- Mostafa Samak added an answer:Has any one tried to induce Hypertrophy in mouse neonatal cardiomyocytes and measure increase in cell area?
I have been using primary cultures mouse neonatal cardiomyocytes (NCM) to study hypertrophy. However, the conventional ways of hypertrophy induction (e.g. by catecholamines, Angiotensin II or Endothelin-1) were previously shown to have very subtle effects in mouse compared to rat NCMs (Deng et al., Circ Res. 2000;87:781–788.). I have personally noticed this, and the best results I got were when I used angiotensin, but yet in very high doses (10 -50 micro M) for 48-72 hours. Increase in cell size, being a widely accepted marker, was not more than 10-15%. Moreover, it was shown that mouse NCMs undergo spontaneous hypertrophy without an inducer. Nevertheless, unlike the cited paper, some papers have published better results of up to 1.5 times increase in cell size. I was wondering if there are some tricks that I can utilize to get a more prominent effect.
Thank you Nai-Kei for the valuable information.Following
- Roberto Flore added an answer:What is preclinical carotid atherosclerosis, how is it defined and what is the marker for it?
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!
hi Li, could the attached review help you?Following
- Vittorio Dorrucci added an answer:Graft İn stent carotid artery restenosis;What are your opinion with this case?
We had reported the case of a 57-year-old male patient with a history of acute amaurosis fugax. Carotid angiography was performed as blood pressure differed between his left and right arms and there was a pan-systolic murmur on the left common carotid artery. Total occlusion of the proximal right brachiocephalic artery and a thrombus occluding 90–99% of the left internal carotid artery were detected by carotid angiogram. We decided to place a graft-covered stent through the lesion first, and contain the plaque and thrombus between the stent and the lumen. Therefore, a graft covered stent (5×13, Direct) was implanted with 12 atm pressure. After removing the distal blockingbased protection system, we opened the selfexpanding stent (7×10×30, Cristallo) (figure 3) and dilated the stent using a post-dilatation balloon5×20, Tarcomgrande).
A self-expanding graft-covered stent was successfully implanted and there were no complications. This case published in BMJ Case Journal “ Covered stents may provide extra protection during carotid artery stenting in high risk patients with an excessive thrombus burden”, Tatli E, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-010258.
However , the patient presented transient ischemic attacks after three years. DSA angiography show 99% instent restenosis in the overleap segment of the both stent.
What are your opinion with this case ?
if I well understand the restenosis was in the overlaping zone where there are two different materials in contact and a different radial force. It's very likely that these two factors have favored the neointimal iperplasia.Following
- Dietrich Klueber added an answer:What are the complication rates for intravascular placed heart valves?
Above method is quite new and due to the high insurance pay happily accepted by heart surgeons. Are there studies, that describe the most important complications rates like: malplacement, secondary displacement, cerebral infarct, other kind of embolism?
Nathan: could you please shortly write the complication rate named in my question in this 5-yrs-study?Following
- David C. Ellinsworth added an answer:Has anyone observed an ability of catalase to attenuate responses to NO donors?
Apparently catalase can bind NO, but every other publication I've seen where this protocol has been used (usually as a negative control for endothelial dysfunction studies) shows negative results, yet mine were very conclusive
I did consider using my colleague's chemiluminescence system to see if NO was consumed by catalase but I was at the end of my studies and simply didn't have the timeFollowing
- Jonathan Skillings added an answer:What is the impact of physical activity, screen time, diet drinks and weather on CV disease?.
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.Following
- Leong chen Onn added an answer:Do you know of any left ventricle or heart localization method for tagged MRI?
I'm currently researching on left ventricle motion quantification. Can anyone suggest me any heart or left ventricle localization method in tagged cardiac MRI images? Appreciate if you can provide me references too. Thanks.
Thanks all. I'm looking for an automated method to define the ROI (left ventricle) for tagged MR images.
To Aymeric Histace, I think the paper you recommended me is useful to me. I'm interested with the mean-std image method which I have personally tried to apply. But I ran into some problem. I've attached the image of the mean-std image below. The mean-std image i generated does not show a a significant contrast between the cavity and the left ventricle wall. I think I'm doing it wrong or missing some steps.
Here are the steps I have taken using Matlab to process the image.
1) compute local mean image using 'conv2' with kernel size N=11
2) compute local std image using 'stdfilt' with kernel size N=11
3) compute uendomap(i,j)=wm.mN(i,j) - wo.ON(i,j) with wm=1/3 and wo=2/3 where wm+wo=1 and wo/wo=2.
Any help is appreciated as I might adopt this method to localize my tagged MR images for my coming paper. Thanks.Following
- Hubert Dabire added an answer:At what percentage of relaxation of acetylcholine to norepinephrine the endothelium of a rat aorta may be considered intact in vitro?
Recently, someone asked here how to remove the endothelium in a rat aorta. I do agree with all answers. My question now is how to check that the endothelium is correctly removed. In other words, at what percentage of relaxation to norepinephrine or other vasoconstrictors (what concentration?) induced by acetylcholine (also what concentration?) one can consider that the endothelium is correctly removed? Conversely, at what percentage of relaxation one can consider that the endothelium is present or intact?
It will be a pleasure to meet you to discuss this subject. How can i contact you?Following
- Vilemar Magalhaes added an answer:Do you agree that high carbohydrate diet may cause heart problem (cardiovascular disease) ?
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.
Most of the specialists do not recommend carbs in the evening not because it van not be digested, but because it is digested too fast and so the person will be sleeping and may store that nutrient as fat. That absortion can be retarded by fat ingestion, then one may need water some time after and he will either have heartburn or will wake up during the night to urinate. There can be thousands of other motives and the ones given above not be true for some individuais. Or even worse it can be true for you today and not tomorrow. Bit as a rule of thumb I would say no to carbs in the evening regardless if you feel bad after having it or not.Following
- Norbi Gabor added an answer:Can LMWH anticoagulation be used before ECV?
What about LMWH anticoagulation (3-4 weeks) without TOE control before ECV? Because in guideline only VKA or NOAC has written, but nothing said about LMWH. What is you opinion?
- David Gross added an answer:What factors may be related to the adaptation of prosthesis in patients with major lower limb amputations?We observed that the prevalence of adaptation to lower limb prostheses was 38%. And patients with a low level of education were the least frequently adapted to the prosthesis.
Thanks, Dee for a very thoughtful and enlightening post.Following
- Mohammad Faramarzi added an answer:What is the most common cause of Acroangiodermatitis of Mali?
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).
Severe chronic venous stasis and failure of the calf muscle pump could have resulted in the elevated capillary pressure causing reactive vascular proliferation and clinically presenting as lesions of acroangiodermatitis.Following
- Marco Marano added an answer:Where can I find references on the alveolar-arterial gradient?
The Alveolar–arterial gradient (A-aO2, or A–a gradient), is a measure of the difference between the alveolar concentration (A) and the arterial (a) partial pressure of oxygen. It seems an useful and interesting parameter in the topic of pulmonary imbibition, but I failed to find published research in last years.
Can you help me?
what a great paper ! what a shame it is historical one !!
What I am looking for it is a blood gas analysis parameter linked to interdialytic weight gain in hemodialysis patients. In my experience, and "of course", in incoming pulmonary edema A-a O2 gradient rises up to 50 mmHg, but I am looking for early gas derangement. Can You suggest me what to look for ?
- Markus M. Mueller added an answer:Is there any information about haemophilia and ageing?
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?
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 email@example.com, I will send you his mail address.
- Khaled Saad added an answer:What is the maximum dose of statins in children with hypercholesterolemia?
Use of statins for treatment of familial homozygous hypercholesterolemia: What is the earliest age for initiating statin therapy and what is the maximum dose used in young children.
Lea S. Eiland, and Paige K. Luttrell, Use of Statins for Dyslipidemia in the Pediatric Population.J Pediatr Pharmacol Ther. 2010 Jul-Sep; 15(3): 160–172.
- Christos P Loizou added an answer:Can anyone help me to find the Database of CCA Ultrasound Video and its ground Truth?
for Atherosclerotic Plaque Segmentation
Dear Emimal, We have a database such the one you are describing, but it is not yet available to download. We have however some other image databases with ultrasound images of the CCA with their Ground Truth available. Have a look at http://www.medinfo.cs.ucy.ac.cy. See under downloads.Following
- Liqun Zeng added an answer:How to determine if an ischmeia heart disease patient is with irreversible ischemia or reversible ischemia?
My understanding is, when the myocadium cells lack of blood supply, the cell will be damaged but to some degree, it's still reversible. When the blood flow recovered, the cell can become alive again. When the ischemia is serious to a certain stage, the cell will die completely. Thus even the blood flow recover, the cell cannot gain live again, call irresversible. (if these are not true, please kindly correct me)
And my question is, for a specific patient, how to judge if his ischemia is reversible, irreversible? E.g. by using some imaging machines??
Thanks for sharing, Dr. Delgado.Following
- Ugo Limbruno added an answer:Is there any role for triple therapy after ACS especially with the increased used NOAC?
Optimal management of patients on NOACs after ACS and PCI with DES.
Latest european guidelines suggest 6 month of triple therapy (no matter if vit K antagonist or NOAC & no matter if DES or BMS) for ACS with HASBLED<3 (IIa indication). Three month triple therapy for all other cases (IIa indication). A WOEST-like strategy of simply dual therapy (OAC/NOAC + clopidogrel) is only a IIb indication despite in this study there was a strong signal towards a mortality benefit. with dual therapy with respect to triple one.
In my opinion, the use of NOAC instead of vit K anagonists might shift net clinical balance towards triple therapy (when compared with a WOEST-like dual therapy) due to the more favourable safety profile of these new drugs.Following
- Parth Shah added an answer:What kind of useful information can be extracted from Wrist-Type PPG signals?
Wrist-Type PPG is very popular right now, but I would like to ask what kind of useful information can be extracted from it (except the head rate)?
Welcome. Feel free to ask any other related doubts.
- Liqun Zeng added an answer:How long will the anticoagulation therapy last after the PTFE-covered stent implant in vein?
I found the the anticoagulation therapy strategy varies with ePTFE material implants in human vessels, such as artificial vascular graft, stent, etc. What are the factors that influence the anticoagulation therapy?
Dear Dr. James Spain, thank you for your comment.
But just out of curious, there is a clinical presenation - deep vein thrombosis. Isn't the thombsis generated from the vein? And for impants in the vein, such as the lead of pacemaker, into the coronary sinus, anticoagulation for a short term, e.g. 3 months at least, is normal in practice. It seems in contradiction with your saying, never used anticoagulation?Following
- Olivier Pétrault added an answer:When we add a drug in an isolated 10 ml organ bath must the dilution be not more than 1:20?
We have Isolated tissue bath, we work on it, herbal, drug blocker....etc
If our krebs solution in organ is 10 ml, I read paper it said you can not adding more than 0.5 ml , is eqaul to 10.5 ml
If more than 0.5 all results become ERROR
Can any one help me ?
I'm agree with the last comment. Osmolarity is a crutial parameter ! Don't forget that ionic channels can be activated with osmolarity changes in particular with salt-based compounds ! In addition, very high concentrations ask us questions of the specificity of your molecule...Following
- Perbinder Grewal added an answer:Any advice on the management of the asymptomatic aorta valve stenosis (Accent on the preoperative time)?
How manage preoperative time of the patients with asymptomatic significant aorta stenosis? Should patient wait for the surgery at home or at the hospital? What criteria for select (home, hospital)? The risk stratification of the sudden cardiac death of the asymptomatic AS patient? And what is your own opinion, practice of the management of the preoperative time?
Hi Peter - I think he means aortic valve stenosis - funny thing is I thought the same as you unitl I was writing out a reply similar to yours - funny how we get clouded by our specialties!Following
- M. Ricky Ramadhian added an answer:How to confirm vascular smooth muscle cell (VSMC) hypertrophy?Recently, we found a decrease in nuclei number and no change in smooth muscle alpha-actin protein expression in aorta of our experiment group. We think this may indicate VSMC hypertrophy. I want to ask whether there is a specific protein or signaling pathways that can verify VSMC hypertrophy in our samples ? I would appreciate any suggestions.
maybe you can have cross section aorta with same level cutting ex: abdominal aorta, you stain with Masson or HE or others satining protocol, and you measure ratio of thickness of tunica media and intima with lumen diameterFollowing
- Mark Cobain added an answer:Is anyone aware of a paper describing a population wide estimation of CVD risk using risk scores?
Estimation of CVD risk using a risk score such as Framingham, SCORE, ASSING, JBS is usually done for an individual. But has this ever been done on a population wide basis, i.e. average risk for CVD is x% in US using the Framingham Risk Score?
If you search for papers by Earl Ford you will find that analyses using NHANES to calculate CVD risk using FRS scores have been published for the US population.Following
- Tausif Alam added an answer:What is the underlying mechanism of low immunity in diabetics?
Mechanism of reduced immunity in Diabetes Mellitus.
You may want to elaborate on your query...
There are several types of diabetes with distinct differences and "low immunity" in what context?Following
- Paulo Eduardo Ocke Reis added an answer:Can anyone help me find information/guidelines for segmental pressure testing s/p bypass graft and stenting?
Good day, I am reaching out to the research community in an effort to find information/guidelines for segmental pressure testing s/p bypass graft and stenting. If there are articles that you may know of on this subject I would appreciate your help.
Dear James Shafer ,
I hope this attached can help you!
- Josef Veselka added an answer:What is the best imaging modality to detect and measure atherosclerotic plaque regression and stabilization?Noinvasive (US, CT, MRI) or Invasive (Angio, IVUS, OCT, Lipiscan, etc.)
Try to use NIRS-IVUS catheters. Near infrared spectroscopy is able to determine the amount of lipids in the plaque and brings another piece of information than more traditional metohods - OCT and plain IVUS.Following
- Paulo Eduardo Ocke Reis added an answer:Can anyone help with a vascular closure system for a Dacron graft after thrombolytic therapy?I am planning a thrombolytic therapy for graft thrombosis of Aorto left femoral bypass (symptoms present for10 days). Do you have any experience with any of the vascular closure systems I can use for a previously placed Dacron graft?
Do you have experience with Exoseal?Following
- Panayot Tanchev added an answer:How frequently do you use novel anticoagulants in the treatment of venous thromboembolism?I am interested in your experience regarding VTE.
Dear Rivaroxaban fans, I can not imagine how patients with severe VTE, and especiially those with severe PE accompanied by hemodynamic failure and pulmonary hypertension would be treated with oral anticoagulants. Those patients need IC, intravenous (easily controlable) anticoagulants or fibrinolysis. In elective cases with massive PE there are indications for pulmonary embolectomy in the conditions of cardio-pulmonary bypass.Following
About Vascular Medicine
Vascular medicine (angiology) is the medical specialty which studies the diseases of circulatory system and of the lymphatic system, i.e., arteries, veins and lymphatic vases, and its diseases.