Maximizing Barrier Coverage Lifetime with Mobile Sensors

Sensor networks are ubiquitously used for detection and tracking and as a result covering is one of the main tasks of such networks. We study the problem of maximizing the coverage lifetime of a barrier by mobile sensors with limited battery powers, where the coverage lifetime is the time until there is a breakdown in coverage due to the death of a sensor. Sensors are first deployed and then coverage commences. Energy is consumed in proportion to the distance traveled for mobility, while for coverage, energy is consumed in direct proportion to the radius of the sensor raised to a constant exponent. We study two variants which are distinguished by whether the sensing radii are given as part of the input or can be optimized, the fixed radii problem and the variable radii problem. We design parametric search algorithms for both problems for the case where the final order of the sensors is predetermined and for the case where sensors are initially located at barrier endpoints. In contrast, we show that the variable radii problem is strongly NP-hard and provide hardness of approximation results for fixed radii for the case where all the sensors are initially co-located at an internal point of the barrier

Lean, Green, and Lifetime Maximizing Sensor Deployment on a Barrier

Mobile sensors are located on a barrier represented by a line segment, and each sensor has a single energy source that can be used for both moving and sensing. Sensors may move once to their desired destinations and then coverage/communication is commenced. The sensors are collectively required to cover the barrier or in the communication scenario set up a chain of communication from endpoint to endpoint. A sensor consumes energy in movement in proportion to distance traveled, and it expends energy per time unit for sensing in direct proportion to its radius raised to a constant exponent. The first focus is of energy efficient coverage. A solution is sought which minimizes the sum of energy expended by all sensors while guaranteeing coverage for a predetermined amount of time. The objective of minimizing the maximum energy expended by any one sensor is also considered. The dual model is then studied. Sensors are equipped with batteries and a solution is sought which maximizes the coverage lifetime of the network, i.e. the minimum lifetime of any sensor. In both of these models, the variant where sensors are equipped with predetermined radii is also examined. Lastly, the problem of maximizing the lifetime of a wireless connection between a transmitter and a receiver using mobile relays is considered. These problems are mainly examined from the point of view of approximation algorithms due to the hardness of many of them

Microglial Inflammation and Cognitive Dysfunction in Comorbid Rat Models of Striatal Ischemic Stroke and Alzheimer\u27s Disease: Effects of Antioxidant Catalase-SKL on Behavioral and Cellular Pathology

Ischemic stroke often co-occurs with Alzheimer\u27s disease (AD) leading to a worsened clinical outcome. Neuroinflammation is a critical process implicated in AD and ischemic pathology, associated with cognitive decline. We sought to investigate the combined effects of ischemic stroke induced by endothelin-1 injection in two AD rat models, using motor function, memory and microglial inflammation in the basal forebrain and striatum as readouts. In addition, we sought to determine the effectiveness of the antioxidant biologic CAT-SKL in one of the models. The early AD model employed the bilateral intracerebroventricular injections of the toxic β-amyloid peptide Aβ25–35, the prodromal AD model used the transgenic Fischer 344 rat overexpressing a pathological mutant human amyloid precursor protein. Motor function was assessed using a cylinder, modified sticky tape and beam-walk tasks; learning and memory were tested in the Morris water maze. Microglial activation was examined using immunohistochemistry. Aβ25–35 toxicity and stroke combination greatly increased microglial inflammation in the basal forebrain. Prodromal AD-pathology coupled with ischemia in the transgenic rat resulted in a greater microgliosis in the striatum. Combined transgenic rats showed balance alterations, comorbid Aβ25–35 rats showed a transient sensorimotor deficit, and both demonstrated spatial reference memory deficit. CAT-SKL treatment ameliorated memory impairment and basal forebrain microgliosis in Aβ25–35 rats with stroke. Our results suggest that neuroinflammation could be one of the early processes underlying the interaction of AD with stroke and contributing to the cognitive impairment, and that therapies such as antioxidant CAT-SKL could be a potential therapeutic strategy

Treating triple negative breast cancer cells with erlotinib plus a select antioxidant overcomes drug resistance by targeting cancer cell heterogeneity

Among breast cancer patients, those diagnosed with the triple-negative breast cancer (TNBC) subtype have the worst prog-nosis. TNBC does not express estrogen receptor-alpha, progesterone receptor, or the HER2 oncogene; therefore, TNBC lacks targets for molecularly-guided therapies. The concept that EGFR oncogene inhibitor drugs could be used as targeted treatment against TNBC has been put forth based on estimates that 30-60% of TNBC express high levels of EGFR. However, results from clinical trials testing EGFR inhibitors, alone or in combination with cytotoxic chemotherapy, did not improve patient outcomes. Results herein offer an explanation as to why EGFR inhibitors failed TNBC patients and support how combining a select antioxidant and an EGFR-specific small molecule kinase inhibitor (SMKI) could be an effective, novel therapeutic strategy. Treatment with CAT-SKL-a re-engineered protein form of the antioxidant enzyme catalase-inhibited cancer stem-like cells (CSCs), and treatment with the EGFR-specific SMKI erlotinib inhibited non-CSCs. Thus, combining the antioxidant CAT-SKL with erlotinib targeted both CSCs and bulk cancer cells in cultures of EGFR-expressing TNBC-derived cells. We also report evidence that the mechanism for CAT-SKL inhibition of CSCs may depend on antioxidant-induced downregulation of a short alternative mRNA splicing variant of the methyl-CpG binding domain 2 gene, isoform MBD2c