Towards Improving the Utilisation of University Teaching Space

There is a perception that teaching space in universities is a rather scarce resource. However, some studies have revealed that in many institutions it is actually chronically under-used. Often, rooms are occupied only half the time, and even when in use they are often only half full. This is usually measured by the ‘utilization’ which is defined as the percentage of available ‘seat-hours’ that are employed. Within real institutions, studies have shown that this utilization can often take values as low as 20–40%. One consequence of such a low level of utilization is that space managers are under pressure to make more efficient use of the available teaching space. However, better management is hampered because there does not appear to be a good understanding within space management (near-term planning) of why this happens. This is accompanied, within space planning (long-term planning) by a lack of experise on how best to accommodate the expected low utilizations. This motivates our two main goals: (i) To understand the factors that drive down utilizations, (ii) To set up methods to provide better space planning. Here, we provide quantitative evidence that constraints arising from timetabling and location requirements easily have the potential to explain the low utilizations seen in reality. Furthermore, on considering the decision question ‘Can this given set of courses all be allocated in the available teaching space?’ we find that the answer depends on the associated utilization in a way that exhibits threshold behaviour: There is a sharp division between regions in which the answer is ‘almost always yes’ and those of ‘almost always no’. Through analysis and understanding of the space of potential solutions, our work suggests that better use of space within universities will come about through an understanding of the effects of timetabling constraints and when it is statistically likely that it will be possible for a set of courses to be allocated to a particular space. The results presented here provide a firm foundation for university managers to take decisions on how space should be managed and planned for more effectively. Our multi-criteria approach and new methodology together provide new insight into the interaction between the course timetabling problem and the crucial issue of space planning.

Monitoring treatment fidelity in a randomised controlled trial of a complex intervention.

Aim. This paper is a report of a study to describe how treatment fidelity is being enhanced and monitored, using a model from the National Institutes of Health Behavior Change Consortium. Background. The objective of treatment fidelity is to minimize errors in interpreting research trial outcomes, and to ascribe those outcomes directly to the intervention at hand. Treatment fidelity procedures are included in trials of complex interventions to account for inferences made from study outcomes. Monitoring treatment fidelity can help improve study design, maximize reliability of results, increase statistical power, determine whether theory-based interventions are responsible for observed changes, and inform the research dissemination process. Methods. Treatment fidelity recommendations from the Behavior Change Consortium were applied to the SPHERE study (Secondary Prevention of Heart DiseasE in GeneRal PracticE), a randomized controlled trial of a complex intervention. Procedures to enhance and monitor intervention implementation included standardizing training sessions, observing intervention consultations, structuring patient recall systems, and using written practice and patient care plans. The research nurse plays an important role in monitoring intervention implementation. Findings. Several methods of applying treatment fidelity procedures to monitoring interventions are possible. The procedure used may be determined by availability of appropriate personnel, fiscal constraints, or time limits. Complex interventions are not straightforward and necessitate a monitoring process at trial stage. Conclusion. The Behavior Change Consortium’s model of treatment fidelity is useful for structuring a system to monitor the implementation of a complex intervention, and helps to increase the reliability and validity of evaluation findings.

Effect of osteoporosis on bone mineral density and fracture repair in a rat femoral fracture model

Osteoporosis (OP) is one of the most prevalent bone diseases worldwide with bone fracture the major clinical consequence. The effect of OP on fracture repair is disputed and although it might be expected for fracture repair to be delayed in osteoporotic individuals, a definitive answer to this question still eludes us. The aim of this study was to clarify the effect of osteoporosis in a rodent fracture model. OP was induced in 3-month-old rats (n = 53) by ovariectomy (OVX) followed by an externally fixated, mid-diaphyseal femoral osteotomy at 6 months (OVX group). A further 40 animals underwent a fracture at 6 months (control group). Animals were sacrificed at 1, 2, 4, 6, and 8 weeks postfracture with outcome measures of histology, biomechanical strength testing, pQCT, relative BMD, and motion detection. OVX animals had significantly lower BMD, slower fracture repair (histologically), reduced stiffness in the fractured femora (8 weeks) and strength in the contralateral femora (6 and 8 weeks), increased body weight, and decreased motion. This study has demonstrated that OVX is associated with decrease in BMD (particularly in trabecular bone) and a reduction in the mechanical properties of intact bone and healing fractures. The histological, biomechanical, and radiological measures of union suggest that OVX delayed fracture healing. (C) 2007 Orthopaedic Research Society. Published by Wiley Periodicals.

Deficiencies of double-strand break repair factors and effects on mutagenesis in directly gamma-irradiated and medium-mediated bystander human lymphoblastoid cells

Using RNA interference techniques to knock down key proteins in two major double-strand break (DSB) repair pathways (DNA-PKcs for nonhomologous end joining, NHEJ, and Rad54 for homologous recombination, HR), we investigated the influence of DSB repair factors on radiation mutagenesis at the autosomal thymidine kinase (TK) locus both in directly irradiated cells and in unirradiated bystander cells. We also examined the role of p53 (TP53) in these processes by using cells of three human lymphoblastoid cell lines from the same donor but with differing p53 status (TK6 is p53 wild-type, NH32 is p53 null, and WTK1 is p53 mutant). Our results indicated that p53 status did not affect either the production of radiation bystander mutagenic signals or the response to these signals. In directly irradiated cells, knockdown of DNA-PKcs led to an increased mutant fraction in WTK1 cells and decreased mutant fractions in TK6 and NH32 cells. In contrast, knockdown of DNA-PKcs led to increased mutagenesis in bystander cells regardless of p53 status. In directly irradiated cells, knockdown of Rad54 led to increased induced mutant fractions in WTK1 and NH32 cells, but the knockdown did not affect mutagenesis in p53 wild-type TK6 cells. In all cell lines, Rad54 knockdown had no effect on the magnitude of bystander mutagenesis. Studies with extracellular catalase confirmed the involvement of H2O2 in bystander signaling. Our results demonstrate that DSB repair factors have different roles in mediating mutagenesis in irradiated and bystander cells. (C) 2008 by Radiation Research Society.

Improving the utilisation of University teaching space

There is a perception that teaching space in universities is a rather scarce resource. However, some studies have revealed that in many institutions it is actually chronically under-used. Often, rooms are occupied only half the time, and even when in use they are often only half full. This is usually measured by the “utilisation” which is basically the percentage of available ’seat-hours’ that are employed. In real institutions, this utilisation can often takes values as low as 20-40%. One consequence of such low utilisation is that space managers are under pressure to make a more efficient use of the available teaching space. However, better management is hampered because there does not appear to be a good understanding within space management (near-term planning) of why this happens. Nor, a good basis within space planning (long-term planning) of how best to accommodate the expected low utilisations. This motivates our two main goals: (i) To understand the factors that drive down utilisations, (ii) To set up methods to provide better space planning. Here, we provide quantitative evidence that constraints arising from timetabling and location requirements easily have the potential to explain the low utilisations seen in reality. Furthermore, on considering the decision question “Can this given set of courses all be allocated in the available teaching space?” we find that the answer depends on the associated utilisation in a way that exhibits threshold behaviour: There is a sharp division between regions in which the answer is “almost always yes” and those of “almost always no”. Our work suggests that progress in space management and planning will arise from an integrated approach; combining purely space issues with restrictions representing an aggregated or abstracted version of key constraints such as timetabling or location, and

Adenosine, inflammation and asthma - a review

Adenosine is a ubiquitous molecule present in every cell of the human body. It has a wide range of physiological functions mediated predominantly through specific cell surface adenosine receptors. Adenosine has both pro- and anti-inflammatory effects and acts on inflammatory and resident immune cells and antioxidant enzymes. The elevation of adenosine in the bronchoalveolar lavage (BAL) fluid of asthmatics combined with its bronchoconstrictor effect on the airways in asthmatics has led to increased research into the contribution of adenosine in the pathophysiology of inflammation and asthma. This review looks at the airway response to adenosine and at the interaction of adenosine with mast cells and basophils.

Regulation of FOS by different compartmental stresses induced by low levels of ionizing radiation

We irradiated different cellular compartments and measured changes in expression of the FOS gene at the mRNA and protein levels. [H-3]Thymidine and tritiated water were used to irradiate the nucleus and the whole cell, respectively. I-125-Concanavalin A binding was used to irradiate the cell membrane differentially. Changes in FOS mRNA and protein levels were measured using semi-quantitative RT-PCR and SDS-PAGE Western blotting, respectively, Irradiation of the nucleus or the whole cell at a dose rate of 0.075 Gy/h caused no change in the level of FOS mRNA expression, but modestly (1.5-fold) induced FOS protein after 0.5 h, Irradiation of the nucleus at a dose rate of 0.43 Gy/h induced FOS mRNA by 1.5-fold after 0.5 h, but there was no significant effect after whole-cell irradiation. FOS protein was transiently induced 2.5-fold above control levels 0.5 h after a 0.43-Gy/h exposure of the nucleus or the whole cell. Irradiation of the cell membrane at a dose rate of 1.8 Gy/h for up to 2 h caused no change in the levels of expression of FOS mRNA or protein, but a dose rate of 6.8 Gy/h transiently increased the level of FOS mRNA S-fold after 0.5 h, These data demonstrate the complexity of the cellular response to radiation-induced damage at low doses. The lack of quantitative agreement between the transcript and protein levels for FOS suggests a role for posttranscriptional regulation. (C) 2000 by Radiation Research Society.