Local false discovery rate facilitates comparison of different microarray experiments

The local false discovery rate (LFDR) estimates the probability of falsely identifying specific genes with changes in expression. In computer simulations, LFDR <10% successfully identified genes with changes in expression, while LFDR >90% identified genes without changes. We used LFDR to compare different microarray experiments quantitatively: (i) Venn diagrams of genes with and without changes in expression, (ii) scatter plots of the genes, (iii) correlation coefficients in the scatter plots and (iv) distributions of gene function. To illustrate, we compared three methods for pre-processing microarray data. Correlations between methods were high (r = 0.84–0.92). However, responses were often different in magnitude, and sometimes discordant, even though the methods used the same raw data. LFDR complements functional assessments like gene set enrichment analysis. To illustrate, we compared responses to ultraviolet radiation (UV), ionizing radiation (IR) and tobacco smoke. Compared to unresponsive genes, genes responsive to both UV and IR were enriched for cell cycle, mitosis, and DNA repair functions. Genes responsive to UV but not IR were depleted for cell adhesion functions. Genes responsive to tobacco smoke were enriched for detoxification functions. Thus, LFDR reveals differences and similarities among experiments

Increasing Power Density of LSGM-Based Solid Oxide Fuel Cells Using New Anode Materials

Chemical reactions between the superior perovskite oxide-ion conductor Sr- and Mg-doped LaGaO3 (LSGM), CeO2, and NiO have been studied by powder X-ray diffraction. The results showed that an extensive reactivity occurs as a result of La migration driven by a gradient of La chemical activity. La migration across the LSGM/electrode interfaces in a fuel cell leads to the formation of resistive phases at the interface, either LaSrGa3O7 or LaSrGaO4. Use of 40 mol % La2O3 -doped CeO2 as an interlayer between anode and electrolyte as well as in the NiO-containing anode prevents all reactions found. Consequently, the air-H2 cell maximum power density was increased to nearly 900 mW/cm2 at 800°C with a 600 μm thick LSGM electrolyte. No sign of degradation was observed at 800°C over 2 weeks for an interlayered cell under a loading current density of 250 mA/cm2

Lifetime Maximization for Amplify-and-Forward Cooperative Networks

[[abstract]]Power allocation strategies are devised to maximize the network lifetime of amplify-and-forward (AF) cooperative networks. We consider the scenario where one source and multiple partners cooperate to transmit messages to the destination. The powers emitted by the users are subject to the SNR requirement at the destination. First, the power allocation strategy that demands the minimum instantaneous aggregate transmit power of all cooperating partners is described and analyzed. The optimal solution results in a form of selective relaying; namely, the user with the best channel condition is selected to help in relaying the message. However, this instantaneous power minimization strategy does not necessarily maximize the lifetime of battery-limited systems. Then, we propose three AF cooperative schemes to exploit the channel state information (CSI), the residual battery energy and the QoS requirement. It is shown that the network lifetime can be extended considerably by taking all these three factors into account.[[fileno]]2030137030021[[department]]電機工程學

Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria.

SCL25A46 is a mitochondrial carrier protein that surprisingly localizes to the outer membrane and is distantly related to Ugo1. Here we show that a subset of SLC25A46 interacts with mitochondrial dynamics components and the MICOS complex. Decreased expression of SLC25A46 results in increased stability and oligomerization of MFN1 and MFN2 on mitochondria, promoting mitochondrial hyperfusion. A mutation at L341P causes rapid degradation of SLC25A46, which manifests as a rare disease, pontocerebellar hypoplasia. The E3 ubiquitin ligases MULAN and MARCH5 coordinate ubiquitylation of SLC25A46 L341P, leading to degradation by organized activities of P97 and the proteasome. Whereas outer mitochondrial membrane-associated degradation is typically associated with apoptosis or a specialized type of autophagy termed mitophagy, SLC25A46 degradation operates independently of activation of outer membrane stress pathways. Thus SLC25A46 is a new component in mitochondrial dynamics that serves as a regulator for MFN1/2 oligomerization. Moreover, SLC25A46 is selectively degraded from the outer membrane independently of mitophagy and apoptosis, providing a framework for mechanistic studies in the proteolysis of outer membrane proteins

The Role of PSR in Zebrafish (Danio rerio) at Early Embryonic Development

During development, the role of the phosphatidylserine receptor (PSR) in the professional removal of apoptotic cells that have died is few understood. Programmed cell death (PCD) began during the shield stage (5.4 hpf), with dead cells being engulfed by a neighboring cell that showed a normal-looking nucleus and the nuclear condensation multi-micronuclei of an apoptotic cell. Recently, in the zebrafish model system, PS receptor played a new role on corpse cellular cleaning for further normal development during early embryonic development, which also correlated with tissues’ or organs’ complete development and organogenesis. In the present, we summary new story that a transcriptional factor, YY1a, in the upstream of PSR is how to regulate PS receptor expression that linked to function of PSR-phagocyte mediated apoptotic cell engulfment during development, especially the development of organs such as the brain and heart. YY1a/PSR-mediated engulfing system may involve in diseases and therapy. This engulfing system may provide new insight into phosphatidylserine receptor how to dynamitic interaction with apoptotic cell during priming programmed cell death

Discrete Power Allocation for Lifetime Maximization in Cooperative Networks

[[abstract]]Discrete power allocation strategies for amplifyand- forward cooperative networks are proposed based on selective relaying methods. The goal of power allocation is to maximize the network lifetime, which is defined as the duration of time for which the outage probability at the destination can be maintained above a certain level. The discrete power levels enable a low cost implementation and a close integration with high speed digital circuits. We propose three power allocation strategies that take into consideration both the channel state information (CSI) and the residual energy information (REI) at each node. By modeling the residual energy of each node as the states of a Markov Chain, we are able to derive the network lifetime analytically by the expected number of transitions to the absorbing states, i.e., the energy states for which the outage probability is no longer achievable. The performance of the three strategies are compared through numerical simulations and a significant improvement in network lifetime is shown, when compared with the case considering only the local CSI.[[fileno]]2030137030010[[department]]電機工程學

Experience with adjuvant chemotherapy for pseudomyxoma peritonei secondary to mucinous adenocarcinoma of the appendix with oxaliplatin/fluorouracil/leucovorin (FOLFOX4)

<p>Abstract</p> <p>Background</p> <p>Pseudomyxoma peritonei (PMP) is a rare condition characterized by mucinous tumors, disseminated intra-peritoneal implants, and mucinous ascites. So far its diagnosis remains challenging to most clinicians.</p> <p>Case presentation</p> <p>A 55-year-old male patient had suffered from acute onset of abdominal pain and abdominal distension for one day prior to his admission. Physical examination revealed tenderness over the right lower quadrant of the abdomen without diffuse muscle guarding. A large amount of ascites was identified by abdominal computed tomography (CT) scan. Paracentesis showed the appearance of sticky mucinous ascites. He underwent laparotomy under the impression of pseudomyxoma peritonei. There was a lot of mucinous ascites, one appendiceal tumor and multiple peritoneal implants disseminated from the subphrenic space to the recto-vesicle pouch. Pseudomyxoma Peritonei caused by mucinous adenocarcinoma of appendiceal origin, was confirmed by histopathology. We performed an excision of the appendiceal tumor combined with copious irrigation and debridement. After the operation, he received 10 cycles of systemic chemotherapy with FOLFOX4 regimen, without specific morbidity. Follow-up of abdominal CT and colonoscopy at post-operative 17 months showed excellent response without evidence of local recurrence or distal metastasis. He made an uneventful recovery (up to the present) for 21 months after the operation.</p> <p>Conclusion</p> <p>This case report emphasizes the possible new role of systemic chemotherapy in the treatment of patients with this rare clinical syndrome.</p