Abstract. Implanted biological sensors are a special class of wireless sensor networks that are used in-vivo for various medical applications. One of the major challenges of continuous in-vivo sensing is the heat generated by the implanted sensors due to communication radiation and circuitry power consumption. This paper addresses the issues of routing in implanted sensor networks. We propose a thermal-aware routing protocol that routes the data away from high temperature areas (hot spots). With this protocol each node estimates temperature change of its neighbors and routes packets around the hot spot area by a withdraw strategy. The proposed protocol can achieve a better balance of temperature rise and only experience a modest increased delay compared with shortest hop, but thermal-awareness also indicates the capability of load balance, which leads to less packet loss in high load situations.

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The development of cardiac hypertrophy in response to increased hemodynamic load and neurohormonal stress is initially a compensatory response that may eventually lead to ventricular dilation and heart failure. Regulator of G protein signaling 5 (Rgs5) is a negative regulator of G protein-mediated signaling by inactivating Gα(q) and Gα(i), which mediate actions of most known vasoconstrictors. Previous studies have demonstrated that Rgs5 expresses among various cell types within mature heart and showed high levels of Rgs5 mRNA in monkey and human heart tissue by Northern blot analysis. However, the critical role of Rgs5 on cardiac remodeling remains unclear. To specifically determine the role of Rgs5 in pathological cardiac remodeling, we used transgenic mice with cardiac-specific overexpression of human Rgs5 gene and Rgs5 −/− mice. Our results demonstrated that the transgenic mice were resistant to cardiac hypertrophy and fibrosis through inhibition of MEK-ERK1/2 signaling, whereas the Rgs5 −/− mice displayed the opposite phenotype in response to pressure overload. These studies indicate that Rgs5 protein is a crucial component of the signaling pathway involved in cardiac remodeling and heart failure.

Abstract-A network of biosensors can be implanted in a human body for health monitoring, diagnostics, or as a prosthetic device. Biosensors can be organized into clusters where most of the communication takes place within the clusters, and long range transmissions to the base station are performed by the cluster leader to reduce the energy cost. In some applications, the tissues are sensitive to temperature increase and may be damaged by the heat resulting from normal operations and the recharging of sensor nodes. Our work is the first to consider rotating the cluster leadership to minimize the heating effects on human tissues. We explore the factors that lead to temperature increase, and the process for calculating the Specific Absorption Rate (SAR) and temperature increase of implanted biosensors by using the Finite-Difference Time-Domain (FDTD) method. We improve performance by rotating the cluster leader based on the leadership history and the sensor locations. We propose a simplified scheme, Temperature Increase Potential, to efficiently predict the temperature increase in tissues surrounding implanted sensors. Finally, a genetic algorithm is proposed to exploit the search for an optimal temperature increase sequence.

Abstract-The thermal environment of data centers plays a significant role in affecting the energy efficiency and the reliability of data center operation. A dominant problem associated with cooling data centers is the recirculation of hot air from the equipment outlets to their inlets, causing the appearance of hot spots and an uneven inlet temperature distribution. Heat is generated due to the execution of tasks, and it varies according to the power profile of a task. We are looking into the prospect of assigning the incoming tasks around the data center in such a way so as to make the inlet temperatures as even as possible; this will allow for considerable cooling power savings. Based on our previous research work on characterizing the heat recirculation in terms of cross-interference coefficients, we propose a task scheduling algorithm for homogeneous data centers, called XInt, that minimizes the inlet temperatures, and leads to minimal heat recirculation and minimal cooling energy cost for data center operation. We verify, through both theoretical formalization and simulation, that minimizing heat recirculation will result in the best cooling energy efficiency. XInt leads to an inlet temperature distribution that is 2 • C to 5 • C lower than other approaches, and achieves about 20%-30% energy savings at moderate data center utilization rates. XInt also consistently achieves the best energy efficiency compared to another recirculation minimized algorithm, MinHR.

Meteorin-like (METRNL) protein is a newly identified myokine that functions to modulate energy expenditure and inflammation in adipose tissue. Herein, we aim to investigate the potential role and molecular basis of METRNL in doxorubicin (DOX)-induced cardiotoxicity. METRNL was found to be abundantly expressed in cardiac muscle under physiological conditions that was decreased upon DOX exposure. Cardiac-specific overexpression of METRNL by adeno-associated virus serotype 9 markedly improved oxidative stress, apoptosis, cardiac dysfunction and survival status in DOX-treated mice. Conversely, knocking down endogenous METRNL by an intramyocardial injection of adenovirus exacerbated DOX-induced cardiotoxicity and death. Meanwhile, METRNL overexpression attenuated, while METRNL silence promoted oxidative damage and apoptosis in DOX-treated H9C2 cells. Systemic METRNL depletion by a neutralizing antibody aggravated DOX-related cardiac injury and dysfunction in vivo, which were notably alleviated by METRNL overexpression within the cardiomyocytes. Besides, we detected robust METRNL secretion from isolated rodent hearts and cardiomyocytes, but to a less extent in those with DOX treatment. And the beneficial effects of METRNL in H9C2 cells disappeared after the incubation with a METRNL neutralizing antibody. Mechanistically, METRNL activated SIRT1 via the cAMP/PKA pathway, and its antioxidant and antiapoptotic capacities were blocked by SIRT1 deficiency. More importantly, METRNL did not affect the tumor-killing action of DOX in 4T1 breast cancer cells and tumor-bearing mice. Collectively, cardiac-derived METRNL activates SIRT1 via cAMP/PKA signaling axis in an autocrine manner, which ultimately improves DOX-elicited oxidative stress, apoptosis and cardiac dysfunction. Targeting METRNL may provide a novel therapeutic strategy for the prevention of DOX-associated cardiotoxicity.

Studies have demonstrated that increased oxidative stress contributes to the pathogenesis and the development of pulmonary artery hypertension (PAH). Extracellular superoxide dismutase (SOD3) is essential for removing extracellular superoxide anions and it is highly expressed in lung tissue. However, it is not clear whether endogenous SOD3 can influence the development of PAH. Here we examined the effect of SOD3 knockout on hypoxia-induced PAH in mice and a loss-of-function SOD3 gene mutation (SOD3E124D) on monocrotaline (40 mg/kg)-induced PAH in rats. SOD3 knockout significantly exacerbated 2 weeks hypoxia-induced right ventricular (RV) pressure and RV hypertrophy, while RV pressure in SOD3 KO mice under normoxic conditions is similar to wild type controls. In untreated control rats at age of 8 weeks, there was no significant difference between wild type and SOD3E124D rats in RV pressure and the ratio of RV weight to left ventricular weight (0.25±0.02 in wild type rats vs. 0.25±0.01 in SOD3E124D rats). However, monocrotaline caused significantly greater increases of RV pressure in SOD3E124D rats (48.6±1.8 mmHg in wild type vs. 57.5±3.1 mmHg in SOD3E124D rats), of the ratio of RV weight to left ventricular weight (0.41±0.01 vs. 0.50±0.09, p<0.05), and of the percentage of fully muscularized small arterioles in SOD3E124D rats (55.2±2.3 % vs. 69.9 ±2.6 %, p<0.05). Together, these findings indicate that the endogenous SOD3 has no role in the development of PAH under control conditions, but plays an important role in protecting the lung from the development of PAH under stress conditions.

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