How Circumcision could reduce the chance for a HIV infection?

This is an interesting question, which has not been answered yet. It is also questionable, if this protective effect is present at all. There are around 40 studies on the topic available which have subsequently undergone meta-analysis. In a meta-analysis all data from recent studies which meet certain quality criteria are analysed together. This gives a much bigger dataset and stronger statistical data. It also helps eliminating the effects of too small test groups.

One of these meta-analysis identified circumcision to have a positive effect on the prevention of HIV infections (reference 1). The authors recommended considering it as a preventive measure.

Two other meta-analysis were more cautious on the topic and either found only a weak link (reference 2) or that only "randomized control studies" (reference 3) would provide clear data. The problem with all these studies is, that they are observational studies, where unknown other effects can play a bigger role than the supposed main effect. It is ethically very difficult to make controlled trials on the transmission of deadly diseases in humans. This is also the reason why all trials on this have been stopped.

There is a hypothesis on how circumcision may help preventing the infection with HIV (when you not get infected in the operation itself due to improper hygienic standards). The skin in the penis contains a large number of immune cells (dendritic cells, CD4/CD8-T-cells) which are the target cells of the HIV virus. It is thought that the virus can more easily penetrate the relatively thin skin of the foreskin. It is also possible, that the surface size is important here, as there are reports which show that men with a larger foreskin also have a larger risk of getting infected. See reference 4.

Another hypothesis has to do with the with the bacteria which live under the foreskin. The number of different strains present is much lower in circumcised men, which led to the conclusion that the dendritic cells, which present these to the immune system have an easier job in the circumcised men and are more likely to prevent the infection with HIV.
See reference 5 and 6 for more information.

References:

Male circumcision and risk of HIV infection in sub-Saharan Africa: a
systematic review and meta-analysis
Male circumcision for prevention of heterosexual acquisition of HIV
in men
HIV and male circumcision--a systematic review with assessment of
the quality of studies.
Male circumcision for HIV prevention: current research and
programmatic issues.
Why Circumcision Lowers Risk of HIV
Male Circumcision Significantly Reduces Prevalence and Load of
Genital Anaerobic Bacteria


Why do living organisms replicate itself or procreate

This is a very interesting question but the answer (or as much of the answer as is known) can fill a few books. There are many many signals that control cell division.

As a horrible simplification, the cell can be compared to a car parked on a slope with a driver's foot on the brake. If she lifts her foot, the car will roll downhill. In the cell, there are various proteins (P53 is the most famous) that have their metaphorical foot on the brake. Various external and internal stimuli can cause these proteins to stop suppressing replication and the cell will then continue its cycle and replicate.

So, a cell's "natural state" is to replicate, there is a complex network of interacting factors (primarily proteins) that actively block replication in resting cells. When the conditions are "right" (what that means depends on the cell in question) the block is removed and the cell replicates.


How to gather life-history traits data on bird species?

Have you tried the Ecological Data Wiki? It's an NSF-funded repository of links to ecological databases and datasets:

Main page:
http://ecologicaldata.org

Find data tab, refined to Taxon=Birds, Ecological level=Species:
https://ecologicaldata.org/search?f[0]=taxonomy_vocabulary_2%253Aname%3ABirds&f[1]=taxonomy_vocabulary_6%253Aname%3ASpecies

The 'Avian body size and life history' dataset on the above page looks relevant to your search.


Why should phospholipid non-polar tails be "protected" in the membrane bilayer?

What should be the correct reason for bilayer arrangement?

I'll answer your second question first, but there is an almost identical question on this site already: Why do cells have a bilayer?

There is water on the extracellular and intracellular side of the membrane. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer formation we know and love emerges.

  why should we protect non-polar part, will it destroy in contact with
  polar part?

To directly address the first part of the question: no, nothing would be destroyed. The word "protect" isn't appropriate (it's a bit too anthropomorphic for my taste!). Here is a video showing the bilayer spontaneously assemble in a molecular dynamics simulation. Read the more thorough 2003 journal article for an idea of early MD simulations of the bilayer formation. As you can see nothing "bad" happens when the water collides with the lipid tails and the lipids aren't destroyed.

Interesting read: MEMBRANE LIPIDS OF THE PAST AND PRESENT. Good animations and explanations of different membrane formations.

For an academic perspective, I'd recommend a couple of reviews: Cournia et al., 2015 and Gerit et al., 2008.


Question about what the liver does NOT do

Liver does all those functions as far as I know. The liver hepatocyctes are stimulated to create the enzyme glycogen synthase which promotes the conversion of glucose to glycogen in the presence of insulin. Glycogen is stored in the liver after its production for further use. The whole process is explained in detail in this page. Regarding the storage of vitamins and minerals, I have a paper which details the absorption and storage of Vitamin A in rat liver.  I am also linking another paper that details the presence of Vitamin B12 in the human liver.


Does the MS2 RNA binding protein have any translational repression effects?

I assume you are talking about the mTAG visualization technique for mRNAs (1). You are probably familiar with it, but the OFR of interest is tagged with MS2L sequence downstream of it and upstream of the 3'UTR. There is also a modified version, in which you can visualize both the mRNA of interest, and the protein that is translated, see the figure below (2). Haim and colleagues found that yeast expressing mCherry and MS2L tagged ATP2 grew on glycerol-containing media, which would require efficient translation of ATP2.

So I would assume that there is no translational repression if you tag the mRNA downstream of the ORF. Unless you have a very good reason to tag the ORF of interest with MS2 upstream of the start codon, I wouldn't do it, because these stem-loop structures would most probably stall translation, as mRNA secondary structure has been implicated in translation initiation efficiency.


How can Valonia ventricosa cells get so big?

Ventricaria ventricosa (previously called Valonia ventricosa) is not exactly a single cell. It has a coenocytic structure with multiple nuclei and chloroplasts. As Jasand Pruski correctly guessed the organism possesses a large central vacuole which is multilobular in structure (lobules radiating from a central spheroid region).

The entire cell contains several "cytoplasmic domains" with each domain having a nucleus and a few chloroplasts (See the figure below). Cytoplasmic domains are interconnected by cytoplasmic "bridges" that are supported by microtubules (like in axons). The peripheral cytoplasm (whose membrane is overlaid by the cell wall), is only about 40nm thick.

  Fluorescent confocal micrograph of a cytoplasmic domain. From Shepherd et al. (2004) Protoplasma 223: 79–91. Here, n is nucleus c is chloroplast and v is vacuole.

So these are not huge cellular balloons that can burst easily. Nonetheless a huge structure like this is susceptible to injuries by shearing forces of water currents and by other organisms like fish which may try to feed on them. These organisms have some mechanisms other than the cytoplasmic organization that allows them to cope up with injuries:

When the outer membrane ruptures, then the cytoplasm contracts with the help of actin filaments that are attached to the former. Subsequently the membrane fuses, protoplasts form and then cell wall is regenerated. This movement is likely to be triggered by extracellular calcium.
A single cytoplasmic domain with nucleus and other essential organelles can regenerate an entire organism.
A muclilagenous layer made up of sulphated polysaccharides coats both the vacuolar and extracellular surfaces. During injury it impedes the movement of water and ions (by retaining them in the form of a gel) and therefore acts like a plug.

Other organisms like this (siphonous algae) also have similar mechanisms. Some even employ calcium carbonate to maintain rigidity.

REFERENCES:

Shepherd et al. (2004) Protoplasma 223: 79–91
Menzel (1988) Protoplasma 144: 73-91


Why do skin and nail go blue in cyanosis?

The skin appears blue due to the diffraction of light through the skin. Blood is either bright red (sufficiently oxygenated) or dark red. "The blue appearance of surface veins is caused mostly by the scattering of blue light away from the outside of venous tissue if the vein is at 0.5 mm deep or more. Veins and arteries appear similar when skin is removed and are seen directly" 1. The color of blood is due to the difference in color between deoxyhemoglobin and oxyhemoglobin.

Let's consider the "blue fugates" of Kentucky. The ancestors of this family have different shades of blue skin tones. Dr. Madison Cawein discovered that the family had a high concentration of FE$^{3+}$ brown methemoglobin. This form is useless to the body so the enzyme diaphorase reduces the methemoglobin to FE$^{2+}$ (hemoglobin that can carry oxygen) [2].

Basically the skin color comes down to light diffraction not the blood changing from red to blue.

Cyanosis is the appearance of a blue or purple coloration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation [3]. Cyanosis is a clinical sign diagnosed visually. Cyanosis is an indication for blood gas testing.

References:

http://en.wikipedia.org/wiki/Venous_blood
http://courses.chem.indiana.edu/c122/documents/Experiment10_BloodandHemoglobin.pdf
http://en.wikipedia.org/wiki/Cyanosis
http://www.webmd.com/lung/arterial-blood-gases


What are the movement mechanisms of thrombus?

This answer aims to list existing models and do meta-analysis about them.
This answer is a draft.

There are many models made based on the thrombus movement.
One of them is proposed by DevashishDas' answer but it seems to focus only on the first stage of hemostasis:

  The model assumes thrombin is generated on the surface of activated
  platelets in the thrombus core and is transported through the fibrin
  network that surrounds the core both by advective flow of fluid
  permeating through the fibrin network and by diffusion through the
  fibrin gel.

and particularly the model keeps these values constant and simplifies

  To calibrate the model, we experimentally determined fibrin clot
  permeability and thrombin diffusion rates through a fibrin network.

which I think should be dynamic (not constant) because of the three endothelium main factors listed below.
Endothelium is a dynamic structure controlling the fibrin clot.

Thrombus Hemodynamics Model

Fibrin Networks Regulate Protein Transport during Thrombus Development by  diffusion-advection equation (Stokes, continuity, Brinkman equations)

which is about the first stage of hemostasis because of its simplification about fibrin clot permeability and thrombin diffusion rates.

Hemostasis

There are three stages of hemostasis altogether which work parallel together:

primary (formation of the platelet plug)
secondary (formation of fibrin through the coagulation cascade)
tertiary hemostasis (formation of plasmin for breakdown of the clot)

Primary hemostasis is the formation of the primary platelet plug.
It involves

platelets
blood vessel wall
von Willebrand factor

Normal endothelium prevents hemostasis.
Injury of endothelium

involves vasoconstriction (local)
enhances adherence of platelets to exposed platelet subendothelial surfaces
and activation of coagulation process

The formation of primary platelet plug involves

Platelet adhesion,
Platelet activation, and
Platelet aggregation.

Main steps in blood coagulation:

Formation of prothrombin activator complex (thrombokinase)
Conversion of plasma protein prothrombin into thrombin
Conversion of dissolved plasma fibrinogen into fibrin (makes filamen- tous skeleton of fibrin clot)

Clot retraction

The platelets in the clot contain contractile proteins.
They bring the edges of the wound together, which also reduces the chance of further bleeding - not vasoconstriction here!
The contraction process also supports the wound healing process as it brings the ends of the wound together.

Clot retraction is the process of getting clot towards fibrinolysis process. Fibrinolysis is the process where a fibrin clot (product of coagulation) is broken down. Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Clot retraction and fibrinolysis are necessary to remove clot so wound healing can proceed.

Myogenic and metabolic autoregulation by endothelium

Myogenic control involves the localized response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relax- ation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

Myogenic and metabolic Autoregulation is the automatic adjustment (local) of blood flow to each tissue in proportion to its needs (oxygen, nutrients, ...), and is controlled intrinsically by modifying the diameter of local arterioles. It involves localised response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relaxation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

There are three types of substances secreted by the endothelium (1):

NO
Endothelium hyperpolarising factors
Endothelins.

where I think the modelling should focus on these three factors.

Sources

My discussion with a researcher in this field 7/2014
My notes in three Physiology courses during years 2011-2014
Costanzo, Physiology, book
Guyton, Physiology, book


Protein binds to DNA and just stays there, what will happen next?

All binding reactions are reversible. The binding and unbinding (association and dissociation) are usually in equilibrium. How much of the protein is bound to the DNA and how much time a single molecule spends in the bound state depends on the kinetic parameters. In case of the non-catalytic Cas, the protein may inhibit transcription if it is bound at the promoter. In fact, such inactive variants have been developed and used for targeted inhibition of transcription (Himeda et al., 2015).

If the CRISPR-Cas is blocking a binding site for a transcriptional activator, then the degree of inhibition would depend on the competition between the activator and the CRISPR-Cas-inhibitor for the binding sites. This competition would be dependent on the kinetic parameters as well as the concentration of the competing species.

Similarly, you can design proteins/RNAs that can bind to mRNAs (at RBS in prokaryotes or Kozak sequences in eukaryotes) and inhibit translation.

Another interesting fact: CRISPR-Cas system has been engineered to work like transcriptional activator, as well (Didovyk et al., 2016).


What is the rest state for eyelids - Open or Closed?

This depends to some extent on how you define "resting state" (it matters).

Innervation of the eye occurs in the brainstem and upper spinal column, so is, like most brainstem functions, on autopilot (like breathing.)

If you define resting state as that which the lids would assume without any innervation, then the resting state of the eyelids is semi-open. This is the state of the eyelids of most people who die.

However, that position is not beneficial to the living eye, as it would lead to corneal breakdown. When people lose eyelid innervation, for example, following a stroke, the lids don't close completely. Ointment must be applied several times daily and the eye is often taped in the shut position to protect the cornea.

If you define resting state as that which occurs in sleep and in most comatose states, the eyes close completely, because innervation of eye muscles is intact and a main function is to protect the cornea, i.e. vision. This is done with a completely closed eye.

Comprehensive Review in Clinical Neurology, Cheng-Ching et al.


This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid?

Well first of all, lets be clear: that is not a study.  Its a review article, basically a paper that summarizes a series of studies published.  The review itself isn't valid or invalid necessarily, it simply takes a series of papers (which may or may not be correct or relevant) and then summarizes them.
As for validity, that is a summary of a lot of obscure papers on mechanisms by which RF fields could interact with cells, rats or in a few cases plants.  Its hard to say if the conclusions are valid, but selecting a few papers at random, they are mostly very obscure journals and many report very specialized measurements that are far removed from demonstrating carcinogenic effects in humans.  Its difficult to draw conclusions that are relevant to human health from that, although it does seem plausible that low frequency fields could have a measureable effect on cells or even rats.

Are low-intensity radio-waves carcinogenic?

Assuming you mean in people, that is a hard question to answer, and not the right question given a review article that does not address effects in people.  A better place to look may be this review article:
Carcinogenicity of radiofrequency electromagnetic fields
published in The Lancet and addressing evidence of carcinogenicity in humans.  To summarize:

The Working Group concluded that there is “limited evidence in humans” for the carcinogenicity of RF-EMF, based on positive associations between glioma and acoustic neuroma and exposure to RF-EMF from wireless phones. A few members of the Working Group considered the current evidence in humans “inadequate”. In their opinion there was inconsistency between the two case-control studies and a lack of an exposure-response relationship in the INTERPHONE study results; no increase in rates of glioma or acoustic neuroma was seen in the Danish cohort study,4 and up to now, reported time trends in incidence rates of glioma have not shown a parallel to temporal trends in mobile phone use.
The Working Group reviewed more than 40 studies that assessed the carcinogenicity of RF-EMF in rodents, including seven 2-year cancer bioassays. Exposures included 2450 MHz RF-EMF and various RF-EMF that simulated emissions from mobile phones. None of the chronic bioassays showed an increased incidence of any tumour type in tissues or organs of animals exposed to RF-EMF for 2 years. An increased total number of malignant tumours was found in RF-EMF-exposed animals in one of the seven chronic bioassays. Increased cancer incidence in exposed animals was noted in two of 12 studies with tumour-prone animals12 and 13 and in one of 18 studies using initiation-promotion protocols.14 Four of six co-carcinogenesis studies showed increased cancer incidence after exposure to RF-EMF in combination with a known carcinogen; however, the predictive value of this type of study for human cancer is unknown. Overall, the Working Group concluded that there is “limited evidence” in experimental animals for the carcinogenicity of RF-EMF.

Note that cancers that people theorize to be associated with exposure to nonionizing EM fields tend to be extremely rare, meaning that studying them is very difficult.  This leads to a lot of uncertainty, because one must try to correlate very rare events with environmental effects. Therefore "limited evidence" does not mean "no", it just means that the effect is hard to measure and may or may not be significant given what we know.


Regulation in plants bearing cleistogamous and chasmogamous flowers

This is a very good question, but I think the reason that it's not being answered is because it is in a sense too broad: different plant groups maintain balances of cleistogamous and chasmogamous flowers, and they modulate that balance through different mechanisms. Many of these mechanisms (genes involved, environmental cues, developmental pathways) may not be fully understood.

Culley and Klooster (2007) categorize cleistogamy depending on the degree to which "the prevailing environment has a say":

In dimorphic cleistogamy CL and CH flower differ in the time or place
of production, with CL flowers produced in conditions (underground,
low light levels, early in the season) that are potentially
unfavorable for outcrossing.
In induced cleistogamy potentially CH flowers that experience conditions such as drought or low temperatures fail to open and self-pollinate, becoming, in effect, CL flowers.

You should check out the Culley and Klooster (available online if you make a jstor login) – they discuss complete cleistogamy which addresses your last question. They report several completely CL species in their Table 1, and give references.

More generally, many different plant groups maintain balances of self-pollination and outcrossing (i.e. "real sex"), through an even more diverse set of mechanisms.

Even more generally, many plants and some animals maintain balances of sexual reproduction and clonal reproduction, through an even more diverse set of mechanisms. For instance, vegetative reproduction (e.g., strawberry runners) is very common in many plant groups; facultative and obligate parthenogenesis in animals also occurs.

Culley, Theresa M. and Matthew R. Klooster (2007). The Cleistogamous Breeding System: A Review of Its Frequency, Evolution, and Ecology in Angiosperms. Botanical Review. Vol. 73, No. 1, pp. 1-30


Do ants or other insects sleep, and if so why?

A quick search on Web of Science yields "Polyphasic Wake/Sleep Episodes in the Fire Ant, Solenopsis Invicta" (Cassill et al., 2009, @Mike Taylor found an accessable copy here) as one of the first hits.

The main points from the abstract:

Yes, ants sleep.
indicators of deep sleep:

ants are non-responsive to contact by other ants and antennae are folded
rapid antennal movement (RAM sleep)

Queens have about 92 sleep episodes per day, each 6 minutes long.
Queens synchronize their wake/sleep cycles.
Workers have about 253 sleep episodes per day, each 1.1 minutes long.
"Activity episodes were unaffected by light/dark periods."

If you study the paper you might find more information in its introduction or in the references regarding why ants sleep, although there doesn't seem to be scientific consens. The abstract only says that the shorter total sleeping time of the workers is likely related to them being disposable.


How would one describe the R-factor in crystallography?

Crystallography requires the collection of many measurements (could be a few thousand to even millions depending on the size of the molecule and complexity of the crystal (technically speaking, the size of the crystal's unit cell is a major determining factor for the size of the data set).  I'm not going to assume this is a small molecule crystal like a salt or a large molecule like a protein.  its not necessary here.

I'll call this a set of intensity measurements, even though what is actually used is the square root of the intensities measured, called the structure factor.

The only way we really know that the molecular structure model is correct is that it generates as accurately as possible the intensities that were experimentally measured.

R, which I believe stands for residual, is a fractional difference between the measured intensities and what any proposed molecular model gives.

The residual is calculated as the absolute value of F(model)-F(measured).  This means that 0.0 is a perfect match while 1.0 is a perfectly awful fit that shows the model is perfectly awful.

In practice 0.60 is usually as bad as random model will give you (there's a statistical argument as to why it doesn't go higher).  Also the measurements are usually not perfect - they contain errors in measurements or artifacts from imperfect crystals or the detector, so an R value of < 0.20 (20%) is typically what you see in a reasonable paper.  I think its commonly less than 0.15 for most structures now in fact.


Help ID this South Indian fruit-bearing tree

This looks like Muntingia calabura, the Jamaica Cherry.

pic source

pic source
It is indigenous to tropical America and often planted in Asia.
It is edible and used in jam, cake and fruit drinks. The bark is sometimes used as rope. Source: "Tropische vruchten, Nowak&Schulz 1999"


You are correct.  Polyketide synthases (PKS) are the enzymes that synthesize polyketides.  PKS are derived from fatty acid synthases via evolution.  Polyketides are of great interest becaus many are of important medical use.


What would happen if a cell is poked by a fine needle?

Generally speaking, there is no effect in microinjections.
This is relevant in the real world example of micro-injections. A video of a pronucleus injection can be seen here, or here is a more thoroughly explained procedure involving cloning. As you can see in the video the membrane, almost no effect will be observed - molecular dynamic simulations show that the membrane can spontaneously reform from fragments in the tens-of-nanoseconds timescale.
1/5 refers to  the question "is the needle small enough?"
The question does include the term "1/5", which is a bit unusual. I guess they want you to recall a specific piece of information about the correct ratio size of needle should be. Here is a video of a microinjection at approximately that ratio. However the exit hole is unintentionally filled with the inserted material and cannot close immediately. The cell disappears out of frame before we can confirm the hole is closed.
Cell diameters are very variable
Cell sizes vary greatly.

From using these values, assuming a cell is a sphere an oocyte has a diameter of approximately 196µm, whereas a neutrophil has a diameter of 8µm. It's a bizarre question given this range because usually micro-needles are between 0.5 and 5 µm diameter in length, except in the case of oocytes where larger needles are used (according to wikipedia). I don't think this is relevant, and it is just arbitrarily picking a needle size that wouldn't completely maul the cell!


Aside from cockroaches and other insects, which species (of all kinds) are 'immune' to ionizing radiation?

According to Paul Stamets, Gomphidius glutinosus is especially well suited to collecting Cesium-137:

  G. glutinosus has been reported to absorb – via the mycelium – and
  concentrate radioactive Cesium 137 more than 10,000-fold over ambient
  background levels.

That article and Stamets' book Mycelium Running have more details on other species.


According to this document (page 11) the shelf life for the cassettes is 1 year. The other ingredients (running buffer, DNA size markers, loading dye) appear to be standard reagents. Of those, the DNA size marker will probably have the shortest shelf life, but it stands to reason that the reagents should have a shelf life at least as long as the cassettes, seeing as only their shelf life is mentioned. It is possible to buy reagent replacement kits.


Do variant callers miss rare variants in reference?

If the reference sequence is associated with a disease or increased susceptibility to some phenotype, the the population you're using to compare against (with a variant) will show protection to it. So either way you're going to find an association, this will just change the sign of the coefficient.


DNA shared by octopuses and modern humans

Octopuses have more chromosomes and genes

Octopuses have 28 chromosomes, and 33,638 protein-coding genes (Albertin et al 2015).
Humans have 23 chromosomes, and 20,365 protein-coding genes (Uniprot).

Octopuses had an expansion of genes in only a few protein families

There is a large number of C2H2 zinc-finger proteins (C2H2 ZNFs) (~1800), interleukin-17-like genes (IL17-like), G-protein-coupled receptors (GPCRs), chitinases and sialins paralogues in the octopus genome.

However, there does not exist a comprehensive analysis of orthologous proteins in the octopus that I can find.
This means that although we can say that there are thousands of genes we only observe in octopuses, there is currently no study comparing orthologues that exist in both humans and octopuses.


What kind of grasshopper-like insect is this?

That is a "cave cricket", in the family Rhaphidophoridae. These are common in basements, and harmless.


Can non-carbonated energy drinks boost alcohol intoxication?

A very well-written question, so I'm sorry if my answer is a bit too simple. Perhaps it will attract attention of somebody with a better answer.

I think the effect could be mainly caused by the fact that sugary drinks slow down alcohol absorption. So while those who drink just alcohol already know they've had enough, those who have had a couple of energy drinks still feel fine and continue drinking, not knowing that they are about to become even more inebriated.

Also, the stimulants in energy drinks can somewhat reverse the sedative effect of alcohol, leading to higher overall activity of the person and thus faster drinking.


Have there ever been as many mammals as there are now?

There can be perhaps 10 trillion rodents and bats on the planet, so the humans and livestock probably are small compared to a rainforest rodents and bats. The biggest bat colony is 40 million, they decline without unmanaged forests, can reach 4-10 bats per hectare, and the world population might normally be in 10s of billions, save for the use of pesticides and deforestation.

Here's a bit of maths to say that we have erased 1 trillion rodent habitats through monocultures and ploughing. Every cow and sheep field would have previously supported 10-20-50 times more rodents, and they aren't adapted for pesticides and ploughs.

37% of the world's land is farmed
Extent of total cultivated land in 2006: 1.5 billion hectares.

If there were 14 mammals per km2 of farmland, then we have displaced 20 billion mammals.

If the pristine habitats previously supported 1 rodent/mammal every 5m2, we would have destroyed the homes of 2000 mice,voles,shrews,squirrels and other mammals by hectare, that's 3000 Billion mammals (worst case scenario) due to monocultures and farming, and 1000 Billion in a best case scenario. Bangladesh rice farms and UK fields both are hostile to mammals.

A 20g mouse for 5m2 comes to the same as one human for 15 square kilometers. A mouse only needs a 3g of seeds/roots/beetles/snails per day to survive, that's about a kilo per year. "blue oak, interior live oak, and black oak respectively produce 2955, 1074, and 616 kg/ha of tree canopy" invertebrates provide 100-300kg/ha.

Perhaps we have erased 1 trillion mammals in the amazon alone.

https://www.worldatlas.com/articles/list-of-primates-by-population.html

Also we have depleted the fish stocks. It is reported that in medieval times, the seas heaved with incredible amounts of dolphins, whales and fish stocks, pristine seal and dolphin numbers could have been about 1 billion. Perhaps today it's about 1/4 of that.

If i had to bet all I own on your theory, I'd say it happened at another time in the previous 60mn years, probably not today.


What is a Archival Tumor Tissue ? For What Purpose is it collected?

When a tumor is removed from a patient, it is usually send to the pathology the make sure that it has been excised completely to make sure there are no residues. Often this tumor is also used to analyze the mutation status of the tumor to determine, which further treatment is possible. For example, this is routinely done for melanoma where the mutation status excludes some drugs for further treatment.

Afterwards these tumors are important material for the scientific tumor research to isolate fresh cell lines or analyze them further. Parts of it are usually stored either frozen or as formalin fixed tissue to build tissue banks. These can be used for later research on this type of tumor and have a high value.

These tissues can then be cut and stained with antibodies or used for nucleic acid extraction (either DNA or RNA) or to test new ideas or methods which where not available to the time when the samples was archived.

Another famous case (although not from tumors) are tissues samples which have been archived from people deceased from the spanish flu in 1918, where parts of the virus was reconstructed using these samples decades later.


It is a green tree python (Morelia viridis)


Sounds like a Curlew (Numenius arquata).

http://www.british-birdsongs.uk/curlew/
https://www.youtube.com/watch?v=q7V25M0szqU


Short answer
The dopamine (DA) hypothesis suggests that excessive DA transmission in the mesolimbic pathway in schizophrenia leads to hallucinations and other positive symptoms. It explains the negative symptoms of schizophrenia (flattened affect, reduced motivation) by reduced DA activity in the mesocortical pathway affecting the frontal cortical regions.

Background
You are referring to the dopamine hypothesis of schizophrenia.

The initial dopamine (DA) hypothesis focused primarily on the positive symptoms of schizophrenia, namely the active psychoses, which includes periods of hallucinations and delusions. These effects can be attributed to hyperactivity in subcortical dopaminergic pathways. Specifically, excessive subcortical release of dopamine is thought to increase D2 receptor activation, disturbing the cortical pathway through the nucleus accumbens (Brisch et al., 2014), called the mesolimbic pathway (Fig. 1). These positive effects can be treated quite effectively with the classical, first-generation anti-dopaminergic antipsychotics such as haloperidol and chlorpromazine.

However, there is another important aspect on schizophrenia, which are the negative symptoms. While the full-blown psychoses occur in waves, these negative symptoms are a more continuous and persistent phenomenon. The symptoms include a flattened affect and dysphoria (reduced pleasure in life). These symptoms are thought to occur due to altered prefrontal cortex (PFC) functioning. Specifically, they are thought to be induced by hypoactivity in dopaminergic D1 transmission (Brisch et al., 2014) in the mesocortical pathway (Fig. 1).

Fig. 1. The dopamine pathways in the brain, including the mesolimbic and mesocortical pathway, implicated in the positive and negative symptoms of schizophrenia, respectively. source: Wikipedia.

These two sides of schizophrenia point to an imbalance in DA activity in the brain, namely hyperactive subcortical mesolimbic D2 activity leading to positive symptoms, and hypoactive mesocortical D1 activity in the PFC resulting in negative symptoms. This imbalance hypothesis is the revised DA hypothesis and it is still an accepted working model (Brisch et al., 2014).

However, as noted by others, schizophrenia is a complex disease and it is thought that besides DA, also serotonin, glutamate and GABA play a role (Olijslagers et al., 2006). The current first line of treatment of schizophrenia are atypical neuroleptics, such as Clozapine. Clozapine is a selective monoaminergic antagonist with high affinity for the serotonin Type 2 (5HT2), dopamine Type 2 (D2), 1 and 2 adrenergic, and H1 histaminergic receptors. Clozapine acts as an antagonist at other receptors, but with lower potency. The broad effects of Clozapine are thought to underlie its potent antipsychotic therapeutic effect. It is believed it mainly works through a combination of antagonistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex. D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms.

References
- Brisch et al., Front Psychiatry (2014); 5: 47
- Olijslagers et al., Curr Neuropharmacol (2006); 4(1): 59–68


How does bacteriorhodopsin differ from the rhodopsin present in mammalian eyes?

Although they are similar in both bacteriorhodopsins  and rhodopsins being retinal-binding proteins, the similarity in their amino acid sequence is very limited.

The key difference between them is that rhodopsin is a G-protein-coupled receptor, and this is not the case with bacteriorhodopsin. A quick Google search on Bacteriorhodopsin vs Rhodopsin will send you to a Wikipedia article that says:

  Bacteriorhodopsin belongs to the microbial rhodopsins. They have similarities to vertebrate rhodopsins, the pigments that sense light in the retina. Rhodopsins also contain retinal; however, the functions of rhodopsin and bacteriorhodopsin are different, and there is limited similarity in their amino acid sequences. Both rhodopsin and bacteriorhodopsin belong to the 7TM receptor family of proteins, but rhodopsin is a G protein-coupled receptor and bacteriorhodopsin is not.

A very good paper if you would like to know more about the two is by H. Gobind Khorana on the Two light-transducing membrane proteins.


Looks like a Malayan Live Bearing snail , fairly common in the US aquarium trade. I have inadvertently gotten them into all my tanks. Common aquarium fish can't eat them ( unless you crush them on the glass). I did not know they can tolerate brackish water. Yhey will get to 1.5 mm.


Calibrating Motic Camera to Stage Micrometer

It looks like the shape is an ellipse rather than a circle. The ellipse has major and minor axes, which are described in terms of half-axes (177 and 175 pixels respectively). Is it possible the software is incorrectly using the half-axis measurements, whereas when you draw a perfect circle it will correctly use the diameter? This is consistent with the x and y scale numbers being different from each other.

So I would suggest re-calibrating with a perfect circle.

Hope this helps.


Is secondary follicle or Graafian follicle arrested in the second metaphase of oogenesis?

Graafian follicle.

The secondary oocyte and thus Graafian follicle are arrested in the second metaphase of oogenesis.
After this the corpus luteum develops from the follicle during the luteal phase of the menstrual cycle.


What are the advantages of heterologous expression systems?

It takes significant resources to establish a cell line. More efficient to use existing lines.

Often cell lines used for expression grow faster. This is why so many proteins are expressed in E coli - they only take a day to grow vs the week or two for mammalian cells, meaning you get a much faster learning iteration in your research.


Why do we think chronic inflammation can cause cancer?

There are good epidemiological data for this.

Links between cancer and inflammation were first made in the
nineteenth century, on the basis of observations that tumours often
arose at sites of chronic inflammation and that inflammatory cells
were present in biopsied samples from tumours.
There are many triggers of chronic inflammation that increase the risk
of developing cancer. Such triggers include microbial infections (for
example, infection with Helicobacter pylori is associated with gastric
cancer and gastric mucosal lymphoma), autoimmune diseases (for
example, inflammatory bowel disease is associated with colon cancer)
and inflammatory conditions of unknown origin (for example,
prostatitis is associated with prostate cancer). Accordingly,
treatment with non-steroidal anti-inflammatory agents decreases the
incidence of, and the mortality that results from, several tumour
types.

Cited from Mantovani, Alberto, et al. "Cancer-related inflammation." Nature 454.7203 (2008): 436-444.
http://www.sld.cu/sitios/reumatologia/temas.php?idv=21500


Why do left and right eyes can require different power of lenses?

Because we have two hands, two feet, two ears, etc., we are tempted to think that we are perfectly symmetrical.  But if you compare the details of your two hands, for example, you will find that the blood vessels are in somewhat different positions, the lines in your palms are different, and the fingerprints of corresponding fingers are different.  The same is true of your eyes: they differ from each other.  These kinds of differences are due to the fact that genetic instructions relating to symmetry during embryo development are not exact; they are approximate.

Probably if you measure the size of the biceps on each arm, or the size of the forearm muscles, you'll find that they are slightly different.  This is partially due to the fact that you use one arm and hand differently from the other: you are right-handed or left-handed.  Similarly, people tend to be left-eyed or right-eyed, using the two eyes differently.  And, people tend to sleep more on one side than the other.  These are differences that emerge due to experiences and habits.

Those factors make it unlikely that the two eyes will ever be identical, and make it likely that eventually they will need different eyeglass prescriptions.


It's didn't disappear.  It's still around today, over 100 years later.  The 1918 influenza virus is the parent virus for all the human seasonal influenza viruses that are around today, as well as for most of the swine influenza viruses out there.

In fact, the presently circulating H1N1 viruses in humans are close enough to the 1918 virus that they probably immunize against each other (Seasonal trivalent inactivated influenza vaccine protects against 1918 Spanish influenza virus infection in ferrets.).

What did happen is that the 1918 virus mutated, becoming less virulent in the process, within a year or so of entering the human population. Why? Presumably because, after infecting virtually the entire human population in its first year, there was so much population immunity that it needed to mutate a little in order to continue to infect. That is, after all, what flu viruses do.

But it continued to circulate for decades, as a very similar H1N1 virus. Also, it almost immediately infected pigs and became endemic in the swine population, only to resurface  after 90 years to cause the 2009 influenza pandemic.

  In 2009, persons who had lived through the first decades of the 1918 pandemic H1N1 era, especially those born before about 1950, were substantially protected from the 2009 pandemic virus by having acquired immunity to the antigenically similar H1 or N1 of the 1918 virus, or both, or to the descendant seasonal H1N1 viruses that circulated over subsequent decades. This is because the 2009 H1 gene was a 1918 viral progeny that had survived for more than 90 years, with minimal antigenic drift, in a domestic pig “time capsule.”

—The Mother of All Pandemics Is 100 Years Old (and Going Strong)! (Am J Public Health. 2018 November; 108(11): 1449–1454)

In 1957 and 1968, the H1N1 virus reassorted with avian viruses to generate first H2N2 and then H3N2 viruses (the great-grandchildren of the H3N2 pandemic still circulate today). But most of the internal genes in those reassortants remained the 1918 versions.

So the 1918 flu never went away. It’s still killing hundreds of thousands of people every year. It’s just that everyone has got used to it, and thinks it’s fine and normal to have hundreds of millions of influenza cases every year.


Why do we use an autoclave at 121°C (250F)? (Origin)

The reason for 121°C and not 120°C is due to how autoclaves work and how they were developed. They sterilize with saturated steam under pressure.  Historically, we measure the pressure generated by the steam. Which leads directly to the answer.
Steam power was the basis of industrial process in the 19th century, and to use it safely required monitoring and controlling boiler pressure. Boiler explosions were not uncommon in the early days of steam power. The Bourdon pressure gauge was invented in 1849 and was a robust technology that yielded reliable and accurate measurement of steam pressure.
https://journals.sagepub.com/doi/pdf/10.1177/002029408702000803
When Chamberland invented the autoclave in 1879 from Papain's earlier pressure cooker, it relied exclusively on pressure measurement for control. Not until 1933 were autoclaves produced that monitored temperature at the drain line to confirm that air was exhausted and the steam was truly saturated.
https://www.steris.com/healthcare/knowledge-center/sterile-processing/everything-about-autoclaves
Study of steam engines was the basis for the development of thermodynamics and the kinetic molecular theory of gasses. Although steam is far from an ideal gas, there is a predictable relationship between temperature and pressure in saturated steam as well as well established properties of heat transfer. These can be found on standard engineering steam tables.
Examples: https://www.engineersedge.com/thermodynamics/steam_tables.htm
Saturated steam is very efficient in transferring heat. This is why scald injuries are so severe compared to simple burns at the same temperatures. It is also how saturated steam kills even heat resistant microorganisms in an autoclave. https://learnaboutgmp.com/good-manufacturing-practices-cgmp/saturated-steam-efficient-sterilization/
One earth atmosphere of pressure at sea level is defined as 14.69 pounds per square inch (psi), though in reality it varies a little bit due to temperature and weather. Because of this variation and because humans using Arabic numerals, arithmetic, and algebra like integer units in 5's; engineers often think of 1 atmosphere of pressure as 15 psi. This amount of saturated steam pressure is well within the capacities of typical steam boilers. This nice round of 15 psi saturated steam will kill even highly resistant bacterial endospores in about 15 minutes. A very reasonable time frame, and a nice mnemonic: 15 psi for 15 minutes.
The temperature of that 15 psi of saturated steam? 121°C.
And that is why we use a very unusual 121°C for typical autoclaving. It's because we are really using a rounded one earth atmosphere of steam pressure. And we did so without concern for direct temperature measurement for the first 50 years of autoclave use. In many ways the temperature of the autoclave was of secondary importance.


Understanding different genetic terminology - Genotype vs SNP

The "IGF1" at the front indicates that the genetic variation is in the gene for Insulin-like Growth Factor 1. The notation (CA)n is used to describe n adjacent repetitions of the two-base sequence CA (Cytosine, Adenine) present in a particular IGF1 DNA sequence. Hence IGF1 (CA)19 / (CA)19 is referring to a genome in which both copies of the IGF1 gene have 19 adjacent repetitions of the CA pair of bases, that is, which is homozygous for IGF1 (CA)19.

Such a repeat is usually called a microsatellite or Short Tandem Repeat (STR). They are common sources of variations in genes because the DNA matching process during meiosis sometimes "slips" one or two repeats over.

The type of test performed by 23andMe reports values for selected SNPs (Single Nucleotide Polymorphisms).  SNPs are a different kind of variation from STRs, so the data available from 23andMe does not allow you to determine the kind of IGF1 (CA)n variant present.


At a glance it looks like a flattened perfectly ordinary dead woodlouse to me.


Why doesn't our immune system react to infused antibodies produced in a horse?

Our immune system does react to horse antibodies, but as with any adaptive immune response it takes some time for the response to develop. In the weeks before our immune response fully responds to the horse antibodies, the infused antibodies can have their effect.

If you then have a second infusion of horse antibodies, the immune response would not only prevent them from having their beneficial effect, but it might case serious adverse effects.  This serum sickness (Wikipedia link) has been known for over a century; here is a paper from 1918 discussing it as a well-known issue:

  The injection of horse serum either in small or in large amounts in human beings is always followed sooner or later by the development of hypersensitiveness of the skin to subsequent injections of horse serum. For the development of this reaction serum disease is not essential.

--THE RELATION OF CIRCULATING ANTIBODIES TO SERUM DISEASE. J. Exp. Med. Published March 1, 1918

Although there aren't many modern situations in which horse (or other non-human species) serum is injected into humans, when it is (as with anti-venom, which is generally produced in non-human animals) serum sickness is still a concern.

  Serum sickness is a delayed immune reaction resulting from the injection of foreign protein or serum. Antivenom is known to cause serum sickness but the incidence and characteristics are poorly defined. ... The primary outcome was the proportion with serum sickness, pre-defined as three or more of: fever, erythematous rash/urticaria, myalgia/arthralgia, headache, malaise, nausea/vomiting 5–20 days post-antivenom.

--Incidence of serum sickness after the administration of Australian snake antivenom (ASP-22). Clinical Toxicology. Published  2016


DISCLAIMER

I know little on the subject. I want to first express my personal views of the existing difficulties at answering this question and then I will attempt to give a short overview of the potential answers I could find.

ISSUES WITH THE QUESTION

Consciousness vs higher cognitive abilities

I personally find it hard to disentangle evolutionary advantage of consciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness.

So, a very important issue with the question is that 'consciousness' is not well defined.

Only few peer-reviewd papers on the subject

While there are a number of ressources in the non-peer reviewed literature (mainly books or popular articles) on the question, I could not find a lot of papers in the peer-reviewed literature. I suppose again that part of the issue that prevents much discussion in the subject is the absent of a commonly agreed upon definition of consciousness. Some of what I'm about to quote is not peer-reviewed and some are not written by biologists but philosophers.

Evolutionary psychology remains very theoretical

One would note as well that most work in evolutionary psychology remains mostly theoretical as it is often hard to perform meaningful empirical testing for the existing hypotheses.

Quoting for safety

As I often failed to make sense of what I just read(!), I will try to quote quite  a bit to avoid misinterpreting other authors.

ANSWER

Definition of consciousness

I recommend having a look at Perlovsky (2007) for a semantic discussion (and opinion) on the concept of consciousness. Quoting their full abstract

  The knowledge instinct is a fundamental mechanism of the mind that drives evolution of higher cognitive functions. Neural modeling fields and dynamic logic describe it mathematically and relate to language, concepts, emotions, and behavior. Perception and cognition, consciousness and unconsciousness, are described, while overcoming past mathematical difficulties of modeling intelligence. The two main aspects of the knowledge instinct determining evolution are differentiation and synthesis. Differentiation proceeds from and unconscious states to more crisp and conscious, from less knowledge to more knowledge; it separates concepts from emotions, Its main mechanism is language. Synthesis strives to achieve unity and meaning of knowledge; it is necessary for resolving contradictions, concentrating will and for purposeful actions. Synthesis connects language and cognition. Its main mechanisms are emotionality of languages and the hierarchy of the mind. Differentiation and synthesis are in complex relationship of symbiosis and opposition. This Leads to complex dynamics of evolution of consciousness and languages. Its mathematical modeling predicts evolution of cultures. We discuss existing evidence and future research directions.

Consciousness as a by-product

To my personal experience, consciousness is in general viewed as a by-product of the selection for specific cognitive abilities. Again, without much of a definition of consciousness it feels to me that selection for specific social skills, such as those requiring the Theory of Mind (ToM) would yield to increase consciousness.

If consciousness and ToM (and other related cognitive skills) are the same thing, then we got our answer, otherwise, the standard view is to consider consciousness as a by-product of the selection for those higher cognitive skills.

On the topic, see for example Judd (1910) (did I really cite such an old paper?) or Dennett (1980) (Dennett is a philosopher, not a biologist).

In the comments the OP said

  To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

I would note that, if taken as an argument, then it would be a logical fallacy called argument from incredulity.

Consciousness as a result of higher social abilities

This opinion seems quite related to the previous one. Quoting from Ingold (2005)

  Becoming a person is thus a matter of gathering social relations into the structures of consciousness: the movement in development, as Vygotsky put it, is ’not from the individual to the socialized, but from the social to the individual’

  [..]

  as relationships unfold in the course of purposive social action, they are
  enfolded in the consciousness of persons, that is, in the structures of the self.
  The connection between social relations and consciousness should thus be
  understood in terms of unfolding and enfolding, rather than in terms of cause
  and effect

  [..]

  This view of sociality, and the theory of direct perception on which it is
  founded, suggests that it is possible for persons to engage with one another on
  the basis of shared perceptual experience prior to the objectification of that
  experience in terms of collective representations encoded in language and
  validated by verbal agreement. Thus sociality is possible in the absence of both
  language and the kind of objective self-consciousness that (probably) depends on language

Conscioussness as result of the logistics of decision making

Quoting from Merker (2003)

  Consciousness will be interpreted as a biological
  function evolved by mobile animals as a solution to neural logistics problems inherent in the
  control of orientation to their surroundings. The interpretation is motivated by the conspicuous
  absence from the contents of consciousness of two significant classes of information known to be
  present in brains, one on the afferent and the other on the efferent side of neural function. In fact,
  the thoroughness of their exclusion from consciousness suggests that their absence represents a
  design feature of consciousness providing important clues to its nature and biological function.
  This in turn helps constrain conceptions of its neural implementation as well as the search for its
  origin in the phylogeny of life forms


Why does my eyes see a red spot when over exposed to light?

You are describing the phenomenon of negative afterimages, a type of physiological afterimage, which is a result of how the cells in the retina work. Specifically, it is a result of the adaptation of photoreceptors.

  According to the opponent process theory of color vision, our
  perception of color is controlled by two opposing systems: a
  magenta-green system and a blue-yellow system. For example, the color
  red serves as an antagonistic to the color green so that when you
  stare too long at a magenta image you will then see a green
  afterimage. The magenta color fatigues the magenta photoreceptors so
  that they produce a weaker signal. Since magenta's opposing color is
  green, we then interpret the afterimage as green.

There is a well-known illusion, called the negative photo illusion, which exploits exactly that. It is required not to move the eyes, because you need to bleach the photoreceptors in an exact place on your retina. This is why you have to fixate on a dot in the middle of a picture, otherwise the bleaching will not occur.

EDIT: I mention a two-axis (magenta-green system, blue-yellow) system, but the exact color system - which would predict which afterimage you would see - is most likely a trichromatic system, which includes red, green and blue channels, based on the principle of the three types of retinal cone cells. It is important to remember that this is a phenomenon in perception, and thus may, in some cases, not be reducible to the fact that there are three types of cone cells, or that bleaching of a photoreceptor has occurred. Please see the comment thread below for some clarification.


From where did the selfish gene get its selfishness?

This is a very introductory question to evolutionary biology. While the book "The selfish gene" is very pleasant to read and directly offer some key notions of modern evolutionary biology, it offers little to no introduction to the basics of evolutionary biology (it is not its goal). I highly recommend that you have a look at a short intro to evolution such as Understanding  Evolution by UC Berkeley for example.

Below, I give a very brief answer to your question but taking an intro course to evolutionary biology would probably be more helpful.

What is evolution?

Evolution is a change in allele frequency in a population through time

An allele is a variant of a gene (or any other sequence at any locus). A locus is a position in the genome.

How do alleles come to existence?

Alleles are created from previous alleles, through mutations. The process of mutation is random in the sense that the effect of the new allele is "unknown from the organism" which create this allele. The mutation just occurs and it just has some effect on the phenotype and the fitness.

What are the forces of evolution?

There are a number of forces that affect evolutionary processes such as genetic drift, migration and natural selection for example.

What is natural selection?

Natural selection is the change of frequency of of the alleles at a given locus caused by differential fitness among the individuals carrying the different alleles.

Why one ought to expect that altruism should not exist in nature?

Here the term selfish and altruism are defined in terms of fitness effects. An altruistic individual is one that is performing a behaviour (or having other phenotypic trait) that is positively affecting the fitness of an individual of the same species while decreasing its own fitness.

Imagine an individual (let's call him the "actor") that has a mutation causing him to be altruistic (in opposition to being selfish). Such "actors" will have a low fitness while its neighbours will take advantage of the altruism of the "actor". There is therefore a differential in fitness between those that are selfish (higher fitness) and those that are altruistic (lower fitness) which ultimately yield to a decrease in the frequency of the alleles causing the altruistic behaviour until it completely disappears from the population.

The above paragraph explains why one would expect that altruism should be absent from nature. However, the story is definitely not that simple. But this extension is a story for another time. You will have to understand the different between "true (lifetime) altruism" and "false altruism", you will have to learn some game theory and finally Hamilton's extension of game theory.

What Dawkins mean by selfish gene

In his books, Dawkins talks about selfish gene often to refer only to genes that are causing meiotic drive (which might be confusing) and to talk about the existence of inter-genomic conflict. There are various mechanisms that can cause meiotic drive. You can learn more about that in Haid and Berstrom 1995, Jeanike 2001 or Jeffrey and Neuman 2002 for examples.


There are several fungi that autodigest  their lamellae  to release spores. Yours seems to be one of them. Due to the black liquid they release during autodigestion, they have the common name inkcap.

As an example, read this Wikipedia article about Coprinus for more details.


Most experiments to try to get at this type of question use stable isotope tracers to measure NADPH production from the various pathways that can make it, and then subtract away the amount that's predicted to be needed for growth/anabolism (based on the observed growth rate and biomass composition). I think this paper is by far the best example:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104482/.

Quote:

  The overall demand for NADPH for biosynthesis is > 80% of total cytosolic NADPH production (Figure 4b), with a majority of this NADPH consumed by fatty acid synthesis. At least in transformed cells growing under aerobic conditions, most cytosolic NADPH is devoted to biosynthesis, not redox defense.

Note that these are fast growing cells without additional oxidative stress. Interestingly, what the authors find is that imposing additional oxidative stress doesn't actually change NADPH production that much, but it slows down growth as more NADPH is used for anti-oxidant defense (Extended figure 9).

For skin cells, the situation might be a bit different, at least in terms of the increase in NADPH production upon oxidative stress. You might look at this paper: http://www.cell.com/molecular-cell/fulltext/S1097-2765(15)00456-6


Short answer
The claim is unclear but is essentially misleading and wrong. However, IMO, for lay people, it is a good approximation to just think that mutations are random!
Here, on Understanding evolution is a great source of information on what it means to say that mutations are random
Long answer
What is a mutation?
Mutation is an event causing an alteration in the DNA sequence where the mutation occurred. There are different types of mutations, consider for example the following Single Nucleotide Polymorphism (SNP)
Original Sequence

ATTATCTG

Sequence after mutation of the 3rd nucleotide

ATGATCTG

Note that mutations can have much more drastic effects such as the duplication of a very long sequence of DNA for example.
You might want to have a look at What is the definition of a mutation? and eventually Effect of mutation on phenotype.
What can be random?
A variable can be random. So is the term mutation a variable?
IS "MUTATION" A VARIABLE
Consider first this discussion about the term house. You can measure the height of the house or the number of windows and both the height of the house and the number of windows so that both the number of windows and the house of houses are variables but house itself is not a variable.
A mutation is an event but, just like with the house, there is no obvious number associated with the term mutations. The number of mutations occurring in a reproductive event is a variable. The effect size on fitness of a mutation is a variable. So claiming that mutations are random is unclear as we don't know what property of the mutation the claim is referring to.
WHAT IS RANDOM
Fully discussing the concept of randomness will require doing quite a bit of math and philosophy. I will not attempt to do so and will intentionally make some oversimplifications here.
The concept of randomness only makes sense if we formalize a model. The outcome of flipping a coing may seem random to you but this is true only if you assume you don't know the forces at play on the coin (the movement of the thumb, the speed of the wind, etc...). A physicist would be happy to consider a coin flip being a perfectly deterministic (deterministic = not random) process.
If a process is deterministic, it means that for a given input there is a single possible output. If a process is stochastic, then there are several (potentially an infinite number) of possible outputs. Now, stochastic does not mean fair or uniformly distributed and therefore a process can be stochastic and yet we can have some predictive power on what range of values the outcome will likely take. For example a weighted die/dice may turn up certain numbers more often, but it's still random, it's just that the distribution of expected outcomes is not uniform.
So, to talk about the claim mutations are random, ideally one would need to fully specify a model of consideration.
RANDOM AS DIRECTIONLESS
Often by random, people mean "directionless" (or "fair"). This is clearly not what the term random means but I will still discuss the case of "direction" (or "fairness") as it is often what people mean. If a mutation is directionless, it means that this mutation is not more likely to increase the value of the variable than to decrease it. For example, if the variable of interest is the height of the individual, assuming that mutations are truly directionless, a mutation is not more likely to increase the height of an individual than to reduce it.
Is the number of mutations random?
VARIATION IN MUTATION RATE
The mutation rate varies dramatically among species and along genomes roughly speaking from a rate of $10^{−2}$ to a rate of $10^{-10}$ mutation per nucleotide. For example microsatellites (repeated sequences) are highly mutable.
EFFECTS OF NEARBY SITES
Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication).
PLASTICITY FOR MUTATION RATE
The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants and bacteria typically) (Chary et al. 1993; Bjedov et al. 2003). The environment affects the mutation rate and the environment can be chosen by some species (avoidance) or even constructed by others (niche construction).
AGE OF THE PARENTS
In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. See the post Gender and age-specific mutation rate in plants (and its references) for more information.
EPIGENETICS
Epigenetic changes (do not concern all species) can also affect the mutation rate and even influence what new nucleotide the old nucleotide will be mutated into (with a given probability).
CONCLUSION
Many things affect the mutation rate. However, the exact number of new mutations an offspring will carry is not perfectly deterministic.
Type of mutations
Mutations are more likely to be transitions than transversions. But again, it is not a perfectly deterministic process.
Effect of mutations on fitness
DISTRIBUTION OF FITNESS EFFECTS
Different mutations have different effects on fitness. We talk about the Distribution of Fitness Effects (DFE).
The DFE varies from one sequence to another. In conserved sequences, mutations tend to have a higher impact on fitness.
ARE MUTATION EFFECTS ON THE FITNESS DIRECTIONLESS?
No, most mutations are deleterious or neutral. Only few mutations are beneficial.
Effect of mutations on the phenotype
Again, some phenotypes are more sensitive to new mutations than others. The increase in phenotypic variance due to mutation at every generation is called the mutational variance.
ARE MUTATION EFFECTS ON THE PHENOTYPE DIRECTIONLESS?
It can be the case, but it is not necessarily true. When mutations are not directionless, we talk about mutation bias (see for example Eyre-Walker 1998, Harr and Schloterrer 2000 or Shah et al. 2010).
Conclusion
Yes, there is some randomness in many of the variables associated with mutation events. However, it would be wrong to think that we have no predictive abilities in the number of mutations or effect of mutations, it would be wrong to think that a mutation is as likely to increase fitness than decrease it and it could be wrong to think that a mutation is as likely to increase a phenotypic trait than decreasing it.
Related posts

Are evolutionary mutations spontaneous?
What are the major causes of mutations in DNA?

Source of information in evolutionary biology
Understanding Evolution by Uc Berkeley is a good, short and very introductory course to evolutionary biology.


Unlike most of the cells in a human body, erythrocytes (or red blood cells) don't have mitochondria (because they are basically O2 carriers), and don't perform Krebs Cycle or Oxidative Phosphorylation. Therefore, they depend exclusively on glycolysis to produce their ATPs.

According to the Genetics Home Reference (from the NIH, National Institutes of Health) page about triosephosphate isomerase deficiency:

  The anemia in this condition begins in infancy. Since the anemia results from the premature breakdown of red blood cells (hemolysis), it is known as hemolytic anemia [...] TPI1 gene mutations lead to the production of unstable enzymes or enzymes with decreased activity. As a result, glycolysis is impaired and cells have a decreased supply of energy. Red blood cells depend solely on the breakdown of glucose for energy, and without functional glycolysis, red blood cells die earlier than normal. (emphasis mine)

Thus, since erythrocytes depend solely on glycolysis as energy source, there is a marked accumulation of DHAP toxic sub-products (Ahmed et al., 2003).

Sources:

Reference, G. (2017). triosephosphate isomerase deficiency. [online] Genetics Home Reference. Available at: https://ghr.nlm.nih.gov/condition/triosephosphate-isomerase-deficiency#genes [Accessed 16 Jul. 2017].
Ahmed, N., Battah, S., Karachalias, N., Babaei-Jadidi, R., Horányi, M., Baróti, K., Hollan, S. and Thornalley, P. (2003). Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1639(2), pp.121-132.


Aligning multiple sequences in heterogeneous group

You can try this:

BLAST each sequence to every other sequence (pairwise).
Every alignment (with some defined cutoff) denotes a connection.
Map all connections.
If a sequence is connected to some other directly or indirectly, it falls in a group. Put all the sequences that seq1 aligns to, in Group-1, then go to the alignments of these sequences; put all the sequences that these align to again in Group-1; so keep populating the group like this.

Methodology:

Install standalone blast (if you don't have many sequences then you can run online BLAST as well)
Make a blast database from your sequences using makeblastdb
Align these sequences against the database. If you are using online BLAST use BL2seq (align two sequences). It is much better and convenient to use standalone. You can also mention if you want plus-plus or plus-minus or both alignments. You might in some cases want only either of the two.
In the standalone BLAST you can specify the output format (which fields to include etc- the format you choose just depends on your requirements).

A tabular output format looks something like this:

# BLASTN 2.2.27+
# Query: TCONS_00036712 gene=XLOC_017996
# Database: ../nt_db/nt
# Fields: query id, subject id, % identity, alignment length, mismatches, gap opens, q. start, q. end, s. start, s. end, evalue, bit score
# 1014 hits found
TCONS_00036712  gi|191174875|emb|CU655970.6|    95.54   202 9   0   423 624 16680   16479   8e-85    324
TCONS_00036712  gi|51491599|gb|AC144709.2|  95.02   201 10  0   424 624 28443   28243   1e-82    316

Ignore the commented (#) lines; the first field is query ID, the second is the subject ID and there is an alignment between the two; the other fields provide information about the alignment (You can choose these fields).

For parsing I use a fast and easy scripting language called awk which is included in all UNIX based systems. It is also available for windows in GNUWin32 package.

What you have to do is check the first two fields and update the group.

# MakeGroups.awk

BEGIN{FS="\t"}     # Declaring Field separator as Tab

!($1 in grp){          # Check if the seq is a parent group. If not...
    k=1
    for(i in grp){
        if($1 in grp[i]){    # Check if the seq is part of any other groups
            parentgrp[$1]=i
            if(!($2 in grp[i]))   # Check if the second field i.e subject already present in the parentgroup
                grp[i][$2]        # if not assign the second field to the parent group
            k=0
            break    # stop checking further
        }
    }
    if(k==1)        # There is no parent group with this label and the seq is not a part of any other group
        grp[$1][$1] # Make a group with the query-id as the label and add this query to this group.
}

$1 in grp{
    if(!($2 in grp[$1]))
        grp[$1][$2]    # If the second field is not a part of the group with first field as label then assign it to that
}

END{
    for(i in grp){
        x++
        print "Group-"x"\n----------"
        for(j in grp[i])
            print j
    }
    print "\n"
}

Run this script like this in the terminal:
gawk -f MakeGroups.awk blastalignmentfile.txt

Note: This script contains multidimensional arrays. It will not work with all versions of awk. Use gawk version >4.0.

As swarnbes mentions in their answer, there are faster algorithms which do this kind of stuff and are used for sequence assembly. What many of them do is to make a graph (networks called deBruijn graphs), where each connection is an alignment, and compute an Eulerian Path. See this review by Pavel Pevzner for details. Overlapping sequences form contigs and you can easily trace back which sequence came from which contig (which you can call a Group). Each contig/Group is a disjoint deBruijn sub-graph.


Why do animal teeth get darker if exposed?

The incisal and occlusal edges of teeth are more translucent since there is only enamel in this area and the dentin core is deeper inside. The dentin is more opaque and reflect the light back and it looks lighter whereas the enamel is translucent and allow more light to pass through and less light is reflected back so it looks darker. Many human teeth the incisal edge is translucent or darker for the same reason.


Is fructose really a poison like alcohol?

Everything is a poison with the right dosage  Here is a fun chart you can use to see what I mean. Even water is poisonous if you drink enough of it.

fructose in no more poisonous than glucose. No study has shown fructose to be dangerous when eaten in normal healthy diet. It is poisonous but only in the sense that water is poisonous if you drink to much of it.

And you should reread your own source the article concludes it is NOT more poisonous than glucose. It also concluded that the paper that claimed so was erroneous because it used animals with different metabolic pathways and the differences were not significant in any case. Nor is it possible to eat a diet high in fructose without it also being high in glucose (see above study) so it would not be an issue even IF Dr. Lustig was right about the lipid metabolism.

News media loves to focus on single isolated studies with odd conclusions which is basically the worst way to represent science, wrong or erroneous things get published all the time and get quickly found out but the media tend to latch on to the former and never report the latter.

Processed sugar is bad for you for completely different reasons, basically the same reasons donuts and bacon are bad for you, they are empty calories, it is just that Americans (and a few others) eat way way more refined sugar than the other two, absurd levels of it, for comparison it is as if you were eating large amounts of bacon for every meal levels of absurd. There is also the aspect of diabetes which has to do with how much and how often we eat sugar not an issue with the sugar itself. (if we instead ate half a pound of bacon grease every day that would be the thing causing problems.)


How does the structure of the pancreatic acinar cell relates to its function?

The secretion pushes the cell organelles to the basal part.

(although the fat cells have no polarity, their organelles have been pushed to one side of the cell:

Comparing to adipose cells, the acinar cells secrete their specific proteins on one specific end of the cell, this is why in contrast with fat cells they have well defined polarity.


The question of what is living is nothing but a matter of definition. We can only tell you what are the standard definitions of what is a living thing but no absolute truth exist behind these definitions. Therefore, I am afraid that all discussions here will bring anything new to your ethic or religion related discussion.

I want to argue that the @user137's answer is very misleading for two reasons. First, he based his discussion exclusively on the "reproduction ability" definition of life. Second because his definition of reproduction might be misleading as well.

Reproduction is not only cell division obviously. Following this same definition one would not consider a human to be a living things but only to be a collection of living (and non-living) things. It is important to understand that a spermatozoid is just one phase of a life-cycle. This phase yield to the next phase. That's it. It seems weird to say that a kid is not alive just because he cannot reproduce. It seems weird to say that a grandmother is not alive because it cannot reproduce. You can say however that a kid is a living thing that cannot reproduce and at another moment of its life cycle it will be able to reproduce (assuming it will survive to this age). One should not think of spermatozoids as something totally detached from the human phase as we know it. These things just form a cycle and it seems to me miseleading to say that a part of this cycle is not alive. Saying such thing would yield someone to think that two living things create non-living things that by fusion will become alive. That seems weird. But again, it is nothing but a matter of definition. I cannot say that user137 is wrong, I cannot only say that his definition seem neither useful, intuitive nor common among biologists.

You may want to have a look to life-cycle and to understand what are the haplontic and diplontic phases with a bunch of wikipedia readings.

Other concepts such as the ability to synthesize its own components, having a boundary between interior and exterior and ability to response to environmental stimulis are often used in order to define what is a living thing and what is not.


Effect and functional role of voltage-gated channels on dendrites

As on axons, one immediate effect of voltage-gated channels on dendrites is the generation of spikes (called dendritic spikes as opposed to action potentials). These typically have higher local voltage thresholds than on axons. They seem to play a major role in long-term potentation. But it's not obvious for me how, and which other "implications in neuronal communication, memory, and learning" they might have.


Deducing amino acid sequence from a DNA sequence

This is a deceptively and badly worded trick question. Your confusion is because it starts with a mention of RNA polymerase, which transcribes DNA into mRNA, but asks about the protein, which is produced by the translation of the mRNA on ribosomes.

The first step in solving the problem is asking what is the sequence of the mRNA produced by the transcription. The question doesn't actually say which strand is copied, but the 5'-end of the mRNA is synthesized first, so you can assume the mRNA is the complement of the bottom strand, which is copied. (The convention of direction presumably tells you the same thing). Thus, the mRNA has the sequence:

  CCACCAUGUUA...

Now you need to go along the sequence (as a ribosome) looking for where to start translating. However the question doesn’t tell you whether this is a prokaryote or a eukaryote (unless you omitted to tell us). In order to solve the problem we have to assume it is a eukaryote where the ribosome normally scans along from the cap to the first AUG to initiate translation (the region italicized above):

  AUG (ATG) = M

  UUA (TTA) = L

  etc

(If it were a prokaryote you’d need to look for a Shine and Dalgarno ribosome-binding site.)

You might wish to raise my criticisms with your instructor (although I doubt that he will thank you for doing so).


What did the evolution of multicellular animals look like?

The life cycle of myxobacteria (e.g., Myxococcus coralloides, Myxococcus disciformis, Myxococcus flavescens, Myxococcus fulvus, Myxococcus macrosporus, Myxococcus stipitatus, Myxococcus virescens, Myxococcus xanthus---for references to the original articles describing these species, see Bacteria I. Taxonomy: Genera and Species) includes the formation of fruiting bodies, which is an obligate multicellular process requiring cooperativity between individual bacterial cells (see, e.g., Cao et al., 2015).


What are some features that do not make an individual better than others without this feature?

Phenotypic effect of mutations

Most mutations have no phenotypic effect and therefore no fitness effect either (fitness is a function of both expected survival and expected number of offspring).

These mutations that have no phenotypic effects are therefore all neutral in terms of their fitness effect. Their probability to be passed on to at least one offpsring in a panmictic population of constant size $N$ is $\left(1-\frac{1}{2N}\right)^{2N} ≈ exp(-1) ≈ 0.36$. A mutation that is beneficial would have a greater probability and a deleterious mutations would have a lower probability. There are a whole bunch of equations for these but I don't want to get too "mathy" in this intro post.

Fitness effect of mutations

Among mutations that have phenotypic effects, some have no effect of fitness, some are deleterious, some are beneficial. The beneficial ones only represent a very small minorities of mutations.

Note that it is important to make the difference between a trait that seems to not be beneficial to you, while whether it actually is or is not beneficial. You cite things like eye color and head shape. Both of these traits can have very important on sexual selection. Try to date someone with a triangular head or with white iris! Also, if I am not mistaken, light colored eyes tend to let more light going through to the retina, hence light colored eyes are better adapted in environment where sunlight exposure is low. Head shape may have important impact too. For example, the jaw bones is an important contributor of the head shape and whether you have a strong or weak jaw is of importance (and the shape of the jaw is under sexual selection pressures).

Examples of neutral mutations

Most mutation that happen at non-coding, non-regulatory regions of the genome will be neutral.

Among the mutations that have phenotypic consequences but no fitness consequence, there are classical genetic markers (such as tongue rolling) that are likely free from any selection pressures. Note, that heritability for such trait is rarely 1.0 (see here for explanations). Maybe earlobes would be a good example, although there might have some sexual selection going one here.

Note also that as many mutations are recessive, the carrier of a single copy of the mutation may not be affected.

What is a gene?

You are using the term gene improperly. A gene is typically defined as a coding region. You might want to study a little the basis of genetics here. You should typically get used to the terms locus, allele and gene copy number. This answer can help you at this endeavour.

A small comment on the frequency of mutations

  If a mutation occurs [..]

Just to make sure you do not have a misconception about how frequent mutations are here, I would like to highlight that, in humans, at every reproduction event, the new born has about 10 to 100 new mutations that were not present in any of both parent. So, mutations are rather common!

Introduction to evolutionary biology

Your question is a very introductory question to evolutionary biology. You might want to have a look at a short introductory course such as evo101 by UC Berkeley.


How to convert FASTQ file format into GTF file format?

You should really read about both these file formats. As swbarnes mentioned, FASTQ and GTF hold different kind of information. GTF stores the annotation of a reference sequence. For example a GTF for a genome sequence will have the information about the locations of features such as genes, transcripts, exons, start codon etc.

FASTQ stores the sequence of a read obtained from sequencing along with the quality scores corresponding to each position.

As mentioned by others, asking for interconversion of these file formats, makes no sense.

I guess what you are asking for is "How to obtain novel annotations with a FASTQ file at hand?"

This also depends on what you want to annotate.

The sixth column in a GTF file refers to a score; you can assign expression values to different features. You can calculate expression using the read counts. If these are RNAseq reads then expression can be measured using packages like tophat-cufflinks, RNAstar or some others.

If you are doing ChIP-Seq then you can generate a GTF with a new feature called TFBS (transcription factor binding site) and annotate the locations. A popular package used for ChIP-Seq analysis is MACS, which takes your reads and outputs the TFBS in the form of a BED file which also stores co-ordinates. You can convert BED to GTF. You can also assign scores based on the read counts at different TFBS.

If you do not have a reference genome or if the annotation of the reference genome is incomplete, then you should first assemble your reads. If you have a reference genome then you can go for a reference guided assembly of the transcripts to obtain novel transcripts or splice variants; Cufflinks does this.

If you do not have a reference genome then you should go for de-novo assembly of your transcriptome and annotate the transcriptome for start codons or other features of processed transcripts. Velvet and Trinity are popular packages that do de-novo assembly.


What negative effects can pinhole glasses have on the body?

Probably not many side effects except in specific instances, but no benefits either. My guess is that there are potential side effects because these glasses reduce the amount of light that the eye receives and restrict the visual field. Therefore, the restricted visual field would be bad for activities such as driving, in which you need your peripheral vision. And the reduced light makes objects appear dimmer, so it is harder to see with them at night. I also imagine (just a guess) that they would be bad for very young infants, who are almost always born without perfect vision and require some visual stimulation to correct.

There are probably many reasons why optometrists use a pinhole occluder for diagnostic purposes, but never prescribe it as treatment...


What can be the reason for yellow and dark marks on leaves?

Yellow leaf spots have various shapes, depending on the cause. Downy mildew starts with angular pale yellow spots. In cucumbers (Cucumis sativus) and other cucurbits, powdery mildew causes pale yellow spots followed by powdery white patches.

The location of the yellow spots may help you determine the cause of the symptom. Some diseases, such as powdery mildew, cause spots on older leaves first and then spread to younger leaves. Yellow spots from powdery mildew can occur on upper and lower leaf surfaces. Downy mildew spots occur on the upper sides of leaves between leaf veins that give the spots their angular shape.

Now lets jump into the causes :-

  1 -Moisture Stress

Over-watering or under-watering are the most common culprits when a plant's leaves turn yellow.
If plants don't receive enough water, they drop leaves to prevent transpiration (essentially, a plant's way of sweating) and conserve water. Before they drop, though, the leaves will typically turn yellow.
Too much water can be just as damaging to leaves. When the soil doesn't drain well, an overdose of water leaves the soil waterlogged and root systems can literally drown. Without oxygen, roots start to die.

  2-Normal Aging

As many plants age, the lower leaves will turn yellow and drop off.

However, to solve this case, don't worry. If the plant becomes too leggy, consider trimming back the main stem to promote new growth and bushiness.

  3-Cold Draft

Now let's first understand what a cold draft is. A cold draft is a current of cold air being drawn indoors.

A plant sitting near it is giving off more heat than it receives from the room. Remember, heat travels from places of higher temperature to places of lower temperature.Cold drafts on tropical plants will often cause the leaves to turn yellow and drop.

To solve this problem, particularly If your plant is near an air-conditioner vent in summer or a drafty window in winter, move it to a less turbulent place.It's also a good idea to mist tropicals that you're overwintering to increase the humidity.

  4- Lack of Light

A plant that is yellowing from a lack of light will typically yellow on the side that is away from the light source.

To solve this, move the plant to a sunnier location and see how it does. If window light is tough to come by in your home—especially in winter—you might need to rig up an artificial plant light or two.

  5- Nutrient Deficiency

This can be caused by too much calcium in the water if you're using hard water, or by a nitrogen deficiency.If this is the problem, the plant's top leaves may be the first to go yellow.

However to solve this issue, since it is species specific, its important to diagnose the problem firstly and them take some remedies.

  6-Viral Infection

If your plant has a viral infection, it might show up as blotchy, spreading yellow patches on leaves throughout the plant. This may be accompanied by deformed leaves and stems, as well as discolored flowers.

To solve this , discard any plants that you suspect are infected since viral infections can not be treated.

  7- Fungal infection

If caused by a fungus, there is nearly always fungus growth of some type in the spot, particularly in damp weather. This fungus growth may be tiny pimple-like structures, often black in color, or a moldy growth of spores.

To solve this, you can use sulphur(in dust form) and milk.

Sources - https://www.thespruce.com/reasons-for-yellow-leaves-on-houseplants-4150680
https://www.hunker.com/12140067/how-to-diagnose-cause-of-yellow-spots-on-leaves
www.uky.edu/Ag/PAT/cat1/leafdis.htm


why do our eyes not go red in response to body temperature?

Skin turns red when light skinned people flush because it contains few absorbers, so photons diffuse through it long distances. During this time green and blue light is absorbed as photons encounter blood vessels. Red photons are not and so the skin appears redder.

The whites of the eyes are strongly scattering and have relatively few blood vessels, so changes in blood flow has a small effect on color.  The (wavelength-independent) scattering dominates over absorption.

The pupils open up on the approximately 22 mm gap between the cornea and the retina. You don't see changes in color here because the entire retina strongly absorbs all colors of light. The few red photons scattered by blood are very unlikely to be exactly aimed at the pupil. Instead most scatter back into the retina and are absorbed. This is compounded by the scattering anisotropy of blood, which causes most incoming red light to be scattered in the forward direction - directly into the strongly absorbing retina.


What would be a reason for a tree to have flowers of different colors?

There are a couple of possibilities for what's going on here:

The most likely explanation is Position Effect Variegation (PEV). Genes are, at the most basic level, organized linearly on chromosomes (very long strings of DNA). Some parts of chromosomes contain stretches of genes that are actively silenced, or turned off, by cells (large silenced regions like this are called heterochromatin). The boundaries of where this silencing starts and ends are sometimes fuzzy. If a gene necessary to produce pigment happens to be next to a silenced region, the silencing can randomly creep in and shut off that gene as well, or creep back to its normal boundary. (This is why it's called 'position' effect variegation: it depends on the physical position of a gene, in this case the pigment gene, on the chromosome, and how close it happens to be to a normally 'silenced' region.) This process is (probably) effectively random, so it won't happen in every cell, which means some cells will produce pigment whereas others won't. A famous example of this happens in fly eyes, as in the image on the left. Importantly, the difference here isn't 'genetic' (the actual content of the DNA), but 'epigenetic' - essentially, the way cells modify and read their own DNA.
Another possibility is an active jumping gene, or transposon: unlike most genes, transposons can move around in the DNA, and can sometimes carry with them a piece of DNA that tells nearby genes to be turned on or off (or are simply silenced by the cell, like in the PEV case above). If a transposon sits right near a pigment gene, it can cause that gene to be silenced. However, if the transposon up and jumps somewhere else at a random time (which active transposons do!), the gene nearby is no longer silenced, and can now cause pigment to be produced again. There's an example of this happening in snapdragons (see middle image). In this case, there is an actual genetic difference between the pink and white cells: one group has a jumping gene sitting next to the pigment gene, and the other doesn't.

Importantly, PEV silencing--like the transposon jumping--is inherited when cells divide, so if a stem cell that eventually makes a whole flower silences the pigment gene (or transposon jumps out), the whole flower will be white. If the silencing happens later in development, maybe when the early divisions forming the flower have happened, then a single petal, or just a sector of a petal, could be white, and the rest pink. Such sectoring is a telltale sign of PEV or transposon-related effects.

In your photo and description, the tree is mostly white, and individual sectors are pink, not vice versa. If the cause of the color switch is PEV, then the pigment gene's 'default' in this tree being silenced, with the silencing randomly moving away from the pigment gene in some cells. Or there could be a particularly active transposon that tends to bring gene silencing along with it at play here.


How did sulfasalazine become a disease-modifying treatment for rheumatoid arthritis?

Question 1:

Why was this "old antibiotic" tested as an anti-inflammatory medicine?

A 2016 publication by the Department of Medicine at both Imperial College Healthcare Trust, and Hammersmith Hospital (both in the UK), titled, "Rheumatoid Arthritis Treatments: A Historical Perspective", states:

"Sulfasalazine: After NSAIDs and Gold, Sulfasalazine (SSZ)
is the third oldest drug class that is still available to use as a
treatment of RA. In 1938, SSZ was the first drug to be synthesized
specifically for RA. The consensus at the time was that RA was
the result of infection and accordingly Svartz et al developed
the DMARD, SSZ (originally known as salicylazosulfapyridin)
by combining the anti-inflammatory, salicylic acid, with the
antibacterial sulfapyridine by an azo bond."

Also, according to a publication by the Department of Medicine at Princeton:

Sulfasalazine was synthesized almost 50 years ago specifically to treat rheumatoid arthritis. At that time bacterial infection was believed to be an important factor in pathogenesis. The linkage of sulfapyridine and salicylate with an azobond was viewed as a method of combining antibacterial and antiinflammatory actions while minimizing gastric irritation. Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery. Subsequent controlled trials have confirmed its efficacy, which may be related to sulfasalazine itself or to the sulfapyridine moiety.

Question 2:

What is the evidence (if any) that sulfasalazine has a disease-modifying effect in the treatment of RA - that it actually slows down the progress of the disease rather than just temporarily reduce symptoms?

A 1995 publication conducted by Adis International affiliates states:

The efficacy of sulfasalazine in RA noted in many noncomparative studies has been confirmed in placebo-controlled trials and comparisons with other disease-modifying antirheumatic drugs (DMARDs). Sulfasalazine therapy produces significant improvements in many clinical and laboratory parameters associated with the disease, including erythrocyte sedimentation rate (ESR), Ritchie articular index (RAI) or number of swollen joints, grip strength and duration of early morning stiffness (EMS).


How to put a gene under the control of a regulable promoter?

If you're expressing the gene in E. coli, then you're almost certain to be using a plasmid or other ectopic gene vector. There are a wide variety of plasmids available, with many different promoters. With a commercial plasmid, you're not adding in the promoter sequence, but the gene sequence. You pick the promoter you want and then clone your gene sequence into the plasmid's multiple cloning site, which is designed to lie downstream the promoter.

There are a variety of tools to design and order plasmids. A common plasmid repository is addgene and my favorite tool for designing plasmids prior to ordering is APE.

Design the plasmid with APE or another tool, to be sure that everything looks good, then you can order the appropriate plasmid vector and enzyme cut site-flanked gene sequence and go to town cloning.


Those are floaters. These are objects floating in the vitreous humour that fills the eyeball. They typically look like: