Beehives deter crop-raiding elephants

By Cody Rogers

A critical analysis assignment based on a seminar given by Dr Lucy E King.

Crop-raiding by African elephants (Loxodonta Africana) poses a combination of social, economic (Figure 1), political and environmental problems. In Tanzania, 60% of farmers rated pests as their primary economic problem (Porter, 1976) and similarly in Zimbabwe, local farmers ranked pests first among 30 obstacles preventing an ideal lifestyle (Wunder, 1997) with farmers displaying ‘ingrained hostility’ towards elephants in particular (Barnes, 1996).

cody rogers picture 4

Figure 1. Direct costs of crop damage on farms by the worst five animals in Uganda (reproduced from Naughton, Rose and Treves, 1999).

The founding of the ivory trade has resulted in an exponential decrease in elephant populations throughout Africa; numbers fell from 129,570 individuals to 15,279 in Kenya between 1973 and 1989 (Douglas-Hamilton, 1989). Human-elephant conflict, due to human encroachment and elephant crop-raiding, has become a major issue and solutions are required in order to mitigate both the effects of crop-raiding and elephant persecution. It is thought that African elephants can be repelled from farms by the presence of African bees (Apis mellifera). Dr Lucy E King has been researching the repellent effects of bees in Kenya and whether or not the presence of bee hives reduces the number of incidents of crop-raiding by elephants. Dr. King, in her first pilot study (King et al. 2009), erected 9 traditional log beehives (Figure 2) along 90m of a trial farm’s northern boundary (Farm A), with Farm B designated as the control with no beehive fence present. Over the 6-week trial period both farmers were able to record crop-raiding events using data sheets. Farmer B gathered daily data on the number of elephants successfully raiding, raid time and the number of elephants that approached his crops and were successfully scared away by traditional deterrent tactics (noise, fire, dogs etc.).

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Figure 2. This diagram shows the construction and application of a traditional log beehive fence. Huts are spaced 6m apart allowing for an 8m space between each hive (reproduced from King et al. 2009).

To evaluate the success of the beehive fences two indicators were formulated; (i) crop-raiding events should be non-existent and (ii) fences should be easy and cheap to create and maintain. During the 6-week trial period the fences were raided on four occasions, causing damage that required minor repairs that could be taken from local resources at no cost, concluding that once erected a hive requires little maintenance. Each traditional log beehive costed approximately US$315 per 100m though multiple harvests of honey has the potential to recover the costs of the beehive fence. Over the study period, a total of 133 raids were recorded at the two focal farms. Farm A had seven successful raids by 38 elephants whereas Farm B experienced twenty-one raids by 166 elephants, including eight failed raid attempts that were prevented by the farmer himself. Additionally, by the end of the harvest season, Farmer B had almost no crops to harvest (with an estimated 90% of his harvest having being destroyed/eaten by raiding elephants), whereas Farmer A was able to harvest successfully.
The perception of the farmers towards the effectiveness of the beehive fences was also an important factor to consider during this study as support from the African community effects the success of such experiments. Attitudes towards the project were positive throughout the trial; group membership increased during the course of the study as word of the trial spread. Also, Farmer A extended (at his own means and cost) the beehive fence to cover a new entrance site after the study. Additionally, following the success of the study all attending members of the beekeeping group displayed interest in having a beehive fence erected around their own farm.

One of the main focusses in Dr. King’s research is the efficiency of the type of beehive used for the beehive fence, ever trying to improve upon previously used beehives. Hives need to be inexpensive to produce and repair, easy to maintain and produce good quality honey that generates a reasonable income. The traditional log beehive used in the pilot study of Dr. King’s work was a basic design, made of hollow logs of bark which are suspended horizontally for safety. These hives are surprisingly light and strong though the coating may split or peel off when the hive is agitated (Vollrath & Douglas-Hamilton, 2002). However, the income that this specific design of hive generates does not equate to the income that other hives produce as the combs cannot be removed unless they are cut which then cannot be returned undamaged to the hive. The Kenyan top-bar hive (KTBH) is a more improved and productive type of beehive (Figure 3) and studies have shown (King, Douglas-Hamilton & Vollrath, 2011) that maintenance is easier and the KTBH improves the quality of the honey harvested from the hives, attracting better prices at the market than honey produced from the traditional log hives. In a later study conducted by Dr. King, the KTBH were used effectively when compared to a traditional deterrent, a thorn bush barrier. A third type of hive, the langstroth hive, has also been developed though this hive costs more to produce, US$800-900 per 240m, and is less favoured.

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Figure 3. Kenyan top-bar hive design – the beehut houses are covered by a rainproof roof made from corrugated iron and is protected from the sun by a flat-thatched roof. Houses are connected by hanging wire which an approaching elephant will instinctively try to pass between, causing the hives to swing erratically often provoking and release the bees (reproduced from King, Douglas-Hamilton & Vollrath, 2011)

The main purpose of Dr. King’s research is finding an appropriate deterrent to stop elephants from crop-raiding farms that are inexpensive and easy to maintain. Previous work studying the effectiveness of deterrents such as elephant warning calls, electrical fencing and trip-alarm techniques have been analysed in various studies throughout the literature. O’Connell-Rodwell et al. (2000) tested the effectiveness of these deterrents and found that only electrical fencing reduced elephant damage at a community level, though the price of erecting the fence, which cost approximately US$5,900, outweighed saving calculations from preventing crop destruction, making this deterrent method unpopular.
More affordable farm-based elephant deterrents, using locally available materials, are becoming more popular due to their cost effectiveness. Graham & Ochieng (2008) trialled a number of these farm-based deterrents which were: (i) Chilli rope fences (ii) Cow bells (iii) Chilli smoke briquettes (iv) Noise makes and (v) Watchtowers and solar powered torches. The study found that though levels of crop raiding declined after the initial introduction of treatments, levels did not decline significantly when compared to control farms (Figure 4). Other studies have shown that chilli-based methods are ineffective, expensive and labour intensive (Karidozo & Osborn, 2014) and that they do not add any significant deterrent effect but do add unnecessary expense and create additional work (Hedges & Gunaryadi, 2009).

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Figure 4. A graph showing comparisons between the number of attempted and successful raids on different treatments (based on Karidozo & Osborn, 2014).

Another deterrent method using capsicum oleoresin spray was tested by Osborn (2002) and it was found that elephants were repelled from fields significantly faster than by traditional methods as the atomised cloud produces a severe irritating effect on any mucous membrane it comes into contact with (Nelson, Bidwell & Sillero-Zubiri, 2003). Osborn & Rasmussen (1995) also tested the spray on wild African elephants in Zimbabwe and all tests gave a positive repellent effect Furthermore, the spray remains effective for 20 minutes and costs US$18 per unit though there are issues with wind dispersal and accidental human exposure.

Recent developments in this area include research into the response African elephants have to undesirable noises such as the sound of disturbed bees. King, Douglas-Hamilton & Vollrath (2007) conducted an experiment investigating the effect that the sound of disturbed bees has on elephant behaviour. In a sample of 18 family subgroups of elephants, the majority reacted negatively – immediately walking/running away, when exposed to the buzz of disturbed bees. Of the 17 families, 16 (94%) left the tree under which they had been occupying within 18 seconds of the bee sound being played. It is possible that this deterrent method, using the sound of bees, can be a less expensive and labour intensive alternative to using live beehives. Additionally, studies looking in to the effectiveness of elephant distress calls as a deterrent have proved inconclusive, sometimes invoking aggression (O’Connell-Rodwell et al. 2000) and inducing habituation (Hoare, 2001; Osborn & Rasmussen, 1995). Furthermore, trip-wire alarms have also been experimented on and elephants are quick to habituate to the noise, though the alarms do serve as a useful warning system to farmers (O’Connell-Rodwell et al. 2000). As well as this, the sounds of domestic cattle have also been played near elephants to gauge reactions; breeding herds retreated though it showed little effect on all male groups (Kangwana, 1996; Hoare, 2001).

The positive effects seen throughout Dr. King studies using beehives suggest that they are a successful deterrent, though using a combination of other effective deterrents such as drum beating, guarding and dogs (Sitati, Walpole & Leader-Williams, 2006) could prove more effective. Though effectiveness as a deterrent is not affected by the type of beehive used, other factors such as maintenance and income generate are affected. Beehive design should be carefully considered in order to ensure that cost is kept to a minimum, maintenance is easy and simple and the income generated is high. Using chilli-based products to spread on interlinking wires (Osborn, 2002) may also be an option but its effectiveness is controversial (Karidozo & Osborn, 2014). Though Dr. King’s studies have only been conducted on small scales, the results produced from them have shown real promise. Conducting a larger scale study which uses both beehives and other cost efficient deterrent methods that have proven to be successful such as capsicum oleoresin spray, may provide an even more successful deterrent method and prevent future crop-raiding incidents by African elephants.

References

Barnes, R. (1996) The conflict between humans and elephants in the central African forests. Mammal Review, 26, 67-80.

Douglas-Hamilton, I. (1989) Overview of status and treads of the African elephants. The ivory trade and future of the African elephant. Oxford: Ivory Trade Review Group.

Graham, M. & Ochieng, T. (2008) Uptake and performance of farm-based measures for reducing crop raiding elephants Loxodonta Africana among smallholder farms in Laikipia District, Kenya. Oryx, 42, 76-82.

Hedges, S. & Gunaryadi, D. (2009) Reducing human-elephant conflict: do chillies help deter elephants from entering crop fields? Oryx, 44, 139-146.

Hoare, R. (2001) A decision to support system for managing human-elephant conflict situations in Africa. IUCN African Elephant Specialist Group Report, 1-110.

Kangwana, K. (1995) Human-elephant conflict: the challenges ahead. Pachyderm, 19, 11-14.

Karidozo, M. & Osborn, F. (2014) Community Based Conflict Mitigation Trials: Results of Field Tests of Chilli as an Elephant Deterrent. Journal of Biodiversity and Environmental Sciences, 3, 1-6.

King, L., Douglas-Hamilton, I. & Vollrath, F. (2007) African elephants run from the sound of disturbed bees. Current Biology, 17, 832-833.

King, L., Lawrence, A., Douglas-Hamilton, I. & Vollrath, F. (2009) Beehive fence deters crop-raiding elephants. African Journal of Ecology, 47, 131-137.

King, L., Douglas-Hamilton, I. & Vollrath, F. (2011) Beehive fences as effective deterrents for crop-raiding elephants: field trials in northern Kenya. African Journal of Ecology, 49, 431-439.

Naughton, L., Rose, R. & Treves, A. (1999) The social dimensions of human-elephant conflict in Africa: A literature review and case studies from Uganda and Cameroon. A Report to the African Elephant Specialist, Human-Elephant Task Conflict Task Force, 1-82.

Nelson, A., Bidwell, P. & Sillero-Zubiri, C. (2003) A review of humane elephant conflict management strategies. People and Wildlife Initiative. Wildlife Conservation Research Unit, Oxford University.

O’Connell-Rodwell, C., Rodwell, T., Rice, M. & Hart, L. (2000) Living with the modern conservation paradigm: can agricultural communities co-exist with elephants? A five-year case study in East Caprivi, Namibia. Biological Conservation, 93, 381-391.

Osborn, F. & Rasmussen, L. (1995) Evidence for the effectiveness of an oleo-capsicum aerosol as a repellent against elephants in Zimbabwe. Pachyderm, 20, 55-64.

Osborn, F. (2002) Capsicum Oleoresin as an Elephant Repellent: Field Trials in the Communal Lands of Zimbabwe. The Journal of Wildlife Management, 66, 674-677.

Porter, P. (1976) Agricultural Development and Agricultural Vermin in Tanzania. Geography of Economic Development. American Association for the Advancement of Science, Boston.

Sitati, N. & Walpole, M. (2006) Assessing farm-based measures for mitigating human-elephant conflict in Transmara District, Kenya. Oryx, 40, 279-286.

Vollrath, F. & Douglas-Hamilton, I. (2002) African bees to control African elephants. Naturwissenschaften, 89, 508-511.

Wunder, M. (1977) Of elephant and men: Crop destruction, CAMPFIRE, and wildlife management in the Zambezi valley, Zimbabwe, Natural Resources and Environment. University of Michigan.

 

Using bacteria for biocontrol: how Pseudomonas fluorescens defeats the common potato scab

By Steven Harris

Based on a seminar given by Dr Tanya Arseneault written in the style of a Letter to Nature summary paragraph.

Common scab is a potato disease caused by the bacterium Streptomyces scabies (1,2). Streptomyces scabies induces common scab disease by the production of extracellular esterases and the toxin thaxtomin A, which damages the surface of potatoes (Solanum tuberosum) (3,4). Common scab disease is ineffectively controlled currently, with hypotheses suggesting the potential for biocontrol measures to be implemented using Pseudomonas fluorescens (4). Yet the implementation of Pseudomonas fluorescens as a biocontrol has not occurred with the success rate of tuberous crop protection requiring further investigation. Here we show Pseudomonas fluorescens sp. LBUM223 produced the antibiotic phenazine-1-carboxylic acid (PCA) to kill Streptomyces scabies soil pathogens and reduce the virulence of Streptomyces scabies. We found that the production of PCA induced a reduction in thaxtomin A production in Streptomyces scabies, the toxin responsible for common scab disease in potatoes (5,6). Moreover Pseudomonas fluorescens LBUM223 was capable of promoting plant growth regardless of Streptomyces scabies presence. We conclude that decreases in the known virulence factor thaxtomin A enable a reduction in common scab symptoms, increasing potato yield5. Our results express the importance Pseudomonas fluorescens LBUM223 has in future biocontrol of common scab disease, illustrating the possible benefits to agriculture and the field of phytopathology Pseudomonas fluorescens LBUM223 possesses.

References

1. Han L, Dutilleul P, Prasher S, Beaulieu C, Smith D. Assessment of Common Scab-Inducing Pathogen Effects on Potato Underground Organs Via Computed Tomography Scanning. Phytopathology. 98(10), 1118-1125 (2008)

2. Takeuchi T, Sawada H, Tanaka F, Matsuda I. Phylogenetic Analysis of Streptomyces spp. Causing Potato Scab Based on 16S rRNA Sequences. International Journal of Systematic Bacteriology. 46(2), 476-479 (1996)

3.Kiss, Z., Dobránszki, J., Hudák, I., Birkó, Z., Vargha, G. and Biró, S. (2010). The possible role of factor C in common scab disease development. Acta Biologica Hungarica. 61(3), 322-332 (2010)

4. St-Onge R, Gadkar V, Arseneault T, Goyer C, Filion M. The ability of Pseudomonas sp. LBUM 223 to produce phenazine-1-carboxylic acid affects the growth of Streptomyces scabies, the expression of thaxtomin biosynthesis genes and the biological control potential against common scab of potato. FEMS Microbiology Ecology. 75(1), 173-183 (2010).

5. Arseneault T, Goyer C, Filion M. Pseudomonas fluorescens LBUM223 Increases Potato Yield and Reduces Common Scab Symptoms in the Field. Phytopathology. 105(10), 1311-1317 (2015)

6. Roquigny R, Arseneault T, Gadkar V, Novinscak A, Joly D, Filion M. Complete Genome Sequence of Biocontrol Strain Pseudomonas fluorescens LBUM223. Genome Announcements. 3(3), e00443-15 (2015)

Role of FTO in adipogenesis

By Amelia Crowley

A critical analysis piece based on a seminar given by Dr Dyan Sellayah.

Historically, obesity was once a sign of wealth that could only be afforded by the likes of iconic characters such as Henry VIII and Queen Victoria (Sugunendran 2012), whilst the rest of the population suffered from malnutrition (Eknoyan, 2006). However, obesity has taken a counter intuitive evolutionary path, which has led to its current worldwide epidemic. This is continuing to worsen; approximately two billion people worldwide are classified as overweight, and one third of this group are considered obese (Seidell and Halberstadt, 2015). This population, who experience poor diet related pathologies, cost the National Health Service (NHS) £5.8 billion a year in the UK alone, meaning obesity has undeniable detrimental impact on the economy (Scarborough et al., 2011).

Obesity occurs when individuals consume nutriment in excess of requirement, which results in increased adipogenesis, and subsequent weight gain. Adipogenesis results in the formation of white adipose tissue (WAT) and brown adipose tissue (BAT), which function in energy storage and wastage respectively. Adipogenesis can be divided into two categories: Developmental adipogenesis which occurs during early life and adult obesogenic adipogenesis, which occurs in adulthood in response to a high fat diet (HFD). The process begins with a precursor cell that originates from the embryonic reticulo-endothelial primitive organ for the formation of both WAT and BAT (Hausman, Campion and Martin, 1980). In developmental adipogenesis, the adipocyte progenitors form mature adipocytes by organogenesis resulting in most gonadal WAT (gWAT) being formed in early postnatal life. Following this, there is no role for developmental organogenesis in adulthood. Weight gain in adulthood is therefore exclusively mediated by obesogenic adipogenesis, where gWAT expands via hypertrophy. The hypertrophic period is short lived, subsides, and is replaced by adipogenesis (Gregoire, Smas and Sul, 1998).

Despite an early obvious link between a HFD and obesity, scientists began to speculate a potential link between genetics and weight gain. This was investigated and supported by various studies, including work done on twins in as early as 1990. This particular study analysed pairs of identical twins that were subjected to a consistent HFD and exercise plan. Weight fluctuation was then observed and the study concluded that there was at least three times more ‘intertwin’ variation when compared with ‘intratwin’ variation, indicating that genetic factors play a role in energy storage (Bouchard et al., 1990).

Based on such initial evidence for the role for genes in predisposing adipogenic potential, scientists began using animal models in order to locate the gene(s) responsible for this effect. Many studies were conducted that identified a specific gene, known as the fat mass and obesity associated (FTO) gene, which has been linked to obesity. A summary of these previous studies and their respective results can be seen in Table 1.

Table 1

Title of paper Author(s) and Year of publication Results from the study
A common variant in the FTO gene is associated with the body mass index and predisposes to childhood and adult obesity. (Frayling et al., 2007) Identification of the FTO gene as a type 2 diabetes susceptibility gene. Predisposes diabetes by increasing body mass index (BMI). Therefore provides initial evidence for the relationship between FTO and weight gain.
Variation in FTO contributes to childhood obesity and severe adult obesity. (Dina et al., 2007) Concluded that a mutation in the first intron of the FTO gene that enhanced its activity, resulted in early onset and higher incidence of obesity in both children and adults.
Genome-Wide Association Scan Shows Genetic Variants in the FTO Gene Are Associated with Obesity-Related Traits. (Scuteri et al., 2007) Various different single nucleotide polymorphisms (SNP) in the FTO gene resulted in increased BMI and weight.
Inactivation of the FTO gene protects from obesity. (Fischer et al., 2009) Demonstrates that knocking out the FTO gene results in growth retardation, a reduction in adipose tissue and a particularly lean body mass.
Overexpression of FTO leads to increased food intake and results in obesity. (Church et al., 2010) Demonstrates that overexpression of the FTO gene results in a dose dependent body and fat mass increase. First direct evidence for FTO overexpression causing obesity in mice.
Table 1. A summary of cherry picked studies and their results to demonstrate important previous research that, together, cemented the link between the FTO gene and obesity.

 

Following the studies in Table 1, as well as various others, the link between FTO gene expression and adipogenesis was evident. This is still relatively new research, and recently scientists have had varying ideas as to exactly how the FTO gene influences adipogenesis. A summary of papers investigating various mechanisms can be seen in Table 2.

Table 2

Title of paper Author(s) and Year of publication Ideas suggested by the study, as well as results
Loss-of-function mutation in the dioxygenase-encoding FTO gene causes severe growth retardation and multiple malformations. (Boissel et al., 2009) That the FTO gene must regulate body weight and fat mass because a mutation in R316Q (catalytic domain of FTO) resulted in growth retardation. Therefore the paper suggests that R316Q is what regulates adipogenesis.
A link between FTO, ghrelin, and impaired brain food-cue responsivity. (Karra et al., 2013) Suggests that the neural response to food is indirectly modulated by the FTO gene. The paper demonstrated that people who are homozygous for the ‘obesity-risk’ version of the FTO gene have disregulated levels of acyl-ghrelin, which usually modulates appetite via neural pathways.
Obesity-associated variants within FTO form long-range functional connections with IRX3. (Smemo et al., 2014) Idea that it is not solely the FTO gene that regulates adipogenesis. Paper proposes that a second gene, adjacent to FTO, named IRX3 also plays a role in its regulation. Results suggest that the FTO gene regulates IRX3, which both work in synergy to regulate adipogenesis.
Hypomorphism for RPGRIP1L, a ciliary vicinal to the FTO locus causes increased adiposity in mice. (Stratigopoulos et al., 2014) Following on from Smemo et al., 2014 (above), this paper suggest that yet another gene, named RPGRIP1L, is also involved in regulating adipogenesis. Results indicate that mice with decreased RPGRIP1L activity are more overweight and hyperphagic (large appetite). These results indicate that RPGRIP1L may be partly responsible, along with FTO and IRX3, in regulating adipogenesis.
FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis. (Zhao et al., 2014) FTO demethylates N6methyladenosine (m6A). Therefore, when this process occurs, as levels of FTO fall, levels of demethylated m6A increase. This increase then promotes an increase in the RNA binding ability of SRSF2. RUNX1T1 is a target for SRSF2, therefore increased activity of SRSF2 results in increased RUNX1T1 activity, which is why adipogenesis is stimulated when FTO is expressed. This paper therefore concludes that FTO potentially acts indirectly, via RUNX1T1 in order to stimulate adipogenesis (in vitro).
Table 2. A table indicating recent research just prior to that of Dr Dyan Sellayah. The table indicates the ideas proposed by various scientists on the mechanism of how the FTO gene is linked to obesity.

 

 

The ideas explored in Table 2 demonstrate how scientists were coming closer to elucidating the mechanism(s) as to how FTO gene expression influences adipogenesis. However, despite this, the process was still unclear. Dr Dyan Sellayah’s work in 2015 provides the latest novel mechanistic insight into how the FTO gene regulates adipogenesis in vivo. His work provides evidence that FTO influences adipogenesis by increasing the levels of the short isoform of the RUNX1T1 protein (RUNX1T1-S) in early adipogenesis. This increase in RUNX1T1-S stimulates various cyclins involved in regulation of the cell cycle, which subsequently function to increase the rate of mitotic clonal expansion (MCE). MCE is a process that occurs within the first 48 hours following adipogenic induction. This stimulation event by heightened levels of RUNX1T1-S results in the increased formation of mature adipocytes from preadipocytes and fibroblasts by adipogenesis, and therefore FTO expression indirectly leads to the stimulation of adipogenesis (Merkestein et al., 2015). His work also demonstrates that there is no role for FTO in adipogenesis following the MCE stage. Since Sellayah’s work demonstrates many other experiments, analyses and respective results, Table 3 has been created in order to compartmentalise his work. The eight experiments carried out in Sellayah’s paper together form a story that leads to the latest, newest research in the field.

Table 3

Experiments/Analyses conducted (with detail) Result from each experiment
1) Experiment demonstrating that FTO promotes adipogenesis in vitro. Mouse embryonic fibroblasts (MEF) were taken and the FTO gene was either knocked out (FTO-KO) or overexpressed (FTO-4). FTO-KO and FTO-4 were given IBMX, dexamethasone and insulin to induce adipogenesis. The ability to undergo adipogenesis was then assessed in each group. FTO-KO cells showed a reduced ability to undergo adipogenesis. This was also accompanied by a reduction in FABP4, C/EBPα, PPARgamma and PLIN1 mRNA levels (which, in normal physiology, have important roles within the process of adipogenesis). PLIN1 and FABP4 protein levels were also lower in FTO-KO cells when compared with a WT control.

 

FTO-4 cells from gWAT tissue showed higher triglyceride accumulation when compared with a WT control, and therefore demonstrated increased adipogenic potential. This was also accompanied by 70, 55 and 50 fold increases in PLIN1, PPARgamma and FABP4 mRNA levels respectively. Protein levels of FABP4 were elevated when compared with a WT control.

2) Experiment disproving the work done by Stratigopoulos et al., 2014 (see Table 2). FTO, IRX3 and RPGRIP1L mRNA expression was measured in WT gWAT cells and MEF’s (FTO-KO and FTO-4). FTO expression was higher than both PRGRIP1L and IRX3 expression in WT gWAT and MEF’s.

 

Significant differences in expression of IRX3 and RPFRIP1L were not observed in FTO-KO MEF’s, FTO-4 MEF’s or FTO-4 gWAT. This demonstrates that differences in adipogenic potential observed for FTO-KO and FTO-4 are independent of both RPGRIP1L and IRX3.

3) Experiment confirming the role of FTO in adipogenesis. This was achieved by assessing the rates of proliferation after applying the induction cocktail and waiting 24 hours. The proliferation rates of FTO-KO and FTO-4 MEF’s were each compared with their respective controls. When compared with a control, FTO-KO MEF’s showed a decreased rate of proliferation.

 

When compared with a control, FTO-4 MEF’s showed an increased rate of proliferation.

4) Experiment demonstrating that FTO regulates MCE in a demethylation-dependent manner. Ie demonstrates that FTO only plays a role in adipogenesis during MCE, and not at any other later point in the process. The FTO gene was knocked down in FTO-4 MEF’s before adipogenic induction, which was then compared with FTO knockdown 48h after induction of adipogenesis.   FTO knock down in FTO-4 MEF’s before the induction of adipogenesis resulted in reduced expression of FABP4, C/EBPα and PPARgamma, when compared with expression before the knockdown event.

 

On the other hand, knocking down the FTO gene 48h after adipogenic induction had no effect on the expression of FABP4, C/EBPα or PPARgamma.

 

These results indicate that FTO solely has a role in initial stages of adipogenesis, specifically during MCE which occurs within the first 48 hours.   

5) Experiment that supported the role of FTO in MCE (above). The expression of CCND3 and CCND1 were assessed, as these two genes are involved cell cycle progression, and their levels are therefore increased following adipogenic induction. FTO-4 MEF’s were transfected and therefore activity was downregulated. This was compared with a FTO-4 MEF’s that were transfected with a control – ie were not altered.

The cyclin gene expression was also assessed in WT MEF’s that were overexpressing FTO.

Transfected FTO-4 MEF’s showed significant downregulation in CCND3 and CCND1 expression at 40h and 24h after adipogenic induction respectively. The control did not demonstrate the same pattern of downregulation.

 

WT MEF’s that were overexpressing FTO demonstrated increased CCND1 expression 24 hours after induction of adipogenesis.

 

This demonstrates that FTO potentially increases the activity of genes that are responsible for regulating cell cycle progression and therefore more FTO expression results in faster cell cycle progression.

6) Experiment assessing whether adipocyte proliferation is definitely dependent on the demethylase activity of FTO, which was an idea suggested by Zhao et al., 2014 (see Table 2). FTO-KO cells were either transfected with WT FTO (restoration of FTO function) or were transfected with FTO that was catalytically inactive. The proliferation rates of the two subgroups were compared. Only the FTO-KO MEF’s that received WT FTO, and therefore had restored function, showed increased rates of proliferation. Transfection with FTO that was catalytically inactive resulted in no increase in cell proliferation.

 

This experiment demonstrates that FTO only has a role in MCE if its demethylation activity remains intact.

7) Zhao et al., 2014 previously suggested that FTO influences adipogenesis by stimulating the production of the short isoform of RUNX1T1, which functions to stimulate adipogenesis. Therefore Merkstein et al, 2015 evaluated this claim. This involved measuring the expression of both the long (L) and short (S) isoforms of RUNX1T1 in FTO-KO, FTO-4 MEF’s and standard MEF’s.     In standard MEF’s, L isoform expression was much greater than S isoform expression. A decrease in the S isoform was observed in FTO-KO MEF’s, yet an increase in S isoform levels were observed in FTO-4 MEF’s.

Levels of L isoform expression were also decreased in FTO-KO MEF’s, but this was a smaller decrease than that of the S isoform. In FTO-4 MEF’s, the L isoform levels did not differ when expression was compared with a control.

 

This experiment provides clear evidence supporting there is a greater role for the RUNX1T1 S isoform in early adipogenesis when compared with the L isoform, and that FTO regulates the expression of the S isoform of RUNX1T1.

8) Experiment aimed to investigate whether increased FTO expression results in a fatter phenotype. Weight gain was measured in mice with an FTO-4 genotype and in WT mice with functioning FTO after both being subjected to the same standard chow diet after the same amount of time.

 

The same experiment was conducted again, but the standard chow diet was replaced with a high fat diet (HFD).

Mice with the FTO-4 genotype showed increased weight gain when compared to WT mice when both exposed to a normal chow diet.

 

The same results were found when both subgroups were subjected to a HFD, but the weight gain was more extreme.

 

Lean mass remained constant, with only fat mass being responsible for the weight gain observed. Results conclude that increased FTO expression does result in a fatter phenotype in mice.

Table 3. Experiments/Analyses conducted by Dr Dyan Sellayah and his team from the paper entitled FTO influences adipogenesis by regulating mitotic clonal expansion, by Merkestein et al., 2015. These experiments collectively demonstrate that FTO influences adipogenesis, as well as the exact mechanisms involved.

 

Each experiment conducted by Sellayah and his team (Table 3) necessitated using chemicals in order to induce adipogenesis. The chemical cocktail selected included dexamethasone, insulin and IBMX. Although this chemical cocktail is successful in inducing adipogenesis, it is known to produce adipocytes that are smaller and more immature when compared with the wild type equivalent (Pantoja, Huff and Yamamoto, 2008), and are therefore not representative of human adipocytes. A recent study conducted in September 2015 has discovered a brand new cocktail capable of inducing adipogenesis that includes rosiglitazone and dexamethasone (Contador et al., 2015). These chemicals induce the production of fully functional, regular sized adipocytes that are therefore much more representative of conditions within the human body. Unfortunately for Sellayah and his team, literature stating the preference for the new chemical cocktail was released after the publication of his work. Therefore, in order to improve the work done by Sellayah, the same experiments should all be conducted again, but the standard induction cocktail should be replaced with rosiglitazone and dexamethasone. This will hopefully verify that FTO affects fully functional adipocytes using the same mechanism as seen in smaller, immature adipocytes.

The C57BL/6 murine model is susceptible to obesity induced by HFD, and therefore represented a sensible model organism for not only Sellayah’s work in Merkstein et al, but also other studies investigating genes involved in adipogenic regulation such as the study by Stratigopoulos et al in 2014 (Details can be found in Table 2). Seven substrains of the C57BL/6 strain exist, and the particular substrain selected by Sellayah is referred to as the C57BL/6J substrain. Although various C57BL/6 substrains are used in adipogenic research, literature has noted that scientists often select their substrain without realising the fundamental differences that exist between them (Mekada et al., 2009). The C57BL/6J substrain used by Sellayah naturally possesses a five exon deletion in the nicotinamide nucleotide transhydrogenase (Nnt) gene (Huang, 2006). This results in a reduction in insulin secretion and therefore a mouse that is glucose intolerant (Freeman et al., 2006). This mutation therefore means that the mice will naturally gain less weight than standard mice given the same diet (Matsui et al., 2010). Although this does not present an issue for experiments one to seven (Table 3), experiment eight in Table 2 aimed to investigate how much more weight was gained in mice overexpressing FTO compared with a WT control when exposed to varying diets. However, seeing as members of the substrain are intolerant to glucose, and subsequently unable to gain weight in a normal way, the weight gain observed by Sellayah may be dramatically underestimated. In order to improve experiment eight, a mouse strain should be used that does not naturally possess a mutation in the Nnt gene. This would allow observation of weight fluctuation that is due to the FTO gene only, without considering the fluctuation caused by glucose intolerance.

The work done by Sellayah and his team has provided the most recent information on how the FTO gene influences adipogenesis, which in itself is exciting research. However, every single conclusion documented in his paper is based on the study of female mice only. This means the novel conclusions ascertained by the study are therefore ambiguous as the FTO gene may not influence adipogenesis in the same way in male mice. In order to unequivocally determine how FTO effects the whole population of mice, experiments one through to eight must be repeated using male mice to see if the results run parallel.

Dr Dyan Sellayah and his team have claimed to provide firm evidence for novel mechanistic insight into how the FTO gene influences adipogenesis. The in vitro work was based on small, immature adipocytes; while in vivo studies were based solely on female mice of a murine strain that already possess other genetic mutations that may alter the role of FTO in adipogenesis. Since this is the case, I believe it is an invalid claim to suggest that the results presented in this paper are representative of a whole population of standard mice, let alone applicable to a human population. Despite this, I do believe that the work has provided excellent foundation for further work to support research into whether this is also the case in male mice, and therefore is potentially the mechanism that occurs during human adipogenesis.

 

References

Boissel, S., Reish, O., Proulx, K., Kawagoe-Takaki, H., Sedgwick, B., Yeo, G., Meyre, D., Golzio, C., Molinari, F., Kadhom, N., Etchevers, H., Saudek, V., Farooqi, I., Froguel, P., Lindahl, T., O’Rahilly, S., Munnich, A. and Colleaux, L. (2009). Loss-of-Function Mutation in the Dioxygenase-Encoding FTO Gene Causes Severe Growth Retardation and Multiple Malformations. The American Journal of Human Genetics, 85(1), pp.106-111.

Bouchard, C., Tremblay, A., Després, J., Nadeau, A., Lupien, P., Thériault, G., Dussault, J., Moorjani, S., Pinault, S. and Fournier, G. (1990). The Response to Long-Term Overfeeding in Identical Twins. New England Journal of Medicine, 322(21), pp.1477-1482.

Church, C., Moir, L., McMurray, F., Girard, C., Banks, G., Teboul, L., Wells, S., Brüning, J., Nolan, P., Ashcroft, F. and Cox, R. (2010). Overexpression of Fto leads to increased food intake and results in obesity. Nature Genetics, 42(12), pp.1086-1092.

Contador, D., Ezquer, F., Espinosa, M., Arango-Rodriguez, M., Puebla, C., Sobrevia, L. and Conget, P. (2015). Featured Article: Dexamethasone and rosiglitazone are sufficient and necessary for producing functional adipocytes from mesenchymal stem cells. Experimental Biology and Medicine, 240(9), pp.1235-1246.

Dina, C., Meyre, D., Gallina, S., Durand, E., Körner, A., Jacobson, P., Carlsson, L., Kiess, W., Vatin, V., Lecoeur, C., Delplanque, J., Vaillant, E., Pattou, F., Ruiz, J., Weill, J., Levy-Marchal, C., Horber, F., Potoczna, N., Hercberg, S., Le Stunff, C., Bougnères, P., Kovacs, P., Marre, M., Balkau, B., Cauchi, S., Chèvre, J. and Froguel, P. (2007). Variation in FTO contributes to childhood obesity and severe adult obesity. Nature Genetics, 39(6), pp.724-726.

Eknoyan, G. (2006). A History of Obesity, or How What Was Good Became Ugly and Then Bad. Advances in Chronic Kidney Disease, 13(4), pp.421-427.

Frayling, T., Timpson, N., Weedon, M., Zeggini, E., Freathy, R., Lindgren, C., Perry, J., Elliott, K., Lango, H., Rayner, N., Shields, B., Harries, L., Barrett, J., Ellard, S., Groves, C., Knight, B., Patch, A., Ness, A., Ebrahim, S., Lawlor, D., Ring, S., Ben-Shlomo, Y., Jarvelin, M., Sovio, U., Bennett, A., Melzer, D., Ferrucci, L., Loos, R., Barroso, I., Wareham, N., Karpe, F., Owen, K., Cardon, L., Walker, M., Hitman, G., Palmer, C., Doney, A., Morris, A., Smith, G., Hattersley, A. and McCarthy, M. (2007). A Common Variant in the FTO Gene Is Associated with Body Mass Index and Predisposes to Childhood and Adult Obesity. Science, 316(5826), pp.889-894.

Freeman, H., Hugill, A., Dear, N., Ashcroft, F. and Cox, R. (2006). Deletion of Nicotinamide Nucleotide Transhydrogenase: A New Quantitive Trait Locus Accounting for Glucose Intolerance in C57BL/6J Mice. Diabetes, 55(7), pp.2153-2156.

Gregoire, F., Smas, C. and Sul, H. (1998). Understanding adipocyte differentiation. Physiological reviews, 73(3), pp.783-809.

Hausman, G., Campion, D. and Martin, R. (1980). Search for the adipocyte precursor cell and factors that promote its differentiation. Journal of Lipid Research, 21.

Huang, T. (2006). Genetic modifiers of the phenotype of mice deficient in mitochondrial superoxide dismutase. Human Molecular Genetics, 15(7), pp.1187-1194.

Karra, E., O’Daly, O., Choudhury, A., Yousseif, A., Millership, S., Neary, M., Scott, W., Chandarana, K., Manning, S., Hess, M., Iwakura, H., Akamizu, T., Millet, Q., Gelegen, C., Drew, M., Rahman, S., Emmanuel, J., Williams, S., Rüther, U., Brüning, J., Withers, D., Zelaya, F. and Batterham, R. (2013). A link between FTO, ghrelin, and impaired brain food-cue responsivity. Journal of Clinical Investigation, 123(8), pp.3539-3551.

Matsui, Y., Hirasawa, Y., Sugiura, T., Toyoshi, T., Kyuki, K. and Ito, M. (2010). Metformin Reduces Body Weight Gain and Improves Glucose Intolerance in High-Fat Diet-Fed C57BL/6J Mice. Biol. Pharm. Bull., 33(6), pp.963-970.

Mekada, K., Abe, K., Murakami, A., Nakamura, S., Nakata, H., Moriwaki, K., Obata, Y. And Yoskiki, A. (2009) Genetic Differences among C57BL/6 Substrains. Experimental Animals., 58(2), pp.141-149.

Matsui, Y., Hirasawa, Y., Sugiura, T., Toyoshi, T., Kyuki, K. and Ito, M. (2010). Metformin Reduces Body Weight Gain and Improves Glucose Intolerance in High-Fat Diet-Fed C57BL/6J Mice. Biological and Pharmaceutical Bulletin., 33(6), pp.963-970.

Merkestein, M., Laber, S., McMurray, F., Andrew, D., Sachse, G., Sanderson, J., Li, M., Usher, S., Sellayah, D., Ashcroft, F. and Cox, R. (2015). FTO influences adipogenesis by regulating mitotic clonal expansion. Nature Communications, 6, p.6792.

Pantoja, C., Huff, J. and Yamamoto, K. (2008). Glucocorticoid Signaling Defines a Novel Commitment State during Adipogenesis In Vitro. Molecular Biology of the Cell, 19(10), pp.4032-4041.

Scarborough, P., Bhatnagar, P., Wickramasinghe, K., Allender, S., Foster, C. and Rayner, M. (2011). The economic burden of ill health due to diet, physical inactivity, smoking, alcohol and obesity in the UK: an update to 2006-07 NHS costs. Journal of Public Health, 33(4), pp.527-535.

Scuteri, A., Sanna, S., Chen, W., Uda, M., Albai, G., Strait, J., Najjar, S., Nagaraja, R., Orrú, M., Usala, G., Dei, M., Lai, S., Maschio, A., Busonero, F., Mulas, A., Ehret, G., Fink, A., Weder, A., Cooper, R., Galan, P., Chakravarti, A., Schlessinger, D., Cao, A., Lakatta, E. and Abecasis, G. (2007). Genome-Wide Association Scan Shows Genetic Variants in the FTO Gene Are Associated with Obesity-Related Traits. PLoS Genetics, 3(7), p.e115.

Seidell, J. and Halberstadt, J. (2015). The Global Burden of Obesity and the Challenges of Prevention. Annals of Nutrition and Metabolism, 66(2), pp.7-12.

Smemo, S., Tena, J., Kim, K., Gamazon, E., Sakabe, N., Gómez-Marín, C., Aneas, I., Credidio, F., Sobreira, D., Wasserman, N., Lee, J., Puviindran, V., Tam, D., Shen, M., Son, J., Vakili, N., Sung, H., Naranjo, S., Acemel, R., Manzanares, M., Nagy, A., Cox, N., Hui, C., Gomez-Skarmeta, J. and Nóbrega, M. (2014). Obesity-associated variants within FTO form long-range functional connections with IRX3. Nature, 507(7492), pp.371-375.

Stratigopoulos, G., Martin Carli, J., O’Day, D., Wang, L., LeDuc, C., Lanzano, P., Chung, W., Rosenbaum, M., Egli, D., Doherty, D. and Leibel, R. (2014). Hypomorphism for RPGRIP1L, a Ciliary Gene Vicinal to the FTO Locus, Causes Increased Adiposity in Mice. Cell Metabolism, 19(5), pp.767-779.

Sugunendran, S 2012, Make a Fortune in the Wellness Industry: How to Initiate, Participate and Profit from the Trillion Dollar Wellness Healthcare Revolution, XLIBRIS.

Zhao, X., Yang, Y., Sun, B., Shi, Y., Yang, X., Xiao, W., Hao, Y., Ping, X., Chen, Y., Wang, W., Jin, K., Wang, X., Huang, C., Fu, Y., Ge, X., Song, S., Jeong, H., Yanagisawa, H., Niu, Y., Jia, G., Wu, W., Tong, W., Okamoto, A., He, C., Danielsen, J., Wang, X. and Yang, Y. (2014). FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis. Cell Research, 24(12), pp.1403-1419.

Predicting invasive species impacts in a changing world

By Katy Ratcliffe

Based on a seminar given by Professor Jaimie Dick written in the style of a Letter to Nature summary paragraph.

In ecology, a functional response is defined as the intake rate of a consumer as a function of food density (7). The ecological process of predation involves several, basic components that underlie all further research (2). Analysing the complexity of predator-prey relationships requires models that provide conclusive findings (5) and have been previously tested (4). Here is shown how assessment of predatory functional responses plays important roles in predator-prey dynamics and how further interactions such as parasitism and higher-order predation, have the potential to modify predator–prey interactions and the ability to predict comparative functional responses (6). Experimentation found that invasive amphipods had a higher predatory impact than native amphipods. Parasitism was shown to influence predation and had the potential to both reduce the impact of the invasive species and increase the impact of the native species. Consumption of prey was similar for both predators and was associated with increasing prey densities (6) in context, this study further supports the application of comparative functional responses in order to predict and assess the impacts of invasive species (3). Continuing to determine the functional responses of predators throughout their life may further improve our understanding and prediction of their impacts in the community (1). The introduction of a more than two species dynamic can also provide a powerful tool when advancing our understanding of how predation and parasitism influence community composition (3).

References

1. Alexandera, M.E., Dick, J.T.A. & O’Connora, N.E. Born to kill: Predatory functional responses of the littoral amphipod Echinogammarus marinus Leach throughout its life history. Journal of Experimental Marine Biology and Ecology. 439, 92 – 99 (2013)

2. Cheng, T.C. Current Topics in Comparitive Pathobiology, Volume 2. Academic Press Incorporated, New York (1973)

3. Gange, A.C. & Brown, V.K. Multitrophic Interactions in Terrestrial Systems. Cambridge University Press, New York. (2009)

4. Holling, C.S. The Analysis of Complex Population Processes. The Canadian Entomologist. 96, 335-347 (1964)

5. Holling, C.S. The Functional Response of Predators to Prey Density and its Role in Mimicry and Population Regulation. Memoirs of the Entomological Society of Canada. 97, 5-60 (1965)

6. Paterson, R.A., Dick, J.T.A., Pritchard D.W., Ennis, M., Hatcher, M.J. & Dunn, A.M. Predicting invasive species impacts: a community module functional response approach reveals context dependencies. Journal of Animal Ecology. 84, 453-463 (2014)

7. Walley, G.S. Review of Edmund M. Walker. The Odonata of Canada and Alaska. The Canadian Entomologist. 91, 291-292 (1959)

Why do epidemics matter?

By Jennifer Maskell

Based on a seminar given by Professor Jeremy Farrar entitled Why Epidemics Matter.

It is inevitable that emerging diseases and epidemics will continue to impact human populations, more so now than previously because as populations grow, native environments are being increasingly penetrated. Epidemiology is a vital for public health action in order to promote and protect the health of the humans which is founded on scientific study, casual reasoning and “practical common sense” (Bisen, 2013). Epidemiology requires the combination of science and public health practice to tests hypotheses related to the occurrence and prevention of illness and death in order to improve the health of populations throughout the world (Bisen, 2013).

Jeremy Farrar, Professor of Tropical Medicine and Global Health at the University of Oxford and the director of the Wellcome Trust, has devoted much of his life to epidemiology and is known as being an “outstanding clinical scientist” whom is “one of the world’s leading figures in the field of infectious disease” (Wellcome Trust, 2013). Professor Farrar presented the ‘Lowry Lecture’ which focussed on epidemics and their importance. He also addressed various infectious diseases and the problems society and science face with diagnosis, treatment and vaccine development, and discussed why quick response to these diseases is so important.

Professor Farrar first introduced the problems lower income countries face (combination of malaria, tuberculosis and other emerging pathogens, as well as drug resistance) with their poor health and research systems. The aspects of drug resistance was also discussed as being the “largest struggle for the 21st century”, as well as environmental and climate changes affecting the vectors for diseases, and massive urbanisation as being the drive for the way in which epidemics occur. The main focus of the seminar was the comparison of the influenza outbreaks in 1918 and 2009 with the Ebola outbreak in 2014. Professor Farrar claimed the epidemics of influenza were due to poor surveillance of the disease, whereas the Ebola epidemic occurred due to the lack of the response to the disease and to the poor communication. The lack and unnecessarily slow response meant that hospitals in the affected areas were not adequately equipped for treatments for 4-5 months, and within 6 months the rural epidemic became a worldwide epidemic. Even though Ebola had a large impact on health systems and on society and their willingness to trust the government, vaccine trials were accelerated to 6 months (instead of a few years) and luck from these successful trials meant a vaccine could be produced. It is clear to see the importance these accelerated vaccine trials had for the decrease in the spread of the disease. Professor Farrar explained that it is normally the human subject research that limits the speed of a response because the research has become so complicated that scientists are frightened of doing it. A process of human research can take an average of 611 days to be granted and it is predicted that these 611 days can allow for 14 epidemics to arise before the human research process even begins. Professor Farrar concluded that priority for human testing is vital, and it is these changes to such things as human vaccine trials that can help to prepare health systems and to protect populations from such devastating emerging epidemics. To apply these changes for a legally fast response to epidemics like Ebola, he believes the United Nations must reform and the Global Health Leadership has to strengthen. Also, the trust between countries needs to be improved so that treatment can be accelerated. Antibiotic resistance is on the increase, epidemics are inevitable but pandemics are optional.

The main focus of the Lowry Lecture was to highlight the problems in response to epidemics and the need of change to the system by evaluating the influenza and Ebola epidemics. The 1918-1919 Spanish Influenza is a good example used by Farrar that demonstrates the effects of devastating epidemics when response is slow, but also shows the positive outcomes it has for society and the government. The 1918 Spanish Influenza pandemic killed approximately 40 million people within 18 months and is said to have spread around the world approximately 3 times (Kamradt-Scott, 2012). Unlike today, during the late 19th century is was a common thought that the governments had little involvement in ensuring public health. This would have encouraged the lack of response and the rapid spread to the pandemic at this time. Even though influenza epidemics and pandemics occurred frequently, surveillance of cholera and typhoid took over due to their high fatality rates and impacts on international trade. It wasn’t until the 1918 epidemic that societal notions about the disease were changed. The disease became the most devastating event in record human history. What made this pandemic different from previous Influenza outbreaks was the speed at which it travelled across the world, despite the lack of air travel, and its high lethality rate of killing 25% of the entire population (Kamradt- Scott, 2012). As Professor Farrar presented, the disease had a rapid increase of cases and death from the months of September 1918, which peaked with 42 days during November 2014 before rapidly declining a few months later (Holtenius and Gillman, 2014). Similarly to the case Professor Farrar made about the reason for the spread of Ebola, it is believed the reluctance to alert the impact of the disease to other countries aided the spread of the disease. Even though the epidemic caused massive loss to human life, the epidemic lead to a dramatic increase in research of the influenza virus (Potter, 1991). Professor Farrar believes that epidemics are important and this can be viewed in this epidemic as the understandings of pandemic influenza and how best to monitor its effects has improved and altered dramatically overtime as scientific advances were made (which lead to the discovery of a virus being the cause of influenza). More importantly, this pandemic stimulated the creation of vaccines and antiviral medicines to stabilise its symptoms (Kamradt-Scott, 2012). The increasing understanding of the Spanish Influenza also helped with the fast response to the H1N1 strain of influenza that caused a pandemic in 2009. Like Professor Farrar explained, the H1N1 strain followed the same infectivity rates as the 1918 influenza pandemic, and although less severe than was originally feared, the virus was detected in multiple countries within weeks. Due to its similarity to the H1N1 strain, response was fast and contingency plans were enforced, emergency committees were assembled and the process of acquiring relevant antivirals and vaccines were initiated (Kamradt-Scott, 2012). This response was only possible due to a comprehensive medical infrastructure and appropriate funding, as well as international and national bodies who kept the public fully informed. They also made a potential outbreak in developing countries a matter of grave concern (Jivraj and Butler, 2013). Although authorities overreacted to this pandemic, like Professor Farrar explained in his seminar, it is good to overreact occasionally to epidemics such as these so that we are able to contain certain diseases that are of importance. For example, this was not the case for the Ebola outbreak in 2014 – as stated by Professor Farrar – that had devastating impacts on health systems, society and the willingness of communities to trust the government. Professor Farrar claimed that the reason for the failure to act on the Ebola epidemic was due to it occurring in a challenging part of the world that had complex government systems (just come out of a civil war). Although this is true, it took the World Health Organisation 3 months to declare the Ebola virus disease as an epidemic (WHO Ebola Response Team, 2014) which suggests that initial recognition and communication about the disease cases, along with the global response were highly inadequate and posed as the initial problems to the spread of the disease. This delay caused postponements in the deployments of experts and medical materials and treatment centres which finally arrived when the virus was already out of control (World Health Organisation, 2014). There were also no known vaccines or efficient vaccines. It is surpsinging that authorities did not respond more quickly to the outbreaks as it spread to communities so quickly and mortality rates were so high. The Ebola epidemic of 2014 did however have a positive outcome (which reflects Professor Farrar’s motives of improving the authority and legality for faster responses to emerging epidemics), in that it lead to accelerated vaccine trials. A process that normally takes a few years, were accelerated to 6 months without compromising the policies for vaccine safety and efficiency (World Health Organisation, 2015). The Ebola vaccine trials took the “risk-based approach” that focuses on a centralised monitoring method (Roca, et al., 2015). It was this approach which (although slightly luck-based) lead to the fast admission of vaccines that has helped to reduce the spread of the disease across multiple affected countries. Due to Ebola’s high mortality rates and the speed at which it spreads, accelerated vaccine trials such as these were granted. This case just proves how vital a fast response is. If authorities had declared the outbreak sooner, this accelerated vaccine trial may either not have been needed, or it could have been initiated much sooner at the start of its discovery which could have later saved thousands of lives.

This topic is something Professor Farrar expressed in the Lowry Lecture – in that changes to response and changes to clinical policy can allow for such dramatic responses. He explains the standards need reforming, and as seen from such a devastating effects of Ebola it is evident to see why this is so important. Without such epidemics and without the problems of response they have raised, the health sector may still react this way to emerging pathogens in years to come. Professor Farrar’s motives are right; transformations are needed in order to successfully and rapidly respond to emerging public health emergencies. Although rapid response and better communication is needed, it is also of importance that health centres are always prepared to care for patients with lethal infectious diseases in order to help prevent the spread of emerging epidemics. Developments in appropriate research protocols approved for clinical research to begin immediately once a future epidemic threatens is going to be vital for the future, especially as antibiotic resistance is becoming a threat to the human population. It should be noted that, as Professor Farrar believes, “experience confirms that the time to act is now” (Dunning, et al, 2014).

References

Bisen, P.S. (2013). Emerging Epidemics: Management and Control. New Jersey, USA: John Wiley & Sons. XV-3

Dunning, J.W., Merson, L., Rohde, G.G., Gao, Z., Semple, M.G., Tran, D., Gordon, A., Olliaro, P.L., Khoo, S.H., Bruzzone, R., Horby, P., Cobb, J.P., Longuere, K.S., Kellam, P., Nichol, A., Brett, S., Everett, D., Walsh, T.S., Hien, T.T., Yu, H., Zambon, M., Ruiz-Palacios, G., Lang, T., Akhvlediani, T.; ISARIC Working Group 3, ISARIC Council, Hayden, F.G., Marshall, J., Webb, S., Angus, D.C., Shindo, N., van der Werf, S., Openshaw, P.J., Farrar, J., Carson, G., Baillie, J.K. (2014). Open source clinical science for emerging infections. The Lancet. Infectious Diseases. 14: 8-9.

Farrar, J. J. and Piot, P. (2014). The Ebola emergency – immediate action, ongoing strategy. The New Englanf Journal of Medicine. 371: 1545-1546.

Holtenius, J. and Gillman, A. (2014). The Spanish flu in Uppsala, clinical and epidemiological impact of the influenza pandemic 1918-1919 on a Swedish county. Infection Ecology and Epidemiology. 17: 4.

Jivraj, N. and Butler, A. 2013. The 1918-1919 pandemic revisited. The Journal of the Royal College of Physicians of Edinburgh. 43: 347-352.

Kamradt-Scott, A. (2012). Changing perceptions: of pandemic influenza and public health responses. American Public Health Association. 102: 90-98.

Potter, C. W. (1991). Chronicle of Influenza Pandemics. London, UK: Blackwell Science. 3–18.

Roca, A., Afolabi, M. O., Saidu, Y. and Kampmann, B. (2015). Ebola: a holistic approach is required to achieve effective management and control. The Journal of Allergy and Clinical Immunology. 135(4): 856-867.
Wellcome Trust. (2013). Professor Jeremy Farrar named new Director of the Wellcome Trust. URL: http://www.wellcome.ac.uk/News/Media-office/Press-releases/2013/WTP052380.htm [Accessed 11/01/2016]

World Health Organisation Ebola Response Team. (2014). Ebola virus disease in West Africa – the first 9 months of the epidemic and forward projections. The New England Journal of Medicine. 371: 1481-1495.

World Health Organisation. (2014). WHO supplies arrive in Guinea to support the Ebola outbreak response. URL: http://www.who.int/features/2014/guinea-ebola/en/ [Accessed: 11/01/2016]

World Health Organisation. (2015). Second WHO high-level meeting on Ebola vaccines access and financing: summary report. URL: http://apps.who.int/iris/bitstream/10665/149045/1/WHO_EVD_Meet_HIS_15.1_eng.pdf?ua=1 [Accessed 11/01/2016]

Welcome to BARS!

Welcome to the Biological Articles for Reading Students (BARS) blog!

Throughout the past year, students have been attending a number of seminars given by some of the UK’s most acclaimed scientists at the University of Reading, Oxford and London. From learning how to save bumblebees, to the development of antibiotic resistance in the food chain, we have had the chance to engage with cutting edge research in Microbiology, Biomedical Sciences, Biochemistry, Evolution and Ecology… And now we can share this with you!

Each fortnight on the first ever School of Biological Sciences blog, we will be featuring exceptional pieces of work completed by our final year students taking the Seminars in Biology module. Every post will be based on a different seminar topic, so whether you are researching into a specific biological field or you’d just like to discover something new, there will be something for you to read and enjoy!

Kirsty Somerscales

With thanks to Dr Francoise Mazet and Dr Renee Lee for making this blog possible and a huge thank you to Emma Reynolds, Ayesha Tailor, Amelia Crowley and Steven Harris for working on the BARS blog committee.