yuna
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Thanks Mytime my sunshine, I will be done with all steps if I could pass this step. Now I am automatically recalling all flashback questions in my mind, that's called PTSD right? Maybe tonight I will get nightmare...so I need you and the sunshine within you...come on 
Edited by yuna on 08/22/07 - 05:06 PM
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| yuna
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I will post some of HY that I missed in my test, or I had to think again and again...
1. Factor V Leiden
In the normal person, factor V functions as a cofactor to allow factor X to activate an enzyme called thrombin. Thrombin in turn cleaves fibrinogen to fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C (aPC) is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.
Factor V Leiden is an autosomal dominant condition in which the coagulation factor cannot be destroyed by aPC. Mutation of the gene encoding factor V�"a single nucleotide substitution of adenine for guanine�"changes the protein's 506th amino acid from arginine to glutamine . Since this amino acid is normally the cleavage site for aPC, the mutation prevents efficient inactivation of factor V. When factor V remains active, it facilitates overproduction of thrombin leading to excess fibrin generation and excess clotting.
The excessive clotting that occurs in this disorder is almost always restricted to the veins, where the clotting may cause a deep vein thrombosis (DVT). If the venous clots break off, these clots can travel through the heart to the lung, where they block a pulmonary blood vessel and cause a pulmonary embolism. Women with the disorder have an increased risk of miscarriage and stillbirth. This disorder does not increase the formation of clots in arteries that can lead to stroke or heart attack, though a "mini-stroke" known as a transient ischemic attack may occur
(source wikipedia)
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| yuna
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2. Hemochromatosis
The crypt epithelial cell expresses HFE on its basolateral surface; complexing of HFE with β2-microglobulin is required for its expression on the cell surface. HFE-β2-microglobulin complexes with the transferrin receptor (TfR) to bind circulating transferring (Tf). Endocytosis ensues; on acidification of the recycling endosome, transferrin-bound iron (Fe(II)) is released and enters into the cytoplasm. High levels of cytoplasmic iron downregulate levels of the iron-regulatory proteins (IRP), a family of proteins with potent effects on nuclear transcription. With low levels of cytoplasmic iron, the IRP content of the cell remains high. IRPs upregulate nuclear transcription of the genes for several proteins required for intestinal absorption of dietary iron: Dcytb (duodenal cytochrome B), DMT1 (divalent metal transporter 1), ferritin (a cytoplasmic iron-binding protein), and FP1 (ferroportin 1).
A mutation in HFE (C282Y) prevents "sensing" of circulating iron levels by the crypt epithelial cell, leading to unregulated expression of these four proteins. The crypt epithelial cell is the precursor cell of the mature absorptive enterocyte on the tip of the villus, through migration up the villus axis. On the apical membrane of the absorptive enterocyte, Dcytb reduces dietary ferric iron (Fe(III)) to ferrous iron (Fe(II)). Fe(II) is then taken up by DMT1 into the enterocyte. Iron can be bound to ferritin (and hence sloughed back into the gut lumen) or transported across the basolateral plasma membrane by FP1 for binding to transferrin and entry into the systemic circulation. In the patient with mutant HFE, the inability to downregulate expression of these four proteins leads to lifelong excessive absorption of dietary iron.
(source Robbins)
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| yuna
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Retinoic Acid Receptors (RARs)
Retinoic Acid receptors (RARs) are nuclear receptors related to the steroid and thyroid hormone Receptors, a family of proteins that function as ligand-dependent transcription factors. Several loci encoding RAR isoforms have been identified in mammals - RAR-alpha, -beta and gamma - as well as novel nuclear receptors known as RXR (Retinoid X receptor), which are distantly related to RARs and respond to high concentrations of RA. The RARs show spatially restricted distribution patterns during embryogenesis, which have led to speculation on a variety of roles for RA in developmental processes. As with other enhancer-binding proteins, nuclear receptors act as transcription factors by binding to specific DNA recognition sequences generally located upstream of responsive genes. Although RARs can activate gene expression through binding to thyroid hormone response elements, a much more specific and potent RA response element (RARE) has been identified recently within the promoter of the RAR-beta gene. This RARE is essential for RA induction of the RAR-beta gene and, when linked to heterologous promoters, can confer transcriptional activation via all three RARs.
Retinoic Acid (RA)
Retinoic acid (RA) may act as a regulator of differentiation at various stages of vertebrate embryogenesis. In particular, the results of exogeneous RA treatment have implicated RA in antero-posterior patterning both along the body axis and in developing Limb bud. A variety of abnormalities, including Neural tube defects, craniofacial abnormalities, and limb defects, have been reported after treatment of pregnant mammals with RA. The recent discovery that RA interacts with nuclear Receptors related to the steroid and thyroid hormone receptors, a family of proteins that function as ligand-dependent transcription factors, suggests that the morphogenetic functions of RA may result at least in part, from activation of developmentally regulated genes by RA receptor (RAR) complexes. An additional feature of retinoid physiology is the existence of a distinct class of molecules, the cellular retinol- and RA-binding proteins (CRBPs and CRABPs), which may modulate the accessibility of RA to the receptors. Representatives of each binding protein also show spatially restricted patterns of expression in the embryo. The complexity of retinoid action was demonstrated further by the recent finding that specific interactions between RARs and other nuclear proteins, including the thyroid hormone receptors and AP-1 transcription factor, can modulate their transcriptional activity.
Retinoic Acid Response Elements (RARE)
TRE-like sequences containing spacers may mediate response to retinoic acid: -GGTAA....[7bp spacer]...TGACC-
Retinoids
Several retinoids can act on activation/repression of Hox- and related genes. These retinoids include All-trans-retinoic acid; 11-cis-retinoic acid and retinol as metabolite of the retinoic acid.
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| yuna
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Telomerase
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| GoodGirl
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Thanks Yuna, you are such a wonderful person, I read everything you put above.
But girl, go enjoy the life, I can imagine, it is hard to change the habits, one day between the books, another all is done, so what to do? Again appreciate what are you doing.
And something else than medical for you :
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| yuna
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Thanksss Goodgirl...If I can do this, and that and this...
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| yoga
usmlelogy professor
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so is it over yuna?? GL on score
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we are all in the gutter but some of us looking at the stars
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| mytime
Kick my butt!
Topics: 39
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OKKKKKKKKKK Am back for SUNSHINE UR WAY!!!!!!!!!!!!!!!!!! Am sure u are done now enjoy and when u are exhausted u can do the HY for us......... The topics are enuff don't spoon feed too much or no one will read!   
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| edie
I can, and I will.
Topics: 26
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No PTDS, no no no!!! Take some time off, you deserve it! Not that I am not grateful for your input, bless you for taking the time to post your HY facts and for your help in the forum. But this is your time now. Enjoy!!!
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| yuna
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Lymphatic drainage of the face. Is it in FA?
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| simi
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wish u a very good score yuna! enjoy ur time
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| ShweHope99.9998
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Lymphatic drainage  hey nice color, where can I get , very Yuna , so colorful, for telomerase too . Like to get both color chart ,plate, do pm or let me know here .
Thanks yuna 1 .
GL from yuna 1.1
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| keepgoing
Forum Guru
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hey congrats on finsihing exam...u have taken step 2 an dcs already??if yes great..all the best..u r almost there now.. thanks for sharing exam experience..and HY stuff w/ beautiful images..thanks..enjoy have great time
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| yuna
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Hi keepgoing, I am on fire now, cheking the Qs and the crazy number of wrong Qs is increasing, even in the easy Qs I think I can do within 10 secs. 
Here is the Cell injury, I think I got this wrong about the sequences
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| GoodGirl
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YOU SHOULD NOT THINK THIS WAY! Actually it is pretty normal what I know, not sure what is the remedy for that, to stop recalling the images and flash backs from the test .
Believe in yourself, I'm sure you did fine.
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| paheli
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hi yuna!! congrats on completing the acid test! also, thanks a lot for the hy facts. very helpful!
now, go enjoy!!!
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| yuna
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How can you differentiate them, when you get a slide of pituitary gland?
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| GoodGirl
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I can not see any image, what did you want to ask?
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| GoodGirl
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Oh, I guess you were talking about pituitary gland cells, basophils, acidophils and chromophobes? ( something like that)
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| yuna
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I mean the acidophils, basophils and all in pituitary gland
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| kity
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Thanks a lot yuna fr high yields.. & dont worry .. we can see your hardwork & god will bless you with great score for sure...
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| GoodGirl
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Hello Yuna,
I really love the image of abdominal wall you posted in my journal! Even I have it in my book, never harm to see it again. Maybe somebody visiting my place would consider it helpful too. No need for apology! There is plenty of space!
Take care ! Must study.
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| mytime
Kick my butt!
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YUNA I just thot of this u better post some pictures on my thread as well coz I remembered that my mom painted a lot the year she was expecting me(she's an artist btw)!!!!!! MAkes my picture side of brain sharper!
So ignore what i said earlier and don't stop!!!!!!!!!!!!! keeep Posting! Love!!!!!!!!!
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| yuna
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Hi , My little one is taking a nap. I am now a babysitter again...
Some good animations (please click)
G protein and Calcium channel
Membrane bound receptors to G protein
Intracellular Receptors (aldosterone)
Feedback mechanism-Estrogen
Good luck, all !
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