Expiring food items is obvious: for fresh food, it's almost always due to bacterial or fungal decay (spoilage).

Oxidization and sunlight doesn't really ruin food; it might alter the taste or decrease its appeal, although it remains edible even by first-world standards. However, it might destroy vitamins and other nutrients.

Medicines are a different matter. Some chemical compounds are slightly unstable, with half-lives measured in years. Instability can cause the compounds to randomly break into subcompounds that are ineffective for treating the intended condition at best and poisonous at worst. Unlike food, it's imperative to keep medicines away from sunlight (and oxidation in some cases) as both of these can further promote instability and breakage into subcompounds.

On the comment that Charles posted about medicine shelf life being much longer than advertised: The reason why they underestimate the shelf life is that it's better to have people throwing out potentially OK medicine than to have it sitting on a shelf for 20 years, going bad and sickening people, and prompting numerous lawsuits against the manufacturer. This type of deliberate underestimation in the name of safety is common in engineering - usually with weight limits advertised below the real weight limit. For example, an elevator able to haul 6000 pounds might be advertised as only 2000 because the manufacturer knows there's always going to be a few idiots who disregard the posted limit.


The situation you are describing where muscles are situated on opposites sides of a joint and produce opposing movements is called "antagonism." Most joints are set up where one or more muscles on either sides will produce such movements (e.g., flexors vs. extensors). Here's a question about muscles without antagonists.

When you contract all the muscles crossing a joint (i.e., when you are "showing off"), the muscles balance each other. If not, the bones would move and the joint angles would change. So taking the elbow as an example, in the image below, Arnold is contracting the elbow flexors (biceps brachii, brachialis) as well as the elbow extensors (triceps brachii). In order for the bones to remain static, the forces must be equal and opposite.


What advantage would the initial 'donor' in horizontal gene transfer by conjugation have received?

The donor bacterium, viewed as a unit, may well gain no advantage from sharing its genes.  The genes that are shared, however, may gain a very substantial reproductive advantage from being able to spread to other strains.  If some of the genes that are capable of being shared also promote sharing, they may be selected for by evolution.

This is a good example of the basic principle of the gene-centered view of evolution, famously popularized by Richard Dawkins is his book The Selfish Gene: evolution selects for genes that are good at spreading themselves.  This may, but need not always, imply helping the organism containing the gene to survive and reproduce.


What does "optimal balance of biological control" mean in nematodes?

It is a long-winded way of saying that these are the only nematode genera that are useful for biological control. In particular the article is referring to Steinernema and Heterorhabditis, both of which genera are used for control of some pest insects.


Is it possible to isolate and analyse intermediates of protein folding?

Theoretically by molecular modeling -- see the works by Harold Scheraga:
https://www.ncbi.nlm.nih.gov/pubmed/?term=Harold+Scheraga%5BAuthor%5D

Note: An unfolded protein is not a random coil.

Fitzkee & Rose (2004) PNAS 101:12497-12502; emphasis mine:

  denatured proteins are biased toward specific conformations, in
  ... conflict with the random-coil model

https://www.ncbi.nlm.nih.gov/pubmed/15314216


Small black slow-moving insect showing up in the home

Based on the hard-looking outer "shell" and elongated nose, this is certainly a type of beetle called a  weevil.

Given the size of the weevil, the time of year and the location of your home (second floor in a large city), I would guess this is certainly some species of nuisance/pest weevil.

Candidates include:

Wheat weevil (Sitophilus granarius)

Range: Worldwide
Food: wheat, oats, rye, barley, rice and corn
Appearance: 3–5 mm long with elongated snouts; reddish-brown
Life History: 36-254 eggs in 5-20 weeks

Rice weevil (Sitophilus oryzae)

Range: worldwide
Food: wheat, rice, and corn
Appearance: 2-3 mm, long nose, brown/black in color with 4 orange/red spots
Life History: 300 - 400 eggs per month [source]
Note: can fly

Maize weevil (Sitophilus zeamais)

Range: cosmopolitan in warmer climes [source]
Food:  corn (maize), wheat, rice, sorghum, oats, barley, rye, buckwheat, peas, cottonseed, other types of stored, processed cereal products (e.g.,  pasta, cassava, other coarse milled grains), and even has been known to attack fruit while in storage (e.g., apples)
Appearance:  2.5 - 4 mm, brown with four reddish-brown spots on elytra, long/thin snout, and elbowed antennae

See this Wikipedia page for a comparison of the rice vs. maize weevils

Life history: 300 - 400 eggs per 36 days

If you've been seeing multiple of them, that likely means they are breeding in some container of grain (wheat, rice or corn perhaps) you have in your home and could be well on their way to an infestation if your grain source is large enough. I recommend you check all sources of dried foods in your home to see if you hear/see weevils in it or coming out of the container.

Given the relatively large number of eggs each female can lay and given the month long generation time, this is an infestation you'd like to stop quickly.

 Note: all info is from the linked/cited Wikipedia pages unless otherwise cited.


Your question would deserve a long essay. R.C. Lewontin wrote a book ("The genetic basis of evolutionary change" - Columbia U.P) on this subject in 1974, right after the neutral theory had been explicitly formulated in the previous few years. The reasons for the controversy over this theory are still alive some 50 years later, despite the enormous advancements in DNA technology. For example the not so hidden polemical tone of this recent paper would not be understandable if some profound ideological issues were not involved; these issues involve something more than "attacks on specific points of neutral theory, (...) or perhaps as attacks on the specific meaning of the term".
In essence, Lewontin argues that the neutral theory has its philosophical roots in the Platonic notion of "ideal" or "type", for which real objects (the genes, in the present case) are only imperfect approximations. This view, applied to the genetic variation in animal species, implies that the role of natural selection is mainly “purifying”, that is, it acts by removing the slightly deleterious mutations that happens continuously and degrade all genomes (when mutations are perfectly neutral, selection does not act at all). As Kimura and Ohta have said, quoting Muller, “the gene through the long course of evolution has finally found itself in man” (quoted in Lewontin, above, p. 30).
The opposite view (can we refer to it as Democritean?) sees all natural populations, man included, as being continuously modeled by unstable and ever-changing environments, so that any attempt to define an “optimum” is intrinsically meaningless. Genomes are highly integrated pieces of firmware, but they are much more fluid, over the generations, than once thought. This means that all genetic variation may have or may acquire meaning, as their molecular or ecological context changes.
Consider an applied consequence of the two views. One of the claims of most anti-racist geneticists is that the variance component among populations of gene frequencies is much higher than the component within populations; this allegedly falsifies the racist argument according to which the differences observed among human population (races) are mostly genetically determined. But if you claim that most of that genetic variation is irrelevant (“neutral”), what remains are the genes responsible for the differences in phenotypic traits, and it becomes obvious that the variance component among populations in the frequency of these genes is lower with respect to the component within populations; and this may be interpreted as supporting a racist view.
It is not automatic that scientists who prefer one theory to the other also support the philosophical implications of that theory. However, the dispute about the neutral theory of evolution cannot be understood without reference to the above conceptual basis.


Which processes are included in the process called cells eating themselves?

So:

the processes are mentioned in the quote you provided: "ubiquitine-proteasome pathway (note: it's proteAsome) and autophagy pathway". As far as I know, apoptosis per se is not utilized for recycling.


Is a female spider, well-fed by sexual cannibalism, less likely to mate again?

It does appear that Wikipedia has not provided the most appropriate reference for that statement, but it is repeated in the article it refers to and that you link to, both in the abstract:

  Male sacrifice may be adaptive because cannibalized males increase their paternity relative to those that are not eaten

and in the  body of the introduction:

  Males that are cannibalized obtain paternity advantages compared to males that survive copulation

These statements do not necessarily contradict the other statement that a well-fed female is less likely to consume her mate, but there might be some nuance missing here in terms of mating versus mate consumption behaviors. However, the authors cite Andrade, 1996 (see below) for the second statement, and this seems like a more appropriate reference for the statement on Wikipedia:

Yes, a female spider who eats her mate is less likely to mate again. Andrade 1996 shows that males who are eaten during copulation mate longer, fertilize more eggs, and the females are more likely to not mate again after eating a mate.

Andrade, M. C. (1996). Sexual selection for male sacrifice in the Australian redback spider. Science, 271(5245), 70-72.


White resin or powder on conifer needles

I believe this is actually crystallized sap which formed on and around the bud as the bud opened up and new leafs emerged.

Note that some coniferous trees have a powdery coating as part of the leaf itself, continuing on throughout the life of the leaf. Blue spruce is a good example of this, as its dark green needles appear blue/gray due to a waxy coating the needles. This wax can be easily scraped off the leaf.


How did the nucleobases in the Murchison meteorite form?

It is interesting to note that, in the Wikipedia article, it states that

  The amino acids were racemic (that is, the chirality of their enantiomers are equally left- and right-handed), indicating that they are not present due to terrestrial contamination".

This implies that, if a 'life form' did create these proteins, they are fundamentally quite different to life on earth. (Particularly in light of the 70 unique amino acids they described!).

We cannot ever 'know' how they were made, unless a pretty revolutionary discovery is made that undisputably confirms evidence for extra-terrestrial life (although this is the best evidence yet!), so we are left to speculation.

The nucleobases either formed 'randomly' in one of the countless celestial events (although the chances of this seem pretty remote given the complexity of the molecules and the homogeneity in the sample), or they were made by extra-terrestrial 'life' (much more exciting, and indeed probably more likely, as we will see). (Or the 3rd option: intelligent design, however this is dramatically less probable than either of the other two).

The Miller-Urey experiment to which you refer has been subsequently enhanced, and evidence for the "catalytic potential of cosmic dust" is now reasonably robust (Hill, 2004). They demonstrate that simple nebular iron silicate catalysts can yield methane and water from CO₂ and H₂, and ammonia from N₂ and H₂. Allowing these to react yields nitrogen-containing organics such as methyl amine.

It is not a huge jump to suppose that with enough time, mass and energy, these reactants could combine and form a molecule (chain of amino-acid-like molecules - a protein) capable of faithfully replicating itself, and thus initiate life. There is no reason to suppose that Earth is unique in this respect; there are billions of suns in our galaxy alone, and billions of years of time for these reactions to take place.


What does it mean to "nucleate multi-protein complexes"?

Here nucleation has a rather physical meaning. mTOR acts as the starting assembly point of the complex.


What's the role of bromelain in pineapple?

Antifungal properties? as tested in below article.

López‐García, B., Hernández, M. and Segundo, B.S., 2012. Bromelain, a cysteine protease from pineapple (Ananas comosus) stem, is an inhibitor of fungal plant pathogens. Letters in applied microbiology, 55(1), pp.62-67. Available here


This page from Cole-Parmer includes everything you could possibly want to know about the adsorption of biomolecules to polystyrene. To summarize:

binding is neither covalent nor ionic, but
it is generally mediated by non-specific intermolecular van der Waals interactions, which generally are about 100X weaker than ionic or covalent bonds
the exception is some hydrogen bonds, which can be 10X stronger than the other types

  Intermolecular attraction forces are based on intramolecular electric polarities of which two types can be distinguished: alternating polarities (AP) and stationary polarities (SP), i.e. dipoles.

these interactions can be both hydrophobic and hydrophilic, depending on the surface chemistry of the polystyrene

If you're interested in the specific chemistry of everything, feel free to read the entire thing, it's quite detailed.

I would to note one thing from your question. In the absence of a specific binding partner like Protein A, antibodies bind to polystyrene completely non-specifically, meaning that not only does the Fc region bind, but Fab as well, including the CDRs (antigen binding domains). An ELISA depends on the fact that not all antibody molecules bind this way, so many or a majority of them have their antigen binding sites available to capture their target.


Sensitivity vs. Limit of Detection of rapid antigen tests

Not necessarily. Sensitivity and specificity are decision criterion-based measures. They are not actually separable from another, they are a consequence of choosing a threshold at which to say "the test reports positive" or "the test reports negative", a consequence of this binary result. As such they are weighed against each other. You can always make a test with 100% sensitivity as long as you always report "Yes". You can always make a test with 100% specificity as long as you always report "No".
Similarly, you can define what it means to have reached a limit of detection, but this need not be the same trade-off as the one you use for sensitivity and specificity. For example, you might declare this as the point where your readout is "significantly greater"  than baseline in a collection of known positives vs known negatives. But if you set your decision threshold right at that level of detection, you may still have, let's say, only 50% specificity at that level and accept too many false-positives, so you set a different decision criteria.
They are apples and oranges, there is no reason they need to correspond.


Do swarm of the same species attack each other?

It will depend on the species and group you're talking about. If the species is territorial, one swarm will tend to chase the other away. If it's a locust, they'll merge until they get to trillions of tons...

A study on wasps (Vespidae) I've read years ago showed an interesting experience. One individual wasp was tied by the waist and put close to different nests. The violence demonstrated by the nest was greater in a different species, median in the same species with a greater genetic distance, and none to her own or related nests.

Some "solitary" bees are very interesting in this respect, because they show many different kinds of sociality in related or even the same species, like many Halictidae and Euglossina (Apidae).


Determining the osmolarity and tonicity of a cell

The efflux of water isn't instantaneous. Since urea is free to move across the membrane, it will (and with a net movement from higher to lower concentration).


What is the name of this plant I found in ROAD HIGHWAY?

It is Fishtail Palm, Example picture look like this:


Do mitochondria simply automatically convert glucose to ATP?

Mitochondria are comprised of ~3000 proteins. However, the mitochondrial genome has only 13-14 protein-encoding genes. The remaining 99.6% of mitochondrial proteins are encoded by genes in the nuclear genome. (Wikipedia) Chloroplast genomes are only slightly larger (~100 genes).

Gene regulation and signaling between the nucleus and mitochondria (and between nucleus & chloroplast in plants/algae) occurs in both directions. Anterograde regulation is the signalling from nucleus to mitochondria and was once thought to be the only method of regulating organelle function. We now also know that Retrograde regulation occurs, in which the mitochondria sends signals to the nucleus.

To answer your question directly (but not thoroughly), both the mitochondria and the nucleus are sensing the environment and needs of the cell and signaling to each other to regulate ATP production.

If you want to learn more about retrograde signaling, googling "retrograde regulation" will bring up lots of papers on this topic in different organisms. This paper also has some diagrams of signalling pathways.


It seems like they are not affected by fluorescent light frequency. I did not find anything about their visual sampling rate. Their hearing is between 0-200Hz with an average of 86Hz so I guess the visual sampling rate is under this, but that's just a guess.

  We conclude that at the illumination levels used in this experiment,
  the hens did not perceive the flicker of low-frequency light or they
  perceived it but did not find it aversive. Low-frequency fluorescent
  light does not appear to adversely affect the welfare of hens.

1996 - Laying hens do not have a preference for high-frequency versus low-frequency compact fluorescent light sources

  It concludes that there is no evidence that fluorescent or high
  pressure sodium lighting, irrespective of intensity or spectral
  distribution, has any consistent detrimental effect on growth, food
  utilization, reproductive performance, mortality, behaviour or live
  bird quality in either domestic fowl or turkeys, nor in the egg
  production of geese.

1998 - Responses of domestic poultry to various light sources

A monochromatic (LED) light can be more beneficial according to this:

  A significant reduction in egg production was observed in all 880nm
  groups; no differences in egg production and quality were found in the
  other groups. Feed consumption was significantly lower by 7% in all
  0.01 W/m2 groups. We suggest that an important reduction in rearing costs of laying hens may be obtained by using this system.

1998 - New monochromatic light source for laying hens


Changes of permeability and driving force during voltage clamp

Relative ion permeabilities determine the equilibrium for a given configuration of ion channels. You can easily understand what is about to happen to the voltage of a cell if you know the permeabilities: if the equilibrium voltage is more positive than the present voltage, then the voltage will increase over time. The rate at which it increases depends on the membrane time constant, which depends on the capacitance of the cell (which is based mostly on membrane area, and stays relatively constant) and the resistance; the resistance is, again, based on permeability.

So permeabilities tell you A) Where you are going, and B) How fast you are going there. This is all relevant if you are living in "voltage land": you can actually ignore currents completely and just think in terms of voltage. This is the situation in 'current clamp' recording and for the most part I would say is the easier way to understand the 'big picture' for a neuron.

If, however, you want to think about currents themselves, then you typically clamp the voltage. Clamping the voltage also keeps the driving force constant (at least over the time scales on which voltage-clamp experiments make sense). In that case, you are right, you can't ignore driving force, however, in that case you are usually setting the driving force (by setting the voltage), and measuring the current. "Driving force" is then only necessary to figure out the permeability.

If you voltage clamp a cell at a depolarized potential for a long time (minutes), eventually yes the ion concentrations will change. Voltage-gated sodium channels tend to inactivate pretty quickly, so you actually won't get much sodium current when you voltage clamp at -20 mV for a long time, at least not in the soma, but you might get more current out in the distal processes that are not clamped well and other ions like calcium. Cells do not hold up well under long-term voltage clamp, however. I believe the main culprit is calcium toxicity, though it might vary by cell type and other particulars of the recording configuration. You can also kill a cell by just disrupting the membrane and making it more leaky: the concentrations change faster than the pumps can keep up with and you get excitotoxic cell death.

I usually recommend Purves' Neuroscience as a basic textbook, and the Methods in Enzymology volume on Ion Channels edited by Rudy and Iverson for patch clamp techniques and related practical wisdom.


Can a person die from over exposure to rain?

Rain per se? No. But when you are wet, your body looses heat more quickly. If it's near freezing, windy, and raining you are in much more danger of developing hypothermia, or low body temperature. If your body temperature falls low enough, you can die. You may hear references to death from exposure, which is shorthand for "exposure to the elements", but the actual problem is hypothermia. If your feet are continuously wet for days and day, you may develop immersion foot, also called trench foot:

  Trench foot is a medical condition caused by prolonged exposure of the
  feet to damp, unsanitary, and cold conditions. The use of the word
  trench in the name of this condition is a reference to trench warfare,
  mainly associated with World War I. Affected feet may become numb,
  affected by erythrosis (turning red) or cyanosis (turning blue) as a
  result of poor vascular supply, and feet may begin to have a decaying
  odour due to the possibility of the early stages of necrosis setting
  in. As the condition worsens, feet may also begin to swell. Advanced
  trench foot often involves blisters and open sores, which lead to
  fungal infections; this is sometimes called tropical ulcer (jungle
  rot).


Diffusion coefficient of cells in blood?

Cells absolutely can be considered as diffusing objects.  However, the origin of the "diffusion" can be very different than for, say, a bead in water.  The reason is that the thermal motion that creates the diffusion of a micron-sized bead can be much less important for a (large) cell.  For instance, the diffusion coefficient due to thermal forces of a sphere in a fluid with viscosity $\eta$ is
$$D_{therm} = \frac{k_B T}{6 \pi \eta R}$$
where $R$ is the cell radius (this is the "Stokes-Einstein" result).  For a white blood cell (say 10 microns in radius), this would - assuming blood is at least as viscous as water - lead to thermal diffusion coefficients around 1 microns$^2$/hour- i.e. we would need many many hours for a cell to travel its own diameter.  This result neglects a bunch of complexities - blood is not perfectly viscous, there is a really high density of red blood cells in blood, etc... but the basic result is that the thermal buffeting that drives the diffusion of a colloidal bead is not enough to drive a cell.
However, cells are not passive beads!  They crawl, both randomly, and (as cancerconnector notes), in response to signals like chemical gradients.  If a cell crawls with a speed $v$ and maintains its orientation over a time $\tau$, it's reasonable to describe its motion (over times much longer than $\tau$ as being diffusive with an effective diffusion coefficient
$$D_{motility} = \frac{1}{2} v^2 \tau$$
which you can get mostly from dimensional analysis, or more rigorous models.  For white blood cells, $v$ is on the order of microns/minute - at least when measured on slides - it might be different in the body.  $\tau$ is a few minutes, so $D_{motility}$ is on the order of many microns$^2$/minute - orders of magnitude faster than mere thermal diffusion.
A good introduction to modeling of this question is probably chapters 9-11 of Leah Edelstein Keshet's "Mathematical Models in Biology" and she cites some classic Lauffenberger papers on macrophage response, etc.  You may have access to this online: http://dx.doi.org/10.1137/1.9780898719147
Also, note that everything I've said so far neglects blood flow - if this is important in your problem (which will depend on the context), things can get more complex (have to include flow in your diffusion equation).  But using diffusion equations to model the spread of randomly motile cells is a very common approach, and there is a lot of literature on it!


What is the process of degradation of proteins into amino acids inside living cells?

There are two major pathways through which proteins are degraded in your generic cell: In a lysosome or in a proteasome.

The Lysosome

It's considered an organelle. It has a lipid bilayer that encloses a potent cocktail of acid hydrolases working at a low pH. The pH is maintained by a Cl-/H+ antiporter(Ref). Acid hydrolases that are being processed in the golgi are targeted to the lysosome through mannose-6-phosphate residues which are recognized by the trans golgi M6P receptors, packaged into clathrin vesicles, and targeted to acidic late endosomes which fuse, forming the lysososome (Ref).

So through endocytosis or phagocytosis, vesicles full of extracellular proteins are uptaken and may fuse with a lysosome. The hydrolases thus digest whatever they can. In a cell stress response cells may also digest their own contents with the aid of lysosomes in a process called autophagy. We can take a look here at some established lysosomal enzymes current to 2009, and if you spot a protease you can generally take a look at it's specific mechanism to see how it works. So I'll pick one out of the bunch (a lysosome has many different hydrolases remember), Dipeptidyl-peptidase I aka Cathepsin C. The mechanism of proteolysis is that of a cysteine protease which follows a bit of a generic mechanism like so:

... and so forth, you can look at a given given protease, and roughly determine how it cleaves peptides.

The proteasome

This one is a a much more directed form of protein degradation. Proteins must be tagged on lysine residues by molecules of ubiquitin, at least 4, referring to the term polyubiquitination. These are added sequentially by proteins denoted E1, E2 and E3 (see proteasome wiki). Proteins that get degraded in this manner are often damaged or come from within the cell, unlike the lysosome where the proteins probably came from outside the cell.

The catalytic domain of the proteasome is a threonine protease which follows the generic mechanism of the catalytic triad, one of the most well-studied protease mechanisms. We can view this generally through the mechanism of a serine protease, like so:

If you read through the whole thing, two notes: (1) the generic term for protein degradation is proteolysis, and (2) The mechanism depends on the protein performing the proteolysis, namely a protease.


What are iPSC cells, and what are their applications?

From this article: iPSC's or induced pluripotent stem cells are somatic cells that have been driven to acquire an induced pluripotent cell state.  Somatic cells can be any cell of the body except sperm cells, egg cells and undifferentiated stem cells. Investigators can induce these cells to 'return' to a stem cell like state by forcing the expression of key transcription factors, and by genome-wide remodeling of epigenetic marks.

There is an entire spectrum of different iPSC's that can be generated, but much is not yet known. Future applications include using them for regenerative medicine, drug discovery, etc.

Recently there were several articles published in nature:

Stem cells: A designer's guide to pluripotency
Genome-wide characterization of the routes to pluripotency

amongst others. Also you can check out http://www.stemformatics.org/ for more information on stem cells and research being done.


How do the first and second law of thermodynamics adhere to breakdown of glucose?

The Second Law of Thermodynamics is intimately linked to the thermodynamics of the breakdown of glucose. By "the thermodynamics of the breakdown of glucose," I mean: is the breakdown of glucose spontaneous, is it thermodynamically favorable?

You may have seen the criteria for the thermodynamic favorability of a reaction in terms of Gibbs Free Energy:

$$\Delta G = \Delta H - T\Delta S\leq0$$
That is, for a reaction to be favorable, the change in Gibbs free energy from the initial state (glucose) to the final state (carbon dioxide, water, and energy) must be negative. This equation is valid for systems at constant temperature and pressure, which is assumed to be satisfied in biological systems. According to Wikipedia, $\Delta G$ for the breakdown of glucose is negative, $\Delta G = -2880$ kJ/mol.

However, there is a nice derivation on Wikipedia that the above equation is nothing more than a statement of the second law of thermodynamics, applied to the case of constant temperature and pressure. So in sum, the second law of thermodynamics is the reason that glucose can be broken down in such a way that useful energy is released in the form of ATP, i.e. that the reaction is spontaneous or thermodynamically favorable. Saying that the Gibbs Free Energy of the breakdown products is lower than that of glucose itself is the same as saying that the breakdown of glucose does not decrease the total entropy of the reaction and its environment.


Would a plant survive if it was watered using hard-water?

It would depend on the content of the hard-water. If the water contained heavier metals like lead or radioactive elements like tritium (Hydrogen-3), the plant would most likely die. Most land plants cannot survive when watered with massive amounts of salt water as the salt would absorb the water from the leaves.


Does X-inactivation lead to expression of sex-linked recessive disorders in half of carrier females' cells?

Yes and No... You are correct that X-Chromosome Inactivation will randomly inactivate the good X-chromosome (i.e. the one NOT carrying the mutation/disease) half of the time. However, this doesn't always seem to be associated with a disease phenotype. It likely depends on the gene and other factors, like the gene allele's function, to determine whether there is a disease phenotype that manifests with inactivation. Check out this paper that looked at Duchenne muscular dystrophy in females that is available freely on PubMed.


What do viruses do during incubation period?

during the incubation period the virus is typically increasing in numbers and spreading between cells. It takes a while for symptoms to become obvious because it takes time for enough damage to be built up in the tissue to become noticeable.
Take for instance the Rhinovirus which causes the common cold, once you become infected it is a day or so before enough damage has been caused to the tissue at at the back of the throat to give you a cough.

In addition some of the symptoms of infection are caused by your own immune system as a way of fighting the infection. For instance inflammation is often a sign of infection but is typically caused by the immune system to allow the movement of plasma and leukocytes into the infected tissue. As the immune system requires time to recognise and respond to a pathogen this leads to the delayed onset in symptoms.

AIDS is actually a syndrome caused by the HIV virus. the HIV lifecycle occurs CD4+ T-Cells, after infection occurs the immune system tries to cope by destroying the infected cells but over long time the infected population increases. The immune system becomes more and more compromised until the CD4+ cell count drops to a level where the patient is diagnosed with AIDS. At this point the immune system is compromised and the chance of a secondary infection by a different organism increases which the patient can no longer fight off. The actual cause of death for someone infected with HIV is rarely the HIV itself but is quite often a different agent.


Burning fat transferred from one part of the body to another

Would the body use this transferred fat for as energy, or would it
  ignore it as it wasn't stored there in the first place?

It would use it as energy source, there is no such thing as "ignored tissue". Fatty acid mobilization is regulated by epinephrine and insulin. These are hormones which are ofc. carried by blood, so every white adipose (fat) tissue is affected by them.

Figure 1 - FFA and glycerol mobilization - source
2003 - Fatty acid mobilization from adipose
tissue during exercise

  Does the body differentiate fat cells stored in different parts of the body?

This is obvious, just check breasts and butts of girls. ;-) (Those are subcutaneous fat depos. They size is probably regulated by estrogen.)

There are other things involved here, we can talk about subcutaneous (fat below the skin), intramuscular (fat in the muscles) and visceral (abdominal fat) white adipose tissue (there are white, brown and beige adipose tissues). The visceral fat is associated with metabolic diseases, obesity etc...

1995 - Pathophysiology and Pathogenesis of Visceral Fat Obesity
2012 - Lower Thigh Subcutaneous and Higher Visceral Abdominal Adipose Tissue Content Both Contribute to Insulin Resistance
2013 - Genomic and epigenomic regulation of adipose tissue inflammation in obesity

The regulation of body fat distribution and amount is complicated and regulated differently by subcutaneous, intramuscular and visceral fat.

  The total transmissible variance ranged from about 40 percent for the
  amount of subcutaneous fat to 60 percent for the pattern of
  subcutaneous fat distribution. Biological inheritance accounted for
  only 5 percent of the variance for subcutaneous fat and the body mass
  index, but 20 to 30 percent for the percentage of body fat, fat mass,
  fat-free mass, and fat distribution. These data suggest that the
  amount of internal fat is influenced by heredity more than the amount
  of subcutaneous fat. Furthermore, we consistently found that
  nongenetic influences are quite important in determining the amount
  and distribution of body fat in the population.

1988 - Inheritance of the amount and distribution of human body fat

  These data suggest that adiponectin concentrations are determined by
  intra-abdominal fat mass, with additional independent effects of age
  and sex. Adiponectin could link intra-abdominal fat with insulin
  resistance and an atherogenic lipoprotein profile.

2003 - Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex

  The FFA storage pathway, which had remained undetected in
  postabsorptive humans until recently, can have considerable,
  long-term, and sex-specific effects on body fat distribution. It can
  also offer a way of protecting the body from excessive circulating FFA
  in obesity.

2011 - Storage of Circulating Free Fatty Acid in Adipose Tissue of Postabsorptive Humans
Quantitative Measures and Implications for Body Fat Distribution

Different colors (white, brows, beige) and orgin (subcutaneous, intramuscular, visceral) originate from different progenitor cells.

  These results reveal a major ontogenetic difference between visceral
  and subcutaneous WAT, and pinpoint the lateral plate mesoderm as a
  major source of visceral WAT. They also support the notion that
  visceral WAT progenitors are heterogeneous, and suggest that
  mesothelium is a source of adipocytes.

2013 - Visceral and subcutaneous fat have different origins and evidence supports a mesothelial source

  Brown and white adipocytes have been shown to derive from different
  progenitors. In this study we sought to clarify the molecular
  differences between human brown and white adipocyte progenitors cells.

2014 - Comparative gene array analysis of progenitor cells from human paired deep neck and subcutaneous adipose tissue

The regulation of fat distribution is under research, and not fully understood yet.

  Fat distribution differs in men and women, but in both sexes, a
  predominantly gluteal-femoral compared with abdominal (central) fat
  distribution is associated with lower metabolic risk. Differences in
  cellular characteristics and metabolic functions of these depots have
  been described, but the molecular mechanisms involved are not
  understood.

2012 - Distinct Developmental Signatures of Human Abdominal and Gluteal Subcutaneous Adipose Tissue Depots


Are bears related to dogs in a similar way to how cats are related to 'panthers'?

No, because panthers are cats, but bears are not dogs. You can see their phylogeny in a figure from one of my papers here: https://www.researchgate.net/figure/Most-likely-phylogram-derived-from-the-Bayesian-Analysis-ln-533753675-Numerals_fig1_6550244

As you can see, Bears are most closely related to pinneped (seals and sea lions), with dogs as sister to that group.


Does cell culturing contribute to dangerous antibiotic resistance to the same degree as livestock?

Antibiotics are used in very different ways in cell culture and in livestock farming.
As you note, in farming, antibiotics are used to manage infection in unsanitary conditions and also to increase animal growth. Farming is essentially an inherently non-sterile environment and so there's not really any good way to keep microbes from spreading and interchanging, potentially carrying antibiotics resistance with them.
In cell cultures, on the other hand, one is typically working with a largely sterile environment, and it has to be maintained that way in order for the cell culture to work. They are far, far more delicate than farm animals---but they also can be entirely enclosed in a sealed vessel. Getting a significant contaminant into such an environment is not a "treat the sick animal" situation but a "sterilize and purge the bad batch" situation. Antibiotics are indeed often used as part of this defense, but the potential modes of infection are very different than with animals, which rules out many classes of pathogen simply because they are adapted for respiratory or gastrointestinal transmission, and a cell culture does not have these things.
Moreover, for most current industrial cell cultures, if the product is not the cells themselves, everything alive including pathogens will generally get killed off during later stages of the process (e.g., pasteurization of wine and beer).
If the cells themselves are the target of mass-scale culturing, e.g., cultured meat, however, then there will indeed be opportunities for antibiotic resistant pathogens to be developed and spread, particularly as increasing scale of operation
offers more opportunities for sloppy operations and regulatory evasion by low-cost operators.
Bottom line: antibiotic resistance is generally far less of a concern with cell culture than with livestock, but may still be at least somewhat of an issue.


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


Is it possible to become pregnant indirectly?

yes this is possible, as long as the sperm make it onto the mucus membrane of the vagina. the LIKELYHOOD depends on the fabric and how much semen is in the fabric, if it's still clotted or not, and environmental factors.


Good question! The way that the carbon budget stays balanced was a bit of a mystery until recently. The amount of carbon in the atmosphere (and the rate at which it was increasing) was lower than models suggested that it should be, given rates of photosynthesis, respiration, and other carbon releasing processes. Somewhere, there was a "missing carbon sink" that wasn't being accounted for. After many years of debating whether the sink was terrestrial or aquatic, it turned out to be a little of both (which is the conclusion to just about every debate in ecology), although somewhat skewed towards the terrestrial (I think). Forests were sequestering more carbon than had been thought, and so were oceans to some extent (although ocean sequestration relied on a chemical reaction that is in danger of reversing if the water warms up too much). For a thorough account, see this article.

But it sounded like you weren't wondering what the missing sink was so much as how there continues to be enough carbon in the air for plants to photosynthesize (if I'm interpreting your question correctly). Carbon gets back into the air for the most part because of cellular respiration, which all organisms, including plants, do. Net primary productivity takes plant cellular respiration into account, but there are still tons of living things on earth eating plants (and thus taking in their carbon) and then breathing it back out after they break down the carbon-containing molecules for energy. There is also natural combustion and volcanoes and such putting carbon back into the air.

EDIT (to address the new part of your question): Oil and coal were produced when large quantities of carbon were buried deep under ground (and thus subjected to lots of pressure) for thousands of years. This is suspected to have happened during the aptly name Carboniferous era, which featured giant plants and, scientists hypothesize, no decomposers to break them down. Since we have much decomposers now, and much smaller plants, oil and carbon are not currently being produced. This is why we call them non-renewable resources. By extracting them from the ground and burning them, we are taken carbon that had effectively been removed from the pool of actively cycling carbon and adding it back in.

The carbon cycle doesn't really have input or output (except the occasional carbon exchange with outer space), because it is defined as already including standing sinks like oil and coal. When we take carbon out of a sink, like oil or coal, it needs to go somewhere else. Terrestrial and aquatic sinks can store some of the additional carbon that we're adding to the not-underground part of the cycle. However, they can't store all of it, so some is staying in the atmosphere instead.


Why does evolution not make our life longer?

Why do we age is a classical question in Evolutionary Biology. There are several things to consider when we think of how genes that cause disease, aging, and death to evolve.

One explanation for the evolution of aging is the mutation accumulation (MA) hypothesis. This hypothesis by P. Medawar states that mutations causing late life deleterious (damaging) effects can build up in the genome more than diseases that cause early life disease. This is because selection on late acting mutations is weaker. Mutations that cause early life disease will more severely reduce the fitness of its carrier than late acting mutations. For example, if we said in an imaginary species that all individuals cease to reproduce at 40 years old and a mutation arises that causes a fatal disease at 50 years old then selection can not remove it from the population - carriers will have as many children as those who do not have the gene. Under the mutation accumulation hypothesis it is then possible for mutations to drift through the population.

Another hypothesis which could contribute to aging is the antagonistic pleiotropy (AP) hypothesis of G.C. Williams. Pleiotropy is when genes have more than one effect, such genes tend to cause correlations between traits, height and arm length probably have many of the same genes affecting them, otherwise there would be no correlation between arm length and height (though environment and linkage can also cause these patterns)... Back to AP as an explanation for aging, if a gene improves fitness early in life, but causes late life disease it can spread through the population via selection. The favourable early effect spreads well because of selection and, just as with MA, selection can not "see" the late acting disease.

Under both MA and AP the key point is that selection is less efficient at removing late acting deleterious mutations, and they may spread more rapidly thanks to beneficial early life effects. Also if there is extrinsic mortality (predation etc.) then the effect of selection is also weakened on alleles that affect late life. The same late-life reduction in the efficacy of selection also slows the rate at which alleles increasing lifespan spread.

A third consideration is the disposable-soma model, a description by T. Kirkwood of life-history trade-offs which might explain why aging and earlier death could be favoured. The idea is that individuals have a limited amount of resources available to them - perhaps because of environmental constraints or ability to acquire/allocate the resources. If we then assume that individuals have to use their energy for two things, staying alive via repair and maintenance (somatic-maintenance) and making offspring (reproductive-investment), then any energy devoted to one will take away from the other. If an individual carries a gene that makes it devote all of its energy to somatic maintenance then its fitness will be very low (probably 0!) and that gene will not spread. If the level of maintenance required to live forever costs more energy than an individual can spare without suffering from low fitness (very likely) or can even acquire and efficiently convert in the first place (also very likely) then high-maintenance alleles will not spread (and aging & death will continue to occur).

To go a little further, it is common for sexes to age differently (this is what I work on) and one possible explanation is that the sexes favour different balances of the trade off between somatic-maintenance and reproductive investment, this can lead to conflict over the evolution of genes affecting this balance and slow the rates of evolution to sex specific optima. This paper provides a good review of the area.

To summarise, evolution has not managed to get rid of death via genetic disease etc. (intrinsic mortality) because the effect is only weakly selected against, and those alleles may provide some early life benefit, and resource limitation may also reduce the potential to increase lifespan due to trade-offs with reproductive effort. Adaptive evolution is not about the survival of the fittest but the reproduction of the fittest - the fittest allele is the one which spreads the most effectively.

EDIT: Thanks to Remi.b for also pointing out some other considerations.

Another thought is that of altruistic aging - aging for the good of the population (the population is likely to contain related individuals, you are related to all other humans to some degree). In this model aging is an adaptive process (unlike in MA where it is just a consequence of weak selection). By dying an individual makes space for it's offspring/relatives to survive (because resources are then less likely to limit populations). This will stop excessive population growth which could lead to crashes in the population and so, by dying earlier, an individual promotes the likelihood that its progeny will survive. Arguments of altruistic sacrifice are often hard to promote but recent work suggests that this is a more plausible model than once thought.

Evolvabilty theories also suggest that aging is an adaptive process. These suggest that populations, composed of a mixture of young and old, have biases in how well adapted the members of the population are - where younger individuals are better adapted (because they were produced more recently it is likely that the environment is similar to the environment they are favoured in). Thus by removing the less well adapted individuals from a population via senescence and freeing up resources for younger better adapted individuals, a population evolves more rapidly towards it optimal state.


By definition, an autosome is a chromosome that is not a sex chromosome. Therefore, as a human diploid cell has a total of 46 chromosomes, including two sex chromosomes, I guess the answer to your question should be 44. I hope it's clear enough for you. :)


The question has been explored in great depth in the cited paper. Have a look.

Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot?. Journal of foot and ankle research. 2011 May 13;4(1):13.

Summary:

Nucleation factors: The site of Gout depends on where the Monosodium Urate (MSU) crystals are likely to form. This process of nucleation depends on a variety of factors. One is temperature, its solubility decreases with temperature and hence the fingers and the toes are more likely sites of MSU precipitation. Further, trauma and pH also affect the nucleation. Repeatedly stubbing a toe makes the first metatarsophalangeal joint (MTPJ) specifically vulnerable.
Cartilage damage and Osteoarthritis(OA).OA sites are correlated with those of higher MSU deposition and cartilage damage (for reasons and evidence, refer to the cited paper). Hence, factors which make MTPJ more susceptible to OA can increase the predilection for MSU deposition. These include "increased concentrations of chondroitin sulfate, degradation of protein-polysaccharide complexes, and epitaxial MSU crystal nucleation and growth on cartilage fragments"

The right sided predilection might be because most people are right-handed, and they might be more likely to injure or stub their right toe.


What is the difference between Reservoir and paratenic hosts?

Reservoir host: The host of an infection in which the infectious agent multiplies and/or develops and on which the agent is dependent for survival in nature; essential host for maintenance of the infection when active transmission is not occurring.
Paratenic host: A host in which a parasite survives without undergoing any additional development (a transport host only)
Source: Diagnostic medical parasitology, pg 1161

and

Any animal that harbors an infection that can be transmitted to humans is called a reservoir host, even if the animal is a normal host of the parasite. Source: Pg no:4

So, we can conclude that paratenic host is different from reservoir host due to following differences:

Paratenic host don't harbour infective stages , if they harbour them, then they would be called as reservoir host but not paratenic host( see second definition)

No development takes place in paratenic hosts, whereas in reservoir host development and multiplication takes place( see 1st definition).

Is a reservoir host a biological vector then?

I too asked the same question, its answer is here.


The terms_id is meant to be a vector of GO or KEGG IDs that annotate to the proteins of interest. As it's described, the method get_term_protein:

  Returns the proteins annotated to belong to a given term.

My substantiation in part comes from the vignettes for STRINGdb that use terms in a separate set of functions like so:

>head(enrichmentGO, n=7)
term_id proteins hits pvalue pvalue_fdr
1 GO:0048545 383 15 2.337593e-07 0.000368020
2 GO:0006952 1286 28 3.806997e-07 0.000368020
3 GO:0002252 405 15 4.756829e-07 0.000368020
4 GO:0010466 234 11 1.767763e-06 0.001025745
5 GO:0045861 330 12 8.407161e-06 0.003765892
6 GO:0010951 228 10 9.735179e-06 0.003765892
7 GO:0002443 141 8 1.224368e-05 0.003839606
term_description
1 response to steroid hormone
2 defense response
3 immune effector process
4 negative regulation of peptidase activity
5 negative regulation of proteolysis
6 negative regulation of endopeptidase activity
7 leukocyte mediated immunity
>head(enrichmentKEGG, n=7)
term_id proteins hits pvalue pvalue_fdr
1 04115 66 6 9.969204e-08 1.475442e-05
2 04610 68 5 3.577966e-06 2.647695e-04
3 05168 174 5 3.254067e-04 1.605340e-02
4 01100 1161 12 5.277721e-04 1.952757e-02
5 04380 123 4 8.399948e-04 2.486385e-02
6 00590 61 3 1.197959e-03 2.638087e-02
7 05161 139 4 1.322517e-03 2.638087e-02
term_description
1 p53 signaling pathway
2 Complement and coagulation cascades
3 Herpes simplex infection
4 Metabolic pathways
5 Osteoclast differentiation
6 Arachidonic acid metabolism
7 Hepatitis B

And so usage would follow, for example, I want proteins that associate with cell growth, I can use c("GO:0016049") as my terms_id to retrieve that list.

library(STRINGdb) #load package

string_db <- STRINGdb$new(version="10", species=9606, score_threshold=0, input_directory="") #set environment, 9606=human

string_db$get_term_proteins(c("GO:0016049")) #use new environment variable to query the database, 0016049 refers to cell cycle just as an example.

Output (annotation column w/ text descriptions removed for brevity):

               STRING_id    term_id preferred_name protein_size
1   9606.ENSP00000002829 GO:0016049         SEMA3F          785
2   9606.ENSP00000211998 GO:0016049            VCL         1134
3   9606.ENSP00000212355 GO:0016049         TGFBR3          851
4   9606.ENSP00000216037 GO:0016049           XBP1          261
5   9606.ENSP00000216911 GO:0016049          AURKA          403
6   9606.ENSP00000221930 GO:0016049          TGFB1          390
7   9606.ENSP00000225792 GO:0016049           DDX5          614
8   9606.ENSP00000230732 GO:0016049         POU4F3          338
9   9606.ENSP00000238682 GO:0016049          TGFB3          412
10  9606.ENSP00000239462 GO:0016049            TNN         1299
11  9606.ENSP00000245479 GO:0016049           SOX9          509
12  9606.ENSP00000255448 GO:0016049          DCLK1          729
13  9606.ENSP00000256951 GO:0016049           EMP1          157
14  9606.ENSP00000258106 GO:0016049           EMX1          290
15  9606.ENSP00000258743 GO:0016049            IL6          212
16  9606.ENSP00000261023 GO:0016049          ITGAV         1048
17  9606.ENSP00000261918 GO:0016049         SEMA7A          666
18  9606.ENSP00000262017 GO:0016049          ITGB3          788
19  9606.ENSP00000263713 GO:0016049        EPB41L5          733
20  9606.ENSP00000263980 GO:0016049         SLC9A1          815
21  9606.ENSP00000264057 GO:0016049           DGKD         1214
22  9606.ENSP00000264279 GO:0016049          NOP58          529
23  9606.ENSP00000265136 GO:0016049           COBL         1261
24  9606.ENSP00000265362 GO:0016049         SEMA3A          771
25  9606.ENSP00000265371 GO:0016049           NRP1          923
26  9606.ENSP00000266058 GO:0016049          SLIT1         1534
27  9606.ENSP00000268182 GO:0016049         IQGAP1         1657
28  9606.ENSP00000270221 GO:0016049           EMP3          163
29  9606.ENSP00000272134 GO:0016049         LEFTY1          366
30  9606.ENSP00000276416 GO:0016049           BIN3          253
31  9606.ENSP00000278671 GO:0016049        LAMTOR1          161
32  9606.ENSP00000281321 GO:0016049         POU4F2          409
33  9606.ENSP00000283027 GO:0016049          NUBP1          320
34  9606.ENSP00000284981 GO:0016049            APP          770
35  9606.ENSP00000296388 GO:0016049         LEPRE1          736
36  9606.ENSP00000296755 GO:0016049          MAP1B         2468
37  9606.ENSP00000296875 GO:0016049           GDF9          454
38  9606.ENSP00000301067 GO:0016049           MLL2         5537
39  9606.ENSP00000303351 GO:0016049          ITGB1          798
40  9606.ENSP00000305133 GO:0016049          SOCS5          536
41  9606.ENSP00000306157 GO:0016049           IL7R          459
42  9606.ENSP00000306662 GO:0016049         ADRA1B          520
43  9606.ENSP00000307156 GO:0016049          LAMB2         1798
44  9606.ENSP00000307272 GO:0016049          RPTOR         1335
45  9606.ENSP00000316357 GO:0016049          USP9X         2570
46  9606.ENSP00000316543 GO:0016049          RAPH1         1250
47  9606.ENSP00000317257 GO:0016049          CPNE1          542
48  9606.ENSP00000322957 GO:0016049           PAK7          719
49  9606.ENSP00000324549 GO:0016049         CYFIP1         1253
50  9606.ENSP00000324560 GO:0016049           ULK1         1050
51  9606.ENSP00000324856 GO:0016049          STK11          433
52  9606.ENSP00000329623 GO:0016049           BCL2          239
53  9606.ENSP00000330382 GO:0016049          PDGFB          241
54  9606.ENSP00000332643 GO:0016049            NDN          321
55  9606.ENSP00000333982 GO:0016049          NDEL1          345
56  9606.ENSP00000334458 GO:0016049          GATA4          442
57  9606.ENSP00000335246 GO:0016049         ENTPD5          428
58  9606.ENSP00000337146 GO:0016049          ENOX2          610
59  9606.ENSP00000337332 GO:0016049          SIRT6          355
60  9606.ENSP00000337697 GO:0016049            DCX          441
61  9606.ENSP00000339740 GO:0016049         CAMK2D          499
62  9606.ENSP00000340820 GO:0016049           MAPT          776
63  9606.ENSP00000341940 GO:0016049           CAV3          151
64  9606.ENSP00000347906 GO:0016049          PRMT2          433
65  9606.ENSP00000348769 GO:0016049          ARIH2          493
66  9606.ENSP00000351049 GO:0016049           PAK4          591
67  9606.ENSP00000351591 GO:0016049          NLGN3          848
68  9606.ENSP00000351905 GO:0016049         TGFBR2          592
69  9606.ENSP00000353362 GO:0016049        CACNA1A         2506
70  9606.ENSP00000353582 GO:0016049           NRP2          931
71  9606.ENSP00000354558 GO:0016049           MTOR         2549
72  9606.ENSP00000354829 GO:0016049          SGMS1          413
73  9606.ENSP00000354877 GO:0016049           ULK2         1036
74  9606.ENSP00000355627 GO:0016049            AGT          485
75  9606.ENSP00000355785 GO:0016049         LEFTY2          366
76  9606.ENSP00000355896 GO:0016049          TGFB2          442
77  9606.ENSP00000357288 GO:0016049        LAMTOR2          125
78  9606.ENSP00000357470 GO:0016049           IL6R          468
79  9606.ENSP00000357494 GO:0016049           ROS1         2347
80  9606.ENSP00000359095 GO:0016049          PRMT6          375
81  9606.ENSP00000359729 GO:0016049         SLC9A6          701
82  9606.ENSP00000360973 GO:0016049          AGTR2          363
83  9606.ENSP00000360988 GO:0016049          LUZP4          313
84  9606.ENSP00000361423 GO:0016049           ABL1         1149
85  9606.ENSP00000362092 GO:0016049          RRAGC          399
86  9606.ENSP00000362717 GO:0016049           LHX2          406
87  9606.ENSP00000363822 GO:0016049             AR          920
88  9606.ENSP00000365663 GO:0016049           NPPA          151
89  9606.ENSP00000366396 GO:0016049           XRN2          950
90  9606.ENSP00000367123 GO:0016049         SLC3A2          631
91  9606.ENSP00000367830 GO:0016049          PRKCZ          592
92  9606.ENSP00000368030 GO:0016049         ATAD3A          634
93  9606.ENSP00000368169 GO:0016049           DVL1          670
94  9606.ENSP00000368683 GO:0016049           EDN1          212
95  9606.ENSP00000369014 GO:0016049           NDNF          568
96  9606.ENSP00000369816 GO:0016049           SHBG          402
97  9606.ENSP00000369960 GO:0016049         ADRA1A          475
98  9606.ENSP00000370330 GO:0016049        ERBB2IP         1371
99  9606.ENSP00000376800 GO:0016049           MTPN          118
100 9606.ENSP00000377823 GO:0016049          NDRG4          391
101 9606.ENSP00000377947 GO:0016049           RARG          454
102 9606.ENSP00000378306 GO:0016049         PPP3CB          525
103 9606.ENSP00000379003 GO:0016049          NUPR1          100
104 9606.ENSP00000385610 GO:0016049          MEX3C          659
105 9606.ENSP00000395359 GO:0016049          CADM1          442
106 9606.ENSP00000411672 GO:0016049       ATP6V0E2          213
107 9606.ENSP00000414303 GO:0016049           BDNF          329
108 9606.ENSP00000419782 GO:0016049           CDK5          292
109 9606.ENSP00000422591 GO:0016049          SLIT2         1529
110 9606.ENSP00000427941 GO:0016049       ATP6V0E1           81
111 9606.ENSP00000430333 GO:0016049          SLIT3         1523
112 9606.ENSP00000465742 GO:0016049        RASGRP4          673


What is called the "area size that an animal usually lives in"?

Are you looking for 'Home range' (see also the definition in Encyclopaedia Britannica)? Generally, 'home range' is defined as the entire area an individual animal uses, while the 'territory' is the subset of the home range that is actually defended from conspecifics (in animals that show territoriality). 'Home range' is often delimited by the types of environments used and movement patterns of individuals.


Is there any way to make protein pass through cell membrane?

Various protein transfection methods are available.

The simplest one is electroporation. By using electric pulses, transient pores can be formed, so that proteins outside can go the inside of membrane.

Several protein transfection reagents are commercially available. I think the mechanism is similar to lipofection of DNA.

http://www.clontech.com/US/Products/Transfection_and_Cell_Culture/Protein_Transfection/Protein_Transfection_Reagent
https://www.neb.com/products/m2563-transpass-p-protein-transfection-reagent
https://www.thermofisher.com/order/catalog/product/89850

Fusion with the transactivating transcription factor (TAT) protein transduction domain from the HIV TAT protein. This 11-amino acid sequence help proteins cross plasma membrane.

http://www.nature.com/mt/journal/v8/n1/full/mt2003155a.html

I am adding a couple of methods here.

Liposomes

Liposomes were designed to deliver drugs to places where the effects are wanted. Drugs are enclosed in liposome vesicles, but when reaching plasma membrane, liposomes could fusion with plasma membrane and release drugs inside of liposomes, although all liposomes are not designed to fuse cellular membrane.  Lipo-fection of DNA is a bit different from this kind of liposomes because DNA is not necessarily enclosed in vesicles.

nanoparticles

This is relatively new. I do not have much knowledge about nanoparticles, but I know they are used to transfect DNA or RNA in vitro and in vivo. I do not know how popular nanoparticles for protein transfection are, but there are publications.

http://www.ncbi.nlm.nih.gov/pubmed/24859743


Strictly speaking the common bread mould Rhizopus sp. does not produce aflatoxin.
The fungus Aspergillus flavus which belongs to the class Ascomycetes secretes aflatoxin. It attacks cereal grains , legumes, tree nuts. The fungi are green in colour and 'mould' like in appearance.
The fungus attacks the food stuffs and storage grains. So under favourable conditions it may grow in your store room if it finds food for its growth. Also Aspergillus can grow at temperatures as high as 48°C and even at low temperatures like 5-8°C.

Edit: On being asked for sources I include some which strongly support my claim
1. For suitable conditions of growth of the fungi visit https://en.m.wikipedia.org/wiki/Aspergillus_flavus and read under the Environment heading.
2. Visit https://bioweb.uwlax.edu/bio203/s2013/ernst_ale2/habitat.htm and read from " Aspergillus flavus is omnipresent " upto " Aspergillus may also grow on or inside walls in homes, especially if the house is damp or has been damaged by flooding. "
3.https://www.moldbacteria.com/mold-types.html this site provides a list of different fungi found in our homes. Here you can find Aspergillus flavus to grow in flower pot soil. Moreover other species of Aspergillus are found in kitchens and bathrooms.


Are there any cases of observed extreme speciation

Could not fit in a comment…

What kind of observations will you accept to be an observation? If we can demonstrate showing genetic data that two current species where actually only one some time in the past would it represent an observation to you? Or does it has to be a lab experiment (experimental evolution)? Experimental evolution with big animals take much time, I am afraid we probably have no evidence (not counter-evidence) of a mammal species that evolve to be phenotypically speaking as different than a fruit fly and a june bug (example coming from your comment). Would you accept considering microorganisms (I have no example in head though right now)?

As you noted yourself I think, it is difficult to know how different (phenotypically or genetically?) should two sister populations (populations who derived from a common ancestral population) be so that you would consider that one of these populations at least evolved into another "kind" (compare to the ancestral population).


What effect does taking antibiotics unnecessarily have on future bacterial infections?

Every time you expose a population of bacteria to an antibiotic, you select for organisms with resistance-granting genes.

Bacteria can pass plasmids full of genes back and forth.  So if you get a nasty E.coli infection, do you really want one of your usual bacteria with a resistance-granting gene sitting right next to it?

Let's say you are so sick you go to the hospital.  Do you think the hospital wants your antibiotic-resistant E-coli around?


It may be a stellate trichome from a plant.

You can find other ones by taking swabs from the onion and nearby plants.

cool images here

wiki info about trichomes


What is the oldest example of DNA identified?

419 million year old DNA from halophilic bacteria.

http://news.discovery.com/earth/oldest-dna-bacteria-discovered.html


Measuring fitness / lifetime reproductive success (LRS) in Drosophila

I haven't done LRS but I don't see a reason why you couldn't make that measurement over only a few days, if you keep this method consistent through out all your populations. Just as a control you might have to do a complete LRS to see if you get any patterns in their egg laying behaviour, which I assume/believe is a decreasing pattern over time but just check the pattern of your WT and make sure your food is the same throughout all your experiments as changes in yeast % can completely distort your results as fly lay eggs like crazy when given yeast!! so use the same batch of fly food.

Although I'm no expert at this, if you look at female ovaries and do some molecular/phenotypic characterisations, you might get some interesting data if you are already observing a huge difference between your populations although you would have to look at the literature for this but having played around with these stuff a little, you find a surprising amount of data! This is in a way nice since you take the males out of the equation as the reproductive fitness could be compromised by either males or females in a population. To determine this you need to cross the males and females of your population of interest to WT flies and count the embryos (although this is slightly dangerous since if males are not performing well, females can lay lots of unfertilised eggs, blanks, and they are indistinguishable from fertilised egg so maybe count the hatched offspring and immediately discard them although that presents its own set of challenges and variables and to be honest its not likely to happen since you usually get this blanks in virgin females that have not yet courtshiped). If you observe lets say no changes in embryo numbers when your male populations are crossed to WT females but significant changes when females are crossed to the WT males, you would know the problem is with the males in your population.

Hope this helps!

EDIT: So I looked a bit further into this and came across this paper (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0024560). If you look at Fig 6, I think it answers your question. I'm basically quoting the paper here. They measured the correlations between adult LRS and cumulative and short-time measures of fecundity and offspring production. Correlations of the short-time measures of fecundity and offspring production with adult LRS were highly dependent on the time of measurement. For young females the correlations were low, but when measured from older females, the correlations were much higher (up to 0.67 for short-time fecundity and 0.83 for short-time offspring production). For both short-time fecundity and short-time offspring production the highest correlations with adult LRS were reached when the female age was about 50 to 80 days. The length of the time frame had only a minor effect: the correlation of the 10-day measure with adult LRS was generally only slightly higher than that of the 2-day measure. The short-time measures performed well in comparison to the cumulative measures of fecundity and offspring production. So in short if you let your females age a bit and measure their fecundity, then it should be representative of their LRS.


Normally in a right handed person the left hemisphere is considered dominant.  However, a new lesion in the left hemisphere can cause loss of this dominance so it is possible that this has occurred.

Alternatively, if the subject is now able to write using both hands concurrently but different material, it suggests that the two hemispheres are disconnected, the so called split brain syndrome which occurs with lesions of the corpus callosum.  However, ambidexterity is not described in that syndrome.

Anyway, you need to consult your physician.


I presume what the author is trying to convey is that as a seed ages, it enters a quiescent phase as a result of natural desiccation. Without more context, I'd guess that the quote you've provided here is referring to secondary dormancy, which is a response to unfavorable germination conditions. By definition, secondary dormancy occurs after the seed is released from the plant.

The mechanisms of secondary dormancy are not well understood, and resumption of embryonic function could be dependent on any number of factors. Generally, dormancy continues until such time as favorable conditions are observed by the dormant seed. For Avena sativa, seeds become dormant if temperatures in excess of the maximum for germination are observed. Other seeds become dormant in response to over- or dehydration, temperature variability, age, other factors, and combinations ad nauseum.

Some of the more common environmental causes of exiting dormancy include afterripening, chilling and lighting.


Why does an electrical shock freeze up muscles?

Interesting question!

An important factor here is the let-go phenomenon, which is defined as the current level in the arm that will cause the hand to involuntarily grip the current source. When the fingers are wrapped around a large cable, most adults will be able to let go with a current of less than 6 mA. At 22 mA, however, more than 99% of adults will not be able to let go.

Nearly all cases of inability to let go involve alternating current. Alternating current repetitively stimulates nerves and muscles, resulting in a tetanic (sustained) contraction that lasts as long as the contact is continued. If this leads to the subject tightening his or her grip on a conductor, the result is continued electric current flow through the person and lowered contact resistance.

Given that the current flow in the forearm stimulates both the muscles of flexion and extension, it seems surprising that one cannot let go. However, the muscles of flexion are stronger, making the person unable to voluntarily let go (similar to the fact that a crocodile's jaws can be kept shut with your bare hands, but one should better not attempt to keep them open like that...).

Direct currents below 300 mA have no let-go phenomenon, because the hand is not involuntarily clamped.

Several different outcomes may occur when a person grasps a conductor giving 10 kV AC hand-to-hand voltage. Within 10 to 100 milliseconds, muscles in the current path will strongly contract. The person may grasp the conductor more tightly. However, mostly subjects are propelled away from the contact, likely due to generalized muscle contractions.

Reference
- Fish & Geddes, J Plastic Surg (2009); 9: 407-21


How does anadromous fish physiology "know" to switch from salt to freshwater and back?

Osmoregulation is a homeostasis regulation mechanism followed by salmons to adapt on both salt and fresh water.

Osmoregulation is the active regulation of the osmotic pressure of an organism's fluids to maintain the homeostasis of the organism's water content; that is, it keeps the organism's fluids from becoming too diluted or too concentrated. Osmotic pressure is a measure of the tendency of water to move into one solution from another by osmosis. The higher the osmotic pressure of a solution, the more water tends to move into it. Pressure must be exerted on the hypertonic side of a selectively permeable membrane to prevent diffusion of water by osmosis from the side containing pure water.

In order to reduce the dehydrating effects of salt water, salmons drink several liters of water per day, but in fresh water salmons doesn't drinks at all. The only water it consumes is that which goes down when it feeds. When an ocean-dwelling salmon drinks, it takes in a lot of salt(NaCl), which exacerbates the salt-loading problem.
In fresh water, the salmon's kidneys produce large volumes of dilute urine, while in the ocean , the kidneys' urine production rates drop dramatically and produce a very concentrated urine.

Salmon use to deal with the NaCl fluxes driven by the gradients between the salmon and its surroundings. In their gill epithelial cells, salmon have a special enzyme that hydrolyzes ATP and uses the released energy to actively transport both Na+ and Cl- against their concentration gradients. In the ocean, these Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the salmon's blood into the salt water flowing over the gills, thereby causing NaCl to be lost to the water and offsetting the continuous influx of NaCl. In fresh water, these same Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the water flowing over the gills and into the salmon's blood, thereby offsetting the continuous diffusion-driven loss of NaCl that the salmon is subject to in fresh water habitats with their vanishingly low NaCl concentrations.
Reference

Reference


What does the hornet do on the ivy blossoms?

Hornets, just like wasp in general, hunt insects to feed their larvae but feed themselves with carbohydrates like nectar (or lemonade). So it is quite probable that the hornets are feeding on the nectar of your ivy. wikipedia


Could we breed a dog to the size of a thumb?

As mentioned above the inbreeding required to select smaller and smaller dogs would be problematic because of the myriad of health problems that would be associated with it (see inbreeding depression).
The question about physiological limitations is interesting. The main reason biological organisms often don't scale is the fact that length, area, and volume don't scale in the same way. E.g. if something is twice as big L to 2L the surface area is L to L^2 and the volume is L to L^3 which means that many systems no longer work or require more energy (see Allometry) . For example in insects the distance for oxygen to diffuse to cells is short enough that simple diffusion is possible, in humans that is no longer the case so we have whole circulatory and respiratory systems to, in effect, help reduce the diffusion distance for oxygen.
I haven't used this kind of analysis in a while so am not very confident applying it here but I would suggest that some issues that could arise due to things scaling with length versus area or volume are:

required heart rate
maintaining body temperature - many small mammals deal with this by falling into periods of cold torpor (sort of like hibernation) where metabolic rate is suppressed
fragility of bones (as Cort Ammon mentions this is actually not a problem: https://jeb.biologists.org/content/207/9/1577)


I am basing my answer on this document issued by one of the departments of the Ludwig Maximilian University of Munich.

Bacillus subtilis:

Doubling time: 30 minutes
Incubation temperature: 37°C
Growth conditions: strictly aerobe

Recommended media:

Luria-Bertani (LB) broth/plates - (for everyday use)
Difco Sporulation    Medium (DSM) - (for long-term storage)

You can find the formulations for the aforementioned media by following the link above.

With regards to the latter part of your question, the easiest way to tell (and doesn't require any "high-tech" lab equipment) whether your cells are multiplying or not is to inoculate a broth and see whether there is turbidity after a certain time of incubation. However, please be aware that you may have cross-contaminated your broth so unless you do further testing you cannot know for certain if it is Bacillus subtilis in your broth.


glycogenesis, glycogenolysis and weight gain or loss

The answer to my question is that the glycogen molecule is extremely hydrophilic. For every gram of glycogen the molecule attracts 3 grams of water. When the glycogen is hydrolysed the attached water is excreted either directly in the liver or through cellular ATP processes.


Why do eyes water in response to particular emotions?

When we are sad, our emotions are in an overdrive and the parasympathetic nervous system triggers lacrimation i.e. tears, and we cry.


Viruses evolve alongside their hosts. If you swapped a human chromosome into a chimp cell for the matching chimp chromosome, there would be a lot of genetic similarities but you would also surface a bunch of incompatibilities because the genes on each chromosome have been evolving independently from the rest of the genome.

Viruses interact with their host genome at many stages. First, they need a way to identify their target hosts (cells) in the environment and gain access to the cells. They do this by recognizing markers on the cell surface. For something like HIV, this identification is far more specific than identifying just humans even: they are identifying particular immune cells.

Once inside, viruses interact with the host to express viral genes, produce and assemble new virions, and get transmitted to subsequent hosts. If an incompatibility occurs at any of these stages, the virus won't be able to replicate.

However, because there is a lot of homology across related species, it is feasible for a virus to infect more than one host. If a virus evolves in a context where it commonly infects multiple hosts, there can be selective pressures for it to maintain those abilities across all the hosts. Alternatively, selective pressures might cause the virus to evolve into separate lineages, one infecting ducks and another infecting sparrows, for example.

For a virus that is specific to a certain host (or range of hosts), it is likely that it will have difficulty in another host outside the context in which it evolved. However, there is also variability in viral genomes, and if many viral copies are exposed to a novel host, there is chance that some of them can survive in that host. This will select for those particular viral genes, and subsequent viral generations will be further selected for traits that help replicate in that host.

Immune reactions could also play a role, but in most cases it is the specialization of the viruses themselves that hold the key to host specificity.

Ahlquist, P., Noueiry, A. O., Lee, W. M., Kushner, D. B., & Dye, B. T. (2003). Host factors in positive-strand RNA virus genome replication. Journal of virology, 77(15), 8181-8186.

Hao, L., Sakurai, A., Watanabe, T., Sorensen, E., Nidom, C. A., Newton, M. A., ... & Kawaoka, Y. (2008). Drosophila RNAi screen identifies host genes important for influenza virus replication. Nature, 454(7206), 890.

Schild, G. C., Oxford, J. S., De Jong, J. C., & Webster, R. G. (1983). Evidence for host-cell selection of influenza virus antigenic variants. Nature, 303(5919), 706.


Species identification: what kind of fungus is this?

I think these are parasitized insects.

Fungi of various types can infect insects.  The end stage produces these fruiting bodies.  Here is an example I found on the excellent site WhatsThatBug.

Here is another example.

http://www.anura.it/the-parasites-parasite-everyone-has-a-bad-day/clasp04/

The second site notes

  Entomopathogenic fungus (Clavicipitaceae sp.) killed a troglophile
  moth, Veins cave (Grotta delle Vene), Italy

I would guess something similar for what you found.

I must say your images are incredible.  The long fungal tendrils on the second image are the most amazing example of this I have ever seen.


I have used both Gibson assembly (what you mean by assembly?) and LCR as replacements for blunt or sticky ended cloning. LCR has, for me, worked better in that a higher proportion of constructs that come out have been assembled correctly and I have noticed no mutations after LCR while I have seen them somewhat often with Gibson.


Found this spider in my bed last night.. can someone help ID?

It seems like an Agelenopsis to me. According to www.spiders.us, the size, the description and the location (Kentucky) match your specimen.

Here is another image (also from www.spiders.us), for comparison:

The mentioned link lists 13 species in the Genus Agelenopsis. It shouldn't be difficult narrowing it down to species (if that's the correct Genus, of course).


How does the brain instinctively know the math behind Newtonian Physics?

Trial and error.

The CNS is very much a living, changing organ system - much more so before you are an adult. While you are a child your neurons fire, muscles contract, and force is exerted on objects - then your CNS modifies itself (either through redistribution of neural contacts or growth of new neurons spurned by chemical changes) to account for the results.

This is why "practice makes perfect." As you continuously perform a task, like throwing a ball, your body is keeping track of the results. Did X muscle fibers contracting in Y muscles overshoot your buddy? You register the failure and compensate by utilizing X-N muscle fibers that contract in Y muscles until you consistently satisfy your goal.

Your CNS is keeping track of everything, all the time. There isn't a single instant in your life - asleep or awake - that's not being monitored, so your body has copious amounts of data to work with when making its estimates.

This is also why simulations take time to adapt to, even if the person is fully aware of the basics behind the physics involved.


If someone were to die on the moon, would their body decay?

I am assuming in spacesuit here, on the face (lit side) of the moon. Bodily degradation involves much more than external fungi and bacteria.

Cells that receive no oxygen or nutrients die. We talk of such tissue death as dry gangrene when it affects extremities, such as fingers, feet, etc. However, we also recognize gangrenous bowel, etc. which results in tissue necrosis.

Such necrotic cell death is the consequence of acute disruption of cellular metabolism, leading to ATP depletion, ion dysregulation, mitochondrial and cellular swelling, activation of degradative enzymes, plasma membrane failure and cell lysis [1]

Lysis is messy and wet. Combined with the fluids in our bodies, what one would end up with is a mushy, smelly degraded body, not a preserved body. For a while, anaerobic bowel bacteria would flourish (which smell terrible).

Add to this the extremes of temperature (253° F in the sun and -243° F in the dark.) The suit would have lost it's heating and cooling mechanisms, so the body would alternately spend 14 days in the heat and 14 days in the freezing cold depending exactly where it was (lets say the equator of the moon.) These freeze/bake cycles would further contribute to degradation through ice crystal formation and thawing.

Eventually, because there was no new substrate, degradation would come to a halt, but I'm not sure at what stage this would be. I assume, though, there would be a vast difference between a mummified body (done by dehydration) and a body left to degrade in a spacesuit.

[1] The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy, John J. Lemasters et. al, Biochimica et Biophysica Acta 1366 (1998) 177-196


How to measure surface area of plated bacteria?

You can count the individual colonies on the plate, with this number being the number of "Colony Forming Units" (CFU), as theoretically, only a single cell is needed to spawn a colony.

To do this though, you will need to do a serial dilution of your liquid cultures before plating, so you would have one plate of 10$^0$ dilution, then 10$^1$, 10$^2$, and so on, generally a ten-fold dilution is performed.

Hopefully this will yield at least one plate with a countable number of colonies, that is - not too many, and not too few - usually 30-300.

cfu/ml = (no. of colonies x dilution factor) / volume of culture plated

This usually yields a very large number, so it is common to then take the log of this number, and report that as your result.

And then you will be able to compare your results between probiotics. It's a very good idea to do replicates of each dilution!


Has medical progress stopped human evolution?

Not at all.

Mutations accumulate independent of medical progress. In fact harmful mutations which would otherwise cause an individual to die can now be "cured" thus if anything increasing the gene pool.
Typically medical progress extends our lives when we are much older, thus we have already passed mutations on to our children before a bottleneck in evolution could occur
We are getting taller, less hairy and women are getting more attractive which is another form of evolution
As new diseases develop the selective pressures on humans are ever changing. HIV which was never as widespread is now pushing certain immunogenetic traits to be favourable, the same is true for malaria (HLA 5701) and many others

In conclusion, whilst there are fewer and fewer strong selective pressures forcing extreme evolution, our bodies are designed to evolve slowly unlike viruses like HIV. Our mutation rates are around 1 in 10^9, allowing us to always slowly evolve as there will always be traits which are slightly more advantageous.


What kind of tree is this — why do its huge leaves change shape and "grow fingers"?

I'm going to take a stab here.  It looks a lot like Artocarpus altilis or breadfruit.  However, the trunk is a bit gnarly for breadfruit, but maybe that is the result of being a street tree.  Also, I can't find any reliable information about the variation in the leaves (heterophylly) for this species.  However, other species in the genus have entire leaves, so perhaps this is hybrid.  Also, Artocarpus chaplasha does show heterophylly related to light intensity and leaf position (online images suggest your tree is not A. chaplasha however).  I think the climate in Taipei is consistent with Artocarpus too.  If it's not breadfruit, I imagine it is a species from the Moraceae.  Finally, in some of your pictures it looks like there is an adjacent tree (possibly a Ficus or Clusia) mixing in -- those leaves are obtuse rather than acute at the tip.
EDIT:
I'm including one of your photos with the leaves of the tree in question circled in yellow, and what I believe to be the leaves of a different tree circled in red (in case my earlier comments were too cryptic).

EDIT 2:
Here is an excerpt of Fig 1 from Jones et al. "Morphological diversity in breadfruit (Artocarpus, Moraceae): insights into domestication, conservation, and cultivar identification" Genetic Resources and Crop Evolution vol 60 no 1 pgs 175-192 (2013) which shows the diversity of leaf morphology in Artocarpus including some hybrids.  I'm convinced you are looking at one of the species in this genus or a hybrid, and looking at the leaves in the panel for A. altilis there is considerable diversity (phenotypic plasticity) w/i that species, so that may be as close as it can be nailed down.
Finally, I can't run it but apparently there is graphical key to Artocarpus species which might be fun to try.

EDIT 3:
@uhoh has verified that all the leaves in the pictures belong to the same tree, so, it's likely we are seeing heterophylly based on the age of the leaves.  I went back to the reference above, and found this sentence would would seem to be consistent with the young leaves being entire and obtuse (and we've already established that the more mature leaves show a lot of variation): "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches".  So I think all the observations and literature point in the same direction, namely good 'ol breadfruit.


What could cause no pain but sense of touch?

I think Congenital insensitivity to pain with anhidrosis might be what you are looking for, it is the closest thing I can think of right now.


Do I need to serially dilute E. coli cultures for optical density measures?

One is not normally required to serially dilute E. coli cultures for spectrophotometric measurements, at least in the experiments where the OD value is important.

For most protein expression work, the consensus is to start the induction at OD 0.6, and for most chemically competent cells, the optimal OD ranges from 0.3 to 0.8 depending on the competency protocol. At no point in time do you need to perform dilutions, as they are all within the linear range of cell count:OD ratio.

The only time you need to dilute the culture is when you want to find the OD of a very concentrated culture (for example after 24 hours of vigorously shaken incubation).


From a purely biological perspective, how does an optimal human diet look?

No, there isn't a single diet that can be recommended from a biological perspective.

The most popular diet from a pseudo-scientific perspective is the Paleo diet, saying we should eat what our ancestors in the Paleolithic were eating, but it makes a mistake of forgetting that our metabolism has evolved since then. There are also numerous other flaws in the Paleo diet but I won't go through them all.

The most notable example to use here would be dairy products, as we're among the few species that can drink milk at adult age. Drinking milk as an adult isn't normal, and yet we evolved the ability to do so. Some individuals can't drink milk, same goes for consuming gluten, nuts, and several other things, but the species as a whole can consume all of the above. Some people must avoid certain foods because of their individual genetic makeup though. Most evolved to process gluten and this ability is greatly responsible for the fact that there are 7 billion of us now. If you read an article "gluten is bad", remember that gluten grew the human race and without it at least a third of the world's population would die through starvation. If you read an article about the Paleo diet, remember we wouldn't be here if the agricultural revolution didn't happen.

The correct answer would be - humans can consume everything that isn't toxic and provides them with energy. We're very capable omnivores, which is probably one of the reasons why we've done so well as a species. In other words, you won't die from eating processed sugar. There are healthier and less healthy foods, but none will kill you.

You are correct, there are numerous answers (or attempts to answer) to this question, and the way the research is concluded definitely doesn't help. Research is mostly conducted through polls designed to prove the scientist's original unverified claim, and virtually no research is conducted on the biological level, e.g. what happens to the body when you consume a certain carbohydrate. The whole field became pseudoscientific. The "food pyramid" is...pretty much wrong.

Body needs proteins, body needs carbohydrates, body needs fat. You could come up with a vague answer if you eliminate the foods that body doesn't need, such as processed sugars, but it's still energy and you won't die from consuming it.

There is no scientific research that consumation of any food, or elimination of any food, affects life span. Meaning, there's no differential survival rate depending on what you eat.

To put things in perspective, imagine a lion preoccupied with attempting to answer whether it would be better for his body to eat an antilope or a gazelle. 10.000 calories is 10.000 calories and if he eats either he'll live another day.


Mutating a protein without mutating the gene?

I assume that you mean changing the amino acid sequence in a single protein in an organism to one that no longer reflects the sequence predicted from the DNA sequence.  In that case, I would suggest using ADAR (Double-stranded RNA-specific adenosine deaminase) or similar enzymes.  ADAR deaminates adenosine to inosine, which is read by the ribosome as a guanine.  I know that it's activity is regulated, but I'm not sure how you could redirect it (perhaps with an antisense RNA that yields a double-stranded binding stretch in the target RNA.


Your question is very awkward.

Let's define Tea as boiling leaves in water. At the end, you remove the leaves and drink the flavoured water.

At this point, the "tea" is still very much water - as in tea is water with dissolved chemicals from the leaves. Note, the word chemicals is not to be interpreted in a negative way because everything (including water) is a chemical.

So, the difference between tea and water are the chemicals that dissolve. What are these chemicals? The answer to that depends very much on the tea. Another difference is the temperature - tea is typically hot.

You can look at this article about chemicals in green tea and their associated health benefits. You can do further searches for other tea types and for each of those chemicals.

In short, no you do not get dehydrated because of tea vs. water. Dry skin can be caused by a lot of different reasons. Oh and no, caffeine doesn't cause any significant amount of dehydration as far as I know.


Why do Hot/Cold drinks taste sweeter once returning to room temperature?

Generally, cold suppresses sweetness. As an example, consider soft drinks that are usually served cold: they taste sweeter when warm (like you said with your examples of drinks).

Our taste receptors send a stronger signal to the brain when activated by warmer substances and so the perception of sweetness, in this case, is lessened when we consume cold food or drinks.

There are taste receptors on the surface of our tongue which refer to the proteins TAS1R2 and TAS1R3 which, which bind to the “sweet-tasting” molecules.
When the molecules bind to the receptors, they trigger a series of actions which increase the number of positively charged potassium ions (K+) in the cell to which the receptor is attached. In order for the signal to continue along to the brain, the cumulative positive charge of the potassium ions must be high enough to activate a TRPM5 channel into the cell, so that calcium ions (Ca2+) can pass through. The Ca2+ ions are required for the release of neurotransmitters which send the signal. This channel requires a much lower positive charge for activation when it is warm than when it is cold.

Now if you were to put, e.g., a cold coke into your mouth, it decreases the temperature of the entire tongue and consequently the TAS1R2 and TAS1R3 proteins, and the TRPM5 channel. This will result in it requiring a greater positive charge in order for the signals to travel to the brain. This means overall also less signals are even received by the brain, thus resulting in us perceiving less sweetness.

Sources:

http://www.ncbi.nlm.nih.gov/pubmed/25963040
http://www.ncbi.nlm.nih.gov/books/NBK236241/
http://www.foodnavigator.com/Science/Food-temperature-affects-taste-reveal-scientists
http://www.ncbi.nlm.nih.gov/pubmed/17180301


I think the key work here is 'evolve'.  Overall GC/AT ratios change by mutations, whose rate is constant.  The probability that given a mutation event that one base will be substituted by another one has been modeled in several ways where the probabilities of different mutations may or may not be the same.

Overall the GC content will tend to close to 50%.  What causes GC rich genomes to become GC rich (60-70%) are that mutations to GC base pairs have selective advantages either in regions or in the genome overall that cause them to be retained. The mutation rate may be no different (or even lower) in GC rich organism (many of them are deep underground or deep underwater.  GC rich genomes occur because AT->GC mutations convey an advantage and they stick around.

The reasons that the GC content migrates away from 50% fall into two categories I will call entropic and selective.

By entropic I mean specifically that coding sequences for genes and other features such as binding sites on the DNA or other features such as centromeres, which will cause the overall ratio to vary from 1 because the sequence is constrained by the information it contains.  While coding regions have a ratio higher than 1, GC content tends to hover around 54%.  Eukaryotes have GC islands and etc, but this also does not overall change the GC content

So gene rich genomes and typical functional features of the genome do not really explain some of the spectacularly high GC contents found; up to the 70% range.  While the link above looks at GC bias in coding regions, its a given that any part of the genome that is merely a spacer between elements with specific functions will freely vary to GC if it is useful.

Selective factors for high GC content include high pressure and temperature environments for instance, which usually strongly bias to high GC content by this mechanism.  You can imagine how this works: high GC content genomes are thermodynamically more stable and can survive the extra molecular collisions of higher energy of those environments more readily.

GC rich genomes are not simple adaptations to live with.  All the genes for DNA oriented processes such as transcription, chromosome packing, DNA polymerase have to adjust a lot. As the organism adapts to hotter temperatures or higher pressures, each individual protein produced will have to also change to be stable and function in the new conditions.  As such, these changes happen only over long evolutionary times.  This is probably a good part of the reason why the archaea niches have not been superseded by eubacteria in all 1+ billion years since life has been on Earth.