Engineering Defects – Costs and Sustainability

Session 18, Paper 1, CIBSE ASHRAE Technical Symposium, Dublin, Ireland, 3-4 April 2014 This paper focuses upon building services engineering defects within industry and how they are perceived and understood. As building services evolve to meet ever growing best practices and sustainable engineering principles it is expected that project defects would be steadily reduced. Within industry this is not always the case, resulting in frustration for all parties. Definitions of defects are explored, why they occur and perhaps more importantly what consequences they carry. The findings suggest that direct and indirect costs applied to defects are considerable. Differences in opinions and responsibilities are common causal factors with lack of communication sitting at the forefront. Defective engineering services not only affect sustainable outcomes and energy efficiency, but also require re-work. Visible costs associated with completing work twice can be significantly high. Indirect costs may be much higher

Is Steam a Modern Heating Medium or a Victorian Hangover?

In the UK many hospitals use steam as a heating medium. It is an accepted fact that steam can carry considerable amounts of heat energy, but is heating by steam really a cost effective and energy efficient method for hospital engineering services? This paper examines some steam and MTHW case studies in terms of energy and operation, and some quantifiable parameters for comparison of the two have been obtained. An important feature revealed by the study is that optimum energy and operational performance for both steam and MTHW systems is directly related to management and maintenance. Other factors affecting the choice of steam are also examined. For example, when choosing between steam and MTHW, how important a factor are those unique hospital applications such as laundries and sterilization equipment, that are traditionally provided for by steam? Interviews were conducted with engineering professionals at a large North-West hospital in order to consider the specialist health service applications for steam. The investigation concludes that although steam retains a Victorian image, in hospital applications its energy and financial performance costs are comparable, and sometimes better than hot water alternatives

Assessment of Energy Consumption in Existing Buildings

There has been general recognition within the construction industry that there is a discrepancy between the amount of energy that buildings actually use and what designers considered that they should use. This phenomenon is termed “The Performance Gap” and is normally associated with new buildings. However, existing and older buildings contribute a greater amount of operational carbon. In response to the Performance Gap, CIBSE have developed the TM54 process which is aimed at improving energy estimates at design stage. This paper considers how the TM54 process can also be used to develop energy management procedures for existing buildings. The paper describes an exercise carried out for a university workshop building in which design energy use has been compared with the actual building energy use and standard benchmarks. Moreover, a sensitivity assessment has been carried out using different scenarios based on operation hours of building/ equipment, boiler efficiency and impact of climate change. The analysis of these results showed high uncertainty in estimates of energy consumption. If carbon challenges are to be met then improved energy management techniques will require a more systematic approach so that facilities managers can identify energy streams and pinpoint problems, particularly where they have assumed responsibility for existing buildings which often have a legacy of poorly metered fuel consumption

A mechanism for extremely weak SpaP-expression in Streptococcus mutans strain Z1

Background: Streptococcus mutans surface-protein antigen (SpaP, PAc, or antigen I/II) has been well known to play an important role in initial attachment to tooth surfaces. However, strains with weak SpaP-expression were recently reported to be found in natural populations of S. mutans. The S. mutans gbpC-negative strain Z1, which we previously isolated from saliva and plaque samples, apparently expresses relatively low levels of SpaP protein compared to S. mutans strains MT8148 or UA159. Objective: To elucidate the mechanism for weak SpaP-expression in this strain, the spaP gene region in strain Z1 was amplified by polymerase chain reaction (PCR) and analyzed. Methods: Allelic exchange mutants between strains Z1 and UA159 involving the spaP gene region were constructed. The SpaP protein expressed in the mutants was detected with Coomasie Brilliant Blue (CBB)-staining and Western blot analysis following SDS-PAGE. Results: The 4689 bp spaP gene coding sequence for Z1 appeared to be intact. In contrast, a 20 bp nucleotide sequence appeared to be deleted from the region immediately upstream from the Z1 spaP gene when compared to the same region in UA159. The 216 bp and 237 bp intergenic fragments upstream from the spaP gene, respectively, from Z1 and UA159 were isolated, modified, and transformed into the other strain by allelic replacement. The resultant UA159-promoter region-mutant exhibited extremely weak SpaP-expression similar to that of strain Z1 and the Z1 complemented mutant expressed Spa protein levels like that of strain UA159. Conclusion: These results suggest that weak SpaP-expression in strain Z1 resulted from a 20 bp-deletion in the spaP gene promoter region

A randomised, open label, active comparator trial assessing the effects of 26 weeks of liraglutide or sitagliptin on cardiovascular function in young obese adults with type 2 diabetes

Aim To compare the effects of a glucagon‐like peptide‐1 receptor agonist and a dipeptidyl peptidase‐4 inhibitor on magnetic resonance imaging‐derived measures of cardiovascular function. Materials and methods In a prospective, randomized, open‐label, blinded endpoint trial liraglutide (1.8 mg) and sitagliptin (100 mg) were compared in asymptomatic, non‐insulin treated young (aged 18‐50 years) adults with obesity and type 2 diabetes. The primary outcome was difference in circumferential peak early diastolic strain rate change (PEDSR), a biomarker of cardiac diastolic dysfunction 26 weeks after randomization. Secondary outcomes included other indices of cardiac structure and function, HbA1c and body weight. Results Seventy‐six participants were randomized (54% female, mean ± SD age 44 ± 6 years, diabetes duration 4.4 years, body mass index 35.3 ± 6.1 kg m−2), of whom 65% had ≥1 cardiovascular risk factor. Sixty‐one participants had primary outcome data available. There were no statistically significant between‐group differences (intention‐to‐treat; mean [95% confidence interval]) in PEDSR change (−0.01 [−0.07, +0.06] s−1), left ventricular ejection fraction (−1.98 [−4.90, +0.94]%), left ventricular mass (+1.14 [−5.23, +7.50] g) or aortic distensibility (−0.35 [−0.98, +0.28] mmHg−1 × 10−3) after 26 weeks. Reductions in HbA1c (−4.57 [−9.10, −0.37] mmol mol−1) and body weight (−3.88 [−5.74, −2.01] kg) were greater with liraglutide. Conclusion There were no differences in cardiovascular structure or function after short‐term use of liraglutide and sitagliptin in younger adults with obesity and type 2 diabetes. Longer studies in patients with more severe cardiac dysfunction may be necessary before definitive conclusions can be made about putative pleiotropic properties of incretin‐based therapies

Network model of immune responses reveals key effectors to single and co-infection dynamics by a respiratory bacterium and a gastrointestinal helminth

Co-infections alter the host immune response but how the systemic and local processes at the site of infection interact is still unclear. The majority of studies on co-infections concentrate on one of the infecting species, an immune function or group of cells and often focus on the initial phase of the infection. Here, we used a combination of experiments and mathematical modelling to investigate the network of immune responses against single and co-infections with the respiratory bacterium Bordetella bronchiseptica and the gastrointestinal helminth Trichostrongylus retortaeformis. Our goal was to identify representative mediators and functions that could capture the essence of the host immune response as a whole, and to assess how their relative contribution dynamically changed over time and between single and co-infected individuals. Network-based discrete dynamic models of single infections were built using current knowledge of bacterial and helminth immunology; the two single infection models were combined into a co-infection model that was then verified by our empirical findings. Simulations showed that a T helper cell mediated antibody and neutrophil response led to phagocytosis and clearance of B. bronchiseptica from the lungs. This was consistent in single and co-infection with no significant delay induced by the helminth. In contrast, T. retortaeformis intensity decreased faster when co-infected with the bacterium. Simulations suggested that the robust recruitment of neutrophils in the co-infection, added to the activation of IgG and eosinophil driven reduction of larvae, which also played an important role in single infection, contributed to this fast clearance. Perturbation analysis of the models, through the knockout of individual nodes (immune cells), identified the cells critical to parasite persistence and clearance both in single and co-infections. Our integrated approach captured the within-host immuno-dynamics of bacteria-helminth infection and identified key components that can be crucial for explaining individual variability between single and co-infections in natural populations

B Cells Regulate Neutrophilia during Mycobacterium tuberculosis Infection and BCG Vaccination by Modulating the Interleukin-17 Response

We have previously demonstrated that B cells can shape the immune response to Mycobacterium tuberculosis, including the level of neutrophil infiltration and granulomatous inflammation at the site of infection. The present study examined the mechanisms by which B cells regulate the host neutrophilic response upon exposure to mycobacteria and how neutrophilia may influence vaccine efficacy. To address these questions, a murine aerosol infection tuberculosis (TB) model and an intradermal (ID) ear BCG immunization mouse model, involving both the μMT strain and B cell-depleted C57BL/6 mice, were used. IL (interleukin)-17 neutralization and neutrophil depletion experiments using these systems provide evidence that B cells can regulate neutrophilia by modulating the IL-17 response during M. tuberculosis infection and BCG immunization. Exuberant neutrophilia at the site of immunization in B cell-deficient mice adversely affects dendritic cell (DC) migration to the draining lymph nodes and attenuates the development of the vaccine-induced Th1 response. The results suggest that B cells are required for the development of optimal protective anti-TB immunity upon BCG vaccination by regulating the IL-17/neutrophilic response. Administration of sera derived from M. tuberculosis-infected C57BL/6 wild-type mice reverses the lung neutrophilia phenotype in tuberculous μMT mice. Together, these observations provide insight into the mechanisms by which B cells and humoral immunity modulate vaccine-induced Th1 response and regulate neutrophila during M. tuberculosis infection and BCG immunization. © 2013 Kozakiewicz et al

Radiation induced angiosarcoma a sequela of radiotherapy for breast cancer following conservative surgery

Radiation induced angiosarcomas (RIA) can affect breast cancer patients who had radiotherapy following conservative breast surgery. They are very rare tumors and often their diagnosis is delayed due to their benign appearance and difficulty in differentiation from radiation induced skin changes. Therefore it is very important that clinicians are aware of their existence. We report here a case of RIA followed by discussion and review of literature

Automated telephone follow-up after breast cancer: an acceptability and feasibility pilot study

Traditional clinical follow-up after breast cancer is inefficient at detecting relapse and is poorly suited to detecting and ameliorating psychological problems. There is interest in developing more effective and efficient methods of follow-up. We report a prospective cohort study of the acceptability and feasibility of remote, automated telephone follow-up after breast cancer. Women with a history of breast cancer were approached at their annual follow-up visit. For participants, the follow-up questionnaire was administered on paper at baseline. In place of a clinic visit following year, the women completed the same questionnaire using an automated telephone system. All patients were given mammograms. A semi-structured interview was then conducted to assess the acceptability. The potential impact on clinic usage was assessed. In all, 110 of 121 women (91%) agreed to participate. Seventy-five patients (71%) completed follow-up using the new automated system 1 year later. Seventy-one of the 75 patients found the system easy to use. Forty-nine of the 75 (65.33%) liked the system and were happy to use it as their sole method of follow-up. A further 12% were happy to use it as part of their follow-up. In only 10.66% of participants were concerns raised which led to clinic attendance. Automated questionnaire-based telephone follow-up is acceptable to women and has the potential to reduce attendance at clinic. Further studies to validate this method further are planned

Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.

Many mutations confer one or more toxic function(s) on copper/zinc superoxide dismutase 1 (SOD1) that impair motor neuron viability and cause familial amyotrophic lateral sclerosis (FALS). Using a conformation-specific antibody that detects misfolded SOD1 (C4F6), we found that oxidized wild-type SOD1 and mutant SOD1 share a conformational epitope that is not present in normal wild-type SOD1. In a subset of human sporadic ALS (SALS) cases, motor neurons in the lumbosacral spinal cord were markedly C4F6 immunoreactive, indicating that an aberrant wild-type SOD1 species was present. Recombinant, oxidized wild-type SOD1 and wild-type SOD1 immunopurified from SALS tissues inhibited kinesin-based fast axonal transport in a manner similar to that of FALS-linked mutant SOD1. Our findings suggest that wild-type SOD1 can be pathogenic in SALS and identify an SOD1-dependent pathogenic mechanism common to FALS and SALS