Evaluation of Staffordshire, Stoke on Trent Allied Health Professionals preceptorship programmes: a mixed method UK study.

AIM: This study aimed to evaluate current preceptorship provision across AHP professions in the Staffordshire, Stoke on Trent (SSOT) region of England to improve consistency, share and optimise best practice. BACKGROUND: Preceptorship, defined as a period of structured transition from newly qualified to an independent practitioner, is thought to improve recruitment and retention of staff and ultimately improve patient care. During the COVID pandemic, SSOT recognised the potential for graduates to lack confidence having had reduced clinical exposure as pre-registration students, and so a likely increased need to support newly qualified staff, and to evaluate existing AHP preceptorship provision. METHODS: An explanatory sequential mixed methods design, utilising a cross sectional survey questionnaire and two subsequent focus groups, explored existing AHP preceptorship in SSOT in 2021. Following ethical approval respondents were recruited via professional networks who completed an online survey questionnaire. Two subsequent focus groups enabled an in-depth exploration of survey results. Descriptive statistics summarised survey data and thematic analysis was used to describe focus group findings. RESULTS: SSOT AHPs (n = 217; 26% preceptees; 47% preceptors) participated in the survey questionnaire and 17 AHPs in the focus groups. 57% of preceptees rated existing preceptorship programmes to be "somewhat, or not effective". Preceptors reported feeling unprepared for their role. Both preceptees and preceptors reported that, post pandemic, most existing programs required revisions to be fit for purpose. Ten pragmatic summary recommendations were made. CONCLUSIONS: Allied Health Professions Preceptorship in SSOT was found to be inconsistent, poorly understood and inadequate. Revisions to preceptorship programs across Staffordshire and Stoke on Trent NHS Trusts have been instigated to reflect changes in AHP practice since the COVID pandemic.

Tau-mediated iron export prevents ferroptotic damage after ischemic stroke.

Functional failure of tau contributes to age-dependent, iron-mediated neurotoxicity, and as iron accumulates in ischemic stroke tissue, we hypothesized that tau failure may exaggerate ischemia-reperfusion-related toxicity. Indeed, unilateral, transient middle cerebral artery occlusion (MCAO) suppressed hemispheric tau and increased iron levels in young (3-month-old) mice and rats. Wild-type mice were protected by iron-targeted interventions: ceruloplasmin and amyloid precursor protein ectodomain, as well as ferroptosis inhibitors. At this age, tau-knockout mice did not express elevated brain iron and were protected against hemispheric reperfusion injury following MCAO, indicating that tau suppression may prevent ferroptosis. However, the accelerated age-dependent brain iron accumulation that occurs in tau-knockout mice at 12 months of age negated the protective benefit of tau suppression against MCAO-induced focal cerebral ischemia-reperfusion injury. The protective benefit of tau knockout was revived in older mice by iron-targeting interventions. These findings introduce tau-iron interaction as a pleiotropic modulator of ferroptosis and ischemic stroke outcome.

Proton-induced cross sections relevant to production of 225Ac and 223Ra in natural thorium targets below 200 MeV.

Cross sections for (223,)(225)Ra, (225)Ac and (227)Th production by the proton bombardment of natural thorium targets were measured at proton energies below 200 MeV. Our measurements are in good agreement with previously published data and offer a complete excitation function for (223,)(225)Ra in the energy range above 90 MeV. Comparison of theoretical predictions with the experimental data shows reasonable-to-good agreement. Results indicate that accelerator-based production of (225)Ac and (223)Ra below 200 MeV is a viable production method.

Reduction of cerebral infarct volume by apocynin requires pretreatment and is absent in Nox2-deficient mice.

BACKGROUND AND PURPOSE: Reactive oxygen species (ROS) derived from Nox2-containing reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity is reportedly detrimental in cerebrovascular disease. However, ROS generation by other Nox isoforms may have a physiological role. No Nox2-selective inhibitors have yet been identified, and thus it is unclear whether isoform non-selective Nox inhibitors would necessarily improve outcome after stroke. We assessed the effect of apocynin on cerebrovascular ROS production and also on outcome following cerebral ischaemia when administered either before ischaemia or after cerebral reperfusion. The involvement of Nox2-containing NADPH oxidase in the effects of apocynin was assessed using Nox2(-/-) mice. EXPERIMENTAL APPROACH: Transient cerebral ischaemia was induced by 0.5 h middle cerebral artery occlusion followed by 23.5 h reperfusion. Mice received apocynin (2.5 mg.kg(-1), i.p.) either 0.5 h before ischaemia or 1 h after reperfusion. In situ superoxide production after cerebral ischaemia-reperfusion was measured in brain sections of wild-type mice at 24 h using dihydroethidium fluorescence. KEY RESULTS: Treatment with apocynin 0.5 h before ischaemia reduced total infarct volume, neurological impairment and mortality in wild-type but not Nox2(-/-) mice. Conversely, treatment with apocynin 1 h after initiation of reperfusion had no protective effect. Cerebral ischaemia and reperfusion increased superoxide production in the brain at 24 h, and pretreatment but not posttreatment with apocynin reduced superoxide levels. CONCLUSIONS AND IMPLICATIONS: Apocynin improves outcome following stroke when administered before ischaemia in wild-type but not Nox2(-/-) mice.

Complex infantile and congenital hip dislocation: assessment with MR imaging.

Twenty-five magnetic resonance hip studies were performed on 19 infants with congenital hip dislocation. These patients had a poor initial treatment response, a teratologic dislocation, or a late presentation. Detailed images of single hips obtained with small surface coils resulted in excellent visualization of all the clinically important soft-tissue and cartilaginous structures of the hip. No other imaging modality demonstrates all of these structures simultaneously.

Isolation and characterization of bone cells from a patient with osteogenesis imperfecta type 1b.

The metabolic defect(s) in bone cells which manifests itself in the disease osteogenesis imperfecta (OI) type 1 is not known. Since this form of the disease displays both a variable tissue involvement and the possibility of remission it is difficult to attribute its expression to a primary mutation in the structural gene for type I collagen (as can the perinatal lethal forms of OI). In an attempt to more fully understand OI type 1 we have isolated and characterized a subpopulation of cells obtained from a sample of bone from a patient with OI type 1b. This subpopulation of cells has been shown to morphologically resemble the osteoblast phenotype, to contain the highest level of alkaline phosphatase of the cells isolated, to synthesize collagen, to respond to bone target hormones such as 1,25(OH)2D3 and parathyroid hormone, and to proliferate rapidly. Moreover, the response of these cells to the vitamin D metabolites, from the standpoint of growth regulation, is qualitatively different from normal bone cells. We intend to use these cells as a model system for studying the defect in OI type 1b.

Congenital subluxation of the knee--an anatomic dissection.

The knee of an infant born with congenital subluxation was dissected to delineate the pathology involved. The primary findings of importance included isolated fibrosis of the vastus intermedius muscle, absence of the gastrocnemius muscle, anterior displacement of the hamstrings and contracture of the anterior joint capsule. Comparison with previously described pathology is discussed.

Assay of bone resorption in vivo with 3H-tetracycline.

3H-Tetracycline (3H-TC) was used to quantify resorption in whole bones of growing rats and dogs. After repeated isotopic labeling of actively growing embryos or neonates, 3H-TC was observed to be distributed homogeneously and in equilibrium with 45Ca. A rapid and large loss of 3H-TC and a small loss of 45Ca occurred during the early weeks of rapid bone growth, suggesting that absolute amounts of 45Ca resorbed from bone, as reflected by losses of 3H-TC, are five to ten times greater than the net amounts of 45Ca lost from bone. Minimal loss of 3H-TC occurred due to nonspecific physicochemical exchange in vivo or in vitro (5%) except with nonradioactive tetracycline, and 3H-TC was not greatly exchanged or reused (10%) in vivo. The data are considered in terms of local and systemic conservation of calcium.