Why does the mass increase in this question? So, on 'http://filestore.aqa.org.uk/sample-papers-and-mark-schemes/2016/june/AQA-BL3HP-QP-JUN16.PDF', question 1.b., they show a partially permeable bag of glucose solution, in a less concentrated solution. Since sugar is more dense than water, why does the bag get HEAVIER, when there's more sugar, and less water?

The reason that dialysis bag A and B will get heavier is due to water diffusing into the bags in order to bring the sugar concentration on both sides of the membrane to an equilibrium. Likewise bag C and D will get lighter as water will diffuse out of the bags in order to bring the system as close as possible to equilibrium. Water diffusion is also called osmosis and can be studied closer here: https://en.m.wikipedia.org/wiki/Osmosis


What is this species of tree? In my city, there is a unique tree, with thorns all over it. I would like to know - what species is this?

I am not a botanist but looking at the flower in the second picture and the thorny trunk and pods it is likely to be part of the Ceiba genus. I cannot however be sure of the exact species.


What elements are a possible basis for life? I've been told that life on earth is carbon-based, Then I got curious about one thing: What are the possible bases for life and under which circumstances could lifr based on other elements exist?

If the existence of a silicon-based life is possible and if it is, under what temperature, pressure, etc?

This is an interesting question, particularly considered in the context that Cairns-Smith (1985) even suggested that clays (silicates in solution) may have had some sort of early selection acting on them due to their surface chemistries.

However, there are a number of major problems with Silicon. Some are chemical and some are astrophysical in nature. For example:

Silicon has a lower electronegativity than carbon and a longer bond length. Silicon can polymerize, but many conformations (such as rings) are highly reactive or unstable.
Silicon lacks chirality. Since biochemical reactions are very specific this may present a fundamental problem for alien biochemistries.
We don't see silicon macromolecules in nature. Large carbon molecules are seen in space such a polycyclic aromatic hydrocarbon rings. The largest silicon molecule seen in space is a chain of SiC_3 (and maybe SiC_4).
On reacting with oxygen (which it does readily) silicon likes to form solids like sand.
Silicon is much less common than Carbon in the Universe. The Solar abundance of silicon is 1/10 that of carbon, and supernova yields suggest that the silicon abundance may be as low as 1/100 that of carbon during nucleosynthesis in low/intermediate mass stars.

To form complex silicon molecules we would probably need to keep it in an oxygen-free environment and somehow maintain it in solution. One possibility would be to hold it at high pressure and temperature such as in the interiors of planets (think deep hot biosphere theory) but this presents another host of problems for conceivable biochmistries and is very speculative.

Apponi, A.J., McCarthy, M.C., Gottlieb, C.A., & Thaddeus, P. 1999, Journal of Chemical Physics, 111, 3911

Cairns-Smith, A. G. (1985) Seven Clues to the Origin of Life  Cambridge University Press, New York, ISBN 0-521-27522-9.

Woosley, S.E., & Weaver, T.A. 1995, Astrophysical Journal Supplement, 101, 181


What happens if you mix brain waves? I was learning about brain waves, i.e. gamma, alpha, beta, etc., and was wondering what would happen if you mixed them together - e.g. I listened to Gamma waves and Delta waves at the same time. Would I get some sort of brain damage or is the brain able to handle that?

Everyone has a mix of ongoing oscillations, of brain waves, at any given point. Some frequencies of waves are more or less likely to co-occur with other types of waves.

In general, brain activity follows roughly a power law distribution - that is, there is more power at lower frequencies and that power decreases in a predictable way as you go to higher frequencies.

When researchers talk about brain waves at a particular frequency, they are talking about a deviation from power law at that frequency - if they say "gamma waves" what they really mean is "there is more energy at gamma frequencies than we would expect if things were random."

Some of these deviations are predictable with changes in brain state - for example, low frequency (delta) activity is greater during sleep, and higher frequency (gamma) activity is higher during cognition.

It should also be understood that these terms really come from a method of data analysis such as Fourier analysis that breaks a signal down into component frequencies. It isn't necessary that a signal is actually produced by combinations of sine waves to break that signal down into component sine waves and describe it that way.


Why these 2 dots frequently occur in dog's eyebrows? Do it serve/served any advantage? It has been wonder me, in spite of so-many variations in color-patterns in dogs; these 2 dots (1 on each eyebrow) remains frequently occurring.

 Dog-1  Dog-1 close up.

this one has a white dot. photographed from Kolkata.

 this one is from Uttarakhand, Western Himalayas. Also has white dots.  I've seen brown dots too, which I have not photographed, so I cite an example from internet (wikimedia: )

Now, my question is; why are these 2 dots are so conserved? Is it associated with some conserved region of a chromosome?  or maybe it has/ had served any purpose or advantage (such as recognition or nonverbal communication or to mislead their prey since if the prey think of them as eyes; then they would miss the gazing direction of actual eye) so that it was selected by nature? Some sort of wolves too have similar paired-spots, so could I guess that once upon a time certain ancestor of all dogs and wolves contained these paired dots?

PS. I've not found helpful discussion about that dots. From this webpage it seems to me, it is being called false-white black and tan atat genotype. Don't know have i understood correct or not...

I suspect but can't prove that these markings are not adaptive, but are accidents or epiphenomena of the general genetic system that determines coat colour.
On the one hand, an Australian Broadcasting Corporation documentary claims that canid eyebrows are adapted for social interaction: they have specialized muscles (which are not present in other carnivorous mammals such as cats), and ...

One study showed foxes who hunt alone had about half the facial expressions of wolves who work in packs. In fact, in wolves and dingoes, the eyebrows are often even a different colour, exaggerating the movement.

(they don't give any primary references).
On the other hand (supporting my guess) a lot of the evolution of these colour patterns seems to have occurred after domestication. These markings (not the eyebrow spots in particular) seem to be called tan points:

Red (tan) appears as pips above the eyes, on the sides of the muzzle extending to the cheeks, as pips on the cheeks, on the front of the neck just below the head, as two triangular patches on the front of the chest, on the lower legs and feet (and inside of the legs), and as a patch underneath the tail (and sometimes along the bottom edge of the tail too).

(I don't know whether eyebrow contrast in animals that aren't strictly brown/black is caused by the same genes ...)
A PhD thesis by Dayna Dreger (some material published in Journal of Heredity 2013:104(3):399–406 doi:10.1093/jhered/est012)

The black-and-tan phenotype, associated with the at allele, is a predominantly eumelanistic phenotype, with phaeomelanin restricted to distinct regions on the lower limbs, cheeks, eyebrows, chest, and around the anus. (p. 7)
Genome wide association study analysis, fine mapping, and sequence analysis identified a 16 bp tandem duplication in intron 5 of the hnRNP-Associated with Lethal Yellow (RALY) gene that segregates with the black-and-tan phenotype, versus saddle tan, in Basset Hounds and Pembroke Welsh Corgis. In breeds that never have the saddle tan phenotype, but frequently have the black-and-tan phenotype, the RALY duplication does not segregate with black-and-tan. This, together with further genotype analysis, suggests a gene interaction of ASIP, MC1R, DEFB103, RALY, and an additional modifier gene is required for expression of saddle tan or black-and-tan. (p. ii)
Neither the coyote nor 9 of the 10 wolves had the RALY duplication and the tenth atypical wolf was heterozygous (+/dup) (Table 5.1), suggesting that the lack of the duplication is the ancestral or wild-type allele (+). It follows then that the saddle tan phenotype is ancestral to the black-and-tan phenotype, despite the relatively limited number of breeds that currently express the saddle tan phenotype, making black-and-tan a modification of the saddle tan phenotype. The popularity of the black-and-tan phenotype across breeds and breed types is likely explained by artificial selection for the striking black-and-tan phenotype over that of saddle tan. Since the saddle tan pattern is found primarily in terriers, scent hounds, and a small number of herding breeds, this finding may also shed light on the development and relation of modern dog breeds, hinting at common ancestors between breed types.


The ermine's colour and geographical range Ermines turn white during the winter, with only the tip of the tail remaining black. However, in the southern regions of the ermine's range it clearly doesn't get so white. Encyclopedia of Life says that:

  However, in the Netherlands, the animals are often only partially white.

Ermine's range is clearly much more southern than the Netherlands:

Wikimedia, stoat range

So I was wondering where does the border go, north of which the ermines are completely white and south of which they remain more brown? I understand it necessarily is not a clear cut line, mountains have impact and subspecies may differ, but I would assume someone must have mapped this. Or is it just weather related, will a southern ermine turn white if the winter is really cold?

I'm just asking this out of curiosity, but the question is rather relevant. Ermine pelt has a long history as an important trade item, and the most valued pelts must have originated on the white side of this line.

The color change of Mustela erminea (more commonly known as ermine/stoat/short-tailed weasel) is both temperature-dependent and photoperiodic (depending on the length of the day). Bissonette 1943 and King and Moody 2012 show that the molting of the ermine happens as a result of the change in daylight lengths.  The King and Moody paper addresses the temperature dependence, using stoats (ermines) in New Zealand as an example:

  In temperate countries such as New Zealand, stoats frequently fail to complete the full change to white. Such animals are not necessarily all caught in the process of moulting. If ambient temperature fell below the threshold for whitening of the lower part of the body but not the rest, new hair would grow white on the tail and flanks and brown on the head and back.

This is a chemical effect of lower temperature (King and Moody):

  Experimental work has established that production of brown hair depends on melanocyte-stimulating hormone (MSH); in cold climates in autumn the synthesis of MSH by the pituitary is inhibited.

They don't provide a specific temperature at which the white color change does or doesn't occur, but I suspect that in nature it'd be very difficult to create a map since temperature is not constant year-to-year. There would most likely be an intermediate zone of partially white animals (both in terms of a mixture of brown and white animals, and a single animal that is not fully white).


High sequence similarity but start codon isn't methionine I have noticed in a particular genome sequence of a prokaryote that various regions in a sequence share similarity which is high(>80%) with known proteins. However, the start is not a methionine. Is this a dysfunctional 'protein' sequence? Or are there alternative codons which translate those regions without a Met or fMet for that matter?

Technically, do all annotations of proteins have to start with a methionine?

There are alternative start codons to AUG used in prokaryotes: GUG and UUG. Those still match the initiation tRNA and encode N-formylmethionine. The rare start codons are matched by wobble pairing.


Sequence alignment scoring The following table is from Deonier's text Computational Gene Analysis at p. 152.
This is an exercise in global sequence alignment and scoring of alternative sequences.
The text proposed a solution (in parentheses). Setting aside the upper left hand portion of the table it seems there may be a better path.

It's more likely I  misunderstand the idea than that there is a typo.

$$\begin{array}{c | c | c | c | c | c | c |}- & -& T & G & G & T & G\\ \hline  - & (0 ) & -2 & -4 & -6  &-8  & -10 \\ \hline
A &(-2)  & -1 & -3 & -5 & -7 & -9 \\ \hline
T &-4 & (-1)  & -2 & -4 & -4 & -6  \\ \hline
C &-6 & -3  & (-2)  & -3 & -5 & -5  \\ \hline
G &-8 & -5 & -2 & (-1) & -3 & -4 \\ \hline
T &-10 & -7 & -4 &-3 & (0)  & (-2 )\\ \hline  \end{array}$$

Just looking at the upper left corner,

$$\begin{array}{c | c | c |} (0) & -2 & -4...\\ \hline -2 & (-1) & -3...\\ \hline  -4 & (-1) & -2...\\ \hline  -6 & -3 & (-2)...\\ \hline  \end{array}$$

which seems to give -7 versus -8 for the book's path. Below are the book's alignment and the one corresponding to my scoring, which may reveal my error.

$$\begin{array}{c | c | c | c | c | c | c |} A: & A & T & C & G & T & - \\ \hline
B: & - & T & G & G & T & G  \\ \hline
\end{array}$$

$$\begin{array}{c | c | c | c | c | c | c |}
A: & A & T & C & G & T & - \\ \hline
B: & T &  - & G & G & T & G  \\ \hline
 \end{array}$$

I had no trouble constructing the matrix just scoring it. it's a small point but I don't like to move on without understanding it.  Thanks for any assistance.

Edit: Both current answer seem clear on this but just for completeness: a match = 1; mismatch = -1; indel = -2.

If I am myself not mistaken, the table shows the paths of least resistance. There are many paths through this table and all of them are not shown only the ones that cost the least. You need to understand that a mismatch between the letters costs -1 (eg - AT), but an empty square  costs -2 (-A or -T). So your solution would cost = -1-3-4-3-2-4 which sums up too -17.
This is a full alignment table. The top value is going diagonal, the second value is going down and the third value is going right.


Why do ants dig surface paths? A few days ago I observed a corridor built and used by ants that went over a path in fields:

Why do they build it? It seems it doesn't bring any considerable protection from the surrounding environment and it certainly costs them a lot of work.

The picture was taken in the morning when the temperature was low so there is no ant activity visible.

I don't have it with me, but the book Adventures among Ants by Mark Moffett, which I highly recommend if you're even vaguely interested in ants, describes the creation of paths such as this. Some ants apparently build underground "highways" of a sort, and such a sunken path is indeed an intermediate step in the construction of such. I can't remember the specific reasons given in the book but I expect protection (if not from the elements, then from other insects and rival ants in particular) and efficiency (it minimizes ants wandering around for that bit of their journey) would be involved. Given how short the path in the photo is it might also be an underground path that the ceiling caved in on for a section.

I am not saying that this is what your photo shows, or even that the ants you were looking at typically make such paths, and I realize that I am technically not even answering your question, but I hope that a confirmation that this is a phenomenon that happens and the recommendation of a book that will answer your question is a decent start.

EDIT - Found the book !

The ant species described in this section is the Marauder ant, a species from India so probably not the one you saw. But the motives described in the book could be transferrable. A few quotes from the chapters "Roads" and "Defense":

  Marauder colonies maintain a fast, steady, well-protected flow of food and labor on their trails. Whereas small ant colonies, like people in small societies, are able to access and distribute the supplies they need without roads, larger groups depend on an infrastructure so complex that in the marauder ant it rivals human highway systems.(...)

  Marauder colonies avoid both gridlock and species confrontations, like that with the Diacamma worker [an encounter described at the beginning of the chapter where killing that errant worker of another species involved major disruption in the flow of traffic], when trails are in good shape. Highway construction efforts are part of the society's logistics, providing supply lines for fresh combatants on the front lines as well as streamlined routes for bringing home the plunder[2]. Trunk trails are well looked after - that's how they can be distinguished from the fleeting paths created by raids

The note after "plunder" points to the following:

  The lower cost to ants of sticking to clear paths rather than going over rough ground is addressed in JH Fewell 1988, Energetic and time costs of foraging in harverster ants, Pogonomyrmex occidentalis, Behav. Ecol. Sociobiol. 22:401-408.

A description of the building of the trails, which matches some of how the picture looks like:

  Each worker size class participates in the creation of the roadways. All the castes eliminate surface irregularities along a trunk: while the medias[medium-sized caste] and majors[big ones] chisel out embedded roots and pebbles, minor workers[little ones] extract grains of soil, establishing the road's slightly concave shape in cross-section. The dross is discarded along the edges of the trail, where it accumulates in embankments(...). When the ground is moist, the minor and media workers build up the ramparts into a complete soil cover, or thin-roofed arcade, fabricated from soil extracted from the trail surface or from mining shafts - blind-ended tunnels near the trail used specifically as quarries.

Giving some reasons for their existence:

  To what use is all this effort? Not, it seems, as protection from the elements. The earthworks fall apart in rain, and disintegrate when the earth is dry. Arcades are thin enough to puncture with a tap of a finger, which means a route is weatherproof only when it travels through an underground tunnel, perhaps dug and then abandoned by other animals. Alternatively, near the nest the ants may make a subterranean route of their own: over time, construction crews can scratch away so much soil from the trail surface that the highway sinks from view, at which point the ants seem to be able to construct a thicker, rainproof cover that becomes flush with the surrounding land.

  The main function of this relentless building is defense. Because trunk trails extend for dozen of meters, they travel through territory controlled by other ant species. Marauder ants must therefore be organized to protect the trunk trails from aggressive neighbors or even from hapless passerby such as the Diacamma.(...)

  ...after an arcade has been completed[,] the Diacamma workers could now walk over the trunk trail, blissfully ignorant of the industry below them. if a trail should sink underground, it is as protected as a passage in an army bunker, safe even from human footfalls.

  Bulwarks constructed over trails and provisions prevent battles among competing marauder ant colonies as well. Where they are absent, combat can last a day and engage thousands of minor workers, which pour along the line of contact between the armies.


What kind bottom feeder is this? It’s about 2 1/2 inches long and had a little tail on the end. Also has short feelers that almost look like a moles.

It's a kind of loach. You have to include the location in your query.
i.e. a black khuli loach:

a weather loach:

http://badmanstropicalfish.com/profiles/profile103.html


Where do mushrooms get their energy from? I'm wondering where field mushrooms get their energy from.
I've heard that they can easily grow on soil in a dark room. So, it seems to me that there wouldn't be any photosynthesizing plants from which they could get energy. Also, as far as I know, they don't have seeds from which they could directly get energy initially.

So, I have two questions:

Where do mushrooms get their initial energy from? (The spores, if that is the right term)
Where do they get their energy from in later stages? (If there is a difference at all)

Mushrooms are the fruiting bodies of fungi. Fungi get their energy by decomposing dead or decaying organic material, such as fallen leaves or dung.

Some background: spores of fungi germinate forming mycelia consisting of threadlike hyphae. When the hyphae of different fungi meet, they may have sex and form mushrooms. The mushrooms produce the spores. See https://en.wikipedia.org/wiki/Fungus.

So, each of these stages get their energy ultimately from decomposition, although the mushrooms get their energy from the mycelium. Spores rely on their internal energy storage to germinate and start decomposing. Even though spores are tiny, the have energy stored, like all cells do.


Is there a theoretical maximum on the number of sexes a given species can have? Background: To the best of my knowledge, most sexually-reproducing species of organism have two sexes, although there are also sexually-reproducing species of organism (flatworms come to mind) which have only one sex. (Depending on one's definition of sex.)

Many species of fungi are both sexually reproducing and apparently have more than two sexes. (Depending on one's definition of sex.)

There are also species of lizards with more than two biologically determined "gender morphs". It is even more debatable than in the case of fungi whether these morphs should be considered separate "sexes" or not, since their mating compatibility network is bipartite.

Question:
Is there a theoretical maximum on the number of sexes a given species of organism can have?

Elaboration:
There would also be a lot of different possibilities -- already with three sexes, one can imagine at least two different means by which sexual reproduction could occur -- any one of three combinations of two individuals from two distinct sexes (most likely in "rock-paper-scissors" fashion), or the combination of three individuals from all three distinct sexes.

How, for example, might either of these two scenarios be maladaptive compared to sexual reproduction of two individuals in species with two or fewer sexes?

I am asking about species with more than two sexes/mating types in general, not necessarily about situations where more than two sexes are involved in a single reproductive event. (Contrast with this related question.) I am also not restricting to animals, or even multi-cellular organisms, or even eukaryotes, since these restrictions might affect the answer. (Contrast with this related question.)

Note that this answer to the second related question implies that we should expect the mating compatibility network of anisogamous sexually reproducing organisms to be bipartite. But note that, as in the example of the side-blotched lizards, this doesn't necessarily preclude having more than two sexes, nor does it give a theoretical maximum to the number of possible sexes. And since I don't want to necessarily restrict to anisogamous sexually reproducing organisms (i.e. isogamous ones would also be fine), then that answer also does not provide a theoretical maximum for isogamous sexually reproducing organisms either.

Well, your question as a whole is quite broad, with a lot of sub-questions or items (and some inaccuracies, as in the case of flatworms) . That being said, in this answer I'll address only your main question (and nothing more), which is ipsis litteris:

  Is there a theoretical maximum on the number of sexes a given species of organism can have?

All the content in this answer is based on this excellent book from Michael Majerus, Sex Wars: Genes, Bacteria, and Biased Sex Ratios:

Unfortunately, I don't have my library anymore and I can't find this book online. So, instead of (boringly) quoting the author, I'll try to summarise his hypothesis. Of course, to a better explanation, you can read the book itself.

Let's start supposing that you're pretty comfortable with the concept of sexual reproduction and sexual types, which I think you are.

Suppose we have two sexual types, called A and B. They have receptors in their gametes' membranes, in such a way that you cannot fusion A + A or B + B gametes, but you can fusion A + B gametes. If the A gamete could fertilize another A gamete, you'll have all gametes in a given gonad fertilising each other, which makes no sense. So, will assume that a given sexual type has mechanisms to avoid fertilising the same sexual type.

So far, what I described is the common system with two sexes, be them "+ and -" or "male and female", it doesn't matter.

Now, let's suppose three sexual types: A, B and C. For this to work, their membrane receptors must be such that A can recognise B and C, but not A. This is theoretically possible (although it is a mess genetically speaking). Thus, the possible matings are:

Sexual type A → A + B and A + C;
Sexual type B → B + C and B + A;
Sexual type C → C + A and C + B;

A system with 3 or more sexes has obvious advantages. Right now, for instance, in a population with two sexual types and the same sex ratio, one has 50% (1/2) of the individuals in that population as potential mate. But, supposing a sex system with 5 sex types (A, B, C, D and E), any individual would have 80% (4/5) of the individuals in that population as potential mate.

So, why cannot we find sexual systems with more than two sex types?

The answer is: we can, but not among species which perform fertilization (animals, plants, most of fungi, most of algae etc...).

This is the problem: in fertilization, or syngamy, the gametes don't simply join their nuclei. It's more complex than that: there is cytoplasmic inheritance, or extranuclear inheritance.

To keep the example among animals, the group you said you know best: mitochondria in the zygote comes from only one gamete (the female one). That happens to avoid what we call heteroplasmy, which is the presence of more than one type of organellar (mitochondrial, in this case) genome in the zygote.

In sex systems with only two sexual types the rule is very clear: "mitochondria comes from this one, but not from that one". That's it, case solved.

But what happens with our system with three (A, B and C) sexual types? If you define that when A mates with B only A donates the mitochondria and, similarly, if you define that when A mates with C only A donates the mitochondria, who donates the mitochondria when C mates with B? Do you see? There is no possible rule here!

Therefore, cytoplasmic inheritance is, probably, what avoids the evolution of more than 2 sexual types.

How can we support this claim?

Let's find what happens in species that perform sexual reproduction, but no fertilization (and, therefore, don't have the cytoplasmic inheritance problem). The best example are protozoans that perform conjugation.

Tetrahymena is a well known example. In these protozoans, according to Umen, 2013:

  An individual Tetrahymena cell expresses one of seven possible mating types (I–VII) that it faithfully and indefinitely maintains during vegetative propagation. After mating each new exconjugant has a recombinant micronucleus formed from its two parents. However, rather than just expressing one of two parental mating types, the sexual progeny of Tetrahymena undergo a kind of genetic roulette that allows them to choose at random up to seven possible mating types. (emphasis mine)

So, we have sex mating types. How that system works? According to Cervantes et al., 2015:

  The unicellular eukaryote Tetrahymena thermophila has seven mating types. Cells can mate only when they recognize cells of a different mating type as non-self.

Thus, if you belong to sexual type I you can mate with someone that belongs to sexual types II, III, IV, V, VI or VII. The same way, if you belong to sexual type II, you can mate with someone that belongs to sexual types I, III, IV, V, VI or VII, and so on...

The record, however, probably belongs to the basidiomycete Schizophyllum commune, with more than 28.000 sexual types! (Whitfield, 2004) To support the idea that cytoplasmic inheritance is in fact the main factor that avoids more than 2 sexual types, it's worth noting that biparental mitochondrial transmission is quite common in fungi (Barr, Neiman and Taylor, 2005).

Sources:

Majerus, M. (2003). Sex wars. 1st ed. Princeton: Princeton university press.
Umen, J. (2013). Genetics: Swinging Ciliates’ Seven Sexes. Current Biology, 23(11), pp.R475-R477.
Cervantes, M., Hamilton, E., Xiong, J., Lawson, M., Yuan, D., Hadjithomas, M., Miao, W. and Orias, E. (2015). Correction: Selecting One of Several Mating Types through Gene Segment Joining and Deletion in Tetrahymena thermophila. PLOS Biology, 13(10), p.e1002284.
Whitfield, J. (2004). Everything You Always Wanted to Know about Sexes. PLoS Biology, 2(6), p.e183
Barr, C., Neiman, M. and Taylor, D. (2005). Inheritance and recombination of mitochondrial genomes in plants, fungi and animals. New Phytologist, 168(1), pp.39-50.


Trypsin and cell culture I am doing an experiment where I have treat the cells with a drug and calculate their counts. I would like to know if is bad to trypsinize the cells in consecutive days i.e. twice within 48 hours. How much time do the cells need to attach again on the surface of the flask? I want to know if I can treat them with drug the same day I add trypsin for counting.

Thanks.

It would be stressful for cells to be trypsinized 24 hours after seeding. After cells are plated, there is a lag time to start growing. Perhaps, during the lag time, physiological state of cells is stabilized. They have to express proteins digested by trypsin and display on the surface etc. Then you could disturb the state again by trypsinizing cells again if you replate cells after 24 hours.
I would not deny some cells are not affected by trypsin much, but you should be carful.

  if I can treat them with drug the same day I add trypsin for counting.

It is not preferable, but in some cases, such a way is taken actually. If you could, you might want to give us more information about which cells and drugs you are going to use.

PS

If you trypsinize cells to count and do not replate them, you do not need to worry about the cell condition, as WYSIWYG says.


Is it the sphincter that flexes when a human pushes a bowel movement? Of course the sphincter muscle is at the exit point. To use a toothpaste tube analogy, if I want to squeeze out some toothpaste, it does me little to no good to jostle the nozzle; I need to squeeze the tube (which is analogous to the colon) to get the paste (payload) to come out.

So when a human is sitting on the toilet squeezing, is that squeezing flexing of the sphincter, or squeezing muscles along the sides of the colon pushing on it as one's fingers push on the tube to get toothpaste to come out.

If it's the sphincter that's getting flexed, how is that helping get a big log out?

The pressure that you apply when you push during a bowel movement derives from an increase in the pressure of the abdomino-pelvic cavity.  You generate this pressure by closing the glottis (the opening to the lungs) and contracting the anteriolateral abdominal muscles (i.e., the external oblique, internal oblique, and transversus abdominus).  This reduces the volume of the (now sealed) abdominopelvic cavity and increases pressure helping to drive feces from the rectum.  This is mechanism is also used to expel urine and during childbirth.

If you do this with the glottis open, then you forcibly exhale because the increased pressure of the abdominopelvic cavity is transferred across the diaphragm and into the thoracic cavity compressing the lungs.


Are there inherent problems in simulating marine environments, as compared to terrestrial systems? We cultivate a number of terrestrial organisms in greenhouses and stables where they live in completely artificial environments. This seems to extend far less to marine organisms, such as fish. Aquariums (especially the salt water variety) seem to be quite unstable and require a lot of maintenance, and commercial scale installations, like salmon farms, are set up in the ocean, rather than in a separate tank.

Are there inherent difficulties in cultivating marine organisms, or is it just that mankind has not tried as hard as with land species?

It probably depends on the type of marine organism you're referring to, some will be much more hardy than others and some will not be able to adapt to change at all. Due to the vast scale of the environment that marine fish come from it's likely that in their natural habitat the conditions they live in are not subject to drastic changes in water chemistry or temperature [1][2]. So recreating those exact conditions for them in man-made habitats, let alone maintaining them is going to be extrememly difficult.  Also, if you think about the conditions that most (there will be some exceptions) terrestrial animals and plants have to deal with on a day-to-day basis they have to be able to cope with some fluctuations in humidity, temperature, weather, light etc and therefore are highly adaptable by necessity.

Other issues can be supplying the correct feed. In artificial settings food may have to be a non-natural substitute and this will likely cause problems for species who require a highly specialised diet. The terrestrial animals we tend to cultivate extensively are omnivorous/herbivorous which are not difficult needs to meet. On the other hand a fish from the sea that requires a particular other kind of fish only found in a particular area and that needs very specific conditions to thrive is going to be problematic.

Check out this article http://www.vliz.be/imisdocs/publications/301.pdf , it might be for a specific fish but it highlights some of the general issues i think you are referring to.

[1] http://www.bestfish.com/saltg.html
[2] http://www.aquaticcommunity.com/marineaquarium/
(both general articles on keeping marine fish)

hope this helps!


Where do kombucha SCOBYs get nitrogen? Kombucha can be brewed even with tiny amounts of inocculate, such as the little bit of sediment at the bottom of store-bought kombuchas. Over 1-2 weeks, this can grow into an inch thick film covering the entire surface of the brew; a very striking accumulation of biomass. Where is the material for this biomass coming from?

It seems like most recipes for kombucha brew consist of:

5.7% sugar
0.7% black tea
10-30% of a previous, "finished" kombucha
SCOBY (optional, the kombucha in the previous step is sufficient)

I can see how the sugar provides carbon, oxygen, hydrogen and energy. Of course, merely providing the elements is not necessarily sufficient, since often enough cells require specific compounds as well. But I'll assume the SCOBY community, in aggregate, is able to transform the sugar into every CHO compound it needs. However, what about nitrogen? The amount of tea seems minute, and tea seems like not a very rich source of protein/amino acids. Sugar doesn't contain nitrogen, and while dead SCOBY constituents from the initial kombucha can conceivably be cannibalized, the cannibalism cannot account for dramatic increase of SCOBY biomass because of conservation of mass.

Short answer:

Nitrogen fixation (i.e, atmospheric nitrogen)

Longer answer:

Nitrogen fixation is the process by which atmospheric nitrogen is converted to forms usable by further biochemical reactions. Some bacteria are capable of nitrogen fixation (and some plants have symbiotic relationships with nitrogen-fixing bacteria); all the others rely on those species directly or indirectly to provide nitrogen.

The microorganisms involve in brewing kombucha tea are actually a collection of different species of bacteria and yeast. The bacteria that are found in kombucha tea include Acetobacter nitrogenifigens and Gluconacetobacter kombuchae, both of which are capable of nitrogen-fixation (and there may be others).

Molasses is also often used as the sugar source for kombucha, and molasses includes some nitrogen-containing compounds.

See the following review for more information:

Jayabalan, R., Malbaša, R. V., Lončar, E. S., Vitas, J. S., & Sathishkumar, M. (2014). A review on kombucha tea—microbiology, composition, fermentation, beneficial effects, toxicity, and tea fungus. Comprehensive Reviews in Food Science and Food Safety, 13(4), 538-550.


How much damage is caused by smoking 2-3 cigarettes on a healthy body? I do not know how bad does 2-3  cigarettes on the average healthy body.

I do not want to include genetic factors on this issue.

So, maybe there is a study or something on this topic.

Does it cause a real damage, or to this quantities the body recovers.

http://tobaccocontrol.bmj.com/content/14/5/315

2-3 cigarettes could make difference absolutely.  It deals 5 points of damage exactly; just kidding.  Hopefully this study provides some insight.


Which step in endocytosis requires ATP? Everybody seems to agree that endocytosis is an energy-using process, and as such requires ATP hydrolysis. However, which particular step requires it? More precisely, which 'molecular machine' involved in endocytosis requires ATP? I cannot seem to find a good answer in the literature.

Endocytosis (specifically you asked about clathrin-mediated endocytosis) is indeed an energy consuming process. the coating of the vesicle may be "spontaneous", but the pinching off of the vesicle, the uncoating of the clathrin, and the transportaion of the vasicle inside the cell all require ATP/GTP hydrolysis.

Dynamin - dynamin forms a spiral around the neck of the vesicle, and uses GTP hydrolysis which in order tighten the coil around the vesicle neck causes it to break and results in the pinching off of the vesicle from the parent membrane.

The uncoating of the clathrin is also ATP/GTP consuming. proteins such as hsp70 chaperon and auxilin is thought to be involved in the ATP hydrolysis. the uncoating process starts after the pinching off of the vesicle.

the tranportation of the vesicle will also cost energy, proteins such as the Myosin family are considered to transport endocytic vesicles into the cell, and use ATP hydrolysis.

Dynamin - Wiki

Myosin  - Wiki

Uncoating process - Molecular Biology Of The Cell ed.6 p.701


Are we evolving to age slower, or to live longer aging at the same rate? I wonder why most of us find senior people lovely and charming. Is it because to love grandpa and granny is vital to our survival as a species, in the same way as we love babies? If so, it would mean that we are either aging slower with time, or being selected somehow to love senior people despite their physical appearance, while they are aging at the same rate but living longer.

Update

Let's say every common characteristic among individuals of the same specie is product of evolution.
Many caracteristics are passed by the individuals to their offspring, but only those that were advantageous in some way or another allowed the offsring to survive and pass that caracteristic to their decendants in turn.
Our love for babies and elders is one of those caracteristics that we as indivudials of  a species have in common.
That make us to want our elders to be with us as much time as posible, just becouse our affinity with them.
This love for the elder have to be an advantaje that worthed to be selected by the evolutionary process, and this caracteristic is reflected in the tendency of the life expectancy to increase generation after generation.
One could say, that those elders that age slower would be more likely to benefit from the love of their offspring, than those that age faster.
On the other hand, to age slower may not make a difference at all, just because we love our elders despicte their physical appearance.
I'm considering the cultural and technological advantages that allow our elders to live longer to be a product of evolution too.

So my question is wheter we are evolving to age slower, or to live longer aging at the same rate?

As a side note, we are becoming more like what they call a super-organism, as most of os can only benefit of a longer life spam by living in society. Just like an anthill or a beehive. If that is true, we are not evolving to age slower.

The question has a more or less official scientific name - the grandmother effect (or hypothesis).   In the rational world of evolutionary biology, children love their parents for the same sort of reason - the parents give them resources to gather their strength and develop as adults so they can have their own children with the most advantage that they possibly can.

Humans are off the charts in the amount of resources we invest in our children - our lives are 1/4 to 1/3 over before we sometimes leave our parents household (in some societies of course they never leave the house, but step into an extended family).  This may be one of the reasons we are so successful as a species - we live in practically every place we possibly could and have no danger of competition from any other living thing excepting ourselves.

The grandmother effect is essentially the idea that if women, who are more attached to the offspring in more cases than fathers, continue to live and help support the grandchildren and make them more successful, then this will allow post menopausal women to have a longer lifespan (which they do).

The evolutionary biologist Sara Hrdy, emeritus UC Davis, has written quite a bit about the nuances of the evolution of the role of motherhood - reading some of her articles or books might give you a deeper sense of how profoundly filial love has shaped human beings.

--- more answer this stuff may or may not be worth reading depending on how broadly you want to understand this question...

Its important to say that many of the expansions of human average human lifespan have not been genetic.  Its commonly cited that sewer systems, clean water, antibiotics and plentiful food are the three most important factors in human lifespan - and before modern developed world nations, the average lifespan of human beings was somewhere in the 30s.  And there are significant lifespan differences in regions where these factors and others (education of women, access to prenatal and early care etc) are available.

Studies continue to be published that examine environmental and lifestyle factors compared to genetics and it seems that environment and lifestyle can make an astounding difference.

But genetics undoubtedly has a role to play here too.  There are probably some individual humans and animals which have evolved to live longer.  This has been found to be genetically related in some humans by demographics and family lines.

Still there are genetic factors that are being identified.  I think its a common misconception that evolution changes the entire species, but its not really true.  There are some who have that tendency and others who do not - at times there will be more of say shorter lived people and other times longer lived individuals will be more common.  It depends upon whether the living conditions of the population really favor one tendency over another.  Usually shorter lived individuals can assume to have other advantages, say the ability to store energy more efficiently.


What is the substrate for glycogenesis? In glycogenesis (i.e. the synthesis of glycogen), are sugar phosphates the direct substrates for glycogen polymerization? I would certainly think so since glucose is phosphorylated and then stuck onto a glycogen chain, but my textbook seems to think no.

A pathway doesn’t have substrates, only a reaction does. And therefore there’s no such thing as a direct or indirect substrate. You can perhaps ask what the precursors are for glycogen (but do you mean immediate or distal), or what the substrates are for the first reaction in the pathway (but only if it is quite clear what the first reaction i).

That’s the trouble with trick questions. They are generally badly worded and tend to lend nothing to biology education.


Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest? In trying to understand the Nernst and GHK equations, I've hit upon a snag somewhere deep in my understanding of the subject matter.

Scenario 1: when calculating the membrane potential of a living cell at rest we use the Goldman equation. This requires us to measure both the concentrations of the ions and the membrane's permeability to said ions, at rest (at least for the concentrations).

Scenario 2: given two cells separated by a membrane (as in Figure 3 here), with a different concentration of KCl in each cell, and having the membrane permeable only to K ions, we can compute the equilibrium membrane potential using the concentrations of the K ions - after the system has reached equilibrium.

So far so good. Here's my question:

Given a living cell at rest with all its ion concentrations, the Nernst equation is used to compute the equilibrium potential of a single ion, using the concentrations at rest. Why is this allowed? As I understand it, the concentrations as measured are what the cell "decides" them to be - it can change the permeabilities of the channels, or create more pumps, etc. - and then we'll measure different ion concentrations at rest. And these concentrations will change if a cell decides to open or close some channels (which is what happens to create the action potential). But the concentrations that are used as input for Nernst's equations should be measured at the actual, not just the steady state, equilibrium (right?).

So, why can we use the steady state measurements to derive the equilibrium potentials?

Excellent question! The answer is actually a really cool and crucially important detail about membrane potentials and the movement of ions. Basically, the electric force is very strong. You don't actually need to move many ions for the membrane potential to fluctuate dramatically. The number of ions that "move" to establish equilibrium is tiny compared to the actual concentrations. That's why the Nernst and GHK equations are so powerful: what really matters is the relative permeability of different ions and the gross concentration differences, not the changes in their concentration that occur when, for example, voltage-gated channels open during an action potential.

You can calculate just how many ions have to move, which depends on the size of the cell. Here is a nice example from the reference I have linked below:

  For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

Therefore to answer your question: why is it allowed to use the resting concentrations? Because the concentrations of the ions don't change by more than 1/100,000 fold with a 100mV swing in potential, and there isn't much impact on the GHK/Nernst equation from a change this small. For example, as the voltage goes from ~-70mV when a fairly typical neuron is at rest (and the membrane is most permeable to K+), up to maybe +30mV at the peak of an action potential (and the membrane is most permeable to Na+), only a "few" sodium ions actually cross the membrane, so maybe the internal sodium concentration changes from 10mM to 10.0001mM. The thing that changes most during an action potential is not the actual concentrations, only the permeability to different ions.

Maybe an additional misconception you have is about the cell "deciding" what the concentrations are. Indeed, if the concentrations of particular ions changed dramatically, it would be necessary to recompute equilibrium potentials. The key concept is that those concentrations don't change much during normal functioning of the cell, and they don't have to change much to observe big changes in membrane potential. An excitable cell uses those swings in membrane potential as the signal, rather than the concentrations of the ions. One exception is calcium, see the note at the end.

Reference:

Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.

(as a side note, movement of ions does matter over a longer time scale, which is why it is necessary for the Na+/K+ pump to constantly operate to keep the membrane potential steady, and some ions like Ca2+ are at such low concentrations normally that the influx of calcium can be substantial relative to the resting concentration, which is partly why calcium is so powerful as a second messenger and why calcium chelating components of the cell are important)


Bioinformatics - DNA binding, sequence-specific protein data I am a computer scientist and we are working on protein function prediction algorithms. Right now, we would like to examine protein-DNA binding properties computationaly. For this, we would make use of datasets about containing DNA-binding proteins and the DNA sequences they bind to. I was looking on Gene Ontology and Protein Databank where I'd expect such informations, but I was unable to find it. Are such data presently difficult to obtain? Or are simply not collected? Or could you give me some direction where to look for such data. Thanks.

You are seeking a database of transcription factor binding specificities. Some model organism databases (which are manually curated), such as Wormbase contain some of this annotation. I suggest you search PubMed for papers by Tim Hughes at the University of Toronto. He has published extensively on this topic over the past 5 years.  Papers he cites, and papers that cite him, will let you bootstrap your way in to the topic.


T-Cell Motility: does motility require direction specific actin polymerization? T-cells have been shown to migrate inside concentration gradients - both in the direction of the source or away. Even under shallow gradients, t-cells move. I argue that, to be able to move in a directed manner, a cell must be able to have a differential response of actin polymerization and philipodia. But I find it hard to believe that it is a differential response unless the sensor resolution not only communicates centrally, but is also extremely sensitive. How does this work?

It's understood at least that leukocyte motility is dependent on cytoskeleton remodeling and actin dynamics. In the blood, as the T cells tumble past the activated endothelium of an affected site, they're grabbed by selectins and integrins expressed on the endothelial surface. These are often illustrated as the adhesion and rolling phases of T cell migration.

Chemokines, which normally form a gradient for T cell chemotaxis, induce changes in the cellular morphology that promote migration into the surround tissues. The cells polarize into a force-generating lamellopodium with a leading edge in the front, and a uropod in the back. It appears as though actin polymerizes in the lamellopodium and juts the cell out toward the direction of the signal, and the uropod contracts in a myosin-dependent manner, releasing molecules bound there, thereby allowing the cell to tug in the direction of the lamellopodia (1, 2).

The mechanism has in fact been characterized by leading-edge redistribution of chemokine receptors such as CCR5 and CXCR4, which may have to do with actin/myosin dynamics and lipid rafts. This makes the receptor distribution asymmetric as well, and so a weaker response to the chemoattractant in the back end of the cell. The best way I could describe it is using the formation of the cSMAC in T cell receptor biology (Figure 1) (3). The SMAC is basically a synapse formed during T cell activation where receptors are concentrated to a particular area where the T cell is meeting the APC.

Figure 1. TCR-mediated cytoskeletal remodeling

The way the authors describe it is the downstream signals from the TCR localize actin pathway molecules to the site of signaling, and causes cytoskeletal remodeling at that particular site.

Studies in neutrophils have shown that polarization leads to a frontness and backness to the cell, regulated by different proteins and inhibit the formation of one another. This is a good paper to read through on that matter, though it's a tougher read in my opinion: https://www.researchgate.net/publication/8957894_Cytoskeletal_remodeling_in_leukocyte_function


What is this whitish jelly-like substance on a branch? I came across this whitish jelly-like substance hanging on a fallen branch. I assume it was growing there and I feel like it might be a fungus or algae of some sort, or maybe an egg sack. I was hiking in a mountain rainforest in Hawaii. The area I found it was shady with adequate indirect sunlight, about 65-70°F at the time. There weren't any others nearby and it was the only one like it that I happened upon during the hike. What is this and if it is living, how does it grow, how does it live?

Looks like a Tremella fuciformis, which is actually a sort of yeast that produces jelly-like fruiting bodies. AKA the white jelly mushroom.


Gene silencing in C. elegans I am trying to silence the tph-1 (tryptophan hydroxylase) gene in C. elegans using the pLT63 plasmid to check if that particular gene has anything to do with the pharyneal pumping or not. Am I using the right plasmid for the purpose?

"pLT63 contains 0.8 kb of the fem-1 gene inserted into the L4440 vector" (1). The gene fem-1 is involved in determining the male sexual trait in C. elegans (you can verify this on uniprot). It may be best, however, to stick to a "normal" plasmid like L4440 that'll just have your tph-1 insert ligated in.


Can upper motor neuron lesions cause hypotonia? I have been taught that hypotonia is always caused by lower motor neuron lesions while hypertonia is by upper motor neuron lesions. However, I recently learned of an entity called central hypotonia, which means hypotonia caused by a central nervous system lesion. This makes it so confusing.

The rule-of-thumb you (and I) were taught reflects the role of the central and peripheral nervous systems in establishing muscle tone. Deprived of CNS regulation, alpha motor neurons increase in their responsiveness to spindle afferents, resulting in hypertonia. Deprived of PNS regulation, muscle spindles are less able to react to input, resulting in hypotonia.

Beyond this rule-of-thumb, things aren't as black-and-white. As you have pointed out, there is such a condition as central hypotonia. In fact, the NINDS includes the CNS as an area where damage can cause hypotonia:

  "Hypotonia can happen from damage to the brain, spinal cord, nerves,
  or muscles." (source)

Purves et al. also note that upper motor neuron syndrome involves an "initial period of 'hypotonia' after upper motor neuron injury" (Neuroscience, 2012, p. 395).

To your question: Yes, the rule-of-thumb is not always accurate and upper motor neuron lesions can cause hypotonia.

If you're looking for a hypothetical mechanism, consider this: Purves et al. also state that hypertonia is "probably caused by the removal of suppressive influences exerted by the cortex" (p. 396). So it is conceivable that overstimulation of these inhibitory control systems by some sort of unique upper motor neuron lesion could result in hypotonia.


Athletes: nature vs. nurture? Having watched a lot of olympians the last few weeks, I was struck by how many of them have actually spent their wholes lives/careers training for their one event (be in running a marathon, or throwing a javelin). This is of course unsurprising - a lot of people take their sport very seriously - but I wondered to what degree these athletes are predisposed to becoming atheletes, and to what degree they just 'happened' to end up doing it.

I've had a bit of a search around, but have been unable to find any studies (although there is an awful lot of media attention to the topic) that actually study the interaction between nature (genetics) and nurture (environment/training etc) in the context of top-end athletes.

It is quite clear to me that the answer is of course 'both', but to what degree? Have any common genetic variants/loci been identified, or is 'athleticism' a far too complex trait for this? Thanks.

For all types of athlete, their ability is determined by both genetic and environmental factors (nature and nurture). The degree to which each contributes ultimately depends on the demands of the sport.

As an example let's compare basketball and golf.

Basketball is likely to have a strong genetic component because players tend to be exceptionally tall (average is over 2 metres and there are only a handful who have played NBA under 1.75m). Because height is strongly genetically (but not entirely) determined by the genes, they have a big influence on whether someone can poses the physical qualities to play in the NBA. However, a large part of their technical capabilities are due to their environment. If you give a basketball to someone who has played 2 games a week their entire lives and ask them to take 10 shots it is likely they would score more than someone who has never seen a basketball!

Comparing basketball to golf, there are all sorts of body types within the PGA tour, and they is no/few obvious genetic traits which golfers tend to have over other people. This would suggest that golfing ability is more affected by environment.

So an easy way to get a rudimentary test of genetic contributions to sporting ability would be to compare frequency distributions of focal traits in the athletes to distributions of regular people. Obviously the phenotypic trait you measure has both genetic and environmental contributions (e.g. childhood diet) which could affect them but it would be a good starting indicator which could give some candidate traits to test.

As a scientist I would also consider sequencing some athletes and some non athletes and seeing which genes the athletes have more often then the regular person's genome. However, such studies are likely to be complex - linking phenotypes (in polygenic traits) to the single allele variants relies on large sample sizes. Generally it will be more difficult if:

There is large variance in the trait
The gene has a small effect (see major and minor effect genes)

Both of these problems going to be positively correlated with the number of genes affecting a trait (how polygenic is it?) which for athletic ability is probably quite a substantial amount of genes.

EDIT:  Here are some possible studies for your further exploration of the topic-

Candidate genes for Specific Genetic Markers of Endurance Performance and o2max

Rowers have an excess of the ACE I allele

Elite Italian footballers with "explosive" leg strength also reveal ACE and other genetic markers

A precautionary tale about Genetic tests for athletic ability


What is meant by the term synaptic targeting? I am studying whether a protein interacts with the mitochondria in the synapses of neurons and I have come across the term "synaptic targeting". I am reading this paper and I have come across the following:

During synaptic development, proteins aggregate at specialized pre-
and postsynaptic structures. Mechanisms that mediate protein
clustering at these sites remain unknown. To investigate this process,
we analyzed synaptic targeting of a postsynaptic density protein,
PSD-95, by expressing green fluorescent protein– (GFP-) tagged PSD-95
in cultured hippocampal neurons.

I am not sure what exactly is meant by the term "synaptic targeting". I have tried Googling the definition but all I get are links to journal papers. I think that synaptic targeting refers to where in the synapse (e.g. presynaptic or postsynaptic ending) a protein is located, but I am not certain. Any insights are appreciated.

PSD-95 is a protein located in the post-synaptic region inside a cell. In fact it's named for this, "post synaptic density-95" referring to the dense appearance of the post synaptic area on an EM microscope and this protein's presence there.
"Synaptic targeting" in this context refers to how that protein gets to where it belongs (the synapse) in the cell, rather than just floating around in the cytoplasm by simple diffusion.


Evolutionary rationale behind migration proteins Tumor cells are able to migrate due to specific migration proteins.
What is their evolutionary origin?
Or are they simply deregulated?

This would be a very long answer but just to give you some hints, the migrational mechanisms are already there and the cancerous cells makes use of them to metastasise. So in short its deregulation. What is under selection pressure tho are cancerous cells themselves to constantly change and evade cellular fail safes which kill (apoptosis) uncontrollably replicating cells. You can find out about this here (http://www.nature.com/onc/journal/v22/n42/abs/1206757a.html)


Do we know if RHEB is more sensitive to some amino acids than other amino acids? RHEB (Ras homolog enriched in brain) senses amino acid levels in order to recruit mTOR.
See this review describing the process of how RHEB recruits mTOR. So does RHEB have differential selectivity towards different amino acids.

We also discussed this in Matt Kaeberlein's class yesterday and I posed this question but no one could answer it (that said, Matt Kaeberlein called it a good question).

RHEB does not sense amino acids. See the abstract of this paper.

  Activation of this pathway requires inhibition of the tumor suppressor
  complex TSC1/2. TSC2 is a GTPase-activating protein for the small
  GTPase Ras homologue enriched in brain (Rheb), GTP loading of which
  activates mTOR by a yet unidentified mechanism. The level at which
  this pathway senses the availability of amino acids is unknown but is
  suggested to be at the level of TSC2. Here, we show that amino-acid
  depletion completely blocks insulin- and TPA-induced Rheb activation.
  This indicates that amino-acid sensing occurs upstream of Rheb.
  Despite this, amino-acid depletion can still inhibit mTOR/S6 kinase
  signaling in TSC2-/- fibroblasts. Since under these conditions
  Rheb-GTP levels remain high, a second level of amino-acid sensing
  exists, affecting mTOR activity in a Rheb-independent fashion.

RHEB also doesn't have any amino-acid binding (or any small molecule binding) domain.


What causes "ear rumbling"? The video Ear rumbling happens below the range of human hearing demonstrates that the "ear rumbling" sound is actual sound and can be recorded by a sensitive microphone near the ear.

What is it exactly that produces this vibration and how is it radiated as sound waves into the air?

If it is subsonic, then why does it sounds like noise rather than being inaudible?

I'm able to create rumbling in my ears at will. Unlike the poster of the video, I don't need to yawn to do so; I can do it without my face appearing to move. I actually discovered this alongside another ability of mine when I was little: the ability to create warmth flowing from the base of my neck outwards into the rest of my body. After some research I figured out that the warmth I'm able to create is actually part of voluntary piloerection (its use for warmth is mentioned here), while the ability to create a rumbling sound is simply the contraction of the tensor tympani, a muscle in the ear. Voluntary control over either one of these things is supposed to be rare, but I've found claims of several other people online who can do both (example1, example2).
Anyways, Wikipedia gives a brief explanation of how the ear rumbling works, which also specifically mentions "yawning deeply" as a trigger:

Contracting muscles produce vibration and sound. Slow twitch fibers produce 10 to 30 contractions per second (equivalent to 10 to 30 Hz sound frequency). Fast twitch fibers produce 30 to 70 contractions per second (equivalent to 30 to 70 Hz sound frequency). The vibration can be witnessed and felt by highly tensing one's muscles, as when making a firm fist. The sound can be heard by pressing a highly tensed muscle against the ear, again a firm fist is a good example. The sound is usually described as a rumbling sound.
Some individuals can voluntarily produce this rumbling sound by contracting the tensor tympani muscle of the middle ear. The rumbling sound can also be heard when the neck or jaw muscles are highly tensed as when yawning deeply. This phenomenon has been known since (at least) 1884.

It also seems like this type of noise can happen with conditions such as Tonic Tensor Tympani Syndrome.
The tensor tympani connects directly to the handle of the malleus, so I'd assume that's why it can be heard by the person doing it. Apparently this also causes the eardrum to move. This means it's classified as objective tinnitus.
Here are some relevant studies I found:

Voluntary contraction of the tensor tympani muscle
and its audiometric effects
Voluntary Eardrum Movement : A Marker for Tensor Tympani Contraction? (paywall)
Tonic contractions of the tensor tympani muscle: a key to some
non-specific middle ear symptoms? Hypothesis and data from
temporal bone experiments (paywall)


How is monoclonality or polyclonality determined? I was reading up Kaposi sarcoma and Robbins Pathology says,

  ..many features suggest that KS is not a malignant tumor despite the ominous name ...spindle cells in many KS lesions are polyclonal or oligoclonal

This is also seen in multinodular goiter where the lesions are polyclonal, but some monoclonal nodules are found.

My question is, how are these determined? By sequencing, is it not that, in cancerous growth there are myriad mutations, how can you map whether the mutations present are due to monoclonal expansion or polyclonal expansion? In non cancerous growths, wouldn't all cells have the same genotype?

Polyclonal and monoclonal expansion in B-cells is clear to me since a polyclonal lineage would have different vdj recombs while monoclonal would have the same. Here also, is it decided by genomic sequencing or the Ig sequence?

There are a few ways to determine clonality. Sequencing-based methods are probably the cheapest, given the current costs of either sequencing, or the even cheaper PCR-based clonality assay. Other methods might include histomorphology, looking for known chromosomal aberrations and/or immunophenotyping, among others. Here's a nice review of some of the clonality testing methods.

Sequencing and PCR would be the most definitive ways to determine clonality of a tumor, since they provide information on the exact sequences of sets of cells.

Exome sequencing would be a good way to determine clonality in a large group of cells, where you don't necessarily know what to look for a priori. PCR is a lot cheaper and more focused and might make a better choice when you do have a specific target to sequence, such as highly polymorphic genes like some androgen receptors and the genes involved in VDJ recombination.


Loss of appetite during fever It is a well-known phenomenon that sickness like the common flu is often accompanied by reduced appetite. Why do sick people stop eating?

The psychologic and behavioral components of sickness represent a highly organized strategy of the organism to fight infection. Sickness is generally accompanied by fatigue, numbness, coldness, muscle and joint aches, and reduced appetite. These symptoms are not simply an effect caused by the pathogen. Instead, it now believed to be an active defense strategy of the body, referred to as “sickness behavior”. Sickness behavior is thought to be an adaptive response that enhances recovery by conserving energy to combat acute inflammation (Maes et al. 2012). It is triggered by the proinflammatory cytokines produced by activated cells of the innate immune system due to the presence of pathogens. These cytokines include mainly interleukin (IL) 1 (IL-1α and IL-1β), IL-6, and tumor necrosis factor α (TNF-α) (Dantzer, 2009; Plata-Salamán, 1998).

One of the sickness behaviors is a loss of appetite. Among a host of other effects, cytokines are believed to inhibit feeding by their actions in the hypothalamus. The hypothalamus is an important neural center that regulates food intake (Plata-Salamán, 1998; Meister, 2000).

I refer you to Maes et al (2012), Plata-Salamán (1998) and Dantzer (2009) for backgrounds and further reading, as cytokine immunology is highly complex and this answer is anything but complete.

References
- Dantzer, Immunol Allergy Clin North Am (2009); 29(2): 247–64
- Maes et al, BMJ (2012); 10: 66
- Meister, Vitam Horm (2000); 59: 265-304
- Plata-Salamán, Semin Oncol (1998); 25(1 Suppl 1):64-72


Efficiency of plasmid DNA isolation from frozen E. coli cell cultures Has anyone isolated plasmid DNA from frozen (at -20degrees) E. coli cell cultures (not pellets)? Has that worked and if so, with what yields? What would be the quality of the isolated plasmid DNA if run on a gel? Would most of it be degraded or intact?

I have done that and it works without any problems. We harvested the cultures at the optimal timepoint (density) and then froze them to do maxipreps later on. Therefore we simply thawed the culture, made sure it didn't got too warm (meaning we worked on ice) and then simply followed the maxiprep protocol. No problems with yield or quality of the plasmide.

What I will do next time is to spin down the culture and take it up in max. 50 ml of medium before freezing. This way freezing will be faster as well as thawing. I have also done minipreps from stock cultures (glycerol stocks of plasmids in E.coli) which accidentally stayed out of the freezer for two days. Here the yields where not so great (but the density of the culture was also much lower), but the quality after standard miniprep was good and the plasmids worked both for subsequent cloning as well as for retransformation to make new stocks.


How many cell membranes are oxygen and carbon dioxide diffuse through in the lungs? In the lungs, oxygen and carbon dioxide pass through cell membranes by diffusion.
Which row is correct?

The correct answer is D, but I think it should be B. I can only think about three layers as maximum which are; epithelium of alveolus, endothelium of capillaries and the membrane of red blood cell. I don't know what are remainings.

Any help would be much appreciated!

Oxigen goes from the alveolar's lumen to the cytoplasm of the erythrocyte, and that's 5 membranes:

the "top" of the alveolar epithelial cell
the "bottom" of such cell
the "top" of the endothelial cell (capillary)
the "bottom" of such cell
the erythrocyte membrane

You got all the cells right, but your only problem was this: oxygen diffuses through the cell membrane entering the cell, moves through the cytoplasm, and diffuses through the membrane again exiting the cell. So, for each cell, you have to count 2 membranes. For the last one, the erythrocyte, you have only 1 membrane (because it is $\ce{O2}$ final destination).

For the $\ce{CO2}$ the situation is a little bit more tricky. We have the same 4 membranes (2x epithelial cell and 2x capillary), but $\ce{CO2}$ can come from 2 locations:

from the erythrocyte, where it is formed from $\ce{H2CO3}$ (by the reaction $\ce{H2CO3 -> H2O + CO2}$) or released from the N-terminal group of proteins, like haemoglobin (where it has previously bound)
from the plasma (around 9% of the $\ce{CO2}$).

In the first case we have 5 membranes, and in the second case just 4.

So, the correct answer is D.


What contributes to the variation of protein sequence across different species? What contribute to the variation of protein sequence across different species (e.g. phenotype, environment, evolutionary pressure) and how do those factors contribute to the variation?

I have tried to search using google + google scholar but they generally show papers discussing why and how the protein conserved across species rather than why/how the protein diverged across species. Please help me on this and references/sources are very important and highly appreciated. Thank you!

An example to clarify my question. The gene CD81 is not identical among human, chimp, rat, chicken based on this identity matrix from ClustalW2. Why is CD81 not identical in all species? What factors cause the different in CD81s? How do those factors cause that (e.g. evolutionary pressure)?
#
#

Percent Identity  Matrix - created by Clustal2.1

#
#

 1: sp|P60033|CD81_HUMAN    100.00  100.00   93.22   82.55
 2: sp|P60034|CD81_PANTR    100.00  100.00   93.22   82.55
 3: sp|Q62745|CD81_RAT       93.22   93.22  100.00   82.55
 4: tr|F1NW06|F1NW06_CHICK   82.55   82.55   82.55  100.00

I have found an acceptable answer for my question. Just post here if any interest in it. Pardon my English.

Source:

Nei et. al. 2010. The Neutral Theory of Molecular Evolution in the Genomic Era. Annu. Rev. Genom. Human Genet.

Evolution and point mutation cause the sequence difference of the same functional protein across species. Neutral theory of molecular evolution shows that speciation level of evolution is an accumulation of molecular level of neutral evolution. In neutral evolution, the mutation only occur at a scope of point mutation in sequence in the manner that the function of the protein is retained. Overtime, speciation occurs yet the function carried out by that specific protein is still necessary and is conserved across species. Difference in protein sequence of the same functional protein is the residuals of random point mutation.


Which animal dug this 5 cm diameter hole deep into mud and build a large mound around it? I noticed the large structure below today at the edge of a very small pond in northern Taiwan lowlands. It is June and it has rained a bit the past few days, and this 15 cm mud dome with a 5 cm diameter hole going straight down looked fresh and wet and glistening.

It is hard to tell for sure but it looks like the borough went deep enough to reach the water line of the pond next to it, but I could not tell because it's dark inside and I did not have a flashlight.

The mound is large, perhaps 15 cm tall and wide, which suggests that a lot of material has been removed and the tunnel could be quite deep.

The pond is only about 3 x 5 meters in diameter.

Question: Snake? Crab? Mole? What further information can I collect about it that would help to identify what produced this?

click images for full size view

A crustacean (land crayfish). There are a lot to choose from.

http://web.nchu.edu.tw/~htshih/crab_fw/fw-crabe.htm


How to get Bacteria to attach to an Object? I have cultured Cyanobacteria (in a media) in a beaker. I want that bacteria to attach to a cloth (e.g. Carbon). My current method is using a syringe to slowly push the bacteria to one side of a cylindric tube and exist through the other end. The cloth is placed stationary inside that tube throughout the process.
Is there a way to get more bacteria to attach to the cloth? (e.g.maybe adding something to the cloth)

You're thinking in terms of making them attach to your cloth, but they want to be attached - there are more nutrients and it is safer.  Make sure they have enough light, but not too much, and their nutrients.  They may be attaching and growing, but just not as fast as you expect.
It is also possible that your strain of Cyanobacteria has lost the ability to attach.  If it has been maintained in liquid culture for many generations, any bacteria attached to the wall of the container were selected against.


Why are two forward and reverse priming sites depicted here? what do they do? This question is in regard to the baculovirus expression system.

(source: amsbio.com)

Why do we need to generate primers for the polyhedrin promoter and the baculovirus?
Primers are needed to amplify DNA regions of interest.Here, why exactly do we need to amplify these regions? and at which steps?

PS : I am not asking about the need for forward and reverse primers.

It's just extra information that you don't need to understand the part above. You could use these primers for colony PCR or sequencing when you'd use the plasmid (after transforming to E.coli for example), but they're not absolutely required.

Compare it with this map for example. There are also some primer sites listed, but you don't actually need those primers for anything.


How to store vegetables in the refrigerator: In plastic bags or not? My wife and I are having a debate similar to this one:

I claim that it's better to take the fresh veggies out of the bags and put them in the crisper with humidity control because:

That's what the crisper with humidity control is for.
If they are in the (plastic) bag, the humidity control is pointless.
It's easier to notice vegetables in their early stage of rotting (it doesn't feel right to throw out an entire bag of rotten cucumbers or zucchinis before we got a chance to enjoy them).
It's more pleasing to the eye. It's more convenient.

She claims that it's better to leave the fresh veggies in their supermarket bags when putting them in the fridge because she could swear she noticed that they rot more slowly when left in their bags.

As you can see from the few links in this question, I tried to conduct my own search on the subject, but all answers seem to be opinions or "experiences", not an authoritative answer based on scientific research or knowledge.

So I am hoping that with the help of biology professionals (or students) I can finally find an authoritative answer to the question: Do vegetables really last longer if they are kept in their (supermarket) plastic bags when put in the crisper?

Update: I found this formal excerpt from the refrigerator's manual:

  Low (open) lets moist air out of the crisper for best storage of fruits and vegetables with skins.

  Fruit: Wash, let dry and store in refrigerator in plastic bag or    crisper. Do not wash or hull berries until they are ready to
  use.    Sort and keep berries in original container in crisper, or
  store in a    loosely closed paper bag on a refrigerator shelf.
  Vegetables with skins: Place in plastic bag or plastic container and store in crisper.

  High (closed) keeps moist air in the crisper for best storage of fresh, leafy vegetables.

  Leafy vegetables: Wash in cold water, drain and trim or tear off bruised and discolored areas. Place in plastic bag or plastic container and store in crisper.

While this seems a bit more authoritative (because it comes from the manufacturer of the refrigerator), it still leaves quite a few questions open:

If leafy vegetables should be "placed in plastic bag or plastic container and stored in crisper", why set the humidity on "High"? How does humidity get the lettuce inside the plastic bag or plastic container? (is it sealed?)

Assuming that some humidity does get into the bag, why is the bag needed? Why not let humidity flow freely?

Based on what I've been able to locate on the USDA website:
Refrigeration & Food Safety

It would be better to take the foods out of the bags and put them in the crisper if you're using the crisper solely for vegetables:

  Some refrigerators have special features such as adjustable shelves, door bins, crispers, and meat/cheese drawers. These features are designed to make storage of foods more convenient and to provide an optimal storage environment for fruits, vegetables, meats, poultry, and cheese.

And:

  Sealed crisper drawers provide an optimal storage environment for fruits and vegetables. Vegetables require higher humidity conditions while fruits require lower humidity conditions. Some crispers are equipped with controls to allow the consumer to customize each drawer’s humidity level.

Therefore, keeping your stuff in the bag would negate the purpose of these specialized compartments. Too bad the USDA doesn't specifically address the issue of bags...


Can Cas13 be used with multiple crRNAs in the same reaction? CRISPR-Cas13 equipped with crRNA (complementary to transcripts of interest) can be designed to target ssRNA transcripts in cells.

Upon successful crRNA and ssRNA binding, a fluorescent domain on Cas13 generates a signal, indicating that target has been found.

As far as I know, this method has been used to find one ssRNA target at a time. If we use different wavelength fluorophores for distinct Cas13-crRNA targets, is it theoretically possible to mix them all in the same reaction and distinguish the presence of different targets based on the different fluorescence wavelengths generated during target binding?

In this paper one fluorescently labeled crRNA is used to detect cleavage of one RNA target through complimentary binding. So is it theoretically possible to use several crRNA, each labeled with a different fluorophore, to cleave and detect several target RNAs?

Answer is no. Because each CRIPSR-Cas(xx) system works as a ribonucleoproteic complex, so they needs to be loaded with a crRNA in order to be working. Functionality is guaranteed while each of the Cas endonuclease domain is associated with a crRNA. You maybe could use multiple Cas13 with multiple crRNA.
In molecular diagnosis is common to use orthogonal CRISPR enzymes with different crRNA, as can be seen in this original research.


What species of duck is this? What species of duck is this? See below photo. Head colour is green like a mallard, but that's pretty much the only similarity. Spotted in Leicestershire, UK.

Probably a domestic hybrid of a mallard.
From Cornell:

If your duck has large patches of white where you didn’t expect it, think domestic duck.

Mallards (Anas platyrhynchos), which have the identifiable green head in the wild, are only 1 of 2 species of ducks that have been domesticated. So it would be no surprise if a strange looking mallard was in fact, well,  a mallard.
Again, according to Cornell:

Another common form [of the domestic/hybrid mallard] is the bibbed version. It has a sort of normal body and head plumage, and a white chest.

Also:

The passion for weird plumage in domestic ducks does not stop with white, but can go the other way too.  Some breeds are darker than normal Mallard plumage

These descriptions both match your specimen quite well.
Although your picture is low quality, it appears to me that the posterior feathers of your specimen also are not straight. Again, quoting Cornell:

Watch for the little curled feathers on the back of the male, above the tail.  Only the Mallard and its domestic descendants have those.

Finally, most hybrid ducks that come from some domesticated origin tend to be larger than  non-domesticated specimens since early domestication efforts emphasized large size for food (vs simply plumage for appearances). Your image has no relative scale, so I cannot comment on whether this applies to your specimen or not.
In terms of a specific "name" for such a hybrid?
I did find evidence that some people refer to domestic-hybrid mallards like your dark-plumage, white-bibbed mallards as "manky mallards", though I'm not sure how ubiquitous this is. For example, see here and here.

Though 10000birds.com claims non-domesticated birds can also occasionally develop bibs similar to those seen on domesticated descendants.


Is gene only the portion of a single strand which codes for a particular protein? I know that gene is a segment of DNA that codes for a specific protein. But is it a segment of a single DNA molecule or a DNA duplex?

The given image shows a section of a dsDNA.

Source of image:https://en.wikipedia.org/wiki/Intron#/media/File:Gene.png

Suppose its the blue portion (5' to 3') that codes for a particular protein.
The figure tells that the blue portion + its complementary red portion make a gene. But if its the blue portion which actually codes for the protein, then shouldn't it alone be considered the gene for that particular protein ?

i.e. Why are portions of the both the DNA strands considered a gene in the figure?

Trust me, every picture on the internet tells the same.

None of the highlighted regions in your figure, is a gene. A gene is a section of DNA which gives rise to a product. Basically, a gene has an orientation (5'→ 3') i.e. it is essentially a single stranded region. However, the strand that mechanistically contributes to RNA synthesis (template) has the reverse-complementary sequence of the gene (in other words, anti-sense). Therefore, a gene, as it is annotated is not a functional entity but a genomic representation of a product. Some viruses (such as M13 phage) have a single stranded genome; for them the transcript is always antisense to the genomic DNA region.

Same section of dsDNA can harbour multiple genes in both orientations and this is clearly seen in viruses which have an highly compact genomes. Other prokaryotic and eukaryotic genomes also have overlapping genes.

Some related posts:

On which DNA strand is TATA box present?
Do transcription factors bind to both strands of DNA?
Which DNA elements belong to the definition of a gene?

  Does that mean only the indicated region of molecule A is a gene? Or,
  does the Indicated portion of molecule A + Complementary portion
  present in molecule B comprise a single gene, such that A is sense and
  B is non-sense strand of the same gene?

If the molecules A and B are expressed from opposite strands, then they are considered products of different genes, even if the gene region overlaps.

The situation is more unclear if both the molecules are expressed from the same strand and the transcribed region overlaps. Sometimes they are classified under the same gene (splice variants) and sometimes they are not.

These are some lines from the human genome annotation file which tells the location of genes in the genome (+ and - denote opposite strands):

chr1    HAVANA  gene    1567474 1570639 .   +   .   gene_id "ENSG00000189409.8"; transcript_id "ENSG00000189409.8"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "MMP23B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "MMP23B"; level 2; havana_gene "OTTHUMG00000074713.4";
chr1    HAVANA  gene    1590786 1594063 .   +   .   gene_id "ENSG00000272004.1"; transcript_id "ENSG00000272004.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.10"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.10"; level 2; havana_gene "OTTHUMG00000185638.1";
chr1    HAVANA  gene    1603429 1604850 .   +   .   gene_id "ENSG00000269737.1"; transcript_id "ENSG00000269737.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.7"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.7"; level 2; havana_gene "OTTHUMG00000182604.1";
chr1    HAVANA  gene    1604714 1605836 .   +   .   gene_id "ENSG00000269227.1"; transcript_id "ENSG00000269227.1"; gene_type "pseudogene"; gene_status "KNOWN"; gene_name "RP11-345P4.6"; transcript_type "pseudogene"; transcript_status "KNOWN"; transcript_name "RP11-345P4.6"; level 1; tag "pseudo_consens"; havana_gene "OTTHUMG00000182605.1";
chr1    HAVANA  gene    1570603 1590473 .   -   .   gene_id "ENSG00000248333.3"; transcript_id "ENSG00000248333.3"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11B"; level 2; havana_gene "OTTHUMG00000078638.4";
chr1    HAVANA  gene    1592939 1624167 .   -   .   gene_id "ENSG00000189339.7"; transcript_id "ENSG00000189339.7"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "SLC35E2B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "SLC35E2B"; level 2; havana_gene "OTTHUMG00000078639.1";
chr1    HAVANA  gene    1634169 1655766 .   -   .   gene_id "ENSG00000008128.18"; transcript_id "ENSG00000008128.18"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11A"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11A"; level 2; havana_gene "OTTHUMG00000000703.14";
chr1    HAVANA  gene    1634175 1669127 .   -   .   gene_id "ENSG00000268575.1"; transcript_id "ENSG00000268575.1"; gene_type "processed_transcript"; gene_status "NOVEL"; gene_name "RP1-283E3.8"; transcript_type "processed_transcript"; transcript_status "NOVEL"; transcript_name "RP1-283E3.8"; level 2; havana_gene "OTTHUMG00000183552.1";

Not evident in these examples but there are many overlapping genes in opposite strands. Anti-sense lncRNAs would be an example to have a quick look at.

Bottomline: A single gene is on one of the DNA strands, not both.


Please Help Identify These Bugs I live in KwaZulu-Natal, South Africa, and the only indoor bugs I've experienced issues with are fleas, as I have two cats (and a big garden). This morning, however, I put on a fleece top that had been lying around somewhere, got a lift to the store, and returned to suddenly feel a crawling sensation. I lifted up my shirt to find these tiny bugs crawling all over my upper body. I did some Googling, went upstairs and carefully observed my bedding and bed, however, the only evidence I found was a few newborn fleas / flea larvae (which I intend to deal with today). I should also mention that a flock of wild Egyptian Geese have been raising five goslings in my yard, and they get very close to me when I'm walking outside at times. My house is also not carpeted, it has oregon pine floors throughout. I tried to take a photo of the critters, however, they're very tiny and move very quickly, so it was difficult to get a clear shot. Any advice would be greatly appreciated.

Yes, this is a book louse (order Psocoptera). They feed on all kinds of organic matter, and are very common. Fun fact - they are called "book lice" because they are often associated with old books, feeding on the organic glues in the bindings. (they are also called bark lice - I'm sure you'd know why).


Are Sloth tongues soft or rough? Are Sloth tongues soft or rough?

Dogs have soft tongues, while cats have rough tongues, so the feeling when they lick e.g. a human hand is quite different. So what about sloths?

This question came up in a recent discussion but I was unable to find any materials as google queries for sloth tongues leads to tons of cute pictures.

Sloths have long, thick, sticky tongues covered in a carpet of tiny, rear-ward pointing spikes that they can pull leaves in with.

So the tongues are quite different from human tongues and likely much less "soft" to touch and more "rough".

According to scanning electron microscopy studies on the topography of a sloth's tongue, the following results were found:

  The results revealed that the rostral part of the tongue presents a
  round apex and covered by filiform and fungiform lingual papillae and
  a ventral smooth surface.


Is oxidative phosphorylation less efficient in gram positive bacteria? Gram negative bacteria perform oxidative phosphorylation in their periplasmic regions, between the inner and outer membrane where a proton gradient is maintained and used by the ATP synthase to make ATP.

Gram positive bacteria do not have a second membrane, but only a porous polysaccharide capsule.  Oxidative phosphorylation then would on try to pump protons to the outside of the bacterium and it could diffuse out into the surrounding environment.  Does this cause gram positive bacteria to operate less efficiency?  does it make them more vulnerable to a basic pH in their environment?

A similar question was already answered at How do Gram + bacteria use a proton gradient for F-type ATPase? . In those answers, there is a general belief that Gram negative bacteria do not have much control over their intermembrane space pH, because their outer membranes have many porins, such as OmpC, which allows free passage both ways for protons and other molecules smaller than 600 daltons. If that is true, there is not much of a difference between Gram positive and Gram negative ability to control pH just outside the inner membrane.

There is a long review at DOI: 10.1016/j.bbamem.2005.09.010 . The first two examples of pH sensitivity are E. coli (divides more slowly when pH goes from 7 to 8.7) and B. subtilis (divides more slowly when pH goes from 7 to 8.5). The first is Gram-negative, the second is Gram-positive. B. subtilis undergoes growth arrested at pH 9, suggesting it might be more sensitive, but again, the difference is just subtle.


Detecting UV by humans From my experience humans can detect UV - not by seeing it but by pain in their eyes. Many people (me too) feel pain when looking at UV lamps. When looking at sun through clouds I still can feel pain very often even if the after -all-image is not very bright (because of the clouds) but when I look at a light bulb or when I look at sun through sun-watching lenses (which cut all UV) I don't feel that pain despite of them being much brighter than the cloudy sun. I also have read about it once or two.

So, can this be true (I mean humans can detect UV with their eyes) or that's just a coincidence? And if it's true, how it happens?

First to address some of the comments:

Concentrated UV damage does hurt your skin, it's called sunburn.  Lighter amounts of UV damage can cause cancer over time.  UV damage can be "felt", as can photonic pressure in extreme cases.  The issue at hand is "what is detection."

Back to your eyes:
As addressed in this answer, the human retina is able to detect UV light if it is not blocked by the lens.

I believe your question, restated slightly, is "can we call the pain experienced by UV damage to our eyes human detection of UV light."  Generically I think the answer is no, because we lack the specificity to determine that it is UV light. Many forms of ionizing radiation can lead to pain, and we would be unable to distinguish between them.  We cannot tell the gradation from UV to gamma, despite the damage they might cause.  Contrast this to the visible light spectrum, where we are quite good at determining the wave length.

Further, you could have similar damage caused by infection, where again you couldn't distinguish between the pain and fuzzy sensation caused by the very beginning of infection vs slight UV damage (though blueberry might help).

Does UV light damage your eyes? Absolutely in large enough doses.  Can it be called detection?  Probably not.  We can deduce UV damage from lots of things, including changes in the color of the pigmentation of your eyes (gold flakes = bad).  When we get to the level of deduction, however, we might as well be using machines to detect UV light and save our eyes (and skin) the trouble.


Does hypothalamus regulate posterior pituitary gland? We have the hypothalamus-anterior pituitary-endocrine axis, but is there a similar chain of command for posterior pituitary gland such that oxycotin and vasopressin are regulated by some tropic hormones?

The difference between secretion of ACTH  and neurohypophysial hormones is that the prior is a two step process, with CRF from hypothalamus stimulating the anterior pituitary. The latter is produced and secreted from the same cell, only in different organs! Magnocellular neurons stretch from the hypothalamus to the posterior pituitary, where they have their neurosecretory endings packed with hormone storing large dense-core vesicles. The same neurons are osmosensitive, regulating their secretion themselves as physiological need arises. Also, they apparently do dendritic secretion as autocrine signalling. Some reading about this: http://www.ncbi.nlm.nih.gov/pubmed/24265070
and
http://www.nature.com/nrn/journal/v7/n2/full/nrn1845.html
Hope it helps.