Do all plants photosynthesize with equal efficiency?

If you mean the efficiency at which plants convert light energy to chemical energy (in sugar or other reduced C compounds) then there is definitely variability between plants, both at the species and individual level. The photosynthetic efficiency WP page gives ranges of between 0.1 and 8% of total solar radiation converted to "biomass", but these values are not cited. In their review, (Zhu et al, 2008) state that the maximum maximum efﬁciency with which photosynthesis can convert solar energy into biomass is 3.5% and 4.3% for C3 and C4 plants (both observed for crops), respectively. Biomass is not a measure of energy, but perhaps they mean potential chemical energy in that biomass.

Its a pretty complicated question though. Photosynthesis is a complex process involving many interdependent chemical reactions and physical processes. All species (or even individuals) of plants have different morphology, physiology, and biochemistry that influences overall photosynthetic efficiency. In addition, they each inhabit different ecological niches and climate space. Therefore, all species or individuals would have a slightly unique maximum potential efficiency. Here are a couple other efficiency related concepts to consider:

There are 2 systems in photosynthesis that work in tandem, the light reaction and the dark reaction.  The light reaction uses light energy, pigments like chlorophyll, and a bunch of electron transport chain proteins to generate ATP and NADPH. These 2 molecules then provide the reducing power for use in the dark reaction (the Calvin Cycle). In the dark reaction, the enzyme RuBisCO joins CO2 and RuBP, creating simple reduced carbon chains which are then used to assemble sugars. This is an over-simplification, as both reactions are very complex systems with lots of biochemical machinery, but this is the basic process used to convert light energy to chemical energy. To operate at peak efficiency, the entire process must not be limited by incoming energy (light), substrate supply (CO2, RuBP), or nutrients used to construct all the needed cellular and molecular machinery (N, P, K, and many others). In reality, there are limits that vary from plant to plant, species to species. For example, a species or individual with a very reflective leaf surface converts less of the light reaching the leaf surface to chemical energy, thus lowering the output of ATP and NADPH. This reduces the chemical energy supplied to the dark reaction and limits the amount of carbon fixed by RuBisCO. So the reflective surface of the leaf, which might be advantageous to the plant in other ways, has a large impact on overall photosynthetic efficiency (compared to a less reflective leaf or leaves).

If you want to search for more information, there are a number of terms that plant physiologists and ecologists use when describing a plant's (or communities of plants) photosynthetic efficiency. Each of these is used in different ways and can have many variations in units.

Light use efficiency: The amount of carbon fixed per unit of light incident.
Water use efficiency: The amount of carbon fixed per unit of water transpired
Nutrient use efficiency: The amount of carbon fixed per unit of nutrient concentration (usually in leaves).

reference:

Zhu, Ort, and Long 2008 "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" Current Opinion in Biotechnology.


What species is this colourful caterpillar?

Just by its appearance and location, that’s maybe a Pale Tussock (Calliteara pudibunda), a kind of moth found in Central Europe.
You can find some observations of that species on iNaturalist: https://www.inaturalist.org/taxa/205294-Calliteara-pudibunda?locale=en-GB


To what extent does loss of neurons in the substantia nigra affect movement?

Great questions!  Here's some quick answers, but I'll give an additional little recommendation at the end if you're interested:

How much of an effect does this destruction of neurons have on movement?

Answer:  A large effect.  The key term here is "Parkinsonism," meaning that the symptoms resemble Parkinson's disease. This often involves motor symptoms like shuffling gait, tremors, rigidity, and bradykinesia (which means slow movement).  While they typically don't result in total paralysis, these symptoms can be debilitating and require treatment, such as L-dopa.

Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Answer:  Generally, these patients were still able to move, but they greatly struggled with controlled movements.  As stated above, Parkinsonism/Parkinson's disease is marked by many motor symptoms, but these do not result in complete paralysis.  Rather, they make voluntary movements more difficult and slower.  According to a paper entitled "The MPTP Story (doi: 10.3233/JPD-179006)" it appears that at least one patient was nearly (if not totally) catatonic and exhibited very little voluntary movement.

If you'd like to know why this is the case in Parkinsonism and Parkinson's disease, I'd encourage you to look up the direct and indirect pathways of the basal ganglia online.  There's likely a good lecture with helpful visuals on how these pathways work to facilitate (direct) and inhibit (indirect) movement by their effects on the thalamus and motor cortex.  Alternatively, you can let me know you're interested via a reply and I'll do my best to explain those pathways on here.  Hope this helps!


What is the molecular basis of hangovers?

First, the hormonal and hemodynamic changes seen in hangover are distinct from those seen in alcohol withdrawal, so the advice to drink more is not good, even if some symptoms are in fact improved. See tables 2/3 in the cited review.

It appears the molecular mechanism of veisalgia (HA, a new word) is not well known.

1. acetaldehyde Part of it may be attributed to acetaldehyde but there is clearly more to it. The liver enzyme alcohol dehydrogenase 1 (ADH1) produces acetaldehyde from ethanol, and aldehyde dehydrogenase 2 (ALDH2) makes acetate from that, so the aldehyde does not exist for a long time, and is rather responsible for short-term illnesses.

2. ADH and diuresis

  Hangover severity is proportional to antidiuretic hormone
  concentration (46). Alcohol inhibits the effect of antidiuretic
  hormone on the kidneys, thereby inducing  diuresis that is out of
  proportion to the volume of fluid ingested. As blood alcohol
  concentration decreases and dehydration persists, the serum level of
  antidiuretic hormone increases, maintaining water retention in
  dehydrated patients with hangover. In our clinical experience,
  hydration attenuates but does not completely relieve hangover
  symptoms.

3. cytokines

  The constellation of hangover symptoms (nausea, headache, diarrhea)
  resembles that seen in conditions related to dysregulated cytokine
  pathways (for example, in viral infections and after administration of
  interferon-alpha). Alcohol alters cytokine production through a
  thromboxane pathway. Levels of thromboxane B2 are elevated during
  experimentally induced alcohol hangover (42), and the administration
  of tolfenamic acid, a prostaglandin inhibitor, at the time of alcohol
  consumption has a small prophylactic effect in reducing hangover
  severity (9).

4. further substances

  Congeners, the byproducts of individual alcohol preparations (which
  are found primarily in brandy, wine, tequila, whiskey, and other dark
  liquors), increase the frequency and severity of hangover (24, 39,
  40). Clear liquors, such as rum, vodka, and gin, tend to cause
  hangover less frequently.

So there are factors that aren't even identified exactly, and these could fit the mixing of drinks observation.

There are several reviews out there, just search for hangover at Google Scholar.

Wiese, Jeffrey G., Michael G. Shlipak, and Warren S. Browner. "The alcohol hangover." Ann Intern Med 132.11 (2000): 897-902. Online at http://dionysus.psych.wisc.edu/lit/topics/Hangover/WieseJ2000a.pdf


The delta refers to a mutant allele, in this case a cysteine point mutant. The -/- refers to a homozygous null allele, in this case a knockout.


Why do we age? or Do we have a theory of senescence?

The 'wear and tear' argument is most likely true but it is also interesting to reason about ageing as inevitable from the evolutionary point of view.

To set up the argument, we need two things:
First, each individual has got a 'reproductive potential' which is realised throughout life. This means a deleterious mutation which has an effect in early life, will affect reproductive value more than a mutation which manifests itself in later life, after the individual has already had offspring. Thus selection will act strongly on genes which are expressed in early life than on those which are expressed later. For that reason, there's no strong selection against diseases such as diabetes or cancer. This argument can be applied not only to occurrence of disease but also to decay of ordinary functions of the body.

Secondly, cells in the body are constantly renewed and defects such as telomeric breaks are repaired. Mutations in the soma are taken care of by the immune system and can be in principle avoided. The fact that they tend to accumulate in later life can be explained by the first point: selection is weaker to oppose telomeric breaks and mutations in later life.

I was trying to be brief here, but there are more sides to the argument (e.g. Williams' antagonistic pleiotropy). Modular Evolution (Vinicius, CUP 2010) provides a good overview of the evolutionary aspect of theory of senescence (and many other interesting evolutionary arguments).


First, count the number of each nucleotide in the sequence, and divide that by the total number of all four nucleotides in the sequence.  For the C. elegans genome these frequencies will be approximately:
A = 0.32
C = 0.18
G = 0.18
T = 0.32
These frequencies should sum to 1.00.

If you select one nucleotide at random from that DNA sequence then those frequencies become the probabilities for selecting a specific nucleotide at that site.  So very roughly you would be twice as likely to get back an A or a T (compared to a G or a C).

Next count the number of each of the 16 possible dinucleotides (e.g., AA, AC . . . TG, TT) in that DNA sequence and divide the numbers by the total number of nucleotides in the sequence.  That will give you the observed frequencies of the dinucleotides. CG (or CpG in your post) is one of these.  If CG occurs proportionally to the frequencies of C and G then if you picked a random dinucleotide from the sequence you would expect the probability to be 0.18 * 0.18.  You can do this same calculation for all of the dinucleotides in a genomic sequence and compare the observed frequencies to the expected frequencies.

If every site is truly random in the sequence then the observed dinucleotide frequencies should be identical to the expected frequencies, and this would be a zero order Markov chain.  In fact, genomic DNA is usually not accurately modeled as a zero order Markov chain.


Can bacteria be killed by purely physical trauma?

My (limited) understanding is that it is quite hard to avoid killing some bacteria even with very gentle physical manipulation. On the other hand, it is quite hard to use physical force to achieve reasonable level of sterilization. Let's bring some examples with a few (hastily found) references.
Pressure
My guess is that most examples the OP mentions (hit with a hammer, knife) will exert their biggest effect on bacteria through a peak in pressure - bacteria are comparable in size to width of a moderately sharp knife edge and thus there will be more "crushing" than "cutting" even with a knife (Science of Sharp discusses that Chosera 1k - a very good stone - will sharpen a knife to 0.5 μm, Wiki has bacteria at 0.5 - 5 μm).
I recently collaborated on a project where initial interpretation of results was wrong simply because putting a glass slip over a sample to inspect it under a microscope caused around 10% of bacterial (B. subtilis) cells to die. Putting a small weight on the slip resulted in roughly 80kPa additional pressure applied and ~ 80% of the cells dying within 25 minutes. But 80% death rate won't do much to e.g. reduce risk of food poisoning - as long as there are nutrients, bacteria will regrow quickly.
As m4rio mentions in a comment to another answer, and in line with The effect of high pressure processing on the microbial, physical and chemical properties of Valencia and Navel orange juice you need to ramp up the pressure to 100s of MPa to achieve high efficacy. And even that may not work so cleanly - e.g., the linked paper mentions that after applying 600 MPa, bacteria regrew to detectable levels after 4 weeks of storage at 4°C. Killing all (or almost all) bacteria is just really hard.
Because it was fun, I'll also link to study showing that High pressure-processed guacamole (4 cycles, 689 MPa, 5 min each) is clean enough to not spoil for 30 days in 25°C.
Note: the two sources above were linked from a commercial vendor of high-pressure products and may thus be biased. While the exact numbers might be problematic, I think the main point is unlikely to be affected.
A review High-pressure processing – effects on microbial food safety and food quality mentions some limitations, e.g.:

Endospores tend to be extremely HPP resistant compared with vegetative cells, withstanding treatments of more than 1000 MPa

ascospores of heat-resistant moulds such as Byssochlamys, Neosartorya and Talaromyces are generally considered to be extremely HPP resistant

It should however be noted that it seems that high-pressure treatment is good enough to be semi-commonly used as the main sterilization for suitable foodstuffs - Current status and future trends of high-pressure processing in food industry reports high-pressure treatment to be FDA approved and USD 10 billion worth of food being treated as of 2015.
Pressure for killing cells previously briefly discussed at Can bacteria or other microorganisms be killed by applying pressure?
Ultrasound
While frequently used for cell lysis in lab, it also doesn't kill all cells. For example The Sterilization of Suspensions Contaminated with MicroorganismsUsing Ultrasound Irradiation reports that roughly 20-30% of bacteria (Bacillus) survived 60 minutes of ultrasound treatment.
Ball mill
This is probably closest to actual "physical trauma" - you put small beads and a suspension with microorganisms into a cylinder and roll it hard. A low energy process for the recovery of bioproducts from cyanobacteria using a ball mill discusses using this process to extract proteins from cyanobacteria. They don't report absolute number of cells killed, just that it varies considerably with the rotation speed, size of beads, .... My interpretation is that in most cases a non-negligible proportion of the cells survive while majority is killed (and their contents extracted for further use).


What advantage does lactose have as the main sugar in milk?

Yes it is thought to provide safer milk, less vulnerable to every bacteria that respires and multiplies on sucrose, and which lets the baby grow faster due to higher sugar content.

Milk has evolved from pouch mucus, antimicrobal secretions of the immune system, Lysozyme in mucus is a glycoside hydrolase which ruptures bacteria cell walls. So the origins of milk are very different than for plants.

Lactose is a larger molecule than sucrose, so it exerts less osmotic effect per unit mass, allowing more carbohydrate to be included in am isosmotic secretion such as milk.

for example:
marsupials have mostly longer oligosaccharides and their milk contains 11-14% sugar,
zebras and and horses with only lactose achieve 7%
humans and other primates achieve 8-9% using milk and polysaccharides.

Another advantage is that it's a molecule rarely produced in nature, and fewer bacteria have evolved the enzymes required to digest it, upgrading the lac-operon to produce galactose-permease, save for beneficial lactobacilli, e-coli, and other mostly mutualist species.

full text.

It is thought that milk evolved from secretory glands in the synapsid egg pouch which helped to protect parchment eggs, with moisture and antimicrobial secretions. In fact, lactose is thought to have come from mucus sugars, which are used to encapsulate and neutralize microbes in the body, "Because α-lactalbumin evolved from lysozyme before the division of amniotes into synapsids and sauropsids (see Figure Figure1),1), the capacity to produce lactose was an ancient trait that preceded its utility in milk synthesis"

Intro to synapsid and sauropsid precursors of lactose.


Why do tails of some lizards break so easily?

It's a self-defense mechanism, the tail falls off during threatening situations, to which the reptile responds by excessively contracting the tail muscles. This process is known as "Autotomy", or "Self-Amputation". Other animals have got "stronger tails" simply because such self-defense mechanism hasn't been developed.
https://science.sciencemag.org/content/20/500/149.2
Check this link for more in depth information!


Where I can find information about the study of animal vision?

Color vision was shown to be dichromatic (sensitivity to two color peaks) by Neitz et al. (1989). For a broader review of color vision of mammals, see Jacobs (1993).

Literature Cited

Jacobs, G.H. 1993. The distribution and nature of colour vision among the mammals. Biological Reviews 68: 413-471.

Neitz, J. et al. 1989. Color vision in the dog. Visual Neuroscience 3: 119-125.


Is solving cancer required in order to avoid aging?

Interesting question. My answer is no, but it requires a rather science-fiction style answer - at least it's beyond current technology, but here goes:

My Assumptions

I make the simplifying assumption that ageing is only related to telomere length. Thus by "avoid ageing" I assume you mean "avoid telomere shortening". Also to clarify things for others, I'll clear up the role of telomeres in aging and cancer:

Telomeres in cancer - it has been hypothesised that telomeres act as "mitotic clocks" - keeping track of how many times a cell can divide before it stops. This "time limit" is supposed to put a halt to cancerous cells before becoming malignant.

Telomeres in aging - Since telomeres set a limit to the number of times a cell can divide this essentially sets a time limit for the organism as a whole - those cells that divide faster (e.g. hair and skin cells) go out first (grey hair and wrinkles) etc.

Short answer

No.

Long answer

All we need to do is come up with a way to somehow "maintain" average telomere length at some "safe" length, i.e. we keep them at a length that is long enough to prevent us from aging but short enough so that a cancerous cell will not be able to proliferate to dangerous numbers.

For example, every now and then we provide "telomere length booster jabs" (this is some abstract fictional idea of course). This is like adding more time to our lives when we are about to run out: "Oh look, I only have three months left!", "Don't you worry, with our new telomere booster jab you will have an extra 3 months!"...


Is the discovery of dominant and recessive genes the only reason Mendel matters?

Independent assortment. Mendel showed that his genetic markers for different traits, or phenotypes are transmitted randomly to the F1 generation. This was before the concept of linkage was discovered, so fortunately he selected unlinked genes.
Segregation of alleles. The dominant and recessive alleles segregate away from each other when the germ cells are created, therefore each parent has two copies of every Gene.
Distinguishing phenotype from genotype in a predictable and testable framework.
The test cross. It was only careful record keeping and back crosses that revealed the recessive copies of mutant alleles in heterozygotes.

One description of his contributions is available on Wikipedia.  Other sites include MendelWeb, Learn Genetics,


What is the effect of the wavelength on the spectrophotometric measurements of protein?

Light absorption happens because of interaction of light with electrons (in a way) such that the energy of the light is transferred to some electrons that moves them to a higher energy state.

As per quantum chemistry (Bohr's model of hydrogen can be referred for a basic understanding), there are distinct energy states (solutions of the Schrödinger equation) and there are no intermediate levels. Therefore, to excite an electron to a higher energy level the energy of the incident light should match the energy gap between the ground state and the excited state.

In a molecule, there are different electrons, that reside in different orbitals and environments; only a few electrons can be exited by the energy that UV-Visible range of the electromagnetic spectrum can provide. These electrons are typically referred to as chromophores. You should refer to a book on spectroscopy for more details. A molecule can have multiple chromophores and each may absorb a different wavelength.

Having said that, there are energy bands (multiple closely spaced energy levels) in the molecule instead of fixed energy state which allows absorption in a range of wavelengths around a value at which the absorption is maximum. The wavelength vs absorption graph will give a peak at the maximum (which usually looks symmetrical but not always necessarily be so).

   From ChemWiki

The width of this absorption band would differ between different chromophores; so in your hypothetical case, some chromophore which has an absorption maximum at 580nm may absorb 530nm while another chromophore with same maximum, may not.

The Beer-Lambert's law will hold for all wavelengths that can be absorbed i.e. the absorbance would be proportional to the concentration of the molecule (unless there are complex phenomena like energy transfers that may be dependent on concentration; this is unlikely in dilute solutions).

As a practical suggestion, I would say that if your spectrophotometer has fixed options then choose the wavelength that is closest to the absorption maximum.

If you see the above example graph and let's say your aim is to quantify nitrophenolate in a mixture of nitrophenol and nitophenolate. Then a measurement at 350nm instead of 400nm would give you erroneous result. In other cases a 50nm difference may not matter (for e.g. measuring at 450 for the nitrophenolate). It all depends on what you are analysing. You should know the molecule that you are analysing.


How would a different solar day affect evolution?

It depends on how different. Day length affects more than just how long the periods of light and dark are. Let's assume a very slow rotation, and a very long day, maybe 1 month light, 1 month dark. The light side would get much warmer while the dark side would get much cooler. At the border between light and dark sides, you'd expect to see powerful storms as the hot moist expanding air moved into the cooler side and had to lose moisture. Any life on a planet like this would have to adapt to surviving in both hotter and cooler temperatures. We can take this to an even worse extreme and look at a planet like uranus. Uranus's axis is tilted at 97.7 degrees, so even though it rotates, the day/night cycle is controlled by it's rotation around the sun. If the earth were tilted like this, then we would 6 months of light followed by 6 months of darkness. Life would either have to keep moving to stay in the moving temperate twilight zones or adapt to hibernate.

If we assumed a shorter day/night cycle, I think the changes would be less significant. Lets say we had a 4 hour day. ( There has to be a speed where things get thrown off the planet, but I don't think 4 hours per day is fast enough ) A 4 hour day would have 2 hours of light with 2 hours of dark. My guess is that circadian rhythms would be less important. Temperature changes from light to dark would be less significant than currently.

It's an interesting thing to think about because the Earth's day is slowly getting longer as the moon exerts a tidal force on our planet, slowing our rotation and escaping further into space, but this change is so slow I doubt it will ever become a problem for humans.


I am putting here the main points from the link given by @WYSIWYG (i.e. this):

  High glucose levels reduce the levels of the powerful vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood pressure and eventually narrows down the vessels...increased modification of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well...the researchers found that there was an increased activity by O-GlcNAc in the blood vessels, which competes with another mechanism for modifying proteins called phosphorylation. In blood vessels, phosphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes more of the blood vessel dilator. O-GlcNAc seems to beat phosphorylation to the punch so there is the opposite result.

Here, O-GlcNAc refers to O-linked β-N-acetyl glucosamine.


Can a living organism run on electricity?

No; the problem is, as you pointed out, that no organism will manage to multiply, grow or even sustain itself without absorbing matter to create new cells and fill metabolic losses.

Even photoautotrophic organisms which get energy from light (which is in fact an E-M wave, so pretty close to electricity) collect matter from the environment -- plants for instance seem to grow out of nothing, but in fact gather significant part of their mass from atmospheric CO_2.


There are some diseases in which a minority population of normal cells can rescue the organism, even in the presence of a majority of mutant cells.  Sort of like a group vacation to Kazakhstan with one friend who can speak Kazakh.  Very different experience from a vacation where none of you speak Kazakh.

Take for example hemophilia A.  Cells have a mutant gene for factor 8.  Without factor 8 blood does not clot properly and people have bleeding trouble.  You do not need much factor 8.  Just a little bit can prevent spontaneous bleeds.  People who are heterozygotes for hemophilia A (carriers) are fine at 50% normal.  So if you edited mutant liver cells such that they could produce factor 8, even if they were only 10% of the total cell population of the liver, having some factor 8 would sidestep the full hemophilia phenotype.

Likewise metabolic mutants - some children are born unable to handle certain substances.  Phenylketonuria is the one you read about every time you drink a diet coke.  If a minority population of cells could be produced that were able to handle phenylalanine, those would rescue these kids even if most of the cells still could not.


Can antibiotic resistant bacteria compete with normal one in an antibiotic free environment?

The antibiotic resistance adds to growth cost. In an antibiotic free medium the antibiotic-susceptible strains will outgrow the resistant ones. See this


Would expression of GroEL and GroES in erythrocytes be a potentially effective therapy for sickle cell disease?

GroEL and GroES are multiprotein chaperonin complexes: Not so easy to ectopically express
Erythrocytes do not have nucleus: you cannot stably express anything in mature erythrocytes.
If your aim is to do a stable gene expression (which would require genomic integration), the better way is to do a gene therapy: culture haematopoetic stem cells, Correct the mutation by homologous recombination. Put the cells back into the bone marrow.


Can a brain be damaged by overstimulation?

(This is such a difficult question to begin answering in any satisfactory manner, though I think can be addressed for pedagogical purposes in line with the aims of this SE.)

Before we address the question, I think it is prudent to think about the difference between stimulation and activity. A neuron can be self-activating without external stimulation, or it can be highly stimulated by sensory input and yet have low or inhibited activity. You do not specify, so I think the discussion must necessarily be very incomplete on this topic.

Your question is also naturally a little unclear and difficult to answer methodically, especially because 'damage' in this case is a very subjective term. As with all biological systems, there are self-protective mechanisms and reflexes and feedback circuits in place to prevent 'you' or your brain from overdoing anything. A dysregulation in neuron activation, or activity, would probably be a state of illness, such as having a seizure. I don't think it is possible for a typical person to expose themselves to sensory extremes without consequently feeling tired or bored as a result (e.g. looking into a strobe light or listening to loud music for inordinate amounts of time), which may be the result of an internal homeostasis, just like blood pH or blood sugar level, though regulated through physiologically-dependent behavior (sleep, concentration levels, apathy, etc.)

More strictly and scientifically speaking, all activity wears all tissues, including the brain. This would make 'brain activity' a process contributing to aging. However, once again, one can interpret anything as 'damaging'; breathing is damaging (oxidation! the cellular definition of wear-and-tear), but it also sustains you. Calories sustain you, but caloric restriction extends lifespan in virtually all animal models.

A recent publication in Nature (Oct 2019) suggests that the global inhibition or decrease of all neuron firing seems to be related to increased longevity which may suggest the opposite case to your question: lower neural activity may lead to extended lifespan. This suggests, though does not demonstrate, that over-activation may contribute more 'damage' and accelerated aging, compared to lower levels of activation. This conclusion is also based on evidence associated with a global - whole-central nervous system - effect, and does not indicate that one should under-stimulate parts of their nervous system to achieve the same result. Also, keep in mind that stimulation and activity are entirely separate things, so such a conclusion does not answer your question.


Help ID this plant with balloon-like feature containing seeds

I searched Google for Lantern plant and came across this http://tabibito.hopto.org/display_one_file.php?article=494

Which is the same plant, but not the best of references, it doesn't give a scientific name and I am not sure Paper lantern plant is their right identification.

It is definitely of the genus Physalis

https://en.wikipedia.org/wiki/Physalis

but as yet haven't been able to find the species that matches your leaf exactly. But I'd thought I'd post for now as it may help you, or others.


Blood finds use in many different dishes as well as biotechnological applications. Research-grade BSA (bovine serum albumin) is derived from cow's blood, there are not special facilities, same cows go for steaks and car seats. So part answer is economical: blood can be processed further. Also it is just easier not trying to preserve liquid inside vessel already opened by slitting the throat. It also seems that blood can rot faster than other tissues, maybe, because in dead animal immune responses are deteriorated and every infection in blood will activate.


Common english name for tissues which are separated from the blood by blood-tissue barriers

I am not aware of any umbrella term: the barriers for each are not identical, the function and reasons for the barriers are not the same.

Often these organs are referred to as "immune privileged" because one of the important consequences of the separation is that immune responses in each of those organs are different than in the rest of the systemic circulation, even though this is of course not the only significance of blood-tissue barriers. The meaning of the term has also shifted a bit, though, and I still see different definitions in different places (for example, the Wikipedia definition is not the one I would use). As a consequence, it is easy to argue that some like the thymus should not be considered immune privileged, so my umbrella suggestion would be to just avoid umbrella terms.


Why is ATP synthase sometimes referred to as ATPase?

The way we were

To understand why you may encounter ATP synthase referred to as ATPase, you need to be aware of the historical context — the experimental work that preceded the knowledge of the structure and function of the enzyme complex that we have today. In a nutshell:

  Original studies of the components of what we now know to be a complex capable of synthesizing ATP could only be assayed by their ability to hydrolyse ATP. Even though these components (F1 and F1FO) were derived from a mitochondrial system that coupled electron transport to ATP synthesis, and the authors believed these components were responsible for ATP synthesis, they were obliged to refer to them by the activity they had assayed: hence F1 ATPase and F1FO) ATPase.

History lesson

It is instructive to consider a paper by Kagawa and Racker, published in 1966, and entitled:

  Partial Resolution of the Enzymes Catalyzing Oxidative Phosphorylation
  VIII. PROPERTIES OF A FACTOR CONFERRING OLIGOMYCIN SENSITIVITY ON MITOCHONDRIAL ADENOSINE TRIPHOSPHATASE”

This work demonstrated that a mitochondrial ‘fraction’ (FO — ‘F’ stood for ‘fraction’) when added to another ‘fraction’ (F1), previously shown to have ATPase activity, could confer sensitivity of the ATPase to inhibition by oligomycin, a compound that inhibits oxidative phosphorylation in intact mitochondria. The title shows clearly that they were aiming to understand ATP synthesis, but were at the stage where all they could measure was the ATPase activity of fractions. It was not until 1973 that Racker and Stoeckenius were first able to  synthesize ATP, and for that they had to use a different system — the light-activated purple membrane of Halobacterium halobium. The key was the incorporation of the membrane — without it there could be no proton gradient to drive the synthesis of ATP, and this was why the isolated F1FO) complex could never catalyse synthesis of ATP on its own.

Those days are gone now

The structure of the components of the ATP synthase finally started emerging in the 1990s, after which no doubt remained that the F1 and FO fractions were part of a synthase.

  Therefore, in describing the enzyme complex as we now know it to be,
  there is no excuse to refer to it as anything other than ATP synthase. Moreover there is a particular need to avoid confusion with a membrane ATPase (below).

In my opinion, any textbook that refers to ATP synthase as ATPase is severely out of date and should be burned.

Of course, I exempt historical accounts, as long as the context is made clear.

The acid test

In some cells there are transmembrane complexes, structurally related to the mitochondrial (or bacterial membrane) ATP synthase, that are ATPases. These are the Vacuolar-type H+-ATPases (V-ATPase) which use the energy of ATP hydrolysis to transport hydrogen ions across the membranes of certain tissues and organelles. Another reason not to refer to the ATP synthase as ATPase!


First, although it only speaks about cases of diploidy, you might want to have a look at Solving Hardy Weinberg problems.

Information given to us

The question gives the same names to the phenotypes than to the alleles which si rather confusing. Let's call the three possible phenotype $P_1$, $P_2$ and $P_3$. We know that the frequencies of these phenotypes are

$$f(P_1) = 0.614$$
$$f(P_2) = 0.306$$
$$f(P_3) = 0.08$$

Compute phenotype frequencies in terms of allele frequencies

Let, $x$, $y$ and $z$ be the frequencies of the three alleles, $A_1$, $A_2$ and $A_3$ (I chose those names to fit with the equations you wrote). The whole difficulty now is to express $f(P_1)$, $f(P_2)$ and $f(P_3)$ in terms of $x$, $y$ and $z$. You should try yourself before looking at the result. Start with $f(P_3)$, it is the easiest.

Here is the solution for $f(P_3)$

   $f(P_3) = z^3$

Here is the solution for $f(P_2)$

   $f(P_2) = y^3 + yz^2$

Here is the solution for $f(P_1)$

   $f(P_1) = x^3 + 3x^2 (y+z) + xyz + xy^2 + xz^2$

Once, you have done that, you have three equations with three unknowns and you just have to solve them. Make sure at the end that $x+y+z = f(P_1) + f(P_2) + f(P_3) = 1$.


How can Pyridostigmine have the indication of Myasthenia?

Pyridostigmine is an analog of neostigmine, so has the same basic mechanism of action. Please forgive me for repeating information you may already know.

There are two main families of acetylcholine receptors: muscarinic and nicotinic. Acetylcholine receptors at the neuromuscular junction (NMJ) are exclusively nicotinic (N1 or NM), so that's the only receptor I'll address.

Myasthenia Gravis is caused by an immune response to nicotinic postsynaptic receptors on skeletal muscle. An antibody can either destroy or block the receptor site. The antibodies destroy the receptor sites more rapidly than the body can replace them. In MG, there can be as much as an 80% reduction in the number of these receptor sites.

Acetylcholinesterase (AChE) is an enzyme that breaks down acetylcholine (ACh) at the synaptic cleft. AChE has a remarkably high specific catalytic activity: each molecule of AChE degrades about 25000 molecules of ACh per second. Any drug which serves to inhibit AChE will increase ACh concentration at the N1 receptor. AChE inhibitors can be irreversible or reversible. Reversible inhibitors, (competitive or noncompetitive) have therapeutic applications; irreversible AChE  modulators are toxic.

Carbamates are organic compounds derived from carbamic acid (NH2COOH). They are reversible AChE inhibitors. This group includes neostigmine, pyridostigmine and physostigmine. Pyridostigmine is an analog of neostigmine, so has the same basic mechanism of action. Because they are not lipid soluble, they are selective for the NMJ; both also have direct action on Nm Receptors. The major difference between them is that pyridostigmine has a slight but significantly longer duration of action.

Drug Bank: Pyridostigmine
NeuroLex.org (get's it's info from PubChem)


I found these skulls in a old bottle in the woods. Can you tell me what they are?

Its a Shrew skull.

Hainault Forest Website

Photographs by © Brian Ecott


Is there any websites that provide the DNA sequences of food samples?

I am not aware of any websites that provide full DNA sequences for food products specifically. In the context of your question, by "food samples" I am assuming you are chiefly referring to meat, fish, and dairy products (the headline-making categories of food fraud), although similar principles are applied to plant products, oils, rice, and other natural products.

PCR

There are a wide variety of genetic techniques used to detect food fraud or adulteration. These techniques do not look at the entire genome of the animal or plant from which it is derived – that would be extremely expensive and unnecessary. Instead, scientists look at particular parts of the genome that they know will likely help them distinguish one species from another.

This is where the primers come in. DNA primers are short segments of DNA that are used to initiate replication of segment of DNA, and is the vital component of PCR that determines which part of the genome will be amplified. Once the PCR product is amplified, it can be analysed by a variety of techniques. For instance, if the PCR products of various species are known, they can simply be run on gel electrophoresis which separates the DNA products by size. Thus if a band of an unexpected size appears on the gel you know there has been some contamination. There are also more automated methods of detecting fragment size via electrophoresis.

Examples of where these techniques has been used has been to detect:

cow's milk in buffalo mozzarella cheese (López-Calleja et al., 2004)
king bolete mushrooms potentially mislabelled as slippery jack mushrooms (Moor et al., 2002)
domestic pig meat in wild boar products (Conyers et al., 2012)

From the López-Calleja study on mozzarella, one of the gels looked like this:

The PCR was run to detect cow's milk in buffalo cheese. Lane 1 corresponds to 100% cow's milk (it is a very bright band), lane 2 is 10% cow's milk, ranging down to lane 6 which has 0.1% cow's milk (a very faint band), and lane 7 is the pure buffalo cheese which shows no band. Therefore, this assay could be useful to rule out contamination with cow's milk.

Real-time PCR

Running gels is a somewhat old-fashioned way of doing things, and there are better ways to make use of PCR technologies on a larger scale. Real-time PCR is the technique now routinely done to detect food fraud. This is a variant of PCR, which (as the name suggests) allows one to quickly see which PCR products are being produced, in what quantity, and there is no need to run a gel.

For example, real-time PCR has been used to detect:

horse and donkey DNA in otherwise-labelled meat products (Chisholm et al., 2005)
pork adulteration in commercial beef burgers (Ali et al., 2011)
Atlantic cod, Atlantic salmon, and European plaice in fish products (Hird et al., 2012)
honey containing pollen from a specific region (Laube et al., 2010)

An example of what the read-out from the real-time PCR is given below. This example is from the Ali study on beef burger adulteration. The letter A was 100% adulterated (i.e. contained 100% pork instead of beef), letter B contained 10% pork, and so-on to E which contained 0.01% pork. F had no pork. The more pork contamination there was, the sooner on the plot (in PCR cycles) the contaminant reached detectable levels:

About the sequence

As you will see from reading about these techniques, it is not so much the sequence itself which is important – it is fragment size or other properties of the region analysed by PCR that is most practically useful. Sometimes the PCR product may be sequenced for comparison purposes, although I do not believe this is done as a routine screening for food fraud.

Keep in mind that PCR is just one of a number of genetic techniques used in food safety. For example, DNA barcoding and SNPs are also useful techniques that are used in this field. The technology is constantly improving and evolving and no doubt more refined and efficient methods are being developed to detect food fraud.


Why does flatulence vary in temperature and smell?

Kind of a bad question but I'm doing my best to answer.

First, the smell will depend on what goes in - primarily a function of what you ate, and conditions in your gut (including the mix of bacteria).

Next, if you ate something containing large amounts of capsaicin (the chemical that makes chili peppers spicy), it's going to "burn" on the way out. Overconsumption of capsaicin can irritate the intestines and cause diarrhea.


Perhaps someone else can answer this with more certainty, but I'd guess that because raphides are essentially sharp crystals that cause irritation-related symptoms, rather than toxic chemicals in the way one might usually think of them, that drinking the water wouldn't pose a problem (actually, I suppose the word "insoluble" might be a clue here). Raphides are defence against herbivory, and chewing raphide-containing leaves is what you want not to do (or not let your pets do).

Veterinary Toxicology p. 889 has more info.


Good source that explains the evolution of single-celled organisms "from scratch"

Origin of Life: Chemical Approach is an edited volume by Piet Herdewijn and M. Volkan Kisakürek.

here is the book's description from the webpage:

  Dedicated to the fond memory of two great pioneers of this science, Leslie E. Orgel and Stanley L. Miller, this compilation of reviews and original manuscripts provides an overview of the current state of the art, written by some of the eminent "players" in this creative domain of "explorative chemistry".
  Since we are still far from finding a definitive answer to the most fundamental of questions in science, "chemistry" here is defined in its broadest sense. It is against this background that the contributions cover such a wide range of theories, including chemistry and selection, evolution of the pioneer organism, chemical aspects of synthetic biology, ribozyme catalysis of metabolism in the RNA world, intractable mixtures and the
  origin of life, the chemical etiology of nucleic acids, interstellar amino acids, and even the chemistry that preceded life's origin.


Animal reproduction when resources are scarce

This is actually a comment, but was not allowed to comment.

I think what you're interested is more in population dynamics and I think what you're really asking about is more in line with what system of  differential equations explains a network of animals and how their populations grow and decrease with the amount of resources and the species population.

I think the problem is that, there's actually no good model, because there are so many factors which seem to contribute to shifts.

@ MIT this year, they had a visiting prof from Tufts give a talk on this, and they're working on models, to try and describe this, and even HE- the prof said, yeah, it gets complicated even for two species.

I would recommend, that if you have time to read up on this?

https://sites.tufts.edu/hening/publications/ <--- a link to his publications

https://arxiv.org/abs/1710.01220

Also, this is probably more a question for the mathematics stack.


Egg shells look as if they're solid, but in fact they're filled with tiny pores through which air can and does diffuse.

  ...up to the time when internal pipping takes place, when pulmonary ventilation is initiated, about 20 liters (O2 + CO2 + water vapor) have passed through 10,000 pores of an 80 gm egg.

--Pores and gas exchange of avian eggs: a review.

  A typical 60-g chicken egg has about 10,000 pores, each with a functional cross section of 150–200 μm^2; therefore, the total pore area is about 1.5–2 mm^2.

--Gas exchange in avian embryos and hatchlings

You only asked about chicken eggs, but chickens have it pretty easy compared to many other avian species.  For example, ostrich eggs have a much larger volume-to-surface area, meaning that exchange is less effective. One way ostriches may compensate is by incubating eggs at lower temperatures, reducing oxygen requirements; more significantly and related, incubation time is relatively slower for birds with large eggs.   Birds at high altitudes have larger total pore size, adapting to the reduced O2 pressure.

Actually, a more serious problem than oxygen exchange is water exchange.  The egg needs to manage water loss (not too much, not too little), and the more gas exchange the more water loss.  Accordingly, birds adapted to different humidities lay eggs with different gas exchange capacities (changing pore densities for the most part); birds in very arid environments, like gulls in Chile's Atacama Desert, have very low gas and water exchange, to the point where their developing chicks are relatively hypoxic:

--Reduced oxygen diffusion across the shell of Gray gull (Larus modestus) eggs.


Electronic cigarettes (e-cigs), any health risks?

Since the question is about risk specific to e-cigarette as opposed to classic cigarettes, what's left is the potential harm from the chemicals in refill-fluids (apart from nicotine): polyethylene glycol, glycerol, alcohol, linalol, flavours. You can find cytotoxicity experiments (e.g. http://www.sciencedirect.com/science/article/pii/S0890623812002833), that show that the most harmful components may be the flavouring compounds. Some other articles (I can't find a reference right now) point out that the moderate heating of the fluid might create harmful byproducts, differently from those in regular cigarette: acroleine, formaldehyde. The use of e-cigarette is probably too recent to have long-term studies that answer your question.


Is Homo sapiens the only extant species of genus "Homo"?

Is Homo sapiens the only extant species of genus “Homo”?

Yes, Homo sapiens is the only species left in the genus Homo. To be more accurate, some even consider all modern humans as being part of the same subspecies Homo sapiens sapiens. In those terms, Homo sapiens sapiens is the only subspecies left in the genus Homo.

There were other lineages before though but they got extinct.

Other Homo lineages that existed

There were other Homo lineages that went extinct. Consider the followings for example

H. habilis
H. gautengensis
H. erectus
H. neanderthalensis (sometimes called H. sapiens neanderthalensis)
H. heidelbergensis

Related posts

Here are two other posts that may be of interest to you

Does it make sense to classify all humans in a single species?
How could humans have interbred with Neanderthals if we're a different species?


The only reason that it shows both colors is due to imperfect manipulation while staining. You cannot count on the majority to determine the result of the stain.

In your specific case, rinsing or decoloration with EtoH was probably not done enough and safrainin wasn't completely eliminated.

The best way to be sure of the result would be to redo the coloring.

A good tip while staining is to have duplicates or triplicates.

Secondly, to answer what you said here:

  I also understand why gram-pos appear purple, --that the crystal
  violet-iodine complex is retained due to thicker cell walls in
  gram-pos..... and thinner cell walls in gram-neg, so they are
  decolorized and appear the color of the counterstain.

Actually it is not only the thickness of the cell wall that will cause the bacteria to retain or not the crystal-violet. Gram positive bacteria have a plasma membrane then peptidoglycan on top while Gram negative bacteria have a plasma membrane, then peptidoglycan and another outer membrane on top. Crystal violet "sticks" primarily to the peptidoglycan.

Decoloring will remove the stain on the outer membrane of gram negative bacteria. You were right with the fact that Gram positive bacteria will have thicker peptidoglycan.

Gram + vs Gram - cell walls http://www.diffen.com/difference/Gram-negative_Bacteria_vs_Gram-positive_Bacteria


How are minerals formed by biological processes?

News to me is that about 4500 of the 4900 minerals on Earth have been created by life.

After reading the article, this isn't what was said.

What was said is that life increases mineral diversity on a planet, most notably through biproducts reacting with existing minerals (like Oxygen - a biproduct of photosynthesis - reacting with iron to create iron-oxide).

So, life doesn't create new minerals, but it does change the abundance of elements at the surface which can undergo reactions with pre-existing minerals to form other minerals.

Not all of the 4500 "new" minerals on the Earth can be attributed to life. We don't know how many new mineral formations have formed because of life, but the article suggests the theory that increased surface diversity of minerals might be a good indicator of life.


Difference between clonal and subclonal mutations

clones means when a cell has the same DNA characteristics as his predecessor so in that case of yours you could say that those cells are clones while for sub-clones I am not that sure, the difference of clone and sub-clone is that a sub-clone is basically a clone who is then remade with a different characteristic(an upgrade if you will) , since cancer are mutated cells you could call them like that but only if you study its DNA, meaning you have to study deep to find out if there are sub-clones in there. AS for the 3 question I didn't quite understood what you meant cuz you just used 2 words with opposite meaning because heterogeneity means a group of organismes with different characteristics and clonal population means organismes with same DNA ( much like a colony of bacteria).


is it necessary that every theca of an angiospermic anther must contain two microsporangia

Is the necessary that stamens have two microsporangia per theca? No. Many species in Cryptocarya group of Lauraceae have microsporangia that have fused such that they have only two microsporangia instead of the typical four (Rohwer et al. 2014). I interpret their description as saying that the microsporangia within a theca but it's not clearly stated as such.

Within the Magnoliidae, one pollen sac of a theca is lost is some taxa (Endress et al. 2008). Evolutionarily, the Hamamelidaceae have reduced the number of pollen sacs from two to one (Endress 1989). I could not find examples of plants with more than two microsporangia per theca.

Why do most plants have two pollen sacs per theca?  It's probably a result of the evolutionary history of plants in general because it is so common. Even those that have only a single pollen sac seems to start out developmentally with two.  It's probably due to the underlying genetics.

The genetics of floral development is complex but being slowly teased apart. The overall development of floral patterns is set by a group of developmental or regulatory$^1$ genes called MADS genes.  Collectively, the MADS genes (along with other regulatory genes) control the overall organization of the flower structure. For example, MADS genes determine the arrangement of floral whorls from sepals (outermost whorl) to petals to stamens to carpals (innermost whorl). Changes in use or timing of the MADS genes can contribute to different types of floral morphology, such as the loss of sepals or big, showy sepals but no petals.

Some of these same MADS genes contribute to the formation of the stamen structure. The review by Goldberg et al. (1993) gives a thorough but now dated review of the developmental genes that control anther development. The figure below (their figure 3) gives a nice overview of the stages that lead to development of the theca with two microsporangia and ultimately to the final stage of fertilization. Even more specific, Bowman et al. (1991) show that AGAMOUS is one regulatory gene that is active during the development of the theca and microsporangia.

I can't speak in detail about how regulatory genes work in flowers (I know a bit more about regulatory genes in animal development, especially from an evolutionary developmental perspective). In animals, regulatory genes often work by concentration gradients, both by the concentration of the regulatory gene itself, by the concentration of other regulatory genes, and by the concentration of the regulated genes. This process helps to determine the anterior-posterior axis in animals with bilateral symmetry, as well as the left and right sides.

I suspect that floral regulatory genes work in a similar fashion.  Changes in regulatory expression can lead to bilaterally symmetric flowers (think of mint flowers, monkey flowers, etc. See Hileman and Cubas (2009 for a good review.). I suspect it is some type of symmetric expression of regulatory genes that leads to the formation of two microsporangia per theca.  Mutations that cause changes in the expression patterns of other regulatory genes can cause the initial expression but subsequent loss of one of the microsporangia, as noted for the Lauraceae and the Hamamelidaceae.

Footnote

Broadly but simply, regulatory genes are genes such as transcription factors that regulate or control the expression of other genes.

Literature Cited

Bowman, J.L., et al. 1991. Expression of the Arabidopsis floral homeotic gene AGAMOUS is restricted to specific cell types late in flower development. The Plant Cell 3: 749-758.

Endress, P.K. 1989. Aspects of evolutionary differentiation of the Hamamelidaceae and the Lower Hamamelididae. Plant Systematics and Evolution 162: 193-211.

Endress, P.K. and L.D. Hufford. 2008. The diversity of stamen structures and dehiscence patterns among Magnoliidae. Botanical Journal fo the Linnean Society 100: 45-85.

Goldberg, R.B., et al. 1993. Anther development: Basic principles and practical applications. The Plant Cell 5: 1217-1229.

Hileman, L.C. and P. Cubas. 2009. An expanded evolutionary role for flower symmetry genes. Journal of Biology 8: 90.

Rohwer, J.G., et al. 2014. A phylogenetic analysis of the Cryptocarya group (Lauraceae), and relationships of Dahlgrenodendron, Sinopora, Triadodaphne, and Yasunia. Phytotaxa 158: 111-132.


Thin layers or laminae that make up a single summer band in tree ring, what are they?

Not as a confident answer but as a comment... to provide image.

The wood TS looks like ring-porous, Oak (Quercus sp.) wood (Not as identification but anatomical features are comparable).

The dark bands (radial here) seems to be xylem fibres, and bright bands (radial here), seems to be xylem parenchyma.

This is a magnified image of wood of post oak (Quercus stellata). .
Source, URL http://www.wood-database.com/wp-content/uploads/post-oak-endgrain-zoom.jpg

where it seems to me

If there is anything wrong in my knowledge, inform me and feel free to downvote this answer. If any better answer comes, I'll delete this answer.


What are the consequences of inbreeding?

You are right. Inbreeding strongly increases overall homozygosity which subjects inbred individuals to diseases caused by rare recessive alleles. In non-inbred individuals the chance is quite low to receive those because many deleterious variants (and in fact, most segregating alleles we can observe) are recessive. Most often, but depending on the dominance coefficient, these 'hide' in healthy heterozygous carriers and when very closely related individuals breed (with a lot of variants that are identical by descent) there is a high chance that some of the 'hidden' deleterious variants are passed to the offspring.

You have to be aware that there are in fact two conceptually different processes that can be both be referred to as inbreeding but are also somewhat continuously linked (see below):

Mating systems that allow offspring between actually related individuals (measured by the degree of relatedness), what in humans often is referred to as incest or consanguinity.
Populations with very low effective population size $N_e$ generally exhibit higher relatedness due to lack of genetic diversity (excess of homozygous sites). Therefore, populations with low $N_e$ are referred to as inbred even if no actually related individuals are mating.

There is some evidence that inbreeding in the first sense is linked to cognitive abilities in humans:

Bashi (1977) investigated the effect of offspring having first-cousin (i.e. between children of siblings) and double first-cousin (i.e. between children of siblings and unrelated siblings, sharing as much variants as half-siblings but with more recombination events) parents while (at least somewhat) correcting for socioeconomic effects. He found an inbreeding depression with respect to cognition that could

  result either from the general increase in homozygosity [...] or from decrease in performance resulting from homozygosity for specific recessive alleles (highlighted by me). The higher variance of the double cousin group in some of the tests favours the second interpretation.

Woodley (2012) presents evidence for slightly lower IQs caused by inbreeding, however, he also mentions that the effect is way smaller than socioeconomic effects:

  Consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.

Fareed and Afzal (2014) investigated verbal IQ, performance IQ, and full-scale IQ and found that all of these IQ parameters are significantly lower in inbred children compared to non-inbred children - actually the difference increases significantly with the degree of relatedness. They conclude that there is

  evidence for inbreeding depression on cognitive abilities among children.

Please keep in mind that, for for sociological/ethical reasons, this is highly controversial, especially when the two concepts above are intermixed - human populations underwent differential and variably strong periods of low $N_e$, i.e. were subject to stronger or weaker inbreeding in the second sense. When reading the citation of Bashi (1977) above carefully, you will notice that he takes good care not to intermix those. Inbreeding in the first sense leaves large runs of homozygosity (ROH, blocks without heterozygous sites, i.e. a clustered and local lack of variation) whereas inbreeding in the second sense increases homozygosity in the genome less selectively. Therefore, the distribution of homozygous sites can be used to infer whether inbreeding is recent (first sense) or old (second sense) (see for example McQuillan et al. (2008) - here you see that both concepts form a continuum: where do you set the cutoff between recent and old? what is an appropriate threshold size for ROH? ...). Regardless, Bashi's findings indicate that effects of inbreeding are caused by recent inbreeding as he presents evidence that his results are rather driven by specific deleterious recessive variants than overall excess homozygosity. Finally, even though the study by Fareed and Afzal (2014) shows rather large effects of recent inbreeding in IQ measures, the results from Woodley (2012) show that one needs to be really careful to separate genetic from environmental components as his study suggests that the latter contribute more to the observed decrease in IQ.


I answered this implicitly in a comment to my answer to: Light and Dark Reaction of photosynthesis?. Anyway:

There is no such thing as NADPH2. There is only NADP+ and NADPH. Consult Wikipedia or a reputable text such as Berg.

The nicotinamide portion of NADP that  undergoes oxidation and reduction is exactly the same as in NAD. The changes undergone are:

The error either comes from confusion with the other redox cofactor, FAD / FADH2, or the fact that two electrons are involved in the reduction of NADP:

  NADP+ + H+ + 2e → NADPH


Basically, yes, cockroaches are very good at avoiding detection. Since you linked to the American cockroach (Periplaneta americana), I'll discuss that species in my answer. I've only twice, in my life, seen an actual cockroach. I don't know what parks you're referring to in your question or if it's that common.

By the time you start lifting up a rock or board to look for a cockroach during the day, it will have already sensed you coming and have left.

  They spend most of their time in narrow, tight cracks and spaces where surfaces touch them on both sides.
  (Cockroaches from the University of Minnesota)

  Cockroaches like to be touched.
  Roaches are thigmotropic, meaning they like feeling something solid in contact with their bodies, preferably on all sides. They seek out cracks and crevices, and will squeeze into spaces that offer them the comfort of a tight fit. And I do mean a tight fit. The small German cockroach can fit into a crack as thin as a dime, while the larger American cockroach will squeeze into a space no thicker than a quarter.
  (10 Fascinating Facts About Cockroaches)

When you understand how thin a crack can be for a cockroach to wedge itself into, you get a better idea how they hide during daylight hours in the outdoors. Many trees have rough bark with enough crevices for them to hide. They could fit in the thin spaces between the bottom of concrete sidewalk pavers and soil, under leaf mulch and many other spaces you may never have noticed before. It takes very little. Best places to look for them in parks would be around trash receptacles where people toss food they didn't finish eating.


These are silver fish (Lepisma saccharina) and harmless. Wikipedia says (image taken from the article):

  Silverfish are nocturnal insects typically 13–25 mm (0.5–1.0 in)
  long. Their abdomens taper at the end, giving them a fish-like
  appearance. The newly hatched are whitish, but develop a greyish
  hue and metallic shine as they get older. They have two long cerci
  and one terminal filament at the tips of their abdomens; the filament
  projects directly off of the end of their body, between the left and
  right cerci. They also have two small compound eyes, despite other
  members of Zygentoma being completely eyeless, such as the family
  Nicoletiidae.

  Like other species in Apterygota, silverfish are completely
  wingless. They have long antennae, and move in a wiggling motion
  that resembles the movement of a fish. This, coupled with their
  appearance and silvery scales, inspires their common name. Silverfish
  typically live for two to eight years. Silverfish are agile runners
  and can outrun most of their predators (including wandering spiders
  and centipedes). However, such running is possible only on horizontal
  surfaces, as they lack any additional appendages, and therefore are
  not fast enough to climb walls at the same speed.[citation needed]
  They also avoid light.


Your fish in question is a zebra danio GloFish; they're genetically engineered to have flourescent coloration. The giveaways for me were the shape of the body (minnow shaped, with zebrafish belonging to the minnow family), its size (small), and the striped pattern running along the body, parallel to the lateral line. Since the fish in your picture is in motion, it's a bit difficult to see, but it's definitely there (can be seen closer to the head).

And here's another image, where the coloration is closer to what you have. (IMO, the previous image has a strong contrast, especially with the black background)

This zebrafish is suffering from a bent spine, which accounts for the misshapen body. (source)

Also, it seems that the fish in the background is a black-skirt tetra.


How does promoter sequence affect initiation?

I agree that it is hard to search for papers but from graduate level classes this is some of the additional insight I have gained. Sequence context of promoters is important. Specific DNA sequences (motifs) can act as binding sites for specific transcription factors and combinations of these transcription factors help recruit RNA pol II to the promoter. These combinations of proteins are spatially and temporally regulated and will help decide if gene that is next to promoter will be activated. A luciferase reporter assay is often used to determine the strength of a promoter.

An example is as follows: A strong promoter might have certain histone marks that would recruit proteins to remodel the chromatin to be more accessible exposing binding sites of transcription factors that help recruit RNA Pol II. A weaker promoter might have less transcription factor binding sites or less chromatin accessibility and thus it is harder for RNA Pol II to be recruited. There are also some kinetics aspects you must keep in mind.


How did mosquitoes expand their habitations to a place they never lived before?

It could be a number of things. Mosquitos need standing water. Look for that. Any changes? Was last year particularly rainy?  One group of mosquitos lays its eggs at the waters edge. They lie dormant until the water reaches them again. If the water was high when the eggs were laid, then recedes, it may be years before the water reaches them again and the eggs hatch, resulting in a bloom of high numbers. Also, other mosquitos breed in containers. Things like tires, or coffee cans, or flower pots in cemeteries. Even a small amount of stagnant water in a container can result in mosquitos. Any changes there? The obvious change is the warming climate, but I would look first to changes in the water.


Why do simulations of dichromatic color vision portray medium wavelengths as yellow rather than green?

Opponent color processing.

https://en.wikipedia.org/wiki/Opponent_process

Studies have shown blue and yellow are opponent colors, as are red and green. We process the colors in opposition, as in perceiving one requires perceiving less of its opponent, equal amounts of both (minus other colors) yields no color in your final visual perception. If you cannot differentiate red and green, than the only two colors you can differentiate reliably are yellow and blue. As a side note this is also why in image processing programs these colors are on paired sliders, it is the simplest way to manipulate color images.

The most common forms of color blindness in humans, and the one all non-primate mammals have prevents them from differentiating red and green.

If you cannot differentiate red and green, and if I show you blue and yellow, you see no color, if I show you red and green you see yellow, becasue your blue cone is not being activated.

The image below is our opponent pairs in our vision.


Does the lack of "mirror life" tell us anything about abiogenesis?

As far as I know, there isn't too much we know about why life is "left-handed". So far the prevailing hypothesis is that in space there may be a tendency for amino-acids to favor one chiral-state over another, and there's some very smart people who are testing this, as opposed to the 50:50 shot here on Earth.

To answer your question, however, the general consensus is that life came from non-living
material. Pan-spermia, intelligent design, and the rest are more fringe ideas, so the question is how life formed from non-life. One of the ideas is that the basic building blocks came from space (likely a comet or meteor), and if the idea that amino acids favor one chiral direction over another in space can help support that hypothesis.


is it possible to visualize coronavirus infection and what type of assays are routinely used?

If you have an antibody against the viral proteins you can do an immuno staining followed by fluorescence imaging. For this type of technique you would need a very specific antibody. I am not aware that this exist at the moment and I don't think anyone had the time to do it for immunostaining purposes.

For FISH it would depend on the genomic nature of the virus (ssRNA, ssDNA, dsRNA, dsDNA), again you would need specific probes to capture it. Again specific is key.

EDIT 01.04.2020: This group says they have found specific antibodies https://www.centivax.com/covid19


Does increasing the value of k in k-fold coverage requires more memory?

In Next Generation Sequencing (or better called 2nd generation sequencing) you are sequencing many many small genome fragments cut from many DNA molecules. Multiplying molecules, cutting them into fragments and amplifying them is known as library preparation (library of fragments to be read). During that process (of which PCR is important procedure) different errors or biases could be introduced.
What you get from a sequencer is many many short reads in form of FASTQ files that you need to assemble into genome sequence (by de novo assembly or more commonly by alignment to reference genome). It is important to know how sure are we for each nucleotide in assembled genome, which depends on how many times (and with what quality score) sequencer read each nucleotide (see image below).

(source: davidson.edu)
Coverage could mean average coverage across whole genome or coverage of some smaller portion of it (different coverage across genome is usually because of mentioned biases introduced in library prep).
To answer question: In final representation you get one whole genome assembled, if all you need is final representation (so answer 2). If you also store reads, then more coverage means more memory, but final genome is of same length.
NOTE: Coverage is even more ambiguous term that I just described, so you should look at this thread for possible different meanings (for example: which portion of whole genome is covered by sequencing).


The wording of the question suggests that it may be useful to clarify the meaning of the numbers in the designations 70S, 50S, 30S etc. These are sedimentation coefficients in Svedberg units as determined in the analytical ultracentrifuge, and are an indication of size.

All ribosomes have two subunits. The reference eubacterial ribosomes from E.coli are 70S with a large subunit of 50S and a small one of 30S. The reference eukaryotic cytoplasmic ribosomes (rat liver, say) are 80S, with large and small subunits of 60S and 40S respectively. The actually sizes (S-values) of the subunits in other eubacteria (say mycoplasma)  and different eukaryotes (say yeast) may differ, but the eubacterial ribosomes share an antibiotic sensitivity (e.g. to streptomycin, erythromycin) which differs from that of eukaryotic cytoplasmic ribosomes (e.g. to cycloheximide) and so it is often convenient to refer to 70S-type ribosomes or 80S-type ribosomes, despite the size difference.

Mitochondrial and plastid ribosomes share some of the antibiotic susceptibility of eubacterial ribosomes (e.g. sensitive to streptomycin, but not to erythromycin) and their rRNA is more closely related to the latter. So they have 70S-type ribosomes with 50S-type and 30S-type subunits. However they vary greatly in size. For example, pig mitochondrial ribosomes are smaller at 55S, with large and small subunits of 39S and 28S, respectively. In contrast, yeast mitochondrial ribosomes are larger at 74S, with large and small subunits of 54S and 37S, respectively. More important, they differ from eubacteria in their ratio of RNA to protein, unlike chloroplast ribosomes, which workers in the field have classified as bacteria-like. This is shown in the table:
 [Adapted from Supplementary Table S1 in Science (2014) vol 343, 1485–1489]

The striking thing about most mitochondrial ribosomes is, whether or not they have undergone a decrease in their rRNA, they have additional proteins with no analogues in bacterial ribosomes. Structural work on both mammalian and yeast mitochondrial large ribosomal subunits show that these additional proteins are associated with an altered exit tunnel for the growing polypeptides, which appears to be tailored to conduct the latter directly to the mitochondrial membrane.

Answers (depending on intent of question)

Yes, mitochondrial and plastid ribosomes have large and small subunits.
No, their sizes are not 50S and 30S, but vary greatly.
Yes, mitochondria and plastids have 70S-like ribosomes, rather than 80S-like ribosomes, but these have evolved considerably from their eubacterial precursors.

Sources

Some of my assertions are based on recent papers and earlier work referenced in them. Also access to them may not be free outside university libraries. Apologies for that — if I find more accessible sources I will add them later.

Mammalian mitochondrial ribosomes: Nature (2014) vol 505, pp. 515–521.
Yeast mitochondrial ribosomes: Science (2014) vol 343, 1485–1489.
Spinach Chloroplast ribosomes: Proc.Nat.Acad.Sci. (2007) vol 104, pp. 19315–19320.
Antibiotics and ribosomes (review): EMBO Reports (2001) vol 2, pp. 318–323.


The name of this plant is:
Ravenala madagascariensis
Check: wikipedia


It's not clear what is 'several database searches with the sequences'. The most obvious solution is blasting your sequence so you can see which part can't be aligned and then blasting the rest. You can choose different implementations (megablast of blastn) and play with algorithm parameters because it may not work for you as-is. But it will work as-is if you'll blast exons separately. This way you can identify origin genes.


Is it possible for human beings to feed through the nose?

Certain vitamins, for example, vitamin B12, can be absorbed through the nasal mucosa by simple diffusion.

Many nutrients can be absorbed through the intestinal mucosa only by the help of specific carriers. These carriers are not likely present in nasal mucosa, so the nutrients in question may not be absorbed there.

The other problem, especially with macronutrients (carbs, proteins, fats), is if the surface area of nasal mucosa is big enough to absorb large amounts of macronutrients (carbs, proteins, fats) needed to meet nutritional demands. In one experiment, only 0.1 mg of glucose from a given dose was absorbed through the oral mucosa.

In another experiment, some amino acids were absorbed from oral mucosa.


Does the octopus have an anus? What does it look like?

The anus of Octopus is channeled into its siphon.

Image taken from Carina M. Gsottbauer

Note:

  Siphon is a tube that leads from the mantle to the outside. Octopuses use their siphon to force water out in jets for propulsion and to flush waste products from the anus.

From Encyclopedia of the Aquatic World, Volume 6
By Marshall Cavendish Corporation


That is some sort of ant. Many species of ants have this huge "nuptial" flights, particularly after rains, where winged males and females leave the nest in swarms. Males die shortly after, while females lose their wings and start a new nest in the soil. I'm not familiar with Australian species, but the fact thatyou can see a "waist" shows you that those are winged ants.


It appears to be a longhorn borer beetle. A more comparable picture is found here. Are there fig trees nearby?

Here you will find numerous images of Longhorn beetles.


Is this flying bug swarm termites? Found in New York city, approx 7mm

Yes it looks to be Reticulitermes flavipes aka the Eastern Subterranean Termite.


Why do some insects constantly move their abdomens?

Insect respiration is passive, with sclerotized tracheal tubes taking oxygen directly to the tissues, and moving carbon dioxide out. By pulsating the abdomen, the movement of gases through this system is accelerated. Wasps, as in your example, are relatively active metabolically, so it is not a surprise that they tend to use this strategy.


It is not really essential that all vital organs should have regenerative potential (for example brain).

The cellular composition of a tissue is a big factor in deciding if the organ/tissue will regenerate or not. Some cells divide while others do not; highly specialized and polarized cells like neurons do not divide perhaps because the act of division itself will compromise their function. That doesn't mean these tissues cannot regenerate; they would need stem cells that can differentiate into the type of cells that died.

So regeneration can happen via:

Division of the tissue cells (skin healing, liver regeneration)
Differentiation of stem cells (erythropoesis, muscle regeneration)

Organs that do not have non-dividing cells can regenerate by simply proliferating whereas others would need to maintain a stem cell niche- which is not possible in all tissues. Maintenance of stem cells also adds up to the cost of metabolism; so there is some tradeoff.


Experimental evidence for the selfish gene vs. the selfish individual

My understanding of this is that the complete reference for molecular centralized evolution is The Selfish Gene itself.  I'm going to cite Alan Grafen's essay here,
Richard Dawkins, proposes that the logical, fundamental unit of evolution is the replicator.

The replicator is the fundamental unit of reproduction - whether these replicators survive or do not defines the properties of the biological system they reside in.  These words were chosen carefully because DNA sequences themselves are not replicators exactly - many individual copies make up the animals in a gene pool and the replication of one copy or another doesn't matter.  The distinction between a physical strand of DNA and the replicator is the bulk of more than one of Dawkins book.  It shows why the life of an individual means nothing to biology or evolution, how the boundaries of genes as transcriptional elements do not define the replicon (commonly misunderstood by molecular biologists).  The replicon (a genetic unit of replication) manifests a behavior or phenotype in the organism that helps it reproduce and is reproduced.  This can be cooperation with other members of your species or egg rolling or killing other sperm and is usually the result of many individual mRNA transcripts working in concert.  A given gene as defined by mRNA transcription commonly participates in multiple replicon type behaviors.

But DNA is in the mind of the molecular biology camp highly intertwined as a replicator because it is the physical medium through which the replicator is passed from one generation to another.  Without DNA, meiosis and the rest there are no replicons.  The earliest replicators were possibly simple transcripts which self replicated and not much more, but over time they have become a network of intertwined molecules working in a system.

To my understanding this is axiom more than proof.  It does not need to be proven because the physical transmission of DNA replication over time is the minimal necessary scenario to picture biology and evolution as we understand it.  The selection amongst groups of genes or groups of cells or groups of individual multicellular animals seem unnecessary given the physical framework of DNA replication.

Certainly that these connections have been shown.  The inspiration for The Selfish Gene is the confirmation of Robert Triver's Selfish Gene hypothesis with the discovery of t a terribly selfish gene which takes up the better part of chromosome in drosophila and increases its chances of showing up in the next generation by showing up in sperm more than half the time.  There are lots of other examples in the Selfish Gene and the Extended Phenotype, which answers many of the common questions about this thesis.  The literature since has been pretty productive. That being understood, its one thing to prove that something is true in biology, and another thing to prove that all other similar mechanisms are simply not true.

Yet even in Dawkins essays we see that the replicator is a bit of an abstraction some practically indefinable group of genes. Even as they each compete against each other, they create phenotypes collectively and the replicon becomes abstracted from the fundamental mechanism of replication.  The most popular example of replication Dawkins creates - the meme - has no relationship to DNA at all - a sticky idea that spreads socially and replicates in the minds of individuals.

When we look at terribly complicated but obviously advantageous behaviors, the connection between the replicator and the competition of individual genes gets muddy.  EO Wilson, having discovered pheromones and started ecology and sociobiology as disciplines still publishes group selection arguments.  Having studied social behavior in insects over his career and co-authored one of the most complete compendiums on the subject, he has put forth consistant arguments since the 70s that group selection still has a place in evolution. Unlike others, Wilson has I think always kept the conversation scientific and isn't jumping off any ideological cliffs (though responses say differently, the whole conversation is still published).

I don't see how an unbiased forum can ignore the fact that the editors of Nature still call this an open discussion.  Some may object, but calling the subject closed is overreaching I feel. There are others besides Wilson; I'm not familiar enough with the whole discussion to go into David Sloane Wilson and the rest, though they publish in reputable places.

I've started in this post since the question has been sitting around for a while. I expect others will post their corrections/objections/views - please do!  Whenever group selection is mentioned it often happens that someone will pop up and say 'this is not appropriate for a scientific discussion of biology here' but never any justification of disqualifying questions - I think that's not really scientific.  The fundamental attraction to academic thought to me is that minority voices that have legitimate observations are tolerated and often result in scientific revolutions, after which they are venerated for their persistence.

Here's a good place to tell us why some questions are beneath discussion in biology.  I personally do not agree; even if a position is intertwined by politics and religion, its the scientific value that should be judged, not by the company it keeps - lest science become just another intolerant clot, not driven by logic, observation and facts.  I ask you, why bother then?


What determines the pathway of a neurological signal?

Short answer
Neuronal signals neither choose where to go, nor do they carry routing flags of some sort to guide them. Instead, neuronal signals are guided by the hard wiring of the nervous system.

Background
Neuronal signals (action potentials) basically follow a one-way path. When they encounter a cross roads, action potentials are simply propagated to all of those alternatives. External effects of neurons, hormones or drugs may alter these signals, for example by inhibiting action potential formation or propagation.

To take the example of the auditory system (Fig. 1):

Fig. 1. Auditory system. Source: New York University.

One can readily see that the signal from the hair cells are routed into the auditory nerve to the cochlear nucleus, from there to the colliculi in the brain stem and further up to the auditory cortex via the medial geniculate. Basically this is a one-way, straightforward route.

There is complexity in the system, however. For example, the fibers of the auditory nerve bifurcate on entering the cochlear nucleus and make synapses on a number of morphologically different types of neuron. Each of the latter sends its axon out of the cochlear nucleus with a distinctive projection pattern that gives rise to further divergence. Specifically, some cochlear nucleus neurons project directly to the inferior colliculus, whereas others project to various divisions of the superior olivary complex and nuclei of the lateral lemniscus, which in turn project to the inferior colliculus (Irvine, 1992).

But even in this complexity the divergence is basically generated by simple bifurcations. An action potential reaching such a junction by default simply gives rise to two parallel signals; there is no choice involved. Regulation is due to other neurons targeting these pathways.

Reference
- Irvine, The Mammalian Auditory Pathway: Neurophysiology Springer Handbook of Auditory Research (1992).


1) I don't think so. I would not assume functionality.

2) People may diverge a bit on the semantics, but here's what I would say (my background is more cell bio and structural bio than biochem or genetics).

Active - Has enzymatic or signalling activity (or some other functional capability). Often proteins have multiple activities, or different active sites, so activity should be with respect to a specific function.
Functional - I interpret this to mean has all of its native activities intact. (I don't take this to mean anything structurally). One could also use this as a synonym for active, especially for a specific functionality.
Native - I take this to mean the protein has not been altered from its form found in nature. This implies it is functional.
Mature - My natural feeling for this is that it means the protein is structurally mature, i.e. it has been folded properly, transported to the correct cellular compartment, post-translational modifications completed, etc... For a non-functional mutant protein, I would hesitate to call it mature though, even if it were not semantically incorrect.
Stable - I interpret this entirely structurally. i.e whether the protein has folded to an energetic minimum or their natural structural state (incl. proteins with disordered domains). People might say, though, that stable means it has a natural lifetime, i.e. the cellular environment or the enzymes present are not destroying it at an abnormal rate.

I'm not quite sure what (3) is asking; if you edit, maybe I can comment.


Blue light in a fridge. Is it really beneficial or just marketing?

Maybe a little bit?

There are two claims here, so let's talk about them individually. I'm not sure how this light is being produced (probably LED), but it'll have a wavelength somewhere between 400 and 500 nanometers.

Reduced bacterial presence:

The intrinsic antimicrobial activity of blue light is well documented. Although the mechanism is not entirely understood and widely debated, the commonly accepted hypothesis is that the blue light triggers the production of reactive oxygen species like singlet oxygen that are highly toxic. However, this has only been observed under high-power light sources, and low levels of light may actually increase bacterial activity. What counts as a high-power source, you ask? The number from this article is $\frac{10mW}{cm^2}$. For a fridge with an internal surface area of >1 meter, such a power source should draw at least 100 W. Given that normal refrigerators use draw 100-200 watts, you'd essentially be doubling your electrical bill for the fridge.

It should also be noted that the above is a best-case scenario. As soon as you add anything to the fridge, you'll reduce the intensity and thus the effectiveness of the light source. Also, the light is unlikely to be on all the time- it probably turns on when you open the door and turns off when you close it. While this helps a lot with power use, it minimizes the effect of the blue light, which is constantly on in experiments.

Larger quantities of vitamins

There's no (reliable) evidence of light of any kind actually creating vitamins, so what the sticker suggests is that it doesn't degrade the vitamins already present as quickly as other kinds of light.

There's a good article here that discusses the stability of various vitamins. It's worth noting that most of these vitamins and essential amino acids are much more likely to be destroyed by cooking than light, which is probably why the fridge focuses its claim on fruits, which are less likely to be cooked.

There's very little research that I was able to find about the effect of different wavelengths of light on the stability of various vitamins, but as a whole I remain fairly skeptical that there's any notable difference. Most experiments that do study degradation of vitamins under light subject pure vitamins to high-intensity light for several days- unlikely to happen in your fridge.

TL;DR:

A claim like this shouldn't be a major factor in your buying decision. The effects of the blue light are probably negligible given the conditions in your fridge, but if you've got two very similar choices this feature could act as a nice tiebreaker. Besides, there's a lot to be said about how cool blue light looks and the confirmation bias present in your purchase.


Can a new plant grow from half a Succulent leaf?

After waiting for a while, I am finally able to answer this question myself:

A part of a Crassula leaf is still able to grow roots and new leaves, even if the part that attached the leaf to the mother plant is missing.

I have tried this out myself. I left the half-leaf depicted in the question on top of soil, watered it occasionally, just to keep the soil humid, but not wet. After roughly 5 weeks the leaf grew a first root from the calloused end. For the photo I have flipped the leaf around, to better show the first root.

In the following month, it grew more roots, and after about a month, the first new leaves started to appear.

At this point there is little doubt that a full plant can grow from this, given the right treatment. It is not different any more from full leaves growing new plants.

Update (June 2018): The plant is now 2 inches tall, and doing well.


What determines the size and shape of a cell?

This is quite a hard to answer question.
There are different cell cycle molecules that, if mutated or knocked out, have shown to cause the cell to have a different shape or "overgrow" in size or not grow at all...

You might find some insight here.

There are lots of factors that influence cell size and shape, thus it is a very complex system to study. For example, cell shape is influenced by the cytoskeleton but also other factors.


Animals as organ donors and organ's life expectancy

tl;dr
Graft survival, even with allotransplantation (human donor to a human host), is not equal to an average human lifespan. It's much shorter (11-16 years on average). Porcine grafts (which often last over 15 years) do not seem to be limited by the average pig lifespan (which, google tells me is 6-10 years). In both allo and xenotransplantation, graft failure and host survival are issues of the immune response to the graft, not of the expected lifespan of the donor.
Full answer:

Will the heart hold-up throughout the lifetime of the human, or will the human need a new heart in say a decade or two?

Lets answer this, first, for a heart transplanted from a human donor, an allograft. Even from a human donor, the heart is unlikely to hold up for a normal human lifetime. Heart transplant survival has improved greatly over the last five decades, but median survival in an adult is now 11 years. In pediatric patients, it's 16 years. The main problems are cardiac graft vasculopathy, malignancy, infection, and immune rejection. Transplant is a treatment, not a cure, and a major challenge of transplant as therapy is managing the immune response. Rejection and graft vasculopathy are (generally) related to immune injury of the transplanted organ. Malignancy and infection are related to immune suppression of the host.
Xenotransplant (transplantation from a non-human donor) adds an additional complication to the challenge of managing the immune response. Here, the range of non-self antigens is even greater, and the graft will be attacked by complement and other aspects of the innate immune system, as well as the adaptive immune system. This leads to graft destruction, often in the first hour after transplant. There have been advancements using transgenic pigs that solve some of these problems, with improvement in survival in pig to primate trials. Personally, I'm skeptical that CRISPR techniques will easily solve all of the problems of transplant immunology, but transgenic animals have moved things forward substantially over the last 15 or so years (see this review)
As far as porcine valves are concerned, they are treated to reduce their antigenicity (a protocol that hasn't worked for cardiac xenotransplants). Paradoxically, graft survival in older patients is quite good, with most valves lasting beyond 15 years. This may have something to do with age related decrease in immune function, but regardless, porcine tissue (at least from a valve), seems to hold up quite well.
There is good access to data on cardiac allotransplant survival (both adult and pediatric) directly from the international society for heart and lung transplant. There is a good review of pediatric transplants here. You can read more about cardiac graft vasculopathy here
As far as xenotransplantation is concerned, there was an excellent issue of the international journal of surgery, november 2015, that has a number of articles reviewing xenotransplant. Many are available without a paywall, and it's a good place to read up on this. This article from that issue discusses immunological challenges in xenotransplantation from pig to primate. You can read more about this here, but it's beyond a paywall. A good discussion of the overall history of xenotransplantation was reprinted in that issue, here


What are some of the known fungi with heat resistant spores

According to Sterflinger, some black yeasts may qualify: http://www.ncbi.nlm.nih.gov/pubmed/10081587

  Rock inhabiting meristematic fungi are extremely tolerant against high
  temperatures, desiccation and osmotic stress. Their temperature
  tolerance increases with increasing dehydration of the fungal thallus.
  Air dried mycelia of black yeasts stand temperatures up to 120 degrees
  C for at least 0.5 hours

More recently, Suryanarayanan et al. (http://www.ncbi.nlm.nih.gov/pubmed/21872180) have published the discovery of several fungal environmental isolates able to survive dry heat sterilization for 2h at 100+ degrees C. Growth testing was done on Potatao Dextrose Agar (PDA).

  Among 25 species of Ascomycota isolated from leaf litter, nine were
  able to grow after incubation in a drying oven for 2 h at 100 °C; the
  spores of two of these species survived 2 h incubation at 110 °C, and
  one survived exposure to 115 °C for 2 h." (...) Craphigera and Phoma sp.
  survived 2 h incubation at 110 °C; the conidia of Bartalinia sp. were
  the most resistant and survived exposure to 115 °C for 2 h

The isolates which survived at least 2h at 100 C were:

Bartalinia sp. (NFCCI 2307)
Chaetomella raphigera (NFCCI 2308)
Curvularia sp. isolate 2 (NFCCI 2311)
Drechslera halodes (NFCCI 2312)
Leptosphaerulina sp.
Pestalotiopsis sp. isolate 1 (NFCCI 2309)
Pestalotiopsis sp. isolate 2 (NFCCI 2313)
Phoma sp. (NFCCI 2310)
Pithomyces sp. (IMTECH 9398)


Shigella's O antigen (PAI synthesised) and passage through host defences

The outer layer of the cell envelope of Gram negative bacteria is the outer membrane, and the outer leaflet of that membrane is composed largely of lipopolysaccharide (LPS). The O antigen is the name given to the outer glycan portion of the LPS - there is a nice diagram at the Wikipedia article I have linked to which makes this clear.

Because this structure is exposed at the bacterial surface it is a target for the immune response, and the serotyping of many bacterial species incorporates this O serotype information.

Table 1 of the review that you link to indicates that PAI SHI-O carries genes gtrA,B,V (originally derived from a bacteriophage - not unusual for a pathogenicity island). These genes encode enzymes which modify the O-antigen via a glucosylation reaction. Presumably this helps the bacteria adapt to an immune response via a shift in serotype. It may be, for example, that an invading population of Shigella includes variants which do or do not express these genes so that a subpopulation can arise which is not recognised by an existing immune response. This is what is meant in Table 1 of the article by "evasion of host immune response". It is a common strategy - examples in Salmonella (flagellar phase variation) and Helicobacter (induced transformation) spring to mind.


A chimeric gene is formed from fragments of other genes whereas a fusion gene is formed from the entirety of other genes. Often in the literature you'll see the term fusion gene used for both cases.