Smart Operations of Air-Conditioning and Lighting Systems in a Government Buildings for Peak Power Reduction

This paper presents the achievements of implementing smart operations strategies for air-conditioning (A/C) and lighting systems in Justice Palace Complex (JPC), Kuwait during the summer 2007. The peak load of this building was 3700 kW. The achievements are summarized as direct savings between 13:00 and 22:00 h by closing supply and return air fans of 52 air-handling units with a connected load 400 kW, and an additional saving of 550 kW during the same period by optimizing the cooling production and distribution. Also an all time saving of 22 kW by de-lamping, and additional saving of 27 kW through TDC of lighting were achieved. In conclusion project achieved an overall reduction in power demand of around 20% between 13:00 to 17:00 h and reduction ranging from 7% to 15% between 17:00 to 20:00 h

Smart Operations of Air-Conditioning and Lighting Systems in Government Buildings for Peak Power Reduction

During the summer 2007 smart operation strategies for air-conditioning (A/C) and lighting systems were developed and tested in a number of governmental buildings in Kuwait as one of the solutions to reduce the national peak demand for electrical power that commonly occur around 15:00 h. The working hours for these building are generally between 07:00 and 14:00 h and their peak demand exceeds 600 MW. The smart operation strategies implemented in these buildings included pre-closing treatment (PCT) between 13:00 and 14:00 h and time-of-day control (TDC) after 14:00 h. Also de-lamping was carried out in some of the buildings to readjust the higher than recommended illumination levels. This paper presents the achievements of implementing these smart operations strategies in Justice Palace Complex (JPC) as a case study. The peak load of this building was 3700 kW. The achievements are summarized as an all time saving of 22 kW by de-lamping, an additional saving of 27 kW through TDC of lighting, direct savings between 13:00 and 22:00 h by closing supply and return air fans of 52 air-handling units with a connected load 400 kW, and an additional saving of 550 kW during the same period by optimizing the cooling production and distribution. In conclusion project achieved an overall reduction in power demand of around 20% between 13:00 to 17:00 h and reduction ranging from 7% to 15% between 17:00 to 20:00 h

Smart Operations of Air-Conditioning and Lighting Systems in a Government Buildings for Peak Power Reduction

This paper presents the achievements of implementing smart operations strategies for air-conditioning (A/C) and lighting systems in Justice Palace Complex (JPC), Kuwait during the summer 2007. The peak load of this building was 3700 kW. The achievements are summarized as direct savings between 13:00 and 22:00 h by closing supply and return air fans of 52 air-handling units with a connected load 400 kW, and an additional saving of 550 kW during the same period by optimizing the cooling production and distribution. Also an all time saving of 22 kW by de-lamping, and additional saving of 27 kW through TDC of lighting were achieved. In conclusion project achieved an overall reduction in power demand of around 20% between 13:00 to 17:00 h and reduction ranging from 7% to 15% between 17:00 to 20:00 h

An Innovative Approach Towards National Peak Load Management

An innovative approach was developed and implemented in eight governmental buildings to reduce their load during the peak demand hours in summer of 2007. The innovative approach implemented in these buildings included pre-closing treatment (PCT) between 13:00 and 14:00 h and time-of-day control (TDC) after 14:00 h for air conditioning (A/C) and lighting systems. PCT realized an overall reduction of 3.43 MW, a saving of 11.7% of the buildings peak power demand; while TDC realized a total savings of 8.67 MW at 15:00 h, a saving of 30.7% of the buildings peak power demand at that hour. The temperature build up inside the buildings due to PCT and TDC was within the acceptable range, which validated the technical viability of these measures. The implementation of the innovative approach in the eight governmental buildings with a total measured peak demand of 29.3 MW achieved a reduction of 8.89 MW. This power is now available to other users leading to financial savings of $13.5 million for the nation towards the cost of constructing new power plants and distribution network equipment. More importantly, this reduction in peak power demand of well over 30$232 million towards the cost of new power generation equipment and distribution network

A New Model for Raf Kinase Inhibitory Protein Induced Chemotherapeutic Resistance

Therapeutic resistance remains the most challenging aspect of treating cancer. Raf kinase inhibitory protein (RKIP) emerged as a molecule capable of sensitizing cancerous cells to radio- and chemotherapy. Moreover, this small evolutionary conserved molecule, endows significant resistance to cancer therapy when its expression is reduced or lost. RKIP has been shown to inhibit the Raf-MEK-ERK, NFκB, GRK and activate the GSK3β signaling pathways. Inhibition of Raf-MEK-ERK and NFκB remains the most prominent pathways implicated in the sensitization of cells to therapeutic drugs. Our purpose was to identify a possible link between RKIP-KEAP 1-NRF2 and drug resistance. To that end, RKIP-KEAP 1 association was tested in human colorectal cancer tissues using immunohistochemistry. RKIP miRNA silencing and its inducible overexpression were employed in HEK-293 immortalized cells, HT29 and HCT116 colon cancer cell lines to further investigate our aim. We show that RKIP enhanced Kelch-like ECH-associated protein1 (KEAP 1) stability in colorectal cancer tissues and HT29 CRC cell line. RKIP silencing in immortalized HEK-293 cells (termed HEK-499) correlated significantly with KEAP 1 protein degradation and subsequent NRF2 addiction in these cells. Moreover, RKIP depletion in HEK-499, compared to control cells, bestowed resistance to supra physiological levels of H2O2 and Cisplatin possibly by upregulating NF-E2-related nuclear factor 2 (NRF2) responsive genes. Similarly, we observed a direct correlation between the extent of apoptosis, after treatment with Adriamycin, and the expression levels of RKIP/KEAP 1 in HT29 but not in HCT116 CRC cells. Our data illuminate, for the first time, the NRF2-KEAP 1 pathway as a possible target for personalized therapeutic intervention in RKIP depleted cancers

Carbonyl reductase as a significant predictor of survival and lymph node metastasis in epithelial ovarian cancer

We have recently reported a novel function for carbonyl reductase (CR), namely, its ability to modulate the metastatic potential of malignant mouse cells. Because there are currently no data addressing a similar function for CR in human cancers, the aim of this study was to assess a correlation between survival and metastasis, and CR level in epithelial ovarian cancer. Using anti-CR antibody, immunohistochemical staining was performed on 73 epithelial ovarian cancers, 13 borderline malignant tumours, and 25 benign ovarian tumours for a total of 111 specimens. The combined rate for strongly and weakly positive reactions for CR was 32.0% for benign tumours, 38.5% for borderline malignant tumours, and 61.6% for ovarian cancers. The CR-positive rate was 35.7% (weakly positive alone) for ovarian cancers with retroperitoneal lymph node (RLN) metastasis and 67.8% for those without RLN metastasis (P< 0.05). The 5-year survival rate was 62.7% for the patients with CR-negative cancer and 86.1% for those with CR-positive cancer (P< 0.05). The present results indicate that decreased CR expression in epithelial ovarian cancer is associated with RLN metastasis and poor survival.© 2001 Cancer Research Campaignhttp://www.bjcancer.co

Estrogen Receptor Silencing Induces Epithelial to Mesenchymal Transition in Human Breast Cancer Cells

We propose the hypothesis that loss of estrogen receptor function which leads to endocrine resistance in breast cancer, also results in trans-differentiation from an epithelial to a mesenchymal phenotype that is responsible for increased aggressiveness and metastatic propensity. siRNA mediated silencing of the estrogen receptor in MCF7 breast cancer cells resulted in estrogen/tamoxifen resistant cells (pII) with altered morphology, increased motility with rearrangement and switch from a keratin/actin to a vimentin based cytoskeleton, and ability to invade simulated components of the extracellular matrix. Phenotypic profiling using an Affymetrix Human Genome U133 plus 2.0 GeneChip indicated geometric fold changes ≥3 in approximately 2500 identifiable unique sequences, with about 1270 of these being up-regulated in pII cells. Changes were associated with genes whose products are involved in cell motility, loss of cellular adhesion and interaction with the extracellular matrix. Selective analysis of the data also showed a shift from luminal to basal cell markers and increased expression of a wide spectrum of genes normally associated with mesenchymal characteristics, with consequent loss of epithelial specific markers. Over-expression of several peptide growth factors and their receptors are indicative of an increased contribution to the higher proliferative rates of pII cells as well as aiding their potential for metastatic activity. Signalling molecules that have been identified as key transcriptional drivers of epithelial to mesenchymal transition were also found to be elevated in pII cells. These data support our hypothesis that induced loss of estrogen receptor in previously estrogen/antiestrogen sensitive cells is a trigger for the concomitant loss of endocrine dependence and onset of a series of possibly parallel events that changes the cell from an epithelial to a mesenchymal type. Inhibition of this transition through targeting of specific mediators may offer a useful supplementary strategy to circumvent the effects of loss of endocrine sensitivity

Childhood acute lymphoblastic leukemia in the Middle East and neighboring countries: A prospective multi-institutional international collaborative study (CALLME1) by the Middle East Childhood Cancer Alliance (MECCA)

Background: Little is known about childhood ALL in the Middle East. This study was undertaken by MECCA as initial efforts in collaborative data collection to provide clinical and demographic information on children with ALL in the Middle East. Procedure: Clinical and laboratory data for patients with ALL between January 2008 and April 2012 were prospectively collected from institutions in 14 Middle East countries and entered into a custom-built-database during induction phase. All laboratory studies including cytogenetics were done at local institutions. Results: The 1,171 voluntarily enrolled patients had a mean age of 6.1±3.9 years and 59.2 were boys. T-ALL represented 14.8 and 84.2 had B-precursor ALL. At diagnosis, 5.6 had CNS disease. The distribution of common genetic abnormalities reflected a similar percentage of hyperdiploidy (25.6), but a lower percentage of ETV6-RUNX1 translocation (14.7) compared to large series reported from Western populations. By clinical criteria, 47.1 were low/standard risk, 16.9 were intermediate risk, and 36 were high risk. Most patients received all their care at the same unit (96.9). Patients had excellent induction response to chemotherapy with an overall complete remission rate of 96. Induction toxicities were acceptable. Conclusions: This first collaborative study has established a process for prospective data collection and future multinational collaborative research in the Middle East. Despite the limitations of an incomplete population-based study, it provides the first comprehensive baseline data on clinical characteristics, laboratory evaluation, induction outcome, and toxicity. Further work is planned to uncover possible biologic differences of ALL in the region and to improve diagnosis and management. Pediatr Blood Cancer 2014; 61:1403-1410. © 2014 Wiley Periodicals, Inc

RKIP Inhibition in cervical cancer Is associated with higher tumor aggressive behavior and resistance to cisplatin therapy

Cervical cancer is one of the most common cancers in women worldwide, being high-risk group the HPV infected, the leading etiological factor. The raf kinase inhibitory protein (RKIP) has been associated with tumor progression and metastasis in several human neoplasms, however its role on cervical cancer is unclear. In the present study, 259 uterine cervix tissues, including cervicitis, cervical intraepithelial lesions and carcinomas, were analyzed for RKIP expression by immunohistochemistry. We found that RKIP expression was significantly decreased during malignant progression, being highly expressed in non-neoplastic tissues (54% of the samples; 73/135), and expressed at low levels in the cervix invasive carcinomas (,15% (19/124). Following in vitro downregulation of RKIP, we observed a viability and proliferative advantage of RKIP-inhibited cells over time, which was associated with an altered cell cycle distribution and higher colony number in a colony formation assay. An in vitro wound healing assay showed that RKIP abrogation is associated with increased migratory capability. RKIP downregulation was also associated with an increased vascularization of the tumors in vivo using a CAM assay. Furthermore, RKIP inhibition induced cervical cancer cells apoptotic resistance to cisplatin treatment. In conclusion, we described that RKIP protein is significantly depleted during the malignant progression of cervical tumors. Despite the lack of association with patient clinical outcome, we demonstrate, in vitro and in vivo, that loss of RKIP expression can be one of the factors that are behind the aggressiveness, malignant progression and chemotherapy resistance of cervical cancer.This work was partially supported by the Portuguese Fundacao para a Ciencia e Tecnologia (grant PTDC/SAU-TOX/114549/2009). Olga Martinho and Sara Granja were recipients of PhD fellowships (SFRH/BD/36463/2007 and SFRH/BD/51062/2010, respectively), and Filipe Pinto and Vera Miranda-Goncalves were recipients of research fellowships (UMINHO/BI/016/2011 and SFRH/BI/33503/2008, respectively), both from FCT, Portugal. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding received for this study

KRAS-mutation status in relation to colorectal cancer survival: the joint impact of correlated tumour markers.

Background:Mutations in the Kirsten Ras (KRAS) oncogene are common in colorectal cancer (CRC). The role of KRAS-mutation status as a prognostic factor, however, is unclear. We evaluated the relationship between KRAS-mutation status and CRC survival, considering heterogeneity in this association by tumour and patient characteristics.Methods:The population-based study included individuals diagnosed with CRC between 1998-2007 in Western Washington State. Tumour specimens were tested for KRAS exon 2 mutations, the BRAF p.V600E mutation, and microsatellite instability (MSI). We used Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between KRAS-mutation status and disease-specific and overall survival. Stratified analyses were conducted by age, sex, tumour site, stage, and MSI. We conducted additional analyses combining KRAS-mutation, BRAF-mutation, and MSI status.Results:Among 1989 cases, 31% had KRAS-mutated CRC. Kirsten Ras (KRAS)-mutated CRC was associated with poorer disease-specific survival (HR=1.37, 95% CI: 1.13-1.66). This association was not evident in cases who presented with distant-stage CRC. Cases with KRAS-wild-type/BRAF-wild-type/MSI-high CRC had the most favourable prognosis; those with CRC exhibiting a KRAS- or BRAF-mutation and no MSI had the poorest prognosis. Patterns were similar for overall survival.Conclusion:Kirsten Ras (KRAS)-mutated CRC was associated with statistically significantly poorer survival after diagnosis than KRAS-wild-type CRC