What would be a single elegant-sounding word denoting controlled increase or decrease? I am a biologist and frequently encounter the words 'upregulated' and 'downregulated' in the literature. Appropriately, these words are flagged by my browser spell-checker; they don't seem to be very widely recognized outside of the biology community, and I find them quite ugly.
I would appreciate any and all suggestions for (ideally) single words or concise phrases that convey the same meaning: increased or decreased in a controlled or causative manner by the action of some external factor.
A general use case: "In experiment A, we determined that gene B was upregulated upon exposure to toxin C, while genes D, E, and F were downregulated."
Of course I could say that 'expression of gene B was increased by/in response to...' but 'B was upregulated' is so much shorter. Surely, though, there must be some way to convey this concisely without using such an annoying construction as 'upregulated'.

There's a reason why you encounter these words so frequently - they are widely understood, concise descriptions that almost any biologist will understand immediately. Almost any other terms you use in their place will only serve to obfuscate the actual biological phenomenon you're talking about.
That said, I've seen the words overexpressed and underexpressed to describe genes that are upregulated or downregulated, but they're not any less cumbersome words, nor are they used any more frequently outside the domain of biology. There are also may be some connotations about the cause of the effect, so there may be subtle differences between upregulation and overexpression depending on who you ask. I don't think there's any better terms than upregulation and downregulation for describing an effect of increased/decreased gene expression.


The pectoral fins of a whale and a shark. Are they analogous organs? Analogous organs: Different origin, same functions,
Homologous organs: Same origin, different functions but same main structure//  right?
So, what is the case for the pectoral fins of a shark and a whale?

Are they analogous organs, because the two animals have different ancestors(shark-Some Chondrichthyes fish, Whale-some mammal) but have organs that do the same thing?

Or are they homologous organs, because the two animals have the same ancestor(A vertebrate animal) and have organs that have a similar structure?(I learned that it is alright for homologous organs to do the same function, for example the wings of a bat and a bird are homologous organs, although they do the same thing)

They are analogous at to function. Whales derive from terresterial animals that "returned" to the sea. Evolution adapted the forearms to fins. Here's a great diagram: http://evolution.berkeley.edu/evolibrary/article/evograms_03

The bat wing and the bird wing are also analogous as to function. Their functional aspects evolved independently. But as forelimbs they are homologous sharing a common ancestor with forelimbs.http://evolution.berkeley.edu/evolibrary/article/evo_09

We haven't yet answered the question of whether the whale fin and shark fin are homologous in origin: http://evolution.berkeley.edu/evolibrary/article/similarity_hs_09


Is the Lucy fossil really what scientists claim it is? The New Scientist has an article talking about how a baboon bone was found in the Lucy skeleton.

Creationist sites like this, https://christiannews.net/2015/04/23/evolutionary-embarrassment-part-of-famous-ape-man-skeleton-actually-came-from-baboon/, and Dr. David Menton are claiming that the Lucy fossil is another hoax like Nebraska man.

Are we sure that the Lucy fossil is not a hoax? (I am not trolling, I really want to know the truth, and when I search, I get mostly creationist sites).

Per the comments, the actual paper seems pretty like a pretty straightforward operation of normal science:

Somebody noticed something that looked off about one of the bones and decided they'd look into it more carefully.
They found that yes, that bone appears to have been an accidental inclusion, and in fact the rest of the skeleton makes more sense without it.
The original conclusions are not weakened in any way, but are in fact strengthened by cleaning up a minor mistake.

It might have come out otherwise, but in this case, as in most cases, careful criticism and examination of scientific work ends up making the whole enterprise more coherent.

It's frankly not even very interesting, scientifically, which is probably why you're finding discussion of it mostly on creationist sites.  Note also that the creationist article linked uses sloppy language like "proof" and "part ape, part human" that tend to indicate a massive lack of understanding of both science in general and evolution in particular.


Anemiaceae etymology What is the etymology of the name Anemiaceae for a family of ferns? I assume that it's from the name Anemia for one of its genera, but that is equally mysterious. Obviously it has no blood, but what fern does? I have been unable to find an answer by searching the internet.

That one is Greek origin from aneimon or "naked, unclad, without clothing" which is to refer to the panicles of the sporangia.


Do micro-organisms survive and live normally in a zero-g environment? Have there been any experiments in space regarding micro-organism behavior? Are they able to move around in a drop of water like they do on Earth? Are they able to eat and reproduce normally?

Edit: by zero-g, I mean an environment where you feel zero acceleration. Orbiting the Earth would be this since you're constantly in free fall. A rotating environment is not zero-g as the things inside will feel a "centrifugal" force pushing them into the wall (though it's actually a centripetal acceleration coming up against your intertia).

Several experiments with microorganisms have been conducted in the ISS (International Space Station), and the results were published in peer-reviewed journals, like this one for instance:

A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space

However, two things have to be clarified:

First, the environment at ISS is not really a zero-g environment. Actually, since the ISS is orbiting at only 400 km from the Earth surface, the gravity in the ship is almost the same of what it is here at the planet surface (89%, to be more precise). What happens is that the ISS is constantly falling, and that endless fall simulates a zero-gravity environment.

For this reason, one doesn't need to go to space to conduct micro-gravity experiments: they can be conducted here, on Earth's surface, in rotating containers (Tirumalai et al., 2017). For instance, this is a device to simulate micro gravity on ground, in a common lab:

Second: most of the experiences conducted on ISS focus on bacteria (and not on other groups of microorganisms, like protozoans and algae), and more specifically on their pathogenicity. The way your question was worded ("Are they able to move around in a drop of water like they do on Earth? Are they able to eat and reproduce normally?") make it seems that you are interested in things like locomotion and phagocytosis in unicellular eukaryotes, but that's not their main concern. Their main concern is that bacteria have different selective pressures in space, modifying their gene expression, and such "new" strains could be potentially dangerous for the crew.

According to Tirumalai (2017):

  Microorganisms impact spaceflight in a variety of ways. They play a positive role in biological systems, such as waste water treatment but can be problematic through buildups of biofilms that can affect advanced life support. Of special concern is the possibility that during extended missions, the microgravity environment will provide positive selection for undesirable genomic changes. Such changes could affect microbial antibiotic sensitivity and possibly pathogenicity. (emphases mine)

And according to NASA (2017):

  scientists have observed that in space, some strains of bacteria appear to exhibit enhanced growth and increased virulence (ability to cause disease).

Therefore, experiments like AES-1 (for "Antibiotic Effectiveness in Space-1") were conducted to compare gene expression from a non-pathogenic strain of bacteria (in that case, Escherichia coli) growing in micro gravity with the same bacteria growing on the ground.

NASA Astronaut Rick Mastracchio using a crank to activate a group activation pack (GAP) onboard the ISS for the AES-1 experiment. (source: NASA,
 2017)

The findings so far show that bacteria growing in micro gravity have less availability of nutrients. Still according to NASA (2017):

  On Earth, the movement of bacterial cells through their media is influenced by the physical properties of the medium, including gravity-driven forces like buoyancy and sedimentation, as well as other forces, such as the viscosity of the medium. As the cells move, they interact with fresh media and absorb molecules of nutrients. The cells also excrete waste products that may sediment down, float up, or trail behind the cells if they move, while simultaneously diffusing away. However, in microgravity, these gravity-driven forces are absent, and ALTERED EXTRACELLULAR ENVIRONMENT MODEL the transportation of nutrients to cells and waste products away from cells are limited to diffusion-only transport. The altered extracellular environment model hypothesizes that the resulting reduction in the movement of molecules leads to less interaction of the cells with fresh media and thus reduced availability of nutrient molecules for absorption.

Analysis of those bacteria showed that they changed their gene expression. The genes over-expressed were mainly associated with:

Low glucose environment
Acidic environment

Also, the experiment showed that such bacteria required a higher concentration of antibiotics to be killed, probably because there is a reduced concentration of antibiotics around the cells.

To finish, a curious device is the "test tube" they use in micro gravity. In space you cannot simply manipulate test tubes like we do here, at 1g. It has to be a special device:

  For the AES-1 experiment, the research team prepared 128 bacterial culture samples to send to the ISS National Lab. The samples were each contained in a fluid processing apparatus (FPA), a test tube specially designed by BioServe Space Technologies for use in microgravity.

This is it:

Sources:

Zea, L., Prasad, N., Levy, S., Stodieck, L., Jones, A., Shrestha, S. and Klaus, D. (2016). A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space. PLOS ONE, 11(11), p.e0164359.
Tirumalai, M., Karouia, F., Tran, Q., Stepanov, V., Bruce, R., Ott, C., Pierson, D. and Fox, G. (2017). The adaptation of Escherichia coli cells grown in simulated microgravity for an extended period is both phenotypic and genomic. npj Microgravity, 3(1). [online] Available at: https://www.nature.com/articles/s41526-017-0020-1
NASA, (2017). [online] Available at: https://www.nasa.gov/sites/default/files/atoms/files/upward_magazine_vol2_issue1.pdf [Accessed 5 Aug. 2017].


Selection marker for a cytoplasmic vector that works at low expression levels? I need to express a selection marker on a plasmid in human cells (e.g. HEK293). However, I am using a cytoplasmic vector derived from a non-human virus with its own mechanism for transcriptional initiation. This means that the expression level of any protein marker will suck: low copy number, very weak promoter, unstable transcripts - these are things that I cannot change in this precise biological context.

Most selection markers (for instance KanMX) come with their own black-box promoter and so I do not know whether they rely on a high number of proteins being produced.

What would be a marker most likely to be selectable despite a very low expression level? I could not find any resource comparing the protein copy numbers of classic markers.

I need to be sure that the cells that cannot survive the selective pressure died because they did not have the marker, and not because the marker was too weakly expressed to protect  cells that have the marker. The standard approach would be to use a regular antibiotic selection and just work with lower concentrations of antibiotics but the number of false positives would most likely be too high.

I can manipulate the host cell to some extent, so I can use antibiotic selection but I can also complement a conditional deletion of an essential gene (auxotrophic marker or non-metabolic genes).

Flow cytometry looking for your plasmid.

These folks labeled their plasmid with a proprietary fluorescent marker, then used flow cytometry to detect cells which had taken up the plasmid.

A novel rapid and reproducible flow cytometric method for optimization of transfection efficiency in cells

  An alternative and more direct method to using fluorescent reporter
  genes is to directly label nucleic acids with fluorescent dyes to
  track their intracellular delivery [16]...
  Using the non-enzymatic Label IT® Tracker TM Kits, any plasmid can be
  custom labeled in a simple one-step chemical reaction before
  introduction into mammalian cells [18]. Thus, both subcellular
  localization of the labeled DNA and expression reporter transgene can
  be monitored simultaneously following introduction of the labeled
  plasmid into mammalian cells [16, 18]...

  Herein, we demonstrate the development of a flow-cytometric assay to
  determine transfection efficiency by labeling a reporter plasmid with
  Label IT® TrackerTM. This method does not depend on co-transfection of
  two different plasmids and simultaneously quantifies cell death,
  uptake of the labeled plasmid during transient transfection, and
  expression of the target protein.

Even if only a small fraction of your cells take up your glowy plasmid, you will sort those out from the rest with flow.


Why are pharmacology studies so experimental? I am a med student, and as far as I see from our pharmacology lectures, pharmacologists work almost completely experimental. Quite typically they take a substance (e.g., from nature), they add, change or remove some chemical groups, and then they test it (either with high throughput screening or on animals), for example to see whether the new drug is active or not. To me, this sounds a bit indirect.

Ideally, we should know exactly what we are targeting, and then custom-make a new drug. For example, if we know which receptor (the 'lock') we wish to activate or inhibit, why do pharmacologists not simply design a fitting key (a plug to block, or a substrate-resembling activator) to the specific lock?

The First thing is that that you can't study any process until it happens. So even if you know the structure of receptor molecule, you can't always be sure that it is completely safe.

It does seem a bit random in beginning but this is how it works. You can't just derive a medicine or drug and send it for mass production. You never know what are the side effects of the drug. For this reason, the drugs are tested on other animals (usually rats because they are quite in number, having short lifespan and not many oppose experiments on rats ethically.)

If the side effects are severe, then the drug is banned from mass production.
But if such drug is produced,more harm will be done than good. Also you can't give it to humans first. If all tests are successful, then only the drug is tested on humans.

So Screening and Testing are indirect but essential steps for studying the effects of it.


What is the genetic background for fast metabolism? I am wondering if it is possible that people with very fast metabolism have some genetic mutation. There are people who can eat a lot while others would definitely get fat with such a diet. In other words, they seem to have very fast digestion and never feel so much full after eating but what's surprising is that they still stay very skinny?

Can it be a result of some disorder/mutation?

The expression "fast metabolism" is very general and makes the question hard to answer. I will hence answer in the most general sense possible and then just give one example.

Yes, it is most definitely the case that there is genetic variation underlying the variation in metabolic abilities in the human population (btw, this post summarizing the partitioning of phenotypic variation might be helpful to you). For example, Greenlandic Inuits have a series of mutations that affect their ability to digest polyunsaturated fatty acids allowing them to cope with the impressive amount of animal fat that is/was found in their traditional diet (Fumagalli et al., 2015).


What is the overall end result of proteins and enzymes binding together? My rudimentary understanding is...

a gene gets transcribed to mRNA
that mRNA is sent off to the ribosome
that ribosome pumps out whatever proteins are coded by that gene
each protein floats around in the cell until it encounters an enzyme that it fits into, and along with other molecules that may have floated into the same enzyme a chemical reaction occurs and one or more products are formed.

I'm assuming "products" are either new protein molecules or maybe the amino acids that made up the original input proteins. What I don't understand is what the overall end result of these reactions are. So there's a reaction, but what does that mean? How does that reaction, lets say, result in some physical attribute of the organism?

Any examples would be helpful.

At a high level, points 1 to 3 are reasonably correct, but 4 is only a special case.

Say we're at end of point 3. You get a protein. Some proteins are enzymes (the majority of enzymes are proteins), others are not. Example of proteins that are not enzymes would be, for example, hemoglobin, which is "just" a (very high-tech) carrier.

Now, each enzyme catalyzes (at a very high level) one reaction, which may or may not involve other proteins:

Reactions without protein other than the enzyme: for example, the cleavage of sucrose into glucose and galactose (two small sugars) performed by an enzyme called sucrase. Such reactions can assemble, cut and modify small molecules or large organic molecules that are not proteins (for example, starch, which is a large polymer of sugar, or even DNA itself)
Reactions mediated by enzymes, that act on non-enzyme proteins: for example, your digestive enzymes can cut proteins from food into building blocks (amino acids) that your body can use to build its own proteins. Similarly, some proteins can ligate proteins together, or add things on them (the proteins on the surface of cells are commonly modified with small sugar chains that control their activity).
Enzymes that catalyze reactions that involve other enzymes: since enzymes are proteins, they can be the target of other enzymes. A very well described example is the cascade of enzymes called kinases. When a cell is stimulated by a hormone, a kinase gets activated by addition of a small phosphate group. Once it is activated, the kinase phosphorylates (i.e. it adds a phosphate group on) another type of kinase, which phosphorylates yet another type of kinase etc; that's a way to amplify small signals.

So the overall result of an enzymatic reaction, regardless of whether it acts on other proteins or not, is usually either

The conversion of a molecule into some other molecule (1 to 1)
The assembly of several molecules into a larger, new molecule (N to 1)
The separation of a large molecule into smaller fragments (1 to N)
The transfer of a fragment of molecule on another molecule (N to N)

Examples of these four types of processes when enzymes act on other proteins:

1 to 1: a "protein disulfide isomerase" can rearrange the topology of the so-called disulfide bridges, that connect cysteine amino acids together in the target protein. This allows a misfolded, non-functional protein to turn into a functional molecular machine.
2 to 1: a "ubiquitin ligase" can covalently attach small proteins (ubiquitin) to old, broken proteins and target them for recycling, thereby preventing the accumulation of dysfunctional proteins in the cell.
1 to 2: a "protease" can cut another protein into two smaller proteins
2 to 2: a "protein kinase" removes the phosphate from a small molecule called ATP, and sticks it on another protein


What is the purpose of an siRNA screen in drug discovery? In the paper "A genome-wide siRNA screen identifies a druggable host pathway essential for the Ebola virus life cycle" by Martin et al. the authors try to disrupt the Ebola life-cycle by screening which human genes participate in it's replications:

In order to identify host factors involved in the EBOV life cycle, we performed a genome-wide siRNA screen comprising 64,755 individual siRNAs against 21,566 human genes to assess their activity in EBOV genome replication and transcription. As a screening platform, we used reverse genetics-based life cycle modelling systems that recapitulate these processes without the need for a BSL4 laboratory.

This helped them find a pathway.
What is siRNA screening and how does it help find a pathway?
The tag [rna-interference] references siRNA:

A post-transcriptional mechanism of gene-regulation/silencing mediated by small RNAs (siRNA)

However, I can't tell if siRNA refers to "small RNAs" or the whole process.

According to the Labome article "siRNAs and shRNAs: Tools for Protein Knockdown by Gene Silencing" siRNA does stand for small interfering RNA.
siRNA is used to silence genes via mRNA degredation:

NA interference (RNAi) is the process by which the expression of a target gene is effectively silenced or knocked down by the selective inactivation of its corresponding mRNA
[...]
The silencing mechanisms can either lead to the degradation of a target mRNA, as induced by small interfering RNAs (siRNAs) or short hairpin RNAs (shRNAs), or the suppression of translation of specific mRNAs, as induced by microRNA (miRNA).

There are also Wikipedia articles discussing these concepts that didn't come up in my search somehow, but a colleague linked me to:

Gene knockdown
Small interfering RNAs


Identification of this species of Toad I found a short video on the Internet of a toad and I wonder if anybody could identify it?

It was posted on a social-media/blogging website called 'Tumblr',

so I don't know much about it (e.g., where the video took place).

EDIT: The original link is no longer active. Here's an alternate link.

Useful for hearing the specimen's "squeak"/scream.

EDIT 2: Here's a gif of some frames from the video for permanence on this site:

P.s. I think it's a toad. Please, don't hesitate to correct me/edit my question, if i'm mistaken.

It looks to me like it's a Pacman frog or Ornate Horned frog, a common pet frog. The specific species, by googling pet websites, my guess is Ceratophrys Cranwelli (common name Brown Pacman frog).


What’s the term used to define a terrestrial being that moves by using six limbs? I know that Bipedal locomotion would describe how beings like humans and ostriches get around.

Quadrupedal locomotion describes how beings like dogs and cats move around.

What about insects, specifically, a cockroach? I believe a cockroach has six “legs”, what would be the term used to describe that type of locomotion?

Hexapedal. From wiki > Hexapedal

  Having six legs

Note that Hexapoda is a taxonomic group including insects and the smaller groups that are Collembola, Protura, and Diplura.


Identify this bug (which looks like a cross between a beetle and a bed bug) I am located in a large Eastern European city. During this summer, a new kind of bug has started appearing in my house (or more specifically, coming into my house from the garden). It's about 1.5-2 cm long, doesn't appear to have any wings, and a relatively strong exoskeleton (makes an audible crack when the bug is squished). Its favorite activities seem to be either sitting in the middle of the floor, waiting for someone to step on it, or sitting on the ceiling and then falling onto somebody's head. Whenever I see one of them, it's almost completely stationary, regardless of the time of day.

Here are pictures of it (sadly, they're very grainy due to my phone's camera's low quality).

That is a weevil. Coleoptera, Curculionidae. Weevils have distinctive snouts, and elbowed antennae. They can be crop pests, and eat seeds, but do not spread diseases to humans. I suspect these have just found their way into your home by mistake. https://bugguide.net/node/view/1126677


Techniques for detecting phosphorylation sites in proteins? I would like to know how phosphorylated sites in proteins are detected in practice. I read some papers where the authors were talking about mass spectrometry techniques.

But my question is that why can't X-ray crystallography or NMR techniques capture phosphorylated sites?

(Note : My background is electronics engineering, so I am not an expert in this area.)

In principle X-ray crystallography or NMR could detect phosphorylation sites but they are much more complex and expensive techniques than mass spec. So for simply figuring out phosphorylation patterns in a protein is much easier using mass spec.

Detailed reasons:

For X-ray you need to crystallize the protein which is often very difficult/impossible and requires quite a lot of sample material. Afterwards you need a good X-ray source (ideally a synchrotron beamline) and record the scattering pattern over an extended range of angles (at least 180 degrees) before your crystal evaporates in the intense X-ray beam. Last but not least, you need additional chemical tricks, elaborate mathematical models and a large amount of computing power to compensate for the fact that in X-Ray crystallography you lose the phase information (because there are no suitable lenses for X-rays).

For NMR, you need large, very strong superconducting magnets, sophisticated radio transmitters and receivers, complicated math and computing power. However even if you have all that, you are still limited to very small proteins because otherwise the NMR spectrum is simply too complicated to be solved.

In contrast, for mass spec, you need a (highly sophisticated) spray gun, a moderate magnetic field and an electron multiplying detector. This is still a very sophisticated machine but much simpler compared to the above. In addition, data analysis is simpler than in the above cases.

Basically if you don't need to know the structural changes induced by phosphorylation (for which you would need to compare the structures of two crystals), you would stick to mass spec.


Question about epinephrine In my class we were told that adrenaline (or epinephrine) causes vasoconstriction.
My question was I had always thought that people took this via an EpiPen when they were having an allergic reaction.

So I thought it would make sense, that it would dilate vessels, because this will allow more air through. Or does the constriction help because it tightens the vessels in the throat allowing a reduction of swelling?

An allergic reaction requiring an epipen can be caused by swelling in the throat and/or bronchoconstriction (spasms decreasing the diameter of bronchioles). Bronchoconstriction can occur in the absence of soft tissue swelling in the lips, tongue and throat, and vs. versa.
Epinephrine reduces pharyngeal edema (swelling) because it is a potent vasoconstrictor in small arterioles and precapillary sphincters in most body organ systems. This is effected through alpha-1 adrenergic receptor activation. While the blood pressure and heart rate increase (due to beta-1 adrenergic effects), the permeability at the capillary level is decreased, relieving swelling.
At the same time, epinephrine relaxes bronchial muscle. It has a powerful bronchodilator action when bronchial muscle is contracted because it is a powerful beta2 adrenergic agonist.
Finally, epinephrine inhibits antigen-induced release of inflammatory mediators from mast cells, and to a lesser extent from diminution of bronchial secretions and congestion within the mucosa. Inhibition of mast cell secretion is mediated by beta2 adrenergic receptors.

Adapted from Simons. Kemp et al. World Allergy Organization Journal 2008 1(Suppl 2):S18-S26   doi:10.1186/1939-4551-1-S2-S18
Epinephrine: The Drug of Choice for Anaphylaxis--A Statement of the World Allergy Organization


How to calculate percentage of DNA that ancestors contributed? In David Reich's book "Who we are and how we got here" there is a graph explaining that more we go back in our ancestors generations, the least we have chances to have any DNA inherited from one of these ancestors because the number of ancestors is doubling every generation while the number of stretches of DNA is only increasing by 71.

In the left side of the graph, there is a percentage indicating how many ancestors contributed to our current DNA. For example : 50% of 1024 ancestors after 10 generations.
I don't understand how this percentage is calculated and it is not explained in the book.
Could someone help me understand it please?

The answer I'm going to give is more or less copied from Graham Coop's post, but I'll try and summarise it here.
A single generation ago, we have 2 ancestors. If we go another generation back, we have 4 ancestors (your 4 grandparents). If we assume that there is no inbreeding within the ancestral population, every time we go back a generation, the number of ancestors doubles.
On the other hand, the amount of your DNA you inherit from each relative halves each generation. You get ~50% of your DNA from your mother and ~50% from your father. These are inherited in large blocks which are split up by recombination events. If you go back a generation, you inherit ~25% from each grandparent.
However, because of stochasticity in how recombination occurs, you don't inherit exactly 25% from each grandparent. What you really inherit is a value distributed around 25%. There is a nice discussion of the ins and outs of it here. As an extreme example, if your parents and grandparents transmit entire chromosomes without recombination, then it is possible not to inherit any DNA on that chromosome from the other grandparent.
It's quite unlikely ($p=4$ x $10^{22}$) that you don't inherit anything from a single grandparent. However, as you go back through generations, it's increasingly likely there are some relatives who don't contribute anything to your DNA.
For example, 8 generations back, there's around a 20% chance that any given ancestor didn't contribute anything to your genome. Therefore, we can say that the number of genealogical ancestors a given generation back is one minus the number of ancestors who contributed nothing. This is why, even though 10 generations back we might have 1024 ancestors, perhaps only around 50% of them will have contributed anything to your DNA.
I'm not entirely sure about how the figures in this book were calculated; whether it was from simulation or not. However, the results should be more or less the same as how Graham Coop calculated it in the above post.


What flying insect is this? Found in Russia. Approx. 7 cm.

This is Crane fly, of the Tipulidae family. They don't bite humans, adults feed on nectar. Larvae prefer moist environments such as wet soil or decomposing vegetable matter and can consume roots and vegetation, damaging plants. Among others, bats and some Coleoptera are its predators.
Further informations can be found in the Wikipedia article linked above.


Manipulating phylogenetic trees I am looking to manipulate manually constructed phylogenetic trees (adding bootstrap values, markers to indicate trate loss/gain etc.) I came across a paper that used Macclade, however, this no longer appears to be a program that will run on almost all computers. Is there a useful alternative software package? I have tried Mesquite, but it does not appear to have the same functionality (although, I have probably just missed understood how to use it effectively).

Any help/recommendations would be appreciated

If you have some knowledge of python, you can do a lot of things with the ETE toolkit.

Disclaimer: I have used an older version of it, but in a very limited manner.


Blocking buffer for actin and fetuin-b in western blot I have been working on western blots for about a month now using actin and fetuin-b primary antibodies to no avail. My background is always high and I only had one good result. I want to know if there is a certain blocking buffer I should use instead of 5% milk with my membranes to get a better result.

I have only used milk for blocking a couple of times but it was always beaten by bovine serum albumin (BSA), casein, or BSA/casein.

My standard blocking buffer is 1 - 5% BSA in tris-buffered saline with 0.1% tween20. I have also used the Western Breeze kits from Invitrogen and in my hands their blocks and alkaline phosphatase detection reagents were very reliable. The preservatives that they include in the stock reagents also allow the block to be reused for up to a week if handled and stored appropriately; keep everything clean, use up to 4 times, and store @ 4 degrees when not in use.

Some antibodies will require specific blocking buffers to perform well.

Background can come from many sources so if you have background with both primary antibodies you should check for other issues as well. Background is a very general term and can be caused by many things, a few I can think of are;

Overheating during transfer
Primary/secondary antibodies binding to the membrane.
Primary/secondary antibodies binding non-specifically to the proteins.
The interaction of detection reagents with buffer components (phosphate and alkaline phosphatase, tween)


Can blood that has had an anticoagulant added to it be boiled without coagulating? If I understood the information I've found elsewhere correctly, you can't boil untreated blood without it coagulating, right? But what if you added an anticoagulant to it? Would it be possible to boil that blood or would it coagulate in spite of it? Thank you in advance!

Coagulation, or clotting, is a proteolytic cascade that generates an insoluble fibrin based protein net, or mesh.

Anticoagulants are things like EDTA (?) that chelate divalent cations required for the clotting cascade.

Boiling blood will denature most, if not all, of the soluble serum proteins, forming an insoluble precipitate.  This is structurally different from a blood clot.

Think about what happens to the white part of a chicken egg when you boil (or heat) it.  That is protein denaturation.


Chicken Genome what are the LGE 'chromosomes'? The chicken genome identifies two "LGE" sequences in the chicken genome.  Are these distinct chromosomes or some highly variable sequence from the genome that is put in a separate sequence? I'm thinking they are not really separate chromosomes.... It would be great to know a little bit about their biology.  the papers didn't seem to help me.

LG stands for "linkage group". It seems the Chicken Genome Sequence group (Hillier et al., 2004) allocated several linkage groups (alleles or genes which tend to be inherited together) to the microchromosomes (tiny chromosomes typical of birds and reptiles), in this case called "linkage group E64" and "linkage group E22....". There are a load more microchromosomes which are the ones numbered 28-31 and 33-38 which haven't yet had their sequences resolved (Burt, 2007).

References:

Burt, D.W. (2007) Emergence of the Chicken as a Model Organism: Implications for Agriculture and Biology. Poultry Science. 86 (7), 1460 –1471. Available from:  [Accessed: 8 February 2012].
Hillier, L.D.W., Miller, W., Birney, E., Warren, W., Hardison, R.C., Ponting, C.P., Bork, P., Burt, D.W., Groenen, M.A.M. & Delany, M.E. (2004) Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution. Nature. 432 (7018), 695–716.


Picking up Plasmid DNA using Nanodrop, but not using Electrophoresis I am currently trying to see if 2 bacteria contains plasmids or not. I had used promega plasmid extraction kit on the bacteria. I ran a gel electrophoresis (.8% gel) with the extract product, however its not showing the presents of any DNA. I also ran the product through Nanodrop (2000) and these where the concentrations I got:

1 : 6.5 ng/ul & 260/280 = 1.56
 2 : 49.4 ng/ul & 260/280: 1.96

Based on experience, I want to say #1 contains no plasmids, however #2 may have a small concentration of plasmids. Please give me your opinion on what to conclude. Also, if there is another test I can try to do to confirm plasmid presents or not, please let me know.

Having a positive reading on the Nanodrop but no band on the gel can be due to a number of different issues (not exhaustive):

An incorrectly zeroed sample
Incomplete staining of the gel
Contamination of the sample
Human errors in loading of samples

You should try to exclude these possibilities by positive controls in order to find out the true reason behind the inconsistent results.


Why is there a difference in the rotation of the tail fin in fish compared to marine mammals? I've been thinking about this one, but I can't seem to find what causes this difference.

All fishes that I've seen have their tail fin positioned vertical:

But all the marine mammals I know have their tail positioned horizontal:

Why is there this difference? Is it because it's mammals compared to fish? Or could fish as well have horizontal tail fins?

While fish tend to move from side to side (lateral undulation) for which a vertical tail makes sense, the land ancestors of marine mammals had their limbs under them and so their spines were already adapted to up and down movement (dorsoventral undulation). When these animals moved to marine environments, they continued up and down movement in their swimming, for which a horizontal tail makes sense.

(The wikipedia article on fins gives some more detail, and links to this webpage on Berkeley.edu. A paper by Thewissen et al. suggests that for cetaceans, dorsoventral undulation as a swimming strategy came first, and the horizontal tail evolved later.

More detail:

In a third example beyond fishes and marine mammals, the icthyosaurs and other aquatic reptiles developed vertical tails, even though like marine mammals they evolved from four-footed land animals. This may be because the legs/spines/gaits of land reptiles differ from those of land mammals, so that the earliest icthyosaurs swam with lateral undulation, as reflected in their spinal modifications.

This blog post by Brian Switek gives a really superb run-down on the issue, with figures and citations. I'll quote this part which deals with the dorsoventral undulation theory:

  ...mammals and their relatives were carrying their legs underneath their bodies and not out to the sides since the late Permian, and so the motion of their spine adapted to move in an up-and-down motion rather than side-to-side like many living reptiles and amphibians. Thus Pakicetus[the pre-cetacean land mammal] would not have evolved a tail for side-to-side motion like icthyosaurs or sharks because they would have had to entirely change the way their spinal column was set up first.

Switek goes on to to talk about exceptions in some marine mammals:

  At this point some of you might raise the point that living pinnipeds like seals and sea lions move in a side-to-side motion underwater. That may be true on a superficial level, but pinnipeds primarily use their modified limbs (hindlimbs in seals and forelimbs in sea lions) to move through the water; they aren’t relying on propulsion from a large fluke or caudal fin providing most of the propulsion with the front fins/limbs providing lift and allowing for change in direction. This diversity of strategies in living marine mammals suggests differing situations encountered by differing ancestors with their own suites of characteristics, but in the case of whales it seems that their ancestors were best fitted to move by undulating their spinal column and using their limbs to provide some extra propulsion/direction.


What is the effect of garlic on intestinal flora? Now that we can compare whole microbiomes, has there been investigations on the effect of garlic (or diallyl disulfide, its main ingredient) on intestinal flora? From the proven antimicrobial activity, it should work like antibiotics. But does it leave "good bacteria" counts untouched?

From studies,

  lactic acid bacteria were found to be more resistant to GP (garlic
  powder) compared to the clostridial members of the gut microbiota.
  While for most bacteria the antimicrobial effect was transient, the
  lactobacilli showed a degree of resistance to garlic, indicating that
  its consumption may favour the growth of these beneficial bacterial
  species in the gut. Once the strains of other bacteria (eg:
  Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium
  nexile A2-232) became resistant, they retained their resistant
  phenotype upon sub-culturing. Garlic intake has the potential to
  temporarily modulate the gut microbiota (reference).

Overall garlic can prove to be beneficial, because it seems to have more of an effect on detrimental bacteria like Helicobacter pylori (H. pylori), even when its strains were resistant to antibiotics. Overall garlic was found to be more detrimental to pathological bacteria when compared to normal gut flora (reference). Garlic’s diallyl disulfide has also been found to effectively cause cell death in Candida albicans which is a fungus in our gut which if not kept in check can cause health problems (reference).

Inulin and fructooligosaccharides present in garlic can also serve as nutrients for the probiotics colonizing your body (reference).


Reasons why living fossils exist? A living fossil is a living species (or clade) that
  appears to be similar to another species otherwise known only from fossils,
  typically with no close living relatives.

A living fossil is considered as a successful organism, which has made its way through many  major extinction events. Also, the morphology of living fossils resemble some species of organisms which we know only through their fossil remains.

What is the reason for a particular type of species to become a living fossil; is the engineering of this particular species extraordinary, in that it can survive any selection process encountered thus far?
Is there not enough selection pressure exerted on this species in order to force it to change morphologically?
Have these organisms modified themselves, so that currently their morphology seems to be similar to a fossil organism?

TL;DR: Living fossils are the children of long-dead fossilised creatures that were good at being alike, other animals are the children that were good at being different.

The boring answer is that living fossils are around because nothing has happened to make them go extinct.

The more exciting answer is a tale of intrigue and lies stretching back hundreds of millions of years:

The lie that is the 'species'

The notion of a species is, of course, a lie. It's a useful lie, and one without which the equally useful field of taxonomy would be impossible, but a lie all the same. Every living thing is ultimately a unique individual unto itself. We group these individuals up and call them things, according to things that are more or less arbitrary, and we arrange these groups into bigger groups and fill books upon books with this method, because it makes it super easy to get a good overview of how life developed.

However, if we want to understand the details, we have to see past species, and look at the lineages.

The shark, our ancestor1

One such lineage that is of interest is that of the shark. Sharks are ancient: They are roughly as old as plants, and older than almost all land fauna. They are vicious, unrelenting killing machines, and all but perfectly suited for being this, with their sleek shape, their conveyor belts of teeth, and rough skin. At some point way back when, however, the lineage of sharks split in two: One branch that leads to fish, amphibians and eventually dinosaurs, squirrels and dolphins, and one that leads to sharks. The forebear to all these things were the early cartilaginous fish of the Cambrian ocean.

To answer the question as posed, we have to compare the success factors of the two lineages.

Why sharks are still around as living fossils

The real answer here is that, in a very real sense, they aren't. Modern sharks are no more alike their long-dead forebears than squirrels are. However, the biological niche inhabited by sharks (apex predator) is a successful one, and sharks, already existing in this niche, have had successful children, made more successful by being superficially and behaviourally alike to their parents, and so, the modern shark presents as a living fossil.

Why shark contemporaries are not still around as living fossils

The real answer here is that, in a very real sense, they are. Morphological differences aside, squirrels are no more different from their long-dead forebears than sharks. Rather, crowded niches have made generation upon generation of increasingly squirrely animals more successful by being superficially and behaviourally different from their parents, and so, modern squirrels have arisen.

Edit: Footnotes:

The shark is not in fact our ancestor, rather Cambrian early jawed fish are. The image of a shark is however far more evocative and easier to talk about.


What causes muscles to generate heat on contraction? I'm curious what the exact cause is of dramatic heat generation that comes along with muscle activity. Can anybody explain this in understandable language?

First, it might be helpful to talk briefly about what heat is. It is a form of energy - molecular energy. Basically, heat is the amount of jiggliness of the molecules of a substance or object. When we look at a hot object, it doesn't apear to be moving any more than a cold object, but on a scale much smaller than we can see, it's molecules are moving faster than in a colder object. Read this for more information if you want.

There are at least two things going on in muscle contraction (as well as in other metabolic processes) which produce heat. The first is the chemical reaction that powers muscle contraction. You probably don't want to get into great detail, but basically there is a molecule which your cells use to store power, which we abbreviate as ATP. When our muscles use that power, an exothermic chemical reaction occurs that "burns" ATP, breaking it into two pieces (ADP and phosphate). That reaction releases energy. Some of that energy is used in the actual movement of the muscle. But some of it just "jiggles" the nearby molecules. Again that jiggling is the very definition of heat.

The second source of heat is probably much smaller: friction. In short, just about any time anything moves, nearby molecules get jiggled some more. Imagine trying to walk through a room packed full of harps. Everywhere you move, some of those strings get plucked and vibrate. It's a little bit like that. When your muscle fibers tighten and flex, they rub past each other and jiggle each others atoms. All of that jiggliness is heat, and the jiggling continues until it can transfer to some other medium, as when, sweat evaporates from your skin.


Why are there no large animals with chloroplasts? Mitochondria and chloroplasts display similarities with bacteria that led to the endosymbiont theory. This theory states that an early ancestor of eukaryotic cells engulfed an oxygen using non-photosynthetic prokaryotic cell. Eventually, the engulfed cell formed a relationship with the host cell 1n which it was enclosed, becoming an endosymbiont (a cell living within another cell). Indeed, over the course of evolution, the host cell and its endosymbiont merged into a single organism, a eukaryotic cell with a mitochondrion. At least one of these cells may have then taken up a photosynthetic prokaryote, becoming the ancestor of eukaryotic cells that contain chloroplasts.

So my question is,  why is it that all the cells that took in the chloroplasts became plants or other simple animals but not large mammalian or reptilian animals?  Is there a limiting factor that restricted chloroplasts from being beneficial to large animals? Why is it that large plants can have both chloroplasts and mitochondria but not relatively larger animals?

I believe the gist of it is that chloroplasts simply cannot create enough sugar from photosynthesis to significantly power the energy-intense needs of any but the simplest of animals. Consider that plants maximize their surface area to the extent possible for a living organism, and still only have enough energy to grow and reproduce - movement is essentially impossible.

Here's a pretty good article I stumbled across a while back:
http://blogs.discovermagazine.com/notrocketscience/2012/09/18/will-we-ever-photosynthesise-like-plants/


How many different protein coding genes are in the Human Biome? There are approximately 20k protein-coding genes found in the human genome. This number is presumably very small when considering all the genomes found in the diverse microbes associated with the human body.

Is there an estimate for the total number of protein-coding genes found in human microbiome?

The Human Microbiome Project collected samples as shown in the image below from healthy volunteers:

They give an estimate of about 8 Million genes in the human microbiome, which is about 360x the number of genes in the human genome. See here for their press release with a lot of information. Additionally these two articles are as well interesting, if you want to dive deeper into the stuff:

A framework for human microbiome research
Structure, function and diversity of the healthy human microbiome


Does the brain store information and personality traits in different areas? I'm aware that muscle memory, language etc can remain largely intact after brain injury that impairs other forms of memory, suggesting that different kinds of memory are stored in different places in the brain.

Are your personality traits also stored separate from memory?

If I'm a bigot, I probably came to be that way because of my experiences and what people who are influential in my life have told me. If I forget those experiences and people due to memory loss following brain injury, will I not be a bigot anymore?
I may have certain nuances in my personality because I'm rich - like body language, or that public transport makes me uncomfortable, never having been used to it. If my memory loss is so severe that I don't recall anything about my life so far, will I still have my nuances?

I think your confusion comes from the fact that you take traits and memory to be distinct from each other. The brain processes information and we know that some of the connections between its cells are altered in the process --some call that memory. You are convinced that this is the only way that traits form, through experience at some developmental stage. You are then asking if cells in areas other than those that change during the formation of traits are affected more by the experience of forming a trait. If that were true, they would by definition be included in the areas that are associated with the trait in the first place. Can you see the problem in the logic of the argument?

Many people have followed similarly flawed reasoning, including trained neuroscientists that have been indoctrinated to believe in extreme forms of functional specialization of the brain, a more subtle version of the now debunked theory of phrenology.


Does Science Say That We Should Die? Excluding situations where you die from accidents, the main reason for death is -generaly- diseases.

And usually it is about an organ which becomes "tired" after many years. These results are all from experience and statistics:

But I've never heard of any study that said: "people can't live longer than x age because the heart can't live longer than that".

From my point of view, I think it's us who control the way we live and consequently someone can live longer than the other. For example, smokers die at an early age.

But even the oldest person in the world, lived for 122 years and 164 days. For me this isn't enough. It seems that someone can't control his age after all.

Basically my question is: Does science provide any limit that a person isn't able to live more than it? For instance can someone live more than 1000 years?

Note: I don't think someone is able to do this because simply even our healthiest habits are not "so" healthy. But imagine someone who doesn't live like any of us as humans, i.e. Can have a very healthy and natural life

Quoting a great biologist Peter Medawar :

  It is by no means difficult to imagine a genetic endowment which can
  favor young animals only at the expense of their elders; or rather at
  their own expense when they, themselves, grow old. A gene or
  combination of genes that promotes this state of affairs will, under
  certain numerically definable conditions, spread throughout a
  population simply because the younger animals it favors have, as a
  group, a relatively large contribution to make to the ancestry of the
  future population.

From Why We Get Sick :

  Imagine that there is a gene that changes calcium metabolism so that
  bone heals faster, but the same gene also causes slow and steady
  calcium deposition in the arteries. Such a gene might well be selected
  for, because many individuals will benefit from its advantages in
  youth, while few will live long enough to experience the disadvantage
  of arterial disease in old age. Even if the gene caused everyone to
  die by age 100, it would still spread if it offered even minor
  benefits in youth. This argument does not depend on the prior
  existence of senescence. Other causes of death—accidents, pneumonia,
  and all the rest—are sufficient to reduce the population at older
  ages. Nor does the theory depend, like Haldane’s, on cessation of
  reproduction.

The message I am trying to get across is that - As organisms are like vehicles which carry DNA and DNA just "madly" wants to replicate itself and pass itself from generation to generation, Natural Selection will favour those traits that maximise reproductive success. These may be traits that provide maximum benefit in youth but cause gradual damage and lead to senescence and death.

You could also think like this - Every machine has wear and tear and must be thrown away after it is irreparable. Same is with our body, it is the most beautiful machine in the world but it is also subject to the same wear and tear.

Also there is the end replication problem. See telomeres if you dont know what I am talking about. There is a limit to number of times a cell can divide.

So all in all I would say that there is a biological limit - a certain age up to which a person may live.


What is this insect in Southern California? I saw this insect flying around in Southern California, USA during the summer. It is about 1.25 cm in length. When it flies, it opens up its wings like a ladybug's.  What is this?

This is a scarab beetle that belongs to the genus Cyclocephala, and has the nickname of "masked shafer" (gallery). There are over 300 different species within this genus, however, the species most common to southern California is C. hirta and C. pasadenae, with me leaning more towards the former.

C. hirta; San Diego County, CA (source)

C. hirta; San Leandro, CA. (source)

C. pasadenae; Vail, AZ (source)

  When it flies, it opens up its wings like a ladybug's.

Ladybug, left; masked chafer, right.


What is the correct nomenclature for expressing a genotype where a recombination event may occur? Given an example punnett square:
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------
 | a-b | A-b/a-b | a-b/Y |
 -------------------------

What is the correct nomenclature to express the genotype prior to putting it into a punnett square? The parent's genotype looks like a-B/A-b x A-b/Y except I want to show that a recombination event can occur, yielding the third row in the punnett square table.
This is relation to my previous question about how to calculate recombination frequencies.

I would suggest "genotype".
A Punnett square is a visualization technique to help us think, it doesn't change the terminology.
If what you mean is the 1N genotypes represented in the rows/columns that combine to make the 2N genotypes, you might consider "haplotype" (haploid genotype). The haploid cells with those genotypes might be called gametes, but that refers to the cell and not to the genotype.
If you are specifically interested in those genotypes/haplotypes in which a recombination event has occurred (or not), you could call them recombinants or non-recombinants. In some cases you can encounter specialized terminology, for example in yeast tetrad analysis you encounter terms such as "tetratype", "nonparental ditype", "parental ditype". But those are not generally used outside the yeast field, I believe.


Why boys who inherit more genes of their mother are not born as girls and girls who inherit more genes of their father not born as boys? If boys as well as girls inherit the genes of the father as well as mother, does it imply that boys inherit more genes from the father to be boys and the girls inherit more genes from the mother to be girls? Or there is some thing else to it that settles the sex of the children? Since girls may inherit more genes of father and less genes of the mother question arises what decides that they are not born as boys or the other way around why the boys who inherit more genes of their mother are not born as girls?

Most genes are not male or female, so receiving more genes from a father or mother would not make a child more male or female. Whether a mammalian embryo grows to be male or female is pretty much determined by a single gene that's found on the Y chromosome. Called the "Testis-determining factor" (TDF), it triggers the development of male characteristics. TDF is a regulatory gene, and its effect is to switch on other genes, which result in the development of testis. All embryos would become female without the intervention of this gene.

The gene TDF is found on the Y chromosome. Male mammals have one Y chromosome and one X chromosome, females have two X. So there's a 50% chance a fertilised egg will inherent an X, and a 50% chance it will inherit a Y chromosome from it's father, which determines its sex.

References:

Testis determining factor, https://en.wikipedia.org/wiki/Testis-determining_factor

General info about sex determination in different animals (it varies a lot),
 https://www.nature.com/scitable/topicpage/genetic-mechanisms-of-sex-determination-314


Can genetically modified genes jump to bacteria in the eater's intestine? The Guardian ran an article a while back talking about GM gene's jumping to bacteria in an eater's intestine. Has other research confirmed this phenomenon?

No.

There is nothing special about a piece of GM DNA when compared to any other random piece of DNA. If this phenomenon happened at any detectable level, we'd have found eukaryotic DNA in bacterial genomes/plasmids long before the introduction of genetically modified crops. And that would be front page news in the field of horizontal gene transfer! Which has many talented people in it!


Bone conduction . Different from the normal hearing phenomena in humans? Bone conduction, is it something different from the normal phenomena of listening through the ears. I checked on some literature . Is it so that Bone conduction has very less to do with the ears and more to do with vibrations of the bones in the skull. Maybe I am mistaken . Please anyone can present a simple picture here and maybe some text to refer .
Thanks !

Prologue: Bone conducted signals are considered to be evoked by the perilymph fluid moving back and forth out of the cerebrospinal cavity, via the cochlear aqueduct, towards the scala tympani. And not by mechanical deformation of the cochlea. “the fact that the bone conduction phenomenon is actually the result of the push-pull movement of the perilymph fluid instead of the presumed deformation of the bony structures.” some text to refer:
Applying physics makes auditory sense.

I am affiliated with this book. I am the co-author of the Appendices.

Year Article Author(s) Source
2010 1 Applying physics makes auditory sense : a new paradigm in hearing
Abstract  |  Full-text Heerens, W.C., Ru, J.A. de Medicine (2010), pp: 1-74

pp: 13:
Objections against the existing bone conduction signal transfer hypothesis: The common model for the transfer of a bone conducted signal is based on the vibration of the temporal bone. However, both the material and the construction of this bony envelope are extremely rigid, while the cochlear shape of the cavity excludes the possibility that parts of this cavity can function as the hypothesized resonators. Therefore, sound stimuli cannot be transferred in such a manner. Certainly not the weak vibration signals with pressure variations of approximately 20 mPa, equal to a pressure variation of
0.2 x 10^-6 atmosphere that are generated by a normal sound stimulus of 60 dB SPL. Hence ‘bone conduction’ must have a cause other than the deformation of the rigid petrous bone that forms the cochlear bony envelope.

The physiological structure data:

• The walls of the cochlear envelope are extremely rigid. Hardly compliant to not compliant at all. So bone conduction based on deformation of that envelope is not possible.

I assume that it is clear, without further explanation that the petrous bone can be regarded as a non-deformable body when confronted with the extremely weak impact of acoustic signals.  We see that for a completely normal 60 dB SPL sound pressure signal, clearly showing that the vibrations of bone in the cochlea offer only extremely small, and therefore completely negligible contributions.  It means that we are talking about deformations which is therefore completely negligible as a possible mechanism for signal transfer. I dare say, no waving arm statements.  Contributions that all result in deformations comparable to an incredibly small fraction, are all leading to naught, one cannot escape the conclusion that there must be another cause for the phenomenon of bone conduction.

Bone conducted signals are considered to be evoked by the perilymph fluid moving back and forth out of the cerebrospinal cavity, via the cochlear aqueduct, towards the scala tympani. And not by mechanical deformation of the cochlea.

pp: 47: It has been established that the rigid cochlear envelope is hardly deformable. This leads to the realistic hypothesis that the ‘bone conducted’ sound signals evoke stimuli by means of a similar process to those of the airborne sound stimuli, namely by means of a push-pull movement of the perilymph, in this case, out of the cerebrospinal cavity via the cochlear aqueduct.

pp: 19-21: Bone conduction: As the petrous bone is the toughest bone in the human body, it is practically impossible for deformation to occur through the vibrating movements that are caused by acoustic pressure changes. Therefore, there must be another means for this signal transfer. A bone conduction audiogram – apart from a reduced transfer of especially the higher frequencies – is not fundamentally different from a pure airborne tone threshold audiogram. It follows that the perilymph movement within the cochlea must somehow also generate the bone conducted signal transfer. And indeed there is such a possibility. The scala tympani is directly connected with the cerebrospinal cavity by means of the cochlear aqueduct, which has its opening in the vicinity of the round window. The cochlear aqueduct enables the perilymph to move backwards and forwards between the cranial cavity and the cochlear channels (scala tympani and scala vestibuli). The perilymph in this cranial cavity is exposed to the alternating pressures caused by the sound induced vibrations of the shell shaped cranial bones that are located in the front and the back of the skull. As a consequence of Newton’s fundamental law of motion we know that when a larger amount of fluid inside the skull must be brought into motion, the effect of these stimuli will be smaller for the higher frequency contributions than for those of the airborne stimuli for similar frequencies. Furthermore, the stapes introduces the airborne signal that results in a backwards and forwards motion of perilymph, in opposite phase to the back and forth motion of perilymph along the
basilar membrane, which is evoked by bone conduction. This results in a slight reduction of the airborne signal, which actually is the stronger of the two stimuli.

pp: 19-21: The alternating movement of perilymph between the cerebrospinal cavity and the scala tympani via the cochlear aqueduct will also be partially directed towards the round window. This splitting up into two directions of the perilymph movement creates a reduced perilymph velocity in front of the basilar membrane, and finally results in a reduction of the bone conduction signal. The rate of reduction depends on the mobility ratio between the oval window and the round window. A further decrease in round window mobility, related to the mobility of the oval window, results in a higher perilymph
movement in front of the basilar membrane, which evokes a higher bone conduction signal, while an increase would result in a lower one.

pp: 19-21: This hypothesis that bone conduction consists entirely of the push-pull movement of perilymph from the cerebrospinal cavity via the cochlear aqueduct, and is evoked by the vibration of the shell shaped bones of the skull, while the rigid temporal bone does not deform at all, is just one logical step further than the functional possibilities indicated by others.


RNA seq: Should non-infected units be used for RNA-seq? I am designing a RNA-seq experiment to study transcriptomic profile changes upon parasite exposure. Some papers I read, mostly extract RNA from the entire treatment group (organisms exposed to parasite), without (seemingly) bothering if all the organisms were indeed affected. Doesn't this practice bias results? Are there any studies on how this could affect results?

It will dilute your signal if you have a pool of samples +/- the parasite prepared as one library prep. It is always better to maximize the number sequencing libraries (usually cost prohibitive) and extract RNA from samples you are confident exemplify the condition of interest, and an equal number of control samples to maximize your statistical power.


What advantage does the pseudostratified epithelial structure type provide over squamous, cuboidal, and columnar? I'm currently and have had difficulty receiving an answer about the role the pseudostratified columnar structure provides.

I understand that that the following have their respective advantages:

Cuboidal: Very tight cell junction
Columnar: Increased Surface Area relative to volume
Squamous: Allows easy passage for materials across

In the tissue we observed from a trachea, the ciliated pseudostratified columnar was responsible for the movement of material across its surface, however it seemed that the cilia provided that, not the structure.

Why not have ciliated columnar tissue? What does pseudostratified bring to the table?

Why not have ciliated columnar tissue?

The respiratory epithelium in the trachea is columnar. The three classifications you bring up in your question: cuboidal, columnar, and squamous, describe the shape of individual cells. The trachea, as you saw in your trachea sample, has columnar epithelial cells (when healthy). The cells are longer along the axis perpendicular to the basement membrane than they are along the axis parallel to it.

You can also classify epithelium according to the number of cell layers between the basement membrane and the free surface of the epithelium. The two possible classifications here are simple (one cell layer) and stratified (more than one cell layer).

The classification pseudostratified means it looks like it's stratified, but it is actually simple. As with any other histological classification, this classification describes structure rather than function. The epithelium in the trachea is simple columnar because all the cells touch the basement membrane, but without knowing that (just by looking at a cross section) it would appear to be stratified because the nuclei of all the different cells do not line up. That is why it is called pseudostratified. The difficulty in distinguishing pseudostratified and stratified from an ordinary cross section of a trachea may be difficult to appreciate without an image. It is not obvious that there is only one cell layer above the basement membrane here, but there is:

As with other simple columnar epithelial tissues, the trachea is specialized for both secretion and barrier formation.

You could speculate on the possible strengths and weaknesses of the pseudostratified structure, but it just happens to be the case that a certain cell population that has nuclei that are closer to the basement membrane (here labeled BC), and a certain cell population has nuclei that are further from the basement membrane (here labeled CC). Those cells with the lower lying nuclei are sometimes called basal cells, and are not terminally differentiated. They provide a reserve for cell replacement in response to normal loss of cells and/or pathophysiological processes like infection and inflammation.

Now, other simple cuboidal epithelial structures, e.g., in the intestine, do not have a pseudostratified structure. If you look at a healthy section of large intestine, the nuclei of the epithelium clearly line up, and it's not hard to see that the structure is a simple epithelium. For those unfamiliar, the epithelium here is only the outer layer. The seemingly disorganized mass of cells deep to the epithelial basement membrane are connective tissue (labeled CT). Look for a thin pink line in each of these slides to help orient yourself to the epithelial tissue. That's the basement membrane.

This simple cuboidal epithelium is also renewed in response to normal loss of cells and pathophysiological processes like infection and inflammation, but doesn't have a pseudostratified structure. This means, clearly, you don't need a pseudostratified structure in order to renew an epithelial surface. So I would caution you not to expect structure and function to be so neatly tied together in histology. It's a descriptive science. You can learn and understand what these structures do, but it's not necessarily a good idea to try to shoehorn the structures into logical rules. The usual answer to "why" in histology, is "because that's what it looks like".

You can read the details in Ross Histology, Chs. 5 (for general classifications and the general concept of pseudostratified epithelium), 19 (for respiratory epithelium and the details on pseudostratified epithelium), and 17 (if you want to compare the respiratory structures to the epithelial structures in the GI tract). Images are from Ross Ch. 5.


Can you measure plasma glucose with a regular glucose meter? I'm wondering if plasma glucose can be measured with a regular glucose meter and strips like this. I know these meters are normally used to measure whole blood glucose, but can they measure plasma glucose levels as well?

Thanks.

Excellent question... "Can you measure plasma glucose with a blood glucose meter?"

Absolutely Not! In my experience, if you try to measure plasma glucose with a whole blood glucose meter the results are highly variable for a number of reasons (mentioned below). Using blood glucose meters to measure plasma glucose is dangerous. The meters are calibrated for whole blood and not plasma, which is chemically different and will yield different results. Depending on the clinical situation (or experimental situation), the results can be significantly different and non-linear across a huge spectrum of concentrations.

Here is a nice link from the University of Virginia demonstrating the basics of how one type of these meters works.

There are a number of types of glucose meters commercially available to the public as well as healthcare facilities. Most of these meters use varying solid-state chemistry techniques to drive the production of an electrical current that can be measured by the glucose meter. In other words, when the blood is taken up by the strip in the meter the glucose takes part in a redox chemical reaction that creates a small "electrical current" that is detected by the meter. The amount of glucose in the sample is proportional to the electrical current produced. However, there are a number of assumptions that the meters make (which can differ between meters). One of the most clinically significant assumptions is that the meter assumes that the hematocrit (i.e. the percentage of blood volume that is erythrocytes) is normal or approximately 45%. If you use these types of meters on plasma (which has no erythrocytes in it), the chemistry is inaccurate because the meter "thinks" all the glucose that it is detecting is actually dispersed within a pool of erythrocytes in a hematocrit of 45%. There are a number of other issues and important points discussed in this review.

When the clinical trials (e.g. NICE-SUGAR) began showing that intensive glucose control was associated with improved mortality, clinical practices changed from keeping blood glucose concentrations in critically ill patients between 150 and 250 mg/dl to a much lower concentrations (i.e. 80-120 mg/dl). As these new guidelines began rolling out, there were a number of subsequent studies that showed that intensive glucose control was actually associated with more frequent hypoglycemia episodes. There were likely a number of issues to explain this, but one of those was that if your meters were not correcting for differences in hematocrit the blood glucose meters would read spuriously higher than what the true measurement was (thus, you could be treating someone with insulin to lower their glucose that was 160 mg/dl - when in true the value was much, much lower).


Crossing white eyed Drosophila with sepia eye So, I'm doing some drosophila experiments with my high schoolers and I had really poor production of wild type individuals for doing the experiment resulting in not enough to cross with everyone... I am trying the following crosses and hoping the kids can still learn from it, but wanted input from any fly-herders on what I can expect with the first two  crosses....

Sepia males x White Eye females

Sepia females x White Eye males

Dumpy males x Wild-type females

Dumpy females x Wild-type males

I don't think the gender separation will make any difference except in the white x sepia crosses since it is X-linked.
What should I get in the sepia x white crosses? Since they both control eye color and are both recessive I'm not sure. Am I correct that w is epistatic, thus should block sepia in an x-linked manner (same as if I had used wild-type instead of sepia)?
I assume the Dumpy x Wild-type will go by the books (F1 all wild-type with F2 3:1 ratio). Fingers crossed.

I posted this on Reddit as well, so credit to km1116 for working this out. Here is his response which follows my original logic (though I'm not sure if he is right):

  female x male:

  w x se

  F1: wild-type females and white males

  F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males, 1/4
  white-eyed females, 3/16 wild-type females, 1/16 sepia females

  se x w

  F1: all wild-type offspring

  F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males; 3/8
  wild-type females, 1/8 sepia females

  wt x dp (either direction)

  F1: all wild-type

  F2: 3/4 wild-type, 1/4 dumpy

My rationale for his answer is the genotype of the cross looks like this:

XwYNN with XWXW nn , where "W" is normal eyes, "w" is white", N is Wildtype and n is sepia.


Breakdown current for human body If I am not mistaken, during exposure to electricity sources it is the magnitude of the current and not the voltage that kills the human body.  If so, what is the order of magnitude of current that human body can sustain, and for what duration?  How do defibrillators exploit this?

According to Wikipedia Electric shock, the Magnitude of electric shock to a body is mainly due to current as well as voltage. Various factor of the environment will also play a major role in damaging the body while under contact. The following quote explains it:

  The minimum current a human can feel depends on the current type (AC or DC) and frequency. A person can feel at least 1 mA (rms) of AC at 60 Hz, while at least 5 mA for DC. At around 10 milliamperes, AC current passing through the arm of a 68 kg (150 lb) human can cause powerful muscle contractions; the victim is unable to voluntarily control muscles and cannot release an electrified object. This is known as the "let go threshold" and is a criterion for shock hazard in electrical regulations. The current may, if it is high enough, cause tissue damage or fibrillation which leads to cardiac arrest; more than 30 mA of AC (rms, 60 Hz) or 300 – 500 mA of DC can cause fibrillation.

To give a clear picture of how various current threshold will affect human body see the image below. (Complete data is available here "Electrical Safety").

Even High Voltage also can be fatal to human body which is enough to cause damage.

  High voltage electrical energy greatly reduces the body's resistance by quickly breaking down human skin. Once the skin is punctured, the lowered resistance results in massive current flow. Ohm's law is used to demonstrate the action.
  At 1,000 volts, Current = Volts/Ohms = 1,000/500 = 2 Amps, which can cause cardiac arrest and serious damage to internal organs.

Now what is the length of time that body is under electrical contact. This length of time exposure is also critical.

  When muscular contraction caused by stimulation does not allow the victim to free himself from the circuit, even relatively low voltages can be extremely dangerous, because the degree of injury increases with the length of time the body is in the circuit. LOW VOLTAGE DOES NOT IMPLY LOW HAZARD!
  100mA for 3 seconds = 900mA for .03 seconds
  in causing fibrillation

(Complete detail is available How Electrical Current Affects the Human Body)


Temperature threshold of a cell While human body as a whole will find a increase in temperature by 2 C fatal, what about individual cells? If temperature of a cell or tissue is maintained at higher temperature via external mechanism , say a sophisticated heating rod, how much temperature rise it can take before dieing? Say, endothelial cells lining blood vessels. Or,any other cell.

Talking about cells in general, the main problem about higher temperatures is the denaturation of proteins (when proteins lose their structure and then they don't work anymore), and every organism has a specific range of temperatures in which its proteins have evolved to work in that determined range.

The most common example of bacteria living at high temperatures is Thermus aquaticus (or others) which proteins are widely used in laboratories for their peculiarity to be able to work at more than 70 °C (e.g. polymerase chain reaction).

In humans the mean temperature is 37 °C, and it's not unusual during severe fevers to get it rising to 39-40 °C (so the assumption that over 39 °C occurs death is incorrect). Of course you can reach higher temperatures but reaching 43-44 °C leads to multi-organ damages. You can find out more in this review.

Another thing to take in consideration is that cells must contain water in liquid phase, so over the 100 °C limit (at atmospheric pressure, so the limit can increase alongside pressure) it's kind of impossible to find living cells.


Number of reading frames in nucleotide sequence In class of molecular biology was posed this question:

"How many reading frames start in sequence of nucleotides 5' ... ATATGAATGATGACAT... 3' ?"

Every nucleotide sequence has six possible reading frames, because each codon (determining one amino acid) consists of a base triplet (3 frames), and there is a complementary strand which could be coding (3 reverse frames).

To find the possible open reading frames contained in your sequence, you have to look for start codons. That is: ATG. But, as said the complementary strand could be coding. So if your known sequence contains CAT, that would be ATG on the opposite strand and might also be an open reading frame.

Count them now and then read on to compare answers.

Your specific sequence contains four start codons (3x ATG and 1x CAT, which makes ATG on the complementary reverse).

5' ... AT ATG A ATG ATG A CAT ... 3'

3' ... TA TAC T TAC TAC T GTA ... 5'


Are a child's traits truly random? To me, there are two definitions of "random" in common usage: effectively random, where predicting the outcome is beyond most reasonable effort (e.g., drawing a card from a deck); and truly random, where predicting the outcome is beyond known science (e.g., radioactive decay/QM).

With this (possibly flawed) perspective, I'm very interested in sources of true randomness. I started thinking about how parents never know exactly what their child is going to look like. Is this because there are aspects of reproduction that are fundamentally unpredictable (true randomness) or because we lack the sophistication/motivation to predict it (effective randomness)?

You true randomness definition is partially wrong! Something does not need to be fundamentally random to be beyond known science.

Also, it is unclear what process you are referring to when talking about a child's trait. I would assume you are thinking about crossover but then, summarizing crossover positions by "child's trait" shows that you misunderstand a number of things!

To my knowledge, outside of quantum physics, in no field of knowledge has it been shown that true randomness has any measurable effect. So, no what chromosome an individual inherits is only random in the sense that it would be necessary to know exactly the position of every molecule in the cell to know where the crossover will happen.


Comparison of examples in incomplete dominance and Co dominance When we consider examples of incomplete dominance we take that of FOUR O CLOCK plant -

We say that alleles for red and white colour of flower are not completely dominant against each other. Hence in hybrid progeny we
Say (as in standard textbooks) that pink colour appears due to "expression of single gene for pigmented flower which produces only pink colour (quantitative inheritance )"

In codominance concept we take example of SHORT HORNED CATTLE which again appears as same case white and red cattle produces roan coloured hybrid progeny but due to "juxtaposition of small patches of red and white colour hair"

The same principle can be applied to four o clock plant too. Suppose pink colour of flower is too due to juxtaposition of red and white coloured elements.

Then where is the difference between the two concepts?

Further the thing which puzzled me more was that - "initially cattle example was considered to be in complete dominance. Later it was CORRECTED to codominance "
Also incomplete dominance is also known as "mosaic dominance" but actually mosaic happens in codominance.
Kindly clarify my doubts

Mosaic dominance

I think your confusion comes from the statement

  incomplete dominance is also known as "mosaic dominance"

I had never heard of mosaic dominance before and I could not find much on this concept. I found a few papers but they either referred to mosaicism (see below) or they did use this term only a few times without defining it. There is an entry for mosaic inheritence in the online medical dictionnary though (here). The definition they give is

  inheritance in which the paternal influence is dominant in one group of cells and the maternal in another.

It is a little vague to me as 1) the phrasing is a little unusual and 2) it does not specify the underlying mechanism. If anything, it feels like a synonym of codominance and not of incomplete dominance.

Mosaicism is a thing in genetics but it is mainly unrelated to the concept of dominance as it refers to genetic polymorphism among cells within an organism.

Where did you read about mosaic dominance? Can you please give a direct quote?

If anything, mosaic dominance sounds like a synonym of codominance and not a synonym of incomplete dominance.

Codominance vs incomplete dominance

Outside the above issue, I think you pretty much define these two terms through your examples. You might want to have a look at the post (although it is a post who did not get much attention)

How is incomplete dominance different from codominance?

In short, codominance implies that the specific phenotypic effect of each allele is being visible in the heterozygote, while incomplete dominance implies that the heterozygote has a phenotype that is somewhat intermediate between the two homozygote phenotypes.


What sea animal is this? I am in a remote village and a young boy (second pic holding tail) says this thing is his friend. This creature is safe, we held it for pictures and released it after. None of us know what this is and we do not know who to contact. The young boy plays with it every day so it is safe but it still is strange.

These are salt water shores, not fresh water.

Someone mentioned a dugong but it is far too skinny I think. I didn't get pictures of the head as we didn't know if it had sharp teeth.
Image is taken in a remote village in Kavieng, Papua New Guinea.

The creature's head looked like this.

Link:
 polartrec.com/files/members/cara-pekarcik/images/dsc_0160.jpg

I'm no expert, but I don't believe seals are in Papua New Guinea, it's almost a hybrid of few things.

It's probably a dugong, based on the location, lack of a dorsal fin, split tail, lack of a blowhole, and narrowing of the snout.

The prominent vertebral column looks unusual, but that might come from the strange posture it is being held in or from malnutrition.

This publication from the Australian government shows necropsy of several dugongs (note, this PDF contains graphic necropsy photographs), including one that was malnourished (see page 53). This individual shows some of the characteristics of the OP, including pronounced vertebral column and a clearly visible neck. The text notes the presence of these features as well.

  Adult dugongs showing signs of malnutrition: a) with neck becoming visible
  and prominent backbone

Sadly, the other dugong pictures I found that look most like this specimen are also ones from news sources that are often dead or injured or needing some other human assistance. Some other examples:

Queensland couple come to rescue of beached dugong
Dugong dies from propeller wounds
Trang fishermen asked to help slow-moving male dugong
Rare Dugong saved in Maliangin Community Marine Sanctuary

Some pictures do show a prominent vertebral column near the tail in animals that seem otherwise healthy, but those images don't show the rest of the animal well (thanks to @theforestecologist):

http://www.oceanwideimages.com/images/11147/large/dugong-58M1444-20D.jpg
http://www.oceanwideimages.com/images/11144/large/dugong-58M1444-17D.jpg

As an extra piece of trivia, dugongs and their manatee cousins have been closely associated with mermaid legends.

Of course, a better picture of the animal's head, especially in profile, would make identification much more clear.


What mechanisms do animals living in groups (herds, packs, swarms) have against spreading contagious diseases? While for example a wolf pack provides protection to a sick wolf, increasing its chance of survival, there is a risk of infecting other members of the pack, decreasing their total chance of survival.

Do animals have mechanisms for preventing that? For example the sick member leaving its group temporarily?

Three proposed mechanisms:

altruistic self-removal (i.e., diseased individuals leave the group to prevent transmission to kin) has been documented in eusocial insects (ants and bees); Rueppell et al 2010 J. Evol. Biol. say:

  altruistic self‐removal by sick social insect workers to prevent disease transmission is expected under most biologically plausible conditions. The combined theoretical and empirical support for altruistic self‐removal suggests that it may be another important kin‐selected behaviour and a potentially widespread mechanism of social immunity.

social distancing/avoidance: This is a commonly used term in human infectious disease epidemiology for the practice of avoiding contact with infected people. I don't know of any great references, but Loehle 1995 Ecology "Social Barriers to Pathogen Transmission in Wild Animal Populations" says:

  Data on animal behavior in this regard [social avoidance] are sketchy. Sick individuals in cattle herds do seem to be isolated somewhat from the group (L. R. Rittenhouse, Department of Range Science, Colorado State University, and Ray Strickland, University of Maryland, personal communication 1988), though whether by chance (failing to keep up with the group due to listlessness), by voluntary isolation, or by avoidance on the part of others is not clear. Edwards (1988) found a higher degree of investigatory behaviors but a lower degree of touching between other group members and mice infected with Trichinella spiralis, though this disease is not transmissible by contact. This example would fit the proposed behaviors perfectly. More study is needed.

seasonal migration has been proposed as a way for group-living organisms to temporarily leave their habitat, allowing the built-up parasite burden in the environment to diminish before they return; it may also have a group-level effect of filtering out diseased individuals.

Folstad et al. 1991 Can. J. Zool. Parasite avoidance: the cause of post-calving migrations in Rangifer?

  Intensities of warble fly larvae, Hypoderma tarandi (L.), were examined in slaughtered reindeer (Rangifer tarandus tarandus L.) from different summer grazing areas of Finnmark County, northern Norway. To test the hypothesis that larval abundance decreases with increase in post-calving migration distance (i.e., distance from calving grounds), herds with differing migration distances were sampled. The prevalence of infection in the total sample of 1168 animals was 99.9%. The study revealed significant differences in larval abundance among herds from different summer grazing areas. Herds with post-calving migrations have significantly lower larval abundances than herds remaining on or near the calving grounds for the whole summer. Between-herds variation in abundance of H. tarandi larvae is assumed to reflect differing densities of the infective stage (adult flies) on the herds' summer ranges. Larval abundance in a herd is in turn negatively correlated with the distance between the main larval shedding areas (i.e., calving grounds) and the areas of greatest transmission (i.e., summer pastures). These results are discussed in relation to transmission of other parasites common to Rangifer and suggest that this host's post-calving migration may be a behavioural adaptation that reduces levels of parasitic infections.

Loehle 1995 also discusses this (qualitatively/speculatively):

  A more subtle effect results from migration. Consider a species that migrates seasonally some large distance. An area that becomes fouled and unsanitary during one season will become largely clean again by the following year. In between, nest and skin parasites such as ticks and fleas will have nothing to eat and will be greatly reduced in number. For example, wide spacing in rabbits results in reduced flea numbers (Mohr 1963) for these same reasons. Excrement piles will decompose between seasons and wash away. Significant benefits could thus accrue to migratory species, even though long distance migratory behavior is not likely to have arisen from this cause alone. (It may result from predator avoidance [Fryxell et al. 1988], or more commonly be due to weather and food supply factors.) Abandonment of rookeries during the non-mating season might, however, be the result of disease avoidance. Another consequence of migratory behavior is the effect on internal parasites ...  Consideration of epidemiology thus leads to some unexpected benefits of migratory behavior.

Hall et al. 2014 J. Anim. Ecol. "Greater migratory propensity in hosts lowers pathogen transmission and impacts" explore a theoretical model of migration effects.


Doesn't the sarcomere contract during isometric contraction? During muscle contraction, the lenght of the sarcomere changes, length of myocyte changes and so does the length of muscle. However, if the length of muscle is not changing length as in isometric contraction does it mean that the sarcomeres are not contracting?

Yes, sarcomeres do contract during isometric contraction, they just don't change the overall length of the muscle. This is due to the tension being transferred to elastic filaments within the muscle that maintain the same muscle length but increase the muscle tension. Thus, this is how sarcomeres can contract while the muscle does not have an overall change in length. (See this link for a paper discussing these elastic elements within the muscle itself; also, this is discussed at this wikipedia link as well).

In an isometric contraction the sarcomere is increasing the tension in the muscle, but without an overall change in length. (Isometric Contraction = No change in length, but INCREASE in tension)

Once a muscle overcomes the tension needed to lift a weight/load, then the tension ceases to increase but the sarcomeres begin to shorten which moves/lifts the load. When the length of the sarcomeres change and the tension remains the same, that is called isotonic contraction. (Isotonic Contraction = No change in tension, but DECREASE in length)

The picture below is from a website discussing these muscle physiology principles and is freely available on the web.


Jamaican/Caribbean insect, plant identification keys/field guides Where can I find plant and insect identification keys and Field guides for Jamaica specifically, or for the Caribbean as a whole?

I've searched Amazon and google for Jamaican and Caribbean identification keys/field guides, to no avail. I'm taking pictures of organisms in my backyard, and I want to identify them and post them to iNaturalist. For my own sake I want to be able to identify them myself, prior to and independent of the (long) wait for a community ID to be given and confirmed.

I've never been to nor botanized Jamaica or the Caribbean, but a quick Google search turned up the following references for Jamaican plants:

Iremonger, S., 2002. Guide to the Plants in the Blue Mountains of Jamaica. University of West Indies Press, 280p. ISBN: 9789766400316
Fawcett, W. and A. B. Rendle. 1910. Flora of Jamaica, containing Descriptions of the Flowering Plants known from the island. Longmans & Company. Found here.

You can also find a list of Jamaican species on Wikipedia and a list of medicinal plants in Jamaica here.


Modelling how much cadmium a cell will be able to chelate with phytochelatins I am involved in a synthetic biology project where I have to do modelling with ODEs. The biological process I want to model is the chelation of Cd2+ with phytochelatins, to know how much can be chelated. I know the basics of ODEs and I already did other modelling tasks, but I never studied anything related to chelation (I am a computer scientist) so any hint about how these kind of biochemical reactions are modelled would be helpful to get started.

One of the best ways that I have found for modeling reaction pathways is to set up a boolean network for that specific pathway. The boolean will give you an idea of the possible different states in that pathway (dependencies) and while not really necessary I find it helps orient you to the system.

The next step once you have yourself oriented is to set up Michaelis-Menten equations which you can then use to run you ODEs. Here is a great primer on how to set up these equations: http://depts.washington.edu/wmatkins/kinetics/michaelis-menten.html

The subsequent modules provided in that link are also helpful in explaining how to set-up quadratic velocity equations and do different sequential models.

Also, I'm sure you know this but, it bears saying: these are all steady-state kinetics. If you are looking for a more accurate model of what is occurring in that reaction you are going to have to set-up stochastic models of your system.

Hopefully, that answers you question. Good luck!

EDIT

I have found a paper that seems to relavent to the process you are trying to model. It goes into a bit more detail than I think you are looking for but the basics seems sound. Mendoza-Cozatl and Moreno-Sanchez, 2006


Are there any fungi that can digest humic acids? Humic acids are a complex group of organic substances, that are generally known to be hardly biodegradable. Fungi as agroup are known for breaking down complex organic matter like cellulose or lignin. But are there any that beak down humic acids as a major contributor to their energy needs?

According to Wikipedia, humic acid (HA) is a product of the biodegradation of dead organic matter. Shown below is a representative structure, but it important to understand that humic acid is a name given to a family of loosely related polymers of the products of biodegradation.

Although HA is resistant to further biodegradation, there are indeed fungi that are able to break it down further.

There is evidence that fungi can break down HA:

  Grinhut et al (2011) Mechanisms of Humic Acids Degradation by White Rot Fungi Explored Using 1H NMR Spectroscopy and FTICR Mass Spectrometry Env Sci & Technol 45, 2784-2754

This paper reports studies of the mechanism of HA degradation by Trametes and Phanerochaete fungi (Basidiomycetes). This degradative property is attributed to the secretion of non-specific oxidising enzymes: manganese peroxidase, lignin peroxidase and laccase. the authors report evidence for "oxidation, a decrease in the aromatic content, and indication of demethylation of the HA during biodegradation.

The paper is also a source of references to earlier work.

The indications are however that these fungi carry out this degradation in the presence of other nutrients, i.e they cannot utilise HA as a major carbon/energy source.