Where do mushrooms get their energy from?

Mushrooms are the fruiting bodies of fungi. Fungi get their energy by decomposing dead or decaying organic material, such as fallen leaves or dung.

Some background: spores of fungi germinate forming mycelia consisting of threadlike hyphae. When the hyphae of different fungi meet, they may have sex and form mushrooms. The mushrooms produce the spores. See https://en.wikipedia.org/wiki/Fungus.

So, each of these stages get their energy ultimately from decomposition, although the mushrooms get their energy from the mycelium. Spores rely on their internal energy storage to germinate and start decomposing. Even though spores are tiny, the have energy stored, like all cells do.


How does one determine intracellular concentration?

In fact the line that you quote doesn't mean that the solution is formulated to be identical to the cytosol. All that it means is that the solution should be buffered to physiological pH (typically slightly alkaline); should contain a relatively high concentration of sodium ions and a low concentration of potassium ions; and should be isotonic (i.e have the same osmolarity as the cytosol) to avoid osmotic effects such as plasmolysis (shrinkage due to loss of water) or osmotic lysis (bursting due to uptake of water).

There are many such solutions, but a commonly used simple one is phosphate buffered saline. Another is Ringer's solution. If the aim is to keep the cells metabolically active these are often supplemented with glucose or lactate, depending upon the cell type.

Addendum in response to comment from OP

According to the WP entry for Ringer's solution, Sydney Ringer determined the requirement for Na, K and Ca salts in a specific proportion when carrying out experiments with perfused frog hearts. This was in the late 19th century. A  Google search measurement of intracellular ion concentrations reveals current methods.

This review starts off with a discussion of early measurements of intracellular pH (see page 298). Basically these all consisted of making cell lysates, with various attempts to prevent post-lytic changes. If you do a Google search determination of intracellular pH you will find lots of current methods.


There are different type of immune cells which falls under either innate or adaptive system.

The cells under the innate are first to respond microbial attack and are able to detect them in extracellular environment by recognizing proteins/peptides called Pathogen-associated Molecular Patterns (PAMPs) on their surfaces; these are only found on microbes.

But when the innate system fails to clear the microbes in time, the adaptive  system is kicked-in. This involves T-lymphocytes and B-lymphocytes. T-lymphocytes are trained to ignore cells that are able demonstrated that they self but B-lymphocytes which produces antibodies/immunoglobulins to the detected antigens do not have a mechanism of ignoring self cells.

So the problem lies with when the immune response gets to the point where antibodies are produced, at that point produced antibodies simply attack without discrimination.

I hope this simplified version would help you.


In my opinion you are pretty close to the exact identification.

I think it is Marauder Ant, which could be Pheidologeton diversus, but probably Carebara affinis as well.

The main feature I can gother from your pictures is Venation of wings which matches with Pheidologeton diversus venation (it would probably match with affinis as well, but I failed to find the picture):

Venation match: the combo picture of the wing from the post and the wing from the reference:

This ant is known as Hong Kong inhabitant -


Can the word phalanx also be used to describe the finger bone plus the soft parts around the bone?

It's a great question, and in my humble opinion, the answer is:

Phalanx (plural: phalanges), (also Cambridge and MedicineNet) is the term for one of the bones (only) in the fingers or toes and not for all the "meat" around it. The Google images search for phalanges is quite convincing.

Someone on https://english.stackexchange.com/ might know a word for the whole bone + "meat" part of the finger.


How efficient is the human body at metabolizing food?

I suspect that what you are actually looking for is the following:

- 1 gram of fat = 9 kcal
- 1 gram of protein = 4 kcal
- 1 gram of sugar = 4 kcal
- 1 gram of alcohol = 7 kcal

Those are general and inexact values. They're just often used to give a rough idea of the amount of energy we get from different types of food.


Was the recent "conservation hunt" of a black rhino supported by science?

Yes it is.  Besides Dr. Knights article which is very focused on the issue and describes numerous benefits, there are other sources of research that show this can be good not only for the animals but also the community.  And specifically that this has worked in Namibia (where the black rhino was hunted) extremely well.

Namibia has encouraged communities to see their local animals as resources to be protected and that they can profit from.  In cases of endangered species, the federal goverment abides by CITES and only allows so many to be killed. Other than that limitation communities are allowed to profit from their local animals both from trophy hunts but also tourism.  This has led to a reintroduction of many of these animals (endangered and not) onto private lands.  The survival and thrival of these animals is now an economic concern to the communities and land holders, and are protected as such.  This has worked for the recovery of many animals in Namibia.  In summary, the selling of a license to hunt one black rhino brings big profits to the community and therefore encourage the people to protect these resources.

The CITES articles are also a good resource when looking at this.  It's very clear in the resolutions to allow quotas for endangered animals that it is not harming the population.

And one other paper, though it's behind a paywall, describes how South Africa's white rhino population went from fewer than 100 to over 11,000 as privatization and legal hunting were legalized.

As a side note, the wildlife conservation department where I live receives almost half its funding from hunting licenses.  Since it has been in operation the deer population has gone from nearly wiped out in the state to over half a million animals.

Flocken's arguments are based on fact but are really targeted at examples of bad wildlife management rather than against the practice of conservation hunting.  There is some concern that allowing the legal killing of any endangered animals will lead to more poaching, but I haven't seen any evidence in the literature of that.


As far as I am concerned L. casei and L. paracasei can be differentiated by the amplification of the 16S rRNA gene of the aforementioned species using PCR - please see the work done by Ward and Timmins (1999). An alignment of the V1 region of the 16S rRNA genes of Lactobacillus casei and Lactobacillus paracasei shows the bases comprising the species-specific PCR primers - screenshot taken from Ward and Timmins (1999):

So, perhaps in your study you have not amplified the correct region of the 16S rRNA gene of L. casei and L. paracasei?

With regards to the classification of these organisms. Just as @skymningen has already mentioned in the comment section, the definition of a bacterial species (not even to mention strains) is somewhat debatable and tricky.

However, here is what Mori et al (1997) suggest:

  The primary structures of the 16S rRNA genes of the type strains of Lactobacillus casei and related taxa were determined by PCR DNA-sequencing methods. The sequences of Lactobacillus casei, Lactobacillus zeae, Lactobacillus paracasei, and Lactobacillus rhamnosus were different. The K nuc values ranged from 0.0040 to 0.0126. On the basis of the K nuc values and the levels of DNA-DNA relatedness among the strains of these species, the L. casei-related taxa should be classified in the following three species: L. zeae, which includes the type strains of L. zeae and L. casei; a species that includes the strains of L. paracasei and L. casei ATCC 334; and L. rhamnosus.


Where can I find these frequencies for several species?

Since most of the genomes consist of double helix DNA, the only meaningful ratio is GC-content. A comprehensive list of the known genomes that includes GC-content data is available at NCBI (note that default Overview tab doesn't contain the GC-content numbers, you need to select another tab, e.g. Prokaryotes). They also provide an FTP access to the raw data, if you need to process the numbers with software.

If you're interested in particular genomes that are not present in this list, you can calculate all frequencies from the sequence. There are a number of programs to do this. For sequences in FASTA format you even don't need a special software, the analysis can be performed with standard tools, e.g. grep (should be installed in Linux/BSD/MacOSX, obtainable for other systems):

grep -v '^>' sequence.fasta | grep -o '[ATGCatgc]' > tmp
# number of AT pairs
grep -c '[ATat]' tmp
# number of GC pairs
grep -c '[GCgc]' tmp


I'm 90-95% certain that the spider in question is a Trachelas tranquillus, more commonly known as a "Broad-faced Sac Spider".

Broad-faced sac spiders are quite distinct in coloring; they have a dark gray/brown head (cephalothorax) with tan/light-gray abdomen, orange/red legs, and distinct pincers (which can be seen if you look closely). These spiders are also quite common for your area, and aren't a major threat to humans.

EDIT: I would like to mention that the images I provided (most likely) have enhanced lighting, and/or are much closer to the spider, so the leg color is (expected to be) lighter than what's depicted in your image.


No enzyme is involved in base-pairing (annealing).

This does happens by chance, but the chances are governed by stoichiometric considerations.

The main such consideration is that the (low molecular weight) primers are added at a high concentration (greater than that of the DNA) and therefore have a greater chance of encountering the appropriate region of the DNA than its complementary strand does. (Reannealing of the denatured DNA strands can occur, but not over the time period of PCR.)


What kind of bug/insect is this? photo attached

I have a doubt we can answer this question with a high level of accuracy: the sample image is very blurred, it is unclear if there are posterior/lower body elements like forceps as well as other significant features which could help with the identification.

My best guess it is baby of Earwig (2000 species): If I look at the posterior part of the body I can "see" the preliminary forceps as well as other similar features, but still the accuracy of the ID is limited.

Enhanced image:

Baby Earwig:


What does the gene name "lexA" stand for?

I'd go with Lambda Excision A. Terms like lex or rec often stand for what'd be termed a mnemonic, where for example rec may stand for recombination, or umu for UV mutator. The naming conventions can be difficult.

Edit: A 1981 study by Roger Brent and Mark Ptashne notes some data from initial studies that showed the lexA repressor downregulated a number of genes including himA, which they note to be required for integration of lambda phage.

http://www.pnas.org/content/78/7/4204.full.pdf


How do crickets get away with being so loud without getting eaten?

They don't always 'get away with it'!  A study by Pascoal et al. (2014) found that field crickets (Teleogryllus oceanicus) on Oahu and Kauai islands of Hawaii have lost the ability to produce sound after an invasive wasp that is acoustically oriented to prey was introduced to the islands within this century. There are a few mutation to the crickets' wing morphology that produces "flat wings" that cannot make sound. Ordinarily, this mutation would reduce fitness through a reduction in competition for attracting mates. However, the selection pressure from the wasp caused independent mutations for flat winds to sweep through the island to the point that the Kauai population was 96% flat wing.
This example illustrates that the deciding factor between 'getting away' with producing so much noise comes down to the selection balance of attracting more mates or attracting more predators.
Reference:
Pascoal, S., Cezard, T., Eik-Nes, A., Gharbi, K., Majewska, J., Payne, E., … Bailey, N. W. (2014). Rapid convergent evolution in wild crickets. Current Biology: CB, 24(12), 1369–1374.


Some thoughts on this. First of all, the positive-inside rule, proposed by Gunnar von Heijne, is an empirical rule based upon observations, not one derived from theoretical considerations, so any explanation is simply an attempt at a rationalisation.

Having said that, here are three of those rationalisations:

the membrane potential is usually negative inside. This will create an electrostatic tendency for basic amino acid side chains to stay inside.
most phospholipid head groups are either neutral or anionic (phosphatidylserine, when the phosphate is included). Again an electrostatic force favouring basic residues inside since to move them out would require overcoming their interaction with the negatively-charged membrane surface
the pK values of the basic side chains (lysine and arginine) are much further from 7 than are those of the acidic side chains, so,  since charged residues must be neutralised to get them through the bilayer, it is more energetically unfavourable to deprotonate basic side chains than it is to protonate acidic ones.


What do we know about the Last Universal Common Ancestor (LUCA)?

Carl Woese has much to say on this subject, including:

  “The ancestor cannot have been a particular organism, a single
  organismal lineage. It was communal, a loosely knit, diverse
  conglomeration of primitive cells that evolved as a unit, and it
  eventually developed to a stage where it broke into several distinct
  communities, which in their turn become the three primary lines of
  descent [bacteria, archaea and eukaryotes].”

There is a 2000 Scientific American article by W.F. Doolittle that discusses much of Woese's (and others') work understanding this question.

Also, see a couple of Woese articles here and here.


What is the lowest common denominator of cancer?

Hanahan and Weinberg's "Hallmarks of Cancer" articles should answer your question.

Their original, highly cited (14k+ citations), [Six] Hallmarks of Cancer article list these six common attributes of all cancers:

Sustaining proliferative signaling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death

The new article, Hallmarks of Cancer: The Next Generation includes additional "emerging hallmarks" and "enabling characteristics" (Figure 3) common among cancers:

The capability to modify, or reprogram, cellular metabolism in order to most effectively support neoplastic proliferation; and
The ability to evade immunological destruction, in particular by T and B lymphocytes, macrophages, and natural killer cells.


The Details
Ecological communities are groups of multiple (2+) species of either plants, animals and/or other organisms that interact in a unique habitat. More accurately (from Wikipedia and corroborated by Begon et al. (2006)), we can define an ecological community as an:

assemblage or association of populations of two or more different species occupying the same geographical area and in a particular time.

These organisms could be interacting in a number of ways:

As you can see, one or both species can be effected either positively, negatively or neutrally (not at all) in these various types of interspecific interactions.
I should note that a community doesn't have to contain all organisms within a certain habitat.

Sometimes we might limit our discussion of a community to a single guild or single trophic level. Other times we might use the terminology simply to describe two interacting species (either within or between guilds/trophic levels).

Really, "communities" are more conceptual "units" used to describe two or more interacting species. More accurately, it's an interaction between populations of 2+ species. In this way, community ecology is an extension of population ecology.

Food webs (i.e., a system of interlocking and interdependent food chains) are essentially summaries of the feeding relationships within an ecological community (Molles, 2010). In other words, they are focused strictly on trophic interactions. These trophic interactions are primarily concentrated within the (+,-) interactions between species. This means that the interactions that dictate a food web are going to consist mainly of consumption (predation/herbivory).

From University of Michigan (my emphasis):

Food webs are graphical depictions of the interconnections among species based on energy flow. Energy enters this biological web of life at the bottom of the [web], through the photosynthetic fixation of carbon by green plants.
Energy moves from lower to higher trophic (feeding) levels by consumption.

Example
An example of a community that does not qualify as a food web:

A community of plants includes just the plants that are competing in the same space and as a result make up (i.e., are classified as) some sort of vegetation type. These species are competing at the same trophic level and do not consume one another. This is classic ecological competition.

If we examine the trophic interaction between each of these plants with each of their sources of energy, each of their consumers, each of their consumers' consumers, etc. then we are talking about a food web.

Final Thoughts
So the term "community" is used generally to describe interacting species of organisms in a given habitat, while "food webs" describe a more specific aspect of a community -- the trophic interactions of the members of that community.

Of course, it could be the case that all species in a given community are represented in a food web, but this is not necessarily the case.

It could also be the case that not all species represented in a food web be part of the same community...

One could also consider food webs to be broader than a community because they can describe the trophic interactions of species/populations across communities. From this perspective, food webs "lie at the interface of community and ecosystem ecology" (Begon et al. 2006).

Citations:

Begon, M., C.R. Townsend & J.L. Harper. 2006. Ecology: From individuals to ecosystems. Fourth edition. Blackwell Publishing Ltd. Malden, MA. pp 469 - 601.

Molles, M.C. 2010. Ecology: Concepts and Applications. Fifth edition.  McGraw-Hill. New York, NY. p. 544.


So the term allele is a broad one, and simply refers to the different versions of any piece of DNA in circulation in the gene pool - it doesn't need to refer to a gene. I can talk about the alleles at a random place in the genome.

But if we proceed with your question and ask - 'do nonsense mutations within coding genes also lead to the creation of different proteins' - the answer is 'sometimes'. A nonsense mutation is just one that introduces a stop codon. The result is an mRNA that codes for a shortened protein. Sometimes, the mRNA will be recognized as faulty and degraded, and so little to no protein gets made. Sometimes, if made, that protein will be unstable, or the result will be as if no protein had been made. Sometimes though, the protein will be stable, and could hang around uselessly, or even do damage.


Allergies are often caused by the immune system reacting to a part of a specific protein, therefore it is in fact a specific protein in the food that is causing the allergic reaction to occur.

Milk allergies are caused by casein and whey (Source: Mayo Clinic)

Oat allergies can be caused by avenin (Source: EJCI)

Soy and egg allergies are caused by their respective albumin proteins. Additionally, egg lysozyme can also cause allergy. (Source: Cleveland Clinic, Food Allergy)


Can skeletal morphology change in adults?

Bone never stops changing.
Your bones are constantly being broken down and reformed on a microscopic level. Your bones are done growing at a certain point but they continue to be reshaped. Remember bone exists to supply calcium (and to a lesser extent phosphorus), to your muscles, Your body needs to break down the surface of the bones for this calcium.*  So bone is dissolved and redeposited constantly, this regulated mineral levels but also allows the bone to slowly reshape itself.
Bone will slowly reshape itself to resist any stress it experiences, for instance if you build muscle the attachment point for the muscle will become more rugged to strengthen the attachment. A runner's leg bones will get thicker and denser to resist the greater stresses. Joint surfaces can even reshape with repetitive motion.
*bone originally evolved as armor but this has been lost in modern vertebrates. Vertebrate muscle requires calcium to function, Vertebrates have lost the armor but not the need for a calcium store, and have repurposed into a structural support. Vertebrates without structural bone need to have massive calcium levels in their body tissue instead.
for continued reading there is a whole series of books by R. Mcneill Alexander that cover bones in fascinating detail.


Is it trivial to assume a version of Hamilton's rule that applies for numerous generations?

I am not sure what you mean by "applies to numerous generations". If the following does not help, can you please clarify what you meant?

Hamilton's rule expresses the condition for which, under a prisoner's dilemna game (see game theory), the stable equilibrium that will be reached is the one where everyone is cooperating. Hamilton's rule is, therefore, a condition to determine the directionality of a dynamic system (the system is dynamic because the state of the system varies over generations).

EDIT

  what if the values of B and C differ depending on [the generation]

In other words, you are asking

  What if the (social or not) environment is changing over time?

Well, under such circumstance, of course, the simplistic rule that consider B and C as constant won't hold.

You could not simply replace B and C by the the arithmetic mean (or by the geometric or harmonic or any other mean) as the system as two stable equilibriums and upon reaching one there would be no way to get out of it (at least as long as the game remains a prisoner's dilemna).


Are all of my ancestors from 400 million years ago fish?

Yes they all were because there weren't any land vertebrates, vertebrates were all fish at 400 million years ago.

It is a close call based on fossil evidence from 395 million years ago, there are footprints of 3 meter tetrapods from littoral/seaside fossils. https://www.sciencedaily.com/releases/2010/01/100107114420.htm

The earliest land vertebrate skeleton is from 375 million years ago. https://en.wikipedia.org/wiki/Tiktaalik

It is technically still a fish, so probably yes, the ancestral species of all land vertebrates were still fish. There are various experimental early quadrupeds, some with 6 fingers, which are cool reading.

They still exist in the form of lungfish.

Here are images of the earliest land vertebrates


Kind of.

What you describe is a cis-eQTL, but the exact distance (1Mb in each direction, 1Mb total, ...) and the definition of the location of the gene (TSS, transcript borders, ...) depend on whoever calculates a cis-eQTLs and are not universal.
The 'cis' part just means the SNP is somehow near the gene, there is no defined limit on the distance.


No, it isn't that simple, because centrifugal force varies with the square of the rotor speed. Have a look at the Wikipedia page for clearing factor.

Those equations are usually used to determine what you need to do if you are going to use a different rotor, but they can also be used to solve your question.

Because you are looking at a situation where the same particles are being centrifuged, the sedimentation coefficient s is the same in both centrifuge runs. Also all of the factors relating to the rotor properties are the same (rmax etc.). So, if you have a set of conditions that work, t1 and RPM1, and you want to choose new conditions t2 and RPM2, you can use the equation:

RPM2 = SQRT(t1/t2) x RPM1

For the example you mention t1 = 10 min and RPM1 = 2500 rpm. If you change the time to 5 min:

RPM2 = SQRT(10/5) x 2500 = 3536 rpm

Because the centrifugal force varies with the square of the rotor speed you don't need to double the speed if you halve the time.


Where do transamination and deamination take place?

According to David H. Vroon and Zafar Israili aminotransferases (transaminases) are widely distributed among tissues, and are found in both cytoplasm and mitochondria, although this may vary between different aminotransferases:

  Aminotransferases catalyze the redistribution of nitrogen between
  amino acids and corresponding oxoacids participating in both protein
  metabolism and gluconeogenesis. They are ubiquitous in their cellular
  distribution.

  Tissue activity for AST (aspartate aminotransferase) is as follows in decreasing concentration:
  heart, liver, skeletal muscle, kidney, pancreas, spleen, lung, and
  erythrocyte. Two distinct forms have been identified: a cytoplasmic,
  or soluble isoenzyme, and a mitochondrial isoform...

  The distribution and relative tissue concentration of ALT (alanine aminotransferase) is similar
  but importantly different. Highest activity is found in the liver,
  followed by kidney, myocardium, skeletal muscle, pancreas, spleen,
  lung, and erythrocyte. ALT activity is found in the cytosol; organ- or
  organelle-specific isoenzymes have not been demonstrated. The
  concentration of ALT in hepatic cell cytoplasm is comparable to AST;
  however, a mitochondrial ALT isoform is not found. In all other
  tissues, ALT activity is significantly less than AST.

As regards deamination, there is a Wikipedia page for glutaminase, which indicates that it is found in the mitochondria of a variety of tissues. There are two isoforms, one especially active in the kidney, and the other in liver (although both are found in other tissues).


What's the mechanism of action of Levomepromazine's analgesic effects?

According to Drugbank and the articles cited below, Levomepromazine is an antagonist of several different receptors: These include dopaminergic 2, dopaminergic 4, alpha-1 adrenoceptor, 5HT-2, histamine type 1 and muscarinic-cholinergic receptors.

References:

Evidence for the use of Levomepromazine for symptom control in the
palliative care setting: a systematic review
Muscarinic cholinergic and histamine H1 receptor binding of
phenothiazine drug metabolites
Levomepromazine receptor binding profile in human brain—implications
for treatment—resistant schizophrenia
Phenothiazine drug metabolites: Dopamine D2 receptor, α1-and
α2-adrenoceptor binding


Can the dendrites of sensory neurons be a meter long?

Short answer
Axons can be over a meter long, but dendrites are never that long. Distance in the body is covered by axons. The dendritic part of skin receptors is generally considered to be the receptor part and the receptor part only. The elongated structure leading to the soma, as well as the axonal part to the spinal cord are generally considered to be one and the same axon, the soma being attached to the axon in this case.

Background
The sensory receptors in the skin have their cell bodies located in the dorsal root ganglia situated adjacent of the spinal cord (Bourinet et al., 2014). In the case of pain receptors it is shown in Fig. 1. The same basic structure holds for the touch receptors in the skin.

Fig. 1. Signaling of pain receptors in the skin. source: Bourinet et al. (2014)

The cell bodies are located in the dorsal root ganglia of the spinal cord. Action potentials are sent from the dendritic region in the skin to the cell body in the ganglion. From there on it is transmitted to spinal interneurons in the spinal cord and up to the brain.

The nomenclature of these sensory neurons is generally as follows: in the cell body the axon splits in two. The afferent part that transmits the pulses from the skin to the cell body and the part that transmits the signal from the soma away from the cell body to the spinal cord are both considered as a part of the axon. The dendritic region is generally considered to be the nerve ending (Fig. 2C). So the axons of peripheral sensory neurons, as well as motor neurons for that matter, can indeed be over a meter long (Lodish et al., 2000).

Fig. 2. Types of neurons. Arrows indicate the direction of conduction of action potentials in axons. (A) Multipolar interneurons. The dendrites receive signals at synapses with several hundred other neurons, and there is a single long branching axon. (B) A motor neuron innervating a muscle cell. Typically, motor neurons have a single long axon extending from the cell body to the effector cell. (C) A sensory neuron in which the axon branches just after it leaves the cell body. The peripheral branch carries the nerve impulse from the receptor cell to the cell body, which is located in the dorsal root ganglion near the spinal cord; the central branch carries the impulse from the cell body to the spinal cord or brain. Both branches are structurally and functionally axons, except at their terminal portions, even though the peripheral branch conducts impulses toward, rather than away from, the cell body. source: Lodish et al. (2000)

References
- Bourinet et al., Physiol Rev (2014); 94(1): 81-140
- Lodish et al., Molecular Cell Biology, 4th ed. New York: Freeman (2000)


What is the actual storage form of energy in muscles? ATP or Glycogen?

This is a typical MCQ which in order to answer you have to have been at somebody’s lectures or be able to read his mind. The antithesis of education! Cells don’t store energy like car batteries.

Glycogen in muscle is a store of carbohydrate. It can be used to generate ATP if it is broken down to glucose and the glucose glycolysed. I wouldn’t have chosen this as an answer.

The concentration of free ATP in the muscle cell is not sufficient for it to act as store of a high group-transfer potential compound (which is presumably what the question means by energy). This is definitely not the right answer.

However if creatine phosphate (a.k.a. phosphocreatine) was a choice on your MCQ, that was probably the answer expected as it is used in muscle as a storage molecule which can be rapidly converted by creatine kinase creatine and ATP.

PS

As you say in your comment that the only choices were ATP or glycogen, then glycogen is what is expected.


That looks like the cast off outer layer of a dragon fly nymph§:

The following resources may be helpful to get a more precise identification:
https://www.fba.org.uk/sites/default/files/EA_specid/ea_specid_mod_8.pdf
https://british-dragonflies.org.uk/odonata/species-and-identification/

§Note: As pointed out by Arthur J. Frost this is actually the exoskeleton left behind when a dragonfly nymph molted and became an adult.


Why is burn feeling 'slower' than touch?

When you touch an object, a compression wave from the collision travels through your body at the speed of sound.  A sensor at any depth in your skin can pick up that signal at roughly the same time as the collision.

When you touch a hot object, heat from it moves into your body via conduction and to some extent radiation.  That heat flow moves much more slowly than the compression wave.  It will take longer for the heat pulse to reach a sensor that is deep in the skin and raise the temperature by a sufficient amount to cause signalling.

There may be further differences in the sensory neurons or in the reaction to the signals.  But there is a physical reason for the temperature signals to lag touch signals from the same object.

"Thermoception and Temperature Regulation" edited by J. Bligh, K. Voigt has some discussion of a study of thermoreceptors in rabbits.  It suggests both that

signal latency increases with increasing depth in skin
while most receptors has short latency, some receptors had much greater latency, and that this disparity in response may aid in determining temperature gradients within the skin, not simply reading instantaneous skin temperature.


Why did some animals evolve inward-slanted legs?

Sorry no references other than illustrations for the moment.
If a running biped has it's feet further away from the line of gravity, then it's got less efficiency in forwards motion and more instability of the line of gravity falling left and right.
When you consider the kinetic downwards weight in kilos that goes into every step, a runner/sprinter who doesn't have aligned steps wastes a lot of energy.
here's are dinosaur footprints:
https://australianmuseum.net.au/Uploads/Images/7919/footprint%20comparisons_big.jpg
The hips joints tend to point sideways to give a strong musculature, lots of running muscle, and a wide base of more than 90 degrees, for a wide birth canal and other reasons.
So the tendency for efficiency of running bipeds is to have aligned footsteps and their hips tend to be a strong and wide base.
That's only the resting position, the walking angles actually vary a bit outwards and straight too, the knee goes outwards when it's rising.
https://cdn.pixabay.com/photo/2016/01/18/02/04/footprints-1145883_960_720.jpg
here is a comparison of ostrich and human bone angles: http://rsif.royalsocietypublishing.org/content/13/122/20160529


Is cannibalism part of mainstream food-chain?

Cannibalism can be found across most animal groups. For some groups of organisms (e.g., spiders, fishes) cannibalism can be common within a single generation. Sometimes it will be between siblings, but more often with other members of their species.

As @heracho pointed out, from a network/food web/flow-diagram perspective, yes, cannibalism is repressed as a negative feedback loop on itself.

Evaluating the statement: "Food chains are found within the population of a species," I interpret is as, within species, there are subgroups that consume subgroups, that consume subgroups. You'd need at least 3 levels for it to be considered a chain (i.e., you don't have a chain with two species/a single link). Cannibalism would be a single link/two species, and not considered a chain. As to whether or not chains exist within a species, I suspect it is not common if it exists at all. If it did, I would guess it'd be found in a group like fishes where prey are often size dependent.


Why does this genetic pedigree show an autosomal dominant allele at one generation but not another?

Why don't the offspring 1, 2, 3, 4, and 5 in Generation III show a similar rate of expression?

Because there are only 5 individuals in that list. The entire generation III involves 8 individuals (all the offspring of one affected and one unaffected parent). The entire pedigree involves 12 offspring of an affected and unaffected parent.

When you look at III 1-5, you see 1/5 affected (0.20).

When you look at III 1-8, you see 3/8 affected (0.375).

When you look at all offspring of an affected and unaffected parent, you see 6/12 affected (0.50).

As you increase the number of offspring you consider, the proportion affected gets closer to the expected value of 0.5. Given a very rare autosomal dominant condition (i.e., I-2 is most likely heterozygous), this is exactly what would be expected. You may have to look at fruit flies, or some other prolific organism, to see it quite so clearly. Mendel looked at tens of thousands of pea plants, if I recall.

Generally, you shouldn't use the proportion of offspring that show a trait to rule out any particular mode of inheritance, especially if you're looking at a small number of offspring. You can state the probability of a particular child expressing a mendelian trait. That doesn't mean a small sample won't deviate from that probability.

You can read more about this in chapter 7 of Thompson & Thompson Genetics in Medicine.


Well SNPs are single nucleotide polymorphisms. Some SNPs are in the coding regions of genes and they can result in changes in the resulting protein. For example, the SNP rs1801131 is a human variation where some individuals have a G instead of an A at position 1515 of the gene MTHFR. When the gene is transcribed and then translated into protein, this variation (the presence of the G nucleotide) causes a Glutamate residue at position 429 of the protein to be a Glycine instead.

So, SNP rs1801131 maps to position 429 of the protein MTHFR.


What is basis of multifunctionality of "master glands" in the endocrine system?

It would seem to me that in the examples that you have listed that proximity to necessary input is the overriding logic behind gland geography. Take the hypothalamus as the first example. This gland receives input from diverse regions of the brain from the amygdala and hippocampus to the retina and brainstem. The brain can tweak levels of various releasing hormones entering the  hypothalamic-hypophyseal portal veins in order to produce a response that is appropriate to the situation perceived by the brain. It makes sense to have all of these co-located because they are all receiving input from the brain. Similarly, it makes sense to have all of cells that are uptaking the releasing hormones close-by to protect these vital peptides from degradation in the systemic circulation. Their collectively unique circumstance makes sharing a specialized vasculature a logical choice.

The pancreas is a good example of the importance of cross-talk within some endocrine tissue. Within the islet, alpha, beta, and delta cells are feeding back on each other to get the balance of insulin and glucagon just right. To whit, glucagon secretion provides a paracrine signal for insulin secretion. This makes sense because the body knows that once glucagon is released the blood sugar will soon rise. Ergo, it makes sense to trigger some insulin secretion as well in preparation. Their co-location makes that possible.

In short, I would say the overriding logic to the placement of each of these glands is their proximity to the necessary inputs and outputs that each of these glands interacts with.


I think that your interpretation is correct, although Principles of Neural Science (Kandel et al.) doesn't mention Peter's rule (which is where I would have hoped to find a simple explanation).

According to Binzegger et al. (2004), the idea behind Peter's rule dates back to Peters and Feldman (1976) and Peters and Payne (1993), though the Rule per se may have been coined by Braitenberg and Schultz (1991; at which point it was still called Peters' rule). Binzegger et al. describe it as:

  They assumed that axons simply connect in direct proportion to the
  occurrence of all synaptic targets in the neuropil. The rule can be
  extended to provide more precise estimates by taking into account the
  detailed morphometrics of the dendritic and axonal trees of the
  different neuronal types.

To paraphrase Binzegger et al., in the simplest form of Peter's rule, the number of synapses in a cortical layer are evenly distributed across the potential target neurons. So there would be a direct proportionality between synapses and targets.

The second sentence of the quote above is the meat of the Binzegger paper. They also present a mathematical model of a more complex and realistic variation of Peter's rule which takes into account different types of postsynaptic neurons and the fact that not all cells receive synapses.

Braitenberg V, Schüz A (1991) Peters' Rule and White's Exceptions. In: Anatomy of the Cortex, pp 109–112. Berlin: Springer.

Peters A, Feldman ML (1976) The projection of the lateral geniculate nucleus to area 17 of the rat cerebral cortex. I. General description. J Neurocytol 5:63–84.

Peters A, Payne BR (1993) Numerical relationships between geniculocortical afferents and pyramidal cell modules in cat primary visual cortex. Cereb Cortex 3:69–78.


Why do I hear beatings with stereo headphones?

Short answer
Dependent on the auditory stimuli used, it sounds like binaural beats to me.

Background
Binaural beats are the resultant perception evoked by the interaction of two auditory tones with different frequencies when presented to both ears (Lane et al., 1998). The presented tones should be below 1000 to 1500 Hz and differ in frequency between 1 and 30 Hz. For example, if a pure tone of 400 Hz is presented to one ear and a 410 Hz tone in the other, an amplitude modulated standing wave with a frequency equal to the frequency difference (10 Hz in this case) is perceived. Note that these 1-30 Hz beat frequencies are below the dynamic range of acoustic hearing. Hence, the beatings are the result of neurophysiological interactions in the brain, and not the result of physical interactions of the auditory stimuli impinging on the inner ear. From an experimental point of view, limiting the sound levels to 60 to 70 dB should prevent gross cross-over stimulation to the other ear.

Binaural beats are thought to be elicited in the auditory brainstem, and specifically in the the superior olivary nuclei, when the two wave forms mesh in and out of phase within the brainstem.

Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52

Source
- Web US

Related post
- How can binaural beats change mental state?


Determining the appropriate bioconjugate

There are general guidelines for cross-linking protein-protein interactions, but specific parameters (i.e. cross-linker sub-types,  spacer length, linker concentration, reaction pH and temperature) are often determined experimentally. Common protein cross-linkers target reactive functional groups that are more likely found on the surface of the protein than in its "active site" or "interface" that is often buried.

Given your relatively hydrophobic, non-reactive binging motif (Tyr/Pro/Met), if you do not need a large amount of cross-linked protein sample, then you could label it with photoactivatable amino acid such as L-photo-Met. Since Met is not often found on the surface, internal cross-linking would stabilize your protein and its binding partner.

If you need a large amount of cross-linked protein (e.g. in mg) for further structural studies, labeling can be costly. You could possibly cross-link the protein (complex) crystal itself (since there were crystals as you mentioned), often just by glutaraldehyde. If the complex is there in the crystal, it would now be as solid as rock.


From what I understand most allergies are detected by a scratch test. from the link below:

"A skin prick test, also called a puncture or scratch test, checks for immediate allergic reactions to as many as 40 different substances at once. ... After cleaning the test site with alcohol, the nurse draws small marks on your skin and applies a drop of allergen extract next to each mark. He or she then uses a lancet to prick the extracts into the skin's surface. A new lancet is used for each allergen. ...About 15 minutes after the skin pricks, the nurse observes your skin for signs of allergic reactions. If you are allergic to one of the substances tested, you'll develop a raised, red, itchy bump (wheal) that may look like a mosquito bite"

More information on scratch tests can be found here:

http://www.mayoclinic.org/tests-procedures/allergy-tests/basics/what-you-can-expect/prc-20014505

After a quick google search,I found a paper from 2014 [1] that seems to speak to the essence of what you are asking, link below.

http://www.tandfonline.com/doi/abs/10.1586/14737159.4.4.539 [1]

In the paper above they propose using a protein microarray technology to find allergies.

I am not sure if there is any way to extract the igE-antigen complex from the patient. But I think it could probably be done with the microarray technology. Although it would be cool to see a picture of the complex.
I hope I have helped answer your question.

[1] Harwanegg, Christian, and Reinhard Hiller. "Expert Review of Molecular Diagnostics." Taylor and Francis Online. Expert Review of Molecular Diagnostics, 09 Jan. 2014.


Species of dinosaur with longest fossile record (no birds!)

Dinosaur biostratigraphy makes it not possible to answer your question through all of history. 8Ma is the highest longevity species I found in a biostratigraphy table. Dinosaurs are faster evolving than crocodilians who have 1/3rd as big a genome as a mouse and 1/6th that of a shark. Adaptive genus existed for 5-30 million years, and well known clades exist for 20-500 Ma.

The most complete geological formations often only cover small spans of history. Generally you will find that paleontologists have few species, and more often groups and genus represented by 10-20 species fragments.

The Hell Creek Formation covers 2 million years of history, and has revealed 400 species, of turtles, dinosaurs, metatherians, mammals, turtles, and a very rich image of life at that time, and 90 percent of the geological time scale is represented by only a fragments of fossils.

So, you won't find a good answer for species, perhaps the best way to find out the longest lived genus (i.e. like a dragonfly, all species are in the same family) is by doing some google tricks:

For genus i can find this:

Plateosaurus 214–204 Ma

Thyreophorans group 199.6–66 Ma

Gryposaurus genus  84-73 Ma

Plesiosaurus genus 199.6–175.6 Ma

Gorgonopsians 265–252 Ma

Dimetrodon 295–272 Ma

Carcharodontosaurus 112-93

Pterosaur 228–66 Ma

Mussaurus : 215–203 Ma

Lesothosaurus : 199–189 Ma

Spinosaurus : 112-93

Kronosaurus genus 125–99 Ma

scorpion 430–0 Ma.

Dragonfly     325–0 Ma

brittle star 499Ma-present

crocodilians 200-0

some shark genus: 100-0

snapping tortoise 100-0

horeshoe crab 455-0

nautilus 488-0

Fossil fields are incomplete, so the HellCreek time period is very well represented with lots of tyranosaurus, and other time periods are incomplete.

Animals with small genotypes Crocodiles and turtles evolve very slowly, and it gives you an idea of evolution speeds prior to the arrival of mammals, who seem can adapt faster than all previous larte animals.

crocodiles have less than 1/3 of the genes of a mouse and a human
tortoises have 2/3rds and so do horseshoe crabs
dragonfly have 1/6th the genome size of a mouse
sharks have twice as big genome


Gene copies vs. gene paralogs - what's the difference?

The general term "copies" has multiple meaning with reference to genes. In diploid organisms for example, we have two copies of each gene (except those on the Y chromosome). However, these copies are called alleles. Copies that are due to duplication are called parlalogs. There is no distance criterion for differentiating copies or parlalogs. Once duplicated, there are two copies. But the consequences of paralogy would depend on differences, so the question is interesting. At the first generation after duplication, if both copies included all of the upstream regulatory elements, it would be hard to identify which of the copies was the original, since they would both be identical. But over time, if one were to evolve a new function or (more likely) accumulate frameshift substitutions, the altered one would be called the paralogous copy (relative to comparisons across species).


Osmosis vs protein-binding in preserving foods through salting

In addition to killing microorganisms, the salt may provide a better environment for some 'beneficial' organisms, and a less beneficial environment for other 'problem' organisms. For instance, in production of kimchi and sauerkraut, salt encourages lactofermentation to the detriment of more harmful bacteria and fungi.


How far is stem cell research from being to generate a new organ?

Sperm can already be generated using stem cells http://blogs.discovermagazine.com/d-brief/2016/02/25/scientists-grow-working-sperm-from-stem-cells/#.V-UADBV94o8
Also, heart, liver and kidney cells as well.
http://www.popsci.com/scientists-grow-transplantable-hearts-with-stem-cells
http://www.ncbi.nlm.nih.gov/pubmed/26458176

Full organs are still far. The main problems are to grow them separately from the rest of the body (embryonic development) and to vascularize them.
One solution is to grow them in other animals http://www.dailymail.co.uk/sciencetech/article-3442818/Growing-human-organs-farm-creatures-takes-step-closer-New-guidelines-allow-research-human-animal-hybrids.html

There are experiments done with some success in using "decellularized" kidneys as a scaffold to "grow" a new kidney by perfusing stem cells into it. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927010/

There are the so-called organoids, very little agglomerates of different organ-specific cells differentiated from stem cells. They are far from being functional organs but it's definitely a start. http://hub4organoids.eu/organoid-technology/

Some labs are experimenting with 3D printing. They use stem cells to derive all the organ-specific cells needed and then they try to rebuild a functional organ by printing cell by cell, layer after layer. http://www.nature.com/nbt/journal/v32/n8/full/nbt.2958.html

Lastly, embryonic stem cells are not strictly needed anymore, they can be substituted (in most of the cases) by iPS that can be derived from many different adult cells (i.e. no embryo is needed).


Source for Specific Models of Birds' Habitat Suitability

A quick google reveals several databases of bird habitats, which appear to be at least somewhat more recent.
I believe that the one closest to what you describe is here (there may not be a single publication but they do have a lot of associated publications on their site). But this climate change geospatial database (with a newer version here) and this more local database may also be helpful.


Our brain doesn't really use cones to detect green light, and detect red light, and detect blue light. Each cone can be excited by many wavelengths; they're just most excited by green, red and blue wavelengths respectively. The brain then uses the different information it receives from all three cones to infer the wavelengths of the light it receives. It doesn't look at the absolute excitation of a cone so much as the relative amounts of excitation different cones get.

So for example, if the brain sees the green cones are very excited and neither the red or blue cones are, the light is green. If the green cones and red cones are equally excited but the blue ones aren't, then the wavelength may correspond to yellow (a wavelength that excites both red and green cones in the same middling way, and blue cones not much at all), or there could be a combination of green and red wavelengths; and in fact both are seen as the same thing by the brain. That's why colors can combine to make other colors.

This is OK insofar as the point isn't to calculate the exact wavelength of incoming light, but to tell the difference between certain wavelength compositions because that provides more information about the world.

So the reason we see white when hit with all wavelengths is the same reason we see any color when hit with any combination of wavelengths.

As for why "color" feels like a single unified perception and not a combination of three numbers, that's a general aspect of perception in general. We don't sense the raw data our brain gathers; we sense how the world is (as guessed at by the brain from the raw data it gathered).

As such, the colors we see aren't even strictly determined by the wavelengths of photons hitting the cones; because colors are a proxy for what the things we see are like, the brain will not only look at the light it receives, but also use its own assumptions about the world (is this thing in shadow, in bright light, mottled light, colored light, near, far...) to guess at what the color "really" is given the wavelengths it has received. This gives us a sense that color is inherent to objects and doesn't depend on lighting conditions, which is generally accurate (an apple's redness is a feature of the chemicals at the surface of its skin, and those don't change with the lighting conditions).

That's where illusions like that of the blue-black or white-gold dress come from: sometimes you get ambiguous stimuli, where the wavelengths hitting the eye could correspond to a black and blue dress in bright light, or they could correspond to a white and gold dress in shadow, and in that case the brain picks one, and you see the dress as the color your brain decided it must be. Except because the stimuli were ambiguous, different brains (or the same brain at different times) will make different guesses, resulting in very different perceptions. But the guessing is actually what happens all the time, it's just that usually the stimuli aren't as ambiguous so all brains agree on their guess, and the guess does correspond to reality, and so the illusion that we perceive the world directly with no filter remains unbroken.


Why don't the apples seeds from grafted trees produce the same kind of apples?

The reason most apples are produced from grafted trees is that apples don't breed true.

In a large number of crops, you have "lines" of crops. Basically, if you breed two plants of the same cultivar together, their offspring are similar enough to both parents that it performs like the parents. The reason for this is that these crop lines have been interbreed with each other for long enough that the population is self consistent, and the important alleles are present in frequencies that mean all progeny are likely to inherit them.

However, the types of apples which are sold commercially are not from these sorts of cultivar lines. Instead, they've been obtained from "sports". That is, the chance production of either a particular hybrid gene set, or sometimes from random mutations that happened on an adult tree of another apple variety. For example, the Granny Smith occurred from a chance seedling which was discovered by Maria Ann Smith.

These apples don't necessarily have "consistent" alleles. For example, it may be heterozygous for certain genes. If you have Aa alleles at one gene, if you self-pollinate the plant, you're going to get a mix of AA, Aa and aa genes in the offspring, the last of these isn't going to be the same phenotype as the parent. Now recognize that this is happening at multiple genes across the entire genome, so there are many chances to get non-parent-like allele combinations. Add to this the issue of co-dominance, where the heterozygote has a different phenotype than either homozygote (that is, BB isn't like Bb), and the chances that an offspring has a gene with a non-parent like allele combination is pretty high.

There's a further complication that some apple varieties like Honeycrisp are self-sterile. Even if Honeycrisp could theoretically breed true, there's no way for it to fertilize itself, meaning that all fertilization events are hybridizations.

Now you can certainly grow apple trees from seed. The planted seed will grow up into an apple tree, but the chances are that the combination of alleles it received by random chance from its parents will not result in an genotype that produces any commecial apple phenotype. Instead, you're likely to get regression to the mean, meaning the apple tree will be like the ancestor of apples - a crab apple, or at least crab apple-like. - But there's a small chance that it will have commercial apple-like properties, which may or may not be like the parent. This is how new apple varieties are formed, after all.

The only way to guarantee that the genotype of an apple tree is close to the parent plant is to propagate it by cloning, and the easiest and cheapest way to clone trees (at least apple trees) is by grafting.

(As a final note, remember that the seeds get their genome from the flowers and the cells which produced the flowers. The genotype of the rootstock - grafted or not grafted - has no bearing on what genes are present in the seeds. You'd have the same issue with apples breeding true even if the parent tree was on its own rootstock.)


Part of the problem is that chromosome is a slippery word. Really it should refer to a single DNA molecule, but since chromosomes came before DNA this sometimes gets a little loose.

This explanation refers to the five Figures in your question as 1-5 from the top.

Figure 1 A pair of homologous chromosomes from a diploid cell  drawn to illustrate their relationship in terms of genes, alleles, centromeres etc. This doesn't really correspond to any biological event. Colour coding is to emphasise that they originated from different parents. I suppose this is what you see in a karyotype.

Figure  2 An homologous pair again, different colours again, but they aren't closely side by side. When each one replicates we end up with pairs of sister chromatids joined at the centromere. These are four homologous chromosomes. At mitosis each of the pairs of sister chromatids will be pulled apart with one chromosome going to each daughter cell. So the daughter cell will end up with a pair of homologous chromosomes, one maternal, one paternal.

Figure 3 is very similar to Figure 2, nothing to add really.

Figure 4 is similar to the right hand half of Figure 2 except that the chromatids are shown not joined at the centromeres. This image is being used to show that recombination can take place between chromatids. This would be during meiosis, but the pairs of sisters would actually  be joined at the centromeres

Figure 5 Up to now the images have been designed to illustrate one chromosome either individually, as an homologous pair or as a pair of sister chromatids. But of course most organisms have more than one chromosome. Leaving aside the X and Y chromosomes your cells have 22 pairs of homologous chromosomes or 44 individual chromosomes. When these replicate the cell  will have 88 chromatids, forming 44 pairs of sisters, corresponding to  22 homologous sets of four.


Are there any creatures that will eat their own limbs or body parts to survive?

What you're describing is actually a well-documented occurrence in individual cells and single-celled organisms. The phenomenon is called autophagy, and Wikipedia has a page about it here. The basic gist is that when cellular components stop functioning or need to be removed for some other reason, the cell essentially digests those components and reuses their parts to make something else. Cells can also consume themselves to prevent the spread of disease or in the case of extreme starvation, when the extra energy might be needed to keep the organism alive.

Self-cannibalism on the macro scale (larger than single cells) is significantly rarer, but it can and does happen. For example, leopard geckos (and maybe some other lizard species? I'm not sure) regularly eat their own shed skin pieces to conserve energy and nutrients. Sea squirts (a type of marine invertebrates) literally digest their own brains as a part of their life cycle, and apparently, some crickets have been known to consume their own wings. Generally, though, unless the limb in question is already damaged and/or rendered unusable, it would be a waste of energy for its owner to consume it, as the energy spent repairing the damage would likely outweigh the energy gained from its consumption in the first place. That is why it's a relatively rare behavior in multicellular organisms.


How are the vitreous humour and aqueous humour of the eye, connected?

Don't be confused by the word "humour": the vitreous body is presented in birth and has very low "exchange" rate of its components, while aqueous is in constant turnover.

Secondly, the vitreous is an organ-like structure and is separated from other eye structures by its membrane, while aqueous is fluid produced by ciliary body processes into the posterior chamber and moves  anteriorly throughout the pupil. Aqueous can move posteriorly in a case of trauma, operations and other non-physiologic states.

ADD (after attachment of the image)

I'd correct some things in the scheme - call Vitreous as Vitreous, not Vitreous humour, change arrow pointing at the ciliary body as on the following image, depict the vitreous body membrane as I did.

In addition learn two terms: Cloquet canal and Berger's space.

Number 9 shows a vitreo-aqueous route which will follow blood, drugs injected to the vitreous (not an only route), etc.


What is the name of the condition where no pacemaker cells are active in the heart for a short-time?

If there are no pacemaker cells active, no muscle contraction will occur. This condition is named asystole. It can be a temporary or definitive condition. Some would call it "extreme bradycardia" in temporary cases, but this is just an euphemism.

Edit:

Ok, so let's try to clear up the confusion a bit. Technically, there is no asystole involved here (not even temporary). This rhythm is regularly irregular (irregular, but has a pattern), while asystole has no pattern by its very nature.

What you are seeing here is not the consequence of low frequency firing from pacemaker cells. The supraventricular extrasystoles (every 3rd QRS complex) are a consequence of early ventricular depolarization not triggered by SA node activity. The P wave that would normally trigger the 3rd complex does in fact occur, but it is synchronous with the abnormal QRS complex, which is why you cannot see it. The compensatory pause is due to lengthening of the hyperpolarized state in pacemaker cells, and is a consequence of the addition of the hidden P wave and the extrasystole in a short time.

In conclusion, this pattern is not the result of delayed pacemaker firing, but of early depolarization of cardiomyocytes by an accessory pacemaker.

I have marked on this strip the maximal time interval of SA node hyperpolarization. Depending on when the P wave hidden in the extrasystole occurs, the real time may be shorter than the above interval.


Does DNA have a phosphate group or phosphoric acid?

The phosphate ion has a negative formal charge and in an acidic solution its appears as a conjugate base of a phosphoric acid. That is the wey the phosphate group found in cells. The nucleotide synthesis can occur de novo or recovery ways. De novo way use phosphoribosyl pyrophosphate, which simple molecules such as amino acid, tetrahydrofolate and carbon dioxide are added.


What bird species is this? (Heron-like waterfowl from China)

I'd go with juvenile striated heron. I ruled out others such as the chinese pond heron because of the spotted wing plumage and slightly different shape of the patch around the eye. The night heron seems to have a more red eye than the striated heron and appears to have a stubbier beak.

Arkive is a good place to see a lot of pictures of birds, this is a good birding site, and otherwise I use generic google searching (e.g. start with "herons china" or "herons asia") - this at least helps narrow down the search quite substantially and is considerably cheaper than having a library of the worlds bird books!


Which sex has higher variance of reproductive rate in modern societies - male or females?

Sperm are cheaper than eggs

According to Bateman's Principle the males of a species are (typically) more able to produce a greater variance in the number of offspring. This is because generally the males can produce many gametes and achieve many matings whereas females are limited by the number of eggs, resources, and time lost to pregnancy. Therefore, just by simple logic, it would appear likely that males have greater variance in mating success (strong/attractive males would be able to mate with many females while weak/unattractive males would have little to no offspring). See Wikipedia for an introduction to Bateman's Principle. Also see this paper about sexual selection and mating success variance.

An Example

An extreme example of higher variance in male mating success is that seen in lekking species. These species form groups of males called leks where females enter and choose mates. Often one/few males will sire the majority of offspring in the next generation. Fallow deer are one lekking species where males have higher mating success variation than expected by chance.

In Humans

Here is a blog post discussing a paper which showed that males have greater reproductive success variance than females in humans. In the paper see table 1 (Vm:Vf column) which indicates the majority, particularly those close to ancestral type lifestyles, have much greater variance in male reproductive success. Only one measured (Finland) is the reverse pattern.


How do you test soil for the nutrients present in it?

Send soil samples to a soil lab (e.g., here).
They will likely use the Mehlich III extractant   method to extract and quantify the nutrients (most importantly the bases such as  Ca, Mg, K, and Na). Will cost less than $25.


Which organism can point us to the evolution of sight?

Which is the least evolved organism that can see?

The term less evolved does not mean anything. Instead one can ask

  Which lineage was the first to evolve the ability to see?

And by "see" of course, I mean detect electromagnetic waves. Seeing does not imply color vision and does not imply accurate vision.

It will be hard to tell really which lineage came up with vision first. But I am sure you'll be interested to know that some cyanobacteria are able to detect electromagnetic waves (reviewed in Nilsson and Colley 2016).


I believe what you are referring to is called 'sympathetic pain,'and the reason you can't find any papers on the subject is because it is not really a well studied concept. That is primarily due to the lack of robustness in the sensation and idiosyncratic nature of the phenomenon. Personally, I'm not too familiar with the concept beyond placebo treatment of patients with such pains.

HOWEVER, I will explain the different types of pains briefly, their biology, and where the pain you have described fits roughly. There are three categories of pain (scientists sometimes argue four, but for our sake let's say three): nociceptive, inflammatory, and neuropathic. Nociceptive pain is the immediate pain reaction you get when you sense something harmful. It's that jerking sensation you get when you touch something hot or you feel something hazardous coming your way. This pain comes from peripheral nerves that link your senses of touch or perception directly to your spinal chord for an immediate knee jerk reaction. Thus, there is no central nervous system (or brain) processing of the pain, just a reaction. You end up feeling the pain more intensely later once the moment has passed. Then inflammatory pain is the pain you get when you cut or bruise yourself, have allergies, stuffy nose, etc. It is the more common and treatable types of pain and is easy to detect. It comes with redness, swelling, and sensitivity to the general area. Biologically your body is stimulating this pain because your inflammatory system is trying to attack any invasive particles or repair damaged sections of the body. There has been much research done in this type of pain (see sources) and is treatable with non-steroidal anti inflammatory drugs (NSAIDs) such as aspirin, Tylenol, etc.

The last type of pain, which is the sympathetic pain falls into, is called neuropathic pain. This pain is more abstract and is often described as constant and idiosyncratic (non standard intervals). In research it is often modeled by inducing diabetes and doing damage to the nerves to cause constant pain signals to the brain. However, the method is controversial in both practice and in efficiency of modeling. This because there are often many different biological ways to induce cognitive pain and it is primarily central nervous system based (aka in the brain), whereas this type of pain is specifically induced by nerve damage (hence neuropathic). This type of pain is often tested using cognitive based test parameters to see if a drug can relieve some of the mental struggles either caused by the pain or causing the pain. There are also such cells called "mirror neurons" that fire when you sense (visual, audio, touch) something and then cause a similar behavior or sensation to occur within the person. It is possible that seeing or feeling someone else's pain causes these mirror neurons to fire for certain people, perhaps due to associate learning or a memory that person has that reminds them of pain they once had. I've attached some literature on the subject for your leisure, but it is a poorly understood science that we are trying to grasp in modern research. Hopefully that answered your question!

Sources

The Principles of Neuroscience by: Kandel, Schwartz, Jessel, Siegelbaum, and Hudspeth (most indepth source)
Pyschopharmacology by Meyer and Quezer
From Mice to Men: Jacqueline Crawley
Pathology Based Pain
Inflammatory Pain Review
Neuropathic Pain Review
Mirror Neurons


Can someone identify this bird? It looks like it has a few deformities

It's an anhinga, as@kmm commented. There's nothing wrong with it; it's not deformed in any visible (to me) way. They spread their wings to dry, as they are darting birds that do not float on the surface of the water, but beneath it.

Here's one drying itself on a turtle.


Why are sugars like mannose expressed on the outside of eukaryotic cell membranes?

The “positive aspect” or reasons why the surfaces of eukaryotic cells contain sugars are various. Major ones appear to be cell adhesion and cell–cell interaction.

In fact, the variation of the sugars in certain cell-surface antigens (blood group antigens and histocompatibility antigens may represent the kind of evolutionary response to infectious agents mentioned in the question. The situation with the major histocompatibility antigen is complex, but variation in blood group antigens is thought to be a response to the malaria parasite — reviewed by Cooling.


Does size correlate with sensory abilities?

Size is not likely to have anything to do with sensory acuity. A simple example can be seen in the fact that rodents have much more sensitive sense of smell than humans, and some birds have much sharper visual senses than humans. It has much more to do with the number of olfactory/light sensors, sensory pathways to the brain and how that information is processed by the brain (i.e how much priority is assigned). Sensory organ size per se is less relevant (think of elephant ears).


There are several nucleotide sequence datbases available. One of the largest is the NCBI GenBank at http://www.ncbi.nlm.nih.gov/genbank/

You may use the search bar at the top to search for nucleotide sequences belonging to a certain organism or gene. For example, searching for "E coli" will give you the full genome sequences for several bacterial species, with a strain of E. coli as the top result. The E. coli genome is about 5 MB large. If you want a single gene sequence, searching for "sonic hedgehog" (without quotes) will return the human hedgehog gene as the top result, which is 1,481 basepairs long.

To get a sequence in raw format, select "FASTA" below the entry. At the page you get sent to  , chose "send" in the upper right corner and under "Choose destination", "file". This will give you a .fasta file, the standard raw sequence format. The first line, starting with ">" will be metadata, while the rest of the file consists of the nucleotide letters only.

Note that in addition to a,t,g and c, you may also find other characters, most often "n". These characters describe ambiguity in the sequence (meaning that the nucleotide at that position could not be determined). For a full description of the FASTA format sequence representation, see http://en.wikipedia.org/wiki/FASTA_format#Sequence_representation


So, I've looked a bit into this and the way you want to do your analysis won't work as you planned it. The main reason for this is that the GO database does not contain any virus species (as fas as I could see). The existence of the species you want to analyse in the database is important, because you need to have a background or reference gene set in order to perform enrichment analysis. Even if you're just interested in the IDs and want to perform the analysis by yourself, this means that you're unlikely to find anything for your genes/proteins in the GO databases.

Your best alternative is to use other annotation databases and either rely on their annotation or map their annotation to GO term ids (here is a list of all databases that allow this).

Your best bet for this is probably the UniProt database, since that should have entries for most of your proteins (though not all will have annotated GO terms). UniProt also offers an ID mapping tool that should be able to convert your RefSeq IDs to uniprot IDs, and also comes with an API for python. Do note that some of your IDs (the YP_ ones) are provisional RefSeq entries and the webpage tool only finds them in the 'UniParc' database (not UniProt KB).

Once you have the the UniProt IDs you should be able to map the available GO terms from there (see the last entries of the first link above).


Mysterious spherical mass of feathers (Reddit)

This is a flap of feathered skin from a Mallard, birds do not shed their skin. The bird in question is likely dead or at the very least, severely injured.

The skin and curved feathers has curled up around itself into a "ball". As it's flattened/separated you can see there is reddish skin with some tissue on it the maggots have gathered on. The feathers here are relatively small and curved and the pattern is SPOT ON for the breast/belly feathers of a Mallard.

While it's not really obvious in the photo of the Mallard below, it is very common for them to have that little bit of pale edging on the dark reddish-brown feathers, as seen in the first photo.

Photo by Jo Garbutt (Flickr: https://flic.kr/p/jVbHwP )


It would be right if there were no recombination (see also crossing over) and no new mutations. However, there are crossover and there are mutations and hence the calculation is wrong.

Segregation

You have solved this problem yourself. You assumed that chromosomes segregate perfectly independently which is a rather sound assumption. The probability is $\frac{1}{2^{46}}$

Recombination

Assuming a genome-wide recombination rate of 22.8 (Wang et al. 2012) and assuming that the number of recombination is Poisson distributed, then the probability of no recombination is $e^{-22.8} ≈ 1.25\cdot 10^{-10}$.

Multiply this number by $\frac{1}{2^{46}}$ and you get about $1.8 \cdot 10^{-24}$. I would note however, that the assumption that the number of crossover is Poisson distributed might not hold (even if it is how it is typically modelled)

Mutation

Now assuming a genome-wide mutation rate of 45 (Rhabari et al. 2016), and assuming that the number of mutations is Poisson distributed, then the probability of no mutation to happen is $e^{-45} ≈ 2.9 \cdot 10^{-20}$.

Hence the probability becomes $\frac{1}{2^{46}} \cdot e^{-22.8} \cdot e^{-45} ≈ 10^{-44}$.

Note that we assumed that the number of mutations and the number of crossovers are independent which is definitely wrong. If we were to know the correlation, we could make better estimates. This would bring our estimate to some higher probability.


How might gene clusters like the lac operon evolve?

Operons, often but not always, contain clusters of genes (under the control of an operator region) which are involved in the same metabolic pathway. There have been several theories for how these groups of genes have arisen but the current feeling seems to be based around the regulation of the genes in question 1. To facilitate co-ordinated gene regulation there may have been strong selection for physical clustering of genes involved in a particular process. By being physically clustered this also means that all the genes within a given operon are probably subject to the same chromatin remodelling and will then be more easily switched on and off under the appropriate conditions i.e. all turned on when they are needed and switched off when they are not.

Operons with similarly arranged genes have been found in different micro-organisms, leading to the thought that the operon was an ancient and evolutionarily conserved arrangement [2]. The figure below from Fani et al. 2005 presents two possible ways of generating the current state of genome organisation for present day proteobacteria.

If the operon is an ancient arrangement we would predict high gene conservation within operons; but genome analysis of different micro-organisms shows this not to be the case (i.e. gene conservation is low and operons are pretty unstable). Accordingly, another author suggests that due to the lack of conservation, operon structure is pretty plastic and can change readily during evolution [3]. Indeed, Fari et al conclude in their paper that the histidine biosynthesis operon has been a construction or re-construction event from scattered genes and not from the descent of an ancient arrangement:

  Our model suggests that the his gene organization in the extant proteobacteria arose from a gene scattering in the genome of the proteobacterial ancestor. The model also predicts that all or most of the his genes (except for hisD) were monofunctional and that they underwent a progressive clustering and compacting which occurred together with gene overlapping and fusion events

They found, as you suggested, evidence for several gene modifications which included elongation, duplication and gene fusions. As for what caused the progressive clustering, see reference 1 again.

Obviously different operons are probably going to have formed in different ways in different organisms and I don't think we can rule out the 'ancient arrangement' argument completely. It's a pretty broad and confusing topic and there's a lot of literature, I hope the examples I picked and have listed are useful!

1 Osbourn, A. and Field, B. Operons. Cell. Mol. Life Sci. (2009) 66:3755–3775

[2] Fani et al. The Origin and Evolution of Operons: The Piecewise Building of theProteobacterial Histidine Operon. J Mol Evol (2005) 60:378–390

[3] Itoh et al. Evolutionary instability of operon structures disclosed by sequence comparisons of complete microbial genomes. Mol Biol Evol (1999) 16(3):332–346


Why is binding energy the difference between ∆G catalyzed and ∆G uncatalyzed?

There's two binding energies in your diagram, and it's the difference between them that's the critical point in understanding enzyme catalysis and the difference between $\Delta G$ catalyzed and $\Delta G$ uncatalyzed?

$\Delta G^R_{bind}$ is the binding energy of the enzyme-substrate complex. That is, it's the difference between the energy of the apo-enzyme and substrate in the non-bound form ("$E+S$") and the enzyme and substrate in the bound form ("$ES$").

The other binding energy is $\Delta G^T_{bind}$. This is the (theoretical) binding energy of the transition state. That is, it's the energy difference between the enzyme-transition state complex (here labeled "$T_{uncat}$", for some reason; it probably should be "$ET_{cat}$") and the apo-enzyme and the unbound transition state ("$E+T_{uncat}$").

Now remember that free energy is a state function. A free energy change ($\Delta G$) is simply the difference between the free energies of the starting state and the ending state - it doesn't depend on the path you take to get there. (The absolute free energies of any given state are unmeasurable, but you can infer information about relative free energies by measuring the $\Delta G$ of transitions between them.)

The two equations at the bottom are derivable from this definition of free energies as a state function. You know that the free energy difference between the $ES$ and the $E+T_{uncat}$ state is the same regardless of the path you take. So if you go first through $ES$ the free energy change ( $- \Delta G_{bind}^R  + \Delta G_{uncat}^\ddagger$) will be equal to that if you go through "$T_{uncat}$" ($\Delta G_{cat}^\ddagger - \Delta G_{bind}^T$) - you don't necessarily need to have physically realizable reactions for the state function property to hold. The second equation is then simply a rearrangement of the first.

In looking at the rate of catalysis, you're primarily interested in how big a free energy change it is to the relevant transition state from the previous state. (This is a basic principle of Transition State Theory.) To speed things up, the enzyme needs to make that energy change smaller - that is, to make $\Delta G_{cat}^\ddagger$ smaller than $\Delta G_{uncat}^\ddagger$. If the enzyme binds the substrate and the transition state equally well, $\Delta G_{bind}^R$ and $\Delta G_{bind}^T$ are the same, and $ES$ and "$T_{uncat}$" are lowered by the same amount, such that $\Delta G_{cat}^\ddagger$ and $\Delta G_{uncat}^\ddagger$ are equal: no catalysis.

But if instead $\Delta G_{bind}^T$ is greater than $\Delta G_{bind}^R$, then the "$T_{uncat}$" state is lowered more than the $ES$ state, making the gap between them ($\Delta G_{cat}^\ddagger$) smaller than the gap between $E+S$ and $E+T_{uncat}$ ($\Delta G_{uncat}^\ddagger$): the enzyme thus speeds up the reaction. This is what that second equation is saying.

This sort of thermodynamic analysis is what leads to the "transition state stabilization" hypothesis of how enzymes work: enzymes speed up reactions because they bind to the transition state more tightly than the substrates or the products.

(P.S. You may be wondering why we have the enzyme hanging around in the uncatalyzed reactions. This is simply a bookkeeping measure to make sure we're using the same reference state for the very start of the reaction ($E+S$). In the uncatalyzed reaction the enzyme doesn't change, and so doesn't really contribute to any free energy change.)


Why does scraped knee hurt more in hot water than cold water.

2 reasons. The first (as anongoodnurse mentioned) is that cold temperatures temporarily knock out dermal surface nerves (in the winter you can verify that your face goes numb after a while outside).

The other reason is that a knee scrape produces inflammation (swelling and increased temperature). Cold water (or anything cold) counters these: stopping the inflammation temperature increase, then freezing out enzymes and proteins needed for inflammation and causing them to slow down or malfunction.


Why does a stomach come before the gizzard in birds?

The gizzard appears to be a structure that bird inherited from a distant ancestor, as the structure is found in dinosaurs (which birds are derived from) and crocodilians.  https://en.wikipedia.org/wiki/Gastrolith

As to why, the bird gizzard is not in a better position, (like say the grasshopper gizzard which is located in front of its stomach), the best reply I think off is evolution is blind.  The innovations that appear, are random and further constrained by the features that the animal already has.

It is probably the same reason why rabbit eat their own poop to better digest their food, even though cows have evolved a four chamber stomach to handle the same problem of digesting grass. Or why no animal has evolved a second set limbs to fly even though it would be super useful to keep arms to catch prey and not sacrifice said arms to be made into wings.

In a sense these questions of why didn't evolution design it better is evidence that the concept of intelligent design is rubbish. Designs in animals (and bacteria) can be really really dumb.


Why do cockroaches burst from soapy water?

As far as I am aware, cockroaches don't burst from being sprayed with soapy water (water + some liquid dish detergent). We previously had many cockroaches in our apartment (some came back after a year of nothing!), and we regularly sprayed the cockroaches with soapy water plus some vineger (more as a disinfectant/cleaner) and they never burst. We've killed at least 30 using this method.

Having said that, what you likely witnessed was the egg sacs dislodging from the back of the female cockroach. As you didn't mention what species of cockroach you were dealing with, I am assuming you had German cockroaches as they seem to be the most common type in non-tropical/hot areas.

According to a number of biology sites, German cockroaches are particularly difficult to control and eradicate is because they carry their egg sacs with them until they are ready to hatch. At which point they drop the sac.

If you are able to catch a few that seem especially big, you will notice that they have a sac at their back.

If you don't have German cockroaches, I have not idea why they would burst...


What happens to drug metabolism when CYP450 enzymes are presented with two substrates

I think the OP is asking the following:

  If an enzyme is not specific one substrate, but is simultaneously presented with a pair of substrates, which one 'wins' and how do we decide?

For example, if an enzyme is presented with a racemate such that the D-form has a 10-fold lower $K_m$ than the L-form, but the L-form has a 5-fold higher $k_{cat}$, which one is preferentially metabolized, and how do we decide?

It was Fersht who first provided the definitive answer, at least for single-substrate enzymes (Fersht, Enzyme Structure and Mechanism, 1977; see also here)

  The kinetic parameter determining the specificity for competing substrates is neither $K_m$ nor $k_{cat}$, but the (so-called) specificity constant: $$\frac{k_{cat}}{K_m}$$

If it assumed that both substrates, considered in isolation, obey the Michaelis-Menten kinetics, then it is very easy to derive (starting with the ratio of the respective Michaelis-Menten equations) the following expression for the initial velocities when both substrates are present simultaneously.

$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{cat}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{k_{cat}^2}}} \ \ \ \ \ (1)$$

(The equation is derived by, among others, Cornish-Bowden (2004, pp 36-39):

If $V_{max}$ is preferred to $k_{cat}$:
 $$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{V_{max}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{V_{max}^2}}} \ \ \ \ \ (2)$$

${{k_{cat}}}\over{K_m}$ has units of a second-order rate constant and, giving it a symbol (${k_{1}^{\prime}}$ for $S_1$ and ${k_{2}^{\prime}}$ for $S_2$) to reflect its status as a fundamental kinetic constant and not just a ratio, allows the following equation to be written:

$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{1}^{\prime}}}\over[S_1]}}  \times{{{[S_2]}\over{k_{2}^{\prime}}}} \ \ \ \ \ (3)$$

This equation provides the answer to the OP question. For the racemate described above, we need only calculate the ratio of the specificity constants to get the answer:

$${
    {
     {
      {v_{i}^{D_{form}}
     }
     }\over{
             v_{i}^{L_{form}}}
            }
    }   =
{
    {
     {
      {k_{D_{form}}^{\prime}\times{[D_{form}]}
     }
     }\over{
             k_{L_{form}}^{\prime}}\times{[L_{form}]}
            }
    } = {
    {
     {
      {k_{D_{form}}^{\prime}
     }
     }\over{
             k_{L_{form}}^{\prime}}
            }
    } =  2 \ \ \ \ \ (4)$$

Much could be written about the specificity constant (diffusion control, enzyme 'perfection', Haldane relationships), but I'll make just one. Considering the single-substrate Michaelis-Menten enzyme, the following holds AT ALL SUBSTRATE CONCENTRATIONS

$$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}][E]}   \ \ \ \ \ (5)$$

When $S_o$ is very low, $[E]$ = $e_o$ (approx) and the following may be written (where,unlike $[E]$, $e_o$ is usually known or may be determined)
 $$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}]e_o}   \ \ \ \ \ (6)$$

  But it is Eqn (5) that is the important one: $k^{\prime}$ (the so-called specificity constant) may be thought of as the second-order rate constant governing the combination of ('free') enzyme with substrate at all substrate concentrations, not just when $S_o$ << $K_m$

Much could be written about this as well

Definitions

I think it is reasonably obvious what everything means. Nevertheless, here is a list:

$K_{m}^1$  is the Michaelis Constant for substrate 1
$K_{m}^2$  is the Michaelis Constant for substrate 2
$k_{cat}^1 $ is catalytic constant for substrate 1
$k_{cat}^2 $ is the catalytic for substrate 2
$V_{max}^1 $ is the maximum velocity for substrate 1
$V_{max}^2 $ is the maximum velocity for substrate 2
$k_{1}^{\prime} $ is the specificity constant for substrate 1
$k_{2}^{\prime} $ is the specificity constant for substrate 2
$v_{i}^{1} $ is the initial velocity due to substrate 1
$v_{i}^{2} $ is the initial velocity due to substrate 2

Reference

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press (London)


Why are successful human rock climbers so dissimilar to Hominidae primates who spend extended time periods climbing?

As a rock-climber myself I’ll attempt to answer:  The selection criteria for competitive rock-climbing is exclusively based on sustain non-resting, extremely challenging moves up a rock-face.  The two most challenging aspects are 1) ability to ‘crimp’ (climbing term) on micro-holds without slipping and 2) being able to keep that up without resting throughout the climb.  I personally have a real problem with the later, because of my weight.

Primates selection criteria is not isolated to non-resting climbs.  They don’t get penalized for sitting on the branch.


allogeneic organ transplant and the immune response

The situation is just as you'd imagine. In an immunocompetant recipient, a host-versus-graft reaction occurs. This is called transplant rejection. Single episodes (acute rejection) are easy to treat and rarely lead to organ failure. Chronic rejection is the leading cause of organ transplant failure. The organ slowly loses its function and symptoms start to appear. This type of rejection cannot be effectively treated with immunosuppressants. Some people may need another transplant.[1]

In bone marrow and other transplants, T cells in the allografts reconstitute T-cell immunity in the recipient. Unfortunately, these T cells recognize the recipient as 'non-self' and employ a wide range of immune mechanisms to attack recipient tissues in a process known as graft-versus-host disease (GVHD).[2]

  Acute GVHD describes a distinctive syndrome of dermatitis, hepatitis, and enteritis developing within 100 days after allogeneic hematopoietic-cell transplantation (HCT). Chronic GVHD describes a more diverse syndrome developing after day 100. In addition to allogeneic HCT, procedures associated with high risk of GVHD include transplantation of solid organs containing lymphoid tissue and transfusion of unirradiated blood products.[3]

GVHD is increasing due to the increasing number of allogeneic hematopoietic cell transplantations (HCT). More than 25,000 allogeneic transplantations performed annually. Given current trends, the number of transplants from unrelated donors is expected to double within the next five years, significantly increasing the population of patients with GVHD.[4] Yet the major complication, GVHD, remains lethal and limits the use of this important therapy.

Long-term immunosuppressants are usually the treatment regimen for chronic GVHD. Fungal, bacterial, and viral infections are a major risk with this treatment since the immune system will be suppressed for a very long time.[5]

[1] Transplant rejection
[2] Graft-versus-host disease
[3] Graft Versus Host Disease
[4] Graft-versus-Host Disease
[5] Graft vs Host Disease: An Overview in Bone Marrow Transplant


How to get conservation of vaccine candidates between hundreds of bacterial strains?

This website will allow you to blast all sequenced microbial genomes:
http://www.ncbi.nlm.nih.gov/sutils/genom_table.cgi

Recovering the full gene sequence might be a bit of a hassle, since BLAST will only allow you to recover the region that matched your query. You may need to set up your own pipeline for this. You may also be able to identify a "protein family" or "cluster of orthologous genes" using the BLAST results.

Once you have the full sequence, you can perform a multiple sequence alignment with CLUSTAL, Muscle, or another program. This will help you to identify the conserved regions.


Can I use grayscale images when working with ImageJ?

There is no evidence that one is better than the other, most likely because it differs from case to case. Neither you, nor your critics, are right. There is a tiny bit of science in a paper on digitizing blots, generalizing from blots of a specific protein (PMID: 19517440), and they use grayscale for no given reason. Come to think, that is the best paper in the field of immunoblot quantification., and it still lacks evidence.

Immunoblot is semiquantitative, meaning it may sort and order bands (and protein amounts), but it fails often at estimating differences and ratios, and may even fail to see differences. Just try your best to find a difference, in the knowledge that if there is no difference in protein amounts, any fiddling with contrast won't create a difference in bands quantitation.

There is almost no difference between color and black-and-white digitized images of an immunoblot. The parts of the blot that are black will still appear in the computer as White = 0, even though a tri-color image file will detail it to Red = 0, Green = 0, Blue = 0. The parts that are nearly black will still be very close to zero.

The only thing that changes a lot between RGB and color is the background.  The background may change, for example, from White = 200, to Red = 190, Green = 190, Blue = 220. There is one consequence of such switching between values for background. (These changes may be induced by switching between grayscale and RGB, but also by altering exposure time etc.) When you use a method where the background gets too close to the blots, the "amplitude" of the blots, the height of the peaks in ImageJ, will be reduced. This loss of contrast should wash out some of the differences between blot bands and lessen support for differences between bands (i.e., for the alternative hypothesis), making you miss a genuine protein difference.

Again, if your blot bands are different enough so that your percent increase / decrease is huge, and your p value is small, you are all set, regardless of the method you chose. Ask your critics to explain your observed differences other than by differences in protein. But if your quantification fails the p test, I think it will be a honest effort, to change the color from grayscale to RGB, or the other way around, just in case your first choice had been the one that dampens contrast.


Those are springtails. Order Collembola. You can find yours here on BugGuide. https://bugguide.net/node/view/258362


If a "parasite" is growing on a dead part of the host or on a completely dead host, does it still count as a parasite?

In parasitic interactions, one species (the parasite) benefits from the interaction while the other (the host) is harmed. So, whether an interaction is parasitic or not really depends on whether on the host species is harmed by the interaction. If something only grows on the dead remains of another organism, but causes no harm to living organisms in terms of growth and reproduction, it would not be a parasite, and might actually be beneficial to that organisms in some ways.
However, dead cells or tissues are not always useless to a still living organism. For example, the vast majority of cells in a mature tree are dead, but are still important for the survival of that tree by providing structure and water/nutrient transport. A hypothetical parasite could feed only on the dead cells inside of a tree and still cause harm to that tree by weakening it's trunk or impairing it's ability to transport water and other nutrients.
Not knowing much about fungal physiology myself, I can't say whether these "hyperparasites" are truly parasitic or not. But it is at least feasible for a parasite to only grow on the dead portions of a host and still cause it harm.


Are all emerging viral diseases of the past 100 years zoonoses?

To my knowledge, yes. A partial list of recently emerged/emerging viral diseases (I certainly could have missed some), with probable reservoir hosts:

Chikungunya* (birds, rodents)
coronaviruses (SARS [bats], MERS [camels], COVID-19 [?? bats ?? pangolins ??])
Ebola and other filoviruses (Marburg): (bats?)
Hendra, Nipah (bats)
Ross river virus* (various mammals)
HIV (primates)
influenza (H1N1, avian) (birds/pigs)
monkeypox (monkeys, duh; also rodents)
West Nile virus* (birds)
Zika* (? "a wide range of animals in West Africa")

Starred examples are vector-borne (so perhaps of slightly lower concern - might not fit your criterion of "capable of causing a global pandemic").

Omitted:

older zoonotic viruses (rabies, dengue, hepatitis, ...)
non-viral zoonoses (malaria, plague, anthrax)

A list of zoonoses; another from US CDC

More generally, the only other place an emerging virus could come from would be from mutation or recombination of existing human viruses. I'm not aware of such an example.


What are the odds of being an albino human and have Down syndrome?

It is correct if (and only if) albinism and Down syndrome are independent events, that is, if albino people is not more nor less likely to have Down syndrome than non albino people (and vice-versa).

However, doing a quick Google search I can't find any source relating albinism and Down syndrome, and therefore independence seems a reasonable assumption unless more information arises and your numbers are right - at least, as right as the sources you are based in.

But beware that your sources are not very representative of what you want to get, or at least not very consistent:

Your source for albinism (and its reference) gives prevalence, that is, number of albino people in the whole population of living people in Europe and USA. Please notice that proportion in living population may differ from proportion of births since albino people may have a different life expectancy.
Your source for Down syndrome gives a "baseline probability" for a given mother age (young) in some unspecified country. For older ages, probability becames larger.

Then, "the chance of giving birth to a child that has both albino and down syndrome" may differ from that you calculated, specially if you want to use it in circumstances that differ from those your data came from.

Anyway, if you just want a rough estimate, you can use your numbers.


Cytogenetic map notation uses the following form:
A[p/q]BC.D
Where A is the chromosome number, p is the petit / short arm, q is the queue / long arm, B is the band, C is the sub-band, and D is the sub-sub-band.
So, 21q21.1-q21.2 designates a region on the long arm of chromosome 21, band 2, sub-band 1, between sub-sub-bands 1 and 2.
Source:  NCBI Genetics Review (archived version)


Are there multiple meanings to "clone" as in "clone a gene"?

"Cloning a gene" also just means making tons of copies of it, like in PCR, so you can sequence it