jsmith613

The problem statement, all variables and given/known data (1) An ideal digital detector only suffers from quantum noise. If, after being exposed to 5 µGy the mean pixel value in the image is 100 and the standard deviation of the pixel values in the image is 5, calculate the SNR? The relationship between pixel value and detector dose is linear. (2) What is the effect on SNR of applying a linear gain of factor 4 to increase all pixel values Attempt at a solution As I understand SNR = 100/5 = 20 (but I am not certain; it could be 100/sqrt(10)) - clarification would be helpful Also I think gain has no effect on SNR (as it increases signal and noise by the same amount) but am not certain. Thanks for your help

I have read that reduing mean pressure in distal arteries (e.g: lower limb) maintains blood flow there. How can this be true if flow=pressure/resistance, and resistance is highest in the arterioles?

Thanks I read about my original question in my Physiology textbook (and my lecturer mentioned it). She said that Bernoulli Principle was IDEAL but was not, in fact, reality because of resistance, as you said

I have been reading about Bernouli's principle and would like to clarify something I have read that the total energy of blood in vessels (assuming a vertical position) is given by the sum of pressure energy, GPE and KE. I have seen two different equations: 1) P + pgh + KE = constant 2) P - pgh + KE = constant I am wondering why the sign associated with pgh changes as I cannot find this out. Thank you

Hello, Please could someone explain why Turner syndrome produces any symptoms at all. As I understand all cells in the female body inactivate one X-chromosome (dosage compensation). As such shouldn't Turner syndrome manifest itself in exactly the same way as all normal cells? thank you

Ok...I think I get it now. thank you both for your help I really appreciate it!

Ok...it seems i've misunderstood something more fundemental. I thought we had 2 of each lobe (2 parietal, 2 frontal...) and each of these lobes were connected my commisural fibres. Is this false? Is there only 1 of each lobe? If so why is it that we have a divide in middle of our brains (middle long. fissure)?

Yes. So the occipital lobe is involved in processing visual information. And as I understand this occurs equally well on both sides. I'm not sure if I am being unclear with my question or if I am just not understanding what your saying but if the occipital lobe processes visual information (equally well on both sides) then who cares if the one of the occipital lobes is damaged? Do we really need both lobes? I thought the right lobe delt with information in the left and the left lobe delt with information on the right So if the reading material was presented to the left occipital LOBE then surely it could transfer to the language centres so it can be processed for intepretation by the brain and comprehension? have I missed something you were saying? thanks again for sticking with me through this problem

Thank you to both of you for your help. I think I get the idea but my confusion lies in the concept of a dominant visual processing lobe hemisphere? I didn't think such a thing existed (as we are binocular)...hence even if information cannot pass from right to left surely visual information reaching the left hemisphere could be intepreted? thanks

Crossman and Neary write that... "Destruction of the splenium of the corpus callosum by stroke or tumour leads to the posterior disconnection syndrome of alexia without agraphia. Such individuals speak and write without difficulty but cannot understand written material (alexia). Disconnection of visual processing in the right hemisphere from the verbal processing of the dominant left hemisphere is thought to explain the syndrome" I thought that visual processing was not dominant to one hemisphere and that if it was it was dominant to the left hemisphere anyway because more people have stronger left eyes. I am aware that language processing occurs mainly in the left hemisphere...but nonetheless I am confused. Why then do people who suffer from splenium tumours find reading difficult? thanks

Is it possible for the ankle to dorsiflex and the foot to plantar flex (e.g: in the heel-contact stage of gait). My lecturer suggests it is possible but I do not understand how? Thanks

I am slightly confused as to why VENOconstriction decreases TPR. TPR = (mean arterial pressure - venous pressure) / CO this equation seems to be saying that increased venous pressure (venoconstriction) = decreased TPR How is this true?

My anatomy teacher said "The liver does not reach under the left hemidiaphragm". All of the images / 3D models I have seen have suggested this is wrong. My question is, am I right in thinking he is wrong or is he correct? If he is correct what seperates the left lobe of the lung from the left hemidiaphragm? Thanks

Why does central venous pressure in the heart determine end diastolic pressure? More importantly for me, why does end diastolic pressure determine end diasotlic volume (rather than volume determinine pressure)? Thanks

When DNA replicates the 5' end of the daughter strand is shorter than the parent strand as DNA polymerase can only work in the 5'-3' direction and RNA primers are eventually removed. 5'__________________________3' 3'_______________________5' If this divides, we SHOULD end up with: 5'__________________________3' 3'_______________________5' and 5'_______________________3' 5'____________________3' So we still have ONE cell with the full strand of DNA and one cell with missing telomeres. so far is this correct (meaning: is it correct to say that the telomeres are NOT removed from the parent strand, so in each generation of divisions, there will always be 2 cells with complete parent strands?) Question 2: Are sticky ends (un-paried bases) removed from a DNA molecule as they probably interfere with coiling? Question 3 is telomerase active in non-embryonic stem cells?

CJD is an example of a disease caused by the misfolding of the protein PrP© I have been researching this disease somewhat and have discovered there are several variants including sporadic CJD and variant CJD. It appears that the different variants of the disease have different risk factors and different physiological effects. Given that they are all caused by the misfolding of the same protein - PrP© - I was hoping someone could explain to me why the physiological effects of each variant differ in some respects [including:median age of death, duration of illness and some clinical signs/symptoms] thanks