What is this long, thin and segmented insect I found in my house in India?

UPDATE:

Based on a comment by ArthurJFrost reminding me of the existence of a group of insects I totally forgot about, AND based on a closer examination of the cerci and what appears to be external mouthparts in the image of the OP's specimen, I think this insect might actually be a webspinner!

These insects would be also about the right size, with the described and shown body plans, but also with short (but non-pincer-like) cerci and external mouth parts as in the OP's image. Female webspinners are wingless [source], as well, as the OP's image also appears to be.

See, for example, the black webspinner (Oligotoma nigra) from New Mexico, USA from bugguide.net:

 Source: bugguide.net

See also here for additional images of Oligotomidae species. (by the way, O. saundersii is the type species of Oligotomidae within the Indian subcontinent).

@ArthurJFrost, since you are more the expert than I on hexapods, PLEASE PLEASE write up an answer detailing how we might all feel more confident knowing that the webpsinner (and not the dipluran) is the better answer. Visually it appears to be the case to me, but I think you'd be able to point out some specifics for us all to learn from!

I will certainly default to you to write up the "official" webspinner answer since my update here on my post is simply to direct away from what I now think is an incorrect answer. I would gladly link to your answer to further emphasize that you came up with this answer.

OLD ANSWER: [Informed guess, but I think it's wrong!]

Based on the thin body plan, extended, segmented abdomen, lack of wings, and pair of posterior cerci, I was immediately reminded of a dipluran (or "two-pronged bristletail").

 Sourcce: Wikimedia

It would be good to know the size of your specimen since most diplurans are smaller than 10 mm  (though some can reach 50 mm!). A better photo would also be appreciated, since diplurans typically have antennae with beadlike segments, and I cannot tell if that's the case in your photo. I will note that many diplurans have much longer and even filamentous cerci, but others (like your specimen) have shorter cerci.

I am not sure why a dipluran would be inside your house, however, since they live in soil or leaf litter. [source]

Other organisms to rule out:

Snakefly (Agulla adnixa) -- no cerci (vs. yours)
Centipede -- too many legs (vs. yours)
I can't rule out earwigs since I am unfamiliar with the species in India. However, your specimen looks longer, thinner, and possessing smaller cerci than the earwigs I am more familiar with. [A clearer image of the thorax would help to determine if wings are present or not, which (if present) would rule out diplurans altogether and suggest it might be some earwig species I don't know).


How can I find a complete human genome file

The National Centre for Biotechnology Information has a link to a genomes FTP site - on that page, there is a file labelled .../genomes/H_sapiens (this a direct link to that directory).

There are numerous files therein.  From the README file:

  Sequence data include chromosomes, contigs, RNAs, and proteins
  generated through the NCBI Reference Sequence and NCBI Genome
  Annotation projects. Map data presented in the Map Viewer resource are
  also provided here.


Jackson Labs offers a service for this for what looks like a reasonable price. I have no experience with the service other than general good feelings about Jackson.

We have a unique selection of mouse single nucleotide polymorphism (SNPs) panels useful for a diverse set of mouse research applications.
Applications of SNP scanning services

Development of congenic mouse lines
Confirmation of C57BL/6 substrain background

[...]
Available custom designed SNP panels specifically tailored for your needs
The right panel for your needs - $179/sample
[...]
C57BL/6 substrain characterization panel distinguishes between C57BL/6J (B6J) and C57BL/6N (B6N) or C57BL/6NTac (B6NTac) genetic backgrounds

--GENOME SCANNING SERVICE
Edit to include some points raised in comments:

"These panels [i.e. the ones Jackson labs offers, noted above] seem to be intended for comparing between known strains, like when you make a transgenic strain and are in the process of backcrossing. It would not be as useful for monitoring drift, or for comparing an unknown C57BL-derived line to a standard one." – Bryan Krause
Any mouse colony will diverge from other colonies, especially if there are relatively few founders.

The identification of two CNVs in the small portion of the genome screened demonstrates that individual mice of highly inbred strains are not isogenic and suggests other CNVs may be segregating within C57BL/6J as well as other carefully maintained inbred strains.

--Genomic copy number and expression variation within the C57BL/6J inbred mouse strain

At the very least, intermittent back-crossing to a mouse from a different source is recommended.

With time, isolation and a little spontaneous genetic drift, a founder pair can produce a new substrain in as little as three generations (something to bear in mind if you're breeding mice in-house without “refreshing” the gene pool with an intermittent backcross to a bona fide C57BL/6J ... Clearly, substrains of C57BL/6 (and other inbred strains) are not all the same.

--All (C57BL/6) Mice are not Created Equal

Simply buying new mice as needed, from the same (reliable and standard) source each time, gives you a better chance of consistency, since a large breeder is less likely to see on-going founder effects.

If you have a solid reason for keeping your own colony, talking to the experts at Jackson Labs would be a good starting point; presumably monitoring strain consistency is something they think about as an ongoing issue, and they can give better advice than we can.


What is the difference between silent and synonymous mutations?

I would say that silent mutations, as they have been defined, are a subset (or perhaps even same as) of synonymous mutations. However, the term, "silent mutation", is not used so much these days. Almost every research paper that I have read pertaining to this topic has always used the term "synonymous mutation" irrespective of whether or not it has a phenotypic effect. It seems that the term, "silent mutation", is confined only to textbooks.

If you consider silent mutations are mutations that are not reflected in the phenotype then there some points that you should consider.

As canadianer mentioned, these mutations can be present in non-coding region. However, mutations in non-coding regions can also affect the phenotype. Moroever, as they mention, synonymous mutations can cause changes in translation rates because of the codon bias which in turn can lead to phenotypic differences (Kimchi-Sarfaty et al, 2007; Waldman et al, 2011; Buhr et al, 2016). These phenotypic differences can arise due to altered protein concentration or altered folding states. So a synonymous mutation is not essentially "silent"
A non-synonymous mutation may not affect the phenotype (neutral mutation).

I would say that this definition should not be used unless the majority of the scientific community agrees on redefining the term. Till then, you can possibly use the term, "neutral mutations", to mean mutations that do not affect the phenotype. Remember that neutrality of "neutral mutations" is defined with respect to fitness. However, if your measure of fitness pertains to the molecular function of the gene then this definition works.


Do single crossovers occur in circular polynucleotides?

Although crossover events can be observed in mitosis (mitotic recombination), they most frequently occur in prophase I of meiosis (crossing over in bivalents). Circular chromosomes are common in prokaryotes, but eukaryotes have linear chromosomes. Remember what meiosis accomplishes and that prokaryotes reproduce asexually. Prokaryotes don't have a need for -- or engage in -- meiotic division, so crossover events in circular chromosomes can really only be observed in instances of mitotic recombination, and I don't know the frequency of this in prokaryotes.

In prokaryote DNA replication, if any entangling of the two product circular chromosomes occurs, it is resolved by DNA topoisomerase. So perhaps a crossover would present a similar situation and the cell would resolve it by similar means.


Expanding the SETI initiative to seek intelligent data within DNA sequences?

Let's extend your idea a bit... Ok, there are conserved sequences that we may not know what their function is. Let's assume that they are indeed not functional and are some kind of message left by an ancient form of intelligence.

How would you go about detecting that? It is already given that they are highly non-random, but this is not surprising and many "non-message" sequences have this property. Also consider that these sequences are quite short, meaning that they will have low information content. This means that if you check enough conversion codes and use imagination, you would probably be able to find several "messages" which are "hidden" there (e.g. "bible codes" etc). In other words, as I am a scientist that deals with probability and pattern recognition frequently, you will have a very hard time trying to convince me that you found a real hidden message... Formally, you don't have a satisfying background model.

The main difference from SETI is that there they know that their background is essentially random noise, so it is much easier to detect "intelligent" messages.


Common genes and enzymes involved in pathogen entry into host

Passing through plasma membrane by remodeling host cell seems reasonable choice but actually most of pathogen use cell's normal functions like endocytosis, phagocytosis, pinocytosis etc to enter (well, indirectly you need actin remodeling for this also but pathogen is not doing it actively. ). Check this review for some 'simple' mechanism pathogen use to enter cell. As far as your question about enzymes, there are lot of common enzymes (specially manipulating kinases) which are important in these pathways.Pathogens use lot of other factors to exploit host. Cytoskeleton remodeling is indirect output of many of these signaling events. Just to put into perspective, recently hiked on social media, Ebola virus use micropinocytosis like mechanism to enter into host cell. Some other representative examples in following figure (Source :Gruenberg and Goot 2006 )


How to refer to person-derived and place-derived species names

According to A Source-Book of Biological Names and Terms by Jaeger, the appropriate terms are the simple, obvious ones:

"Geographical" for place-derived names and

"Personal" for person-derived names.


Why were wisdom teeth not eliminated by evolution?

Reductions in the size of our lower jaw that result in wisdom teeth sometimes becoming impacted result from changes in our diet, and are not the direct result of the evolution of a smaller jaw. This means that natural selection has had at most 8000 years to act on the phenomenon, which occurs in people in their mid to late 20s (who, historically, probably would have already reproduced if they were going to), and so the selective advantage of lacking wisdom teeth has not had enough time or been strong enough to cause the no-wisdom-teeth phenotype to spread throughout the human population.

Global human mandibular variation reflects differences in agricultural and hunter-gatherer subsistence strategies - Cramon-Taubadel, PNAS (2011)

Before Agriculture, Human Jaws Were a Perfect Fit for Human Teeth - Smithsonian.com (2015)

Incongruity between Affinity Patterns Based on Mandibular and Lower Dental Dimensions following the Transition to Agriculture in the Near East, Anatolia and Europe - PLOS One (2015)


Hormonal effects of Luteinizing hormone on endometrium

Both FSH and LH are indirectly involved in endometrial thickening:

GnRH regulates release of the gonadotropins- luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from specialized cells (gonadotropes) in the anterior pituitary gland
LH and FSH promote ovulation and stimulate secretion of the sex hormones estradiol (and estrogen) and progesterone from the ovaries.
As estradiol levels increase, the intact basal layer regenerates the endometrium to its maximum thickness late in the ovarian follicular phase (proliferative phase of the endometrial cycle).     ...{1}

Again, wikipedia{2} says the same:

...In both cases, the endometrium initially proliferates under the influence of estrogen.

The difference between the hormones, of course lies in their other functions. You can see this for more on that. To clarify again, the endometrium does not thicken 'differently' under the influence of each.
{1}-https://www.msdmanuals.com/professional/gynecology-and-obstetrics/female-reproductive-endocrinology/female-reproductive-endocrinology?query=lh
{2}-https://en.wikipedia.org/wiki/Endometrium#Cycle


HPV. How do viruses persist outside the body?

bob1's answer is good, but I was already working on this one so I'll go ahead and post the parts that aren't redundant:
What does it mean for a virion to lose infectiousness?
To be 'infectious' a  virus particle perform a set of tasks that result in more virus particles. A simplified list for HPV could be: attach to receptor on host cell > enter cytoplasm > enter nucleus > make proteins > copy DNA > assemble new virions from protein and DNA > exit cell. The first four tasks must be performed by proteins in the virion; if enough of these are degraded, the corresponding task cannot be completed, and the virion cannot infect a cell. This means that there are many different routes by which any particular virus might be inactivated. One of the references in the question suggests HPV can be inactivated by gunk from dead cells sticking to the otherwise-viable virions:

The greater inactivation of the virions in the extracts at 56 C may be due to denatured cellular protein, which visibly aggregated at 56 C and above, interfering with infection.

Viruses are not metabolically active on their own!
This means that damage cannot be repaired, and also that a functional protein cannot be 'reset' after it changes shape. To use the SARS-2 spike protein as an example, the spikes have energy stored in them like a mousetrap. If the transition from open to closed is triggered while the spike is bound to ACE2 on a host cell's membrane, the motion of the spike protein changing shape will bring the viral membrane in contact with the host membrane, fusion occurs, and the virion contents enter the host cytoplasm. If the transition is triggered before the spike is bound to a host receptor, that spike is 'dead'. SARS-2 virions have many spikes, but if all of them trigger prematurely, the virion as a whole becomes uninfectious. The transition from the high energy 'prefusion' state to the lower energy 'dead' or 'postfusion' state has to be energetically accessible in order to be triggered by the new host cell. This means that the risk of premature triggering is inescapable. Therefore, damage or premature transition of all copies of some viral protein that changes shape to allow cell entry is a likely candidate for inactivation for any viral species. This hasn't been investigated systematically, though, so there's no reference I can cite for this.
In papillomaviruses:
Unlike coronaviruses, HPV doesn't have a membrane that can fuse with the host's for cytoplasm entry. Instead, it is absorbed by endocytosis, then the capsid disassembles, and L2 disrupts the endosome membrane. The details of how this happens aren't known, but it's likely that L2, which is protected inside the capsid most of the time, becomes exposed by structural changes to L1 which occur in the endosomes. This suggests to me that degradation of L1 is the main cause of viral inactivation outside of the cell. That hypothetical structural change of L1 would need to be identified before you could start to investigate if it's present in inactivated particles.


Does carbon dioxide from carbonated drinks enter the bloodstream?

Is there enough CO2 to matter?

A can of soda contains about 2.2 grams of carbon dioxide (see this question from Chemistry.SE).

A human outputs about 1 kg of CO2 daily from respiration, though the rate can be much higher during physical activity. So, even if all of the CO2 content of a can of soda was absorbed into your blood, that's only 0.2% of your ~resting daily CO2 output.

A normal range for [partial pressure of CO in blood] is about 38-42 mmHg.

Gas exchange

The surface area of the lungs is something like 50-75 m2.

The surface area of the stomach is much smaller, closer to 1 m2.

Therefore, gas exchange is going to be much more efficient in the lungs than at the stomach.

Result

Any CO2 is going to be fairly efficiently cleared from expiration if it gets into the blood from the stomach. It's unlikely that you could detect any appreciable change in CO2 levels beyond what happens naturally as blood travels through the circulation and picks up CO2 from the periphery, and it's even less likely this difference would be greater than the difference between rest and exercise. That isn't even accounting for the buffering capability of the blood and diffusion into other tissues (both would smooth out any rise of CO2 over time) as well as not all of the CO2 will even make it to the stomach, and the gases that make it there can also leave via the esophagus.

As a sidenote, the Mythbusters partly addressed this issue in their episode on Mentos+coke. One of the factors they discussed is that much of the CO2 doesn't even make it to the stomach because it is released in the process of drinking, though they didn't quantify it. Therefore, CO2 is likely to have even less of an effect than described above.


Can rapid eye blinking induce epileptic seizures?

“Self-induction” in photosensitive epilepsy is a well-described and fascinating  phenomenon. Photosensitivity itself is rare, occurring in only ~5% of patients with epilepsy.1 Among this group it has been estimated2 that 25% self-induce epileptiform activity. The most common methods appear to be passing a hand with open fingers repeatedly across the visual field and, as you query, blinking.

Quoting from a classical paper on the topic by Andermann et al:3

  The method of inducing seizures varies
  both in detail and in principle. Light contrasts are always brought about, but they may either be applied to and alternate for the whole visual field—an effect produced by blinking or batting the eyelids and induced by any flickering light—or else the attack is elicited by the spatial displacement of brightness and darkness  over the retina.

This phenomenon is most common in epileptics with established photic triggers, and the scenario triggering an attack is often in the context of bright sunlight. However, this has also been described in epileptics who are not otherwise photosensitive. See, for example, “Seizures triggered by blinking in a non-photosensitive epileptic.”4
Notably, some authors have questioned whether blinking and other “triggers” are actually themselves ictal phenomena (i.e. representing the initial phase of an epileptic event) rather than a form of voluntary self-induction. For more on that hypothesis, see Ames, 1971.5

Presuming that this is, in fact, self-induction as has been traditionally postulated, the question of why such patients repeatedly self-induce seizures is perhaps the most interesting aspect of this. There has been some research2 considering the psychiatric factors underlying the behavior. Quoting Andermann3 again:

  The reward a patient seeks by self-stimulation may lie in escape from unwanted situations, in attracting attention, in punishing those around him, or, indeed, in deriving pleasure from the attack.

References

Kasteleijn-Nolst Trenité DG. Photosensitivity in epilepsy. Electrophysiological and clinical correlates. Acta Neurol Scand Suppl. 1989;125:3-149.
Ng BY. Psychiatric aspects of self-induced epileptic seizures. Aust N Z J Psychiatry. 2002 Aug;36(4):534-43.
Andermann K, et al. Self-induced epilepsy. A collection of self-induced epilepsy cases compared with some other photoconvulsive cases. Arch Neurol. 1962 Jan;6:49-65.
Rafal RD, Laxer KD, Janowsky JS. Seizures triggered by blinking in a non-photosensitive epileptic. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):445-7.
Ames FR. "Self-induction" in photosensitive epilepsy. Brain. 1971;94(4):781-98.


How likely is it that Earth has millions of different species?

We can be reasonably certain that ALL species that exist today share a common ancestor, a common origin. Every single species we have even encountered, for example, uses a long chain of nucleotides (DNA or RNA1) to store its genetic information. If life had arisen through multiple independent sources, we would expect to find different solutions to the problem of passing genes to offspring.

To put it another way, all forms of life we have found can be placed in one of three main classes (superkingdoms): eukaryotes, prokaryotes and archea. All other types of life come under one of those three categories (viruses are special and not really considered alive2):

Now, any organism we have ever seen uses the same basic systems of storing its genetic information. In fact, there are even certain genes that are conserved (similar in sequence) across all domains of life (see my answer here for some examples). That is why this version of the tree has a common root. All lines start from a single original line (commonly known as the Last Universal Common Ancestor, LUCA).

In summary, all the evidence we have points to a single origin of life. There are too many shared features to assume multiple origins. Despite their enormous diversity, all organisms share certain very basic systems.

NOTES

As far as I know, only certain viruses use RNA instead of DNA, all truly living creatures use DNA. Even if I'm wrong about this, the differences between RNA and DNA at this level are small enough that the common origin still holds.
See here for more in why viruses are not alive.


MLE estimation with Mk model in ape or phangorn?

From reading though the documentation, the Mk model does not appear available.

Although the JC69 model is, which this source describes as a slightly less generalized form as Mk.  The JC69 model still assumes equal substitution rates and equal base frequencies.  To use the JC69 model in phangorn set the model to "JC" and in ape set the model to "JC69".


Living tissues are not usually transparent. Obviously, the crystalline lens needs to be in order to let light go through. This is done by a fairly complicated system that requires active pumping of ions in and out. When that system stops, the lens becomes opaque resulting in that white cloudy appearance. This can happen in living animals (including humans) too, such as in cataract.


Why is it advised that infants are fed mother's milk?

The phrase "Breast is best" is a hotly debated one (source: The Guardian and personal communications with many folks). The reason why we don't want to feed infants cow's milk is, however, anything but debated, because

Cow's milk does not provide enough:

Vitamin E
Iron
Essential fatty acids

And because it contains too much:

Protein
Sodium
Potassium (source: NIH's MedLine)
Further, mother's milk is generally free of pathogens, cow's milk may not be (source: Australian Unity). However note that, unfortunately, HIV can hitchhike within the maternal white blood cells to the infant (Quintanilla, 1996)

There are many benefits to mother and infant of breast milk. These benefits are, however, typically compared to the benefits over formula. No study will compare the benefits of mother's milk over cow's milk, simply because infants should never be fed cow's milk.

The benefits of breast milk for the infant are the following:

Breast milk a nearly perfect mix of vitamins, protein, and fat, all provided in an easily digestible form, as compared to formula;
Breastfeeding lowers baby's risk of having asthma or allergies;
Plus, babies who are breastfed exclusively for the first 6 months, without any formula, have fewer ear infections, respiratory illnesses, and bouts of diarrhea. They also have fewer hospitalizations and trips to the doctor (source: WebMD).
Breast milk contains a variety of growth factors, including EGF, BDNF and GDNF that may promote vascularization and neural development (Ballard & Morrow, 2014).

There are a host of immunoprotective factors present in breast milk. These proteins offer protection against diarrhoea, food allergies and infections. The immunoprotective components of human milk include, but are not limited to:

Lactoferrin : binds to iron, thus rendering it unavailable to viruses, fungi and bacteria, which is an effective means of inhibiting their growth (Ballard & Morrow, 2014);
Lysozymes: destroy viruses and bacteria by disrupting their integrity (source: NIH's MedLine);
Secretory IgA: immunoglobulins that destroy viruses and bacteria. Secretory IgA is believed to survive the harsh conditions of the intestines, especially in infants and is therefore active in the intestines of the baby. IgA can bind to pathological viruses and block their receptors necessary to invade the epithelial cells lining the intestinal wall. It also clumps bacteria together through cross-linking, which may affect their dispersion. Bacterial cell membranes, like shown in Salmonella, may be disrupted by IgA binding (Mantis et al., 2011). As mentioned by anongoodnurse in the comments; because mother and baby share the same habitat and hence encounter the same pathogens, the antibodies produced by the mother will be more beneficial to the baby than any other mammal on earth;
Human milk contains a variety of chemokines and cytokines that can cross the intestinal barrier, where they communicate with baby's cells to influence immune activity. Many cytokines and chemokines have multiple functions, and milk-borne cytokines may be grouped broadly into those that enhance inflammation or defend against infection, and those that reduce inflammation (Ballard & Morrow, 2014);
Bifidus factor: promotes the growth of beneficial bacteria in the gut and limits the growth of disease-causing bacteria (source: NIH's MedLine).
A variety of immune cells, including macrophages, T cells, stem cells, and lymphocytes. In early lactation, the breastfed infant may consume as many as 1010 maternal leukocytes per day. They can differentiate into dendritic cells that stimulate infant T-cell activity (Ballard & Morrow, 2014).
Breast milk changes in composition according to the infant's needs, something cow's milk can never accomplish; The first fluid produced by mothers after delivery is colostrum, which is distinct in volume, appearance and composition. Colostrum is produced in low quantities in the first few days postpartum and is rich in immunologic components such as secretory IgA, lactoferrin, leukocytes, as well as developmental factors such as epidermal growth factor. It contains relatively low concentrations of lactose, indicating its primary functions to be immunologic and trophic rather than nutritional. Levels of sodium, chloride and magnesium are higher and levels of potassium and calcium are lower in colostrum than later milk (Ballard & Morrow, 2014).

For more complete reviews on the immunochemistry of breast milk, please refer to Ballard & Morrow (2014) and Mantis et al. (2011)

The mother also benefits:

Breastfeeding burns extra calories, so it can help mothers to lose pregnancy weight faster;
Breast feeding releases the hormone oxytocin, which helps the uterus return to its pre-pregnancy size and may reduce uterine bleeding after birth;
Breastfeeding lowers the risk of breast and ovarian cancer. It may lower the risk of osteoporosis;
Breastfeeding has been linked to higher IQ scores in later childhood in some studies (source: WebMD);
During lactation, menstruation ceases, offering a form of contraception;
Mothers who breastfeed are less likely to develop breast cancer later in life;
Breastfeeding is more economical than formula feeding;
Hormones released during breast-feeding create feelings of warmth and calm in the mother (source: NIH's MedLine).

In terms of bonding:

Skin-to-skin contact during breastfeeding, and eye contact all help a baby bond with the mother and feel secure.
Oxytocin release is known to promote the bonding with bubba. A newly born person can cause dramatic changes in the life of mommie (and daddy!), and a steady release of oxytocin promotes the bonding and love of mommie for the bubba (source: WebMD).

References
- Ballard & Morrow, Pediatr Clin North Am (2013); 60(1): 49–74
- Mantis et al., Mucosal Immunology (2011) 4: 03–611
- Quintanilla, Nurs Times, (1996); 92(31): 35-7


Well the simplest way is to cut the gene at the both ends from operon by means of proper restriction enzymes but in case that you get more than one recognition site then you can use microRNA or proper oligo to make a hairpin loop and break that part
If you only want to silence the operon then you just need to cut it nearly at middle of the gene and ligate it with a nonsense sequence, then it will loose it's functionality.


What is meant by "complexity of carbon sources"?

Consider all the different types of carbon molecules one can find on earth.

Proteins.  Sugars like cellulose and starch.  Alkanes like methane and tar.  CO2.  Alcohols.  A boatload of variety.

Now think of how each one is used or can be used by an organism.  I will chow down on a potato.  And some alcohol. Termites eat cellulose.  Anaerobic bacteria use methane.  Plants eat up the CO2.

One carbon nothing eats is CaCO3 or limestone.  I am not sure why.  Oh - also diamond.  Not many things can metabolize a diamond.  Although maybe they don't get the opportunity to try...


What happens to the cut-out introns from a pre-mRNA?

Yes. Ribonucleases (RNAses) break down the spliced RNA strands back into mononucleotides, and these building blocks can be reused.

They will be broken down into nucleotide monophosphates, so they will have to be re-phosphorylated to triphosphates before they can be reused for transcription.

Here are a couple of reasonable reviews of the mechanisms:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177198

Note: this one also mentions that sometimes introns are not fully degraded to single nucleotides, but instead can serve as signaling molecules.

http://www.sciencedirect.com/science/article/pii/S0092867409000671


No, there is not. Cells in the bloodstream reach most areas in the body, but there are certain privileged areas which stop cells, drugs and macromolecules from leaving the bloodstream and entering the tissue. These privileged areas are thought to exist in sensitive or important areas for their own protection:

  Immune privilege is thought to be an evolutionary adaptation to protect vital structures from the potentially damaging effects of an inflammatory immune response. (Wikipedia)

The most common example of such an area is the blood-brain barrier, but there other barriers to privileged areas, including the blood–testis barrier, the blood-retinal barrier and the blood-ocular barrier. Cells do not pass from the blood through these barriers, except in disease (Larochelle et al. 2011).

Related reading:

The first chapter of Blood Groups and Red Cell Antigens has a decent high-level overview of different types of blood cells and their roles in the bloodstream and the immune system.

How do immune cells overcome the blood–brain barrier in multiple sclerosis? Larochelle et al. 2011


What is the exact frequency of Delta brain waves during Slow Wave NREM Sleep?

Periklis Y. Ktonas and Atul P. Gosalia performed such an analysis. It was published in 1981 under the heading "Spectral Analysis vs. Period-Amplitude Analysis of Narrowband EEG Activity: A Comparison Based on the Sleep Delta-Frequency Band"

The bins were quite wide but their analysis showed peak power spectrum moved between 0.84 and 1.96 Hz at different times.

I think the paper would serve you well, as it highlights the difficulty in achieving what you have set out to achieve. The frequency is not constant, even over short timescales. It depends for the most part on a balance between the intrinsic, basal polarity of thalamocortical neurons, and the effect of synchronising, inhibitory input from the reticular nucleus. The latter is in turn subject to cortical feedback. There are huge numbers of neurons involved. The period between bursts, and the number of action potentials per burst, is quite variable.

Perhaps it might be possible to set up a device that alters the round in real time, based on the EEG measurement.

With regards to your 'bonus' questions:

(1) The video posted does show an effect on the thalamic rhythm, which is surprising, as it had been thought that in deep sleep, sound has no effect on the thalamocortical circuit, since it is gated at the thalamus. This shows the plausibility of the hypothesis. However, the video does not provide any evidence that this alteration in rhythm is beneficial. It is possible that it is not and this possibility should be eliminated.

(2) Clearly the sound has an effect on the rhythm, so it seems entirely plausible that there is an optimal sound to maximise the effect.

(3) It will be hard to organise the phase, given the continuous, rapid shifts in period, unless done in combination with EEG in real-time.

(4) I am not aware of any research attempting to correlate thalamic rhythms with heart beat, although it would be quite easy to do. However it is highly unlikely there is a correlation, since the thalamocortical period has a lot of variation moment to moment, whereas the heart rhythm does not. Also the thalamocortical rhythm is generaly somewhat faster.


You have to scale amounts of all PCR components proportionally depending on the volume of the reaction. The polymerase is no exception in this respect, the only difference is that you measure it in terms of activity - units. So in your protocol you have 0.025 U/µl and you have to maintain this concentration when changing the volume.


Can Helicobacter pylori be eradicated naturally?

H.pylori is a bacteria that is a cause for Peptic ulcer disease of human being. It helps to create more acidic product and causes ulcer. But human body is naturally protected to H.pylore, but excess stress,irregular life style etc helps H.pylori to growth and causes ulcer. Simple measure can escape you from this infection. 1. Intake enough water 2. Maintain oral hygiene is very Imp, 3, at bed time gurgle by H2o2 ( Hydrogen per Oxyde) 3. If you are infected then triple therapy for 3 weeks is the choice of treatment


Large plasmid ligation: do I need alkaline phosphatase?

A plasmid vector will always be prone to recircularisation when a single restriction enzyme has been used, but recombinant plasmids will also be formed during the ligation. Alkaline phosphatase treatment can be used as you describe; you can also  simply make sure that the insert fragment is present in high molar excess and be prepared to work harder at the end to find the recombinant plasmids. Neither approach is correct or incorrect, they both have their limitations.

Of course the best approach is to avoid this type of cloning altogether.

Added later

Incidentally, the wording of your question suggests that you think you may have more of a problem because the plasmid vector is a little larger than usual. Not so! Circularisation is favoured because the two ends are tethered so the effective concentration of each is high with respect to the other. As the plasmid gets bigger the tether is longer and the tethering effect will be less.


The regulation of tear production (lacrimation) involves reflexes initiated by sensory neurons in the cornea. Corneal pain receptors (nociceptors) and mechanoreceptors detect damaging stimuli and induce tearing to cleanse the ocular surface (and, hence, Shigeta is right as tear gas stimulates pain receptors). Corneal neurons sensitive to drying of the ocular surface also appear to increase tearing. These neurons also respond to cooling and hyperosmotic stimuli (Kurose & Meng, 2013). The tear duct is necessary to drain the tears away from the eye into the nasal cavity (Fig. 1).

Fig. 1. Tear glands and tear ducts. Source: Mayo Foundation for Medical Education and Research.

Strong emotional responses like crying can result in an overflow of tears (epiphora). Epiphora is mediated by the limbic system (the emotional center of the brain), especially the hypothalamus. Such strong parasympathetic stimulation is accompanied by other symptoms, like reddening of the face and convulsive breathing (University of Minnesota, Duluth).

Reference
- Kurose & Meng, J Neurophysiol (2013); 109(10): 2517-22


There has been a study by Jackson, Meltzoff & Decety (2005) who investigated the neurocorrelates involved in the perception of pain.
In order to assess this, they carried out an fMRI study in which their subjects were shown photographs of of feet and hands in situations that are likely to evoke pain and also a control set of photos that were free of any pain evoking stimuli.

Their results display that with the experimental photographs, there is a strong increase in bilateral changes in several regions that we know are involved in the perception of pain, namely:

  the anterior cingulate, the anterior insula, the cerebellum, and to a lesser extent the thalamus

Notably, the activity of the anterior cingulate was most strongly correlated with the participants rating of the other persons pain, which suggests that the anterior cingulate is especially modulated according to the subjects reactivity to pain of others.

Source:

Jackson, P. L., Meltzoff, A. N., & Decety, J. (2005). How do we
perceive the pain of others? A window into the neural processes
involved in empathy. NeuroImage, 24, 771-779.
doi:10.1016/j.neuroimage.2004.09.006


How many proteins could participate in a complex

The problem with coming into bioinformatics from a non-biological background is all too apparent in your question, and very real. You are dealing with a category of object called a protein complex, you suspect that it will be reasonable to exclude a proportion of them, but as you don’t really know what they are (other than at a basic level) you don’t understand the implications of doing so. As generally in such cases, you need to find an appropriate biologist to help you.

All I can do is try to make an analogy. Consider an entity that the biologist who knows nothing about computing calls a ‘program’. As a surrogate for the number of components, let us consider that it is written in Java and so that one can judge its complexity by counting the number of classes. (I know that the examples I am giving are not all normally written in Java, but in theory they could be.) I could write a simple program that just parses a file and outputs a second file in a different format. That would use very few classes (especially without a GUI interface). Then I might write a modest web application to query a database and return biological information to the user. That could have perhaps two dozen classes. A more sophisticated commercial web application would have more. And then we get into commercial desktop applications from the relatively modest utilities to the monsters like Microsoft Word.

But just classifying computer programs on the number of Java classes would have severe limitations, just as would an alternative approach such as programming language (python for scripts, C++ for large applications). What I would really need to decide is what kind of program to include or exclude.

Likewise with protein complexes. I am not familiar with Corum (I just checked the website on my phone) but one might assume that the protein complexes it contains range from basic enzymes and proteins with two different subunits (perhaps in two or more copies, generally in a regular structure) like haemoglobin or immunoglobulin G, through proteins that interact with several species and posses half a dozen different subunits, to what are in effect machines of greater or lesser complexity, like the ribosome, the two subunits of which may together have 70 to 80 proteins.

So, yes, it would be reasonable to exclude the relatively small number of very large complexes which constitute a class of “machines” (and your size distribution suggests where the cut-off might be). But for your work to be valid you need to know specifically what class of complex you are excluding so as to be able to state that you had deliberately decided to ignore large complexes like ribosomes, splicesomes etc. And name them.

It’s tough at the moment, I know, but in my opinion you do need to sit down with a biologist and have this explained in more detail, reviewing the names of the complexes in the Corum list that you are considering excluding.


Can epigenetic changes affect reproductive success?

This article deals with the effect of phenotypic variation brought on by epigenetic patterns, and how these are inherited to the next generation. Their conclusions?

Our results show that epigenetic variation is inherited in chickens, and we suggest that selection of
favourable epigenomes, either by selection of genotypes affecting epigenetic states, or by selection of methylation
states which are inherited independently of sequence differences, may have been an important aspect of chicken
domestication.

However, I personally prefer this article, as it has a more profound implication on reproductive success and addresses your question specifically. They found the there is a species-level difference in DNA methylation between humans and chimps, but more importantly that this difference is responsible for the causation of numerous lethal diseases/conditions, which has a direct impact of the fitness of the species as a whole.

Finally, we found that differentially methylated genes are strikingly enriched with loci associated with neurological disorders, psychological disorders, and cancers. Our results demonstrate that differential DNA methylation might be an important molecular mechanism driving gene-expression divergence between human and chimpanzee brains and might potentially contribute to the evolution of disease vulnerabilities. Thus, comparative studies of humans and chimpanzees stand to identify key epigenomic modifications underlying the evolution of human-specific traits.

In summary, evidence has shown that epigenetics does seem to play an active role in the evolution of species, although the exact mode of inheritance of DNA methylation from generation to generation is unknown.

References

Nätt, Daniel, Carl-Johan Rubin, Dominic Wright, Martin Johnsson, Johan Beltéky, Leif Andersson, and Per Jensen. “Heritable Genome-wide Variation of Gene Expression and Promoter Methylation Between Wild and Domesticated Chickens.” BMC Genomics 13, no. 1 (February 4, 2012): 59.

Zeng, Jia, Genevieve Konopka, Brendan G. Hunt, Todd M. Preuss, Dan Geschwind, and Soojin V. Yi. “Divergent Whole-Genome Methylation Maps of Human and Chimpanzee Brains Reveal Epigenetic Basis of Human Regulatory Evolution.” The American Journal of Human Genetics 91, no. 3 (September 7, 2012): 455–465.


Will humans and animals be harmed by frequencies outside their hearing range?

The only sensible answer to these questions is "sometimes".

The reason: even a simple monotone must be described by both frequency and amplitude. Any frequency can cause harm with enough amplitude, and any frequency can be harmless when the amplitude is low enough. If you want to actually quantify the damage, you'll need something like an equal-loudness curve, but for damage rather than loudness. As a proxy, you could use the pain threshold of the equal-loudness curve.

As for the second question, there is nothing magical about 20kHz: physical damage will always fall on a spectrum, there is no single frequency and/or amplitude at which damage begins. If you set an oscillator to constant amplitude and slowly turn up the frequency, you'll notice that the sound slowly dies out around 20kHz. The damage threshold will behave the same way.


Nope, not true.  It's a pretty common myth; that paper cites a  reference from 1932 in primates claiming to show that the ovaries alternate.  A few papers before this, in particular this one from 1991 showed that ovulation was not alternating, but this was the first to do so in actually fertile woman.  In particular,

  Alternate ovulation occurred in 61 of the 119 succeeding ovulations (51.3%, not significant) which means that there was no consistent tendency to alternation.

Alternation only occurred half the time.  Neither did they find a difference between side preference; right-side ovulation occurred in just over 50% of the cases, not significantly different.

FSH, follicle-stimulating hormone, and LH, luteinizing hormone, stimulate each ovary equally, but one ovary will get slightly ahead.  Ovulation (and indeed pregnancy at times) is a positive-feedback loop, meaning the response will be exponential; if one ovary is even just slightly ahead it will rapidly dominate the other.  The less-developed one quickly senses the other is ahead of the game and ceases to respond.


Long-term-potentiation and memory. Where do we stand?

Is there clear evidence that LTP is involved in long-term memory (not
  counting 1 hour as long-term...)?  Has LTP/LTD been shown in vivo
  after long period of time (e.g. months).

This Journal of Neuroscience paper shows LTP in vivo measured out to one year:  Abraham WC, Logan B, Greenwood JM, Dragunow M. 2002. Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. The Journal of neuroscience : the official journal of the Society for Neuroscience 22: 9626–34.


The answer to this question emerges from an examination of the structure of tyrosine — or, more strictly, the tyrosyl residue, which is how it exists in proteins, the concern of the question:

  It has both hydrophobic and hydrophilic features and can exhibit both
  behaviours depending on the circumstances.

The ring is aromatic and hydrophobic, but the hydroxyl substituent is hydrophilic.

It is important not to try to fit things into rigid classifications that may not be appropriate for them. Indeed, one should ask how useful a particular classification is in any circumstance, and be aware of its limitations.

The classic illustration of the importance of these dual properties of tyrosine is in Perutz’s description of the differences between the oxy- and deoxy- structures of haemoglobin, where oxygenation of the haem cause the movement of tyrosine from the hydrophobic interior of the protein to the hydrophilic surface. This movement is associated with breaking of ionic bonds between the subunits in the overall change in quaternary structure:

(This is a modified version of Fig. 3 of the original, produced many years ago for teaching purposes. The wiggly line is a cartoon representation of the polypeptide chain of the α-subunit of haemoglobin between His-F8 and the C-terminal Arg residue. For clarity, the preceding region is not shown but its continuation indicated by an arrow head.)


Is every protein encoded by just one gene?

There are proteins encoded by more than one gene.

It would be a heterodimer protein of quaternary structure. One famous example would be haemaglobin, which is assembled from alpha and beta sub-units.

Also, one gene is capable of coding for multiple proteins!

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

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

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


Doubling the concentration of extracellular calcium hyperpolarizes a neuron. Why?

This paper and this paper supports the second possibility I hypothesized. That is a increase in external Calcium concentration leads to an increase in conductance of Potassium.

While the increasing the external Potassium concentration can be shown to depolarize the cell with by calculating the Nernst potential for the Ion, the Calcium Ion has a non-intuitive effect. This means if one increases the outside concentration of Calcium Ions then inevitably there will be a small increase in the internal concentration of Calcium ions on the inside. This will slightly bias the Calcium Activated Potassium Ions to be a little more open. Thus raising the conductance of Potassium. This will mean there is a net hyperpolarizing current keeping the cell less excitable.


Human genetic diversity in Africa in comparison with the rest of the world

Here is a tree based on mitochondrial DNA variations in human populations.

van Oven M, Kayser M.  Hum Mutat. 2009 Feb;30(2):E386-94.
Updated comprehensive phylogenetic tree of global human mitochondrial DNA variation.

Looking at genetic distance between populations via mitochondria DNA, all nonafricans are descended from a founder in one mtDNA group (L3).  All the other L groups are African populations: L0 is the San people, L1 is Mbenga pygmies, L5 is Mbuti pygmies, and the others are other African groups.

If one considers each L haplogroup to represent genetic variation then 5/6 (83%) of human genetic variation is from African populations.

From a different source looking at genetics differently   A map of human genome variation from population scale sequencing Nature. 2010 Oct 28; 467(7319): 1061–1073

  Populations with African ancestry contributed the largest number of
  variants and contained the highest fraction of novel variants,
  reflecting the greater diversity in African populations. For example,
  63% of novel SNPs in the low coverage project and 76% in the exon
  project were discovered in the African populations, compared to 20%
  and 33% in the European ancestry populations for the exon and low
  coverage projects respectively.


Can crows see in ultraviolet? If so, does their plumage look different in UV?

Corvids (and raptors) are reported to not see UV Håstad et. al. 2005.

However, American crows are reported to recognize sex-specific differences in plumage that are invisible to humans Eaton 2006.

Unfortunately, I don't have access the latter paper so I don't know what the basis for that discrimination is or how to reconcile that result with those of Håstad et. al.

You might also find this well referenced blog post that summarizes these results to be of interest.


What kind of spider is this and is it dangerous?

That's a nice female Nursery Web Spider, related to the Fishing Spiders.  They're rather pretty animals, and like almost all spiders, quite harmless to anything that's too big to eat.  The very rectangular cephalothorax ('head' end) pattern and the simple wavy line down the abdomen are the key clues for this one.  They also like to sit with the front legs arranged in pairs.
https://bugguide.net/node/view/2919/bgimage


Does apoptosis occur more at a particular time of day?

Your question is quite well-formed, however all I can say so far is: I don't know. Maybe it is known, however I could not find any information on this in the literature. In general, little is known about the crosstalk between circadian rhythms and apoptosis. It is known that circadian rhythms regulate DNA damage repair, so I would assume that the same is true for other maintenance functions such as apoptosis of redundant or damaged cells.

I don't know which research tools are available to you, but if you want to look at the effect of the clock on apoptosis signalling in a simplified setting, I would recommend synchronising the clock of culture cells with dexamethasone (you'll find a lot on that in the literature) and then using the apoptosis read-out of your choice on samples of these cells taken in regular intervals. I recommend taking samples every 4 h over the course of 24-48 h. You can make this less tedious by synchronising separate batches at different time points. As read-out for apoptosis I recommend Caspase-3 / -7 activity, ideally by Western Blot or an enzymatic activity assay using Ac-DEVD-AMC or something similar.

If you want to have a look at the effect in a more complex, physiological model, you will have to use mice.

I hope I could help you a little. Good luck!


Do pet animals and humans perceive good and bad smells differently

TL; DR Mostly no.

On a molecular basis, cats' and dogs' noses look quite similar to ours. Most of what we know about smell comes from studies on non-human mammals, and is supposed to apply to humans too. So, big similarity, but...

Cats and dogs distinguish far more kinds of than humans. It's likely they know more kinds of bad smells and good smells, possibly including from things that we think lack odour.
Many animals also have a working vomeronasal organ, that is, a sensing organ similar to the olfactory mucosa we use for sensing common smells. The vomeronasal organ detects pheromones, the smell-like signals used for communication between animals. We, humans, are at least deficient, if not completely unable to use the vomeronasal organ and pheromone signals. It is debatable whether animals conflate regular smells with pheromones. Pheromones are very efficient in conveying information about potential sexual partners, rivals, and so on. So these are a completely different set of bad and good smells, available only to animals. That is, if we can call those sensations smells, a big if.
On the other hand, humans evaluate smells culturally. Some people learn to enjoy offensive smells that people from other cultures carry on disliking. Since dogs have limited ability to manipulate smells and to convey information to another dog, I doubt they can form these cultural constructs of smell. We sense sensuality in a perfume; the dog senses a bunch of pungent flowers, neither good, nor bad.


Can the brain influence gene expression?

As has been pointed out in comments, the brain can certainly affect gene expression; but so can anything in our bodies, because the blood stream is super good at carrying stuff around the body to wreak havoc.

But I'm going to take a somewhat uncharitable view of this question1; and assume that what you are asking about is high-level mental processes affecting gene expression throughout the body, which is not a thing that happens.

The basic concept to bring forwards here is that the brain is hell-a layered. The brain is an extremely complicated organ, and while it's not a complete mystery, it's not an organ that we generally can be said to understand, at least not on the level that we can be said to understand in major terms how, say, the liver, kidney or spleen works.

What we do know is this: The brain forms a massive network of neurons; the shape of which informs our personality, memory and cognitive functions. Even our simplest thoughts involve, by necessity, thousands of neurons, and anything more complicated than 'Fire!' involves tens, hundreds or thousands of thousands (millions) of neurons.

At the same time, it's important to understand that our brain does a lot of things that we're not directly cognisant of. For one, our brain controls our breathing. As you're reading this, you'll discover that you take control of your breath, but also that you haven't done so for several hours at the very least, and maybe not for days or weeks, and you haven't died from hypoxia yet. Our brains do these kinds of things all the time, and we hardly ever notice.

Genetics are a very, very, very low-level thing. Way lower of a level than mere breathing, genetics is the engine that drives decision making at a cellular level; which is so far removed from consciousness that it's hardly imaginable.

And this is where layering really comes into play: While recent research indicates that brain cells have hijacked DNA replication techniques to store memories, most of our actual thoughts exist only on levels that are so much higher than the nuts-and-bolts of our brains that the physical structure of our brains don't even come into play.

Essentially, thought as we understand it doesn't exist within individual neurons, but only within the relationship between neurons. When it comes to cognitive or metacognitive processes, things like genetics becomes an implementation detail isolated from the higher-level system as a whole. The underlying physical structures can affect gene expression, but do so not as a response to thoughts or subconscious desires, since these don't exist in the individual neurons; but as a response to primal needs like "more sugar for the brain!" or "more oxygen for the brain!" or "more protein for the brain!".

In other words: While the (sub)conscious mind can affect gene expression, it does so in terms of resource management, not in terms of how body tissues act, because the mind as it is has no physical concept of bodily function.

1: Uncharitable, yes, but it does make the question more illuminating and interesting, IMHO.


Is there a distinction between the fisherian runaway theory and Fisher's sexy son theory?

The Fisherian runaway is the observed phenomenon of an "arms race" of features and traits in sexual dimorphism, the Sexy sons hypothesis is the theory of why it happens. One is factual/known data and the other is a hypothetical explanation as to why we see that data.


Where can I find SARS-CoV-2 genome sequences for the UK?

Oxford University's Bugbank project is designed to collect SARS-CoV-2 samples (and other microbial cultures) from UK Biobank participants for sequencing. Once completed this data will be available to researchers through the UK Biobank:

  We originally developed this system as a pilot study to determine the feasibility of prospective microbiological culture collection from UKB participants to create a microbiological biobank (‘bugbank’) for joint studies of epidemiological, human genetic and pathogen genomic risk factors for infection. In light of the COVID-19 pandemic, we have repurposed the system to provide near-to-real-time data on SARS-CoV-2 positive and negative test results for UKB participants.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank (2020) *

* Disclaimer: I have worked on this project.


What is meant in biology by the term "evolved"?

"More evolved" is actually meaningless in all contexts. See terdon's answer for a good explanation.

In the strictest sense, an organism can be said to be more divergent than another when comparing both to an outgroup, such that there is an inferred most common ancestor in reference to which to make the comparison. In this case, one organism is more divergent if there are more changes to this organism than the other, relative to the reference point.

However, when speaking, many people get lazy, and use "more evolved" as shorthand, wishing it to mean something like "more divergent". Even "more divergent" is meaningless in the following contexts:

when there is no outgroup understood
when describing increasing complexity (obligate parasites have lost complexity and have had more evolutionary changes than their non-parasitic relatives)
when the outgroup is poorly chosen. Mammal vs reptile comparisons should not, in general, use prokaryotes as the outgroup.

Edited 2013/12/06 to reflect the precision in the answer by terdon.


Since there are 2 alleles of each gene and 3 different genes, 2EE3 = 8? Let's test this by making a table, for 1 gene there are two different kinds of gametes, so 2EE1 = 2, for 2 genes there are 4 different kinds of gametes (AB, Ab, aB, ab) so 2EE2 = 4, and you already did the calculation yourself for 3 genes, and 2EE3 =  8.

Why don't you try working it out yourself for 4 genes and see if you come up with 16 different kinds of gametes?

Two words: Punnett Square. In this case for a trihybrid cross:

That is a Bernoulli coin-flipping probability. If you are flipping a true coin three times in a row, how often will you get three heads in a row? 1/8? All the events are independent, right? what about the Punnett square? Does it give the same result somehow?

Here is the answer worked out for you.


What is the X-chromosome responsible for?

Here is the list! There are about 900 protein coding genes and about 500 non-coding transcribed sequences. It is not going to be feasible to explain you the function of every single one of those genes. Your question is hence too broad.

You will find here on wikipedia a small subset of those ~900 genes.

If your question was

  Are all genes that are on the X chromosome related to sex?

Then, the answer is "no". Most of them have nothing to do with gender specific traits.


How do scientists discover a new antigen and its epitope?

Okay, you have a few questions building on top of each other (rephrased the questions for clarity):

  How do scientists discover a new antigen?

There are multiple ways to this, which are applied for different purposes.

In order to discover a natural antigen, which is recognised by an antibody normally produced by the immune system, one would first have get hold of this specific antibody. This would be an approach to reproduce or understand the effective response of the immune system against a pathogen (e.g. a virus).

In order to get hold of the antibody (and ideally the coding DNA sequence for it), researchers have to use the pathogen, or parts of it and find the antibodies (or B cells) that bind to it. To do this the pathogen (particles) could be fixed to a column and after running blood through the column the respective antibodies and B cells will remain in the column. Then the DNA of these cells can be sequences, or the antibody can be further purified.

In most cases however, scientists want to find a not-yet existing antibody against an antigen, which leads us to:

  Do scientists try to inject antigens to the body to see if it causes an immune response or not?

Yes, this is done - but only with animals (mostly rats, rabbits & goats). Polyclonal antibodies can be extracted directly from the blood of these animals, but most often monoclonal antibodies are needed for research or medical purposes. The process required for these is much more complicated, but leads to a cell lines which can then be used to produce the desired antibody in greater quantities.

  How do scientists know the corresponding epitope to an antibody?

There are multiple ways to find the exact epitope of an antibody, all of which are commonly described as epitope mapping.

The most common methods are based either on site-directed mutagenesis of the antigen to see which positions (amino acids) are crucial for binding of the antibody, or on peptide fragments of the antigen, which can still be bound by the antibody.


Can animals that rely heavily on sonar sense colour?

Any animal using sound cannot sense color though sonar directly, though these animals are not entirely blind and can probably see colors in the infrared we can't.

  Even on the darkest night there is some light around and all bats use this. Old World fruit bats have colour vision, which is useful to them as they are often quite active in daytime, roosting on trees in exposed positions, rather than tucked away in dark crevices like most microbats, which can see only in black-and-white.

Dolphins have additional senses in addition to seeing they can sense electrical fields.  So if an animal has its eyes covered, they will seem to be able to do things you would not expect.  Its not the same as seeing the color though.

Such animals using sonar can additionally sense density and hardness as well as other material attributes which would cause the acoustic properties of the material as well as movement.

  A hard-bodied insect produces a different quality of echo from one with a soft body, so bats can distinguish between some different groups of insects in this way. They can also determine the size of the object.

What's really interesting is that even human beings can experience this unusual sense.  Blind people have learned to echolocate by making clicks with their mouth, and there is a movement to teach this skill.

Anyone can try it.  In just an hour or two I was able to tell how close I was to a wall, whether the wall was concrete.  I couldn't play video games (2:20 on the link) or see colors though.


Studies on model organisms suggest effects begin quickly, within 6-8 hours of exposure. Rat studies suggest liver absorption of dioxin reaches a maximum from 8-24 hours, with Cytochrome P450 protein expression levels peaking afterwards. Another study uses a comet assay that measures DNA damage after six hours of dosing, and damage is tied to dose level.

Epigenetic changes to sperm and eggs are heritable, passed along to offspring. These result from histone deacetylation and methylation, which in turn change how DNA are packed and unpackaged for protein expression, and change expression itself.

A summary article on epigenetic dioxin (TCDD) toxicity suggests that there are specific effects on protein expression involved in embryonic development in model organisms, which result in birth defects and immune system damage.

In addition to controlled lab experiments on rats and mice, the United States of America and Monsanto conducted a massive, uncontrolled science experiment on humans, dropping dioxin in great quantities on millions of Vietnamese civilians during the Vietnam War.

Children of exposed victims suffered spinal bifida and other birth defects. US military exposed to dioxin in the course of deploying this chemical weapon also had their children suffer greater rates of similar birth defects.


I think the author was just trying to make a point that while the "central dogma" is indeed key, there is more to it than that and that understanding of molecular biology has advanced beyond being simplified to that one tenet. Without having the passage in front of me, the ideas you gleaned from the paragraph make sense, though others such as epigenetics seem like they would fit as well.

As you've noticed, this term is difficult to find anywhere else, it isn't a standard term and therefore doesn't really have any meaning unless it is defined in the source. I wouldn't recommend using it yourself unless you plan to define it. The Wikipedia page for central dogma that you linked has a whole section on information transfer not included in the "central dogma" - I think you can safely assume the author was referring broadly to these items.

This all may be a bit of a joke, as well, given the definition of "dogma" and it's somewhat inappropriate use in the context of the central dogma of molecular biology - again, the Wikipedia article you linked talks about the problematic use of the word "dogma" in this scientific context.


Is the quiescent centre only found in monocot roots?

Note that quiescent centers are typically defined by cell division activity not anatomical placement and are not confined to monocots.

For example, this paper discusses the quiescent center in Arabidopsis roots1.

Reference:
1: Doerner, P. (1998). Root development: quiescent center not so mute after all. Current Biology, 8(2), R42-R44.


How do lilies sense day and night and open and close their flowers?

The three main cues for flower opening/closing used by plants are temperature, light and humidity (van Doorn & van Meteren 2003, freely available pdf), with the first two being most common. Plants with daily opening and closing of flowers can be divided into nocturnal (open at night) and diurnal (open at day). There exists several different mechanisms for how flowers open and close, and these include e.g. reversible expansion and contraction of cells by changes in water balance and differential growth of cells due to temperature (in either the petals themselves or cells at the base of flowers). See the previously referred paper for examples.

The evolutionary advantages and molecular mechanisms (along with the circadian clock of plants) behind opening and closing of flowers are open research fields. Several evolutionary hypothesis exists for explaining different flowering strategies, and these often deal with efficient pollination (close when good pollinators are absent), protection against frost, conservation of resources (e.g. water) or predator/pathogen defence.

I do not know what the specific mechanism in lilies is, and it can possibly/probably differ between different species.


Yes, this is still considered mRNA. A lack of stop codon is usually due to a so-called readthrough mutation, where DNA sequence changes within the stop codon and after transcription it can no longer be recognized by release factors. But yes, ribosomes still recognize the mRNA molecule and start synthesizing abnormal proteins, usually until the ribosome stalls on the 3' end of mRNA and can neither go further nor detach. There are various mechanisms converting this "stalling signal" to a chain of intracellular reactions that lead to degradation of that protein and that abnormal RNA.

Bacteria for instance have a very curious mechanism of solving that problem, namely a tmRNA molecule that is targeted to a stalled ribosome by some specific proteins and acts as an aminoacyl-tRNA as well as mRNA template. It resumes translation, allowing addition of a peptide tag to the malformed protein, which will serve as a marker for degradation. More on that here:
https://en.wikipedia.org/wiki/Transfer-messenger_RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358797/


Is α-keratin a fully functional protein?

What we call as protein is the final quaternary structure. Whether it is translated from a single gene or from multiple genes (as in haemoglobin), always the structure with all bonds and interactions taken into account. Similarly here the alpha- Keratin forms Disulfide bonds to form a functional protein.


How to convert bwa mem output to BAM format without saving SAM file

For directly outputting a sorted bam file you can use the following:

bwa mem genome.fa reads.fastq | samtools sort -o output.bam -

Optionally using multiple threads:

bwa mem -t 8 genome.fa reads.fastq | samtools sort -@8 -o output.bam -


Why don't our cells merge when their phospholipid membranes touch each other?

Phospholipid bilayers found in cells are usually negatively charged. The phosphate groups repel each other by like charges and prevent two membranes from coming too close to each other. Membranes are also full of proteins and often coated with carbohydrates, which serve to keep membranes from interacting too strongly. See this diagram of a membrane bilayer:

Even this diagram is probably cleaned up.

From a more physical chemistry perspective, the energy barrier for flipping a lipid in a bilayer is pretty high, since the polar head group doesn't like passing through the hydrophobic layer. Bringing two membranes together would require overcoming the charge-charge repulsion and flipping around the inner two layers of lipids, so you go from 4 layers to 2.

Interestingly, there are mechanisms for fusing membranes, such as using cationic lipids. These would turn charge repulsion into charge attraction. The lipid ion pairs tend to have shapes that don't support bilayer formation, and tend to prefer micelle or inverted micelle shapes. These have been utilized to break down vesicle membranes and allow large molecules to pass through, like DNA or proteins, and are used in genetic modification of cells.


What is the maximum amount of different bacteria in the drinking water in Europe?

No, your colleages are right: There should be no coliforms in drinking water in Europe following the Council Directive 80/777/EEC.
This PDF from the Northern Ireland Environment Agency (which follows the directice mentioned above) shows this a bit nicer.
It makes sense, since coliforms are a sign of mixing sewage and fresh water. Nothing you want to have happening.

This is the relevant table from the linked PDF:


According to Yossef Braslevi, "HaYadata Et HaHaretz - Yam HaMelach Saviv Saviv" ("And you shall know the land - The Dead Sea and its Surroundings", 1956, Vol. C, page 199 -- the answer is positive. There were native addaxes in the Land of Israel.


Why do humans not have a powerful sense of smell?

Humans' poor sense of smell is a myth, borne of 19th century speculation rather than actual data. This is described in an excellent recent paper in Science , "Poor human olfaction is a 19th-century myth" by John P. McGann. Quoting from a recent blog post of mine,

  The myth dates to the work of the pioneering and hugely influential
  anatomist and anthropologist Paul Broca, who concluded that the
  relatively small olfactory bulbs in humans and other primates enabled
  the occupancy of this space by facilities of intelligence and even
  free will: “…it is no longer the sense of smell that guides the
  animal: it’s intelligence enlightened by all the senses… This is the
  cause of the atrophy of the olfactory apparatus of primates." This
  presumed “atrophy” and poor sense of smell however, were not based on
  any actual data on primates’ sense of smell! The myth propagated and
  expanded in the 20th century, becoming dogma. Back in the 19th, even
  Freud weighed in, noting that the lack of a strong sense of smell
  contributed, in humans compared to other animals, to sexual repression
  and mental disorders.

Humans, when trained, smell quite well, and can for example follow scent trails through grassy fields. Interestingly, the number of olfactory neurons is very similar in humans and other mammals (plotted in the aforementioned post).


Is there evidence to suggest that sleeping requires more energy than watching TV?

From Harvard Health Publishing. The weights are in pounds, and the energy is shown in calories. These values are for over a 30 minute period.

This suggests that the claim is false; watching TV uses more energy than sleeping does.


Is there a possibility that medicine will affect the efficiency of natural selection?

Summary:  Yes it can, but not the way you might think.

Humans aren't under a lot of selective pressure on a large scale right now.  We have a lot of control over our environment, and you're accurate that disease (or I'd add massive, fatal natural disasters) are the biggest ways we would see a large genetic shift.  (Or genocide, which is an extremely unnatural, artificial selection, but some of our species have historically been horrific enough to try to do this.)

Small local natural selection has happened in areas where Malaria is endemic: many people die from malaria. some people die early from homozygous sickle cell anemia, but those who are heterozygous have "sickle cell trait" (because of incomplete dominance) and have deformed enough RBC that malaria isn't able to infect them well.  So the survival advantage is enough that the prevalence of sickle cell alleles in these areas is higher.  There's a similar story with Glucose-6-phosphate dehydrogenase deficiency.

But on a scale you might be thinking of, the primary mechanism would be a global pandemic infection that targets people with a specific trait.  For example, if suddenly an incurable contagious, virulent, highly pathogenic, and fatal virus/bacteria that was only fatal to those with an allele for blood type A were to emerge.  Theoretically it would cause a genetic shift to eliminate type A blood from the gene pool, and reduce prevalence of type B (by eliminating AB due to the A).  Or if it attacked only one location of the world, but that's highly unlikely due to global travel.

Medicine could theoretically catch it in time - mitigate impact and prevent a large shift by creating a vaccine or cure that is effective and easily mass-produced.  The most likely to succeed would be a vaccine (yay for public health!).

Variations on this have happened to reduce or eliminate pathogens (such as polio and smallpox because of the vaccine) and their effect on mankind, but those have little to do with selection for human traits that would cause genetic shift.


No. When a signal is sent through a myelinated axon, the Nodes of Ranvier act as repeaters in electronics. The signal/action potential will disperse down the axon, the Node of Ranvier will pick up the signal, amplify it, and send it to the subsequent Node of Ranvier. I think you're thinking of the Nodes of Ranvier as cracks in the myelin/axon rather than as mini re-amplification sites.


What light intensity starts melatonin release in humans?

The question piqued my interest, but after hunting through the literature for a bit, I hadn't found any direct answers.  Then I went back and read the mouse study you cited a bit more carefully. The mouse study only made a reference to mice being affected at 4 lux, ~100x more sensitive than humans.  However, for that number it cited a paper in Science that has a direct answer.

http://www.sciencemag.org/content/210/4475/1267

    Melatonin concentrations decreased 10 to 20 minutes after the subjects were exposed to 2500-lux incandescent light and reached near-daytime levels within 1 hour (Fig. 1). After the subjects resumed sleeping in the dark, the melatonin concentrations increased immediately and within 40 minutes were at the levels measured before exposure. The fluorescent light (500 lux) did not reduce melatonin, and there was no change after the return to darkness. In the two subjects who were exposed to 1500-lux incandescent light, melatonin concentrations decreased to levels intermediate between those measured during exposure to 500 and 2500 lux (Fig. 2). The return to normal nighttime concentrations after subjects were exposed to 1500 lux was similar to that occurring after their exposure to 2500 lux. The concentration of melatonin in subjects awakened and exposed to 500-lux fluorescent light did not differ significantly from that measured while they were asleep in the dark.

Since that was the granddaddy study of the subject, I just checked the recent citation list on that page for modern articles.

Using pure blue LED lights at 446-477 nm wavelengths, West et al. measured light intensities necessary to induce melatonin suppression. Table 1 of that study converts LED irradiance/lux into retinal irradiance (uW/cm2) based on mean pupil size.  Figure 2 shows plasma melatonin falling (p<0.05) at 20 uW/cm2 of corneal irradiance (then curve fit to 14.19 uW/cm2). It's at least twice as powerful as white light, which didn't show significant suppression at 40 uW/cm2, but was "numerically similar" to 10 uW/cm2 exposure.  If I've got the conversions right, 20 uW/cm2 is about 136 lux, which is about the brightness of an overcast day or half the brightness of typical office lighting.

http://jap.physiology.org/content/110/3/619.full

As for the discrepancy between the two studies (1500 lux vs. 136 lux), I would blame it mostly on technological advances since 1980.  The original study used gas chromatography. You can see the huge error bars and noisy data in the Figure.  The modern study uses a radioimmuno assay using antiserum, and is presumably far more sensitive.

I was also going to mention a nice review paper that summarizes more findings, but apparently I can only post 2 links as a new user.  So I'll just paste the abstract and citation.

    Light is a potent stimulus for regulating the pineal gland's production of melatonin and the broader circadian system in humans. It initially was thought that only very bright photic stimuli (≥ 2500 lux) could suppress nocturnal melatonin secretion and induce other circadian responses. It is now known that markedly lower illuminances (≤ 200 lux) can acutely suppress melatonin or entrain and phase shift melatonin rhythms when exposure conditions are optimized. The elements for physical/biological stimulus processing that regulate photic influences on melatonin secretion include the physics of the light source, gaze behavior relative to the light source, and the transduction of light energy through the pupil and ocular media. Elements for sensory/neural signal processing become involved as photons are absorbed by retinal photopigments and neural signals are generated in the retinohypothalamic tract. Aspects of this physiology include the ability of the circadian system to integrate photic stimuli spatially and temporally as well as the wavelength sensitivity of the operative photoreceptors. Acute, light-induced suppression of melatonin is proving to be a powerful tool for clarifying how these elements of ocular and neural physiology influence the interaction between light and the secretion of melatonin from the human pineal gland.

Photic Regulation of Melatonin in Humans: Ocular and Neural Signal Transduction
Brainard, Rollag, and Hanifin
J Biol Rhythms December 1997 vol. 12 no. 6 537-546

If you need more information, I'd start by checking the papers cited by the second paper. Alternately, there's probably more historical information available by looking at papers which have cited the first one.


Blast output - program to count the number of hits

This script, named blast2table.pl is from the code accompanying the Blast book by Korf & Yandell (there is a 3rd author whom I haven't met).

#!/usr/bin/perl -w
use strict;
use Getopt::Std;
use vars qw($opt_p $opt_b $opt_e $opt_m $opt_n);
    getopts('p:b:e:m:n:');
    my $PERCENT = $opt_p ? $opt_p : 0;
my $BITS    = $opt_b ? $opt_b : 0;
    my $EXPECT  = $opt_e ? $opt_e : 1e30;
my $START   = $opt_m ? $opt_m : 0;
    my $END     = $opt_n ? $opt_n : 1e30;

my ($Query, $Sbjct);
my $HSP = "";
    while (<>) {
        if    (/^Query=\s+(\S+)/) {outputHSP(); $Query = $1}
        elsif (/^>(\S+)/)         {outputHSP(); $Sbjct = $1}
        elsif (/^ Score = /) {
            outputHSP();
            my @stat = ($_);
            while (<>) {
                last unless /\S/;
                push @stat, $_
            }
            my $stats = join("", @stat);
            my ($bits) = $stats =~ /(\d\S+) bits/;
            my ($expect) = $stats =~ /Expect\S* = ([\d\.\+\-e]+)/;
       $expect = "1$expect" if $expect =~ /^e/;
            my ($match, $total, $percent) = $stats =~ /Identities = (\d+)\/(\d+) \((\d+)%\)/;
            my $mismatch = $total - $match;

        $HSP = {bits => $bits,
                    expect => $expect,
                    mismatch => $mismatch,
                    percent => $percent,
                    q_begin => 0,
                    q_end => 0,
                    q_align => 0,
                    s_begin => 0,
                    s_end => 0,
                    s_align => ""};
        }
        elsif (/^Query:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{q_begin}  = $1 unless $HSP->{q_begin};
            $HSP->{q_end}    = $3;
            $HSP->{q_align} .= $2;
        }
        elsif (/^Sbjct:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{s_begin}  = $1 unless $HSP->{s_begin};
            $HSP->{s_end}    = $3;
            $HSP->{s_align} .= $2;
    }
}
outputHSP();

sub outputHSP {
    return unless $HSP;
        return if $HSP->{percent}  < $PERCENT;
        return if $HSP->{bits}     < $BITS;
        return if $HSP->{expect}   > $EXPECT;
        return if ($HSP->{q_begin} < $START or $HSP->{q_end} < $START);
        return if ($HSP->{q_begin} > $END   or $HSP->{q_end} > $END);
        foreach my $field ('percent', 'q_align', 'mismatch', 's_align', 'q_begin', 'q_end', 's_begin', 's_end', 'expect', 'bits'){
        print "$field not defined\n" if not defined $HSP->{$field};
        }
        print join("\t", $Query, $Sbjct, $HSP->{percent}, length($HSP->{q_align}), $HSP->{mismatch}, countGaps($HSP->{q_align}) + countGaps($HSP->{s_align}), $HSP->{q_begin}, $HSP->{q_end}, $HSP->{s_begin}, $HSP->{s_end}, $HSP->{expect}, $HSP->{bits}), "\n";
    $HSP = "";
}

sub countGaps {
    my ($string) = @_;
        my $count = 0;
    while ($string =~ /\-+/g) {$count++}
        return $count;
}


What's the distinction between a tetrad and a synaptonemal complex in meiosis?

As far as I can tell there is a distinction.

A tetrad refers to the entire group of four chromatids after they have come together for crossing over in Prophase I (synapses).

A synaptonemal complex as you would expect is formed in synapses.  This is a protein-RNA complex that connects the intervening regions of matched chromosomes in some circumstances - it is not required. Mutated yeast that can not form this complex has still been shown to be able to exchange genetic information.

In other words, you can have a tetrad without a synaptonemal complex, but not vice versa.


Large Alpine Hymenopteran Seen in the White Mountains

Looks like some sort of cimbicid sawfly. Thanks @ArthurJFrost !


Is urine dirty as soon as it leaves the human body?

It was believed for a long time that urine stored in the urinary bladder is sterile. However, Wolfe et al(1). recently found evidence of bacterial presence in the urine extracted from bladders of healthy women. In an article just published, Hilt et al. found that at least some bacteria found in the bladder of healthy women are viable and can be grown in a laboratory after extraction from the bladder).2 (Paywall). They expect that the same is the case for men.

From the Hilt et al. paper:

  Thirty-five different genera and 85 different species were identified
  by EQUC. The most prevalent genera isolated were Lactobacillus (15%),
  followed by Corynebacterium (14.2%), Streptococcus (11.9%),
  Actinomyces (6.9%), and Staphylococcus (6.9%). Other genera commonly
  isolated include Aerococcus, Gardnerella, Bifidobacterium, and
  Actinobaculum.

Note that these species for the most part (Actinobaculum being one exception, as a possible uropathogen) appear to be part of the normal microbiome (collection of microorganisms) in healthy people in the same way as bacteria inhabit other parts of healthy persons. Additionally, the recovered organisms required special care to achieve growth:

  Most of the bacteria isolated required either increased CO2 or
  anaerobic conditions for growth, along with prolonged incubation, and
  they often were present in numbers below the threshold of detection
  used in routine diagnostic urine culture protocols.

Thus, fresh urine is non-sterile but probably unlikely to cause infection in healthy persons.

In the process of leaving the body, there is a chance of contamination from organisms living in the urinary tract or on the surface of the body. However, if organisms picked up from the urinary tract made you sick, I except that you would already be having symptoms of an urinary tract infection, as the stomach is hardly a more forgiving environment. The risk of contamination from the surface of the body would depend on personal hygiene.

See also this question on https://outdoors.stackexchange.com/questions/264/is-drinking-urine-safe

Edit: This might go without saying, but apart from possible pathogens, there are of course other aspects of urine which makes it unfit for general consumption.


Does having to urinate imply that you are becoming dehydrated?

There are two parts to answer this question. "How does my body know when to pee? Do diuretics affect that, or my hydration?"

Does wanting to pee imply dehydration?

In summary: Not necessarily. Your body might have plenty of water, but the bladder is full. Alternatively your body might be dehydrated, but the caffeine and normal body functions have filled the bladder and you'll need to pee.
Caffeine as a diuretic.
Caffeine belongs to the Xanthines, and inhibits reabsorption of Na+ by cells, and increases flow rate of filtered fluid through the kidneys. This reduces water content in your body. In other words diuretics do dehydrate you, specifically caffeine will. Coffee and tea (very low doses of caffeine) are mild diuretics.
Bumetanide, Furosemide, and Torsemide are examples of stronger diuretics, and hydration should be monitored closely.
On the other hand, the colour of your urine may indicate your hydration.
The below image is a crop of this Cleveland Clinic infographic.

How does my body know when to pee?
The bladder is hollow and slightly elastic, so as it fills with urine it expands. A healthy bladder can hold up to 2 cups of urine comfortably for several hours. When the bladder approaches its maximum capacity, signals are sent to the brain, letting the body know that it is time to urinate.
But it's critically the kidneys that are controlling the production of urine.
Caffeine increases the production of urine from the kidneys, and fills the bladder quicker. However, the increase in production of urine from a cup of coffee is more than offset by the water in the coffee.


"Twig-with-leaf"-like insect in central Mexico

That is a Mexican/Texas unicorn mantis, which is of the species Phyllovates chlorophaea.


Can you increase the microbiota in an insect?

The answer is absolutely yes.
There are 3 main ways:

Faecal transplant: faecal sample from other insect could be
transplanted in order to colonize the gastro-intestinal tract
Injection of bacterial culture into the desired tissue
Use of functional foods to increase the abundance of specific bacterial
genus.

See this review for more detail


1. What was the original research paper?

This one appears close: Hyperphagia in rats produced by a mixture of fat and sugar (PubMed, 1990)

  Experimental groups were fed sugar (sucrose), fat (corn oil), or a
  sugar-fat mixture as an option to chow; options were in the form of
  water solutions or emulsions. The control group was fed only chow. The
  sugar-fat group displayed a robust hyperphagia (greater than 36%),
  relative to the control group; the hyperphagic response was greater
  than that observed in the fat group but not in the sugar group. The
  sugar-fat group selected more calories from the option than the other
  two experimental groups. Body weight gains were also greater in the
  sugar-fat group than in the fat and sugar groups. Addition of
  saccharin to the fat emulsion increased fat and total intakes to
  levels close to those of the sugar-fat mixture. In a second
  experiment, the relative palatability of the plain and sweet fat
  emulsions was assessed with two-bottle preference tests. The sugar-fat
  mixture was preferred to the saccharin-fat mixture, which in turn was
  preferred to the plain-fat emulsion. These results suggest that the
  sweetness of the sugar-fat mixture contributed to the pronounced hyperphagia and obesity obtained with this diet option.

2. Have there been any related new results with other mixtures like sugar/salt fat/salt?

A free-choice high-fat high-sugar diet induces changes in arcuate neuropeptide expression that support hyperphagia (PubMed, 2010) (a study in rats)

  Our data suggest that the specific combination of saturated fat and
  a 30% sugar solution results in hyperphagia-induced obesity.

Snack food intake in ad libitum fed rats is triggered by the combination of fat and carbohydrates (PubMed Central, 2014)

  Thus, it can be concluded that the combination of fat and
  carbohydrates is a major molecular determinant of potato chips
  triggering hedonic hyperphagia.

Fat/carbohydrate ratio but not energy density determines snack food intake and activates brain reward areas (PubMed Central, 2015)

  We conclude from our behavioural data that the ratio of fat and
  carbohydrates, but not the absolute energy density, is the major
  determinant of the palatability and intake of snack food during
  short-term two-choice preference tests in rats.

Which Foods May Be Addictive? The Roles of Processing, Fat Content, and Glycemic Load (PubMed Central, 2015) (a human study)

  In summary, the current study found that highly processed foods,
  with added amounts of fat and/or refined carbohydrates (e.g., sugar,
  white flour), were most likely to be associated with behavioral
  indicators of addictive-like eating. Additionally, foods with high
  GL [glycemic load)] were especially related to addictive-like eating
  problems for individuals endorsing elevated symptoms of “food
  addiction.”

In conclusion, it can be either a combination of fats and sweetness (due to sugar or non-sugar sweeteners) or a combination of fats and high glycemic carbs (sugar, white flour, potatoes) that can induce overeating.


Are four-leaf clovers mutations, developmental errors, or something more complicated?

A recessive gene for four leaves has been identified (Tashiro et al., 2010). The clover is a tetraploid species and together with the fact that environmental conditions may also suppress the development of the fourth leaf, it indeed takes a lot of luck to find one. If it will bring you any is another question though.

In fact they are aiming at making a four-leaved cultivar (source: New Scientist).

Reference
- Tashiro et al., Crop Sci (2010); 50: 1260–8


1. Carrion crow (Corvus corone)

The plumage of carrion crow is black with a green or purple sheen, much greener than the gloss of the rook. The bill, legs and feet are also black. It can be distinguished from the common raven by its size (48–52 cm or 19 to 20 inches in length as compared to an average of 63 centimetres (25 inches) for ravens) and from the hooded crow by its black plumage

3. Hooded crow (Corvus cornix)

ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.

2. This one is a bit more difficult, but I think it is also a hooded crow or possibly a hybrid  Carrion crow × Hooded crow (Corvus corone × Corvus cornix).

 Hybrid
At first glance, #2 looked somewhat like a Western jackdaw (Corvus monedula) because the grey feathers travel fairly high up on its neck and because the bird appears to be somewhat smaller.

Measuring 34–39 centimetres (13–15 in) in length, the western jackdaw is the second smallest member of the genus Corvus...The cheeks, nape and neck are light grey to greyish-silver, and the underparts are slate-grey. The legs are black, as is the short stout bill.

However, C. monedula has fairly conspicuous grey eyes and its feathers travel up the neck/head almost as far superiorly/anteriorly as the eyes. Neither appear to be the case in your specimen.

All three species are common in Europe.


Purpose of K+ channels in action potential

Great question! However, your question is based on some misconceptions about what polarization means and how ion movement is involved, as well as the difference between equilibrium and the time it takes to get there. That's okay - it's a mistake that many many people learning about neurophysiology make, including instructors.

Na+/K+ concentrations actually change very very little during an action potential. The Na+/K+  pump establishes the concentration gradient, not the resting membrane potential. The resting membrane potential is caused by the concentration gradient plus the relative permeability of different ions via the Goldman equation: specifically, that permeability to K+ is much much higher than Na+.

When you open voltage-gated Na+ channels during an action potential, the relative permeability to sodium increases dramatically, so the new "equilibrium potential" is closer to the reversal potential for sodium (again, use the Goldman equation). There will be a net flow of ions (mostly Na+ coming in) until that new equilibrium potential is reached.

However, voltage-gated Na+ channels inactivate quickly, so that equilibrium isn't really reached. Instead, as the Na+ channels close, the new equilibrium potential is back near the original resting potential (for a third time, use the Goldman equation), because the primary permeability is to K+ through leak channels, and therefore the net current flow direction changes.

Okay, so what's the need for the voltage-gated potassium channels in all this? Well, the rising phase (sodium phase) of the action potential is fast because there is a really high conductance to Na+ so lots of Na+ can flow quickly in. In comparison, there is a lot less conductance of K+ through the leak channels. If all you have are leak channels, it takes a long time to return to rest. Equilibrium potential is just that: the equilibrium. It takes time to get to equilibrium. Voltage-gated K+ channels speed up that return to rest.

What if you had no K+  conductance, including no K+ leak channels? Well, then it doesn't matter at all what the relative concentration of K+ is inside and outside the cell: check the Goldman equation! You can't really have no conductance to anything at all, but if there is no dominant ion then the membrane potential will be something around zero. In that condition, the charge imbalance of the Na+/K+ pump process can contribute a couple mV, but nothing more than that.

All that said, to address your specific questions:

  I understand that they serve to repolarize the neuron after the Na+ influx. What I don't understand is why this is important.

It's important for speed and for the minimum refractory period between action potentials. Nervous system activity would slow way way down if action potentials could only occur every 100 ms.

  Instead, we have to wait until the Na+/K+ pump can restore the proper intra-/extra- cellular balance between them. And then the neuron can fire again.

  But don't we have to wait until the Na+ concentration is restored before we can fire again anyway?

Na+/K+ pump is only needed to maintain ion balance over a very long term. On the time course of a single action potential, the concentrations of Na+ and K+ do not change appreciably. That's not what repolarization is.

  So what do we really gain by having a way to restore the charge differential?

Speed!

You can also see my answers on some related questions:

Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?

Why does K+ moves out of the cell?


What fills the space between the alveoli in the lungs?

Alveolar tree is like a bunch of grapes. If you put a bunch of grapes into a plastic bag and put this bag into another bag, you can imagine how the lungs are covered.

Alveoli form the surface of the lungs. There is a membrane called visceral (or pulmonary) pleura that covers the alveoli and this membrane continues into another sheet called parietal (or thoracic) pleura that covers the inner side of the thoracic wall. The space between the membranes is called pleural space.

Here you can see how visceral pleura continues into parietal pleura:

Picture 1. Pleural space (source: sdstate.edu)

Picture 2. from page 1117 of "Cunningham's Text-book of anatomy" (1914) (source: Flickr)


How to clean and preserve a cicada's molted exoskeleton (exuvia)?

The exuvia is made of cross-liked chitin, and will not decay. You don't need any special preservatives as all. If you need to get the mud off, just rinse it as you said, in soapy water, let it dry, and you are done. Simple.