VICAR-DIGITAL image processing system

Computer program corrects various photometic, geometric and frequency response distortions in pictures. The program converts pictures to a number of elements, with each elements optical density quantized to a numerical value. The translated picture is recorded on magnetic tape in digital form for subsequent processing and enhancement by computer

Transient but not genetic loss of miR-451 attenuates the development of pulmonary arterial hypertension

<b>Rationale:</b> MicroRNAs are small non-coding RNAs involved in the regulation of gene expression and have recently been implicated in the development of pulmonary arterial hypertension (PAH). Previous work established that miR-451 is up-regulated in rodent models of PAH.<p></p> <b>Objectives:</b> The role of miR-451 in the pulmonary circulation is unknown. We therefore sought to assess the involvement of miR-451 in the development of pulmonary arterial hypertension.<p></p> <b>Methods:</b> Silencing of miR-451 was performed in vivo using miR-451 knockout mice and an antimiR targeting mature miR-451 in rats. Coupled with exposure to hypoxia, indices of pulmonary arterial hypertension were assessed. The effect of modulating miR-451 on human pulmonary artery smooth muscle cell proliferation and migration was analysed.<p></p> <b>Measurements and Main Results:</b> We observed a reduction in systolic right ventricular pressure in hypoxic rats pre-treated with antimiR-451 compared to hypoxia alone (47.7 ± 1.36mmHg and 56.0 ± 2.03mmHg respectively, p<0.01). In miR-451 knockout mice following exposure to chronic hypoxia, no significant differences were observed compared to wild type hypoxic mice. In vitro analysis demonstrated that over-expression of miR-451 in human pulmonary artery smooth muscle cells promoted migration under serum-free conditions. No effect on cellular proliferation was observed.<p></p> <b>Conclusions:</b> Transient inhibition of miR-451 attenuated the development of pulmonary arterial hypertension in hypoxia exposed rats. Genetic deletion of miR-451 had no beneficial effect on indices of pulmonary arterial hypertension, potentially due to pathway redundancy compensating for the loss of miR-451.<p></p&gt

UK hospital patient discharge: the patient perspective

Objectives: Hospital discharge is a complex process that can result in errors and delays for patients, particularly around the supply of medicines and communication of information. To improve patient discharge, patient perspectives of the discharge service must be explored to determine where patients feel problems arise. This study aimed to explore inpatient perceptions and experiences of the current discharge process. Methods: This study involved questionnaires with patients at a large city centre teaching hospital. Results: A total of 104 inpatients participated, 60% (n=62) were male with an average age of 55 (age range 19-93). Participants were from a range of medical, surgical and admissions wards. The majority, 71% of respondents (n=74) took regular medicines, with 65% (n=48) taking five or more medicines daily. Most patients, 89% (n=87) were satisfied with their hospital discharge but felt that it took too long. The perceived main cause of delay was waiting for medicines. Other highlighted issues included lack of counselling by pharmacists and the need for more patient involvement throughout the discharge process. Conclusions: This study shows that certain aspects of the discharge process need improving to provide safe, quality care for patients and improve patient experience of discharge. The findings from this study will inform the development of a new model of care for patient discharge from hospital

Development of A “PharmaComm” Serious Game for Teaching Pharmacist Communication and Drug Administration in a Virtual Hospital Setting

Practical experience is crucial in pharmacy education, but it can be difficult to provide pharmacy students with a sufficient level of experience during their education due to a number of challenges. Video games might provide a platform where students can gain positive learning experience in a virtual environment. Serious games have been used successfully across many industries, which suggest that a well-designed serious game can have positive learning outcomes. Increased engagement and motivation are mentioned by experts as some of the main benefits of serious games. Being able to practise skills before utilising them in real-world scenarios is another advantage identified. In this paper, we present a virtual patient simulator which is designed specifically teaching pharmacy students patient communication and administration of drugs. A pilot study and an expert review were carried out to evaluate the effectiveness of the application and its findings are presented

Hospital patient discharge process: an evaluation

Objectives Medication discrepancies for patients after discharge from hospital are well documented. They have been shown to cause unnecessary harm to patients and can result in hospital readmission. To improve patient discharge, the current process of discharging patients from hospital (the discharge process) needs evaluating to determine where and why medication issues occur. This study aimed to identify and evaluate the discharge process used in a range of acute National Health Service hospitals across the North West of England. Methods This qualitative study involved semi-structured telephone interviews with 13 chief pharmacists or an appropriately nominated member of the hospital pharmacy team. Thematic analysis of the transcribed interview data was performed. Data analysis revealed eight main themes which all impacted on the discharge process. Results The study was successful in identifying the discharge process across the range of hospitals as well as key issues and examples of good practice. The hospitals involved in the study were found to have similar discharge processes with issues common to all. One significant finding was a lack of patient involvement in the discharge process. Conclusions To improve the patient discharge process, innovative solutions are required to overcome the current issues. In future work, the study findings will be used to develop a new model of care for patient discharge from hospital

The serotonin transporter promotes a pathological estrogen metabolic pathway in pulmonary hypertension via cytochrome P450 1B1 pulmonary circulation

Pulmonary arterial hypertension (PAH) is a devastating vasculopathy that predominates in women and has been associated with dysregulated estrogen and serotonin signaling. Overexpression of the serotonin transporter (SERT+) in mice results in an estrogen-dependent development of pulmonary hypertension (PH). Estrogen metabolism by cytochrome P450 1B1 (CYP1B1) contributes to the pathogenesis of PAH, and serotonin can increase CYP1B1 expression in human pulmonary arterial smooth muscle cells (hPASMCs). We hypothesized that an increase in intracellular serotonin via increased SERT expression may dysregulate estrogen metabolism via CYP1B1 to facilitate PAH. Consistent with this hypothesis, we found elevated lung CYP1B1 protein expression in female SERT+ mice accompanied by PH, which was attenuated by the CYP1B1 inhibitor 2,3',4,5'-tetramethoxystilbene (TMS). Lungs from female SERT+ mice demonstrated an increase in oxidative stress that was marked by the expression of 8-hydroxyguanosine; however, this was unaffected by CYP1B1 inhibition. SERT expression was increased in monocrotaline-induced PH in female rats; however, TMS did not reverse PH in monocrotaline-treated rats but prolonged survival. Stimulation of hPASMCs with the CYP1B1 metabolite 16α-hydroxyestrone increased cellular proliferation, which was attenuated by an inhibitor (MPP) of estrogen receptor alpha (ERα) and a specific ERα antibody. Thus, increased intracellular serotonin caused by increased SERT expression may contribute to PAH pathobiology by dysregulation of estrogen metabolic pathways via increased CYP1B1 activity. This promotes PASMC proliferation by the formation of pathogenic metabolites of estrogen that mediate their effects via ERα. Our studies indicate that targeting this pathway in PAH may provide a promising antiproliferative therapeutic strategy

Friction between human skin and incontinence pads in the presence of barrier protection products

This novel experimental work aims to bring further knowledge of frictional performance of common barrier products used in the treatment of incontinence-associated dermatitis and determine how the skin-pad interface changes when a treatment is applied to the skin. Key data is reported and there is an in-depth analysis into friction profiles which reveals great differences between how different skin-pad tribosystems operate when exposed to commercially available barrier treatments. In a wet-pad state Barrier cream A (3M™ Cavilon™ Barrier cream) reduced friction and had much lower dynamic and static coefficients of friction than the other barrier treatments (Barrier cream B (Sorbaderm Barrier cream) and the Barrier spray C (Sorbaderm Barrier spray)). Barrier cream A provided stable friction coefficients in reciprocating sliding, whereas the other treatments, and untreated skin, did not display this unique characteristic. The barrier spray gave rise to high static friction coefficients and exhibited the most stick-slip. All three candidate barrier protection products were found to reduce directional differences in the static coefficient of friction: indicative of reduced shear loading. Knowledge of the desirable frictional properties would drive innovation in product development, and benefit companies, clinicians and users

Dexfenfluramine and the oestrogen-metabolizing enzyme CYP1B1 in the development of pulmonary arterial hypertension

<p>Aims: Pulmonary arterial hypertension (PAH) occurs more frequently in women than men. Oestrogen and the oestrogen-metabolising enzyme cytochrome P450 1B1 (CYP1B1) play a role in the development of PAH. Anorectic drugs such as dexfenfluramine (Dfen) have been associated with the development of PAH. Dfen mediates PAH via a serotonergic mechanism and we have shown serotonin to up-regulate expression of CYP1B1 in human pulmonary artery smooth muscle cells (PASMCs). Thus here we assess the role of CYP1B1 in the development of Dfen-induced PAH.</p> <p>Methods and results: Dfen (5 mg kg−1 day−1 PO for 28 days) increased right ventricular pressure and pulmonary vascular remodelling in female mice only. Mice dosed with Dfen showed increased whole lung expression of CYP1B1 and Dfen-induced PAH was ablated in CYP1B1−/− mice. In line with this, Dfen up-regulated expression of CYP1B1 in PASMCs from PAH patients (PAH-PASMCs) and Dfen-mediated proliferation of PAH-PASMCs was ablated by pharmacological inhibition of CYP1B1. Dfen increased expression of tryptophan hydroxylase 1 (Tph1; the rate-limiting enzyme in the synthesis of serotonin) in PAH-PASMCs and both Dfen-induced proliferation and Dfen-induced up-regulation of CYP1B1 were ablated by inhibition of Tph1. 17β-Oestradiol increased expression of both Tph1 and CYP1B1 in PAH-PASMCs, and Dfen and 17β-oestradiol had synergistic effects on proliferation of PAH-PASMCs. Finally, ovariectomy protected against Dfen-induced PAH in female mice.</p> <p>Conclusion: CYP1B1 is critical in the development of Dfen-induced PAH in mice in vivo and proliferation of PAH-PASMCs in vitro. CYP1B1 may provide a novel therapeutic target for PAH.</p&gt