By definition, will some children always be stunted? I had a question about stunting i.e. height-for-age. The WHO defines at as any child whose height-for-age is 2 standard deviations below the median height-for-age.

Given this definition, wouldn't there always be stunted children? I must have misunderstood the definition because this seems like one of those challenges that needs to be "fixed" but my current understanding means its sort of unfixable.

Any insight is appreciated.

You are correct, that under that definition; unless there were no variation (which would be impossible), there would always be individuals that fall below 2 standard deviations. However, "stunted" under this definition would not be a problem if variation was extremely low. So yes, it would be unfixable by definition, but if variation fell, then the "problem" would be fixed, because it would no longer be a problem.


Why do large neurotransmitters travel faster down the axon? I understand that with large neurotransmitters, like neuropeptides, the precursor neurotransmitter and the enzymes are produced in the soma and quickly travel down the axon to be modified in the axon terminal.

With the small molecule transmitters, the enzymes are made in the soma and then transported slowly down the terminal to the terminal where they synthesize the small transmitters.

Why is it that the precursors and enzymes for large neurotransmitters travel fast down the axon, whereas the enzymes for the small transmitters travel slowly? Is there a specific reason?

I presume you are referring to fast versus slow axoplasmic transport.

I presume by "small neurotransmitters," you are referring to "small molecule" neurotransmitters like GABA, glutamate, acetylcholine, and the catecholamines like dopamine.

For the "large" neurotransmitters, I assume you are referring to peptides.

(for a quick reference on these two categories you can see this book blurb)

Although local protein synthesis is possible outside the soma, particularly in dendrites, and there is even evidence for protein synthesis in axons, including neurotransmitter peptides, most protein synthesis still seems to occur in the vicinity of the nucleus, at the soma. Synthesis anywhere else means you need to transport the mRNAs and translation machinery instead, since the mRNA needs to be made at the nucleus. Even the "large" neurotransmitters, which are peptides, need to be synthesized just like bigger proteins.

Back to axoplasmic transport... There are two main mechanisms for moving things down the axon. The faster version of this transport is really for the transport of vesicles. To transport a neurotransmitter peptide in this fashion, you fill a vesicle full of the peptide and send it on its way along the microtubules via kinesin and dynein motors.

Larger, non-membrane bound proteins, however, are often not transported in vesicles, but by the slower transport mechanism. Note that this transport is still pretty fast, way faster than simple diffusion, it just isn't as fast as the "fast" transport. The exact mechanisms of slow transport are still an active area of research and not fully understood.

To get back to your question, "is there a specific reason?" The reason isn't so much about the speed, but about the mechanism of transport. Small peptides and membrane-bound proteins move in vesicles via fast transport. Large proteins not bound in membranes move via slow transport. The enzymes that synthesize the small neurotransmitters fall into this latter category. Importantly, although the neurotransmitters may be small, the enzymes themselves can be big, at least certainly bigger than the small peptides that are equivalent to the "large" neurotransmitters.


Can excessive carbonated drink consumption lead to elevated red blood cell levels? I've recently had a blood test and the results displayed elevated levels of erythrocytes as well as hemoglobin. (As a result my hematocrit levels were also above average)

At my workplace there is a water cooler which also has an option to dispense carbonated water (this is just regular ol' carbonated tap water) and usually over the course of the day I tend to drink quite a lot of the stuff.

Since erythrocytes/hemoglobin deals with O2 and CO2 transport, I was wondering if my daily consumption of carbonated water is a plausible cause for the additional erythrocytes that are being pumped out?

The main regulatory input into erythrocyte production is hypoxia. The response to elevated CO2 levels in the blood (hypercapnia) is mainly to increase ventilation (i.e. more and/or deeper breaths) so that the excess can be "blown off".

I think that some carbon dioxide could pass into the bloodstream from the stomach since gases tend to be quite good at diffusing across membranes, but this would be easily dealt with by the physiological mechanism described above.


Why are there N's after Sanger sequencing? After sending a DNA sample for sequencing, the resulting sequence had N's in the beginning and end of the sequence.  I know the N's mean that the computer can't tell what the base pair is, but why is this?

Typically Sanger sequencing will run into a few errors. Sometimes the traces will overlap as below in red and the computer will call N. If you truly wanted to figure out the correct basepair, you can look at the trace.


Why can't plasma proteins migrate from capillaries? Why can't plasma proteins shift from capillaries to connective tissue but WBCs can be very rich in connective tissue even though obviously the WBCs had to go through capillaries.  Another example: in alveolar sacs neutrophils are there in the lumen  despite the presence of epithelia of alveolar sacs,  and it can only reach there via capillaries. So, how can they get into lumen despite the epithelia lining? Histology textbooks say that no plasma proteins can enter or leave capillaries, but WBCs (which are much larger than proteins) can move to connective tissue via capillaries?

Cells of the endothelium are joined by tight cell junctions which are impermeable or selectively permeable. Generally, proteins can only migrate through the endothelium via active transcytosis.
Leukocytes (specifically neutrophils, lymphocytes and monocytes) express various adhesion molecules and cytokine receptors which allow them to interact with endothelial cells and facilitate their movement (diapedesis) either between (paracellular) or through (transcellular) the cells. The process of leukocytes leaving the endothelial lumen is known as extravasation.

Carman CV. 2009. Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'. J Cell Sci 122:3025-3035.
(C,D) The process of diapedesis, whether during intravasation or extravasation, can occur by two distinct pathways: paracellular or transcellular. (C) Paracellular diapedesis. Leukocytes and endothelial cells coordinately disassemble endothelial cell-cell junctions and open up a gap between two or more endothelial cells (Muller, 2003). (D) Transcellular diapedesis. Leukocytes migrate directly through individual endothelial cells via a transient transcellular pore that leaves endothelial cell-cell junctions intact. Note that the two individual endothelial cells in C and D are distinguished by different shades of pink.


Complete metabolic map of humans Do we have the complete metabolic map for humans? Do we know from the genome what enzimes are expressed and what each enzime does?

As Armatus notes, we don't know ALL human metabolites and the enzymes + metabolic reactions that produce them. Identifying small molecules is hard and metabolism is dynamic, it depends on what is being fed into the system.

The virtual metabolic human (VMH) is an attempt at compiling the information that we do know. You can read their paper here. The human build currently includes (and links together);

13 543 metabolic reactions
4138 metabolites
3695 genes (enzymes)

It also attempts to compile all known metabolic reactions that result from the gut microbiome, nutritional metabolic pathways and genetic diseases that alter metabolism. Everything is linked via stable identifiers which is a real challenge.

The human metabolic database (HMDB) is also very good. It contains more metabolites than the VMH as it includes many partially or poorly characterised metabolites. The HMDB is really useful if you are working to identify metabolites while the VMH focuses on how they connect to one another.


Is there a difference between macroevolution and group selection? I encountered two different attitudes towards macroevolution:

The first one included long-term microevolution such as the evolution of Cetacea.
The second one included only macroevolution in terms of group-selection - that is for example the evolution of altruistic behaviour (the groups - families or tribes survived more likely if they were altruistic and shared the resources).

What about for example evolution of the parental instinct? Would it be considered a macroevolutionary (because it is about the evolution of families) or a microevolutionary trait?

And in general, am I getting macroevolution right with the second attitude?

Is there a difference?

Yes, they are quite different things.

What is group selection?

Group selection is an view of evolution where selection acts at the level of the group, rather than the individual. It suggests that selection is mediated by fitness of the population, and leads to conclusions of things occurring for "the good of the species". It is generally excepted that group selection arguments can rarely be invoked (but see haplodiploid social insects and kin selection). There is a long and controversial history to group selection and it's well worth reading about in further detail if you are interested in the history of science!

What is macroevolution?

Macroevolution is the evolution which occurs at larger scales, things like speciation, extinction, and the history of life. It often involves comparing species or lineages for example.

  "Macroevolution generally refers to evolution above the species level."

Microevolution on the other hand is, generally considered, evolution which occurs within lineages, or (more often) within populations. Researchers of microevolution would consider problems of adaptation for example.

  "Microevolution is evolution on a small scale — within a single population."

Macro- or microevolutionary trait?

I've never heard anyone refer to something in this way, traits can be studied in both micro- and macroevolutionary contexts.


What is the family of this insect caught by my Drosera? I am currently trying to find out what type of flies are flying around in my home. If they are fruit flies, fungus gnats or something else.

Currently my Droseraa caught one of them and I am currious what species it is.

It is a small fly, like fruits flies and fungus gnats. As seen in the third photo the length is about 1,5 to 2mm (The distance between each line is 1mm).

The location is Stockholm in Sweden (in my apartment).

Could you help me identifying it?

This is a Dark-winged fungus gnat (family Sciaridae); the European species of the family are dealt with by Menzel, F.; Mohrig, W., 1999, Revision der paläarktischen Trauermücken (Diptera, Sciaridae) [A Revision of the Palaearctic Black Fungus Gnats (Diptera: Sciaridae)], Studia Dipterologica Supplement, (6):761 pages; copies are sold by Ampyx-Verlag (see http://www.ampyx-verlag.de/lilac_cms/de/4852,,refz,rd,368,2914,12/index.html).  Some species of the family have economic importance, but identification to species usually requires male specimens which must be at least temporarily mounted on microscope slides.


What is the name of this tree with compound leaves? Can anyone tell me what is the name of this tree?

It was found in Northern US.

(click on image to enlarge it)

It is Cussonia spicata,  It is one of the favorite foods of wild elephants.

The attractive leafs grow from the end of thick branches to form rounded heads.

Source

Wikipedia


Mitochondrial DNA and recombination Firstly I could do with a brief description of mitochondrial DNA. How does the structure of DNA in mitochondria compare to animal DNA (for the sake of simplicity let's say human - some animals might have unusual DNA structure) and what living organism is the mitochondrial genome most akin to? (Circular like bacteria maybe?) and are the mitochondria within a single human homogenous?

Secondly, and most importantly to my aim, does the mitochondrial genome recombine in anyway? Is the process of recombination affected by its structure? Are there any patterns/rules in mitochondrial recombination? Is there DNA transfer between mitochondria which could have a similar effect?

I am trying to think about how male deleterious alleles can spread differently in diverged populations given potential recombination to female beneficial (or recombination away from female deleterious mutations).

Mitochondrial DNA is circular, like bacterial DNA, and around 16.6 Kb long. It codes for 37 genes in total but the majority of these are simply the machinery for gene expression (curiously, mitochondria have a slightly different codon->amino acid translation 'table' to nuclear DNA) and so just 13 code for proteins. Single mitochondria usually have multiple copies of the DNA.

Mitochondria are thought to be most closely related to the bacteria Rickettsia, an obligate intracellular parasite that causes typhus. Mitochondria are so degenerate, however, that they've lost nearly all the genes that normal bacteria have.

While there is some small level of heterogeneity in mitochondria in a single person because mitochondria are exclusively transmitted down the female line most people typically only start with a single clonal population of mitochondria. Because of this, there is no other mitochondrial population present that the mitochondrial DNA could undergo recombination with.

Mitochondrial DNA does undergo recombination with nuclear DNA, however, in that genes can be transfered from the mitochondria to the nuclear DNA and because of this the majority of genes necessary for mitochondrial function are now coded not on the mitochondrial DNA but on the nuclear DNA and their protein products transported into the mitochondria after translation.


What is the closest species to humans in animal kingdom? I presumed chimpanzees were the closest relatives of us. However, after watching this TED Talk, it seems bonobos are closer to us both in skeleton and behavioral similarity than chimpanzees. I once read in The Magic of Reality that we share quite a lot of common FOXP2 gene letters with chimpanzees, but there isn't any mention on similarity between us and bonobos in that book. Here is the excerpt:

  You can tell that FoxP2 is the same gene in all mammals because the
  great majority of the code letters are the same, and that is true of
  the whole length of the gene, not just this stretch of 80 letters. Of
  the total of 2,076 letters in FoxP2, the chimpanzee has 9 letters
  different from ours, while the mouse has 139 letters different.   And
  that pattern holds for other genes too. That explains why chimpanzees
  are very like us, while mice are less so. Chimpanzees are our close
  cousins, mice are our more distant cousins. 'Distant cousins' means
  that the most recent ancestor we share with them lived a long time
  ago.

  Monkeys are closer to us than mice but further from us than
  chimpanzees.   Baboons and rhesus macaques are both monkeys, close
  cousins of each other, and with almost identical FoxP2 genes. They are
  exactly as distant from chimps as they are from us; and the number of
  DNA letters in FoxP2 that separate baboons from chimps is almost
  exactly the same (24) as the number of letters that separate baboons
  from us (23).

So which species is closest to us, chimpanzees or bonobos?

Others have given great answers, so I'll just support their answers with this diagram and a little further background on how to think about relatedness in evolutionary context.

Since the author in this excerpt makes no mention of Bonobos, I would imagine that, by chimpanzee, he really meant the genus Pan, which includes both Bonobos and Common Chimps. But that does not necessarily matter.

Relatedness, in modern taxonomy, depends purely on common ancestry, not necessarily on similarity of specific traits. As others have explained, we make theories about ancestry relationships based on many criteria and logic, not just variation in one gene. In this tree, you should think of A, B, and C as theoretical, extinct common ancestors of the species below them in the tree. The list of apes at the bottom represent the relevant extant species species only. Bonobos and Common Chimps have a more recent common ancestor (C) than either Bonobos and Humans (B) or Common Chimps and Humans (B). This is why @mgkrebs said that both qualify equally as most closely related, because the common ancestor of each pair is the same.

Few would disagree that Bonobos do seem to be more similar to humans than Chimps are to humans, but that actually does not mean they are more closely related evolutionarily! Theoretically there are two ways this could happen even if Bonobos and Chimps are equally related to humans, either our common ancestor with Chimps and Bonobos also shared the traits we have in common with Bonobos and Chimps changed, or Bonobos and Humans happened to develop these similarities independently. The former is a simpler explanation, but either are possible for each similarity. Again, the key in understanding this is in thinking about the theoretical ancestor species, B and C. The only way Humans could be more closely related to Bonobos than chimps is if the common ancestor, B, was a descendant of C, which seems extremely unlikely and as far as I know is not supported by the genetic research in this area.

Our common ancestor with Gorillas (A) on the other hand is much "earlier" than our common ancestor with Chimps and Bonobos, so Gorillas are less closely related to use than the group containing Bonobos and Chimps.


Understanding the concept of a "Place Field" and the difference between place cells and grid cells I have 3 questions that are interrelated:

After reading the proper literature on the subject, my understanding of the place field is that it's a place in space to which an animal's place cell reacts by firing. Then there might also be another place in field to which the same place cell reacts by firing. Is this understanding correct?

1.1 Why is it called place "field," what does the "field" actually imply, etymologically speaking?

1.2. The Wikipedia Grid Cell Page says that:

  By contrast, if a place cell from the rat hippocampus is examined in the same way (i.e., by placing a dot at the location of the rat's head whenever the cell emits an action potential), then the dots build up to form small clusters, but frequently there is only one cluster (one "place field") in a given environment, and even when multiple clusters are seen, there is no perceptible regularity in their arrangement.

So then what are those "clusters", i.e. I guess the place fields, are they the ones I highlighted in red on this picture (sorry, I am a very visual learner!) and also, why do they fire in clusters?

The Wikipedia Page has the following description of this picture but I am still not sure I am understanding it correctly:

  Spatial firing patterns of 8 place cells recorded from the CA1 layer of a rat. The rat ran back and forth along an elevated track, stopping at each end to eat a small food reward. Dots indicate positions where action potentials were recorded, with color indicating which neuron emitted that action potential.

The first question stems from the second and the main one I am confused about: what is actually the difference between the place cells and the grid cells, in a layman terms (beyond the obvious structural differences, i.e. that the place cells are pyramidal neurons and the grid cells fire in a hexagonal pattern)?
In terms of their functional differences, is the difference mainly in the fact that the grid cells are theoretically responsible for path integration, whereas "The place cells are thought, collectively, to act as a cognitive representation of a specific location in space, known as a cognitive map" ( O’Keefe John, 1978 ).

What is the physiological or anatomical difference between.... Available from: https://www.researchgate.net/post/What_is_the_physiological_or_anatomical_difference_between_place_cells_and_grid_cells_in_the_hippocampus [accessed Aug 16, 2017].

O'Keefe, John (1978). The Hippocampus as a Cognitive Map. ISBN 978-0198572060.

Yes, that's correct. Mostly, place cells fire in different places in different contexts, and they don't necessarily share the same spatial relationship in different contexts (like in your picture, the "yellow" cell comes right before a "cyan" cell; those place fields wouldn't necessarily be adjacent in a different context.

1.1. "Field" is just a term that refers to a region of space. I'd say the Merriam-Webster definition closest is #6:

  a region or space in which a given effect (such as magnetism) exists

1.2 The picture you have is probably a schematic, but what it depicts is a recording from several different cells. Each cell is assigned a color. Every time the cell fires a spike, there is a dot placed at the location in space where the animal was at the time of the spike. You let the animal run through the maze and get a record of lots of these points, and you see that they cluster together into place fields.

2&3 - These questions are getting to be a bit too broad and also you are only supposed to ask one question per submission, so I'll be very brief here. Grid cells are located in an entirely different part of the brain, the entorhinal cortex (part of neocortex), although this part does project to the hippocampus where place cells are found.

Grid cells fire in regular patterns in a spatial field, like in this image:
https://en.wikipedia.org/wiki/Grid_cell#/media/File:Autocorrelation_image.jpg

They also keep their relationship of firing locations relative to each other constant across contexts. You can think of them like a nested coordinate system.

Place cells do not do this. For a given environment, they seem to be somewhat randomly arranged relative to each other. Most likely, what actually happens with place cells is that if you could record from all of them, there would be a unique combination of cells active at any location, and this location could then be associated with other information like "I found food here."

Perhaps you could think about grid cells like a GPS location, but place cells are like a map marker.


Data for giraffe subspecies population change over the time. Is there a historical data for the number of animals in the wild for every subspecies of the giraffe and where it could be found?

In a recent paper in Current Biology, Fennessy and colleagues conclude that there are four species of giraffe and that their numbers are declining in Africa. Giraffes (Giraffa camelopardalis) are presently classified as one species, with nine subspecies, which are considered ‘Vulnerable’ on the IUCN Red List. The present consensus of one species divided into nine subspecies has previously been questioned (Supplemental information), and Fennessy and colleagues provide another viewpoint on giraffe taxonomy. The fundamental reason for different taxonomic interpretations is that they are based upon different datasets that adopt different statistical techniques and follow different criteria for nomenclature.
Its basically a form of evolutionary process.
Living giraffes were originally classified as one species by Carl Linnaeus in 1758. He gave it the binomial name Cervus camelopardalis. Morten Thrane Brünnich classified the genus Giraffa in 1772. The species name camelopardalis is from Latin.
The giraffe is one of only two living genera of the family Giraffidae in the order Artiodactyla, the other being the okapi. The family was once much more extensive, with over 10 fossil genera described. Their closest known relatives are the extinct deer-like climacocerids. They, together with the family Antilocapridae (whose only extant species is the pronghorn), belong to the superfamily Giraffoidea. These animals may have evolved from the extinct family Palaeomerycidae which might also have been the ancestor of deer.
The elongation of the neck appears to have started early in the giraffe lineage. Comparisons between giraffes and their ancient relatives suggest that vertebrae close to the skull lengthened earlier, followed by lengthening of vertebrae further down.One early giraffid ancestor was Canthumeryx which has been dated variously to have lived 25–20 million years ago (mya), 17–15 mya or 18–14.3 mya and whose deposits have been found in Libya. This animal was medium-sized, slender and antelope-like. Giraffokeryx appeared 15 mya in the Indian subcontinent and resembled an okapi or a small giraffe, and had a longer neck and similar ossicones. Giraffokeryx may have shared a clade with more massively built giraffids like Sivatherium and Bramatherium.
Further on researches are also being made till now!


Are the sympathetic and parasympathetic nervous systems exact opposites? Suppose mechanism existed that could block function of the PNS. Would this just mean then the sympathetic nervous system would become overly active?

Do the sympathetic and parasympathetic systems act as opposing forces?

The Autonomic Nervous System is composed of the sympathetic and parasympathetic nervous systems. Each are dominant under different conditions - both are always active but one is dominant.
An important way to understand the the autonomic nervous system is in considering the effects of pharmaceutical drugs.
Sympathomimetic drugs enhance adrenergic function.
Sympatholytic drugs interrupt adrenergic function.
Parasympathomimetic drugs enhance cholinergic effects.
Anticholinergic drugs inhibit cholinergic effects.
For example:
Muscarinic antagonists are parasympatholytic (Anticholinergic) drugs - which reduce the effects of parasympathetic system.
But it is not that simple. They also increase sympathetic tone.
But again it is not always that simple. E.g. for sympathomimetic drugs (enhance adrenergic function) - there is no parasympathetic nervous system effect.
To answer your question, the sympathetic and parasympathetic nervous systems oppose each other sometimes. It depends on which receptors are activated and where.
(E.g.Alpha 1 receptors, Alpha 2 receptors, Beta 1 receptors & Beta 2 receptors).
Source & further reading on pharmaceutical interventions
Source & further reading on receptors


Are any organisms known to use meiosis I to create non-identical offspring asexually? So, there are numerous species of animals who use parthenogenesis, but to my knowledge the reproduction is clonal. That is, the offspring are identical to the mother. Are there any documented cases where a female goes through meiosis one to produce varied cells that are now diploid and these cells do not go through meiosis two, but rather develop in to a diploid organism? It would seem an effective reproductive strategy in that it generates genetic variation without a mate (at least more-so than strict asexual reproduction). Is my logic flawed in some way?

In automixy the meiotic cells give rise to diploid offsprings. This can happen by diploidization of the haploid cell (1n->2n), which will produce homozygotes or endomitosis prior to meiosis (4n->2n) which produces heterozygotes. Examples:

Cnemidophorus uniparens : 4n->2n
Sphyrna tiburo: 1n->2n

I don't know of any case where there is fusion of similar gametes to form a diploid cell. It is difficult for two ova to fuse in natural conditions because the vitelline membrane has to be dissolved.
Experimentally a haploid ES-cell can be fused to ovum to form a progeny. Haploid ES cells undergo diploidization and when injected in blastocyst, can develop properly (Ref). In fact haploid androgenic-ES cell line had been made in this study by injecting sperm into an enucleated oocyte. These androgenic-haploid cell lines can be fused to ovum to give rise to viable offsprings.

Also see this question. Similar topic


What is the difference between abundance and dominance in an ecosystem? I was reading Hydroperiods of created and natural vernal pools
in central Ohio: A comparison of depth and duration
of inundation by Debra L. Gamble and William J. Mitsch (2008), and I came across this statement:

  The dominant tree species in the vernal pool area were Acer saccharinum and Quercus palustris, while Ulmus americana, though smaller in diameter than the other trees listed, was the must abundant species...As at the New Albany, the most dominant tree species in the vernal pool area was Acer saccharinum, followed by Fraxinus pennsylvanica, while Fagus grandifolia was the most abundant species.

There seems to be a distinction between the terms dominance and abundance in the context of ecology. I've read some of the wikipedia articles on them, but I can't seem to find the difference in their meanings. They seem to both deal with the frequency that a species is in a population.

Any help is greatly appreciated.

There is a difference between dominance and abundance in vegetation science, and your citation is about vegetation.

Abundance is the relative representation of a species in a particular ecosystem. It is usually measured as the number of individuals found per sample.

Ecological dominance is the degree to which a taxon is more numerous than its competitors in an ecological community, or makes up more of the biomass.

In vegetation science, abundance is usually measured as the number of individuals or the percentage of coverage of that species in a plot. An abundant species would typically have a lot of individuals in the plot. A dominant species dominates the other species, so typically covers more than 50% (up to 100%) of the plot. Doing this, it also takes away space (and light!) for other plants.
Usually abundant species also cover a lot, but small species (for example grasses) can be abundant without becoming dominant while large species (like trees) can be dominant with relatively few individuals.


Can the human body create glucose out of fat? I read conflicting views about whether or not the human body can create glucose out of fat. Can it?

Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.

This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).

The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)

So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.

Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).


Does the magnitude of gene-expression changes decrease the more downstream a gene is from the origin of change? If I have a decrease or increase in expression in one gene, will the decrease/increase in expression in the downstream genes always be of a magnitude lower than the previous ones, or can they be higher?
I’m thinking in terms of signal propagation in a network. If I, for example, knockdown gene $X$ to 40% of its basal level, and it influences genes $Y$ and $Z$ in the following manner:
$$X → Y → Z,$$
Will I expect genes $Y$ and $Z$ to suffer lower decreases/increases than the previous gene, for example:
$$X: 40\% ~⇒~ Y: 60\% ~⇒~ Z: 80\%$$
Or could I have a scenario where a small change in one gene’s expression can lead to higher magnitude changes in downstream ones, for example:
$$X: 40\% ~⇒~ Y: 20\% ~⇒~ Z: 10\%$$
I suppose that in some networks the signal will always decrease in magnitude the farther it is from the source, but I’m wondering if, in a biological network, that will also happen and consistently in each step. I read papers with knockdowns all the time, but I never stopped to analyse if knockdowns always create lower magnitude changes in downstream genes or not. So I was wondering if this intuitive notion holds empirically or not.

Gene expression can be very well described by Hill functions, i.e.:
$$c_Y(c_X) = \frac{c_X^n}{1+c_X^n}$$
when $X$ activates $Y$ and
$$c_Y(c_X) = \frac{1}{1+c_X^n}$$
when $X$ represses $Y$ (omitting units and all sorts of constants for simplicity). For the common case that $n>1$, these functions look like this:

As you can see, they are far from linear, but sigmoids. For $n→∞$, these become perfect step functions.
As a result, gene regulation mostly works like a switch:
As long as you are not close to the critical concentration ($1$ in the above example), changes in the regulator have a less than proportional effect.
For instance in the above example, it doesn’t matter whether the concentration of your activator is $2$ or $10$, the protein production is pretty much $1$.
Therefore, “signals” in gene-regulation networks get stabilised instead of diluted.
There are also some other self-regulation effects contributing to this such as genes that self-regulate, the availability of amino acids, and the limits of the translation apparatus.
Note that without these sigmoidal relationships, you would also have big influences of the inevitable fluctuations of the regulator.
As a result, it would be impossible to keep the metabolism in some stable state – the only stable state in a linear system is death.
Simply put, you would have to keep a very precise and regular diet, lest your body stops working.


Population Genetics Using WGS: How do I know when I have enough individuals? I am having a difficult time finding information about a minimum threshold for number of individuals to use in wgs pop gen analyses. Are there software or formulas/theory available to determine what number total number of haplotypes/individuals you need to get theta estimates, make a linkage map, run mk tests etc based on inputs such as genome size, read depth per individual, sequencing platform? Obviously there can be financial constraints and considerations to make for non-model organisms when choosing how many individuals to sequence. Any advice would be appreciated. Thanks!

I think that many of the applications that you mention require wildly different numbers of individuals. It would help to know more about goals, questions, organism details, etc.
For example, for simple population statistic estimates, you can depend on the large number of sites in the genome to get an accurate estimates (such as Watterson) from a single individual, if you are working in a diploid organism, as you can use heterozygosity. See the first Neandertal genome paper for what you can do with one single not very good sequence.
For applications such as linkage maps, you will need a rather larger number of individuals, as you need to sample a large number of recombinations. However, "large" is relative, as a centimorgan-level resolution of the human genome was achieved with a mere 110 humans and ~6000 loci. For finer linkage analysis you may need more individuals; however, with WGS your loci will be much less limited.
For McDonald-Kreitman tests or such-like, it is possibly more important to have more individuals. But you don't need WGS of every individual, in principle you could just find the gene(s) of interest and Sanger it for every individual, which is in most cases still much cheaper.
Obviously each of these has its own power and precision added by more samples, more could be said of each. General resources can be found here and here and here and here, in case it is helpful.


How many nucleotides are there in the LMO1? Dr Maris at CHOP has linked the cause of high-risk neuroblastoma to a common SNP in  LMO1. How many nucleotides are there in the LMO1 gene?

1274bp

http://www.ncbi.nlm.nih.gov/nuccore/NM_002315.1

If you need to know gene size and are confused w search results, search for gene name + "cDNA"


What does "nesting failure" mean? According to the Wikipedia article on swans, swans are mostly monogamous but may sometimes separate, particularly after a "nesting failure". What "nesting failure" may mean is not entirely clear to me. Does it mean that they they have literally failed to build a physical nest? Or is it that they have failed to produce offspring? Or is it something else entirely?

Actually, nesting failure means that nesting trial fail before offspring could even leave the nest. In case of precocial species (where chicks leave nest immediately after hatching, like swans) it means that eggs was destroyed or parents abandoned nest, as @nico point out. In case of altricial birds (offspring stay in nest) nesting failure may also mean that all nestlings died before leaving nest.

for example among House wrens (Belles-Isles & Picman 1986):

  About 81%
  of nesting failures (n = 30) were due to predation (contents disappeared before the expected fledgingdate). Females abandoned seven nests, and starvation (presumably because
  of desertion by parents) accounted for one nesting failure.


List of Asymmetric Animals The (male) Fiddler Crab is a famous example of an animal whose morphology exhibits neither mirror nor radial symmetry:

(Image source)

List of animals featuring external asymmetry is a Wikipedia article showcasing a few more animals with this property.

Is there a comprehensive list of all such animals that have been described?

1) Pareas iwasakii has asymmetric mandibles.  A few more examples of asymmetric snakes (reference)

Pareas iwasakii skull

2) Camels have an asymmetric penis (reference)

3) You could find quite a few in this article titled Animal asymmetry

Hope that helps. I am sure there are more but these are some I could find.


How do t-lymphocytes become mature if thymus has lost its function? The development of t-lymphocytes are done by thymus and we also know that the thymus degenerates before puberty and we also know the maximum lifespan of WBC's is 15 days. So, how do t-lymphocytes become mature if thymus has lost his function?

A few points, I'll expand on this later and add references if I have time:

The thymus starts degenerating at puberty but continues to function in thymocyte maturation for decades, albeit at a lower level
Many mature T cells can live for years
Through homeostatic proliferation, peripheral T cells maintain their population size
Immune surveillance generally decreases with age

Note that extended lifespans and homeostatic proliferation (points 2 and 3) don't contribute to TCR diversity but only maintain the existing repertoire.


What can be the reason for yellow and dark marks on leaves? The plant in our office started to have this strange marks, what can be the reason for that kind of marks? how can we cure the lovely plant?

Yellow leaf spots have various shapes, depending on the cause. Downy mildew starts with angular pale yellow spots. In cucumbers (Cucumis sativus) and other cucurbits, powdery mildew causes pale yellow spots followed by powdery white patches.

The location of the yellow spots may help you determine the cause of the symptom. Some diseases, such as powdery mildew, cause spots on older leaves first and then spread to younger leaves. Yellow spots from powdery mildew can occur on upper and lower leaf surfaces. Downy mildew spots occur on the upper sides of leaves between leaf veins that give the spots their angular shape.

Now lets jump into the causes :-

  1 -Moisture Stress

Over-watering or under-watering are the most common culprits when a plant's leaves turn yellow.
If plants don't receive enough water, they drop leaves to prevent transpiration (essentially, a plant's way of sweating) and conserve water. Before they drop, though, the leaves will typically turn yellow.
Too much water can be just as damaging to leaves. When the soil doesn't drain well, an overdose of water leaves the soil waterlogged and root systems can literally drown. Without oxygen, roots start to die.

  2-Normal Aging

As many plants age, the lower leaves will turn yellow and drop off.

However, to solve this case, don't worry. If the plant becomes too leggy, consider trimming back the main stem to promote new growth and bushiness.

  3-Cold Draft

Now let's first understand what a cold draft is. A cold draft is a current of cold air being drawn indoors.

A plant sitting near it is giving off more heat than it receives from the room. Remember, heat travels from places of higher temperature to places of lower temperature.Cold drafts on tropical plants will often cause the leaves to turn yellow and drop.

To solve this problem, particularly If your plant is near an air-conditioner vent in summer or a drafty window in winter, move it to a less turbulent place.It's also a good idea to mist tropicals that you're overwintering to increase the humidity.

  4- Lack of Light

A plant that is yellowing from a lack of light will typically yellow on the side that is away from the light source.

To solve this, move the plant to a sunnier location and see how it does. If window light is tough to come by in your home—especially in winter—you might need to rig up an artificial plant light or two.

  5- Nutrient Deficiency

This can be caused by too much calcium in the water if you're using hard water, or by a nitrogen deficiency.If this is the problem, the plant's top leaves may be the first to go yellow.

However to solve this issue, since it is species specific, its important to diagnose the problem firstly and them take some remedies.

  6-Viral Infection

If your plant has a viral infection, it might show up as blotchy, spreading yellow patches on leaves throughout the plant. This may be accompanied by deformed leaves and stems, as well as discolored flowers.

To solve this , discard any plants that you suspect are infected since viral infections can not be treated.

  7- Fungal infection

If caused by a fungus, there is nearly always fungus growth of some type in the spot, particularly in damp weather. This fungus growth may be tiny pimple-like structures, often black in color, or a moldy growth of spores.

To solve this, you can use sulphur(in dust form) and milk.

Sources - https://www.thespruce.com/reasons-for-yellow-leaves-on-houseplants-4150680
https://www.hunker.com/12140067/how-to-diagnose-cause-of-yellow-spots-on-leaves
www.uky.edu/Ag/PAT/cat1/leafdis.htm


What is the Shine–Dalgarno sequence? I am trying to understand the Shine–Dalgarno sequence. I currently know it is related to ribosomal binding sites, it is only found in prokaryote cells and it is in front of the initial codon. Also, how do you recognize a Shine-Dalgarno sequence?

According to this Wikipedia article:

  "The Shine-Dalgarno (SD) sequence is a ribosomal binding site in
  bacterial and archaeal messenger RNA, generally located around 8 bases
  upstream of the start codon AUG.1 The RNA sequence helps recruit the
  ribosome to the messenger RNA (mRNA) to initiate protein synthesis by
  aligning the ribosome with the start codon.

  The Shine-Dalgarno sequence exists both in bacteria and archaea. It is
  also present in some chloroplast and mitochondrial transcripts. The
  six-base consensus sequence is AGGAGG; in Escherichia coli, for
  example, the sequence is AGGAGGU..."

I hope this gives the insight that you needed.


Solitary wasp larval behavior Once placed in proximity to its future meal, how long does it take for the larva of a solitary parasitic wasp to begin feeding? I have several books on wasp behavior, but none address the time involved. An internet search also proved fruitless. I am asking out of curiosity and also to ensure accuracy in a story I am working on. I am sure it varies, I am just trying to get a general idea. For example, is it possible for larvae to begin feeding as soon as they are deposited?
(Edit: I added details to this question thanks to the first answer I received on this question)
(Edit: I've spent some more time looking into this and thought I'd share some information, should anyone be interested. Indeed, larvae can begin feeding within two days of being deposited. The larvae of Cicada-Killer Wasp (Sphecius speciosus), for example, begins feeding in 2 to 3 days, according to "The Strange Lives of Familiar Insects" by Edwin Way Teale. In "The Hunting Wasp" by John Crompton, the introduction sets a general range of 2 to 3 days, although I have read online of some wasp larvae taking longer.)

It depends on species and situation.
There are a lot of different solitary wasps, the kind you are referring to are parasitic wasps, that lay their eggs in or on a host for the larvae to feed on before they pupate to reach the final stage of their lifetime.
Some larvae that consume a host in groups take as little as twelve days to consume their host and eat their way out.
However, this wasp species can even have their larvae remain in the larval stage through winter and adapt through seasons. it's entirely dependent on what sort of wasp you're asking for what the time span would be for a larva to mature.


What genes are required to make E. coli photosynthetic? "All" of the genes for bacterial photosynthesis were discovered in a gene cluster almost 40 years ago. Marrs, J.Bact.  What more is needed to make E. coli photosynthetic?

I think the crux of the answer is only hinted at in WYSIWYG's answer. The crux of photosynthesis is partitioning coupled reactions.

Photosynthesizing plant cells have sub-cellular structures called chloroplasts; their membranes are especially important for the compartmentalization of different functions and chemical processes for the entirety of photosynthesis to even be possible. Partitioning is difficult to achieve in E. coli, and that to me seems a necessity for achieving true heterologous, truly ectopic photosynthesis... Even photosynthesizing cyanobacteria (photosynthesizing prokaryotes) possess thylakoids, membrane-bound compartments where the magic happens. Photosynthesis though can certainly proceed and be made more efficient in single cells (example).
That leaves us with a simple answer: engineering E. coli with thylakoid-like structures is not really practicable. Why not simple use cyanobacteria instead?
Further reading: review on single cell photosynthesis in single cells.


How can you develop a bacterial infection when taking antibiotics for another area of the body with a bacterial infection? How can you develop a bacterial infection when taking antibiotics for another area?
For example, "if someone was prescribed an antibiotic for a bacterial infection of the throat and while taking the antibiotic tablets they developed a bacterial infection in their toe.  Explain why the antibiotics taken for the throat did not prevent the growth of the bacteria in the toe".
Is it because the bacteria in the toe is a different type and didn't respond to the bacteria developing the toe (don't think so, but not sure), or
was It because antibiotics don't prevent the development of bacteria they only inhibit it once grown and kill it, or
something else?

Your first assumption is mostly correct

  Bacteria in the toe is a different type and didn't respond to the
  [antibiotic taken for the throat infection].

the reason being because it outlines some essential characteristics of "antibiotics" and antimicrobial drugs in general.

Selective Toxicity and Mode of Action

A very important characteristic of an antibiotic is its selective toxicity. An ideal antibiotic has a high level of selective toxicity meaning that it will only target the bacteria that is causing an infection while not damaging the host tissue (cells) and the person's biota (resident microorganisms). This characteristic generalizes antibiotics into two categories; broad-spectrum (low selectiveness) and narrow-spectrum (high selectiveness). For example, a broad-spectrum antibiotic will target both gram-positive and gram-negative bacteria while a narrow-spectrum antibiotic will either target gram-positive or gram-negative not both.

Another characteristic of an antibiotic is its mode of action or in other words the area of a bacterium that it targets to inhibit/kill it. Most commonly antibiotics target one or more of the following areas/processes:

Cell wall synthesis,
Cell membrane function,
Protein synthesis, and
Nucleic acid synthesis

It is important to know this because mode of action goes hand in hand with selective toxicity, for example an antibiotic that targets membrane function might prove ineffective against bacteria that form capsules another themselves.

So to answer your question

  why [did] the antibiotics taken for the throat not prevent the growth of
  the bacteria in the toe?

We can reason that the selective toxicity of the antibiotic taken for the throat was narrow or that its mode of action only targets the bacteria causing the throat infection but not the bacteria causing the toe infection.


Hundreds of Red Spiders in Individual Webs I live in the USA in south Louisiana. I woke up this morning to find my yard covered in hundreds of spider webs.

Each of those little white puffs is a spider web. Inside of each web is one little red spider.

The spiders are pretty small. Less than half an inch long.

Anyone know what they are?

It is a black-tailed red sheetweaver, Florinda coccinea.

Identified by its red body colour , location (USA) and black caudal
tubercle.

More images to be found on bugguide.net

  It is a species of web-building spider belonging to the family Linyphiidae. It is the only species in the genus Florinda. It is sometimes known as the red grass spider. This species is common in the southeastern United States, inhabiting grasslands, lawns, and agricultural fields.

Reference: Wikipedia


What are garlic's effects on DHT? Most antiandrogens inhibit DHT. DHT is connected to testosterone. [1] shows a beneficial effect on prostate cancer which can be caused by DHT. However, according to [2] garlic also increases testosterone.

What are the effects of garlic on Dihydrotestosterone (DHT) or 5α-dihydrotestosterone? Can it be used as an antiandrogen?

[1] Hsing AW, Chokkalingam AP, Gao YT, et al. Allium vegetables and risk of prostate cancer: A population-based study. Journal of the National Cancer Institute 2002; 94(21):1648–1651.

[2] Oi, Y; Imafuku, M; Shishido, C; Kominato, Y; Nishimura, S; Iwai, K (Aug 2001). "Garlic supplementation increases testicular testosterone and decreases plasma corticosterone in rats fed a high protein diet". The Journal of nutrition 131 (8): 2150–6.

Garlic may affect testosterone metabolism. Its beneficial effect on prostate cancer is not attributed to this, but it is attributed to the direct effect on prostate cancer cells.

What is garlic's connection to DHT?

Cytochrome P450 enzymes. Diallylsulfide, a constituent of garlic, suppresses oxidative demethylation by competitively inhibiting cytochrome P450 2E1, an enzyme that activates carcinogens. Since testosterone metabolism occurs through the mixed function oxidase cytochrome P450 system, garlic may affect the rates of metabolism of testosterone and dihydrotestosterone. The metabolism of testosterone is catalized by inducible P450 1A1, 1A2, 3A3, 3A4 and 3A5 enzymes. These mixed function oxidases can be modulated by a wide variety of environmental facts and dietary constituents. Little is known about the potential for modifying testosterone risk or its treatment modality by administration of garlic constituents [1].

S-allylcysteine (SAC), a potent compound derived from garlic, suppressed the proliferation of PC-3 cells and led to cell cycle arrest at the G0/G1 phases, as well as induced cell apoptosis, which was accompanied by the decreased expression of Bcl-2 and increased expression of Bax and caspase 8. This demonstrates the chemopreventive activity of SAC in vitro, and that SAC may be a promising candidate for prostate cancer treatment [2, 4].
Diallyl disulfide (DADS) is another major component of an oil-soluble allyl sulfide garlic (Allium sativum) derivative. Inhibitory effects of DADS on prostate carcinoma LNCaP cells motility and invasiveness were found to be associated with increased tightness of the tight junctions (TJ), which was demonstrated by an increase in transepithelial electrical resistance (TER) [3, 4].

References:

Paul A. LaChance. Nutraceuticals: Designer Foods III: Garlic, Soy and Licorice. John Wiley & Sons, 2008. Pages 177-180.

Liu Z, Li M, Chen K, Yang J, Chen R, Wang T, Liu J, Yang W, Ye Z. S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells. Mol Med Rep. 2012 Feb;5(2):439-43. doi: 10.3892/mmr.2011.658. PubMed PMID: 22052207.

Shin DY, Kim GY, Kim JI, Yoon MK, Kwon TK, Lee SJ, Choi YW, Kang HS, Yoo YH, Choi YH. Anti-invasive activity of diallyl disulfide through tightening of tight junctions and inhibition of matrix metalloproteinase activities in LNCaP prostate cancer cells. Toxicol In Vitro. 2010 Sep;24(6):1569-76. doi: 10.1016/j.tiv.2010.06.014. PubMed PMID: 20600798.

Bhandari P. Dietary botanicals for chemoprevention of prostate cancer. J Tradit Complement Med. 2014 Apr;4(2):75-6. doi: 10.4103/2225-4110.130371. PubMed PMID: 24860728.


Genome Project Focusing on gene ADRB2? I am not sure which project database to use UCSC or Ensembl for my asthma study about ADRB2 gene (Arg/Arg-16 genotype).

I am using the original Human Genome Project database at the moment.
However, I think Ensembl may be better suited for me.

Which genome database is good for Asthma research for Single Nucleotide Polymorphism (SNP variations)?
I am looking for something which has existing visualisation tools or one where you can easily write one yourself.

If you are looking for variations in a gene, there are a few databases you an consult.

You can of course use the usual genome browsers, search for your gene and then select the variations listed. For ADRB2 this looks like this on Ensembl. If you plan to retrieve and compare data from different genomes/genes, I really recommend learning how to use Biomart, as this is a very powerful tool.

Then you can use specific databases or search engines, which only target SNP's. Examples would be: DBSnp and SPSmart (which queries different databases).


Why do humans have only two nipples? If other animals have more than 2 nipples, then why do humans have only 2 nipples?

Even my pet dog has more than 2 nipples.

Questions of the type, "why does organism X have feature A?" invite teleological (just so) explanations which are difficult to substantiate. For example, the number of teats on a cow are difficult to explain in terms of providing milk to humans!

We should look to evolutionary history to explain human traits, not "just so" stories. The simple answer is that humans are primates, and primates have similar bodies and lifestyles. If there's a single pressure that lead to the number of teats in primates, it's likely the arboreal niche, not the mean litter size. Indeed, litter size is usually a plastic trait, even in primates, and is certainly not an accurate predictor of the number of teats.

There are no strict restrictions on nipple numbers in humans; they can occur anywhere on the milk line. So humans tend to have two nipples because that's what primates tend to have, because of our evolutionary history.

A better answer than this one would locate a candidate common ancestor to the primate and non-primate lineages and make reference to the embryonic development of the mammary tissue.


ID flying insect found in Belgium I live in Belgium, and I've just witnessed a weird looking wasp/fly flying around in my room. Here's a picture:

So, what's this? It's still in my room, just chilling there. It zooms like a wasp, and flies VERY FAST. You can see white vertical stripes on his upper body, and then golden vertical patches. I couldn't get the camera to focus, so it's not really full-hd.

[Edit (better picture)]

This is a hoverfly! Specifically in the genus Helophilus.  A lot of species of hoverflies exhibit Batesian mimicry of wasps/bees, as we see here, while they mainly feed on pollen and nectar.  So please, don't worry about it trying to bite you.

As far as species go, I think it is probably a Helophilus trivittatus.  I am basing that on location and a lot on the banding patterns on the thorax as well as the markings on the prominent terga.  Here is a picture below for you to compare.


To which negatively charged components of the cell envelopes do the crystal violet complexes bind in gram staining? The gram positive have negative components in the peptidoglycan layer in the form of teichoic acid phosphodiester bonds, and the gram negative have negative components in their outer membrane in the form of lipopolysaccharide. Is that where the crystal violet binds?

The gram staining relies on the differences in the bacterial membranes. The gram positive bacteria have a thick peptidoglycan layer on top of the cell membrane, the gram negative bacteria have a lipid layer on the outside followed by a thin peptidoglycan layer and then the cell membrane. See the image for clarification (from here):

Crytall violet dissociates into a positively charged dye molecule (CV+) and chloride (Cl-). The CV+ travels between the membrane layers (outer and inner membrane) and is trapped there by the addition of iodine. This is used to form large crytal violet-iodine complexes which are retained during the destaining process.

In the destaining process, the peptidoglycan layer of gram positive bacteria is dehydrated and therefore shrinks which prevents the staining from being washed out. In the gram negative bacteria, the outer lipid layer is removed and the peptidoglycan layer (which is much thinner) exposed which allows the removal of the stain. The teichoic acid is important for the rigidity of the membrane but not for the binding itself.

References:

Gram staining
The Gram Stain after More than a Century
Use of the Gram stain in microbiology


Why might food spoil faster in Ireland than the US? An American is staying in my house for the summer and claims that food (specifically, bread and milk) spoils a lot faster here than at home in California. Is there a significant difference in chemical content (preservatives etc.), or other factors, that might explain this?

I would think added preservatives are the most likely candidate, for example, Azodicarbonamide is frequently added to bread in the US, but banned in Ireland and most of the rest of the EU. Since it has a preservative effect it is a reasonable candidate for a specific causal factor.

But as Keegan points out there are an awful lot of possible factors so it's impossible for us to say with any certainty.


Nomenclature of substrates for DNA synthesis I have read in my school textbooks that both deoxyribonucleoside triphosphate and deoxynucleotide triphosphate are used in DNA Replication as substrates.
However, it is unclear to me whether the terms refer to the same molecule as one uses the term nucleotide and the other uses nucleoside. What confuses me is that nucleoside is a compound with a purine or pyrimidine base and a sugar and a nucleotide is the same but with the inclusion of a phosphate group.
Is it possible that the “deoxynucleotide triphosphate“ is used in artificial DNA replication as in PCR, and “deoxyribonucleoside triphosphate“ is the natural substrate for the replication of DNA within cells?

Summary
The systematic chemical names of many important biological molecules are too long to write routinely in full, and in any case were preceded historically by abbreviated forms which generally stressed the distinguishing features of importance to those studying their metabolism. Thus, as the poster points out, a molecule such as dATP (image below) has a base-(deoxy)sugar-phosphate(s) structure, and can be termed a deoxynucleotide. Adding triphosphate provides the additional information that there is more than one phosphate. A base-sugar(deoxyribose) combination is, as the poster states, a deoxynucleoside, but by extending this name to deoxyribonucleoside triphosphate, one indicates the addition of phosphates, so that one is, by definition, describing a deoxynucleotide. The reference to ribonucleoside indicates that the sugar is ribose, a specification lacking from the other definition. However, in practice these two terms are used to describe the same entity, one which might a little more completely describe as 2′-deoxyribonucleoside triphosphate (to indicate the position of the reductive change). This answer attempts to explain with precision the aspects of the nomenclature that are likely to be important to the biochemist or molecular biologist.
Disclaimer
The original question might be considered not to represent a biological problem, and one might argue for closing it on that account. However because of the very nature of trivial nomenclature, it is difficult for those without experience of the usage in a field to find the answer. In answering it I have tried to broaden the scope to include the aspects of structure that I feel are most likely to be to biological students.
Answer
It is convenient to start with ribonucleoside triphosphates (rather a deoxy- ribonucleoside triphosphates), and I have chosen a specific example in the molecule that is generally known as ATP:

Alternative names for this ribonucleoside triphosphate, in decreasing order of complexity, include:

[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methoxy-hydroxyphosphoryl] phosphono hydrogen phosphate
9-β-D-ribofuranosyl adenine 5′-triphosphate
adenosine 5′-triphosphate
adenosine triphosphate
ATP

Of interest to us are the three components of the molecule: a purine base (adenine), a sugar (ribose), and three linked phosphates. This is not reflected in the chemical nomenclature (1), so let us focus on the, albeit rarely used, biochemical nomenclature (2).

The ‘9’ specifies the position of the adenine ring that is linked to the sugar. This is not of particular interest in the context of the question.  (The numbering of the ring is, however, relevant to describing differences between or modifications  of the purine and pyrimidine bases1.)
The D-ribofuranosyl is a form of ribose (see below). The ‘D’ indicates that it is D-ribose enantiomer rather than the alternative, L-ribose. However, as all natural sugars are ‘D’ this is generally omitted (although discussions of why all natural sugars are ‘D’ abound2).
Ribofuranosyl indicates that the ribose is in the five-membered hemiacetal ring form (rather than the straight chain or the six-membered pyranose ring), but this is always the case in nucleosides, and so is not of particular interest.
The 5′ specifies the position of the sugar ring to which the phosphates are attached, the prime (′) indicating that the numbering is for the sugar ring (not that of the base). This is important, as it is relevant to the linkage in the (asymmetric) phosphodiester bond made to the 3′-OH:

The image above is for DNA, but before addressing the nomenclature there, we would point out:

The common α, β, γ designation of the three bond phospho-ester bonds. This is very relevant to the formation of polynucleotides (DNA and RNA) from their substrates, and in general to the utilization of the free energy the hydrolysis of these bonds for other processes3.

Finally we come to a structure of interest to the poster, dATP:

In the designation, 2′-deoxyadenosine 5′-triphosphate, the 2′-deoxy indicates that it is the 2 position in the ribose ring (′) that has had the oxygen removed (deoxy), i.e. OH is reduced to H. Although common knowledge, it is important that the student new to the subject understands this, as if it were the 3′ position that was reduced, it could not form the phosphodiester bonds of DNA. And it is relevant in many other contexts. For example the chain-termination method of DNA sequencing uses 2′,3′-dideoxy nucleotides to inhibit such bonds forming4, the single difference between ribose and deoxyribose allows us to understand the profound affect on the susceptibility of RNA to alkaline hydrolysis in nature5, and certain RNA molecules are hydroxy-methylated at this position.

Related information in SE Biology answers
1 Topical example related to base modification
2 Speculation on the origin of biological homochirality — not SE Biology
3 Why does ATP sometimes produce ADP and sometimes AMP?
4 Sanger sequencing by chain termination
5 Difference in stability of DNA and RNA


Is this black locust? This grows in Modiin, Israel. The leaves look like black locust (Pseudoacacia robinia) to me, but the branches are very knobby. Can anyone identify it?

Although the photos are less than ideal, and I can't see any flowers or fruit, I can clearly see that the leaves are "evenly pinnate" and rounded distally (not pointed). The wood structure also looks bumpy.  Given Israel as the neighborhood, it is likely to be a carob tree (Ceratonia siliqua) which is native to the Mediterranean region.  This tree is sometimes mistakenly called a "locust" tree.  See Links below.

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

http://tree-species.blogspot.com/2008/04/carob-tree-ceratonia-siliqua.html


Do both Carbamazepinum and Lamotriginum increase glutamate threshold? I have in my notes that:

Carbamazepinum increases threshold for glutamate
Lamotriginum delays release of glutamic acid

I would like to simplify these sentences into a single line. I would like to know if it would be correct to say the following:

both Carbamazepinum and Lamotriginum increase glutamate threshold?
"both affect glutamate function" should at least be correct

Do both Carbamazepinum and Lamotriginum increase glutamate threshold?

Characterizing those drugs.

A = group, B = mechanism of action and C = indications.

Carbamazepinum
A. Anticonvulsant, antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line of Epilepsy grand mall seizures, bipolar disorder, trigeminal neuralgia.
Lamotriginum
A. Unique antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line Epilepsy - generalized, partial and absence - all types. Bipolar disorder - depression stage. Neuropathy.

Short answer
Both carbamazepine and lamotrigine are listed as Na+ channel blockers. Carbamezipine's action is mainly associated with inhibition of postsynaptic neural activity, while lamotrigine is thought to inhibit glutamate release. Given that glutamate is the principal excitatory neurotransmitter in the brain, and if you insist of using a one-liner I would go for:

  Both lamotrigin and carbamazepine can be said to inhibit glutatamatergic neurotransmission, albeit carbamezipine does so in a non-specific way.

Background
My two most beloved drugs in one question!

First off, this answer is formulated from the perspective of both drugs being used as anticonvulsants in generalized tonic-clonic epilepsies. As anti-epileptics, Both lamotrigine (Lamictal) and carbamezipine (Tegretol) are listed as Na+-channel blockers.

Carbamezipine does so quite specifically, and it inhibits sustained repetitive firing by blocking sodium channels. It does so in a very clever way, as it only binds to Na+-channels of rapidly firing neurons, which is exactly what makes it a good anti-convulsant (Courtney & Etter, 1983). It also is believed to have anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties (Drug bank). Hence, your note that it increases the threshold for glutamate is true in the sense that it is likely to increase the firing threshold of glutamate-activated neurons.

However, note that carbamezipine (nor lamotrigine) does not increase the threshold for glutamate - glutamate has no threshold and hence it cannot be raised. It is incorrect word use.

Lamotrigine is also listed as a Na+-channel blocker, but the exact mechanism(s) behind its anti-convulsive and mood-stabilizing effects are unknown. In vitro pharmacological studies suggest that lamotrigine's inhibiting effects on voltage-sensitive Na+ and/or Ca2+ channels stabilizes neuronal membranes and consequently modulates presynaptic transmitter release of excitatory amino acids (e.g., glutamate and aspartate). It has also been shown to enhance K+ currents and GABA-ergic inhibition (Coulter, 1997). Hence, your note that it decreases glutamate release is correct.

References
Coulter, J Child Neurol (1997); 12: S2-9
Courtney & Etter, Eur J Pharmac (1983); 88: 1-9.


Can organisms like Noctiluca be commercially exploited? Scientists think that Noctiluca flashes to startle or scare away its predators. The bioluminescence might also attract bigger predators to eat Noctiluca’s predators, just like a burglar alarm that alerts the police to come to someone’s house to catch a robber.
 It takes energy to make the chemicals that allow them to glow. It would be a waste of that energy to glow during the daytime
But the question is whether we can commercially exploit this for human welfare??

Well, scientists have been developing Bioluminescent Plants to use as a future road light source. Also, there is a way that Bioluminecent algae can be used as medicine.


Vectors for genetic engineering Well can a bacterium be used as a vector?I have learnt that Agrobacterium tumifacian can be used to deliver a gene of interest in plant cells but on a book in a multiple choice question it says that only plasmid and bacteriophage can be used and not the bacteria to deliver a gene of interest to a host cell.

Yes, Agrobacterium is indeed a very widely used vector in plants. So it wouldn't be wrong to consider bacteria as vectors. Just to add, it's worth noting that in recent times, bacterial vector options have been explored in the case of humans also, especially in the case of gene therapy for cancer treatment, though its success hasn't been demonstrated yet. Refer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056088/ for more information on this.

To conclude, bacteria can be considered as a vector undoubtedly.


Does a neuron ever generate an action potential without stimuli? Most accounts I read involving action potentials and synapses and the like tend to focus mostly on the action potential as a mere automatic reaction to another similar event happening upstream.

From a more theoretical point of view, it would be nice to know if (and under what circumstances) a neuron would be able to generate an action potential, in the absence of an upstream neuron firing first.

I suspect that the nervous system, at least in higher animals, is not simply a relay system that processes and transmits information from senses to actuators like the limbs. The relay system picture is fine for short-timescale, reactionary behavior but it is hard to imagine any longer-timescale learning processes happening this way. This is what motivates my question.

Neurones fire when they're sufficiently depolarised past their threshold. In the sensory system this is in response to an external stimuli which sets of a chain reaction. Then motor neurones may relay signals back and in this case the signal or initial depolarisation is occurring in the brain. However this is still caused by a stimuli even if indirectly. If we take an action it is generally because we thought which action we should take because of some sort of stimuli e.g. we are cold so we put a coat on.

But anything which depolarises neurones can set of an action potential. However there's always something which causes it to depolarise, perhaps a drug or a stimulus or another neurone. If any of these don't count as a stimuli depending on your definition, there's your answer.

Or perhaps if you consider cardiac muscle which can intrinsically depolarise. Not a neurone but there's an action potential. They just naturally depolarise over time and action potentials are set of regularly with no stimulus required.

As for learning, where the structure of neurones can change so they connect to new neurones or not to old neurones or vary in the strength of their connection.


Are there any methods to quantify H2O2 (hydrogen peroxide) which don't rely on horseradish peroxidase? I can't use HRP since my substrates interfere with it and I need a real-time method because I want to measure kinetic parameters of some oxidases.

Amperometric detection of H2O2 can be performed without HRP, and gives high-resolution real-time readings.

You will find many different type of electrodes that are used in the literature to detect H2O2, including for instance MnO2-coated carbon paste microelectrodes or gold electrodes derivatized with cytochrome c.

Commercial electrodes also exists. For instance these from WPI are based on derivatized carbon fibers (although they do not specify with what, so I would not exclude HRP...)

Another option is that of using the H2O2-sensitive dye H2DCF (dihydro-dichlorofluorescein).


What is neuronal computation? Can someone give me a good explanation of what is neuronal computation and some examples of its use in neuroscience investigation?

The term neural computation is basically synonymous with computational neuroscience.  It is the science of studying how the brain processes information by creating realistic mathematical models. Unlike general study of artificial neural networks (ANNs), neural computation heavily relies on biological accurateness. However, it may use models from ANN research, and vice versa.

Also see this course description of the PhD level course "Neural Computation" at Carnegie Mellon University  (CMU) :

  Neural Computation is an area of interdisciplinary study that seeks to
  understand how the brain computes to achieve natural intelligence. It
  seeks to understand the computational principles and mechanisms of
  intelligent behaviors and mental abilities -- such as perception,
  language, motor control, and learning -- by building artificial
  systems and computational models with the same capabilities. This
  course explores how neurons encode and process information, adapt and
  learn, communicate and compute at the individual level as well as at
  the levels of networks and systems. It will cover basic concepts in
  computational and neuronal modeling, information theory and coding,
  neural networks and learning, neural data analysis and decoding,
  signal processing and system analysis, statistical learning and
  probabilistic inference.

(Emphasis mine)


Is there a relationship between Melatonin, Norepinephrine and depression in humans? I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". This particular paragraph caught my attention and I would like to better understand what it means:

  The requirement of intact beta-receptor function for melatonin
  synthesis, and the stimulatory effect of norepinephrine on melatonin
  synthesis and release, point up a theoretic relationship of melatonin
  to depression.

I've been looking at the biosynthesis of norepinephrine  and tryptophan metabolism and do not see how the two cycles are connected. Is there a connection between the norepinephrine system and the melatonin synthesis in humans?

This answer addresses your question about a link between norepinephrine and melatonin, but I have nothing to say about depression.

In vertebrates, the link between norepinephrine (NE) and melatonin lies in the regulation of the melatonin biosynthetic pathway.

Arylalkamine N-acetyltransferase (AANAT) is an enzyme in the biosynthetic pathway for melatonin, and controls the diurnal rhythm of melatonin production in the pineal gland. NE is released as a neurotransmitter by neurons innervating the pineal gland, and which themselves are regulated by the circadian pacemaker of the hypothalamus. One of the effects of NE on the pineal gland is to elevate the transcription of the AANAT gene via adrenoreceptors and cAMP levels.

The paper cited below describes this, and other relevant diurnal rhythms in the viscacha, a rodent of the chinchilla family. This animal was chosen because it has an interesting diurnal behaviour pattern with two apparent peaks in melatonin biosynthesis. It's a good starting point for further research into the literature on this topic.

  Calderon,C et al. (2008) Daily rhythms of norepinephrine, β1-adrenoceptor mRNA, serotonin, arylalkylamine N-acetyltransferase mRNA, arylalkylamine N-acetyltransferase and hydroxyindol-O-methyltransferase activities, and melatonin in the pineal gland of viscacha. Biological Rhythm Research 39: 93-107


What does the species name 'fistula' mean? Cassia fistula is tree with yellow flowers. As a medical student what amazes me is that the word fistula implies other meanings. A fistula, at least in medical science refers to a tract with two epithelial openings.

The botanic and medical term fistula is directly derived from the latin word fistula meaning tube or pipe.

Both the medical fistula and the fruits of the Cassia fistula tree show phenotypes similar to a tube.

I will spare everyone the medical example picture, but here are the fruit of Cassia fistula, which are sold as "manna":


Are a bonsai tree and its normal version the same species? I would like to know if bonsai type of a tree is a separate species from its normal version. Do they differ by genes, or is it just a matter of different physical care?

Can I grow a bonsai tree from seed of a normal outdoor tree (of course, I understand that not every species will endure being dwarfed)? Can I grow a normal outdoor tree from some seeds labeled "bonsai"?

Yes. For any species that it is possible to grow as a bonsai tree, it is also possible to grow that species as a non-bonsai tree. The process of creating a bonsai tree involves growing a tree in a severely restricted pot with a minimal amount of soil, and trimming both the roots and branches to maintain a desired shape and size. It is the small growing space and regular pruning which keeps bonsai trees small, not the genetics of the tree.

You may wish to check the list of species used in bonsai on Wikipedia to get a sense of which species make good bonsai plants.


Type of plant cell that builds a secondary wall in between two primary walls? I read that there is this type of pattern in cell wall synthesys. What is the type of cell that does that and in what kind of scenario?

Secondary cell walls are found in many plant cells especially ones used in for structural functions, such as the lignified cell walls in xylem such as in wood. This occurs in a mature plant cell, where the cell constructs a second wall between the primary cell wall and the plasma cell membrane, which is made up of strong cross-linked cellulose microfibrils, which are then lignified.

The secondary cell wall adds additional support to the cell, enabling it to carry out effective structural functions in the plant such as transportation of water and mineral ions in xylem from the roots to the leaves.

Occasionally, there is a tertiary cell wall located on the inner side of the secondary cell wall adjacent to the plasma cell membrane. This is usually very thin and is made up mainly of xylan with a small ratio of cellulose (unlike the primary and secondary cell walls which are mainly cellulose). It can be found in the xylem tracheids (usually found in the wood) of gymnosperms (e.g. conifers, ginkos). As for purpose, again, it strengthens the cell even more and sometimes contains nutrients ready to pass through the membrane into the cell.


What is the course of inter auricular line? BACKGROUND: The interauricular line is the line connecting two auricles.

I wish to know the exact route through which this line passes. I want to be sure whether it passes through the parietal prominences, or in front of them.

Up front - I have never heard of this term and I could not find information on the interauricular line. The only thing I was able to dig up was the term auricular line, which is (Fig. 1):

  [The] [l]ine pass[ing] perpendicular to the anthropological baseline,
  through the cent[er] of the external auditory meatus.

Fig. 1. Auricular line. source: Radiology Key

The anthropological line being (Fig. 2):

  [The] [l]ine join[ing] the infraorbital margin to the superior border
  of the external auditory meatus.

Fig. 2. Anthropological line. source: Radiology Key


Can a reservoir host act as a vector? Is it possible to get an infection by contact with a reservoir host ?

Can a reservoir host act as a vector ?

What is the distinction between these two concepts (reservoir host vs vector) ?

A reservoir host most obviously is a long-term carrier organism of a given pathogen that doesn't exhibit the disease caused by the pathogen.

A vector is literally any agent that transfers the pathogen to another organism. If you think about it, a reservoir doesn't have to be a vector i.e. there's no route of transmission they participate in, but a vector can certainly be a reservoir, such as bats, who often act as a vector for the pathogens they house (think Rabies). On the flip side, ticks are common vectors for Lyme disease, but small rodents actually act as the reservoir for B. burgdorferi (1).


What is meant by "Expression" of Non-Coding RNA? I was having a look at lncRNAdb and its help says:

  The ENCODE project gene annotation list, GENCODE, has predicted that the human genome contains 14,470 lncRNAs whereas only a small proportion of these have been shown to have function.

  We have examined thousands of publications in order to find and
  manually annotate lncRNAs that have been shown to be functional by
  overexpression or knockdown experiments.

What is meant by Overexpression of a Non-coding RNA here? Even if you have a look at any lncRNA in the DB, its entry has a column for "Expression":

With many non-coding RNAs, the RNA is the functional endpoint. Therefore, ncRNA "expression" simply refers to the production of that functional component. Similarly to with proteins, this involves looking at differential tissue production of that noncoding RNA (i.e. in which tissues the RNA is produced).

Gene expression is defined in the Oxford Dictionary of Biology as:

  The manifestation of the effects of a gene by the production of the
  particular protein, polypeptide, or type of RNA whose synthesis it
  controls.

In other words, gene expression means the same thing whether the functional product is a protein or a noncoding RNA. Of course, there is no translational component to expression of ncRNA.


Will fruit/seed of a bonsai yield another bonsai plant/tree? With practice one can create a bonsai; no complicated modification of the DNA in a high-end lab required. The bonsai will even beget bonsai fruit.

What I am curious about is - if such bonsai fruit is planted again, will it give rise to a normal, or a bonsai tree?

No, seed from a bonsai tree will not automatically produce another bonsai tree. Bonsai are dwarfed due to restriction of root growth in their small containers - unless the offspring are also grown in environmentally dwarfing conditions, they will tend to grow normally.


Why do we find flowers attractive? Given that we (humans) are not evolutionarily closely related to bees, why do we find flowers attractive?

Sure, flowers can be sign that the fruit is underway as @JonathanMoore said and viewing any trait as a result of selection is probably what the OP was waiting for. Thinking that if an organism produces a behaviour, then this behaviour must have been selected is wrong though.

The reality is that specific behaviours are affected by evolution of other behaviours and other traits as well as an by our environment (incl. social environment). It will be particularly difficult to hypothesize as for the different selection pressures that may have existed on a specific behaviour especially in animals with such high cognition as humans. Maybe we like flowers because we like colour contrast and maybe we like colour contrast because face with stronger colour contrast is more attractive because it is a sign of health. Maybe we like sunset because we like flowers. Maybe we like colour contrast because we like fresh fruits. Maybe, we like complex design because it makes us think about the possible complexity of shapes. Maybe we like complex shapes because we like to explore. Maybe we like simple design because we like clear skins. Maybe we like flowers because of the diversity of shapes. Maybe we like flowers because they are a sign of the end of the cold winter. Maybe we like flowers because we are being told that they are pretty things. Maybe we like flowers because it symbolizes abundance and reproduction. Anyone could formulate loads of hypotheses. Maybe we like flowers because we like any smell that is not the smell of something that is rotting. Maybe we like flowers because we like trees, leaves, mountains, rivers, lakes and pretty much anything else in our natural surrounding. Maybe we like flowers because flowers is a sign that there is not no pests in our garden or simply that the plant we are growing is healthy.


Can HIV be transmitted via mosquitos? It is known that HIV is usually transmitted by direct blood or body fluid contact between an infected individual and a healthy person (like blood transfusion or needle sharing):

Suppose a mosquito bites an individual suffering from AIDS and in the process sucks up some T cells infected with HIV along with RBCs. Then it bites another person not suffering from the disease, and transfers these infected T cells. Isn't there a high probability of the second individual contracting HIV?

No, this is not possible. There are a few reasons for that, but most important are that the only thing a mosquito injects is its own saliva, while the blood is sucked into the stomach where it is digested.

To be able to infect other people HIV would need to be able to leave the gut intact and then also be able to replicate in the mosquitos which it cannot do, due to the missing of the CD4 antigen on the surface of the insect cells. These are needed as a surface receptor for the virus to bind and enter the cells. This is also true for other blood sucking insects like bed bugs or fleas.

Other pathogens can do this, examples would be Yellow fever or Malaria. In Yellow fever the virus first infects epithelial cells of the gut, then enters the blood system of the insect to finally end up in the salivary glands, where the virus is injected together with the saliva into the biten person. In Malaria the pathogen is also able to leave the gut region and mature in the salivary glands.

HIV can only be transmitted through blood (either through direct transmission, operations etc.), through semen (cum), pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, and breast milk. See reference 3.

References:

Why Mosquitoes cannot transmit AIDS
Can we get AIDS from mosquito bites?
HIV Transmission Risk:  A Summary of Evidence


Identify this spider from Bangladesh Location: Jahangirnagar university, Savar, Bangladesh

EDIT: Here is the video from which image is taken

It  is a jumping spider. Could be Genus Epocilla sp. .

Jumping spiders have their posterior lateral eyes placed high up the cephalothorax and the rest three pairs in a typical arrangement as observed in your specimen.

An image of Epocilla sp. from Wikipedia.

Your specimen more closely resembles the E. calcarata .


How is cartilage immunised? How is human cartilage immunised (protected) against pathogens since it does not contain lymphatic vessels?

I also had this relevant problem, when I was learning about cartilage tissue.

Generally, cartilage tissue has no blood supply. But it is a traversable  tissue, therefore nutrients, and breathing gases can enter into the tissue without any problem.

But the problem is how does it immunized while there is not containing of lymphatic cells.

The perichondrium, has a presence  of blood vessels. It pulls/stimulate  the necessaries for enter to the cartlage tissue. That's how, the  tissue get immunized.


Why do Mangoes have a single large seed, and not multiple small ones? I was just thinking about this, wouldn't it make more sense for a mango to have multiple seeds, as it would allow more seed propagation?

It is an interesting question and it applies to other fruits with big seeds as the avocado as well. It is very likely that these fruits evolved to be spread by large animals (like big birds or large mamals) which existed for a relatively long time, but are extinct today. These animals swallowed whole fruits and excreted the seeds afterwards (most of these seeds are slighty laxative) together with dung to support the growth.

They are called "evolutionary anachronisms" and there is a very interesting book about them, called "The ghosts of evolution: nonsensical fruit, missing partners, and other ecological anachronisms." (which can be found as a PDF online)
Two interesting articles about this phenomenon can be found here:

The Trees That Miss The Mammoths
Anachronistic Fruits and the Ghosts Who Haunt Them


Bacterial capsule vs. slime wall I've read that the bacterial capsule protects the bacterium from phagocytes and prevents water (and nutrients, possibly?) leakage from the bacterium.

A less organized and less dense version is called a slime layer. It seems that the slime layer has similar functions, according to Wikipedia.

What are the differences between the effects a capsule and a slime layer bring to a bacterium?

I thought about the followings:

The capsule covers most part of the bacterium, so adhesion proteins and transport proteins on the plasma membrane do not work effectively, whereäs with a slime layer, more proteins on the plasma membrane are exposed to the exterior, making them work more effectively.
Maintenance of the capsule takes more energy than that of the slime layer simply because there are more glycoproteins in the capsule.
Bacteria with capsules are less likely to lyse than those with slime layers.

Is there anything else significant that goes on this list? Or are there any points I made that are not true?

According to the Wikipedia section on bacterial capsules, they're made of the same thing:

  When the amorphous viscid secretion (that makes up the capsule) diffuses into the surrounding medium and remains as a loose undemarcated secretion, it is known as slime layer.

Todar's Online Textbook of Bacteriology synonymizes "slime layer" and "biofilm":

  A true capsule is a discrete detectable layer of polysaccharides deposited outside the cell wall. A less discrete structure or matrix which embeds the cells is a called a slime layer or a biofilm.

This makes sense with what I remember learning about slime walls--the main difference I saw was that the capsule was directly associated with/only protects a single bacterial cell, whereas the slime layer is associated with/protects multiple bacteria. I'm not sure that I'd call it a biofilm though, as those are notoriously difficult to remove; their removal in hospital and food processing sysyems is a current research topic.

Regarding your three points above, I might instead argue that the slime layer provides another layer of protection in addition to the bacterial capsule.


Re-establishment of Hardy Weinberg Equilibrium After Selection I have been given this question:

In a population of 2500 mice, light-colored fur is dominant to dark-colored fur. 2400 mice originally have light-colored fur. However, an owl species moves into their environment, preying mainly upon the light-colored mice as they are easier to spot when hunting at night. When the owls finally leave, 80% of the dark-colored mice are left, and only 10% of the light-colored mice. After many generations, Hardy-Weinberg equilibrium is re-established. Approximately what percentage of mice now have dark-colored fur?

Answer choices are:

A) 10%
B) 15%
C) 20%
D) 25%
E) 30%
F) 35%

My thought process goes as such:
When the owls leave, the groups are 240 light mice and 80 dark mice.
$q^2 + 2pq + p^2 = 1$
q is recessive allele, p is dominant allele.
$0.5^2 + 2*0.5*0.5 + 0.5^2 = 1$
Apply fitness:
$0.8*(0.5^2) + 0.1*(2*0.5*0.5) + 0.1*(0.5^2) = 0.275$
(0.8 and 0.1 correlate to the fitness of dark and light mice, respectively)
Now divide everything by 0.275 to figure out new allele frequencies:
$0.727 + 0.182 + 0.091 = 1$
This means that 0.727 = 73% is the new frequency for homozygous recessive (dark) mice.
However, the correct answer is B) 15%
Any idea what I did wrong/how the correct answer is achieved?

Revised to add complete solution

Before the owls arrive, 100 out of the 2500 mice are dark-colored. This ratio provides the frequency of the recessive allele

$$q^2 = \frac{100}{2500}$$

So $q$ is 10/50 or 0.2. This means that the frequency of the dominant allele $p$ is 1 - 0.2 or 0.8.

Knowing these frequencies, it is possible to calculate the number of each allele

$$AA = (0.8)^2 \times 2500 = 1600$$
$$Aa = 2 (0.8) (0.2) \times 2500 = 800$$
$$aa = (0.2)^2 \times 2500 = 100$$

Of the light-colored mice, 2/3 are AA and 1/3 are Aa. The same proportions hold after the owls leave, but the total humber has been reduced. The dark-colored mice are all aa.

$$AA = \frac{2}{3} \times 240 = 160$$
$$Aa = \frac{1}{3} \times 240 = 80$$
$$aa = 80$$

From these values, the total number of each allele may be calculated

$$A = 2 \times 160 + 80 = 400$$
$$a = 80 + 2 \times 80 = 240$$

These numbers provide the frequency of each allele post-selection

$$p = \frac{400}{640} \approx 0.63$$
$$q = \frac{240}{640} \approx 0.37$$

Applying Hardy Weinberg for the new equilibrium

$$aa \approx (0.37)^2 \approx 0.14 $$

which is, "approximately" 15%.


What are calories and how to burn them? What exactly is a calorie? When burning calories, do we always lose fat?

I have tried many apps to measure calories, do they give exact amounts? How many calories should be taken a day?

A calorie is a measure of energy. In nutrition, we usually mean the kilocalorie (kcal), which is the same as about 4.2 kJ (kilojoule). A average person needs about 2,000--2,500 kcal per day, but this of course varies quite a bit between people, depending on size (muscle mass, particularly) and level of physical activity (physical work, exercise).

Nutrition guidelines found on the labels of food products give a pretty good summary of the amount of energy they contain. I'm not sure what applications you have been using, but they most likely rely on the same basic data, so the values should be similar. You can use these values to figure out roughly what your calorie intake is, and to spot very calorie-rich foods. But counting calories exactly is actually quite difficult --- you need to carefully weigh everything you eat and keep track of lots of numbers, and it's easy to make mistakes.

Burning calories does not always mean burning fat. Fat is a long-term energy storage form in the body. When exercising, the body tends to burn stored carbohydrates (glycogen) first, and turns to burning fat when carbohydrates are exhausted. Therefore, prolonged, low-intensity exercise like long walks are usually better for burning fat than short "sprint" type of exercise. The body also burns fat during normal daily activity if your energy intake is lower than the daily need (when dieting). But it is also possible that some muscle mass is degraded (to amino acids) and used for energy as well.

See also Wikipedia articles on food energy and exercise. Please note that "how to burn calories" is a heavily debated issue, there is an entire industry of weight loss methods, and various claims about "easy" methods or products to lose weight quickly are generally not true. The only reliable method to lose weight is to reduce food intake and increase exercise, for a long period of time.


Is Sanger sequencing still used in labs, and therefore worth learning? If iI were to have access to funds for research, would learning this technique be a boon for me? Or are next-gen sequencing methods all the range now? My knowledge of both are limited.

Sanger sequencing is still used in the labs today - and not only on the side. Next-generation sequencing has its strength when it comes to sequencing very large amounts of DNA (basically whole genomes or exomes).

Sanger sequencing is used when you want to sequence smaller regions or portions of a genome/plasmid. Typical read length is (depeding on the machine and the skills of the operator) 600-900bp. This is enough to verify site directed mutagenesis, the presence of inserts you cloned as well that they are correct (if the insert is longer you will typically nest the single sequence reactions to cover the whole sequence) or look for a polymorphism. There are endless possibilities.

Additionally it is relatively cheap to sequence single samples (which is not really working on the next-gen machines), one sample comes between 8 and 10$ (at least the last time I sent this out). And you don't even have to do it yourself as there are a lot of service providers available. The technique itself is not hard to learn either.