Does this recording sound like the pulses emitted by bats?

Though I cannot be 100% sure from the sound quality, it certainly does sound/seem like bats are making the calls you are hearing/seeing. I spent a number of years as a bat bioacoustics researcher and I came across similar sounds frequently and was able to confirm they came from foraging bats.

I'll have to see if I can find any old spectrograms or recordings on an old data hard drive. If I can find clear examples similar to yours I will add them to my answer. (Though I haven't seen that hard drive in years, so don't get your hopes up!).

These sounds can likely be explained by one of the following:

Some bat species have been known to echolocate using calls that sweep into human hearing range (i.e., below 20kHz; Fenton, 2015; other sources already mentioned).
Many bats actually emit calls during flight that differ in structure from echolocation calls; these calls, often referred to as “social calls,” may occur between echolocation calls and often consist of broadband calls with low-frequency components and multiple syllables (Altringham and Fenton, 2003; Wright et al., 2013).
Some bats use special sounds to avoid collisions with each other while in flight (Fenton, 1983).

You can see and hear examples of some social calls (used broadly in this case) for a pipistrelle bat in Britain here.

I copy a spectrogram of one of these social calls from the above link (see the middle call signature):

Wright et al., 2013 also provide a spectrograph demonstrating all the various call signatures they recorded from various Eptesicus fuscus (big brown bats) in the United States:

Purchasing some bat bioacoustic analysis software should assist with your recordings and call interpretation. I recommend Sonobat (best, but expensive) or SCANR (from Binary Acoustic Technology). There are other less used options as well (e.g.,the Echo Meter Touch Bat Detector for Apple, for which I picture an example screen shot below):

I also want to provide some information and citations about bat echolocation to help inform those interested in this question. I would include this in the comments, but it's too long:

Bat Acoustics 101

Shorter wavelengths (higher frequencies) provide a better resolution of target detail allowing the bat to receive a more detailed picture of its target (Fenton, 1983).
Acoustic energy reflected from a target is theoretically greatest when incident wavelengths of calls are near the same size or smaller than the target (Jones and Rydell, 2003); otherwise, if the object is smaller than the wavelength, the sound will be scattered instead of reflected (Yalden & Morris, 1975).
Bats need to be close to objects to "see" them: range is typically 1-5 m for frequencies around 20 kHz and increasingly closer for higher frequencies (Jones and Rydell, 2003).
In addition to target range, bats perceive target shape and texture from the delay of multiple reflections (echoes).
Calls contain base frequencies, but they can also add harmonics & overtones to the bandwidth of the calls, which can enhance target ranging and localization (Jones and Rydell, 2003) and thus increase acuity (Fenton, 1983). They can also suppress certain harmonics and use variations of combinations of tones.
Bats can also vary the amplitude, or loudness, of their calls (Yalden & Morris, 1975).
Bat calls can be composed of frequency modulated (FM) or constant frequency (CF) components or a combination of both types of calls (Jones and Rydell, 2003).

FM = each signal, consisting of discrete pulses of sound (Fenton, 1983), starts at one frequency and sweeps down to another. Sweeping through a range of frequencies allows bats to achieve some protection from errors associated with Doppler shifts; in addition, the modulation of frequencies helps to tell the bat about the texture of the target (Fenton, 1983).
While foraging, FM bats create a series of repeating ultrasonic pulses in various phases.  There are three major phases, each with an increase in repetition rate.   The change in rate across the phases can go from 4-5 pulses per second to 200 pulses per second.

The signals bats produce may serve multiple functions; they can be used for echolocation as well as for communication, whether intentionally or unintentionally.

Use echolocation calls of others to locate roosts, and eavesdropping also allows a territorial bat to distinguish between another bat trying to steal its food or just one passing through its territory (Fenton, 1983).
“Social calls" (Altringham and Fenton, 2003; Wright et al., 2013).
Collision avoidance sounds (Fenton, 1983).
Alarm calls and distress calls when in stressful situations.
Mother-young communication.


To obtain a full survival curve (basically a full life table) you would need to make quite a number of assumptions, since the data for paleolithic societies is scattered and probably biased. This is however not a field I know well, but I can point you to one recent paper (White, 2014) that explores how the ratio of young and old individuals in a population relates to demographic rates, using agent-based models. Using such a model you can obtain smooth survival curves and also explore how different assumptions will affect the survival curves.

There are also data from recent or current hunter-gatherer societies that can be used to approximate what the survival curves looked like during the paleolithic. For instance,  Hewlett (1991) (pdf here) has compiled survival rate data for individual hunter-gatherer societies (along with other demographic rates and data from other types of pre-industrial societies). The child mortality rate (deaths before age 15) often lie in the range 40-50% in active (mobile) and sedentary hunter-gatherer societies, with an infant mortality rate usually between 10-30% (death before 12 months of age). This indicates a fairly steep survival curve, which is the reason why the average age of paleolithic people is often estimated to ~25 years. This doesn't mean that most people died around the age of 25, just that the distribution of ages was very skewed and non-normal. Many died young, but people that survived to adulthood could become much older than 25.


To answer your bigger question:

Yes, most of this is possible - under some conditions -, and animals and animal cells can acquire chloroplasts, and use them.

E.g.: see Elysia chlorotica whose cells actively take up chloroplasts and use them, and keep them alive (though not replicating). - Though some genes of algae are also contained in the Elysia chlorotica genome - which may be considered as partial replication.

Also there are salamanders that have replicating algae within them (since embryogenesis) - even algae (with chloroplasts) within animal cells - though here the algae might be rather understood as symbionts or "cell types", and the animal cells don't have the chloroplasts by themselves.


How do butterflies defend themselves from other creatures when they don't have the ability to sting or some other offensive/defensive mechanism?

Butterflies have a number of defence mechanisms, even if they don't have the ability to sting (as adults - see spines in larvae below). Here is a non-comprehensive list of some defensive mechanisms:

Toxins or repellents, which can be present in both adults and larvae.
Aposematism (warning coloration)
Mimicry, both in the form of resembling other poisonous species and using features such as eyespots.
Spines, bristles or long hairs, often in larvae (see google images), to make ingestion highly unpleasent or dangerous. See the Pine processionary moth (Thaumetopoea pityocampa) for an nice example of defensive larval hairs.
Camouflage/hiding
Sound clicks used to startle or disorient predators. This is most often known from moths to prevent bat attacks (see e.g. Cycnia tenera and Fullard et al, 1994).
Conspicuous features at the edge of wings to make them targets of attack, e.g. eyespots or appendages, which are used to lure predators to attack non-essential body parts (see Olofsson et al, 2013 for an example).


Fats include free fatty acids and their compounds with glycerol: mono-, di- and triglycerides.

In a cooking context, fats refer to solid fats, and oils to fats that are liquid at room temperature. Most of them contain triglycerides.

Fats belong to a broader group--lipids--, which are substances that are usually not soluble in water and usually soluble in certain organic solvents, such as ether or acetone. Besides fats, lipids include sterols (cholesterol, plant sterols), waxes, lipid-soluble vitamins (A, D, E, K) and steroid hormones (aldosterone, corticosterone, etc).

Examples of complex lipids are phospholipids, glycolipids and lipoproteins.

Fats and lipids are often used as synonyms. However, you usually say dietary fats and blood lipids.

http://www2.chemistry.msu.edu/faculty/reusch/VirtTxtJml/lipids.htm
http://biology.about.com/od/molecularbiology/ss/lipids.htm


It basically means, that the body gets used to certain drugs and that you need to raise the dose to reach an effect. This is for example true for a number of anesthetics or pain medications as morphine.

Permanent application leads to a down-regulation of the drug receptor (for morphin this is the mu-opiod receptor) and the activation of counteracting signaltransduction pathways. To still get an activation you will need a higher drug concentration.
For more details have a look at these articles:

Opiate tolerance and dependence: receptors, G-proteins, and
antiopiates
Cellular neuroadaptations to chronic opioids: tolerance, withdrawal
and addiction


Why doesn't the human skin grow back exactly how it was before being damaged?

Human skin is made up of three layers [1]:

Epidermis; it contains no blood vessels; it has 5 cellular layers (starting from surface):

stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum germinativum

Dermis; it is separated from the above by the basal membrane; made up of connective tissue (with blood vessels and nerve endings)
Hypodermis - it is not even considered part of the skin

"Gray940". Licensed under Public domain via Wikimedia Commons.

  Why (and how) is regenerated skin different from original ?

Why? Skin is a very important organ. It protects from pathogens, it maintains body temperature, it keeps body water [1], etc. How? That depends on what causes the regeneration. I've emphasized two terms in the above list.

Stratum corneum represents the "skin cells that becomes the dust in our homes and it always grows back to full thickness". It is lost during a physiological process called desquamation [2]. The cells that are lost are non living corneocytes. Their only purpose is to from a protection barrier [3].
Basement membrane holds the germinativum layer of the epidermis. Injuries that do not affect it are repaired by complete regeneration of all destroyed layers. However, if the injury destroys membrane continuity, the germinative cells on the edges will fail to "reconnect" with each other, thus the layers derived from them will follow the same rule. A process of fibrosis is triggered. The result of  extensive fibrosis is a scar, containing collagen secreted by the granulation tissue with dermal origins. Yet, the germinative layer tends to join back together [6], but probably the excess collagen production, without the limiting basement membrane, bulges into the epidermis and limits germinative layer extension. That's why keeping the edges of the tissue close to each other reduces excessive fibrosis and allows germinative layer regeneration, thus resulting in none to small, barely visible scars.

How deep should an injury be in order not to affect basement membrane? No more than 0.06 to 0.08 mm [5].

  What about skin transplants ?

Skin grafts contain at least a part of dermis [4], which will allow granulation tissue formation thus permitting revascularisation and making the graft stick. Otherwise it would fall off and/or be lost by necrosis.

References:

Wikipedia contributors, "Skin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Skin&oldid=619454074 (accessed August 4, 2014).
Wikipedia contributors, "Desquamation," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Desquamation&oldid=614028888 (accessed August 4, 2014).
Wikipedia contributors, "Stratum corneum," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stratum_corneum&oldid=615247326 (accessed August 4, 2014).
Wikipedia contributors, "Skin grafting," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Skin_grafting&oldid=603324006 (accessed August 4, 2014).
Sandby-Møller J, Poulsen T, Wulf HC. Epidermal thickness at different body sites: relationship to age, gender, pigmentation, blood content, skin type and smoking habits. Acta Derm. Venereol. 2003;83(6):410-3. doi: 10.1080/00015550310015419. PubMed PMID: 14690333.
Dawn A. Tamarkin, Ph.D. Repair of skin. 2011 STCC Foundation Press. Available from http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm (accessed 04.08.2014)


Manifestations of open foramen ovale in adults

A fully patent foramen ovale (pfo) is rare however a partial or small pfo is present in about 30% of the population.

Now the manifestations you described are partially correct. A pfo causes a left to right shunt in the adult whilst a right to left shunt in the fetus. In the fetus this is normal. In the adult, it is left to right because the left atrium is at higher pressure than the right. Due to this some of your manifestations are the wrong way round but still correct.

For example you mentioned hypertension, but presumably you meant systemic hypertension. It is more common at least in the early stages to get pulmonary hypertension. The pressures in the left atrium cause the pressures in the right atrium to increase when there is shunting. This is frequently seen when pressures in the left are increased due to factors like systemic hypertension. Coronary artery disease can also worsen the shunt and increase pressures in the right atrium and pulmonary pressures because the left ventricle can be stiffer.

Despite all this the more common presentation of a clinically significant pfo is right heart failure. Volume overloaded,the right heart dilates and fails. This will cause the usual presentation of right heart failure i.e. peripheral oedema, ascites and hepatomegaly.

Of course increased pulmonary pressures also causes strain to the right heart and can also cause right heart failure.

They then may go on to develop congestive cardiac failure and the exertional dyspnoea that comes with it. The inadequacy of the right heart can lead to excess strain to the left heart through a number of mechanisms that leads to it also failing. Dilation of the right heart can also lead to atrial fibrillation which in turn leads to stroke all being other possible presentations.

Cyanosis usually doesn't occur at least early in the disease as there isn't a shift from right to left (unoxygenated to oxygenated) but the other way round.

The severity of the pfo will lead to the severity of the clinical manifestation and how early it is picked up. Most people have routine checks of their heart (the murmur is usually pretty loud) so it is frequently corrected before any clinical disease manifests. In patients with small pfos they may never notice unless they become hypertensive or put strain on their heart during pregnancy. Yes they have a slight disadvantage as they lose some oxygenated blood but not anything noticeable.

If anything is unclear or you have more questions, please ask.


Why are oceans said to have "low productivity" in terms of photosynthesis?

First, we have to know which are the most important criteria for photosynthesis to occur; these are: light, CO2, water, nutrients.
docenti.unicam.it/tmp/2619.ppt
Second, the productivity, you are talking about, it should be called "primary productivity" and it is calculated, dividing the amount of carbon converted per area (m2) by the time.
ww2.unime.it/snchimambiente/PrPriFattMag.doc

So, thanks to the fact that oceans occupy the larger area of the world, the marine microorganisms can convert lots of inorganic carbon into organic (principle of photosynthesis).
A big problem in the oceans is availability of nutrients; these tend to deposit or react with water or other chemical compounds, even though the marine photosynthetic organisms are essentially found on the surface, where, of course, light is present. This reduces as a consequence the  photosynthetic productivity potential of oceans.


Can DNA & RNA be considered as nature's programming language?

This question can't be answered with a simple yes/no, but I would say that the analogy of DNA being the "code" used by cells is a reasonable one, if taken with a number of other considerations.

DNA function

When Watson and Crick first described the structure of DNA (being a double-stranded sequence  of the nucleotides Adenine, Cytosine, Guanine and Thymine) this led to what is known as the Central Dogma of Molecular Biology [1], which posits that DNA makes RNA makes Protein (figure from [2], as originally produced by Watson).

As you correctly point out, less than 2% of the genome is protein-coding, however our understanding of the rest of the genome is increasing manifold due to projects like ENCODE [3], which are discovering not only the "regulatory" regions that control the expression of protein-coding genes, but also the discovery of non-coding RNA's, many of which are totally uncharacterised [4].

The point of this section is to clarify that although only 2% of the genome codes for protein, it is incorrect to say the rest is "junk" or non-functional. The Central Dogma described above is now an outdated model - certainly some DNA makes RNA makes Protein, but not all; many RNA molecules are functional in their own right.

You could argue that proteins and non-coding RNA molecules are the product of "scripts" in the DNA that are run or performed by cells, although you are unlikely to find any genomic scientists talking in these terms.

Epigenetic control

Where the analogy breaks down is that all* the cells in an organism have the same genome, yet they are vastly different to one another. These differences are due to epigenetic processes, which are described as non-coding modifications to the DNA that affect expression of transcripts. A basic overview can be found here [5].

These modifications come in several forms and include:

DNA methylation

the addition of a methyl-group to cytosine nucleotides that can affect binding of transcription factors etc,

Histone modifications

DNA is actually a 3-dimensional structure, and is wrapped around proteins called histones, which wrap together to form chromatin and the characteristic chromosomal structure.

The availability of DNA to transcription factors is completely dependent on these modifications to the DNA, which are specific to individual cell types and prevent retinal cells, for instance, expressing liver enzymes. (Below figure from [6])

Overview

In short, genetics and the DNA sequence can certainly be thought of as the blueprint for an organism - changes to this sequence can profoundly affect phenotype - however it is too simplistic to imagine that the sequence alone provides all the information needed.

Not only are there many non-coding molecules essential for functioning in cells, there is exquisite control over expression by DNA modifications that do not affect the sequence of nucleotides and are essential for cellular differentiation.

The ENCODE (Encyclopedia of DNA elements) project [7] is making headway into the interpretation of the non-protein-coding elements of the DNA, but there is still a long way to go.

* not quite all, for instance B-cells have a hypervariable region to enrich antibodies for variation [8]

http://www.ncbi.nlm.nih.gov/Class/MLACourse/Modules/MolBioReview/central_dogma.html
http://sandwalk.blogspot.co.uk/2007/01/central-dogma-of-molecular-biology.html
ENCODE Project Consortium, “The ENCODE (ENCyclopedia Of DNA Elements) Project.,” Science, vol. 306, pp. 636–640, 2004. PMID: 15499007
http://www.nature.com/encode/threads/non-coding-rna-characterization
http://www.whatisepigenetics.com/fundamentals/
http://www.eusem.com/main/CH/epi
http://www.genome.gov/encode/
http://www.anaptysbio.com/technology/somatic-hypermutation/


Why are hard boiled eggs so homogeneous?

Disclaimer: This is my understanding of the egg anatomy as a general biologist. There is most certainly better references and sources out there to explain this (please add better references if you know of any).

If I understand you correctly, your question is why we do not see cell organelles in a cracked or boiled egg. If so, your question seems to stem from a misunderstanding of what the egg white and egg yolk represents. A chicken egg is not simply an enlarged cell, and the egg yolk is not the cell nucleus.

When an oocyte matures in the chicken ovary, it stores yolk inside the cell and therefore enlarges. The yolk is therefore part of the oocyte cytoplasm. However, as it enlarges, the yolk is separated from the germinal disc, which holds all the other cell organelles (including the nucleus). The germinal disc is seen as a small white area on the egg yolk. Eventually, when the oocyte has accumulated enought yolk, it disattaches from the ovary (ovulation) and goes into the hens oviduct. This process is happening continuously, and oocytes of different stages of maturation are present on the ovary, which can be seen in this image:

(image from Chickscope: Formation of the Egg. University of Illinios)

When the oocyte passes through the oviduct it builds up layers of egg white (albumen) and other supporting structures. The shell is formed last in the shell gland, which is located at the end of the oviduct. Therefore, the egg white and the shell is formed externally of the oocyte and the egg yolk.

So the reason why we do not see more structures in a boiled egg is that the majority of the egg is yolk and egg white, which are both structures to store energy ment for a growing embryo (mainly protein and fat). It should also be noted that oocytes in most (all?) animals contain yolk granules, but the storage of yolk is most extreme in birds (see this webpage on animal development from State university of New York for a short comparison).

It should also be noted that an egg that is fertilized will naturally contain more than one cell, since the embryo will have started growing.

References:

Chickscope: Formation of the Egg. University of Illinios (webpage)
Chickscope: The yolk. University of Illinios (webpage)
Chapter "Eggs" in Johnson et al. 2002. Molecular Biology of the Cell. 4th ed. Garland Science, New York
Wikipedia: Egg
Animal development. State university of New York (webpage)


Proteins evolve and have different sequences between species, so you would have to define what you mean with "same protein". One option would be to use an orthology database like eggNOG. (eggNOG has the same protein identifiers as STRING.) Then you could figure out 1:1 correspondences between proteins.

You probably also want to read up on Roded Sharan's work, e.g. Global alignment of protein-protein interaction networks.


Can I change the genetics of a group of plants naturally?

Of course, you can place a population of anything (incl. a population of plants) into a specific environment and you could expect this population to slowly adapt to it.

Most plants don't have a particularly fast generation time and therefore, the evolutionary experiment might take longer than your lifetime. The experiment would be much faster if you choose some unicellular algae such as Chlamydomonas reinhardtii for example.


Interbreedability between current humans and his ancestors

Short answer
Considering only post-zygotic isolation and based on below discussion, I would tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA for safety.
Long answer
Concept of species
The post How could humans have interbred with Neanderthals if we're a different species? makes a good introduction to the difficulties behind the concept of species.
Pre-zygotic isolation
Anatomically speaking, it is probably possible to get a spermatozoid cell from a 20th century man start fusing with a Homo abilis ovule (and vice-versa). The potential pre-zygotic isolation will rather be caused by aesthetic appearance.
To the risk of sounding posh, I would say that Homo abilis hairy face does not exactly fall within my standards! I suspect it will be the same for many of us, humans of the 20th century. It is hard to really know how much time one needs to go back to consider that we don't disgust each other enough to refuse mating together. There are a few reasons why this is hard

Reconstruction (esp. facial reconstruction) is often too inaccurate to really allow to tell how ugly their faces were.
It is going to be super hard to tell what they would just about our faces today! I bet they'd laugh at our ridiculously small jaws!
It is hard to fully separate the environment from the person. In middle-age (in Europe at least) people would bath a few times in a life-time. Again I would consider this not in my standards!

But let's focus on post-zygotic isolation.
Post-zygotic isolation
Humanzee

The humanzee (Homo sapiens sapiens × Pan) (also known as the chuman or manpanzee) is a hypothetical chimpanzee/human hybrid. An unsuccessful attempt to breed such a hybrid was made by Ilya Ivanovich Ivanov in the 1920s. There have been occasional reports of human-chimpanzee hybridization, notably regarding a performing chimp named Oliver during the 1970s, but none of them have been confirmed. Similarly, the possibility of a chimpanzee–gorilla hybrid, known as a koolakamba, also remains unsubstantiated.

There is no evidence of humanzee but it is important to realize that the idea of such hybrid is not fully unthinkable. Human and chimpanzee share a common ancestor about 6 millions years. So, if a humanzee is consider eventually possible, I would quite definitely consider that a H. abilis (~1 MYA) or H.erectus (~2 MYA) and 20th century human could well interbreed if we were to live at the same time.
Sumatrans and bornean orangutans can hybridize (Malinson, 1984) despite that their lineages have split about 1.3 MYA!
So putting all of that together and follwing some vague intuition, I would personally tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA (MRCA with gorillas). But really, it is a rather vague intuition.
See also CrashCourse > How to Make A Humanzee


Can Bioluminescence drive photosynthesis?

Yes and no. Yes as in the energetics do work out and you will be going down a small but non-trivial driving force as long as you continue to provide the luciferin to the algae.

However, the wavelengths of light by which photosynthesis absorbs its energy are well defined and narrow. As a result, light sources for photosynthetic organisms have to be fairly strong and bright to cover the whole spectrum to provide the necessary light. As a result, your bioluminescent algae will also have to emit light at the desired wavelength to achieve a high photochemical efficiency and provide light to both Photosystem II and Photosystem I which have different wavelength requirements.

(source: gsu.edu)


Long term effects of "brain freeze" on the cerebral vasculature

I do not have a source for the following as it was taught to me in neuroanatomy classes, the explanation given for brain freeze is that it is  referred pain through the trigeminal nerve. The  meninges (the tissue lining the central nervous system) is innervated by the trigeminal nerve in the head. Therefore the pain feels as though it is like a headache from meningeal irritation but is in fact benign.

Given that the mechanism is through referred pain rather than any vascular event it should not put you at any increased risk.

This being said if you experience repeated headaches and are unsure of the cause it would be wise to consult your doctor.


Why does alcohol cause the hemolysis of RBC in a large proportion?

Well, it turns out the situation is more complex. I had assumed the answer was what rwst suggests or something to do with osmotic pressure. It seems that we don't really know that well.

In a paper from 1991, Chi and Wu suggest the following possible mechanisms :

Membrane fusion during the shedding of exovesicles might produce a transient decrease of the permeability barrier.
Increase of lipid dynamics by the alcohol could decrease the packing of the
bilayer. The membrane barrier behaves like a soft polymer, which can sieve solutes. The meshes in the polymer might become larger if its packing density is
reduced.
Lateral phase separation of lipids could induce packing defects in the lipid domain. This has been observed for long chain alcohols and postulated to be responsible for the increase of membrane permeability by amphiphiles.
Increase of the dielectric constant of the membrane by the alcohol would also increase the partition of hydrophilic solutes into the membranes. Such an increase has been postulated to be responsible for the increase of the permeability by aliphatic alcohols.
Modification of the intrinsic membrane domain might follow modification of the membrane skeleton by the alcohol. Accordingly, aggregation of intrinsic proteins might cause membrane modification mentioned under point 2 to 4.

The authors state that it is not possible to decide between the
various possibilities, but they seem to prefer point 5:

  Although it is not possible to decide between the various
  possibilities from the present data, we showed that the
  release of membrane fragments from ethanol-treated RBC was not a
  requirement for the creation of membrane pores since it occurred at a
  time much later than the detection of K ÷ leakage. In addition, we
  found that changes of membane rheological properties preceded the
  permeability increase. These properties have been related to
  the membrane skeletal protein spectrin. Moreover, ethanol has
  been shown to affect the skeleton. The processes leading to
  the formation of pores in ethanol-treated RBC may thus relate to a
  deranged cytoskeletal network, followed by the aforementioned
  alteration of membrane properties.

The plot thickens, apparently, low concentrations of alcohol protect erythrocytes from hemolysis while higher concentrations can cause it. The following are extracts from Tyulina et al:

  The seeming paradox between the direct haemolytic effect of ethanol on
  erythrocytes (Fig. 1) and the stabilizing effect of ethanol on
  erythrocytes undergoing NaOCl-induced haemolysis (Fig. 2) could be
  explained by the relatively small destabilizing effect of ethanol
  which is observed (<1% haemolysis) over 16 h. This effect would be
  negligible in the short time period (generally <10 min) assay for
  NaOCl-induced haemolysis where 100% of the cells are haemolysed. An
  alternative explanation for this paradox is that the mechanisms of
  haemolysis induced by ethanol and NaOCl are different.

  It therefore appears that ethanol does not induce significant
  oxidative stress in the human erythrocyte, and these data are in
  agreement with previous studies (Seeman et al., 1971), in which it was
  found that low ethanol concentrations could protect erythrocytes
  against haemolysis. Although the mechanism for this protective effect
  is unknown, it has previously been suggested (Halliwell and
  Gutteridge, 1999) that ethanol can serve as a hydrogen donor in the
  elimination of the hydroxyl radical with formation of water and the
  2-hydroxyethyl radical.

The authors then state (emphasis mine):

  In summary, we conclude that the damage to erythrocytes which occurs
  on in vitro exposure to ethanol may be caused, at least in part, by
  unmetabolized ethanol directly, rather than by the oxidation of
  ethanol to acetaldehyde or its conversion to FAEE.

I would guess this "direct effect" is something very much like what rwst suggested but the fact that the authors, who clearly work in this field, do not say so makes me think that the situation is more complex.

So, in conclusion, the exact details of alcohol's hemolytic properties don't seem to be understood in great detail. Admittedly, neither of these articles is very recent, if anyone can find a more up to date account I would love to read it.

REFERENCES:

Chi LM, Wu WG. Mechanism of hemolysis of red blood cell mediated by ethanol.
Biochim Biophys Acta. 1991 Feb 11;1062(1):46-50.

Tyulina OV, Prokopieva VD, Dodd RD, Hawkins JR, Clay SW, Wilson DO, Boldyrev
AA, Johnson P. In vitro effects of ethanol, acetaldehyde and fatty acid ethyl
esters on human erythrocytes. Alcohol Alcohol. 2002 Mar-Apr;37(2):179-86.

Trandum C, Westh P, Jørgensen K, Mouritsen OG. Association of ethanol with
lipid membranes containing cholesterol, sphingomyelin and ganglioside: a
titration calorimetry study. Biochim Biophys Acta. 1999 Aug 20;1420(1-2):179-88.


What is the use of futile reaction cycling such as Fruc-P to Fruc-BP?

As far as I am aware there are various regulatory mechanisms (allosteric regulation, hormonal control) in place to minimise futile cycling by ensuring that phosphofructokinase (glycolysis) and fructose 1,6 bisphosphatase (gluconeogenesis) are not both active at the same time.

See this Wikipedia article for a starting point.

  The precise regulation of PFK1 prevents glycolysis and gluconeogenesis from occurring simultaneously. However, there is substrate cycling between F6P and F-1,6-BP. Fructose-1,6-bisphosphatase (FBPase) catalyzes the hydrolysis of F-1,6-BP back to F6P, the reverse reaction catalyzed by PFK1. There is a small amount of FBPase activity during glycolysis and some PFK1 activity during gluconeogenesis. This cycle allows for the amplification of metabolic signals as well as the generation of heat by ATP hydrolysis.

The last two sentences of the quotation are probably what you remember reading about. There is a theory that having some cycling provides an element of regulatory responsiveness. See here for example. I'm not enough of a mathematician to explain this idea well.


What purpose do the opening(s) serve in diapsid and synapsid skulls?

It is believed that originally the holes evolved to give the jaw muscles a place to expand into as they contract. They evolved as the the  otherwise larger jaw muscles are trapped between the bones and cannot contract properly. I say "believe" because the original function is still debated, and it is not something that can be easily tested.

Diapsids likely evolved from early synapsids, however the evidence is tentative at best and it is just as likely that they both evolved independently from anapsids.

Birds are diapsids. However many modern birds have lost the bony partition between the two holes, separating them by cartilage and soft tissue only. Just as some mammals have lost the bony partition between the jaw muscles and the orbit. Additionally in many mammals and birds the expansion of the braincase makes it harder to identify the holes for the laymen as they are pushed down and to the side.


The amino acids asparagine and glutamine have hydrolysable amide groups on their R groups, as shown here:

Note the leftmost amide group on both amino acids. When exposed to acid, these groups would hydrolyse, releasing ammonia.

This was of interest when people used to determine amino acid compositions by acid hydrolysing purified proteins (example paper which does this) and then running them through HPLC or mass spectroscopes. This method, however, fails to distinguish asparagine/aspartate and glutamine/glutamate due to their acid-unstable nature.

So to answer your question, an acid-stable amino acid is any amino acid that does not degrade under acid treatment.

Additional amino acids that degrade under such treatment can be found here, and includes serine, threonine, tyrosine, tryptophan and cysteine in addition to the two above amino acids. These amino acids degrade by alternative pathways distinct from the one by which the above amino acids degrade.

Finally, assuming you are talking about amino acids in dietary supplements, the reason acid-stable amino acids are reported is because acid hydrolysis is usually the method used to hydrolyse the proteins into amino acids, and therefore the manufacturer would not be able to produce acid-unstable amino acids by this method, leading to that label on your supplements.


How are Antibody and T-cell receptor different?

B cell receptors (BCR) work on a similar paradigm, but a different mechanism than the TCR completely, structure aside. When a B cell encounters an antigen that binds to it's BCR, the receptor-antigen complex is internalized where it's processed onto class-II MHC.

Source: UP Manila Lecture, Marilen Parungao (link)

The peptides have to be processed to ~22-residue fragments to load on MHC-II, and the whole antigen is thus fragmented on the extrinsic processing pathway. To be specific, one antigen becomes many different peptides on many different MHC-II on the same B cell. You can imagine this produces some diversity among peptides suitable that at least one Th cell with similar specificity might bind. Class switching and somatic hypermutation that the B cells undergo help them attain greater utility and specificity, and the membrane-bound BCR is alternatively processed so that the c-terminus domain traffics antibodies to be secreted (2).

On the other hand, the TCR is specific with a little wiggle room to a particular MHC-I or II loaded peptide, with the exception of yδ T cells which have been shown to be largely MHC-independent (3). The same situation follows, however, that your antigen presenting cell or APC has many different peptides of the same antigen loaded on MHC, just as cells expressing MHC-I might, which means that the T cells are also not recognizing the same exact peptide sequence. Since they originate from the same antigen, however, your cytotoxic and helper T cells can be specific for the same "target."


Which cells produce HCl produced in stomach? Don't these cells get destroyed by HCl?

Since your first question is a quite basic one (the answer is oxyntic cells) and asking two or more questions in the same post is a reason to close ("Avoid asking multiple distinct questions at once"), I'll address only your second question:

  [Why] don't these [oxyntic] cells get destroyed by HCl?

First, it's important to understand that oxyntic cells (from the greek ὀξύς, meaning "sharp" or "acid") do not produce HCl. They actually secrete two separate ions, Cl− and H+ (and, since HCL is a strong acid, one can say that technically there is — almost — no HCL in the lumen, because the ions keep dissociated).

You can find this in any physiology book, but there is a good explanation of the steps in Scientific American (2017):

Potassium ions, K+, diffuse passively from the parietal cell into the lumen.
An active transport pump brings K+ back into the parietal cell,
simultaneously secreting H+ from the cell to the lumen. As much K+
returns by this route as leaks in (1).
Chloride ions, Cl−, diffuse passively from the cell to the lumen, and their negative charges balance the positive charges of the secreted H+.
An exchanger on the opposite face of the parietal cell balances this
loss of Cl− by importing Cl− from the blood in exchange for
bicarbonate ions (HCO3−).
Within the cell, water reacts with carbon dioxide (CO2) to form carbonic acid (H2CO3), which dissociates into H+ and HCO3−.

This image from Lodish (2000) summarises it very well:

Of course, the important factor in lowering the pH (and in eventually killing the oxyntic cell) is the H+ concentration, not the Cl− one. Regarding that, it's worth mentioning that, despite the H+ concentration in the lumen keeps rising, cytoplasmic H+ concentration is never as high as the luminal one, because H+ is being pumped out of the cell.

Second, why don't the HCl (actually Cl− and H+, as explained above) already present in the lumen destroy the mucosa? The answer is the mucus layer.

Still according Scientific American (2017):

  HCl in the lumen doesn't digest the mucosa because goblet cells in the mucosa secrete large quantities of protective mucus that line the mucosal surface. Basic electrolytes, such as HCO3−, trapped inside the layer of mucus neutralize any HCl that penetrates the mucus.

By the way, a similar mechanism explains why doesn't the lysosome has its membrane destroyed by the enzymes it contains.

Sources:

Lodish, H. (2000). Molecular cell biology. New York: Scientific American Books.
Scientific American. (2017). Why don't our digestive acids corrode our stomach linings?. [online] Available at: https://www.scientificamerican.com/article/why-dont-our-digestive-ac/ [Accessed 30 Jul. 2017].


What is the connectivity between on-center & off-center bipolar cells?

First off, the post is quite lengthy and contains various sub-questions. I will answer the first two questions in detail, but only after starting with an abstracted overview of photoreception in the retina. By the looks of it, your basic understanding of photoreceptors and secondary visual neurons is incorrect. Clearing the general neurophysiological workings of the retina up should get you on your way in understanding questions 3 - 6.

Synopsis of information flow in the retina: sensation of light
In Fig. 1 a schematic of the retina is shown. It basically consists of three layers. Layer one contains the photoreceptors, namely the rods and the cones. These primary sensory neurons absorb the light with photopigments and generate electrical signals in response to that. The photoreceptors, in turn connect to the second layer, namely bipolar cels, horizontal cells and amacrine cells. These cells are responsible for the center-surround structure of the receptive field of the last layer of cells (Fig. 2), namely the retinal ganglion cells in the front of the retina, whose axons pass across the surface of the retina and form the optic nerve (Kolb, 2017).

Fig. 1. Retina. source: Quasar Group

Note that there are no light-sensitive cells in the retina besides the rods and cones (barred the retinal melanopsin ganglion cells, but please forget that for the sake of simplicity). This one detail should basically clarify the sub-questions 3 - 6 in your post. The first two questions I will address next.

Fig. 2. ON and OFF center responses. source: McGill University

Regarding the retinal bipolar system and your first two questions:

  Do rod-photoreceptors only form synapses with on-center bipolar cells (and on-center ganglion cells in the next step)?
  and
  Why do rod-cells only connect to on-center cells, while the cones connect to both on- and off?

Rod bipolar cells in the mammalian retina are of the ON type. In contrast to the cone system, rod bipolar cell signals are split into ON and OFF components by amacrine cells. The cone system piggybacks then on the cone system; Rod ON signals flow from rod bipolars to amacrine cells to ON cone bipolar cells. Rod OFF signals are generated between amacrine cells and OFF cone bipolar cells (Nelson & Connaughton, 2017). See Fig. 3 for an overview of the retinal connectivity between rod and cone bipolar cells.

Fig. 3. Retinal circuitry. source: Nelson & Connaughton (2017)

References
- Gouras, Color Vision: In: Webvision: The Organization of the Retina and Visual System (2017)
- Kolb, Simple Anatomy of the Retina. n: Webvision: The Organization of the Retina and Visual System (2017)
- Nelson & Connaughton, Bipolar Cell Pathways. In: Webvision: The Organization of the Retina and Visual System (2017)


MathsBio is quite a large field. It is an interdisciplinary branch having utility in a lot of branches in biology like biophysics, biomedical, genetics and molecular biology. Applied  Mathematics is generally used in modelling and understanding biological phenomena where we have to deal with large amount of data, for example the use of graph theory for analysing biochemical networks. Systems biology is an emerging field which uses a lot of mathematics.

You should pick a book depending on the field in which you want to use mathematics, though having knowledge of elementary biology is necessary. I am suggesting some books which cover wide application of mathematics in biology.

Mathematical Biology: I. An Introduction by JD Murray

For systems biology:

Mathematical Modelling in Systems Biology: An Introduction by Brian Ingalls


What makes a rotator cuff tear symptomatic in humans?

The underlying reason is difference in the rate of firing of torned and intact muscle in movement of shoulder joint.

Asymptomatic patients had minimal pain (<3 on the visual analog scale and no loss of active range of motion compared with the contralateral side); symptomatic patients had pain greater than 3 on the visual analog scale and decreased range of motion compared with the contralateral side (>10 degrees of motion loss). Electromyographic activity from 12 muscles and kinematic data were collected simultaneously during 10 functional tasks. Both symptomatic and asymptomatic cuff subjects demonstrated a trend toward increased muscle activation during all tasks compared with normal subjects. During the internal rotation tasks, asymptomatic patients had significantly greater (P<.05) subscapularis activity than symptomatic patients (65% maximal voluntary contraction [MVC] vs 42% MVC). During the carrying task, asymptomatic patients demonstrated significantly less (P<.03) upper trapezius muscle activation than symptomatic patients (16% MVC vs 50% MVC). During shoulder elevation tasks, symptomatic patients had significantly greater supraspinatus (52% MVC vs 28% MVC, P<.03), infraspinatus (32% MVC vs 16% MVC, P<.05), and upper trapezius (39% MVC vs 20% MVC, P<.04) muscle activation compared with asymptomatic patients. During heavy elevation (8 lb), asymptomatic patients showed a trend toward increased activation (P<.06) of the subscapularis compared with symptomatic patients (34% MVC vs 21% MVC). Differential shoulder muscle firing patterns in patients with rotator cuff pathology may play a role in the presence or absence of symptoms. Asymptomatic subjects demonstrated increased firing of the intact subscapularis, whereas symptomatic subjects continued to rely on torn rotator cuff tendons and periscapular muscle substitution, resulting in compromised function.

Source: Kelly, Bryan T., Riley J. Williams, Frank A. Cordasco, Sherry I. Backus, James C. Otis, Daniel E. Weiland, David W. Altchek, Edward V. Craig, Thomas L. Wickiewicz, and Russell F. Warren. "Differential patterns of muscle activation in patients with symptomatic and asymptomatic rotator cuff tears." Journal of shoulder and elbow surgery 14, no. 2 (2005): 165-171. https://www.ncbi.nlm.nih.gov/pubmed/15789010


Photosynthesis: What Powers the Splitting of Water?

Catalysis is about reducing the free energy barrier (aka. activation energy) of a reaction, so it does not require any energy. In photolysis (e.g. splitting water) you get the energy from the absorbed photons.

The exact process is called the Joliot-Kok cycle:

Figure 1 - Joliot-Kok cycle - source

So the photon separates the charges on the P680, after that the activated P680 activates the Yz intermedier, which forces the enzyme to the next step (Sx) in the reaction.

2012 - Transmembrane Electric Potential Difference in the Protein–Pigment Complex of Photosystem 2
2006 - The Manganese-calcium oxide cluster of Photosystem II and its assimilation by the Cyanobacteria

  The overall process comprises three types of reaction sequences: (a)
  light-induced charge separation leading to formation of the radical
  ion pair P680+QA(-) ; (b) reduction of plastoquinone to plastoquinol
  at the QB site via a two-step reaction sequence with QA(-) as
  reductant and (c) oxidative water splitting into O2 and four protons
  at a manganese-containing catalytic site via a four-step sequence
  driven by P680+ as oxidant and a redox active tyrosine YZ acting as
  mediator.

2007 - Photosystem II: structure and mechanism of the water:plastoquinone oxidoreductase.

So the process does not involve ATP or NAD or something like that just the "redox active tyrosine YZ". ATP and NADPH are created after the PS2 part of photosynthesis.

Figure 2 - Light-dependent reactions of photosynthesis - electron transport chain - source

The photolysis of water is about storing the energy coming from the photons (light) in ATP and NADPH. In the Calvin cycle the cells use the stored energy to reduce CO2 into carbohydrates. For instance glucose can be delivered to the cells in the root, which can use it as food.


In insects, does the Alanine repeat occur on the homeodomain sequence of the abdomen or does it occur on a different sequence?

Some background:

  The new work involved misexpression of the Drosophila Ubx protein in the presumptive thorax of transgenic fruitfly embryos. Limb development was suppressed because of repression of Dll. By contrast, the misexpression of onychophoran and crustacean Ubx proteins did not interfere with Dll expression and the formation of thoracic limbs. These results raised the possibility that the Drosophila Ubx protein is functionally distinct from Ubx in onychophorans and crustaceans. One study suggests that Drosophila Ubx has acquired an alanine-rich peptide that mediates the repression of gene transcription; this peptide is lacking in onychophorans. The other study provides evidence that the crustacean Ubx contains an additional peptide that modulates the activity of the alanine-rich peptide, and possibly other repression domains, in crustacean Ubx.

  Insect-restricted sequences include four regions N-terminal to the
  homeodomain (I1–I4), a peptide motif (QAQAQK), and an extended run of
  alanine residues C-terminal to the homeodomain

  The onychophoran Ubx protein might function as an activator of appendage development. When the onychophorans and arthropods diverged,
  Ubx acquired an alanine-rich repression domain near its carboxy
  terminus. This domain mediates constitutive repression in insects.
  But in crustaceans the addition of the regulatory peptide causes it to
  function in a conditional fashion. As a result, Ubx does not suppress
  limb development in crustaceans. But it eliminates abdominal limbs in
  insects, greatly reducing the overall number of appendages compared
  with crustaceans.

You can read about it here:

Levine, Mike. "Evolutionary biology: how insects lose their limbs." Nature 415.6874 (2002): 848-849.

Galant, Ron, and Sean B. Carroll. "Evolution of a transcriptional repression domain in an insect Hox protein." Nature 415.6874 (2002): 910-913.


Does all of life on Earth use the same DNA compounds for all species?

Yes, there are no variations on this. There are 3 domains of life; Archaea, Bacteria and Eukaryota. All use these identical nucleotides. All use all four of them, and this is one of many lines of evidence for the single origin of life on Earth.


Is there an organism which has a common English name which overlaps with another organism's scientific name (or vice versa?)

One great example I know of is the duck-billed platypus (Ornithorhynchus anatinus),  often simply called a platypus, which shares its name with the Platypus genus of ambrosia beetle.

Wikipedia gives a brief history of the taxonomy of the duck-billed platypus:

  The common name "platypus" is the latinisation of the Greek word πλατύπους (platupous), "flat-footed", from πλατύς (platus), "broad, wide, flat" and πούς (pous), "foot". Shaw assigned it as a Linnaean genus name when he initially described it, but the term was quickly discovered to belong already to the wood-boring ambrosia beetle genus Platypus. It was independently described as Ornithorhynchus paradoxus by Johann Blumenbach in 1800 (from a specimen given to him by Sir Joseph Banks) and following the rules of priority of nomenclature, it was later officially recognised as Ornithorhynchus anatinus. The scientific name Ornithorhynchus anatinus is derived from ορνιθόρυνχος (ornithorhynkhos), which literally means "bird snout" in Greek; and anatinus, which means "duck-like" in Latin.


No genes' ID in peak annotations during ChiP-Seq with ChIPpeakAnno R package

I had the same problem.
This how I solved it, I found the solution somewhere here, I don't remember where, and it worked for me.

macs.anno <- annotatePeakInBatch(gr_broadPeak, AnnotationData=TSS.human.GRCh38,
                                     output="both", maxgap=5000L)
 macs.annoL=addGeneIDs(macs.anno,"org.Hs.eg.db",c("symbol", "genename","entrez_id"))
 macs.annoDF=as.data.frame(macs.annoL)
   result=macs.annoDF[which(macs.annoDF$symbol!="NA"),]


Can enzymes catalyze thermodynamically unfavorable reactions?

Enzymes can catalyze a thermodynamically unfavorable reaction by coupling it with a thermodynamically favorable reaction. Most often, enzymes use ATP hydrolysis reaction (energetically favorable) as a source of energy (in simple terms) to drive the unfavorable reaction forward. One important point to keep in mind here is that enzymes don't drive a reaction equilibrium forward or backward; they just help in achieving the reaction equilibrium faster. Also pay attention that enzyme itself does not change the thermodynamics of a reaction (as you say, ∆G of the concerned reaction remains the same, except at equilibrium), coupling of a favorable reaction with an unfavorable one only helps in making the overall reaction favorable. This phenomenon, of one reaction changing the rate of another reaction, is called induced catalysis and has nothing to do with the enzyme itself.

I will talk about how enzymes do this using examples, while the other answer talks about the semantics. An example which will help you understand this concept is ATP synthase. It is an enzyme found in the inner mitochondrial membrane which allows the movement of H+ from the inter-membrane space towards the mitochondrial matrix, using the energy of movement (since this is favorable and exergonic) to generate ATP. The reaction would look like this:

$$\ce{ADP + P_i + 3 H^+_{IMS} \rightarrow ATP + 3 H^+_{matrix}}$$ (remember that exactly 3 H+ are not required, this is a simplified version)

But, ATP synthase does not drive the reaction forward; it just helps in reaching the following equilibrium faster:
$$\ce{H^+_{IMS} \leftrightharpoons H^+_{matrix}}$$ i.e. keeping the amount of H+ in inter-membrane space and matrix the same. This is why a constant gradient is required to keep them in working condition. For this, the electron transport chain continuously throws H+ into the inter-membrane space to maintain an electrochemical gradient. Along with this, enzymes ATP-ADP translocase and phosphate carrier continuously take out ATP from the matrix and throw in ADP and Pi. However, this lowers the electrochemical gradient (exchanging ADP3- for ATP4- in inter-membrane space, while phosphate carrier catalyzes electroneutral reaction), making the final reaction: $$\ce{ADP + P_i + 4 H^+_{IMS} \leftrightharpoons ATP + 4 H^+_{matrix}}$$

However, since the enzyme just helps in maintaining equilibrium, it can also work backwards i.e. it can also transport H+ against electrochemical gradient (unfavorable), coupling it with ATP hydrolysis (favorable) to reach equilibrium. The enzyme is now called ATPase and the reaction becomes: $$\ce{ATP + 4 H^+_{matrix} \rightarrow ADP + P_i + 4 H^+_{IMS}}$$

There are many more such enzymes which couple ATP hydrolysis (or other favorable reactions) to catalyze reactions which are either unfavorable or very slow (i.e. require a source of activation energy) under normal cellular conditions. Another factor, as the other answer explains, which helps in this is changing the concentration of products. As seen above, ATP-ADP translocase and phosphate carrier continuously decrease the concentration of products (ATP) and increase concentration of reactants (ADP and Pi) so that the overall equilibrium shifts forward and the enzyme keeps on driving the reaction forward (this, again, has nothing to do with with the enzyme itself, it is called Le Chatelier's Principle). Again, the other answer focuses on this issue.

References:

Enzyme - Wikipedia
Cellular Respiration


How and when did a dedicated immune system evolve?

Immunity has probably evolved more than once as it is completely necessary for survival.  You might even argue that defenses such as antibiotics and predatory behavior are immune defenses for single celled creatures.

As you point out, plants have a different immune system than animals do.  Insects do too.  They don't have innate immune memory which many animals have, where pools of cells embody the immune response to a specific antigen.  (i.e. encode for a specific immunoglobin or a tCell Receptor variant).

I found this reference that this appears to be the collective property of jawed vertebrates.  Even so, there are many late innovations in the immune system, where reptilian and mammalian immune responses vary substantially.

Its not clear to me whether other animals have the insect system. Animals that branched off before insect lines such as radiates probably have their own way of dealing with immune response.  That's just a guess though.


On what basis is each chromosome given a number?

Chromosomes are generally ordered by size in terms of number of nucleotides. The first chromosome is the biggest. Note that when there are sexual chromosomes (as it is the case in mammals or birds for example), the pair of sexual chromosomes are typically considered last irrespective of their sizes.

Note that in some species the ordering has been decided and further studies have shown that the actual size order does not perfectly match the ordering. This is for example the case in humans, where chromosome 11 is actually bigger than chromosome 10 (thanks @canadianer).

Numbering is mainly just a simple naming system. It is just handy to be able to refer to a chromosome as chromosome 3 rather than having to somehow describe this chromosome for other to understand what we are talking about.


Does an allergic reaction kill body cells?

Is it possible that the human body actually kills its own cells in the
  process?

Yes it is. It is happens not only as a result of allergic reactions (see comment of @terdon). But in case of allergy our body have 3 methods for killing own cells.

Cytotoxic, antibody-dependent (Type 2 hypersensitivity) The antibodies produced by the immune response bind to antigens on the patient's own cell surfaces.These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.
Immune complex (Type 3 hypersensitivity) Occurs when antigen-antibody complexes that are not adequately cleared by innate immune cells accumulate, giving rise to an inflammatory response and attraction of leukocytes
Cell-mediated immune memory response (Type 4 hypersensitivity) is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

See Wiki about types and diseases and about Hypersensitivity


Why is knowledge of bacterial pathogenesis important?

Because it is first important to understand a mechanism before you can think about using it for drugs. Take melanoma for example: A large subset of melanoma has a mutated and constitutive active BRAF kinase which permanently signals towards the nucleus and thus deregulates gene expression. Once this mutation was found it was possible to design inhibitors which only work on this specific mutation, which are available in the clinic today.

The same is true for example for activity of antibiotic on bacteria and the fight against resistance. Once it was known that the enzyme beta lactamase inhibits beta lactam antibiotice (penicillin or ampicillin for example) it was possible to find an inhibitor of the enzyme. The clavulanic acid works as a specific inhibitor and has been added to beta lactam antibiotics subsequently to overcome resistance. The same is true for changing antibiotic molecules chemically so they evade the established resistance mechanisms.

The contributions of basic research is the basis for applied research and drug design. Without them, this wouldn't work. Besides that it is also the curiosity of humans which drives science - without having any particular application in mind. These often come much later.


Genetic linkage greater than 50 centimorgans

Understanding the statistics we use when talking about recombination rate is an important question that is unfortunately too often dismissed in an intro course to evolutionary biology or population genetics and that is misunderstood by many. I have a partial understanding of it but hopefully, I'll manage to write a decent answer.
#Short answer
A recombination rate and a genetic distance (in centiMorgan) are two different things. While the recombination rate is bounded between 0 and 0.5, the genetic distance is bounded between 0 and infinity. There is a one-to-one function from the genetic distance to the recombination rate. For small recombination rate, the recombination rate and the genetic distance take very similar values but for greater values, the recombination rate is much lower than the genetic distance.
#Long answer
There is a tiny bit of math below. These equations are mainly for curiosity as one can understand the answer without understanding the maths behind it.
Definitions of $r$ and $M$
You are getting confused between two different statistics

The rate of recombination $r$ between two loci
$r$ is the probability for two loci to remain in the same gamete after recombination occurred. This probability cannot be greater than 0.5 ($0 \le r \le 0.5$).
The distance in Morgans $M$ (or more commonly in centiMorgans) between two loci. $M$ is the expected number of cross-over that occurs between the two loci.

Morgans and centiMorgans
You will note that I talk in Morgans rather than centiMorgans, which is not typical in the literature, but it helps at conveying the intuition of what it means. If $150$ centiMorgans $=$ $1.5$ Morgans. For two loci distant by 1.5 Morgans, the expected number of cross-over between the two loci is 1.5 (by definition). Below are some more explanations on these two definitions with some drawing :)
Case study with loci A and B
While $M$ and $r$ are closely related, they are not exactly the same thing. Consider the following sequence with the loci A and B
---[A]------------------[B]---

Let's assumed the two loci are very far apart and $M=2$. The probability of having exactly $k$ crossovers is therefore given by a Poisson distribution with rate $M=2$
$$P(k) = \frac{e^{-M}M^k}{k!}$$
Let's say for a given case that $k=1$ (a single cross-over occurred). This cross over is represented by a "/" below
---[A]-------------/----[B]---

Here clearly the two sequences at loci A and B will be separated. Let's say now that $k=2$ (two cross-over occurred).
---[A]---/-----/--------[B]---

Here, even if crossovers have occurred, the two sequences at loci A and B will remain together. Only the sequence in between the two cross-overs will come from the homologous chromosome.
Relationship between $r$ and $M$ - in words
You might see it coming from the previous section. The probability $r$ of these two loci A and B to be separated via recombination is the probability of an odd number of recombination events to occur between them (knowing that $M$ is the expected number of cross-overs).
Relationship between $r$ and $M$ - in equation
Let's calculate first the probability $p_{even}$ that an even number of cross-overs occur. This probability is just
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!}$$
, where I just added the constant $2$ before $k$ at both the numerator and denominator. With some algebra and trig, one can show that
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!} =
e^{-M}\sum_{k = 0}^{\infty}{M^{2k} \over (2k)!} = $$
$$e^{-M} \: cosh(M) = e^{-M}\left ( \frac{e^{M} + e^{-M}}{2}\right ) =
{1 + e^{-2M}\over 2} $$

As, $r = p_{odd} = 1 - p_{even}$,
$$r = 1 - {1 + e^{-2M}\over 2} = {1 - e^{-2M}\over 2}$$
Here we go! We have our relationship between $r$ and $M$! Let's graph it
#Relationship between $r$ and $M$ - on a graph
I just graphed the above equation in Mathematica (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 5}])

Here is the same graph but zoomed on lower values of $r$ and $M$ (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 0.1}])

We clearly see from the graph that for low values of $M$, as $M$ increases $r$ increase quasi linearly ($M≈r$). For greater values of $M$, $r$ still increases but slower and slower until reaching an asymptote / plateau at $\frac{1}{2}$. $r$ is indeed bounded between 0 (when $M=0$) and $\frac{1}{2}$ (when $M=\infty$).
Note, the fact that the sum of probabilities of every even $k$ in a Poisson distribution is always lower or equal to 0.5 is an interesting math fact in itself!


How were we able to determine the age of the first cell?

I can't imagine a team finding a fossilised cell and shouting "We've found the first cell !"

Well... not the very first cell, but one old cell, yes!

Most of these very old fossils are microorganisms found in seafloor hydrothermal vent precipitates, in stromatolite or in very old sedimentary rocks typically in Greenland but also in eastern Canada. There were also very old fossils found in sandstone in Australia.

  Might it have something to do with a well determined evolutionary rate conjectured to be constant and leading back to that particular time ?

No, that's now how we do. We just look for very old fossils. The reason we can't do such simple regression is three-fold.

As measure of 'evolutionary rate', we would typically use the substitution rate at neutral loci. The method is referred to as "molecular clock". The principle is easy (the stats and detailed implementation are a bit less easy). Consider a diploid population of size $N$. Each generation $2N\mu$ mutations are being created at a given locus, where $\mu$ is the mutation rate at this locus. If those mutations are neutral, then a fraction of $\frac{1}{2N}$ of these mutations are going to fix (fixing means reaching a frequency of 1 in the population). This result can be demontrate with a number of technics (incl. diffusion equations and branching processes) but I am not going to detail that now. This means that $2N\mu \frac{1}{2N} = \mu$ mutations will fix every generation in a population. If each substitutions occur at a new locus, then the number of substitutions accumulated over $t$ generations is $2t\mu$. For the substitution rate at neutral loci to scale with time we need constant mutation rate.

The assumption of constant mutation rate is very likely violated on such time interval.
For very distantly related lineages, substitutions won't always occur at new loci. There are tricks to deal with that but there's a point after which, all substitutions will occur at loci that have already received substitutions and there is no signal left to analyse.
We need two lineages to compare their number of substitutions but there is no reason to think that the oldest forms of life quickly separated in different lineages that would have survived until today

Was it really 3.8 billions years ago?

The date of 3.8 billions years ago that you got from CrashCourse (or that you may have read somewhere) is not as accurate as the Green brothers (authors of CrashCourse) may have made you think it is. There is much more than a 100 million years of wiggle room. The only think we can do is find a very old fossil of something that looked like a living thing, date it and claim that life is at least as old as this fossil is.

We think life appeared after the formation of the ocean (which happened 4.41 billions years ago), so any fossil older than that would be quite an extraordinary discovery. The earth was formed about 4.54 billions years ago, so of course we won't find any fossil older than that.

Papineau et al. (2017) is good read on very old fossil (and potential fossils) that we've found. From their abstract

  Here we describe putative fossilized microorganisms that are at least 3,770 million and possibly 4,280 million years old in ferruginous sedimentary rocks, interpreted as seafloor-hydrothermal vent-related precipitates

You will notice that we don't quite know the exact date of when abiogenesis happened. I recommend you having a look at this paper if you want to learn more.


Why do drugs which are hormones have long half-life?

The question is a bit vague, but in general a drug formulation is made of the active principle plus a series of other non-active compounds call excipients.

Excipients have multiple roles such as:

They act as fillers to add volume to the drug. Often only very small amounts of the active compound are present in each pill/capsule/etc. and it would be complicated for the patient to handle these very small amounts.
They act as binders to keep everything together and avoid the pill to crumble.
They can modify the pharmacokinetics of the active principle by speeding up or slowing down its release.

(there are many more resons to add excipients, see the relevant Wikipedia page for a longer list)

This last point is what you are looking for. If the hormone (or any other molecule, it doesn't really matter) is complexed with excipients it will be released in the blood or metabolized slower/faster depending on the specific molecules/formulations/mode of administration.


The answer depends a lot on the polymerase you are using. Some are engineered for better processivity, by fusion of a processivity-enhancing domain (Wang et al, Nucleic Acids Res. 2004), but even the best one will struggle after a few tens of kilobases.

You can push the length of the amplicons a little by playing around with conditions but to produce something significantly larger than the average limit of your polymerase, you will usually need to amplify smaller fragments, and then assemble them together. This is the strategy that was used to synthesize the 1079kbp synthetic genome of M. mycoides JCVI-syn1.0, the first "artifical genome" (Hutchison et al, Science 2016); the authors first amplified many fragments of 1.4kbp, and assembled them in vitro. To easily assemble large fragments in vitro, common one-pot enzymatic techniques include the so-called Gibson assembly (Gibson et al, Nature Methods 2009) and Golden gate assembly (Engler et al, PLoS One, 2008) for example.


Relationship between membrane current and voltage in neurons

This is a bit of a strange way to plot out these data, I think Figure 3.2 is easier to understand, but basically these are data plotted from early voltage-clamp experiments trying to walk you through how the Hodgkin-Huxley model was developed.

They step the voltage to a particular point and look at the current. There are two phases to this current: an early transient and a later plateau.

The shape of the "early" component ultimately results from the multiplication of two functions: the gating curve of the voltage-gated sodium channels and the reversal potential for sodium around 50 mV. If the voltage gated channels were simply open all the time, you would just have a straight line through +50mV, it would follow the right-side shape of the curve. The left-side of the curve is due to more channels opening as you depolarize more.

For the late component, which comes from voltage-gated potassium channels, all of the dependence is on voltage, because the plateau is at a point where all the potassium channels are open. You will also notice, however, that the slope changes a bit in time: it's steeper at the higher voltages, because the potassium channels open more quickly (and also sodium channels inactivate; the combination of the two would make it hard to separate them here).

Your picture is a bit different from these traces plotted in time: figure 3.3 is showing the peak of each component as a function of the voltage step. I think it would be better to present 3.3 as a series of data points rather than a smooth curve to make this more obvious.

Note that the actual numbers here are a bit different than one would see in a mammalian cell, because these original experiments used the squid giant axon which has some differences in voltage dependence, gating, and ion concentrations.

The reason sodium and potassium can be seen separately in these voltage clamp experiments is because:

A) Sodium channels open really fast early on, and then inactivate

B) Therefore, in the long term the potassium current dominates the sodium current.

If you blocked the potassium current and VG sodium channels didn't inactivate, the "early" part would look like a mirror image of the "late" part of the voltage-clamp traces. As-is, the early component is mostly sodium but also includes some voltage-gated potassium current as well that cancels it out and makes it appear smaller than it would otherwise be.

If you look at the late curve in your original figure, it's mostly straight from the point that all the K channels are open. For the late component, the K permeability is at max by -30mV so after that it's all linear from driving force. The little curve at the bottom up to about -30mV is the range at which not all the K channels are open, otherwise it would be a completely straight line, and it would reverse at the K reversal potential instead of asymptoting around zero. But it's not exactly zero because there is also some leak which is mostly potassium, and that does reverse around the K reversal.


Does the minimum spanning tree tell us anything useful about evolutionary ancestry?

Your graphic is omitting nodes of the tree, branching points, which are essential for trees and phylogeny.

When you read the data file, you should count the brackets ((( ))) because they signify where the tree has nodes, common ancestors.

You should generate simple phylogeny trees, prior to doing complex data mining for similarity. The names are in latin? there are genetic distance numbers? What format and data are you using? You have given the common animal names. you may have to use a database of common-and-latin-names to be ables to search "tiger"... that database will return "panthera tigris tigris"... And then you can start crawling up and down the tree branches to search for animals related to tigris tigris, by counting brackets and marking species close to that name.

To prevent the tree exploding to 5000 animals, you can
1/define a search depth. Depth 5, Five, will not go further than five brackets: (((((panthera_tigris_tigris)(lion)(cheetah)))))
2/represent a random fraction of the species (1/100 gives 50 animals from a 5000 tree)
3/use statistics measures to select certain animals based on data mining.

If you want to travel from whales to monkeys, you will have most of the mammalian family, and you will be able to count nodes and brackets by the dozens.

Not that parsing 5000 species has a big computational load that can take 1 hour to read through once, let alone 40 times!

Whichever statistics you are using to measure similarity, number of brackets / genetic distance numbers, you should have once represented trees as branches, nodes and leaves, because that is what tree data is meant to represent.

I'd recommend that you draw a tree using nodes and random animal selection, like 1% chance the animal is drawn in the final tree. When your tree has branches and is drawing OK, change the 1% selection line for the complex MST / MCD selection.


You'll probably have to titrate it down yourself. You might be able to estimate: The detection limit for ethidium bromide staining is about $1 ng$ per band. The insert says it's at "1 $\mu g/ \mu l$", but that's for all 40 bands and they're clearly not all at the same concentration. Depending on which bands you care about (1600 and below are dim), you might be able to get away with $(\frac{1}{25})^{th}$ their recommended concentration (1 $\mu g / 40$ bands = 25 $ng$) -- but I would titrate a small amount and see what works.


why male penis not considered as cartilage?

feel the tip of your nose. Mush it around, It's got a certain stale gummy bear feeling to it. Now feel your ears, all over. The outer edge, the back, the hard part in the front where the ear meets the face. Feel your adam's apple. This is cartilege.

When you feel your penis, does anything even feel close? Nope. It's just soft. Soft tissue, to be precise.

When stimulated, there are comparmemts within the penis which engorge with blood.

When they fill up with blood, the penis gets hard. That's all there is to it. No bones, no cartelidge.

If you have any questions, noe's the time to ask.


Why does the membrane of a neuron not stay at its depolarized state?

Three facts:

The K+ ions are heavily concentrated on the inside while the Na+ ions are heavily concentrated on the outside

The Na+/K+ ion pump is unidirectional. It can only pump K+ ions inside the cell while expelling the Na+ ions.

Finally only the Na+/K+ ion pumps can restore the ionic equilibrium.

The full scene:

Once the threshold is reached the Na+ voltage gated channels open up. So Na+ ions rush in, causing depolarisation.

Then the Na+ channels close while the K+ channels open. This causes rushing of K+ ions outside, thus slowly reducing the potential difference starting the process of repolarisation

Now the Na+/K+ ion pumps are geared up as the extracellular concentration of K+ and intracellular concentration of Na+ ions are high (which is the ideal environment for the pump to work.

PS:
Without the high extracellular concentration of the K+ ions the pump can't function any faster than the basal rate even though the intracellular concentration of Na+ ions exceed the normal value by many times. High concentration of K+ ions in the extracellular environment is essential for restoration of the ionic equilibrium.

Edit:
I meant unidirectional in the sense that when actively pumping sodium is always pushed out while potassium is always pushed in.
Thanks to AliceD for pointing out that when the gradient is reversed, the pump synthesizes ATP due to forced movement of ions in the opposite direction.


Why did the indigenous peoples of northern Asia and America not evolve the same physical characteristics as people of Nordic ancestry?

If you look at the Wikipedia image from their lovely article on human migration, you'll notice that after arriving from Africa, some humans went west and others went east.  The ones who went east went on to most of the arctic regions, except in Western Europe.  The physical differences between these groups probably can be explained as random variation, though we may never know what social and environmental factors (such as the behavior of predators or prey) might have driven adaptive changes.
Previously some might have suggested different levels of Neanderthal ancestry could be involved, but this seems even harder to credit in light of recent evidence that all humans have a small but significant degree of Neanderthal heritage.


Identifying statistically significant gene rich and gene poor regions

Interesting question. I don't myself know how to do this but a literature search returns some older papers on how this was achieved for pig and chicken genomes over a decade ago. The best way to do this today is to look through annotated genomes (like the mouse mm10) and use a gene density metric. You can achieve this with R code, writing your own code, trying to use some of the rich features provided in-browser at the UCSC genome browser (for mice, otherwise start here), or perhaps try to search literature for gene density stuff. I defer to others for more specialized answers.

PS. Since you're also interested in determining statistical significance, you probably will need to apply this over a sliding window across chromosome lengths, and this kind of question has been answered often elsewhere on SE (example). Sorry I can't be of more help; good luck!


Is the minicolumn the unit of the neocortex?

I am skipping the background information (I will amend my question later) for now.

So, what is known about minicolumn?

The term was coined by Ramon y Cajal who saw narrow stripes, running from white matter to the surface (reference) in his preparation with Nissl staining.
The hypothesis about minicolumns to be anatomical units was proposed by Mountcastle in 1957, known as "columnar hypothesis" in neuroscience (reference).
It has been shown that minicolumns grow from progenitor cells within the embryo (reference), and don't require brain functions to emerge.
Minicolumns  contain neurons within multiple layers of the cortex (reference).
One of the latest review on the topic (Buxhoeveden & Casanova, 2001) contains 121 references to experimental papers on this topic.

I wouldn't say that these columns are developmental relic, for there is a known heterogenity among these structures (like hypercolumns, macrocolumns and segregates) and it is rather improbable that all these types are relics.

So, as long as we stick to the term "anatomical unit", I see no problems why columns (with all possible types and sizes of them) should not be it.


How much genomic variation one usually find within a given bacterial species?

Genetic variation within bacterial species can be much higher than one might expect.

First, this can be a difficult question to answer quantitatively because even just testing whether two strains are part of the same bacterial species is difficult: the "gold standard" method is actually experimental and involves whole-genome DNA-DNA hybridization (with a cutoff of 70% relatedness). Modern sequencing approaches have shown this usually corresponds to around 95% average nucleotide identity (ANI) (see here).

However, an ANI of 95% does not actually mean that the genomes are 95% identical: it means that of the shared sequences, one expects 95% of the nucleotides to be the same. The percent of the sequences that are actually shared in the first place can be much, much lower. For example, this paper compared 61 sequenced strains of E. coli. Out of the ~15K genes observed in at least one genome sequence, only 6% of genes were observed in all strains. Variably-present genes made up around 80% of a typical E. coli genome. This is a high level of variability, but not outrageous: an analysis of only nine P. putida genomes, for example, showed a core of at most 33% (ref).

So, if a gene is indeed indeed present in two strains of the same bacterial species, then it is likely to be highly conserved. But there is also little guarantee of finding the exact same set of genes in two strains of the same species. This means you cannot naively take chromosomal coordinates from one strain and apply it to another: you need to actually figure out which sequences correspond to one another in your genomes.


Systems Biology of triacylglycerol (TAG) synthesis in Jatropha

Triacylglycerol synthesis in plants is probably highly conserved.  The metabolic pathway is here.

The Jatropha genome sequence is also available.

Given this some effort has been made to figure out how these genes are regulated.  This is a microarray study of Jatropha focusing on fatty acid and TAG biosynthesis.   This gives some idea of how TAG genes respond to one another, but of course will not find the promoter sequences or the transcription factors themselves.

Having spent a summer going over fatty acid synthesis, I can only say that there has been a lot of wet lab work done on these pathways which would probably be conserved in the Jatropha plant.  The literature would be quite extensive.  Integrating all of that is more like a paper for publication than an answer on stackexchange.  This sort of outlines the procedure... do you have a more focused question?

I'll outline one way of approaching this - there are an uncountable number of variants if you tweak it.  There are other ways to get this, most notably looking for defective mutants, the method which is still used in plants quite a bit.

Anyway here is a genome based approach:

1) Identify genes in the pathway of interest. choose 10 or so genes that you think constitute your network.  This is an editorial decision. Ultimately if you start looking at genes regulated by the same transcription factors as being included in your network, you will eventually take in the entire genome and the work will be impossible to accomplish.

2) find candidate promotor binding sites. look at the upstream promotor regions for all these genes.  you can look at how these are conserved between similar plants by examining the same gene promotor regions aligned against each other.  This doesn't work very well.

2b) Another way of finding these is to do a pull down experiment where transcription factors are bound to DNA and a DNAse digestion is done and remaining fragments identify the binding sites.  All this somewhat assumes that you kind of know which transcription factors are responsible for each gene. That is probably not the case here.

3) find the transcription factors important for the plant pathway.  this is not easy - one way is to try knock outs of the TF genes.  I imagine this plant has 4000 + of these genes.  around 1-2% may be involved.

So far these methods have been use for the ENCODE project as well as some bacterial genomes.  a plant is a new scenario which will have issues of its own.


Why does olfactory sensation need lateral inhibition?

Here is the paper which directly answers your question.
Urban NN. Lateral inhibition in the olfactory bulb and in olfaction. Physiology & behavior. 2002 Dec 31;77(4):607-12.
A few salient points:

It is true that the spatial gradient of sensory attributes is not as clear in the olfactory bulb-neuronal topography as it is at other places with lateral inhibition, but lateral inhibition still seems to serve a similar purpose in all these cases, namely sharpening the perceived stimuli. It is not settled how is this "edge enhancement" brought about in a nontopographical system ( "...Specific inhibitory connections between groups of cells with similar receptive fields may allow for functional lateral inhibition in such nontopographic systems, but no evidence for such specificity has been provided in the olfactory system...").

Unlike say for example in the Retina, where lateral inhibition creates the on/off centres, the lateral inhibition in olfactory bulbs is more widespread. That is, the area inhibited is relatively more expansive. This fact, coupled with the highly localised excitation caused by odours, suggests that "....lateral inhibition will be most effective at suppressing signals with low spatial frequency, in other words, signals that involve activation of broad regions of the olfactory bulb...". This is what I assume was meant by your source while referring to background odours.

The overall neurological effects of lateral inhibition is not settled, and the evidence is scanty. To quote the aforementioned paper, "... A simple prediction for the effects of lateral
inhibition on olfactory behavior would be that impairment
of lateral inhibition should impair performance on olfactory
discrimination tasks, and perhaps that these effects should
be strongest for tasks involving discrimination of very
similar odorants. Such a result has been obtained in experiments
in the honeybee in which inhibition is blocked by
picrotoxin. However, in these experiments, the blockade
of inhibition did not affect the odor-evoked firing rate of
the cells recorded, suggesting that the impairment of discrimination
ability was independent of a broadening of
tuning curves..."

Have a look at the cited paper, and the papers quoted therein, for further information.


Is it possible to induce erysipelas to treat cancer, under the condition that the patient is to be given antibiotics to control the erysipelas?

Before any experimentation on humans, any treatment undergoes an extensive testing on animal models.

Besides, there must be some degree of confidence in the potential curative effect of a remedy in order to start experiments in the first place. An experiment like the one you describe would not be approved by your institute's animal ethics commission (there is such an unpleasant but important thing) unless you prove with some line of evidence and prior knowledge that the suffering of the animals is likely not going to be in vain.

It is now also customary to provide an official approval from the ethics commission during publication submission. [You would not need such an approval for flies or worms, but for rodents (which would likely be your first test object in the case in question) or primates you would.]


How can 3' end polyadenylation protect cellular RNA from ribonuclease degridation?

According to my book Molecular Biology Principles of Genome Function by Craig et al, eukaryotic RNA degradation does not have an initiation, as in bacteria where pyrophoasphate hydrolase hydrolyses the 5'-triphosphate to 5'-monophosphate, and is therefore the initiatior.

In eukaryotes the polyA-tail is shortened by a deadenylase enzyme complex which contains a 3'to 5' exonuclease called CCR4. But deadenylation of polyA-tail doesn't necessesarily need to lead to degradation since it is reversible by post-translational readenylation.

Poly A tail protects the mRNA by not letting the nucleases reach the mRNA itself. As long as poly A tail is degraded, its just fine, since it can readenylate back again. The figure below shows the degradation of mRNA in eukaryotes, which can be either in 5' to 3' direction or 3' to 5' direction.

What you are thinking of is ubiquitination of proteins, which is a post-translational process which can mark the proteins for degradation.


Identifying a thin, black, worm-like creature with a hammer-shaped head

Hmm, I don't believe I have ever seen that before, but it looks  like a Hammerhead Worm (Bipalium kewense).


It isn't just humans that have fused sacral vertebrae. Animals on the phylogenetic tree ranging from Squamata (lizards), to Aves (birds), to even Monotremata (egg-laying mammals) all have fused sacral vertebrae. The fused vertebrae can serve as a stronger, weight-baring structures for animals that do land locomotion, including humans. Any bones that have evolved to withstand extensive force will also be thick or fused together: and example is the fusion of the radius and ulna in frogs. This fusion of bones allows for the forearms to withstand the force of landing after a large leap.

Photo references:

Bird Sacrum: http://www.discussfossils.com/forum/uploads/842/sacrum_2.jpg

Frog Radioulna: http://classconnection.s3.amazonaws.com/573/flashcards/4420573/png/appendicular_skeleton-frog-142D89D722717E64724.png


Multiple studies have found moths along with most other insects to be significantly more attracted to lamps that emit smaller wavelengths such as ultraviolet (UV). Some species of moth appear to be more attracted to shorter wavelengths than others. The visibility of the light to the moth, the distance between the moth and light, and the brightness of the light are also contributing factors in whether the moth will be attracted to light.
Why Moths are Obsessed with Lamps | Nat Geo Wild

Langevelde et al. found that actinic lamps with a mean weighted wavelength of 382 nm (lamp type a) were the most attractive to moths in both abundance and species richness when compared to other lamps that emitted longer wavelengths. The lamp types used along with the data they collected are displayed below:

References & Further Reading
Hsiao, H. (1972). The attraction of moths (Trichoplusia ni) to infrared radiation. Journal of Insect Physiology, 18(9), 1705-1714. doi:10.1016/0022-1910(72)90100-x
Google Scholar | Crossref
Owens, A. C., & Lewis, S. M. (2018). The impact of artificial light at night on nocturnal insects: A review and synthesis. Ecology and Evolution, 8(22), 11337-11358. doi:10.1002/ece3.4557
PubMed | Google Scholar | Crossref
Somers-Yeates, R., Hodgson, D., McGregor, P. K., Spalding, A., & Ffrench-Constant, R. H. (2013). Shedding light on moths: shorter wavelengths attract noctuids more than geometrids. Biology Letters, 9(4), 20130376-20130376. doi:10.1098/rsbl.2013.0376
PubMed | Google Scholar | Crossref
Truxa, C., & Fiedler, K. (2012). Attraction to light - from how far do moths (Lepidoptera) return to weak artificial sources of light? European Journal of Entomology, 109(1), 77-84. doi:10.14411/eje.2012.010
Google Scholar | Crossref
Van Langevelde, F., Ettema, J. A., Donners, M., WallisDeVries, M. F., & Groenendijk, D. (2011). Effect of spectral composition of artificial light on the attraction of moths. Biological Conservation, 144(9), 2274-2281. doi:10.1016/j.biocon.2011.06.004
Google Scholar | crossref


How does a biologist decide when she has enough results to publish a paper?

When you do science you start with a question or a hypothesis. How is Gene A regulated? Or "does hormone B have an effect on the immune system". Or whatever.

Then you start by thinking how you can prove or disprove your question/hypothesis with experiments. You then do your experiments and see if they are enough to prove your question. It often happens that you have to do additional experiments to cover side-questions which appear during the work or to exclude some side-effects which may also be important. If you have done all this (with replicates) and looked from different angles on your problem, then you can start writing an article.

This includes some introduction from the literature and a classification of your results into the things already known. If you make strong claims, then you will need a lot of arguments (=results) to prove your point. It is quite hard to argue against "common knowledge".

The question of how much research is enough is quite philosophical, since you usually don't "finish" a topic. You look only at certain aspects from a certain angle. This can be quite different for other researchers.


People who think in creationism or think about species rigidly might have a bit problem with that, so let me describe an example:

When are humans "adult"?
Legally, at 18 (or your national equivalent). However, everyone understand that people are becoming adult gradually. Sometimes, they "age" very quickly after some harsh experience (16 years old student who parties all days because parents pay for it vs 16 years someone whom father died and he has work to help feed his small sisters as family did depend on father's wage).

Now imagine that you don't have all this information, but very incomplete "images" or "screenshots" of this kind of development. There would be quite a mess from it. You have image of one kid at 13 who is still young, another kid at 19 who is partying, single image of this 16 year old adult who has to feed his family and image of 48 year old gentleman.

If you go with this mindset that most of species that ever lived you can't get and you are just guessing something from a few snapshots that are themselves incomplete as well (e.g. we often don't have whole skeleton but just single bone from a lot of species), your idea on what to expect will change. This is a first step. Then you need to realize that most of fossils that shows some transition do not form lineage, but instead branches that are related. Finally, when you understand this (and modify your expectations and "what to look at", you can take any relatively complete and well-studied set of fossils like human ones. On human lineage (with great apes), we can see gradual increase of brain and in the case of human, gradual decrease in size of jaw. Development of hip bone is nice as well as it shows gradual process of adaptation to upright walking.

Another line of examples, but again, you need to redefine your expectations, is to point on dogs. If we had dogs in our fossil records, there would be large amount of species, instead of one "dog" species.

Or you can just point out at plants and say that "species" does not really mean anything.


the population tends towards infinity

Well yes, Hardy–Weinberg principle is based on several assumptions one of them being "population size is very(infinitely) large". Another being "Mating is random".

However, even if the population is small your version of calculation does not make much sense biologically.
If we talk about civets (gonochorists) the probability an offspring has two blue eye color alleles is
(probability mother gives him blue eye allele copy)*(probability father gives him blue eye allele copy).

The two probabilities are not connected. What allele individual gets from mother has no influence over which allele they get from father. This is assured by "Mating is random" assumption.

To calculate the probability we should calculate:

(allele proportion in all possible mothers)*(allele proportion in all possible fathers)

In your example there is no information about sex of individuals, so the best approximation we have for allele proportion in females/males is the overall allele proportion in the whole population (20%) therefore the best calculation is 20%*20% = 0.04

  but doesn't that assume replacement of alleles!

It seems you think that there is some rule that each parent allele copy is used only once in next generation. This is not true. Under random mating some parents can produce many children and some have none. Some allele copies get replicated several times some don't get replicated at all. In large populations the resulting random changes to allele frequency even out. In small populations allele frequency drifts.


Physiological reason why leaves got twisted when treated with indole acetic acid

Disclaimer: Not my area of research

Since IAA (auxins) can induce growth, partially acting through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), it seems likely that the explanation to your result is differential growth/elongation rates on the upper and lower side of the leaves. This could result from uneven spraying, e.g. by spraying the leaves from the top. Faster growth on the top part of the leaf would lead to downward twisting, which seems to be what is happening most of the time.

You could test if this is the case by doing a simple experiment where you carefully apply IAA with a brush on both sides of the leaves for some plants, while others are sprayed. If uneven application is the cause you should see twisting when spraying but not when applying with a brush.

However, auxin is toxic to plants at high concentrations, so you also need to consider the concentration you are using.