Can galls be formed from mutualistic relationships? According to Wikipedia, galls (cecidia) are formed by parasitic insects and mites like gall wasps (Neuroterus albipes). At some metamorphic stage, these organisms alter cell division processes in meristematic tissues of their host plants, which creates a tumour on (typically) the surface of leaves, branches or roots. These organisms use the galls as their habitat and/or food source (exploiting the sugars present).

However, I also know that bullhorn acacia and ants form an interspecific mutualistic relationship (with galls), so apparently galls don't need to be parasitic. Are there any other specific plant-insect pairs that have the same type of mutualistic gall relationship as the acacia-ant system?

From what I know of ant-Acacia mutualisms, I've never heard of an ant gall in an Acacia. The link in your question also never mentions a gall. You've likely confused either domatia or Beltian bodies as a gall. Both differ greatly from galls in that domatia or Beltian bodies are created by the plant and not by the insect.

Domatia are small plant-made chambers that house mutualistic insects (though are often invaded by non-mutualists).

Beltian bodies are a type of food body (or plant-made structures containing nutritional substances (often high in protein) that attract a mutualist species of ants in Acacia).

See here or here for more info about galls.

To answer your overarching question of whether there are mutualistic galls, I would have to say no. I do not know of any instances of which this is the case. Further, galls are inherently parasitic (not mutualistic). Even if the swollen cells do not interfere with normal plant function (e.g., as is common in Solidago spp.)1, the parasitic insect (or other arthropod) is still required to chew its way out of the gall. Last I checked, chewing on your host's tissues is never very mutualistic.

 1: Crutsinger, G.M., Habenicht, M.N., Classen, A.T., Schweitzer, J.A. and Sanders, N.J., 2008. Galling by Rhopalomyia solidaginis alters Solidago altissima architecture and litter nutrient dynamics in an old-field ecosystem. Plant and soil, 303(1-2), pp.95-103.


History: Building a "Phylogenetic network" of famous evolutionary biologists Seems like many of the famous evolutionary biologists are somehow related to each others. For example (and I might be mistaken), Ronald A. Fisher was mentored by a descendent of Charles Darwin. Joe Felsenstein did undergraduate research with James Crow and wrote his doctoral thesis under Richard Lewontin. Muller was mentored by Huxley, friend of Darwin. Brian Charlesworth was mentored by John Maynard Smith who was himself mentored by J.B.S Haldane.

Is there anyone who is crazy enough and interested in the history of evolutionary biology enough to draw a network of relationships between most famous evolutionary biologists since Charles Darwin?

An arrow between any two evolutionary biologist might represent a relationship of the kind family, PhD supervision or friendship. Of course there is no limit to the number of famous people to include and there is no good distinction of who should be included. But a network of the 20 (or 50 if you feel courageous) most famous evolutionary biologist would be awesome!

Maybe not exactly what you are searching for, but you should look at the evolutionary biology version of Academic tree. This provides family-tree type relationships between researchers, but mostly (only?) of supervisor-student relationships.

As an example, the tree for Joe Felsenstein includes links to e.g. Dobzhansky, Lewontin and Sewell Wright. You should be able to find much of the information you are looking for at this site.

Here is a small cutout of Joe Felsenstein's tree, just as an example:


What happen's to a virus's capsid after it injects its genetic material into the host cell? After a virus (one of the varieties which infects the cell via injection and not endocytosis) injects its genetic material into the host cell, what happens to its protein coat? I would guess that it just falls off. However, since it is now outside of a cell, there are no protein-digesting enzymes -- or are there?

What happens to it now? I'm guessing it doesn't just float around for all eternity.

Interesting question and actually I haven't found a real answer here yet. The phages seem to bind rather hard, since the need to be blended (subjected to relatively high forces) to shear off. This was used in the Hershey-Chase-Experiment to find out what the genetic material of the cell is. It doesn't matter though, since most of the cells which are infected get destroyed anyway. If not, they are most likely taken up and broken down inside the cell, as it happens with other membrane proteins.
This is only valid for viruses which inject their genetic material into the host cell, while the capsid stays outside. This happens mostly for Bacteriophages.

There are a few other possibilities for viruses to enter cells where this is no problem:

Viruses which have a membrane envelope can enter the cell via membrane fusion. To make the fusion happen, either the membranes have to get very close, or the virus first binds receptors on the cell surface and then fuses its membrane with the cell. This causes the interior of the virus to be released into the cell. The picture below shows the fusion (from the Wikipedia article on membrane fusion). An interesting article on this topic is: "Membrane fusion."

Another possibility for a virus to enter a host cell is via endocytosis. Here the virus uses the uptake of material from the surrounding of the cell to get inside. This can either happen together with resources inside a vacuole.
Or it happens via the binding of specific receptors, which are internalized into the cell upon binding of the specific ligand. Here the virus mimics the ligand of the receptor to get internalized into the cell.
In both cases the virus needs to escape from the vacuole before it get broken down because the vacuole is turned into a lysosome.


Is arachnophobia connected to lower immunity against spider toxins? Are arachnophobics more subceptible to toxical effects coming from spider toxins?

This is an interesting question and may stem from the fact that spider phobias tend to run in families and thus have a genetic link - assuming susceptibility to toxin levels can be passed from parent to offspring.  However, instead a study found that the fear of spiders was caused by social learning of disgust reactions.

Source: https://www.psychologytoday.com/blog/why-we-worry/201407/why-are-we-afraid-spiders

Directly from source:

  In relation to the first question, it has been known for many years
  that spider phobia tends to run in families. It has often been assumed
  that this may represent a biological predisposition caused by the
  transmission of genes between parents and offspring. However, we found
  that this relationship was considerably more complex and indirect. We
  found that the only significant predictor of a child’s spider fear was
  not the level of spider fear in the parents, but their levels of
  disgust sensitivity. One interpretation of this finding is that spider
  fear may be transmitted within families as the result of social
  learning of the nature and intensity of disgust reactions–including
  disgust reactions to spiders.

Link to study abstract: http://www.sciencedirect.com/science/article/pii/000579679390041R


How does the peptidoglycan layer of a bacterial cell wall help prevent osmotic lysis? I recently read that penicillin works by damaging the peptidoglycan layers of a bacterial cell wall causing osmotic lysis, which is when the bacteria cell bursts due to osmotic pressure.

I just would like to know how peptidoglycan prevents this. Thanks for any responses!

Peptidoglycan is formed by the linkage of molecules of NAM ( N-acetylmuramic acid) and NAG (N-acetylglucosamine) into a polysaccharide structure.  Many of these structures are then formed into a lattice by crossbridges of polypeptides.  In gram + bacterial cell walls many layers of this lattice are stacked up forming a rigid structure, that is external to the plasma membrane, and provides more resistance to osmotic lysis than the plasma membrane alone posesses.

Penicillin interferes with the final linking of the peptide crossbridges which results in a weaker cell wall that will make it more likely that the cell will undergo osmotic lysis.

Gram - bacterial cell walls are quite different than gram + cell walls.  They do contain peptidoglycan but the peptidoglycan layer is thinner - only one, or very few, layers of peptidoglycan with some structural differences also.  Therefore, gram - bacterial cell walls are weaker than gram + bacterial cell walls.

"Microbiology, an introduction" Tortora, Funke and Case 11th EDition pp 84-86


Chiral (a)symmetry of curly hair (and fur) Some people have curly hair, as well as fur of some animals can be curly.
However, shapes which are curly are not mirror symmetric, much alike screws or chiral molecules.

The question is whether curly hair in a given species (say, humans, but I don't stick to this example) are in the same proportion left-handed and right-handed?

One can easily imagine that chirality of molecules (e.g. keratin) gives rise to macroscopic chirality of curly hair. However, it is far from obvious whether this effect is strong enough.

EDIT:

I am interested mostly in data. It might be easy (yet misleading) to convince oneself that there should (or there shouldn't) be relation of microscopic to macroscopic mirror symmetry (or lack of it).

(E.g. in some other cases there is such effect - e.g. with left/right orientation of body organs like heart, or asymmetry of left and right brain.)

Microscopic chirality is not at all necessary to explain curly hair (or other objects).  All that is required is flexibility. Once hair gets long enough, it collides with itself, and is pushed off to one side or another, forming a chiral curl.

For some anecdotal evidence against microscopic chirality, find someone with large diameter hanging curls in their hair. Those seem to often curl straight back on to themselves. A more compelling anecdote is that curled objects, including hair and telephone cords (if anyone still remembers those) can be pulled through themselves and chirally inverted. Sometimes there will be some resistance, but that could be the keratin or plastic or whatever having set in its shape over time, rather than being preferentially formed that way.

These are obviously both anecdotal though, and the idea that there is some slight chiral preference isn't ruled out. I'm not even opposed to the fundamental idea of transitive chirality through several orders of superhelicity (look at DNA), but it just hasn't been my empirical experience. As Ryan points out, if it were a strong effect, all hair would curl the same way, and straight hair wouldn't exist at all.

Just to provide a bit of data, this paper demonstrates that hair curvature is based on the distribution of 4 different cell types in a follicle. The keratin (and many other proteins associated with) intermediate fibrils were associated with curvature, but only to the extend that their compositions were different in the 4 cell types. But the curvature was based on the distribution of the cells themselves.  Chirality wasn't specifically studied in the paper, but I think (given that they were staring at individual fibers with an electron microscope) that they would have noticed it had it existed.

Cortical cell types and intermediate filament arrangements correlate with fiber curvature in Japanese human hair
http://www.sciencedirect.com/science/article/pii/S1047847708002980

  Naturally straight and curved human scalp hairs were examined using fluorescence and electron microscopy techniques to determine morphological and ultrastructural features contributing to single fiber curvature. The study excluded cuticle and medulla, which lack known bilateral structural asymmetry and therefore potential to form curved fibers. The cortex contained four classifiable cell types, two of which were always present in much greater abundance than the remaining two types. In straight hair, these cell types were arranged annularly and evenly within the cortex, implying that the averaging of differing structural features would maintain a straight fiber conformation. In curved fibers, the cell types were bilaterally distributed approximately perpendicular to fiber curvature direction with one dominant cell type predominantly located closest to the convex fiber side and the other, closest to the concave side. Electron tomography confirmed that the dominant cell type closest to the convex fiber side contained discrete macrofibrils composed of helically arranged intermediate filaments, while the dominant cell type closest to the concave side contained larger fused macrofibrils composed of intermediate filament arrangements varying from helical to hexagonal arrays approximately parallel to the longitudinal fiber axis. These findings concur with the current hypothesis of hair curvature formation and behavior.


Why is atropine a CNS stimulant, although it blocks the muscarinic receptors in the brain? I know that atropine is a muscarinic  antagonist, so why does atropine have excitatory actions on the brain while it is blocking muscarinic receptors?

Short answer
Atropine inhibits an inhibitor and hence its effects are excitatory.

Background
According to the wiki page on muscarine M2 receptor:

  M2 muscarinic receptors act via a Gi type receptor, which causes a
  decrease in cAMP in the cell, generally leading to inhibitory-type
  effects.

Atropine is an antimuscarinic (anticholinergic) drug.According to the wiki page on atropine:

  [R]eactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, dizziness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, dry mouth and potentially extreme confusion, deliriant hallucinations, and excitation especially among the elderly.

So atropine blocks inhibitory muscarinic receptors, and hence causes excitation.


Cranial Nerve Decussation I want to get my head round this once and for all so if you guys could help me would really appreciate it! I understand lesions to the optic nerve. It is the other nerves that I find difficult.

So far this is my understanding, please correct me if I'm wrong. The cranial nerves do not decussate generally with exceptions being CN2, CN4, CN7 and CN12. That means if a lesion affects Cranial Nerve 1, 5, 8, 9 and 11 or the respective nucleus there is either sensation loss or atrophy of the muscle (dependent on what the nerve does) of the ipsilateral side. For example in a lesion affecting CN6, the eye cannot look out in the side of the lesion.

In the case of CN4, I'm not too sure what happens but I imagine if there is damage to the nucleus the opposite side is affected (meaning superior oblique in the contralateral side will not work). If the nerve is affected, it is typically the ipsilateral side. The same I imagine is true for CN12.

In CN7, the forehead is bilaterally innervated so if the upper motor neurone is affected eyebrows can be raised but the lower side of the face is affected ipsilaterally. In a lower motor neurone lesion, there is complete loss of one side of the face ipsilaterally.

Am I correct?

As you mentioned, the resulting impairment depends on the level of the injury: nuclear, fascicular, central / peripheral. So, you should differentiate lesions inside the brain tissue (which can be at nucleus, at any location of a tract, before crossing or after, and outside. From this, the first thing we should explain is the normal anatomy.  From normal anatomy we can understand the pathology.

One interesting fact you probably wanted to know is that Optic Nerve it not a real nerve in a classic definition, because it begins outside the brain as grouping axons of RGCs (retinal ganglion cells) and after leaving the eye becomes a “nerve”. From this, you can understand its damage better, because the damage to the visual fields depends on the level of insult.

IV nerve is the only cranial nerve that completely crossed (decussated). Thus, the lesion before the crossing/decussation (you were right mentioning the nucleus, but we extend the “region” until the decussation) will cause palsy and consequent atrophy contralaterally to the lesion. After the decussation the palsy and atrophy will be ipsilateral.

Considering cranial nerve XII we should speak about nuclear-infranuclear and supranuclear damage and with this notion supranuclear damage will cause contralateral transient tongue paresis. Nuclear-infranuclear damage will cause more permanent palsy, which is mostly bilateral because the nuclei are close to each other.

Considering VII pair, nuclear-intranuclear damage (“peripheral”) will cause ipsilateral hemifacial palsy including the brow and eyelid, while supranuclear (“central”) lesion will cause contralateral facial palsy with brow/eyelid sparing.


Alternatives to commercially available flow cytometric analysis software for use in cell cycle analysis? I know that many labs use either FlowJo or FCS Express to plot and analyze their flow data. These seem like the two standards for most labs (and I have used FlowJo before). However, my current funding does not cover software licenses and I'm not keen to pay $500-2000 out-of-pocket for a license.

Are there alternatives that approach the quality of FlowJo/FCS Express but are open-source/free with an academic license? I'm looking for an approach which will allow me to fit G1/S/G2-M curves to my data.

Sounds like you should look into Bioconductor's flow suite.  I actually really like doing flow analysis in R, but it takes some practice and getting used to.

The biggest problem you will run into (in my opinion) is gating.  It's not easy to setup a GUI point and click gate.  Rather, you'll be more forced and inclined to set limits with algorithms or hard value limits.

I found .Net Bio to be fun, but not nearly as powerful as Bioconductor.

Meta note, couldn't think of a less opinion oriented way to answer other than just to say "It can be done in R utilizing Bioconductor."  If this is still off, I'm fine with deletion.


Species identification, tree from Ecuador This tree is recently photographed in Quito, Ecuador. It grows everywhere. I'm new to South American flora, so I'd like to know what the species it is?

Your plant appears to be Chionanthus pubescens, the pink fringe tree, which is native to Ecuador and Peru. The genus has a number of species. It belongs to the family Oleaceae, which includes well known plants like jasmine, forsythia, ash trees and olives. I could not find much biological information on the pink fringe tree but plantlist.org contains a number of links to various databases that may be helpful if you want to dig deeper.


Are all known germs benign in small enough quantities? i.e. Why do we wash our hands? We know that we wash our hands because germs can get into our body through the nose, the mouth, the eyes, cuts, etc. But I doubt we can completely clean our hands of germs every time we wash them, down to the individual bacterium or virion, even if we use anti-septic soap. So chances are, even if we keep up with our hygiene, germs still get into our body, only in very very small quantities. So here are some questions:

In theory, is there a dividing line where we can say "ok, at this non-zero count of bacteria or virion, there is still (an arbitrary probability) that a normal healthy person won't get sick" for every germ known to man? If not, are there germs that are known to cause havoc in a healthy person even if he comes into contact with a single individual bacterium or virion?
Do we know a certain trend based on the classification of the germ?
How about the most commonly found germs (whichever they are)?
How about some of the most feared, but not so common, virii known to man, like HIV, ebola, SARS?

I think that without being able to answer some of these questions, especially #3, hygiene would be nothing but a ritual activity (because "it just works").

There is a Wikipedia page  which gives some typical values for infectious doses of bacteria. I suspect that lot of these have been taken from this slideshow which confirms the values on the Wikipedia page, gives more interesting details of how they have been arrived at, and also mentions a few viruses.

It seems from the slideshow that infectious dose isn't estimated in the way that the OP envisages - "What is the probability of infection if I ingest one cell?".

What is clear is that the infectious doses for some bacteria can be less than 10 cells (e.g. Shigella flexneri, E. coli O157:H7). Conversely for many other pathogens such as other strains of E. coli the estimate is >106 cells, so standard hygiene precautions will always offer some protection.


What is this large brown bug with pincers? What is this large, brown insect with pincers? Seen in Waltham, Massachusetts.

You probably have a specimen of a stag beetle.

In Europe we have a very big one: Lucanus Cervus
but it seems to be absent in US.

Then I found an interesting web-site referring to the different stag beetle and mentioning the link to the European one.

In this above site, they mention you have to look into the antenna and as they are not very visible on your picture I think it would be difficult to define precisely what is the exact taxon of the one you found.

For specifically Massachussets region, I found this interesting link.

and they refers to Lucanus Cepreolus, but I would not be 100% sure it is this one as the antennas are not present on your picture.

References

http://beneficialbugs.org/bugs/Ground_Beetles/stag_beetles.htm
http://bugguide.net/node/view/3104/bgpage
http://www.insectidentification.org/insects-by-type-and-region.asp?


How can you design a drug to modify apoptosis to treat a disease such as cancer? How can you design a drug to modify apoptosis to treat a disease such as cancer? Im in highschool so can someone please explain in simple terms. Thankyou.

The new cancer drugs are custom designed antibodies that have a cell-killing agent attached to them. These antibodies specifically attach to the cancer cells, and kill them. Other methods, like traditional chemotherapy target cells that are actively dividing, like hair in addition to cancer. Cancer cells are defined by uncontrolled cell division. But traditional chemotherapy, in simple terms, stresses the body to near death, differentially killing actively dividing cells. The new targeted methods are much less toxic.


How do you go from virus infection to disease? I heard on the radio a few days ago1 a discussion on viruses and diseases (go figure why :)).

The guest was very precise in how the virus enters a cell, how its RNA merges with the cell's one and how it turns the cell into a "virus factory" (roughly speaking).

The question which was not accurately answered was "and so what? how does this makes someone actually sick?"

One of the points vaguely confirmed by the virologist (following a question from the journalist) was that the immune response of the body (notably the raised temperature) was what we perceived as the disease.

Since their time was short, there were no more deliberations on that interesting point.

My question: what happens that turns the "virus replication" activity into disease? I understand that the raised temperature is a direct effect of the immune system fighting these foreign bodies (the virus) but there are other effects such as headache, cough, etc.

Are all of these a consequence of the immune system fighting back? Or is the virus changing the way the cells function, and therefore they fail at their intended activity?

1 French radio France Culture, the guest was Olivier Schwartz, director of the Dept of Virus and Immunology of the Institut Pasteur, link to the podcast (in French, obviously)

In viral infections, the disease (on the cell/tissue level) is mainly due to immune response that results in inflammation, for example, of the throat mucosal lining, which can trigger symptoms, such as dry cough.

Each symptom has its own trigger. For example, in flu:

  The mucous membranes lining the nasal and sinus cavities can become
  inflamed when infected with the flu virus. This results in increased
  pressure around the eyes and face, which may lead to a magnified
  headache (National Headache Foundation).

and

  The immune reaction to the viral infection and the interferon response
  are responsible for the viral syndrome that includes high fever,
  coryza, and body aches (StatPearls).

How viruses cause symptoms is a broad question - it depends on the virus and exact symptom, so just few more examples:

In viral pneumonia, immune response triggers inflammation in the lung alveoli, which can result in shortness of breath (StatPearls).
In AIDS, HIV virus destroys CD4 lymphycites and thus impairs cell-mediated immunity, which makes the infected person vulnerable for infections, so most symptoms are from those infections, for example, oral thrush due to overgrowth of Candida yeasts in the mouth (MerckManual).

Viruses usually do not cause disease or symptoms by merely changing the function of the cells, but by damaging them, so it's more about "injury" than just a changed function. The damage of the cells and the viruses themselves trigger inflammation and most of symptoms usually originate from it.


Which fish species is it? Today we found this kind of fish on the shore of Baltic Sea near Gdansk (PL). It is a very thin "fish" with some kind of a needle in place of nose. It was about 5 cm long and very lively. What is the name of the species?

PS. Kids caught it into a bucket just to take a pic - we released the creature just after the photo session :)

This looks like a pipefish, possibly a straightnose pipefish.

See also. But the size suggests a juvenile?


Tissues in plants and animals What is the equivalent connective tissue in plants?

Connective tissue in animals are mostly made up of collagen.

What about in plants?

Connective tissue in animals are mostly made up of collagen

Tissue is not like a simple chemical mixture ; rather tissue means a group or assemblage of cells, obeying certain defining-characteristics.
Animal connective tissues contain collagen mostly in the extracellular matrix. There are also other cell-constituents like phospholipid(membranes), DNA, RNA, etc.  Blood is a liquid connective tissue which do not contain collagen in its matrix (plasma)

  What is the equivalent connective tissue in plants?

Connective tissue is defined as all the tissues originated from the mesoderm layer of the animal embryo.

Now plants have a different mode of development than animals (plausibly due to evolution in separate route). So no part of a plant-body is homologous with a part of animal-body. It is impossible to bring a compare.

However; plants too; have their extracellular matrix; which is more popular as plant's cell wall (that contain cellulose, hemicellulose, etc.) as well there are intercellular spaces.

Still, if you forcefully want to bring a comparison; then the ground-tissue system of plant maybe called as a rough analogy with connective tissues in animals ( Similarly epidermal tissue of plant maybe a rough analogy with epithelial tissue of animals)


What is bilateral symmetry in "bilateria", an actual symmentry Wikipedia defines bilateria as :

  animals with bilateral symmetry, i.e., they have a head ("anterior") and a
  tail ("posterior") as well as a back ("dorsal") and a belly
  ("ventral"); therefore they also have a left side and a right side.

By symmetry, I understand that divisions of the body along some plane be similar. Now, if you have a head and tail, isn't the horizontal symmetry lost (head and tail look different) ? Similarly, for a vertical division, a different looking belly and back also destroys symmetry along this axis.

An organism whose head and tail are exactly the same (you can't even make out if something is head, and the other, tail), is perhaps "actually" bilaterally symmetrical (along the horizontal axis).

What am I missing here ?

You are missing that "bilateral symmetry" does not mean "the divisions are the same on some arbitrary plane" it means "the divisions are the same on one specific plane".

That specific plane for animals with bilateral symmetry is on the mid-saggittal plane that divides the body into left and right. You won't get symmetry if you bisect in any other plane. If you do get symmetry in a different plane, then you are no longer talking about bilateral symmetry but rather some other type of symmetry, such as radial symmetry, spherical symmetry, or biradial symmetry.

Note also that although many animals do not have perfect bilateral symmetry in their internal organs (humans, for one), they are still considered to be bilateral symmetrical, because the bilateral symmetry is the main organizing feature of the whole animal.


What's the difference between reaction norms and phenotypic plasticity? I'm trying to understand better these two concepts, but I cannot see a clear difference yet.

Reaction norm: "set of phenotypes that can be produced by an individual genotype when exposed to different environmental conditions"

Phenotypic plasticity: "ability of individual genotypes to produce different phenotypes when exposed to different environmental conditions"

Are phenotypic plasticity changes temporary changes in genes; are they an extension of the reaction norm?

Phenotypic plasticity, as you define in your question, is an ability or a property of the organism (a given genotype) to manifest different phenotypes in different environments (Pigliucci et al., 2006).

Reaction norm is an analysis of the pattern of phenotypes exhibited in different environments. In other words it is an analysis of the phenotypic plasticity.


Are human beings evolved to eat meat? I know humans can cook and prepare almost anything, but are humans specifically adapted to eat meat?

One of my doubts humans are not particularly well adapted to eat meat because they lack canine teeth. I read more reasons for this here.

What does an evolutionary biologist have to say on this matter? Perhaps evolutionary biology is the field related to this?

Some links supporting my doubt:

http://www.peta2.com/blog/humans-supposed-eat-meat/
http://mindfullybliss.com/humans-are-designed-to-eat-meat/

First, the correlation between canine teeth and carnivory isn't absolute. Gorillas have fearsome canines, and they're herbivores. Humans are the only primates capable of rotary chewing, thanks to our small canines. (Encyclopedia Britannica: Canine Tooth)

Even with our small canines, some groups of humans live almost entirely on meat. However, humans are clearly omnivores in general.

Our closest living relative is the chimpanzee. Chimps are primarily herbivores, but they love meat.

Mastering the art of tool (and weapon) making, made our ancestors more efficient hunters. Meat became an especially important source of food for people living in colder climates, where plants were scarce in winter or year round. It was thus presumably more important during the Ice Age, which was an important chapter in our evolution.

But humans remain adapted to an omnivorous diet, ranging from herbivory (veganism) to carnivory.


Are the transverse septum in sharks and the diaphragm in mammals homologous structures? Are the transverse septum in sharks and the diaphragm in mammals homologous structures?

I have searched on Google Scholar and Web of Science, but haven't found substantial evidence to prove or falsify the claim.

A beginning of answer here below, I hope. Please first consider that many structures are involved in the question here, the diaphragm (UBERON:0001103), the diaphragmaticus muscle (UBERON:0036071) and the septum transversum (UBERON:0004161). At Bgee (bgee.org) we aim annotating relations of similarity between anatomical structures, please have a look at our GitHub
https://github.com/BgeeDB/anatomical-similarity-annotations

We already annotated 'diaphragm' as a mammalian structure, not homologous in Amniota (please see https://raw.githubusercontent.com/BgeeDB/anatomical-similarity-annotations/master/release/similarity.tsv). In our next release, you will see the annotation for the 'diaphragmaticus muscle' which is an analog organ in Crocodylians (and Turtles) but not homologous to the mammalian diaphragm either. See here for more details about this new Uberon class:
https://github.com/obophenotype/uberon/issues/1229.

Based on the comments here above, I would say that currently we can argue that there is no evidence for a homologous relationship between the 'septum transversum' in sharks and the mammalian diaphragm. Please note that UBERON:0004161 septum transversum describes the (mammalian) embryonic structure that will give rise to the central tendon of the diaphragm, while here you are talking about a adult structure closer to a 'diaphragmaticus muscle'-like septum, as far as I understand.
But anyway thank you for your interesting question that points out a very exciting and rapidly evolving evo-devo field, as this recent paper also suggests
https://www.ncbi.nlm.nih.gov/pubmed/?term=27859325


Mushroom Identificaton(USA) I need help identifying a perculiar species of mushroom found in my yard today. Color is orange-yellow, around 3-4 inches total radius, its a cluster of tiny to medium mushrooms. They were found near an oak tree. Location is southern Georgia, USa.

These could be specimens of Omphalotus Illudens based on the orange/yellow color, the time of the year, their association with decaying wood (an oak in this case) and your location (eastern North America)

You can read more about these species in this reference: Messiah College


What's the smallest animal with hemoglobin running in its veins? What's the smallest known animal with hemoglobin running in its veins?

Here I mean an animal that on its own is able to produce the hemoglobin that is running in its veins. For that reason this excludes mosquitoes that have filled themselves with blood from another creature, for example.

With smallest I mean either by mass or by spatial dimensions. Either would be interesting.

It depends how different from human hemoglobin it can be and still count as hemoglobin.  Here is a cool evolutionary tree of globins.

http://www.mhhe.com/biosci/genbio/enger/student/olc/art_quizzes/genbiomedia/0329.jpg

Here is the worlds smallest fish.  Fish have hemoglobin similar to that of humans.
from Wikipedia:  The world's smallest fish is Paedocypris progenetica1 from Indonesia, with mature females measuring 7.9 mm (0.31 in).

But I think bloodworms are even smaller. They have hemoglobin too.  It is evolutionarily more distant from us but they use it for the same reason we do.

from https://www.prestoninnovations.com/img/media/Seq-7.jpg

http://www.allaboutworms.com/the-basics-of-blood-worms

  Blood worms are red because their blood plasma contains haemoglobin,
  like human blood. Also spelled “hemoglobin,” haemoglobin increases its
  ability to take up oxygen. The larvae commonly burrow in the
  oxygen-poor mud bottom of pools and rivers, so haemoglobin is of great
  value to the larvae.

If you are going to allow very distant relatives,  I think this snail is even smaller than the smallest bloodworm.  Less than 1 mm.  Molluscs have hemoglobin too.

from https://www.slideshare.net/fmoretzsohn/texas-seashellsmore-than-you


What culture medium should we use for tap/drinking water bacteria? We are a group of high school students from Manila who is performing an investigatory project on a topic that we chose which, at first glance, seemed simple, but turned out a bit complicated. We're trying to test the effectiveness of SODIS of solar water disinfection in killing bacteria.

I previously asked a  question here at Stack Exchange and we consulted our teacher about the answer we received. According to her, at our level, it is best to use culture media. Our testing will be qualitative. We won't be identifying the specific type of bacteria. Rather, we will observe culture media if anything grows in there.

She gave us an assignment to research about what medium to use. Due to inexperience and lack of knowledge on what we find on the internet, we resorted to ask here again.

For bacteria commonly found in tap water, what culture medium do we use? We found mentions of Legionella, Salmonella,  E. coli, and Anabaena sp. in our research.

In this article, we found different types of culture media. TSA captured our attention because it is a "general type." Nonetheless, we're not that sure about what "general" means if it means it can be used for the bacteria I mentioned above. There's also EMB that appears to be used in two of the bacteria we mentioned.

Edit:
It appears that not all culture media is good for student use. According to this article, only LB Agar, Nutrient Agar, and Tryptic Soy Agar can be used by students. Among these three, is there something I can use?

Usually when culture-based methods are used to test drinking water a range of selective culture media are used (media that favor the growth of a specific category of bacteria, e.g. the MacConkey Agar mentioned in the article you linked to). This is because the aim is to test for the presence of known harmful bacteria.

I would suggest that any of your suggestions (LB agar, Nutrient Agar or Tryptic Soy Agar) would work just fine.

On another note: How are you inoculating the agar? The concentration of bacterial cells in tap water is very low, to test for bacteria usually a large volume (~ 1 liter) is passed through sterile filter paper which is then pressed onto an agar plate to transfer the bacteria.


Are there examples of animals being sexually attracted to another species more than to their own? I just thought that from the perspective of a female domestic cat, a male bobcat probably looks like the archetype of a perfect mate. As tall, strong, muscular and mighty as it possibly gets. Clearly preferable to any of these boring male domestics.

Has anyone ever done any research on this topic, like presenting a male cat and bobcat to a female in heat and scientifically evaluating her response? (I'm not exclusively asking for cats and bobcats, but for any type of animal, and I'm just using the cat-bobcat-example to better explain the question.)

Here are a few examples. All are open to debate as to whether it answers your question.

Zoophilia in humans

When asking of example of a "species" that does something, it is easy to forget about the diversity of behaviours among individuals of that species. It raises the question of how frequent must the behaviour be in that species to accept that the species is representative of this specific behaviour. Many might be tempted to disregard humans as examples thinking that zoophilia (sexual fixation of a human on non-human animals) is very rare but the reality appears quite different.

The Kinsey reports (1953) estimated that 8% of men and 3.6% for women had sexual interaction with animals at some point in their lives. More recent studies tend to find somewhat similar results (of the order of a few percents). These numbers seem to go way higher for people living near farms. Although these numbers seem debated, the Kinsey reports (1953) estimated that 40–50% of people living near farms have had sexual interaction with animals at some point in their lives.

Given the prevalence of zoophilia, I would argue that humans could be considered an example of a species where (some) individuals are sexually attracted to individuals of another species.

Many animals have sex with about anything

In my life I have seen many dogs, rabbits and bulls attempt to have sex with inanimate objects. If a dog can be sexually aroused by a pillow (poor pillow), then I am pretty sure it can be sexually aroused by individual of another species.

Here is a picture of a moose trying to mate with a statue of a bison

Note btw that I am talking here about animal species that have a very high cognition, so below is a funny example with a beetle.

A tragic love story

In Australia, a species of Buprestidae (family of beetles) called Julodimorpha bakewelli has gone through an important decrease in population size. The blame is on people throwing their empty bottles of beers on the side of the road. Why? Males are attracted by the brown shiny color of the females and it turns out that many glass beer bottles have this same exact color. Hence, males started to spend all their time mating with beer bottles rather than with females causing a decrease in the species population size.

Sure a beer bottle in not another species but it shows how individuals of a species can be more aroused by something else than individuals of its own species (and the example is funny; the study won the IgNobel prize in 2011).

Amazon Molly

The Amazon molly is a fish species in which there is no males. All Amazon mollies are females. However, the amazon mollies need sperm to reproduce. How is it possible?

The females have to seek for sperm in a sister species in order to activate the development of the eggs. They mate with males of this sister species but don't use the genetic material of the father from the sister species (otherwise they would not be two different species). The amazon mollies are therefore only sexually aroused by individuals of another species. See Kokko et al. (2008).


Difference between aerosol and droplet transmission for airborne diseases I've been doing some pandemic reading and can't find why there is a distinction between transmission by aerosols and by droplets. Some articles give a size cutoff of 5 microns; how is that important?

Aerosols were also mentioned to be either wet (small droplets) or dry (dry remains from an evaporated droplet). Does that mean droplets can evaporate enough to count as an aerosol?

An Aerosol is a suspension of droplets or particles in air. A "suspension" means that the droplets or particles are suspended in the air and do not just fall down with gravity. Very tiny droplets can be suspended in this way by the Brownian motion of the air molecules: The air molecules move around randomly (their speed indicates the air's temperature) and hit these tiny droplets back and forth and prevent them from falling down as they would normally do because of gravity. But larger droplets are too big, the air's Brownian motion is not powerful enough to keep them suspended against gravity, so larger do fall down and do not create an aerosol.

So, if the coughed-up droplets are big, they will quickly fall down - and as a result the disease will be hard to transmit (the healthy person needs to stand close enough to the infected person to inhale the droplets before they fall down). However, if the droplets are smaller than some size, they form - as I described above - an aerosol. Such an aerosol can be suspended in the air for a long time, which can mean that a person who walks into a room where a person previously sneezed will get infected. It can also mean that the aerosol can float around the room, and infect a person standing pretty far away from the source.


What did we learn with Nazi human experimentation? Was there actually any useful knowledge gained from the Nazi experiments on human test subjects? Wikipedia cites freezing and phosphine gas reactions, but I would like to know other potential results from the Nazis.

At a first glance, it looks like the problem is that, in addition to the obvious ethical issues, there was also a lack if scientific rigor. Is this true or can some results actually be of some use?

Basically nothing.  The Nazis did unfathomably terrible things of little value, and they did it poorly.

This* is a fascinating, albeit long, read.  It goes through some of the ethics of the data, but first lists some more of the "experiments" the Nazis performed.  To add to your list: high-altitude, sea water potability, tuberculosis, poisoning, artificial insemination, and numerous woundings.  They also did terrible things to twins.  Aside from being torturous and cruel, the "experiments" rarely if ever used anesthetics and were usually designed to kill the prisoner.

The article goes on to list a few case studies where some of the Nazi works came up and could have been considered, but were repeatedly shot down.  It then details a number of reasons why the "experiments" were worthless.  In particular,

"[I]t is doubtful that physiological responses of the tortured and maimed victims represented the responses of the people for whom the experiments were meant to benefit."
Nazi "researchers" were racists who were looking to validate their own beliefs.  No good science comes from that.
The results weren't ever actually published.
The "data" are inconsistent.

The article moves into ethical arguments and hypotheticals, but ends up saying theoretically some of it could be considered, or that "Absolute censorship of the Nazi data does not seem proper, especially when the secrets of saving lives may lie solely in its contents."  It's a complicated scenario where that would arise.

Editing a few years later to add this discussion from the NY Review of Books.  It's a little removed in tone, and is over-generous as regards the intent of the Nazi torturers, but makes the interesting point that one good thing to come out of the experience was the first codified guidelines for human experimentation:

  As part of the judgment, the court issued the celebrated Nuremberg Code in 1947—the first, shortest, and in many ways most uncompromising of the major ethical codes and regulations for the conduct of medical research on humans. Although the code had no legal authority in any country, it had great influence on ideas about human experimentation, and subsequent international codes and legislation.

In particular, the concept of "informed consent" is directly traceable to the Nuremberg Code:

  The first provision of the Nuremberg Code is unqualified: “The voluntary consent of the human subject is absolutely essential.” No exceptions are permitted... Furthermore, the code is clear that consent must be given by subjects who are fully informed.

*I should note that the article is from a Jewish law website, so some may discount that as not a perfectly neutral source.  Which is silly.


What's the state of the art in designing and creating your own life forms? What's the state of the art for solving the following problem. You imagine a set of features that you want a life-form to have. Just to take an arbitrary example, say you want your life-form to have a) a strong sense of smell, b) the ability to fly and c) a comfortable couch shaped saddle on its back. What's the sequence of steps you need to take so that you can create this life-form in the lab?

I realize that we are probably far away from solving this very general problem. But perhaps there are some smaller subproblems that we do know how to solve.

For example, as far as I gather, you can probably make any living being fluorescent green in color by inserting into its genome the gene responsible for expressing the Green Fluorescent Protein. So may be if we limit the set of features one is allowed to choose from, the above problem can be solved. So my first question of the set of questions is:

1)  What features can be easily inserted into almost any organism easily?

Next, I imagine that to design and create an artificial life-form will consist of three steps:

Figure out which proteins will give rise to those feaures,
Design a genome that will express those proteins in the right quantities and
Implant that genome into a cell and actually let the being grow.

2)  Is the above sequence of steps correct, or am I missing something?

3)  What is the state of the art for each of these steps?

Finally, in light of the recent spur in the open source biology groups and DIYbio enthusiasts, I feel that there might be some very simple but really cool things related to my question that you can already do in your garage. For example, may be there is some very simple single-cell life-form that's so well understood that you can add or subtract tons of features from it with a budget of a few hundred dollars. So my final question is:

4) What is the cheapest experiment you can perform at your own home without access to a biology lab which involves changing the genome of a living organism in a way that's functionally visible? (An arbitrary example: Can you create an apple that's blue in color with a budget of $500? By create, I mean you should be able to hold the blue apple in your hand.)

The problem is of course very complex so take my answers as simplifications.

Most transgenesis so far has been done on unicellular beings (bacteria, yeast), which we can change as much as we want fairly "easily", plants, insects and some mammals. Notably, for the latter case, mice are the species which has been used the most for transgenesis, as they are cheap (compared to, say, using pigs), do not take lots of space, have big litters and a quick reproductive cycle (~20 days). Aside from mice we've seen GFP rats, pigs, dogs, cats, sheep and probably there is more, but I will mostly restrict my answers to mice (as far as I know there are big technical difficulties in applying transgenics procedures to something bigger than a mouse, but to be honest I could not explain you the details on this as I have never done it).

  What features can be easily inserted into almost any organism easily?

Well, essentially, it is easy to give rise to monogenic traits (i.e. traits that depend on a single gene). Generally speaking, when you want to have more traits, or need more than 1 gene to have the trait you create single transgenics and then breed them together.

So, if your phenotype depends on the presence of gene A and B you will generate a (mouse) line expressing A, one expressing B, you breed them together and, if you are lucky, a part of the pups will be expressing both.

  Next, I imagine that to design and create an artificial life-form will consist of three steps: 1. Figure out which proteins will give rise to those feaures, 2. Design a genome that will express those proteins in the right quantities and 3. Implant that genome into a cell and actually let the being grow.
  Is the above sequence of steps correct, or am I missing something?

No, that is not how it is done!

There has been, to my knowledge, only one (very impressive) attempt to do that, a project led by Craig Venter at Celera Genomics. The project resulted in the creation of the first synthetic life form, named Mycoplasma laboratorium (see also the original paper on Science). Doing this for a multicellular being is, presently, science-fiction.

What normally you would do is to insert or remove just the piece of DNA you need in the genome.

There are different approaches to do that: for instance, you can start from embryonic stem cells, from fertilized oocytes or from spermatozoa.

This is the general process for making a transgenic mouse:

Source: https://web.archive.org/web/20161212170103/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/T/TransgenicAnimals.html

Now, depending on how you inject your gene you can distinguish between transgenics and knock-in mice. In a transgenic mouse you insert the gene somewhere in the genome and, although there are method to understand where it ended up you generally do not know.
Knock-in animals, instead, target a specific region of the genome. This is usually used in order to change an existing gene, to improve its function or to remove its function (knock-out animals). This process, called gene targeting relies on the biological process called homologous recombination.

So, why don't we just synthesize a new genome each time?
Aside from Venter's dream, the process would:

have incredibly high cost
be extremely complicated technically
be extremely long (mostly for reason 2)
suffer from the problem that there is so much we do not know about genome regulation in a bacteria, let alone in a mouse! You have to think that the genome is not just a series of genes one after another: there is a big part of regulatory regions that define things like the 3D form of the genome, which determines when and how much genes are accessible for transcription, when and where they are activated and so on. Also, more and more attention is now drawn to something called epigenetics marks, modifications of the DNA, or its associated proteins that can also modulate its transcription.

  What is the cheapest experiment you can perform at your own home without access to a biology lab which involves changing the genome of a living organism in a way that's functionally visible? (An arbitrary example: Can you create an apple that's blue in color with a budget of $500? By create, I mean you should be able to hold the blue apple in your hand.)

Quick answer: no you cannot.

Health authorities will be not very happy if you start to produce transgenic organisms in your garage
The sole cost of the reagents which you will need to create the transgene will be >$500. You would then need various machines (e.g. a thermocycler, probably a spectrophotometer, a hood, etc etc.).
I personally don't have a clue how one creates a transgenic plant, but I suspect it is not much easier than an animal. And definitely you don't want a mouse colony in your garage, do you?

An easy experiment you can do is extracting (fairly unpurified) DNA with stuff you have at home. More than that it gets really complicated.


What is the advantage of having multiple pathways to activate complement? We all know there are three pathways to activate complement: classical pathway, lectin pathway and alternative pathway. What is the advantage of having multiple pathways?

There can be many reasons for this, but generally redundancy in biological systems is very important in that it makes the system more robust. If one pathway fails, due to mutation or some environmental factors, the other(s) can compensate and the function of the pathway remains. In some cases it can also be used to tune the degree of activity or speed of activation.

Article on pathway redundancy


When is it better for a gene to cause a biased sex ratio? Because genes are selfish and want to maximise their transmission from generation to generation, if they can distort a population's sex ratio, isn't it always in their interest to cause a biased sex ratio? Or are there cases when distorting the sex ratio isn't in their interest because they decrease the overall fitness at the higher level, i.e., incur too much damage in the individual/population? Their main priority is still to subsist in a population before spreading, right?
Thanks in advance :)

Well first if a gene is not on a a sex chromosome there is little advantage in changing the sex ratio. This is why most of the ultra-selfish genes we know about are on sex chromosomes. A gene is not helping itself spread if makes more Male offspring unless one of two things is true, it is on the Y chromosome or there is already a bias making male offspring more successful. the latter actually helps keep populations rex ratios stable since if there are more of one sex generally having offspring of the other sex is an advantage.
The most impactful sex ratio altering genes we know about result in selfish sweeps where populations can collapse as they take over and eventually prevent mating entirely. but up until that final generations with no mates the gene in question has an advantage, evolution does not care about the survival of the species or population, if a gene can improve its own ability to spread at the cost of the population then so be it. fitness at higher levels is basically irrelevant. A gene is perfectly capable of spreading by favoring itself and driving the species/population extinct. In many ways run away sexual selection is this in a nut shell, detrimental to the individual and population but beneficial to the gene.


What is the difference between sequence alignment and sequence assembly? I read the wikipedia page about sequence alignment and sequence assembly but I have not been able to find any difference between the two. What is the difference between sequence alignment and sequence assembly? If there is no different why are the terminologies different?

Sequence alignment
It is done for checking sequence similarity between two or more different sequences. This will give information about how two sequences are different, what is their evolutionary relationship, which residues are conserved etc. Take a look at following sequence alignment between different sequences. (Image courtesy: Wikimedia Commons)

You can see conversation of different amino acid residues in variety of organisms like human, mouse, rat etc.
Sequence Assembly
It is done for creating long consensus sequence from short fragments of same sequence. Generally you would do sequence assembly after sequencing some genome or large DNA fragment. Take a look at following representative image of sequence assembly (Image courtesy: Wikimedia Commons)

Here black sequence is your original sequence which you wanted to sequence. However because of technical difficulties you can't sequence all at once. Hence you fragment and sequence different fragments 9which are shown in red, blue and green). Looking at overlapping region between different sequenced fragments you calculate consensus (shown in Cyan). Here you are ideally sequencing only one large sequence and assembling it.


How does Humira work when injected into patients with rheumatoid arthritis? OK, I have rheumatoid arthritis and I've been injecting Humira 2 times a month for the last 8 months.

As far as I know rheumatoid arthritis is simply an immune system disorder which makes the immune system produce more proteins called Tumor Necrosis Factor alpha which regulate body disorders.
When I inject Humira I actually import a protein called Adalimumab which is a TNFα inhibitor.

So far so good but my question is

Does my body throw this protein away after some time? How is this protein removed from my body?

What about the way Adalimumab inhibits TNF, does it bind to TNF?

Also the details of how rheumatoid arthritis appears are not well known but the main reason is because of the patients DNA isn't it?

Adalimumab is an antibody that binds to tumor necrosis factor alpha. Antibodies have high-affinity binding sites for their antigen, and for a small antigen such as TNF-alpha, would bind to it and prevent it from binding to its target receptors. Antibodies, like all proteins, degrade after a certain period of time and are removed from circulation, and since the body does not produce more of this antibody, it must be re-administered every few weeks.

The mechanism of this pharmacological is in a sense somewhat ironic in that in nature the chief role of antibodies is binding and neutralization of foreign and potentially dangerous antigens, however, this antibody binds and neutralizes a feature of the immune system itself. This element of the immune system is a cytokine, TNF-alpha, whose function is to promote inflammation, which draws white blood cells to the site of the inflammation and activates them. TNF-alpha also induces fever, and suppresses tumor formation and viral replication by activating programmed cell death pathways.

Aggressive immune responses always cause collateral damage to surrounding tissues, however, in autoimmune diseases such as rheumatoid arthritis the damage is compounded by the fact that the target of the immune response is an element of the body itself. A central function of the immune system is to induce tolerance to self; sometimes tolerance fails and while there are genetic components involved, the process is yet to be well-understood.


How does the eye know whether to focus further out or nearer in order to bring a blurry object into focus? If the eye sees an object, but the object is out of focus, the eye could be focusing too near or too far. How does the eye (or the brain) distinguish one situation from the other?
How does it know whether to focus closer or further?

I'm interested in the case when:

only one eye is open (There must be another way besides parallax clues).
The object is an unfamiliar size
The object is an unknown distance from the eye.

Ideas so far

Does the eye try focusing either a little nearer or further and then if that doesn't help to make the object clearer then the eye focuses in the opposite direction?

Or is there some light-sensitive apparatus that is always a focused a little nearer or further than the rest of the eye, and so for instance if the cells which are focused further out are giving a clearer picture than the other cells then the eye knows to focus further out?

Or is the blurriness of a object closer than the focal point a distinguishably different sort of blurriness than an object beyond than the focal point?

Or is there some other mechanism altogether?

The neurology of vision is an extremely complex subject and is difficult to describe with any brevity, because there is so very much going on in so many parts of the brain. It is estimated that about 50% of the pathways of the brain, and about 30% of the cortex are involved in vision (where only 8% of the cortex is devoted to touch, and 3% to hearing). Some research estimates that eighty to eighty five percent of our perception, learning, cognition and activities are mediated through vision.1

The ability to accurately focus on an object, sustain that focus, and to change focusing when looking at different distances is called accommodation. That happens with the pupil size, the lens shape, etc. but it doesn't tell us how the brain chooses on what to focus. The short answer is that it's much more than focusing like a camera lens. We have retinal areas that simultaneously pay attention to further and closer areas, light/dark, edges, and more, all going on at once. That and much more information carried to the brain is processed, and efferently focus is honed. It's even more complex when two eyes are involved.

There are so many aspects to sight that an enormous number of kinds of optical illusions exist. They are involuntary. That's why they're fun. In fact, if you weren't tricked, it would indicate a problem in part of your brain. Here's one that relies on processing contrast:

As you scan looking at the white dots, your peripheral vision seems to be able to see black dots, but it's clear on scanning them one row at a time that there are no black dots.

In the following illusion, the red vertical lines are parallel.

The following are summaries of the neuroanatomy of vision.

Eye, Brain and Vision
Anatomy and physiology of the afferent visual system

1 Vision Is Our Dominant Sense


What is this plant with hardened fruits on the beach in Mozambique? We saw these near the Barra and Tofinho beaches in the Inhambane province in Mozambique, in July. They were hard and leathery and dry to the touch, long past something resembling edible fruit.

Anybody have an idea what they might be? (just curious)

Edited: Here is some context around the tree.

I will take a guess that it is Ficus racemosa which is found in that area. More info. If you have pictures of the rest of the tree that would be helpful.


Looking for Kelly Chibale's paper on Malaria cure From National Geographic, there has been a lot of hype on Kelly Chibale's work from University of Cape Town on the aminopyridine MMV390048. Unfortunately, this was from an announcement from an internal meeting so there is very little literature on the compound.

So I ask, does anyone have good literature on the compound?

This may be the paper you are looking for:

Ongaroraa DSB, Gutb J, Rosenthalb PJ, Masimirembwac CM, Chibale K. 2012. Benzoheterocyclic amodiaquine analogues with potent antiplasmodial activity: Synthesis and pharmacological evaluation. Bioorganic & Medicinal Chemistry Letters, 22(15): 5046–5050, doi:10.1016/j.bmcl.2012.06.010.


Bird species ID in the Northern Territory, Australia I was visiting Darwin, NT, Australia a few years back and I encountered this bird. I must say it was in Darwin's Botanical Gardens, so I can't be absolutely positive the Northern Territory is its original habitat. However, I'm pretty sure it's a NT native, as the whole Gardens were packed with, and dedicated to NT's wildlife.

The photo is kind of dark and a bit fuzzy due to poor lighting conditions. I already tried to digitally enhance it by removing shadows and so forth.

I tried Google Images reverse search to ID this bird, but I'm not a hero with that tool. Although it looks a bit like it - it's definitely not a Jabiru.

That's an Australian White Ibis (Threskiornis moluccus).

It's widespread across much of Australia:

You can find more info on Wikipedia.


What could live inside a pillow? I have a phobia of bugs (or other small creatures) living inside my pillow and crawling into my ear in the night. It might seem silly, but bare with me.

Recently I got wondering, what organisms could actually live inside a casual foam pillow?
I machine-wash it every now and then to keep it clean.

Bed bugs (wiki)! However, you will definitely be able to notice when they are around by bite marks and blood residues.


Biology Intuition and Origin of the "facts" I am a graduate physics student but also taking biology classes. I am new to the field of bio. Most of what we do in class seem like memorizations and stating-facts. I am wondering:

How can I develop intuition for biology? (Aside from memorizing and practicing.) I am not even sure what intuition would be like in the case of biology?
Where are all the known facts in biology (and chemistry) come from? Have to be from EXPERIMENTS though, I hope to understand the origins of the I-was-being-told-this-way facts such as the composition of DNA and the types of bonding. By understanding, I don't necessarily mean the exact experimental procedure, but the general idea of how everything came about. (I am mainly interested in molecular and cell bio).
Much appreciation for any input!

Googling "landmark experiments in biology" came up with a lot of hits, what was wrong with the experiments cited in any of those works?  Mendel's pea experiments should be easy enough to understand.

Honestly I don't see how it will benefit you to know the organic chemistry work that went into determining the chemical structure of adenine.


Is there a good field methods book that covers terrestrial ecology? In the past I have used Limnological Analysis by Wetzel and Likens and Methods in Stream Ecology edited by Hauer and Lamberti to develop labs and research methods for courses and projects with an aquatic focus.

These books detail the standard methods of lotic and lentic ecology with some emphasis on utilizing the methods in undergraduate or graduate level courses.

I am now developing a biogeochemistry course that is not limited to aquatic systems and I am looking for a summary of field methods for terrestrial systems.

Is there a book that summarizes terrestrial field ecology methods similar to Wetzel and Likens and Hauer and Lamberti?

Take a look at Field and Laboratory Methods for General Ecology by James E. Brower, Jerrold H. Zar, and Carl N. von Ende.

If you are only interested in plant sampling techniques, an great resource published by U.S. Bureau of Land Management is Measuring & Monitoring Plant Populations by Caryl L. Elzinga, Daniel W. Salzer, and John W. Willoughby.

Another great resource that covers wildlife research and management techniques (2 volume set) is The Wildlife Techniques Manual published by The Wildlife Society and edited by Nova J. Silvy.


How can just random mutations explain mimicry? I have been reading this article on drug resistance which explained that how random mutations in a bacterial colony can lead to development of drug resistance among some organisms in that colony.

A thought occurred to me that if mutations are just random (by random what I know (or think)  here is the number and time of a mutation occurring in an organism in a normal environment may not be fixed but random) events arising from copy errors during DNA replications then how come some animals in nature mimic their surroundings to save themselves from predators or catch prey?

Let's consider for the time being that an animal exhibiting mimicry have evolved through natural selection, after suffering a mutation in their DNA which made them well adapted to their environment, and also saved them from their predators. Now we know a fit organism, in the struggle for existence, produces offsprings which can withstand the adversities of the surroundings and thus increases in numbers. In this way we may assume that due to many such helpful mutations led to the evolution of a new species.

This may sound simple but it actually seems to me as an over simplification of the events that lead to the development of 'that' new species. First of all not all mutations are helpful. Some are lethal as well. Also mutations may often be silent due to the degeneracy of the genetic code and presence of introns in the eukaryote. But let us consider here that the mutation suffered by our test organism was neither silent nor harmful, that too leaves us with infinite number of mutation possibilities to get a favourable organism from an unfit (to the surrounding in which our test organism is struggling) parent generation. Thus I think nature may not test each and every kind of possibility to select the fit one because in that case the test organisms will be far too many in number. Also if we consider that the fit one emerged just by chance out of million other possibilities then its sure that it was either too lucky or there is some other factor except 'just' mutation which can explain mimicry. Thus can only general mutation explain mimicry or we need something more to explain it?

/how come these animals (below) show such striking resemblance with their surroundings/

You are looking at the culmination of millions of generations of these insects.  The mutations are random, but only the helpful ones (of all the random ones) produce an advantage for the organism and so persist in the species.   If a random mutation caused an insect to look slightly more like its environment, that insect might do better at avoid predators or catching prey.   Thus it would be more likely to produce offspring which would also have its mutation.  Random mutations that caused an organism to look some other way would not confer any benefit as regards producing more offspring.

In each generation, if there is some random mutation that made the organism more similar to its environment, it could produce better fitness.  The end result, over thousands (even millions) of years, is an organism which looks very much like its environment.

Fitness is what drives evolution.  Read more at the link if you are interested.  The more offspring I have the more I pass along my DNA and the better my fitness is.  If I have a mutation that lets me have more offspring, that improves my genetic fitness.


What is the advantage of restriction enzymes cutting only at specific sites? Bacteriophages have sequences which often do not have specific sites for restriction enzymes of bacteria to cut at and so can attack the bacteria.

Wouldn't it be better if bacteria had something "universal" like an enzyme that simply cuts the nucleotide sequence "randomly"? Is there any particular advantage of cutting at only a few restriction sites?

Such universal restriction enzymes would be very dangerous to leave lying around even if contained within a vacuole. Remember that bacteria are prokaryotes and have no nuclear membrane to protect their DNA.

The analogy would be having a burglar alarm capable of burning down the house in order to protect it against thieves.


Intuitive explanation for Kin- and Group- selection It is known from theoretician in the field of kin selection that kin selection (inclusive fitness theory) and group selection are actually two sides of the same coin. In other words, these two concepts are actually only one single process.

Questions

Is group selection equivalent to kin selection for any evolutionary game or exclusively for the prisoner's dilemna?
Can you please provide an intuitive explanation of why kin- and group-selection are the same thing?

First of all, there is a very heated debate about this in the field of social evolution at present, and you aren't likely to get a conclusive answer. One theorist may give you one answer, but another will vehemently disagree. I'll start by logically answering your questions in reverse order!

Question 2: Can you please provide an intuitive explanation of why kin- and group-selection are the same thing?

The first formal 'proof' that they are the same came from a paper by Queller in 1992. Let me give you the gist of what he found without being ultra rigorous. I won't focus on relatedness, since that was answered nicely by @falsum, "Price's equation tells us that this happens when the genetic variance between-groups is higher than the genetic variance within-groups. This is equivalent to saying that altruists tend to interact with other altruists and, accordingly, that the coefficient of relatedness increases."

Queller explored the change in mean additive genetic (breeding) value for a trait over a single generation using Price's equation

$
\Delta \bar{G} = \mathrm{Cov}(W,G)
$

where $G$ is the additive genetic value, and $W$ is relative fitness. Now, the key question is, how should we define fitness? If we treat it as a random variable, we can do a linear regression of fitness on a set of explanatory variables. What should we choose for the explanatory variables? One natural choice might be to predict the fitness of a focal individual based on the phenotype of the focal individual itself, and the phenotype of the individuals the individual interacts with socially:

$
W_{i} = w_{0} + \beta_{direct} P_{i} + \beta_{social} P_{j}
$

where $w_{0}$ is baseline fitness, $P_{i}$ is the phenotype of the focal individual, and $P_{j}$ is the phenotype of the focal individual's social partner. However, another way to predict the fitness of a focal individual might be to focus on the average phenotype of individuals in the focal individual's group, and the deviation of the focal individual's phenotype from the mean phenotype of individuals in the group

$
W_{i} = w_{0} + \beta_{deviation} (\bar{P}_{group} - P_{i}) + \beta_{group} \bar{P}_{group}
$

These regression equations for fitness hold exactly (only for a single generation), independent of the 'true' form of the fitness functions (they can be as non-linear as you like). What these allow us to do, however, is partition fitness effects into those that are due to benefits of a behaviour, those that are due to costs of a behaviour (and unmodelled residuals or 'noise').

From a kin-selection perspective, it turns out that the benefit in Hamilton's rule is

$
\beta_{social} = B
$

and the cost in Hamilton's rule is

$
\beta_{direct} = C
$

From a group-selection perspective, it turns out that the benefits and costs in Hamilton's rule are distributed over deivation and group effects

$
\beta_{deviation} = C - B
$

and

$
\beta_{group} = C + (N-1)B
$

Thus, we find that it possible to write fitness equivalently in two different ways that relate the change in frequency of individuals to benefits and costs associated with a social phenotype.

Question 1 Is group selection equivalent to kin selection for any evolutionary game or exclusively for the prisoner's dilemna?

They are always equivalent no matter what game is being played or how the population is structured if you are happy use the regression methods described to define fitness, benefits, costs, and relatedness. Many people have issues with the regression methods though. See Allen et al for a discussion of this. Others argue that kin-selection holds in every case and that the problems with kin-selection stem from a misunderstanding of the methodology. See Gardner et al for a discussion of this.

Many biologists find the debates in social evolution about kin/multi-level selection unhelpful (at best), and choose either framework to work in based on the question at hand. A few are very partisan on either side. There is a great deal of misrepresentation floating around about both, so read papers making strong claims with skepticism and caution.


What phenotypes can arise from gender-related aneuploidy? Humans normally have 46 chromosomes (two copies - one from each parent - of each of the 24 chromosomes: [1:22] + [XX or XY]).

Aneuploidy is an abnormal number of chromosomes - Down's syndromes is an example of this, where individuals have an additional copy of chromosome 21.

I have read a little about gender-related aneuploidy, where individuals can have additional sex-specific chromosomes (for example XXY).

I was wondering what (roughly) the prevalence of the different combinations are, what the specific phenotypes are, and what (if any) medical complications can arise from these combinations, or indeed, what advantages could be conferred by the additional chromosome!

47,XXX
47,XXY
47,XYY

My question also stretches to whether the different combinations display a hermaphroditic phenotype?

Note that anyone with a Y chromosome is considered a genetic male. Also, aneuploidy is usually a result of nondisjunction (but can have other causes as well) and is usually not inherited.

47,XXX is called Triple X syndrome and occurs in approximately 1 in 1,000 female births. These individuals usually appear normal, but may have tall stature, a small head, and delayed development. According to this case report, the tall stature is possibly due to SHOX gene triplication, in some cases. The short stature homeobox gene (SHOX) gene is a gene on the X and Y chromosome and is associated with short stature if a copy of the gene is missing or mutated. The case report states, "The enhancing effect of SHOX gene triplication on growth was ascribed to the concomitant absence of gonadal steroids in cases of gonadal dysgenesis, allowing a prolonged period of growth."
47,XXY is called Klinefelter's syndrome. Here is an image/diagram of symptoms. These people may have gynecomastia (enlarged breasts), less muscle, less body hair, and hypogonadism (decreased testicular function, also resulting in smaller testicles and penis) due to lower testosterone production. These symptoms become more obvious after puberty, because individuals with Klinefelter's have less "masculinization" (for lack of a better word). Cognitive problems are usually present. It occurs in roughly 1 in 500 to 1 in 1,000 male births.
47,XYY is XYY syndrome and has an incidence of 1 in 1,000 male births. They appear normal but may be slightly taller than average. This study looked at the cognitive and motor phenotypes of boys with Klinefelter's and XYY syndromes. It found that both groups have generalized cognitive impairment, but XYY has more profound language impairment and Klinefelter's has more significant motor impairment. Their hypothesis is that "the more severe language-based cognitive phenotype in XYY versus KS is likely to be genetically determined on the basis of abnormal dosage of specific Y chromosome genes, but not abnormal levels of testosterone because XYY is not associated with testicular failure."

There's also 45, X0 (Turner syndrome), in which girls have a webbed neck,  broad chest, low-set ears, short stature, gonadal dysfunction, and often other conditions such as a bicuspid aortic valve, coarctation of the aorta, and vision problems. Image of symptoms. It occurs in 1 in 2,000 live births. Individuals usually have 1 X chromosome, but may also have 2 X chromosomes, with 1 of them being incomplete (source). The single copy of the SHOX gene (mentioned above) has been linked to the short stature in Turner syndrome.

Interestingly, people with 47,XYY and 47,XXX people often have normal fertility, but not in the other two cases. My uneducated guess is that the extra "normal" chromosome (for the person's sex) doesn't disrupt gonadal function.


Living on pure glycogen? I was recently fascinated when I learned about polysaccharides (I am a biology newbie) and was wondering about some of their properties. After doing some googling I was unable to find any information regarding this scenario.
This is purely theoretical, I am not insane enough to actually try this.

If my only source of carbohydrates was ingestion of pure glycogen,
could I live healthily? (assuming I obtain all other necessities for
life)
Approximately how many grams of glycogen would I need to live for a
week (assuming I weigh 150 lbs)? Is this even possible to calculate?
What does pure glycogen taste like?

You asked three questions here, so I'll answer them one by one.

Yes, you can survive with glycogen as the only source of carbohydrates, assuming that you also take other nutrients like proteins, fats, vitamins, etc. also because carbohydrates cannot supplement all of them. See this article:

There are three macronutrients: carbohydrates, protein and fats. Macronutrients are essential for proper body functioning, and the body requires large amounts of them. All macronutrients must be obtained through diet; the body cannot produce macronutrients on its own.

No, there's no way to calculate this. If we were talking about glucose, a definite range could be given. But since glycogen is a polymer with variable amount of glucose molecules linked together (at least I couldn't find an exact number),  its not possible to tell how many glycogen molecules are needed for the daily metabolism in the body.

Glycogen is an organic, non-polar polymer, insoluble in water just like starch. It does not have a specific taste, but once you eat it, an enzyme called salivary amylase will break it into glucose, maltose and limit dextrins, causing it to taste a bit sweet. See this article:

This enzyme acts on starch, glycogen and related polysaccharides and oligosaccharides producing beta-maltose by an inversion.

Source


Why aren't genetic triplets roughly evenly found in DNA? Sorry, the page I linked to is huge and you'll need to do a text search for "CG" to find the part I'm talking about.

I found a graph on this page (http://www.oftenpaper.net/sierpinski.htm) showing that the eight DNA sequences including CG, i.e. four *CG and four CG* sequences are much rarer than the others in a human X chromosome. I realise that this is only for one sample of a human X chromosome (not even all human chromosomes) but I was wondering why this is? Obviously, if *CG is rare CG* will be too.

From my limited understanding the equivalent RNA sequences would be *GC (redundant codes for four amino acids) and GC* (the only codes that produce Alanine). According to the Wikipedia page on Alanine it accounts for 7.8% of genetic amino acids, well over the average.

Is this representative across all DNA? Across all human DNA? What does DNA have against coding CG sequences, even if only in the X chromosome? Do other chromosomes have an abundance of CG sequences but are rare in others?


H O N C alternatives for organic life? Most organic structures built from hydrogen, oxygen, nitrogen and carbon. They are represent 1-,2-,3-,4- bond relations (chemical valence) which allow to build variety of chain structures.

Are there exist some replacements for these elements to create complex structures that theoretically can create life (self-reproduced or be a part of cell as organelle)?

UPDATE

Is there a common chemical model for life in the universe?
Arsenic-eating microbe may redefine chemistry of life
A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus
https://en.wikipedia.org/wiki/DNA#Alternate_DNA_structures
https://en.wikipedia.org/wiki/Arsenic_DNA

Its not scientifically or logically possible to say 'this is impossible' but since this is a speculative question, I'll hazard an opinion.

I'd like to argue that, at Earth standard pressure temperature and atmospheric conditions, C H O and N are not really replaceable.  Throw water into the mix as the most common liquid and replacing any or all of these elements is hard to imagine.

One can think about this by looking at the formation of long hydrocarbon chains.  Silicon can form polymers, but they tend to fall apart. Silcone-oxide polymers [SiR2-O-SiR2-O-] are more stable, but do not resemble hydrocarbon polymers as readily.

Carbon is much more versatile, capable of forming either chain, or including sulfur, nitrogen in stable chains that don't seem to really have any length limitations.

At thousands of atmosphere's pressure, temperatures of 70 Kelvin or in a sea of sulfuric acid, its easy to imagine other sorts of chemistry would dominate - phosphate , arsenic chains or germainium lattices, but on Earth most of these would fall apart.

Even if/when life is discovered elsewhere , it will certainly feature chemistry that will completely amaze us; unlike anything here.  But even so, its hard for me to imagine it being completely exclusive of these four elements.  I just want to point out that by a wide margin, hydrogen is the most common element of the universe.   Nearly all the other light elements like C, O and N are the next most common.  This is simply because they take fewer nuclear fusion events to create.  Hydrogen is pretty useful no matter what chemistry you are looking at.  These four are probably going to be there somewhere - most planetary atmospheres have Ammonia, CO2 and methane in them as well - at least as far as we've seen.


What is the least costly method to generate sequential amino acid deletions? I'm looking to generation sequential deletions from a gene of interest. The total size of this region is 8 amino acids. I'm trying to determine which portion of this region is necessary within the gene.

For example, if this is my sequence:

ABCDEFGH

I want to generate:

BCDEFGH, CDEFGH, DEFGH, and so on.

What is the least expensive way to do this (by minimizing primer use, enzyme use, etc). I already have this gene sub-cloned into an expression vector.

Thanks!

Deletions may make sense if you are analyzing the N-terminus or C-terminus of a protein. If you are looking at an internal region however, keep in mind that the more AAs you delete, the more likely you are to disrupt the overall protein structure. If you delete any random selection of 8 AAs within a protein, there's a chance you'll knock out activity by changing the protein fold or stability. That's not useful information.

This question is usually first addressed by alanine scanning - sequentially or additively changing amino acids to alanine. This is much more informative than deletions. Even better, you can choose to replace wild-type AAs with other AAs of similar size but differing charge or hydrophobicity. Then you are most likely to change the function of a region without changing the structure.

The quickchange kit works great, but if cost is an issue you can do whole plasmid mutagenesis PCR with your own reagents. And make your own competent cells.

In my experience though, whole plasmid PCR can be tricky - if it doesn't work the first time it can be difficult to troubleshoot. If time is an issue, I'd recommend doing overlap extension PCR with the same mutagenic primers, plus one set of amplification primers at the 5' and 3' end of your gene. Make a large batch of digested vector, test as a negative control, and use it for ligation of all of your different inserts.


How can we differentiate between respiration and breathing? I am a student of 10th grade, and I eagerly want to learn biology. What is the difference between respiration and breathing?

There are two uses of the term respiration: physiological respiration and cellular respiration

Physiological respiration involves the intake of outside oxygen and its distribution to the tissues of the body. Breathing is a part of physiological respiration and functions to bring oxygen into the lungs and expel carbon dioxide.

Cellular respiration is a chemical process by which energy is obtained within individual cells from biomolecules like glucose. In aerobic respiration, oxygen is used. Cells can also use fermentation and, for some, anaerobic respiration to obtain energy.


Does Mn always exist in Photosystem II? I had the impression that PSII (photosystem II) always has four Manganese atoms
(4 Mn). Is there any reason that these atoms are needed?

Is Mn or Fe also present in bacteria LH1 or LH2?

Manganese is part of the oxygen-evolving complex and is essentiell for the oxidation of the water to generate electrons, protons and oxygen. This is done by changing the oxidation state of the mangane from +2 to +4, as shown in the figure (from here):

These manganese atoms are the center of the reaction - important here are the different oxidation states they can take, other examples are copper (in tyrosinase for example) or iron (hemoglobin) which are also present in the active center of enzymes.
For more information see references 1 and 2.

Anoxygenic bacterial photosynthesis also needs metal ions in the bacteriochlorophyll, this is magnesium (as in the chlorophyll of green plants), the light harvesting complexes contain iron-sulphur complexes.
For a general overview see reference 3, for more detail on the reaction centers and their evolution, see reference 4.

References:

Where water is oxidized to dioxygen: structure of the photosynthetic
Mn4Ca cluster.
Reduction-induced inhibition and Mn(II) release from the photosystem
II oxygen-evolving complex by hydroquinone or NH2OH are consistent
with a Mn(III)/Mn(III)/Mn(IV)/Mn(IV) oxidation state for the
dark-adapted enzyme.
Bacterial Photosynthesis
Reaction centres: the structure and evolution of biological solar
power.


Protein that exit from the cell - as marker Searching for some protein, that I could use as extracellular marker for mammalian cells. I need to insert mRNA to cell, and to detect the protein outside the cell (not on membrane) if the mRNA successfully enter and been translated. (not GFP, I need protein that exit from the cell in big numbers)

Thank you.

You can always express GFP or your favorite protein in a secretory vector like pSecTag or pSecTag2 from Invitrogen/Life/ThermoFisher/SuperUltraBioMegaMart. There are probably others, but those were the first ones I came across. They contain the mouse Igκ signal sequence for efficient secretion (so the website says, I've never used it).

I don't know the details of your experiment, but are you sure you want to use a secreted protein as a transfection marker? Remember, it's possible that only a small fraction of your cell population will take up the vector (or mRNA, if that's what you're using, but there are issues with that), but you will see secreted protein regardless of the number of cells that take it up.


During interphase, is DNA wrapped around histones? Are histone proteins present around DNA in the nucleus during all of interphase (including G1) or do histone proteins only form later on when chromosomes are condensing into chromatids?

Thanks in advance!

Yes, DNA is always wrapped around histones.

DNA condensation using histones is not only meant to form the chromatids for mitosis/meiosis, but also one of the factors that control gene expression. Tightly packed heterochromatin is not being expressed, whereas unpacked euchromatin is transcriptionally active. The process of condensation is controlled by enzymes such as histone actelytransferase (HAT) and deacetylase (HDAC) that change the electrostatic properties of the histone proteins. Positively charged lysine in heterochromatin histones allows condensation with negatively charged DNA. By acetylation of these lysines, they become neutral and the heterochromatin turns into euchromatin, which, provided the necessary activators etc., can now be translated. To silence gene expression, the process is reversed.

Gene expression control is very complex and histone acetylation is only one factor out of many. Nonetheless, you see that histones are a crucial part of the chromosomes and are not only formed during mitosis or meiosis.

3.0.jpg

Source: https://en.wikipedia.org/wiki/File:Histone_acetylation_and_deacetylation.jpg


Difference between strand-specific and not strand-specific RNA-seq data I would like to ask the difference between strand-specific and not strand-specific dataset.

As far as I know, strand-specific data means that we know which strand the transcript is from.

I do not have biological background. Please confirm whether it is correct. If we have a transcript, which is from sense strand, when RNA-seq is producing reads, is that first the cDNA is synthesised. Then this cDNA is used for PCR to amplify the sample? Then the reads generated could be from both strands of the original DNA?

For strand-specific protocols, what is different?

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

Follow up.

Please correct me if I am wrong. There are multiple protocols to produce strand-specific RNA-seq libraries. The basic process is like:

Get the RNA;
Get its cDNA;
Somehow mark the cDNA as sense or antisense when amplifying (PCR?) (here comes the differences between different protocols);
Then REMOVE all antisense (or sense) cDNAs;
Read the reads from clean cDNA library.

The result is that, the reads from this RNA can be used to assemble the sense cDNA. And for not strand-specific libraries, using the reads would be able to assemble both the anti-sense and sense cDNA.

Am i right about this problem? Thanks.

It may be worth checking out the paper "Comprehensive comparative analysis of strand-specific RNA sequencing methods".

The most common techniques sequentially ligate different RNA adapters to the 5' and 3' ends of each RNA molecule prior to cDNA synthesis.  You will end up with an RNA molecule that looks like this (where A and B are the two adapters):

  5'-AAAAAA---------------BBBBBB-3'

These adapters are then used for cDNA synthesis and library preparation.  Finally, since each adapter is ligated to a specific end of the RNA the library can be generated in a stand-specific fashion; ie. the reads derived from the antisense strand should align to the antisense strand of the genome.

** Note that there are other variations of this technique but Illumina's protocol is one of the most popular.


What are some good books on oncology? I'm looking for some book suggestions on oncology, preferably I want them to be fairly recent. I am not worried if they are fairly technical, as long as they have good accurate content and layout.

You could try DeVita, Hellman, and Rosenberg's Cancer: Principles & Practice of Oncology. It has detailed information on both biological and clinical aspects of cancer. Apparently, the publishers regularly release online updates to cover the latest developments in oncology.

Reference to the current edition:

DeVita VT, Rosenberg SA, Lawrence TS, editors. DeVita, Hellman, and Rosenberg's cancer: principles & practice of oncology. 11th Edition. Philadelphia: Wolters Kluwer; 2018. 2432 p.


what is the name of this fish? ]2
fishes are of length 2 to 3 inches.

Looks like Jewel Fish, a cichlid that has been kept for a long time. Hemichromus bimaculatus , native to west Africa a bit different from "African Cichlids" which are from east Africa. Source : Exotic Aquarium Fishes by W. T. Innes ( the guy neon tetras are named after), 1937 ; But I don't think you can find it online .


Which came first in hominid evolution: language or bipedalism? I suspect both language-use and upright-posture have anatomical consequences. So does the fossil record show which came first?

NOTE: To the folks who marked this question "homework": This is certainly not an actual homework question. I have been an accomplished biologist for over 30 years and I am genuinely interested in the evidence for the timing of these critical human attributes. If you feel that the answer is so trivially obvious, that I should have been able to find out with only modest research, could you please leave a comment explaining, as if to a child, exactly how it is so obvious?

This article by Philip Lieberman On the subcortical bases of the evolution of language, page 22, he asserts the neurons associated with language may have developed based on the demands of bipedal posture. While there's no concrete data to support when we see the first languages, here we see evidence of arches (and presumably bipedal posture) in Australopithecus afarensis. So there are still some dots that need connecting.