I was reading "Adventures among Ants", by Mark Moffett, to see if he said something about the length of the trails of Argentine ants and I was about to give up and give a general answer based on the other information about Argentine ants in the book, when I hit upon this quote by "Physicist turned biologist Jean-louis Deneubourg":

  The Argentine ants' exploratory behavior is exceptional in that they mark continually and explore collectively. Whereas other recruitment trails are constructed between two points (e.g., nest and food), their exploratory trails have no known destination, progressively advancing into the unknown. They rapidly lead new explorers to the frontier between the just explored and the about to be explored zones, avoiding situations where ants will end up exploring the same zone twice, and help returning explorers reach the next directly. A wide corridor of the chemically unmarked area is thus systematically "swept' and marked in a minimum time with maximum economy.

The things to know about Argentine ants are, they form supercolonies in which all ants from the same supercolony can mingle indifferently, regardless of the nest they are from. There is no theoretical limit on the size of such a supercolony; if there is one, it is over thousands of kilometers:

  The largest [Argentine ant supercolony] extends from Italy to Spain's Atlantic coast, a distance approaching 2,000 kilometers

This means that the length of an Argentine ant trail is definitely not limited by ant exhaustion or chemical evaporation, depending on what we mean by "trail". If interconnected trails can be counted as a single one you could theoretically have a 2000-km Argentine ant trail that is maintained by ants all along its length. In practice the trail lengths are probably still limited, but by their purpose instead of hard physical limitations. The Deneubourg quote says recruitment trails are built between two specific points, such as a nest and food: this example clearly implies a distance limited by nest density (the trail between a nest and food will be from the nest closest to the food, so if nests are all 10m apart the length of the trail will be 5m at most). This would be true of any trail that has a nest as an endpoint, and what other kind are there?

He also says exploratory trails have no fixed destination, but that doesn't mean they cover unlimited distance either: the exploratory front as described clearly moves forward gradually and deliberately, and as Argentine ants are constantly building nests within the territory of the colony, the exploration front will always be a certain limited distance from the nearest nest.

Then again we could also argue that nest density is itself determined by a physical limit on maximum trail length, which could indeed be ant exhaustion (or ant loss of efficiency at least), risk of the trail being perturbed, chemical evaporation (as in, a longer trail would need more ants to maintain it), etc. I can't speak to that.

Trying to find numbers on Argentine ant nest density I fell upon this paper, which gives more information about ant colony structure and gives the closest thing I think you will find to a definite answer to your question:

Nest connectivity and colony structure in unicolonial Argentine ants

  In experiments using labeled food, and in a 3-year census of nests and trails, we found that food was shared and nests were linked by trails at distances up to 50 meters.

Note that this is "path distance", i.e. the length of interconnected sets of trails. I couldn't find statements on a single trail, but they show a figure and the longest trail on it is between nests that are about 12m apart.

As an aside, this very interesting paper breaks up the "supercolony" concept a bit; while supercolonies are defined by seeing which ants will attack one another, meaning you can legitimately drop an ant from one end of the colony into the other end and it will go to work unmolested as if it were home, the authors of this paper looked at actual worker movement and food sharing, and found that

  Argentine ant populations do not function ecologically as single, large supercolonies, but instead as mosaics of smaller, distinct colonies consisting of groups of interacting nests.

It also says the distribution pattern of nests is seasonal (Argentine ants have very ephemeral nests to begin with); this could give some clue as to what determines nest density and whether physical limits on trail length play a role.


Why does the sweat of children not smell like adults?

There are two types of sweat glands: (1) eccrine sweat glands and (2) apocrine sweat glands.

Eccrine sweat glands are present from birth in humans and secrete sweat that is mostly water and functions in evaporative cooling.
Apocrine sweat glands are found in the armpits and groin regions and become active in humans at puberty (although the distribution appears to be broader fetally). These sweat glands secrete an oily substance containing lipids and proteins that through interactions with bacteria on the skin (e.g., bacteria digesting lipids), lead to the "smelliness" of adults (including body odor).

So it's not really the sweat that smells, it's the action of bacteria on apocrine sweat that becomes prevalent after puberty.


Why can't our eyes smoothly transition from side to side without focusing on a moving object?

Short answer
Smooth pursuit is driven by retinal slip, which is determined by external input registered peripherally in the retina.
Background
The smooth pursuit system is a system designed to minimize retinal slip, i.e., the movement of an image across the retina. Saccades are rapid eye movements meant to fixate quickly on a new target (Purves et al., 2001).
Both movements are readily apparent when sitting in a train and staring outside; the eyes focus on a distant object and pursue that object. Once it exits the field of view, the eyes target a new object via a saccade and smooth pursuit is again initiated (the train window phenomenon).
Saccades can be triggered both involuntary (due to a sudden, unexpected stimulus) and voluntarily (Walker et al., 2000).
The smooth pursuit system cannot be voluntarily controlled, barred in some highly trained observers (Purves et al., 2001). Instead, it is guided by eye movements dependent on the movement (slip) of the fixated target on the fovea (Thier & Uwe, 2005). Hence, this system is controlled by external stimuli, not by internal ones. Retinal slip can of course be voluntarily manipulated by moving the eyes away from the target, for example by moving the head. The smooth pursuit system detects this by registering retinal slip, and keeps the eyes fixated on the target, through smooth pursuit which is involuntary.
References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)
- Thier & Uwe, Curr Opinion Neurobiol (2005); 15: 645–52
- Walker et al., Exp Brain Res (2000); 130: 540–4


What does it mean when you "extract the filtrate with ethyl acetate three times?"

This procedure is referring to chemical extraction, which is a separation process used in chemistry (and biochemistry) to isolate compounds of interest by using two immiscible phases in which the compound of interest has differential solubility.

For example, in a liquid-liquid extraction, often one of the phases contains a polar solvent like water, and the other phase contains a nonpolar solvent like oil. Water and oil won't mix, but after stirring them together and waiting some time, the more polar molecules in solution will tend to concentrate in the water, and the less polar molecules will tend to concentrate in the oil. Because the phases are immiscible, it is relatively straightforward to separate them once equilibrium has been reached.

Ethyl acetate is a fairly non-polar molecule often used in organic extractions. In the process that you described, the result will be that non-polar contents of the fermentation broth will be extracted into the ethyl acetate, and hydrophilic contents will remain in the aqueous phase.

Because this process is never 100% efficient (the efficiency will depend on the concentrations of the solutes and relative affinity for the two phases), it is often repeated several times to improve the extraction.


Cancer is caused by the mutations in cells.

Cancer exists because of the failure of cell cycle checks which could actually allow cells to survive with erratic genomes. However, that alone does not cause cancer.

Cancer is the uncontrolled proliferation of cells. That only happens when cells have accumulated enough errors during cell division and each cell division goes undetected to the point that cells refuse to commit apoptosis; they are no longer receptive to the body's control mechanisms.

Cancer cells are also malignant. That means that cancer cells cannot be called cancer cells until they are invasive. That means a few cancerous cells cannot be caused cancer because they don't take nutrients from the body . Also, tumour  suppressor  genes can also cause cancer when they turn proto-oncogenes into oncogenes.


How do Gram + bacteria use a proton gradient for F-type ATPase?

Protons are pumped out of the bacterial cell by the electron tansport chain. This creates a protonmotive force with two components, one due to the difference in proton concentration, the other due to the membrane potential that is created. In bacteria and mitochondria it is the membrane potential component that provides most of the driving force to pull protons back in through the ATP synthase. Thus the fate of the protons outside the cell doesn't matter too much. Even if you were to buffer the exterior absolutely, the fact that charge had moved out would drive ATP synthesis.


Why arent mosquitoes found near neem trees?

The growing accumulation of experience demonstrates that neem products work by intervening at several stages of an insect's life. The ingredients from this tree approximate the shape and structure of hormones vital to the lives of insects (not to mention some other invertebrates and even some microbes). The bodies of these insects absorb the neem compounds as if they were the real hormones, but this only blocks their endocrine systems. The resulting deep-seated behavioral and physiological aberrations leave the insects so confused in brain and body that they cannot reproduce and their populations plummet.

In case of a regular (house) mosquito, the effects of neem are as follows:
1. Retardation of growth
2. Inhibition of feeding
3. Eggs are unable to hatch

Apart from this, larvae of a number of mosquito species are sensitive to neem. They stop feeding (as mentioned above) and die within 24 hours after treatment.

Studies regarding your question are still in process so it's hard to narrow down to one exact reason.

Sources referred: The National Academies Press


Can parents' learned traits be transmitted genetically?

Strictly speaking no. There are ideas about cultural inheritance though that seem relevant here: see http://www.ncbi.nlm.nih.gov/pubmed/11425279.  Cultural inheritance theory uses the plasticity of the human brain as the evidence for the underlying genetics of culture.  I.e. we aren't born with the ability to speak English because our parents learned it but we have an the underlying brain structure that is controlled by genetics to learn cultural traits.  It seems far more likely that the phenomenon you describe with holocaust survivors is more related to some environmental effects (from their parents) than anything genetic.  In the comments stress hormones in pregnant mothers were mentioned.  Any impact these have on the offspring are not truly "genetic", they're termed "maternal effects" in the evolution literature.  In fact most selection studies go to great lengths to control for them or eliminate them.  They aren't truly genetic because these traits would never get passed down to the grandoffspring of the original mother.


Is it possible to grow E. coli K12 with algal amino acids as the sole carbon source?

E.coli can do that and in fact does this a lot in a commonly used bacterial medium: The popular LB Medium. This is composed of three components:

Tryptone, a peptide mix made by digesting milk casein with the peptidase Trypsin (10g/l)
Yeast extract, made by autolysis of the cells (5g/l)
Sodium chloride (10g/l)

The original formulation of Bertani from 1951 (see reference 1) also contains 1g/l Glucose, which was later discarded, since the handling is easier without it (glucose cannot be autoclaved as it degrades).

Since the medium does not contain any other utilizable sugars as a carbon source, the bacteria use free amino acids (and small peptides up to 650 Da in size) for their growth. The reason for this limit is the exclusion size of the bacterial porin channels which allows the uptake of the peptides and free amino acids (see reference 2 for details).

Once these are exhausted, the growth stops, which is the reason why LB Medium is actually not very good suited to get really high densities (that's why SOC media are used for some applications). Read the excellent paper in reference 3 and the also excellent article in reference 4 if you want to know more about the topic.

I don't think it matters from which source your amino acids are coming. Regarding the concentration I haven't found any data, but in reference 4 it is estimated that only about 25% can be used by the bacteria. Since the mixture contains about 15 grams of protein lysate, this would roughly mean about 4 grams of free amino acids or more.

References:

Studies on Lysogenesis I.
Size Restriction on Peptide Utilization in Escherichia coli
Escherichia coli Physiology in Luria-Bertani Broth
The Limitations of LB Medium


What is the meaning of the "d(...)2" notation when writing a DNA sequence?

Assuming that you were referring to this specific usage of d(CGCTAGCG)2, the image provided for the crystal structure clearly shows that the structure refers to the fact that two strands of deoxy-ribonucleotide oligos were dimerised to each other.

Had the same structure been formed by double-stranded RNA instead, the resultant dsRNA duplex helix would be referred to as r(CGCTAGCG)2


The definition of life is a controversy in itself, and as it is simply a word that can be understood by everyone however they wish, there is no "correct" definition. It is thus not really possible to give a "correct" answer to your question, but here are a list of things you may want to consider:

Replication of DNA is probably the most agreed common feature to all life on earth. Most organelles do not contain their own DNA but are simply lipid and protein constructs.
Independence is a difficult criterion of life, as parasites require a host for reproduction. However, while the organism may require a host, its cells individually can replicate without a host.
Cells are able to replicate when removed from the body - under the right conditions. (We are getting better and better at culturing all sorts of cell types, for example to avoid having to use animals for research.) Most organelles are not able to replicate under any conditions.
In nature, there are single living cells. In fact, the majority of organisms on earth consist of one cell only. There are no organelles living in nature.

Mitochondria and plastids make a complicated exception to these, as they are originally derived from bacteria themselves. It is indeed debatable whether they could be considered alive, as they possess DNA and it is replicated in order for them to divide, like individual cells do. However, the machinery required is not produced by themselves but rather by their "host" cell, making them subject of a similar argument as viruses.


That's a silverfish (order Zygentoma) https://bugguide.net/node/view/79 This individual is not in great shape, and probably got crushed, however you can see it had the cerci in its tail. The individual is lacking antennae, which are usually long, but the eyes  are also very characteristic. You can see a similar picture on this thread (https://bedbugger.com/forum/topic/here-we-go-againcame-home-now-and-found-this-id-please-silverfish. They are fairly common in homes and are harmless. They feed on fibers and detritus in your home.


In vivo, does it take energy to move double bonds from cis to trans in long chain unsaturated fatty acids

As I understand it the question refers to mammalian oxidative degradation of dietary polyunsaturated fatty acids, as the diet is the major source of such fatty acids. Its concern is with two different aspects of this process neither of which involve the use of ATP. The proposition in the final paragraph is therefore incorrect.

The first aspect is not explicitly stated, but seems evident in the mention of the crowding of fatty acids with cis double bonds and the repetition of “in vivo”. I would rephrase it as:

  How is the agglomeration of lipids disrupted so as to be available to
  the enzymes that degrade it?

This is as much physiology (not my field) as biochemistry, but there are many accounts available (e.g. this I found at random) regarding the emulsification of lipids by bile salts in the small intestine and their conversion to chylomicrons in the lymph and blood. The latter are either processed and stored in the adipose tissue and later oxidized when needed, or oxidized directly, in the mitochondria, especially of the liver.

The disruption of fatty acid aggregates is purely a physical process facilitated by the chemical environment in which they find themselves. This alone allows oxidative enzymes access. (In passing, I would say that it is difficult to conceive of a mechanism by which ATP could be used to disrupt a hydrophobic aggregate — see Appendix.)

The only stage at which ATP is required is the conversion of free fatty acids to fatty-acyl CoA by fatty acid thiokinase before reaction with carnitine and entry into the mitochondria in the form of acyl carnitine. In relation to the handling of hydrophobic molecules in a hydrophilic environment (or vice versa for membrane transport) it may be worth mentioning in passing that carnitine is a zwitterion.

The second aspect of the question is more straightforward. In chemical terms what the question refers to as “moving double bonds” is called isomerisation. So the question is:

  Does cis-trans isomerisation of unsaturated fatty acids require ATP?

This is described in standard biochemistry texts such as Berg et al., from which the diagram below is taken.

No ATP is involved.

Of course a reductase is required to catalyse the reduction of double bonds using NADPH as a reducing agent, regardless of whether they are cis or trans. As the related NADH can be oxidised in the electron transport chain to produce ATP by oxidative phosphorylation, this could be regarded as equivalent to using ATP. However this has nothing to do with the isomerisation.

Appendix: ATP and energy — concepts and  misconceptions

Although this question includes some chemically correct references (the need for cis-trans isomerisation for unsaturated fatty acids to act as a substrate for acyl CoA dehydrogenase), it does raises some suspicions of an incomplete grasp of the factors affecting the viability of biochemical reactions and the role of ATP. If this is correct — and shared by others — I suggest reading an account of how the concept that the Gibbs free energy change of a chemical reaction determines whether or not it proceeds, and how the negative free energy change in the hydrolysis of ATP can be coupled to reactions that have an (otherwise unfavourable) positive free energy change.

Two points relevant to the question are worth mentioning in this regard. Although ATP can be used to cause motion, this involves motor proteins like myosin, kinesin and dynein interacting with large molecular structures. Thermal vibration and thermodynamics are the normal drivers of motion in a cell. The second is that many biochemical isomerisation reactions have standard free energy changes close to zero as, in isolation, the alternative structures have similar energies. What normally prevents the reaction proceeding is the activation energy barrier for the interconversion reaction of one isomer to the other, which is where enzymatic catalysis is comes in. The actual free energy change depends on the concentration of reactants and products, so if the cis isomer builds up and the trans product is removed by reaction then the reaction will proceed in the cis-to-trans direction.


Can we use differential equations for population that is discrete?

You can make the continuous approximation when the population size is large. As mentioned by arboviral, there are algorithms that allow you to perform stochastic simulations with discrete variables. However, these are computationally much more intensive than integration of ODEs. Moreover, analytical solutions for the master-equations (time evolution of probabilities) are very difficult to calculate. Therefore, whenever possible, people go for ODE-based continuous models.

These models would give incorrect representation of the dynamics for small populations and fail to explain phenomena such as extinction. However, they can explain the dynamics of large populations fairly well. So the choice of the modelling approach depends on the questions you want to ask and the complexity/computational cost of the model.


Short answer
It is believed that low water levels occurring several times during the last ten million years facilitated migration and divergent evolution of the felids. The North-American ocelot, lynx, puma, leopard cat, and domestic cat are believed to have evolved from a common ancestor that crossed the Bering land bridge between 5 to 9 million years ago from Eurasia. Note that Pangea broke apart 175 million years ago, way before the Age of Mammals even started, 65 million years ago.

Background
It is believed that modern felids arose in Asia with the divergence of the genus Panthera 10.8 million years ago (Mya) and the bay cat lineage 9.4 Mya. These dates correspond to the low sea levels that occurred during the late Miocene (Fig. 1). Between 8.5 to 5.6 Mya a progenitor of the caracal lineage arrived in Africa. The common ancestor to five felid lineages (ocelot, lynx, puma, leopard cat, and domestic cat) migrated across the Bering land bridge to North America, referred to as the New World migration. This period is also believed to have facilitated migrations of the Eurasian carnivores (ursid, procyonid, mustelid, and saber-toothed felids) to North America.

Additional Pliocene/Pleistocene migrations paved the way for the differentiation of the cheetah, originating from the North American puma and migrating to central Asia and Africa. Reversely, Asian Panthera species spread into America (jaguar, lion) and subsequently into Africa (lion and leopard).

Fig. 1. Global migrations of felids. source: Johnson et al., (2006)

Reference
- Johnson et al., Science (2006); 311: 73-7


What is this crow eating, and is it a common part of the corvid diet?

Crows are omnivorous, and will eat almost anything they find or can kill.

In this case the prey looks like a Yellow-Shafted Flicker.


What’s the reason for isovolumic contraction and isovolumic relaxation?

To put it in very simple words the reason for isovolumetric contaction and relaxation is to make the necessary pressure changes that is necessary to allow blood to flow into or flow out of the ventricles.

The basic formula you need to remember to understand this is:-

  Fluids flow from high pressure area to low pressure area along the pressure gradient (Eg: Injecting a drug into blood stream - as the pressure in the syringe is higher than the pressure in blood vessel, the drug flows into the blood vessel)
  Pressure is inversely proportional to volume (when temperature is constant) - this is Boyle's law. In a container with a fixed amount of fluid an increase in the volume of container will cause a proportionate amount of fall in the pressure in the container and vice-versa

Isovolumetric contraction:

The end-diastolic pressure in the aorta is in the range of approximately 90-100 mm of Hg. For blood to flow from left ventricle to aorta, the pressure in the left ventricle should exceed the pressure in the aorta.

As long as the pressure in the left ventricle is lesser than the pressure in the left atrium, the blood flows from Left Atrium to Left Ventricle. When Left Ventricle starts contracting the pressure in the LV rapidly overcomes the pressure in left atrium leading to closure of the mitral valve.

Now the pressure in the LV is greater than the pressure in the LA. So no blood flows in. At the same time the pressure in the LV is not sufficient to overcome the pressure in the aorta. So the semilunar valve remains closed. The ventricle continues contracting causing a time period in which there is increase in pressure without volume change as both inlet and outlet are closed. This period is called period of isovolumic contraction.

The isovolumic contraction ends when the pressure in the left ventricle becomes higher than the pressure in the aorta, which will cause the semilunar valves to open and blood to flow from left ventricle to aorta.

Isovolumic Relaxation:

The reverse happens in isovolumic relaxation.

As the blood volume in the ventricle decreases and the left ventricle starts relaxing the pressure in the left ventricle falls. When the pressure gets below that of the aorta, the semilunar valve closes. But the pressure in the ventricle is still higher than the pressure in the left atrium. So the mitral valve remains closed. So here too both the inlet and outlet are closed but as the ventricle is relaxing the pressure keeps falling. So till the pressure in the left ventricle falls below that of the left atrium, there is a time period volume is constant and the pressure keeps falling - this is called Isovolumic Relaxation.

This period is followed by opening of the mitral valve (as the pressure in the LV falls below that of the LA) and blood flows into the ventricle.

Take a look at the phonocardiogram linked in Majid's answer. It will help you understand what I explained.

Hope this explains your question


Can fruit tissue be cultured and grown independent from the plant?

Plants are not a strong suit for me, but in general the answer is yes.  What I know mostly comes from animal tissue, so someone may have a better answer than I...

Botanists have been cloning plants from cuttings for thousands of years.  More recently, propagation from cell lines around for much longer than for animals.  Entire plants can often be grown from a plate of cells.  So you can grow roots or an entire plant from cells right now, but I can't find any mention of anyone trying to grow fruit without the rest of the plant, and there might not be any research for this.  Let me explain why this may be...

Bioengineering animal tissue and organ growth has been an intensive area of research for the past 15 years or so.  In some cases, such as the growth of skin or liver, the technology has proven to be exceptionally valuable and useful.

Using plastics with biological growth factors attached and 3D printing, even more complex organs such as bladders and tracheas can be grown from the patients own cells, which avoids the problems of rejection and the complexities of donor matching.

More recently growing muscle tissue in an animal free culture has been tried, which would relieve some of the environmental and ethical problems of raising meat animals.

All this has been driven by a strong cost-benefit payoff.  A transplanted organ is highly valuable and improving that process and making organs more broadly available for patients has a high economic value.  The more often the structure is related to the tissue around, the more structurally complex, the more difficult it is to imagine growing that organ independently of the host organism (brain and eyes come to mind).  Other transplant worthy tissue cultures look quite promising.

Right now, it seems as if plant fruit like an apple or a kiwi might be difficult/expensive to grow in the lab as opposed to just picking them off the tree.  I think that growing a banana pulp or an apple sauce might be possible, though.  Who knows what we might be doing in 50 years or more though?


Are the bacteria doing the same photosynthesis as plants do?

Photosynthesis is always about using solar energy to oxidize a mineral molecule and reduce an organic molecule, which becomes an energy source for the photosynthetic cell.

Bacteria and plants have different types of photoreceptors. It is not always the same chlorophyll, maybe even no chlorophyll at all ! The different colours in algae come from the different pigments they are using to do photosynthesis.

Plant cells carry out photosynthesis in chloroplasts, which are organites, whereas bacteria carry it out in their plasmic membranes.

Plants do aerobic photosynthesis, which means they reduce dioxygen into water. Some bacteria do anoxic photosynthesis, which means they can reduce hydrogen sulfide into sulfur.


I'm not sure to understand your query. I can say that in my lab we are also using fluorescent dye (for SSR detection). But we are doing it with a one step approach:

Our forward primers are like yours preceded by the fluo sequence (M13-forward primer). But instead of making a second PCR, we add directly the fluo primer (let's called it M13-FAM) in the first PCR. It is REALLY important to put your M13-forward primer in lower quantity than the reverse one (factor 10 for me). To achieve that I use 0.1mM primer solutions and I mix my primers before

For 96 wells (20µL/well)

Primer Mix

1.25 µL of M13-F primer
12.5 µL of R primer
240 µL of water

PCR Mix

200 µL of Primer Mix
20 µL of M13-FAM
Master Mix 1mL
Water 1mL


How are large snails able to climb trees?

The foot of the snail secretes a sticky mucus which allows the snail to climb even the smoothest surfaces. The mucus have two states: one in which it is almost liquid to lubricate motion, and the other - a very viscous one, in which the mucus is sticky and "glues" the snail to the surface. The mucus can alternate between these two states via the pressure the snail activates on it. The gluey state sticks the snail to the surface via adhesion.

Researchers discovered nearly 30 years ago that snail mucus has some unusual properties. It allows the animal to stick to a surface while moving, with the mucus changing its characteristics according to how firmly the snail presses on it.  The slime initially acts like glue, sticking the snail to the surface. But when the snail's foot presses down hard enough on the mucus, it becomes more liquid, allowing it to flow underneath the moving snail. Existing theories assumed that this special characteristic of snail mucus was always necessary for the snail to push off and move forward.

Cited from: https://news.stanford.edu/news/2011/april/snail-slime-trails-040611.html


I know that ENSEMBL, PDB and the Human Atlas give known locations for many proteins at different levels of certainty, but such data is far from complete. Also experimental indication of a proteins localization does not prove the absence at other locations. Dependent on your scientific questions it might still be valid to theoretically look into specific scenarios of a proteins localization and to assume a certain pH of that sub-cellular context. SO to answer your question: Higher pH-resolution than the hypothesized cellular sub-localization is unrealistic, and the justification of the assumption of localization depends on your specific plan.


How would one go about identifying unknown cell cycle checkpoint proteins (i.e., cyclins)?

I've actually been involved in a hunt for checkpoint proteins in diatoms (a type of eukaryotic algae), the cyclin family has been greatly expanded in these organisms and we were trying to figure what these extra cyclins were sensing/signalling[1].

In a nutshell, the first author looked at different conditions which were likely to affect cyclin expression. Most of these conditions prevented cell division (e.g. lack of nutrients, G2/M chemical inhibitors or light) and samples were taken before and after the blocking conditions were removed. Afterwards mRNA's were quantified of suspected cell cycle genes. As the checkpoint genes' mRNA and protein cycles extremely transiently this took some doing. Cyclins that reacted to the conditions were characterised using complementation assays and other techniques.

Afterwards yeast two hybrid assays were used to identify interacting proteins to build up the network[2]. In general, these experiments were not that straightforward and messing with essential genes causes a lot of trouble but it still nothing compared to the original yeast cyclin work where they were slogging through mountains of temperature sensitive mutants defective in their cell cycle (see the work of Lee Hartwell and Paul Nurse who got the Nobel prize for this in 2001 with Tim Hunt).


How do susceptible organisms prevent parasites from overcoming resistance?

In an environment where all plants are resistant to certain parasites, a rare breed which has a mechanism against this resistance has free play - lots of food and no competition. However, in plants which do not have the resistance, this rare parasite breed may be at a disadvantage compared to parasites who do not have the mechanism against that resistance (even if only because they do not waste energy on a defensive mechanism they don't need).

By mixing resistant and unresistant plants, it is probably possible to maintain high enough a competition of parasites without that defensive mechanism to prevent the ones with the mechanism from developing. It's natural selection at work :)


Which organs/tissues are defined as "peripheral organs/tissues"

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

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

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

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


Why are my calculations for O2 requirements of daily metabolism so far off?

The math was correct, but there was a misunderstanding in what some of the numbers represent. The energy expenditures listed for RMR include resting dietary thermogenesis in addition to the actual ATP energy used for work. You can see that the same is done for reporting Calories in food (e.g. 4 per carb) at http://www.fao.org/docrep/006/Y5022E/y5022e04.htm

When this is taken into account, we use 686 kcal/mole of glucose to get similar oxygen numbers. This includes the energy for the ATP and the energy from heat.


Why is fructolysis independent of glycolysis?

Summary

The mechanistic reason why fructose is converted to fructose
1-phosphate by fructokinase rather than fructose 6-phosphate by
hexokinase is explained in terms of the Km values of fructose and
glucose for the latter enzyme.
A possible general rationale for the two distinct pathways of
metabolism is to allow them to operate and be regulated independently
of one another. Although plausible, I am unaware of further data
support this idea.
The manner in which the fructokinase pathway evolved is a matter for
conjecture. I discuss what types of approaches to this question may
be valid, and the types of arguments that I consider invalid.

“Why?” Questions — A Note of Caution
Before addressing this question I think it important to consider what is meant by a “Why?” question in biology. This can be a trap for the unwary if one is not clear whether a question is answerable objectively or only speculatively. There are two main types of “Why?”questions:

Mechanistic “Why?” questions. For this SE Question this would seem to be: “What is the mechanistic explanation of the fact that
fructose is converted to fructose 1-phosphate, rather than to
fructose 6-phosphate, in liver?”
Rationalization “Why?” questions. In this case it would seem to be
“How can one rationalize the fact that a separate pathway for
fructose metabolism exists?”

Mechanistic questions can be answered objectively if there are sufficient experimental observations. Rationalization questions cannot.
Rationalization is helpful to try to make sense of observations — to provide a framework for further experimental work. It is useful in teaching and learning, which is why one encounters it frequently in text books. But just because it is in text books it should not be regard as on a par with the facts described therein. It is just an opinion, an interpretation, which should be regarded critically. There is a danger in accepting an inadequate explanation, just because it is the only one that has been proposed for something that is difficult to understand but we think that must have an explanation.
Rationalization “Why?” questions are often confused with questions about how something Evolved. These should be clearly distinguished. Rationalization explanations refer to the functional utility of a system, not its evolutionary history. If the only explanation is in terms of evolution, then there may be a plausable evolutionary explanation but no rationale.
An Answer to the Mechanistic Question
Fructose is not converted to fructose 6-phosphate in the liver because it has a much higher Km for hexokinase than glucose does. Furthermore, glucose is present normally at a higher concentration and will therefore act as a competitive inhibitor. Instead, as the poster writes, there is a specific fructokinase, which converts it to fructose 1-phosphate and a further enzyme converting to the fructose 1-phosphate to glyceraldehyde and dihydroxyacetone phosphate. The glyceraldehyde is phosphorylated to glyceraldehyde 3-phosphate.

Trying to Answer the Rationalization Question
“How can one rationalize the fact that a separate pathway for fructose metabolism exists?” The explanation given in the Encyclopedia of Human Nutrition — that it allows separate regulation of glucose and fructose utilization — seems possible, but fails to explain the circumstances in which it would be advantageous for fructose to be converted to pyruvate, but glucose to, say, glycogen. In the absence of this I would say that there is no convincing explanation, and that one should carefully consider a number of different possibilities:

It is chemically difficult to create a enzyme specific for fructose
to catalyse the formation of fructose 6-phosphate.  This seems
unlikely — we are not dealing with two molecules as similar as serine
and threonine.
Fructose 1-phosphate has functions (metabolic fates or regulatory
roles) other than energy generation in the latter stages of
glycolysis. The Kegg pathway map doesn’t suggest anything in the
former respect, but the entry in the Encyclopedia of Human Nutrition
states: “As fructose-1-phosphate is formed, it feeds forward and enhances the activation of pyruvate kinase thereby facilitating the passage of fructose carbon to pyruvate and lactate.” I do not have access to the book, so cannot say whether this argument is developed further. However as pyruvate kinase is also activated by fructose-1,6-bisphosphate (generated from fructose 6-phosphate) there would seem to be no regulatory difference between fructose and glucose metabolism in this respect.
Fructose 1-phosphate lacks some regulatory role of fructose
6-phosphate (or fructose-1,6-bisphosphate) and hence results in
different flux of fructose and glucose through glycolysis. This is
the converse of the previous possibility. It is true that
phosphofructokinase is activated by fructose 2,6-bisphosphate, which
is formed from fructose 6-phosphate, and so there is a feed-forward
effect when the concentration of fructose 6-phosphate is high.
However the fact that fructose 1-phosphate does not have this effect
would not seem to have any significance as it does not use
phosphofructokinase. Another possibility is proposed in the
Encyclopedia of Human Nutrition: “Since fructose enters the glycolytic pathway [later than the phosphofructokinase reaction] it does not exert an inhibitory effect on the gluconeogenic rate-limiting enzyme, fructose-1,6-bisphosphatase” As the only
relevant molecule that regulates fructose-1,6-bisphosphatase is
fructose 2,6-bisphosphate — inhibiting it — the argument would seem
to be that the entry of fructose into glycolysis through fructose
1-phosphate allows more glucose production for other tissues. Why
this would be a “good thing”, however, is not clear to me.
Unphosphorylated glyceraldehyde has other roles in metabolism, so its
production independently of glyceraldehyde 3-phosphate is more
energy-efficient. Unfortunately the other metabolic fates of
glyceraldehyde are specialized and minor, and do not seem to support
this possibility.

In conclusion, I personally cannot see a rationale for the separate pathway of fructose metabolism to pyruvate, although I believe that there must be one.
The Evolutionary Question
Let us use the question to consider arguments in this area. The approaches that I suggest may — in principle — be valid are those relating to actual mechanism. One can consider the number of evolutionary events that need to occur for a new pathway to evolve — the more steps, the more difficult. (I have used a similar argument in another SE answer). In this question the implicit argument is:

“The evolution of the pathway from fructose to glyceraldehyde
phosphate via fructose 1-phosphate requires three steps, whereas that
for a highly specific enzyme that converted fructose to fructose
6-phosphate would require only one.”

If one accepts this argument, it would suggest that there is some rationale for the fructose 1-phosphate pathway that has escaped us. Although this also seems likely for other reasons, one needs to ask whether the argument is correct. Did three separate enzymes really evolve to accomplish this, or were perhaps some of the enzymes already present and serving other purposes?
Two examples of common type of argument that I think are invalid are in the original question.

“As there are several disorders that arise from the deficiency of
enzymes used in fructolysis, wouldn’t there be a selection pressure
against two separate metabolic pathways?”

Selection pressure against causes of a human disease require them to have a severe effect on the survival of the species, to cause death before the individual is of a reproductive age, and to be relevant to early humans. Minor enzyme deficiency disorders of fructose metabolism, or even disorders arising from modern over-consumption of sucrose would exert absolutely no selective pressure. As it turns out fructokinase (EC 2.7.1.3) is widely distributed in nature — If one looks up fructose metabolism in fruit flies on KEGG one can follow a trail to a long list of species in which the enzyme is present. The point that I think this demonstrates is that for biochemical evolution, one needs to think when and where the pathway might have evolved.
The second example of argument that I think are invalid is

“Wouldn’t it be more economical to use a single reaction, so
everything would be easier to regulate?”

I refer to this type of argument as “playing God” or “second guessing Nature” as to me it presumes that one is in a position of such knowledge and wisdom that one is able to propose the optimal design for life.
Economical in what sense? Is our concept of economy the over-riding feature driving mammalian evolution? Multiple reactions and isoenzymes abound in the metabolism of animals. Apparently ‘wasteful’ energy- or material-consuming reactions like splicing are everywhere. And the regulation of intermediate metabolism is mind-boggling in its complexity. Regulation clearly evolved after the pathways, and “ease” of doing this does not seem to have been a driving force in evolution.
The lesson I draw from this is that even the most knowledgeable molecular scientist is in a poor position to say what is economical or efficient, and to predict the outcome from the cost/benefit tradeoff Nature will make or has made to do things “better”. And it is difficult to say what is “better”.


Is a pampa an example of ecological succession?

This is a difficult question to answer. I would say that is uncommon (though not improper) to think of questions of ecological succession at the biome scale. In this case, the pampa is probably a good example of a climax community (if we exclude human-caused changes). After the rivers changed course there would have been a lot of bare substrate. Over time different plant species would establish and then  be replaced by other plant species. After thousands of years you would get to the somewhat stable state of the pampa biome. It is important to note that this biome is maintained by fire and grazing (Vignolio et al 2003). Fire/grazing prevent trees and shrubs from establishing in high densities and maintains the open grasslands of the pampa. In general, every place in the world that has natural life would be the result of ecological succession. Succession is a process that happens as life establishes and ecological communities change.
As for why other places are also called pampas, the word "pampa" apparently comes from a Quechua word for plains, that was then adopted into Spanish. Since Peru and Bolivia both have Quechua speaking populations, it seems reasonable that this work was applied to plains areas in those countries.
Edit in response to comments
Comment about biome scale
The reason behind the scale comment is that typically we observe succession for a given habitat. Part of this stems from the origin of the succession ideas, where Frederic Clements posited that climate was the major driving factor of successional trajectories (Clements 1916). This would actually fit well with the biome view of succession, however in order for this model to explain all the variation we see in the world (eg. why a tree grows in location X but not location Y 4 metres away), you devolve into splitting the world into infinitesimally small micro-climates. Henry Gleason proposed a more individualistic model, which suggested that climate was just one influence, and that each plant species responds to a myriad of different environmental cues (Gleason 1927). The sum of these responses results in the community at a given location. This seems to fit better with our current understanding of succession but is not without problems. In a Gleasonian model, any variation can be expected to result in a different community. Since it would be strange for the pampas region to be homogeneous over 1.2 million km2, there are likely distinct communities within the biome, each developing as a result of factors like soil moisture, soil chemistry, climate, wind exposure, and herbivore use. One can still talk about succession at a biome scale, but at that scale we would be thinking about what factors lead the pampas region to become a grassland, rather than what factors lead grass X, tree Y and forb Z to coexist next to each other.
Factors maintaining grassland type ecosystems are fairly uniform globally. You need some sort of event that will kill woody vegetation but not kill grasses and forbs. Fire and grazing are natural examples (Briggs et al. 2002), but mowing would also maintain grassland (Fidelis et al. 2012). Earthquakes are unlikely to maintain grassland as trees and shrubs are likely to survive earthquakes.
Comment about global pampas
Yes, and no. There are other wet grasslands in the world that would have similar moisture regimes and productivity levels seen in the pampas of South America. However, these are likely not called pampas. Temperate grasslands in Canada and the US are typically called prairies or plains, while the same kind of system is called a steppe in Eurasia. Ecologically they are very similar in function, though they may have very different species present. Perelman, Burkart, and Leon (2003) use prairie and steppe to refer to different sub-communities of the Pampa. Perhaps the closest analogue would be the Great Plains of North America. There is no other area called the Great Plains, but since the great plains are made up of prairie, steppe, and savannah (Oesterheld et al. 1999), there are many other areas globally that exhibit similar ecological function. This can get confusing, as there are cultural usages of these terms to refer to places, and there are ecological uses of these terms to refer to grassland sub-types.
I am not sure I understand how you are relating chaparral/Mediterranean forest to this. Both of those ecosystems will have much higher presence of trees and shrubs than pampas/prairie/steppes (Hanes 1971, Palahi 2008). Chaparrals tend to be dominated by evergreen drought tolerant shrubs, while Mediterranean forests will have more trees present. All of these systems are influenced naturally by fire and drought, so they are similar that way.
Sources
Briggs, John M., Alan K. Knapp, and Brent L. Brock. "Expansion of woody plants in tallgrass prairie: a fifteen-year study of fire and fire-grazing interactions." The American Midland Naturalist 147.2 (2002): 287-294.
Clements, Frederic Edward. Plant succession: an analysis of the development of vegetation. No. 242. Carnegie Institution of Washington, 1916.
Fidelis, Alessandra, et al. "Short‐term changes caused by fire and mowing in Brazilian Campos grasslands with different long‐term fire histories." Journal of Vegetation Science 23.3 (2012): 552-562.
Gleason, Henry Allan. "Further views on the succession‐concept." Ecology 8.3 (1927): 299-326.
Hanes, Ted L. "Succession after fire in the chaparral of southern California." Ecological monographs 41.1 (1971): 27-52.
Oesterheld, M., et al. "Grazing, fire, and climate effects on primary productivity of grasslands and savannas." Ecosystems of the world (1999): 287-306.
Palahi, M., et al. "Mediterranean forests under focus." International forestry review 10.4 (2008): 676-688.
Vignolio, Osvaldo R., et al. "Effects of fire frequency on survival, growth and fecundity of Paspalum quadrifarium (Lam.) in a grassland of the Flooding Pampa (Argentina)." Austral Ecology 28.3 (2003): 263-270.


If the flu vaccine is the exact same as last year, would it still offer protection this year?

If one flu strain wouldn't change between the years (meaning there wouldn't be any new mutations in it) and the same strain would circulate again in the following year, the "old" vaccination would protect people. This is the same as with other viruses which do not change, once you reached a protection (usually one basic immunization and one booster), this protects for a long time (see measles vaccination as an example here).

There are surprisingly little articles available on how long the immune response after a vaccination lasts. There is a difference between the livettenuated influenza vaccine (LAIV) and the inactivated influenza virus (IIV), with the former giving a less good protection (see reference 1).
Data for the LAIV suggests that there is protection for at least one year after the vaccination (see reference 2).

However, there is evidence that the immunity against the flu after an infection against this specific strain might last life-long, as a paper demonstrated on survivors of the 1918 flu epidemic (see reference 3).

Having the flu against being vaccinated against it is a complete different thing (higher exposure, probably more antigens), but the question is if the immune response against vaccinations may also for a longer time.
The problem with the flu vaccination are:

The strain circulating in a year is changing.
The stains are mutating, making them different from the virus used for vaccine production. Depending on how different these mutations make the circulating strain, it can render the vaccine more or less useless. This is something what happened this flu season.
The flu vaccine is prepared from different flu strains to cover a broader range. In a tri-valent vaccine these are typically 2 Influenza A and one Influenza B virus strains, in tetra-valent vaccines 2 A and 2 B strains. The composition is based on a prediction (from epidimiologic data) which strains are likely to circulate in the next season and is done early in the year for the following season (production takes time, etc.).

Because of these problems, researchers are working on a universal flu vaccine; which is based on virus parts which do not change and should protect against all virus strains. Then only the basic vaccination would be necessary as with other vaccinations.

With all these limitations, it is still advisable to get a flu vaccination, as it is a pretty severe infection.

When not challenged (i.e. upon infections) antibodies are cleared from the blood within a few weeks, but there are low amounts produced (which are enough for detection). The immunologic memory is maintained by memory B cells which can ramp up production of the highly specific antibodies in a very short time - this is the reason for the protection by immunizations.

References:

Modest Waning of Influenza Vaccine Efficacy and Antibody Titers
During the 2007-2008 Influenza Season.
Longevity of B-cell and T-cell responses after live attenuated
influenza vaccination in children.
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors


Is there a difference between pig and cow anatomy that makes religious slaughter of the latter less painful?

Difference between kosher and non-kosher animals

Rabbi Zamir Cohen, in his book The Coming Revolution - Science Discovers the Truths of the Bible, quotes modern day scientists that have made an incredible discovery of a major difference in the way the blood flows in the species that are kosher and those that are not. In non-kosher mammals, the vertebral arteries flow directly to the brain through the rete mirabile. However, in cloven-hoofed, cud-chewing mammals and permitted foul, the vertebral arteries drain into the carotid artery and do not have any direct flow to the brain. There will therefore be an immediate drop in blood pressure at the time of shechita that causes the animal to lose consciousness, thus feeling no pain.


Cloning two fluorescent proteins with different promoters in the same plasmid?

If you want to express them in an operon, make sure you have an RBS at the 5' end of each coding sequence. If you place one 10bp downstream without it having an RBS, it will be transcribed, but not translated... If you want more help, paste the DNA code of each as a comment.


Can anyone tell me what tree does this leaf belong to?

maybe it is from tulip-tree (Liriodendron tulipifera)

use one of this applications to identify plant species:

http://www.plantsnapp.com/#theapp
https://itunes.apple.com/gb/app/id957861141?mt=8
https://itunes.apple.com/gb/app/flowerchecker-plant-identification/id916709270?mt=8
https://play.google.com/store/apps/details?id=cz.thran.flowercheckerplus

and many others here


Does the cellular response to every receptor work the same way?

It's a complicated answer. More than 200 cell types, each type of cell inherits a unique expression of receptors, internal and external. Diffusion of signals through the plasma membrane and/or nuclear compartment may act directly as cofactors, activators, etc. The specific sequestration, and pattern of expression of external receptors also influence what signals become bound and relayed. The cell will also have a motif of internal/cytoplasmic/nuclear proteins expressed that complex or become directly activated by interaction with any of the above, etc. So the currently expressed set of internal, and external proteins determine not only how the cell interprets the signal, but also how they respond.

As for the actual genetic material, you'll find inherited motifs like DNA methylation, histone acetylation patterns etc. influence what parts of the DNA can actually be accessed. Per the above schema of signaling pathways, the signals received by each individual cell differ based on the actual cell type. In any case there are patterns of activators/repressors, enhancers/silencers that are switched on or off by these signals. Some journals are also introducing evidence insoluble receptors like EGFR+ligand can actually internalize and translocate to the nucleus and act as transcription regulators.

The final note, is that due to alternative splicing and transcription of proteins that promote or repress splicing sites, in a combination with the above concepts a cell can regulate for thousands of genes. This is a very general answer, however. The concept to take home, though, is that differentiated cells have their own specific motifs they express that make "reading" different signals possible, and also makes differing responses to what could be the same signal possible. These motifs also allow for the accurate expression of the relevant portions of the genome (not all genes are expressed at all times in all cells).


Do electromagnetic waves outside the visible spectrum have any role in photosynthesis?

Photosynthesis is nearly all visible light. There's usually not enough UV and thermodynamics more or less rules out infrared. Chris covered that pretty spectacularly, but that nearly is significant.

There is some evidence that certain kinds of fungi can use gamma rays or other ionizing radiation for energy, but they're not particularly common. Melanin is used instead of chlorophyll, but apparently 'tooling up' for radiosynthesis(is that a word?) is fairly hard on the cell. It was assumed the melanin was a protective pigment(like it is in humans) and produced only when necessary(also like humans), but these particular ones were discovered growing in the Chernobyl reactor and apparently evolved to continuously produce melanin and absorb ionizing radiation for food. They don't stop producing melanin even on the verge of starvation. Other melanized fungi live in high-radiation environments, like mountaintops and the poles, where there is more UV and cosmic rays and things.

Fun fact aside: Fossilized melanized fungal spores turn up at the K-T boundary when the earth had no magnetic field and therefore higher radiation flux at the surface (see paper linked above and Hulot & Gallet, 2003 for more).


Is it possible to move your arms above your head when handcuffed in the back?

This is not normally possible or would be extremely painful if done. But there are special cases.

  Atraumatic dislocation.
  This occurs when the shoulder dislocates with minimal force such as reaching up for an object or turning over in bed. Usually it will 'pop' back in itself or with a little help. Normally this type of dislocation does not need reducing in A&E. It can occur regularly throughout the day and will be associated with certain positions the arm is placed into. This type of dislocation is associated with people that have 'lax' joints, for example people who hyper-extend their knees and elbows and can get the palms of both hands onto the floor with ease.  This joint laxity is normal for these people and the onset of dislocation can be associated with a change in how the muscles around the shoulder are interacting with each other or a change in posture/ position of the arm. This can produce an imbalance in the control of the joint. Referral for appropriate physiotherapy is the initial form of management. The physiotherapist should look at the way in which the muscles and shoulder joint is moving and posture aiming to restore the balance. Treatment can 'cure' the problem as long as the exercises and advice is continued, but in some cases there is only minimal or nil benefit. At this point surgical intervention is indicated.
  Positional Non-traumatic dislocations.
  This group of people can dislocate their shoulders without any form or history of trauma. Some may have started out dislocating their shoulder as a party trick; others may have always had shoulders that just 'fall' out of joint. This type of dislocation is usually painless and can be put back in easily. Both shoulders are typically involved. The cause of this type of dislocation is usually a result of what we call 'abnormal muscle patterning' which means the strong muscles around the shoulder joint are not working in the correct order causing them to pull the shoulder out of joint with active movement in the particular direction such as lifting the arm forward above the head or out to the side and above the head.  The main treatment for this is physiotherapy that looks at re-sequencing the muscles in order to prevent further dislocations.  Occasionaly surgery in the form of thermal capsular shrinkage or plication may be neccessary.

Taken from here such people would be able to dislocate then get their hands in front and relocate.

The body can be trained to be quite flexible through training like gymnastics etc...


Proteins are polymers of amino acids. Each amino acid has a side chain. Many of these side chains contain ionisable groups. The ionization state of these groups is dependent on the pH. A group that is protonated at pH=2 and neutral, for example, may become deprotonated at pH=8 and become negative. See the Henderson-Hasselbalch equation.

Protein structure is held together by many intermolecular interactions: dipole-dipole, hydrophobic, electrostatic, etc. The correct protein structure is necessary for function. At different pH levels, the protonation and deprotonation of ionisable amino acids affects the intermolecular interactions within the protein and its conformation will change. At a certain pH, the conformation of the protein will be optimal for its function and this is where it will have maximum activity. As pH deviates to either side of the optimum, the conformation changes and the structure will no longer be correct for proper function.

The ionization state of amino acids is also important in the active site but not only because of conformational changes. Catalytic residues must have certain properties to catalyze their specific reactions. As an example, two Asp residues (which have carboxylates on their side chains) in the active site of DNA polymerase are responsible for coordinating two magnesium ions that promote polymerization. If the pH were to decrease to a point where the Asp residues were protonated, they could no longer bind the Mg2+ ions and the enzyme would not function.


Many genetic studies in this area have found that variation in serotonin receptors associates with differences in a number of personality traits. That one gene, or a very small number, turns up time and time again for something so complex as human personality makes me a bit suspicious.

Other factors at play:
Family dynamics
Culture and cultural norms
Society and societal norms (these could clash with the above two)
Exposures - drugs, toxins, diet, and many others
Traumatic events


Why don't bees sting hornets for defense?

Smithsonian mag says that the bee stings can't penetrate through the predator hornet's armor, which is simply a case of the hornet's armor being tougher than the blunt barb of the bee sting. https://www.smithsonianmag.com/smart-news/invasion-murder-hornets-180974809/
Here's a good research:"

To examine their behaviors of penetrating into different materials, we performed penetration–extraction tests and slow motion analyses of their insertion process. In comparison, the barbed stings of honey bees are relatively difficult to be withdrawn from fibrous tissues (e.g. skin), while the removal of paper wasp stings is easier due to their different structures and insertion skills. The similarities and differences of the two kinds of stings are summarized on the basis of the experiments and observations.

Some research suggests that bee stings have evolved to ward off vertebrates, physically and chemically. Wasps have more slender stings and perhaps that's why the hornets prefer bees nests.
Actually, a lot of insects have phenomenally hard keratin, beetles and the bulldog raspy cricket, as far as i know, even parasitoid wasps which have specialized stings evolved to cope specificially with insects are more common on caterpillars and spiders than strongly armored animals like big beetles.


What does a hornet nest foundress feed on?

I used the below articles to get the information.
1. the queen does collect both carbohydrates (nectar mostly) and protein (often bee flight muscles).

Only found one case study of one nest for this, so not sure. The queen did leave the nest during the period when it would be expected to have larvae. The articles I read did not mention food storage in the nest.
Same case study, the queen left the nest probably for longer than four weeks.

The developmental period was about 4I-42 days (egg 6 days, larva about 15 days, pupa about 20-21 days.
 from "Taxonomy, distribution and nesting biology of the Vespa bicolor group" (Hym., Vespinae) (1994) by Michael E Archer. found at https://www.academia.edu/4236740/Taxonomy_distribution_and_nesting_biology_of_the_Vespa_bicolor_group_Hym._Vespinae_1994_

This review article has a good overview. "Vespa velutina: a new invasive predator of honeybees in Europe" by Karine Monceau, Olivier Bonnard, and Denis Thiery.  DOI 10.1007/s10340-013-0537-3. accessed at https://www.doc-developpement-durable.org/file/Elevages/apiculture/maladies&parasites/Vespa%20velutina_frelon%20asiatique/Vespa%20velutina%20a%20new%20invasive%20predator%20of%20honeybees%20in%20Europe.pdf

A case study of a captured nest (one queen, four workers) found that the queen stayed inside the nest permanently after 27 more days.

From "Observations on the colony activity of the Asian hornet Vespa velutina
Lepeletier 1836 (Hymenoptera: Vespidae: Vespinae) in France" Article in Annales- Societe Entomologique de France · January 2009 DOI: 10.1080/00379271.2009.10697595 downloaded from ResearchGate

There are also other articles that may have the answer, but in languages that I could not read.


How sterile is working next to a bunsen burner?

For doing bacterial work on an open bench, this is standard "Sterile Technique." The updraft from the heat generated by the Bunsen Burner should create a relatively sterile field with which to work, so long as you aren't breathing directly on your plates.

Also part of sterile technique is to "flame" all of your pipets, agar plates, and the openings of bottles to remove any contaminants from those areas, and also to protect them from getting into sterile mediums. Every time you uncap or cap a media bottle or test tube you are suppose to quickly pass it over the flame. Obviously these days, plastic equipment makes that a little less practical, but it still can be done if you pass quickly and aren't too close to the flame.

Disposable serological pipettes should remain covered until just before use and then the "banana peel" method of removing the wrapper should be used. If the tip touches anything it should be discarded.

The true test of your sterile technique is whether or not you are getting contamination. Some labs that work with recombinant bacteria don't even bother with sterile technique for bacteria work as they are using antibiotic selection, and contamination becomes much less of a concern. That being said, an ounce of prevention is worth a pound of cure, so if you keep your work space clean, and there isn't a risk of fire, i.e. you don't have organic solvents in the area or the stack of lab reports you are supposed to grade spilling over onto your bench, then it doesn't hurt to light up a burner even if you are using selection.

You are also supposed to have cleaned your work space prior to lighting the burner with 70% ethanol, which will rather quickly kill most bacteria on the surface. Wearing gloves and proper glove technique also helps keep contamination to a minimum. Keeping hair tied back and wearing a clean lab coat can also help, though lab coats are usually more for your protection and for the protection of others (not transmitting hazardous materials on your personal clothing) than to prevent contamination.

Most people get the false impression about BSL-2 Laminar flow cabinets or glove boxes are suppose to be sterile and prevent contamination. Their real purpose is to keep things in, not really to keep things out. Laminar flow hoods will keep aerosolized particles within them from getting to you, so long as you keep the hood area fairly clear and do not block vents, but as you pass your hands through the flow, you are bring whatever is on you and has tagged along for the ride into to work field. Glove boxes can maintain a sterile field, so long as it, and everything going into it, other than your samples have been sterilized, and your sample hasn't already been contaminated.


Except for protecting ears from cold air, does a woollen cap provide any other significant advantage in winters?

This article is what you need: http://www.bbc.com/future/story/20130708-is-most-heat-lost-from-your-head . Citing an excerpt from it:

[H]aving your head immersed in cold water only adds 10% to your overall heat loss in a cold pool. And given that the head accounts for 7% to 9% of the body’s surface, that doesn’t seem excessive.
But before you throw your collection of woolly hats in the bin, there’s another finding to bear in mind: when the head is allowed to get cold and the body is effectively insulated, the body’s core temperature drops a lot more rapidly than most people would expect.

In the end, wearing a woollen cap prevents the body's core temperature to drop too low. So if the rest of your body is well covered, you can skip the cap and put just your comfy headphones on; if, on the other hand, your clothes don't protect you well, putting a woollen hat on may be the easiest way to not feel cold.


Is this plant lantana camara? If not what is it?

It is Lantana camara, you can check here: https://en.wikipedia.org/wiki/Lantana_camara


How many kg of seed can one expect from 230 kg of cotton fiber?

According to this document (pdf) the rate is around 700 lb seed per 500 lb of fibre.

seed = 1·4 × fibre

230 kg fibre ≅ 320 kg seed

(Strangely, the rate has fallen over time.)


I don't think, there is a precise answer about the evolutionary mechanisms, but "mechanically":

mammals have principally just two types of pigments: eumelanin and pheomelanin, both of which have their color variants, but within a known range. Bird pigments, besides melanins, include carotenoids and porphyrins. Arthropods generally have carotenoids, melanins and ommochromes [and other pigments?]. E.g. carotenoids and ommochromes alone can create rather "exotic" coloration from a mammal point of view (green, pink, violet).
both birds and insects actively utilize iridescence. With fur it seems to be technically much more difficult to achieve than with feather or scales.
many (most?) mammals do not differentiate colors. Birds have much better vision abilities in this respect. From a selectionist point of view this cuts out a considerable part of selection acting upon coloration, which could otherwise produce broader spectrum of phenotypes.


Why do the proportion of predators increase at mass extinction events?

The data used in the graph you posted seems to be from Bambach. 2002. Supporting predators: changes in the global ecosystem inferred from changes in predator diversity (in Kowalewski & Kelley. The Fossil Record of Predation) - see fig 19b - and, if so, is specifically dealing with marine predators.

I don't have time to look at that paper closely (it is quite long), and paleoecology is not my field, but a couple of relevant sections are:

  However, the diversity of predators and the proportion
  of total faunal diversity composed of predators have both increased over time, implying that ecosystems have
  increased their ability to support either more predators or more specialization among predators. Also, turnover
  in diversity dominance among predator groups, with more energetic predator taxa replacing or being added to a
  fauna of less energetic groups, implies that the energy available in marine food webs has increased.

and

  If
  the efficiency of energy transfer between levels in
  the food pyramid has stayed nearly constant (and
  there is no evidence that it has not), then a reasonable
  hypothesis for the increased proportional diversity
  of predators is that either the biomass of prey species
  has increased or the populations of prey taxa have
  become more stable (or both), permitting greater
  specialization by predators on more reliable food
  supplies. Thus, predators could increase their
  proportional share of total diversity by specializing
  on fewer prey taxa.

So according to the author, energetics, energy flow and predator specialization seems like likely reasons for the change. However, the paper also discuss factors such as rates of fossilization and also the fact that predators are generally rarer than prey means that there is probably more stochasticity in the fossil occurence process, which could affect estimated turnover rates and maybe also the proportion between predator and prey. You'll have to look at the entire paper for a fuller picture, and maybe somebody more knowledgeable can fill in later. I also think that you need to look at radiation patterns in certain taxa to fully understand these stepwise changes, and also to consider oxygenetion events as possible underlying reasons, but these are just my speculations.

The reasons given above also in one sense echoes the "biotic" explanation for the latitudunal diversity gradient (see e.g. Gaston, 2000 and Mittelbach et al, 2007), where high levels of primary production can support more specialized predators/parasites in more complex food webs, then leading to higher species diversity. So there might be interesting connections to contemporary patterns and processes of biodiversity as well. However, I haven't seen a compilation of %predators over different biomes or latitudes to match the graph in the question. Also, the "biotic" explanation for the latitudunal diversity gradient has been criticized and is not without problems (see papers above for more).


Do somatic cells alter their own nucleotide sequence?

One case where human cells alter their DNA occurs in the immune system.  In the early stages of the continuing production of B-cells and T-cells, the developing cell recombines (shuffles) genes in a particular DNA region which codes for what are called Variable, Diverse, and Joining gene segments.  This shuffling is called somatic recombination or V(D)J recombination.  This rearrangement gives the cell a genetic template for a random instance out of a enormous set of possible antigen-recognition proteins used by the immune system to recognize foreign molecules (in order to fight infection).


It’s not the fault of the database, it’s the fault of the individual scientists that described the epitopes. O.K. in a perfect world the curators would have gone through the entries and tried to standardize the descriptions. But they probably lack the time or expertise. I sympathize with them.

So what can you do? You have to use your own expertise or that of experimental scientists you are working with and make your own decisions, some of which will be incorrect.

This is a general problem with databases compiled from papers or individual submissions, and is a headache for data mining: misspellings, spaces or no spaces, hyphenated or not, different names for the same entity. Unfortunately there’s no fairy with a magic wand to solve the problem for you.


Why do dog's eyes glow green on a photo?

Dogs, cats, and many other mammals have a Tapetum lucidum which reflects light back through the retina to help with night vision. Humans don't have this layer. The tapetum is probably reflecting green light that would have normally been absorbed.


LacZ' selection: blue colonies despite ligation of insert

Most inserts will disrupt beta-gal expression (by shifting the reading
  frame and introducing stop codons) and therefore remove the enzymatic
  activity required to cleave X-gal and produce the blue color.

Your source is agreeing with you - inserting a stop codon will stop translation (not transcription) and keep the white color.


Try this article as a starting point;

Stringer, Chris B., and Peter Andrews. "Genetic and fossil evidence for the origin of modern humans." Science 239.4845 (1988): 1263-1268.

It is old, but it has been cited 918 times to date. That should be more than enough of a breadcrumb trail to find what you are looking for. Also if you click through to the Science Magazine page, it also has a list of relevant articles below the abstract. You may need a membership to AAAS or library access to get a copy of the actual article.

Also try a Google Scholar search for Modern Human Fossil Record. The above article is the second article referenced in this search.


It's a type of begonia. With 1800 species in the genus, it's hard to say which it is, but the leaves which seem palmate would place it in the aconitifolia species. Your leaves don't appear to be variegated, and your flower is deeper pink, but it's the same flower species.


How is excretion of metabolic wastes from a cell related to its size?

The critical element here is that building materials that need to be absorbed, or waste materials that need excretion have to cross the cell membrane. The larger the surface of the cell's membrane relative to its volume, the faster the exchange rate.

The book section you linked in the comments mentions the following on p.14:

  The volume [of a spherical cell] increases by a factor calculated by cubing the radius, [...] the surface area increases by a factor calculated by squaring the radius. [...] This means that a large cell has relatively less surface area to bring in needed materials and to rid the cell of waste [...]. Cells are limited as to the size they can attain [...]. Cells that are larger [...] have modifications that allow them to function efficiently. This is accomplished by shape changes such as from spherical to long and thin, [or] have infoldings or outfolding to increase their surface relative to their volume.


Why some parts of the human body have immune privilege?

The immune privilege is happening for brain, CNS, eye, testis and the uterus. All these tissues (or structures) share that they cannot be regenerated once they get damaged by an overshooting immune reaction. Infections in the eye followed by a strong immune response often lead to the loss of the eye, in rodents loss if immune tolerance against the fetus leads to abortion.

So basically this is a protective mode for these tissues to protect them from a stong immune reaction. See the references for some more details (especially on how this works).

References:

See no evil, hear no evil, do no evil: the  lessons of immune
privilege
What is immune privilege (not)?
Immune privilege or privileged immunity?
Immune Privilege and the Philosophy of Immunology

  Each immune privileged tissue has a unique function. The eye must protect the light path and signals that stimulate the retina, and photoreceptors to preserve vision. The testis has to protect the sperm as they proceed to the epididymis where they mature. The maternal reproductive tract has to protect its eggs both before and after fertilization and thus has developed specialized mechanisms to modify the body’s response to foreign antigens. These unique challenges require different solutions and lead to unique immune privilege mechanisms. However, although microenvironment and the stromal cells that carry out the particular function may vary between tissues, and consequently the mechanisms that promote regulation may be unique to that cell or tissue, the goal is the same: limit collateral damage to preserve tissue integrity and maintain homeostasis to the extent possible, without compromising host defense.


Pancretic Acinar Cell - ATP, calcium concentration data

In this study, even though they have used fluorescence based method, they have reported concentrations.

  When we studied basal intracellular calcium concentrations in acini from control rats they were in the low nanomolar range (140 ± 5 nmol).

For ATP concentrations you can see here.

  Is it possible to find this information in a specific book or website, to avoid trawling though vast amounts of literature?

There is the human metabolome database. However, it doesn't have data for all cell types. Either more studies are required or the database needs updation.

Similarly there is the yeast metabolome database (you may not require it for your query but just another piece of information that I thought is worth adding).


How can (GPCR) signaling be spatially encoded?

Terse explanation: During endocytosis the G protein-coupled receptor can be spatially constrained.
Your paper refers to: "Fulfilling the promise of “biased” G protein-coupled receptor agonism", by Luttrell LM, Maudsley S, and Bohn LM, in Mol Pharmacol. 2015;88(3): 579-588. https://doi.org/10.1124/mol.115.099630.

Abstract: The fact that over 30% of current pharmaceuticals target heptahelical G protein–coupled receptors (GPCRs) attests to their tractability as drug targets. Although GPCR drug development has traditionally focused on conventional agonists and antagonists, the growing appreciation that GPCRs mediate physiologically relevant effects via both G protein and non–G protein effectors has prompted the search for ligands that can "bias" downstream signaling in favor of one or the other process. Biased ligands are novel entities with distinct signaling profiles dictated by ligand structure, and the potential prospect of biased ligands as better drugs has been pleonastically proclaimed. Indeed, preclinical proof-of-concept studies have demonstrated that both G protein and arrestin pathway-selective ligands can promote beneficial effects in vivo while simultaneously antagonizing deleterious ones. But along with opportunity comes added complexity and new challenges for drug discovery. If ligands can be biased, then ligand classification becomes assay dependent, and more nuanced screening approaches are needed to capture ligand efficacy across several dimensions of signaling. Moreover, because the signaling repertoire of biased ligands differs from that of the native agonist, unpredicted responses may arise in vivo as these unbalanced signals propagate.".

A relatively simple explanation is offered in another paper: "Temporal Bias: Time-Encoded Dynamic GPCR Signaling", by Manuel Grundmann and Evi Kostenis DOI: https://doi.org/10.1016/j.tips.2017.09.004:

"The notion that information is not only encoded by the chemistry of the signaling components but also by their spatial and temporal occurrence, brought about the term of ‘spatiotemporal signaling’ $^{[3]}$. Signal transduction can thus be categorized into at least three dimensions, (i) quality (which substances take part), (ii) space (where the event takes place) and (iii) time (when the event takes place). The interplay between these dimensions will hereinafter be designated as ‘dynamic signaling’ or ‘signaling dynamics’. Dynamic signaling is deeply entrenched in GPCR signal transduction as an increasing number of reports provide us with a glimpse into spatiotemporal aspects of receptor function $^{[4, 5, 6, 7, 8, 9, 10]}$.".
[3] Kholodenko B.N. et al. Signalling ballet in space and time. Nat. Rev. Mol. Cell Biol. 2010; 11: 414-426
[4] Irannejad R. Functional selectivity of GPCR-directed drug action through location bias. FASEB J. 2017; 31 (664.2)
[5] Mullershausen F. et al. Persistent signaling induced by FTY720-phosphate is mediated by internalized S1P1 receptors. Nat. Chem. Biol. 2009; 5: 428-434
[6] Irannejad R. et al. Conformational biosensors reveal GPCR signalling from endosomes. Nature. 2013; 495: 534-538
[7] Eichel K. et al. β-Arrestin drives MAP kinase signalling from clathrin-coated structures after GPCR dissociation. Nat. Cell Biol. 2016; 18: 303-310.
[8] Thomsen A.R. et al. GPCR-G protein-β-arrestin super-complex mediates sustained G protein signaling. Cell. 2016; 166: 907-919
[9]  Jean-Alphonse F.G. et al. β2-Adrenergic receptor control of endosomal PTH receptor signaling via Gβγ. Nat. Chem. Biol. 2016; 13: 259-261
[10] Plasma membrane localization of the μ-opioid receptor controls spatiotemporal signaling. Sci. Signal. 2016; 9: ra16

See: "Spatial encoding of GPCR signaling in the nervous system", by Zara Y Weinberg, Stephanie E Crilly and Manojkumar A Puthenveedu, DOI: https://doi.org/10.1016/j.ceb.2018.12.006:

"Several GPCRs, including receptors previously thought to signal primarily from the cell surface, have been recently shown to signal from many intracellular compartments. This raises the idea that signaling by any given receptor is spatially encoded in the cell, with distinct sites of signal origin dictating distinct downstream consequences.".

During endocytosis the G protein-coupled receptor can be spatially constrained.
See: "Spatial resolution of cAMP signaling by soluble adenylyl cyclase", by Giusi Caldieri and Sara Sigismund
DOI: https://doi.org/10.1083/jcb.201606123 which offers a easy to understand image:

Figure 1. Spatial and temporal control of GPCR signaling by ACs. In hippocampal neurons, CRHR1, upon binding to agonist CRH, activates the trimeric G protein complex, composed of α, β, and γ subunits. Stimulatory Gα subunit is released and activates tmAC and cAMP production (Irannejad and von Zastrow, 2014). In parallel, activated GPCR can also induce local Ca$^{2+}$ release that activates sAC, followed by an increase in cAMP levels (Inda et al., 2016). (1) These two sources of cAMP at the PM contribute to the early phase of ERK activation via the effectors protein kinase A (PKA) and EPACs (Inda et al., 2016). Activated GPCRs once released from the G proteins are phosphorylated and recruit β-arrestin (β-ARR) to be internalized via clathrin-coated pits (CCPs; Irannejad and von Zastrow, 2014). (2) At the endosomal station, GPCRs activate sAC to trigger a second wave of cAMP production and to sustain Erk signaling in an EPAC-dependent fashion. sAC activation at the PM and at endosomes requires Ca$^{2+}$ and bicarbonate (not depicted for simplicity; Inda et al., 2016). The signaling cascade leading to Ca$^{2+}$ and bicarbonate release (particularly at the endosomal station) and the exact mechanism of action of sAC are not completely characterized. The different forms of ACs, and the corresponding cAMP gradients generated by them, are depicted in different colors to highlight their different roles. Whether this specificity reflects different isoforms and/or regulation remains to be clarified.

"The work reported by Inda et al. in this issue integrates and expands our emerging knowledge of localized GPCR signaling at the endosomal level. In a previous work, these authors showed that Erk activation by corticotropin-releasing hormone receptor 1 (CRHR1) signaling is biphasic, with an early response originating from the PM and a late response that is endocytosis dependent (Bonfiglio et al., 2013). In their new work, Inda et al. (2016) reinforce these findings, showing that distinct cAMP sources are differentially involved in the two phases of Erk signaling. Whereas tmAC and sAC both contribute to the acute Erk signaling response, sAC is specifically involved in the sustained “endocytic” phase of Erk signaling in hippocampal neuronal cells (Fig. 1).".

Note phase 1 and 2, targeting one phase or another, rather than continuous action, is spatially encoded.


In which way would the yeast cell cope with the excess amount of methionine in the growth media?

In humans, cysteine first fills the glutathione pool (which itself is a reservoir for cysteine, apart from reduction equivalents and biotransformation). Excess cysteine can go three ways,

oxidation to sulfoalanine and further hypotaurine and taurine, via still unknown enzyme(s)
degradation to lanthionine and toxic H2S
degradation to serine and toxic H2S

Since cystathionine gamma lyase which (its L-cysteine desulfhydrase activity) catalyses 2 and 3 has homologues in yeast, my guess is that H2S is produced there too. Further oxidation of H2S happens through an ancient mitochondrial pathway which is highly conserved as well, yielding sulfite and sulfate. Sulfate then makes for a bit acidic environment but else is non-toxic.

I have linked to reactome.org entries where you can find references. Filling up the yeast's glutathione pool (if it happens) would move the NAD+/NADH balance to the NADH side, i.e., fill up reduction equivalents, too.


Do both Carbamazepinum and Lamotriginum increase glutamate threshold?

Short answer
Both carbamazepine and lamotrigine are listed as Na+ channel blockers. Carbamezipine's action is mainly associated with inhibition of postsynaptic neural activity, while lamotrigine is thought to inhibit glutamate release. Given that glutamate is the principal excitatory neurotransmitter in the brain, and if you insist of using a one-liner I would go for:

  Both lamotrigin and carbamazepine can be said to inhibit glutatamatergic neurotransmission, albeit carbamezipine does so in a non-specific way.

Background
My two most beloved drugs in one question!

First off, this answer is formulated from the perspective of both drugs being used as anticonvulsants in generalized tonic-clonic epilepsies. As anti-epileptics, Both lamotrigine (Lamictal) and carbamezipine (Tegretol) are listed as Na+-channel blockers.

Carbamezipine does so quite specifically, and it inhibits sustained repetitive firing by blocking sodium channels. It does so in a very clever way, as it only binds to Na+-channels of rapidly firing neurons, which is exactly what makes it a good anti-convulsant (Courtney & Etter, 1983). It also is believed to have anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties (Drug bank). Hence, your note that it increases the threshold for glutamate is true in the sense that it is likely to increase the firing threshold of glutamate-activated neurons.

However, note that carbamezipine (nor lamotrigine) does not increase the threshold for glutamate - glutamate has no threshold and hence it cannot be raised. It is incorrect word use.

Lamotrigine is also listed as a Na+-channel blocker, but the exact mechanism(s) behind its anti-convulsive and mood-stabilizing effects are unknown. In vitro pharmacological studies suggest that lamotrigine's inhibiting effects on voltage-sensitive Na+ and/or Ca2+ channels stabilizes neuronal membranes and consequently modulates presynaptic transmitter release of excitatory amino acids (e.g., glutamate and aspartate). It has also been shown to enhance K+ currents and GABA-ergic inhibition (Coulter, 1997). Hence, your note that it decreases glutamate release is correct.

References
Coulter, J Child Neurol (1997); 12: S2-9
Courtney & Etter, Eur J Pharmac (1983); 88: 1-9.


Why do alpha-gal allergies only occur after a tick bite if alpha-gal is already present in red meat?

In order for the immune system to respond to an antigen, beyond recognition of that antigen, there needs to be a signal that there is something wrong. Co-stimulation can take a few different forms, but it requires the involvement of more than just one arm of the immune system, and generally helps prevent our immune system from what I like to call the Dr. Strangelove effect (a psychotic lone general can just decide that there is a problem and launch an attack). Here, costimulation might be from (or downstream of) the tick bite and other invaders associated with the tick bite, or from an allergy to peanuts. You can read about this in the first chapter of Sompayrac's How the Immune System Works, as well as the first chapter of Abbas Basic Immunology.


Is there theory that connects longevity, time-scale of environmental disturbance, and adaptation?

If the disturbance is short compared to a species' lifespan, then it's would be difficult for any adaptations to that disturbance to become fixed. Say an individual with a novel mutation is born during the disturbance that would impart some benefit under such conditions; since the species lifespan is much longer than that disturbance, by the time the individual reproduces, the disturbance will no longer be in effect and thus that allele will no longer be beneficial. In fact, this is seen in the thrifty phenotype in humans. When the mother experiences a period of duress during her pregnancy (say, the Dutch Hunger Winter of 1944), the fetus will undergo epigenetic changes that signal, in effect, that food is scarce and resources should be used sparingly. When those children grow up, they find themselves no longer under harsh conditions and this thrifty phenotype becomes a disadvantage, causing diabetes, obesity and so on.

If the disturbance is on the order of the lifespan of the species or slightly larger and especially if it is cyclic, polyphenism would be advantageous. This might also impart some resistance against long-term change, at least up to a certain point. For example, the butterfly Bycyclus anynana shows marked differences when born in the cool, dry season versus the warm, wet season: different body mass, different resting metabolic rate, different wing patterns and so on. This is controlled by hormonal switches in response primarily to temperature.

It seems that the best strategy in the face of long-term change would be gradual evolution due to progressive selection on traits that impart resistance to the disruption, at the cost of being vulnerable to future reversions in the conditions.

But of course, none of this can be "planned for" by the species. In the face of a new change in environmental conditions, be it gradual or sudden, the species can only work from its current genetic background. So whether there is a specific theory that deals with this (aside from the examples given above) is not clear. I would think that what we will see with strong-but-gradual climate change is a progressive loss of biodiversity (due to the inability to adapt in time) followed by rapid expansion to fill newly opened niches. To that end, I guess Gould's "Wonderful Life" would be appropriate to read. Any book on Evo Devo would lend insight into understanding how species might be able to rapidly adapt to a slowly changing environment, albeit in an indirect/abstract manner (i.e. "food for thought"); I like Sean B. Carroll's "Endless Forms Most Beautiful".


Does gene editing have any technical cross-species limits?

So, I'll assume that you are talking about gene editing in a laboratory (e.g. using a technique like CRISPR).

Theoretically, there are almost no limits to what you can do - or at least try. Fundamentally DNA is the same in all living (and non-living) things on earth, so you can absolutely take a gene from a plant and "paste" it into a human cell/genome (with some additional work needed to make the pasting work). You probably even go further and try to isolate whole chromosomes from one organism and (literally) inject them into cells of another one.

The problem with this radical approach to gene editing is, that it probably won't do much (good). A human cell likely doesn't recognise a plant gene as a gene and so just ignores it (it might still cause indirect problems for the cell though) and if you start making very drastic changes like adding chromosomes the chances that your cells will just die are super high.

This means that in practice you either need to (heavily) modify a gene you want to insert to match the structure and 'expectations' of the target organism - you basically have to make a humanised version of a given plant gene - or you can only use genes from similar enough organisms: as a general rule genes from the same kingdom (bacteria, archaea, plants, fungi, animals) are likely to retain some degree of function in another species (but how much exactly or even a general effect is almost impossible to predict).


Mechanical pressure, stress, strain or distortion are mechanical cues. In general, cues sensed by mechanoreceptors are mechanical cues!


You won't find a good book that presents the 'weaknesses' of the theory of evolution, and for good reason. There has to date been no convincing challenge to the theory, whilst it has been supported by experimental and circumstantial evidence as well as clear logic over and over and over again, as well as actually being observed taking place numerous times. The closest to what looking for is a book which presents our best understanding of how evolution works, or which discusses competing ideas about how evolution works - there's no question about whether it works.

The Selfish Gene by Richard Dawkins, whilst it contains some errors, has some very clear thinking about evolution in it, and in particular explains why group selection is a misguided idea.

The Logic of Chance: The Nature and Origin of Biological Evolution by Eugene Koonin is a more up-to-date coverage of our current understanding of evolution, in particular with insights from modern genomics.

There are plenty of terrible books about the weaknesses of evolution, but they are deeply flawed. Pick one and I'll be happy to debunk it for you.


Does pre-operational exercise affect recovery from surgery? Statistical Analysis

Regarding your first question, the effect size is not invalid if the confidence interval (CI) crosses 0. The effect size is a point estimate. When the CI -a range estimate of the coverage probability- includes 0, the probability that the range of the effect size can include 0 cannot be rejected at the $1-\alpha$ level of confidence.

Regarding your second question, from the definition of Hedge's g:

$$g = \frac{\bar{x_1} - \bar{x_2}}{sd_{pooled}}$$

we can see that if $\bar{x_2}$ is larger than $\bar{x_1}$ then $g$ will be negative. So, the sign only determines which of the estimates is larger and that will depend on which estimate is considered as the reference.