Science topic

Atherosclerosis - Science topic

Atherosclerosis is a thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Questions related to Atherosclerosis
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Dear All,
Have You ever faced problems with atherosclerotic plaque staining? Yesterday I stained mice aortas full of plaques. Very few of them are not stained. So then I repeated the whole process again, but the results are the same. Do you have any advice?
#atherosclerosis #plaques #plaque #LDLrKO #aorta #ORO #staining #problems
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I was staining lipids in atherosclerotic plaques.
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Can we explain the increased mortality of COVID-19 parallel to the increased age with the well-known disseminated atherosclerotic process in elders?
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Dear Dr Mehmet Rami Helvaci . See the following very useful RG link:
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the role of phytochemicals on cardiovascular diseases in specific mention to atherosclerosis, lipid profile
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Atherosclerosis is a specific type of arteriosclerosis.
Atherosclerosis is the buildup of fats, cholesterol, and other substances in and on your artery walls. This buildup is called plaque. The plaque can cause your arteries to narrow, blocking blood flow. The plaque can also burst, leading to a blood clot.
Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis can be treated. Healthy lifestyle habits can help prevent atherosclerosis.
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As we know that Fat , cholesterol and other substances like Calcium , are the building block for the formation of plaque inside the lumen of coronary arteries , partially or totally block the blood flow to heart , leads to Ishaemia or infarction. There is no specific novel biomarkers to assess the progression of atherosclerosis. Besides the usual novel biomarkers like BNP , NT-Pro BNP , tropinin HDL-c , HDL function ,now researcher are eager to find out the novel biomarkers( produced by cardiac tissues) like miRNA , protein , fat by use of new technologies like Mass spectroscopy ,pcR bases array and MS based lipidomics
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Hello
It is been a long time I have been trying to stimulate vascular smooth muscle cells (MOVAS) for ROS generation. I am using DCFDA assay for ROS detection....
Everything I tried, has failed to stimulate it! LPS (short and long incubation time), high and low concentration!, Iron (Fe3+), glucose (25 mM 50 mM etc), Beta-glycerophosphate (up to 10 mM).... none works!
Does anybody have any idea what is happening?
Extremely frustrating cycle of trial and failure !!!
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If you need a positive control, just treat them with H2O2. Otherwise nicotine or high calcium (3.6 or 5.4 mM) worked in my hands, in primary human vascular smooth muscle cells.
The problem might be in the MOVAS cells themselves? Maybe the fact that it's a cell line makes them insensitive to stimuli.
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I was wondering whether CD8 T cells that are present in the spleen are also present in the para-aortic lymph nodes during atherosclerosis. I can not find any article that studies the specific cells (CD8 T cells that express granzyme K) in de para-aortic lymph nodes, and I thought that if the cells were present in the spleen, they might also be present in the para-aortic lymph nodes since they are both lymphoid organs.
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Yes, dear Fa Ro they can present in lymph node.
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what is better: duplex for CCA or ICA or ECA?
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I agree with Benito jonas Baldauf.
To add, the measurements should be taken at the anterior, posterior, medial and lateral walls and the average of the measurements to be taken.
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A proinflammatory cytokine is a cytokine that promotes systemic inflammation. Examples include IL-1 and TNF alpha. They produce fever, inflammation, tissue destruction, and, in some cases, shock and death. The anti-inflammatory, like IL-10, Il-4, Il-6, etc., cytokines are a series of immunoregulatory molecules that control the proinflammatory cytokine response. Some author says that a cytokines ma behaves Pro as well as anti-inflammatory. So, My question is...
Is there any anti-inflammatory cytokine that acts as a pro-inflammatory cytokine in atherosclerosis? Please provide me a list of those cytokines that act as pro as well as anti-inflammatory cytokines and some references.
Thank you
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Thank you sir@ Daniel P. Moriarity
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I isolated LDL from human plasma by ultra centrifugation followed by dialysis overnight. Now I want to oxidize a part of the native LDL with CuSO4 but 24 hrs after oxidation at 37 degrees, I can't find any change in the absorption (formation of dienes) at 234 nm between oxidized and native LDL. What should I do ? I am trying to do this for the second time but it does not work.
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It is difficult to find out the LDL oxidation process at 234 nm. You will get nice conformation by Thiobarbituric Acid-Reactive Substances (TBARS) assay.
  • Preparation of Oxidized LDL :-
  • Dissolve LDL (5 mg) in PBS (1 mL). Add PBS (1 mL) containing CuSO4 (10 μM). Transfer to 3.5 cm sterile plastic culture dish and incubate for up to 48 h at 37°C. Dialyze against 12 L PBS for 48 h at 4°C (two changes of 6 L each). Determine protein content by the Lowry method.
  • Measurement of LDL Thiobarbituric Acid-Reactive Substances (TBARS) in Oxidized LDL . Add LDL (50 μg) to NaCI (150 mM, 1.5 mL) in a 13×10 cm culture tube. Add TCA (20% w/v, 0.5 mL) and TBA reagent (0.5 mL). Boil at 95°C for 1 h. Cool with tap water. Add butan-1-ol (2.0 mL) and vortex mix vigorously. Centrifuge at 4,000 g for 15 min. Remove top layer and measure fluorescence (excitation at 515 nm, emission at 550 nm).
  • For more detail protocol is written in our recent published journal. See the link below.
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In most of the communities especially are owned by lower socioeconomic status.Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.
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Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.
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Chronic kidney disease (CKD) is commonly defined as reduction in eGFR value < 90 ml/min/1.73 sq. m. Several studies have reported a significant association between CKD and cardiovascular events. Oxidative stress, inflammation, and endothelial dysfunction are important phenomenons in atherosclerotic CVD. Oxidative stress is also observed in patients with CKD. Thus, it further related to atherosclerosis and CVD events.
While doing a CVD risk assessment, I am curious about using the CKD as a surrogate endpoint of CVD events. Can we do that? Is it possible to use CKD as a surrogate biomarker of CVD and other vascular comorbidities including stroke?
Paper that shows the association between CKD and CVD is available at:
DOI: 10.1056/NEJMoa041031
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First I would recommend being crystal clear in language.
You may have cardiovascular disease (CVD) and cardiovascular events, maybe say CVE. Events are occurrences that happen more or less at once, while a disease is a continuous condition.
Endpoints are usually events. Maybe you can use clear-cut conditions that are correleted with immediate risks, not with long-term risks, to define a substitute endpoint.
It appears that the aspect risk should also be carefully considered. Risks are not endpoints!
Having said this and not being an expert in that field I could imagine that hospitalisation or certain intensive care measures related to renal conditions could be defined as endpoint(s), rather as substitute endpoint(s).
The lab condition you mentioned above I would rather consider as marker of risk.
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I am trying to analyse the blood flow simulation through atherosclerosis arteries. The structure consists of 3 layers with different hyperelastic property materials. Now in this present case the blood flow simulation is done and the pressure obtained in the Fluent simulation is to be coupled with structure. When it is done with system coupling option using ANSYS workbench, we are unable to open the results.
The system currently we are using is with 32 GB RAM with 32 cores and NVIDIA graphics with 2400MHz.
How effectively can we run the simulation for FSI and obtain best results.
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I am also looking for the same answer
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Dear scholars, researchers, and colleagues, I am waiting for your opinions. Many thanks for your contributions in advance.
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I think that the main cause of atherosclerosis is the high level of cholesterol and triglycerides in the blood and this is known and personalized this leads to high level of oxidized low density lipoproteins
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In some article, it is mentioned that arteries with diffuse atherosclerosis is easily regarded as ''normal'' arteries and are underestimated its severeness, compared to focal stenosis. I wonder why it would happen because plaques can also be observed in CTA graph.
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Coronary angiography is a luminogram and that explains low sensitivity for diffuse disease
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Could it be that the glycated cells are under such force in the arterial vessels of the heart that plaque builds up quickly in the damaged lumens more rapidly than other arterial vessel locations? It seems to me that a red blood cell that is highly glycated can cause a lot of damage when accelerated at such close proximity of the pressure wave of the left ventricle. A glycated cell cannot slip in between tissues in a normal function and maybe it scratches the lumens along the path to distal locations that have slower circulatory surges (speed in the vessels of circulation). 
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Which are better cell lines to study the atherosclerosis model in vitro
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Smooth muscle cells (generally primary isolated cells, but there are also cell lines). I have worked with rat media and intima smooth muscle cells, endothelial cells, monocyte/macrophages typ M1, and more, depending on the interest!
There are now provider offering "atherosclerosis on the chip"!
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is rabbit no longer use or representative for atherosclerosis model?
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Dear Ermin Rachmawati, I'm sending you 3 articles' references which can help to clarify your question.
1. Fan, J., Kitajima, S., Watanabe, T., Xu, J., Zhang, J., Liu, E., & Chen, Y. E. (2014). Rabbit models for the study of human atherosclerosis: from pathophysiological mechanisms to translational medicine. Pharmacology & therapeutics, 146, 104-19.
2. Recommendation on Design, Execution, and Reporting of Animal Atherosclerosis Studies A Scientific Statement From the American Heart Association. Alan Daugherty; Alan R. Tall; Mat J.A.P. Daemen; Erling Falk; Edward A. Fisher; Guillermo García-Cardeña; Aldons J. Lusis; A. Phillip Owens III; Michael E. Rosenfeld; Renu Virmani. Arterioscler Thromb Vasc Biol. 2017;37:e131–e157. DOI: 10.116
3. Arq Bras Cardiol. 2010 Aug;95(2):272-8.
Experimental atherosclerosis in rabbits.
[Article in English, Portuguese]
Dornas WC1, Oliveira TT, Augusto LE, Nagem TJ.1/ATV.0000000000000062.)
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and which cell lines should one prefer?
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Atherosclerosis is a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls, by definition you can't induce atherosclerosis in the cell lines but you can induce the marker or components of atherosclerosis in the cell line, in addition there may be some 3D model of atherosclerosis available that you can use to study the lesions.
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Hi, I'm trying to evaluate a paper that looks into IL-1, MMP3 and atherosclerotic plaque stability and would really appreciate advice if anyone has read this paper or knows about the subject ; "Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice"- Journal of Clinical Investigation.
1. Are the brachiocephalic artery and aortic root the most representative vessels to look at when studying the role of proinflammatory cytokines on plaque stability?
2. Does it provide enough evidence to suggest clinical therapies that promote IL-1 should be used and how representative is the mouse model?
Also, other opinions on this paper are also greatly welcomed.
Thank you.
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2. The major interest of the article you refer to is that they found opposite results as compared to what the authors were expecting.
In fact, there are multiple studies that point in the opposite direction, that is: IL-1 and IL-2 show pro-atherosclerotic effects. Very recently, the large RCT CANTOS showed that inhibition of IL-1 beta prevents cardiovascular events in patients with previous Myocardial Infarction.
These intriguing results just raise the point that things are a bit more complex than previous hypotheses.
On this basis I don't believe it justify the development of a therapeutic approach.
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Statins reduce further deposition of lipid and in some cases with very high dose statin, some marginal reduction in atheroma may be seen.
In patients with substantial atheroma, one wants appreciable reversal and removal of lipid. Statins cannot do this
Initial studies with HDL infusions have shown promising results, but problems exist with immunogenicity .
Can HDL be rendered less immunogenic and is it a potential game changer in the world of cardiovascular disease and death?
Can we one day 'clean out' the atheroma from our arteries with this intervention?
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The point is not just raising HDL, but the efficacy of the oxLDL uptake at the site of atheroma and removal by the liver. That blocking CETP didn't work was logical from this point of view Just putting more garbage collecting trucks on the road while not improving the uptake at home nor delivery at the destruction site just creates traffic jams.
This was most clearly addressed in the apo-I Milano study where a population was found with extremely low HDL levels and still no atherosclerosis. So, better understanding of the reverse LDL transport system is of uttermost importance.
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Has anyone else investigated the PTP1B inhibitor trodusquemine (TD) and its potential to reverse atherosclerosis? A mouse study showed that a single exposure of TD reversed atherosclerosis.
TD has been shown to be safe for humans.
It has been studied in addressing Type II diabetes with a successful result. A breast cancer study was in process but the sponsor went belly-up financially, terminating the study.
TD, by the way, is responsible for salamanders, dogfish sharks and other animals being able to re-generated an entire limb.
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Interesting
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I am looking for antibodies against the protein Puromycin N-acetyltransferase.
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I have found some that work for Western but not for IMF.
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Please go through these 3 references:
1. An excerpt from wikipedia: (https://en.wikipedia.org/wiki/Lipid) reads:
"A few studies have suggested that total dietary fat intake is linked to an increased risk of obesity (Astrup, 2005; Astrup et al., 2008) and diabetes (Astrup, 2008). However, a number of very large studies, including the Women's Health Initiative Dietary Modification Trial, an eight-year study of 49,000 women, the Nurses' Health Study and the Health Professionals Follow-up Study, revealed no such links (Beresford et al., 2006; Howard et al., 2006). None of these studies suggested any connection between percentage of calories from fat and risk of cancer, heart disease, or weight gain."
2. Watch the video, Sugar the bitter truth by Robert H. Lustig, MD, UCSF professor of pediatrics in the division of endocrinology (https://www.youtube.com/watch?v=dBnniua6-oM).
Analogy: So is it logical to exonerate sugar and indict fat cholesterol as the major causes of heart diseases, increase in blood pressure, obesity, type 2 diabetes etc?
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I spent some time in eastern Africa as an environmental officer, my home was in Nairobi. On an assignment to Uganda, I ran across an old Brit MD and we discussed heart and vascular disease. He commented that the local diet was high in fat but that the prevalence of heart disease was low but had increased following the establishment of sugar plantations and refineries.
The fat may impact the ability of the endothelial cell to generate NO and the sugar generate ROS, thus pro inflammatory transcription factors, hence upregulation of ICAM-1
See, for example: Mitochondrial Reactive Oxygen Species Mediate Lysophosphadylcholine-induced Endothelial Cell Activation, by Xinyuan Li, et al.
Dr Edo McGowan
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Fat induced hepatic injury.
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Yes according to a recent work done by my collaborator. Nonpublished yet.
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Currently, I work in a lab that does research on Diabetes, Atherosclerosis, and Osteoporosis. I am the research specialist and am not involved in the hypothesis or theory of our project, I am just the technician. However, I love to read and learn more about our project and how it can be applied in other fields. In on our models we will be studying the mechanisms of S1P related to the disease models I mentioned earlier. I am just curious how or why you would be studying these interactions and if there is a future implication for human health or if it just a biological question. Would you have time to refer me to any literature? Or, If you have time to merely answer the question that works too! Thank you for your time and I wish you the best in your research!
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I am a PhD student in my first year working in a lab that searching for naturaceutical as a therapy for atherosclerosis. For example my project is on Pinolenic acid (PNLA) as PUFA have anti-atherogenic action on LDL, monocyte migrations etc... in vitro. Following this going to work on mouse model to see the effect of PNLA on atherosclerosis
. Regards Sphingolipids I have no idea really. Thanks Joseph for providing an answer. As soon as I finish my mini viva and getting more results I ll plot any update . Thanks all and best wishes.
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The exact cause of atherosclerosis isn't known. However, certain traits, conditions, or habits may raise the risk of the disease.
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In addition to what our colleagues wrote, I mention chronic Inflammatory conditions like Psoriasis, autoimmune diseases causing arteriitis, and also linked to metabolic syndrome, as well as Hypercoagulation syndromes. In addition risk factors like Lp(a), Fibrinogen, pHcy.
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what the main gene responsible for atherosclerosis?
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Dear
I think this article help you
  • Munir MS, Wang Z, Alahdab F, Steffen MW, Erwin PJ, Kullo IJ, Murad MH. BMC. The association of 9p21-3 locus with coronary atherosclerosis: a systematic review and meta-analysis. Med Genet. 2014;15:66. [PMID: 24906238; PMC4074865].
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Hi,
Does anybody have any experience with histologically processing arterial plaque tissue which may contain calcified regions?
  1. I understand decalcifying agents such as EDTA can be used however what techniques can be used if you want to keep the calcified region (without dislodging during microtome slicing) in your histological slices for staining?
  2. Additionally, if anybody had a working protocol for decalcifying atherosclerotic tissue, it would be a great help?
All advice is welcome!
Robbie
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Decalcification is necessary to get a fine paraffin section. Otherwise, the section will tear. If you want to skip decalcification, you could try plastic/ resin sectioning approaches.
Assuming you want paraffin, just trim and fix tissue as you normally would, then transfer to decalcification solution for 24-48 hours. These are sold commercially (we use 'Cal-Ex' from Fisher Scientific) or you can make buffered solutions of HCl and/or EDTA, which is what these solutions usually contain.
Note that the solution only takes out the calcium ions, not the cells or other cell products. Your atherosclerotic plaque region will still be present, but no longer crystalline.
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I have developed an non invasive risk assessment tool to estimate the stenotic risk of atherosclerosis to detect asymptomatic individuals. The carotid duplex will be the standard measure.
My question is:
For tool validity, should l apply the tool and carotid duplex on two groups (diseased and at risk) or only for one group ( at risk) ?
Second question:
Is fisher et al.,1998 the best sample size equation for this study
n = z²pq/d²
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Dear our Prof .. Hello ,
using screening 2 x 2 table for sensitivity and specificity to know the validity of the test.
In other words we need to critically appraise the article on a diagnostic test?
In such article we are looking for the following:
Have the researchers compared the test to a reference [Gold Standard]; which means that patients have undergone the two tests.
Example: Gold standard [ The carotid duplex ]
Example of Screening Test: A non invasive risk assessment tool
Blinded comparison: The results of one should NOT be known to those who are applying and interpreting the other
How have the researchers justified the selection of the Gold Standard?
in the attached files : nomogram
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If I,m going to asses reliability of new tool developed by me to estimate the risk of atherosclerosis through a cross sectional study how to calculate sample size avoid confounders make randomization
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Hi Arwa
I strongly suggest you get some advice from a biostatistician. You need more help than can be provided here.
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Dyslipidemia is related to the progression of atherosclerosis. Although treatment of dyslipidemia is beneficial in decreasing the number of coronary events its effect on infarct size and myocardial remodeling are still to be assessed. What is the best strategy in terms of preserve myocardial function after AMI?
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Dear colleagues
Thanks for the informations
I agree with you and we have to use statins in high doses to improve microvascular function and reduce systolic dysfunctio.
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Any paper related to clinical trails or related to research based on nano-particle and related to atherosclerosis will be helpful.
Any suggestion will be highly appreciated?
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Hello everyone could someone give some help or some interesting articles related to: <<The application of inorganic nanoparticles in drug delivery.>>?
Thank you in advance!
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I am planning to feed rats with radioactive calcium. Is there any evidence that the radioactive uptake prefers the bone sites of the body in comparison to vasculature ?
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Yes, it will eventully end in bone for the most part.
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I recently analyzed RT PCR data for NASH livers. Oil red O staining revealed that my experimental group has exacerbated NASH/ lipid content. This group also demonstrates lower RNA expression of Srebp2, Hmgcr, and Hmgcs. However the gene expression of Ldlr is drastically increased. These results should be validated with western blot analysis also but does anyone know why this might be? PCSK9 is a post transcriptional inhibitor of Ldlr, so this wouldn't affect Ldlr on a transcriptional level.
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Thank you so much! I will definitely look into this.
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I was looking into a study on the inhibition of atherosclerosis in diabetic pigs using anti alphavbeta3 antibody. I just wanted to know...
Is it possible that integrin alphavbeta3 could be replaced by another integrin when antagonised with an antivbeta3 antibody? for example alphavbeta1
Is inducing diabetes with streptozotocin a bad idea..for example Is it possible that using such a drug could have an effect on atherosclerotic lesion...I found that SIRT1 is increasingly expressed following the use of streptozotocin which has been found to exhibit anti-aging effects.
What would be the most appropriate controls to use for such a study.
would an IgG F(ab)2 antibody be appropriate or are there better controls to utilise?
Any help would be greatly appreciated..Please see the paper I am referring to in the link attached...
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Hi Jonathan i have send u a message on your watts app, let me know mate thanks 
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Staging of portal hypertension is not clear but important for prediction of first bleeding episode. Do you have any evidence (as we obtained) of splenic artery increased blood flow may be a possible predictor?
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Thank you, it is really interesting high quality article. Good day. With respect, Sergii.
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For the qunatitaive study of atherosclerosis in mice, is gelatin embedding of heart important or can we do snap freeze with isopentane?
My understanding is that, to study atherosclerosis, we need to do Oil Red O staining to study the foam cells and also the journals now ask for cell types present in the atherosclerotic plaque.
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There is a mistake on this question. I am not an author of this article. Sorry about that.
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Just a question I came across whilst going through readings. 
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Statins have pleotropic properties encompassing anti inflammatory effects, countering of smooth muscle proliferation and prothrombosis. It has been reported to also cause some blood pressure reduction. These ameliorate atherosclerosis even if hypolidaemic effect is not great
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I would like to feed STZ-injected mice (type 2 diabetes) on cholesterol diet for 28 weeks. Is this period enough to induce atherosclerosis? since wild type mice are resistant to atherosclerosis
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Thanks all
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in a patient with diabetes type 1 with lactic acidosis is it possible to have a false positive test for ethylene glycol?
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I think these articles can help you
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How to address cholesterol efflux in primary residential macrophages? We can't access radioactivity so the classical approach couldn't be used. Any suggestions are welcome.
Thanks
Vivek
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You can use the fluorometric methods using BODIPY-cholesterol or NBD-cholesterol.
See these papres:
A sensitive assay for ABCA1-mediated cholesterol efflux using BODIPY-cholesterol.
The implication of cigarette smoking and cessation on macrophage cholesterol effl ux in coronary artery disease patients.
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how strong are the data that K2 supplements can reverse coronary calcium buildup? What doses are needed?
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I don't see what would the mechanism for such a proatherogenic cause consist of?
Is there any experminetal/observational evidence for the correlation of Vit. K antagonists intake and atherosclerosis build-up? Since there are a lot of patients taking warfarin, there must've been something noticed, if that's what happens?
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The compound is a Tyrosin Kinase Inhibitor (type 1). Can also reduce ROS (in HUVEC, TNF-a induced). I need to know which factors are required to be considered/proved in vitro and in vivo to show that the compound is a potential one against atherosclerosis. 
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ROS is directly associated with arthrosclerosis. If your compound is able to attenuate ROS, I believe you can target and portray ROS pathways. You can approach via anti-oxidant mechanisms for example: Renin induced hypertension and testing your compound. Screening of mitochondrial damage by ROS induction and testing your compound would also be an excellent approach.
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is there any optimum time frame for that? 
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In that case put them on diet for 6-8 weeks depending on the age of your mice, because ApoE-ko can develop lesions on normal Chow diet as well.
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i would like to test my compound in vitro. which cell line should I use to generate atherosclerosis?
to prove my compound's (Kinase inhibitor) potency which assays would be rational ?
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Obviously, there is no good model for a complex process such as atherosclerosis in a cell culture system.  However, you could test your compounds in isolated cells in culture or co-culture if you have a predicted mechanism of action.  For instance, if you expected an effect on monocyte targeting, you could examine monocyte adhesion to the endothelium (preferably under flow) in response to an atherogenic stimulus such as oxLDL treatment.  However, the model will be limited to the specific process you are trying to reproduce in culture.
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Hi i am currently doing research on ApoE-/- mice and I am wondering if anyone here can point me to the the current gold-standard method for quantifying total lesion area of the aorta and likewise to identify and quantify specific morphology of a plaque - fibrous caps, necrotic cores, macrophages etc.
Thank you, your suggestions would be very much appreciated :)
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J Pharmacol Exp Ther. 2005 Oct;315(1):320-8. Epub 2005 Jul 14.
Calcium channel blocker inhibits Western-type diet-evoked atherosclerosis development in ApoE-deficient mice.
Kyselovic J1,
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If someone is working on Probiotics, specifically Gut microbiota and share some new identified probiotics. I need some species and may if possible can work and will be considered as a contributor in my research work. will work together and share some knowledge and experience 
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Doing a PK study on rosuvastatin in parrots
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Dear Hugues Beaufrere,
I am really sorry that i have not your expected data ...i do not get a sound scope for working on this field .
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Is it important to coat the flask / tissue culture plates etc with ECM like gelatin or collagen while culturing HUVEC or doing experiments with HUVEC. My cells adhere much better when I culture them on non-coated flask. I have my cells from LONZA, and I am using the EGM-2 media from LONZA as well.
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Dear researchers,
Endothelial cells are polar cells with apical and basolateral domains which has to do with their attachments to the substratum, usually a basal lamina consisting of various types of collagen, fibronectin, laminin etc. Thus it is essential to grow them on a coated surface because glass surface is not known to these cells in their natural environment. I believe this will help us to deal with cells that are sane in our experiments.
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If you are interested in knowing about a gene (not necessarily the protein) and its relationship with a disease, try DisGeNET. (http://www.disgenet.org/web/DisGeNET/menu;jsessionid=15gl6du1cmyrv77xqzmqt2b1a)
It links articles which may have suggested association or functional aspects of a given gene with the disease. 
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We are looking for any lab who has experience with ES cells differentiation to Macrophages. We are interested in cholesterol efflux in Macrophages.
Thank you in advance.
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Dear Dr. Yakala,  You can try to contact the 
You can try to contact the  following groups
  1. Prof. Megumu K. Saito, Department of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan
  2. Jerome A. Zack, Mailing address: David Geffen School of Medicine, University of California at Los Angeles, 173 BSRB, 615 Charles Young Drive South, Los Angeles, California, 90095. Phone: (310) 825-0876; Fax: (310) 267-1875; ude.alcu@kcazj
  3. Christopher D. Gregory from University of Edinburgh/MRC Centre for Inflammation Research, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 2TJ, UK
1 and 2 for human human ES cells and 3rd is for murine ones
All the best,
Tushar
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My lab is new to atherosclerosis research, and I am trying to do oil red o staining of aortic roots from mice that we induced kidney disease and then fed a high fat diet for an extended period. We didn't use the LDLr or ApoE ko mice yet, because we wanted to see if the mice would get atherosclerosis without genetic knockout. My boss is unable to give me feedback on some of the problems I am having with the staining. I have attached a ppt with points pointed out that I specifically have questions about. If you guys have any insight into my problems, or have any other additionally critiques please let me know! 
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Dear Cassi, we´re doing ORO staining from aortic root cryosections following this protocol: 60´air dry, 3x wash H2O, circumvent section using pap pen, dehydration 5-10´in 100 % propyleneglycol, 60´filtered ORO at RT, 2x3 min dips in 85 % propyleneglycol, 3x wash H2O and counterstaining. Make sure your ORO is filtered properly, in case you dont see red stained droplets, increase time and or temperature. Good luck!
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Helo
is there any research that have done exam in umbilical artery to see any atherosclerosis lesion such as foam cell, plaque atherosclerotic or thickness of tunika intima regarding obese maternal
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thank you for answering my question.
have you ever heard about IHC for defining the lesion. I want to use CD68 for checking the foam cell, VCAM-1 antibody and also thickness of tunika intima,Is it possible to do that in umbilical artery??
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Hello, does anybody know if there is any commercially available hyperlipemic serum for cell culture? It would be rather easier to obtain (and presumably more standardised) than serum from WHHL rabbits or rats/rabbits on high fat diet. I would like to check the effect of such serum on the MSC in vitro differentiation. There are lipid supplements available (eg. from Sigma) but they do not represent the whole repertoire of lipids and lipoproteins found in the sera of atherosclerotic patients. 
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I know that the Harefield Hospital trust near Uxbridge has a centre for LDL apheresis of familial hypercholesterolemia patients - not sure if you can recover the LDL after the procedure or if this would be suitable for your experiments...
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What are the sex differences in susceptibility to atherosclerosis in mice?
Could you correlate this to humans and highlight important differences? How would you comment on translational values of studies on atherosclerosis in mice?
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Gregory and Ali, 
Thank you for your comments! It seems that there are some quite complex differences between atherosclerosis risks in mice and humans, but a lot of research papers still translate results obtained on mice to humans. Gender differences are particularly interesting. I have seen several explanations and I feel this is important area of research that may not in the beginning yield results that can directly be translated to human practice, but definitely give us knowledge about shared pathophysiological pathways. How would you comment on the fact that female mice are more susceptible to atherosclerosis than male mice. 
Best regards,
Jan 
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Atheromatous plaques are commonly seen in the coronaries, carotids and aorta. Despite sharing the same risk factors only certain sites are predisposed. Even in the same individual, despite similar blood vessel size, hemodynamic stress and blood flow patterns, plaques are often unilateral and seem to spare vessels sharing similar stress. 
Why this variation?
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Atheroma site specificity correlates strongly with regions of disturbed shear stress, I.e. on the outer wall at a flow divider, e.g. bifurcation - where shear is low, or at regions of vessel curvature, e.g the aortic arch. Also, contrary to popular believe, shear is not uniform across the circulation. In fact, it is considerably higher in small arteries and especially arterioles. Also, between species there is an inverse relation between shear and body mass, e.g. shear is around 15 times higher in the abdominal aorta of a rat than the same region in a human. Coincidence that rats don't spontaneously develop atheroma?? Notably, shear is a powerful inducer and suppressor of the genes pertaining to vasodilation and vascular disease. 
Hope that helps,
Dave
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Obesity is a critical public health problem as it is a risk factor for many human diseases, including diabetes, atherosclerosis and cancer. The cross-talk between mTOR, an ancient nutritional cellular sensor critically involved in cell growth and metabolism, and neuro-immune-endocrine metabolic controllers, to regulate and
integrate signals of energy balance, lipid metabolism and inflammation opens new avenues in the study of the molecular mechanisms involved in the pathogenesis of obesity-related atherosclerosis and cancer. A better understanding of the molecular and cellular mechanisms involved in obesity-induced atherosclerosis, may lead to identification of potential targets for therapeutic interventions.
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Si estoy de acuerdo que la obesidad es un proceso generalizado de inflamación generalizada, que origina enfermedades diversas en toda la economida del organismo y que se debe realizar un tratamiento intensivo para mejorar el IMC
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I have been studying anti-atherosclerosis effect of one well known DPP-4 inhibitor. For observing MMP-9 activity I am using rat SMC primary cell but I could not get the clear expression. Now I want to switch primary cell to cell line for observing MMP-9 activity by zymography method, could any one please recommend me specific cell line for this study? I am using 20 ng/ml TNF-a as stimulant.   
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I confirm that HT1080 with TPA is a good way to recover MMP-9 in conditioned medium.
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Is it possible that freshly secreted (pre beta) HDL particles aren't (oxidatively) modified whereas larger (alpha 4, alpha 3,..) HDL particles are? In other words; is there a certain time needed after the secretion of lipid free ApoA-I for it to become oxidized / ...? 
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In general I would expect that freshly secreted HDL particles are not modified, within the ER and the Golgi system no oxidation should occur. As soon as the particle enters the blood (or the cell culture medium if you are working with isolated cells) its open for modifications and the time scale depend on several parameters (O2 saturation of the blood, antioxidant conc., free radicals, enzymatic activities in the blood and on the HDL particle itself ...).
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Vegetarian diets are promoted, even by scientists, that these diets are safe unlike the non-vegetarian diets which over the years lead to development of arteriosclerosis (atherosclerosis). But research does not show any substantial proof. Did any one look at the properties of blood vessels at various ages ? Do the vessels lose their ability to repel the lipids flowing 
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the question has many answers, all -more or less- plausible. First, there are many different vegetarian diets, which act differently in different races and in different individuals. The reaction is, usually, detached. Second, there is no "vegetarian diet" but the product of an eating habit (and its variability during the life) for a certain time, at a certain stage of life, in interaction with numerous genetic, epigenetic and environmental factors. Third, we must not forget that atherosclerosis is a systemic disease, proliferative and degenerative, slowly progressive, but reversible, which extends along the life, and that ATS is one of the rate-limiting step in the life span of individuals and in growth of populations. Fourth, the experimental methods available currently are not correct and do not provide answers to multidimensional problems with hundreds of variables. Fifth, there is no need to assume that the study of "average trends" (as in controlled clinical research) can help to predict individual responses. Fifth, predictive medicine and medicine of complexity models (i.e. so called System Medicine) have not yet suitable to solve the problems, nor sufficient computing power. (we hope for the future)
So, from the empirical point of view, how would the Doctors of Salerno School of Medicine, many centuries ago, we can say that we have enough evidence to say that certain dietary habits may be healthy. We also know well enough evil: that some diet errors can cause illness. But we should not expect too much from a science that is still in its infancy. From a practical standpoint, we have to go to a few elements essential and I shared when we give instructions to our patients, limiting the essential advice to those trying to customize them also on the basis of elements of clinical and physiopathological  reasoning  NOT encoded by the guidelines or the EBM ( cave canem,  without giving too much weight to a myriad of studies and experiments, each one seemingly plausible but all together completely impossible. For example: if you do the sum of all the proven benefits in GCP published (on dietetic products and nutraceuticals) you will always result in eternal life and perfect health in all men, and yet.........
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In atherosclerosis disease, secretory IgM (sIgM) is important for protection. Atherosclerosis levels were significantly increased in sIgM-/-LDLR-/- mice than sIgM+/+LDLR-/- after 12 weeks WD feeding. However, there is no significant difference in atherosclerosis after 12 weeks WD feeding in sIgM-/-ApoE-/- mice when compared with its control group sIgM+/+ApoE-/- mice.
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Prasad, The original description of the sIgM -/- mice is described here. The apoE -/- and LDLR -/- background should not directly affect the immune system. You may be observing differences in the mechanism of atherosclerosis development. Have you considered the comparing atherosclerosis in the 2 different apo E -/- mice on a chow diet where the development of atherosclerosis will be slower?    http://www.jimmunol.org/content/160/10/4776.full.pdf+html
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Kindly give references for the same if possible; also kindly quote any clinical trials done/in progress, with regard to the same. Thanks in advance !
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Thank you julian
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AMPK boosts a cascade of events within cells that are all involved in keeping energy homeostasis.
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In my view first of all see its interaction with the ligand already attached with the complex at pdb database or you can visualize it on chimera or some other visualiztion software.
In order to assess its activity docking can be done on different ligands or biomolecule that enhance the or decrease AMPK activity. Docking score will give us an idea or extent at which this molecule is expressed in different condition
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Measuring the amount of epicardial adipose tissue (EAT) can be a novel parameter that is inexpensive and easy to obtain and may be helpful in cardiovascular risk stratification. However, the relationship between epicardial fat and cardiac function and that between epicardial fat and cardiac risk factors is less well described.
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The  topic  is  worth  investigating.
With  echocardiography  the  epicardial  fat  thickness  can  be  easily  quantified  in  a  reproducible  manner.
Establishing  a  cut  off  value  for  predicting  metabolic  syndrome  and  coronary  arterial  disease  may  need  a  triad  study  involving  epicardial, visceral  and  subcutaneous  adipose  tissue  and  then  correlating  them  individually  with  certain  biomarkers,  in  a  longitudinal  study.
This  triad  study  will  involve  2D  or  3D ultrasound  for  visceral  and  subcutaneous  adiposity  and  echocardiography  for  epicardial  adiposity. It  would  be  reasonable  to  do  it  that  way  to  be  sure  of  the  best  predictor   for  metabolic  syndrome  and  coronary  artery  disease.
We  did  a   little  work  on  visceral  adipose  tissue  quantification  with  ultrasound  which  will  still  be  developed  in  future. 
The  link  below  may  be  helpful.
Thank  you.
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Macrophages are known to be an active player in MS. They are involved in active demyelination and myeline uptake, which leads towards the development of foamy macrophages with M2-like properties. But can they migrate out of the brain/lesion before they become necrotic and cause a pro-inflammatory respons (cfr. atherosclerosis)?
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Foamy macrophages (gitter cells) do migrate out of the MS plaque into the perivascular space and then into the blood stream.
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Hi, dear all, can you please help me with the follow questions: How to define preclinical carotid atherosclerosis? and what is the marker of it? If carotid intima-media thickness >1mm, may I say this patient already have carotid atherosclerosis, or I should say the patient is in the status of preclinical carotid atherosclerosis?
Thank you all very much!
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hi Li, could the attached review help you?   
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Some studies showed that eNOS-derived reactive oxygen species play an important role in atherosclerosis progression and restoration of eNOS functionality by upregulation of GCH1 is a rational therapeutic approach. GCH1 transcription has been shown to be upregulated by cytokines, insulin, statins and ARBs. Could be this the next frontier in treatment of atherosclerosis?
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Dr. Kar thanks for the answer. We will be waiting for the manuscript to better understand the mechanisms involved.
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There are controversies about size and levels of HDL to predict atherosclerosis. Due to its strong association with cholesterol acceptor capacity, high-density lipoprotein size has been appointed as a potential risk marker and can challenge the efficacy of traditional risk markers.  What are your opinions about this?
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I believe in it. Do you think it is possible to develop strategies to measure the diferents sizes of HDL and establish its impacts in the development of atherosclerosis?
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LDL cholesterol remains the proven target. Many alternatives have been presented. The possibilities debated involved cholesteryl ester transfer (CETP) protein inhibitors, apolipoprotein B (apoB) mRNA antisense oligonucleotides, microsomal triglyceride transfer protein (MTP) inhibitors and proprotein convertase subtilisin/kexin type 9 (PCSK9) antibodies, which one would be better? 
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Thank you Dr. Mishra for yours considerations, with which I agree. Let's wait for the new studies to establish the behavior improvements .
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The essential logic is to decrease the time of exposure to cardiovascular risk factors with genetic insights providing strong justification for this approach. Lifetime exposure to lower concentrations of cholesterol specifically, plasma levels of low-density lipoprotein (LDL) cholesterol, is shown to be associated with larger reduction in the risk of coronary heart disease. The decrease in risk is related to the genetic variants of receptors that remove cholesterol from the circulation matched with individuals who do not carry such variants. For a known reduction in LDL cholesterol, there was much more impact on reduction in cardiovascular disease risk than that reached with pharmacotherapeutic modulation in late life. Several studies have shown that the adoption of a healthy life , the act of not smoking, weight control and perform regular physical activity , with the reduction of cholesterol levels can be more effective than drug therapy of known effectiveness. How best to link these two strategies and show people that the protection of their coronary health goes beyond the use of drugs ?
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Stop researching risk factors and get into prevention. If you want to research risk factors, find a disease we haven't already studied to death. 
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Data from population studies dating back from the Framingham study/substudies among others demonstrated quite clearly that a sedate lifestyle and a diet high in calories were risk factors for the development of atherosclerosis. I am not aware of any studies looking specifically at "screen time" which I assume you mean computer screen time but any such activity, whether watching TV, playing video games or what have you that limit physical activity will have the same effect of classically measured low activity lifestyles. I am not aware of a US study on the effects of weather but the Scandinavians may have conducted a few.
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Congratulations, you discussed a very interesting issue. I agree with the individualized therapeutic approach, especially in the patients with mild haemophilia phenotype. I would like to discuss the management of elderly haemophilia patients with atherosclerosis, obesity, smokers who have undergone an episode of arterial thrombosis. What do you think about the combination of replacement and antiplatelet therapy? How many haemophilic patients with diabetes and other conditions such as cancer do you have? 
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Dear Peter,
an expert in your field of interest would be Dr. Wolfgang Miesbach, head of the hemophilia clinic at the university clinics of the Goethe University in Frankfurt/Main, Germany.
If you can send an email directly to m.mueller@blutspende.de, I will send you his mail address.
Best,
Markus
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I would like to know the changes in statin prescription rates and cholesterol treatment guidelines over time (i.e. from the introduction of statins until the present time in the United States and Europe). I am especially interested in the context of secondary prevention of embolic stroke. Are you aware of any published data or do you know where I can find out-dated versions of cholesterol treatment guidelines? Thank you for your suggestions.
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Each organissation develops their own clinical guidelines. Depending on your research you should target each country and the national organisation in charge of developing the guidelines. For Spain you can find the information on this website: :http://portal.guiasalud.es/web/guest/guias-practica-clinica. they collect all the different clinical guidelines developed by the different regional governments (17 in Spain), so usually if they exist you can find them on this website, if not I;m afraid that you should contact each autonomous community  one by one.
You could contact Guia Salud (through the website)and ask if they keep track of old guidelines.
For European Countries having different regional health governments (Germany, Italy) you will probably face the same problems of non-centralised information.
For UK, they use the guidelines of NECP , ATP III, as mentioned ,through the NIH you can find them easily on their website, the one I found is from 2002 and I also  found an 2004 update in an interesting  article: http://www.nhlbi.nih.gov/files/docs/guidelines/atp3upd04.pdf    ,page 237
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In order to screen the hypolipidemic drugs, Triton induced hyperlipidemic animal model is being used. In most of the papers, Triton WR 1339 (tyloxapal) was used to induce hyperlipidemia. However, in some paper Triton X 100 was used. Which Triton is best or ideal to induce hyperlipidemia in rat model.
Thanks in advance for replies.
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Triton WR-1339 reliably induces hyperlipidemia in rodents treated with it without fatalities unlike triton X-100 which kills animals as a result of its attendant hemolysis for which it is notoriously reputable. 
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Lipoproteins can be separated by these two techniques, one another by molecular size and density, but the fractions obtained are not identical and may not be equivalent análisis.
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From the perspective of mechanistic systems biology and kinetic modeling, we always want to know what separation technique was used to define lipoprotein fractions. Michael's answer is right on target for ultracentrifugation because protein composition will change in the ultracentrifuge. 
A related question that we worry about is: Shouldn't we expect a continuous distribution of lipoprotein size at least for the apoB100-containing lipoproteins? Since LPL and LCAT and PLA2 and CETP and other intravascular processes are constantly modifying lipoprotein composition, we build our models with each lipoprotein species (defined by density or size or apoprotein composition) permitted to have variable lipid composition. The question then becomes: Can we account for the measured compositional and kinetic data given what we know about the intravascular processes AND the characteristics of each subfraction as defined by the separation technology?
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When studying some metabolic parameters in elderly people, it seems difficult to distinguish which ones are caused by aging per se or by age-related diseases. In particular, circulating IL-6 is known to increase with age but is it a relevant biomarker of aging since it is also elevated in metabolic diseases such as obesity or atherosclerosis. Then, is there a very specific biomarker of aging?
How can we characterize healthy elderly? For the recruitment of such cohort, do we exclude all kind of diseases or can we tolerate some?
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I am not unbiased, as you can imagine. The answer also depends on your objectives. I am skeptical about the distinction about aging and age-related diseases and also try to avoid going to semantics. There are many biomarkers of aging but all they are "weak", in a sense. Using the frailty index approach we can find a summary measure that is much superior to any single biomarker.  Aging is a systemic property of the organism therefore any assessment should also be systemic, i.e. to combine available information.  Such information can be based on clinical assessment  or even self-reports but also can be more "objective". Take a look at the recent paper Howlett et al. BMC Medicine, 2014 where the lab tests were combined together in a FI-Lab. To go in this direction you should not hate math, although math is very basic.
Arnold
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Thrombus in the non-aneurysmal, non-atherosclerotic descending thoracic aorta (NAADTA) could explain a little part of the 20% of non-cardiac causes of peripheral and visceral emboli. The presence of aortic mural thrombus in NAADTA is an extreme rare condition: whether this is explained by either under-diagnosis or true low prevalence, or both, might be debated. The optimal management of these patients is still controversial. I am actually managing an asymptomatic thombus in a descending thoracic aorta without any sign of atherosclerosis or aneurysm. It is about a 7x20 mm thombus with a little peduncular portion. Have you any experience in such cases? How do you managed it?
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Many of these originate in the stump of the ductus and are grossly mobile. They usually are discovered because of embolic presentation. Many can be very large. We resect these by open operation.
The ones that are just layered along the more distal aortic wall we watch with serial CT scans. We do not really know a cause for these.
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Recent studies suggest that there is still a benefit without significantly increasing side effects, but I'm not convinced that long term or in certain subgroups of patients, the metabolic change that we generate with very aggressive treatment is safe.
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The original question was what do we have to monitor with high statin therapy. If we use other therapies may other metabolic Parameters would also have to be considered. In statin therapy I would monitor lipids, glucose and HbA1c, ALAT, may be  CK (at least at the beginning) and eventually hsCRP.
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In addition to its anti-inflammatory effects, the
PPAR-gsystem affords protection from oxidative stress. But the mechanism of its anti-oxidant effect is not well studied. Whether PPAR-γ enhancing
the transcription of  antioxidant genes such as Nrf2 contributes to this effect.
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PPAR gamma regulates genes involved in fatty acid uptake and triglyceride storage in cells (adipocytes as well as other cell types).
Fatty acids can either be stored in neutral lipid deposits, as triglycerides or oxidized for energy through mitochondrial beta oxidation. Mitochondrial metabolism usually shifts between oxidizing glucose and fats for fuel to produce ATP, depending on the time of day (sleep/wake, postprandial state etc) and metabolic demands of the organism (eg exercise, fasting).
Reactive oxygen species (ROS) are an inevitable biproduct of oxidative metabolism and are usually neutralized by tightly regulated antioxidant defense mechanisms within cells (which are regulated at the transcriptional level by other PPAR isoforms, particularly ppar delta).
Fatty acids contain more energy than carbohydrates (4 vs 9 kcal/gram) and so oxidation of fatty acids produce more ROS than oxidation of glucose.
Models of metabolic disease (obesity, diabetes) exhibit metabolic inflexibility-- The ability to switch between oxidizing glucose and fats for fuel is impaired at the cells, tissues and the whole animal level. In diabetic states, where glucose uptake is reduced, fatty acids are abundant and are the primary fuel source. Excessive oxidation of fatty acids results in accumulation of reactive oxygen species. Inhibiting fatty acid oxidation, or altering fuel preference to favor glucose oxidation decreases ROS production.
PPAR gamma activation reduces oxidative stress, by promoting fatty acid storage in neutral lipid droplets.
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Endothelial dysfunction is first step of atheroma progression in atherosclerosis.
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TNF-alpha,  IL-1 beta
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Literature shows that there are correlations between the heart anatomy and physiology on the one hand and the level of performance on the other hand in humans. Also in humans, coronary dominance is researched in the context of, for example, atherosclerosis. But should it be possible that the coronary dominance is also a factor which influences the level of cardiac performance in men and horses?
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It is true that a lot of factors play a role and also that the morphology of coronary dominance will probably not influence directly the pump rate. But i can imagine that one or another morphology can influence the blood flow of some smaller parts of the myocardium (for example in the interventricular septum) and in that way some parts can get their oxygen in a more efficient way than other parts. Which could have its repercussions on sustained efforts. These are just assumptions, but I thought to myself that it might be interesting to look at coronary dominance in this context. Gr Tim