I'm guessing here - some type of flagellate? [often helps to know more details about the specimen, e.g., magnification?]

I agree with the above comments. For some genes we know that there are likely hundreds of allelic variations, e.g., there are over 100 described for the metabolic enzyme cytochrome P450 2D6 (CYP2D6: this enzyme metabolises many common pharmaceuticals such as some beta-blockers), the numbers steadily increasing with the use of the latest DNA sequencing methods.

For this particular gene a repository has a set of criteria that have to be met for an actual allelic variation - see http://www.cypalleles.ki.se/criteria.htm, e.g., to be assigned a unique allele designation the “sequence should contain at least one nucleotide change that has been shown to affect transcription, splicing, translation, posttranscriptional or posttranslational modifications or result in at least one amino acid change.” Note that many non-functional variations are not designated.

I would imagine that this border has been highlighted due to a combination of factors - e.g., population dynamics, antimalarial usage and plasmodium control measures which could all contribute to multidrug resistance problems. A WHO leaflet on this region - see http://www.who.int/malaria/publications … y_2012.pdf - highlights population migration, and malaria-endemic- and high-transmision-areas.

Proteins are usually broken down by proteolysis which involves the action of enzymes. Most but not all (e.g., ribozymes) enzymes are proteins themselves, and enzymes can act proteolytically on enzymes to tightly control target enzyme activity. Some enzymes (e.g., protein convertases) act on larger protein precursors by cleaving at dibasic amino acids to yield smaller, biologically active peptides/hormones - this is quite common for neuropeptides, examples include the processing of pro-hormones to yield beta-endorphin, vasopressin and oxytocin. Enzymes degrade proteins at different rates (e.g., minutes to days to months) for different proteins, what we usually refer to a protein’s half-life. As Bernard mentions proteins can also be degraded by non-enzymatic proteolysis such as changes in pH and/or temperature.

As a 'supporting' neuronal cell, astrocytes often participate in changes in the 'functional plasticity' (which can involve alterations in cellular phenotypes) of various brain regions. In addition to David's suggestion you could also search something like 'astrocytes water deprivation', 'astrocytes hypothalamo-neurohypophysial system', 'atrocytes brain injury' or the like.

Searching 'kangaroo spleen' there is a cool link:

'On the structure and use of the spleen' by Henry Gray (1854) that has a description of the spleen from the kangaroo and a few other species.

David, from what I can gather from a very brief search, compared to many other animals the marsupial spleen is considerably smaller in relation to body size.

The process of transcription and translation is covered exhaustively (at A level and beyond) via a Google search, e.g., see - http://www.chemguide.co.uk/organicprops/aminoacids/dna3.html,
and there are many images that clearly depict the mechanism(s).

I think all should be clear if you note that the template for transcription is complementary to the coding (in your example the sense 5’-3’) strand. So the mRNA is complementary to the strand that is read!

Note also that the coding strand does not always have to be the ‘top’ (sense) DNA strand (labelled in the 5’-3’ direction) - there is extensive antisense (‘bottom’) strand transcription in the mammalian genome.

Kangaroo anatomy is not my forte, but how about the spleen? The spleen of rodents (rats, mice) is 'riddled' with white 'spots' (under the surface) comprising the white pulp (areas of lymphocyte activity), not too dissimiliar from the appearance of your tissue.

[if spleen, I doubt it would actually be attached to the stomach]

Yes, pepsin cleaves IgA. IgA secreted in the gut is accompanied by a ‘J (joining) chain’, which regulates its polymer formation, and a ‘secretory component’ which wraps around IgA molecules and protects them from proteolytic cleavage by the gastric acids and enzymes.

G’Day O: It is difficult to answer this question. Fish don’t ‘hold their breath’ when out of water - wet gills will allow for some oxygen exchange to occur (and/or some fish have a labyrinth organ which enables them to breathe surface air). Depending on the size of the fish and local conditions (e.g., humidity) it is probably minutes, bearing in mind that the longer the fish is out of water the stress it endures will reduce survival when it is released. Here is a previous link that mentions the stress to catch-and-release fish - http://www.askabiologist.org.uk/answers … p?id=13113

Changes in core body temperature, due to heat or cold, impact our homeostatic control to maintain temperature equilibrium. A whole host of mechanisms can come into play as temperatures increase, especially during a prolonged fever. For example, not only are enzymes implicated, but molecules such as cytokines (e.g., interleukins) and chemokines synthesized (which will involve enzyme activity) as a by-product of peripheral immune system activation that can directly or indirectly impinge on the brain. These substances can also be produced by brain cells themselves, such as microglia, endothelial cells and neurons, and can influence cognitive processes such as memory by changing neurotransmitter tone, e.g., altering glutamate, GABA, acetylcholine and dopamine release in brain regions such as the hippocampus. Prolonged fever may act as a chronic stress to activate the hypothalamic-pituitary-adrenal axis to release cortisol - this can alter cognition. Dehydration activates neurotransmitters and neuromodulators to conserve body water, e.g., vasopressin will help maintain water balance by increasing water resorption from the kidney, but it also has antipyretic effects in the brain and can alter cognitive processes.

Similarly, hypothermia can alter neurotransmitter release. As an aside hypothermia is considered neuroprotective in certain situations (e.g., in some types of traumatic brain injury and cerebral hypoxia/ischemia).

MacConkey agar was one of the first ‘selective’ (for gram-negative and enteric bacteria) culture medias developed. Bacterial growth and colour development depends on the bacterial strain being cultivated, and may be reduced if the media is old (way past its ‘use-by date’), or has been exposed to light or extremes in temperature. At 37 degrees C you should see some growth after about 24h; bacteria will likely take longer to grow in your case since you are incubating your plates at 25 degrees C (higher than room temperature). The bacteria will continue to grow until they have used up local nutrients; if the plates are a bit dry this will likely reduce the amount of growth.

There are some basic experimental considerations here that you should discuss with your teacher! e.g., what is the bacterial growth like on other students’ plates?. By the way, in the lab we may include plating a bacterial strain of known concentration as a ‘positive’ control for our reagents and procedure. If you do a Google search you will find plenty of information on the types of bacteria that grow on this type of medium.

(posted in Birds)

To add, DTT and a number of its metabolites also act as ‘xenoestrogens’ or ‘endocrine disrupters’ that mimics endogenous estrogen by binding to the classical estrogen receptors (alpha and beta) and estrogen-related receptors.

I agree with Reetika, it will depend on the neurotransmitter and its local environment (including storage vesicles and neuronal 'activity') where there will be rapid diffusion, enzyme-decay (where relevant) and re-uptake (and transporters can be 'promiscuous' having binding capacities for more than one neurotransmitter). Although the absolute levels of neurotransmitter(s) released at most synapses may not be known, I would not be surprised if someone has arrived at an estimate based on quantal release, but as far as I am aware quite a few assumptions have to made depending on the technique used (see - http://www.ncbi.nlm.nih.gov/pmc/article … 8087.pdf).

P.S. e.g., here's a paper on some estimates of local neurotransmitter concentrations (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777263/) but no mention of what 'gets lost'! There are also references to the book 'The Biochemical Basis of Neuropharmacology' by Copper, Bloom, Roth (2003) saying that 80 percent of dopamine is retrieved from the extracellular fluid by re-uptake - I guess the remainder is broken down enzymatically and/or diffuses (I can't imagine much is bound to pre- or post-synaptic dopamine receptors)?

The DNA is what it ‘says on the tin’ - it is ‘naked’, not associated with proteins to form chromatin in chromosomes (unlike eukaryotic DNA).

David makes an important point about well-nourished individuals, changing diet and brain function  - e.g., with all the studies and 'press' about the beneficial effects of omega-3 fatty acids - check out the canned tin of fish in your supermarket!! - I think the scientific conclusion to date is that there are more studies needed on larger groups. There are a number of reports that have not shown a beneficial effect of omega-3 supplements on cognitive function in cognitively healthy people.

G'Day George: Yes, many of the major small molecule neurotransmitters such as the 'amino acids' glutamate, glycine and gamma-aminobutyric acid (GABA), and the non-protein catecholamines (e.g., dopamine, serotonin, noradrenaline) have 'gathering' (re-uptake) mechanisms, often driven by transporters. I have seen the statement from on-line advocates of diet changes to alter neurotransmitter levels that all neurotransmitters are made up of proteins - this is incorrect. Many neuropeptides (proteins of varying sizes) are sometimes considered 'neurotransmitters', 'neuromodulators' or 'neurohormones' - the issue is hotly debated - and the majority of these are inactivated by enzymes rather than re-cycled as intact proteins. A change in diet is sometimes recommended for people with suspected neurotransmitter deficiencies - an example of that could be supplementing your diet with L-tryptophan, an amino acid essential in serotonin synthesis. However, establishing whether there are mearsureable neurotransmitter imbalances in various conditions in the first place is often difficult!!

There is some evidence that ‘psychological’ stress can influence the immune response to vaccines (see - http://www.ncbi.nlm.nih.gov/pubmed/9629291; http://www.ncbi.nlm.nih.gov/pubmed/11139000), although in these studies the ‘stress’ in caregivers of patients with dementia was relatively ill-defined. A review on the subject (http://kungfu.psy.cmu.edu/~scohen/cohmillrab01.pdf) suggests that psychological stress may affect the secondary antibody responses to immunization, but the data is by no means conclusive which is not surprising due to a number of factors including: nature of, and predisposition to the stress; type of immunogen; methological differences in measurements of immune activation. Psychological stress can certainly alter stress hormones such as cortisol which can impact immune cells such as lymphocytes.


On the flip side immunization itself can cause a stress response via activation of the hypothalamic-pituitary-adrenal axis at various levels, releasing corticosterone, and an anticipatory activation of this and the sympathetic nervous system to release adrenaline.

(posted in General Biology)

I agree with Reetika although I would guess that the bioluminescence of the 'brightest' organisms would be luciferin/luciferase-based. There are other considerations such as organism size, how and where light emission is measured, and sample variability. Here is one comment based on photon measurement - http://entnemdept.ifas.ufl.edu/walker/u … r_29.shtml

Speaking from personal experience on the east coast of USA the light emission from the firefly, especially in numbers, is really impressive!!

As far as I am aware they are one and the same! see - http://www.ncbi.nlm.nih.gov/books/NBK21570/

Astrocytes have often been regarded as ‘mere’ supporting cells for neurons, responding locally to intense synaptic activity, but that view has changed dramatically over a number of years. For example it appears that astrocytes can release neuroactive molecules, often called ‘gliotransmitters’ (e.g., glutamate), that can modulate activity at functional synapses - whether this is excitatory or inhibitory will depend on the type of the molecules released and the nature of the synapse (e.g., acting on presynaptic or post-synaptic receptors).

Calcium transients in astrocytes themselves are often driven by ligands binding to G protein-coupled receptors on the cell surface of these cells - they can exhibit calcium oscillations independent of synaptic transmission.

In the clip it looks like the main image is of a cell body of a single astrocyte in a brain (caption says hippocampus) slice. It is showing fluctuations in intracellular calcium - there are also calcium fluctuations in its fine processes which perhaps is less evident at this resolution. The calcium changes in the astrocyte cell body often have different dynamics than those found in processes - see http://www.nature.com/nrn/journal/v15/n … n3725.html for commentary. Intracellular calcium rises can occur from an influx in calcium and/or release from intracellular stores.

I guess that the cell has been loaded (e.g., through bulk-loading, or into the individual astrocyte via a ‘patch’) with something like a calcium-sensitive fluorescent dye or genetically-encoded calcium indicator. The stimulus? It is likely that a neurotransmitter such as glutamate released from the neurons is acting on glutamate receptors present on the cell surface of astrocytes, which in turn can regulate synaptic transmission (e.g., see - http://onlinelibrary.wiley.com/doi/10.1 … 72864/pdf) and any number of other processes such as local blood flow. The astrocyte can also re-cycle glutamate to maintain excitatory neurotransmission. Note that neurons will release other molecules like potassium ions and/or perhaps other modulators/neurotransmitters such as neuropeptides.

Cone snails are not uncommon in the waters off Northern Queensland in Australia, with about a third of all species found there. They can release a number of different types of toxins, and there have been the occasional bites - see http://www.abc.net.au/news/2015-06-09/c … nd/6533710

As far as I am aware the harpoon is like a disposable, hypodermic needle, and once it is used to inject venom it is discarded. The cone shell can lock and re-load another harpoon to strike again. Here is an article and as site that may also interest you - http://www.nature.com/nature/journal/v4 … 798a.html; http://grimwade.biochem.unimelb.edu.au/cone/index1.html

Shawn, just to add that a colleague who is an expert in microscopical imaging here at Bristol says that "clarity of image will depend a great deal on cell type and use of preparation techniques. Resolution limits are not really dependent on whether 'analogue' or 'digital' image capture techniques are used but primarily on optical properties of the lenses used."

G'Day Jennifer: Normally the moiety you are referring to is the label that is incorporated into the DNA or RNA probe - but sometimes you have people referring to the actual nucleotide to be labelled as a moiety itself! The labelling moiety can be any number of molecules that can be detected in a number of ways including chromogenetically (e.g., digoxegenin, biotin - hence DIG or biotin moiety), fluorescently (a dye) or autoradiographically (a radioactive molecule). These molecules can be introduced into a stretch of DNA (or RNA) by a variety of methods - e.g., labelling roughly every fourth nucleotoide (as in incorporating a DIG moiety into RNA using DIG-UTP with RNA polymerase off a DNA template - a 'transcription' reaction), or labelling of a DNA oligonucleotide at either end (‘tailing’ - e.g., adding a stretch of DIG-labelled nucleotide to the end of a DNA probe).

Usually we want to introduce as many labels into the DNA or RNA probe as possible because that increases the detection sensitivity, e.g., 100 labels in a stretch of RNA 400 nucleotides long can be better (higher 'specific activity') than 25 labels introduced onto the end of a DNA probe by tailing. So highly-labelled probes are usually preferred to detect less abundantly expressed RNAs. But there are limits; e.g., a probe as large as say 600 nucleotides may not penetrate a tissue section as well as a 48 nucleotide probe, if you are doing a technique like in situ hybridization histochemistry. The sensitivity of many of the strategies can be increased by various techniques so that the activity of one labelled moiety can be amplified. Hope this helps!

Also, a simple google search will provide a lot of info on microscopes/microscopy, eye pieces and lenses. For example, microscope vendors will often cover digital versus analog (or analog plus digital) microscopy see - http://www.olympusmicro.com/primer/digi … sics.html; https://www.microscopyu.com/articles/di … intro.html

Bear in mind that even if you have a lovely microscope with all the bells and whistles for high resolution viewing the way the sample is mounted is critical. For example, you should consider the sample thickness, the mounting medium and the coverglass thickness. For the latter most people in the lab use something like number ‘1’ (a bit less 0.17mm thick but the refractive index of the mounting medium is also factored in) - the objective(s) you have on your microscope should offer some guidance about optical characteristics, e.g., see - http://www.microbehunter.com/about-the- … objective/

I hope your microscope has a decent specimen holder! Sometimes for these types of microscopes the specimen holder on the stage will not hold a slide firmly in place - you would want to move the specimen around easily without any manual manipulation (especially at high magnification under oil).

G’Day Ellie: This is a very interesting question (and EPQ topic)! Epigenetic silencing is a ‘natural’ process, e.g., it can contribute to the differential pattern of gene expression in the brain. It is also regulated by ‘stress’ such as adverse early life experiences which can alter gene expression in the young that appears to persist for life, and may be transmitted to future generations.

In terms of climate change as an environmental stressor in animal populations, there are studies to suggest that some genes are turned on or off (which may involve some epigenetic modifications) in reef fish to assist in adaptation to increased water temperature (see - http://www.nature.com/nclimate/journal/ … 724.html). Stable epigenetic changes to cope with increased temperatures can also occur in plants (http://mbe.oxfordjournals.org/content/27/11/2465).

Searching something like ‘genes switched off/on climate change’ on Google or PubMed will likely retrieve further examples. You will find a lot more studies on plants and animals which are easier to study relatively quickly under controlled conditions compared to characterising human cohorts. Bear in mind that climate change may have ‘positive’ or ‘negative’ adaptations, and direct and indirect consequences. For example it could lead to disruption of the food chain such as crop failure and malnutrition in parts of the population in some places of the world. Depending on the scope of this it may lead to epigenetic changes. Some of the best-characterised epigenetic changes in the human population are those that are presented by Dutch individuals who were prenatally exposed to famine caused by food embargos towards the end of WWII (named the Dutch Hunger Winter; e.g., see - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2579375/). Good luck with your research!

Myxomatosis is caused by a virus and I think it is mainly transmitted by biting insects. In terms of 'manmade' it was introduced into at least one country, Australia, to combat the large rabbit populations. Growing up in Southern Victoria I remember the often unpleasant sight of acutely infected rabbits - swollen faces and inflamed eyes were characteristic, the latter often leading to blindness.

Fine, but perhaps we should also draw the distinction (and some similarities) between passive/active transport across the G-I tract, lung, etc epithelia where a drug may be absorbed and the actual site where a drug may be ‘active’ (i.e., often via receptors on the target cell membrane).

No-one is saying that various 'drugs' cannot enter cells. It is well-known that some compounds can be actively or passively transported across the cell surface membrane. In addition, it has also been well-established for decades that adrenal and sex steroids such as cortisol and oestrogen cross the cell membrane and bind 'classical' nuclear/cytoplasmic receptors - there is evidence that these compounds can also bind receptors at the cell surface. Compounds such as cannabinoids can also cross the cell membrane, irrespective of whether they bind to the CB1 and/or CB1 GPCRs on the cell surface. There is a growing body of evidence that a number of endogenous ligands can also cross the cell surface and act at intracellular receptors. David's comment was that 'in many cases the drug does not get into the cell" - this remains true, as does compounds can cross the membrane with and/or without active transporters, and with/without binding to a cell surface receptor.

Ectopic pregnancies can occur outside the uterus (e.g., in a fallopian tube). Fertilization of ova with sperm outside the body is the basis of in vitro fertilisation (e.g., in a petri dish containing special medium) - see this link for one of the original references: http://www.ncbi.nlm.nih.gov/pubmed/6775685

I agree with David - as an example in many cases ligand binding to G protein-coupled receptors, the largest family of cell surface receptors in the mammalian genome and towards which a large proportion of pharmaceuticals are targeted, activate intracellular signal pathways without apparently entering the cell. The receptors on the other hand can be internalised upon ligand-binding.

I should add that many pharmaceuticals act as antagonists that inhibit the binding of an agonist to a receptor, transporter or channel.

It appears that you have some pent-up emotions here! Fish scales have a number of uses, including protection (which may include some scale shedding) from injuries, parasites and predators. Some (perhaps most?) scales have a hydrodynamic function in drag reduction to reduce water resistance, something that swimwear manufacturers have tried to mimic in the past, especially for elite swimmers. Sorry, I am not familiar with fish that may have scales under the skin...but that doesn't necessarily end, or preclude any discussion by others on this site!

It really depends on the dose ingested. Acetic acid is corrosive and acts as an irritant to many our biological barriers including skin, and the stomach if it is swallowed. High concentrations of acetic acid can change blood acidity and be quite harmful, but the general public is rarely exposed to such concentrations, even if people enjoy vinegar on their fish and chips!. The wikipedia entry on acetic acid is quite informative.

Latent DNA can be recovered from various samples quite some time after it has been deposited, even under what we might call 'adverse' conditions, and forensically analyzed depending on what type(s) of DNA markers are being investigated - e.g., see - http://onlinelibrary.wiley.com/doi/10.1 … x/abstract

As David says it is at the police's discretion whether to pursue this any further.

The important point about 'manufacture the same primer sequence exactly' is quality control. Yes there are any number of companies that have large-scale oligonucleotide production, and some guarantee 100% accuracy. Varying degrees of purification are provided, such as HPLC which may remove truncated sequences. Purity may sometimes be checked by mass-spec. Reetika's comment about 'work and specific' may not necessarily refer to actual (i.e., exact) primer sequences. As far as I am aware, for most primers the precise DNA sequence (e.g., rather than DNA content) is not confirmed at source, and is usually verified by sequencing a product (e.g., PCR) in which the primer sequence(s) has been incorporated, or by other methods such as checking restriction enzyme cleavage sites that may be present in the primer(s) sequence.

Your primer sequence can be inputed directly (e.g., if it has been entered electronically when you order your primers) into their oligonucleotide synthesis machine, or it can be entered manually. See a previous post - http://www.askabiologist.org.uk/answers … hp?id=8603

I agree with Alistair’s comments - a fish caught by hook and line usually constitutes a major acute stress, activating the equivalent of the mammalian sympathetic nervous system to release catecholamines and hypothalamic-pituitary-adrenal (inter-renal in fish) axis to release cortisol. How this plays out will depend on many of the same factors in mammals such as stress nature (e.g., location of hook, bait or artificial lure), intensity, duration (e.g., either acute or repeated landing time) and perhaps even adaptation to certain stressors, prior exposure to stress, genetic predisposition/stress susceptibility/species, age and perhaps even gender, and the environment (e.g., chemical composition of the water, extremes in water temperature) and can have short and long-term (e.g., reproductive) effects. In terms of catch-and-release you also have to consider the time spent out of water, and any facilitated recovery. Here is another short article on this matter - http://www.acuteangling.com/Reference/C … ality.html - walleye are briefly mentioned in a couple of tables.

It is usually standard practice in molecular biology labs to keep bacterial strains on agar plates for a few weeks-months at 4 degrees C. Sterile technique in plating and opening plates helps minimize contamination, as does a tight seal (e.g., with clingfilm and tape) when the plates are stored. Even then you might end up with spurious growth (of different colours!!). Most of us keep glycerol or DMSO frozen stocks (ideally kept at -80 degrees C but -20 degrees C will suffice for shorter term (perhaps less than a year) storage) to replenish cultures as a safeguard against cross-contamination from other bugs used or present in the lab (yeast is often a culprit), or from mutations that may render bacteria antibiotic resistant. You can take scrapes for years from the frozen stocks to set up new cultures.

I do not routinely (or purposely!) grow Staph but here is an article on general culture techniques and antibiotic resistance testing - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070006/

I’m sure that there are animals that have head/shoulder movement similar to, or with even a greater range than humans. One point is that animals like cats, deer and horses with ‘independent ears’ do not have to move their bodies as much to detect sound, perhaps an evolutionary adaptation that allows quick responses to sound from such things as predators whilst, e.g., feeding.

As noted in the post from which you quote, the outer ear has functions that are less important in humans compared to other animals, such as thermoregulation, and outer ear shape can also effect the range of sound frequencies that can be detected. Our auricula are functional (e.g., collect and funnel sound) and some people are capable of moving their ears independently. Others on this site may be able to comment on the apparent lack of evolutionary pressure for humans (in general) to have independently moving ears, but there is evidence that our outer ear shape may have evolved to mirror acoustics in the natural environment (see -http://www.pnas.org/content/111/16/6104.abstract).

There is a rare outer ear condition called ‘moving ear syndrome’ but I think this usually presents as involuntary movement - I do not know whether it is accompanied by any changes in hearing.

A very good question! You can certainly have neurons that receive both excitatory and inhibitory input from multiple neurons. I asked a neuro-electrophysiologist colleague and he recalled that during early development some GABAergic neurons can function as excitatory but when mature are inhibitory (see - http://www.nature.com/nrn/journal/v3/n9 … 920.html). It also appears that POMC (pro-opiomelanocortin, the precursor for ACTH and beta-endorphin) neurons in the arcuate nucleus can release both GABA and glutamate (as well as other neuromodulators) to affect downstream neurons in the arcuate (http://www.jneurosci.org/content/32/12/ … l.pdf+html) - there may be other examples, but I have no idea of the excitatory/inhibitory ratio and I guess that the neurotransmitter release may be subject to differential regulation!

Anti-idiotype Abs as a concept has been around for many years - I think I am right in saying that the idea of these Abs in molecular mimicry harkens back to the days of Neils Jerne’s anti-idiotype network theory, a view on the regulation of immunoglobulin (Ig) production. There are quite a few reviews on anti-idiotype Abs, Igs that bind to the antigen-combining site of another Ab, e.g.,

http://www.ncbi.nlm.nih.gov/pubmed/7821758
http://www.ncbi.nlm.nih.gov/pubmed/3111984
http://www.ncbi.nlm.nih.gov/pubmed/2481210
http://www.ncbi.nlm.nih.gov/pubmed/2901298

There are a number of interesting applications of anti-idiotype Abs (e.g., see -https://www.abdserotec.com/anti-idiotypic-antibody.html), including (but certainly not restricted to) racotumomab (commercial name Vaxira), an anti-idiotype monoclonal Ab that induces an Ab response to an antigen present in several tumours, and omalizumab, an anti-IgE treatment for severe allergies.

And if you are still interested in marine biology in a few years try applying for work experience at a marine centre/aquarium.

To provide some brief background to David’s question, oxytocin (OT) and vasopressin (VP) released from the hypothalamus into the pituitary portal blood circulation acts on the anterior pituitary cells, e.g., VP acting on corticotrophs to aid in the release of corticotrophin (ACTH); OT stimulating prolactotrophs to release…uhm, prolactin! (and maybe even acting on gonadotrophs and sommatotrophs), depending on the nature of the stress (noting of course, that there can be individual variations in the predisposition to stress, including social stress).

I guess you are referring to OT released into the peripheral circulation, David, which is a pertinent question. As well as being released into the blood vessels that bathe the pituitary, OT and VP can also be secreted into the peripheral circulation, again stimulus (or stressor)-dependent. The traditional physiological roles of circulating VP (water retention) and OT (contracting smooth muscle of the reproductive tract) released in response to physiological manipulations such as dehydration (which is a stress) and during parturition and sexual activity, respectively, are well-known. OT also has direct actions on non-reproductive peripheral tissues. It has renal (e.g., increasing glomerular filtration rate), and metabolic and perhaps cardiac effects (e.g., lowering blood pressure - see http://www.ncbi.nlm.nih.gov/pubmed/21981277), actions on the G-I tract, and there are OT receptors present in other areas such as bone and immune tissues. Some of OT’s effects may be mediated by VP receptors, such as the V1a subtype which is present in many peripheral tissues. The actions of OT on peripheral tissues may have some behavioural consequences.

OT and VP released into the circulation do not appreciably cross into the brain in physiologically relevant amounts. The general consensus appears to be that OT can be released within the brain to inhibit HPA activity. Furthermore, it (and VP) can be released into the hypothalamus and other brain areas to affect social behaviour like affiliative and maternal behaviour, social recognition, fear, and aggression, and reward- and anxiety-like behaviour (e.g., see http://www.nature.com/news/neuroscience … in-1.17813 for commentary).

A final point about the role of peripheral and/or central OT. There have been a number of recent clinical studies on the effects of intranasal OT (usually very high concentrations) on social behaviour, especially in autism spectrum disorders (i.e., can OT improve behavioural deficits seen in these and other conditions? see http://www.sciencemag.org/content/347/6224/825 for commentary). These studies have garnered a lot of attention amongst behavioural scientists and in the press. It is worth pointing out, however, that the execution and robustness of some of this work has been questioned, and the site of action of intranasally administered OT, i.e., peripheral or central, is hotly disputed - see http://www.ncbi.nlm.nih.gov/pubmed/26049207 for a balanced argument.

Good question Katie, and you have got this about right! For many mammals, including rodents, there would be an 'anticipatory' rise in catecholamines such as adrenaline in the predator, and likely also a rise in corticosterone due to activation of the hypothalamic-pituitary-adrenal (HPA) axis. There would often be a further increase in these hormones when the predator 'engages' (e.g., starts running and makes 'contact') as it exerts itself physically. In fact, even in social interactions (moreso when we meet someone who we have not met before) without an 'aggressive' component  there can be activation of the sympathetic nervous system and HPA axis.

For an EPQ I think David's recommendations are very good - for neurogenerative conditions you would want to concentrate on something quite specific (e.g., one gene) that will encompass many of the general concepts of necrosis and apoptosis. I think the same focussed approach is also applicable to depression for which there are any number of underlying theories, ranging from 'faulty' brain wiring to brain atrophy. For example, you could give an overview on the activation of the hypothalamic-pituitary-adrenal axis (stimulating the release of adrenal steroids like cortisol) in chronic stress and anxiety, that could lead to some forms of depression. As I'm sure your biology teacher would tell you, focus and clarity are key.

This article - http://www.ncbi.nlm.nih.gov/pubmed/24932483 (or http://journals.plos.org/plosone/articl … e.0098078) - states that at sexual maturity female great whites (at 4.5-5.0m) are larger than males (at approx. 3.6m), citing the following refs -

Boustany AM et al., Expanded niche for white sharks. Nature 415: 35-36, 2002; Francis MP, Reproductive strategy of white sharks Carcharodon carcharias. IUCN Shark Specialist Group, Shark News 9: 8-9, 1997.

Testosterone and other androgens are produced by the Leydig cells in the testis, not the Sertoli cells or sperm (either immature or mature). They are secreted into the blood - if you remove the testis there will be androgens associated with testicular cells and vascular elements, and perhaps minute amounts of androgens bound to testicular cells and sperm. As far as I am aware androgens, in particular dihydrotestosterone, are found in seminal fluid (e.g., see - http://www.ncbi.nlm.nih.gov/pubmed/12711017) although this is probably better known as a rich source of substances such as mucus, other hormones and nutrients, many of which are produced by the bulbourethral gland, seminal vesicles and prostate. Its composition can change with diet and age.

I do not know the fate of ingested androgens, but it appears their levels are increased in the blood (see - http://www.ncbi.nlm.nih.gov/pubmed/16888459), which are not necessarily associated with anabolic effects and may indeed have a wide range of unwanted side-effects!

Your entire life! I’ve have had a look for an authoritative source and can’t find one - maybe someone else will have more luck! There are lots of comments of this type attributed to Steve Jones and others that go back to 2000 or earlier (and are continually recycled), which is interesting given that as far as I can see the first draft of a banana genome was published in 2012 (see - http://www.nature.com/nature/journal/v4 … 241.html). If there is a value of around 50% gene-share between banana and humans, it would be interesting to know how the DNA was actually compared! Presumably by ‘genes’ people are referring to the predicted protein-coding genes, approx 36,000 in the banana genome which is more than that predicted in humans.

There will obviously be some banana (or plant)-specific genes, and bananas won’t be ‘special’ i.e., you would suspect a high degree of nucleotide identity between human and plant house-keeping genes (e.g., involved in basic cell machinery such as transcription and translation). I’ve seen values of around 40-50% gene match between drosophila (fruit fly; around 14,000 genes) and humans (e.g., see - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082451/) - in this case I think people are generally referring to the overall identity at the nucleotide level between homologs (not all genes!). I doubt bananas will outdo flies at this level!

An example of what David is referring to is the Brattleboro (di/di) rat which has a single base deletion in exon B coding for the neurophysin II part of the vasopressin precursor gene - this animal is unable to concentrate its urine because of the lack of circulating vasopressin. In humans, familial neurohypophysial diabetes insipidus is often caused by numerous different types of mutations within the vasopressin precursor gene, which again is associated with decreased vasopressin release and excessive (dilute) urine production.