CO2 - Based Demand-Controlled Ventilation Control Strategies for Multi-Zone HVAC Systems

CO2-based demand-controlled ventilation DCV strategy offers a great opportunity to reduce energy consumption in HVAC systems while providing the required ventilation. However, implementing CO2-based DCV under ASHRAE 62.1.2004 through 2010 is not simple as it was under previous versions due to the changes in breathing-zone ventilating rate calculations. This paper discusses the difficulties in the CO2-based DCV and proposes an alternative strategy based on the supply air CO2 concentration. The proposed strategy offers great benefits in terms of better indoor air control and improved energy efficiency and could be easily implemented for multi-zone HVAC systems. To evaluate the strategy, energy simulations were performed on various USA locations and for a typical two-story office building conditioned by a VAV system. The results show that the cooling saving could be up to 23% by implementing the proposed strategy as compared to the design-occupancy ASHRAE Standard 62.1 2010 procedure

On the H\'enon-Lane-Emden conjecture

We consider Liouville-type theorems for the following H\'{e}non-Lane-Emden system \hfill -\Delta u&=& |x|^{a}v^p \text{in} \mathbb{R}^N, \hfill -\Delta v&=& |x|^{b}u^q \text{in} \mathbb{R}^N, when $pq>1$, $p,q,a,b\ge0$. The main conjecture states that there is no non-trivial non-negative solution whenever $(p,q)$ is under the critical Sobolev hyperbola, i.e. $\frac{N+a}{p+1}+\frac{N+b}{q+1}>{N-2}$. We show that this is indeed the case in dimension N=3 provided the solution is also assumed to be bounded, extending a result established recently by Phan-Souplet in the scalar case. Assuming stability of the solutions, we could then prove Liouville-type theorems in higher dimensions. For the scalar cases, albeit of second order ($a=b$ and $p=q$) or of fourth order ($a\ge 0=b$ and $p>1=q$), we show that for all dimensions $N\ge 3$ in the first case (resp., $N\ge 5$ in the second case), there is no positive solution with a finite Morse index, whenever $p$ is below the corresponding critical exponent, i.e $1<p<\frac{N+2+2a}{N-2}$ (resp., $1<p<\frac{N+4+2a}{N-4}$). Finally, we show that non-negative stable solutions of the full H\'{e}non-Lane-Emden system are trivial provided \label{sysdim00} N<2+2(\frac{p(b+2)+a+2}{pq-1}) (\sqrt{\frac{pq(q+1)}{p+1}}+ \sqrt{\frac{pq(q+1)}{p+1}-\sqrt\frac{pq(q+1)}{p+1}}).Comment: Theorem 4 has been added in the new version. 23 pages, Comments are welcome. Updated version - if any - can be downloaded at http://www.birs.ca/~nassif/ or http://www.math.ubc.ca/~fazly/research.htm

An Efficient Bandit Algorithm for Realtime Multivariate Optimization

Optimization is commonly employed to determine the content of web pages, such as to maximize conversions on landing pages or click-through rates on search engine result pages. Often the layout of these pages can be decoupled into several separate decisions. For example, the composition of a landing page may involve deciding which image to show, which wording to use, what color background to display, etc. Such optimization is a combinatorial problem over an exponentially large decision space. Randomized experiments do not scale well to this setting, and therefore, in practice, one is typically limited to optimizing a single aspect of a web page at a time. This represents a missed opportunity in both the speed of experimentation and the exploitation of possible interactions between layout decisions. Here we focus on multivariate optimization of interactive web pages. We formulate an approach where the possible interactions between different components of the page are modeled explicitly. We apply bandit methodology to explore the layout space efficiently and use hill-climbing to select optimal content in realtime. Our algorithm also extends to contextualization and personalization of layout selection. Simulation results show the suitability of our approach to large decision spaces with strong interactions between content. We further apply our algorithm to optimize a message that promotes adoption of an Amazon service. After only a single week of online optimization, we saw a 21% conversion increase compared to the median layout. Our technique is currently being deployed to optimize content across several locations at Amazon.com.Comment: KDD'17 Audience Appreciation Awar

Switching the sphingolipid rheostat in the treatment of diabetes and cancer comorbidity from a problem to an advantage

© 2015 Nikolas K. Haass et al. Cancer and diabetes are among the most common diseases in western societies. Epidemiological studies have shown that diabetic patients have a significantly higher risk of developing a number of different types of cancers and that individuals with comorbidity (cancer and diabetes/prediabetes) have a poorer prognosis relative to nondiabetic cancer patients. The increasing frequency of comorbidity of cancer and diabetes mellitus, mainly type 2 diabetes, has driven the development of therapeutic interventions that target both disease states. There is strong evidence to suggest that balancing the sphingolipid rheostat, ceramide - sphingosine - sphingosine-1-phosphate (S1P) is crucial in the prevention of diabetes and cancer and sphingosine kinase/S1P modulators are currently under development for the treatment of cancer and diabetes. This paper will highlight some of the complexities inherent in the use of the emerging sphingosine kinase/S1P modulators in the treatment of comorbidity of diabetes and cancer

The Impact of CO2-Based Demand-Controlled Ventilation on Energy Consumptions for Air Source Heat Pumps in Schools

There have been increasingly growing concerns for many years over the quality of the air inside buildings and the associated energy use. The CO2-based demand-controlled ventilation DCV offers a great opportunity to reduce energy consumption in HVAC systems while maintaining the ventilation requirements. Thus, the paper discusses the applications of CO2-based demand-controlled ventilation DCV strategy for air source heat pumps in schools, investigates its impact on the annual energy consumption, and determines the potential savings achieved in different USA locations. The study includes detailed energy analysis on an existing middle school through whole building simulation energy software. The simulation model is first calibrated and checked for accuracy using the actual monthly utility data. This model is then used for saving calculations resulted from CO2-Based DCV and with various occupancy profiles and locations. The results show a significant saving could be obtained as compared to the actual operating strategy implemented in the existing system and this saving depends mainly on the actual occupancy profile and building locations

“Dicing and splicing” sphingosine kinase and relevance to cancer

© 2017 by the authors. Licensee MDPI, Basel, Switzerland. Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or “non-oncogenic addiction”. Here we discuss additional theories of SphK cellular mislocation and aberrant “dicing and splicing” as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics

Mammalian sphingosine kinase (SphK) isoenzymes and isoform expression: challenges for SphK as an oncotarget.

The various sphingosine kinase (SphK) isoenzymes (isozymes) and isoforms, key players in normal cellular physiology, are strongly implicated in cancer and other diseases. Mutations in SphKs, that may justify abnormal physiological function, have not been recorded. Nonetheless, there is a large and growing body of evidence demonstrating the contribution of gain or loss of function and the imbalance in the SphK/S1P rheostat to a plethora of pathological conditions including cancer, diabetes and inflammatory diseases. SphK is expressed as two isozymes SphK1 and SphK2, transcribed from genes located on different chromosomes and both isozymes catalyze the phosphorylation of sphingosine to S1P. Expression of each SphK isozyme produces alternately spliced isoforms. In recent years the importance of the contribution of SpK1 expression to treatment resistance in cancer has been highlighted and, additionally, differences in treatment outcome appear to also be dependent upon SphK isoform expression. This review focuses on an exciting emerging area of research involving SphKs functions, expression and subcellular localization, highlighting the complexity of targeting SphK in cancer and also comorbid diseases. This review also covers the SphK isoenzymes and isoforms from a historical perspective, from their first discovery in murine species and then in humans, their role(s) in normal cellular function and in disease processes, to advancement of SphK as an oncotarget

Mammalian sphingosine kinase (SphK) isoenzymes and isoform expression: Challenges for SphK as an oncotarget

Copyright: © Hatoum et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The various sphingosine kinase (SphK) isoenzymes (isozymes) and isoforms, key players in normal cellular physiology, are strongly implicated in cancer and other diseases. Mutations in SphKs, that may justify abnormal physiological function, have not been recorded. Nonetheless, there is a large and growing body of evidence demonstrating the contribution of gain or loss of function and the imbalance in the SphK/S1P rheostat to a plethora of pathological conditions including cancer, diabetes and inflammatory diseases. SphK is expressed as two isozymes SphK1 and SphK2, transcribed from genes located on different chromosomes and both isozymes catalyze the phosphorylation of sphingosine to S1P. Expression of each SphK isozyme produces alternately spliced isoforms. In recent years the importance of the contribution of SpK1 expression to treatment resistance in cancer has been highlighted and, additionally, differences in treatment outcome appear to also be dependent upon SphK isoform expression. This review focuses on an exciting emerging area of research involving SphKs functions, expression and subcellular localization, highlighting the complexity of targeting SphK in cancer and also comorbid diseases. This review also covers the SphK isoenzymes and isoforms from a historical perspective, from their first discovery in murine species and then in humans, their role(s) in normal cellular function and in disease processes, to advancement of SphK as an oncotarget