P4_5 Atmospheric ODSTs

In this paper the maximum acceleration on the ODST and the pod was found to be $-4g$, with a braking thrusters force of $14100$ N during the last $50$ m of descent. This deceleration brings the impact velocity of the pod to below velocity of $1$ ms$^{-1}$, should the braking thrusters fail to fire the pod will hit the ground with a velocity of $43.2$ ms$^{-1}$ killing the trooper

P4_3 Light Ordnance

In this paper we consider a weapon system that fires a laser at an interplanetary vessel. We calculate the energy required to melt through a vessel’s armoured hull, of thickness 0.254 m, from a shot from a laser with a calibre of 16 inches. The energy required is found to be E = 34449 J. Using this energy, the recoil of the laser firing was calculated to be ρ = 1.15x10−4 kgms−1

P4_6 Wind swept

This paper discusses the plausibility of the thruster in the Iron Man suit being used as weapons to push a human back. It was determined that the shock-wave produced by the change in temperature due to the thrusters would produce a force of $183$ kN on a person it was shot at, this would cause the person to accelerate at $2614$ ms$^{-2}$ killing the person

P4_2 How to fly your dragon

In this paper we calculate the minimum area and length of a dragon’s wing for it to be able to fly. The minimum area was calculated to be 224m^2 and the length was 35.6m

P4_4 Snorlax used Body Slam

In this paper we consider the maximum strength of Ash's Snorlax, from the Pokemon original TV series, this will occur when the Snorlax jumps as high as it can. The maximum height of the jump was calculated to be 41.8 m, the velocity it impacts the ground with is 28.1 ms^-1 and the momentum of the Snorlax when it hits the ground is 12,900 kgms^-1

The potential for dietary factors to prevent or treat osteoarthritis

Osteoarthritis (OA) is a degenerative joint disease for which there are no disease-modifying drugs. It is a leading cause of disability in the UK. Increasing age and obesity are both major risk factors for OA and the health and economic burden of this disease will increase in the future. Focusing on compounds from the habitual diet that may prevent the onset or slow the progression of OA is a strategy that has been under-investigated to date. An approach that relies on dietary modification is clearly attractive in terms of risk/benefit and more likely to be implementable at the population level. However, before undertaking a full clinical trial to examine potential efficacy, detailed molecular studies are required in order to optimise the design. This review focuses on potential dietary factors that may reduce the risk or progression of OA, including micronutrients, fatty acids, flavonoids and other phytochemicals. It therefore ignores data coming from classical inflammatory arthritides and nutraceuticals such as glucosamine and chondroitin. In conclusion, diet offers a route by which the health of the joint can be protected and OA incidence or progression decreased. In a chronic disease, with risk factors increasing in the population and with no pharmaceutical cure, an understanding of this will be crucial

The cellular microscopy phenotype ontology

BACKGROUND: Phenotypic data derived from high content screening is currently annotated using free-text, thus preventing the integration of independent datasets, including those generated in different biological domains, such as cell lines, mouse and human tissues. DESCRIPTION: We present the Cellular Microscopy Phenotype Ontology (CMPO), a species neutral ontology for describing phenotypic observations relating to the whole cell, cellular components, cellular processes and cell populations. CMPO is compatible with related ontology efforts, allowing for future cross-species integration of phenotypic data. CMPO was developed following a curator-driven approach where phenotype data were annotated by expert biologists following the Entity-Quality (EQ) pattern. These EQs were subsequently transformed into new CMPO terms following an established post composition process. CONCLUSION: CMPO is currently being utilized to annotate phenotypes associated with high content screening datasets stored in several image repositories including the Image Data Repository (IDR), MitoSys project database and the Cellular Phenotype Database to facilitate data browsing and discoverability

Counteractive effects of antenatal glucocorticoid treatment on D1 receptor modulation of spatial working memory.

RATIONALE: Antenatal exposure to the glucocorticoid dexamethasone dramatically increases the number of mesencephalic dopaminergic neurons in rat offspring. However, the consequences of this expansion in midbrain dopamine (DA) neurons for behavioural processes in adulthood are poorly understood, including working memory that depends on DA transmission in the prefrontal cortex (PFC). OBJECTIVES: We therefore investigated the influence of antenatal glucocorticoid treatment (AGT) on the modulation of spatial working memory by a D1 receptor agonist and on D1 receptor binding and DA content in the PFC and striatum. METHODS: Pregnant rats received AGT on gestational days 16-19 by adding dexamethasone to their drinking water. Male offspring reared to adulthood were trained on a delayed alternation spatial working memory task and administered the partial D1 agonist SKF38393 (0.3-3 mg/kg) by systemic injection. In separate groups of control and AGT animals, D1 receptor binding and DA content were measured post-mortem in the PFC and striatum. RESULTS: SKF38393 impaired spatial working memory performance in control rats but had no effect in AGT rats. D1 binding was significantly reduced in the anterior cingulate cortex, prelimbic cortex, dorsal striatum and ventral pallidum of AGT rats compared with control animals. However, AGT had no significant effect on brain monoamine levels. CONCLUSIONS: These findings demonstrate that D1 receptors in corticostriatal circuitry down-regulate in response to AGT. This compensatory effect in D1 receptors may result from increased DA-ergic tone in AGT rats and underlie the resilience of these animals to the disruptive effects of D1 receptor activation on spatial working memory.The authors’ research is funded by the Wellcome Trust (grant number 086871/Z/08/Z), the MRC (G0701500), a joint award from the MRC (G1000183) and Wellcome Trust (093875/Z/10/ Z) in support of the Behavioral and Clinical Neuroscience Institute at Cambridge University, and an MRC strategic award to the Imperial College-Cambridge University-Manchester University (ICCAM) addiction cluster (G1000018).This is the final version of the article. It first appeared from Springer at http://dx.doi.org/10.1007/s00213-016-4405-8