Thermocline management of stratified tanks for heat storage

Stratified tanks are useful for maximising the thermal energy efficiency of non-continuous and semi-continuous processes. Liquid at two or more dissimilar temperatures is stored within the same tank to provide a buffer for variations in heating and cooling loads. Control of the thermocline between the hot and cold fluid regions is needed to minimise thermocline growth and maximise operation of the storage tank. An experimental programme using a scale model of an industrial stratified tank (aspect ratio 3.5) and Perspex tank (aspect ratio 8.2) is reported. The behaviour and growth of the hot-cold thermocline under various operating conditions is presented. A siphoning method to re-establish the thermocline without interrupting the use of the tank is tested. Siphoning of the thermocline region from either 20%, 50% or 80% of the tank height is an effective strategy for uninterrupted interface re-establishment. However, the rate and position of siphoning and the load balance of the exit streams are critical variables for minimising the time for effective re-establishment of the two temperature zones

Mining Medical Data: Bridging the Knowledge Divide

Due to the signi¯cant amount of data generated by modern medicine there is a growing reliance on tools such as data mining and knowledge discovery to help make sense and comprehend such data. The success of this process requires collaboration and interaction between such methods and medical professionals. Therefore an important question is: How can we strengthen the relationship between two traditionally separate fields (technology and medicine) in order to work simultaneously towards enhancing knowledge in modern medicine. To address this question, this study examines the application of data mining techniques to a large asthma medical dataset. A discussion introducing various methods for a smooth approach, straying from the `jack of all trades, master of none' to a modular cooperative approach for a successful outcome is pro-posed. The results of this study support the use of data mining as a useful tool and highlight the advantages on a global scale of closer relations between the two distinct fields. The exploration of CRISP methodology suggests that a `one methodology fits all approach' is not appropriate, but rather combines to create a hybrid holistic approach to data mining

Endogeneity: How Failure to Correct for it can Cause Wrong Inferences and Some Remedies

This is the peer reviewed version of the following article: ABDALLAH, W., GOERGEN, M. and O'SULLIVAN, N., 2015. Endogeneity - how failure to correct for it can cause wrong inferences and some remedies. British Journal of Management, 26(4), pp.791-804, which has been published in final form at http://dx.doi.org/10.1111/1467-8551.12113. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.Although researchers in business and management are becoming increasingly aware of the importance of endogeneity affecting regression analysis, they frequently do not have the right methodological toolkit to adjust for this issue. This paper discusses such a toolkit. There are also areas in business and management research which to date seem to be mostly oblivious about the endogeneity issue. This paper highlights such an area, which studies the question as to whether firms that are cross-listed on a foreign stock exchange are charged premium fees by their auditors. When the same methodology (pooled ordinary least squares) as in the existing literature is used, the existence of an audit fee premium for cross-listed firms seems to be confirmed. However, once methodologies are used which adjust for the various types of endogeneity (i.e. omitted variable bias, simultaneous and dynamic endogeneity) there is no longer support for the existence of such a generalised premium. Hence, this paper not only illustrates that failure to adjust for endogeneity has severe consequences such as drawing the wrong inferences, but it also reviews various ways to control for the different types of endogeneity

Engineering tendon and ligament tissues : present developments towards successful clinical products

Musculoskeletal diseases are one of the leading causes of disability worldwide. Among them, tendon and ligament injuries represent an important aspect to consider in both athletes and active working people. Tendon and ligament damage is an important cause of joint instability, and progresses into early onset of osteoarthritis, pain, disability and eventually the need for joint replacement surgery. The social and economical burden associated with these medical conditions presents a compelling argument for greater understanding and expanding research on this issue. The particular physiology of tendons and ligaments (avascular, hypocellular and overall structural mechanical features) makes it difficult for currently available treatments to reach a complete and long-term functional repair of the damaged tissue, especially when complete tear occurs. Despite the effort, the treatmentmodalities for tendon and ligament are suboptimal, which have led to the development of alternative therapies, such as the delivery of growth factors, development of engineered scaffolds or the application of stem cells, which have been approached in this review

Targeting KSHV/HHV-8 Latency with COX-2 Selective Inhibitor Nimesulide: A Potential Chemotherapeutic Modality for Primary Effusion Lymphoma

The significance of inflammation in KSHV biology and tumorigenesis prompted us to examine the role of COX-2 in primary effusion lymphoma (PEL), an aggressive AIDS-linked KSHV-associated non-Hodgkin's lymphoma (NHL) using nimesulide, a well-known COX-2 specific NSAID. We demonstrate that (1) nimesulide is efficacious in inducing proliferation arrest in PEL (KSHV+/EBV-; BCBL-1 and BC-3, KSHV+/EBV+; JSC-1), EBV-infected (KSHV-/EBV+; Raji) and non-infected (KSHV-/EBV-; Akata, Loukes, Ramos, BJAB) high malignancy human Burkitt's lymphoma (BL) as well as KSHV-/EBV+ lymphoblastoid (LCL) cell lines; (2) nimesulide is selectively toxic to KSHV infected endothelial cells (TIVE-LTC) compared to TIVE and primary endothelial cells (HMVEC-d); (3) nimesulide reduced KSHV latent gene expression, disrupted p53-LANA-1 protein complexes, and activated the p53/p21 tumor-suppressor pathway; (4) COX-2 inhibition down-regulated cell survival kinases (p-Akt and p-GSK-3β), an angiogenic factor (VEGF-C), PEL defining genes (syndecan-1, aquaporin-3, and vitamin-D3 receptor) and cell cycle proteins such as cyclins E/A and cdc25C; (5) nimesulide induced sustained cell death and G1 arrest in BCBL-1 cells; (6) nimesulide substantially reduced the colony forming capacity of BCBL-1 cells. Overall, our studies provide a comprehensive molecular framework linking COX-2 with PEL pathogenesis and identify the chemotherapeutic potential of nimesulide in treating PEL

Nrf2-dependent persistent oxidative stress results in stress-induced vulnerability to depression.

Stressful life events produce a state of vulnerability to depression in some individuals. The mechanisms that contribute to vulnerability to depression remain poorly understood. A rat model of intense stress (social defeat (SD), first hit) produced vulnerability to depression in 40% of animals. Only vulnerable animals developed a depression-like phenotype after a second stressful hit (chronic mild stress). We found that this vulnerability to depression resulted from a persistent state of oxidative stress, which was reversed by treatment with antioxidants. This persistent state of oxidative stress was due to low brain-derived neurotrophic factor (BDNF) levels, which characterized the vulnerable animals. We found that BDNF constitutively controlled the nuclear translocation of the master redox-sensitive transcription factor Nrf2, which activates antioxidant defenses. Low BDNF levels in vulnerable animals prevented Nrf2 translocation and consequently prevented the activation of detoxifying/antioxidant enzymes, ultimately resulting in the generation of sustained oxidative stress. Activating Nrf2 translocation restored redox homeostasis and reversed vulnerability to depression. This mechanism was confirmed in Nrf2-null mice. The mice displayed high levels of oxidative stress and were inherently vulnerable to depression, but this phenotype was reversed by treatment with antioxidants. Our data reveal a novel role for BDNF in controlling redox homeostasis and provide a mechanistic explanation for post-stress vulnerability to depression while suggesting ways to reverse it. Because numerous enzymatic reactions produce reactive oxygen species that must then be cleared, the finding that BDNF controls endogenous redox homeostasis opens new avenues for investigation