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COVID-19: gender inequalities during pandemics.

Gender inequalities are widened during pandemics, yet policies and public health efforts fail to reflect  this1. These inequalities are also evident in the COVID-19 pandemic where women carry higher  vulnerability to the physical, mental and economic impacts of this outbreaks2. Although data for COVID-19 show similar numbers of confirmed cases in men and women in most countries  which have provided data3, it should be noted that many  lower- and middle-income countries (LMICs) have no available COVID-19 sex-aggregated data and gender inequalities tend to be more prevalent within  these regions 4. However, data do suggest that men develop more severe cases of COVID-19, hence, have higher death rate5. Reasons for this could be due to higher rates of smoking in men compared to women6. Although death rates appear to be higher in men, the issues faced by women during this pandemic go beyond the primary health  impacts of COVID-19 and it is crucial that such secondary impacts, such as less publishing by women in STEM7 to sexual and reproductive issues, are investigated to produce  equitable interventions worldwide.

Women make up around 70% of the world’s global health and social sector workforce already putting them at an increased risk during pandemics8. However, women are also the primary caregivers and take on the role of providing health care within their families, particularly in low- and middle-income countries1. Such roles are often socially constructed in societies and cultures which view the role of women to be housemakers1. This places women in a position where social distancing measures are not an option, and many lack the appropriate resources and equipment to be able to safely care for their family during outbreaks. Women in developing countries are disproportionally affected due to limited education and literacy. Literacy rates are among the lowest in West and Central Africa and in South Asia9. Females making up 59% of the illiterate youth population worldwide9. Thus, health information is not comprehended or implemented by many women. Nevertheless, policies and guidelines introduce universal public health measures, such as social distancing and lockdown, which fail to recognise the unique needs of women and may negatively impact them if they are not implemented appropriately.

The COVID-19 pandemic has disrupted access to essential services such as sexual and reproductive health and gender-based violence services10. With lockdown in many countries, women are vulnerable to gender-based violence trapped at home in abusive relationships, which may be exacerbated by the increasing financial difficulties caused by job loss. Reports around the world show a surge in domestic violence rates. In South Africa, authorities state there were around 90,000 cases of violence against women during the first week of lockdown11. Countries like Lebanon, Malaysia, China and France are all witnessing a rise in the number of calls for help from homes. This, along with counselling and support systems being striped back to due resources being funnelled towards emergency care, may result in detrimental physical and mental health impacts on women.

Such abuse often includes sexual violence resulting in unplanned pregnancies bringing its own set of challenges. Pregnancy puts women at an increased risk to infections due to immune and anatomic alterations and more frequent hospital visits12. However, globally, women may fear going to antenatal clinics compromising their health during pregnancy and the health of their unborn baby. In rural areas of low- and middle-income countries antenatal care is commonly provided by non-governmental organisations. During pandemics, restrictions on travel and movement nationally prevent such organisations to provide effective care for pregnant women in rural areas. The Ebola epidemic in 2014-2016 saw a reduction of access to antenatal care by 50% and 18% in Liberia and Sierra Leone, respectively13,14. There was a 34% increase in the facility maternal mortality ratio in Sierra Leone13. If governments and global health institutions do not act fast and put in place appropriate services for women, the COVID-19 pandemic may see similar devastating results in maternal health. Further analysis is required on gender and maternal health impacts of COVID-19, with increased efforts to collect data and implement socially and culturally appropriate strategies for the most vulnerable in developing countries.

Want to read more? Click on the links below!
1. Overcoming the ‘tyranny of the urgent’: integrating gender into disease outbreak preparedness and response. 
2. COVID-19 requires gender-equal responses to save economies.
3. Sex, gender and COVID-19
4. Girls’ hidden penalty: analysis of gender inequality in child mortality with data from 195 countries.
5.  Gender and COVID-19: Advocacy brief.
6. Why are men more likely to get worse symptoms and die from COVID-19.
7. Are women publishing less during the pandemic? Here’s what the data say.
8. The COVID-19 pandemic could have huge knock-on effects on women’s health, says the UN.
9. UNICEF Literacy Data.
10. Women, girls, health workers must not be overlooked in global COVID-19 response.
 11. Global Lockdown resulting in ‘horrifying surge’ in domestic violence, U.N. warns. NPR.
12. Maternal health care management during the outbreak of coronavirus disease 2019 (COVID-19). doi: 10.1002/jmv.25787
13. Effects of the 2014 Ebola outbreak on antenatal care and delivery outcomes in Liberia: a nationwide analysis. doi: 5588/pha.16.0099
14. Women and babies are dying but not of Ebola: the effect of the Ebola virus epidemic ion the availability, uptake and outcomes of maternal and newborn health services in Sierra Leone. 

By Nafisa Insan
I am a PhD student in Population Health Sciences researching global maternal mental health. I am also on the committee for Students for Global Health Society. 

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Brewing is a science not an art?

Maybe you’re finding yourself making a lot more coffee now you’re stuck at home. Maybe you shelled out on an espresso machine. Maybe you’re just a coffee enthusiast. Brewers at Frisky Goat coffee have partnered with analytic companies from Switzerland and the UK, and researchers from Cambridge, Huddersfield, Limerick, Portsmouth, and the USA, to pin down some fundamental improvements to making expresso in a recent article in the journal Matter.


The article: Systematically Improving Espresso: Insights from Mathematical Modeling and Experiment, lays out their thesis for a perfect cup of Joe. The goal of the study was not to tell baristas what a good coffee tastes like, hopefully they knew that already. Rather, the team aimed to reduce waste by finding the conditions in which perfect coffees could be reliably made using less water or dry coffee. They targeted several important brewing parameters for their study, such as grinder setting (fineness of the coffee ground) and extraction yield , while considering the espresso machines water pressure and how this combines with coffee particle size to affect the flow rate through the grinds. They monitored extraction yield – the ratio of dry coffee going in, to concentration of coffee in the espresso shot – which typically ranges from 17% – 23%. Coffees over 23% tend to taste bitter, whereas those under 17% tend to taste sour. They recommend that baristas identify conditions where their coffees taste good to them – the “tasting-point” – and then use their recommendations to calculate a more material effective way of producing the same espresso. The article claims that espresso is the coffee style most vulnerable to fluctuations in brewing and beans that might affect quality. And argue that there is a clear need for guidance in this area from the scientific community.


Coffee grind setting was identified as being very important. Courser grinds create more variably sized (and shaped) particles of coffee, which in turn produce larger pore spaces for water to flow through. This increases flow rate but decreases the surface area of coffee the water is exposed to. The particulate size was identified as being bimodal – having two peaks. The smaller peak represented the fines produced from the point of fracture of the bean and a larger peak was the large coffee boulders which peaked around the largest size at which they could escape the burr grinder. Although more of the coffee ended up boulder-sized the majority of the flavour comes from the finer material. However, the article warns against grinding too fine and identifies that a minimum grind size for homogenous extraction exists, a grind below this results the machine becoming partially clogged and highly inefficient. Tamping pressure and machine pressure are also important parameters.


The final recommendations include locating the “tasty point” of the coffee and then identifying the best combo of grind setting and either added water, or grind volume needed to achieve an equivalent tasting, less wasteful coffee:      
“Thus, a barista is able to achieve highly reproducible espresso with the same [extraction yield] as the 20g espresso by reducing the coffee mass to 15 g and counter-intuitively grinding much coarser. This modification may result in very fast shots (<15s), a reduction in espresso concentration, and a different flavour profile.”

The article declares no conflicts of interest, though this is highly suspect as we could all benefit from knowing the secrets of a better brew.


Want to know more: Cameron et al., Matter 2, 1–18, 2020 Elsevier Inc.

By Justin Byrne | {react} Committee Member

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Uncategorised

Modelling COVID-19 – Imperial versus Oxford

With COVID-19 affecting all aspects of our lives, mathematical models have been thrust into the limelight as the main way decisions are being made regarding the crisis. Models are a way to simulate possible outcomes in the real world and are useful when key information about a phenomenon is unknown. They are based on a series of assumptions and these assumptions are what determine how accurate our model is. In the case of COVID-19, these can include how likely you are to get infected to how people interact with others and their movements. We cannot predict human behaviour with 100% accuracy, nor do we know all the parameters that affect this particular outbreak, so there will be some error in any model we create, however a level of simplification is necessary for efficient computation.

A simple example of an outbreak model is the SIR model, which stands for “susceptible”, “infected” or “recovered”. The model assumes that everyone starts off susceptible – which is a reasonable choice given the information we have about COVID-19 and if you come into contact with an infected person you have a certain chance of getting infected. Since this is a relatively simple model that we will use, it does not take into account any organised travel such as travelling to a central place in a community (shops, places of worship etc), but these things can be implemented into the model. This also does not consider mitigation methods such as self-isolation, in this model, infected individuals act as susceptible individuals would. After infection you become “removed” or commonly known as “recovered”, this category refers to those who can no longer pass on the disease whether they overcome the illness or die from it.

Firstly, people are assigned to the “susceptible”, “infected” or “recovered” groups. We usually have two parameters which we can change, β and γ. The maths behind the SIR model – without births and deaths independent of the infection – is described by a set of differential equations as follows:

*No new people enter the population. This would not be the case for a model where we allow for births and migration.

Below we have the results of a simple simulation as an example SIR model. Between the three simulations, we have kept γ constant and only changed the value of β. As you can see the last plot with the highest value of β = 5 has a very quick spike as a large proportion of the population get infected very quickly. If we decrease our parameter β = 2, we see that the infections decrease quite significantly and we have started to “flatten the curve”; you may think of this change as perhaps increased hygiene measures or self-isolation. In the first plot, we have decreased β further to β = 0.5 and we see that the infection does not really manage to get a hold, and, in fact, in most simulations, the infection does not really start, as now the R0 is below one. The main takeaway from this small simulation is how sensitive the model is to the small changes in parameters and why measures such as simple as better hygiene have been recommended.

The Imperial College London Model

The Imperial College London model was what was cited for the policy decisions regarding the UK’s response to COVID-19. The simulations looked at both UK and the US but here we will mainly consider the results surrounding the UK. The study looked at the effects of mitigation (slowing the growth of the epidemic) and suppression (reducing R0 < 1) methods on the number of cases in the country and whether it is possible to keep cases below ICU bed capacity.  The model was a modified simulation model used for pandemic flu planning but the crux of it is individuals being simulated in a similar manner to SIR. The model does, however, contain more variables such as moving people to isolation and specific movement behaviours to take into account the country’s specific challenges. For example, contact was made with individuals in households, schools and at work as well as the wider community, which was not accounted for in our simple SIR model. Clearly, if a member of your household gets infected you are more likely to also get infected than if an arbitrary person in your community is infected. The model also took into consideration demographical data such as age to determine the number of critical care beds that will be occupied. In the model, the incubation period was assumed at 5.1 days and infectiousness was assumed from 12 hours before the onset of symptoms but with reports of asymptomatic people spreading the virus, we do not know how accurate this assumption is at this moment. R0was placed at around 2.4, which is in line with estimates from Wuhan. The mitigation options that were considered in the study were case isolation in the home, voluntary home quarantine, the social distancing of those over 70 years of age, social distancing of the entire population and the closure of schools and universities. These variables all have their own assumptions on the decrease of contact due to them however an interesting assumption was that 25% of universities would remain open.

Mitigation strategy scenarios for GB from Impact of non-pharmaceutical interventions (NPIs) to reduce COVID- 19 mortality and healthcare demand. Image taken from: Ferguson et al., 2020, p. 8

What we can see from the simulation is that in all considered scenarios we exceed the critical care bed capacity significantly, a minimum peak demand of 8 times higher than capacity.

The best outcome is seen from a combination of school and university closure, case isolation and general social distancing, however it is predicted that when restrictions are lifted that the epidemic will reach a peak later in the year.

Suppression strategy scenarios for GB showing ICU bed requirements from Impact of non-pharmaceutical interventions (NPIs) to reduce COVID- 19 mortality and healthcare demand. Image taken from: Ferguson et al., 2020, p. 10

The Oxford Model

The Oxford model gained publicity after headlines suggested up to 50% of people may have been infected. This was not quite the full story and has been contested by other scientists. The yet to be peer-reviewed Oxford paper is less modelling what will possibly happen and more a set of hypothetical scenarios given what we know right now. What the team did was use an SIR model, with the usual assumptions, with some added assumptions that deaths due to the disease were well reported and only occurred in the vulnerable subset of the population. The model also assumed R0 (the basic reproduction number) as between 2.25 and 2.75, which is where other professional estimates lie, so this seems reasonable. The other parameter which changed was the proportion of the population at risk of serious disease, this just seems to range from 0.001% to 0.1% of the population arbitrarily. The model was fitted to the first 15 days after the second death recorded to avoid the effect of control strategies put in place. Then, given a number of deaths and a proportion of the population that was at risk of these deaths, reverse engineered the model to show how many people are likely to be currently infected. Where the headlines come in is that if the proportion of vulnerable people was 0.001% then over 50% of the population must have been infected by March 15th to give us the number of deaths that we have.

This has been controversial as over 1 in 8 people in the UK are over 70 with many of those having underlying health conditions so it is unlikely that only 0.001% of the population is at risk of dying from COVID-19. What we have to bear in mind is that, in the end, we do not know how many people have already been infected as we are not doing the antibody tests to determine that.

The team themselves tweeted, saying their “results are not forecasts,” and that the country doesn’t “know the current state of the epidemic because we do not know the parameter ρ,” (the proportion of the population that is vulnerable).

In the end, modelling allows us to see the effects of our strategies quickly, before we even implement them. It’s obvious, however, that even small changes to the parameters of these models, which represent simplified versions of reality, can have large effects on the outcomes. Therefore it’s critical that we continue to gather more real-world data, by monitoring the outcomes of other countries, or measuring the real spread of the virus in the population through testing. It’s vital too that we understand the statistics behind the headlines and maintain a healthy scepticism of sensationalist stories.

By Laura Etfer

Laura is a third-year Maths and Statistics student interested in medical statistics and infectious diseases. Outside of university, she helps to run a team of charity volunteers and is working on perfecting her lemon cake recipe.

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William Gan

Complement: Past, Present and Future?

by William Gan

(Image source: Pixabay)

The immune system, the body’s defense mechanism, is what protects us against pathogenic infections. In a nutshell, it is a complex network of specialized cells and proteins that interact with one another, generating unique signals to eliminate foreign pathogens. In the world of research, immunologists are the people that strive to unravel the secrets that lurk within the many different aspects of immunity.

One of these stories began in 1891, when Hans Ernst August Buchner discovered a blood serum factor responsible for killing bacteria, naming it ‘alexin’, later renamed as ‘complement’ by Paul Erlich at the turn of the 20th century. As part of the innate immune system, complement enhances the ability of antibodies and other immune cells to clear pathogens, also playing roles in inflammation and killing of microbes.

The complement system is simply a collection of small proteins, dispersed in blood plasma in their inactive forms like mines in a minefield, waiting to be triggered by immune complexes, foreign material, damaged cells, etc. All three activation pathways in this complex system lead to the generation of C3 convertase, a protease made up of other activated complement protein fragments, cleaving C3 to make C3a and C3b.

C3b covalently binds to pathogenic surfaces, marking a target to be eliminated by phagocytes. Most importantly, it associates with its ‘maker’ to form C5 convertase that drives the terminal pathway, ultimately creating a membrane attack complex that literally rips a hole on a targeted membrane! In this chaotic cascade of protein-protein interactions, regulatory proteins exist to inactivate complement and prevent ‘unwanted explosions’, much like a dedicated bomb defusal squad.

When cells go boom! (Image source: Pixabay)

But imagine if these ‘bombs’ could somehow go rogue, perhaps through mutations that result in an altered protein function, or autoantibodies against regulatory proteins that tip the balance of complement control. The involvement of complement is the reason behind complications such as age-related macular degeneration, atypical haemolytic uraemic syndrome (aHUS) and especially paroxysmal nocturnal haemoglobinuria (PNH), characterised by complement-mediated destruction of red blood cells!

A major breakthrough in complement therapeutics came in 2007, with the release of eculizumab (Soliris), a terminal pathway inhibitor that proved to be effective in treating aHUS and PNH. However, drawbacks such as high costs and risk of meningococcal infections presents limitations to treatment but paves the way for next generation drugs like ravalizumab. C1 esterase inhibitors ie. Cinryze, Berinert and Ruconest, function to completely switch off complement and are currently used to treat hereditary angioedema.

The therapeutic landscape is constantly changing with the many possible innovations to improve future therapies ie. alternate drug administration routes, physiological barrier crossings, etc. But in the end, complement-mediated diseases constantly beg the question of the level of inhibition required, raising much interest as an ideal therapeutic choice. By modulating and reducing complement activity rather than turning it off, homeostasis could be restored thus treating disease while simultaneously maintaining the role of complement in immune defense!

 

Inspired by my final year research project and this simple, easy-to-understand video on complement:
https://youtu.be/BSypUV6QUNw

Compendium of current complement therapeutics. (Newcastle researchers involved!) –
https://www.ncbi.nlm.nih.gov/pubmed/31446305

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Liza Olkhova

Unhealthy diet leads to a higher risk of death and disability than tobacco smoking

by Liza Olkhova

Image source: Pixabay

It is no longer surprising to hear that diet is just as important as lifestyle choices we make that determine our quality of life and longevity. With obesity levels rising globally, higher death rate and disability rise alongside this. An urgent need to raise awareness regarding imbalanced and damaging diet choices in children and adults is required in order to tackle this global problem and reduce its socio-economic impact.

More evidence comes to light to unequivocally support this notion from decades-long extensive study. A Lancet article published in April 2019 summarises a global study conducted worldwide in 195 countries from 1990 to 2017. The study assessed what risks are associated with lifestyle choices including suboptimal diet and tobacco smoking, alongside major diseases such as cancer.

It turns out that high blood pressure is the biggest killer with over 10 million deaths per year attributed to hypertonia. On the second place, however, is diet-related death with almost 9.5 million deaths per year. Surprisingly, tobacco smoking came third following diet.

Diet-related death is most commonly caused by cardiovascular disease, cancer and diabetes that have developed as a result of poor diet choices. For instance, high sodium content, consumption of red meat, processed food and sugar-packed beverages as well as low intake of health-boosting foods such as grains and fruits all attributed to the majority of death and disability cases.

How can we move away from this problem? Extreme changes to the diet in many countries have to be made on the national level, but of course, on the global level too. This includes education of children and public through campaigns, policy reforms to provide appropriate food labelling and price regulation, implementation of balanced diets in schools and universities, changes in taxation of various products (such as a recent ‘sugar tax’ in the UK on high-glucose drinks).

There is also evidence that substituting meat protein with plant-based protein source reduced the level of cardiovascular disease. Therefore, it could be worth letting people know about the healthy alternatives to their current diets instead of notifying them of what is unhealthy.

 

Read the Lancet article in full: https://doi.org/10.1016/S0140-6736(19)30041-8

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Annie Derry

Prioritising sleep is much more important than you think

by Annie Derry

Prioritising sleep is much more important than you think

A really good 7- or 8-hour sleep seems elusive for many people in the working world. A lack of sleep is sometimes even bragged about as if being ‘too busy’ to sleep equates to success. In our fast-paced environment with constant work, endless Netflix series to binge-watch, and phones that we never put down – it is easy to see why it’s harder than ever to get some shut-eye… or any peace for that matter.

In his recent TED Talk, “Sleep is your superpower” and his popular science book “Why We Sleep”, Professor Matthew Walker from University of California, Berkley, hones in on the benefits of having good ‘sleep hygiene’, and the sometimes-detrimental effects of lacking it.

Image source: Pixabay

Throughout the day our bodies work tirelessly at a molecular level to keep us moving, working, thinking, breathing – living. There is a constant stream of reactions going on that allow us to do this. A lot of these reactions produce chemical by-products along the way, which can be harmful if they are not removed. During the time that we sleep, one of the many activities going on in the brain is the removal of these waste products, in a sort of cleaning process that ‘washes’ the brain. Along with this, sleep is important for the consolidation of connections between neurons, allowing information from the previous day to be processed and stored.

What are the effects when these sleep tasks cannot be carried out?

Late nights; at your own risk:

1.Cognitive ability and memory function

It is fairly common knowledge that our higher cognitive processes are impeded on the day after a poor night’s sleep. Sleep deprivation has been found to impair attention and working memory, as well as long term memory and decision making. Prolonged wakefulness decreases alertness and ability to concentrate through the fact that it causes slowed responses and lapses – brief moments of inattentiveness. This is one of the reasons why driving a car or taking an exam with a severe lack of sleep is generally a very bad idea.

2. Long-term disease risk

In recent years there has been a growing link between a lack of sleep and the protein implicated in Alzheimer’s Disease, beta-amyloid. A build-up of this protein has been found in Alzheimer’s patients and, independently, in people reporting sleep disorders. It is thought that a lack of sleep contributes to a vicious cycle, where the brain is less able to wash out toxic proteins like beta-amyloid, as it usually does this during non-REM sleep. This could therefore contribute to the increased levels seen and lead to disease progression.

3. Higher risk of cardiovascular problems

There were some alarming results in a study which monitored the effects of losing an hour of sleep when the clocks go forward in the Spring (Daylight Saving Time, DST). Researchers found that the incidence of heart attacks reported by hospitals increased by 24% in the days following the time change. The opposite effect is seen when we gain one hour of sleep as the clocks go backwards in the Summer – the number of heart attacks reported decreases by 21%.

4. Immune function

Some of the most eye-catching statistics from Matthew Walker’s research were from his studies into the effect of sleep on our immune system. We have a number of cell types that all work together in order to fight off infection by recognising and killing foreign microorganisms like bacteria and viruses. Among the cells that are important in this, the natural killer cells (NK cells) are vital in the process eradicating threatening microbes. It was found that when sleep was reduced to 4 hours, even just for one night, there was a 75% reduction in NK cells in the blood of patients the next day. This indicates at least an association between our sleeping habits and how well we could fight off an infection, even a common cold, if exposed after a poor night of sleep.

 Don’t panic

Studies in to sleep do have alarming conclusions sometimes, but we cannot assume that sleep is the isolated causative variable contributing to the negative effects seen. As with almost all studies they must be taken as an indication, rather than a conclusive result. It also must be considered that some people may be genetically (or otherwise) predisposed to restless nights of sleep – we cannot assume that one person needs exactly the same number of hours to see out a healthy life.

That being said, it wouldn’t do any harm to try and pay more attention to the needs of our body and to allow ourselves to sleep as much as we really need to.

How to prioritise getting more/better quality sleep?

  • Reducing screen time at night
  • Reducing artificial lighting in the bedroom
  • Using apps like Headspace in order to practice mindfulness (and as a useful tool to get back to sleep if you wake up in the night)
  • Reading before bed to help to wind down
  • Going to sleep and waking up at a similar time every day

FYI… Matthew Walker received his PhD in Neurophysiology at Newcastle University in 1999.

This blog post was based on:

“Why We Sleep” – Matthew Walker

“Sleep is your superpower” – TED Talk by Matthew Walker

https://www.ted.com/talks/matt_walker_sleep_is_your_superpower?language=en

Sleep deprivation: Impact on cognitive performance – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/

 

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Liza Olkhova

How can the past experiences of your ancestors can alter the way you behave and your gene expression?

by Liza Olkhova

Photocredits: Pixabay

Epigenetics – the study of how gene expression is altered without altering the gene sequence itself – may hold the key to how gene expression can be modified in the offspring of parents exposed to environmental factors such as severe stress, without offspring being exposed to the same factors. This can revolutionise the way we assess and deliver children healthcare

Gene expression regulation depends on various chemical modifications of the genetic code without alteration of the code letters themselves (mutations). Various chemical modifications of genes can either facilitate or hinder gene expression by altering the amount of protein synthesised from a gene.

So the question is, can these gene chemical tags be passed down to the next generations?

It has been shown that they are wiped out in egg and sperm cells, however small non-coding RNA (sncRNA) may be present in sperm and may affect the regulation of RNA levels in zygote and the developing embryo. Moreover, sncRNA molecules can be modulated by stress.

How could the trans-generational changes induced by stress be modelled in vivo? To answer this question, various mouse models were developed, in which mice were subject to stress. Surprisingly, changes in the RNA dynamics were passed on not only to the first generation of offspring, but also to further generations. These gene expression changes were accompanied by behavioural abnormalities, for example, more risk taking behaviour. Rodent behaviour was tested using a specially designed maze that assesses rodent exploratory behaviour.

The next aim is to explore how changes seen in sncRNA molecules in rodent models could be compared to changes in human physiology. For instance, a study involving analysing blood samples of soldiers before and after deployment showed increased levels of different types of sncRNA molecules with some of them correlating to post-traumatic stress disorder (PTSD).

Currently, the science is at the dawn of fully understanding epigenetic changes within human genome and how these changes could potentially be transmitted through to further generations. We have yet to witness more detailed and advanced human studies in order to gain a clearer perspective.

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Emma Kampouraki

Biology: significantly more efficient than technology

by Emma Kampouraki

Photo credits: Biohm (https://www.biohm.co.uk)

For thousands of years, the only true driving force of life on Earth has been evolution. Among the population of every species, only those with the strongest characteristics survive, leading them to selectively pass on these characteristics to their ascendants, in an attempt to adapt better to the changing environment.

Humans, having evolved as a result of the same process, are now taking nature as an example for the construction of their own habitat. Recently, I had the opportunity to meet the Founder and Director of Innovation at Biohm in a Pint of Science event. Biohm could – and may – have been derived from the combination of bio and home; otherwise construction using natural materials. Mostly considered as waste nowadays, organic matter is well re-used in nature, through a process facilitated by decomposers; organisms that break down dead or decaying organisms, absorbing nutrients for their own growth and development. Could we do the same with our homes?

Ehab Sayed from Biohm says yes. The company collects organic waste and holistically sustainable natural materials (which sometimes include organisms, for example fungi) and turns them into building materials, which are satisfactorily durable and stable for a number of years before they are replaced (for free) with new ones. Durability is mainly down to the specific material or mixture of materials used, and stability depends on the particular structures constructed. Their novel and revolutionary construction system is called Triagomy and is basically the way they assemble the materials together which gives them great stability and the ability to be self-assembled. The team consists of researchers, engineers, architects and experts in circular economy and sustainability. The perfect blend for green buildings and the advent of the recycled construction industry.

If we can convince ourselves to think out of the box, use what we have effectively and respect the environment as a priority, we will ultimately facilitate and speed up evolution in our own habitat. Evolution will bring growth and better adaptation. More importantly, it will solve the problems of plastic pollution, waste management, toxic construction materials and deteriorating health in Earth’s ageing population.

 

Declaration: This is a non-sponsored blog, inspired by a novel idea for a circular economy and recycle, facilitated by scientific knowledge.

 

 

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Joanna Ciafone

The Pint of Science Festival is here!

by Joanna Ciafone

It’s that time of the year again! Next Monday the 20th of May, the Pint of Science festival kicks off, bringing three nights of fantastic speakers to venues around Newcastle. Local researchers will be sharing their cutting-edge work in a fun, accessible format. This year, you can sip on a pint and hear thought-provoking talks on diverse topics, including how to grow a ‘living’ city and understand how animals feel pain. Other exciting events feature scholars of consumer psychology, immunology, human sexual behaviour, archeology, artificial intelligence, and more!

Tickets for the 18 events are still available but going fast! Grab yourself a ticket and have a great night out next week!

Contributors from {react} will be cosying up to the bar next week so keep an eye out for blog posts on their experiences coming soon!

 

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Joseph Smith

Bursting the bubble

by Joseph Smith

In my last blog post I discussed the use of a gene-editing technology, termed CRISPR, and the controversy surrounding its potential for use in human studies. Today I will talk about an experimental gene therapy, distinct from CRISPR, that has been used to restore the immune systems of young children with X-linked severe combined immunodeficiency (SCID-X1).

SCID-X1 is caused by mutations in the gene that encodes interleukin 2 receptor common gamma chain (IL2RG), located on the X chromosome. As a result, these children are unable to produce two essential types of immune cell, T cells and natural-killer (NK) cells. Furthermore, functional T cells are required for the proper development of B cells and so these patients also possess a defective B cell population. For those that suffer from this disease the lack of a functional immune system means that infection with viruses or bacteria, that a healthy individual will often fight off, can actually be fatal. As a result, unless they are cured, these children are destined to a life of isolation.

The current gold standard in therapy entails undergoing a bone-marrow transplant from a matched donor. However, this is not always possible and so scientists around the world have sought an alternative therapy, for almost two decades. One potential treatment involves delivering a functional copy of the IL2RG gene into the children’s cells using a viral transporter, consequently restoring their immune system. Historically, trials utilising this method have had mixed results, leading to only partial restoration of immune function. Moreover, early trials led to some children developing leukaemia through unintentional activation of proto-oncogenes, highlighting the risks associated with the technology.

On the 17th April scientists published the results of a study wherein 8 infants with SCID-X1 were treated using the same approach; however, researchers utilised a different virus. This version is better at delivering IL2RG to slowly-dividing stem cells, which will eventually form the patients’ immune cells. Encouragingly, all of the children who underwent this treatment went on to produce the essential cell types required for a functional immune system, T cells, B cells, and NK cells. Furthermore, up to 2 years after treatment the children are showing no signs of leukaemia. The results of this study mean that these children, that would otherwise be unable to leave the protective confines of specialist hospital facilities, are now living normal and healthy lives.

This study represents a landmark improvement in the treatment of patients with SCID-X1. However, it is too early to tell whether this treatment is a permanent cure for the disease. It is not known how these children’s immune systems will function in the long-term. Is it possible that the effects will wear off? For now, the restoration of immune function alongside improved quality-of-life is an indisputable success for these patients.