Not much is known about the mechanisms involved, but they do appear to differ significantly from parasite to parasite. I'll discuss a few different examples here, and try to provide as much information as is currently known about how the parasites are doing it.

There are likely to be many more different examples and mechanisms than these, and researchers may well revise the below hypotheses over time. For this reason, I'm thinking about either splitting this answer into multiple separate answers or changing it into a community wiki.

Example 1 - Toxoplasma gondii and rats as an intermediate host

The Toxoplasma gondii parasite infects multiple hosts during its lifecycle. At one stage, it is hosted by a rodent, which must be eaten by a cat if the parasite is to use the feline's gut in the next stage of its life cycle. Somehow, the parasite causes the rodent (I know that rats are affected, but I don't know if mice or other rodent species are) to behave in a less risk-averse way around cats, making it more likely to be eaten by them.

Exactly how Toxoplasma influences its rodent hosts is unclear. An article in Nature ("Parasite makes mice lose fear of cats permanently") mentions that the parasite creates cysts within the rodent's brain cells, increasing their production of dopamine, which may be one of the causes for the change in behaviour. However, the researchers quoted in the article found that the risk-taking behaviour persisted even without the cysts and dopamine.

Link to that research paper: "Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance".

One theory is that the parasite simultaneously infects the ovaries/testes of the rodent, causing increased testosterone levels in the male and thereby causing it to engage in more risk-taking behaviour. A lot of the literature relevant to this theory is behind paywalls, but as far as I can tell studies have shown that:

Male rats with their testes removed are not affected by the behavioural changes, although I do not know if the orchiectomies were performed before or after infection.
Male rats in general are affected.
Female rats are affected by the behavioural changes, whether or not their ovaries have been removed.

This suggests that the parasite has more than one means of inducing the behavioural changes in the rodent, and that the behavioural changes in female rats have a different cause to the same behavioural changes in males. In the case of the male, it is believed that epigenetics play a part. The increased testosterone levels lead to reduced methylation in genes in a certain area of the brain, and this in turn leads to increased production of the chemical "arginine vasopressin" (AVP). I know nothing about AVP, but the increased levels of it are supposed to cause the behavioural changes, according to this theory.

As I mentioned, the presence of paywalls is giving me some difficulty in studying the relevant research for this particular theory, but a link to one paper is provided in the "Sources" list below.

Another theory is that the parasite infects the white blood cells and causes them to produce excess quantities of a chemical that acts as a neurotransmitter, affecting the brain through the increased levels of said chemical. The research paper is "GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii".

There's also a New Scientist article: "Parasite makes mice fearless by hijacking immune cells")

Example 2 - Ophiocordyceps unilateralis (fungus) and carpenter ants

A recent article in Ars Technica ("Zombifying fungus bypasses the brain to make ants its puppets, study finds") described research into another example, the Ophiocordyceps unilateralis fungus that parasitizes carpenter ants. The researchers had found that the fungal cells in the ant's body effectively disconnected its brain and linked up to act as a replacement brain to move the host's limbs.

Link to the research paper: "Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants"

(If I understand correctly, the brain's disconnection might be due to damage caused to it by chemicals emitted by the fungus. It may be the case that the original brain and fungal network are both able to move the ant's limbs during the early stages of infection, I'm not sure.)

Even then, one piece at least of the host's altered behaviour wasn't in fact due to this, but due to the fungus destroying a protective membrane on the ants' jaw muscles - leading to the famously strong "death grip" as the infected ant bites a high leaf, dies, and is held in place by the grip of its jaws.

The O. unilateralis fungus extending soma stalks and fruting heads from the bodies of dead ants. Image taken from https://en.wikipedia.org/wiki/File:Ophiocordyceps_unilateralis.png. The image was posted under a Creative Commons Attribution 2.5 Generic license and is credited to David P. Hughes and Maj-Britt Pontoppidan.

The research paper for the jaw membrane is, unfortunately, behind a paywall. If you have access: "Zombie ant death grip due to hypercontracted mandibular muscles"

The "cut off and replace the brain" part of this was also covered by a 2017 article in The Atlantic ("How the Zombie Fungus Takes Over Ants’ Bodies to Control Their Minds").

Example 3 - Dicrocoelium dendriticum and ants

For the actual host/parasite pairing that OP was asking about, not as much is known. One fascinating aspect of this infection is that the ant's behaviour is only changed during the evening/nighttime hours. As day approaches, if the ant has not already been eaten, and if the temperature exceeds a certain threshold, the ant climbs back down to ground level. It rejoins the colony (which does not reject it) and continues to function normally until night falls again, whereupon it climbs back up to the top of the blade of grass.

(In some situations, it may climb up a flower stem and attach itself to a petal.)

A team of researchers used micro-CT scanning to examine the brains of infected ants, publishing their results in a 2018 Nature article ("3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host")

Most of the parasites are situated in a region of the ant's abdomen known as the "gaster". At this stage in their lifecycle, they are known as "metacercariae". At least one of the parasites, however, will enter a region of the ant's nervous system known as the "suboesophageal ganglion" (SOG). In the brains examined by the researchers, one (and only one) of the parasites in that area would attach its "oral sucker" to the brain tissue of the host ant. This would occur in "the ventral-anteriormost region of the SOG".

The parasites in the gaster are contained within cysts. Some or all of the ones in the brain may not be. The parasite that has attached its oral sucker is not. This one is informally nicknamed "the brain worm".

What is so significant about the SOG region? For one thing:

  dendrites of the 10–12 motor neurons that stimulate the fast muscle fibres of the mandibular closure muscles in ants share the same neuropil in the ventral-anteriormost region of the SOG24 – the precise location where non-encysted D. dendriticum metacercariae are located. Thus, by targeting this region of the SOG, D. dendriticum has the potential to directly interfere with ... the action of the mandibles.

Thus we see another mechanism used by a parasite to force its ant host to grip something tightly with its mandibles.

The SOG also has some connection to locomotive activity - presumably getting the ant to climb the blade of grass and/or stopping it from climbing down too soon:

  Site-selection and development of non-encysted metacercariae within the SOG can provide a direct pathway for the manipulation of locomotory activity.

And even more...

  The SOG is a major part of the nervous system-wide network for neuromodulation in insects, evidenced by the many different neuromodulators expressed in neurons that reside in this region of the brain [25,26,27]. The effects of these neuromodulators ... are diverse and far reaching, from flight modulation, visual dishabituation and olfactory learning to mediation of the fight-or-flight response and the control of aggression ... FMRFamide-like peptide is implicated both as a neurotransmitter and a neuromodulator and affects the nervous system as well as skeletal muscle [25]. Thus, any influence exerted by metacercariae on the activity of neuromodulatory neurons in the SOG could have far reaching consequences for the behaviour of infected ants.

The researchers noted that they did not know if the "brain worm" was in contact with the SOG all the time, or just when the temperature was low enough to induce the changed behaviour. Further research was needed.

Sources:

Ingram WM, Goodrich LM, Robey EA, Eisen MB (2013). Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance. PLoS ONE 8(9): e75246. https://doi.org/10.1371/journal.pone.0075246
Abdulai-Saiku, S., Vyas, A. Loss of predator aversion in female rats after Toxoplasma gondii infection is not dependent on
ovarian steroids. Brain Behav. Immun. (2017), http://dx.doi.org/10.1016/j.bbi.2017.04.005
Fuks JM, Arrighi RBG, Weidner JM, Kumar Mendu S, Jin Z, Wallin RPA, et al. (2012). GABAergic Signaling Is Linked to a Hypermigratory Phenotype in Dendritic Cells Infected by Toxoplasma gondii. PLoS Pathog 8(12): e1003051. https://doi.org/10.1371/journal.ppat.1003051
Fredericksen MA, Zhang Y, Hazen ML, Loreto RG, Mangold CA, Chen DZ and Hughes DP. (2017). Three-dimensional visualization and a deep-learning model reveal complex fungal parasite networks in behaviorally manipulated ants. Proceedings of the National Academy of Sciences Nov 2017, 114 (47) 12590-12595; DOI: 10.1073/pnas.1711673114
Mangold CA, Ishler MJ, Loreto RG, Hazen ML and Hughes DP. (2019). Zombie ant death grip due to hypercontracted mandibular muscles. Journal of Experimental Biology 2019 222: jeb200683 doi: 10.1242/jeb.200683
Martín-Vega D, Garbout A, Ahmed F. et al. 3D virtual histology at the host/parasite interface: visualisation of the master manipulator, Dicrocoelium dendriticum, in the brain of its ant host. Sci Rep 8, 8587 (2018) doi:10.1038/s41598-018-26977-2


Why are dogs so selective about choosing a spot to defecate?

Marking territory with faeces

Despite urine being the most common way for dogs to mark territory, they also can use faeces to do so. Not only the faeces have a unique scent for the dogs, but, most importantly, it contains secretions from the anal glands, which are very important in dog communication. In fact, when you see two dogs sniffing each other "behinds", they are smelling the other dog's anal glands secretion.

So, being selective about the place to defecate is indeed an expected behaviour in dogs.

Magnetic sensitivity in dogs

However, if you are specifically talking about the dog spinning around after it — more or less — decided where to defecate (which makes the dog seem like it had not yet decided if it is going to defecate or not) one factor that plays an important role is that dogs like to eliminate with their bodies aligned to the North-South axis.

According to Hart et al. (2013):

  Dogs preferred to excrete (sic) with the body being aligned along the North–South axis under calm Earth's Magnetic Field (MF) conditions. This directional behavior was abolished under unstable MF. The best predictor of the behavioral switch was the rate of change in declination, i.e., polar orientation of the MF.

So, the dog has to spin some times until it finds the desirable orientation, which explains the behaviour.

It's worth mentioning that the interesting aspect of this research is not the fact that it explains why dogs spin around before eliminating, but the fact that it shows that dogs have magnetoreception!

Still according to Hart et al. (2013):

  It is for the first time that (a) magnetic sensitivity was proved in dogs, (b) a measurable, predictable behavioral reaction upon natural MF fluctuations could be unambiguously proven in a mammal, and (c) high sensitivity to small changes in polarity, rather than in intensity, of MF was identified as biologically meaningful.

Source: Hart, V., Nováková, P., Malkemper, E., Begall, S., Hanzal, V., Ježek, M., Kušta, T., Němcová, V., Adámková, J., Benediktová, K., Červený, J. and Burda, H. (2013). Dogs are sensitive to small variations of the Earth’s magnetic field. Frontiers in Zoology, 10(1), p.80.


Can paper/plastic currency serve as a medium for pathogens?

TB is an extremely poor example, because as has been mentioned, it usually requires prolonged contact.
But lets go with something with a low required infectious dose, that's friendly to surface contamination, and persists in the environment: Norovirus.
Can norovirus serve as a medium for pathogens? Absolutely. To be blunt, almost anything will serve as a medium for the right pathogen with some level of efficacy. This is a presentation from the New York Federal Reserve on what contaminates money, but given the outlandish things that can be contaminated with infectious material, there's no reason to suspect money isn't among them.
Wash your hands.


Why are bacteria and archaea in different domains?

The reason that Archaea were determined to be a separate (and only the third) kingdom so late (1977 according to this reference) was because archaea often completely resemble eubacteria.  They are unicellular and have no organelles and appropriately they were grouped with other prokaryotes because of their morphology and cellular physiology.

But by the 1970s phylogeny becoming based on the sequence of DNA and RNA which were just becoming more available.  Based on a simple comparison of the sequences of 18S rRNA of 13 fungi, bacteria and archaea, Woese and Fox showed that the bacteria and the archaea were about as different from the eukaryotes than from the bacteria.  (see table 1).

Since then, the differences between bacteria and archaea have continued to be great.  The wikipedia diagram below is not to scale- the divergence of the three kingdoms is so far back that they pre-date the emergence of eukaryotes entirely. But you can see that fungi and other eukaryotes are more similar to archaea than the bacteria.

BTW, the idea that archaea are extremophiles is not entirely true - they are pretty much exclusively the only kingdom found in these conditions, but archaea have been found to coexist with bacteria and eukaryotes in the open sea and their detection heretofore in most environments may be only due to the fact that archaea are difficult to grow in the lab.

Just found this retrospective from Woese himself, who passed away recently.


Your question is based on a misunderstanding. You have a single strand, lets assume it's the red sequence in the image. The linear sequence along this strand is not limited by base-pairing rules.

The base-pairing rules (A-T, G-C) apply to the complimentary strand, given in blue in the image.

It's convention to only give the sequence for one strand because the base-pairing rules allow us to infer the complimentary sequence.


Hair becoming white in one night after tremendous stress

The physiological condition you are looking for is commonly called Marie Antoinette Syndrome.

Under extreme psychological stress, the hair of the person does turn white but not in a single night (takes place slowly over successive days; in a matter of weeks) and cases of this has been reported worldwide generally in warzones.

Contrary to what you suggest, this phenomenon is extremely rare and I doubt many soldiers experience it.

Source- http://archderm.jamanetwork.com/mobile/article.aspx?articleid=712060

Another interesting tidbit the author mentions is whether Marie Antoinette herself suffered from it or not. The author goes in depth on the topic; regardless the syndrome is definitely real with documented cases. It is also known as canities subita.

Most in the scientific field now refer to it as an acute episode of diffuse alopecia areata. Alopecia areata is patchy hair-loss. This syndrome is referred to as such because the white hair eventually fall off.


Comprehensive biology or anatomy wordbank

So I found a good list. Behold: wikipedia:

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


What recovers normal polarisation after hyperpolarisation?

Remember that the action potential gets more positive in the first place, so increasing positivity is achievable. Net Na+ movement into the cell makes the potential more positive. This occurs as the Na+ gate (right on the image below) are open. The key message is that the membrane can move charge to cause an increase in either positive and negative potential.

Imagine one side becomes more negative. The Na+ diffusion will correct this to reach an equilibrium around 3 to 4 milliseconds (ms) after the stimulus to reach the resting potential
 (as alluded to my @MCM in the comments).

There are some great animations demonstrating this principle on the University of Bristol's website. They clearly show how positive charge can be conferred over the membrane.

A (now deleted) comment linked to the below image that shows the potential and when the gates are opened and closed. I would still go to the bristol website too to see it in action, but this figure is a quick go to once you get your head around the timing of ion flux.

As with most biology, it is a little more complicated than that overly simple model. There are entire books on how neurones control their charges.

Note: The key terminology is somewhat muddled and there doesn't seem to be a standard term. I have seen this "recovery" phase called undershoot, overshoot (and overshoot rather unhelpfully also refers to another part of the action potential), the refractory period, and discussed as part of hyperpolarization. The go to term is afterpolarisation if you want to research this more thoroughly.


Maternal immunity without prenatal vaccination?

tl;dr

If a woman was vaccinated when she was a child, will she be able to provide passive immunity to her children?

It depends on the vaccine. Generally, if the mother still has high levels of protective IgG  during the third trimester (especially if it's type 1 or 4), those antibodies will cross the placenta and provide passive immunity to the newborn. In whooping cough, though, good levels of newborn IgG require vaccination in the third trimester.
Maternal immunizations
Immunizations are given to adult women prior to conception, while pregnant, and after delivery to protect the mother from infection, protect the fetus from infection, protect the fetus from congenital anomalies associated with maternal infection, and to protect the newborn from infection through passive immunity and through decreased exposure to infected contacts. The exact recommendations differ for different vaccines and different levels of maternal risk. From the same recommendation, you can see that some vaccines are recommended only if maternal antibody titers are negative and some are recommended regardless of maternal antibody titers or prior immunization.
Passive immunity of the newborn
IgG undergoes active transport from the maternal circulation to the fetal circulation across the placenta.

The reference linked above is an excellent review of transplacental antibody transfer and the science that underpins maternal immunization recommendations for passive immunization of the newborn (especially in the case of whooping cough). Key points here include:

Newborn IgG levels correlate with maternal IgG levels (i.e., the active transport mechanism isn't saturated in most cases). This suggests that low IgG for a particular antigen in the mother will result in low IgG for that same antigen in the newborn.

Antibody transport begins as early as week 14, but both the total transport and the rate of transport increases over the length of the pregnancy. This suggests an hypothetical optimum time for an intervention that would temporarily boost the level of any antibody.

Pertussis example
Whooping Cough, or pertussis, the illness caused by Bordetella pertussis, an encapsulated bacteria, is quite dangerous in the newborn. A few years ago recommendations for vaccination against pertussis were updated to immunization in the third trimester, regardless of the mothers prior immunization status. This recommendation is based, in part, on the understanding of transplacental transfer of IgG described in the article I linked in the earlier section, and in part on data on the association between timing of maternal immunization and fetal, all in the context of increased pertussis case rates.
Shortly after these recommendations were updated, additional, more thorough data confirmed this recommendation, though it suggested a slightly narrower window for the ideal time of Tdap administration (from 27-36 weeks to 27-30 weeks).
An aside re: the relationship between passive immunity of the newborn and childhood immunizations
Passive immunity from antibodies transferred to the fetus during pregnancy declines pretty sharply after birth. By 8 months the maternal IgG contribution is effectively gone. This is passive immunity because only the products of B-cells (the antibodies) are transferred. Immunization of the child, on the other hand, provides active immunity, because they develop the capacity to produce their own antibodies. I'd refer you to the allergy and immunology chapter of Bernstein and Shelov's Pediatrics for Medical Students, a surprisingly good general reference.
How should we interpret the linked article in the OP
This article is a comment on a very interesting study in baboons. It doesn't present any new data, but does comment on epidemiological data from a natural Swedish cohort between the discontinuation of whole-cellular pertussis vaccine 1979 and introduction of acellular pertussis in 1996. They reference this data through a misinterpretation of yet another study that analyzed infection rates between 1986 and 2007. The misinterpretation is as follows:

The (1996) drop was pronounced in infants too young to be vaccinated (Fig. 1A), itself a clear indication of herd immunity.

This is incorrect. That figure represents the decrease in infection rates for infants under 1 year of age at the point when vaccine was re-introduced. This included infants who were vaccinated (at 3 and 5 months).
The data before the re-introduction of vaccine, e.g., in 1995, though, does provide a good natural experiment for the epidemiology of pertussis in a non-immunized and immunization remote population. It had been 16 years since the use of whole-cell pertussis and you can clearly see the waning immunity in the population incidence as a whole. If you are really interested in digging into these questions, this cohort is a good place to start. Sweden is very good at collecting important data, so it may be out there.


Do blood vessel walls have blood vessels in them?

Yes, they do: the vasa vasorum.

When a blood vessel is too large, like the aorta or the cava, it has vessels to supply blood to their outer layers (where the cells are too far away from the lumen), not only to the Tunica adventitia (if by wall in your question you mean only that most external layer), as you can see in this image:

(note: this image is from a quiz in McGraw-Hill site, and the legend is not correct, "intima" and "media" are swapped)

Those vessels inside vessels are thus called vasa vasorum, which in Latin means exactly this: a vessel ("vasa") of a vessel ("vasorum"). You can read more about them in this Wikipedia page.

  If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall?

No, they do have their own walls. Despite being inside another vessel, the vasa vasorum have the same basic structure of any other vessel with their same width.

Therefore, vasa vasorum vary in size, from vessels with single or multiple smooth muscle layer(s) to simple endothelial channels.

Interestingly, vasa vasorum are normally found next to nerves and lymphatics (see the image above). This close structural relationships "provide evidence that adventitial vasa, nerves, and lymphatics provide arteries and veins with nutrition, neurohumoral input, and an effective pathway to remove waste products from the parent vessel" (Williams and Heistad, 1996).

(source: Williams, J.K. and Heistad, D.D. (1996) "Structure and function of vasa vasorum", Trends in Cardiovascular Medicine, 6(2), pp. 53–57).


Why are we using upper teeth and lower lip on labiodental sounds?

The alternative articulation, called dentolabial, is more difficult to articulate, so it is very rarely used in human language. However, it apparently is common enough in disordered speech to be allocated an ExtIPA diacritic.

The reason labiodentals are easier: Humans normally have a slight overbite.

When the jaw and lips are in a "neutral" position, the lower lip is close to or touching the upper teeth, so with a small vertical movement of the jaw (together with tensing the lip) one can articulate a labiodental. Articulating a dentolabial requires moving the jaw a fair distance forward, to go around the upper teeth before reaching the upper lip. As Ben pointed out in the comments, front-back jaw movement is unusual, a less "common movement in terms of other vocalisations and eating".

Furthermore, since labial articulations are directly visible to observers, learners are especially likely to imitate others' exact articulation. Thus even though labiodentals and dentolabials sound similar, everyone in the population of speakers uses the same articulation (rather than having both articulations in free variation).

Perhaps dentolabials would instead be more common if most people were like this:


Quantification of various amino acids from bacteria?

A good approach could be to use GC-MS to identify cytosolic metabolites. When focussing on cytosolic amino acids, it might be useful to precipitate the proteins in a purification step and continue with the soluble fraction. Subsequently, a derivatization is done. The mass spectrometry helps to better identify the amino acids. This article by Phelippe et al. can give a good start.


First, I am no expert on this topic, I am simply synthesizing several different sources of information along with the very good work of others.  Since the "thing" featured in this question has appeared elsewhere, it deserves an answer.

These appear to be eggs of Chironomous midges (wikipedia).  This conclusion is based largely on reading the three-part blog by Tom of askanaturalist.com
Part 1, Part 2, Part 3 which is very thorough.  In the last part of that blog, it is stated "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical." Looking at the pictures here and on the other SO questions (here and here) it appears that the eggs are indeed elongated rather than spherical.  Hence they are apparently Chironomous midge eggs.


It seems to me that they are not summing the changes correctly in this page.

They are summing the lengths of the paths to the root (and for the fig 2, they assume that the terminal branches, from left to right are of lengths 3, 2, 1 and 1). This doesn't make sense to me.

The correct way to count changes using parsimony is to consider each site in the alignment, and try to put the minimum number of mutations on the tree to explain the states observed at the terminal branches. Then, sum the number of mutations across alignment sites.

Here, for figure 1, I get:

site 1: 1 mutation, either on the left (T->A) or on the right (A->T) internal branch.

site 2: 1 mutation on the 4th terminal branch (T->C)

site 3: 0 mutations (all terminals have C)

site 4: 1 mutation on the 2nd terminal branch (G->C)

Total: 3

for figure 2:

site 1: 1 mutation on the branch leading to the most recent common ancestor of the two right-most terminals (A->T)

site 2: 1 mutation on the right-most terminal branch (T->C)

site 3: 0 mutations (same reason as for figure 1)

site 4: 1 mutation, either on the left-most branch (G->C) or on the branch leading to the most recent common ancestor of the 3 right-most terminals (C->G)

Total: 3

The trees are equi-parsimonious.

I hope I did not make any mistakes.

There exist algorithms to do this. For instance, Wagner parsimony.

Don't trust a course on phylogeny that resides on a medical center web page.


What is allelic effect sizes and direction?

These two concepts are different from penetrance.

Allelic effect size

An allelic effect size is the magnitude of the effect of an allele on a phenotype.

The detailed definition seems a little bit trickier than it sounds I think (and I would love confirmation by other users on what follows and or a reference). For example, a phenotypic trait might be influenced by 20 QTL. At one such QTL (say QTL8), you may observe two alleles in the population: QTL8_A and QTL8_B. The effect size is the absolute phenotypic difference between two individuals differing exclusively at QTL8. I suppose it is also possible to define an allelic effect size as the average difference between the phenotype of QTL8_A and QTL8_B over all possible genetic background (eventually weighted by the average frequency of each background in the population at a given instant). In the case of a QTL that contains more than two alleles, then the allelic effect size can be defined either between each pair of alleles or between one allele and the average effects of all the others. Strong epistasis make the whole thing more complicated if one wants to average over all possible genetic backgrounds.

Direction of an allelic effect

The direction of an allelic effect is the direction (add or subtract) that an allele has on a phenotype.

Talking about direction makes sense only in the absence of sign epistasis.


Circulation through the liver in light of drug metabolism

Yes, the blood from the hepatic artery (proper) and the portal vein mix in the sinusoids of the liver. The hepatic vein supplies about 75% of the blood to the liver, and the hepatic artery the remaining 25%. Because the portal vein provides such a large part of the blood supply to the liver, then any disease that causes the blood to build up can cause portal hypertension.

The hepatic artery carries oxygen-rich blood from the heart. The portal vein is part of the portal system and connects the capillary beds of the gastrointestinal tract to those of the liver. Because of the larger volume through the portal vein, I think that each vessel carries about half the oxygen supply to the liver.

For drugs introduced through an injection, for example, metabolism occurs throughout the circulatory system and in the liver. Remember that it's all the same blood supply, but the first-pass effect just refers to the blood that goes to the liver before entering the systemic circulation (by which it can travel to its target).


Why is stimulation of nerve tissue with a negative pulse called "cathodic" stimulation?

The answer to your (excellent) question is a matter of definition, which has its roots in the 18th century.

A cathode is the electrode where conventional positive current leaves a current source. Conventional current is positive, due to historic reasons. Around 1750, Benjamin Franklin described the flow of current between wool and wax after electrostatically charging the former. He defined the flow of current as being positive, flowing from the surplus side (which he defined as positive) to the current sink (defined as negative). This unfortunate choice is sometimes referred to as the Franklinian approach to electricity, and is still widely used today to describe electronic circuits and referred to as the conventional flow notation (Fig. 1) (Efron, 1960).

Fig. 1. Franklinian approach: the conventional flow of current still in use today for electronic circuits. Source: All about circuits.

The electrical current was only later found to consist of negatively charged particles, namely electrons. The work of Luigi Galvani on electrical stimulation in frog muscles around 1780 and the invention of the electric battery by Alessandro Volta in 1800 eventually led to the discovery of the electron in 1897, attributed to J.J. Thomson and his work on cathode rays shown in Fig. 2. As the figure shows, the true flow of electrical current is the reverse, namely an electron current flowing from from negative to positive. In the meantime, however, the convention of positive current flowing from the positive pole (cathode) to the negative (anode) was already established. Note that this holds for a discharging device. In a charging device, such as the battery, the cathode is negative, and the anode is regarded as positive.

Fig. 2. Cathode ray showing electron flow. Source: TutorVista

Hence, in a stimulating (discharging) device, the cathode is in truth negative, because it is the source of negative current (electrons). Cathodic stimulation therefore means electrical stimulation with a negative current. A cathodic pulse is therefore injection of a negative current pulse.

Reference
- Efron. Chapman & Hall London, Rider Publisher New York (1960)


Nernst equation and equilibrium potential

The Nernst equation should be:

RT/(zF)*ln(Out/In) = 2.3 RT/(zF)*log10(Out/In)

You substituted for 2.3 RT/F (approximately 60 or 61 mV: use 60 because your instructor asked you to), but forgot about z. Calcium is divalent (and positive) so for calcium z=2. Substitute this and you can see how you get your answer.

(Also note the "out/in" which is how you get negative numbers when z is positive and out < in )


How many people are required to maintain genetic diversity?

Actually it is a very important question for laboratory animals (and, I imagine, endangered species) and was calculated to be 25 couples.

With any number of animals (including humans), there is always some inbreeding happening, but you can reduce it with the number of breeding pairs and careful pairing. When you get to 25 pairs (50 animals) and have complete control over pairing, you can sustain the genetic diversity practically infinitely (especially if you take into account spontaneous mutations).

Of course, such control over who can have children with who (plus whether one is at all allowed to procreate and what will be the sex of their children!) would be questionable morally, so in case of populating a distant planet, we would need a larger group, to provide for sexual preferences, fertility problems etc.

Some information on laboratory outbred stocks.


Excellent question!

You would definitely be able to find quite a few sequences of DNA that are undamaged (in fact most of them would be undamaged), but it is very unlikely that any cells in his/her body would have a perfect copy of the entire original genome.
I'm sure that cells closer to the skin (exposed to more radiation) would have more mutations, but beyond that most everything depends on where you live, your habits, etc. (if you're a smoker you will obviously have more mutations in your lung cells).
Under regular circumstances (low levels of mutagens), about 3 nucleotide mutations occur in the human genome per cell per division (DNA replication) (from http://www.ncbi.nlm.nih.gov/books/NBK26881/). The rest of the math would be a very rough estimate, seeing as you'd need to make a lot of assumptions (cell division rate average, other mutagens an organism may encounter, life span, the list goes on), but however you want to do it, there's the number you need to start with.

I hope this helps.

CDB


Why are there 10 base pair steps, not 16?

Unlike RNA, where the sense of the molecule is unique, DNA is double stranded, with the two strands having the opposite sense. In the sense of chemical stability it odesn't matter, which sense is considered positive, and which is negative.
Thus, if we consider a base pair step WX|YZ, we have Y folowing W on the positive sense strand (W->Y), and X following Z in the negative sense (antisense) strand (Z -> X). This means that, if we labeled the strands differently, we would have Z->X on the positive strand and W->Y on the negative one, i.e., we would have base pair step ZY|XW. I.e., the general symmetry rule is
$$
WX|YZ \rightarrow ZY|XW
$$
In particular, this means that CG|CG is identical with GC|GC, whereas TA|AT is identical with itself, rather than with AT|TA.
Visually, this symmetries are obtained by rotating the image of the base pair step by 180 degrees, as can be readily seen in the image provided in the question.


the Genus Cuscuta has over 200 species varying in color from yellow, to orange, and purple (sometimes but rarely can also be green).
The organism in the photo is not likely to be a subspecies of the usual dodders you find in your area, instead it is likely to be a different species entirely (while still belonging to the same genus).
The rope dodder (Cuscuta compacta) is very possibly the species you are looking at. However, I am also convinced that Cuscuta europea is a possible candidate, particularly due to this photo of the species that I got from the European Nature Information System (EUNIS) web site:

I must admit that I do not know nor have access to photos of all the different species of the Cuscuta genus to make a truly objective analysis of your image however I hope this information as a minimum leads to some new insight on the matter.


You should purify your RNA after transcription from any buffer/enzyme contaminants. There are several kits available in the market for that. One is GeneJET DNA & RNA Cleanup and Concentration that uses standard silica-beds packed columns to absorb nucleic acids. You can then elute them in pure water and you should be ready to go. Once the RNA is purified you will use the vivo-jetPEI for the delivery.


Penguins (and many birds) recognize their offspring and mate thanks to vocalizations.
It's called individual vocal recognition, it's like when you recognize your friend voice among a group of chatting people.
Scientific article references for penguins:
http://www.sciencedirect.com/science/article/pii/S0003347299910862
http://rspb.royalsocietypublishing.org/content/267/1448/1081.short


No.  The CDC recommends using a hand sanitizer at at least 60% ethanol.  Most preparations used in the lab are 70% ethanol.  Humans start to risk death somewhere around the 0.3% alcohol level (BAC), especially around 0.5%.  People have gone higher, but even 1% BAC would be completely useless against bacteria.  You'd be dead long before the bacteria died.  Besides, if you've got bacteria in your blood, you've got bigger problems than a simple infection.

In a pinch, though, it can be used as a topical antiseptic, as per this fun article.


Why can't we propose a solid theory regarding origin of life?

First of all, we do have some solid theories to explain the origin of life. That said, the main thing missing in order to be able to accept one of these theories with a decent amount of certainty is the ability to run a planetary scale experiment for a few billion years.

The theories are fine, the problem is that we cannot really test them. In order to test a theory that describes the origin of life, we will have to recreate the original conditions (think of a test tube the size of the Earth) and then pump energy into the system and watch what happens over the next few billions of years. This is not really feasible, for obvious reasons. I really doubt you will be able to get funding for an experiment that will run that long.


Paleontology is the main scientific branch, which study fossils and prehistoric times.

Paleozoology studies the fossils and biology of prehistoric animals.
Paleobotany studies fossils and biology of prehistoric plants.
Paleobiology studies the biology of prehistoric organisms.
Paleoecology studies the prehistoric ecological systems and ecology.

In fact, putting the prefix "paleo-" turns every scientific branch of biology to a branch concentrating on this subject but in prehistoric times.


Why does Rigor Mortis occur after death?

You are right that ATP is needed in relation to Rigor Mortis: This for ion pumps to maintain concentration gradients in cells. Without a constant supply of ATP to the pumps, calcium starts to diffuse from the extracellular matrix (and other intracellular compartments with high concerntations of calcium) into the sarcomere where it binds to troponin, a regulatory protein in skeletal muscles. This holds myosin the actin filaments together creating the effect of rigor mortis.


What is the science behind the inaccurate perception of colors?

First recall that pink is white minus green, more or less.
Now, your perception can be explained by adaptation: Neurons try to control their gain (amplification factor) to have roughly the same range of output. So if there's a lot of stimuli they like, they will reduce their gain, and vice versa. It can be thought of as a form of fast time-scale homeostasis in this case.

While you were in the green room, your neurons that represent 'green' gets less sensitive to green stimuli due to strong green input (adaptation). Additionally, the 'non-green' representing neurons become more sensitive, since there's less visual stimuli that they like. When you suddenly come out of that room, now the green neurons do not respond as strongly as the non-green neurons in response to white, hence your perception of pink.


How can I normalize mRNA samples for sequencing?

I found the link to a commercial product by Evrogen here:
http://www.evrogen.com/technologies/normalization.shtml

They claim their method is compatible with nextgen sequencing platforms:

  cDNA normalization using duplex-specific nuclease (DSN) is a highly
  efficient approach that can be applied for normalization of
  full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
  2005). The resulting cDNA contains equalized abundance of different
  transcripts and can be used for construction of cDNA libraries and for
  direct sequencing, including high-throughput sequencing on the next
  generation sequencing platforms (Roche/454, ABI/SOLiD or
  Illumina/Solexa).

And the most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503


I guess confusion comes from either:

Inclusion vs exclusion of H2O (free AA vs in chain)

Averaging with
equal weight between all AA vs weight of their relative
occurrence

Does this help?


Are there any drugs that target the lipid envelope of viruses?

The lipids in the viral envelope come from chunks of the host cell membrane. Therefore, something targeting those lipids is unlikely to be virus-specific, and not suitable for use in a living animal.

Out in the environment where the virus is found in surfaces and such, sure, one can target the lipid envelope using soaps/detergents and such, but you wouldn't want to take those internally.


Accessing Expression Levels for Genes of Interest from GEO Experiments

You could look at supplementary and methods section of "The Landscape of Long Noncoding RNAs in the Human Transcriptome" paper. They've collected RNASeq samples from TCGA, ENCODE and MCTP and processed it with their pipeline (most of it are filtering and GSEA) to detect novel lncRNAs and associate them with cancer pathogenesis. Their statistics, processing and cross-validation look clean and accurate.
To extract signatures from GEO, you could use GEO2Enrichr. Then calculate the differential expression of tissue-specific libraries in Enrichr. Also, you could submit gene list to Enrichr's Crowd libraries and find GEO entries with a reasonable number of mapped genes first.


Which proteins are most sensitive to electric fields?

There are various proteins sensitive to changes in electric field. More precisely, they are activated by changes in voltage (surrounding the protein), and immersed in water, as all cells are mainly composed of an aqueous solution. You are correct that most charges in the side chains of the proteins' amino acids are 'masked' by the dipole character of water molecules, but the electrochemical potential of the cell is primarily due to ions, and not to the interaction between side chains in a protein. However, it is important to note that within these proteins sensitive to changes in the electrochemical field, there are domains that contain charged aminoacids (i.e. not covered by water), very important to be able to 'sense' the changes in voltages.

You can check out some of the voltage-sensitive ion channels, which participate in different cellular pathways, including the generation and transmission of the action potential in neurons:

Wikipedia has a good entry about them.


Regulation of V. cholerae virulence factors

Virulence factors of V cholerae is regulated by a hierarchical regulatory system. The proteins you listed in your question are part of this system. In this paper it is said that the actual activation of TCP and CT is done by ToxT- thus this could be your "key" protein. I'd also like to note that just because these are two different genes does not necessarily mean that there has to be two key factors - this assumption of yours if a bit faulty.

Also because the activation of the virulence factors are regulated by a chain of events, each link is can be considered equally important, because if one of them fails the whole chain is dysfunctional.

The short description of the regulatory chain taken from the article linked above:

  The ToxR regulon is a hierarchical regulatory system that activates virulence gene expression in response to environmental stimuli (2). Induction of the ToxR regulon starts with activation of tcpPH expression by AphA and AphB (4, 5). AphA and AphB are cytoplasmic regulatory proteins that cooperatively bind to the tcpPH promoter and activate its expression. Once TcpP is produced, it functions in conjunction with ToxR to activate toxT expression. TcpP and ToxR are structurally similar membrane-bound DNA binding proteins that are thought to modulate gene expression in response to external stimuli (6, 7). When stimulated, TcpP and ToxR bind to the toxT promoter and activate its expression. ToxT then directly activates the expression of the genes that encode for CT and TCP production (8).

This paper might also be helpful. Unfortunately I could only access the full text this way (through researchgate):

Regulation of virulence in Vibrio cholerae: the ToxR regulon.
Brandon Childers, Karl E Klose
Future Microbiology (Impact Factor: 4.02). 07/2007; 2(3):335-44.
DOI: 10.2217/17460913.2.3.335

This paper provides details of regulation and mechanism of ToxT.

Taken from the third linked paper. As you can see the final activator of CT (termed CTX in the picture) and TCP is indeed the ToxT, but as I wrote it earlier each link in the chain is important.


How is human biological clock modelled in modern science?

The situation is quite complex, and there are certain things that we do not fully understand, but I will try to give you an explanation.

First of all, at the cellular level, you have the genetic components of the circadian clock, the clock genes and their protein products.

You can divide clock proteins into positive and negative regulators: the positive regulators modulate transcription of clock-controlled genes and are inhibited by the negative regulators in a loop that lasts approximately 24 hours (in Latin: circa = around and dies = day).

For instance the Clock and Bmal1 nuclear proteins, when present in sufficiently large amount, will dimerize and act as transcription factors on a series of genes that contain a region in their promoter element called E-box. Amongst these are the Period (Per) genes.
Per is then synthesised, and exported to the cytoplasm. Here, if in a sufficiently large amount, it can heterodimerize with the Cryptocrome (Cry) proteins: the dimer will then enter the nucleus and inhibit the transcription actions of the Clock/Bmal couple. This will in turn, block the transcription of Per, that will therefore not be able to dimerize with Cry and stop the inhibition of Clock/Bmal and so on. All of this takes approximately 24 hours.

This basic loop (and some more) is nicely schematised in this review by Reppert and Weaver

Coordination of circadian timing in mammals. - Reppert and Weaver, Nature. 2002 Aug 29;418(6901):935-41.

I report here the legend of the figure:

  The clock mechanism comprises interactive positive (green) and negative (red) feedback loops. CLOCK (C, oval) and BMAL1 (B, oval) form heterodimers and activate transcription of the Per, Cry and Rev-Erbalpha genes through E-box enhancers. As the levels of PER proteins increase (P, blue circle), they complex with CRY proteins (C, diamond) and CKIε/CKIδ (ε/δ, circle), and are phosphorylated (p). In the nucleus, the CRY–PER–CKIε/CKIδ complexes associate with CLOCK–BMAL1 heterodimers to shut down transcription while the heterodimer remains bound to DNA, forming the negative feedback loop. For the positive feedback loop, increasing REV-ERBα levels (R, circle) act through Rev-Erb/ROR response elements in the Bmal1 promoter to repress (-) Bmal1 transcription. CRY-mediated inhibition of CLOCK–BMAL1-mediated transcription de-represses (activates) Bmal1 transcription, because REV-ERBα-mediated repression is inhibited. An activator (A, circle) may positively regulate Bmal1 transcription (?) alone or by interacting with mPER2. There are probably kinases (?) other than CKIε and CKIδ that participate in phosphorylation of clock proteins.

The clock machinery, however, is even more complex than this and different tissues need to integrate different signals (e.g. light, hormonal concentrations and so on).

However, as nice as this may be, our bodies are not constituted by one single cell... if we "zoom out" a little bit and we go to the tissue or the whole body level, we see that circadian rhytms are present in all sorts of tissues and involve all sorts of different physiological processes. A very interesting question is then: how do cells from different organs coordinate each other so that the interrelation of different circadian processes is always the same? For instance, the release of cortisol peaks in the morning, our body temperature has a peak in the late afternoon and a trough in the early hours of the morning, and our heart rate is higher during the daytime.

In 1972, an article by Moore and Eichler was published, showing that lesioning the suprachiasmatic nucleus (SCN) of the hypothalamus (a region at the base of the brain) resulted in the "breakage" of the circadian rhythm of corticosterone (the stress hormone).

Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat. - Moore and Eichler, Brain Res. 1972 Jul 13;42(1):201-6

The fact that lesioning a bit of the brain resulted in loss of circadian rhythm in the adrenal gland was obviously a very big deal: the central circadian clock of the organism had been discovered.

I will not going too much into that but, since 1972 many advances have been made and nowadays we know that, although the role of the SCN is very important, it is not the only clock in the body. Several peripheral clock exist, in organs such as the pituitary gland, the liver or the pancreas. How all these clocks communicate between each other and what is their contribution to the generation of non-circadian rhythms (ultradian and infradian) are questions that still have to be solved.

A few interesting papers on the matter:

A riot of rhythms: neuronal and glial circadian oscillators in the mediobasal hypothalamus. - Guilding et al., Mol Brain. 2009 Aug 27;2:28.

A clockwork web: circadian timing in brain and periphery, in health and disease. - Hastings et al., Nat Rev Neurosci. 2003 Aug;4(8):649-61.

Peripheral circadian oscillators in mammals: time and food. - Schibler et al., J Biol Rhythms. 2003 Jun;18(3):250-60.


Probability of carrier for recessive trait given parents are carriers and sister affected

Assuming the trait is caused by a single gene, she would indeed have a roughly 50% chance of being a carrier. If both parents are carriers but unaffected they will both be Aa (with a being the recessive mutation). For your girlfriend to be a carrier she will have to be Aa, of the 4 possible combinations her parents could have passed on (AA,Aa,aA,aa) two lead to this outcome, thus 1/2. If you are sure that she is unaffected the aa option is eliminated and she thus has a 2/3 chance of being a carrier.

If you are not a carrier but your girlfriend is it will be impossible for your child to express the trait (but would still have a 50% chance to be a carrier!). If you are both carriers you loop back to the original situation of her parents, your child would have a 25% chance of being affected and have a 50% chance of becoming a carrier. I must emphasize that real life genetic inheritance is more complex than these textbook calculations, chromosomal crossing over and whatnot can seriously alter these percentages.

I am not a health professional, consult your physician and/or get your girlfriend tested (if possible).


Based on various comments, I've expanded this answer. Though long, I cannot cover the depth of the topic of sleep but I tried to address the issues asked in the original question while broadly highlighting various aspects about sleep research. I welcome any suggestions for improvement.

What is sleep?

To know what it means to be awake, you must know what it means to be in a state of sleep. These are two alternative states for animals that sleep.

Finding a concise scientific definition of sleep is difficult, probably because sleep is a very complex process. For example, Diekelmann and Born (2010) state that,

  Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory...

and later

  Sleep is characterized by the cyclic occurrence of rapid eye movement (REM) sleep and non-REM sleep, which includes slow wave sleep (SWS, stages 3 and 4) and lighter sleep stages 1 and 2....

Most attempts to explain what sleep is include the four stages of sleep along with REM (rapid eye movement sleep). The stages are nicely explained by this National Institutes of Heath website on Brain Basics: Understanding Sleep. Each stage of sleep can be identified by specific types of brain waves, shown below (image from here).

Notice that the first wave pattern is characteristic of being awake.  The wave patterns change as an individual becomes drowsy and then falls asleep. While asleep, the brain cycles through the different stages, each with its characteristic brain waves.  Associated with these stages are changes in metabolic activity and physical capabilities. For example, the Brain Basics site notes that we become less responsive to external stimuli and metabolic activity slows. During REM, breathing becomes rapid and we can't move the muscles in our arms or legs. Similar states are found in other invertebrate and vertebrate organisms, which suggests that these are common indicators of sleep or a sleep-like state. Some examples of these states are given in the citations and links below.

Defining "awake" seems just as difficult as defining "asleep" but once again neural activity seems to be key indicator. As shown in the figure above, being awake has characteristic wave patterns in the brain that are distinct from the wave patterns associated with sleep. In addition, none of the physiological/physical states associated with sleep stages are present when you are awake.

In both cases, asleep and awake, the indicators seem to be based on characteristic neurological activities in the brain or, in the case of some invertebrtes, the organized nervous system.  This interpretation is important when considering whether organisms without any type of nervous system is capable of sleep or the alternate state: awake.  More on this at the end.

Why sleep?

Science magazine, in the 125th anniversary issue, made a list of 125 big questions that remain to be answered by scientists. One of those questions was "Why do we sleep?" The role of sleep remains elusive but many ideas have been put forth about the role of and the evolution of sleep. The leading idea seems to be memory consolidation. This article by Kavanau (1997) reviews ideas about the function of sleep and why it evolved.  He suggests that sleep and memory evolved as as ways to improve or maintain effective connections among the nerve cells in the brain. Some circuits are used frequently, such as those used to process sensory information like vision. Other circuits are used less frequency, such as circuits that can be used to store memories. Sleep may allow those infrequently used circuits to be activated and used without causing conflict with the circuits used during "restful waking." In other words, sleep may allow the lesser used circuits to be exercised, which can help to consolidate memories. So, at least one function of sleep may be to help maintain efficiency in how information is moved around the brain by maintaining the brain circuitry.  See also this review by Siegel (2005) and the previously mentioned article by Diekelmann and Born (2010).

This Scitable article has a nice overview of the importance of sleep for humans, as does the Brain Basics site.

What organisms sleep or have sleep-like activity?

Sleep has been well-studied in vertebrates, from fishes (Marshall 1972) to mammals (Pace-Schott and Hobson 2002). However, not all vertebrates necessarily sleep (Kavanau 1998). For example, continuously swimming fishes like some sharks and blind cave fishes may not sleep. These are just three references of many about sleep in vertebrates.

Sleep and sleep-like activity has not been as well studied in inertebrates. As noted in this thread, there is evidence for sleep in at least some insects. Cephalopods like octopuses show signs of sleep (Mather 2008). Caenorhabditis elegans, a nematode worm and model biological system, shows sleep-like states tht are similar to mammals and fruit flies (Raizen et al. 2008). The most basal organism that shows evidence of sleep-like patterns is a jellyfish called Chironex fleckeri (Kavanau 2006). Cnidarians like jellyfishes are the basal (most "simple") group of organisms with an organized nervous system. Interestingly, C. fleckeri process a lot of visual information obtained through their 24 eyes. Twelve of the eyes are simple, light-receiving structures but 8 of the eyes are camera-like, meaning they have a lens.  Kavanau (2006) argued that sleep (up to 15 hours) in this jellyfish allows time for its simple nervous system to process the visual information obtained while it is awake. The presence of sleep-like activity in jellyfish and nematode worms suggest that sleep is an evolutionarily ancient phenomenon.

This Wikipedia page on sleep in non-humans overviews evidence for sleep in vertebrates and invertebrates. It's not clear whether androids sleep or what they dream about if they do sleep.$^1$

Do single-celled organisms sleep?

This is (to me) a tricky question. Sleep is associated with specific types of neural activity in the brain or nervous system. In addition, sleep-like neural activity has been found in diversity of organisms with some type of nervous system, and seems evolutionarily old. I therefore think that any organism that has some form of organized neural center (brain, brain-like organ or centralized nervous system) has the potential to show some type of sleep-like patterns.

In contrast, organisms lacking any type organized nervous system would not be capable of sleep, at least as currently defined. If they do not sleep, then they also cannot be awake because being "awake" seems to be recognized as neural activity not typical of sleep.  Therefore, it seems to me that single celled organisms like bacteria and paramecium are neither sleeping nor awake.  Plants are neither sleeping nor awake. They are metabolically active but they are neither asleep nor awake because they do not have any type of neural activity.

I'm not a sleep researcher (but sometimes I am a sleepy one) nor am I a neurophysiologist. I just walked through my train of thought. I welcome contrary views along with the supporting science.

Literature Cited

Diekelmann, S. and J. Born. 2006. The memory function of sleep. Nature Reviews Neuroscience 11: 114-126.

Kavanau, J.L. 1997. Origin and evolution of sleep: Roles of vision and endothermy. Brain Research Bulletin 42: 245-264.

Kavanau, J.L. 1998. Vertebrates that never sleep: Implications for sleep's basic function.

Kavanau, J.L. 2006. Is sleep's 'supreme mystery' unraveling? An evolutionary analysis of sleep encounters no mystery; nr does life's earliest sleep, recently discovered in jellyfish. Medical Hypotheses 66: 3-9.

Marshall, N.B. 1972. Sleep in fishes. Proceedings of the Royal Society of Medicine (abstract).

Mather, J.A. 2008. Cephalopod consciousness: Behavioral evidence. Consciousness and cognition 17: 37-48.

Pace-Schott, E.F. and J.A. Hobson. 2002. The neurobiology of sleep: Genetics, cellular physiology and subcortical networks. Nature Reviews Neuroscience 3: 591-605.

Raizen, D.M. et al. 2008. Lethargus is a Caenorhabditis elegans sleep-like state. Nature 451: 561-572.

Siegel, J.M. 2005. Clues to the functions of mammalian sleep. Nature 437: 1264-1271.

Footnote

I could not resist.


The change in gel migration distance is due to the conformational changes due to the binding of the ion, and have nothing (detectable) to do with the ionic radius of the ion.

The left image shows calmodulin with no ligand bound, and the right image shows it with calcium and peptide bound to it.

As you can clearly see, the unbound calmodulin is significantly thinner, and therefore can migrate faster through the gel. The change in charge on the protein due to cation binding in native PAGE may also affect the result.

Since the calmodulin conformational change is enhanced by both a peptide and calcium cations, as well as its phosphorylation state, it would be reasonable to investigate the contributions of these factors to your result. Reading the original paper again to see what you missed the first time may also be helpful.


Are there single-celled organisms that have evolved from multi-cellular ones?

I would consider HeLa cells to be an example of a unicellular eukaryotic organism that evolved from humans. It can survive independently and replicate within cell culture plates, but cannot survive in the wild, however.

HeLa cells are, like in your example, cancer cells, in this specific case human cervical cancer cells. They were propagated as an immortal cell line, and completely match the replication characteristics of eukaryotic cell lines when propagated in the laboratory.

It can be even considered the case that HeLa cells are actually a kind of unicellular eukaryotic model organism not unlike S. cerevisiae, since they are widely used in experiments involving human-like cells.

As WYSIWYG has said in the comments, some biologists have even assigned the binomial name Helacyton gartleri to the cells (albeit with some controversy).


The heart of a Pigmy Shrew beats 1300 per minute then why is it so fast?

There is a correlation between the heartbeat and the life expectancy as you can see below.

(source: medcan.com)

This relationship is not linear (the y-axis is on a logarithmic scale) and is negative, that is, the faster is the heart beat, the lower is the life expectancy. You'll note the outlier (human) that has a life expectancy that is twice as high as you wold expect from the regression. This shift toward the right is caused by medicine, food quality and hygiene.

Correltation vs causation

Note that correlation doesn't imply causation. Typically, you'll notice from reading the species names on the first graph that species that have a fast heartbeat (and therefore a low life expectancy) are small in size.Allometry  is the study of the relationship of body size to shape, anatomy, physiology and behaviour. You might want to have a look at the wiki page.

  can we consider faster heartbeat is not good for health?

No! it is wrong to think from from those data that the shrew (that has low life expectancy and fast heartbeat) that if they were to have a slower heartbeat, they would live longer. This is wrong. Shrews have the heartbeat they need to have. If one shrew (due to a mutation or some environmental developmental effect) had a slower heartbeat, it would die very early.

In other words, such inter/species correlation doesn't tell anything about intra-species correlation. To reuse the example of the relationship between mass and life expectancy: Body mass and life expectancy are positively correlated among species (see above) but the mass at which life expectancy is maximized in humans is average. The below graphs shows the relationship between body mass and Relative Risk (RR) of coronary heart disease.

(source: revespcardiol.org)

Health ≠ life expectancy ≠ adaptation

Life expectancy, health and high fitness (biological sense) are three concepts that are eventually related but that are very different. While life expectancy can compare health in inter-species comparison, it makes little sense to compare health of different species. Note also, that natural selection may well favour short lifespan (as suggested by @RioSiv, you might want to have a look at life-history r/K selection theory).


When something "smells moldy" what are we really smelling?

The vast majority of the things you smell are odorants, or volatile molecules; not spores. They are light compounds that have high vapor pressure (are airborne), and that interact with your chemoreceptors in your nose (can be smelled). The most-often reported microbial volatile organic compounds in living environments according to this study are as follows:

2-Methyl-1-propanol
3-Methyl-1-butanol
3-Methyl-2-butanol
2-Pentanol
3-Octanol
1-Octen-3-ol
2-Octen-1-ol
3-Methylfuran
2-Hexanone
2-Heptanone
3-Octanone
2-Methylisoborneol
2-Isopropyl-3-methoxy-pyrazine
Geosmin
Dimethyl disulphide

Geosmin is probably the most moldy-smelling and is detected very sensitively by olfactory systems of animals that want to avoid contaminated food. To me it smells muddy, or earthy, like soil after a rain shower. In our lab, about half the people find it a pleasant smell. It can be smelled in wine, it's the earthy taste found in vegetables, it's the smell of dead bacteria, and so on and so on. The term petrichor describes the odor and geosmin is a major contributing odorant for this.


If an organism is supported only by cartilage, does it have an endoskeleton?

From wikipedia

  An endoskeleton (From Greek ἔνδον, éndon = "within", "inner" + σκελετός, skeletos = "skeleton") is an internal support structure of an animal, composed of mineralized tissue.

Cartilage is a mineralized tissue so it counts as a skeleton from this definition. A bit further in the wikipedia article it says

  The vertebrate endoskeleton is basically made up of two types of tissues (bone and cartilage)


Would short term increases in oxygen lead to beneficial effects?

Humans are pretty well suited to a 21% oxygen atmosphere (at STP). It's what our lungs are used to dealing with, and it's what brings the appropriate amount of oxygen to our brain (in particular, most organs are more forgiving, although not a lot more).

A lower concentration grows quickly and strictly deleterious, leading in short order to hypoxia, subsequently death. A higher concentration is also deleterious, leading initially to an oxygen high (as seen with Oxygen Bars), but also causing vision problems, seizures and death.

Oxygen is also highly reactive, and increased concentrations for even short bursts could, if frequent, lead to cancers, especially lung cancer. (The primary cause of lung cancer prior to asbestos and smoking? Breathing.).

There are cases in which increased oxygen concentration can be beneficial, but they are rare and specialised.


Normal cell diffusion in normal organism?

In a healthy body, cells travel.
But this is very dependent of the cell type. Some cell type will travel in all the body (lymphocytes, plasmocytes, etc) while other do not have any migration capability.

The concept of diffusion is wrong to apply here, indeed the scales at which you are looking are not molecular.

Moreover, there are very active mechanism to keep cell type in place, for example, a concept called preferential attachment will maintain the cells grouped by cell type. If you take two balls A and B and A attached more to A and B to B, and you shake, you will see appearance of clusters of A and clusters of B. But that is only one such mechanism and a lot of other take play here.

see this: http://www.ncbi.nlm.nih.gov/books/NBK26937/

Thus, the probability of finding a cell type NOT at its normal position (that is one that does not travel) is maybe not zero, but so close to it that you will not find a cell outside of their normal position.

I hope this answers your question ?

Reference
Cooper GM. The Cell: A Molecular Approach. 2nd ed. Sunderland (MA): Sinauer Associates; 2000


How can you design a drug to modify apoptosis to treat a disease such as cancer?

The new cancer drugs are custom designed antibodies that have a cell-killing agent attached to them. These antibodies specifically attach to the cancer cells, and kill them. Other methods, like traditional chemotherapy target cells that are actively dividing, like hair in addition to cancer. Cancer cells are defined by uncontrolled cell division. But traditional chemotherapy, in simple terms, stresses the body to near death, differentially killing actively dividing cells. The new targeted methods are much less toxic.


In plasmid-based transient transfection of mesenchymal stem cells, do I have to select for transfected cells and verify GOI expression via a reporter?

No and Yes, respectively.
No, you don't need to select for and generally you can't unless you use something like FACS to sort and capture cells expressing your marker/GOI.
Transient transfections are generally not selected for, if they are it is to make a more stable line, and either requires integration of the marker site into the genome (most common) or in some cases use of a plasmid and cell system that supports propagation of the plasmid.
With transient transfection it is normally a good idea, at least for the first few times, if not every time, to confirm that the plasmid is expressing as you expect. You can do this by immunological methods, most commonly western blotting (WB) or immunocytochemistry (ICC). ICC will give you a percentage transfection, which can be useful in assessing how well you would expect an overall population to respond to a stimulus and how well you can see that effect - what if only 10% of your cells transfected compared to 50% or 90%, but it can't tell you how much protein is being expressed. ICC can also tell you how cytotoxic your transfection is - commonly used methods like the Lipofectamine family of reagents are often in the 20-50% cell-death range. WB on the other hand gives you how strong your expression is - how much protein is there, but it can't tell you how many cells were transfected or how much cell-death there is.
In theory at least FACS can do both number and strength, but it would require calibration of your antibody by both western and ICC.
You can also look at RNA expressed off the plasmid, but this may not bear a direct relationship to how much protein is produced.


How far in can non-extremophiles live, in Earth?

Welcome to Biology.SE and what a great project, it sounds fascinating!

A few years back there was an expedition that drilled down to the deepest layer of the ocean's crust. Down there they found hundreds of different species of bacteria (mostly Proteobacteria) surviving largely on hydrocarbons and other minerals found in the rock. The deepest (that was sequenced) was found 1391.01 mbsf (meters below sea floor) and survived at a temperature of about 102°C (215°F). Like I said, there were several species sequenced, so you could really use any of them that match your needs as at least a start to your organism.

This is the deepest point I know of that we have found life, and, considering your project, I don't think you have need to go much deeper. I assume Kepler-422b has liquid water (obviously not at the surface, but perhaps a few miles down)? If so, there is a chance that the water goes relatively close to that depth already.

I hope this helps and good luck!

CDB

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974637/

Edit: If you are looking for a multicellular organism that survives deep enough underground to rely on core warmth, I suggest Halicephalobus mephisto, a nematode living about 1.3 km underground at about 32°C (90°F). This is still considered an extremophile, however it is multicellular with a digestive tract, nervous system, etc. I apologize for the confusion in my initial answer and thanks to jamesqf for noticing my mistake. If you are not content with any extremophiles (even multicellular) please let me know and I will do my best to find something else. Again, I am very sorry for my error.


What's the relationship between snail movement and rain?

The movement of organisms towards water is termed hydrotaxis. 'Hydro-' refers to water and '-taxis' refers to movement. Hydrotaxis has been investigated in animals such as the nematode Caenorhabditis
elegans (Wang et al., 2016) and, closer to snails, the gastropod Littorina
littorea (Gendron, 1977). Animals may sense the water content of their surrounding environment and moisture content in the air to move where they are more comfortable.
Animals need specific amounts water in their bodies to allow effective metabolism. We can control our bodily water content by taking a drink but simpler animals aren't afforded that luxury so they need to move towards/away from water. Your snails likely moved because the water levels in their bodies dropped as they 'dried out' over the week. They could then have sensed a gradient in the moisture content of their surroundings and moved towards it. Mechanisms in animals' bodies can give animals responsive behaviour, as seen here. For instance, C. elegans uses its cGMP pathway, neurons and biochemistry to respond to water content with movement (Wang et al., 2016).
References

Wang et al. (2016). cGMP Signalling Mediates Water Sensation (Hydrosensation) and Hydrotaxis in Caenorhabditis elegans.

Gendron, R. P. (1977). Habitat selection and migratory
behavior of the intertidal gastropod Littorina
littorea. J. Anim. Ecol 46 79-92


What are the limiting factors of pathogen population size in human populations?

One of the limiting factors is how many uninfected hosts exist. As a pathogen becomes more widespread, the probability of someone infected with it infecting someone else decreases, as it's more likely that the person will spread the disease to someone who already has it instead of someone who doesn't have it, preventing the virus's population size from increasing. See this for more information.

Also the more common a pathogen is, the more likely it is that people will take actions against it, for example by being more sanitary or getting vaccinated against it.


Why are compost worms sensitive to light?

It will sounds counter-intuitive you but earthworms do sense light with their skin. They don't have eyes but they have specialized nerve ending equipped with photoreceptor cells. They are all over skin but concentrated towards first segment of worm. Prostomiun are main light sensing organ in worms. Following image shows their position in first segment of earthworm. (Image source: cronodon.com).

Closer look of above image taken from same website,

Structure of photoreceptors

Earthworm have microvillar photoreceptors like insects (Rohlich et al 1970). Detailed structure is discovered long back.

There is not much information about phototrasnduction in worms but it is well characterized in it's close relative C. elegans (Ward et al 2007).

Now coming to why part, you might wonder if they are spending most of time buried why do they need photoreceptors ? @AMR has guessed it correctly. They use this as protective system. Photoreceptors helps them providing information about how near they are to surface because UV radiation will harm them or probably kill. If there is higher light sensing, they go back to darker regions. You can find similar information from UMICH press release.


Is genome recurrence possible like in Jupiter Ascending?

Various types of genetic variation exist in natural populations. One is the single-nucleotide polymorphism (SNP), which is where different nucleotides are present at the same location in the genome of different individuals in a population (with variation present in a nontrivial number of people; the threshold is usually set arbitrarily at 1%).

Even just considering SNPs and ignoring other types of variation, what you talk about would be effectively impossible.

The human genome is about 3 billion base-pairs long. Along the whole genome, according to Chen et al 2012, between two individuals there is something like 3 million SNPs. Imagine two people flipping a coin and the result is exactly the same every time, 3 million times. Now imagine instead of heads or tails, there are 4 options.

Only 1 result of the series of 3 million 1 in 4 chances is identical to the original series.

$\frac{1}{4^{3000000}}\approx\frac{1}{\infty}$ = 0

Go ahead, try it on your calculator.

Now, there are also variations that are beyond SNPs between individuals that cause much more variation between two people. These can cause even more "unprobability". Since we already require infinite people before this event is likely to happen, I think we can just call this event impossible.


Is this 12+ foot plant a sunflower or hogweed?

The plant in your photo is a sunflower (Helianthus annuus).  The large, heart shaped leaves and stiff, hairy stem are very characteristic of the sunflower as seen in your plant. These form a single flower head on top when mature - about 90 days after planting.  They typically grow to 10 feet in height, so 12 feet would not be unusual.  The tallest recorded specimen was apparently 30 feet in height. Please see links below for more information.

https://en.wikipedia.org/wiki/Helianthus_annuus#Cultivation_and_uses

https://homeguides.sfgate.com/time-year-sunflowers-bloom-67915.html

http://www.illinoiswildflowers.info/prairie/plantx/an_sunflowerx.htm


In which direction does ATP synthase rotate?

Short answer
The direction of rotation depends on the viewing point of the observer and the reaction catalyzed by the ATP synthase. When synthesizing ATP, and viewed 'from the bottom' (observer faces the intermembrane space looking into the mitochondrial matrix) it rotates clockwise.

Background
ATP synthase is a membrane bound enzyme with two large subunits; F0 and F1. F0 is inserted in the membrane and funnels H+ ions from the intermembrane space into the mitochondrial interior (Fig. 1). The stalk region connection F0 and F1 contains the γ subunit, which basically forms a rotating shaft powered by the flow of H+. This causes the entire F1 unit to rotate during ATP synthesis.

Now importantly to know before continuing; enzymes basically work two ways, as they merely establish equilibrium. As such, any ATP synthase is also an ATP hydrolase. When it synthesizes ATP, the γ subunit runs in clockwise direction when observed from the “bottom” (the side closest to the F0 and the membrane, see Fig. 2). When it hydrolyzes ATP (e.g., under non-physiological laboratory conditions) it runs counter-clockwise as the reaction, as well as the movement of the γ subunit reverses (Nakamoto, 2008).

The direction in which the rotation takes place is dependent on the steps involved (Fig. 3). In this figure, ATP hydrolysis is shown and that can be compared to burning fuel in a combustion engine. Now the direction of H+ reverses, against its concentration gradient and needing energy (the road speeding below a car if you like). Because ATP binding, hydrolysis and release of waste (ADP + Pi) each cause a 120o turn of the rotor, the F1 subunit rotates one full turn in each cycle (Yoshida, 2001). During ATP synthesis the opposite direction is established, as waste (ADP + Pi) is taken in and phosphorylated to ATP, during which the flow of H+ reverses (akin to a car going downhill, only combustion engines cannot generate gas from carbon dioxide and water, unfortunately).

Fig. 1. ATP synthase subunits. source: Penn State University

Fig. 2. ATP synthase. source: Noji, 2004

Fig. 3. ATP synthase compared to a combustion engine. A combustion engine converts fuel energy into rotation of a rotor. It can drive the intake of the fuel gas, compression, ignition and exhaust sequentially just by a simple rotation of the central rotor (right panel). The F1 gamma-subunit has and three reaction chambers (the catalytic beta-subunits (left panels). The three reaction sites each go through three cyclic steps in a 120° phase difference to cause rotary motion, very similar to a combustion engine. source: Yoshida, 2001

References
- Nakamoto, Arch Biochem Biophys (2008); 476(1): 43–50
- Noji, Biohistory journal (Winter, 2004)
- Yoshida, Nature Rev Mol Cell Biol (2001); 2: 669-77


Most accurate depiction of cortical homunculus?

Be sure to distinguish exactly what the diagram is showing. Your first reference is sensory cortex mapping. The second reference is motor cortex mapping. The text of the second reference is admittedly confusing about this, a search for "Wilder Penfield motor cortex" verifies.

It seems reasonable the feet would show sensory response similar to the hands. Stepping on a nail is just about as bad as bumping your hand into one. Motor control is different. Muscles are not all innervated the same. In some of the large muscles, say in the legs, one nerve can control hundreds of cells. In other cases, particularily in the face, one neuron might control only six muscle cells. Thus a greater number of neurons, and a larger portion of the brain, is needed for control in these delicately controlled areas. It would make sense a greater part of our brain would be needed for motor control in our hands versus our feet.


In adverse effects of Heparin, why is bleeding from deeper organs more common?

Skin is extraordinarily tough compared to much of our internal tissues; it has to be to protect us. To bleed, skin integrity must be breached, which usually involves sharp objects.

Think for a moment that most splenic or hepatic injuries (even complete ruptures) occur from blunt force trauma without breaking the overlying skin. For a more common example, if someone hits your thigh with a baseball bat, you will get a large bruise, maybe even a broken bone, but the skin will usually remain intact (if badly bruised) from blood vessel damage beneath and within the skin.

Many organs are delicate, and damage within them is not rare. Bleeding within/from some bodily organs is fairly common: runners bleed from their kidneys, and many, many people bleed from somewhere in their GI tract. High blood pressure may cause bleeding in the brain (a stroke) but it won't cause bleeding from the skin.

Just add to all the above the effect of anticoagulation (what heparin does.) I hope that explains things. If it doesn't, please leave a comment.


How does the helicase enzyme break the hydrogen bonds between the strands of DNA?

Im not sure if there is a decided helicase mechanism but the ‘backbone stepping motor’ model has been proposed for
helicase translocation and unwinding. Helicases contain two domains that are analogous to a set of ‘pincers’ (motor domain), when ATP is present, there is only a distance of two nucleotides between the
pincers and so they are closed, whereas when ATP is absent, there is a distance of three nucleotides between the pincers and so they are open. The motor domains interact with the
nucleic acid through contacts between threonine residues on the pincer terminus and phosphoryl oxygen on the nucleic acid. ATP binding weakens these interactions, allowing a pincer to move one nucleotide closer to the second pincer. A third domain (D3), that is part of the helicase but not involved in the binding of ATP, also interacts with the nucleic acid using a threonine residue. As the motor domains move along, tension builds up between the motor domain and D3 and after the motor domain has moved three base pairs, the protein contracts like a spring, pulling D3 toward the motor domains, disrupting the DNA in between. The structures responsible for prying apart the DNA are called “pins” or wedges”, which act as a physical barrier between the two strands of nucleic acid, prying apart its structure. The single
stranded regions are stabilised by helicases as well as other proteins such as single stranded DNA binding proteins, which prevent the reformation of the double stranded nucleic acid.

For more information and good images see: “Translocation and unwinding mechanisms of RNA and DNA helicase”


Why doesn't the Tsetse fly wipe out all animal life in its range?

Firstly, as Remi.b points out, although Trypanosoma brucei infection is invariably fatal in humans, the same is not true for all host species. Domestic animals, particularly cattle, are an important reservoir of T. brucei rhodesiense and can also be infected with T. brucei gambiense (although it's not clear how important a reservoir they are for gambiense).

Secondly, just because all hosts in an area get bitten by tsetse does not mean they all become infected with trypanosomes. Even in endemic areas most vectors never become infectious. The transmission cycle for trypanosomes and other insect-borne pathogens requires an incubation period in the insect vector which is often longer than the median lifespan of the insect, so even if all insects get infected early in life, most will never survive the incubation period to become infectious. The later the average time of first infection gets, the higher the fraction of hosts that will have the opportunity to reproduce before dying.

Finally, it isn't entirely accurate to say "there is no way to prevent being bitten"; it is possible to reduce exposure to insects behaviourally. For example, in most endemic areas local residents will know which areas are most heavily infested and should be avoided.


Functionality of vitamin A, Bx, C, D, E, K as used in cosmetics for the skin?

Vitamin A: One study conducted in the 60's claims that vitamin A acid prevents formation of comedones in Acne Vulgaris [1]. Another one conducted in the 70's found no significant improvement of plantar warts when vitamin A acid was applied topically [2].

Vitamin D: Agents like calcipotriene associated with topical steroids are effective against psoriazis [3]. They inhibit keratinocyte proliferation, normalize differentiation and modulate the activity of immune cells [4]. Active form of vitamin D is also effective against vitiligo [5].

Vitamin E: It reduces skin damage induced by UV [6, 8], but it shouldn't be applied on scars [7].

Vitamin K: It prevents bruising after laser treatment and reduces the severity of eventual bruising [9, 10].

Vitamin B12: It is an effective treatment for atopic dermatitis [11] and children with eczema [12]. It could also potentially improve olfactory function when associated with corticosteroids [13].

Vitamin B1: It doesn't protect you from mosquitoes [14].

Vitamin B3: It improves fine lines/wrinkles, hyperpigmentation spots, texture, red blotchiness and sallowness [15, 16].

Vitamin C: It improves wrinkling by new collagen formation [17]. It is useful in sun-induced skin ageing [18, 19] where it increases density of dermal papillae [20].

And here are the results of a study [21] which assessed multiple vitamins:

  Vitamins A, C, E, and B3 have been shown to have potent antioxidant and anti-inflammatory properties, but to achieve optimal effectiveness, products must be delivered in appropriate formulations. Products containing alpha-tocopherol (vitamin E), L-ascorbic acid (vitamin C), retinol (vitamin A), and niacinamide (vitamin B3), are effective for the treatment of photoaging. These compounds have also shown effectiveness in the treatment of inflammatory dermatoses, acne, and pigmentation disorders and wound healing.

The same study [21] also concludes that combinations are better:

  There is emerging evidence that combinations of vitamins have additive effects that provide enhanced efficacy compared with individual compounds.

References:

Kligman AM, Fulton JE, Jr., Plewig G. Topical Vitamin A Acid in Acne Vulgaris. Arch Dermatol. 1969;99(4):469-476. doi:10.1001/archderm.1969.01610220097017.
de Bersaques J. Vitamin A acid in the topic treament of plantar warts. Dermatologica. 1976;150(6):369-71. PubMed PMID: 1201813.
Devaux S, Castela A, Archier E, Gallini A, Joly P, Misery L, Aractingi S, Aubin F, Bachelez H, Cribier B, Jullien D, Le Maître M, Richard MA, Ortonne JP, Paul C. Topical vitamin D analogues alone or in association with topical steroids for psoriasis: a systematic review. J Eur Acad Dermatol Venereol. 2012 May;26 Suppl 3:52-60. doi: 10.1111/j.1468-3083.2012.04524.x. PubMed PMID: 22512681.
Tanghetti EA. The role of topical vitamin D modulators in psoriasis therapy. J Drugs Dermatol. 2009 Aug;8(8 Suppl):s4-8. PubMed PMID: 19702030.
Gorman S, Judge MA, Hart PH. Immune-modifying properties of topical vitamin D: Focus on dendritic cells and T cells. J. Steroid Biochem. Mol. Biol. 2010 Jul;121(1-2):247-9. doi: 10.1016/j.jsbmb.2010.02.034. PubMed PMID: 20211255.
Burke KE, Clive J, Combs GF, Commisso J, Keen CL, Nakamura RM. Effects of topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. Nutr Cancer. 2001;38(1):87-97. doi: 10.1207/S15327914NC381_13. PubMed PMID: 11341050.
Baumann LS, Spencer J. The effects of topical vitamin E on the cosmetic appearance of scars. Dermatol Surg. 1999 Apr;25(4):311-5. PubMed PMID: 10417589.
Krol ES, Kramer-Stickland KA, Liebler DC. Photoprotective actions of topically applied vitamin E. Drug Metab. Rev. 2001;32(3-4):413-20. doi: 10.1081/DMR-100102343. PubMed PMID: 11139138.
Shah NS, Lazarus MC, Bugdodel R, Hsia SL, He J, Duncan R, Baumann L. The effects of topical vitamin K on bruising after laser treatment. J. Am. Acad. Dermatol. 2002 Aug;47(2):241-4. PubMed PMID: 12140470.
Cohen JL, Bhatia AC. The role of topical vitamin K oxide gel in the resolution of postprocedural purpura. J Drugs Dermatol. 2009 Nov;8(11):1020-4. PubMed PMID: 19894369.
Stücker M, Pieck C, Stoerb C, Niedner R, Hartung J, Altmeyer P. Topical vitamin B12--a new therapeutic approach in atopic dermatitis-evaluation of efficacy and tolerability in a randomized placebo-controlled multicentre clinical trial. Br. J. Dermatol. 2004 May;150(5):977-83. doi: 10.1111/j.1365-2133.2004.05866.x. PubMed PMID: 15149512.
Januchowski R. Evaluation of topical vitamin B(12) for the treatment of childhood eczema. J Altern Complement Med. 2009 Apr;15(4):387-9. doi: 10.1089/acm.2008.0497. PubMed PMID: 19368512.
Heilmann S, Just T, Göktas O, Hauswald B, Hüttenbrink KB, Hummel T. [Effects of systemic or topical administration of corticosteroids and vitamin B in patients with olfactory loss]. Laryngorhinootologie. 2004 Nov;83(11):729-34. doi: 10.1055/s-2004-825676. PubMed PMID: 15538662.
Holzer RB. [Protection against biting mosquitoes]. Ther Umsch. 2001 Jun;58(6):341-6. PubMed PMID: 11441693.
Bissett DL, Miyamoto K, Sun P, Li J, Berge CA. Topical niacinamide reduces yellowing, wrinkling, red blotchiness, and hyperpigmented spots in aging facial skin. Int J Cosmet Sci. 2004 Oct;26(5):231-8. doi: 10.1111/j.1467-2494.2004.00228.x. PubMed PMID: 18492135.
Bissett DL, Oblong JE, Berge CA. Niacinamide: A B vitamin that improves aging facial skin appearance. Dermatol Surg. 2005 Jul;31(7 Pt 2):860-5; discussion 865. PubMed PMID: 16029679.
Fitzpatrick RE, Rostan EF. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatol Surg. 2002 Mar;28(3):231-6. PubMed PMID: 11896774.
Humbert PG, Haftek M, Creidi P, Lapière C, Nusgens B, Richard A, Schmitt D, Rougier A, Zahouani H. Topical ascorbic acid on photoaged skin. Clinical, topographical and ultrastructural evaluation: double-blind study vs. placebo. Exp. Dermatol. 2003 Jun;12(3):237-44. PubMed PMID: 12823436.
Farris PK. Topical vitamin C: a useful agent for treating photoaging and other dermatologic conditions. Dermatol Surg. 2005 Jul;31(7 Pt 2):814-7; discussion 818. PubMed PMID: 16029672.
Sauermann K, Jaspers S, Koop U, Wenck H. Topically applied vitamin C increases the density of dermal papillae in aged human skin. BMC Dermatol. 2004 Sep 29;4(1):13. doi: 10.1186/1471-5945-4-13. PubMed PMID: 15456516.
Burgess C. Topical vitamins. J Drugs Dermatol. 2008 Jul;7(7 Suppl):s2-6. PubMed PMID: 18681152.


Why does caffeine consumption cause one to urinate more?

Caffeine inhibits the secretion of the antidiuretic hormone (ADH), so it increases diuresis, but this effect is small and transient.
http://en.citizendium.org/wiki/Vasopressin

Caffeine in amounts up to 400 mg/day (~4 cups of coffee) does not results in net dehydration, since the amount of water lost due to slightly increased diuresis is much smaller than the amount of water in coffee.
http://www.ncbi.nlm.nih.gov/pubmed/19774754

In some people, caffeine may irritate the bladder and thus trigger more frequent urination, but this is not increased diuresis and the total volume of the urine is not increased.


What would need to be discovered to prove there is extraterrestrial life?

Curiosity is on the Martian surface and is equipped with a slew of laboratory equipment.

But not, incidentally, equipment to detect life.

  What would Curiosity need to discover to prove there is or has been life on Mars? Would it have to find DNA …?

No. In fact, DNA would be lousy evidence of life on Mars, it would almost certainly be a contamination from Earth.

Lacking equipment, I’m not even sure how Curiosity would go about finding traces of DNA but assuming that it did (through some sort of chemical assay), it has no way of telling the origin of said DNA.

And even if the genetic material could be sequenced there are a number of scenarios. It could be very similar to what is found in extremophiles on Earth, in which case we wouldn’t necessarily know the origin (but due to the aforementioned contamination risk, the prior probability of it being Earth life would be very high). If it were completely different, that might be compelling enough to consider it extraterrestrial.

But maybe not: estimates for the number of existing species on Earth vary drastically. One thing is certain, though: we’ve only scratched the surface of prokaryotic life in particular. So if we find something new, that wouldn’t even be very surprising.

More interesting would be an alternative genetic material, neither DNA nor RNA. So far, we haven’t discovered anything like this on Earth (despite earlier hopes) so it would be more likely of extraterrestrial origin. But again, as the refuted study shows, we cannot entirely exclude the possibility of such life being found on Earth either.

All this is just to show that proving microbial life to be extraterrestrial is quite hard. It would be much easier if we were to find non-microbial life on Mars (i.e. something multicellular). However, I don’t know of any serious scientist who seriously entertains this possibility.

But the reason to prefer such a discovery is simple: the bigger the life form, the less likely that we haven’t found it yet on Earth, and the smaller its viable niche. So if we find multicellular life adapted to the surface of Mars there aren’t many places on Earth where it could have originated from, never mind the low chance of having survived the ride aboard the probe.


In C. elegans, why does knock-down of cco-1 in some tissues increase lifespan, and knock-down of cco-1 in other tissues decrease lifespan?

Let us first answer the question: what is the effect of cco-1 knock-down in C. elegans. Durieux J., Wolff S. and Dillin A. in their paper "The cell-non-autonomous nature of electron transport chain-mediated longevity". Cell 144:79-91 (2011) provide the following explanation:

  The life span of C. elegans can be increased via reduced function of
  the mitochondria; however, the extent to which mitochondrial
  alteration in a single, distinct tissue may influence aging in the
  whole organism remains unknown.

So, by slowing-down the mitochondria function you manage to slow-down the normal wear-and-tear of the mitochondrial enzymes, which are normally responsible for the so-called respiratory chain -- one of the fundamental biological process for storing energy in cells (despite the common belief, ATP is rarely to store energy, but mostly to transfer it to the target!).

If we group the tissues where the knock-down leads to similar effects we will get muscle cells opposed by neurons and intenstine cells.

This is just my suggestion, but if we approach those groups with the idea of energy storage and re-use in mind, we'll see that muscle cells have much higher turnover of energy (for contraction and even more for dilation), whereas nerve and intestine cells are not that dependent upon energy and have much lower baseline of energy consumption and turnover.

Now we can suggest that cco-1 knock-down decreases the functions of mitochondria in muscle cells below the acceptable level and the decreased life span is due to depletion of mitochondrial energy storage under light stress conditions which would have been easily coped with under normal conditions. And vice versa, nervous/intenstine cells requiring a constant energy source at a much lower level just help the animal to cope with stress more effectively even during old age, leading to increased life span.