The clinically led worforcE and activity redesign (CLEAR) programme: a novel data-driven healthcare improvement methodology.

BACKGROUND: The NHS is facing substantial pressures to recover from the COVID-19 pandemic. Optimising workforce modelling is a fundamental component of the recovery plan. The Clinically Lead workforcE and Activity Redesign (CLEAR) programme is a unique methodology that trains clinicians to redesign services, building intrinsic capacity and capability, optimising patient care and minimising the need for costly external consultancy. This paper describes the CLEAR methodology and the evaluation of previous CLEAR projects, including the return on investment. METHODS: CLEAR is a work-based learning programme that combines qualitative techniques with data analytics to build innovations and new models of care. It has four unique stages: (1) Clinical engagement- used to gather rich insights from stakeholders and clinicians. (2) Data interrogation- utilising clinical and workforce data for cohort analysis. (3) Innovation- using structured innovation methods to develop new models of care. (4) Recommendations- report writing, impact assessment and presentation of key findings to executive boards. A mixed-methods formative evaluation was carried out on completed projects, which included semi-structured interviews and surveys with CLEAR associates and stakeholders, and a health economic logic model that was developed to link the inputs, processes, outputs and the outcome of CLEAR as well as the potential impacts of the changes identified from the projects. RESULTS: CLEAR provides a more cost-effective delivery of complex change programmes than the alternatives - resulting in a cost saving of £1.90 for every £1 spent independent of implementation success. Results suggest that CLEAR recommendations are more likely to be implemented compared to other complex healthcare interventions because of the levels of clinical engagement and have a potential return on investment of up to £14 over 5 years for every £1 invested. CLEAR appears to have a positive impact on staff retention and wellbeing, the cost of a CLEAR project is covered if one medical consultant remains in post for a year. CONCLUSIONS: The unique CLEAR methodology is a clinically effective and cost-effective complex healthcare innovation that optimises workforce and activity design, as well as improving staff retention. Embedding CLEAR methodology in the NHS could have substantial impact on patient care, staff well-being and service provision.

PROCESS AND SYSTEMS: The WRaPT process - a novel and patient-centred approach to workforce planning by a clinically active workforce.

The concept of supply and demand is well established within the health economy of the UK. However, complex health and social care needs, associated with an ageing population, pose a novel challenge to NHS resources and, in particular, its workforce. Although existing strategies adopt a more linear approach to clinical activity and workforce demands, the Workforce Repository and Planning Tool process draws upon the principles of 'realist' data evaluation to combine -empirical evidence, practical experience and clinical theory to offer transformation strategies for an NHS workforce that is fit for purpose and its patients.

The association of noise and surgical-site infection in day-case hernia repairs.

INTRODUCTION: Surgical-site infections (SSIs) are associated with an increased duration of hospital stay, poorer quality of life, and an marked increase in cost to the hospital. Lapses in compliance with aseptic principles are a substantial risk factor for SSI, which may be attributable to distractions such as noise during the operation. The aims of this study were to assess whether noise levels in the operating room are associated with the development of SSI and to elucidate the extent to which these levels affect the financial burden of surgery. METHODS: Prospective data collection from elective, day-case male patients undergoing elective hernia repairs was undertaken. Patients were included if they were fit and at low risk for SSI. Sound levels during procedures was measured via a decibel meter and correlated with the incidence of SSI. Data analysis was performed with IBM SPSS (IBM, Armonk, NY). RESULTS: Noise levels were substantially greater in patients with SSI from time point of 50 minutes onwards, which correlated to when wound closure was occurring. Additional hospital costs for these patients were £243 per patient based on the National Health Service 2013 reference costing. CONCLUSION: Decreasing ambient noise levels in the operating room may aid in reducing the incidence of SSIs, particularly during closure, and decrease the associated financial costs of this complication.

Pubic lice: an endangered species?

UNLABELLED: The incidence of pubic lice infestations is estimated to be between 1.3% and 4.6%, with an average incidence of 2% worldwide. It is also estimated that 70% to 80% of adults now remove pubic hair in part or entirety, using a variety of methods. It is hypothesized that the destruction of this pubic hair habitat may account for the falling incidence of pubic lice and may possibly lead to its eradication or atypical presentation. AIM: To report the changing incidence of pubic lice infestation from our unit over the last 10 years and assess its association, if any, with pubic hair removal of any kind. METHODS: Assessment of medical records and questionnaires were used to identify the incidence of hair removal and pubic lice infestation over a 10-year period. Data were anonymized and analyzed to identify any correlation. RESULTS: A significant and strong correlation between the falling incidence of pubic lice infections and increase in pubic hair removal was observed, with a Pearson correlation r value of 0.9686 (95% confidence intervals, 0.88-0.992). The P value is less than 0.0001. CONCLUSIONS: The increased incidence of hair removal may lead to atypical patterns of pubic lice infestations or its complete eradication as the natural habitat of this parasite is destroyed.

In an in vitro model of human tuberculosis, monocyte-microglial networks regulate matrix metalloproteinase-1 and -3 gene expression and secretion via a p38 mitogen activated protein kinase-dependent pathway.

BACKGROUND: Tuberculosis (TB) of the central nervous system (CNS) is characterized by extensive tissue inflammation, driven by molecules that cleave extracellular matrix such as matrix metalloproteinase (MMP)-1 and MMP-3. However, relatively little is known about the regulation of these MMPs in the CNS. METHODS: Using a cellular model of CNS TB, we stimulated a human microglial cell line (CHME3) with conditioned medium from Mycobacterium tuberculosis-infected primary human monocytes (CoMTb). MMP-1 and MMP-3 secretion was detected using ELISAs confirmed with casein zymography or western blotting. Key results of a phospho-array profile that detects a wide range of kinase activity were confirmed with phospho-Western blotting. Chemical inhibition (SB203580) of microglial cells allowed investigation of expression and secretion of MMP-1 and MMP-3. Finally we used promoter reporter assays employing full length and MMP-3 promoter deletion constructs. Student's t-test was used for comparison of continuous variables and multiple intervention experiments were compared by one-way ANOVA with Tukey's correction for multiple pairwise comparisons. RESULTS: CoMTb up-regulated microglial MMP-1 and MMP-3 secretion in a dose- and time-dependent manner. The phospho-array profiling showed that the major increase in kinase activity due to CoMTb stimulation was in p38 mitogen activated protein kinase (MAPK), principally the α and γ subunits. p38 phosphorylation was detected at 15 minutes, with a second peak of activity at 120 minutes. High basal extracellular signal-regulated kinase activity was further increased by CoMTb. Secretion and expression of MMP-1 and MMP-3 were both p38 dependent. CoMTb stimulation of full length and MMP-3 promoter deletion constructs demonstrated up-regulation of activity in the wild type but a suppression site between -2183 and -1612 bp. CONCLUSIONS: Monocyte-microglial network-dependent MMP-1 and MMP-3 gene expression and secretion are dependent upon p38 MAPK in tuberculosis. p38 is therefore a potential target for adjuvant therapy in CNS TB.

Mycobacterium tuberculosis-infected human monocytes down-regulate microglial MMP-2 secretion in CNS tuberculosis via TNFα, NFκB, p38 and caspase 8 dependent pathways.

Tuberculosis (TB) of the central nervous system (CNS) is a deadly disease characterized by extensive tissue destruction, driven by molecules such as Matrix Metalloproteinase-2 (MMP-2) which targets CNS-specific substrates. In a simplified cellular model of CNS TB, we demonstrated that conditioned medium from Mycobacterium tuberculosis-infected primary human monocytes (CoMTb), but not direct infection, unexpectedly down-regulates constitutive microglial MMP-2 gene expression and secretion by 72.8% at 24 hours, sustained up to 96 hours (P < 0.01), dependent upon TNF-α. In human CNS TB brain biopsies but not controls the p38 pathway was activated in microglia/macrophages. Inhibition of the p38 MAP kinase pathway resulted in a 228% increase in MMP-2 secretion (P < 0.01). In contrast ERK MAP kinase inhibition further decreased MMP-2 secretion by 76.6% (P < 0.05). Inhibition of the NFκB pathway resulted in 301% higher MMP-2 secretion than CoMTb alone (P < 0.01). Caspase 8 restored MMP-2 secretion to basal levels. However, this caspase-dependent regulation of MMP-2 was independent of p38 and NFκB pathways; p38 phosphorylation was increased and p50/p65 NFκB nuclear trafficking unaffected by caspase 8 inhibition. In summary, suppression of microglial MMP-2 secretion by M.tb-infected monocyte-dependent networks paradoxically involves the pro-inflammatory mediators TNF-α, p38 MAP kinase and NFκB in addition to a novel caspase 8-dependent pathway.

Mycobacterium tuberculosis upregulates microglial matrix metalloproteinase-1 and -3 expression and secretion via NF-kappaB- and Activator Protein-1-dependent monocyte networks.

Inflammatory tissue destruction is central to pathology in CNS tuberculosis (TB). We hypothesized that microglial-derived matrix metalloproteinases (MMPs) have a key role in driving such damage. Analysis of all of the MMPs demonstrated that conditioned medium from Mycobacterium tuberculosis-infected human monocytes (CoMTb) stimulated greater MMP-1, -3, and -9 gene expression in human microglial cells than direct infection. In patients with CNS TB, MMP-1/-3 immunoreactivity was demonstrated in the center of brain granulomas. Concurrently, CoMTb decreased expression of the inhibitors, tissue inhibitor of metalloproteinase-2, -3, and -4. MMP-1/-3 secretion was significantly inhibited by dexamethasone, which reduces mortality in CNS TB. Surface-enhanced laser desorption ionization time-of-flight analysis of CoMTb showed that TNF-alpha and IL-1beta are necessary but not sufficient for upregulating MMP-1 secretion and act synergistically to drive MMP-3 secretion. Chemical inhibition and promoter-reporter analyses showed that NF-kappaB and AP-1 c-Jun/FosB heterodimers regulate CoMTb-induced MMP-1/-3 secretion. Furthermore, NF-kappaB p65 and AP-1 c-Jun subunits were upregulated in biopsy granulomas from patients with cerebral TB. In summary, functionally unopposed, network-dependent microglial MMP-1/-3 gene expression and secretion regulated by NF-kappaB and AP-1 subunits were demonstrated in vitro and, for the first time, in CNS TB patients. Dexamethasone suppression of MMP-1/-3 gene expression provides a novel mechanism explaining the benefit of steroid therapy in these patients.