Science topic

Hypertension - Science topic

Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
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Guillermo Zalba is not part of the team of the article, plese delete his name
Best regards
Alejandra Guillermina Miranda-Díaz, MD, PhD
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!!!!!!!!!!!!!!!!!!!!!!!+++++++++++++++++++++++
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Dear researchers , I have an issue with Revista Latinoamericana de Hipertension journal which published my paper with another authors names . I emailed the journal many times but there is no answer. How can I get my rights with my paper ? any suggestions ...
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Thank you for your advices , the Journal finally answered.
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I am interested in comparing the fecal samples of Nomotensive, Pre-Hypertensive and Hypertensive patients through the findings from genesequencing and culture. The gene sequencing will be sample from the lab work while the culture process will involve, serial dilution, culturing the sample on different plates and observations will be taken.
How can I determine the sample size before going out to carry the experiment? Kindly help please.
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If you know the mean and standard deviations, then something like G*Power could help; Universität Düsseldorf: G*Power (hhu.de).
You could read published work and take a guess at the right (publishable) sample size, or you could run a preliminary trial designed to estimate the appropriate sample size. There are economic and personal costs to having a large sample size that needs to be weighed against the risk of project failure costs if your sample size is too small.
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There is an increasing concern about non-communicable diseases. How can we (clinicians and researchers) bring change and facilitate people through digital applications and software? How can we conduct a research based on this specially in Low Middle Income countries?
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Obesity and diabetes are major source of non-communicable diseases. Research finds that socioeconomic condition is a responsible factor for obesity, diabetes and diabetes associated diseases. One can collect information in cooperation with technical staffs working in diabetic center or in diagnostic center in a systematic way. Technical assistants may help the researcher to collect information from patients/ visitors visiting the center. Visitors of a week or visitors of alternate day/ week may be interviewed according to predesigned questionnaire.
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Hypertensive crisis is an umbrella term for hypertensive urgency and hypertensive emergency. These two conditions occur when blood pressure becomes very high, possibly causing organ damage.
Hypertensive Urgency Hypertensive urgency occurs when blood pressure spikes -- blood pressure readings are 180/110 or higher -- but there is no damage to the body's organs. Blood pressure can be brought down safely within a few hours with blood pressure medication.
Hypertensive Emergency Hypertensive emergency means blood pressure is so high that organ damage can occur. Blood pressure must be reduced immediately to prevent imminent organ damage.Organ damage associated with hypertensive emergency may include:Changes in mental status, such as confusion Bleeding into the brain (stroke) Heart failure Chest pain (unstable angina) Fluid in the lungs (pulmonary edema) Heart attack Aneurysm (aortic dissection) Eclampsia (occurs during pregnancy) Hypertensive emergency is rare. When it does occur, it is often when hypertension goes untreated, if the patient does not take their blood pressure medication, or they have taken an over-the-counter medication that exacerbates high blood pressure.
Symptoms of Hypertensive Emergency Symptoms of a hypertensive emergency include:Headache or blurred vision Increasing confusion Seizure Increasing chest pain Increasing shortness of breath Swelling or edema (fluid buildup in the tissues)
Diagnosing Hypertensive Emergency To diagnose a hypertensive emergency, your health care providers will ask you several questions to get a better understanding of your medical history. They will also need to know all medications you are taking, including nonprescription and recreational drugs. Also, be sure to tell them if you are taking any herbal or dietary supplements.Certain tests will be performed to monitor blood pressure and assess organ damage, including:Regular monitoring of blood pressure Eye exam to look for swelling and bleeding Blood and urine testing
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Most commonly used tool for screening blood pressure monitoring is Home monitoring Blood pressure (HMBP) and Ambulatory monitoring Blood pressure (AMBP) . Home monitoring Blood pressure usually performed by classical Cuff Pressure BP instrument or Automated BP instrument. Ambulance Blood pressure monitoring can be performed byOmron Heartguide, which has an extra-stiff band that inflates to measure BP like a normal blood pressure cuff as well as Checkme cuffless blood pressure monitoring device based on pulse transit time.22,23 Both devices are able to synchronize data with smartphone apps. Besides that Dietary modification like low salt intake, Daily aerobic exercise, avoid use of Low K containing Food isost important .Last but not the least, avoid the stressful situations
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In an epidemiological study (eg: the effect of alcohol on Hypertension), if the value of the odds ratio is less than 1 (eg:0.45) but it is statistically significant. Does it mean that consumption of alcohol is playing a protective role in hypertension? please let me know the correct interpretation of this kind of result.
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Do you actually mean the relationship between alcohol and hypertension? I think that is the most meaningful way of getting information for you.
If that is the case, then it means the association between variable n and variable m is 0.45. It does not really mean it is protective, however.
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Scenario : Will cases diagnosed with pheochromocytoma, and on prazosin and metoprolol, with no concurrent comorbidities suggestive of autonomic dysfunction have increased incidence of usage of vasopressors intraoperatively, if magnesium sulfate is given prior induction with an aim to curtail hypertension?
Main Articles :
James MF, Beer RE, Esser JD. Intravenous magnesium sulfate inhibits catecholamine release associated with tracheal intubation. Anesth Analg. 1989;68:772–776 : Another consideration during magnesium sulfate administration is that it may cause cardiovascular depression by acting as a calcium channel blocker. The consequent inhibition of catecholamine release reduces plasma epinephrine and norepinephrine concentrations after endotracheal intubation, and therefore reduces hypertensive responses during anesthesia induction.
Do SH. Magnesium: a versatile drug for anesthesiologists. Korean J Anesthesiol. 2013;65(1):4-8. doi:10.4097/kjae.2013.65.1.4 : Thus, magnesium sulfate should be used with caution in hypovolemic patients and in those with limited cardiac capacity.
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Pre-induction and intraoperative use of Mg as bolus f/b infusion will reduce hypertensive response to intubation and surgical stimuli. It is unlikely to increase vasopressor requirement if the Mg infusion rate is titrated carefully with direct intra-arterial BP monitoring. Moreover, Mg should be stopped just before the removal of the pheochromocytoma tumor.
However, other concerns of Mg remain. It can potentiate neuromuscular blockade and therefore muscle relaxants should be dosed as per TOF monitoring. Secondly, Mg can accumulate in patients with kidney dysfunction. So better to avoid Mg in AKI or CKD patients and monitor urine output intraoperatively.
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Seniors in the world with diabetics and hypertension and heart diseases are millions ,and they are facing covid.therefore we should give them advices and precausions to face covid 19,this vquestion concentrate on this important situation,
he risk for severe illness with COVID-19 increases with age, with older adults at highest risk. Severe illness means that a person diagnosed with COVID-19 may require hospitalization, intensive care, a ventilator to help them breathe, or may even die. Here’s how to reduce your risk and what to do if you get sick.take medicines for diabetics and hypertensions and heart.problemsso how to deal with sickness for seniors?
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The mechanism
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The catecholamines, epinephrine, and norepinephrine bind to B1 receptors and increase cardiac automaticity as well as conduction velocity. B1 receptors also induce renin release, and this leads to an increase in blood pressure. In contrast, binding to B2 receptors causes relaxation of the smooth muscles along with increased metabolic effects such as glycogenolysis.
Beta-blockers vary in their specificity towards different receptors, and accordingly, the effects produced depend on the type of receptor(s) blocked as well as the organ system involved. Some beta-blockers also bind to alpha receptors to some degree, allowing them to induce a different clinical outcome when used in specific settings.
Once beta-blockers bind to the B1 and B2 receptors, they inhibit these effects. Therefore, the chronotropic and inotropic effects on the heart undergo inhibition, and the heart rate slows down as a result. Beta-blockers also decrease blood pressure via several mechanisms, including decreased renin and reduced cardiac output. The negative chronotropic and inotropic effects lead to a decreased oxygen demand; that is how angina improves after beta-blocker usage. These medications also prolong the atrial refractory periods and have a potent antiarrhythmic effect.
Beta-blockers classify as either non-selective and beta-1 selective. There are also beta-2 and beta-3 selective drugs; neither has a known clinical purpose to date. Non-selective agents bind to both beta-1 and beta-2 receptors and induce antagonizing effects via both receptors. Examples include propranolol, carvedilol, sotalol, and labetalol. Beta-1 receptor-selective blockers like atenolol, bisoprolol, metoprolol, and esmolol only bind to the beta-1 receptors; therefore, they are cardio-selective.[2][3][4]
Beta-blockers lower the secretion of melatonin and hence may cause insomnia and sleep changes in some patients.[5]
Alpha-1 receptors induce vasoconstriction and increased cardiac chronotropy; this means agonism at the alpha-1 receptors leads to higher blood pressure and an increased heart rate. In contrast, antagonism at the alpha-1 receptor leads to vasodilation and negative chronotropic, which leads to lower blood pressure and decreases heart rate. Some beta-blockers, such as carvedilol, labetalol, and bucindolol, have additional alpha-1 receptor blockage activity in addition to their non-selective beta receptor blockage. This property is clinically useful because beta-blockers that block the alpha-1 receptor have a more pronounced clinical effect on treating hypertension.[6]
Farzam K, Jan A. Beta Blockers. [Updated 2021 Dec 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532906/
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When I fit a linear mixed-effect model, I would apply the splines function to control for the potential nonlinear association. For example, the model goes like lmer(hypertension~PM2.5+ns(temperature, df= i )+(1|ID), data=mydata). I would like to use the AIC value to select the df of temperature. However, as the df rises, the AIC value of the model drops. It seems like the larger the df is, the better the model is, which really distrubes me.
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Mohamed I. Riffi Thank you for your answer. It makes sense.
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Literature suggests cutoff for Pre-eclampsia being 0.3 gm/24hrs while it is more 0.5gm/24 hrs for Chronic hypertension with superimposed with pre-eclampsia . Any justifications?
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If a patient with chronic hypertension with proteinuria due to hypertensive nephropathy there will high cut off value to define proteinuria with eclampsia
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I would like to measure the inner diameter, the outer diameter, and then a measure of the thickness between the inner and outer diameter. I have created several regions of interest (ROIs) but am not certain about the output from ImageJ. Someone, please assist me.
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Hi! Not sure if ImageJ has an equivalent plugin, but I find the 'Incremental Distance' tool on Image-Pro Premier very useful for measuring vessel wall thickness between two irregular shaped lines or polygons. Drawback though is that it's a paid software... a free version will definitely be useful to the general community. Good luck!
Video on its use on YouTube:
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Dear community of researchers,
I am currently working on a small research project that will explore community- and patient-led strategies for increasing referral of diabetes and hypertension and raising awareness of these two diseases in Mozambique, a highly resource-constrained country.
I would like to ask:
- does anyone have knowledge on patient-led referral strategies and advocacy activities? If so, could you please share any relevant links and/or are you aware of any recommendations on this from international health organisations?
- do you believe that involving patients in such activities would be ethically appropriate? Why/ why not?
Thank you in advance for any replies.
Regards,
Chiara
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Thank you very much Jehan for sharing your perspective, that is very helpful.
To be more clear, with "referral" I referred to the identification by T2D patients of individuals with risk factors for T2D, such as being overweight and having excessive thirst or urination, and their referral to healthcare professionals.
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May I have any help about this? I can see some hyaline areas but what is that cell infiltration?
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Thanks Rodrigo, it was the idea I had. We made immunostaining for macrophagues but not PAS. We will try. Thank you
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Is hydralazine a first line drug in the management of hypertensive emergencies
or urgencies?
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Hydralazine for Use During Hypertensive Emergencies
The guidelines recommend the use of intravenous antihypertensive drugs during hypertensive emergencies. These mainly fall in two groups:
1. Vasodilators: Sodium nitroprusside, Nicardipine, Fenoldopam, Nitroglycerine, enalaprilat, and Hydralazine
2. Labetalol, Esmolol, and Phentolamine
However, due to availability, expense, and toxicity issues commonly employed drugs used intravenously to reduce BP during hypertensive emergencies have been Labetalol, Nicardipine, Nitroglycerine, and Furosemide. In source poor settings Hydralazine is commonly used.
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Hypertension urgency is condition of hypertension crisis
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please see the link. I hope this might be helpful for better understanding.
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I have searched the article but most of it gives DOCA by injection subcutaneously, Is it possible to carry out Deoxycorticosterone acetate (DOCA) induced hypertension by oral administration in experimental?
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Can oral administration of Deoxycorticosterone acetate (DOCA) be used in experimental animals (rats) to induce hypertension?
No. You can have a look at the experimental details in these articles below (1-2) where the DOCA was used subcutaneously as an injection.
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Plaques form due to a self-healing mechanism of blood vessels and will increase over time. When entering blood vessels, they block blood flow, lead to hypertension and decrease blood flow to organs such as the heart. To get rid of these plaques, we need to boost the good cholesterol such as HDL or improve health of liver to produce enzymes that move these plaques. So, what other ways to get rid of these plaques without using invasive methods?
Thanks and best regards.
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The following RG link is also very useful:
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Stations in preeclampsia 
Treatment or prevention
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Thanks alot for this valuable information
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Is it medically possible to have a single treatment for all diseases? One way to proceed about it is anti-aging. Aging is a process of accumulation of impairments of aging throughout life and ongoing damage of aging. If we can nullify it, our body intrinsic ability to heal would tale over, and provide a healthier system.
Kindly answer to this question with best of your knowledge. For the ongoing covid pandemic and upcoming chronic disease epidemic, we can provide a better treatment if this method works.
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Also check please the following useful RG link:
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Hypertension is often called " Silent Killer", because it often goes undetected for years. However, when the treatment starts, even missing few doses of medication shoots the blood pressure to dangerous levels. So why human body did not produce any symptoms for years before medications starts and reacts violently when the treatment starts and missed few doses ?
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لاتظهر الاعراض سابقا على مرضى ضغط الدم وذلك لقلة الضغط النفسي اذا ان العامل النفسي له تأثير كبير جدا على المريض
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No doubt Arjuna has many medicinal properties like antioxidant, anti-inflammatory and antimicrobial, strengthens and tones the heart muscles, helps in proper functioning of the heart. Arjuna tree also has strong anti-hypertensive property and helps reduce high blood pressure. In this context my request is to know that is there any scientific study or proof regarding the removal of the plaque/ reversal of plaque in the arteries by the use of Arjuna (any form).
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Please visit the following RG link for insights.
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We see reduction in PA pressure after mitral commissurotomy and MVR
Does it persist in certain subset of patients?
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Dear Naeem Hameed,
It is an excellent question.
Mitral Stenosis is quite prevalent in our part of the world. In some patients with mitral stenosis pulmonary hypertension persists (PPH) after balloon valvoplasty or MVR.
Studies have shown PPH occurs more frequently in patients with residual significant gradient. Atrial fibrillation, old age, preexisting higher pulmonary hypertension, mitral regurgitation after procedure and left to right shunt created by septostomy etc. So it is difficult to say if there is permanent changes in pulmonary vascular bed in these patients as cause for pre or post capillary PH persist in many patients . Autopsy study have found plexiform change in the arteriole of these patients, but those reversed after procedures.
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Hello
I have 10,000 data related to Covid patients who have 2,000 blood pressure and 8,000 do not have high blood pressure.
My main goal is to study the risk factors for death in patients with high blood pressure with Covid 19. On the other hand, I want to find the risk factors in patients who do not have high blood pressure and compare it with the group that has high blood pressure. As in the table below.
I want to make two separate coxs for both data. Do you think this comparison are correct? Do I need to make adjustments to compare the final risk factors so that I can make the right comparison?
(I can not match here.)
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A couple of questions :
First – I presume that you know the status of each person, that is whether or not they died. With relatively small death rates you might think of Poisson regression (with robust standard errors) or negative binomial regression (ditto).
Second, do you want to see if hypertension modifies the effect of other risk factors? If so, you don't want separate regressions. You want to use an interaction term.
Third : hypertension is a tricky variable because it takes a continuous variable like BP and divides it into two categories, while the underlying effect on risk is, of course, continuous. Have you got BP measurements? Why not start with looking at them before you prematurely lose all that variation by collapsing into categories.
Fourth : People with previously detected hypertension are a problematic group made up of treated and untreated hypertensives and of those treated there will be those with well and poorly controlled BP. Given the interest in the effects of statins and metformin on the course of Covid, the nature of the hypertensive medication is also of interest. As you well know, there are several types of drug here.
Finally, I hope you are not planning on a data-dredging exercise like the one you showed above. It looks horribly as if someone did a stepwise regression.
Please tell us a little more. It's an interesting area but one that I think needs a certain amount of thought to define what question(s) the analysis should answer. Once those are clear, the methodology should be easier to work out.
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Our research world has become dependant on research output.
Many academic jobs depend on a certain sustained level of research.
Is this unhealthy?
Does it stunt creativity? Does it create pointless research? Does it lead to plagiarism?
Should we have different outcome measures eg a Research Quality Score per article, rather than number of articles?
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Publication is necessary for sharing knowledge, but publication because you are in an academic race is wrong, it creates Journals and publication houses who thrive on the need.
You need to pull out academicians from this race, by providing ample time and resources for quality research, instead of counting number of publications for career advancement.
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The ideal is to have both functioning well, but in many medium to low resource countries, this has become an Either/Or decision for Health Administrators.
Primary Health care to reduce the burden of disease and complications of disease and thus reduce the need for specialized care and it's cost.
Specialised care follows all the latest trends and innovations, but usually are very costly. Costs are likely to come down over time, though.
So FOMO medicine: Specialised....
or Affordable rimary Health Care....?
What is your view?
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The concept of PHC is to provide comprehensive package of health care services in the form of preventive, promotive, curative, rehabilitative, emergency, palliative, responsive, sensitive to the need of people. Now universal health care to everyone everywhere which should be accessible, available, acceptable & affordable. Through this wide network including ASHAs , interface with community & political will can make it possible.
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Hi all
My work led me to found some of the proteins interacting with some other proteins involved in hypertension. Now, I want to decipher if there is direct or indirect interaction between such interacting partners. Please suggest to me the direction that I should move in.
Thanks.
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Hi Dr Gaurav Kumar . I think this can be done by methods such as co-immunoprecipitation (co-IP), pull-down assays, crosslinking, label transfer, and far–western blot analysis is critical to understand protein function and the biology of the cell. See the link: https://www.thermofisher.com/uk/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/overview-protein-protein-interaction-analysis.html
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We have a situation where use of a device is resulting in exposure to sodium above the the IOM recommended UL value of 2300 mg. We can justify these small increases over the limit for non hypertensive subjects but what about risk to people with hypertension?
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People with hypertension has to limit their sodium consumption of less than 1500mg. Any increase of sodium intake above this level will increase both systolic and diastolic blood pressure. The DASH trial clearly had demonestrated the benefit of sodium restriction to reduce the BP.
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One of my relative admitted in hospital. he had angioplasty. Interventional Cardiologist recommended him to take medicine Ramipril BP (Controls Blood pressure) and Rosuvastatin (Controls cholesterol) for his entire life. My question is If a cardiac patient control the daily diet (lowers intake of salt and avoid cholesterol containing food) is it still necessary to use Ramipril BP and Rosuvastatin? Thanks in advance
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Yes, he needs to continue those drugs in addition to diet and life sthle medication. Drugs, lifestyle modifications and risk factors control all together may give ardsult equivalent to bypas surgery or sngioasty in patients with stable coronary hesrt disease.
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Why are there high mortality rates post operatively among patients with severe portopulmonary hypertension, after undergoing a liver transplant? This can also be put as : why severe portopulmonary hypertension, a contraindication to liver transplant?
Main Article : Krowka and associates divided 36 patients with portopulmonary hypertension who had undergone liver transplant into 3 groups according to mean pulmonary artery pressure: > 50 mm Hg, 35 to 50 mm Hg, and < 35 mm Hg. Mortality rates of the 3 groups were 100%, 50%, and 0%.
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Although exact csuse yet to be estsblished, one of the presumed csusre for high mortality after liver transplsntation in patients with port pulmmonary hypertension is right ventricular failure.
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Noise pollution is detrimental to humans and animals as it impacts their health. It may induce hearing damage, anxiety, heart disease, sleep disturbance, and hypertension.
Noise pollution is described as any unexpected or distracting sound which may be distressing or harmful to one's health and well-being. It seems to be an invisible threat as its present cause detrimental health impact on biodiversity both in land as well as under the water.
Strict rules and regulation are keenly needed to minimize noise pollution. With this, we have to raise public awareness about the bad impacts of noise pollution.
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Noise pollution is the most dangerous pollution of a man’s environment which adversely affects the human health.
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As stated I am currently interested in the field of Mobile Health and it's effect on Medication adherence in the Hypertensive population. That is why I am respectfully inquiring on the status of this study.
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M group has worked on the gene database of AD, PD, SZ, SZ and ALS. I wonder if there is any gene database compiled for hypertension, diabetes, or other comorbidities. Please let me know.
An example of the analysis is available at:
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I find, for example, diabetesgenes.org (https://www.diabetesgenes.org/), but it does not have a list of the genes but more processed information. I would like to learn human genes with meta-analysis or some kind of risk assessment. I would appreciate it.
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i want to analyze data regarding uncontrolled hypertension and its risk factors but don't know how to acess and analyze
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Dear Mohd Maroof,
1. You can select the list of what risk factors relating uncontrolled hypertension you are looking for.
2. We can then collect the data from nfhs4 _data (if those factors are there at all) for both controlled and uncontrolled hypertensive groups.
3.Then chi-square test can be done between the groups. If you want to propose new risk factor then you may have to do the logistics regression test to find if it has significantly related to uncontrolled hypertension.
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Taxometric analysis is commonly done for psychiatric diagnosis to assess discrete categories vs dimension or dimensions + categories. But has it been done for medical diagnoses with similar characteristics. The best example I can think of is hypertension (HTN). I have attached a graphic file looking at the most recent systolic BP recommendation and the distribution of blood pressures in the population. I also searched available literature for taxometric analysis of hypertension and could find nothing.
Is it possible that all polygenic, quantitative rather than qualitative disorders (HTN, asthma, diabetes, etc) produce the same results as psychiatric disorders in general? (I have found one study of metabolic syndrome.)
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I can mention one study with taxometric analysis in parastic disease:
Anshu Malhotra et al. Taxometric analysis of helminths of marine fishes 1.Pedunculacetabulum spinatum n. Sp., from chlorinemus mandetta and wenyonia rhincodonti n. Sp., from Rhincondon typus. Journal of parastic diseases, 2011:35(2):222_9.
DOI. 10.1007./s12639_011_0049_0
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Deoxycorticosterone acetate (DOCA) is commonly used to induced hypertension in experimental animals after the left kidney has been removed. is it possible to induced hypertension with DOCA without the left kidney being excised.
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Yes, I thought for a long time that uninephrectomy was necessary, but it is not.
We have just been giving a Doca pellet and 1% salt to drink. Blood pressure increases similarly to the one kidney model. One does not see the massive renal hypertrophy which accelerates and complicates evaluation of the effects of hypertension on the progression of kidney disease.
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Global Longitudinal Strain parameters in this particular case is within normal range. Biplane ejection fraction is also normal.
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Dear Meen Sumathy,
Much now has been learnt about diastolic dysfunction during this time..
Particularly for this patient
2 additional mechanism can be considered.
1.Mycardial fibrosis (we need to know about comorbidity like obesity, sleep apnea etc)
2. Coronary microvascular disease.
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How can one understand hypertension, with about 20 percent immediate drop in systolic and diastolic when switching from lying on left side or back, to right side? BP measurements being taken on left arm.
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Dear Moshe Rogosnitzky,
At a times in critically sick patients, you may have to monitor the patients, in the way you have mentioned. But in those casrs BP is monitored continously by automated non invasive BP, which is attached to the monitor and are constantly monitored. Many a time in such case, recordings show fluctuations of BP ( mostly due to technical csuses). In those cases BP is measured manually to get the BP. Allthogh in some situations BP can be monitored invasively by an invasve arterial catheterization when it is much needed.
Generally the highest BP rcorded is the real BP, meaning your patience BP in supine position to be taken as the true value. And still if are interested to know the BP in the right postion you have to readjust the total measuring procedure. As Albert Manfredi rightly mentioned the measring instrument should be kept at the level of heart.
Yes much morre engineering components are there in cardiac patients_civil, mechanical, elctrical.
Dear Fatema the properly trained CCU or ICU nurses are best in this regards.
In your country you have MSc in csrfiac nursing and they do an excellent job for the cardiovascular patients.
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Could non-alcoholic fatty kidney disease (NAFKD) the cause of gout, hypertension and CKD in metabolic syndrome?
I am pleased to share free access to my published hypothesis on the cause of gout and high Uric acid in obesity and metabolic. Please, feel free to post your opinion
Anyone clicking on this link before February 12, 2021, will be taken directly to the final version of your article on ScienceDirect, which they are welcome to read or download. No sign-up, registration, or fees are required.
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Dear Mohammed Abrahim,
In metabolic syndrome, diabetes hypertension, coronary artery disease, Hyperurecimia obesity, microalbuminuria etc clusters togdther. Common soil hypothesis states insulin resistance (IR) could be the link. NAFLD is atleast twice as common with IR. And may have common origin. NAFLD again shown to be associated with NAFKD and subsequent renal failure. Chronic inflammation and oxidative stres are in the centre of pathogenisis linking all these diseased togrther.
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Hi
Calcium is naturally present in water. It is a determinant of water hardness. The high level of calcium can be reduced by ion exchange such as adding sodium. Ionization replaces calcium and magnesium by sodium. So, the sodium content would be increased after ionization. High amount of calcium and magnesium in drinking water can cause health problem such as high blood pressure (Hypertension) and kidney stone. High amount of calcium can be treated with a water softener that uses ion exchange process, but it increases the level of sodium.
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Calcium and magnesium in drinking water do not cause hypertension, on the contrary they lower blood pressure. Sodium rises blood pressure.
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Confused because it seems that more protein intake can increase satiety. But I also found an article that have data shows people with high protein diet get HT more. Why?
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I have found two teachings from different sources. One they said about blood volume increase and therefore the patient has oedema and hypertension. But, another source says when there is high blood volume, low osmolality, it decreases the aldosterone, which promotes natriuresis and water excretion which in results euvolemic hyponatremia and oedema and hypertension does not occur? Which is true?
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Although SIADH is euvolemic hyponatremia, in reality patients are in the upper zone of euvolemia evident but continuously elevated urine sodium but this level of subclinical volume expansion should not be enough to give edema unless a different mechanism exist (primary salt retention) or there is chronic venous insufficiency which would precipitate lower limb edema.
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ABSTRACT
Worldwide, hypertension remains one of the most significant causes of morbidity and mortality. Despite the substantial public burden of hypertension coupled with the sustained government efforts in controlling the disease among hypertensive patients, there is still slow progress in the prevention and control of the ailment. The majority of patients still have uncontrolled blood pressure levels, with a significant number having life-threatening complications. The malady continuously subjects patients to immense suffering as it affects their health, predisposing them to life-threatening complications such as heart failure and even stroke in their 50s. Most countries, especially in the global south, have reported uncontrolled blood pressure levels among hypertensive patients despite anti-hypertensive drugs. This study, therefore, aims to investigate the clinical management of hypertension in adult patients by healthcare providers in Kakamega County, Kenya. The Specific objectives will be threefold: To assess patients' factors that influence the clinical management of hypertension in Kakamega County. The second one will examine the health care provider's factors that influence the clinical management of hypertension in Kakamega county. The third specific objective is to determine health system factors influencing clinical management of hypertension in Kakamega county based on clinical guidelines of 2018. The researcher will employ a cross-sectional analytical study design in multiple study sites. The pilot study will be carried out in the Vihiga county referral hospital. The primary study will be carried out in both tier 2 and tier 3 public, together with private hospitals in Kakamega County. Data will be collected from both the patients and the health care providers. The study will employ the use of a questionnaire and an observation checklist. Analysis of the collected data will be by the Statistical Package for Social Science (SPSS) version 28. Logistic regression will be used to identify factors associated with uncontrolled blood pressure and prognosis. Research participants will be required to sign a written consent.
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I am a PhD student and I am trying to establish "renal artery ligation model for renal hypertension". i am facing three main problems: 1) separation of renal artery from the vein (usually i fail and it ends with venous injury and massive bleeding), 2) high mortality rate after surgery (usually 2 from 3 rats die 3-4 days after the surgery), 3) unstable blood pressure (the blood pressure increases after the surgery then falls again nearly 4 weeks after the surgery)..
any tips regarding these three issues ?
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Weight gain due to anemia and other metabolic factors is the main cause of mortality in renal artery ligation model of hypertension.
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For example: Cardiometabolic risk factors (Hypertension, Obesity, Dyslipidemia and fasting hyperglycemia) as outcomes
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It depends on your research question. For example: Do risk factors (Hypertension, Obesity, Dyslipidemia, fasting hyperglycemia) increase the incidence of heart attacks? If you want to compare those 4 risk factors, you need to have enough participants in all groups. So your sample size will be e.g. 4x 20 individuals.
Here you have the best program to determine sample size: https://www.psychologie.hhu.de/arbeitsgruppen/allgemeine-psychologie-und-arbeitspsychologie/gpower.html. You will find many tutorials on how to use it on youtube.
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Using parenteral iron preparations for the management of anemia accompanied by several side effects some of the recently published articles said its hypotension rather than hypertension. Do you notice any significant blood pressure changes during your daily practices ?
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Dear Dr. Muhammad Yousuf at first I am so grateful for your kind contribution
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A 42-year-old patient with history of diabetes, hypertension and ischemic heart disease where coronary angiography with stent was done for him before presented to ED with chest pain and fatigue
What is your diagnosis ?
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Mobitz Type I (Wenckebach) second degree heart block with complete LBBB in the setting of recent STEMI.
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I've heard garlic and high nitrate foods like arugula or beets typically occupy high ranking here. What others do you know of or recommend? What's your top 10 list, based on what research? Thanks.
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When I eat lemon, lower my blood pressure
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Hypertension, diabetes, and cardiovascular disease are the most prevalent comorbidities in patients with COVID-19. Although they do not appear to affect the infectivity of the virus, they do increase disease severity. One of the common mechanisms of this effect is said to be the renin-angiotensin-aldosterone system (RAAS). What is the role of RAAS in this condition?
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Acei and ARBs are proven to be beneficial in covid 19 patients who also have underlying cardiovascular conditions according to prominent institutions such as European of science association.
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ACEI beneficial against SARS-CoV-2 infections
European Medicines Agency. (2020). EMA Advises Continued Use of Medicines for Hypertension, Heart or Kidney Disease During COVID-19 Pandemic.
European Society of Cardiology. (2020). Position statement of the ESC Council on Hypertension on ACE-inhibitors and angiotensin receptor blockers. ESC.
Hubei by Patel and Verma (2020) show that mortality rates are greatly reduced when ACE inhibitors are used.
Guzik, T. J., Mohiddin, S. A., Dimarco, A., Patel, V., Savvatis, K., Marelli-Berg, F. M., ... & Nicklin, S. A. (2020). COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. Cardiovascular research.
ACEI worsens SARS-CoV-2 infections
ACE inhibitors and angiotensin II blockers (ARBs) may worsen COVID-19 infections since they upregulate the expression of ACE2. (Diaz, 2020)
Diaz, J. H. (2020). Hypothesis: angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may increase the risk of severe COVID-19. Journal of Travel Medicine.
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Thanks for your explanation.
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As we know,the pulse propagates in wave form and the velocity of wave propagation depends on the propagation medium features. So,Is it possible to use the measurment of velocity of pulse propagation in the body to diagnose cardiovascular problems such as hypertension and hypotension?
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Obesity puts people at risk for a whole host of conditions, including Type 2 diabetes, high blood pressure and sleep problems. But is obesity itself a disease?
Doctors are divided on the issue. Some say obesity is indeed a disease, with causes beyond eating too much and exercising too little, and consequences that harm the body like any medical condition. In addition, they say referring to obesity as a disease would improve care for patients, and ensure treatments are covered by insurance plans.
Others argue obesity is a risk factor for health problems, but not a disease itself. They say calling obesity a disease would stigmatize a huge population, and categorize some people as "sick" who actually may be healthy.
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Obesity is a disease per se and is also a risk factor for all other disease as well. The main risk factor for obesity is sedentary lifestyle and over eating.
The life style modifications need to be inculcated since childhood and adolescence and it will help in long run.
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Generally, We have been told to make social distancing and all others rules to follow, and we have been following since the pandemic situation started in whole world as our government advised. But, why it is more dangerous for the people who are 60 or more than 60 years, also if they are diabetics or they have high blood pressure. What kind of precaution they can take, if they visit to doctors or emergency work.
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COVID-19 is more harmful for older people because of associated co- morbidities such as hypertension, diabetes, chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD).
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The neutralisation of the coronavirus has been much discussed in recent weeks, including antiviral medication used for HIV, HCV and anti malarial drugs with variable outcomes (potent antiviral drugs, such as remdesivir, chloroquine, or lopinavir/ritonavir) also convalescent plasma and IgG. However, inflammatory mediators appear to impact the progression of disease in COVID 19 patients.
Viral infection require precise regulation of the innate immunity by inflammatory immune mechanisms but over-activation of these processes can cause immunopathology with further complications to infected patients. Some significant clinical feature or patients with coronaviruses include, dyspnea, hypoxemia, and acute respiratory distress, lymphopenia, and cytokine release syndrome. This suggests that homeostasis of the immune system could play an important role in the development of COVID-19 pneumonia. Some plasma cytokines and chemokines are increased in COVID 19 patients, including IL-1,2,4,7,10,12,13,17, GCSF, MCSF, IP10, MCP-1, MIP-1, hepatocyte growth factor, IFN-γ and TNF-α.
The protective barriers of mast cells of the submucosa in the respiratory tract are activated by the virus and release histamine and protease and later activate IL-1 and IL-33. Could IL-1 receptor antagonists be helpful?
Histamine, as well as affecting vascular and bronchial responses, is increasingly identified with modulation of immune responses, including a variety of lymphocytes, such as T cells. Could antihistamines have beneficial effects on immune dysregulation and tissue remodelling during COVID 19 infection?
Virus particles invade the respiratory mucosa firstly and infect other cells, triggering a series of immune responses and over-activation of lymphocytes by apoptosis or necrosis of infected cells and the production of a cytokine storm causing a systemic T cell response in the patient, which may be associated with the critical condition of COVID-19 patients. COVID 19 attaches to pulmonary host cells by ACE2 then fuses to the membrane and releasing viral RNA. Lower levels of granulocytes are observed in the severe group than the mildly infected.
The development of inflammatory complications may be associated with the genetic individuality of a patient’s innate immune responses, resulting in different phenotypes. Considering the balance of IL-10/IL-12 expression influences the Th1/Th2 responses and imbalance in airway mucosa plays an important role in immune responses to viral infections and asthma development, IL-10 drives a humoral response and IL-12 drives a cytotoxic T cell response. Whereas Th2 responses are linked to the development of atopy, Th1 differentiation is often associated with the pathology of certain autoimmune processes. Patients with asthma viral infections tend to promote a Th2 response and increased eosinophilia exacerbates symptoms of the disease leading to breathing difficulties. Patients with chronic airway inflammatory diseases have impaired or reduced ability to promote Th1 cytotoxic responses to neutralise the virus. Could this be an implication for IL-12 therapy for anti-viral responses in patients not able to clear COVID 19?
In the severe group, CD4+ cells with lower IFN-γ and TNF-α and levels of granzyme B and perforin in CD8+ T cells were higher in the severe group than in the mild group. Could IFNγ as an antiviral therapy, despite its rather unpleasant side effects?
Further, Zinc supplementation showed benefits, shortening the duration of oxygen desaturation, tachypnea, and clinical symptoms in children with pneumonia, showing a Th1 response with the increase of IFNγ and IL-2 cytokines.
Chloroquine also seems to act as a zinc ionophore, thereby allowing extra cellular zinc to enter inside the cell and inhibit viral RNA dependant RNA polymerase.
Please contribute to this discussion.
Suggestions for anti-inflammatory considerations
  1. Antihistamines administered early in infection may reduce excessive cytokine proinflammatory storms.
  2. Zinc supplementation of population
  3. IFN-γ
  4. Introducing anti-inflammatory cytokines and/or monotherapy blocking IL-1 cytokine or receptor, inhibiting IL-1 may inhibit the inflammation.
  5. IL-4,6,10,11 and 13 are anti-inflammatory cytokines
  6. IL-1 receptor antagonists
  7. Chloroquine, the antimalarial drug that inhibits lymphocyte proliferation. As well as anti-viral activity. US have approved this therapy.
References
  • Marone G, Granata F, Spadaro G, Genovese A, Triggiani M. The histamine-cytokine network in allergic inflammation. J Allergy Clin Immunol. 2003;112(4 Suppl):S83–S88. doi:10.1016/s0091-6749(03)01881-5
  • Yan-Rong Guo, Qing-Dong Cao, Zhong-Si Hong, Yuan-Yang Tan, Shou-Deng Chen, Hong-Jun Jin, Kai-Sen Tan, De-Yun Wang, and Yan Yan The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak – an update on the status. Mil Med Res. 2020; 7: 11.
  • Zheng, H., Zhang, M., Yang, C. et al. Elevated exhaustion levels and reduced functional diversity of T cells in peripheral blood may predict severe progression in COVID-19 patients. Cell Mol Immunol (2020). https://doi.org/10.1038
  • Front. Pediatr., 14 November 2019 | https://doi.org/10.3389/fped.2019.00431). /s41423-020-0401-3).
  • J A Carr, J Rogerson, M J Mulqueen, N A Roberts, and R F Booth. Interleukin-12 exhibits potent antiviral activity in experimental herpesvirus infections. J Virol. 1997 Oct; 71(10): 7799–7803.
  • Jorge Alberto Acevedo-Murillo, Miguel Leonardo García León, Verónica Firo-Reyes, Jorge Luis Santiago-Cordova, Alejandra Pamela Gonzalez-Rodriguez2 and Rosa María Wong-Chew, Zinc Supplementation Promotes a Th1 Response and Improves Clinical Symptoms in Fewer Hours in Children With Pneumonia Younger Than 5 Years Old. A Randomized Controlled Clinical Trial. Front. Pediatr., 14 November 2019 | https://doi.org/10.3389/fped.2019.00431
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Thank you so much, Ruediger, for your contribution. I made a few notes on mast cell activation, particularly IgG involvement as over the last year mast cells have been a particular interest for me and am preparing a paper on the subject.
Mast cells
They originate from CD38+, being granulocytes derived from myeloid stem cells. MCs are also associated with neuro-immune systems. As innate immune cells, MCs are phenotypes that are tuned by cytokines and other micro-environmental stimuli. They also play a role in transplantation immunology but this will not be further discussed in this review.
As members of the innate immune system, MCs are located in places like skin, lung, and intestinal mucosa, which are in close contact to the outside world and they have an immediate activated response to parasite infections and antigens involved in allergies. In the case of parasites and allergens, these long-lived MCs defend against parasites maintaining an immune protection on the physical barriers in the body and are activated by the antigens. The response is mediated by a cross linking of FceR1 by immunoglobulin E (IgE), which results in the degranulation of the MCs. This particular linkage is used in MC detection by applying high infinity IgE. Staining the MC granules with toluene blue also characterises the cells.
There are a wide variety of receptors expressed on the surface of MCs that enable them to be activated by several different ligands, such as, endogenous cytokines, IgE, TLR ligands and IgG immune complexes. The inflamed tissue contains many of these ligands. A number of mediators including chymase, tryptase, histamine and other cytokines and chemokines are released, dependent on the route of activation.
An in vivo experiment with rats found that IL-3 wa involved in the recruitment of MCs and there were differential effects, dependant on the target tissue and time of exposure to the chemoattractant (de Cássia Campos MR 2014). Other mediators that stimulate MCs and trigger degranulation, proliferation and release of mediators include, IgG, complement components, TLR ligands, neuropeptides, cytokines, chemokines as well as other inflammatory products. Migration and differentiation are also stimulated by these inflammatory components. Thus the true versatility of MCs is recognised through them responding to a wide repertoire of different stimuli and not just IgE involvement (Yu Y 2016).
The MRGPRX2 MC receptor is important in the activation of MCs by peptide stimuli with abundant positive charges and aromatic/aliphatic amino acids (Lu L 2017).
The activated MC response results in the release of a broad spectrum of proinflammatory mediators, proteolytic enzymes and chemotactic factors that attract other immune cells. Proteolytic induce rapid inflammation and tissue remodelling.
MCs also are important in wound healing releasing factors and promote the recruitment of leukocytes, platelet activation and fibrogenic processes. Although the pathogenesis of RA is not fully understood, joint destruction possibly occurs due to the recruitment of neutrophils and monocytes that facilitate the damage of joint related cartilage when they activate osteoclasts. Histamine is a mediator that is involved in the activation of osteoclasts.
Clearly, in the case of allergies this immune response is detrimental and can cause asthma, even promote anaphylaxis. The MC is rich in granules of histamine and heparin, all-important in the fenestration of epithelium to enable other immune cells, such as, lymphocytes to migrate to the source of supposed infection. Other mediators of immune response from MC granules are leukotrienes causing shortness of breath, prostaglandins, tryptase, interleukins, heparin and TNF-alpha (Jennings S 2014), (Afrin LB 2013), (Valent P 2012), (Theoharides TC 2015).
MCs promote anti-inflammatory mediators as well as proinflammatory processes. They can act as antigen presenting cells and express a large array of co-stimulatory molecules. MCs are able to tolerate the introduction of some antigens without eliciting an inflammatory immune response in certain sites of the human body, described as having immune privilege to tissues with T-regulatory cells and are essential elements in fibrotic conditions.
In allergic responses, MCs are a potential source of chemokines and cytokines, important in inflammation. As well as IgE activation, MCs can be activated by Toll-like receptors and/or IL-1, which can be inhibited by IL-37 whereas IL-36 is a powerful proinflammatory cytokine (Gallenga CE 2019). IL-1 activates the release of inflammatory chemical mediators from MCs.
There are many known triggers for MC activation in addition to Infections (viral, bacterial or fungal)-
· Stress: emotional, physical, including pain
· Stress: environmental (i.e., weather changes, pollution, pollen, pet dander, etc.)
· Food or beverages, including alcohol
· · Heat, cold or sudden temperature changes
· Exercise
· Fatigue
· Drugs (opioids, NSAIDs, antibiotics and some local anaesthetics) and contrast dyes
· Natural odours, chemical odours, perfumes and scents
· Venoms (bee, wasp, mixed vespids, spiders, fire ants, jelly fish, snakes, biting insects, such as flies, mosquitos and fleas, etc.)
· Mechanical irritation, friction, vibration
· Sun/sunlight
Typical symptoms experienced during mast cell activation in allergy are flushing; itching, diarrhoea and hypotension are all mediated by histamine. Leukotrienes cause shortness of breath and prostaglandins are responsible for pain, brain fog, cramping and also flushing. In addition, MCs induce cytokines that cause fatigue, weight loss and enlarged lymph nodes. MCs are also implicated in autoimmune pathology as well..
Perhaps patient histamine levels may be used as an early indication of COVID 19 disease severity or outcome by measuring the COVID 19 patient levels of histamine in serum and urine to assess the possible degree of mast cell involvement in the cytokine storm.
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Thank you to KG for bringing this to my attention this evening. Colby Cosh In the National Post March 21, 2020: “If you take drugs for high blood pressure, you might have noticed some nervous speculative mumbling about possible interactions between the virus and the drugs.” He raises a similar question about corticosteroids. Is it possible?
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Any drugs that lower the immunity can lead to increased risk of SARS-COV-2 infection and COVID-19 deaths.
The major groups of patients who are using these medications are:
1. Collagen vascular diseases (SLE, Rheumatoid arthritis, Polymyositis etc) - using corticosteroids, Azathioprine, Cyclophosphamide, Methotrexate etc.
2. Patients with cancer and on chemotherapy - all these drugs suppress the immunity
3. Patients having organ transplantation (Kidney, liver, heart, bone marrow) on drugs to avoid rejection of the donor organ
4. Certain skin, blood, and vascular disorders who also need these drugs
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Discussion on the best options for management of hypertension, T2 diabetes mellitus in the context of macroalbuminuria is sought to get an insight into the matter.
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I would definitely include SGLT-2 inhibitors in the treatment algorithm early on in the care of such patients.
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I'm going to do research, but my funding is not enough, can anyone tell me how to get funding? My research is about hypertension?
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There has been some discussion about the comorbidities, including cardiovascular disease and diabetes, which often qualify for angiotensin inhibitor (ACEI) therapy, which significantly increase mRNA expression of cardiac ACE2 and on this basis that the treatment may exacerbate the severe course of COVID 19 infection. The European and American Societies of Cardiology, now express that ACEIs and ARBs are safe and should be continued and prescribed according to established guidelines during COVID 19 infection.
Angiotensin receptor blockers (ARBs) have recently been suggested as a useful strategy to inhibit COVID 19 infection.
It is understood that COVID 19 attaches to pulmonary host cells by ACE2, the angiotensin receptor, then fuses to the membrane and releasing viral RNA and is postulated that the current angiotensin blocker drugs may inhibit this mechanism of viral attachment to pulmonary cells.
Such drugs as losartan or candesartan cilexetil (long-lasting, effective angiotensin II type 1 receptor blockers) are well tolerated in normal cohorts and well evaluated in clinical studies with patients with primary hypertension, including elderly and does not aggravate co-existing risk factors like hyperlipidaemia or glucose intolerance.
ACE expression is known to affect myeloid cells activity in both infection and malignancy, modulating both innate and adaptive immune responses, including macrophage and neutrophil function.
Common ARBs may exert anti-inflammatory mechanisms by modulating the immune system directly.
rhACE2 completely binds to virus S-protein may protect the lungs from virus attack and an improved understanding of this class of pharmaceutical, with regard to its anti-inflammatory properties, may inhibit COVID 19 virions pulmonary cell entry via the ACE receptor.
Are there any indications yet that this protcol for COVID 19 therapy is successful?
References-
· Coronavirus Disease 2019 (COVID‐19): Do Angiotensin‐Converting Enzyme Inhibitors/Angiotensin Receptor Blockers Have a Biphasic Effect? Journal of the American Heart Association. 2020;9:e016509
· Gurwitz D. Angiotensin receptor blockers as tentative SARS‐CoV‐2 therapeutics. Drug Dev Res. 2020 doi: 10.1002/ddr.21656. [CrossRef] [Google Scholar]
· Tobaiqy M, Qashqary M, Al-Dahery S, et al. Therapeutic Management of COVID-19 Patients: A systematic review [published online ahead of print, 2020 Apr 17]. 2020;100061. doi:10.1016/j.infpip.2020.100061
· Bernstein KE, Khan Z, Giani JF, Cao DY, Bernstein EA, Shen XZ. Angiotensin-converting enzyme in innate and adaptive immunity. Nat Rev Nephrol. 2018;14(5):325–336. doi:10.1038/nrneph.2018.15
· Marshall TG, Lee RE, Marshall FE. Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b. Theor Biol Med Model. 2006;3:1. Published 2006 Jan 10. doi:10.1186/1742-4682-3-1
· Zhang J, Xie B, Hashimoto K. Current status of potential therapeutic candidates for the COVID-19 crisis [published online ahead of print, 2020 Apr 22]. Brain Behav Immun. 2020;S0889-1591(20)30589-4. doi:10.1016/j.bbi.2020.04.046
· Talreja H, Tan J, Dawes M, et al. A consensus statement on the use of angiotensin receptor blockers and angiotensin converting enzyme inhibitors in relation to COVID-19 (corona virus disease 2019). N Z Med J. 2020;133(1512):85–87. Published 2020 Apr 3.
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It may lead to positive results, but it takes a long time to confirm its effectiveness
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Best cell-free fetal DNA isolation kit for serum/ plasma samples? anyone doing estimation of cell free fetal DNA in Pregnancy induced hypertension ?
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thank you Alexander Sasha Vlassov , will check if it is available in India.
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Garlic is a plant for human consumption and it is said to have health benefits.
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Highly interesting paper on SARS-CoV transmission via Ace2.
Could this be a possible link to the increased mortality among hypertensive patients. These patients are often treated with ace-inhibitors that conceivably may cause up regulation of ace expression.
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Good morning,
Thank you for your interest. Some say that ACE inhibitorshave have a "permisive" role for COVID 19. And not only them but also angiotensine II receptor inhibitors. On the other hand, some authors consider that there is not enough study to sustain these opinions. So, in my vision, I consider that changing current medication is not good, taking into consideration the benefits they provide. But keep in mind the side effects. The patient with high blood pressure should respect all the preventing rules, like all of us.
All the best to you.
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I have recently got my Bachelor's degree in medicine and surgery and I have finished step 1 USMLE recently. I am looking for a research opportunity in cardiology or cardiology-related basic science. I have good research experience. I can help in databases searching, statistic work or manuscript writing.
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For sure, we can collaborate together.
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The high blood pressure is on the rise. We found 2.1% of school going students having raised blood pressure. Most of the studies on high blood pressure are done in adults. It is important to understand high blood pressure among youth so that preventive meaures for modifiable risk factors are taken early to live a healthy and complication freeadult life.
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Dear Rodolfe, I am so sorry that I am not able to understand your comments due to my inability to read and understand it . Could somebody please translate this comment in English? Thanks
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White coat syndrome and cuff-inflation hypertension are 2 distinct phenomena seen in patients at clinic. What is the best way to deal with cuff-inflation hypertension?
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see this link
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SARS-CoV-2, the causative agent of COVID-19, seems to use ACE2 as a portal of entry into the lungs.
Drugs used to treat hypertension and/or prevent remodeling in heart failure (mainly ACE inhibitors and angiotensin II receptor blockers) increase ACE2 levels
Could this partially explain the relationship between increased fatality rate of COVID-19 in patients with cardiovascular diseases, including hypertension? Is anyone aware of a study that has looked into the use of ACE inhibitor or angiotensin II receptor blockers and mortality?
Thanks.
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Thank you all. Great input. To sum it up:
- ACE2 expression is increased in patients treated with ACE inhibitors, ARB, ibuprofen or thiazolidinediones
- ACE2 expression could influence the course of COVID19 in 2 different ways: increased expression leads to increased mortality (by promoting viral entry) or increased expression leads to decreased mortality (due to ACE2 anti-inflammatory effects that could prevent ARDS development)
- some data may even suggest that viral load is not related to disease severity, so maybe ACE2 expression isn't the issue here, but rather some other mechanism (such as bradykinase-bradykinin balance)
Once again, thank you all. And good luck fighting this. We are beginning to see a explosion here in Portugal...
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Hypertensive patients with CKD are at increased risk of many complications such as anemia, peripheral edema, hyperkalemia, and heart disease. How frequently should these patients monitor their blood pressure outside of the office? Should these patients opt for a 24-hours ambulatory blood pressure monitoring (ABPM)? If so, how frequently should it be done?
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You are welcome
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Arginine is the substrate for nitric oxide synthesis, which is pivotal to vascular homeostasis and linked to the insulin response, it has long been posited that supplemental arginine could benefit cardiometabolic health. So administration of arginine can be effective in the treatment of hypertension as well?
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Please take a look at the following RG link and a PDF attachment.
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Hypertension is very common disease in many places and millions are suffering .It has very link to potassium nin blood , Hypertension remains the leading cause of cardiovascular disease (CVD), affecting approximately 1 billion individuals worldwide [1]. More than 72 million Americans, or nearly 1 in 3 adults, are estimated to have hypertension but only 34% achieve blood pressure (BP) control [2–5]. Nearly 70 million more adults are at risk of developing prehypertension, BP between 120/80 mm Hg and 140/90 mm Hg. Over 90% of adults in the United States will probably develop hypertension, especially systolic elevations, by age 65 [3]. Hypertension is associated with an increased risk of morbidity and mortality from stroke (cerebrovascular accident, CVA), coronary heart disease (CHD), myocardial infarction, congestive heart failure, and end-stage renal disease. Poor BP control is even more of a challenge for patients with diabetes and chronic kidney disease, who have lower recommended BP goals [6]. Hypertension remains the most common reason for patient visits to physician’s offices and is the primary reason for the use of prescription antihypertensive drugs, with an annual cost of almost $20 billion. Diet in the Prevention and Treatment of Hypertension Several epidemiologic studies [7–10] suggest that diet plays an important role in determining BP. So how potassium is playing?
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can I get the tools like the research title? that I have sent the file
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I think family education about hypertension can empower the family members to facilitate hypertension control
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SD runs a very chronic course like that of Diabetes or hypertension but SD is not asymptomatic. It produces many symptoms. Pruritus is one of them which is sometimes unbearable. Many treatment options are there but none produces long term remission. What could be the most effective therapeutic option for SD in a diabetic and hypertensive adult male?
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Good afternoon everyone.
I have a big database where every year there are different number of patients diagnosed with hypertension. The hypertension is a categorical variable (hypertension=1, hypertension absent=0). The years from 2001 to 2010 are scaled. I have another categorical variable depending what kind of instance they have. Let's say 1=employee insurance, 2=private insurance, 3=no insurance.
My question is how do I calculate the p value for people with and without hypertension depending whether have private insurance or not. I want to see if there is a trend across the years from 2001 to 2010 and if it's significant or not?
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You can do this using logistic regression, with insurance coded 1 for yes, 0 for no. The odds ratio from logistic regression gives you the rate of change in the odds of having insurance per one-year increase in year.
I am totally bewildered by
Rodolfo Vega Candelario
's dump of an entire paper as an answer to your question. Perhaps he pasted the wrong thing into the box and pressed the add button before he realised what he had done. In any event, there is nothing in it that would justify you reading it. Indeed, it contains a number of very peculiar statements, such as "The punctual prevalence rate of high blood pressure was 111.5 × 103". I have no idea what this means. Maybe
Rodolfo Vega Candelario
can explain how the paper answers your question.
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Taurine might also improve heart failure because it seems to lower blood pressure and calm the sympathetic nervous system, which is often too active in people with high blood pressure and CHF.
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Taurine could have both hypotensive and hypertensive properties.
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Many study suggest that elevated liptin level in obese individuals cause hypertension, l may disagreed with them, it has protection mechanism against hypertension. As it's a potent vasodilator
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please look in this link , it will help you
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What do you think that Noise Pollutant affects you the most?
(A) On Heath
o Effect on hearing
o Other health issues
o Disturb sleep
o Result in deafness
o Mental health disorders
o Any other, please mention
(B) On Life
o Reduce Working Efficiency
o Interfere with communication
o Cause annoyance
o Any other, please mention
(Other health issues may include like High Blood Pressure, Hypertension, cardiovascular effects, Heart Disease, Stress
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Headaches mostly .and occasionally it triggers my dormant anger.
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I am performing a logistic regression. I have a number of independent variables (age, hypertension, BMI, diabetes and a sleep risk score which is a function of (age, hypertension, BMI and other sleep related factors) to test the association their association with dependent variable (diastolic dysfunction). Can I include this risk score, if it is partly a function of some of the independent variables?
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