̽��ֱ�� of Cambridge - Department of Experimental Medicine and Immunotherapeutics

Thousands of pregnancies tracked in UK’s biggest study on pre-eclampsia

Anonymous — Wed, 19 Jul 2023 10:16:45 +0000

̽��ֱ��POPPY study (Preconception to pOst-partum study of cardiometabolic health in Primigravid PregnancY) is funded by Wellcome and is being led by a team from Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust (CUH) and the ̽��ֱ�� of Cambridge. ̽��ֱ��study is also being carried out in Glasgow and up to four other research centres in London.

In the first large scale study of its kind in the UK, women are being monitored before, during and after their first pregnancy to see what factors might be influencing the health of their placenta and their long-term cardiovascular risk. It’s hoped that by understanding this risk, the health of women who develop placental complications can also be improved over their lifetime.

Placental complications affect around 1 in 10 pregnancies and includes:

pre-eclampsia (high blood pressure with kidney/liver/brain involvement)
gestational hypertension (high blood pressure in pregnancy)
fetal growth restriction (baby being small).

These conditions can lead to serious complications for both mother and baby if not monitored or treated.

High blood pressure (hypertension), diabetes, autoimmune conditions, age and being obese before pregnancy are just some of the factors likely to increase the risk of pre-eclampsia and placental dysfunction, but it’s unclear exactly why and whether there are other causes.

In addition, women who experience placental complications are twice as likely to develop heart disease and diabetes later in life, compared with women who have a healthy pregnancy.

It’s not clear however whether placental complications cause heart disease and diabetes directly, or whether these conditions happen in women who already have some underlying and/or unknown health issues before pregnancy.

Women thought to be at high risk of developing pre-eclampsia are advised to take a 75 to 150mg daily dose of aspirin from the twelfth week of pregnancy until birth to reduce the risk of developing this condition. If a woman develops pre-eclampsia, the only way to cure it is to deliver the baby, normally at around 37 to 38 weeks of pregnancy, although this can be earlier in more severe cases.

Dr Bernadette Jenner is a medical registrar in obstetric medicine and clinical pharmacology at Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust (CUH) and is leading the POPPY study in Cambridge. She said:

“This study is going to be monitoring thousands of women from before they become pregnant for the first time and will track them through to birth and beyond to try and discover why some develop placental conditions and others don’t. We also hope to find out whether or not these conditions trigger longer-term health issues such as heart disease and diabetes.”

“We have a significant lack of understanding when it comes to placental conditions, especially when you consider how common they are, and the serious impact they can have on women and babies, which at times is life-threatening. To prevent pre-eclampsia and other placental conditions we need to know what really causes them and why. We have some big gaps in our knowledge and this study hopes to find answers.”

Professor Ian Wilkinson is leading the POPPY study and is a clinical pharmacologist and Professor of Therapeutics at the ̽��ֱ�� of Cambridge. He said:

“ ̽��ֱ��POPPY study is a world first and will help us to better understand why common complications of pregnancy adversely affect women’s long term cardiovascular health. This is the key to reducing this risk and may also allow us to prevent pregnancy complications before they occur.”

"Unfortunately, many women who suffer from pre-eclampsia, or one of the other placental complications, are not aware of the potential long term risks, and very few of them are actively followed up after birth - despite recommendations by NICE.”

“Therefore, whilst we await the findings of the POPPY study it is important that women who have experienced one of these complications are seen by a medical professional in the months after delivery to ensure that their blood pressure and other cardiovascular risk factors are checked and treated if necessary."

̽��ֱ��POPPY study is now open at Addenbrooke’s Hospital in Cambridge. Two more sites will be open soon at Glasgow Royal Infirmary NHS and Imperial College Healthcare NHS Trust, with further sites in London to start in the coming months.

Participants must be planning their first pregnancy and live in Glasgow, Cambridge or London where the study is taking place. Participation will involve monitoring alongside regular pregnancy checks and tests.

Find out how you can take part on the POPPY Study website.

Adapted from a press release by CUH

Up to 3,500 first time mums are due to take part in a study led by Cambridge researchers to understand why some will develop pre-eclampsia and placental complications during pregnancy and whether it effects their long-term health.

We have a significant lack of understanding when it comes to placental conditions, especially when you consider how common they are, and the serious impact they can have on women and babies, which at times is life-threatening

Bernadette Jenner

POPPY study | Dr Bernadette Jenner

Suhyeon Choi

Pregnant person holding her stomach

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Lab-grown beating heart cells identify potential drug to prevent COVID-19-related heart damage

cjb250 — Thu, 05 Aug 2021 08:35:20 +0000

̽��ֱ��heart is one the major organs damaged by infection with SARS-CoV-2, particularly the heart cells, or ‘cardiomyocytes’, which contract and circulate blood. It is also thought that damage to heart cells may contribute to the symptoms of long COVID.

Patients with underlying heart problems are more than four times as likely to die from COVID-19, the disease caused by SARS-CoV-2 infection. ̽��ֱ��case fatality rate in patients with COVID-19 rises from 2.3% to 10.5% in these individuals.

To gain entry into our cells, SARS-CoV-2 hijacks a protein on the surface of the cells, a receptor known as ACE2. Spike proteins on the surface of SARS-CoV-2 – which give it its characteristic ‘corona’-like appearance – bind to ACE2. Both the spike protein and ACE2 are then cleaved, allowing genetic material from the virus to enter the host cell. ̽��ֱ��virus manipulates the host cell’s machinery to allow itself to replicate and spread.

A team of scientists at the ̽��ֱ�� of Cambridge has used human embryonic stem cells to grow clusters of heart cells in the lab and shown that these cells mimic the behaviour of the cells in the body, beating as if to pump blood. Crucially, these model heart cells also contained the key components necessary for SARS-CoV-2 infection – in particular, the ACE2 receptor.

Working in special biosafety laboratories and using a safer, modified synthetic (‘pseudotyped’) virus decorated with the SARS-CoV-2 spike protein, the team mimicked how the virus infects the heart cells. They then used this model to screen for potential drugs to block infection.

Dr Sanjay Sinha from the Wellcome-MRC Cambridge Stem Cell Institute said: “Using stem cells, we’ve managed to create a model which, in many ways, behaves just like a heart does, beating in rhythm. This has allowed us to look at how the coronavirus infects cells and, importantly, helps us screen possible drugs that might prevent damage to the heart.”

̽��ֱ��team showed that some drugs that targeted the proteins involved in SARS-CoV-2 viral entry signiﬁcantly reduced levels of infection. These included an ACE2 antibody that has been shown previously to neutralise pseudotyped SARS-CoV-2 virus, and DX600, an experimental drug.

DX600 is an ACE2 peptide antagonist – that is, a molecule that specifically targets ACE2 and inhibits the activity of peptides that play a role in allowing the virus to break into the cell.

DX600 was around seven times more effective at preventing infection compared to the antibody, though the researchers say this may be because it was used in higher concentrations. ̽��ֱ��drug did not affect the number of heart cells, implying that it would be unlikely to be toxic.

Professor Anthony Davenport from the Department of Medicine and a fellow at St Catharine’s College, Cambridge said: “ ̽��ֱ��spike protein is like a key that fits into the ‘lock’ on the surface of the cells – the ACE2 receptor – allowing it entry. DX600 acts like gum, jamming the lock’s mechanism, making it much more difficult for the key to turn and unlock the cell door.

“We need to do further research on this drug, but it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus, particularly those who already have underlying heart conditions or who have not been vaccinated. We believe it may also help reduce the symptoms of long COVID.”

̽��ֱ��research was largely supported by Wellcome, Addenbrooke’s Charitable Trust, Rosetrees Trust Charity and British Heart Foundation.

Reference
Williams, TL et al. Human embryonic stem cell-derived cardiomyocyte platform screens inhibitors of SARS-CoV-2 infection. Communications Biology; 29 Jul 2021; DOI: 10.1038/s42003-021-02453-y

Cambridge scientists have grown beating heart cells in the lab and shown how they are vulnerable to SARS-CoV-2 infection. In a study published in Communications Biology, they used this system to show that an experimental peptide drug called DX600 can prevent the virus entering the heart cells.

Using stem cells, we’ve managed to create a model which, in many ways, behaves just like a heart does, beating in rhythm. This has allowed us to look at how the coronavirus infects cells and, importantly, helps us screen possible drugs that might prevent damage to the heart

Sanjay Sinha

Beating heart cells infected with virus

sbtlneet

Heart

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Repurposing existing drugs for COVID-19 a more rapid alternative to a vaccine, say researchers

cjb250 — Thu, 07 May 2020 08:25:58 +0000

Since the emergence of the SARS-CoV-2 virus in late 2019, more than 3.5 million people are known to have been infected, leading to over 240,000 deaths worldwide from COVID-19, the disease caused by the novel coronavirus. ̽��ֱ��race is on to find new drugs to treat COVID-19 patients and to develop a vaccine to prevent infection in the first place.

A team of researchers representing the International Union of Basic and Clinical Pharmacology today say there will be no ‘magic bullet’ to treat the disease and argue that a multi-pronged approach is needed to find new drugs. They caution that an effective and scalable vaccine is likely to take over a year before it can used to tackle the global pandemic.

When a virus enters our body, unless we have already developed immunity from previous infection or vaccination, it will break into our cells, hijacking their machinery and using it to replicate and spread throughout the body. Often, the symptoms we see are a result of our immune system fighting back in an attempt to clear the infection. In severe cases, this immune response can become overactive, potentially leading to a so-called cytokine storm, causing collateral damage to organs along the way.

“Any drug to treat COVID-19 will need to focus on the three key stages of infection: preventing the virus entering our cells in the first place, stopping it replicating if it gets inside the cells, and reducing the damage that occurs to our tissues, in this case, the lungs and heart,” said Professor Anthony Davenport from the ̽��ֱ�� of Cambridge, one of the authors of the review.

̽��ֱ��review looks at potential therapeutic drug targets – the cracks in the virus’s own armour or weak spots in the body’s defences. Two key targets appear to be proteins on the surface of our cells, to which SARS-CoV-2 binds allowing it entry – ACE2 and TMPRSS2. TMPRSS2 appears to be very common on cells, whereas ACE2 is usually present at low levels that increase depending on sex, age, and smoking history.

“As we know these two proteins play a role in this coronavirus infection, we can focus on repurposing drugs that already have regulatory approval or are in the late stages of clinical trials,” said Professor Davenport. “These treatments will have already been shown to be safe and so, if they can now be shown to be effective in COVID-19, they could be brought to clinical use relatively quickly.”

One promising candidate is remdesivir, a drug originally developed for Ebola. Although clinical trials found it to be insufficiently effective at treating Ebola, clinical trials in the USA have suggested the drug may be beneficial for treating patients hospitalised with COVID-19, and the FDA has now approved it for emergency use. There have also been promising findings from studies of monoclonal antibodies, but this type of drug is expensive to produce and therefore less likely to be scalable.

“While we're waiting for a vaccine, drugs currently being used to treat other illnesses can be investigated as treatments for COVID-19 – in other words repurposed,” said Dr Steve Alexander from the ̽��ֱ�� of Nottingham.

“There’s unlikely to be a single magic bullet – we will probably need several drugs in our armoury, some that will need be used in combination with others. ̽��ֱ��important thing is that these drugs are cheap to produce and easy to manufacture. That way, we can ensure access to affordable drugs across the globe, not just for wealthier nations.”

̽��ֱ��team say that we need to move quickly to identify existing drugs that are effective in clinical trials so that we can begin treating patients as rapidly as possible, but also because cases are likely to fall during the summer meaning there will be fewer people who can be recruited to clinical trials ahead of an anticipated second wave of the disease in autumn. They estimate there are currently more than 300 clinical trials taking place worldwide, though many of these investigational drugs are unlikely to be effective for widespread use because either it is not clear which part of the disease pathway they are targeting or they cause unpleasant side-effects.

They also advise patience for the promise of developing an effective vaccine against the virus anytime soon. Even after a new vaccine candidate has been shown to offer immunity against the coronavirus in humans, it needs to be tested in larger numbers of people to ensure it is safe to use. Manufacturing and distributing a vaccine at the scale needed to tackle this pandemic will also present significant challenges.

“Although there are a lot of vaccines being developed around the world, which we hope will be successful, it's still going to take a long time before those vaccines are shown to be effective and can be manufactured at the scale needed to make an impact,” said Dr Steve Alexander.

“Some of the vaccines may not work, so the more drugs that can be tested and the more we know about the targets, the more likely we are to get something which is effective. ̽��ֱ��very specificity of vaccines means they are limited in which viruses they can neutralise. ̽��ֱ��lessons we learn and the drugs we generate will hopefully provide a greater degree of protection, not just against the COVID-19 virus, but also against the next viral threat.”

Professor Davenport is a member of the Department of Medicine, ̽��ֱ�� of Cambridge, and a Fellow at St Catharine’s College.

Reference
Alexander, SPH, et al. A rational roadmap for SARS-CoV-2/COVID-19 pharmacotherapeutic research and development. British Journal of Pharmacology; 1 May 2020; DOI: 10.1111/bph.15094

Repurposing existing medicines focused on known drug targets is likely to offer a more rapid hope of tackling COVID-19 than developing and manufacturing a vaccine, argue an international team of scientists in the British Journal of Pharmacology.

"[Repurposed drugs] will have already been shown to be safe and so, if they can now be shown to be effective in COVID-19, they could be brought to clinical use relatively quickly"

Anthony Davenport

PIRO4D

Coronavirus

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Strategic partner: AstraZeneca

skbf2 — Mon, 11 Nov 2019 16:20:03 +0000

Scientists at AstraZeneca, a global biopharmaceutical company, have been working with Cambridge ̽��ֱ�� for more than two decades. What are the secrets of their success?

Drugs: how to pick a winner in clinical trials

lw355 — Mon, 26 Jun 2017 11:00:12 +0000

“Did not meet primary endpoint.”

Prosaic words, but they can mean a billion dollar failure has just happened.

̽��ֱ��average cost of taking a scientific discovery all the way through to a drug on a shelf is enormous – last year it was estimated at $2.6 billion by the Tufts Center for the Study of Drug Development.

One reason the figure is so high is because it also includes the cost of failure. Recent years have seen some very high-profile failures of drug candidates that either did not meet the ‘primary endpoint’ (they didn’t work) or had their trials halted owing to serious side effects.

“It’s only natural that some drugs will fail in clinical trials – the process exists to ensure that treatments are safe and effective for patients,” says Professor Ian Wilkinson, Director of the Cambridge Clinical Trials Unit (CCTU) on the Cambridge Biomedical Campus. “But what’s unexpected is the high number of drugs that fail in phase III. You’d think that by this stage the molecule would be a sufficiently good candidate to make it through.”

He explains that failures in phases I and II – when the drug is tested for safety and dosage in healthy volunteers and patients – are inevitable. However, a great many molecules don’t make it through phase III, the stage at which the drug’s effectiveness is tested in large numbers of patients before regulatory approval is given. In fact only 10–20% of drugs that enter phase I are ultimately licensed.

“ ̽��ֱ��problem with failing at phase III is it’s very expensive – a single drug trial can cost around $500m.”

He continues: “There’s a human impact for the thousands of patients who enrolled on the trial. For patients with cancer, it’s sometimes their last available treatment option,” says Wilkinson. “It’s also really unhelpful economically. Pharma companies have less money to put back into R&D, and it becomes even harder to fund drug development.”

This is why Wilkinson, along with a team of clinicians, scientists and pharmaceutical collaborators, together with statisticians at the Medical Research Council Biostatistics Unit, has been taking a hard look at the early phases of clinical trials. Their aim is to ask what can be done to get an early indication that a potential drug will make it to market.

“Traditionally, clinical trials have been organised to test safety first and efficacy last,” he explains. “It’s a cautious step-by-step approach adopted to ensure that pharma companies can satisfy regulators that the drug is safe.

“For many drugs this has worked well. But we are in a landscape where drug targets are more challenging – think for instance of conditions like psychiatric disorders and dementia. Leaving questions of whether a drug is effective to the final stages is now too risky and expensive.”

On any one day, the CCTU (one of the UK units accredited by the National Institute for Health Research) might be coordinating up to 20 trials in various phases for potential treatments for cancer, stroke, infections, dementia, heart attack, and so on.

Many of the trials are now designed with what Wilkinson calls “added value” built in at very early stages to give indications of whether the drug might work. This could include a biomarker that shows a drug for cirrhosis is reaching the liver, or a drug for heart disease is lowering cholesterol. “These are read-outs. They don’t show the drug works for the disease, but if the results are negative then there’s no point in progressing to later stages.”

̽��ֱ��trials are also run ‘adaptively’. “We look at data for each person as it comes in… once we have enough information to guide us, we make a decision that might change the trial. It’s a quite different approach to the traditional rigidity of trials. It maximises the value of information a trial can yield.”

In recent years, pharmaceutical companies like GSK and AstraZeneca (AZ) have championed the need for rigorous trial design to weed out likely failures earlier in the process.

GSK has its only trials unit in the UK in the same building as the CCTU. There, GSK researchers work alongside Cambridge clinicians and scientists on first-in-man studies. A more targeted approach to testing medicines in patients is a key component of a Strategic Partnership between GSK, the ̽��ֱ�� of Cambridge and Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust (CUH), which has the long-term ambition of jointly delivering new medicines to patients in the next five to ten years.

A few years ago, AZ analysed its drug pipeline before embarking on a major revision of its R&D strategy to increase the chance of successful transition to phase III and beyond. One area AZ identified as being crucial to success is to identify a causal relationship between target and disease. This might seem obvious but so-called mistaken causation has led to late failures right across the drugs industry. ̽��ֱ��usual cause is confounding – where a factor that does not itself cause a disease is associated with factors that do increase disease risk.

Professor John Danesh and colleagues at the Department of Public Health and Primary Care have pioneered a new way of finding evidence for causality before a patient is ever involved. Called ‘Mendelian randomisation’, it’s akin to a trial carried out by nature itself.

“Misinterpreting correlation as causation is a big problem,” explains Dr James Peters, who works with Danesh. “An increase in a protein biomarker in patients with atherosclerosis might suggest it’s important in the disease, but it’s not a valid drug target unless it plays a causal role. ̽��ֱ��conventional way to test this is to block the protein with a drug in a clinical trial, which is expensive, time-consuming and not always ethical.

“In phase III trials, the randomisation of participants helps to average out all differences apart from whether they are receiving the drug. Instead, we take advantage of the natural randomisation of genetic variants that occurs during reproduction.”

Some genetic variants can increase or decrease certain proteins that have been linked to a disease. If these variants can be identified – by computationally analysing enormous genetic datasets – then researchers can compare groups of people to see whether having the variant also increases the risk of a disease.

̽��ֱ��team has used this method to look retrospectively at why two phase III trials for a potential cardiovascular drug failed. “ ̽��ֱ��genetic evidence showed that the drug target was not valid,” says Peters. “We would have advised against taking this drug to a clinical trial.”

But it’s not just about predicting failures, Danesh’s team is picking winners. Evidence for the role of an inflammatory protein in atherosclerosis has now resulted in a clinical trial to see if an arthritis drug can be repurposed for atherosclerosis.

̽��ֱ��researchers are helping industrial collaborators to prioritise potential drug targets and predict side effects. They also hope to expand their capabilities to test large numbers of variants for different potential targets in an automated fashion – a high-throughput approach to therapeutic target prioritisation.

Meanwhile, Wilkinson is planning ahead to avoid a different type of limitation: expertise. “There is a lack of individuals trained to design and deliver innovative clinical trials, and this is now impacting on drug development,” he explains.

Last year, an Experimental Medicine Training Initiative was launched to train medics how to run innovative clinical trials. Wilkinson is its Director and it’s supported by the ̽��ֱ�� in partnership with CUH, Cambridge Biomedical Research Centre, and AZ/MedImmune and GSK.

“We all believe that the failure rate for drug candidates making it through phase III is unacceptably high,” he says. “Less than one in a thousand molecules discovered in the lab make it through to being a drug. We want to be sure that we can answer the billion dollar question of which are most likely to be winners.”

Read more about research on future therapeutics in Research Horizons magazine.

When a drug fails late on in clinical trials it’s a major setback for launching new medicines. It can cost millions, even billions, of research and development funds. Now, an ‘adaptive’ approach to clinical trials and a genetic tool for predicting success are increasing the odds of picking a winner.

We all believe that the failure rate for drug candidates making it through phase III is unacceptably high. We want to be sure that we can answer the billion dollar question of which are most likely to be winners.

Ian Wilkinson

Gatis Gribusts

Medication

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New research allows doctors to image dangerous ‘hardening’ of the arteries

cjb250 — Fri, 10 Jul 2015 08:21:49 +0000

̽��ֱ��technique, reported in the journal Nature Communications, could help in the diagnosis of these conditions in at-risk patients and in the development of new medicines.

Atherosclerosis – hardening of the arteries – is a potentially serious condition where arteries become clogged by a build-up of fatty deposits known as ‘plaques’. One of the key constituents in these deposits is calcium. In some people, pieces from the calcified artery can break away – if the artery supplies the brain or heart with blood, this can lead to stroke or heart attack.

“Hardening, or ‘furring’, of the arteries can lead to very serious disease, but it’s not clear why the plaques are stable in some people but unstable in others,” explains Professor David Newby, the BHF John Wheatley Professor of Cardiology at the Centre for Cardiovascular Science, ̽��ֱ�� of Edinburgh. “We need to find new methods of identifying those patients at greatest risk from unstable plaques.”

̽��ֱ��researchers injected patients with sodium fluoride that had been tagged with a tiny amount of a radioactive tracer. Using a combination of scanning techniques (positron emission tomography (PET) and computed tomography (CT)), the researchers were able to track the progress of the tracer as it moved around the body.

“Sodium fluoride is commonly found in toothpaste as it binds to calcium compounds in our teeth’s enamel,” says Dr Anthony Davenport from the Department of Experimental Medicine and Immunotherapeutics at the ̽��ֱ�� of Cambridge, who led the study. “In a similar way, it also binds to unstable areas of calcification in arteries and so we’re able to see, by measuring the levels of radioactivity, exactly where the deposits are building up. In fact, this new emerging technique is the only imaging platform that can non-invasively detect the early stages of calcification in unstable atherosclerosis.”

Following their sodium fluoride scans, the patients had surgery to remove calcified plaques and the extracted tissue was imaged, this time at higher resolution, using a laboratory PET/CT scanner and an electron microscope. This confirmed that the radiotracer accumulates in areas of active, unstable calcification whilst avoiding surrounding tissue.

Dr James Rudd, a cardiologist and researcher from the Department of Cardiovascular Medicine at the ̽��ֱ�� of Cambridge adds: “Sodium fluoride is a simple and inexpensive radiotracer that should revolutionise our ability to detect dangerous calcium in the arteries of the heart and brain. This will allow us to use current treatments more effectively, by giving them to those patients at highest risk. In addition, after further work, it may be possible to use this technique to test how well new medicines perform at preventing the development of atherosclerosis.”

̽��ֱ��Wellcome Trust provided the majority of support for this study, with additional contributions from the British Heart Foundation, Cancer Research UK and the Cambridge NIHR Biomedical Research Centre.

Reference
Irkle, A et al. Identifying active vascular microcalcification by 18F-sodium fluoride positron emission tomography. Nature Communications; 7 July 2015.

Researchers at the ̽��ֱ�� of Cambridge, in collaboration with the ̽��ֱ�� of Edinburgh, have shown how a radioactive agent developed in the 1960s to detect bone cancer can be re-purposed to highlight the build-up of unstable calcium deposits in arteries, a process that can cause heart attack and stroke.

Sodium fluoride is a simple and inexpensive radiotracer that should revolutionise our ability to detect dangerous calcium in the arteries of the heart and brain

James Rudd

̽��ֱ�� of Cambridge

Imaging atherosclerotic calcification or ‘hardening of the arteries’ using positron emission tomography

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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