How do plants benefit from their seeds being buried? Common planting advice, when starting many plants from seed, is to bury the seed some small distance under the soil.  It seems like most plants (at least members of class Dicotyledonae) will grow a root, lift the seed casing out above the surface, then the cotyledons push off the seed coat.

My question then is: why is it recommended to put the seeds below ground at all?  It would seem that dirt only serves to interfere with the first stages of growth.

I can guess at a few reasons:

To keep moisture around the seed
To make sure the root hits dirt no matter which way the seed is oriented
To prevent predators from eating the seed
To keep the seed in place

Absent these reasons, is there any reason to have soil sitting on top of a seed?

Excellent question!

The main reason why us humans bury seeds seems to be to keep seed-eaters from finding them, though any historical evidence that could conclusively prove why we started doing that is probably lost to time, since we discovered agriculture before we began writing things down. Beyond that, you've rightly identified a number of advantages to burying seeds.

First, it may be helpful to note that no physical substrate is even necessary for plant nutrition. We can actually grow plants in mid-air, but for the fact that we would still need something to keep them still. Seeds will germinate if you simply spray nutrients at them - see aeroponics. This is because plants take in what would be soil nutrients via cation exchange and diffusion, as opposed to more a more active process like phagocytosis. By surrounding the seed with nutrient rich substrate, we inadvertently improved germination by exposing more of their surface area to nutrients.

As far as soil seeking behavior goes, Thomas Knight demonstrated that plants can actually find the ground by following gravity. He did this by sticking seeds onto a rotating disc to simulate gravity in another direction and germinating them there. The seeds responded by growing roots away from the center and sprouting stalk towards the center.

Of course, burying seeds too deep means that they may run out of energy before they can break the surface. However, it seems that many varieties of seed have a better chance of germinating in darkness.

Resources

On the Direction of the Radicle and Germen during the Vegetation of Seeds
A Reversible Photoreaction Controlling Seed Germination


Is the reason that flies can perceive things faster because their brains are smaller? We know that flies can perceive changes in the world around them up to seven times faster than a human - we appear slow to them.

I'm wondering how this is possible. Is it just that information travelling is limited by the speed of light, and it has a shorter distance to travel across a flies brain? Or is there some metabolic or other biological reason for this?

(It would be great to speed up a human's brain - but I'm sure there are a million reasons why that is not possible).

My question is: Is the reason that flies can perceive things faster because their brains are smaller?

Fly neurons aren't like human neurons. They have different nerves that transport signals faster than human nerves. So they can see your hand moving towards them faster than we can see for ourselves, which makes them able to avoid being squashed (most of the time).


Translation of RNA into proteins What's the least number of tRNA molecules needed to form a polypeptide chain that contain 50 amino acids of 15 types?

  I know that each type of amino acid has at least one unique type of tRNA that recognizes it and transport it, so according to my understanding the 15 types of amino acids need at least 15 tRNA molecules of different types unless there was a reason that prevents one tRNA molecule from transporting two identical amino acids (two alanine) to the same polypeptide chain

•In other words:
Can one tRNA molecule carry two identical amino acids (ex: two alanine) to the same polypeptide chain that's being synthesized or not?

In the basic model of protein synthesis the events involving tRNA and amino acids are as follows (see any standard text, e.g. Lodish et al. section 4.4):

An amino acid is attached to the appropriate tRNA (the one with the anticodon that recognizes a codon for that amino acid) by one of twenty specific amino acyltRNA synthase enzymes in a reaction requiring ATP. This is called charging or aminoacylation of tRNA.
The tRNA corresponding to the mRNA codon is brought to the ribosome by an elongation factor (EF1) and the peptidyl transferase activity of the large ribosomal subunit catalyses the formation of a peptide bond between the growing polypeptide chain* and the amino acid of the tRNA, releasing deacylated tRNA.

I am unclear why you are concerned with this problem, but if there were two alanine codons in the mRNA, in theory after a particular discrete tRNA molecule had inserted the first alanine it could be recharged by the aminoacyl tRNA synthetase and then be used to insert the second alanine. However the concentration of tRNA molecules in the cell needed to support protein synthesis is such that the actual probability of this same discrete molecule being used, rather than another tRNA carrying alanine, is remote.

*A real-life complication is that a polypeptide chain has to be initiated by an initiator methionine-tRNA that is distinct from the methionine-tRNA that inserts internal methionines (see Lewin et al. section 4.5).


Is there any kind of antibiotic effective against fungi? I know that antibiotics usually have properties affecting specifically bacterial cells, like by inhibiting peptidoglycan synthesis. but do any antibiotics exist affecting eukaryotic cells, like yeast or other fungi? I read in a text that "most" eukaryotic cells are resistant against antibiotics and that confused me.

Regardless of whether it can be used against bacteria or not, is there any kind of antibiotic effective against fungi, or any kind of eukaryotic cell?

Yes. The antibiotic (general microorganism “targeter”) you’re looking for is an antifungal. There are fewer ways to target fungi as opposed to bacteria, but we can target them nonetheless.

The fungal cell membrane has ergosterol to regulate its permeability whereas the mammalian cell relies on cholesterol. Fungi have cell walls which are not present in mammalian cells and are different in chemical composition to bacterial cell walls. A fungal cell wall is made of chitin whereas, as you mentioned before, a bacterial cell wall is made up of peptidoglycan.

We rely on these differences to target fungi. Some antifungals bind to ergosterol (e.g. Polyenes like Amphotericin-B) whereas other agents inhibit ergosterol synthesis altogether (e.g. Azoles like Triazole). Other antifungal agents target the fungal cell wall by inhibiting the synthesis of chitin (e.g. Echinocandins like Caspofungin).

There are more ways to target fungi, like introducing nucleotide analogues (“look alikes” that don’t work) to disrupt their nucleic acid synthesis (e.g. Fluorocytosine 5-FC). Another method is to disrupt the fungal microtubule’s aggregation during mitosis (e.g. Griseofulvin), thus “arresting” the fungal cells in metaphase.

Recommended Textbooks:

Hugo & Russell’s Pharmaceutical Microbiology 8th edition, Wiley- Blackwell. Edited by S.P. Denyer et al.
ISBN 9781444330632
Essential Microbiology for Pharmacy and Pharmaceutical Science, Wiley- Blackwell. By Geoffrey Hanlon and Norman Hodges
ISBN 978-0-470-66534-3 (pbk.)


Where does the exudate comes from during inflammation? During inflammation transudate and exudate is formed by vessels. I would like to make sure if it comes from arterioles, venules, or both, and the reason why.

exsudates almost exclusively come from the capillary compartment. If you think about the structure of the vessels, this appears logical.

The capillary compartment :

has vessels only several microns thick
has only the endothelial and basal lamina layers
spans an enormous surface, far greater than arterioles or venules

So when the fenestrations and tight junctions of the capillaries are impaired, serum directly passes into the extracellular medium.
A good example of that would be advanced anaphylactic shock. In this situation, the general inflammatory state causes a loss of endothelial integrity. Adrenaline given in such a state will have an inotropic and chronotropic effect on the heart, will cause vasoconstriction, but will also act to restore endothelial integrity. This last element is the main reason why allergic people carry an epinephrine syringe at all times.


How do multiple replication forks function without 'colliding', and what is the benefit of this method? I'm currently reading a little about DNA replication, and have come accross the following statement;

  Replication starts from a fixed point and is bi-directional ... In Eukaryotes, there are multiple replication forks, each progressing in a bi-directional fashion.

If there is a single, long strand of DNA in a Eukaryotic cell, I see potential problems with this:

These forks involve opening up a section of double-stranded DNA, and each strand becoming a double strand in a newly synthesised piece of DNA. At some point, before any single fork has become two new double-stranded molecules, another fork could 'collide' with this, causing it to attempt to replicate the non-finished section.

Simply, how can one replication fork meet another without either exponentially increasing the number of strands being replicated?

Also, on a more general level, I would be quite interested to know the actual benefit of this, when, typically, only a single copy of the double-stranded molecule needs making.

To get to the exponentially increasing number of strands, the replication would have to be started on the already replicated strand, and not on the original strand. Replication in eukaryotes is tighly controlled and such an event is prevented by the regulation.

How can the cell prevent re-replication of the strand that is currently synthesized? By timing the steps of the replication in strict order and preventing any replication outside of that order.

Replication starts at defined origins of replication. In the G1 phase, pre replication complexes (pre-RCs) are assembled at the origins of replications. At these pre-RCs the replication can be initiated, but pre-RCs itself cannot be assembled in the later phases of the cell cycle. When the replication starts, the pre-RC is converted to a post-RC which can't initiate the replication anymore, preventing re-replication.

The benefit of multiple origins of replication is replication speed. Eukaryotic genomes can be much, much larger than those of simple bacteria. Replicating them using a single origin of replication would take a very long time.

Some further reading material:

Genomes, 2nd edition, chapter 13
Cell Cycle Regulation of DNA Replication


What makes an E.coli an E.coli, genotype or phenotype? According to this paper, among 61 strains of E. coli they studied only 6% of the genes are common in all. Which means that the overwhelming majority of the genes are not shared.

And wikipedia defines E. coli like this:

  ... is a Gram-negative, facultative anaerobic, rod-shaped, coliform bacterium of the genus Escherichia that is commonly found in the lower intestine of warm-blooded organisms (endotherms).

Which is a phenotypic  definition. My question is: what defines E. coli as a species: its genotype or its phenotype?

The context for identifying E. coli is primarily clinical Microbiology, and in the clinical lab the identification is primarily phenotypic, based on various properties such as growth and morphology on selective media, Gram stain appearance, biochemical characteristics, etc - only under unusual circumstances is genetic testing done. The latter is problematic because of extreme genetic diversity within the species and some overlap with others (even other genera).

The problems with the notion of "species" in E. coli in the context of 16s sequencing, horizontal gene transfer, mobile genetic elements, plasmids, etc is discussed at some length in Quammen's recent book The Tangled Tree.

For now, phenotypic species identification is the norm, as illustrated by the "Nomenclature" guidance to authors of the Journal of Bacteriology, a publication of the American Society for Microbiology.


Is it PSI-BLAST or BLASTP if I use PSI-BLAST for only one iteration In my case, I used PSI-BLAST in the local BLAST+ to search queries against the self created database. After the first search, I added the searched result to the database and then conducted the multiple sequence alignment myself with MUSCLE to get the conserved parts. Then, I searched the queries against the consensus sequence obtained from the multiple sequence alignment (without gap). In this process, I did not calculate a PSSM, while the first iteration of PSI-BLAST uses a constant matrix, which is much similar to BLASTP. So what did I actually use in the process – PSI-BLAST or BLASTP?

You simply used BLASTP against a consensus sequence. The first iteration of PSI-BLAST is identical to BLASTP.


How to do multiple sequence alignment? I have a DNA sequence that makes protein 1. but now I have asked to:

compare the amino acid sequence of protein 1 with nine homologous proteins and make a multi sequence alignment (MSA) of the sequences.
Determine a consensus sequence for the proteins based on the MSA.
Find any specific parts of the proteins that are conserved, then explain why these parts are conserved.

MSA Tools

compare the amino acid sequence of protein 1 with nine homologous proteins and make a multi-alignment of the sequences.

EBI have a portal for many MSA tools and there are also other MSA tools available elsewhere.
In research, it's good practice to use several alignment techniques and look at which generates sensible indels. Usually, this is the lowest number of indel events.
Clustal Omega is probably the most sophisticated MSA tool hosted on the EBI site, however, it is relatively new and isn't as established as T-coffee or MUSCLE.
Note that these tools are updated fairly regularly. This question and top answer about "cutting edge" MSA tools from 2014 refer to a paper from 2011 that attempts to benchmark MSA tools. As you can imagine the state-of-the-art tools change rapidly (for example, clustal-w2 was released, and now clustal omega since that benchmarking paper). For most researchers though, it's a personal preference, and different MSA tools are "better" for different situations (speed of computation, number of alignments, similarity of sequences, complexity of secondary structure, local vs global alignments etc.).
Consensus sequence

Determine a consensus sequence for the proteins based on the
multialignment.

This depends entirely on the information from your alignment.
A common way to make a consensus sequence is to just take the most abundant residue at each position in the MSA. I don't like this approach because it heightens the significance of abundant residues, and diminishes the appearance of less abundant residues. This distorts the biochemistry and can easily lead to sequences that would be impossible or useless in biology. I would always rather see a raw alignment.
Conservation amongst alignments

Find any specific parts of the proteins that are conserved, then explain why these parts are conserved.

Conservation usually implies function, and hopefully you'll have a homologue that has a categorised function. Perhaps in your case one could attribute this function to a conserved sequence in the other homologues.
One brilliant tool is called consurf.

You can upload your MSA file to it and it will colour code regions of conservation from purple to blue. A purple region implies an evolutionary selection to not change that region, implying that it is a "functional" region.
Consurf works better with more sequences, so perhaps it isn't appropriate for this project. Instead try loading the alignment in Jalview and show "sequence conservation".

Caution.
When performing an MSA remember that the algorithm assumes that the sequence is homologous and that assumption can produce errors. If it looks wrong, it probably is!


Hardy Weinberg Explanation I am able to calculate frequencies for allele and genotype, but I don't understand how to tell if the population is at equilibrium. Or how to determine how many generations of random mating would be needed to reach HW equilibrium. I thought the proportions didn't change from generation to generation?

number of individuals: TT-200, Tc-200, cc-600
observed frequencies : TT-0.2, Tc-0.2, cc-0.6
HW frequencies       : TT-0.05, Tc-0.35, cc-0.60

p=.33, q=.77

The answer is logical if you understand the reasoning behind Hardy-Weinberg. I recommend that you to have a look at the post Solving Hardy Weinberg problems and try to answer the question yourself. Once you've done that, you can hover over the yellow zone below for the answer to compare against what you've understood.

The answer:

   If the assumptions of Hardy-Weinberg are respected (see Assumptions of Hardy-Weinberg rule), incl. random mating, then a population is back to Hardy-Weinberg equilibrium at the beginning of any single generation. H-W equilibrium is directly caused by the random sampling of gametes. This random sampling is happening at every single generation and therefore a single generation is enough to get back to H-W equilibrium.


How can antibiotics damage the ear? What is the mechanism by which aminoglycoside antibiotics (such as streptomycin and gentamicin) damage the mechano-sensory hair cells of the auditory and vestibular system? (Could this be seen as evidence for Lynn Margulis' theory that these cilia are descended from bacteria?)

This phenomenon is called Ototoxicity, which literally means "toxic for the ear". Mostly the cochlea or the auditory nerve are affected and almost all these cases are connected to medications as gentamicin or cisplatin.

The reasons for this are that the cells are either driven into apoptosis or necrosis. This is caused by destroying mitochondria and releasing calcium and cytochrome c which triggers apoptosis or by deregulating the the JNK-signal transduction pathway and causing necrosis. This image gives a nice overview:

For further reading you can start with the Wikipedia page on ototoxicity and then also read these two papers which are both freely available (the figure above is from the first):

Intracellular mechanisms of aminoglycoside-induced cytotoxicity.
Gentamicin rapidly inhibits mitochondrial metabolism in
high-frequency cochlear outer hair cells.

To answer the question why this occurs in the ear, it seems that there is some genetic predisposition for this, see this paper: "Aminoglycoside-induced ototoxicity." Mitochondrial damages leading to hearing loss is also not uncommin, see here. Noise seems to play an additional role here and is probably the "last drop" to cause hearing loss.


How do honeybees requeen themselves? It is said that beehives once queenless try to rear a new one by themselves. Beekeeping resources, books, websites, youtube videos, etc. have a very pragmatic human-centered view to the issue: what should the beekeeper do and don't. Some say, that the beehive can potentially rear a new queen on their own. I've also heard from beekeepers that they can be helped by introducing an extra brood comb from another hive.
I am interested in knowing the details on how this re-queening process takes place without human intervention.
Queens, like workers are female, hence they must come from diploid eggs. Hence only a mated queen can provide the egg needed to produce a new queen. Also it is known that queens are reared inside special queen cells which lie in vertical position in the comb.
It is known and it can be easily observed, that if the queen dies unexpectedly, the hive prepares for a substitute by building queen cups (will be queen cells).
But I wonder how do they actually get a queen from those cells.
The workers must either

carry an egg, previously laid by the former queen, from a worker cell into the cup,
or build the queen cup around a cell that already has an egg, or a young larva.

I can't imagine any other possible way.
So, how does exactly the requeening processes takes place?
Update. To be more specific about the details of the process of requeening I would like also to add the following questions:

Do they start breeding a queen from an egg or a young larva?
Do they choose this egg/larva at random?
Do we know a probability distribution for queen hatching dates? ie. the probability of a queen emerging (starting from a 0-day egg) after 15 days, 16 days, 17 days, etc.
What's the attitude of worker bees with respect to queen cells? Can a queen cell be destroyed by worker bees under certain circumstances?

Thanks to @S-Pr I found the answer on wikipedia. On the Supersedure section of the article it is written the following:
If a queen suddenly dies, the workers will attempt to create an "emergency queen" by selecting several brood cells where a larva has just emerged which are then flooded with royal jelly. The worker bees then build larger queen cells over the normal-sized worker cells which protrude vertically from the face of the brood comb. Emergency queens are usually smaller and less prolific than normal queens.
Although, There is no reference to a source. Maybe one of the citations at the end of the page has the answer.


Selection for less efficient egg transfer in Human Botfly life cycle I have heard that the Human Botfly transfers its eggs through other invertebrates, and it strikes my curiosity that if an insect could simply land on its host directly to deposit its eggs, then why have intermediate hosts?

I have speculated that the vectors may be better specialized for penetrating hosts, and that penetrating hosts may be difficult, or that approaching hosts is risky. Another speculation on my part is that the Human Botfly may be filling a niche where it does not need to compete.

In multi-host complex life cycles (CLCs), an intermediate host often aids in the dispersal of offspring.

In general terms, an animal, say a botfly, have an ultimate "purpose" or 'goal'  to spread their genetic information as much as possible. This could mean producing a large number of offspring and hoping some survive or it could mean having one offspring, investing a lot of energy and ensuring it does survive. Regardless, spreading genetic information often requires offspring to disperse (or be spread) a great distance, which may allow the individuals' genetic information to dominate an new region.

In the case of botflies, having an intermediate host means the genetic information can be spread a great distance.

If you're looking for a more thorough explanation of complex life cycles, this paper describes it well. There is also this site more specific to the botfly which is not peer reviewed, but well-researched and descriptive.


does life make or break? Ok, this question seems like it may be impossible to answer, but would be interesting to see if anyone has an idea.

Throughout the course of a human life, do we make more molecular bonds than we break, or vice versa?

Metabolism ≈ Anabolism + catabolism

Metabolism is the set of all chemical reactions happening inside a living body. These reactions can either breaks down big molecules and build up big molecules. The set of reactions the breaks down big molecules is called catabolism. The set of reactions that build up big molecules is called anabolism.

Energy

Generally speaking, anabolism cost energy and catabolism yield energy. The molecule that is directly used to transfer this energy is Adenosine triphosphate (ATP).

Any energy transfer is coupled with some loss of energy from the system (see Energy conversion efficiency).

Entropy

For any chemical reactions, there is always an overall increase of entropy. As a consequence, a living organism increases the entropy in its surrounding. In other words, it breaks more than it builds.

Your question

  does life make or break?

Life does both! But on average, it mainly breaks things up (just like any other chemical reaction).

Want to learn more?

The concepts of energy and entropy are studied in physics and chemistry but not so much in biology. I cannot really give you a good source of information.

Khan Academy offers a very good introductory course on metabolism (here), you should have a look!


Is Bramble (blackberry bush) carnivorous? I have come across this video which put forth the hypothesis that bramble actually qualifies as a carnivorous plant.  The observations that have led to the hypothesis are:
1. Sheep getting caught frequently in bramble
2. Sheep will die  without human intervention.
3. The rotting corpse of the sheep will nourish the plant for many days.
4. The thorns angle inward -- supposedly evidence for adaptation that helps trap prey animal.

I agree , on the surface it looks plain silly but that is a reflexive reaction, not an argument.  Is this a plausible hypothesis? If not , please give reasons.

Even if the adaptations to tangle were well supported, brambles would still not be carnivorous.

Carnivorous plants release digestive enzymes to digest their prey or have other adaptations specifically to pull nutrients from the things they kill. Brambles would have to rely on something else to rot the carcass and pick up whatever trace nutrients that get released into the soil like any other plant. Brambles tendency to tangle could just as easily be a defensive adaptation meant to encourage herbivores to avoid it. Without any specific adaptations to uptake the nutrients from killed animals, classifying them as carnivorous would be premature.


Is there any clear relationship between physical characteristics and patterns in the genome? Given that for example humans have five fingers on each hand, is there a region in the genome with a sequence of five similar subregions, one for each finger? Is the region on the genome that encodes for the right hand near another region that encodes for the left hand?

This kind of question is what developmental genetics is all about. The answer turns out to be, in general, 'no'. There is no neat mapping between spatial dimensions of an organism and its genome. (There is one exception to this in some organisms called the Hox cluster, but they are kind of a freak case).

The reason for this is that in general you should think of the genome as being a recipe for a developmental process, rather than a description of the end product. You might have, say, a specific set of genes which is active in all limb buds, which are the structures that become limbs and fingers etc. These genes would be active at different levels, at different times and places, in your different fingers. E.g. length of time one gene is on could control how long the finger grows for and thus how long it gets.

There are some genes which are only active in specific parts of the body, but you don't necessarily need a particular set of genes for each distinct finger/limb etc. And these genes certainly don't need to be in the same place in the genome. Your left and right hand are going to have identical gene expression for instance.


Map gene IDs to Ensembl gene ID Forgive me if this question is too trivial.

I have the gene IDs of the following type

EOG6STSR2
EOG60ZRJB
EOG6SBFJ2
EOG6P5KX3
EOG6B5PRW

from the first supplementary file in Comparative validation of the D. melanogaster modENCODE transcriptome annotation .

I'm not sure as to the type of the IDs. I learned that IDs beginning with EOG are Eukaryotic Orthologous Group IDs but I couldn't find these particular ones in any of the databases.

Is it possible to map them to Ensembl IDs or any of the other commonly used ones?

These are not gene ids, but groups of orthologous genes -- try to search for the ids on Google, I can find this page http://cegg.unige.ch/orthodb6/fasta.fasta?ogs=EOG6STSR2&swaptree= and thus you should be able to download the sequences and ids from OrthoDB.

Note that, strictly speaking, the are no Ensembl ids for Drosophila, only FlyBase ids that are also used by Ensembl.


Understanding the brain: how are neurotransmitters released in the brain? I have a basic knowledge of how neural networks work. A potential difference is created that forces sodium, potassium, chloride, and calcium ions to flow which carries an electrical signal to the end of a synapse. From there, the presynaptic neuron releases neurotransmitters creating a potential difference to the postsynaptic neuron.

What I don't understand yet are the mechanics of which neurotransmitter will be released. Do the vesicles of each type of neurotransmitter have an energy threshold? If yes, when the highest energy threshold of a vesicle is achieved, does this mean all the other vesicles will release the encapsulated neurotransmitters?

The release of neurotransmitters is a very specific type of SNARE mediated exocytosis. The action potential from the influx of sodium propagates along the axon and reaches the axon terminal, containing the calcium channels. This causes the calcium cations (ions) to travel down the electrochemical gradient. The Ca2+ then binds to a protein. The vesicles containing the neurotransmitter called synaptotagmin (Ca sensors), would cause conformational changes leading to the formation of a SNARE complex. Some good animations can be seen here and here.

Regarding whether there is an energy threshold: there is a threshold on the amount of Calcium needed to cause the activation of synaptotagmin, as with all types of SNAREs.

See this article: http://www.pnas.org/content/93/23/13327.full.pdf

Past a certain calcium threshold, all the neurotransmitter should in theory be released, but whether they cause a response would depend on the receptor and on the postsynaptic membrane, as each synapse is specific in the neurotransmitters and receptors it expresses.


Species identification - what kind of worm is this? I am finding these worms in my bathroom since summer arrived. I have been finding these on floor, walls and damp towel I left hung overnight in bathroom couple of times. When these worms are squished, a bang like sound is produced. Can you help me identifying this, is it something to be taken seriously & requires immediate action? Average length of these worms is ~ 1-1,5 inches.  Please find a closeup picture I managed to capture with mobile camera.

I moved into this house last winter so don't know previous summer history. Anyways I think I should get bathroom drain cleaned.

Edit: Just noticed it has very tiny hair thin, white/ transparent legs, many of them. These legs are barely seen with naked eye. May be they are just hair like things not legs (I don't know proper terminology).

Edit2: origin is Lahore, Pakistan. It's far from sea, open agricultural terrain. Climate is hot.

About movement, no they don't move like earth worms (shortening in length and then stretching). Neither it's snake like. It kinda straight. They also don't have legs as centipedes do, on their sides.

This is almost certainly not a millipede as it has no antennae and moves by compressing its body. My money is on insect larva, possibly a drain fly (which would make sense if you regularly see them in the bathroom).

It would be interesting if you could put one in a jar and see what it develops into.


How are reflexes suppressed? What neurophysiological process keeps reflex arcs in check? For example, the withdrawal reflex causes the hand to jerk back when the fingers touch something painfully hot incidentally. However, that reflex can be voluntarily suppressed when one deliberately touches that same hot object on purpose. What neural process is involved in conscious suppression of reflexes?

Short answer
The pain withdrawal reflex can only be suppressed when touching something painful on purpose. Deliberate, conscious contraction of the extensor muscle before reflex initiation can prevent the contraction of the flexor muscles once the reflex is started.

Background
The pain withdrawal reflex arc (Fig. 1) receives input from sensory neurons that enter the dorsal part of the spinal cord via the dorsal root of the spinal nerve and synapse onto interneurons within the spinal gray matter. The interneurons in turn synapse onto motor neurons, which send axons that exit the cord via the ventral root. They conduct information to the muscles. The resulting withdrawal reflex is initiated by activating motor neurons of the flexor muscles (agonist), and simultaneous inhibition of the motor neurons to the extensor muscles (antagonist). This loosening of the antagonist while the agonist is being contracted is referred to as reciprocal inhibition (Crone, 1993). More important to the question is the fact that the motor response is well under way before the signals responsible for the conscious sensation of pain (which exit the reflex pathway in the spinal cord) ever reach the brain (Cornell University).

Fig. 1. Schematic of the pain withdrawal reflex arc. Source: Washington Uni.

Hence, the reflex pathway is initiated even before we are aware of any pain. The only possible way to suppress a reflex that is faster than perception is to start counteracting the agonist (flexor) before the reflex is initiated, i.e., by contracting the antagonist (extensor) before touching the painful object.

Reference
- Crone, Dan Med Bull (1993); 40(5): 571-81


Why will tissue from identical twin be rejected in some cases? Also, transplants from one identical twin to another are almost never rejected.
[ Source: Medline Plus ]

Why can a tissue from an identical twin be rejected ?

This was too long for a comment, but I have absolutely no evidence for what I'm about to say :)

It looks like that sentence was a little bit of hand-waving, as the author didn't want to categorically state that identical twin tissue would never be rejected. I suspect that in the early days there may have been reports of organ failure (esp. kidneys) in the recipient that were incorrectly identified as rejection episodes. I suppose there's also the slight possibility that one twin could have a mutation event very shortly after the separation of the twins in utero (when all the cells are still pluripotent) that could somehow change or (more likely) silence one or more of the HLA or other surface antigens involved in transplant rejection. This would almost certainly have to happen when the separated twin was a single cell. The mutated twin would therefore not express an antigen the non-mutated twin did, and if the non-mutated twin donated a kidney or other organ to the mutated one, its immune system wouldn't recognize the silenced antigen and could potentially result in rejection.

Like I said earlier, all pure conjecture :)


Is this a valid principle of curing HIV? I have a set of questions actually, it will be very helpful if you answer them in order.

Where does the HIV virus hide (during incubation period)? Let answer be X cell.
Is X cell in the bloodstream?
What parts of the HIV are constant for all its version? (I suspect it's Reverse Transcription Protein, Glycoprotein 120 and 41) Let answer be Y.
Is there a chemical that can destroy Y?
Is Y present in the normal Human body?
If Answer to question 2 is yes and that to question 5 is no can we inject the said drug into the bloodstream so that it can wipe out the virus?

HIV hides in a number of known cells and unknown cells. Although most of the damage of HIV is caused by its infection of shorter lived cells, long lived cells which it infects includes anything with adequate receptors including memory T cells, dendritic cells, macrophages and some glial cells too. These cells are found widespread in the body from tissues to the blood stream. HIV also infects an as of yet unknown pool, which is thought to be the cause of rebound after HART (Highly Active Retroviral Therapy) is stopped.

The constant parts are not exactly there. Every part of HIV can essentially mutate and does. In functional HIV particles (which surprisingly make up a tiny proportion of total HIV particles in an infected individual), the epitopes you mentioned are mostly constant.

Destroying them is impossible as of yet and hence no cure for HIV. It is hard to destroy a particular protein. We could make HIV that doesn't make these proteins (it would then rapidly mutate until it did, or be non-functional to the point it was an awful vaccine not inducing a particularly adept CD8 response). Otherwise we could block either these proteins themselves or that which they bind. There is a group of individuals with the delta 32 mutation which blocks CCR5 preventing infection, however this is rare. For the most part most individuals are susceptible as CD4 and CCR5 are highly conserved amongst humans. We would benefit therefore from inhibitors of these proteins themselves, however due to glycosylation generally our antibodies are terrible at inhibiting the glycoproteins. Reverse transcriptase inhibitors exist and are in fact very important as part of HART.

HIV came from chimpanzees. In their natural host the HIV equivalent (SIV) doesn't cause immunosuppression. HIV doesn't infect quite a few primates due to restriction factors which do not exist in humans or do not target the same things. Then of course there's the matter of the lack of the correct receptors. There's ongoing research if there's a chemical that does cure HIV however there isn't a subset of individuals where this occurs to study. HIV resistance is normally due to elite control of the virus due to specific genetic features that make the immune system target the best least variable, most deleterious (if HIV mutates them to escape) epitopes. If we could get everyone to respond to these epitopes that would be great (see a billion vaccine trials for HIV) otherwise if we could flush out the cells where it hides latently integrated (our current therapy and the immune system can only target cells where HIV is constantly replicating).


What kind of spider is this? I spotted this spider in my garden (Northern UK). The body is about 20mm long, and it's made a sizeable (50cm) web on a wall.

There's another semi-identical one on a nearby hedge.

What kind is it?

Thanks for the pictures! That's the European Garden Spider (Araneus diadematus)

They are most commonly seen from June to October, but they reach a peak around right now.  This species is all over UK, and is widespread in gardens, woodland, and meadows.  Here is another picture for reference:

Fun Fact: After laying their eggs in late autumn, the females die and only the eggs make it through winter.  Upon hatching, they look quite different from the adults:


Photosynthesis and its subtopics Which of the following statements about photosynthesis is true?

a.  Photosynthesis is an energy consuming process

b.  The light-dependent reactions produce the energy-rich compounds that are used up in the light-independent reactions.

c.  The light independent reactions can only occur in night

d.  Photosynthesis and respiration cannot take place together in plants

I think both c and d are incorrect, but I'm unsure whether a or b is the correct option.

The reason why I think a is correct is that sunlight is used during photosynthesis and b because the hydrogen of $NADPH$ produced during light phase is used to combine with $CO_2$ by utilizing ATP (which again was produced in the light phase ) to make $C_6H_{12}O_6$ in the presence of enzyme Rubisco.

Which of the following is true about photosynthesis?

a.  Rate of photosynthesis is directly proportional to concentration of $CO_2$ in the air.

b.  Photosynthesis takes place only in the visible spectrum of the electromagnetic radiations.

c.  Rate of photosynthesis would be highest under the green light

d.  Structure of leaf has no effect on the rate of photosynthesis

Here I am also stuck between either a and b.

The reason why I think a is correct is that when $CO_2$ concentration increases the rate of photosynthesis also increases until the concentration reaches 0.1 % and it could be b because photosynthesis takes place in the presence of sunlight, not any other radiation.

First question:

B. The net gain of ATP in Photosynthesis is 0, so it cannot be A. C & D are obviously not true.

Second question:
B. D is not true, C is not true (it is actually the opposite- Chloroplasts absorb all BUT green, so only green would be bad). Like another commentator said, the level of CO2 only aids the rate to a point, at which the rise is not great.
http://www.rsc.org/learn-chemistry/content/filerepository/CMP/00/001/068/Rate%20of%20photosynthesis%20limiting%20factors.pdf


Protein denaturation and edible toxins As a protein denatured, it may lose its functions.
So theoretically if I heat some type of biological toxins like poisonous mushroom to 100 oC or higher temperature, will I able to eat it? (I know peoples still death after eat them even boiled to 100 oC, but why?)
Is there anyway to make them edible?

Update: i know some protein can survive in high temperature, for example: taq polymerase. Can i destroy it functions by boil it to higher temperature like 140-160 oC at higher atmosphere pressure and then return back to normal temperature?

Update2 : i found some information on the internet by searching keyword "toxin destroyed by heat" : http://aggie-horticulture.tamu.edu/food-technology/bacterial-food-poisoning/

The botulinum toxin is destroyed by boiling the food for 10 minutes.*
.
So it's depend on the type of protein, the heat and time.

So is there any way/formula to predict the temperature and time to destroy a protein? Or is there any absolute temperature and time to kill most type of protein ?

Why people still die after eat them even boiled to 100 oC, but why?

Well not all toxins are protein based. Some are just small molecules that fit into some vital protein in your body, causing  it to stop and death not long later. Some are cyclic peptides and are not denatured by heat. The peptide is simple, and has many carbon bonds to stablize its structure (it is a ring and has carbon bonds linking internally) https://en.wikipedia.org/wiki/%CE%91-amanitin

  Or is there any absolute temperature and time to kill most type of protein ?

Autoclaving.. 134 °C (274 °F) for 18 minutes in a pressurized steam can destroy prions. And prions pretty tough. https://en.wikipedia.org/wiki/Prion


What information do microarray image convey? OK I have read that a cell generates 4 kinds of digital (to be precise discrete) data namely DNA, RNA, Protein (sequences that can be encoded as string sequences of nucleotides/ amino acids) and micro array image. I am not a biologist, but my interest is in the statistics and information theory of these data. I would like to know what information do DNA micro array image convey? For example after processing it with the aid of a suitable software, what sort of information we do obtain?

Sample micro array image:

Each spot overlaps with an oligonucleotide probe, that is designed to identify a specific nucleic acid sequence. Gene expression arrays have probes which are complementary to sequences derived from the exons; therefore they will hybridize with these sequences.

Before hybridization the cDNA (in this case) is labeled with a fluorescent molecule such as Cy3 or Cy5 (two dyes can be used to differentiate treated and control). Note that each spot will have many probe molecules.
Fluorescent intensity is proportional to number of hybridized DNA strands, which in turn is proportional to its expression in the sample.

Extensive amount of texts are available on microarray data analysis which you can find quite easily.


How do bats distinguish between day and night? How do bats distinguish between day and night? Do they hunt at night - if yes, how they know that?

Are they afraid of sunlight?

Bats distinguish day and night the same way that other animals do, with an internal circadian clock and by environmental cues (dawn and dusk).

Most bats (over 1000 different species total) are nocturnal, meaning that they are out of their roost and foraging at night. This includes that vast majority of bats, which also echolocate. Some bats, notably pteropodid "Flying foxes" are diurnal, meaning they are active during the day and sleep at night, like humans. These bats are typically fruit-eating. There are, of course, exceptions, but these general patterns hold.

Bat Conservation International has good educational information about bats.


When does DIFFUSION occur and not OSMOSIS, and the otherwise? For example, I do know that red blood cells have both the Na+/Cl- co-transporter and Aquaporin (water channel) that allows both Na/Cl and water molecules to pass through. But why in biology textbooks they imply that osmosis occurs instead of the diffusion of Na/Cl molecules, though red blood cells have the channels for them, too? (that leads into crenation or lysis of the cells)

NOT ion PUMPS, but ion CHANNELS (those that don't require energy). The Na+/Cl- co-transporter works along with the gradient (not against!).

If an RBC is to put in a hypertonic solution, why wouldn't it absorb the excess NaCl using this channel instead of letting the water out?

I do know in the case when we put cells in a hypertonic/hypotonic glucose solution, osmosis will occur instead because the cells need insulin to allow glucose in (via GLUT4).

But when does exactly osmosis occurs instead of diffusion?

But when does exactly osmosis occurs instead of diffusion?

These processes are not mutually exclusive. Both can happen simultaneously. Their rates depend on different parameters such as permeability of the membrane towards water and the solutes. A semi-permeable membrane has different permeability for different molecules. There are cases when one of these two processes may happen but not the other (again, a function of the parameters):

Osmosis+/Diffusion-
When there are no solute transporters expressed in the membrane of the concerned cell. For e.g. RBCs do not express the Sodium-Chloride symporter. It is expressed in the distal convoluted tubule of the nephron.

Osmosis-/Diffusion+
When the osmolarity of the cytosol is same as that of the ECF and the cell expresses ion channels. The action potential in a neuron would be an example of this phenomenon.


Are females more flexible than males in all mammals? It's common that human females have a more flexible body than males, (but I don't know why, so it'd be helpful if someone answers why so as well!) but does this apply to all mammals?

Try birthing a child for once. You need to be flexible to accommodate the growth of another organism inside you.

Take a look at some pictures of the mothers spine during the course of a pregnancy, you will have no further questions. Same with belly size, breast size and vagina size upon birth.

This video is a nice explanation of this. Also includes the different centers of gravity for males and females (human).

http://www.youtube.com/watch?v=WO8DtsZO1nA


Gestation period of African savanna elephants? I found out it is 22 months for African bush elephants, but is this also true for African savanna elephants?

The African bush elephant and the African savannah elephant are the same species (i.e., they are just different names for Loxodonta africana).

According to here and here, the African savanna/bush elephant (Loxodonta africana) has a gestation period of 22 months.

The only other African species of elephant, the African forest elephant (*Loxodonta cyclotis), has a gestation period of 20 - 22 months (see here). Both Wikipedia and this source corroborate this higher expected range of 22 months, but with the latter source adding:

  from zoo data a gestation length averaging 660 days has been determined while the average in one wild population (Amboseli) was 656 days.

And for fun, click below for a video of an elephant fetus!


What is a good Microbiology atlas for Bacteriology as online version? I am looking for a online atlas for Bacteriology, the cost does not matter.
I have been searching SpringerLink, and Amazon but no good online version found.

What is a good atlas for Bacteriology as a online version?

Not sure what you are exactly looking for? If you change the question or comment I can update my answer...

NCBI's taxonomy site has a listing of bacteria.  Encyclopedia of life is also great.

Then there's UCSC's microbial genome browser.

Biocyc is  great reference for bacterial genes.  to get into E coli, which is the model bacterium there's Port Eco featuring 130 E coli genomes.

Am Soc Micro has an excellent E coli/ Salmonella site based on their classic reference - you have to pay for access though.


How long before robin no longer needs the nest on my porch? A robin has made a nest on my porch. Unfortunately, the nest is on my weed wacker which I might want to use at some point this summer. Currently, there are two eggs in the nest.

How long will it be before the robin is done needing the nest?

Location is Eastern Massachusetts.

-- Update May 13 --

I think one of the eggs must have hatched. The robin no longer sits in the nest, she just stands on it constantly.

According to Cornell's All About Birds website, you will have to wait about a month for the nest to be cleared.

The egg incubation period is 12–14 days.
Following hatching, the nestlings will remain in the nest for another 13 days (i.e., the "nestling period" is 13 days).

However, there are two caveats to this:

A typical robin clutch size (i.e. the # of eggs in the nest at once) is 3-5 eggs. Since you only have two eggs, that could suggest that more eggs are about to be laid very soon, which may extend the nest occupancy another day or so.
Some robins use the nest more than once!

  An American Robin can produce three successful broods in one year.

Here's a visual of what the nestling period (approximately) looks like so that you can track your nest visually :) :

 Source: L. Birnbaum


Can swallowed fingermails, hair, or skin get caught in your appendix? There is a common saying in my place: If you eat your skin, hair or nails, it will be deposited in the cecal (Vermiform) appendix, and can cause appendicitis. (This is mostly told to children to discuourge them from eating their own.)

Is there any reality in this statement? In the case of hair and nails they are dead cells, but what is the issue with skin? Skin is normally living and the cells are active.

So is there any problem digesting ones own skin?

Do nails, skin and hair must be trapped in Vermiform appendix?

Skin is safe to chew, and digestible. Fingernails are not digestible, so really shouldn't be swallowed if avoidable. In the medical literature, there are at least 225 cases of foreign bodies in the appendix. They include:

a metal drill bit that was ingested unintentionally 3 months earlier
pins (81  cases)
lead shot (81 cases)
seeds (34 cases)
bones (16 cases)
eggshell
glass
teeth
nails (hair causes problems with bezoar formation)
a die (dice)
the clinical end of a thermometer.

Most (71%) patients were symptomatic, typically with intermittent abdominal pain for months or years. Pins were most likely to elicit symptoms (93% of cases).

So it seems there is some truth to this nugget of folk wisdom.

The above were found over many, many years. Since most cases are asymptomatic, it's likely there are many cases that never come to light, but not remarkably so (lots of appendices are removed and examined every year!).

Foreign Bodies in the Appendix


Hardy-Weinberg for triploids Problem:

A certain species has somatic cells with ploidy 3n (the organism inherits
three sets of homologous chromosomes from each of three parents). At a certain locus, there are three possible alleles A 1 , A 2 , A 3 , which are
completely dominant in the order A 1 > A 2 > A 3 . The proportion of organisms
exhibiting traits A 1 , A 2 , and A 3 are respectively 0.614, 0.306, and 0.08. In
addition, the proportion of organisms that are completely heterozygous
(genotype A 1 A 2 A 3 ) is 0.18. Which of the following are allele frequencies of A 1 , A 2 , and A 3 , respectively?

Answer Choices:

A. f(A 1 ) = 0.5, f(A 2 ) = 0.3, f(A 3 ) = 0.2

B. f(A 1 ) = 0.3, f(A 2 ) = 0.5, f(A 3 ) = 0.2

C. f(A 1 ) = 0.3, f(A 2 ) = 0.4, f(A 3 ) = 0.3

D. f(A 1 ) = 0.6, f(A 2 ) = 0.2, f(A 3 ) = 0.2

E. f(A 1 ) = 0.7, f(A 2 ) = 0.2, f(A 3 ) = 0.1

Correct Answer:

A

Solution:

No clue. I'd guess that the solution follows a hardy-weinberg model for polyploids. For simplicity, I will refer to A1, A2, and A3 as x, y, and z, respectively.

(x + y + z)^3 = x^3 + 3x^2y + 3xy^2 + y^3 + 3x^2z + 6xyz + 3y^2z + 3xz^2 + 3yz^2 + z^3

Given that z^3 = 0.08, shouldn't z (A3) equal the cube root of 0.08 = 0.43?

That doesn't match any of the answer choices, so I will assume that my steps were incorrect.

Any suggestions?

First, although it only speaks about cases of diploidy, you might want to have a look at Solving Hardy Weinberg problems.

Information given to us

The question gives the same names to the phenotypes than to the alleles which si rather confusing. Let's call the three possible phenotype $P_1$, $P_2$ and $P_3$. We know that the frequencies of these phenotypes are

$$f(P_1) = 0.614$$
$$f(P_2) = 0.306$$
$$f(P_3) = 0.08$$

Compute phenotype frequencies in terms of allele frequencies

Let, $x$, $y$ and $z$ be the frequencies of the three alleles, $A_1$, $A_2$ and $A_3$ (I chose those names to fit with the equations you wrote). The whole difficulty now is to express $f(P_1)$, $f(P_2)$ and $f(P_3)$ in terms of $x$, $y$ and $z$. You should try yourself before looking at the result. Start with $f(P_3)$, it is the easiest.

Here is the solution for $f(P_3)$

   $f(P_3) = z^3$

Here is the solution for $f(P_2)$

   $f(P_2) = y^3 + yz^2$

Here is the solution for $f(P_1)$

   $f(P_1) = x^3 + 3x^2 (y+z) + xyz + xy^2 + xz^2$

Once, you have done that, you have three equations with three unknowns and you just have to solve them. Make sure at the end that $x+y+z = f(P_1) + f(P_2) + f(P_3) = 1$.


Are mitochondria dead? In the video "What is Life? Is Death Real?", the subject of mitochondria is raised at 2:58. At 3:12, the narrator says "[mitochondria] are not alive any more: they are dead."

What currents of thought lead to this affirmation?

When I search for mitochondria are dead on Google, I get many links about the role of mitochondria in cell death, but I don't see anywhere that the assertion in this video is discussed.

SolarLunix posted an excellent answer detailing the criteria for being classified as "alive", and showed that by those criteria, mitochondria could be considered as "dead".

However, I would argue that the narrator's statement in your video does not make any sense. The currently-accepted theory of the evolution of mitochondria (and possibly other organelles) from free-living prokaryotes is called symbiogenesis and postulates that the mitochondrial progenitors began living symbiotically with the precursors to eukaryotes some 1.5 billion years ago. Life originated on Earth about 3.5 billion years ago, so eukaryotic cells (carrying mitochondria) have been around for a little less than half of that time.

In that incredibly large span of time (if you counted 1 number per second, you'd reach 1.5 billion in about 47.5 years), what used to be an independent organism (we assume) has become an organelle - an integral part of the eukaryotic cell. It absolutely could not survive outside the cell on its own, and relies on signals from the cell (mainly, the cell's energy needs as detected by "sensor" proteins to key molecules like glucose and ATP) to reproduce.

Therefore, it is most appropriate to think of mitochondria simply as another organelle, just like the endoplasmic reticulum, lysosomes, or the nucleus. It doesn't make sense to think of those other structures as "alive" or "dead", just as it doesn't make sense to think of mitochondria in the same way. Yes, they used to be independent, but are no longer; instead they are a well-integrated part of the whole cell.


How do I find samples/patients in TCGA (the cancer genome atlas) that had radiation therapy? I want to correlate the expression of a gene (for sample the KRAS gene) with survival and if the patient received radiation therapy using any suitable TCGA (the cancer genome atlas) dataset. However, I have so far been unable to figure out what patients have received radiation therapy.

Any suggestions?

The process is slightly painful but here is how you do it.
Go to UCSC Xena, then launch the browser, hit the Visualize tab, pick your cohort of interest, then in the next menu pick phenotype, and then type radiotherapy in the box and pick the radiotherapy related columns you want. Then, once it has loaded the annotation bar, you can hit download and the downloaded spreadsheet will have this information along with the TCGA barcodes. As for clinical data, https://www.synapse.org/#!Synapse:syn7343873/wiki/412112 is a very good pancancer source.


Why do we only initially feel the bending of a hair? In my neurobiology class, my professor prompted us to take the tip of our pencil and fold or push down a single strand of hair on our arm or leg in the opposite direction that it grows in. He then commented on how we are able to detect the initial stimulus, but how after a while we no longer feel the hair being bent.

My question is thus, why does this occur? Why would we suddenly no longer be able to feel the stimulus of the hair being forced back?

Short answer
Touch receptors become unresponsive after continuous stimulation, a process called neural adaptation.

Background
There are various touch receptors in the skin (Fig. 1). One of them is the hair follicle receptor. These receptors form sensory nerve fibers that wrap around each hair bulb. Bending the hair stimulates the nerve endings.

All the afferent fibers of the skin receptors in the skin show neural adaptation. A rough classification of the various skin receptors is grouping them in rapidly and slowly adapting fibers.

Rapidly adapting fibers respond mainly to pressure changes. Typical examples are the Pacinian and Meissner's corpuscles, but also the hair follicle receptor.

Fig. 1. shows a static stimulation of the various receptors. Upon initial stimulation, the hair follicle receptor (Fig. 1a) vigorously fires action potentials. Because the hair follicle receptor rapidly adapts, however, it soon stops responding when the hair is continuously, statically bent in that same direction. Once the stimulus is removed it fires another volley of action potentials because the hair moves again.

In other words, the hair follicle receptor responds to strokes, stretch and skin vibrations, as it is a novelty detector; it detects change, just like Pacinian and Meissner's corpuscles do (Fig. 1b,c). This opposed to Merkel cells and Ruffini endings (Fig.1d,e) - these receptors are designed to continuously fire action potentials upon a static pressure stimulus (Fig. 1), although even these receptors eventually give up and become unresponsive.

Fig. 1. The skin receptors and neural adaptation. source: Delmas et al., (2011)

Reference
- Delmas et al., Nature Rev Neurosci (2011); 12: 139-15


Is 100% antibacterial resistance possible? The quest to develop antibacterial and antibiotic substances has often been described as an arms-race, as bacterial life develops resistance, requiring us to develop novel agents which can effectively kill said microbes.

My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?

There is only so much information-capacity in microorganism DNA to encode the means of resistance to various substances. If we climb the arms-race ladder high enough would a highly-advanced bacteria somehow "forget" how to defend against penicillin, for example?

...or are we utterly boned?

This is a theoretical question, which I can't answer, because genetics is not my favorite topic. In practice we only have about a dozen antibiotic classes. There are already panresistant bacterias, which are resistant (as far as I know) all of these classes of antibiotics, so we have already lost.

The causes of our defeat is more interesting I think:

Pharmaceutical industry does not have enough interest in the antibiotics research, since it is not as profitable as for example cholesterol reducers. Antibiotics are cheap, and you usually heal after the first treatment, while the research and the clinical trials are really expensive, it is hard to find working chemicals, which do not have severe side effects.

  “We  need  to  shift  from  the  concept  of  the  pharmacy  as  a
  ‘shop’  and  build  a  culture  of  pharmaceutical services. This is
  already happening  in some countries, but we need to make it  the
  rule  everywhere,”  says  Zsuzsanna  Jakab,  WHO  Reg ional  Director
  for  Europe.  “As  pharmacists  dispense  medicines  to  patients,they
  are   important  allies  in  our  fight  against  antibiotic
  resistance.  As  such,  they  need  to  be  ena bled  to  deliver
  accurate  information  and  counselling on proper antibiotic use.”

  Over  40%  of  antibiotic  prescriptions  are  inappropri ate,  recent
  studies  found.  This  relates  especiallyto antibiotics prescribed
  for the common  cold and sore throat; these most oftenresult  from
  viral infections,on  which antibiotics have no  effect. Further, in
  some countries, there is  atendency towards self-medication.
  Inappropriate an tibiotic use is the major driver of growing
  antibiotic resistance.

Pharmacists have decisive role in combating antibiotic resistance, says new WHO European survey
People with Mycobacter infections does not always do the treatment long enough, so Mycobacters can become resistant to antibiotics.

  Most people with TB are cured by a strictly followed, six-month drug
  regimen that is provided to patients with support and supervision.
  Inappropriate or incorrect use of antimicrobial drugs, or use of
  ineffective formulations of drugs (e.g. use of single drugs, poor
  quality medicines or bad storage conditions), and premature treatment
  interruption can cause drug resistance, which can then be transmitted,
  especially in crowded settings such as prisons and hospitals.

http://www.who.int/features/qa/79/en/
There is no global regulation of how to use antibiotics, so in some countries you can buy them without consulting a doctor and get a prescription. On top of this you can buy antibiotics without prescription on the internet if you want. This leads to overuse of antibiotics, and overusage leads to resistance.

  Self-medication is more common in developing countries due to factors
  such as ready availability of antibiotics without prescription, the
  unrestricted access to antibiotics,lack of regulation over drugs, and
  physicians and pharmacists prescribing and dispensing antibiotics
  without regard to the cause of infection

http://article.sapub.org/10.5923.j.cmd.20110101.02.html#Sec3.3.4

  We found 138 unique vendors selling antibiotics without a
  prescription. Of those vendors, 36.2% sold antibiotics without a
  prescription, and 63.8% provided an online prescription. Penicillins
  were available on 94.2% of the sites, macrolides on 96.4%,
  fluoroquinolones on 61.6%, and cephalosporins on 56.5%. Nearly all,
  98.6%, ship to the United States.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746509/

  These results demonstrate that, although illegal, the sale of
  antibiotics without a prescription continues in Spain.

http://cid.oxfordjournals.org/content/48/10/1345.full
Some of the antibiocstics are used by agriculture industry, which leads to antibiotics resistance as well.

  They identified bacteria able to shrug off the drug of last resort -
  colistin - in patients and livestock in China.

  It is likely resistance emerged after colistin was overused in farm
  animals.

http://www.bbc.com/news/health-34857015

  Nutritive and therapeutic treatment of farm animals with antibiotics,
  amounting to half of the world's antibiotic output, has selected for
  resistant bacteria that may contaminate the food produced.
  Antibiotic-resistant enterococci and staphylococci from animals are
  found in food when they survive the production processes, as in raw
  cured sausages and raw milk cheeses1. The broad host ranges of some
  plasmids and the action of transposons in many bacteria allow
  antibiotic-resistance genes to be communicated by conjugation between
  different species and genera2,3. A multi-antibiotic resistance plasmid
  from a lactococcus found in cheese provides a historical record of
  such events.

http://www.nature.com/nature/journal/v389/n6653/abs/389801b0.html

  About 2/3 of the antibiotics are used in animals.

https://youtu.be/iLJAleLjJv8?t=3m47s

So the problem is with not enough motivation in development and the lack of proper regulation of usage. Regulation is the business of the politicians, so its their fault as always. :D


Are antihistamines considered to be psychoactive substances? I have heard many times that the widely used antihistamines are not considered to be psychoactive drugs. Yet their impact on ones cognitive functions can be substantial. According to some sources, sedatives are also attributed being psychoactive, but not antihistamines. What is the difference?

UPDATE

Some links for the "cognitive effects" that I am referring to include hallucinations as well as drowsiness, anxiousness and irritability.

Besides that, it is well known that antihistamines cause drowsiness and sleepiness which are artificially altered states of mind because they are 1) not naturally-occuring, 2) have different mechanics and flow than their natural counterparts.

from experience I know these effects can be very strong, up to the state when one sees dreams while being awake. I can't find any scientific papers on that, but I have found many reports on the web and among people I've talked to.

Short answer
First-generation anti-histamines are psychoactive, second-generation equivalents may not be*.

Background
According to WHO, psychoactive substances are:

  [...] substances that, when taken in or administered into one's system, affect mental processes, e.g. cognition or affect. This term and its equivalent, psychotropic drug, are the most neutral and descriptive term for the whole class of substances, licit and illicit, of interest to drug policy. ‘Psychoactive’ does not necessarily imply dependence-producing, and in common parlance, the term is often left unstated, as in ‘drug use’ or ‘substance abuse’.

Antihistamines are used to treat allergies. First-generation antihistamines readily cross the blood-brain-barrier and have been associated with performance deficits on tests of attention, working memory, vigilance, and speed. By contrast, second-generation antihistamines that do not readily reach the brain do not have these side-effects (Kay, 2000).

Since attention, working memory and vigilance are mental cognitive processes, first-generation antihistamines fall into the classification of WHO as being psychoactive.

Reference
- Kay, J Allergy Clin Immunol (2000); 105(6-2): S622–7

Note
*I am not an MD and data on 2nd generation drugs are based on a single study with a limited number of tests. Consult a medical professional for prescription of the appropriate treatment.


Excessive sweating in dry heat It's pre-monsoon season here in India. The temperatures in the Northwest of the country really take a spike around mid April. Apparently the heatwave-like conditions seem to have announced themselves quite early this year. The mercury is at 42°C for most of this past week.

I'm new to this region and even though the relative humidity is quite low, such weather conditions prove unbearable to me. A few minutes walk down the Avenue and I start to sweat in bucket loads.  However, I find locals here don't sweat too much even in this hell of a weather. They say this weather is still bearable and that the monsoon phase proves to be the worst.

Having witnessed monsoon in other parts of the country I find favorable weather conditions prevailing at that time. The rain brings down the temperature and the air seems to get cooler. Most people here and elsewhere in the world would disagree with me on that. They say humidity is the worst and than dry heat can be combated by drinking enough fluids. I also see people sweating more in humid conditions compared to in temperatures of 42°C. The opposite applies to me. I barely break a sweat in temperatures of mid 30s despite there being high humidity.

What is this anomaly? Is there evidence that some bodies are just meant to excel in certain weather conditions while finding life difficult in others? Kindly help me understand the science behind it all.

My assumption is that if you're sweating excessively, you could also be suffering from a condition called hyperhidrosis. This is a condition whereby your hands and feet sweat excessively. I would suggest that you try looking into using a solution like an iontophoresis machine to be able to treat this condition. I too have suffered from sweaty hands for a long time, and after trying different options, I found that using an iontophoresis machine provided me with the best results.


Do plants with non-green leaves have chlorophyll and photosynthesis? Is it even possible that plants with non-green leaves have chlorophyll, and do such non-green leaved plants carry out photosynthesis?

Yes, it is possible, but not necessarily the case.

Non-green leaves with chlorophyl: There are leaves that don't appear green, but do have chlorophyl and therefore can conduct photosynthesis. (See, for instance, refraction effects in white caladiums or the link in the answer by Resonating).

Non-green leaves without chlorophyl: There are leaves that don't appear green because they have no chlorophyl, and so do not conduct photosynthesis. (See, for instance, parasitic plants like the Oronbanche linked by Cactuswoman or this Monotropa)


Doubling the concentration of extracellular calcium hyperpolarizes a neuron. Why? I was doing some back of the envelope calculations to try to answer this question in more mathematical terms. Essentially the question states: Why does increasing the extracellular potassium concentration depolarize a neuron, while increasing the extracellular calcium concentration hyperpolarize the neuron?

My initial thought was that there is a change in the equilibrium potential for each ion. Working this out however I realized I was wrong in my reasoning; my math proved me wrong.

Doubling the concentration of extracellular potassium makes the equilibrium potential of potassium 17.8 mV more positive. For calcium, it increases the driving force by 8.9 mV (based on room 300 K temperature). What this means to me is that both will cause the resting potential of the neuron to become slightly more positive, though calcium less so.

This is indeed obvious: adding more positive ions to the outside of the cell increases the driving force for that ion, and assuming there is any conductance (albeit small) then there will be some depolarization of the neuron.

This makes me think that this is not a phenomena explained by a neuron at rest. Some other mechanism is responsible for increased extracellular calcium causing the neuron to hyperpolarize.

My possible guesses:

If the calcium concentration is doubled, then the driving force for calcium increases, so there is more influx of calcium and thus the internal calcium concentration will increase. Because the concentration of calcium ions on the inside was previously near zero, now that internal concentration will rise to be some significant number, thereby hyperpolarizing the neuron.
The internal concentration of calcium rises slightly, but instead of (or perhaps in conjunction with) lowering the resting potential directly, there is more activation of calcium-activated potassium channels, thus raising the conductance of potassium ions, and thus ultimately hyperpolarizing the neuron.

Am I on the right track or am I missing something?

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

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


why do overweight individuals sweat more than ordinary people? A common phenomenon that I have noticed while traveling in buses is that overweight individuals seem to sweat a lot more than people with ordinary weight. Is this a coincidence or is there some science behind this?

Well there are some overall, simplified answers, but every individual is ..well.. individual.

First there is the ratio of volume to area. As interaction between two mediums normally is depended on their common/shared surface. If we state, that an overweight person A has more volume than a skinny person B of same height, A also has a larger surface as B, but not in the same scale the volume is increased.

The easiest way to describe is with spheres, let's assume bellies are kind of spherical ;-) . A sphere with diameter 2r=1d (hint: one dimension) has a surface of π4r²=πd² (hint: 2dimensions; 2nd power 2²=4; d²=(2r)²=4r²) and a volume of $$\pi\frac{4}{3}r^3=\pi\frac{8}{6}r^3=\pi\frac{1}{6}d^3$$ (hint: 3dimensions; 3rd power 2³=8).
So, if we manipulate r it's manipulated to the 2nd power for surface and to the 3rd power for volume.
So, if we double the radius, we have 4 times the surface, but 8 times the volume.

Humans are biochemical machines, we take an energyform we can exploit to fuel our processes keeping us alive. These processes also produce heat, which is kind of a nice sideeffect allowing us to operate in cold climate. But in hot climate we need to get rid of the heat.

As I stated before, interaction is surface based. Person A has a lot more heat producing volume than B, but the surface isn't that much bigger, so A's surface has a higher urgency to interact with the medium around than B's surface (so more sweat for example). Also more tissue produces more heat. But again disclaimer: different tissues have different activities.

Furthermore fatty tissue has an insulating effect, which reduce interaction even more. Other way round the heatloss of an overweight person isn't as dramatic as for a skinny person in sudden cold.

But these are simplified answers, there's much more to it. Like bloodpressure, thyroid, biological activity. Which can be influenced by so many more things.


What species have had their genomes sequenced/are being sequenced? The human genome project released it's first complete genome nearly ten years ago. Since then many species have also been sequenced.

I am trying to find a list of completed (and possibly ongoing/initiated) projects sequencing other species along with some very basic summary data such as number of genes (divided amongst the sex chromosomes and autosomes), length of DNA, number of chromosomes etc.

This is for a presentation I am giving at a conference and would make a nice addition to my talk.

The GOLD database (Genomes Online DB) contains data on the sequencing status, and also some stats (number of chromosomes, genome size) -- but this extra data is not available for all species.


Why hasn't life on Earth reached an evolutionary stable strategy? I heard in some YouTube video that cheetahs only existed 5,000,000 years and according to https://en.wikipedia.org/wiki/Extinction, extinctions are occurring all the time so I assume life on Earth hasn't reached an evolutionary stable strategy. I know some species like ants are in an evolutionary stable strategy and most species are close to their evolutionary stable strategy because the system of the rest of the species is changing so slowly but why hasn't the system of all life on Earth reached an evolutionary stable strategy. Could it be that it's destined to never reach one? That doesn't necessarily mean there isn't one. According to https://en.wikipedia.org/wiki/Evolutionary_game_theory, the side blotched lizard has 3 forms undergoing cyclic evolution so it's destined to never reach an evolutionary stable strategy if the state of the rest of the species on Earth doesn't change. There's another case of cyclic evolution where rabbits outcompete wolves when there are very few rabbits and wolves outcompete rabbits when there are a lot of rabbits? Why are there so many species that have existed for no more than 5,000,000 years instead of the system of all life on Earth being stable with a few species undergoing cyclic evolution? What's causing the current state of all life on Earth to keep on not being evolutionary unstable?

Because the environment on earth is not stable on the long run.

Antarctica was on the tropics. However plate tectonics has moved the continent from that location to south pole. And in time the continues will leave the poles and move toward the tropics again.

So a perfectly evolved animal in tropical Antarctica 200 million years ago, would have to continue evolving or it would have gone extinct as Antarctica moved southwards. And the animals living on Antarctica today will have to evolve as the continues continues with its motions.

Also predator-prey relationships... are red queen type relationship. They may appear stable on the outside, but both parties are actually under selection pressure to evolve, to counter the advantages of the other party. They are in an arms races. Pressure to out run the predator. Pressure to outwit the prey. Pressure to better camouflage. Pressure to detect prey from multiple senses (sound, sight smell).

So on the long term, the strategy that a predator uses will change as its prey evolves. And vise versa for the prey.


Is it possible to knock out a gene in adults? gene knockout is mainly used in creating newborn animals... right? Well can you do it to already-adult animals or humans so that they themselves would experience change in their body and not just their off springs?

Actually, Cas9 system might be a possible method to achieve your aim in the future, research teams are trying to utilize cas9 in vivo, which means maybe someday we can doing some genetic modification in body cell precisely. However, this is only a future direction and we still can not say its fit for a knockout.(Patrick D. Hsu, Eric S. Lander, and Feng Zhang, (2014) Development and Applications of CRISPR-Cas9 for Genome Engineering. Cell 14(6): 1262-1278)
And for editing some cell gene in a limited area, some research are on going for therapeutic purpose (Liqun Zhang et al.CFTR Delivery to 25% of Surface Epithelial Cells Restores Normal Rates of Mucus Transport to Human Cystic Fibrosis Airway Epithelium), but haven't seen research are trying to built KO cell in vivo.


What is the difference between transverse section and longitudinal section? Can anyone explain the difference between transverse and longitudinal section?

Or are they the same?

For an animal with bilateral symmetry, a longitudinal section is parallel to the anterior-posterior axis (labelled central axis in the image below). Sections through or parallel to either the sagittal or coronal (also called frontal) plane are longitudinal. A transverse section is perpendicular to the anterior-posterior axis and is also called a cross section.

image source


Does repolarization of muscle fibers mean that the muscle bundle is relaxed? If I flex my bicep and continue to contract it does it mean that the muscle cells are in depolarizing state and not repolarizing?

No, macroscopically human muscle works by oscillation. This means that when a muscle is contracted (isometric contraction), some fibers alternatively contract through the actin/myosin process while some others relax at the same time. The end result is that the muscle as a whole keeps the same length, although it still does consume energy to stay in that state. That is why you get tired after some time of isometric contraction. To directly answer your question, it means that muscle in isometric contraction state will have some fibers depolarized, and others in resting state at any moment.


What goes into a vaccine placebo, typically and in the specific case of Pfizer's SARS-CoV-2 vaccine trials? I am curious about what actually goes into a vaccine placebo formulation, given that there were apparently some reactions reported by trial subjects who received the Pfizer SARS-CoV-2 placebo.
From what I've been able to find out online, the actual vaccine contains as principle ingredients (simplified):

mRNA (active ingredient) to make the target antigen (spike protein)
lipids (to protect the mRNA and facilitate its delivery into cells)
salt(s) to adjust pH and match the salinity of blood
sugar to address issues which occur when the vaccine is frozen

An injectable placebo could be as simple as a saline solution... if so, how could reactions be explained? Is it entirely psychosomatic?  Is the Pfizer SARS-CoV-2 trial placebo the complete formulation (or some subset of vaccine components) minus the active (mRNA) ingredient?
The lipids have been implicated in allergic reactions to the actual vaccine; would they have been present in the placebo and account for the placebo reactions?

Simple answer: This vaccine trial compared their trial vaccine against saline.
See the original publication by Biontech and Pfizer in the New England Journal of Medicine linked below. The relevant information can be found in the methods section:

TRIAL PROCEDURES
With the use of an interactive Web-based system, participants in the trial were randomly assigned in a 1:1 ratio to receive 30 μg of BNT162b2 (0.3 ml volume per dose) or saline placebo. Participants received two injections, 21 days apart, of either BNT162b2 or placebo, delivered in the deltoid muscle. Site staff who were responsible for safety evaluation and were unaware of group assignments observed participants for 30 minutes after vaccination for any acute reactions.

As far as I followed up the case of the allergic reactions, two of these have been observed in England. Both people had an epipen injector for such cases by hand, making it possible that they have underlying problems with allergies (as this is not a medical device people usually have at hand), no such cases have been reported from the trial. Allergic reactions are always a small risk with vaccinations which is the reason why this is done in a controlled medical environment.
As for the vaccine reactions in the placebo group, this can be caused by the nocebo effect, where expecting negative effects leads to a more negative reaction. As @BryanKrause mentioned, all possible effects reported in such trials are recorded as possible side effects. This leads to a lot of things being recorded which happened at the same time as the vaccination but have no connection to it.
Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine


What is the strength of human cornea? What is the difference of pressure a human eyeball cornea (cornea, lens and other elements separating vitreous body from air) can handle? Or asking differently: what the outside pressure should be to "blow up" a healthy man's eyeball?

Normal pressure in the eye1,2 is between 10 and 21 mmHg (somewhere around 1.3-2.8 kPa or 0.01-0.03 atm) with pathology occurring at around 30 mmHg.3  Clearly the cornea can handle that, but how much more?  There's a lot more evidence as far as I could see for how well surgeries hold up, with 150-300+ mmHg (20-40 kPa, 0.2-0.4 atm).4  One source5 from 1998 cites work supposedly showing that the stroma:

  gives the cornea 100 times more strength than is necessary to withstand the maximum intraocular pressure under physiological conditions.

So maybe around 200 kPa, for just the stroma?  Interestingly, a new eye layer was discovered earlier this year; this Dua's Layer is incredibly thin - 15 microns - but can withstand pressures of around 100-200 kPa (750-1500 mmHg, 1-2 atm).6,7  The large range there is due to some conflicting numbers in those links; the 200 kPa is the more widely reported one, but again, that's just for one layer.

Then, of course, there is this: a beautiful 2009 thesis by Jill Aliza Bisplinghoff from Virginia Tech which thoroughly examines the issue.  As an answer to your question, it includes the following such gems:

  The high rate pressurization of 20 human eyes resulted in a mean rupture pressure of 0.97 ± 0.29 MPa (7275.60 ± 2175.18 mm Hg)... A student T-test revealed that the difference in the rupture pressure between the equatorial mean of 0.93 ± 0.30 MPa (6975.57 ± 2250.19 mm Hg) and the meridional mean of 1.13 ± 0.21 MPa (8475.70 ± 1575.13 mm Hg) was not significant (p=0.16)

and

  A pneumatic cannon was used to impact eyes with a variety of projectiles at multiple velocities... The projectiles selected for the test series included a 6.35 mm diameter metal ball, a 9.25 mm diameter aluminum rod, and an 11.16 mm diameter aluminum rod... A range of internal eye pressures were produced that varied from 1256 mmHg (24.3 psi) to 22843 mmHg (442 psi)... [and] resulted in zero globe rupture.


Is O4I2 sufficient to reprogram cells (ie induce pluripotency)? Is exposure to the chemical O4I2 (ethyl 2-((4-chlorophenyl)amino)-thiazole-4-carboxylate) sufficient to reprogram an adult cell back to pluripotency?

They sell this chemical online for pretty cheap. My question is, if I wanted to start a colony of induced pluripotent stem (iPS) cells, would I only need to buy this or are other reprogramming materials required?

No, the chemical O4I2 (thats a name, not a chemical formula btw) only helps to induce production of the Oct-4 transcription factor. Even if just this chemical is sufficient to express Oct-4 (which it might not be, I'm not really sure about that), you still need to induce transcription of other genes (usually Sox, cMyc & Klf4) to obtain iPS cells.


Mites on ginger root I was just looking at some mouldy ginger found in the fridge under the microscope and was horrified/delighted to find (what looked to be) mites growing in it. I have searched the web and can only find references to red spider mites which these are certainly not. They were clear white and under 40x zoom about less than a mm across - does anyone know what they could be? Furthermore, what are they feeding on (ginger root is only ~15% carbohydrates - is that enough?) and has a minimal (~1%) amount of protein.

Here is a picture (sorry for the quality but the white thing looks to be a mite).

Does this look like the same bug to you ?

.

This one is a bulb mite, Rhizoglyphus robini, see here.


Can retroviral delivery systems "overwrite" genes? As the question states, what are the limits of retroviral genetic delivery systems?

Are they limited to adding additional gene sequences to a cell, or can they actually overwrite specified segments of DNA?

Or, more aptly described, can they remove one segment of DNA, and insert a new segment (whether the same or different length) in the spot where the old segment used to be?

Retroviruses, such as HIV, have a genome that is composed of RNA.  Once inside the host cell, that RNA is reverse-transcribed into DNA; it is that DNA which is inserted into the host genome.  All retroviral genomes are integrated through insertion; there is never any replacement.

Some retroviruses do, however, disrupt normal gene function.  Mouse mammary tumor virus (MMTV) or Human T-lymphotropic viurs (HTLV) will often insert inside or near host genes termed "oncogenes," that, when disrupted, can lead to cancer formation.1,2  Viruses could cause up to 15% of cancers in humans.3  So, no actual genetic replacement, but there can definitely be genetic disruption and a deleterious functional change.

This ability, to insert new genes, has recently been touted as a new way to cure many diseases.  Here's the most recent case, where the researchers used a retroviral backbone to insert a functional gene into some children; i.e., genetic engineering (Side note: Every time you see an article saying how scientists used HIV to cure a disease or something, this is what they mean.  It's akin to calling dental X-rays "giant death lasers that fight cavities.").  With luck we will get better and better at it, but right now it's only successful in limited cases for very specific diseases; massive genetic engineering of humans is still far off (unless you count bone marrow transplants).


why do chaperones bring protein into mitochondria? why would mitochondria need protein? Sounds trivial? Please help to sort out. I saw this picture while looking at dehydration reactions and cell revision.

And proceeded to the reference web page.

  Protein Folding and Processing in the ER: Various changes occur to proteins in the ER.
  Chaperones and Folding: Polypeptides must assume the correct folding pattern in order to function properly. The correct folding of a protein is mediated by chaperones (they also are proteins--chaperones are abundant in the ER lumen). A completed polypeptide will assume the correct folding pattern spontaneously, however before translation is complete, it could assume an incorrect formation or it could aggregate with other partially made polypeptides. To prevent this, chaperones in the ER (and cytosol) bind to the nascent polypeptide and keep it from interacting with anything until the polypeptide is completely synthesized. (Chaperones bind to polypeptides destined for mitochondria then release them as they pass through the mitochondrial membranes. Chaperones on the inside of mitochondria bind until these polypeptides have completely entered.)

With regards to protein synthesis and folding, this kind of info is not in my textbook. Not in couple of the online open textbooks either. I even search for where do protein fold? to find out if there was a relationship. It doesn't say protein fold in mitochondria and turns out it's a question most scientist are looking for answers.

For whatever protein synthesis I have learnt so far, there was no mentioning of protein strands going into mitochondria but mitochondria as a power houses. What's going on here?

Why would a protein go into a mitochondria? How does it exit and where to?

As you probably know, mitochondria (together with chloroplasts) are a very interesting organelle: they are a result of an endosymbiotc relationship that took place more than 1 billion years ago.

And, because of that, mitochondria have their own (circular, as a prokaryote) DNA. And here comes the common misconception: a lot of students think that mitochondria (and chloroplasts as well), because they have their own DNA, can synthesise all proteins they have (the most famous ones are the enzymes of Krebs cycle and Respiratory chain). But that's not correct.

What happened is that, generation after generation, along a very big period of time, mitochondrial genes were, little by little, transferred to the host's nucleus. According to Nature (2017):

  During the course of mitochondrial genesis, many genes were transferred from the genome of the mitochondrial endosymbiont to the genome of the host.

Thus, today, a human mitochondria has only 37 genes:

From those 37 genes, only 13 code for respiratory proteins. Therefore, those mitochondrial genes are responsible for only a minor fraction of the proteins present in a human mitochondrion. So, where do the other proteins come from?

They come from the nucleus, encoded in the nuclear DNA. Those proteins are synthesised in the cytosol and, using peptide signals, are transferred to the mitochondria. According to Dudek, Rehling and van der Laan (2013):

  Most mitochondrial proteins are encoded in the nucleus. They are synthesized as precursor forms in the cytosol and must be imported into mitochondria with the help of different protein translocases.

According to the Human Protein Atlas, 1070 proteins have been detected in the human mitochondria. Thus, since 13 of them are from mitochondrial origin, we conclude that at least 98.7% of the mitochondrial proteins are imported from the cytosol.

Sources:

Nature.com. (2017). Origin of Mitochondria | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/the-origin-of-mitochondria-14232356 [Accessed 5 Aug. 2017].
Dudek, J., Rehling, P. and van der Laan, M. (2013). Mitochondrial protein import: Common principles and physiological networks. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1833(2), pp.274-285.
Proteinatlas.org. (2017). Search: subcell_location:Mitochondria - The Human Protein Atlas. [online] Available at: http://www.proteinatlas.org/search/subcell_location:Mitochondria [Accessed 5 Aug. 2017].


Determine percentage of crow hybrids We had in class following question which I had no idea how to get to the correct answer:

  The carrion crow and the hooded crow are fertile together,  but their
  reproductive success is reduced by 50%. In a certain region exist
  two populations of both species of roughly the same size. Thus,
  mixed couples occur in about 10% of all cases. What is the percentage of
  hybrids in the F1-generation?

(Translated from German.)

I thought it would be something like 5/95 = 5,3% but apparently the answer is 1%. Why?

In order to make your reasoning clearer, you should use more formal notations and explain your thinking step by step. Here's a proposition.

Let's use the following notations :

$C$: the total number of couples (mixed and not mixed)
$r$: the reproductive success
$F1_h$: the number of hybrids in the F1 generation
$F1_{nh}$: the number of non hybrids in the F1 generation

You are looking for the percentage of hydrids in the F1 generation, which is:
$x = \frac{F1_h}{F1_h + F1_{nh}}$

You know that $10~\%$ of the couples are mixed couples and that their reproductive success is reduced by $50~\%$. This can be written:
$\begin{cases} 0.9\cdot C \cdot r = F1_{nh} \\ 0.1\cdot C\cdot \frac{r}{2} = F1_h \end{cases}$

Thus: $\displaystyle x = \frac{F1_h}{F1_h + F1_{nh}} = \frac{0.05\cdot C\cdot r}{C\cdot r\cdot 0.95} = \frac{0.05}{0.95}$

This is indeed the result you suggested. So the correction you were given might not be correct. Or maybe there was some more information in your homework that you ignored...


What is an accessible book about plant evolution for a non-biologist? I have an acquaintance interested in learning about the evolution history of plants. This person has a wide knowledge on botanics, from personal reading and taking care of plants, but E is neither a biologist or a biology student.

Based on this, which is an accessible book to non-biologist that can be used to learn about the evolution of plants?

I have Fossil Plants by Paul Kenrick and Paul Davis, published by The Natural History Museum in London.  It takes the reader through a well-researched but accessible illustrated history of the evolution of plantlife from the beginnings to now.  There are photos of many key fossils, and artist's renderings of what the landscapes of the past would have looked like.


Meaning of "Antibody is 50% w/w pure of interfering proteins" From Google Patents, "Preparing antibodies from cho cell cultures for conjugation":

  An isolated antibody or ADC is typically at least 50% w/w pure of interfering proteins and other contaminants arising from its production or purification but does not exclude the possibility that the monoclonal antibody is combined with an excess of pharmaceutical acceptable carrier(s) or other vehicle intended to facilitate its use. Sometimes monoclonal antibodies or ADCs are at least 60%, 70%, 80%, 90%, 95 or 99% w/w pure of interfering proteins and contaminants from production or purification.

Does it mean that even after purification the antibody solution may have an amount of impurities totaling to up to 50% of the antibody itself, in terms of weight? That the total weight of impurities may reach 50% of the antibody weight?

Maybe "an isolated antibody" is an antibody just after it has been produced? But the mention of "purification" confuses me. Why then such a high impurity content?

Patents are not the best source for reliable information, and obviously are not that readable. In this case they mean that of the purified product (usually that what comes of a protein A column I think), at least 50% of the weight is antibody. Or less (silly patents).

Commercial purification of antibodies (and proteins in general) is usually not that thorough. Most of the times what you'll get is just culture supernatant with cells removed, maybe some ammonium sulfate precipitation fraction or if it's thermostable just the proteins that are left after the production-solution is heated.


Can canines communicate with each other using gaze direction? After researching why humans have white scleras when most primates have dark scleras, I stumbled upon the cooperative eye hypothesis. It proposed that white scleras may have evolved on behalf that it is an effective form of communication in that it makes the iris stand out and enables another to clearly see where the eye is looking so as to read expressions.

I noticed that dogs, which also have white scleras, use eye direction periodically for expression. Does the cooperative eye hypothesis apply to canines as well? If not, then for what reason might dogs utilize eye movement as they seem to do? Might such a thing be learned behavior?

It is hypothesized that the starkness of white sclera against darker colors of the pupil and iris is a unique mutation in primates that have become prevalent in human beings because it enhanced our ability to communicate with other humans and animals, including dogs, by more clearly communicating where we are looking.

However, it has not yet been established that dogs use this communication with each other, communicating more commonly with other means such as body language, head direction, vocalizations, etc. Some dogs, especially domesticated ones, do have white sclera and it is proposed that this is due to unintentional selection by humans who have a preference for such features.

What is extremely fascinating is that this 'mutation' occasionally occurs in chimpanzees and apes, too, but has not become prevalent in their respective populations.

Sources:

Secret Life of Dogs- BBC Film
Do the Eye Have It?-Academia
Common feature in domesticated dogs-CARTA
Juvenile features-NIH