119 research outputs found

    Technology and maritime security in Africa : opportunities and challenges in Gulf of Guinea

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    This research was supported by funding from the St Andrews Research Internship Scheme (StARIS).Maritime security threats undermine safety and security at sea and, in turn, coastal states’ efforts to harness the resources in their maritime domain. This assertion is true for coastal states and Small Island Developing States (SIDS) on the African continent, where limited maritime enforcement capabilities have increased security threats at sea, such as illegal, unreported and unregulated fishing, piracy and armed robbery at sea, toxic waste dumping and other illicit activities. African navies and their foreign partners are taking advantage of the opportunities that technology provides to improve safety and security. Technology has led to the identification of criminals at sea, their capture and prosecution, making it crucial in enhancing maritime security. As such, the merits of its use for maritime security are undeniable. However, using technology comes with challenges that need to be considered. With this in mind, our research makes an original contribution by exploring the opportunities for using technology to advance maritime safety and security in Africa, successes and challenges with an emphasis on the Gulf of Guinea region. Drawing from questionnaire data from maritime law enforcement personnel, agencies supporting the implementation of the Yaoundé Code of Conduct (2013), and a review of relevant literature and policy documents, we contend that technology has significantly improved maritime domain awareness and the effective implementation of maritime safety and security in the Gulf of Guinea. However, addressing existing limitations and enhancing human capacity is imperative to sustain this progress.Publisher PDFPeer reviewe

    Applying a socio-ecological model to understanding the needs of children and young people bereaved by intimate partner homicide across their life course

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    Purpose: To develop a socio-ecological understanding of the immediate and long-term effects on, and the needs of, children and young people (CYP) in the UK and Ireland bereaved by parental intimate partner homicide (IPH).Method: The study draws on in-depth interviews from three different informants: those with lived experience (LE) (10); caregivers (12); and professionals (10). In addition to the 10 interviews with those bereaved by maternal IPH, experiences discussed include a further 23 cases of bereavement due to IPH during childhood(when aged under 18). We used thematic analysis to code and extracted themes into the relevant five dimensions of the socio-ecological model.Results: The circumstances in which the homicide/suicide took place, were crucial in shaping children’s life trajectory. We identified circumstantial predictors in branching of trajectories: witnessing the murder; relatedness to perpetrator; and assumptions on biological relatedness. We found the need for life-long accessto therapeutic care to support CYP essential during various developmental stages and life transitions. We recognized that both kinship and foster carers, required support in dealing with the complexity of grieving children. For kinship care, carers require help in managing their own grief, in addition to financial support toaccount for the new caring responsibilities. We also observed that children’s voice was rarely elicited, with no opportunities to exercise their agency.Conclusion: Our findings highlight the importance of contextual circumstances for tailored support and the identification of appropriate carers and supporting them holistically. Finally, we highlight the importance ofchild centered policies and dedicated resources to support relevant services dealing with CYP bereaved by parental IPH

    Δ9-TETRAHYDROCANNABINOL IS PROTECTIVE THROUGH PPARγ DEPENDENT MITOCHONDRIAL BIOGENESIS IN A CELL CULTURE MODEL OF PARKINSON'S DISEASE.

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    Cannabinoids such as Δ9-tetrahydrocannabinol (Δ9-THC) are neuroprotective in animal and cell culture models of Parkinson's disease (PD). In a PD cell culture model we recently demonstrated that Δ9-THC is neuroprotective through activation of the nuclear receptor peroxisomal proliferator-activated receptor γ (PPARγ). Furthermore, activation by specific agonists rosiglitazone and pioglitazone, has also been found neuroprotective. PPARγ is a nuclear receptor whose activation can lead to the expression of proteins involved in the de novo synthesis of mitochondria. One such protein is the PPARγ co-activator 1 α (PGC1α) as it co-activates NRF-1 mediated gene expression which is essential for the production of nuclear encoded, mitochondrial proteins. Here we investigate the effect of Δ9-THC and pioglitazone on mitochondrial biogenesis

    Application of Sensing Techniques to Cellular Force Measurement

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    Cell traction forces (CTFs) are the forces produced by cells and exerted on extracellular matrix or an underlying substrate. CTFs function to maintain cell shape, enable cell migration, and generate and detect mechanical signals. As such, they play a vital role in many fundamental biological processes, including angiogenesis, inflammation, and wound healing. Therefore, a close examination of CTFs can enable better understanding of the cellular and molecular mechanisms of such processes. To this end, various force-sensing techniques for CTF measurement have been developed over the years. This article will provide a concise review of these sensing techniques and comment on the needs for improved force-sensing technologies for cell mechanics and biology research

    Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi

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    The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation results in the synchronized response of cell migration on the villi. We conclude that cell proliferation within the crypt is the primary force that drives cell migration along the villus. This methodology can be applied to interrogate intestinal epithelial dynamics and characterize situations in which processes involved in cell turnover become uncoupled, including pharmacological treatments and disease models

    Writing in Britain and Ireland, c. 400 to c. 800

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    Schizophrenia as a disorder of disconnectivity

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    Schizophrenia is considered as a neurodevelopmental disorder with genetic and environmental factors playing a role. Animal models show that developmental hippocampal lesions are causing disconnectivity of the prefrontal cortex. Magnetic resonance imaging and postmortem investigations revealed deficits in the temporoprefrontal neuronal circuit. Decreased oligodendrocyte numbers and expression of oligodendrocyte genes and synaptic proteins may contribute to disturbances of micro- and macro-circuitry in the pathophysiology of the disease. Functional connectivity between cortical areas can be investigated with high temporal resolution using transcranial magnetic stimulation (TMS), electroencephalography (EEG), and magnetoencephalography (MEG). In this review, disconnectivity between different cortical areas in schizophrenia patients is described. The specificity and the neurobiological origin of these connectivity deficits and the relation to the symptom complex of schizophrenia and the glutamatergic and GABAergic system are discussed
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