Why is selfishness the 'obvious' strategy?

It basically comes down to a question of the unit of selection.

From the common viewpoint, in which natural selection is seen as acting on individual organisms, it's almost a tautology that the organisms favored by selection are those that maximize their own reproductive fitness.  Thus, the possibility that some organisms might engage in acts that help another organism at their own expense may seem like a paradox, or at least a puzzle in need of explanation.

One solution to this puzzle is offered by the gene-centered view of evolution, where selection is viewed as acting on genes, with organisms being merely convenient (and usually, but not always, cooperative) collections of genes that (usually) reproduce together.  From this viewpoint, it is not at all surprising that evolution might favor genes that cause an organism to help other organisms, provided that there's a statistical tendency for those other organisms to also be carrying the same gene.

Other mechanisms for the evolution of cooperation do also exist.  For example, organisms with sufficiently advanced cognitive capabilities may indeed engage in reciprocal altruism, where they help others only if those others have shown themselves willing to help them in exchange.  Such exchanges, being mutually beneficial, do indeed help both participating organisms, and are thus selected for even at the organism level.  However, to persist (in the absence of gene or group level selection effects), they generally need some form of enforcement and/or learning mechanism — if cheaters can keep receiving help without ever helping anyone else, they'll do better than the cooperators and eventually displace them.

Also, in some situations, an organism acting simply to help itself (e.g. by modifying its environment to be more suitable for itself) may also end up helping other organisms that just happen to be nearby.  In such a situation, selection indeed favors cooperative behavior in isolated organisms by default, with the evolution and persistence of "freeloaders" (who spend less effort on improving their surrounding, relying instead on others to do the work) being only possible as long as there are sufficiently many cooperators around.

Of course, none of these mechanisms are mutually exclusive.  Indeed, the presence of some gene-level selection effects tends to be unavoidable in any realistic situation involving cooperative interactions; it's hard to come up with a setting in which no two interacting organisms ever share genes, and obviously the fact that two organisms share a common genetic predisposition to cooperate makes them more likely to do so when they meet.

(However, one not-so-realistic theoretical limit case where that does happen is that of an infinitesimally rare cooperative mutant invading an infinitely large and well mixed population.  The popular use of this simplifying limit assumption in classical models of evolution may be one reasons why cooperative behavior is so often seen as something remarkable and hard to explain by evolutionary theorists.)


What animal has the longest juvenile period?

As you indicate in your question, the average age of sexual maturity is probably the best way to approach this, since immaturity is usually how juveniles are defined. Age of puberty is also different in boys and girls (the same goes for many animals), and has also decreased in the 21 century. However, as an historical average for humans 15 years is probably fair, even though there is a lot of variance. That is high compared to most animals, but there are some that have similar or higher ages of maturation, e.g.:

Cicadas in the genus Magcicada, which can have a 17 year life cycle
Elephants reach sexual maturity at about an age of 8-15 years, but usually dont start to breed until they are at least 18-20 years (see e.g. elephantsforever.co.za and Association of Zoos and Aquariums). Males mature and start reproducing later than females, and in practice it is mostly older bulls that reproduce.
The Nile crocodile, which reach sexual maturity at at an age of 12-16 years (largely dependent of body size though).
Some species of Tortoise reach maturity at ages 13-16 years (e.g. Gopherus
sp, see Germano, 1994), and, again, which is largely due to body size and growth rate. Captive bred individuals can mature more quickly.

As you can see, there is a difference between sexual maturity and reproductive age. To actually be able to reproduce, especially in some male mammals, you often need experience and size, which means that reproduction is delayed in practice. Whether this period from sexual maturity (with respect to producing mature eggs/sperm) to reproductive age should be defined as least partially as "adolescence" will affect how humans compare to other animals. In my examples, I have focused on sexual maturity (which usually has less variation between individuals).

For other examples, you might want to look at insects other than Cicadas that have delayed larval stages. This does for many woodliving beetles, where development times can be very variable, and under poor conditions take up to 20-30 years. This is usually not the norm though.

When searching for other examples, use the terms "age of maturation, "reproductive age", "sexual maturity" etc, to focus on sexual maturation and not gestation.


It is clearly a Theridiid (cobweb) spider, but it doesn't look like the Parasteatoda tepidariorum I'm familiar with here in the US.  The egg sac it's holding indicates it's a mature female, and the regular pattern on the abdomen is both distinctive and unlike the variable, blotchy pattern of tepidariorum.  Unfortunately, not being familiar with Eurasian spiders likely to be found in your area, I can't be of much help as to what it might be, beyond limiting it to the Theridiids.
Oh, yes - it's pretty clearly not one of the Widows (Latrodectus spp.), and since those are the only medically significant Theridiids we know, it's not dangerous.


What did Richard Feynman contribute to molecular biology?

According to Gleick, Feynman spent the summer of 1960 in Delbrück's lab at Caltech and discovered intragenic supression.

This is where the expression of a gene which has been knocked out by a mutation may be restored by a second mutation within the same gene.

Fenynman worked with the rII mutant of phage T4 and was looking for back mutations in E.coli strain K.

He noted some unusual plaques which he labelled idiot r's.

Feynman correctly deduced that these revertants were due to a second mutation which cancelled the effect of the first, but he did not publish the result, possibly because he had no molecular explanation for what was going on.

The Delbrück lab referred to these revertants as Feyntrons.

Cricks and co-workers in Cambridge, UK, correctly explained the phenomenon.  If, for example, a mutation caused a gene to be read out of sequence (a frameshift mutation) then a second mutation within the same gene could put the message back 'in phase', thus cancelling out the effect of the first mutation.

All the above is taken from James Gleick (1992) Genius.  Richard Feynman and modern physics, a great book.


Why do bulls-eye rashes look like they do?

The spreading of the rash is caused by dissemination (migration) of the Lyme spirochetes (Borrelia) through the skin out from the initial site of infection.

The spirochetes trigger a immune reaction that involves macrophages entering the skin and releasing pro-inflammatory factors.

The clear areas (when present) apparently represent areas where macrophages have been cleared from the skin and thus are no longer triggering a inflammatory response.

The different patterns associated with the rashes can be explained by differences in how fast macrophages are cleared from the skin.

Reference:
Vig, D. K., & Wolgemuth, C. W. (2014). Spatiotemporal evolution of erythema migrans, the hallmark rash of Lyme disease. Biophysical journal, 106(3), 763-768.


Do disaccharidases require a cofactor or coenzyme to function?

Apparently not for lactase and β-galactosidase, as one might expect for this sort of hydrolytic reaction. There are also Wikipedia entries for maltase, sucrase and trehalase with references you can follow up to check yourself.


Why does carbon dioxide diffuse easier through the bilipid layer than oxygen?

After diffusion the partial pressure of both O2 and CO2 in arteries become almost equal to the atmospheric values(100mmHg and 40mmHg), regardless of partial pressures in veins. Rate of diffusion through membrane is roughly the same, it's the solubility that is different, as CO2 is about 22 times more soluble than O2 (it can be stored is water as HCO3-).
  However, oxygen still can easily enter and stay inside the blood vessel because it's bound to hemoglobin inside the erythrocyte. Hence there is no significant difference between the diffusion rates.


Is vision a vestigial sense for deep ocean species?

I can't answer your third, but I can answer your first two. With one word, in fact:
Bioluminescence
http://brightnepenthe.blogspot.com/2010/08/palate-cleanser-90.html

That's the deep ocean at night for ya. Unlike underground environments and caves, it's not pitch black pretty much anywhere in the ocean. There are things to see everywhere, and they play an important role in predator/prey relationships and/or mating. The absence of natural light does make things harder to see, but that's why you see the enormous eyes on species which live far down. So, nope! The eyes on deep ocean critters are not vestigial. They're very functional (and, if anything, probably increased in sensitivity).
The basics are summed up here: http://www.lifesci.ucsb.edu/~biolum/functions.html


recolonize earth desert with plants : which plants first?

This is a big idea that's gaining momentum in many people's minds across the world.  This is a brief and probably inadequate survey and hopefully other answers / comments will fill out a better picture.

Most of the plans to reclaim arid regions are not completely hands off.  It seems that the current thinking is that if we waited for microbes and lichen to reclaim arid soil, it would take too long.  Most of them focus on trees.

Trees are fantastic because they can grow in climates that have minimal water once they are established.  They can claim moisture from the air, remove pollution from the air, reduce the ground temperature, sequester carbon, prevent erosion, and make the environment more accommodating to other plants.

Some estimates are that to curb the expansion of deserts worldwide, 30 billion trees should be planted every year for the next decade.

The tree one plants varies depending on the place and application, but the selection of the plant is more than just a climatic choice.  Trees are grown in nurseries when their needs for water are most intensive, and then need to be cared for until they are established enough to survive on their own.

The Green Belt project was the focus of the 2004 Nobel Peace Prize.  Its success in rolling back desertification was because of its understanding of the causes of desertification in many cases as a social effect.*  People harvest the trees, graze the land dry, burn grassland etc.  Green Belt created networks of local people and incentivized them to grow trees, selecting trees which had agricultural and economic value so that they would help the local economy.

The Great Green Wall project is a successor to this idea.  Attempting to contain the Sahara desert's spread across the continent of Africa.   Their plan is to have a different organization in each country, including automation of sorts to collect water from the air and rain for more continuous support of young trees.

there are arguments that ultimately the animal ecosystem needs to be involved.


Edman method to identify peptides with Phenylisothiocyanate (PTH)

The short answer is that the Edman degradation is a multi-step process. The Wikipedia page has a decent picture of the mechanism. In practice, the peptide is reacted with phenylisothiocyanate (PTH) under mildly basic conditions to give a thiourea, which is stable. The excess PTH is separated from the thiourea intermediate. The thiourea is then treated with acid to cleave the N-terminal residue from the peptide. The PTH is no longer present, so there's no concern about reacting with the second residue.


As 3cat already stated, the terms actually refer to the pollinators. While solitary and social describe the behavioural traits (see this wikipedia article), diploid and haplodiploid give information about the chromosome number of the pollinators (see here and here).

The descriptions in the article depict different combinations of both characteristics.


How do Mockingbirds find each other during mating season?

Wildlife biologist Daniel Edelstein implies as much here: he says that there are in fact variations in tone and context that distinguish mockingbirds from other birds they imitate. (He was writing about the possibility of mockingbirds attracting the birds they are imitating, which doesn't happen. I can't find much about what specifically attracts female mockingbirds, except for the variety he alludes to.)


Laying eggs vs giving birth: is there a connection with internal vs. external ears?

You are quoting from Imam Ali,

  "The animals who have their 'EARS' outside their body give birth to
  their young ones and the animals who have their 'EARS' inside their
  body lay eggs."

And in short the answer is that is wrong. Giving birth to live young is called vivipary. When a species lays eggs it is called oviparity. There are other mechanisms too.

  Ovuliparity: fecundation is external (in arthropods and fishes, most
  of frogs)

  Oviparity: fecundation is internal, the female lays zygotes
  as eggs with important vitellus (typically birds)

  Ovo-viviparity: or
  oviparity with retention of zygotes in the female’s body or in the
  male’s body, but there are no trophic interactions between zygote and
  parents. (Anguis fragilis is an example of ovo-viviparity.) In the sea
  horse, zygotes are retained in the male’s ventral "marsupium". In the
  frog Rhinoderma darwinii, the zygotes developed in the vocal sac. In
  the frog Rheobatrachus, zygotes developed in the stomach.

  Histotrophic
  viviparity: the zygotes developed in the female’s oviducts, but find
  their nutriments by oophagy or adelphophagy (intra-uterine cannibalism
  in some sharks or in the black salamander Salamandra atra).

  Hemotrophic viviparity: nutriments are provided by the female, often
  through placenta. In the frog Gastrotheca ovifera, embryos are fed by
  the mother through specialized gills. The lizard Pseudomoia
  pagenstecheri and most mammals exhibit a hemotrophic viviparity.

Though it is true that most typically we would associate egg laying with animals with ears "inside" such as birds and snakes, there are some examples that are not this way. Boa constrictors are one species which gives birth to live young rather than laying an egg and being a snake their ears are 'inside their body'. However I should point out that this is Ovoviviparity, not viviparity. For an example of a lizard with viviparity see the Pseudomoia lizard genus.


What's the Evolutionary Purpose of Religion?

In terms of genetic evolution, religion itself cannot really be considered to have an evolutionary advantage or disadvantage, as it is not anchored in any genes. This means that it is not an evolutionary trait and hence the principles of evolution do not apply to it. However, religion is a product of underlying capabilities of the brain (for example imaginative capacity?), and these are genetic and evolutionarily advantageous. Aside from this, asking for the 'evolutionary purpose' of anything is the wrong way to approach the topic, as things do not evolve to have a purpose but they simply evolve and stick around unless they produce a net disadvantage compared to a competing version of the same trait.

You could look at religion from a memetic point of view however, i.e. as an idea which competes with other ideas. The idea of religion has many aspects to it that would help it to 'survive', i.e. not be forgotten. These include the drive to tell other people about it, ease of understanding, the claim of exclusivity, addressing many social cravings, and filling in gaps of knowledge for which explanations are desired.


I have finally figured out what these are, and it turns out I greatly misunderstood their relationship with snails.
These worms are annelids of the genus Chaetogaster, specifically Chaetogaster limnaei limnaei.

Source: Page 653 of "Fresh-water biology" (1918)
Ch. l. limnaei is unique in its genus in that lives on the bodies and in the shells of snails, including Physa spp. like the Physa acuta snails in question. While the relationship was originally thought to be parasitic by early researchers, it turns out that it's actually commensalistic (or even mutualistic in some scenarios).
From this vantage point the worms feed on various microorganisms, such as rotifers and algae, and small particles stirred up by the host snail scavenging for food. They also feed upon the cercariae and metacercariae of fluke species that parasitize the snails, even able to protect the snails from getting infected in the first place.
That said, it's not all good-- Snails with heavy infestations of Ch. l. limnaei have been shown to be less active, spending more time in their shells rather than out and foraging for food (Stoll et al., 2013). Additionally, worms have been experimentally shown to consume tissues of their hosts when food is low or nonexistent (Stoll et al., 2013).
To respond to a few points from the question:

These worms are highly specialized, and do not seem to affect ramshorn or pond snails, which I have numerous of in the same tank, in the slightest. It's only the bladder snails that end up infested.

Ch. l. limnaei is not restricted to bladder snails, and will happily live on pond snail and ramshorn species. It's possible that the bladder snails had more severe fluke infestations which the worms found preferable.

My theory at this point is that the young penetrate snails, grow inside of them, emerge and hang onto the host for a while, and then eventually dismount as free-living adults. Adult worms seem to be independent, while smaller worms hang off of the host the snail (feeding off of it?) until they're large enough to live freely.

This worm is able to reproduce both asexually through budding, but also sexually as shown here. Sexual reproduction often occurs in the winter, where the worm lives freely and reproduces sexually before returning to snail hosts in the spring.

I would like to eliminate these worms if possible

I found a blog post by someone struggling with the same problem:

One day (do not know it exactly, probably few months later) I noticed that all worms disappeared. I did not know why they were gone.
Later I found the reason in the 1974 thesis. Chaetogaster limnaei limnaei is highly sensitive to temperatures above 24 °C. Such a temperature reduces or completely eliminates these worms. Therefore, If you transport worms from their natural environment to your tropical aquarium, there is no need to worry. If you have aquaria with aquarium heater, they are bound to be killed by high temperature. Worms are killed in summer heat as well.

This seems to be accurate, as with the onset of the summer heat, I no longer have any of these worms present on my snails. Now knowing what they were, it almost feels like a shame-- They were protectors, not foes.
References

Density-dependent relationship between Chaetogaster limnaei limnaei (Oligochaeta) and the freshwater snail Physa acuta (Pulmonata)


Measuring the electrical signals (=nerve signals) from the heart is frequently done in medicine, it is called electrocardiography. It looks like this (from the same article):

Influencing the heartbear can also be done and is done by pacemakers. Depending on the patients necessities the can permanently stimulate the heart or do this only, when certain criteria are met which makes an intervention necessary to prevent cardiac arrest. Wrong stimulation can in fact kill people, since they go into cardiac arrest when the stimulation of the heart is not correct. This is why pacemaker patients have to stay away from strong magnetic fields which make their pacemakers fail and leave them without proper stimulation.

This technique of influencing the heart from outside is used by defibrillators, which use an electric shock to influence the heart beat. It is used for treating cardiac dysrhythmias, ventricular fibrillation and pulseless ventricular tachycardia, which all lead to death if left untreated. A special form are automated external defibrillators, which measure the an electrocardiogram and then decide by the form of it, if an electric shock is needed.


@JM97 is correct.

According to National Geographic >>

The gestation period of a Red Kangaroo is 33 days and it's baby at birth weighs a mere 0.03 oz. To put it into a more precise perspective, on birth, the baby weighs 1/100,000 of an adult red kangaroo's weight.

Second place goes to the baby of a Giant Panda; at birth it weighs 3.2oz which is 1/900 of an adult giant panda's weight.


What is the impact of prolonged electromagnetic exposure on human health?

Actually the applications of magnetism to organic systems is new to Science.  Duke Univ in NC is currently experimenting with humans sticking their heads into large electromagnetic coils while electrodes are attached to the outside of the skull. A small amount of research has been done with magnetism and plant physiology (my interest), but in the main very little published research is available on the topic.  I might direct you to use Scholar.Google to find more technical articles rather than just using Google itself.


Has an ape ever drawn/painted something?

Yes. The objective clarity of what constitutes representation is not certain, but here: https://www.youtube.com/watch?v=nSHQyLsPm4Q you can see something relatively convincing. The elephant really slays this, but your question is about apes; I don't know how species-specific you intend to be. I find that non-biologist laypersons assume that finding humanoid traits necessitates searching in human-like animals. Often not so! In fact, I wouldn't be surprised if someone came up with an octopus capable of a transformative masterpiece.


This might be a good article to read: http://www.ncbi.nlm.nih.gov/pubmed/24497635

Robert Kerns's lab has been doing a lot of work on fluoroquinolines, so look into his other work as an entry to the literature. And apparently X-ray crystals have been done for at least parts of this complex. There is some evidence for fluoroquinolines binding to DNA, then moving into the protein as it moves along the DNA.


Why E.Coli get bigger if they replicate faster?

Rapidly dividing bacteria contain more than one bacterial chromosome, and often more than two. The chromosomes take large amount of space in the cytoplasm and also attach to the cytoplasmic membrane. More chromosomal DNA requires larger cytoplasmic surface area; larger surface, larger volume.


Parental care

What you call "parenting" is called "parental care" and "parental care" is any investment of the parent to improve the fitness of their offspring. Parental care can take many forms from niche building for the offspring to parental feeding passing by placing plenty of ressources in the egg.

Issue with the definition of parental care

Given the vastness and eventual lack of a strict enough definition of the concept of parental care, it will likely be difficult to really know what you would consider as being parental care. Below I am suggesting two possible cases. If you were expecting to another answer, you will need to provide a nice and strict definition of parental care.

Mutation rate

Under a very broad definition of parental care, one could argue that first examples of parental care would be found in very early organisms (bacteria/archae, eventually viruses) that would at some point (for a given lineage) reduce its mutation rate to ensure transmitting a good genome to its offspring cells.

Nutrients in eggs

If you feel unhappy with me using such a broad definition, you might want to consider the first examples of parental care as being the existence of anisogamy (see here), where females (by definition) produce large eggs filled with nutrients, proteins, mRNA and other things. I doubt we know what lineage first evolved but it could be an ascomycota eventually.


Determination of genes to be modified in epigenetics

Mutations are not performed targeting a specific new phenotype. There is no way an organism can "know" the impact of a specific future mutation anyway. A mutation is just a mistake in the replication process. As a consequence the majority of mutations are deleterious and only a handful of mutations are beneficial.

It is true though that the mutation rate can be affected by the environment or the stress induced by an individual (Agrawal 2002). It seems more intuitive that these are just a consequences of the cost of the DNA replication machinery and DNA repair machinery but it is not impossible that such changes in mutation rate could eventually evolve as a bet-hedging strategy. In the extreme case where the same types of environmental change happen over and over again, it is not impossible that a lineage could evolve the ability to modify the mutation rate at a particular locus. However, to my knowledge this has never been found.

You might want to follow an introductory course to evolutionary biology. You might also want to read this post too that gives a mixture of related information


I'm not sure if this is what you're asking for, but in the following image, allele K (or k) is linked to B while A (or a) and B are independent.

Again, this is just a guess because your question seems a bit unclear to me.


What are Some Classical Examples of Local Adaptation?

Adaptation is a change in a trait as a response to selection. As you ask for local adaptation I assume you want examples where sub-populations have either come under different selection and adapted differently, or cases where sub-populations have come under similar selection but not all have had the necessary genetic variation to evolve, i.e. selection has caused differentiation between sub-populations. Local adaptation can lead to varying degrees of divergence, so some for some examples it may be worth exploring speciation events. Here's some examples:

Galapagos Tortoises

There are two general shapes to the shell of tortoises on the Galapagos Islands. On islands with little low-lying vegetation the tortoises seem to have evolved long necks & limbs and different shell shapes which allow them to reach up more easily.

  "The shell distortion and elongation of the limbs and neck in saddlebacks is probably an evolutionary compromise between the need for a small body size in dry conditions and a high vertical reach for dominance displays."

Silent Crickets

Marlene Zuk has some very famous work on crickets that evolved to be silent on a Hawaiian island where parasitic flies were using the call as a targeting method. It's a great example of rapid adaptation occurring under observation in the wild. During the 1990's the population of crickets was in decline as a result of parasitism. At some point a mutation arose where the crickets no longer produced song, and this allele spread rapidly and cricket numbers bounced back strongly.

Other possible examples. Some of these are not "classical examples" but serve as interesting examples nonetheless.

Peppered moth colouration in response to the industrial revolution
Sickle cell anaemia and Malaria
Artificial selection in crops, livestock, and domesticated animals
Darwin's Finches
Antibiotic resistance in diseases; resitance to pesticides and herbicides; resistance to diseases unique to/more prevelant in sub-populations
Seasonal and continuous breeding by species present in both temperate and tropical climates
The Stephens Island Wren adapted to life without predators, and then failed to adapt to life with predators
Barn owl colouration across Europe
Predator-prey co-evolutionary dynamics as demonstrated by Guppies in Trinidad and Tobago
Drosophila melanogaster and adaptation to starch and maltose based foods
Adaptation to different salinity across gradients in marine organisms


This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.

Without further evidence/details, it's hard to narrow down to a species.

One possibility is Larinioides sclopetarius (the bridge spider or gray cross spider).

 Source: Ed Nieuwenhuys

 Source: Eurospiders.com

Description:

  Prosoma grey to grey-brown. Opisthosoma grey to grey-brown, dorsally with pronounced, white margined pattern. [Source: University of Bern]

See University of Bern for detailed drawings of anatomical structures.

Size: females = 10-14 mm ; males = 8-9 mm.
Web: orb webs can have diameters of up to 70 cm.
Ecology: often lives on briges or near water; often found on steel structures.
Range: holoarctic including Ottawa, Canada

What it's NOT

Although visually similar, this is not
Nuctenea umbratica (walnut orb-weaver)

 Source

This species is confined to Europe, Asia and Africa.

The specimen is also unlikely Larinioides ixobolus, which generally has a black outline (vs white) on their backs And is constrained to Europe/Asia:

 Source


Does the modern synthesis theory of evolution deny that acquired characteristics can be inherited?

Generally, yes, this is not part of theory of evolution as it is generally accepted by most of the scientific community.

For a trait to be subject to natural selection over several generations, it needs to have heritability, meaning it needs to show up in offspring (or their offspring). Generally, what is called an "acquired trait" does not fit that criterion. What's passed on is the genetic material of the parents and that doesn't change when the parent acquires these traits.

For example, bonsai trees are kept small by environmental conditions, as such, their height could be called an acquired trait. Their offspring does not naturally grow as a bonsai tree. Giraffes did not grow longer necks because they stretched them, but because those giraffe ancestors with longer necks (which just happens randomly through mutation - you have varying neck lengths in a population) could reach food more easily and could survive when those with shorter necks didn't. The giraffe example is a classic one that was proposed by Jean-Baptiste Lamarck, whose theory of evolution (called Lamarckism) was superceded by Darwin's.

There are traits where acquired versus genetic traits are hard to differentiate - while a good athlete does not have children who are athletic because their parent did sports, they are often also good athletes. For one thing, the parent might be genetically "suited" for sports and has passed these genes on. Another reason is that they will probably train their children and want them to become more athletic.

I know of one example where something that could be called an acquired trait is passed on to offspring - methylation patterns. Those are modifications of the genetic material that happen during an organism's lifespan and aren't modifications of the actual genetic code - they can be passed on to offspring. Since these patterns influence gene expression, they have an effect on the offspring. However, that's usually not what people mean when they talk about acquired traits.

Lamarckian inheritance


how is the plasma membrane repaired after endocytosis?

You have one misconception about the endocytosis: In the process no hole in the membrane is generated. It works in principle like in the figure below (it is of course more complicated, but this should explain it):

The membrane forms a vesicle around the particle which shall be integrated until it is completely surrounded by a membrane. At this point the vesicle is detached from the cell membrane and inside the cell. To accomplish internalization, the particle binds to certain receptors which regulate this process. See the Wikipedia for more details.

Exocytosis works in principle the other way round. Here are the visicles detached from the Golgi apparatus (mostly at least) and are directed to the cell membrane. Here the fuse with the membrane and form a pit which has its opening to the outside, releasing what was in the vesicle. It works like this (image from here):

In this process you have to differentiate between permanent unregulated exocytosis and regulated endocytosis (for example for the release of hormones) which are regulated by signal transduction pathways.


Did the eugenics program in Nazi Germany have a measurable effect?

As most of the comment have pointed it out, It's nearly impossible to find out. This is my try:

Dr. L Alexander wrote in his paper, Medical Science under Dictatorship:

  Hitler issued the first direct order for euthanasia in Germany on
  September 1, 1939, as his Panzers moved on the Blitzkrieg of Poland.
  Organizations with humanitarian-sounding names were immediately set up
  to execute "health" programs, again, under deceptively, euphemistic
  terms. For example, questionnaires collected by a "Realm's Work
  Committee of Institutions for Cure and Care" gathered and reported
  information on patients who had been ill five years or more and who
  were unable to work. "On the basis of name, race, marital status,
  nationality, next of kin, whether regularly visited and by whom, who
  bore financial responsibility, and so forth," decisions were made at
  key universities about which patients should be killed by
  psychiatrists who had themselves never seen the patients.Likewise, the
  "Realm's Committee for Scientific Approach to Severe Illness Due to Heredity and Constitution" was exclusively devoted to the killing of
  children with congenital anomalies or chronic illnesses. In all,
  275,000 people were put to death in these killing centers before the
  Nazi Holocaust.

Law for the Prevention of Offspring with Hereditary Diseases (July 14, 1933)

  Anyone suffering from a hereditary disease can be sterilized by a
  surgical operation if, according to the experience of medical science,
  there is a high probability that his offspring will suffer from
  serious physical or mental defects of a hereditary nature.    Anyone
  suffering from any of the following diseases is considered
  hereditarily diseased   under this law:

  1. Congenital mental deficiency,

  2. Schizophrenia,

  3. Manic-depression,

  4. Hereditary epilepsy,

  5. Hereditary St. Vitus’ Dance (Huntington’s Chorea),

  6. Hereditary blindness,

  7. Hereditary deafness,

  8. Serious hereditary physical deformity.

  Furthermore, anyone suffering from chronic alcoholism can be sterilized.

If anyone is trying to get the statistical evidence that Eugenics have even remotely successful, have look at this table:

Current Top 50 death causes of Germany. (Rate = $\frac{death}{1000}$)

They have started various ways to brainwash people, one of them was movies.

$\text{Ich klage an}$

(source: filmportal.de)

Plot: A woman suffering from multiple sclerosis pleads with doctors to kill her

Current Scenario: Germany Rank $18^{th}$ in the world in death due to Multiple sclerosis

Source:

Alexander L. Medical science under dictatorship. N Engl J Med 1949;July 14.
http://www.life.org.nz/euthanasia/abouteuthanasia/history-euthanasia6
Table: WHO, World Bank, UNESCO, CIA and individual country databases for global health and causes of death.


Why was cotton chosen to grow on the moon?

China's state-run Xinhua News Agency mentions the reasoning for most of the species they sent:

Why were these species chosen?
Xie [the chief designer of the experiment] said potatoes could be a major source of food for future space travelers. The growth period of Arabidopsis, a small flowering plant related to cabbage and mustard, is short and easy to observe. Yeast could play a role in regulating carbon dioxide and oxygen in the mini biosphere, and the fruit fly would be a consumer of the photosynthesis process.

While this doesn’t mention cotton, it seems very likely to me that, like potatoes, it’s just a very useful crop.
According to another article, the goal for China is a moon research base:

“We’ll use the Chang’e-8 to test certain technologies & do some preliminary exploration for jointly building a research base on the moon,” Wu said.


How can tooth enamel feel pain when drilled by a dentist?

Yes you are right. It is the dentin.
Enamel has got no nerves.
So when the dentist use his/her instrument, initially there is no pain (if the enamel is intact).
The next layer is dentin. As you said, dentin has got dentinal tubules containing dentinal fluid.
Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.

Reference

Reference

There are three main theories of dentine hypersensitivity:
Direct Innervation (DI) Theory
Odontoblast Receptor (OR) Theory
Fluid Movement/Hydrodynamic Theory

The Hydrodynamic or Fluid Movement theory is one of the main theories in dentistry to explain the mechanism by which a tooth perceives the sensation of pain. It is currently the most widely accepted theory used to explain tooth sensitivity.

Reference
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
Hence anaesthesia is required.
Hope I have answered your question :)


What is the evolutionary rationale for palm sweating?

As @Ben states, every theory of 'why' we evolve a trait is just a guess and never more than part of the story.   But there are theories.
The palms of our hands are a major source of heat transfer out of our body.  For bears it is the nose and pads of their feet, for dogs it is their toungue, for us a major portal for heat out of our body is the palms of the hands.

Black bears are extremely well-insulated animals, equipped with a heavy coat of fur and a thick layer of subcutaneous fat that help them maintain their body temperature as they hibernate through winter. But once spring arrives and temperatures rise, these same bears face a greater risk of overheating than of hypothermia. How do they dump heat without changing insulation layers?
Heller and Grahn discovered that bears and, in fact, nearly all mammals have built-in radiators: hairless areas of the body that feature extensive networks of veins very close to the surface of the skin.
Rabbits have them in their ears, rats have them in their tails, dogs have them in their tongues. Heat transfer with the environment overwhelmingly occurs on these relatively small patches of skin. When you look at a thermal scan of a bear, the animal is mostly indistinguishable from the background. But the pads of the bear's feet and the tip of the nose look like they're on fire.
These networks of veins, known as AVAs (arteriovenous anastomoses) seem exclusively devoted to rapid temperature management. They don't supply nutrition to the skin, and they have highly variable blood flow, ranging from negligible in cold weather to as much as 60 percent of total cardiac output during hot weather or exercise.

Given this, one could see how the palms of our hands are more likely to react to emotional situations where the heart rate elevates and sometimes we get hot under the collar.  The AVAs will
I am not physiologist, but the quote above comes from an article I stumbled upon a few months ago.  They use the AVAs to reduce the swelling associated with exercise and got some amazing results.  I guess that's another story though.


How significant is RNA degradation with removal of cap/polyA's in eukaryotes, or UTR's in prokaryotes?

Removal of 5' cap is essential for degradation by 5'→3' exonucleases such as Xrn1/2. Xrn1/2 is constitutive and degradation of uncapped RNAs would be quite fast (don't have a reference for the exact lifetime). Deadenylation generally precedes 3'→5' degradation by exosome but I am not sure if that is a prerequisite. However tailless mRNAs can be stabilized by tethering Pab1p (Poly-A binding protein) to the 3'UTR. See this paper.

Figure 4 of the linked paper.

  Tethered Pab1p stabilizes mRNAs that do not receive a tail. (A)
  Strategy. The HDV self-cleaving ribozyme was inserted into the 3′ UTR
  of MFA2/MS2 RNA, yielding an mRNA without a poly(A) tail (A0) in vivo.
  (B) Oligo(dT) cellulose chromatography. RNAs were extracted from cells
  carrying the ribozyme-containing construct depicted inA, or the
  control plasmid used in previous figures. RNAs were fractionated by
  oligo(dT) cellulose chromatography, then analyzed by Northern
  blotting. The ribozyme-containing RNA is not retained by the column,
  whereas the control RNA is retained. (T) Total RNA prior to
  fractionation; (+) retained by the column; (−) not retained by the
  column. The mRNA runs slightly faster in the oligo(dT) retained (+)
  sample than in the total (T) RNA, because less RNA is loaded per lane.
  (C) S1 nuclease analysis. The 3′ end of mRNA prepared from a strain
  carrying the ribozyme-containing RNA was determined by S1 nuclease
  mapping. The position of undigested probe (65 nucleotides) and of the
  protected species (43 nucleotides) are shown. The prominent 3′
  terminus lies at the expected position for ribozyme cleavage. (D)
  Decay of ribozyme-cleaved RNA by a transcriptional pulse-chase
  experiment and Northern blotting. The turnover rate of
  ribozyme-cleaved reporter mRNAs was determined in strains with (left)
  or without (right) MS2/Pab1p. Time (in min) following transcriptional
  repression are given directly at top; half-lives are at bottom. (E)
  Quantitation of results. Amounts of mRNA were normalized to the level
  of 18S rRNA, at bottom of each lane in D. (•) MS2/Pab1p; (○) vector
  alone.

Prokaryotic UTRs do not have any general paradigm. To have a controlled inactivation of a mRNA in a prokaryotic system you can use riboswitches or  cis-repressive RNA (RBS complementary RNAs). RNA-guided RNA degradation is also possible in prokaryotes using the CRISPR-Cas system. See this paper. Proteins Cmr-1,2,3,4 & 6 are required for this activity.


Do all gene mutations in pathogens lead to more harmful consequences for humans?

Mutations are random; the (pathogenic) bacteria (or any living being) will randomly acquire mutations that may be beneficial, deleterious or neutral to its fitness. Only beneficial and neutral mutations will survive the selection. Random mutations and survival of the fittest are not two independent mechanisms. The random mutations can alter the fitness as I mentioned and natural selection ensures the survival of the fittest.

Many pathogens have reduced genome (number of genes) compared to their free living relatives (Weinert and Welch, 2017). This is because they lack most of the genes required for synthesis of different metabolites required for survival. They rather obtain these metabolites from the host and hence they have the parasitic lifestyle. It is not possible for the pathogens to acquire that many genes to stop being pathogenic and become a free-living organism. It may be possible via lateral gene transfer wherein a bacteria may obtain an entire gene (or a set of genes) from another bacteria but the likelihood of that happening to convert a pathogenic bacteria to a non-pathogenic bacteria is negligible.

It is certainly possible that pathogens might lose the activity of some of the pathogenic genes (for example those required for toxin production) due to mutations. However, they may no longer be efficient pathogens and would be outgrown by the others who still retain those genes.


Dataset of microscopic images before and after staining?

Virtual fly brain (http://www.virtualflybrain.org/site/stacks/index.htm) is an excellent database of fly (Drosophila) brain sections, which can be electronically processed/annotated/highlighted on the fly to show different areas of the fly brain as an overlay on top of the original images.

Alternatively, you can use BrainTrap (http://fruitfly.inf.ed.ac.uk/braintrap/) for the expression of proteins in the fly (Drosophila) brain using brain sections. Another database which has silver stains of Drosophila brain sections is the flybrain (http://flybrain.neurobio.arizona.edu/Flybrain/html/atlas/) database. This database also contains 3D models of different fly brain structures and much more!

I'm sure there are many many similar databases, but these are the ones I knew of, which are widely used in the Drosophila community.


It is C. During S-phase the DNA of each chromosome duplicate and the two sister chromatids formed get attached by cohesin proteins. These sister chromatids separate at Anaphase-II of Meiosis.

From wikipedia:

  A sister chromatid refers to either of the two identical copies (chromatids) formed by the replication of a single chromosome, with both copies joined together by a common centromere. In other words, a sister chromatid may also be said as 'one-half' of the duplicated chromosome. A full set of sister chromatids is created during the synthesis (S) phase of interphase, when all the chromosomes in a cell are replicated.


What tool to use to map reads (samtools, sequencher,...)?

Samtools is not an aligner; it is used to analyse alignments. FastQC is for analysing the read qualities and average composition. You can get to know the adaptor sequence by running FastQC.

The next step is adaptor trimming. There are many tools that do that. Trimmomatic is currently popular. You can find the adaptor composition of each read by subtracting the read length post trimming from the read length pre-trimming (this would be same for all reads).

Then you have to align your trimmed reads to a reference, using an aligner. Again, there are many aligners available; Bowtie, STAR and now a new one called HISAT. STAR and HISAT are faster than Bowtie.

Since you already have the alignments (aln.bam) to hg19, you do not need to perform alignment. You want to know, to which genes do these reads map to. This information is not available unless you have the genome annotations. The annotations are available in the form of GTF/GFF files. You can obtain the association between genomic locations and the reads using the BEDOPS toolkit as mentioned in this Biostars post.

I don't have much experience with this tool. What I would do is convert the BAM to SAM (using samtools) or to BED (using bedtools:bamtobed) and parse the columns of the SAM/BED file describing the read locations with the GTF file. See this link for the details on the SAM format. You can use any scripting language like awk or perl to parse.

Samtools does have an option to filter the reads according to regions specified in the BED format but it will not automatically annotate them.

samtools view -hL regions.bed aln.bam > aln_filtered.sam


Is there any completely Computation Drug ever launched in market?

Yes, there are a few. Mostly they are designed in combination with X-ray crystallography of the target which should be inhibited. Then molecules are designed which fit specifically into these targets.

The oldest example I could find is Dorzolamide which acts as a carbonic anhydrase inhibitor. See here: "Application of the three-dimensional structures of protein target molecules in structure-based drug design."
Some more examples are names in the Wikipedia article on drug design.

While looking for an example, I found these articles, which also look interesting:

Molecular Modeling and Computer Aided Drug Design. Examples of their
Applications in Medicinal Chemistry
Computer-based de novo design of drug-like molecules
Recent advances in computer-aided drug design

I am also not sure, to what extent the modern small molecule inhibitors like Vemurafenib (PLX4032) and others are designed using computers. At least to some extent this should be true.


Does sample buffer require EDTA for protein separation on SDS PAGE?

EDTA is a complexing agent for bivalent cations and is usually used to inhibit enzymes (proteases, nucleases) which need these ions in their active center to work. Without it they do not attack the sample.

The presence of EDTA in the sample buffer is interesting, since Laemmli's original paper from 1970 ("Cleavage of structural proteins during the assembly of the head of bacteriophage T4.") doesn't use it and I think it is not necessary.

The reason for this is simple: Protein samples are usually generated in buffers which contain different protease inhibitors, which protects the samples. Additionally the purpose of the sample buffer is to denaturate (at least for the standard SDS gels) the protein sample completely, so it will run uniformly. Both steps ensure that proteases are either inhibited or completely denaturated, which will both protect the sample.

The only reason I can think of for using EDTA is that it can help to destabilize your target protein, when a co-factor which is important for the structure is complexed by EDTA and thus keep it in solution after the denaturation.

There are of course ressources which state that EDTA is necessary for protein integrity, but they only say it is there to inhibit proteases by complexing metal ions (see here for example).

As a 2x sample buffer, I use the following recipe (this can also be made 5x if necessary), which contains EDTA, but can also be done without. If you prefer β-Mercaptoethanol, you can use it in the same concentration as the DTT (which has the advantage of being less smelly):

2x sample buffer:

4% SDS
20% glycerol
2 mM EDTA (ethylene diamine tetraacetic acid) - can be made without
100 mM Tris-Cl, pH 6.8
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye


The Cicada

A careful study of the noise-making apparatus of the cicada can be found in a 1994 paper by Young and Bennet-Clark.$^1$ The authors generated sounds at about 0-16 kHz at peaks on the order of 100 dB using cicadas in various stages of deconstruction.  The cicada uses a resonant organ-system called the tymbal which buckles and unbuckles rapidly to produce sound. The buckling-in is caused by muscle contraction and is louder than the buckling-out (relaxation) phase. Air sacs (a feature of many other small noisemakers) serve to amplify the sound.  The tymbal itself, for the species in this paper, has a resonant frequency of about 4kHz (Young, page 1017). The song of the cicada as modified/amplified by air sacs and other structures, is often around 10kHz.$^{2}$

Pure Tone vs. Diffuse Tone?

The vocalizations of large vertebrates are a complex superposition of waves that in the frequency spectrum are somewhat spread out. To the extent that a frog or a bird emits a pure tone, the energy will be confined to a narrow frequency range and this may be a strategy for achieving greater amplitude. Given comparable audio sensitivity, however, the intensity of pure tones will depend on amplitude (intensity), regardless of frequency.$^{3,4}$

Other Small Loud Animals

While the songs of cicadas are intense, especially in concert, on an individual level there is competition from other species. According to a Gizmodo article quoting assorted scientists, the snapping shrimp produces a transient snap that is around 200 decibels, a level that one site describes as "deafening." For perspective, dolphins can emit short chirps of 220 dB but these are outside the range of human hearing. The lion emits a roar of 115 dB which is sustained and audible 5 miles away, according to the article. Elephants also are capable of 117 dB cries, as are howler monkeys.

Both the shrimp and the cicada use non-vocal vibration to create their sounds. The shrimp uses a "spring-loaded claw" (the spring is muscle). The localized force of one part of the claw hitting the other generates a bubble (this is known as inertial cavitation). When the bubble collapses it generates a shock wave (noise) that stuns fish (prey).$^5$ The noise of frogs is produced as air passes from the lungs through the larynx, amplified by distended air sacs which resonate. Birds can produce up to 135dB (the Mollucan Cockatoo). They generally force air past (membranes and) a specialized organ called the syrinx located at the bottom of the trachea (see the Wikipedia note on bird vocalization).

Micronecta scholtzi, a 2mm-long aquatic insect, is for its size the loudest known animal. It creates a sound of 99.2 dB intensity which (despite being largely lost in transition from water to air) is audible to humans ashore. According to the Wikipedia note it creates this sound by "stridulating a ridge on its penis across corrugations on its abdomen." The area involved is about 50$\mu m$ across. Details of the mechanism are poorly understood. The article's comparison of the sperm whale's 236 (underwater) dB song gives perspective, as a sperm whale can weigh 14 metric tons.

A Common Aspect of Sound Intensity: Cavity Resonance

Descriptive studies of sound-creation by small animals (with the possible exception of the snapping shrimp) do not fully explain why a one-gram bug can make a bigger noise than a lion. Purely vocal methods of larger vertebrates produce sustained noise on the order of 100 dB but the non-vocal instruments of smaller creatures are capable of short bursts of amazing intensity.

It is difficult to generalize but because air sacs are part of many sound-making schemes, cavity resonance probably plays an important role. Like spring-mass systems or RLC circuits, cavities have resonant frequencies at which amplitude of a signal may be increased (the policeman's whistle is a familiar example). Another paper by Bennet-Clark and Young gives a sketch of a theory along these lines. At resonant frequencies the impedance of the instrument falls sharply and instead of being dissipated (generally as heat) the energy emerges as sound.$^6$

$^1$ Bennet-Clark and Young, The Role of the Tymbal in Cicada Sound Production, J. of Experimental Biol. (1995) 198, 1001-1019.

$^{2}$ The frequency of cicadas is variable, mostly on the order of 10kHz but occasionally very low (< 1kHz), mostly due to body size. See this article.

$^3$ Sound--essentially a compression wave--diminishes with distance. So when the Wiki article on noise levels compares noise levels it includes the distance from the object. For example, 100 db (comparable to the cicada) is the level of noise associated with a jack-hammer at 1 meter away.

$^4$ Audible range for humans is roughly 15 Hz-16000 Hz. As mentioned below, the dolphin can emit very intense high-pitched sounds that we don't hear at all, so the analogy to EM waves (higher frequency = higher energy) doesn't help predict perception. See Pfaff and Stecker, Loudness and Frequency Content of Noise in the Animal House, Lab. Animals (1976) 10, 111-117.

$^5$ M. Versluis, B. Schmitz, A von der Heydt & D. Lohse (2000). "How snapping shrimp snap: through cavitating bubbles". Science 289 (5487): 2114–2117.

$^6$ Bennet-Clark and Young, Short Communication, The Scaling of Song Frequency in Cicadas, J. Exp. Biol. 191, 291-294 (1994).


Protein structures given in PDB and SNP's

Swiss PDB Viewer allows you to mutate residues in an existing structure and explore the effects.

I'm pretty sure that UCSF Chimera does too.


The midpiece has a central filamentous core with many mitochondria spiralled around it, used for ATP production for the journey through the female cervix, uterus and uterine tubes. This is a good article explaining more about this topic: http://genetics.thetech.org/ask-a-geneticist/mtdna-comes-only-mom


Do I need primers if ordering from a DNA synthesis provider

Only if you intend to subsequently amplify the DNA you've ordered. I tend to never fully trust anything I don't confirm myself so primers to sequence the insert in the construct they give you might not be a bad idea either.


What did cyanobacteria gain from photosynthesis?

But cyanobacteria do not seem to use polysaccharides in the same way as plant cells do (building materials, for example)

The Calvin-Benson cycle produces glucose which is the starting
material for a lot of biosynthetic pathways including that of the
nucleotides (ribose from the pentose-phosphate pathway). Glycolytic intermediates are also involved in the synthesis of amino
acid, isoprenoids etc. Essentially all the carbon that cyanobacteria
contains comes from fixation of carbon (from CO2) via
photosynthesis.
Cyanobacteria also store starch as an energy reserve (Suzuki et
al., 2013). They also produce other polysaccharides (Phillipis
and Vincenzini, 1998). Moreover, the peptidoglycan cell wall has a "glycan" part which is a glucose derivative (a polysaccharide).
Moreover, cyanobacteria cannot produce ATP via the photosynthetic
electron transport chain in the dark and ATP in dark conditions
is generated (though significantly less) via substrate level phosphorylation in glycolysis.


Why does autosomal trisomy have more adverse effects than sex choromosome monosomy or trisomy?

It has to do with dosage compensation:

The Y chromosome contains relatively few genes. Interestingly, chromosome 21 and 18, which are over represented in the most common viable trisomies, are also relatively small.
Humans already possess a mechanism to compensate for additional X chromosomes: X-inactivation. Normally this inactivates one of the two X chromosomes in females but can also inactivate two in cases of X trisomy.

  Humans are much more able to tolerate extra sex chromosomes than extra autosomes. … Compared to autosomal trisomies, … sex chromosome trisomies are fairly benign. Affected individuals generally show reduced sexual development and fertility, but they often have normal life spans, and many of their symptoms can be treated by hormone supplementation. The ability of humans to tolerate supernumerary sex chromosomes is quite remarkable, as individuals can survive with as many as four sex chromosomes. This tolerance most likely relates to both X inactivation and to the small number of genes on the Y chromosome. In fact, when cells from individuals with more than one copy of the X chromosome are analyzed under a microscope, all but one of the X chromosomes appear as condensed Barr bodies, the cytological manifestations of X-chromosome inactivation. Supernumerary copies of the Y chromosome may be tolerated because the few gene products of the Y chromosome are not required for survival.

From: Chromosomal Abnormalities: Aneuploidies by Clare O'Connor (emphasis added)

An added bonus (and I feel as though I should actually write something myself), I recently read a paper studying trisomy 21:

Jiang J, Jing Y, Cost GJ, Chiang JC, Kolpa HJ, Cotton AM, Carone DM, Carone BR, Shivak DA, Guschin DY, Pearl JR, Rebar EJ, Byron M, Gregory PD, Brown CJ, Urnov FD, Hall LL, Lawrence JB. 2013. Translating dosage compensation to trisomy 21. Nature 500(7462):296-300.

Using zinc finger nucleases, they inserted a XIST transgene into chromosome 21 of cells derived from Down syndrome patients. XIST is a gene centrally involved in X-inactivation. They found that, by inserting it into chromosome 21, they were able to silence one and revert the trisomic cells to a more normal phenotype.


Why can't bacteriophages survive inside the human body thus negating the possibility of using them against bacteria?

This question cannot be answered, because the assumption behind your question is wrong. I haven't found a source to claim that bacteriophages cannot survive in the human body. Bacteriophages can and are, in fact, used as a treatment against human bacterial infections, it's called "phage therapy" (1,2,3).

This is, nevertheless, a rather uncommon procedure for a number of reasons:

Availability: Compared to antibiotics, which you can easily get from any doctor/pharmacy, phage therapy requires special facilities, because very specific phages need to be produced for each disease.
Safety and regulation: Virus handling requires special safety measures and using them in humans requires a lot of paperwork, safety tests and clinical trials.
Money: Due to the reasons above, phage therapy is a lot more expensive than antibiotics.
Lack of research: Thanks to the availability of antibiotics there was no urgent need to develop the application of phage therapy. We know comparably little about how the immune system might react to bacteriophages in the blood or bacterial toxins released by lysed bacteria. We haven't found a way to e.g. quickly engineer bacteriophages for diseases.

With a growing concern about multi-drug resistant bacteria, developing new ways to combat diseases has become more important. Maybe phage therapy will be one way to deal with this more regularly in the future.


Would prehistoric humans have been considered negroid or australoid by modern standards?

The first question to answer might be: Has phenotypic diversity in humans increased or decreased since prehistory?  It might be the case that prehistoric humans were as diverse as modern humans, or more so, since there have been a number of diversity-reducing bottlenecks in our evolution.


Activation of Glycogen Synthesis by Insulin - mechanism and cellular location?

Insulin, like glucagon, binds to receptors on the surface of muscle cells and illicits a response that is transduced to produce changes of phosphorylation in the enzymes controlling glycogen turnover. Unlike glucagon it does not initiate an enzyme phosphorylation cascade, but its binding to the receptor causes autophosphorylation on tyrosine residues, resulting in protein–protein interactions which lead to the activation of various enzymes through subsequent phosphorylations.

I would recommend you go to Berg et al. in NCBI Bookshelf online — rather than Wikipedia — for this kind of thing. It is a best-selling biochemistry textbook which is produced with great care (even if the edition online is out of date). Thus in Section 21.5.2 you will find:

  How is glycogen synthesis stimulated? As stated earlier, the presence of glucagon signifies the starved state and initiates glycogen breakdown while inhibiting glycogen synthesis. When blood-glucose levels are high, insulin stimulates the synthesis of glycogen by triggering a pathway that activates protein phosphatase 1 (Figure 21.20). The first step in the action of insulin is its binding to a receptor tyrosine kinase in the plasma membrane. Multiple phosphorylations again serve as the instigation for a regulatory wave of dephosphorylations. The binding of insulin to its receptor leads to the activation of an insulin-sensitive protein kinase that phosphorylates the RGl subunit of PP1 at a site different from that modified by protein kinase A. This phosphorylation leads to the association of the RGl subunit with PP1 and the glycogen molecule. The consequent dephosphorylation of glycogen synthase, phosphorylase kinase, and phosphorylase promotes glycogen synthesis and blocks its degradation.

I am assuming that you are familiar with the pathways of glycogen synthesis and breakdown. (If not, search for this in Berg et al.) At the risk of violating copyright, I reproduce Figure 21.20 below:

You can read more about the insulin receptor in Section 15.4.1 of Berg et al.

Addendum

Insulin also affects glycogen synthesis indirectly by stimulating/activating the glucose transporter, GLUT4. The mechanism by which this is accomplished is less well established than that described above.


Is the number of protons in the mitochondrion sufficient for ATP synthesis?

The question, as amended, can be summarized as:

  If there are 2–8 protons in the mitochondrial matrix (as calculated
  from a pH of 8) is this sufficient for ATP synthesis, if 2–3 hydrogen
  ions are required for each molecule of ATP synthesized?

The initial deficiency in the argument was that it did not consider the inter-membrane space, and my answer was:

According to the generally accepted Mitchell Hypothesis, the generation of ATP in the
mitochondrion is due to an electrochemical gradient between the
mitochondrial matrix and the inter-membrane space.
This gradient is predominantly a pH gradient — the [H+] is
higher in the inter-membrane space than in the matrix
The flow of protons down this gradient is responsible for the
production of ATP.
The H+ gradient is maintained by protons being pumped across the inner mitochondrial membrane by the flow of electrons through the electron transport chain. (i.e. The H+ concentration is kept low in the matrix and high in the inter-membrane space, even though protons are continually flowing into the matrix.

i.e. For ATP synthesis to occur there is no requirement for a high steady-state concentration of hydrogen ions in the mitochondrial matrix — quite the opposite (as is reflected by the pH 8). A relatively high concentration of hydrogen ions is only required in the inter-membrane space — as is indeed found.

The amended question assumes a pH of 6.8 for the inter-membrane space, and calculates 8.9 protons to be in this compartment.

The poster still does not state specifically what the problem is — there is still a concentration gradient of hydrogen ions, and a vast body of experimental evidence shows that it is this gradient of hydrogen ions that drives ATP synthesis.

So the implied question does not seem specific to ATP generation, but to the concept of pH in cellular compartments of small volume. There is obviously something wrong here, and the paper quoted — which addresses this question — suggests some possible explanations:

That the pH measured is incorrect because of the methodology
That the hydrogen ions are not free but associated with negatively charged species (possibly phosphate ions) from which they may be released, as required.

The latter point had occurred to me before reading the paper. In summary:

The steady-state hydrogen ion concentration gradient is sufficient to drive ATP synthesis, with many hydrogen ions at any time passing through the membrane in one direction or another.
Many of the hydrogen ions in both compartments will be buffered in a manner that allows there release
The naive calculation is likely to be an underestimate because the pH in the inter-membrane space may be much lower.

If I were an ox-phos person I would know how many molecules of the ATP synthase complex there are per mitochondrion and the number of protons pumped into the membrane space per unit time. Such information would, presumably, bear on the problem.


Why are there two abrupt changes in the genome sequencing price curve?

This graph from the Broad's Opinionome blog (ugh) is somewhat more annotated:

As noted elsewhere, the precipitous drop in 2007 is almost certainly due to maturing next-gen sequencing (NGS), in particular Illumina.  Illumina acquired Solexa in 2007, which offered gigabase-level sequencing ability.  In 2014, President of Illumina Francis de Souza essentially said as much:

  During the EmTech conference, De Souza said Illumina’s success was due to a “hard pivot” the company made in 2006, when it got into the DNA sequencing business by acquiring Solexa, a U.K. startup, and bet its fortunes “on a technology with no sales, that no one knew if it would work.”

Essentially, by 2007/2008 you had stellar technology+company hard-selling it = adoption

I'm less certain about the less-dramatic drop in 2014/2015, but I agree with Franck that it's likely largely be due to the introduction of the Illumina HiSeq X Ten in early 2014.  You can read some corporate spam, but it was indeed a big deal.  There were other technologies that probably played a role (new PacBio system released in 2013, etc.) but Illumina was and is top-dog.

None of this takes into consideration increased interest in such research, or the faster computers, larger SSDs, and expansion/normalization of multi-core systems that makes working with such data easier.


Photosynthesis results into formation of a carbon skeleton (a 3C or 6C skeleton). These newly formed carbon skeleton can be used to form a large number of bio-molecules which are required by a cell. For example the glucose can enter into aerobic respiration and the intermediates thus formed are used for synthesis of several molecules.

As you can specifically see from the above figure, alpha ketoglutarate is converted into glutamate which is then used for synthesis of proteins.

Alpha ketoglutarate is a keto acid can easily be aminated to give rise to amino acid.


Is there any alternative to x-gal white/blue screening for the monitoring of pseudomonas aeruginosa beta-galactosidase activity on agar plate?

I think your problem will be even worse when you'd use MacConkey or Endo plates. You can see differences between different kinds of bacteria / expression of certain enzymes on those plates, but the coloring / decoloring is based on soluble compounds that easily diffuse.

Hydrolysis of xgal creates an insoluble product that's staying more or less at your colony. Of course it's not perfect and after a while you have a completely blue plate, but this would happen much faster with a soluble compound.

Try adjusting your conditions so you can look at the plate before it's completely blue. Things you could try: look earlier, plate them a little bit more dilute so colonies are further apart, use less xgal so your final coloring is less intense, look for some papers that use xgal for screening and steal their tricks.


Multiple sequence alignment - how to align everything to 1 gene sequence?

Your question is not very clear, but I think what you are trying to do is align sequencing results to a reference gene sequence.

Your total gene sequence spans ~2500 bp. It sounds like you have a forward sequence at the start of gene, reading only about 1000 bp and the reverse strand reading in 1000 bp from the end (if this is Sanger sequencing, you likely only have 800-900 bp of accurate base reads by the way). Therefore, you have a gap of about 500 bp in the middle of your gene of interest.

There are (at least) two ways to do the alignment, and I would suggest the manual method if you are trying to verify gene sequencing.

Manual Method:

In a word processing document, paste in your gene-of-interest (or the recombinant gene you are trying to make), as well as the base reads from the forward strand, and the reverse complementof your reverse strand. Make sure you remove any whitespace like line breaks and spaces as this will disrupt the rest of the process.
Manually select a small portion of your forward read (20-30 bp for example) and search for the same "phrase" in your gene-of-interest. If you find it, highlight it in both the sequence it came from and the gene-of-interest so that you know you have already matched them.
Carry on with adjacent bases for the forward strand. Repeat for the reverse complement of the reverse strand.

Semi-Automated Method:

Go to NCBI Blast, and under the heading Basic Blast, click "nucleotide blast".
Check "Align 2 or more sequences."
Enter your Query Sequence as your 1000 bp sequences, entered in FASTA format. FASTA format will allow you to enter multiple sequences, but if you just enter one at a time, that will work perfectly well. Results will only display one at a time anyway.

For example:

> sequence name here
ATCGATCGATCGATCGATCGATCG....

Enter your gene of interest as your Subject Sequence. Format does not matter here, but for consistency, I use FASTA format.
Keep "Highly similar sequences (megablast)" selected. You shouldn't need to play with these parameters, they just change how the alignment method penalizes alignments for gaps and mismatches.
Hit BLAST.
Interpret your results. I've included an example of BLAST results below.

At the top of this window is a schematic, showing exactly how much of the the query sequence aligns with the subject sequence. The longer the line, the more bases align. Similarly, the closer the colour of the line is to right of the scale (e.g., red), then the more continuous the segment is indicating a longer, continuous alignment.

Below the graphic is a table of results. Briefly, the table highlights all possible alignments that the BLAST algorithm has found, including how much coverage there was, confidence of the alignment and length of alignment coverage.

Below the results table, are the detailed results which were summarized in the table. This detailed report shows you exactly which bases align or mismatch, or any gaps. The top line is the subject sequence; the bottom is the query sequence. The other thing to keep in mind here is the Strand line. In this case, it says "Plus/Plus, meaning that the aligned sequences were the forward sense, or plus strand, of each of subject and query sequence, respectively. If you entered a reverse complement sequence instead (such as the reverse sequencing results) then this would change to "Plus/Minus".

From here, you will still need to manually line these results up to your gene of interest to determine exactly which portion of the gene is missing sequence coverage, as well as any mutations that may have cropped up in the cloning process.


That is not a bed bug. The picture is rather poor, which makes an ID difficult, but I think it might be the beetle Ptinus fur (spider beetle), or another species from the same genus. This species is found all over the world, and often indoors (they can e.g. feed on dry foods).

Reasons for this suggestion is the body shape (incl relatively hidden head), color ("reddish"),long legs with thick femurs, long hind legs, and long antenna. The long legs together with the long antenna (the antenna can look similar to a fourth set of legs), as well as the hidden head (so the body look two-segmented) is what makes it look somewhat like a spider .

(picture from bugguide.net)

(from weedimages.com)


Food allergen-related skin reactions and intestinal inflammation?

Afaik the most probable trigger of IBDs (Crohn's, colitis ulcerosa) are changes in the gut microbiota due to western lifestyle (high intake of some nutrients e.g. milk fat). These changes cause an inflammation in the susceptible (genetic factors) people. So the cause of IBDs is very likely not an allergic reaction.

According to wikipedia IBS is not an IBD (inflammatory bowel disease). It is a functional disorder of the bowel, so not so serious as the IBDs. Its possible causes are low grade inflammation of the bowels and neuroendocrine disregulation. It has genetic factors as well. The pathomechanism is not fully understood yet.

There are many bowel diseases which can be caused by specific foods, e.g. celiac disease, lactose intolerance, and so on, the list is long, many of them can be caused by food protein intolerance. It is my understanding of protein sensitivity that skin conditions are caused by B-cell (IgE) mediated immune response, while bowel conditions are caused by T-cell mediated immune response. Ofc. there is connection between them, so it is possible that a certain type of protein induces skin symptoms and intestinal symptoms as well. Based on the current studies I think food sensitivity is not related to IBDs, and probably not related to IBS as well.

  CD is associated with dramatic changes in the gut microbiota and this
  was particularly evident for individuals with ileal CD.

2008 - Molecular analysis of the gut microbiota of identical twins with Crohn's disease

  Molecular profiling of faecal bacteria revealed abnormalities of
  intestinal microbiota in UC and IBS patients, while different patterns
  of Bacteroides species loss in particular, were associated with UC and
  IBS.

2010 - Ulcerative colitis and irritable bowel patients exhibit distinct abnormalities of the gut microbiota

  Breakdown of the normal microbial community increases the risk of
  pathogen infection, the overgrowth of harmful pathobionts and
  inflammatory disease. Understanding the interaction of the microbiota
  with pathogens and the host might provide new insights into the
  pathogenesis of disease, as well as novel avenues for preventing and
  treating intestinal and systemic disorders.

2013 - Role of the gut microbiota in immunity and inflammatory disease
2014 - Role of the gut microbiota in inflammatory bowel disease
pathogenesis: What have we learnt in the past 10 years?

  Crohn's disease and ulcerative colitis are idiopathic, chronic,
  relapsing, inflammatory conditions that are immunologically mediated.
  Although their exact etiologies remain uncertain, results from
  research in animal models, human genetics, basic science and clinical
  trials have provided important new insights into the pathogenesis of
  chronic, immune-mediated, intestinal inflammation. These studies
  indicate that Crohn's disease and ulcerative colitis are heterogeneous
  diseases characterized by various genetic abnormalities that lead to
  overly aggressive T-cell responses to a subset of commensal enteric
  bacteria. The onset and reactivation of disease are triggered by
  environmental factors that transiently break the mucosal barrier,
  stimulate immune responses or alter the balance between beneficial and
  pathogenic enteric bacteria. Different genetic abnormalities can lead
  to similar disease phenotypes; these genetic changes can be broadly
  characterized as causing defects in mucosal barrier function,
  immunoregulation or bacterial clearance. These new insights will help
  develop better diagnostic approaches that identify clinically
  important subsets of patients for whom the natural history of disease
  and response to treatment are predictable.

2006 - Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis.
2011 - Proinflammatory Cytokines in the Pathogenesis of Inflammatory Bowel Diseases
2014 - Role of Regulatory B Cells in Chronic Intestinal Inflammation: Association with Pathogenesis of Crohn's Disease
2013 - Effects of Enteral Nutrition on Crohn’s Disease: Clues to the Impact of Diet on Disease Pathogenesis

  The composite human microbiome of Western populations has probably
  changed over the past century, brought on by new environmental
  triggers that often have a negative impact on human health1. Here we
  show that consumption of a diet high in saturated (milk-derived) fat,
  but not polyunsaturated (safflower oil) fat, changes the conditions
  for microbial assemblage and promotes the expansion of a
  low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2.
  This was associated with a pro-inflammatory T helper type 1 (TH1)
  immune response and increased incidence of colitis in genetically
  susceptible Il10−/−, but not wild-type mice. These effects are
  mediated by milk-derived-fat-promoted taurine conjugation of hepatic
  bile acids, which increases the availability of organic sulphur used
  by sulphite-reducing microorganisms like B. wadsworthia. When mice
  were fed a low-fat diet supplemented with taurocholic acid, but not
  with glycocholic acid, for example, a bloom of B. wadsworthia and
  development of colitis were observed in Il10−/− mice. Together these
  data show that dietary fats, by promoting changes in host bile acid
  composition, can markedly alter conditions for gut microbial
  assemblage, resulting in dysbiosis that can perturb immune
  homeostasis. The data provide a plausible mechanistic basis by which
  Western-type diets high in certain saturated fats might increase the
  prevalence of complex immune-mediated diseases like inflammatory bowel
  disease in genetically susceptible hosts.

2012 - Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice

  The pathogenesis of IBS seems to be multifactorial, with the following
  factors playing a central role in the pathogenesis of IBS:
  heritability and genetics, dietary/intestinal microbiota, low-grade
  inflammation, and disturbances in the neuroendocrine system (NES) of
  the gut

2012 - Irritable bowel syndrome: Diagnosis and pathogenesis
2014 - Melatonin Regulation as a Possible Mechanism for Probiotic (VSL#3) in Irritable Bowel Syndrome: A Randomized Double-Blinded Placebo Study
2012 - Irritable Bowel Syndrome: Methods, Mechanisms, and Pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome


I believe it is a Red Wag Platy (Xiphophorus maculatus)


How do a particular arrangement of atoms become self aware?

You are skipping too many steps.
$Atom \rightarrow \color{red}{molecule \rightarrow structure \rightarrow cell} \rightarrow organ \rightarrow organism$
The following is a proposed speculation regarding the steps in red on the above:

How life originated and how the first cell came into being are matters of speculation, since these events cannot be reproduced in the laboratory. It was first suggested in the 1920s that simple organic molecules could form and spontaneously polymerize into macromolecules under the conditions thought to exist in primitive Earth's atmosphere. At the time life arose, the atmosphere of Earth is thought to have contained little or no free oxygen, instead consisting principally of $CO_2$ and $N_2$ in addition to smaller amounts of gases such as $H_2$, $H_2S$, and $CO$. Such an atmosphere provides reducing conditions in which organic molecules, given a source of energy such as sunlight or electrical discharge, can form spontaneously. The spontaneous formation of organic molecules was first demonstrated experimentally in the 1950s, when Stanley Miller (then a graduate student) showed that the discharge of electric sparks into a mixture of $H_2$, $CH_4$, and $NH_3$, in the presence of water, led to the formation of a variety of organic molecules, including several amino acids.

Although Miller's experiments did not precisely reproduce the conditions of primitive Earth, they clearly demonstrated the plausibility of the spontaneous synthesis of organic molecules, providing the basic materials from which the first living organisms arose.
The next step in evolution was the formation of macromolecules. The monomeric building blocks of macromolecules have been demonstrated to polymerize spontaneously under plausible prebiotic conditions. Heating dry mixtures of amino acids, for example, results in their polymerization to form polypeptides. But the critical characteristic of the macromolecule from which life evolved must have been the ability to replicate itself. Only a macromolecule capable of directing the synthesis of new copies of itself would have been capable of reproduction and further evolution.
Of the two major classes of informational macromolecules in present-day cells (nucleic acids and proteins), only the nucleic acids are capable of directing their own self-replication. Nucleic acids can serve as templates for their own synthesis as a result of specific base pairing between complementary nucleotides. A critical step in understanding molecular evolution was thus reached in the early 1980s, when it was discovered in the laboratories of Sid Altman and Tom Cech that RNA is capable of catalyzing a number of chemical reactions, including the polymerization of nucleotides. RNA is thus uniquely able both to serve as a template for and to catalyze its own replication. Consequently, RNA is generally believed to have been the initial genetic system, and an early stage of chemical evolution is thought to have been based on self-replicating RNA molecules—a period of evolution known as the RNA world. Ordered interactions between RNA and amino acids then evolved into the present-day genetic code, and DNA eventually replaced RNA as the genetic material.
The first cell is presumed to have arisen by the enclosure of self-replicating RNA in a membrane composed of phospholipids.

Phospholipids are the basic components of all present-day biological membranes, including the plasma membranes of both prokaryotic and eukaryotic cells. The key characteristic of the phospholipids that form membranes is that they are amphipathic molecules, meaning that one portion of the molecule is soluble in water and another portion is not. Phospholipids have long, water-insoluble (hydrophobic) hydrocarbon chains joined to water-soluble (hydrophilic) head groups that contain phosphate. When placed in water, phospholipids spontaneously aggregate into a bilayer with their phosphate-containing head groups on the outside in contact with water and their hydrocarbon tails in the interior in contact with each other. Such a phospholipid bilayer forms a stable barrier between two aqueous compartments—for example, separating the interior of the cell from its external environment.
The enclosure of self-replicating RNA and associated molecules in a phospholipid membrane would thus have maintained them as a unit, capable of self-reproduction and further evolution. RNA-directed protein synthesis may already have evolved by this time, in which case the first cell would have consisted of self-replicating RNA and its encoded proteins.

Source: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9841/


In DNA sequencing, is "mate pairs" synonymous with "paired ends"? If not, how do they differ?

Paired-end is the name of the sequencing approach.

Mates refer to the read pairs that correspond to the same insert, but sequenced from opposite directions.


Do cuttlefish know how to mimic animals since the moment they are born or do they learn by observing?

I haven't been able to find any definitive research/answers, but, based on the usage of their mimicry (camouflage and sexual), and some of its features (alteration of the surface texture of their skin, electric camouflage, development+change through lifetime), I'd hypothesise that it's most likely a mixture of the two. They likely have a large innate capacity to use the form of mimicry young cephalopods do, which is further developed socially/as a learned behaviour, which subsequently causes the change in the nature of their mimicry.

Cuttlefish texture change (Primary research article)

Transient sexual mimicry (Summary article (Nature))

Research has shown that cuttlefish mimicry develops and changes as they grow; it has also been shown to differ based on the location of the creature. There is also evidence of cephalopods learning socially, so it does indicate that their behaviour is at least partially learned. (Source + additional references- reed.edu ->Visual Mimicry in Cephalopods -> Ontogeny)


What happens when the parietal cells of gut epithelium becomes partially non-functional?

Parietal cells are responsible for acid secretion (HCl) in the stomach.

pH is inversely correlated to H+ concentration; the higher the H+ concentration, the lower the pH.

If the stomach's parietal cells become partially non-functional, there will be less acid secreted into the stomach (a lower H+), and the pH will rise.

Answer (b)

  (b) The pH of the stomach will fall abruptly

is the opposite of what would be expected to occur.

The correct answer is d), for the reason you listed.

  Proteins will not be adequately hydrolysed by pepsin into proteoses and peptones.

Regulation of Acid Secretion


Is anaerobic activity during ketosis possible?

You are correct in thinking that fatty acids cannot be metabolised anaerobically. However, in the type of metabolic state that you are describing, blood glucose will be maintained by the liver to support tissues or cells which are more or less dependent upon anaerobic metabolism. The classic example of such a cell type is the red blood cell which as no mitochondria and so cannot use the TCA cycle. The brain is also heavily dependent upon glucose.

The liver exports glucose that it has produced via gluconeogenesis from amino acid skeletons, as well as from glycerol produced as a result of fat metabolism.


Genes that were once functional but no longer are are called pseudogenes (as Corvus pointed out in the comments).

Many genes that are similar today (homologs) are hypothesized to have come from duplication events in the past.  In most cases, these duplicates diverge.  The divergence can happen in several ways:
1) one retains the original function while the other obtains a novel function
2) a dosage response occurs where both (keeping the original function) become necessary for that function
3) one retains its function while the other loses all functionality.

This third group are the pseudogenes.  This isn't the only way pseudogenes come to be, but it is probably the most well-characterized.

There are several resources for lists of these.  I'll just point you in that direction.  I assume you are interested in a particular group (i.e. genes important in development or patterning), so that you can dig more deeply into:

http://seqanswers.com/forums/showthread.php?t=32054
http://www.genomebiology.com/2012/13/9/r51


What is the actual chance of sibling incest child suffering from a genetic disorder?

Usually when we talk about genetic disorder risks for closely related pairings, the concern is the high probability of homozygous recessive alleles.

Lazarin et al. 2013 screened ~23,000 individuals for 108 genetic diseases and found 24% were carriers of a known allele for some disease. Including carriers of multiple alleles, the total frequency comes to about 38% (this is a lower bound because only known alleles can be screened; there may be many other variants that are not known to science that cause the same symptoms).

That means about a 62% chance that one of an individual's parents carries one of these alleles (1-.62*.62 - note that this 62% has nothing to do with 1-.38, just a mathematical coinicidence with rounding).

If a parent is a carrier, each sibling would have a 50% chance of also becoming a carrier; the probability that both siblings are carriers would be 25%. The probability that an offspring from those siblings would be homozygous recessive would be another 25%. .62*.25*.25=3.9% (note that these are all lower bounds, the chances would be much higher if there were multiple recessive alleles present or if both parents were carriers for the same gene).

However, this is limited to Mendelian mutations just for this subset of known alleles. There are many many more conditions and disorders that have more complicated genetics that we may or may not understand, so that the original question becomes nearly unanswerable. In fact the paper I cited only paid attention to what were considered "major" disorders and even left out the Mendelian alleles known to cause more minor issues (including clotting disorders that can easily lead to death in the right circumstances). There are also many mutations that don't cause a clearly defined disorder but cause some other more limited issues that could predispose the offspring to other illnesses.

Lazarin et al. 2013 refers to estimates that each individual carries about 4-5 lethal recessive mutations. Given that siblings are very likely to be carriers of the same particular recessive mutations, this would significantly impact any offspring well beyond the estimates for the known disease alleles.

References

Lazarin, G. A., Haque, I. S., Nazareth, S., Iori, K., Patterson, A. S., Jacobson, J. L., ... & Srinivasan, B. S. (2012). An empirical estimate of carrier frequencies for 400+ causal Mendelian variants: results from an ethnically diverse clinical sample of 23,453 individuals. Genetics in Medicine, 15(3), 178-186.


Where do the electrons and protons formed from biological reactions go?

I've reproduced the diagram that you linked to. It shows the oxidation of a pair of thiols to create a disulphide. What is missing from this scheme is the accompanying oxidising agent. So for example this could be carried out without catalysis in a reaction with molecular oxygen, in which case hydrogen peroxide would be formed. So the electrons and protons have ended up on the oxygen.

In a biological system this oxidation would usually be carried out by an enzyme, in which case the oxidising agent would probably be FAD (flavin adenine dinucleotide) or NAD+(nicotinamide adenine dinucleotide). These are by far the most commonly used redox cofactors. In a typical eukaryotic cell these would end up either (a) being reduced either by the mitochondrial electron transport chain (in which case the ultimate electron acceptor would again be oxygen); or (b) when they were used as a reducing agent in a metabolic reaction.


Questions regarding serial passage of virus through animals arising from the paper The proximal origin of SARS-CoV-2

No. Serial passage through animals attenuate the virulence of a virus In It's ORIGINAL Host. it can cause and will cause an increased virulence in the animals that were used in serial passage, and, if the animals have similar receptors as humans, increase the virulence in humans as well. like the two experiments that passed bird flu across ferrets until they become virulent and airborne across them.
https://www.cidrap.umn.edu/news-perspective/2014/04/experiments-render-h7n1-virus-more-contagious-ferrets
https://www.scientificamerican.com/article/pandemic-bird-flu-studies-public/
https://science.sciencemag.org/content/336/6088/1534.full
https://jvi.asm.org/content/88/12/6623


Chromosome splits (or fusions for that matter) might not mean that much for reproductive success since genes can still line up and recombine. To quote the science blogger P.Z. Myers:

  [C]hromosome numbers can change dramatically with no obvious effect
  on the phenotype of the organism.

He illustrates it thusly:

So to answer your first question, changes in the number of chromosomes aren't always fatally deleterious (as you seem to think).

As for how a change in chromosome number might spread, the explanation is likely random drift and inbreeding. To quote P.Z. Myers again:

  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant.

"Evolution" by Mark Ridley, p. 361 similarly points out that reproduction will be an uphill battle until the new variant becomes more common (often through inbreeding or drift in small populations):

  When a new chromosomal fusion mutation arises, it will be selected
  against because of its disadvantage in heterozygous form. But if it
  drifts up to a locally high frequency, as may easily happen in a
  local, small, and perhaps inbreeding, mouse population, natural
  selection will favor it. Natural selection favors whichever
  chromosomal form is locally common[.]

This might in the end lead to speciation due to the two populations becoming incompatible.


Autoclaving media with carbohydrates (or sugar solutions on its own) is not a good idea for two reasons:

The Maillard reaction: This occurs when you heat mixtures of amino acids and sugars. The amino group of an amino acid reacts with a carbonyl group of a sugar, fusing the two molecules together. This is a common reaction in the kitchen which is for example responsible for making the bread crust brown. It also changes flavors.
Caramellization: This is the heat induced breakdown of sugars - also leading to brown products, but much more undefined than the Maillard reaction. What products arise depends on pH, temperature and other reactands.

Both reactions may lead to products which can be inhibitory to microbe growth and should be avoided. There is also a paper which analyzed the effect of autoclaving on sugars which might be interesting to read in this context (see reference below).

So prepare a higher concentrated stock solution of your sugars, which can then be added under sterile conditions to your autoclaved and cooled down media or the agar solution (still warm enough to pour).

Sterilize this solution by filtrating it through a 0.2µM filter - depending on the volume either through syringe filters or through bottle top filters.
Make sure to maintain sterile conditions.

References:

Sugar degradation during autoclaving: Effects of duration and
solution volume on breakdown of glucose


Looks a lot like a radish seedling to me.

However, if I'm not mistaken, it doesn't even have its first true leaves yet, making identification very tenuous.

It can also be any number of brassica species, e.g. mustard (l) or cabbage (r):

If you can't wait to see what it grows into, smash one of the "leaves" between your thumb and a finger. If it's a radish, it will smell like one. If it does, taste the other leaf. If it tastes radishy, you have your answer without waiting. If you want to wait, however, doing that would kill the seedling.

Brassica seedlings will also taste spicy, but not like a radish.

Based on the number of "weeds" in the brassica family, I'd guess it belongs in that group.

I included these diverse possibilities to illustrate how difficult identifying a plant without true leaves is. :)


Cellular specific mass (in grams-dry-weight per pico liter)?

Density of a variety of cell types is rather well known. It can been measured directly by examining buoyancy (tendency to float) in liquids of known density, and also by microfluidic methods. But the results depend on the osmolality of the solution in which the cells are kept, since cells tend to "swell" (take up water) in low osmolality (hypotonic) medium.

Using a microfluidic technique, this paper reports a density of 1160 $\pm$ 1 pg/pL for E.coli at 290 mOsm, and 1139 $\pm$ 3 pg/pL for red blood cells. At comparable osmolality and using a gradient centrifugation method, this paper gives a density of 1095 pg/pL for E.Coli. So the results clearly differ a bit depending on experimental conditions (possibly the medium composition was different). For budding yeast, this paper estimates a density of 1103 $\pm$ 3 pg/pL, compared to 1113 pg/pL by gradient centrifugation.

In all cases, cells are heavier than pure water (1000 pg/pL), and larger eukaryotic cells seem to be slightly more dense. As macromolecules are more dense than water, this would suggest that eukaryotes have lower water content.