoted to see what the authors suggest. However, to my knowledge, such atrophy has not been widely discussed in the cocaine literature but I could be wrong.

For further information see Sulzer. 2011. How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission.

Cocaine hits the brain with dopamine creating the desired high, which, the users seek. When used repeatedly, the brain begins to confuse it's own production with the user's introduction. Slowly, the brain begins to depend on the user's introduction and slows its own production to the point where it no longer produces it. This lack of production causes the part of the brain responsible for dopamine to shrink. It shrinks because it is tissue that is not being used and therefore doesn't get the proper blood flow to it and begins lose its health. Blood stimulation is lost, cell health is lost and size is thereby lost.

The brains of heavy cocaine users display little to no age-related brain shrinkage as compared to non-users because their brain has already shrunk to its limit. The shrink is due to lack of fresh blood stimulation. It is like a sponge that no longer is getting water and shrivels. After 2 days the sponge stops shrinking, it doesn't eventually shrink to a dust particle. It shrinks to its water-free size, the same way the cocaine user's brain shrinks to a blood-stimulation-free size. Age can't further shrink what's already maxed out in shrinkage.


Why don't mammals have more than 4 limbs? Arthropods have 6 or more limbs and arthropods with 6 limbs appear to move faster than arthropods with 8 limbs so I wonder whether this might have something to do with fast and efficient locomotion. But, this is just a guess. I wonder what the official explanation is, if it exists.

Number of legs in terrestrial vertebrates

Not only do mammals have four legs but actually all terrestrial vertebrates (which include mammals) have four legs. There are slight exceptions though as some lineages have lost their legs. Typically snakes have no legs anymore. Apesteguia and Zaher (2006) discuss the evolution of snakes legs reduction and report a fossil of snakes with a robust sacrum. Cetaecea (whales and friends) have lost their hind legs but we can still spot them on the skeleton. See for example the orca (killer whale, easily recognizable to its teeth) on the picture below. Pay attention to the small bones below its vertebral column at the level on the left side of the picture.

I also want to draw attention to the importance of the definition of legs. I guess that we would call something a pair of legs if it is constructed using a similar developmental pathway than current existing legs. If we are using some broader definition, then a prehensile tail as found in some new world monkeys, for example, could be considered as a leg (but only a single leg, not a pair of legs obviously). A list of animals having a prehensile tail can be found here (Wikipedia).

Did you say Natural Selection?

I think (might be wrong) that you have too selectionist a view of evolution. What I mean is that you are wondering why mammals have four legs and you're looking for an explanation of the kind "because mammal have this kind of need of locomotion and for this purpose four is the most optimal number of legs". Consider the following sentence: "If there is a need, natural selection will find a way!". This sentence is wrong! Evolution is not that easy. This false view of evolution is sometimes referred to as panselectionist.

The reality is that it is not easy to evolve such a developmental pathway as drastic as having an extra pair of legs that are well integrated into the body of the carrier of this new trait. Such an individual would need a brain, a nerve code, a heart and some other features that are adapted to have extra legs. Also, assuming such a thing came to existence it is rather complicated to imagine how it could be selected for. To go slightly further, you have to realize that there are many stochastic processes in evolution (including mutation and random variation in reproductive success) and an organism is a piece of complex machinery and is not necessarily easily transformable to some other form that would be more efficient (have higher reproductive success). Often going from one form to another may involve a "valley crossing" meaning that if several mutations are needed, intermediate forms may have low reproductive success and therefore a high amount of genetic drift (stochasticity in reproductive success) to cross such valley of low reproductive success. See shifting balance theory. Finally, even if there is selection for another trait, it may take time for the mean trait in the population to shift especially if there is only little genetic variance. A complete discussion on why the sentence "If there is a need, natural selection will find a way!" is wrong would fill up a whole book.

Gould (1979) is a classic article on the subject and is very easy to read even for a layperson.

Why 4 legs?

Terrestrial vertebrates have four legs because they evolved from a fish ancestor that had four members that were not too far from actual legs (members that could "easily" evolve into legs). This is what we call a phylogenetic signal. The explanation is as simple and basic as that. You can have a look at the diversity of terrestrial vertebrates here (click on the branches).

Number of legs in invertebrates

Arthropoda (Spiders (and other chelicerata), insects (and other hexapods), crustaceans (crabs, shrimps…) and Myriapoda (millipedes) and Trilobite as well)) evolved from a common ancestor who had a highly segmented body. From this ancestor, many groups have fused some segments. In these taxa, each pair of legs is attached to a particular segment (I don't think the segments are still visible in spiders today). In insects, for example, all 6 legs are attached to the thorax but to 3 different segments of the thorax, the pro- meso and meta-thorax (see below).

As a side note, it is interesting to know that the wings in insects did not evolve from the legs (as it is the case in birds and bats). There are two competing hypotheses for the origin of insect wings. Wings either developed from gills or from sclerite (chitine plate, the hard part of the insect). When insect first wings, they actually evolved three pairs of wings (one on each segment of the thorax). At least one pair has then been lost in all modern species. In the diptera, a second pair of wings have been lost and are replaced by halteres, particularly easy to spot in craneflies (see below picture). In millipedes, the link between segmentation and legs is even more obvious (see picture below). You can have a look at the diversity of Arthropoda here (click on the branches).

Pictures

Update 1

Asking how likely it is for a given population to evolve a given trait is extremely hard to answer. There are two main issues: 1) a definition of the question issue and 2) a knowledge issue. When asking for a probability one always needs to state the a priori knowledge. If everything is known a priori, then there is nothing stochastic (outside quantum physics). So to answer the question one has to decide what we take for granted and what we don't. The second issue is a knowledge issue. We are far from having enough knowledge in protein biophysics (and many other fields)  to answer that question. There are so many parameters to take into account. I would expect that creating a third pair of legs would need major changes and therefore one mutation will never be enough in order to develop a third pair of legs. But, no I cannot cite you any reference for this, I am just guessing!

Following the wings example in insects. Insects have had three pairs of wings. While some mutation(s) prevented the expression of the third (the first actually) pair many of the genetic information for this third pair remain in the genotype of insects as they still use it for the two other pairs. Taking advantage of that, Membracidae (treehoppers) developed some features using a similar biochemical pathway than the one used to develop wings. Those structures are used as protection or batesian mimicry.

Update 2

Let's imagine that an extremely unlikely series of mutations occur that create some rodent with 6-legs. Let's imagine this rodent with six legs has a larger heart in order to pump blood to these extra legs and it has a brain that is adapted to using six legs and some changes in its nerve cord so that it can control its 3rd pair of legs. Will this rodent have higher reproductive success than other individuals in the population? Well… let's imagine that with its six legs, it can run faster or whatever and has a very high fitness. How would the offspring of a six-leg mother (or father) and a four-leg father (or mother) look like? Will it be able to reproduce? See the issue is that it is hard for such trait to come to existence because 1) it needs many steps (mutations) and 2) it is hard to imagine how it could be selected for. For those reasons, there exist no vertebrates with 6 fully functional legs.

Well, let's assume it does and in consequence, after 200 generations or so, the whole population is only made of 6-legged individuals. Maybe the species got extinct then and no fossil record has ever been found. This is possible. It is not because something has existed that we necessarily find something in the fossil record.

Don't forget the laws of physics...

Yes, tetrapods (mammals, birds and herptiles), may have initially inherited genes for two pairs of limbs from their fish ancestors, but why do fish themselves have limited numbers of fins, rather than sixteen or 400?

Moreover, some tetrapods have lost one or even both pairs of limbs.

To put it in perspective, how many invertebrates can you think of that have just two pairs of legs? If vertebrates can lose limbs, so can invertebrates. Yet Nature seems to favor greater numbers of limbs among invertebrates.

I don't know exactly why, but I suspect it could be something as simple as physics. Imagine an elephant with six massive, pillar-like legs. The animal would be significantly heavier and therefore slower. Plus, it would need more nutrition to support the extra limbs.

So I would argue that the answer is a combination of genetics and "physics," in the broad sense of the term.


Insect identification: Fly with eye strip Location details:
Country - India,

State - Tamil Nadu,

District- Chennai.

Found this fly in my backyard keen to know its exact name. Thanks for the help

Definitely Stratiomyidae, probably genus Odontomyia. Very widespread and species-rich genus.
Here is an example of Odontomyia - not the same species - https://www.flickr.com/photos/63075200@N07/sets/72157632905103705/.


Why do I only breathe out of one nostril? I was just sitting with my hand next to my nose and I realized that air was only coming out of the right nostril. Why is that? I would think I would use both, it seems much more efficient. Have I always only been breathing out of my right nostril?

Apparently you're not the first person to notice this; in 1895, a German nose specialist called Richard Kayser found that we have tissue called erectile tissue in our noses (yes, it is very similar to the tissue found in a penis). This tissue swells in one nostril and shrinks in the other, creating an open airway via only one nostril. What's more, he found that this is indeed a 'nasal cycle', changing every 2.5 hours or so. Of course, the other nostril isn't completely blocked, just mostly. If you try, you can feel a very light push of air out of the blocked nostril.

This is controlled by the autonomic nervous system. You can change which nostril is closed and which is open by laying on one side to open the opposite one.

Interestingly, some researchers think that this is the reason we often switch the sides we lay on during sleep rather regularly, as it is more comfortable to sleep on the side with the blocked nostril downwards.

As to why we don't breathe through both nostrils simultaneously, I couldn't find anything that explains it.

Sources:
About 85% of People Only Breathe Out of One Nostril at a Time
Nasal cycle

As others have said, this phenomena is called the nasal cycle, a process controlled by the autonomic nervous system that alternants congestion between your nostrils. Mentalfloss of all places has an article about this that explains:

  ...it makes our sense of smell more complete. Different scent
  molecules degrade at different rates, and our scent receptors pick up
  on them accordingly. Some smells are easier to detect and process in a
  fast-moving airstream like the decongested nostril, while others are
  better detected in the slower airstream of the congested nostril.
  Nasal cycling also seems to keep the nose maintained for its function
  as an air filter and humidifier. The alternating congestion gives the
  mucous and cilia (the tiny hairs up in your nose) in each nostril a
  well-deserved break from the onslaught of air and prevents the insides
  of your nostrils from drying out, cracking and bleeding.

link: http://mentalfloss.com/article/30363/why-does-your-nose-get-stuffy-one-nostril-time


What actually happens when my leg 'falls asleep'? Most people have experienced the temporary loss of feeling and tingling in their leg resulting from sitting in an abnormal position for a short while. Usually you get a loss of feeling in your leg while it is being compressed/constricted at some point and then the tingling sensation as the pressure is removed. But what is actually happening? I understand the the blood vessels are probably constricted from the pressure, but how does this lead to loss of feeling and later the strange tingling sensation? Are there any other things that extended compression on the leg does to cause this? What exactly are the requirements to get the sensation of a one's leg or other limb falling tingling in that manner?

The feeling you describe is called "paresthesia," and according to the NINDS info page, it happens "when sustained pressure is placed on a nerve."

The explanation in the link Polynomial posted is essentially correct.

Whenever there is a reduced or blocked blood supply (ischaemia) to your extremities, the 'five P's' can occur: pulselessness, pain, pallor (colour), paresthesia (numbness) and paralysis (or weakness).(1).

The numbness and weakness happen after the blood flow have been reduced for a particularly prolonged period.

Cells in our body require a blood supply to stay alive (think about a stroke or heart attack for example). So a reduced supply can cause them to function abnormally or after a time (depending on the cell or tissue type) die.

So with a 'sleeping leg', staying in an awkward or particular position where arterial blood supply is blocked or reduced to the leg, the muscle, nerve tissue etc all lack supply hence causing sensory disturbance and weakness.

The possible buildup of metabolites could also contribute to the symptoms (pain).

Hope that helps!

Miller's Anaesthesia - Miller.


How do gory images lead to nausea? How do gory images lead to nausea?

Yesterday my friend visited shock sites (a website). He said that he got nauseous sensation within seconds after viewing the gory images. However, I don't understand how seeing such sights can lead to nausea? Eyes are present at the top of the head and the digestive tract is present below the mouth. They aren't physically connected.

The connection between eyes and food pipe had to do nothing with the motion sickness because the visual inputs and outputs to these sensory information are processed in the brain itself, So there is not need for eyes and food pipe to be connected together in order to cause nausea.

  Vasovagal response or vasovagal response or vasovagal attack (also called neurocardiogenic syncope) is a malaise mediated by the vagus nerve. When it leads to syncope or "fainting", it is called a vasovagal syncope, which is the most common type of fainting.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

This case is most commonly seen in adults and adolescents. There are several syndromes which comes under the vasovagal syncope which consists of symptoms like loss of consiusness,lightheadness,nausea,sweating,tinnitus,confusion,altered heart rate,fuzzy thoughts,cloud like spots in vision etc.

  Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

Several pshychiatric disorders can cause vasovagal response like,

Agoraphobia
Obsessive–compulsive disorder
Social anxiety disorder
Blood-injury phobia
Hemophobia
Traumatophobia
Trypanophobia

http://www.nwocc.com/Pt%20Education/neuro_syncope.pdf http://en.wikipedia.org/wiki/Vasovagal_response

  When it comes to seeing red, the faint feelings could be tied to a phenomenon called blood-injury phobia. According to WebMD, this condition evolved as a way for humans to cope with threats:

  "The idea is that back in time, when someone was coming at someone else with a sharp stick or rock, a kind of genetic variation allowed certain people to faint in response," explains Tyler C. Ralston, PsyD, a clinical psychologist in Honolulu, who treats people with blood-injury phobias. Warriors who fainted looked dead and were passed over during battle. The blood pressure drop also might have helped those who were wounded avoid bleeding to death. Survivors then passed on the "fainting" gene.

(from: http://www.popsugar.com/fitness/Why-Sight-Blood-Makes-You-Feel-Faint-3061135)

"Overcoming Obstacles in CBT" written by Yvonne Tone and Michael McDonough states a condition about a patient having similar psychological problem described in the question. Here the patient's panic is associated with "gory images" of injury or illness, and his responses included intense nausea, pale skin, sweat and sometime fainting. He also reports avoiding gory scenes on TV/filim and medical programmes. The problem is identified as co-morbid panic/agoraphobia and blood injury phobia.

http://books.google.co.in/books?id=1uIYqkKgKRYC&pg=PA44&dq=nausea+and+gory+images&hl=en&sa=X&ei=qLZ2VJPMJ420uAS8qoHIBA&ved=0CB0Q6AEwAA#v=onepage&q=nausea%20and%20gory%20images&f=false

The connection is almost certainly psychological.  For me, I can watch Grey's Anatomy, Spartacus, or any number of bloody shows while eating, but while researching microsurgery I came across an image of a hand cut in half and it bothered me for an entire day.  Therefore, for me at least (and likely others) nausea from gore is context dependent and therefore likely psychological.

Then again, there may be some biological basis.  From https://en.wikipedia.org/wiki/Disgust#Neural_basis :

  Functional MRI experiments have revealed that the anterior insula in the brain is particularly active when experiencing disgust, when being exposed to offensive tastes, and when viewing facial expressions of disgust.

That Wikipedia article links to this Letter to Nature: http://www.nature.com/nature/journal/v389/n6650/full/389495a0.html which provides more detail.

Also, the part of the brain that actually controls vomiting is called the Area postrema.

So...  in short, my answer is "The insular cortex of the brain is responsible, though there is a large psychological component."


When a muscle contracts, but not all the muscle fibers are activated, what happens to the remaining muscle fibers? I understand how motor neurons work, but I would like clarification on what exactly is going on when a muscle contracts. For the sake of simplicity, let's just use the bicep as an example. If I do a bicep curl with a weight that is the maximum weight my bicep can lift, all the muscle fibers in my bicep will be activated and contract(more or less). If I remove the weight and do the same bicep curl, now only a small percentage of the muscle fibers in my bicep will be activated and contract, because that extra force isn't needed. But, the whole bicep muscle is still contracting! It must be, otherwise wouldn't the other muscle fibers staying at regular length prevent the bicep from contracting?

So the only thing I could think of is that the unactivated muscle fibers are pliant and DO contract, they just don't initiate the contraction, but instead go along for the ride. So if you looked at the level of sarcomeres, in the activated muscle fibers, the myosin heads pull on the actin, causing contraction. In the unactivated muscle fibers, myosin heads are NOT pulling on the actin, but the sarcomeres are still contracting, due to the forces from the activated muscle fibers. Is this a correct interpretation of what's going on or am I wrong?

I don't think the unused sacromeres will contract though because every time you contract, it requires ATP and so it will be really expensive if you contract when you don't need to. I believe the unused muscle fibre will just be compressed or bent, since cells have a certain degree of compliance. I am guessing that is also why you won't feel your muscle as hard if you are not doing MVC


Where are the evolutionary "inbetweeners"? The problem I've always had with evolution is the actual lack of variation between animals. More specifically, the lack of observable gradual change between species.

Take for example the hammerhead shark. It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right? As far as I understand, evolution works by random mutation in a child being somehow slightly beneficial to that animal so it get's to live longer and reproduce more, eventually resulting in it's genetic material in dominating the inferior ones before it. But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now? On the other hand, if it wasn't beneficial, how come the hammerhead still exists?

Furthermore, I feel like some characteristics of a certain animal can't really have gradual benefits. There's a lizard that shoots blood out of it's eyes. The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life. So for it to actually become beneficial, it seems to me that there had to be a ton of lizards that had a disadvantage of bleeding slightly. In fact, there had to be so many that they evolved even further in the same direction and kept doing that until they bled so much it's an actual benefit (sorry for this turning so gross). So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

More specifically, the lack of observable gradual change between species.

Most significant phenotype differences occur over several thousand generations, which means several thousand years on up. While we certainly can create experiments where a controlled form of evolution occurs within a very small time-frame, I'm going to assume that you're not interested in closed laboratory experiments given the nature of your question.

  It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

The data below does answer you question, but in reverse. Hammerheads are much older than most of their relatives; so their cousins have actually grown smaller heads... but there are certainly intermediates.

From Andrew Martin (1993 - mtDNA data) via Elasmo-research.org:
*The circles represent the head-width vs. body-length ratio.

Martin's conclusion: "...the hammer appeared rather suddenly and fully formed, and was later optimized along different lines to suit various selection pressures."

  I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right?

Not necessarily. Single Nucleotide Polymorphisms (a.k.a. - "SNPs" - a change in one nucleotide) can have pretty wide-ranging effects.

The vast majority of humans, for instance, are lactose intolerant in adulthood. However, lactose tolerance evolved twice from two different SNPs in two different human populations: One European and one African. One gene. One regulatory mechanism change. Massive benefits (essentially opening up a whole new resource in adulthood).

Significant differences in phenotypes (the physical appearance of something) can require more gene mutations, or not. It depends on where the mutation is in the genome and what the gene does.

  But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now?

The simple answer is because either there wasn't enough selective pressure that the rest of the shark phenotypes succumbed to that the hammerhead avoided, or that the hammerhead design doesn't give enough of an advantage to completely dominate the gene pool. An alternate, but more abstract answer, is that there simply hasn't been enough time for the hammerhead design to dominate the shark phenotype. Remember, evolution works by generations - not years. It would take unknown thousands of generations for a weakly-advantageous design to dominate an entire niche - if it ever would.

Also, it is worth it to point out that evolution doesn't only select for advantageous mutations. Mutations that aren't very detrimental can still exist within a population as long as the detriment doesn't prevent resource exploitation and offspring production. Think Huntington's Disease which severely restricts a person's survivability, but only after their mid-30's (in general) - plenty of time for the person to have sex and raise a kid into semi-adulthood. It is a genetic defect which sticks around only because it allows humans to reproduce before it seriously affects them.

  The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life.

Maybe, maybe not. Maybe it shot something else before blood, and then a mutation caused it to shoot blood instead - but the overall effect (deterring predators) was the same so it doesn't really matter.

You're correct that some traits might appear very awkward if they had evolved gradually, but the question then becomes: Did they evolve gradually? Sometimes we simply do not know.

  So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

Like I said above, just because a trait is detrimental doesn't necessarily mean it will be eliminated. As long as the being can survive long enough to reproduce successfully with the trait, the trait might not be eliminated for a very, very long time- if ever.

As for in-betweeners dying out - it's difficult to think of it like that. You're talking bout LCAs ("Last Common Ancestors") of extant (currently-living) species. While some LCAs just die out for some reason or another, it's more common that the LCA simply continued to evolve and become a genetic relative due to some sort of isolation.

Think of it like the in-betweeners coming to a fork in the road. Some choose right, some choose left. There isn't anybody left behind - merely two populations that are changing over time that were once one group until they don't really mate between each other anymore (or can't). Heck, even Biologists have trouble deciding at what point a population is considered a different "species" because of discoveries in the last 50 years - so right now a firm answer like "It takes 15% of the genome to change for a new species to emerge" isn't possible as it doesn't really work like that.

We'll get to it eventually, but for the time-being, it might be easier to say that everything currently living on Earth is an in-betweener of something else in the future. Everything in its current iteration will eventually die off, but not before something else emerges from our offspring which may or may not be significantly different from us due to however many genetic mutations our offspring have from us. It could be one that opens up a whole new realm of possibilities (like lactose tolerance) or an accumulation due to selective pressures (like Phoemelanin production and pale skin in humans [Redheads] to produce more Vitamin D3 at higher latitudes).

If an inbetweener offers a slight advantage to survival, and if the full-fledged trait even more so, then once the full-fledged population becomes sufficiently large, they will have the advantage and the inbetweeners will die out.


In Darwinian evolutionary theory, does the environment has any role? In Darwinian evolutionary theory, does the environment has any role?

To state it clearly:

Suppose I have an isolated system. First, I place several types of entities (organisms) in an environment. According to Darwin, eventually, the fittest will survive.

Next time, I place Only one organism. Will it survive this time as there's no one else in the system?
If not, did Darwin also consider the whole environment as another entity, so that in the above case, there are two entities, the organism and the environment. The environment is more evolved and it survives, other dies?

Moreover, if the climate is favourable and the organism reproduces sexually results in the same fate as the case if climate is unfavourable, organism reproduces asexually, what conclusion does it leads to?

"According to Darwin, eventually, the fittest will survive"

Darwin never said this. Fitness and survival are two separate concepts.

In a simplistic version, fitness is measured by reproductive output. Survival is, well, survival. You can have higher output than your brother, but have a lower chance survival. In fact, the very act of producing offspring can negatively affect your ability to survive.

No, the environment is not an other organism, in any context. It is the place (stage, arena, etc) in which the measure of fitness (reproductive output) can be measured. The environment can directly influence and affect fitness, and other organisms (inter and intraspecific) ARE part of that environment.

A single isolated organism does not evolve, but can have offspring. However, you need a more than one organism for fitness to have any meaning in a Darwinian model.


Are there any substance that are more dangerous at low dose than at higher dose? It is commonly admitted that

  The dose makes the poison

which means as a person, the more I take a substance, the more risk I take for my health.

There is even an indicator called LD50 (see Median Lethal Dose), which specifies the 'lethal dose' at which 50 percent of subjects will die.

This might seems a stupid question but: are there any substances for which it is more dangerous to take at low dose than at higher dose? For example, you have to ingest at least 1µg of XXX because if you ingest less you will have health problem...

Yes. Taking antibiotics (and by extension antivirals and antineoplastics) at low doses is dangerous, as this creates an evolutionary pressure to evolve antibiotic resistance (or rather, incorporate through horizontal gene transfer). This is dangerous because an infection resulting from these bacteria will then be harder to treat.

In the paper "Experimental evolution of resistance to an antimicrobial peptide", Perron et al. gave E. coli the chance to evolve resistance against a novel antibiotic. When given a high dose initially, most bacteria died. When exposed to low doses, the bacteria evolved resistance in 600 to 700 generations.

For the same reason it is strongly advised to finish a course of antibiotics even after symptoms fade.

First of all, that is an excellent question! Secondly, please excuse the lack of thorough sourcing for this post. I only like to share some pointers...

Q: Can substances do more harm in a mammal at a lower dose than at higher dose?

A: Yes.

Some may know the example of the blood thinner, and widespread NSAID Acetyl-salicylic acid (Aspirin). I will use this example because Aspirin is one of the most known and used drugs in the world, with a long and interesting history. As being part of the class of nonsteroidal anti-inflammatory drugs (NSAIDs) it has recently gotten a bad wrap for blocking an enzyme which is crucial for prostaglandin synthesis and processes that maintain  a healthy stomach wall in the presence of an potentially harmful bacterial and chemical milieu. On a sidenote, as an acid, Aspirin actually hardly dissolves directly in the acidic stomach.

To quote wikipedia (DOR: 28/09/2012):

  Salicylates are excreted mainly by the kidneys as salicyluric acid
  (75%), free salicylic acid (10%), salicylic phenol (10%), and acyl
  glucuronides (5%), gentisic acid (< 1%), and 2,3-dihydroxybenzoic
  acid.[148] When small doses (less than 250 mg in an adult) are
  ingested, all pathways proceed by first-order kinetics, with an
  elimination half-life of about 2.0 to 4.5 hours.[149][150] When higher
  doses of salicylate are ingested (more than 4 g), the half-life
  becomes much longer (15–30 hours),[151] because the biotransformation
  pathways concerned with the formation of salicyluric acid and salicyl
  phenolic glucuronide become saturated

Aspirin can interfere with a lot of drugs, including Ibuprofen. The known list of drugs is so high, in part due to the widespread application of aspirin, and in part due to the chemical composition of this very small drug with two functional groups. A functional group is a sort of chemical feature that determines how and with what probability a chemical interacts in a given milieu.

As a certain metabolic degradation pathway may get saturated, other pathways can take over and lead to different potentially harmful metabolites resulting in damage to the excretion/clearance organs such as the liver (hepatotoxic) and kidney (nephrotoxic).
A metabolite is the product of metabolism ( a weak back-referencing definition). metabolic pathways are a sequence of chemical reactions within a cell, and metabolism is the entire set of metabolites and pathways.

Liver/Kidney Toxicity is believed to result from an interplay of a) high concentrations of metabolites or direct toxins (=parent chemicals) within specialized high-concentration-forming cells, and b)  the non/covalent  binding of cellular macromolecules to interfere with their normal function and/or production of reactive oxygen species (ROS).

Another example (from memory) is the interaction pharmacokinetics of theobromine (from cacao) and other xanthines (unverified).

There are many more examples. I hope this example and mechanism serves you well as a starting point...

From a biochemical standpoint:

In fact drugs may act differently at different concentration thresholds at different times at different places within an organism and its cells that make it up. Evolution exploited this very early on and used it for things like body segmentation along defined axis during development.
Drugs may interact with each other differently at different levels of concentrations, say as binary, ternary, and higher order complexes. The rate of formation of such complexes is denoted through the dissociation constant - which is a type of equilibrium constant such as pH is.

The dissociation constant describes the propensity of a chemical species to separate reversibly and, - this is crucial! - is concentration dependent. This is accounted for by the use of so called activities or the apparent concentrations, as a result of incomplete hydration of the chemical and other effects of a "crowded environment". Now don't just think of chemicals, but macromolecules as well. In immunology for instance new molecular features can arise on the surface of a macromolecule, due to the association (complexation) with a small molecular drug. This in turn can lead to an immunological reaction, even anaphylaxis ( a so called Type I hypersensitivity reaction) and ultimately shock. Such drugs are classified as haptens.

Important in an organisms sensitivity and susceptibility to drugs however, is the current allometric growth rate and types of organs and cells available. As such a fetus is more susceptible than an adult.

I hope a simple yes accompanied by this admittedly to-long to really read post gave you some insight into what scientist across many, many fields are dealing with. Naturally, the issue is more complex.

Personally I believe the issue of dosing and drug reactions will improve significantly over the coming decade...


What is the reason behind choosing the reporter gene when experimenting on your gene of interest? I noticed within example experiments in class that different reporter genes are chosen to be inserted near your gene of interest to prove whether or not the gene is being expressed. For example, you may insert the gene for fluorescence next to your gene of interest so you know if it is transcribed or not by whether the organism's cells are fluorescent and to what degree they are fluorescing at.

I have noticed in some experiments that have multiple versions that in one case they use the fluorescent gene and in the next a different gene (for example lactose). Both portions of the experiment use almost the exact same steps so why would they not choose the same reporter gene?

Different genes will serve different purposes. For example, if you want to perform colocalization studies, then fluorescent genes like eGFP and DS-Red (or any variation of those, namely Emerald, mCherry, etc) will be quite useful, since you can use different filters on your microscope for the various fluorophores. For morphological assessments, perhaps a LacZ gene or alkaline phosphatase may be better suited, since the detection of these enzymes is compatible with standard histological techniques and you get usually much better contrast than with fluorescence. For quantification purposes, you would use probably firefly luciferase or CAT, since there are very good quantitative assays for these enzymes.

The decision will also depend on the degree of experience of the lab with each detection technique and even in the availability of the constructs. If a reporter is already made by the lab next door and if it fits your needs, you'll just use it, instead of creating your own, even if the reporter gene would not have been your first choice.

Reporter genes have become an invaluable tool in studies of gene expression.A gene consists of two functional parts: One is a DNA-sequence that gives the information about the protein that is produced (coding region). The other part is a specific DNA-sequence linked to the coding region; it regulates the transcription of the gene (promoter). The promoter is either activating or suppressing the expression of the gene.
The purpose of the reporter gene assay is to measure the regulatory potential of an unknown DNA-sequence.So it is quite helpful,it;s kind of reverse engeneering the function and then let know what exactly it does.