Cambridge scientists uncover key protein in Zika virus pathology

The recent Zika virus outbreak has had a devastating global impact on human health, with at least 70 countries reporting infections since 2015.1 Zika virus is spread to humans by mosquito bites, although it can also be passed from person to person via sexual contact or bodily fluids, and from mother to foetus via the placenta. In children and adults, the virus causes only a mild illness. However, in pregnant women it can have devastating consequences for foetal neurodevelopment.

In the Americas, over the past two years, more than 3,500 babies have been confirmed to have congenital malformations associated with Zika virus infection.2 Perhaps the most tragic consequence of Zika virus on the unborn baby is microcephaly; a serious birth defect where the brain fails to develop properly, characterised by an abnormally small head.

Until recently, it was not known how the Zika virus caused neonatal microcephaly. However, scientists at the University of Cambridge have provided an insight into the mechanism by which the Zika virus may ‘hijack’ neural stem cells to cause this devastating brain condition.3 Their research showed that, in order to replicate, the Zika virus interacts with a neural stem cell protein called Musashi-1. In developing embryos, Musashi-1 is an RNA-binding protein that binds to target genes to regulate neural stem cell function. The interaction between the Zika virus and Musashi-1 disrupts this process and damages the foetal neural stem cells. Ultimately, neural stem cells die and the brain fails to develop to normal size.

Although, transmission of Zika virus may finally be slowing down, in the Americas at least,4 we are starting to understand the way that Zika virus causes microcephaly, giving scientists hope that, someday, we may be able to treat this devastating disease.

1. European Centre for Disease Prevention and Control. Rapid risk assessment: Zika virus epidemic, tenth update. 4 April 2017.

2. Pan American Health Organization/World Health Organization. Zika cases and congenital syndrome associated with Zika virus reported by countries and territories in the Americas, 2015–2017. 21 September 2017. [Accessed September 2017]

3. Chavali PL, Stojic L, Meredith LW, et al. Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication. Science 2017; 57 (6346): 83–88.

4. Pan American Health Organization/World Health Organization. Regional Zika Epidemiological Update (Americas) August 25, 2017. [Accessed September 2017]

Ciara Whitty

Ciara Whitty  PhD

Editorial Project Manager

Oct 2017

Much ado about nothing?

Assessing the value of placebo treatment in clinical trials

Clinical trials often involve placebo treatment. Use of a placebo tests the influence of study procedures themselves on treatment outcomes, thus helping to isolate the ‘true’ effect of the investigational product.

Placebo-controlled clinical trials are commonly used to evaluate the efficacy and safety of medicinal products. However, in situations where an approved treatment already exists, the use of a placebo essentially denies patients access to a proven effective treatment. Withholding treatment can result in long-lasting harm; in schizophrenia, for example, progressive relapses may lead to irreversible brain damage.1 Is it ethically acceptable to switch a patient from an effective intervention to placebo treatment, and observe the resulting rate of decline?

The use of an active comparator is an alternative method, whereby a new treatment is compared with one already deemed effective, rather than with a placebo. This method illustrates relative efficacy versus a current approach, and does not involve withholding treatment. However, the very act of being treated can result in remarkably high response rates – the so-called ‘placebo effect’ – and so, in an active-comparator study, it is impossible to tell how much of the treatment response is due to the activity of the drug, and how much of a response would have been observed if patients had only received a placebo.

How, therefore, can we weigh up whether or not placebo treatment is justified? Millum and Grady emphasise that methodological reasoning alone is not enough to warrant using a placebo; rather, any additional risks associated with placebo treatment must be balanced by the additional societal value of the study, relative to using other study designs.2

Unfortunately, the concept of “societal value” is by no means clear-cut. Compared with placebo-controlled studies, demonstration of efficacy in active-comparator studies requires a greater number of patients, thus exposing more patients to any risks associated with the new treatment. Is a smaller risk to a greater number of patients better societal value than a greater risk to a smaller number of patients? Furthermore, enrolment of fewer patients may translate to lower study costs,2 and saved costs could help fund future research, although it is certainly debatable whether a patient would consider pharmaceutical company finances an acceptable reason for risking their health.

In another avenue of debate, how should we assess the value of a study if the patients involved may not personally benefit in the long run? Or, put another way, how do we balance societal value and personal value?

Some argue that patients should consider participation in clinical studies ‘for the greater good’; others suggest that clinical research should only be conducted if its intent is to benefit the population from which the study participants are drawn.2

Ultimately, the benefits of placebo-controlled studies must undoubtedly outweigh the risks, but exactly how to evaluate benefit and risk in the unpredictable world of clinical research is a difficult decision to make.


1. Andreasen NC, Liu D, Ziebell S, et al. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013; 170 (6): 609–615.

2. Millum J, Grady C. The ethics of placebo-controlled trials: methodological justifications. Contemp Clin Trials 2013; 36 (2): 510–514.

Liz Kelly

Liz Kelly  BSc (Hons)

Account Manager

Jul 2017

Treating Alzheimer’s disease in an era of intelligent drug design

Given the major advances in the treatment of cancer, it is frustrating that the same progress has not been achieved in the field of Alzheimer’s disease and dementia.

In the early 1970s, a diagnosis of cancer meant a 50:50 chance of surviving for one year; for patients diagnosed in 2010, that 50:50 chance of survival had extended to ten years.1 This increase in the duration of survival is impressive considering that cancer is an aggressive and belligerent disease. However, there is still more work to be done in order to improve the treatment of cancer, and certain types in particular (for example, lung and pancreatic cancer) still show very low survival rates.1 The improved chance of survival observed over the past 50 years is due to therapeutic advances as a result of researchers gaining a more in-depth understanding of the disease process. Today, many of the new drugs in development target specific pathways, such as those involved when cancer cells evade the immune system, or when cancer cells generate their own blood supply. These targeted therapies would not be possible without a detailed appreciation of the disease pathology.

The situation for Alzheimer’s disease is quite different. Despite decades of work on the underlying disease pathology, the formation and testing of the ’amyloid hypothesis’, and the interrogation of the function of tau protein, little is known about the underlying cause of Alzheimer’s disease. This paucity of knowledge has led to a horrific attrition rate for drugs in development for Alzheimer’s disease – between 2002 and 2012, of 244 compounds assessed, only one was approved for marketing (99.6% attrition).2 Many of the diseases of middle and older age are being alleviated or cured, and so there is a growing population of older individuals who are susceptible to dementia. Consequently, the need to find an effective treatment for Alzheimer’s disease should be met with the rising urgency it deserves.

Quite why Alzheimer’s disease is so intractable to understanding remains a mystery but, if it were a simple problem, it would have been solved already. If a solution is ever to be found, society must not lose hope. We cannot be as fatalistic as Lyall Watson, who once said: “If the brain were so simple we could understand it, we would be so simple we couldn’t.”


1. Quaresma M, Coleman MP, Rachet B. 40-year trends in an index of survival for all cancers combined and survival adjusted for age and sex for each cancer in England and Wales, 1971–2011: a population-based study. Lancet 2015; 385 (9974): 1206–1218.

2. Cummings JL, Morstorf T, Zhong K. Alzheimer’s disease drug-development pipeline: few candidates, frequent failures. Alzheimers Res Ther 2014; 6 (4): 37.

Christopher Edge

Christopher Edge  PhD

Scientific Consultant

Nov 2016

Should prevention play a greater role in modern healthcare?

Over the past few decades, huge strides have been made in the treatment of HIV infections. There was a time when a diagnosis of HIV was a death sentence – now, highly active antiretroviral therapy (HAART) is a viable treatment allowing HIV-positive individuals to live full and satisfying lives. However, the disease is still spreading; in Europe, 2014 saw the highest number of newly diagnosed infections in a 1-year period, since monitoring began (in the 1980s).1 Despite the efficacy of treatment, there is clearly an unmet need for drugs that can help to prevent the spread of the HIV pandemic. The old bromide goes ‘prevention is better than the cure’, so why, then, is PrEP (pre-exposure prophylaxis) not more widely available in healthcare systems across Europe? PrEP is a method whereby HIV-negative individuals who are at a high risk of contracting HIV are given antiretroviral therapy (ART), in order to reduce the risk of infection (when used in conjunction with other preventative measures).2

Of course, there are always other ways of looking at the same problem. I can remember James Watson (a man never shy of controversy) giving a talk at my institute arguing that science should be focussed on curing late-stage cancer, nothing else. If we can cure cancer in its latest stages – he reasoned – then we need not worry about early detection, screening programmes, and maintaining a healthy lifestyle. The same argument can be applied to HIV – if science focusses on treating and curing AIDS, then prophylaxis is unnecessary. However plausible this theory may appear, it shows complete disregard for an individual’s quality of life, which should be of paramount importance for treating physicians and for clinical researchers. Quality of life is not served by allowing patients to progress to the late stages of debilitating conditions, nor is it served by allowing HIV to spread when preventative measures like PrEP have been developed.

As we move into an age where disease management aims to provide holistic benefits that extend beyond the traditional approach of symptomatic treatment, we may see a greater acceptance of preventive medicine into healthcare systems.


1. World Health Organization. Highest number of new HIV cases in Europe ever. 26 November 2015. Accessed 22 June 2016.

2. Terrence Higgins Trust website. Accessed 22 June 2016.

Christopher Edge

Christopher Edge  PhD

Scientific Consultant

Aug 2016

Can a simple blood test change the way we treat depression?

Despite the many treatment options that are available for depression, patients often struggle to find a drug that works for them. Patients may try many different antidepressants before settling on a particular medication, and some patients never find a satisfactory treatment. Such trial and error approaches to therapy are inefficient and expensive, as well as exposing the patient to unnecessary side effects. Fortunately, a recent scientific breakthrough indicates that it may be possible to predict whether or not a patient will respond to antidepressants before they have taken their first dose.

The test for potential non-responders is based upon levels of ‘inflammatory biomarkers’ in the blood. Inflammation is the term used to describe the body’s response to harmful stimuli, such as infection or injury. During inflammation, the body releases chemicals into the blood that help to fight the cause of the harm, as well as to repair or remove damaged tissue. Measuring the levels of these chemicals, or ‘biomarkers’, in the blood, enables doctors to gauge the degree of inflammation in a patient.

While depression itself cannot be diagnosed with a blood test,a studies have shown that depressed patients who are resistant to standard antidepressants have higher blood concentrations of certain inflammatory biomarkers than those patients who are not resistant to antidepressants. It is thought that a high degree of inflammation can interfere with particular biological processes that are crucial for antidepressants to exert their therapeutic action.

The latest breakthrough expands this research by identifying biomarker concentration cut-offs that accurately predict non-response to antidepressants. Patients with biomarker levels below the cut-offs are likely to benefit from standard antidepressants, whereas patients with levels above the cut-offs may require additional treatment with other antidepressants, or perhaps with anti-inflammatories. Thus, in the future, a doctor may be able to perform a simple blood test before prescribing the appropriate antidepressant medication – thereby eliminating months of suffering and uncertainty for the patient.


Cattaneo A, Ferrari C, Uher R, et al.; MRC ImmunoPsychiatry Consortium, Pariante CM. Absolute measurements of macrophage migration inhibitory factor and interleukin-1-beta mRNA levels accurately predict treatment response in depressed patients. Int J Neuropsychopharmacol 2016 [Epub ahead of print].

aDepression is diagnosed based upon symptoms such as low mood and loss of interest in daily activities.

Chris Watling

Chris Watling  PhD

Senior Medical Writer

Jul 2016

The beginning of the end for HIV?

During my time as an undergraduate student, I wrote an essay arguing that HIV could never be cured by drugs because it readily mutates within the body, and that it could never be eradicated by vaccination for essentially the same reason. Fortunately, my reasoning failed to anticipate the revolutions in technology that would be of benefit to the medical field.

Viral infections, such as HIV, are notoriously difficult to treat. Recently, there has been a drive to apply one of the great nascent medical technologies – CRISPR – to the treatment of HIV infections.1 CRISPR (clustered regularly-interspaced short palindromic repeats) is a gene-editing technology used to cleave DNA at specific locations (see an earlier blog entitled ‘Medicine in an era of genetic control’).

The technique has been used by one research group to target the HIV virus within T-cells but, despite an initial reduction in HIV replication, certain strains of the HIV virus managed to escape the attack (those with mutations around the CRISPR target site).2,3 The team have described this finding as only a ‘minor setback’, and they continue with their efforts to implement CRISPR in the ongoing fight against HIV.1

It is easy to see that, with some fine tuning, CRISPR (and subsequent technologies) could become a powerful weapon in the battle against viruses. Maybe, as an undergraduate, I should have hedged my bets when weighing my opinions against the totality of the future?


1. Pharmafile. HIV successfully overcomes CRISPR gene-editing technology. Available at: Accessed 6 May 16.

2. Wang Z, Pan Q, Gendron P, et al. CRISPR/Cas9-derived mutations both inhibit HIV-1 replication and accelerate viral escape. Cell Rep 2016; 15 (3): 481–489.

3. Wang G, Zhao N, Berkhout B, Das AT. CRISPR-Cas9 can inhibit HIV-1 replication but NHEJ repair facilitates virus escape. Mol Ther 2016; 24 (3): 522–526.

Christopher Edge

Christopher Edge  PhD

Scientific Consultant

May 2016

Combination of gene therapy and radiotherapy shows promise as a treatment for prostate cancer

A novel approach to the treatment of prostate cancer combines gene therapy and radiotherapy; the result is a synergistic effect on the anti-tumour immune response.1 An adenoviral vector, containing a herpes simplex thymidine kinase gene (ADV/HSV-tk), is used to render tumour cells vulnerable to valacyclovir, an anti-viral prodrug.1 Phosphorylation of valacyclovir mediates the effect of ADV/HSV-tk, which produces a cytotoxic nucleotide analogue, killing the tumour cells.1 Consequently, tumour-associated antigens are released, and an immune response is triggered.1 Administration of Intensity-modulated radiotherapy (IMRT) enhances the response of the immune system.1 This combination of therapies has been investigated as a treatment for prostate cancer, through a Phase II trial.

The trial enrolled 66 men with prostate cancer.1 They were treated according to the severity of their disease – Group A comprised patients with less severe disease; Group B comprised those with more severe disease.1

Gene therapy sessions of four ADV/HSV-tk intraprostatic injections, 14 days of oral valacyclovir, and IMRT were given twice to patients in Group A, and three times to those in Group B.1 Patients in Group B also received hormone therapy after the first injection.1 The primary endpoint was freedom from failure (FFF), where failure was defined as a rise by greater than or equal to 2 ng/ml above the nadir prostate-specific antigen (PSA).1,2 Five-year FFF rates of 94% and 91% were observed in Groups A and B, respectively.1 Overall survival, a secondary endpoint, was 97% for Group A and 94% for Group B.1

Further evaluation of this strategy is warranted and, indeed, a randomised trial is ongoing.1 However, the development of this and other immunotherapies represents a paradigm shift in cancer management.


1. Teh BS, Ishiyama H, Mai W-Y, et al. Long-term outcome of a Phase II trial using immunomodulatory in situ gene therapy in combination with intensity-modulated radiotherapy with or without hormonal therapy in the treatment of prostate cancer. J Radiat Oncol 2015; 4 (4): 377–386.

2. Roach M 3rd, Hanks G, Thames H Jr, et al. Defining biochemical failure following radiotherapy with or without hormonal therapy in men with clinically localized prostate cancer: recommendations of the RTOG-ASTRO Phoenix Consensus Conference. Int J Radiat Oncol Biol Phys 2006; 65 (4): 965–974.

Oliver Fleck

Oliver Fleck  BSc (Hons), MRes

Editorial Project Manager

Apr 2016

The latest trends in e-learning

At Cambridge Medical Communication we create e-learning courses on a wide range of medical and scientific topics. We start by thinking about the desired aims and outcomes of the e-learning, before developing a detailed specification of the structure and content. Medical writing, editing, and all the usual review loops and checks for accuracy and scientific integrity are undertaken. The final e-learning package can then be built using software such as Adobe Articulate.

We recognise the importance of keeping up to date with current ideas and technologies in the creation of e-learning materials. Consequently, this month, members of our team participated in the FutureLearn online course, ‘Designing e-learning for health’.

The course, run by the University of Nottingham’s Health E-Learning and Media (HELM) team, introduced the ASPIRE process as a framework for the creation of high-quality ‘reusable learning objects’. Throughout the course, we were reassured to find that the value of the core principles by which we work at Cambridge Medical Communication is reflected in other people’s experiences. For example, we are not the only ones who shy away from the use of jargon, and we also recognise the importance of interactivity – a key feature that we embrace in our e-learning courses, to engage the audience and to facilitate understanding of the programme content.

Ultimately, an effective e-learning programme is one that is designed with clear objectives, with learners at the forefront, and with a relentless insistence on accuracy. These drivers are at the heart of the e-learning programmes that we deliver at Cambridge Medical Communication.

Contact us to discuss your next e-learning project

Christopher Edge

Christopher Edge  PhD

Scientific Consultant

Mar 2016

Embracing the devil in the detail

Being meticulous about grammar could be considered indicative of an individual’s general attention to detail. Indeed, someone with a tendency to “scatter commas into a sentence with all the discrimination of a shotgun” may disregard the value of detail in other aspects of their work, whether or not it is related to writing.1 Here at Cambridge Medical Communication, we keep our shotguns at bay.

Over the last few weeks, I have been working on scientific posters that will be presented at the European Crohn’s and Colitis Organisation (ECCO) congress later this month. My part of the project involved reference checking the draft text, editing the content for accuracy and clarity, and working with designers to prepare an eye-catching layout.

As with all aspects of our work, these tasks require an impeccable attention to detail. Have the facts and data been checked and cross-checked? Do the posters effectively and unambiguously communicate the study findings, and the value of the work? Is the writing style consistent, and is the text grammatically correct? Do the layout, colour usage and line weights adhere to specified branding guidelines? I could go on…

We take great care to address these questions. Ultimately, we are communicating details that may inform the treatment of patients. It is therefore vital that the content is accurate, and that the messages are clear.

At Cambridge Medical Communication, we believe that our drive for accuracy provides the foundation for scientific integrity, which is fundamental to the clear and imaginative communication materials that we produce. This commitment to delivering excellence reflects the true passion that we hold for our work.


1. Wiens K. I won’t hire people who use poor grammar. Here’s why. 20 July 2012. Accessed 2 March 2016.

Liz Kelly

Liz Kelly  BSc (Hons)

Account Manager

Mar 2016

Should I aim for 7 hours of sleep per night?

Barely a week seems to go by without a story in the news about how much sleep we should be getting. While these articles tend to agree that too little sleep, or too much sleep, is bad for your health, they do not always agree on what amount of sleep is optimal. What’s more, the precise relationship between sleep and health tends to be skimmed over in the popular press. Does poor sleep cause poor health, does poor health cause poor sleep, or is there a hidden third factor that affects both our amount of sleep and our health?

A meta-analysis published this week has attempted to gather together all studies correlating night-time sleep duration with risk of all-cause mortality. Over one and a half million adult participants were included from sleep studies around the world.

A U-shaped relationship was found between sleep duration and risk of mortality, meaning that the further from 7 hours of sleep one goes, the greater the risk of premature death. At either end of the range, 4 hours of sleep was associated with a 7% increase in risk, and 11 hours with a 55% increase in risk.

The authors of the meta-analysis were careful to state that amount of sleep may be just a marker of health status, rather than being directly linked to mortality. For example, a person with depression may sleep too much, and may also have a premature death. However, looking at only those patients without chronic diseases, a similar U-shaped relationship was found. Thus, it appears that both long and short night-time sleep duration are independent predictors of all-cause mortality.

These results are potentially affected by publication bias, since studies with null results tend not to be published, and therefore were not included in the analysis. However, as the best evidence available, it appears that we really should be aiming for 7 hours of sleep per night in order to minimise the risk of premature death.


Shen X, Wu Y, Zhang D. Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Sci Rep 2016; 6: 21480.

Chris Watling

Chris Watling  PhD

Senior Medical Writer

Feb 2016

Let value drive your communications

What makes effective value communication?

Effective value communication is essential to gaining market access. At Cambridge Medical Communication, we believe that creating a successful ‘value story’, for any product, relies on finding its niche within the healthcare system. Building on this foundation, our medical writers can then communicate the true value of a product that resonates, not just with payers, but with the wider audience of healthcare professionals, policymakers, and patients/caregivers. In an era where value messaging is becoming more payer-focussed, this ‘holistic’ approach reflects the ‘real-world’ value of a product.


Our value communication experience

In 2015, we used our experience to help clients communicate the value of their products at different stages in the lifecycle.

For pre-launch products, we worked alongside our clients to help them develop their value strategy. These close collaborations and the insight gained were pivotal in our development of supporting communication materials – value propositions, value messages, value stories, global value dossiers, negotiation guides – that aligned with the value strategy, and which ensured that the value of the product was communicated, consistently, throughout.

For mature products, we analysed the current situation and identified changes relevant to the market, the therapeutic area, the product and competitors. Key evidence was used to advance value strategy and to bring communication materials up-to-date.



We deliver value

We pride ourselves on delivering genuine value to our clients; this is what they say.

“I have worked with a number of agencies over the years and my experience with Cambridge Medical is that they are the best agency that I have worked with. I am extremely pleased with the quality of the work they deliver, even under very challenging timelines. I find them to be extremely good ‘value for money’.”

“…thank you for wonderful collaboration and absolutely great work…”

“As always we do very much appreciate your great efforts”

We can help you

To find out how we can support all of your communication needs, please contact us.

Mary Read

Mary Read  PhD, MBA

Operations Director

Feb 2016

Medicine in an era of genetic control

The potential of CRISPR technology in drug development

At a fascinating and wide-ranging talk on the future of the pharmaceutical industry, Menelas Pangalos, Executive Vice President of AstraZeneca, discussed the exciting new technology, known as CRISPR (clustered regularly-interspaced short palindromic repeats). CRISPR is a ground-breaking technique that can edit a cell’s DNA, subtly, and with precision.

Genetic modification was once seen as the Holy Grail of medical science. The idea that inborn errors of metabolism could be corrected, and the person cured, was fantastic. However, early attempts at gene therapy using viral-vectors resulted in some horrific off-target effects. CRISPR, on the other hand, has the potential to be much more targeted.

In the more immediate future, CRISPR technology may be used to improve the efficiency and safety of drug development. Using CRISPR to generate cell lines expressing specific genetic defects, the merits of targeted pharmacological treatments can be tested in more pathologically relevant pre-clinical models, thereby reducing candidate drug attrition.

Gene therapy may become a viable medical tool in the future but, in the meantime, CRISPR opens wonderful new worlds of possibility for drug development.

Based on a talk entitled “The challenge and excitement of discovering new medicines” given by Menelas Pangalos, at Churchill College, Cambridge, for the Cambridge Society for the Application of Research.

Further reading:

Lander ES. The heroes of CRISPR. Cell 2016; 164 (1–2): 18–28.

Savić N, Schwank G. Advances in therapeutic CRISPR/Cas9 genome editing. Transl Res 2016; 168: 15–21.

Dominguez AA, Lim WA, Qi LS. Beyond editing: repurposing CRISPR-Cas9 for precision genome regulation and interrogation. Nat Rev Mol Cell Biol 2016; 17 (1): 5–15.

Christopher Edge

Christopher Edge  PhD

Scientific Consultant

Feb 2016

Using 3D-printing to help save lives

Mapping cerebral blood vessels with 3D-printing

Surgery to save a woman from a life-threatening brain aneurysm has been performed successfully, thanks to a 3D-printed map of her cerebral blood vessels.1,2

Brain scans had revealed that the blood vessels surrounding the aneurysm were severely twisted, meaning that, in this instance, the usual surgical approaches would not work.1,2 To help surgeons plan an optimal approach to treating the aneurysm, a 3D model of the blood vessels was printed using a polymer with similar biomechanical properties to human tissue.1,2 Surgeons were then able to perform the surgery successfully, saving the patient’s life.1,2

Doctor Siddiqui, who directed the treatment, said that relationships between hospitals and 3D-printing companies are, increasingly, being established to assist surgeons.1 Indeed, the use of 3D-printing in medicine is growing: research has demonstrated that 3D-printing could be used to create personalised medicine.3

Another blog, written by Oliver, on the use of 3D-printing in medicine can be found here.


1. Stratasys. Jacobs Institute Case Study. Accessed 7 January 2016.

2. BBC. 3D printing helps surgeons plan life-saving operation. Accessed
7 January 2016.

3. Yuang K, Pu S, Pu M. 3D printing for precision drug therapy: an initial proof of concept study. Poster presented at American Heart Association Scientific Sessions 2015. 8–10 November; Orlando, USA. A17443.

Oliver Fleck

Oliver Fleck  BSc (Hons), MRes

Editorial Project Manager

Feb 2016

A ‘natural’ coronary bypass?

Insights into the developing heart suggest new approaches in heart disease

Cardiovascular disease is the leading cause of death worldwide, and most commonly occurs when coronary arteries become blocked or narrowed due to a build-up of fat (atherosclerosis).1 This reduces oxygen supply to heart muscle, which can be fatal.

Current treatment focuses on redirecting blood flow using coronary artery bypass surgery, or by widening diseased arteries.1 However, current surgical approaches are limited by the risk of post-operative adverse cardiac events.2

Recent research conducted by Stanford University suggests that the adult heart could be stimulated to generate new coronary arteries.3 Using various labelling techniques on cells derived from an embryonic mouse heart, the team found that coronary artery cells developed from precursor cells called pericytes.3 Crucially, pericytes were also found to be present in the adult heart.3

Although in its early stages, this research highlights the possibility that adult pericytes could be stimulated to grow new arteries, diverting blood flow without the need for surgery. In essence, a natural, non-surgical coronary bypass.


1. World Health Organization. Cardiovascular diseases (CVDs). WHO 2015. Fact sheet 317. January 2015.

2. Diodato M, Chedrawy EG. Coronary artery bypass graft surgery: the past, present, and future of myocardial revascularisation. Surg Res Pract 2014; 2014: Article ID 726158.

3. Volz KS, Jacobs AH, Chen HI, et al. Pericytes are progenitors for coronary artery smooth muscle. eLife 2015; 4: e10036.

Liz Kelly

Liz Kelly  BSc (Hons)

Account Manager

Jan 2016

3D-printed medication

A new dimension for personalised medicine

3D-printing is an increasingly useful technique, and is now being considered for a variety of medical applications, from replacement organs1 to inexpensive prosthetics.2

A proof-of-concept study presented at the American Heart Association’s Scientific Sessions 2015 has suggested that 3D-printing may be the key to producing oral therapies tailored to a person’s medical and biological profile.3 Researchers have developed an algorithm that adjusts the concentration of an oral therapy based on patients’ biomedical data, including age, race, weight, and glomerular filtration rate.3 This algorithm computed patient-specific doses, and 3D-printing data for 80 pills across five doses were produced.3 Testing showed little variability between pills.3

Additional research is needed before personalised 3D-printed therapeutics become commercially available. However, the US FDA recently approved the first 3D-printed oral pill, as an adjunctive therapy in epilepsy.4 This new development indicates that the future of healthcare will have a more personal touch.


1. Murphy SV, Atala A. 3D bioprinting of tissues and organs. Nature Biotechnology 2014; 32 (8): 773–785.
2. Gretsch KF, Lather HD, Peddada KV, et al. Development of novel 3D-printed robotic prosthetic for transradial amputees. Prosthet Orthot Int 2015 [Epub].
3. Yuang K, Pu S, Pu M. 3D printing for precision drug therapy: an initial proof of concept study. Poster presented at American Heart Association Scientific Sessions 2015. 8–10 November; Orlando, USA. A17443.
4. Aprecia Pharmaceuticals. Press release: FDA approves the first 3D printed drug product. Blue Ash, Ohio: 2015.
/pdf/2015_08_03_Spritam_FDA_Approval_Press_Release.pdf. Accessed 20 November 2015.

Oliver Fleck

Oliver Fleck  BSc (Hons), MRes

Editorial Project Manager

Nov 2015