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1.
Br J Nurs ; 33(15): 726-733, 2024 Aug 13.
Article in English | MEDLINE | ID: mdl-39141334

ABSTRACT

BACKGROUND: Nursing students often face anxiety and cognitive overload, leading to high attrition rates; meanwhile, traditional pastoral interventions have proved insufficient. A novel, digitally enhanced learning environment named The Wellbeing in Student Education (WISE) Room, was introduced as an alternative at a UK university. AIMS: This study investigated the impact of The WISE Room, a 4m × 4m digital platform containing touch-interactive walls, co-created with students and academic staff, designed to promote insight through immersive experiences beyond traditional learning settings. METHODS: A mixed-methods approach was adopted, collecting data from nursing students, healthcare staff and academic faculty. Data were collected at three stages, each corresponding with the iterative development of The WISE Room, including an evaluation of the intervention. RESULTS: Feedback from 240 participants was positive. In Phase 2 of the study, 93% of the 79 students and 21 staff who visited the room and completed a survey were satisfied with the room's suitability in three key areas: emotional wellbeing, academic readiness, and placement preparedness. CONCLUSION: The WISE Room has proved effective in supporting nursing students' wellbeing, and educational and placement preparation requirements. Its multisensory, digital and experiential nature is beneficial for students throughout their learner journey. Additional trials and content development will be required to enhance the learning and teaching experience further.


Subject(s)
Students, Nursing , Humans , Students, Nursing/psychology , United Kingdom , Education, Nursing, Baccalaureate/methods , Education, Nursing/methods , Learning , Female , Male , Adult
2.
J Vis Exp ; (207)2024 05 17.
Article in English | MEDLINE | ID: mdl-38829135

ABSTRACT

The blood-brain (BBB) is a crucial system that regulates selective brain circulation with the periphery, as an example, allowing necessary nutrients to enter and expel excessive amino acids or toxins from the brain. To model how the BBB can be compromised in diseases like vascular dementia (VaD) or Alzheimer's disease (AD), researchers developed novel methods to model vessel dilatation. A compromised BBB in these disease states can be detrimental and result in the dysregulation of the BBB leading to untoward and pathological consequences impacting brain function. We were able to modify an existing technique that enabled us to inject directly into the Cisterna magna (CM) to induce dilatation of blood vessels using elastase, and disrupt the tight junctions (TJ) of the BBB. With this method, we were able to see various metrics of success over previous techniques, including consistent blood vessel dilatation, reduced mortality or improved recovery, and improving the fill/opacifying agent, a silicone rubber compound, delivery for labeling blood vessels for dilatation analysis. This modified minimally invasive method has had promising results, with a 19%-32% increase in sustained dilatation of large blood vessels in mice from 2 weeks to 3 months post-injection. This improvement contrasts with previous studies, which showed increased dilatation only at the 2 week mark. Additional data suggests sustained expansion even after 9.5 months. This increase was confirmed by comparing the diameter of blood vessels of the elastase and the vehicle-injected group. Overall, this technique is valuable for studying pathological disorders that affect the central nervous system (CNS) using animal models.


Subject(s)
Blood-Brain Barrier , Disease Models, Animal , Animals , Mice , Blood-Brain Barrier/metabolism , Pancreatic Elastase , Cerebrovascular Disorders , Cisterna Magna , Male , Dementia, Vascular
3.
Neuropsychopharmacology ; 47(7): 1421-1427, 2022 06.
Article in English | MEDLINE | ID: mdl-35383319

ABSTRACT

Converging evidence points to the significant involvement of the immune system in autism spectrum disorders (ASD). Positron emission tomography (PET) can quantify translocator protein 18 kDa (TSPO), a marker with increased expression mainly in microglia and, to some extent astroglia during neuropsychiatric diseases with inflammation. This preliminary analysis explored, for the first time, whether TSPO binding was altered in male and female participants with ASD in vivo using full kinetic quantification. Thirteen individuals with ASD (IQ > 70 [n = 12], IQ = 62 [n = 1]), 5 F, 25 ± 5 years) were scanned with [18F]FEPPA PET. Data from 13 typically developing control participants with matching age and TSPO rs6971 polymorphism (9 F, age 24 ± 5 years) were chosen from previous studies for comparison. The two tissue compartment model (2TCM) was used to determine the total volume of distribution ([18F]FEPPA VT) in four previously identified regions of interest (ROI): prefrontal, temporal, cerebellar, and anterior cingulate cortices. We observe no significant difference in [18F]FEPPA VT relative to controls (F(1,26)= 1.74, p = 0.20). However, 2 ASD participants with higher VT had concurrent major depressive episodes (MDE), which has been consistently reported during MDE. After excluding those 2 ASD participants, in a post-hoc analysis, our results show lower [18F]FEPPA VT in ASD participants compared to controls (F(1,24)= 6.62, p = 0.02). This preliminary analysis provides evidence suggesting an atypical neuroimmune state in ASD.


Subject(s)
Autism Spectrum Disorder , Depressive Disorder, Major , Adult , Anilides/metabolism , Autism Spectrum Disorder/diagnostic imaging , Autism Spectrum Disorder/metabolism , Brain/diagnostic imaging , Brain/metabolism , Depressive Disorder, Major/metabolism , Female , Humans , Male , Positron-Emission Tomography , Pyridines , Receptors, GABA/genetics , Receptors, GABA/metabolism , Young Adult
4.
Br J Nurs ; 30(12): 706-710, 2021 Jun 24.
Article in English | MEDLINE | ID: mdl-34170729
5.
Antioxidants (Basel) ; 9(8)2020 Aug 13.
Article in English | MEDLINE | ID: mdl-32823544

ABSTRACT

Neurodegenerative disorders, such as Alzheimer's disease, are a global public health burden with poorly understood aetiology. Neuroinflammation and oxidative stress (OS) are undoubtedly hallmarks of neurodegeneration, contributing to disease progression. Protein aggregation and neuronal damage result in the activation of disease-associated microglia (DAM) via damage-associated molecular patterns (DAMPs). DAM facilitate persistent inflammation and reactive oxygen species (ROS) generation. However, the molecular mechanisms linking DAM activation and OS have not been well-defined; thus targeting these cells for clinical benefit has not been possible. In microglia, ROS are generated primarily by NADPH oxidase 2 (NOX2) and activation of NOX2 in DAM is associated with DAMP signalling, inflammation and amyloid plaque deposition, especially in the cerebrovasculature. Additionally, ROS originating from both NOX and the mitochondria may act as second messengers to propagate immune activation; thus intracellular ROS signalling may underlie excessive inflammation and OS. Targeting key kinases in the inflammatory response could cease inflammation and promote tissue repair. Expression of antioxidant proteins in microglia, such as NADPH dehydrogenase 1 (NQO1), is promoted by transcription factor Nrf2, which functions to control inflammation and limit OS. Lipid droplet accumulating microglia (LDAM) may also represent a double-edged sword in neurodegenerative disease by sequestering peroxidised lipids in non-pathological ageing but becoming dysregulated and pro-inflammatory in disease. We suggest that future studies should focus on targeted manipulation of NOX in the microglia to understand the molecular mechanisms driving inflammatory-related NOX activation. Finally, we discuss recent evidence that therapeutic target identification should be unbiased and founded on relevant pathophysiological assays to facilitate the discovery of translatable antioxidant and anti-inflammatory therapeutics.

6.
Healthcare (Basel) ; 7(4)2019 Nov 01.
Article in English | MEDLINE | ID: mdl-31683839

ABSTRACT

Healthcare Organisational Culture (OC) is a major contributing factor in serious failings in healthcare delivery. Despite an increased awareness of the impact that OC is having on patient care, there is no universally accepted way to measure culture in practice. This study was undertaken to provide a snapshot as to how the English National Health Service (NHS) is currently measuring culture. Although the study is based in England, the findings have potential to influence the measurement of healthcare OC internationally. An online survey was sent to 234 NHS hospital trusts, with a response rate of 35%. Respondents who completed the online survey, on behalf of their representative organisations, were senior clinical governance leaders. The findings demonstrate that the majority of organisations, that responded, were actively measuring culture. Significantly, a wide variety of tools were in use, with variable levels of satisfaction and success. The majority of tools had a focus on patient safety, not on understanding the determining factors which impact upon healthcare OC. This paper reports the tools currently used by the respondents. It highlights that there are deficits in these tools that need to be addressed, so that organisations can interpret their own culture in a standardised, evidence-based way.

7.
Nurs Stand ; 31(7): 36, 2016 Oct 12.
Article in English | MEDLINE | ID: mdl-27762955

ABSTRACT

As a third-year nursing student my final placement was with an anaesthetic team. Two months into the placement, the emergency telephone rang at 4am, with the message 'obstetric airway emergency' - a call that no nurse or midwife wants to receive.


Subject(s)
Empathy , Midwifery , Students, Nursing , Emergencies , Female , Humans , Pregnancy , United Kingdom
8.
Clin Cancer Res ; 15(4): 1192-8, 2009 Feb 15.
Article in English | MEDLINE | ID: mdl-19228725

ABSTRACT

PURPOSE: Single-agent chemotherapy is largely the treatment of choice for systemic therapy of metastatic melanoma, but survival rates are low, and novel adjuvant and systemic therapies are urgently required. Endoplasmic reticulum (ER) stress is a potential therapeutic target, and two relatively new drugs, fenretinide and bortezomib (Velcade), each acting via different cellular mechanisms, induce ER stress leading to apoptosis in melanoma cells. The aim of this study was to test the hypothesis that apoptosis of melanoma cells may be increased by combining clinically achievable concentrations of fenretinide and bortezomib. EXPERIMENTAL DESIGN: Three human melanoma cell lines were used to assess changes in viability and the induction of apoptosis in response to fenretinide, bortezomib, or both drugs together. A s.c. xenograft model was used to test responses in vivo. RESULTS: Fenretinide and bortezomib synergistically decreased viability and increased apoptosis in all three melanoma lines at clinically achievable concentrations. This was also reflected by increased expression of GADD153, a marker of ER stress-induced apoptosis. In vivo, fenretinide in combination with bortezomib gave a marked reduction in xenograft tumor volume and an increase in apoptosis compared with fenretinide or bortezomib alone. The cell cycle stage of tumor cells in vivo were similar to that predicted from the effects of each drug or the combination in vitro. CONCLUSIONS: These results suggest that fenretinide and bortezomib, both of which are available in clinical formulation, warrant clinical evaluation as a combination therapy for metastatic melanoma.


Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Boronic Acids/administration & dosage , Endoplasmic Reticulum/drug effects , Fenretinide/administration & dosage , Melanoma/drug therapy , Pyrazines/administration & dosage , Animals , Apoptosis/drug effects , Bortezomib , Cell Division/drug effects , Cell Line, Tumor , Cell Survival/drug effects , Drug Synergism , Endoplasmic Reticulum/metabolism , Female , G2 Phase/drug effects , Humans , Ki-67 Antigen/analysis , Melanoma/pathology , Melanoma/secondary , Mice
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