Science topic

Vascular Diseases - Science topic

Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.
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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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The origin of many, if not all, vascular diseases can be correlated with endothelial cells (ECs) mechantransduction. The mechanosensory of ECs is strongly linked to the physics of blood flow. CFD models of vascular blood flow can provide insightful information about the hemodynamic environment associated with different vascular disease. Hence, CFD can contribute to the research on ECs mechanotransduction. However, since blood flow is inherently multi-harmonic pulsatile flow and vascular geometry have complex 3D morphology, CFD models require rigorous validation practice in order to ensure that their results are as valuable as they are considered to be.
I would like to discuss the previous efforts conducted to provide consistent, reproducible and physically meaningful validation procedure for CFD models of pulsatile flow for vascular hemodynamics applications. Is there any validation resource available for public access? What would a good and reliable validation database include?
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Thank you Dr. Kartik Jain for the informative response. I have used many of these validation datasets in my early CFD work on turbulent combustion modeling. However, pulsatile flow is quite different from fully developed flow, especially when it comes to transition to turbulence. The FDA nozzle benchmark is dealing with fully developed flow too.
As to the mesh convergence tests, of course it's a good way to establish benchmark for evaluating the numerical error in a CFD model. Similar to Richardson extrapolation or any of its variants, mesh convergence estimates the error resulting from discretization scheme. Validation, on the other hand, aims at estimating the error resulting from the physical model and assumptions in the governing equation (such as viscosity closure).
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Acroangiodermatitis has been described in amputees (especially in those with poorly fitting suction-type devices), in patients with paralyzed legs, in patients undergoing hemodialysis (from arteriovenous shunts distally), and in association with hepatitis C. It has been documented in chronic venous insufficiency and in vascular malformations (eg, Klippel-Trenaunay syndrome, Stewart-Bluefarb syndrome, Prader-Labhart-Willi syndrome).
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Acroangiodermatitis of Mali is usualy caused by chronic venous
insufficiency
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For how long? Just 2-4 weeks? And is topical steroid necessary? Or it the patient can be on other medications without fearing complication? I.E does topical steroid prevent any serious complications? Or just treat the symptoms like Erythema?
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Dear Dr. Elsersy.
Long term use of topic steroids is not recommended for stasis dermatitis. It can be used as a short course to reduce the inflamation. Treatment aimed to correct the hemodinamic abnormality in venous system responsable for skin changes is most important. Treatment plan also includes elastic and non-elastic compression and veno-active drugs.
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I am using survival analysis for vascular disease of lower limbs and need to categorize patients according to a risk factor eg hypertension. is there a minimum number of patients that needs to be in one specific group eg on one drug only?
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You need to sit with Biostatistician and discuss with him/ her what you want to do. (project details) before that you need to go through literature review and search similar studies, their methodology, sample size and techniques and specific outcomes (results) of those studies. it is important to know estimated positive outcomes of your study objective inorder to calculate sample size. (you may use WHO sample Size Calcultor with help of your Biostatistition)
Generally when we divide the study population in more groups via stratification our sample size increases so that we can justify results with atleast 95% confidence and margin of error <0.05%.
Authenticity of your study results depends on how confidently you can generalize your results.
Objective of study should be SMART
specific
Measurable
Attainable
Relevant
time bound.
Hope you got the answer
Regards!
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Any paper or help that can assist with predicting the life course of primary vasculitis of the skin if left untreated ?
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This depends upon the cause of skin vasculitis. The most common skin vasculitis is small vessel vasculitis of the variety known as leucocytoclastic vasculitis. This can have varying caused ranging from infections, drugs to associated systemic vasculitis with internal organ involvement. The ones related to drugs and infection might be self limiting. The skin vasculitis associated with systemic vasculitis especially medium vessel vasculitis in the form of large ulcers or pyoderma gangrenosum like lesions or cutaneous infarcts need aggressive immunosuppressive therapy
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In this scenario, I'm interested in Daflon (Trade name). Could misdiagnosis be harmful and turn the Pharmacological and therapeutic effect of a drug (Daflon) into an adverse reaction? We know that Daflon is used in case of chronic venous insufficiency as it helps with capillary permeability, etc..But is it dangerous for someone with healthy veins to ingest Daflon? Does decreasing capillary permeability in case of healthy veins(someone who is healthy) affect it in a negative way? And if so, is it imperative that drug shouldn't be given unless we are 100% sure of the diseased state, so when given the drug, it'll return normal? And how can I know when the drug pharmacological effect can be turned into an adverse reaction?
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The undesirable effects that may appear are those well described: digestive disorders (frequent), nervous system (rare) and immuno-allergic (rare). They are related to flavonoids.
The pharmacological effects are likely to be expressed in the healthy subject (AGRAWAL AD, 2011. Pharmaceutical activities of flavonoids: a review. International Journal f Pharmaceutical Sciences and nanotechnology). In my opinion, they will not have any clinical expression.
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Beta carotene 15 mg twice per day, and Daflon 500 and both failed to treat this rash.
Medical history:
Atrial Fibrillation
Allergy related to temperature changes
Hemorrhoids
Medications:
Bisoprolol 2.5 mg once per day
Cetirizine 5 mg once per day (Sometimes, to treat allergy related symptoms like shortness of breath)
Daflon 500 once per day (Hemorrhoids, and was given previously to treat this rash)
Multivitamin supplement from time to time
Age: 52
Gender: Female.
What is the diagnosis?
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Dear dr. Mostafa,
For diagnosis, a detailed history of the lesion and its systemic association is needed. The lesions could be a type of small vessel vasculitis, rash of hypercoagubility state, embolic rashes (given the history of AF) or circulatory insufficiency. These can be differentiated by taking biopsy. But it could be a dermatological dyspigmentation problem, so it is worth to take dermatological consultation as well.
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Cerebrovascular and cardiovascular events are the causes of more than 50% of deaths in developed countries. Atherosclerosis is a diffuse vascular disease, which may have a common mechanism of stenosis in both coronary and carotid arteries.
However, several reserches show that presence of plagues in carotid artery has low correlation with coronary artery disease.
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Thank You Sergey for such interesting data.
In this case the threshold 0.09 ml is concerned to plaque volume by 3-D, though in most studies intima-media thickness (IMT) is used as atherosclerotic marker (as a part of carotid vessel with 50% more than nearest intima-media).
Sillesen et al. reported that 3-D plaque burden was highly correlated with coronary calcium and TPA, but not IMT, further, they reported that plaque
burden was as predictive of events as coronary calcium.
Because carotid plaques are focal, and grow along the artery 2.4
times faster than they thicken, and also progress and regress
circumferentially, carotid plaque can change in three dimensions.
IMT changes only in thickness.
Measurement of Total Plaque Area (TPA) can also be used.
The advantage of TPA for risk stratification was shown clearly in the Tromso studythe , a population-based study in over 6000 participants, with measurement of IMTand TPA at baseline, and long-term FU. Plaque area strongly predicted risk, but IMT in the CCA did not predict MI or stroke. Progression of IMT does not predict events, whereas progression of TPA is strongly predictive of cardiovascular events: after adjustment for age, sex, BP, cholesterol, smoking, DM, total homocysteine and treatment of BP and cholesterol, patients with plaque progression despite treatment had twice the 5-year risk of stroke, death or myocardial infarction, compared to patients with stable plaque or regression.
E.B. Mathiesen, S.H. Johnsen, T. Wilsgaard, et al., Carotid plaque area and
intima-media thickness in prediction of first-ever ischemic stroke: a 10-year
follow-up of 6584 men and women: the Tromso study, Stroke 42 (2011)
972 e 978
Best regards!
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I am interested in the oxidative stress response in ECs and I have noticed that after treatment with H2O2, cells are going into cell cycle arrest and are down-regulating DNA replication and repair mechanisms - is this a symptom of senescence? I'm not sure why they would go into arrest if not to repair DNA. 
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If the DNA damage response is persistent and cannot be repaired then cells can become senescent, possibly promoting immune clearance of these damaged cells rather than undergoing apoptosis.  Lower levels of H202 would likely promote transient growth arrest because the DNA damage can be repaired.  
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Hi all, does there any score system by DSA OR angiography to assess the CVT? Or standard to calculate the venous phase which indicate the venous flow is slow? 
Plz provide references, thanks!
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Great point! Thank you Szaniewski.
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can anyone give me suggest what happen with this aorta?proliferation, hypertrophy, hyperplasia? i give it NaCl 8%
I have picture with 400x magnification in microscope of aorta with HE staining
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I want to compare with wild type picture :)
Anyway, it looks like medial hyperplasia (between elastin lamina). 
Trichrome stain is helpful to detect elastin lamina.
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plaque classification obejective
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Just contact the people at the BiKE biobank at the karolinska (Ulf Hedin).
Note that most stable lesions are probably FCPs (stabilized lesions) according to the Virmani classification and not stable lesions (LFA, Virmani classification)
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Every DVT event is the result of an "abnormal" surface, an abnormal "equilibrium" for plasma coagulation proteins and factors and sometime platelet reactivity (yes, even on the venous side). A local slow flow is an aggravating factor. But a generally reduced microcirculatory flow is a tremendous aggravating factor. Bad microcirculatory flow = low conversion of Protein C to Activated Protein C. Lack of APC leads to increase procoagulative state, decrease protection against platelet aggregation, and less profibrinolytic drive. It is only one factor, look to the antithrombin III content, the other inhibitors and factors and the game becomes very very complex. In cancerous states, some abnormal proteins are often exposed and trigger the coagulation processes, illustrating the surface role.
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I am looking for How lungs have got an association with liver..what is the underlying mechanism that causes Intrapulmonary dilatations from portal hypertension????
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It is not just dilation. there is also aberrant vasculogenesis in HPS; probably VEGF driven. The basic connection seems to be an overflow of the factors driving splanchnic vasculogenesis to reduce portal hypertension, into the pulmonary system leading to undesired aberrant vessel formation and dilation of existing vessels. This is seen in experimental models.
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I had a case of deep cervical artery anastomosis with occiptal artery because of internal carotid stenosis in the right side.
Have you ever seen a case like this?
Thanks,
Artur J. Rocha Lima, M.D.
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Yes I did have a case like that, I will look for the case and send you images.
Best...
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Does diabetes contribute significantly in pathogenesis of vascular dementia or are those two diseases with separate pathophysiological processes?
1/ If they're linked, what are these links?
2/ Should cognitive assessment be preformed on regular check-ups for patients with diabetes mellitus?
3/ Since Alzheimier disease (AD) is also recognized as diabates mellitus type 3, is diabetes mellitus type 2 generating a pathophysiological process towards AD, vascular dementia or both?
4/ How does chronic glucose regulation affect cognitive performance and would some other substances rather than glucoregulation per se improve diabetic patients cognitive status?
5/ Why isn't cognitive performance reported more in studies involving diabetic patients?
Hoping to get some answers to these questions. Related recent literature is in links, but doesn't provide answers to these questions.
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Dear Toljan,
First of all I appreciate you for asking such brain storming questions. The questions highlight your interest in the subject. I would like to answer a few of youur queries:
1/ Diabetes is basically a microangiopathy causing damage at the level of micro-vessels. These microvascular damage predisposes to micro-infarcts that may eventually lead to the development of vascular dementia. Hypertension is considered to be a more damaging risk factor for vascular dementia than diabetes. So, microangiopathy can a link between diabetes and vascular dementia.
2/ Though we do not have guidelines available today that recommend us to do this cognitive testing in diabetic patients. But it is advisable that if a diabetic patient presents with some neurological deficit of any kind, that patient must be checked for cognitive testing as well. We may have to wait for sometime and see the upcoming guidelines on this subject.
3/ Research is going on on this subject. And a substantial amount of research and evidence will be needed before declaring AD as DM type 3. As more and more pathophysiological processes become evident, we may be in a better position to describe an underlying relationship between these identities.
5/ Every research is done with a background and with a clearlt defined objective. So, it is quite possible that recent and future studies may be done with this point in mind to check cognitive status of the diabetic patients. 
Your post may turn out to a brain storming key for researchers on the subject and may lead to incorporation of your novel ideas in future studies.
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A 34 years old  female presented with cyanosis  and pain of the right hand. Her patient angiography has been shown in Figure 1.
What is your diagnosis ? and  What can we manage this patient ?
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Structurally it appears that the radial artery is occluded sacrificing arterial supply to the thumb, index, and middle finger.  Without more history or more information, etiology may be difficult to ascertain.
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I have a patient who has gross clubbing of fingers and toes, who is smoking cannabis for last 15 years, 10 cigarettes a day. He is underweight with BMI of 22.5. I also noted epigastric mid line hernia.
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Go for the same symptoms as in nicotine smoker, as the volatile, active compound do not play a big role in development of clubbing
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The choice of the more appropriate method of SFA recanalizazion represents a very interesting and actual topic. This is particularly relevant in claudicant patients. It is reasonable the use  in these cases of a covered Stent  ?
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I think that the risk is very small, and should not affect your decision to technically optimize your procedure.  However as I said in CLI pts with diffuse SFA disease and probably poor tibial runoff I would avoid implanting a covered stent.
 
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I'm specifically interested in whether anyone has observed differential expression of Nox1, 2, 4 and/or 5 in the endothelium at regions of disturbed shear, I.e at vessel branchpoints and bifurcations, compared to straight sections of the downstream vessel or the preceding feed artery. Also, comparisons between small and large vessels, and similar sized vessels from different beds.
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The Antioxidants Red Signal review you quoted, while being a very good review, does not appear to answer my specific question. 
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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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Reference : Harrison's principles of internal medicine
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Shankar sir. Surely makes so much sense now !! Thankyou.
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Pulse wave velocity is the best predictor of cardiovascular events. So why don't we use it in outpatient clinic? Can you support this idea? Are you ready to use it in your daily practice?
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A simpler and clinically applicable method is the radial pressure wave form, obtained invasively or by tonometry. The second peak in the radial pressure wave (rPW) is clearly visible in hypertensive patients (see Pauca et al. Chest 1992; 102(4): 1193-8, Pauca et al. Brit J Anaesth. 2004) and is directly related to the degree of aortic stiffness (Wang et al. Am J Physiol Heart Circ Physiol. 2003; 284(4):H1358-68, Davies et al.. Am J Physiol Circ Physiol. 2010; ;298(2):H580-6). This occurs because the aortic pressure wave has two clear deflections: the first peak produced by the initial flow from the LV and the second by the distention of the proximal aorta. The higher the rigidity, the higher the peak (Davies et al. Artery Research. 207; 1(2):40-45). Hughes et al. Hypertension. 20008; 51(6):e45-46 have explained the equivalence of the second peak in radial and aortic PWs. This equivalence had been found by comparing these waves produced by the same ventricular contraction with identical pressure transducers. It was found that the second peak in radial and aortic PWs was equivalent (which explained the mechanics of the less than 4mmHg difference) whenever the systolic pressure was represented by the second peak in the radial PW. This is easily recognized because the apex in the radial PW is on the right, before the incisura. These findings have been fiercely disputed by investigators who believe that the second peak is produced by reflected waves from distal aorta. This belief is traditional, but has never been demonstrated (Baksi et al. J Am Coll Cardil. 2009;54(22) 2087-92.  
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Dear all,
I am working on an experimental ex-vivo protocol that involves induction of hyperglycemia on Wistar rats. We have tried to incubate the aorta and mesenteric arteries for 3h or 4h in 25mM D glucose then we did the bioassay vasoactivity, but there was no endothelium dysfunction observed. Another protocol we tried 20h incubation in 25mM glucose in Krebs or DMEM medium then we did the bioassay vasoacitivity, but the vessels didnt relax at all after 20h. We use D glucose powder and Krebs 11mM glucose, DMEM with 10% FBS Penicilin / Streptomycin.
Any advice or reference would be greatly appreciated! Many thanks in advance.
Phuong Nga
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Phuong,
Below is a reference that uses isolated vessel preparation from Wistar rats and examines the mechanism for dysfunction of vasoreactivity in a "diabetic" environment.  You might be able to wean some of the methodology to be applicable to your needs. The full article can be access for free on the web.
Best,
Jorge Jacot, Ph.D.
Diabetologia
Diabetologia. 2010 May; 53(5): 989–1000.
Published online 2010 Feb 26. doi:  10.1007/s00125-010-1677-0
PMCID: PMC2850524
Hyperglycaemia-induced impairment of endothelium-dependent vasorelaxation in rat mesenteric arteries is mediated by intracellular methylglyoxal levels in a pathway dependent on oxidative stress
O. Brouwers,1 P. M. Niessen,1 G. Haenen,2 T. Miyata,3 M. Brownlee,4 C. D. Stehouwer,1 J. G. De Mey,2 and C. G. Schalkwijk 1
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Would you advise against use of cortical or whole brain slices for in vitro I/R studies? Why?
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Yes.... the larger is your explant, worst is the media (and gas) perfusion/exchange. So, as you increase the size of your explant, higher is the risk of cell death by hipoperfusion, specially those cells located in the middle of the tissue (central area). 
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Airborne particulate matters are the major air pollutants responsible for many cardio vascular diseases.
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By mention of cardiovascular diseases I suspect you mean PM10 and PM2.5. You may find an impact on cardiovascular systems from other particle sizes but that may be down to particle composition (i.e. does it contain heavy metals, VOCs, PAHs etc) as opposed to size.
As Satoshi points out, it would be good to know whether you need to just identify particle size or if you need to collect samples, because collection methods vary significantly depending on which one is most suitable.
If you're looking for pollutants contributing to cardiovascular disease don't forget to look at the gaseous pollutants (e.g. NO2, Ozone etc.) too. They're very important.
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I want know how many genes for responding cardio vascular diseases, diagnosis and what are the genes expressed  myocardial infarction and coronary artery disease can tell me whom are working these relevant working
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Accumulating evidence suggests frequent consumption of select foods rich in certain flavonoids is important for optimal health
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Ajwa dates are one of the most expensive dates in its raw form in Saudi Arabia. One kg cost about 80/SR. Its look is unique and taste is superb. Dates are also rich in natural fibers. Modern medicine has shown that they are effective in preventing abdominal cancer. They also surpass other fruits in the sheer variety of their constituents. They contain oil, calcium, sulfur, iron, potassium, phosphorous, manganese, copper and magnesium.The dates are highly nutritious, full of sugar (60%), and small quantities of fat (2%), proteins (2%), and minerals (2%). In other words, one date satisfies the minimum requirements of a balanced and healthy diet. Because Ajwa date is fiber rich and for digestion of fiber more bile will be used, because bile contains salts of cholesterol ring, hence step by step Ajwa dates will consume extra cholesterol mainly biliary as well as bad cholesterol LDL streaming in the blood.
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For examples; in hepatocellular carcinoma, it can be classified into 3 categories; small size below 3 cm. , intermediate size 3-5 cm. and large size >5cm.
they showed that Microvessel density (MVD) in small size is lower than intermediate size. on the other hands, the MVD in intermediate size is not larger than the large size. 
Thanks you so much
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In solid tumors, the oxygen supply to tumor cells is frequently reduced or even abolished owing to their deteriorating diffusion geometry (abnormal micro-vessels and thus poor micro-circulation) leading to hypoxia. In hypoxic state, the mitochondrial oxygen consumption rate as well as ATP production are reduced leading to hindrance in tumor growth.
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In the last two years have been published about 5 original articles that describe the equation to calculate Apolipoprotein B from various other 2 - 3 - 4 lipid parameters. Does anyone have experience using the calculated Apo B in clinical practice or research?
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Dear Rudolf, 
you can determine the content of ApoB in LDL directly through a simple and easy colorimetric protein assay as ApoB-100 comprises >95% of total protein in LDL. ApoB also exists in chylomycrons and VLDL, but if you're interested on inferring the content of ApoB based on triglycerides and cholesterol then please beware it will be an estimated value. To date, it is not yet fully understood what are the structural features in OxLDL responsible for its atherogenicity, whether it's modifications to the protein or lipid moieties that activate macrophages and formation of foam cells. Hope this helps, Ana
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In patients with exhausted upper limb options or subclavian vein stenosis is a HeRo device preferable to lower limb access
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Today I put HeRO grafts in sick, elderly patients who I think will probably die in a year or two and I do  femoral vein fistulas (Superficial Femoral Artery to transposed femoral vein) in healthy patients expected to live for several years.
I recently presented a paper "Fewer HeRO Grafts and More Thigh Fistulas: Our Changing approach to Management of Bilateral Central Venous Stenosis". I am working on the manuscript. My presentation is attached.
Eric
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I am used to growing human primary bronchial smooth muscle cells in DMEM - high glucose medium + 10% FCS, which works very well. Now I am planning to start growing primary human vascular smooth muscle cells (e.g. coronary artery), but I am uncertain if I can use the same medium or need to switch to commercial smooth muscle cell medium . Does anybody have information on this? Thank you in advance.
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Hi Martijn!
In my previous job I used to work for almost 10 years within the vascular bioloy research, especially with ASMCs, and culture both primary cells and cell lines. I managed to grow primary VSMCs in both DMEM and specific SMC-mediums. I remember using always at least 20% FBS and sometimes purposedly culturing endothelial cells together with VSMCs, since the SMCs grew notably faster by coculturing the endothelial cells with them. In addition to the high serum concentration and some antibiotics, starting the culture from the smallest possible well also helped and fastened the growth remarkably. There are also some collagen- or other protein-coated dishes and multiwell-platesin the market that promote the growth of VSMCs. Good luck to you and have a nice summer!
Best regards, Annamari
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Or, how and by which mechanism can hydrogen sulfide modulate endothelial dysfunction?
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It depends on what you mean by endothelial dysfunction. In our work in the newborn we are showing a significant link between microvascular flow and hydrogen sulfide. In addition H2S interacts with and is interacted by the other gasotransmitters, CO and NO at both genomic and enzyme levels. Whilst this can have adverse consequences ( see stark et al) it is probably more function than dysfunction. Several publications are on the way...watch this space.
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I want to stain for inflammatory markers in the endothelium and I have some times the problem that after mounting there are some kind of lipids or tissue on top which makes patchy the microscope view and difficult to get a complete view.
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There are many ways to image and based on what you have said I have some suggestions. You state that you are imaging on face so I assume you want to image the the endothelium. The protocol I use is simple and effective it can be used for epiflorescence but is better suited to confocal microscopy. While this simple method would work because of the "ribbed" intimal surface of arteries an initial perfusion fixation would improve clarity.
1. Clean Aorta of all connective tissue
2. Pin to a sylgard dish throughout the process (you can use an O ring to create a low volume chamber). Use small vannas scissors to cut open, pin out with EC layer (luminal layer) facing upward at fix in 2-4% PFA for 1-2 hours or overnight at 4 degrees
3. wash for 1 hour in blocking buffer (at least 3x wash during the hour)
4. Add primary antibody leave at 4 degrees overnight up to 48 h
5. wash 1 hour in blocking buffer then add secondary for 2 hours
6. Wash 1 hour in blocking buffer then one ws in PBS and mount onto slide EC facing upward and add coverslip - coated slides like superfrost are good for this, vecta shield or prolong are good mounting reagents. Use a weight to improve slide fixation and leave over night
If you want to image smooth muscle in the aorta I would recommend a transverse section the adventitia and the EC/thick internal elastic lamina (which has autoflorescence) of the aorta will make en face imaging of the medial layer hard even with a good confocal, pointless with epifloresence.
I have never had a problem with connective tissue or lipids doing this. Links to tow papers using this method are below.
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A lot of research is carried out in vitro and using rats but not a lot of literature on human studies.
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Dear Emily,
See for instance the following publication:
Pripp A. H., 2008, Effect of peptides derived from food proteins on blood pressure: a meta-analysis of randomized controlled trials. Food Nutr. Res., 52, DOI: 10.3402/fnr.v52i0.1641
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I used the formulas from this article.
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Either you have used the formula wrongly or we have edited it wrongly. Cos shouldn't be greater than 1. I will pass this question on to our matematician Linda Ingebrigtsen.
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The PVR related to resistance in both pulmonary artery and vein.
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If the pulmonaries veins have normal anatomy, the participation in pulmonary artery hypertension is a manifestation of the left ventricle or left atriun dysfunction.
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What is better, endo or open?
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I agree that endovascular procedure must be a recommendation but only after remission of inflamatory phase of disease .
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In peripheral interventions: Do you make any difference in use of antiplatelet therapy after bare metal stent / drug eluting stent / drug eluting balloon / covered stents? What is your regime like?
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Without other concomitant vascular diseases our procedures for peripherals are:
For BMS we give 4 weeks clopidogrel 75 and ASS100, followed by life-long ASS.
In case of propaten-covered prothesis (gore - viaban) we give ASS100 and clopidogrel 75 for 6 mths, followed by life-long ASS100.
In case of DEB we give ASS100 and clopidogrel 75 mg for 3 mths, followed by ASS100 life-long - due to the prolonged "epithelial wound". For DES same procedure like propaten-covered prothesis.
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Estimating and quantification of the amount of wave reflection should provide a better understanding of the pathophysiology of cardiovascular disease and a better assessment of cardiovascular risk in patients with hypertension, arteriosclerosis or peripheral vascular diseases. But where are the reflection sites for arterial pressure waveforms? I need help with physiological explanations.
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Dear Jonathan Mynard,
Thanks very much. Your answer help me a lot.
It is important to research indeeply at any aspect of this issue and make sure it could contribute for the current studies. I will work on it!
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I would like to know if there is an established chronic hindlimb ischemic model in mice especially for new angiogenic / arteriogenic therapy. Since most researchers use an acute femoral artery ligation model in healthy mice, results from these studies are difficult to be translated to the clinical patients. Thus, there should be a consensus regarding a reliable model and reliable end-points that could be measured in a timely fashion in vivo (angiography, tissue perfusion, and molecular imaging). Are there any suggestions or comment?
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Dear Dr. Zhaung,
You ask an insightful question. Many therapies that have been shown to have significant effect in murine models have failed to show benefit in clinical trials. This has led many to conclude that murine models do not mimic the human condition of PAD. However, many of the murine experiments used conditions that were very different from those that exist in humans with PAD. For example, young healthy mice have been used when humans afflicted with PAD typically have multiple risk factors and comorbidities. Also, some murine models have gone to extremes to produce sustained severe ischemia by excising long segments of limb arteries and veins which of course does not represent the human condition. Vascular compensation to arterial occlusion in humans is impaired with age and other risk factors. We have had some success in mice with vascular risk factors in mimicking impaired compensation(e.g. FASEB J, 25: 1092.17.) The specific model you might use will depend upon a number of factors, including the stage of human disease you want to mimic (e.g subcritical or critical limb ischemia), and the parameters you want to study. We have offered some suggestions for improving the relevancy of murine models for testing novel therapeutics in our review article entitled "Marvels, Mysteries, and Misconceptions of Vascular Compensation to Peripheral Artery Occlusion" PMID: 20141596. One suggestion is to administer treatment beginning several weeks after model creation when any natural compensation has mostly occurred. The specific endpoints you study will depend upon your objective but ideally would include functional reserve or maximal flow capacity as addressed in the review of preclinical PAD models by Waters et al PMID: 15107408.
Best wishes,
Joe
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They are both related to deep vein thrombosis,
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The coerulea dolens is a rare condition but much severe because can cause the amputation of limb. It is the only venous condition that can provoce that. It is due to complete block of arterial microcirculation with ischemia and gangrene. The alba is a massive deep venous thrombosis with a poor collateal superficial circle.
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I have been infusing rats with angiotensin II, which causes severe vasoconstriction and probably should induce systemic hypoxia. How could I prove my hypothesis? I’m looking for a molecule or something that I could determine by ELISA. Does someone have experience with systemic hypoxia and HIF expression in the body?
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Hypoxia is a relative term. In a "normoxic" organism breathing air, many organs are "hypoxic". Moreover, ischemia implies local (not always systemic) hypoxia but the reverse is not rue. So, there is no established marker of hypoxia, but many markers of the response to hypoxia are available: most if not all of them have been listed above. So my suggestion would be to use the marker related to the "hypoxic" response you are investigating in your specific research. Good luck!