A comparison of the nursing competence of graduates and diplomates from UK nursing programmes

This paper reviews the literature on nursing competence measurement and reports the results of a comparative quantitative study of the competencies of Project 2000 diplomates and BA (Hons) Adult Nursing graduates from two UK nursing programmes. The findings reveal that graduates appear to overcome any initial limitations and become more competent than the diplomates in certain areas. Attention to social awareness and participation is necessary in both pre-registration programmes, whilst greater attention could be given to graduates' leadership and management development. Diplomates need support in their professional development if they are to achieve the same level of competence as graduates during the first post-qualifying year. There are implications for the level of support afforded to qualifying nurses in their first staff positions; preceptorship programmes could be an important means of assisting newly qualified staff to gain confidence. More research on nurse competencies with larger samples drawn from programmes across the UK is needed

MCP-1 and murine prion disease: separation of early behavioural dysfunction from overt clinical disease

Prion diseases are chronic, fatal neurodegenerative conditions of the CNS. We have investigated the role of monocyte chemoattractant protein-1 (MCP-1) in the ME7 model of murine prion disease. MCP-1 expression increased in the CNS throughout disease progression and was positively correlated with microglial activation. We subsequently compared the inflammatory response, pathology and behavioural changes in wild-type (wt) mice and MCP-1 knockout mice (MCP-1?/?) inoculated with ME7. Late-stage clinical signs were delayed by 4 weeks in MCP-1?/? mice, and survival time increased by 2–3 weeks. By contrast, early changes in affective behaviours and locomotor activity were not delayed in onset. There was also no difference in microglial activation or neuronal death in the hippocampus and thalamus of wt mice and MCP-1?/? mice. These results highlight an important dissociation between prolonged survival, early behavioural dysfunction and hippocampal/thalamic pathology when considering therapeutic intervention for human prion diseases and other chronic neurodegenerative condition

Hepatic CC chemokines control the magnitude of the inflammatory response within the injured rodent brain

Hepatic CXC chemokines, behaving as acute phase proteins, regulate neutrophil mobilisation and recruitment following focal IL-1h-mediated inflammation to the rat brain. To determine whether this response was specific to CXC chemokines or whether it represented a more generalised response to acute brain inflammation, we examined brain and liver production of MCP-1, a CC chemokine, when rats were microinjected with TNF-a into the brain. As early as 2h after the TNF-a challenge, MCP-1 mRNA and protein were observed in the liver by Taqman RT-PCR and ELISA. The serum MCP-1 level was also elevated between 2 and 4 h, which was consistent with maximal mobilisation of leukocytes into the blood. Monocyte recruitment was most marked in the liver after 6 h, but was delayed in the brain until 24 h. Elevated hepaticand serum chemokines are implicated in the control of leukocytosis and leukocyte recruitment to the brain and liver, since dexamethasone pretreatment attenuated the hepatic MCP-1 response, modulated leukocyte mobilisation and reduced monocyte entry not only to the brain but also to the liver. Thus hepatic chemokine production controls and amplifies the CNS response to inflammation by controlling the rate, timing, magnitude and composition of leukocyte recruitment to the damaged brain