Examples of animals with 12-28 legs? Many commonly known animals' limbs usually number between 0 and 10. For example, a non-exhaustive list:

snakes have 0
Members of Bipedidae have 2 legs. Birds and humans have 2 legs (but 4 limbs)
Most mammals, reptiles, amphibians have 4 legs
Echinoderms (e.g., sea stars) typically have 5 legs.
Insects typically have 6 legs
Octopi and arachnids have 8 legs
decapods (e.g., crabs) have 10 legs

....But I can't really think of many examples of animals containing more legs until you reach 30+ legs in centipedes and millipedes. Some millipedes even have as many as 750 legs! The lone example I am aware of, the sunflower sea star, typically has 16-24 (though up to 40) limbs.

So my question is: what are some examples of animals with 12-28 legs?

As a couple of counterexamples, species in the classes Symphyla (Pseudocentipedes) and Pauropoda within Myriapoda have 8-11 and 12 leg pairs respectively, so between 16 to 24 legs (sometimes with one or two leg pair stronlgy reduced in size).

(species in Symphyla, from wikipedia)

Another common and species-rich group with 14 walking legs (7 leg pairs) is Isopoda.

(Isopod, picture from wikipedia)

You also need to define 'legs' for the discussion to be meaningful. As you say, decapods have 10 legs on their thoracic segments (thoracic appendages), but they can also have appendages on their abdomens (Pleopods/swimming legs), which will place many decapods in the 10-20 leg range.

(Decapod abdominal appendages/legs in yellow, from wikipedia)

So overall, in Arthropoda, having 12-28 legs doesn't seem all that uncommon. There are probably other Arthropod groups besides those mentioned here that also have leg counts in this range.

However, for a general account, the most likely answer (if there is indeed a relative lack of 12-28 legged animals) is probably evolutionary contingencies and strongly conservative body plans within organism groups.


Can concentration of a protein be determined from a gel quantitatively (rough estimation)? I've got a His-tagged protein in 6M urea, 500 mM imidazole buffer that needs to be quantified before dialysis to ensure there's enough protein worth dialysing. I ran out of my elution buffer which should be used for blanking. I made a fresh buffer with the same contents, it started giving me false results. I could interpret that problem is with the buffer (probably because of change in chemical batch) from the readings I got in BCA and Bradford assays. Hence, I ran a gel to get an idea of presence of protein. Are there ways to estimate protein concentration quantitatively from the gel?

Yes, you can use SDS-PAGE as a semiquantitative estimate of protein concentration. You need to create a standard curve with a protein of known concentration to compare against. Quantification is done by densitometry. It's a quick and easy process, but keep in mind some limitations:

Band intensity depends not only on the amount of protein but also on the amino acid composition of the proteins and the dye used
The unknown protein and standard should be run on the same gel to remove variations in gels, electrophoresis, staining, destaining and imaging
Densitometry can be quite qualitative depending on how it's done

I'm not sure if you're looking for a protocol, but it's relatively straight forward. I usually load 2, 4, 6, 8 and 10 uL of 100 ng/uL BSA as a standard and 2, 4 and 6 uL of the protein of interest (based on past experience with my proteins and their purification). The gel is stained with Coomassie and the band intensity estimated with a program called ImageJ. A standard curve is created by plotting intensity as a function of mass, from which the concentration of the unknown can be found.


Pros/cons: linear vs. circular DNA Why did Eukaryotes evolve to have linear DNA and not circular like Prokaryotes? What are the pros and/or cons?

This question has been asked before: Is there an advantage to linear chromosomes?

Firstly, I should state that the generalisation that ALL prokaryotes have circular genomes is incorrect. A growing number of prokaryotes have been discovered which have linear chromosomes, such as Borrelia burgdorferi ,which causes Lyme disease, members of the Streptomyces family and Agrobacterium tumafaciens, which has both a circular and a linear chromosome.

Anyway, on to the question being asked:

Generally, my feeling is that large circular chromosomes would have much greater supercoiling and related torsional problems, making it difficult to unwind them for transcription, replication or repair. This limitation on physical size limits the amount of genetic information that can be carried in a single chromosome, thereby limiting complexity of the organism.

You could increase the number of circular chromosomes to compensate for their lack of size, but again, you end up having a physical limitation (size of the nucleus or size of the cell for anuclear organisms) on how many chromosomes you can pack into the cell.

Linear chromosomes are just a more efficient shape when it comes to larger sizes.

=====================

Here are a few good references to dig further, if you're interested:

A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10802162
Why do we have linear chromosomes? A matter of Adam and Eve. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10422538 -- Proposes that meiosis was the driver for linear chromosomes.


What are the movement mechanisms of thrombus? I am thinking how thrombus (veins, arteries and heart) can move.

Secondary mechanisms come to my mind only:

some enzyme which lyses it, probably adhesion mechanism.
Blood circulation (flow rate) is one secondary measure, I think.

I am not sure if there exist any primary mechanisms:

In veins, there are valves which probably can help thrombus go forward by pushing.
Veins can also dilate so dilation of vessel can help.

Arteries do net dilate their diameter.
So aim would be there to maximise laminar flow, and decrease turbulence.

So probably the question is related somehow to the laminar flow which could help thrombus to move.

How can thrombus move in veins, arteries and heart?

This answer aims to list existing models and do meta-analysis about them.
This answer is a draft.

There are many models made based on the thrombus movement.
One of them is proposed by DevashishDas' answer but it seems to focus only on the first stage of hemostasis:

  The model assumes thrombin is generated on the surface of activated
  platelets in the thrombus core and is transported through the fibrin
  network that surrounds the core both by advective flow of fluid
  permeating through the fibrin network and by diffusion through the
  fibrin gel.

and particularly the model keeps these values constant and simplifies

  To calibrate the model, we experimentally determined fibrin clot
  permeability and thrombin diffusion rates through a fibrin network.

which I think should be dynamic (not constant) because of the three endothelium main factors listed below.
Endothelium is a dynamic structure controlling the fibrin clot.

Thrombus Hemodynamics Model

Fibrin Networks Regulate Protein Transport during Thrombus Development by  diffusion-advection equation (Stokes, continuity, Brinkman equations)

which is about the first stage of hemostasis because of its simplification about fibrin clot permeability and thrombin diffusion rates.

Hemostasis

There are three stages of hemostasis altogether which work parallel together:

primary (formation of the platelet plug)
secondary (formation of fibrin through the coagulation cascade)
tertiary hemostasis (formation of plasmin for breakdown of the clot)

Primary hemostasis is the formation of the primary platelet plug.
It involves

platelets
blood vessel wall
von Willebrand factor

Normal endothelium prevents hemostasis.
Injury of endothelium

involves vasoconstriction (local)
enhances adherence of platelets to exposed platelet subendothelial surfaces
and activation of coagulation process

The formation of primary platelet plug involves

Platelet adhesion,
Platelet activation, and
Platelet aggregation.

Main steps in blood coagulation:

Formation of prothrombin activator complex (thrombokinase)
Conversion of plasma protein prothrombin into thrombin
Conversion of dissolved plasma fibrinogen into fibrin (makes filamen- tous skeleton of fibrin clot)

Clot retraction

The platelets in the clot contain contractile proteins.
They bring the edges of the wound together, which also reduces the chance of further bleeding - not vasoconstriction here!
The contraction process also supports the wound healing process as it brings the ends of the wound together.

Clot retraction is the process of getting clot towards fibrinolysis process. Fibrinolysis is the process where a fibrin clot (product of coagulation) is broken down. Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Clot retraction and fibrinolysis are necessary to remove clot so wound healing can proceed.

Myogenic and metabolic autoregulation by endothelium

Myogenic control involves the localized response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relax- ation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

Myogenic and metabolic Autoregulation is the automatic adjustment (local) of blood flow to each tissue in proportion to its needs (oxygen, nutrients, ...), and is controlled intrinsically by modifying the diameter of local arterioles. It involves localised response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relaxation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

There are three types of substances secreted by the endothelium (1):

NO
Endothelium hyperpolarising factors
Endothelins.

where I think the modelling should focus on these three factors.

Sources

My discussion with a researcher in this field 7/2014
My notes in three Physiology courses during years 2011-2014
Costanzo, Physiology, book
Guyton, Physiology, book


Purifying large amounts of PCR product I have had trouble purifying very large quantities of pure PCR product. We are using these as templates for the reconstitution of nucleosomes and I require hundreds of micrograms to milligrams of template.

Here are some methods I have tried:

1) QiaexII slurry--typically I use the entire slurry for one purification then regenerate the resin by washing in 1M HCl then re-equilibrating with water. This way has worked best for me so far but the yield tends to be fairly low (~100 ug from 100 PCR reactions).

2) Phenol-chloroform extraction. This method seemed to work great, however I believe I have phenol contamination at the end--the yields are often much higher than they should be even if I chloroform back extract before the ethanol precipitation. When I run it out on a gel it looks like the apparent concentration I get is off. I have not tried this too many times so perhaps it could be optimized.

3) Spin column purification. I've used the DNA Clean and Concentrator from Zymo and the yields seemed quite low, even for the columns with an apparent 100 ug capacity.

Another option I have explored is large scale purification of the parent plasmid followed by digestion to liberate the small insert. However I still run into the issue of purifying away the parent plasmid. I've seen a few protocols using FPLC and/or size exclusion but I'm not sure how effective this would be.

Anyone have any ideas?

We had to do this frequently. What I would first recognize is that all of your current methods only work for at the small scale and that for you to purify mg quantities of DNA, you need to work with mg scale equipment.

First of all, you should examine your "upstream" process. Are you doing your PCR at scale? Typically, we have scaled out by going with multiple PCR reactions rather than one large PCR reaction. Generally the reactions max out at 50uL depending on your thermocycler. If you're getting around 1ug/10uL, scale up to a 96 well plate with 50 uL reactions and get ~500 ug of material. Make sure that you mix your dNTPs! Scale-up accordingly.

To start, the DNA Clean and Concentration is designed for really small reactions. It's much better to use the next level of purification by maxiprepping everything. The  The binding capacity of those columns go up to 1 mg. Using the QIAEX II slurry works but you should make sure that you scale up correctly. Make sure that you complete your regeneration. This protocol works well.

Alternatively you can ignore the column and just ethanol precipitate everything to remove your nucleotides. I suggest following Ethanol precipitation of nucleic acids from OWW. We had to make a lot of linear template and for most applications this works great.

As with all things related to molecular biology, there is a lot of voodoo. Some things that supposively work is to chill your ethanol mixture at -20C for at least an hour (or overnight), generally, you'll see your DNA fall out of solution and that's your sign that things are working. At this scale you should be seeing your DNA pellet; that's a good sign if things are working. While eluting anything from the columns, we would warm up our elution buffers. Thermodynamically this would make sense since it would reduce the barrier for unbinding. You would also get away with a lower residence time.

I would frankly avoid using FPLC unless you're working with gram quantities of DNA. You're not Moderna.


Are cytotoxic (killer) T-cells always present or are they only produced during a cell mediated immune response? The book I'm studying says the following
"During a cell mediated immune response, the release of IL-2 by helper T-cells is resposible for stimulating the production of Cytotoxic T-cells, which have receptors that match the anti-gen of the infecting pathogen."

I'm not exactly sure if this is impliying that cytotoxic T-cells are only produced and present during an immune response or not, since I also have an older version of the book that simply says "the IL-2 released by helper T-cells activates cytotoxic T-cells" which seems to indicate that they are normally always present, but just inactive

Naive T cells are regularly matured in the thymus where they're released into the blood. A majority are CD4+, but many are also CD8+. As a caveat, many are TCRαß+, and few are TCRyδ+ (outside the scope here but fun to look up and read).  From there, they home to the lymph node where they hang in the T cell zone until blood trafficking signals coax them into the blood. T cells regularly navigate the body in response to signals from different cells such as blood vessel endothelium, lymphaptic vessel endothelium, epithelial cells, and so forth (1).

The basic process behind an adaptive immune response is that antigen-presenting cells get ahold of foreign antigens and head back to the lymphoid organs like lymph nodes. By the time they get there, they've matured into "licensed" professional antigen-presenting cells. They interact with both CD4+ or helper T cells, and CD8+ or cytotoxic T cells. It's more complex than that, but the point of the helper T cell is to produce "help" signals. These include IL-2, and other cytokines which not only assist the CD8+ T cells in their activation, but also determine a lineage they'll take based on other factors.

So they're both there, in the lymph node at the time the antigen-presenting cell, such as a dendritic cell, arrives to activate the lymphocytes in that region. Take home point: the naive lymphocytes are there until they are activated, in which you would be correct in your last line. But they do actually do things other than sit there, other take home point. They aren't simply anergic and waiting.


Why our body does not produce polyunsaturated fatty acids? Our body does not produce two polyunsaturated fatty acids (PUFA): linoleic acid and alfa-linolenic acid.

I am thinking reasons for it.

Saturated fatty acids have more energy than unsaturated.
Saturated fatty acids do not need NADPH and some many other enzymes as unsaturated in beta oxidation.
This means that less storage places in the body needed to have energy in the form of saturated fatty acids such as for muscles and heart.

There are four main reasons why our body does not use PUFAs as the primary source of the energy but saturated:

PUFAs lower metabolism and interfere with thyroid function
PUFAs spontaneously oxidize, speed up the process of glycation, since too much glucose
PUFAs decrease mitochondrial respiration - more oxygen and CO2, less lactate

where one reason is missing.

One complication of PUFA is

PUFAs promote diabetes, cancer, inflammation and biological stress

which cannot be thought as a reason why our body does not use PUFAs as the primary source of the energy.

There are positive sides of the PUFAs when they are used in other way.
- PUFAs replace trans fats and saturated fats in certain types of foods.
- PUFAs can help your body to eliminate high cholesterol levels
- PUFAs decrease the risk of heart disease

There are also some types of essential fats that your body cannot produce on its own - omega-6 and omega-3 fatty acids.
PUFAs are used to create these.
You can get PUFAs from vegetable oil, fish and nuts for instance.
Balanced diet is essential.

Normal lipid metabolism depends directly on food lipids.
Both the essential fatty acids and right amounts of PUFAs can be obtained from food.
Body converts the essential fatty acids to long PUFAs, which serve as the precursors of prostaglandins and leucotrienes for instance.

There are so many reasons why our body does not produce polyunsaturated fatty acids.

Why our body does not produce polyunsaturated fatty acids?

Simply, it’s because our bodies add double bonds in MUFAs by delta 9 desaturase which adds double bonds between delta 9 and delta 10 carbons, hence additional double bonds can be formed between existing double bond and the carboxilc group but cannot be formed between the existing double bond and the omega carbon. As a result, our body cannon synthesize parent omega 3 alpha linolenic acid and parent omega 6 linoleic acid, but can form timnadoneic acid which is an omega 3 PUFA


Regulation of V. cholerae virulence factors So I know that several different environmental signals, such as pH, bile, and temperature, regulate virulence gene expression in V. cholerae. Specifically, they control expression of the genes encoding the toxin co- regulated pilus (TCP) and cholera toxin (CT).

But what are the two key (main) transcriptional regulatory proteins that control TCP and CT expression, and where is each localized in the bacterial cell? Also, what does each protein do?

I know that the proteins involved are ToxR/S, ToxP/H, and ToxT, but I don't know which are the MAIN ones and why...

Virulence factors of V cholerae is regulated by a hierarchical regulatory system. The proteins you listed in your question are part of this system. In this paper it is said that the actual activation of TCP and CT is done by ToxT- thus this could be your "key" protein. I'd also like to note that just because these are two different genes does not necessarily mean that there has to be two key factors - this assumption of yours if a bit faulty.

Also because the activation of the virulence factors are regulated by a chain of events, each link is can be considered equally important, because if one of them fails the whole chain is dysfunctional.

The short description of the regulatory chain taken from the article linked above:

  The ToxR regulon is a hierarchical regulatory system that activates virulence gene expression in response to environmental stimuli (2). Induction of the ToxR regulon starts with activation of tcpPH expression by AphA and AphB (4, 5). AphA and AphB are cytoplasmic regulatory proteins that cooperatively bind to the tcpPH promoter and activate its expression. Once TcpP is produced, it functions in conjunction with ToxR to activate toxT expression. TcpP and ToxR are structurally similar membrane-bound DNA binding proteins that are thought to modulate gene expression in response to external stimuli (6, 7). When stimulated, TcpP and ToxR bind to the toxT promoter and activate its expression. ToxT then directly activates the expression of the genes that encode for CT and TCP production (8).

This paper might also be helpful. Unfortunately I could only access the full text this way (through researchgate):

Regulation of virulence in Vibrio cholerae: the ToxR regulon.
Brandon Childers, Karl E Klose
Future Microbiology (Impact Factor: 4.02). 07/2007; 2(3):335-44.
DOI: 10.2217/17460913.2.3.335

This paper provides details of regulation and mechanism of ToxT.

Taken from the third linked paper. As you can see the final activator of CT (termed CTX in the picture) and TCP is indeed the ToxT, but as I wrote it earlier each link in the chain is important.


Why can't we call dog breeds different species? I understand this question might fall into opinion based, but I'm trying to write it so that it meets the "Many good questions generate some degree of opinion based on expert experience" part and not get closed.

A closed creationist question about directly observing the evolution of new species made me think about just declaring dog breeds as new species just to provide an answer to that question. Turns out I'm not the first one to think of it, and to be honest I probably read that article and forgot about it.

That article quotes geneticist Jerry Coyne as saying:

  “If somehow the recognized [dog] breeds existed only as fossils,
  paleontologists would consider them not one species but
  many—certainly more than the thirty-six species of wild dogs that live
  in nature today.”

There is also this question about breeds of dogs being different enough they can't breed. The answer posted to that question discusses attempts to breed beagles with irish setters, and having great difficulty.

I'm aware that the commonly used definition of different species is individuals who can't interbreed and make a fertile offspring. However the Scientific American article I referred to above mentions that animals are often classified as separate species because they are separated by a geographical barrier, and if they could mingle they would make fertile hybrid offspring. The same articles mentions fruit fly research that bred two different species of fruit fly and made fertile offspring, even though they would never interbreed in the wild.

This is speculation, but let's imagine taking an island and putting several breeds of dogs on that island. Many of those breeds would easily interbreed and create mutts. But I'm pretty sure there would some sorting, the large dogs like st. bernards and great danes aren't going to easily interbreed with tiny dogs like chihuahuas. If we came back to this island after 50 or 100 years, we'd probably see small dogs and large dogs (assuming the island had decent ecological niches for both sizes of dogs to survive in)

Creationists like to ask why we haven't observed the evolution of a new species and don't want to listen to arguments about the fossil record or DNA sequences. If we just define some dog breeds as different species, we'd have an easy answer. I think some dogs would at least come close to meeting that definition for these reasons:

Dog breeds with large size differences would have great difficulty breeding.
Some pairs of breeds seem to have trouble interbreeding (Beagles + Irish Setter).
Some animals recognized as different species can create fertile hybrid offspring.

So why don't we recognize some dog breeds as different species?

I don't enjoy the idea of comparing people to dogs, but this is a bit akin (please note the bit) to asking if people who are genetically short (or "little people", both proportionate and disproportionate dwarfism), pygmies, short people, normal sized people, tall people, very tall people, and people with acromegaly (gigantism) can be called different species. I compare because it's fairly clear to most individuals that we are all the same species: homo sapiens. About breeding, it is very likely that a reproductive specialist would be quite concerned (I certainly would be) about a woman with drarfism carrying the child of a very tall person (who had very tall parents), but not the opposite pairing.

Below is a photograph of the wedding of Tom Thumb and Lavinia Warren. That union produced no children. Her bridesmaid Minnie, (her sister), who was only 27 inches tall, also married a little person (Edward Newell). She became pregnant with a normal-sized child, but died during the birthing of a 6 pound baby (her baby died as well).

Are they a different species? No. A paleontologist (a good one) would be able to tell that the bones of a little person was actually of the same species based on certain conformations, just as I believe paleontologists today could distinguish prehistoric small cats from very large cats. Size matters, but not nearly as much as the type and distribution of teeth, the shape of the jaw, etc.  In other words, I strongly disagree with the following:

  If somehow the recognized [dog] breeds existed only as fossils, paleontologists would consider them not one species but many—certainly more than the thirty-six species of wild dogs that live in nature today.

That statement is based on a fairly profound error in thinking: a cognitive bias that is mistrustful of science in general due to a lack of familiarity with the rigors involved in the scientific methods of paleontologists in particular. I say this without rancor or animus of any kind; where I settled down (in the deeply religious region), the vast majority of my children's friends' parents are creationists, and the vast majority of our friends are fundamentalists. We argue about science all the time; I know the basic arguments. I'm familiar with their websites. I personally find myself in the camp of Christian thinkers like geneticist Francis Collins, M.D., Ph.D., the director of the Human Genome Project, who understand genetics and find no threat to their faith in evolution or science. (E.g. Creationists reject all science which indicates the age of the Earth is >~6000 years.)

The truth is that the definition of a species is not that easy, even for prokariotes. Difficult as well is a pure definition of life.

Finally, about size. The domestic dog exhibits greater diversity in body size than any other terrestrial vertebrate. This is due to a small number of (or perhaps even a single) alleles: the IGF1 Allele. It's hard to argue difference of species on the basis of a small number of alleles: we allow much more variability for other alleles without wanting to classify as different species: eye color, hair color, hair length, straight vs. curly coat, degree of tail curl, ear morphology, etc.

A Single IGF1 Allele Is a Major Determinant of Small Size in Dogs
Lessons learned from the dog genome
A species definition for the modern synthesis
Single-Nucleotide-Polymorphism-Based Association Mapping of Dog Stereotypes
Canine Genetics Facilitates Understanding of Human Biology
How many species of prokaryotes are there? (PNAS)
Ernst Mayr and the modern concept of species (PNAS)
Hybridization, ecological races and the nature of species: empirical evidence for the ease of speciation
Is it Useful to Have a Clear-cut Definition of Life? On the Use of Fuzzy Logic in Prebiotic Chemistry


Why do we like music? Music is, of course, just a sequence of sounds. Sounds are vibrations in the air, which our ears detect. So why do we find certain sequences of sounds to be appealing? What makes us want to hear these sounds (turn on a radio, for example), or make these sounds on our own (sing/play an instrument)?

Heck, why do we even move our body strangely when we hear certain music (dancing)?

According to the article Why do we love music?, "No one knows why we love music, or what function, if any, it serves."

Of course, that article was published in 2013, so it's possible someone has found an answer since then. ;)

Some have argued that music is merely an evolutionary byproduct that serves no really important purpose. (Type "auditory cheesecake" into Google.) In a similar vein, one might speculate that music did serve an important purpose at one time (e.g. a mating ritual).

In this spirit, we might ask how one defines music and then ask if we humans are the only species that makes music. When we hear frogs croaking or crickets chirping, are they merely communicating, or are they making music - or are they doing both at the same time?

Though your question focuses on music people listen to, a similar question could be asked about dance. Except I think music is more universally popular than dance, which doesn't interest everyone.

In summary, I haven't really answered your question - which probably can't be answered with any accuracy at this time. But there are actually lots of references on the Internet that offer clues to the puzzle. I suspect there's some overlap between the love of music and the love of poetry, painting, etc.

I just discovered an interesting term - evolutionary musicology - along with another theory to explain music's popularity: It may simply be a welcome break from silence, which may be associated with danger.

Yikes, I know I'm doing a lot of rambling, but here's another thought:

Some researchers believe music served as a sort of group bonding tool. In other words, a particular tribe might have produced a certain kind of music that helped unite members of that tribe. In other words, music could be a form of symbolism, similar to flags.

As a huge fan of Latin music, I've come to appreciate the association between specific genres and their places of origin. For example, flamenco is a product of Spain, while cha-cha-cha and mambo are forever linked with Cuba. There's a fierce debate about the origins of salsa, which was officially born in New York City but which is clearly derived from mambo.

No one can deny that country music sucks. Yet I love a lot of country music, which I was exposed to when I was growing up in rural West Dakota.

What I'm trying to say is that music probably helps us identify with a particular group and connect with our roots.

P.S. It's worth noting that other species do indeed enjoy music. Check out the article What type of music do pets like?


Which organs/tissues are defined as "peripheral organs/tissues" In the following paper [1], I encountered one term "peripheral organs". Literally, based on my understanding, it should be related to the organs/tissues, such as skin, hair and ear in the human, and wing, antenna and leg in the insect. However, in reference [1], fat body, oviduct and hemocytes are listed as peripheral organs. Is there specific definition of "peripheral organ/tissue"?

Thank you!

[1] Verlinden, H., et al. (2010). "The role of octopamine in locusts and other arthropods." J Insect Physiol 56(8): 854-867.

The most common usage of "central" vs "peripheral" organs/tissues is: central nervous system (brain/spinal cord) vs all other organs/tissues:

"B cells in peripheral organs and the CNS" (from the article linked in the comment)
Nervous system includes central nervous system (brain/spinal cord) and peripheral nerves (spinal and all other nerves) (Central nervous system and peripheral nervous system).
n-3 PUFA and obesity: from peripheral tissues to the central nervous system (PubMed)
Atrial natriuretic factor receptors: distribution and regulation in central and peripheral tissues (PubMed)

However, depending on the context, different organs/tissues can be considered peripheral:

From the liver metabolism viewpoint, liver can be considered central and muscles and fat peripheral (Apoptosis and insulin resistance in liver and peripheral tissues...).
From the intestinal absorption viewpoint, gut can be central and all other organs peripheral (From the gut to the peripheral tissues...).


Knockout and knockdown of gene Out of curiosity, I got this question whether knocking out (deletion) of a gene on one side and knocking down (RNAi) of the same gene on the other side will affect the cell in a similar manner or not.

If not why?
If yes, is it applied to every gene?

Knock out of a gene will correspond to no expression (gene deletion) in the cell, which can be appropriate to confirm the functional specificity, to observe processes which are affected in its absence and some other processes which are compensating the absence of the gene.

Knockdown of a gene will result in expression defect by decreasing the level of the transcript (mRNA silencing).

Now, the points which I am wondering upon are:

no mRNA presence and silenced mRNA will create two different environments for the cell to deal with or not.
whether the whole amount of transcript should be targeted to have the same phenotype as of gene knockout.

This is a fascinating set of questions.  The only one I can comment on is: is KD qualitatively similar to KO?

My answer is: sometimes yes, in general no.  To understand why, I like to think of a hypothetical plot of "phenotype of interest" on the y axis, and "expression of gene" on the x axis.  You can imagine that this plot could be monotonic, i.e. that the phenotype continuously increases or decreases as expression increases.  Or it is also possible that this plot could have one or more minima or maxima in it.  One example of KD giving dissimilar results from KO is for essential genes.  If they are knocked out, they of course kill the organism.  However, there may be some levels of essential gene knockdown for which the phenotype is actually increased relative to wild-type!

I will selfishly share one of my articles where I observed something like this.  We found that ADH1 knockdown improves butanol tolerance in yeast, but that ADH1 knockout was highly detrimental to butanol tolerance.  http://dx.doi.org/10.1007/s10295-015-1713-7


Are "constraint trees" in phylogenetic analysis cheating? How can I correctly use them? How do phylogenetic experts evaluate results which use constraint trees? Are there examples in the literature where phylogenetic experts detail how they use constraint trees?

Here is my problem. I have 500 samples. These are five different "categories" of species A, B, C, D, E, 100 samples each.

Category A: A1, A2, A3, ..., A100
Category B: B1, B2, B3, ..., B100
Category C: C1, C2, C3, ..., C100
Category D: D1, D2, D3, ..., D100
Category E: E1, E2, E3, ..., E100

There are two classes of which these "categories" fit in: Class 1: A and B, Class 2: C, D, and E.

For the purpose of this discussion, let's say A=whale, B=dolphin, C=mouse, D=gerbil, E=hamster

When I do the analysis, there are some problems. The output tree resolves the samples into two classes which meet my expectations; it splits the samples into two groups: ( A & B) and ( C & D & E ). That's great. However, it doesn't resolve the species into separate categories, e.g. it mixes together "whale" samples with "dolphin" samples, and mixes together all the individual C, D, E . I see

(A1, B3, A27, B23, B2, A2, A3, A4, ....), (C3, C5, D72, D3, E1, E2...).

This would mean whale1 is more evolutionarily "related" to dolphin3 than whale 27.

I try to use a constrain tree instead to constrain each of these groups, using the form

((A1, A2, ..., A100), (B1, B2, ..., B100), (C1, C2, ..., C100), (D1, D2, ..., D100), (E1, E2, ..., E100))

Sure enough, my tree now resolves each "category" A, B, C, D, E into a distinct category.

Question 1: Isn't this cheating? I feel like I stipulated "resolve the tree in this manner I expected" and RAxML output that.

Question 2: How do I evaluate whether this is correct?

Question 3: For experts, could direct me to published literature which used this approach? Which papers used RAxML constraint trees?

Thanks for any help. I'm happy to clarify things.

I understand where you are coming from when you say that it feels like cheating. However, there are a coupled of things to keep in mind. First let's consider why your tree topology might not reflect concordance with intuition/species trees:

1) Presence of artefacts such as long-branch attraction

2) Lack of sufficient phylogenetic signal/presence of non-phylogenetic signal (due to, for example, convergent evolution in the sequences)

3)Horizontal gene transfer (unlikely in animals).

4) Incomplete lineage sorting/deep coalescence (hemiplasy).

Only in the case of 3 and 4 does your tree reflect true relationships among taxa that genuinely differ from the species tree. Cases 1 and 2 are artefactual. In cases 3 and 4, it would not be appropriate to use a constraint tree to get a species-tree concordant topology because the resultant topology would not reflect the 'true' relationships among taxa (i.e. would be 'cheating'). In cases 1 and 2, I would argue that it is appropriate to use a constraint tree to get the species-tree concordant topology (depending of course on what you want to use the tree for) because you know that the your current topology is species-tree discordant because of artefacts and is therefore not reflective of the 'true' relationships among taxa. Of course, you are unlikely to know a priori what factors (1-4) are causing your bad topology (though you can do some tests for long-branch attraction for example -- see Cladistics 21 (2005) 163–193).

What you can do is test whether the log-likelihood of your non-constrained tree and your constrained tree differ significantly. You can use tree topology tests such as the  Kishino and Hasegawa (KH) test. I don't know about RaxML, but IQ-TREE has excellent topology testing: http://www.iqtree.org/doc/Advanced-Tutorial. If your constrained topology is significantly different (statistically) from the ML topology, then you probably should not use the constrained tree. I am by no means proficient in phylogenetics concepts so I would take my advice with a grain of salt, hopefully some of the other members can illuminate the issue a bit further.


Pathway mediates nitroglycerin-induced relief from angina pectoris what kind of Pathway mediates nitroglycerin-induced relief from angina pectoris,please provide some idea...

The effect of nitroglycerin on the cardiac tissue is similar to nitric oxide (NO),  which forms in the endothelium of blood vessels from arginin metabolism products.

So, the general scheme can look like this:

R-NO2 is converted to R-NO outside of the cell (glutathion-SH-dependent reaction). NO is lipophilic and rapidly penetrates into the cell where it activates guanylate cyclase. From this moment you can see the resulting influence on myosin and actin on this picture:


If you measure the O.D. of cells at one wavelength, is it possible to find its equivalent O.D. at another wavelength? For example, I measured the optical density (O.D.) of some cells at wavelength 550 nm but I should have used 600 nm. Is there a way of converting my O.D. to its equivalent in another wavelength?

O.D. can mean 30 different things, many of them being related to science and to optics (see here)! I'll assume you mean absorbance (for Optical Density I'd guess) or light scattering as @canadianer said

Each substance has its own absorption spectrum and reflectance spectrum. Knowing only the absorption is a given wavelength does not tell much about the absorption at another wavelength (at least not without some other a priori knowledge about the substance studied).

So, the answer is 'no'.


A poor man's COVID-19 vaccine? If person A is infected (COVID-19) and person B is not, could the following work as a vaccination?  Person A exhales (coughs?) into a a transparent bag.  The bag is radiated for a long time with a strong ultraviolet (UV) light as is found in some residential well-water systems.  Person B inhales the contents of the bag.

I am curious mostly about how virus particles are damaged at the molecular level by UV light and how this relates to how vaccines are manufactured today.

Short answer: probably not.

Long answer: for your body to build immunity against something, it needs to identify it as something harmful to you. Otherwise, how would it know if this is just some random particle in your environment that it should ignore? There are molecular clues that your body uses to recognize better whether something is likely a pathogen (that means it should try to build immunity against) and those are some of the additives (known as adjuvants) present in man-made vaccines.

Also, the route of administration is also important. Things that you eat or breath in are triaged by the waldeyer ring because maybe you just ate something that is alive, but not exactly a pathogen. Dysfunctions in this process (thinking a normal protein is part of a dangerous pathogen) is believed to be one of the possible causes of allergies. Injecting it into your blood-stream often makes it more effective (but there are exceptions: polio vaccine however can be orally administered).

A nice read about this topic is this: The dichotomy of pathogens and allergens in vaccination approaches.

This is perhaps a must read on this topic: What to expect of a good vaccine and how to achieve it.

I'm not really sure what else to tell you. The process you described is a part of the manufacturing of some vaccines, so you are on the right track. But vaccines are hard to make, you can't do it for every disease and involves a lot of experimenting.


Do we have evidence of heritable personality traits in chimpanzees? I have read that chimpanizees have distinct personalities. Do we have evidence of heritable personality traits in them?

There has been some research in order to explore this direction, for instance, see this reference:

A. Weiss et al. - "The Heritability of Personality Factors in Chimpanzees", Behavior Genetics, Vol. 30, No. 3, 2000.,

in which the authors study five human-like factors - Surgency,
Dependability, Emotional Stability, Agreeableness, and Openness.

Quoting verbatim their findings:

  Only Dominance ... was significantly heritable. Dependability showed evidence that it might be heritable, but the parameter estimates were not statistically significant ... Two other personality traits, Agreeableness and Emotional Stability, showed positive heritability estimates but the parameter
  estimates were nonsignificant and small. Openness and Surgency showed no evidence of heritability.

In fact, the statistical correlation between dominance and heritability makes a strong sense.  Here's what I make out of this - this was a correlation based study, or kind of an experiment, hence the stress on statistical significance. But the question it raises is - is there a causal relationship between the two, i.e. does there exist any proper mechanism for the inheritance of "dominance". Finding such a mechanism was clearly beyond the scope of this study, but I believe the requisite answer for your question is if one stumbles on to such mechanisms, and not statistical correlations, which are mere pointers.

But on the basis of the study at least, all that one can safely conclude is - statistical correlations suggest that inheritance of "dominance" appears plausible, but the exact mechanism of how this implements out in practice, is beyond the scope of this study.


Can a gene-expression or epigenetic 'user-history' be found in the body? (EDITED - a lot of what I am saying is implicit and simplified. I'm not looking to recreate the numerous textbooks and scientific papers on how DNA works).

As far as I can understand it, an organisms basic building blocks (proteins) are made up of DNA, Genes, and Chromosomes. The most basic form of this is DNA, made up of molecules in double helix strands. DNA carries all the instructions for the body in a simple 'database' or 'blueprint' form. Genes are chunks, or sequences, of the DNA telling the body 'what to do'(1) by reading the 'DNA database' in a myriad of unique coding sequences. Genes naturally(2) switch on and off throughout an organisms lifespan allowing amongst other things for an organism to grow from young to old. DNA is essentially(3) stored in Chromosomes.

External and environmental factors can influence the expression of genes, and the information stored in the DNA (4) - the study of which is Epigenetics. These Epigenetic factors can change over time, switching genes on and off. (5)

Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?

Apologies, I do not have a background in Biology. (6)

EDIT NOTES

(1) what to do, how to do it, when to do it. not necessarily all life supporting instructions but also the minute-to-minute, day-to-day processes etc.

(2) naturally. there is no black and white in nature, only shades of grey.

(3) essentially. not exactly and not in all cases but mostly.

(4) As in, factors influence the expression of genes (which in turn are made up of DNA information). I am not suggesting that external factors can influence the 'DNA database' itself but rather just how they are 'read', sequenced and expressed as genes.

(5) again, naturally. no sharp on/offs but variations of concentrations.

(6) I may not have used the correct terminology.

First Paragraph - let's debunk what was poorly phrased

Many sentences you wrote are quite misleading. You should have a look at an introduction to molecular genetic to have a better understanding such as what you can find on Khan Academy. In short:

  the double helix DNA strands are the building blocks of an organism

This sentence is very opinion based. as a matter of proof, one could for example replace the term double helix DNA by "cells" (or other terms) and many would still be satisfied with the sentence.

  Genes are chunks of DNA telling the body what to do.

A gene is a part of DNA which contains regions coding for proteins. There are many sequences which are not coding for any proteins that are essential for the individual survival (such as regulatory sequences or sequence coding for rRNA for examples).

  Genes naturally switch on and off.

The regulation of gene expression is actually much more continuous than just on/off. Also, regulation of protein concentration can occur at different levels and not only by regulating gene expression.

  DNA is essentially stored in Chromosomes.

This sounds like chromosomes are boxes in which one can find DNA. In reality, DNA is a type of molecule which can be found under different forms. In humans (and other eukaryotes) most of the DNA (but not all) is present in the form of chromosomes.

Second Paragraph - What is epigenetics?

  External and environmental factors can influence the expression of genes,

This is correct

  and the information stored in the DNA

This is wrong. Environmental factors do not affect the sequence of base pairs of the DNA. It only regulate its expression. Such regulation of expression can last for a long time and even be transmitted to the offspring. The term epigenetics is loosely defined. In short epigenetics refers to the set of mechanisms that affect gene expression at short and long term. The classic mechanism of interet in epigenetics in the methylation of histone tails (quickly speaking, histones are proteic structures around which DNA is wrapped).

Your question

  Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?

As explained above, some of the molecular mechanisms yielding to changes in gene expression can have long term consequences on gene expression (which can even be inherited). But there is not data bank (or other centralized or not source of information) that specifically record the expression of each gene at any one time in the history of the cell life.


Is there any advantage of having mitochondria for aerobic respiration? If we consider the pathway of breakdown of glucose which includes glycolysis, the citric acid cycle and the electron transport chain, all these processes takes place in some  prokaryotes and eukaryotes. In prokaryotes all these processes take place in cytoplasm while in eukaryotes the last two processes take place in mitochondria.

So is there any advantage of performing the last two processes in the mitochondria? Does it yield more energy? If there is no advantage, what is the point of having a mitochondria (at least for this process)?

From the evolutionary point of view, the eukaryotes acquired these metabolisms (except glycolysis) from their prokaryotic endosymbionts. Not all prokaryotes have the ETC. The free living ancestor of mitohondria is supposed to be the alpha-proteobacterium.

Now, glycolysis is a common pathway in lot of lifeforms perhaps because of abundance of glucose. TCA cycle is coupled with ETC at certain steps which makes it essentially a part of aerobic metabolism.

The reason for having a dedicated organelle for respiration

ATP synthesis is a membrane process. Imagine a large prokaryotic cell- as big as an animal cell. Such a cell cannot take care of its energetic demands which primarily consists of protein synthesis with the given area of membrane i.e it needs much more ATP-synthases than it can have to cope up with the energy demands of maintaining such a huge cell (this index is approximated based on surface to volume ratio). Therefore it is wise to harbor multiple efficient organelles i.e. mitochondria which themselves have just a small essential genome and proteome to maintain.

For a better understanding, please read this article. I just loved it.
There is also a book by the same author about mitochondria called Power, Sex, Suicide.


Gene expression for mathematicians: where to start? I am a PhD student in mathematics, and I will be involved on a project that aims to cluster (i.e. automatically group) people according to their gene expressions.

Well, the project looks very nice, but I have no idea of what gene expressions are and consequently how to model them mathematically. So here are my questions.

Is there a "Gene expression for dummies" manual that I can read, considering that my last studies of biology move back to the high school (10+ years ago)? Any suggestion, also divulgative books?

Is there a good reference to study how gene expressions are modeled under the mathematical point of view?

I suppose you first need to learn the basics of genetics before investigating the stats behind gene expression clustering. I will based my recommendations on Khan Academy, that is generally speaking a good very introductory source of information for biology and other fields.

Basics of genetics

Here are a few questions for you:

What exactly do we call the genetic code?
Are you aware that genes are transcribed into mRNA that are translated into proteins?
What is an allele?
Do you know what is an exon and an intron?
Do you know what is a TATA box?

If you answered no to any of these question I would recommend that you have a look at Khan Academy > Central Dogma.

Gene regulation

Then, you should have a look at Khan Academy > Gene regulation

Other

Don't hesitate to have a look at other sections in the biology series of khan academy if you want to broaden your understanding of e.g. what DNA looks like, what is happening at reproduction, how do genes segregate, or other things such as evolution. Typically, Khan Academy > biotechnology could also be helpful as to give you a rough feeling of the methods used to investigate gene expression

Gene expression clustering

The literature on clustering gene expression is very rich (see google scholar).


What is the effect of flash pasteurisation on Maillard reactions or production of AGEs in milk? Does flash UHTP homogenision and pasteurisation change significantly the extent of maillard reaction in milk compared with traditional batch pasteurisation? If this is significant does this effect the nutritional value of the milk?

Initial research; i have found via my wikisearch  http://www.food-info.net/uk/colour/maillard.htm and on pub med an abstract: J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S57-69.Influence of processing on protein quality.
Mauron J.
Source University of Fribourg, Switzerland.  i dont have full access to pubmed papers.

background to question.I have developed a sensitivity or intolerance to UHT and typical homogenised and pasteurised milk in the supermarket and any products with milk solids. I can consume non homogenised batch pasteurised milk from the specialty organic store, thus the curious chemist in me was alert. Either my body doesn't produce sufficient of the necessary enzymes ,ruled out by the latter scenario,  or the composition of the milk has changed in modern high throughput pasteurisation.

In Flash pasturisation we have P.T and V all being varied to increase proximity and likelyhood of collisions of reactants as well as temporary emulsification.

There is another term AGE see http://agefoundation.com

This is only an partial answer, as I do not have the time now to look for other references.

In the chapter about milk, Harold McGee's beautiful book "On Food & Cooking" says (pg. 21 of the 2004 edition, bold is mine):

  Flavors from cooking
  Low-temperature pasteurization slightly modifies milk flavor by driving off some of the more delicate aromas, but stabilizes it by inactivating enzymes and bacteria, and adds slightly sulfury and green-leaf notes (dimethyl sulfide, hexanal). High-temperature pasteurization or brief cooking - heating milk above 170°F/76°C - generates traces of many flavorful substances, including those characteristic of vanilla, almonds and cultured butter, as well as hydrogen sulfide. Prolonged boiling encourages browning or Maillard reactions between lactose and milk proteins, and generates molecules that combine to give the flavor of butterscotch.

He continues by speaking about the different types of pasteurization, and says (pg.22-23)

  The third method of pasteurizing milk is the ultra-high temperature (UHT) method which involves heating milk at 265-300°F/130-150°C either instantaneously or for 1 to 3 seconds, and produces milk that, if packaged under strictly sterile conditions can be stored for months without refrigeration. The longer UHT treatment imparts a cooked flavor and slightly brown color to milk; cream contains less lactose and protein, so its color and flavor are less affected.
  Sterilized milk has been heated at 230-250°F/110-121°C for 8 to 30 minutes; it is even darker and stronger in flavor, and keeps indefinitely at room temperature.

So, it appears as if indeed there may be some Maillard reaction going on in UHT, although it is probably minor (otherwise the milk would be much darker in color, as it is the case for sterilized milk).

The book also speaks about homogenization, but it does not mention anything specific about Maillard reaction there (homogenization is not carried on at high temperatures, so it does makes sense not to have it).

To answer your question:

  Does this effect the nutritional value of the milk?

Well, according to this presentation (but, be warned, it does not cite any reference!) it seems that it does, although I don't think the Maillard reaction is specially involved.

http://www.slideshare.net/Aslal_saja/effect-of-uht-treatment

Specifically it says that the irreversible changes that occur are:

Whey protein denaturation (35 to 100% of denaturation of $\beta$-lactoglobulin)
Slight increase in the size of casein micelles
Whey protein-casein micelle interaction
Maillard reactions
Fat globule composition changes (although no changes in nutritional value of milk fat)
Vitamin content changes (20-30% loss in vitamin B1 and B12. Markedly reduced content in vitamin C and folic acid if high level of oxygen were present during the treatment, no changes in vitamins A, D, E and beta-carotene).

It also says that:

  Biological value and net protein utilization of UHT milk were lower for stored milk than directly used milk. Lysine loss during UHT is high but not significant to affect milk nutritional values.

I don't know whether the fact that you have problems when drinking UHT milk has anything to do with Maillard reaction or any of the other modifications brought by UHT treatment, and I will not venture in there, as I am not an MD and prefer not to give any sort of medical advice.


What are the differences between mammal and insect digestion of cellulose? I know that digestion of cellulose is difficult in mammals and requires a lot of steps. But I am fascinated by the idea of one day achieving human digestion of cellulose.

Which got me thinking about how insects digest cellulose much faster than mammals, how is this possible?

Update 2 (interpreting "faster" in terms of efficiency because it seems easier to measure)

The question has been updated but I still don't see a reference for insects being more efficient than mammals. Therefore I investigated this and did not find convincing evidence that it is the case.

Granted, the means of measuring efficiency are not necessarily comparable, but nonetheless it appears that ruminant cellulose digestion efficiency is comparable to overall distribution of cellulose-digesting bacteria.

(Overall, in both clades, the vast majority of species do not appreciably digest cellulose, so I focus on those that do.)

This paper suggests that while termites have remarkable ("nearly 99%") efficiencies they are a dramatic outlier among insects. In different groupings efficiencies range from 12-68%, 40-90%, and 11-50%.

This paper suggests that the "digestibility" of cellulose by cattle is in the range 0.7-0.8 (that is, 70%-80%). It is observed that the rate is higher in sheep (and goats?), though comparable figures are not provided. Other figures in the paper are in terms of animal body weight gain, which is unfortunately a poor measure due to the high energy cost of just living for warm-blooded animals.

If I interpret these numbers correctly, this means that ruminants in fact compare favorably to most celullolytic insects in their cellulose digestion efficiency. The very high efficiency of termites specifically is likely a facet of their being little microbial factories with legs; they are definitely an outlier among insects.

In conclusion, I don't think that there is any particular intrinsic advantage for insects in cellulose digestion.

Update

I went back and read the linked post and realized that much of my answer was covered there and thus somewhat duplicative.

What is not covered is the insect/animal comparison. I do not see the source material for the assertion that insects are more efficient at cellulose digestion, it might be true or be somewhat trivially true but I would need to see where you got this information to assess it.

I would suggest doing a little initial research to maybe get closer to an answer. For example, here is a review on cellulose digestion in insects, and here is a resource for mammals, here is a comparison between the two.

Original

Neither insects nor mammals (as far as I know) have the appropriate digestive enzymes to digest cellulose efficiently on their own. However, some special animals like termites and ruminants have assemblages of microbes in their gut that can break down cellulose. These enzymes are called cellulases.

However using these assemblages efficiently requires an extremely specialized gut system such as the rumen.

So you might get humans to digest cellulose by making transgenic humans with cellulases in their digestive system or completely redesigning the human digestive system. Possibly there would be a way to supplement with cellulase the way some people do with lactase.

A different concern might be that human physiology isn't set up to support that style of nutrition. For example I imagine that diabetes incidence would increase. But it's hard to predict.

If the idea is to feed a growing population of earth in a less carbon-intensive way, there are likely less complicated ways to do that by altering diet to e.g. less meat, popularization of sea vegetables, etc. But that's just my opinion, maybe you had something else in mind.

Hope that helps.


Why are plants referred to by their Latin species names, and not by their popular names? Often the names of herbal ingredients in certain cosmetics products are given by their scientific names like Anthemis nobilis instead of chamomile or Lavandula angustifolia instead of lavender.

Is there any reason why this practice is followed? Wouldn't those who have allergies to certain plant materials be better off reading "coriander leaf extract" instead of scratching their heads over what "Coriandrum sativum leaf extract" is? Why put something more complex when something simpler would be more beneficial to the consumer?

The use of a genus-species notation gives more exact information. For example there are multiple species of chamomile: There is Roman chamomile (Chamaemelum nobile), German chamomile (Matricaria recutita, or Chamomilla recutita) and Dyer's chamomile (Anthemis tinctora). The first two species are appraised for their medicinal properties and help to calm upset tummies and to aid sleep, among other things. The latter species, however, does not have these properties and is used for dyeing. This illustrates the fact why 'chamomile' alone is insufficient.

Popularly, classifications of living organisms arise according to need and are often superficial. Anglo-Saxon terms such as 'worm' have been used to refer to any creeping thing including snakes, earthworms and intestinal parasites. The term 'fish' is used in shellfish, crayfish, and starfish. However, there are more anatomical differences between a shellfish and a starfish than there are between a bony fish and man.

In science it has been the convention to use the genus-species notation since Carl Linnaeus introduced it in the 1700's. This formal classification serves as a basis for a relatively uniform and internationally understood nomenclature. A uniform classification system simplifies cross-referencing and retrieval of information. The Linnaean taxonomical system aids in this purpose and is widely used. The genus-species system can be extended by including subspecies and varieties. Many (plant) species don't even have an (English) trivial name. Taking your lavender example: there are some 39 Lavendula species known and obviously, many of them don't have a trivial name. Here one has to fall back to the Latin names to be sure what it is.


What are the atmospheric requirements for large dinosaurs? What are the atmospheric requirements for large dinosaurs? and are the atmospheric constituents for supporting large dinosaurs any different from the atmosphere today?

Oxygen levels have changed greatly throughout Earths's history starting with very little atmospheric oxygen and gradually increasing as photosynthetic activity appeared until all the oxygen sinks such as minerals had been filled, then taking off, reaching as high as 35% of the atmosphere during the carboniferous period 3. The reasons behind this sudden increase in O₂ has to do with the development of bark covered wooden plants, a feature made possible by the molecule lignin, which strengthens the trunks of trees and makes tall plants possible. However, lignin was hard for microbes to digest, and the dead trees built up, never returning their carbon to the atmosphere as CO₂. So the oxygen they had made while alive stayed in the air 4.

The plot shows the upper (red) and lower (green) estimates for O₂ concentration over time. The data for this plot was taken from a review of analysis of sulfur, carbon, iron, and manganese deposits 2. If you're interested in how isotopic analysis can give information about atmospheric oxygen, read that paper, it's detailed.

That spike in the plot is the carboniferous. This period in history is interesting because of the appearance of large invertebrates, such as 3 foot wide dragonflies and 6 foot long centipedes 5. Since these animals move oxygen through a series of tubes called trachea, where air just moves through by diffusion, it was speculated that the higher concentration of oxygen allowed this growth. Recent research indicates that insects can force air through their trachea, and that competition between predators and prey could have explained most of the size 6.

So how does this affect dinosaurs? The carboniferous period was about 350-300 million years ago, which corresponds with the spike on the graph. Dinosaurs appeared in the Triassic, which was about 250-200 million years ago, but oxygen levels were at 16% of the atmosphere at the time 7 ( current O₂ levels are about 20% ) If we move into the Jurassic, about 200-150 million years ago, oxygen levels rise to about 26% 8. In the Cretaceous, about 150-65 million years ago, O₂ was at about 30% 9. The O₂ percentages are taken from the infoboxes on the right side of the wikipedia articles, which in turn take the number from a plot very similar to the plot I posted here, despite being in German 10.

I compiled lists of heaviest and lightest dinosaurs by going through the wikipedia article on dinosaur size 11 and going to the article on each dinosaur and checking if it was Triassic, Jurassic, or Cretaceous.
If we look at the heaviest dinosaurs, most of them appeared during the Cretaceous:

Heaviest Dinosaurs
Theropods                           Metric Tons     Period
Spinosaurus aegyptiacus             7-20.9          Cretaceous
Carcharodontosaurus saharicus       6.1-15.1        Cretaceous
Giganotosaurus carolinii            6.1-13.8        Cretaceous
Tyrannosaurus rex                   6-9.5           Cretaceous
Oxalaia quilombensis                5-7             Cretaceous
Acrocanthosaurus atokensis          5.6-6.2         Cretaceous
Tyrannotitan chubutensis            4.9-5.6         Cretaceous
Suchomimus tenerensis               2.7-5.2         Cretaceous
Therizinosaurus cheloniformis       5               Cretaceous
Tarbosaurus bataar                  4-5             Cretaceous

Sauropods                           Metric Tons     Period
Amphicoelias fragillimus            122.4           Jurassic
Argentinosaurus huinculensis        60-90           Cretaceous
Antarctosaurus giganteus            69-80           Cretaceous
Mamenchisaurus sinocanadorum        75              Jurassic
Sauroposeidon proteles              40-60           Cretaceous
Paralititan stromeri                59              Cretaceous
Brachiosaurus altithorax            28.7-56.3       Jurassic
Puertasaurus reuili                 50              Cretaceous
Ruyangosaurus giganteus             50              Cretaceous
Alamosaurus sanjuanensis            50-60           Cretaceous
Futalognkosaurus dukei              38.1-50+        Cretaceous
Turiasaurus riodevensis             40-50.9         Jurassic/Cretaceous
Camarasaurus supremus               47              Jurassic
Diplodocus hallorum                 30-42.5         Jurassic
Supersaurus vivianae                32-40.2         Jurassic
Elaltitan lilloi                    42.9            Cretaceous
Tehuelchesaurus benitezii           41.3            Jurassic
Apatosaurus louisae                 18-41.3         Jurassic

Ornithopods                         Metric Tons     Period
Shantungosaurus giganteus           9.9-22.5        Cretaceous
Iguanodon seeleyi                   15              Cretaceous
Saurolophus angustirostris          6.6-9           Cretaceous
Iguanodon bernissartensis           8.3-8.6         Cretaceous
Edmontosaurus annectens             3.2-7.6         Cretaceous
Brachylophosaurus canadensis        4.5-7           Cretaceous
Saurolophus osborni                 6.6             Cretaceous
Lanzhousaurus magnidens             6               Cretaceous
Parasaurolophus walkeri             3-5.1           Cretaceous
Charonosaurus  jiayinensis          5               Cretaceous
Barsboldia sicinskii                5               Cretaceous

Ceratopsians                        Metric Tons     Period
Triceratops horridus                5-14            Cretaceous
Triceratops prorsus                 6.5-11          Cretaceous
Titanoceratops ouranos              6.5-11          Cretaceous
Eotriceratops xerinsularis          10              Cretaceous
Pentaceratops sternbergii           3-4.8           Cretaceous
Pachyrhinosaurus canadensis         3-4.4           Cretaceous
Styracosaurus albertensis           4.2             Cretaceous
Agujaceratops mariscalensis         2.6             Cretaceous
Centrosaurus apertus                1.1-2.5         Cretaceous
Coronosaurus brinkmani              2               Cretaceous
Rubeosaurus ovatus                  2               Cretaceous
Achelousaurus horneri               2               Cretaceous
Pachyrhinosaurus lakustai           2               Cretaceous
Chasmosaurus belli                  2               Cretaceous

Thyreophorans                       Metric Tons     Period
Dacentrurus armatus                 5-7.4           Jurassic
Ankylosaurus magniventris           1.7-6           Cretaceous
Stegosaurus stenops                 2.6-5.3         Jurassic
Cedarpelta bilbeyhallorum           5               Cretaceous
Hesperosaurus mjosi                 3.5-5           Jurassic
Tuojiangosaurus multispinus         4.8             Jurassic
Wuerhosaurus homheni                4               Cretaceous
Niobrarasaurus coleii               4               Cretaceous
Stegosaurus ungulatus               3.5             Jurassic
Gobisaurus domoculus                3.5             Cretaceous
Nodosaurus textilis                 3.5             Cretaceous
Palaeoscincus costatus              3.5             Cretaceous
Sauropelta edwardsi                 3               Cretaceous
Edmontonia rugosidens               3               Cretaceous
Edmontonia schlessmani              3               Cretaceous
Edmontonia longiceps                2.3-3           Cretaceous
Tuojiangosaurus multispinus         2.8             Jurassic
Euoplocephalus tutus                2-2.7           Cretaceous
Jiangjunosaurus junggarensis        2.5             Jurassic

This isn't exactly a fair way to do it, but I didn't want to calculate average dinosaur mass over time. I know that some groups, such as the ceratopsians didn't appear until the late Jurassic, skewing the results, and I didn't make any attempt to differentiate between late or early periods. However I also noticed that many of the smallest dinosaurs appeared in the Cretaceous as well. Pay attention to the units, even the smallest sauropods are measured in metric tons.

Lightest Dinosaurs
Theropods                           kg              Period
Parvicursor remotus                 0.137           Cretaceous
Epidexipteryx hui                   .164-.391       Jurassic
Compsognathus longipes              0.26            Jurassic
Ceratonykus oculatus                0.3             Cretaceous
Juravenator starki                  0.34-0.41       Jurassic
Ligabueino andesi                   0.35            Cretaceous
Microraptor zhaoianus               0.4             Cretaceous
Sinosauropteryx prima               0.55-0.99       Cretaceous
Rahonavis ostromi                   0.58            Cretaceous
Mahakala omnogovae                  0.76-0.79       Cretaceous
Xiaotingia zhengi                   0.79            Jurassic
Mei long                            0.85            Cretaceous
Microraptor gui                     0.95-1.50       Cretaceous

Sauropods                           Metric Tons     Period
Pleurocoelus nanus                  0.5             Cretaceous
Magyarosaurus dacus                 0.75            Cretaceous
Europasaurus holgeri                0.8-1           Jurassic
Bonatitan reigi                     1               Cretaceous
Lapparentosaurus madagascariensis   1.4             Jurassic
Lessemsaurus sauropoides            1.8             Triassic
Lirainosaurus astibiae              1.8-4           Cretaceous
Shunosaurus lii                     2.2-6.7         Jurassic
Ampelosaurus atacis                 2.5             Cretaceous
Amargasaurus cazaui                 2.6-3.8         Cretaceous
Hypselosaurus priscus               2.7-8           Cretaceous
Euhelopus zdanskyi                  3.4             Cretaceous
Neuquensaurus australis             3.5-6.1         Cretaceous
Rinconsaurus caudamirus             4.1             Cretaceous
Atacamatitan chilensis              4.3             Cretaceous
Dicraeosaurus hansemanni            4.4-5           Jurassic

Ornithopods                         kg              Period
Gasparinisaura cincosaltensis       1-13            Cretaceous
Yueosaurus tiantaiensis             3.9             Cretaceous
Fulgurotherium australe             6               Cretaceous
Notohypsilophodon comodorensis      6               Jurassic
Yandusaurus hongheensis             6.6-7.5         Jurassic
Hypsilophodon foxii                 7-21            Cretaceous
Thescelosaurus sp.                  7.9-86          Cretaceous
Valdosaurus canaliculatus           10              Cretaceous
Haya griva                          11              Cretaceous
Agilisaurus louderbacki             12              Jurassic
Drinker nisti                       20              Jurassic
Changchunsaurus parvus              20              Cretaceous
Qantassaurus intrepidus             20              Cretaceous
Zephyrosaurus schaffi               20              Cretaceous
Oryctodromeus cubicularis           20              Cretaceous
Orodromeus makelai                  20              Cretaceous

Ceratopsians                              kg        Period
Liaoceratops yanzigouensis                2         Cretaceous
Yamaceratops dorngobiensis                2         Cretaceous
Psittacosaurus sinensis                   4.1       Cretaceous
Psittacosaurus lujiatunensis              5         Jurassic
Yinlong downsi                            5.5       Cretaceous
Micropachycephalosaurus hongtuyanensis    5.9       Jurassic
Chaoyangsaurus youngi                     6         Jurassic
Xuanhuaceratops niei                      6         Jurassic
Bagaceratops rozhdestvenskyi              7         Cretaceous
Psittacosaurus meileyingensis             8         Cretaceous
Psittacosaurus neimongoliensis            8-8.4     Cretaceous
Archaeoceratops oshimai                   10        Cretaceous
Psittacosaurus mongoliensis               12.1-20   Cretaceous
Psittacosaurus sibiricus                  15        Cretaceous

Thyreophorans                       kg              Period
Scutellosaurus lawleri              3               Jurassic
Emausaurus ernsti                   50              Jurassic
Scelidosaurus harrisonii            64.5-270        Jurassic
Animantarx ramaljonesi              300             Cretaceous
Struthiosaurus transylvanicus       300             Cretaceous
Struthiosaurus austriacus           300             Cretaceous
Gargoyleosaurus parkpinorum         300             Jurassic
Mymoorapelta maysi                  300             Jurassic
Minmi paravertebra                  300             Cretaceous

So what does this mean for the relationship between oxygen levels and dinosaur size? Higher oxygen levels in the Jurassic and Cretaceous probably allowed for larger animals to exist, however as time went on Dinosaurs became more diverse in general, including size. Many of them evolved to become smaller, despite being allowed to become larger by higher levels of oxygen. We should also note that even though oxygen levels were still lower than they were during the carboniferous, the animals were much larger, most likely due to their more efficient oxygen transport systems (lungs, 3(4?) chambered hearts, sealed circulatory systems, hemoglobin).

If we think about what could drive species to become larger, competition for food and protection from predators comes to mind. Sauropods that could reach the leaves in taller trees had distinct advantages over those who could not. Prey animals stood a better chance at fighting off predators if they were bigger. Likewise, predators could kill larger prey if they became larger too. Oxygen didn't drive them to become larger, it simply allowed them to.

To actually answer the question, could the modern atmosphere support animals as large as dinosaurs? It probably could. The heaviest living animal today is the blue whale, at an average mass of 110 metric tons, is heavier than all but 1 of the sauropods on the list I compiled. The heaviest land animal living today is the African Elephant, with average mass of 4.9 metric tons and as high as 10 metric tons, would be a respectable competitor with many of the dinosaur groups I listed 12.

Another interesting question is not how oxygen affected the size of organisms, but how it affects it their metabolism. Cold blooded animals don't need as much oxygen because they don't spend as much energy. Warm blooded animals must constantly expend energy to maintain body heat, and this requires greater consumption of oxygen. Obviously being large and warm blooded would force you to need even greater levels of oxygen than 1 or the other. It may be that the advantages of being warm blooded outweighed the advantages of large size, but I don't want to dig into that question right now.


Why is offspring of identical twins not identical? When identical twins marry identical twins, the children of the couples will be full genetic siblings but why are they not genetically identical?

They are not identical for the same reason full siblings are not identical.

A simplistic Mendelian setup would be the following:

X1/X2 = Mothers
X3/Y = Fathers

That means the children could be:

X1/X3
X1/Y
X2/X3
X2/Y

So children born to two married couples composed of identical twins only have a 50/50 shot at being the same gender, much less have the exact same set of genes and express them in the same way.

Now, the simplistic view above only concerns 4 alleles - but the human genome is composed of thousands. By the end, the chances of genetically identical offspring from a set of identical twins is still very, very low.

And you haven't even began to include epigenetic variations, which often arise as a response to the environment! One cousin might be shorter due to their diet as an infant, one might have allergies the other does not depending on if they played outside as a child, and for non-Mendelian traits (incomplete dominance, co-dominance, phenotypes that rely on more than one allele [especially hair, eye, and skin color]) there's even more opportunity to introduce differences!


Why digest proteins into peptides for Liquid Chromatography - Mass Spectrometry? Digesting (trypsin or whatever other proteolytic enzyme) proteins generates multiple peptides  so the degree of complexity of the sample, at the peptide level, increases a lot. In addition there is the problem of infering the original protein from its constituent peptides.
Why is this digestion step needed when you have to go back to protein level ? Is it just technological limitation?

This is going to be a very long answer but to give a short response.

You have to consider that MS for peptide detection works on the bases/principle of mass to charge (m/z) to detect an AA molecule, which is then normalised and analysed etc etc (http://en.wikipedia.org/wiki/Mass_spectrometry). Once you have the amino acids, then you just look at the order in which they get through and then you have your peptide sequence. Please read about the B, A and Y-type ions although this page is slightly technical (http://www.matrixscience.com/help/fragmentation_help.html). If the proteins was not digested then it would be far too big to be analysed since it would be read as one massive blob of m/z, which could be anything! So once you have your spectra from a peptide, you need to compare it to a model spectra, and based on that you predict what the sequence is as fragmentations peaks can be anything. Look at SEQUEST (http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software). Now there are tons of correction algorithms that are applied, which you can look up.

Now RP-LC is carried out before MS to prevent all the sample rushing into the MS machine all at once as the machine can not cope if too much sample is inserted hence the flow rate is controlled. What I think you are thinking in terms of the set machine limit, is the (digested) peptide fragment that enters the machine, before undergoing electrospray. Now the experts that run the MS machines do set a peptide mass upper and lower limit, for what size/mass of fragment to accept and what size/mass to ignore. Look at this theoretical digest example (http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest). This happens frequently with trypsin digest as it recognises specific AA before cleavage (http://en.wikipedia.org/wiki/Trypsin). Now a days, MS has advanced so much that we have machines such as Orbitrap (http://en.wikipedia.org/wiki/Orbitrap), which can cope with peptides, digested with elastase, which cleaves non specifically, which means you are less likely to get peptides that are far too big for analysis, hence increasing the protein coverage.

Hope this helps!


Do ring species exist? In trying to understand evolution better, I have been looking at examples of speciation, and have thus come across the topic of ring species.  I have tried to find concrete examples of how these work, but have been unable to.  This paper deals with one of the frequently quoted examples of ring species, but concludes:

  In conclusion, although ring speciation is theoretically
  possible, the few well-studied examples suggest that it
  occurs infrequently, because the dynamics of species’
  ranges are more likely to result in fragmentation, i.e. periods of allopatry, before the slow process of isolation by
  distance leads to sufficient divergence to allow for circular overlap.

The paper does, however, cite an article on a bird that appears to be a strong example of a ring species, but buying access to it is more expensive than a year´s supply of toilet paper.

Is there hard evidence that ring species exist?  And if so, what is the evidence and what does it teach us about the nature of speciation?

While no perfect example exists, there are various different 'ring species' in nature where you have which species are able to interbreed with closely related populations, but there are least two "end" populations in the series. Examples include:

Alauda arvensis, A. japonica and A. gulgula: Species of Skylark birds that coexist around Central Asia

In central Asia, a northern form,, arvensis, a southern form,gulgula, and Oriental,japonica , coexist without interbreeding.These forms are separated
by a gap in distribution in northern China, but a morphologically intermediate
form, japonica, occurs in Japan. Northern japonica are similar to arvensis and
southern japonica resemble gulgula. -Ring species as bridges between microevolution and speciation

Lalage leucopygialis, L. nigra, and L. sueurii: Species of triller birds that coexist on Sulawesi Island.

The existence of ring species like this can, as biologist Ernst Mayr puts it, illustrate "how new species can arise through 'circular overlap', without interruption of gene flow through intervening populations…" and offers proof of speciation through a method other than allopatric speciation: speciation that happens when two populations of the same species become isolated from each other due to geographic changes.


Plants with no chlorophyll If chlorophyll or chloroplast is needed for the process of photosynthesis then how do non green plants with no chlorophyll get food

As @AlexDeLarge mentioned, all non-photosynthesizing plans are holoparasites because they lack the mechanisms for autotrophy. Although it is worth mentioning that it is not always chlorophyll that is doing the photosynthesis in all plants, and that even "non-green" plants can still photosynthesize (see note below).

There are generally two classifications of holoparasitic plants: those that require fungal mycorrhizal hosts called myco-heterotrophs and those that require other plants as hosts. Some examples of non-photosynthesizing myco-heterotrophic plants include those in the genus Monotropa. Examples of plant-specific holoparasitic plants include those in the genus Boschniakia.

In both cases, the parasite is partitioning nutrients directly from its host plant through a specialized root called the haustorium that penetrates the host's roots or hyphae, essentially bypassing the need for its own photosynthetic production. Technically, those parasites that attack other plants are still relying on photosynthesis (of the host), although indirectly.

This is a good review paper on some of these species:
Leake JR. 1994. The biology of myco-heterotrophic ('saprophytic') plants. New Phytologist 127(2): 171-216.

Note: For instance, when deciduous trees turn yellow and red in the fall, they are relying on the carotenoids, xanthophyll and carotene. So, while the plant is not utilizing chlorophyll to absorb light, the carotenoid compounds are incapable of transferring light energy directly to the photosynthesis pathway themselves, and thus still require chlorophyll as a pass-thorough.


If someone's arm is cut off, how does that affect blood circulation throughout their body? Essentially what I'm asking is that if someone's arm is amputated, doesn't that cut off a significant part of their blood flow because the blood vessels that normally flowed up to the hand of the amputated arm and back can't anymore?  If it heals, does that mean the body has to grow more vessels to sort of complete the circuit again?  Does the body just compensate by putting more stress on the rest of the body's blood vessels?

If I understand your question correctly, you ask how does the body deals with released blood volume after the removal of part of blood vessels?

The simple answer is the body decreases the blood volume. Our body is able to alter blood volume significantly in response to different factors.

For example, take a look at this paper: Blood volume changes in normal pregnancy. It states that:

  A healthy woman bearing a normal sized fetus, with an average birth weight of about 3.3 kg, will increase her plasma volume by an average of about 1250 ml, a little under 50% of the average non-pregnant volume for white European women of about 2600 ml.

So, after the arm cutting, an organism will decrease its blood volume. Although it will take some time, blood volume altering is more probable way than new vessels generation.


How is breathing involuntary if the muscles that control it are skeletal? How is breathing involuntary if the muscles that control it are skeletal?  Breathing is involuntary. However, the muscles that control it are skeletal: intercostal muscles and the diaphragm. Are there other muscles involved? Is it that these skeletal muscles are being controlled and/or acting involuntarily?

Humans can both continue to breathe while asleep, and they can also intentionally take a deep breath.

How is breathing be an involuntary act, that can also be controlled?

Breathing is controlled by both the Autonomic nervous system and the voluntary nervous system. You see this in instances where our breath rate increases in flight or fight situations glide to the secretion of Adrenaline and also when we intentionally increase the breathing rate when undergoing high levels of activity. This is due to the fact that the involuntary aspect of breathing is controlled by the medulla oblongata and the voluntary aspect s controlled by the cerebral cortex. The fact that it is controlled by skeletal muscles has nothing to do with how it is innervated. For example, Cardiac muscles are innervated by both the hearts own conducting system and by the Autonomic nervous system.
If you're wondering why the skeletal muscles dont get fatigued, it's because there is a small but significant rest period between each Breathing cycle (inhalation and exhalation). Therefore the skeletal muscles have a rest period. However if a high rate of breathing does occur for a sustained period, they will fatigue and that's why you get cramps after a marathon or a sprint.


Why is selection less effective in small populations than in larger? I can understand that the genetic drift has a higher impact on smaller populations, but what does it mean for the selection to be less effective in small populations than higher?

This question seems to be about negative/purifying selection, judging by the wikipedia quote. Positive selection can often (but not always) occur more slowly in smaller populations, but 'efficiency/effectiveness' of selection generally means the rate at which deleterious variants are purged from the population, so I'll skip out taking about positive selection (unless you did mean that).
First, genetic drift: Genetic drift is the stochastic change in allele frequencies caused by random differences in the survival of different individuals. For example, a mouse might get struck by lightning and not transmit any of its genes to the next generation. Whether or not it was struck by lightning probably wasn't related to its fitness, it was just 'bad luck'. As population size increases, genetic drift becomes weaker because the larger the population, the smaller the proportional impact of each random event that concerns just one individual
Negative selection tends to be less effective in smaller populations because random fluctuations in allele frequency (drift) may lead to deleterious alleles reaching higher frequency. The rate at which deleterious alleles are removed from a population depends on mutation, dominance, linkage, and demography and can vary across populations. Therefore, the average fitness over time may become reduced. Kimura in 1963 was one of the first people to show this.
In reality, 'low efficiency of selection' and 'strong drift' in small populations are the same thing.


How do large herbivores get enough protein? The food they eat seem extremely low on protein. Do they need less protein per mass unit than carnivores? Most of them grow quite a lot in the first year, is most of that from the mothers milk?

It boils down to the anatomy.

Herbivores are very good at digesting plant matter, which us monogastrics are not particularly good at. Many herbivores (such as ruminants) have large, highly developed gastrointestinal tracts containing symbiotic bacteria to allow them to digest plant matter. Once the cellulose in the plant cell walls is digested, the animal can then access the nutrients  contained in the plant matter to a degree we cannot. Ruminants (such as cows) are even better able to absorb nutrients in this way than monograstric herbivores (such as horses). Rumen microbes are also an important source in ruminants for production of amino acids.

There's also a reason why the GI tract of these herbivores is so big. In the cow, it's an enormous rumen. In the horse, it's a massive colon for hindgut fermentation. To get all the nutrients they need - such as amino acids - these herbivores have to consume and ferment vast quantities of plant matter. A carnivore can generally get all the nutrients it needs in a much smaller meat meal, meaning it does not need such an extensive GI tract.

Different species, of course, have different metabolic demands and corresponding nutritional needs. Cows and other herbivores cannot synthesize all the amino acids they need, meaning they have to be consumed through the diet. Though it is somewhat dated, an interesting discussion on this subject is Protein and Amino Acid Requirements of Mammals (PDF) by Anthony Albanese (1950). The author goes through in great details the different protein requirements for various species, but I will bring your attention to one interesting table on p 116 as it is pertinent to your last question:

As you can see, the protein content of milk seems to correspond with the time to double birth weight. Cats with a high protein milk grow very quickly, while cows, horses, and humans grow comparitively more slowly (and thus have lower protein milk).

All animals have to get protein or amino acids through the diet, but they just have different methods to satisfy their metabolic requirements. For carnivores, they consume small protein-packed meals. For large herbivores, they have to consume and digest large quantities of plant matter to meet their needs.


Why do humans stop growing? Humans grow most quickly when young, and to a lesser extent in preadolescence and early adolescence. However an equilibrium is then reached in adulthood, typically at around 1.6/1.7 meters tall.

I have found the age at which people "stop growing", meaning that they are at their tallest hight, is around the age of 21-25.

Why is it beneficial for humans to grow to 1.6/1.7 meters?

Why is there so so much variation in this, with some reaching there full height in there early teenage years?

Human bones grow in length due to the effects of human growth hormone on the epiphyseal plates near the ends of the bone. Over time these two growing margins decrease in size, or width, until those special cells are either gone, or can no longer respond to hGH. At that point the body has no mechanism to increase the size of the skeleton, and growth stops. In females this tends to happen earlier than in males; approximately 2 years after the onset of puberty for females.


I would like to know what this insect is please Noted on the side of a tree in the Brazilian Atlantic Rainforest in Oct 2017. About 3-4 cm long . Middle of a very hot day.

That is a planthopper, order Hemiptera, suborder Auchenorhycha, Superfamily Fulgoroidea. It looks to be in the Genus Phrictus. Very similar to a picture I saw on the web of Phrictus diadema.


What kind of spider is this? Bolivia Can anyone help me identify this spider found in Cochabamba, Bolivia. It is quite small. This photo shows it on a normal mortar layer between brick.

It's a (possibly subadult) female Black Widow. Subadult females often have some level of red or red and white markings on the upper surface of the abdomen, and females of some species retain those markings even into adulthood - the notorious Redback (Latrodectus hasselti) being an examnple of that. Black and red is a very common "Danger!" signal in nature, so you should be a little leery when you see it.  This one looks like Latrodectus mirabilis, which Garb, Gonzalez and Gillespie have marked in the area of Bolivia. I know almost nothing of this Widow, but since most Black Widows are pretty similar in their habits and venoms, I feel pretty confident in saying that you probably do not want to get bitten by this spider. It would be extremely painful, and would probably give you a couple of very bad days until the effects eased up. Widows don't usually tend to bite unless physically injured, but you probably want to shake out your boots in the morning before putting them on..

Here's the link to the Garb paper:

Garb, J.E., González, A. and Gillespie, R.G., 2004. The black widow spider genus Latrodectus (Araneae: Theridiidae): phylogeny, biogeography, and invasion history. Molecular phylogenetics and evolution, 31(3), pp.1127-1142.

And here's a nice Spanish language blog
that features this photo of L. mirabilis: