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