Hypertension - Science topic

Good day!

I am looking for a risk stratification tool that can identify high-risk individuals among those with diagnosed/subclinical hypertension, diabetes mellitus, and/or dyslipidemia. Ideally, the tool is age-standardized, region-specific (Asia/SE Asia in my case), easy to utilize, and cost-effective, but it's not necessary to fulfill the first two criteria.

I have looked into SCORE2, MUS, etc., but most of these models are appropriate only for apparently healthy individuals. WHO cardiovascular risk stratification charts are useful but their use is limited only to patients aged 40-75 y/o.

So far, it appears my best candidate would be the risk stratification heat map presented in the 2007 ESH-ESC Practice Guidelines for the Management of Arterial Hypertension since it encompasses the three cardiometabolic conditions I've specified.

I would just like to ask if you could recommend a more optimal risk stratification tool than the heat map I've mentioned? Thank you very much!

What are the latest findings on the topic: Effect of hypertension (high blood pressure) on mouse retina structure? I can barely see articles on this topic, rather than ocular hypertension or human retina.

If you have something to look at, please contact me!

Blood Pressure (BP) in Atrial Fibrillation (AF)

1. Whether the (so called) modest elevation in BP, which increases the risk for incident AF, and subsequently, concomitant hypertension and AF accounting for a multiplied cardiovascular risk enhancement – remain to vary (significantly) – depending on individual’s metabolism?

2. What exactly we mean by “optimal BP” (corresponding to an individual), which requires lowering BP for mitigating risk for cardiovascular morbidity and mortality; and for those individuals, with the coupled effect of AF & hypertension?

Feasible to deduce the optimal BP for an individual from home BP & 24 h ambulatory BP monitoring?

Do we always have a positive correlation between ‘left ventricular hypertrophy’ and ‘left atrial size’ with ‘ambulatory BP monitoring’?

3. Do we have a control over hemodynamic changes associated with AF, that in turn, causing variations in BP? Or Could we track the reasons for ‘changes in BP’ in the absence of considering hemodynamic changes?

4.  If the accuracy of automated BP measurements in AF patients in an out-of-hospital setting remain to be suspicious, then, the development of AF detection algorithms implemented in an automated BP devices would successfully serve the intended purpose? How about false positives?

5. In the absence of details on a recorded sleeping hours of a concerned patient, what exactly we mean by daytime and night-time measurements of systolic & diastolic BP, Mean Arterial Pressure & Pulse Rate?

Whether, Pulse Pressure in such cases, would remain to be the simple difference between systolic BP & diastolic BP (irrespective of the HR being lesser or greater than 90 bpm)?

In the context of BP measurements, whether HR would remain to be critical at all, if it is less than 120 bpm?

Suresh Kumar Govindarajan Professor (HAG) IIT Madras

I haven't seen one in a while so I wondered if that journal prohibits that form of redistriibution.

What are the main differences between chronic hypertension and gestational hypertension in fetal growth? Do these babies grow differently?

How to treat it

This is for a presentation on Hypertension in blacks.

I'm trying to compare prevalence of hypertension over the years in Nigeria

Hypertension

My dear teachers

Can you please guide me to find a scale to measure stress level that is relevant for patients with high blood pressure, except (the Perceived Stress Scale or DASS 21)

I want to ask about the usage of parametrical and non-parametrical tests if we have an enormous sample size.

Let me describe a case for discussion:

- I have two groups of samples of a continuous variable (let's say: Pulse Pressure, so the difference between systolic and diastolic pressure at a given time), let's say from a) healthy individuals (50 subjects) and b) patients with hypertension (also 50 subjects).

- there are approx. 1000 samples of the measured variable from each subject; thus, we have 50*1000 = 50000 samples for group a) and the same for group b).

My null hypothesis is: that there is no difference in distributions of the measured variable between analysed groups.

I calculated two different approaches, providing me with a p-value:

Option A:

- I took all samples from group a) and b) (so, 50000 samples vs 50000 samples),

- I checked the normality in both groups using the Shapiro-Wilk test; both distributions were not normal

- I used the Mann-Whitney test and found significant differences between distributions (p<0.001), although the median value in group a) was 43.0 (Q1-Q3: 33.0-53.0) and in group b) 41.0 (Q1-Q3: 34.0-53.0).

Option B:

- I averaged the variable's values over all participants (so, 50 samples in group a) and 50 samples in group b))

- I checked the normality in both groups using the Shapiro-Wilk test; both distributions were normal,

- I used t Student test and obtained p-value: 0.914 and median values 43.1 (Q1-Q3: 33.3-54.1) in group a) and 41.8 (Q1-Q3: 35.3-53.1) in group b).

My intuition is that I should use option B and average the signal before the testing. Otherwise, I reject the null hypothesis, having a very small difference in median values (and large Q1-Q3), which is quite impractical (I mean, visually, the box plots look very similar, and they overlap each other).

What is your opinion about these two options? Are both correct but should be used depending on the hypothesis?

Mr. Guillermo Zalba did not participate in the research of the article "Prevalence of Hypertension and Obesity: Profile of Mitochondrial Function and Markers of Inflammation and Oxidative Stress". I ask you please to remove it from your information

Best regards

Alejandra Guillermina Miranda-Díaz, MD, PhD

Please explain the action of diuretic drugs can decrease blood pressure

Empirical studies on the knowledge level of adults on cholesterol and risk of hypertension

I want to write a case-report about my condition, which is unusual for someone my age - I have mild high blood pressure. I'm not sure if it's okay for me to write about myself like this. Are there any rules against it? I understand that there might be concerns about being honest and unbiased since I'm the patient, but I could write objectively and have others review my work to make sure it's fair and neutral. Would that be okay?

Guillermo Zalba is not part of the team of the article, plese delete his name

Best regards

Alejandra Guillermina Miranda-Díaz, MD, PhD

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 ...

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.

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?

I have a pre-post research design with control group. i have an educational program for the intervention group where i measure their knowledge, perceptions and practice towards hypertension before and after the intervention. at the same time i have a control group who receive the regular practice without any intervention. i measure their knowledge, perceptions and practice at the same period that i measure for the intervention group. i have calculated the sample size that was 350 patients. my question is whether this number is for both groups (175 for each group) or i should have 350 patients in each group? many thanks in advance.

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

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.

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?

The mechanism

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.

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?

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.

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

May I have any help about this? I can see some hyaline areas but what is that cell infiltration?

Is hydralazine a first line drug in the management of hypertensive emergencies

or urgencies?

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?

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.

Stations in preeclampsia 

Treatment or prevention

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.

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 ?

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).

We see reduction in PA pressure after mitral commissurotomy and MVR

Does it persist in certain subset of patients?

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.)

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?

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?

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.

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?

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

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.

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.

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:

i want to analyze data regarding uncontrolled hypertension and its risk factors but don't know how to acess and analyze

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.)

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.

Global Longitudinal Strain parameters in this particular case is within normal range. Biplane ejection fraction is also normal.

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.

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.

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.

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?

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?

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.

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 ?

For example: Cardiometabolic risk factors (Hypertension, Obesity, Dyslipidemia and fasting hyperglycemia) as outcomes

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 ?

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 ?

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.

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?

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.

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.

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.

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.

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

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?

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.

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?

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?

· 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.

Best cell-free fetal DNA isolation kit for serum/ plasma samples? anyone doing estimation of cell free fetal DNA in Pregnancy induced hypertension ?

Garlic is a plant for human consumption and it is said to have health benefits.

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.