Xalatan

Yep I agree with Endy. Metastasis may occur via haematological, lymphoid, or transcoelomic spread. Some of these processes seem like passive processes rather than active motility-based activities - for example being carried via the blood or lymph vessels to the liver or local lymph nodes. The key histological feature may thus be breaking through the protective basement membrane rather than EMT per se - if you look at the definition of carcinoma in situ, it's often defined as a glandular or epithelial tumour being confined to the epithelium or epidermis, since the submucosa or dermis contain the blood and lymph vessels that enable metastatic spread. I guess EMT is one means to break through the basement membrane barrier but not the only.

Are they all folluculitides? Can an inflamed epidermoid cyst be considered an ectopic intradermal infundibular folliculitis?

A lot of the grey matter of the brain is found on the outer surface of the brain (ie. The cerebral cortex). So if you are asking for pure anatomical localisation of the conscious mind it could be the cerebral cortex.

I see the maze procedure indicated for catheter refractory atrial fibrillation, is it performed for ventricular arrhythmia too? From what I read poststabilisation management of VT/VF goes from radio-frequency ablation to ICD. Is it not somewhat palliative? No room for a more curative cardiothoracic approach in between? http://emedicine.medscape.com/article/159075-treatment#d9

Many thanks for asking, my IOP is fine :') a friend suggested the nick name for me, she thinks it sounds like an alien star system XD

Aspirin is a cox1 inhibitor. It irreversibly stops prostaglandin and thromboxane A2 synthesis. TXA2 mediates platelet GPIIbIIIa activation and the formation of the primary platelet plug. But you get the side effects of aspirin from prostaglandin inhibition. Lack of production of stomach mucous lining is the most commonly cited s/e. Anti inflammatory effect may be another - prostaglandin is a paracrine signalling molecule for all kinds of tissues in the body, you'll have to look it up, and you may find lots of idiosyncratic effects from aspirin. For one, xalatan, or latanoprost is a prostaglandin analogue to lower intraocular pressure as glaucoma treatment. So I wouldn't be surprised if aspirin increases IOP in a case series. This isn't medical advice, you should ask your doctor if you are taking aspirin, usually there is good reasons why patients are on aspirin prescription with all the benefits and risks weighed. This is purely an academic discussion from my part.

http://forums.studentdoctor.net/threads/hypokalemia-repolarization-qt-prolongation.313878/ Apparently IKr channels are gated by extracellular potassium, and Ke determines the conductance of IKr channels. This supposedly explains why counter-intuitively hypokalaemia prolongs the QT interval and increases the risk of early afterdepolarisation and torsade de pointes. Can someone with insight kindly explain how this gating works at the molecular level? Input would be really appreciated. Is there a pocket on the extra cellular domain of the IKr channel that binds potassium agonistically? I'm thinking along the lines of the GABA-A channel having a modulatory domain for benzodiazepines.

Yep as you guys point out, some plants have digestive systems. Interesting topic. http://www.scientificamerican.com/article/how-does-the-venus-flytra/ I wonder if being a heterotroph is considered more evolutionarily advanced than being an autograph. I guess it depends on which form of nutrient acquisition is more efficient in a particular circumstance.

The only mechanistic issue I can see is, hanging generates a pressurising injury that presses down on the cerebellum, through the foramen magnum. A penetrating gunshot injury may depressurise the brain rather than pressurise it, since the bullet would go through the brain. How could a hole in the brain, especially an exploding injury, generate the necessary intra cranial pressure to cone the brain? This is probably why you haven't read the priaprism phenomenon after a gun shot injury. In your novel you may need to think about how the firearm injury is being delivered, it should be blunt rather than penetrating trauma.

I'd say it's possible. The basis of penile erection is cutting off blood return from the penis rather than increasing blood flow to the organ as you proposed. This cutting off effect is mediated by the pelvic splanchnic nerve coming out of the S2-4 spinal cord, releasing nitric oxide to dilate the penile arteries, and compressing the penile veins that drain blood from the penis. So, similar to the effect of hanging, as long as there is head or neck injury severe enough to induce tonsillar herniation, there will be mechanical pressure on the spinal cord and thus the pelvic splanchnic nerve to stimulate an erection. This could be an entirely postmortem reflex not requiring brain or heart function - as long as there is no pelvic injury that damages the spinal cord or ruptures the perineum and the causes existing blood to leak out of the penis, I can see a spinal reflex that induces postmortem Prisprism secondary to gun shot head injury. Disclaimer: For me this is purely an academic discussion and I only share my personal views and opinions.

Actually to reinforce my point, there is a set of channelopathy diseases related to potassium, sodium, and calcium ion channels called periodic paralysis. So I'd say manipulating electrolyte composition may allow controlled paralysis. https://en.m.wikipedia.org/wiki/Hypokalemic_periodic_paralysis

http://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/restless-legs-syndrome/what-is-rls/causes.html Unexpectedly, Iron deficiency can cause restless leg syndrome. Supposedly iron may be needed by the neuromelanin cells in the substantial nigra to synthesise dopamine. How does this work? Is iron a co-factor for tyrosine hydroxylase or dopa decarboxylase? Also does this imply iron supplements may help extrapyramidal akathisia when using antipsychotics?

Based on wiki's definition, none of pons, thalamus, and hypothalamus are part of the cerebrum. https://en.m.wikipedia.org/wiki/Forebrain Cerebrum = cerebral cortex, underlying white matter, and basal ganglia. Telencephalon = cerebrum. Diencephalon = thalamus, hypothalamus, epithalamus. Forebrain = telecephalon + diencephalon. Hindbrain = rhombencephalon = pons, medulla, cerebellum.

Also, chromosomal disorders like Down's, Turner's, Klinefelter's, as well as diseases of genomic imprinting like Prader-Willi, Angelman's syndrome almost always develop sporadically during meiosis and spermatogenesis.

The spermatocytic DNA is not always perfect, there can be sporadic mutations that develop in individual sperm cells as a result of imperfect DNA repair. I learned it on this forum too, but there is a genetic condition called Smith-Magenis Syndrome that develops due to sporadic mutations in sperm or ovum or early zygote. There is a thread about it on this forum. https://ghr.nlm.nih.gov/condition/smith-magenis-syndrome

How is the PPRF wired for vertical gaze, and how does this apply in Supranuclear Ophthalmoplegia? Can't find a good clear explanation for this piece of neuroanatomy, would really appreciate if someone can describe. Thank you!

The reason anaesthetics work is because they are sodium channel blockers. In theory, biochemically you may be able to achieve the same by altering the electrolyte composition of the extracelluklar fluid - eg. Controlled hyponatraemia, or controlled hypercalcaemia. I wouldn't try hypokalaemia because it's probably not safe to play around with serum potassium concentrations, unless you did it super slowly. But sodium and calcium levels may be more adaptable. No sure how you could limit the electrolyte changes to a specific part of the body though.

This is interesting - so the assumption is size correlates to function and reducing the R amygdala should alleviate the agoraphobia to a degree. Psychosugery has greatly fallen out of favour in modern medicine - I guess gamma knife radiotherapy is the lesser evil, maybe it will catch on, but I'm not sure if there is enough evidence yet to back up this kind of invasive intervention for panic disorder. You didn't think about deep brain stimulation? Would you continue with antidepressants and would you think about further therapy?

Over training will lead to sports injuries - most runners will have experienced plantar fasciitis, shin splints, knee sprains etc. to varying degrees. As you build up muscle power and endurance it becomes less frequent. Degenerative osteoarthritis over time. Other problems like exercise induced asthma too. I don't think you need to worry about free radical damage from running. Molecular oxygen is stable, your arterial oxygen tension may increase with increased ventilation but your bodily cellular mitochondrial function is intact, and cells have a physiological reserve of antioxidants like glutathione to mop up excess radicals. It's not like the case in ischaemic reperfusion injuries where damaged cells are exposed to oxygen.

Actually the liver metabolises and secretes ketoacids, acetoacetate and beta hydroxybuturate. They convert to acetone in the body, which is why in Diabetic keto acidosis patients develop acetone breath. I'm not sure if an organ can store acetone to great concentrations - the metabolic process to synthesise acetone produces organic acids, and at higher concentrations it may lead to acidotic poisoning.

BTW you're so admirable going for neurosurg :,) Most of my friends would be more than happy with neuropsych or ophthalm. I guess treating stroke or glaucoma or depression just aren't enough, it's gotta be draining those haematomas and chopping out the pituitary adenomas huh. Back surgery looks insanely difficult!

Yep you are correct. It's the vestibular system that uses Ach (and histamine) signalling, which is why schopolamine and cyclizine work. CTZ uses 5HT, DA, and Neurokinin, so it's probably more relevant for antiemetics like ondansetron and domperidone. Interesting piece of physiology here :')

I'm not an expert on virology nor am I a clinical microbiologist, and have never worked with HIV in vitro, so this is just my personal opinion and you should best seek professional advice from Oraquick for a clear response - there is a 24/7 confidential line you can call for information. Should there be contaminated blood present in the buffer, HIV has been known to survive in blood for upwards of weeks. However, bear in mind there has not been a case of HIV reported from being in contact with spilled blood or bodily fluids. http://mobile.aidsmap.com/Survival-outside-the-body/page/1321278/ Also, Triton X-100 is a detergent so it may hopefully solubilise the lipid envelope of any HIV viruses present. But as Charon said, it may also be a matter of titre and viral load in the potentially contaminated fluid. Third, if there was HIV contaminated blood in the buffer solution, it cannot cross healthy skin barrier to infect.

Unless you have a photographic memory, it's very hard to memorise the entire textbook with all the fine details. What works for me is understanding the material enough to have working knowledge of the information, which allows me to function effectively at what I do. Everything else can be referenced from text books when required.

To induce cancer the EMR has to induce genetic damage and mutations. For example, UVB causes thymine dimers and cross-links nitrogenous bases of nucleotides. This requires high energy EMR that is able to penetrate tissue to reach the genetic material. Microwave is sitting on the wrong end of the EM spectrum with its long wavelength and lower energy. It doesn't make a case esp compared to the likes of UVC, X ray, gamma ray.