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Old 01-13-2012
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Smile Mechanisms Guys Mechanisms !!

Share the concepts and mechanisms which you found it interesting while you were learning today. This would help us to strengthen our concepts. Lets add at least one concept everyday.

Nobody knows everything, but everybody knows something

Good luck guys
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Old 01-13-2012
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I am adding mine :


2,3 DPG normally alters beta chain of adult hb. and reduces its affinity for o2. That is Hb-o2 dissociation curve shift to right

Since fetal hb have gamma chain instead of beta chain, 2,3 DPG has no effect on it. And hence their affinity is high for o2
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Old 01-14-2012
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Share some concepts guys ........
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Old 01-14-2012
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Metabolic and respiratory alkalosis causes albumin to liberate H+, rendering albumin more negative.

The extra negative charges on albumin bind ionized calcium leading to hypocalcemia. However, total serum calcium remains constant.


I know this is probably very basic but I have been a lousy student and I was happy to finally find out about it
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Old 01-14-2012
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Default keep up, Moske! :D

Quote:
Originally Posted by moske View Post
I am adding mine :


2,3 DPG normally alters beta chain of adult hb. and reduces its affinity for o2. That is Hb-o2 dissociation curve shift to right

Since fetal hb have gamma chain instead of beta chain, 2,3 DPG has no effect on it. And hence their affinity is high for o2
2,3-DPG is significant in birds, as they have to fly up high in cold air current, thats the mechanism how they keep warm and sufficient O2 at the same time. As 2,3 DPG binds to the beta chain of Hb, O2 is released and heat is also released.

Fetal Hb a2g2 has the highest affinity for O2. In what adults can we see a2g2? Sickle cell dz(defective beta chain of Hb again).The 6th aa is changed from Glu to Val, making the deoxyHbs stick together even stronger, sickling RBCs (basically a bag of Hbs). So what is the Tx for sickle dz? Increase the proportion of fetal Hb, a2g2, keeping RBCs oxygenated and normally-shaped so that they wouldn't occlude microvessels. L&G, here comes HYDROXYUREA!

I have nothing to contribute now, but will keep up soon.
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Old 01-14-2012
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RB and P53 are tumor suppressor genes....
They stop the cell from going from G1 to S phase and let it go only when required!!!


RB gene stops the cell from going from G1 to S phase, its is inhibited when Cyclin D kinase 2- cyclin D phosphorylate it. other wise it keeps a brake on the cell going from G1 to S,

Cyclin D kinase is kept in control by P53 so that it doesnot phosphorylate RB and let it keep the cell arrested in G1 unless when required....

In Retinoblastoma this Rb gene is mutated so the cell starts replicating like mad.... and in cancers associated with p53, e.g Li- Fraumani this p53 control is lost.....
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Old 01-14-2012
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A bit detailed version of wat i put in my last post:

RB, P53 and p16 are tumor suppressor genes ....
They stop the cell from going from G1 to S phase and let it go only when required!!!


1) RB gene stops the cell from going from G1 to S phase, its is inhibited when Cyclin D kinase 2- cyclin D phosphorylate it and forms E2F-RB complex, other wise it keeps a brake on the cell going from G1 to S,

2)Cyclin D kinase 2 is kept in control by P53 so that it doesnot phosphorylate RB and let it keep the cell arrested in G1 unless when required.... When required P53 is phophorylated by AtR kinase and ATM kinase, this causes upregulation of p21 which allows CDK2-cyclin D complex to form and do the above mentioned reaction of forming E2F-Rb complex

Third mechanism at this checkpoint is:

3) P16 gets phopshorylated which inactivates CDK4/6- cyclin D causing a stoppage at this checkpoint.

In Retinoblastoma this Rb gene is mutated so the cell starts replicating like mad.... and in cancers associated with p53, e.g Li- Fraumani this p53 control is lost.....
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Old 01-21-2012
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Ape thumb in chronic median nerve injury is due to loss of function of opponens pollicis. So thumb tends to lie in the same plane as other digits as in an ape
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