Improvement in photovoltaic performance of rutile-phased TiO2 nanorod/nanoflower-based dye-sensitized solar cell

An improved dye-sensitized solar cell (DSC) of rutile-phased titanium dioxide (TiO2) electrode with increased power conversion efficiency was successfully fabricated. Rutile-phased TiO2 nanorods and nanoflowers were grown directly on fluorine-doped SnO2 (FTO) by simple aqueous chemical growth technique using one-step hydrothermal process. The solution was prepared by mixing hydrochloric acid, deionized water, and titanium butoxide used as precursor. In the preparation of DSC, both TiO2 nanorods and nanoflowers, platinum (Pt), ruthenium dye N719, and DPMII electrolyte were used as photoelectrode, counter electrode, dye solution, and liquid electrolyte, respectively. The prepared rutile-phased TiO2 nanorods and nanoflowers samples were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM). The DSCs were fabricated based on the rutile-phased titanium dioxide nanorod and nanoflower photoelectrodes. For their energy conversion efficiency, I-V characteristics and electrochemical impedance spectroscopy were studied. We also investigated the effect of cetyltrimethylammonium bromide (CTAB) reaction times 2, 5, and 10 h in the preparation of rutile-phased TiO2 nanoflowers for DSC. CTAB is one of the capping agents that cover the refine surface of nanoparticles and prevent them from coagulation or aggregation. In our final result, the combination of rutile-phased TiO2 nanorod- and nanoflower-based DSCs showed best efficiency at approximately 3.11% due to its good electron transport of TiO2 nanorods and increased surface area by the TiO2 nanoflowers that had increased dye absorption

On the Deformation of a Hyperelastic Tube Due to Steady Viscous Flow Within

In this chapter, we analyze the steady-state microscale fluid--structure interaction (FSI) between a generalized Newtonian fluid and a hyperelastic tube. Physiological flows, especially in hemodynamics, serve as primary examples of such FSI phenomena. The small scale of the physical system renders the flow field, under the power-law rheological model, amenable to a closed-form solution using the lubrication approximation. On the other hand, negligible shear stresses on the walls of a long vessel allow the structure to be treated as a pressure vessel. The constitutive equation for the microtube is prescribed via the strain energy functional for an incompressible, isotropic Mooney--Rivlin material. We employ both the thin- and thick-walled formulations of the pressure vessel theory, and derive the static relation between the pressure load and the deformation of the structure. We harness the latter to determine the flow rate--pressure drop relationship for non-Newtonian flow in thin- and thick-walled soft hyperelastic microtubes. Through illustrative examples, we discuss how a hyperelastic tube supports the same pressure load as a linearly elastic tube with smaller deformation, thus requiring a higher pressure drop across itself to maintain a fixed flow rate.Comment: 19 pages, 3 figures, Springer book class; v2: minor revisions, final form of invited contribution to the Springer volume entitled "Dynamical Processes in Generalized Continua and Structures" (in honour of Academician D.I. Indeitsev), eds. H. Altenbach, A. Belyaev, V. A. Eremeyev, A. Krivtsov and A. V. Porubo

Regulation of Neuronal Cell Death by c-Abl-Hippo/MST2 Signaling Pathway

BACKGROUND: Mammalian Ste20-like kinases (MSTs) are the mammalian homologue of Drosophila hippo and play critical roles in regulation of cell death, organ size control, proliferation and tumorigenesis. MSTs exert pro-apoptotic function through cleavage, autophosphorylation and in turn phosphorylation of downstream targets, such as Histone H2B and FOXO (Forkhead box O). Previously we reported that protein kinase c-Abl mediates oxidative stress-induced neuronal cell death through phosphorylating MST1 at Y433, which is not conserved among mammalian MST2, Drosophila Hippo and C.elegans cst-1/2. METHODOLOGY/PRINCIPAL FINDINGS: Using immunoblotting, in vitro kinase and cell death assay, we demonstrate that c-Abl kinase phosphorylates MST2 at an evolutionarily conserved site, Y81, within the kinase domain. We further show that the phosphorylation of MST2 by c-Abl leads to the disruption of the interaction with Raf-1 proteins and the enhancement of homodimerization of MST2 proteins. It thereby enhances the MST2 activation and induces neuronal cell death. CONCLUSIONS/SIGNIFICANCE: The identification of the c-Abl tyrosine kinase as a novel upstream activator of MST2 suggests that the conserved c-Abl-MST signaling cascade plays an important role in oxidative stress-induced neuronal cell death

Coevolved mutations reveal distinct architectures for two core proteins in the bacterial flagellar motor

Switching of bacterial flagellar rotation is caused by large domain movements of the FliG protein triggered by binding of the signal protein CheY to FliM. FliG and FliM form adjacent multi-subunit arrays within the basal body C-ring. The movements alter the interaction of the FliG C-terminal (FliGC) "torque" helix with the stator complexes. Atomic models based on the Salmonella entrovar C-ring electron microscopy reconstruction have implications for switching, but lack consensus on the relative locations of the FliG armadillo (ARM) domains (amino-terminal (FliGN), middle (FliGM) and FliGC) as well as changes during chemotaxis. The generality of the Salmonella model is challenged by the variation in motor morphology and response between species. We studied coevolved residue mutations to determine the unifying elements of switch architecture. Residue interactions, measured by their coevolution, were formalized as a network, guided by structural data. Our measurements reveal a common design with dedicated switch and motor modules. The FliM middle domain (FliMM) has extensive connectivity most simply explained by conserved intra and inter-subunit contacts. In contrast, FliG has patchy, complex architecture. Conserved structural motifs form interacting nodes in the coevolution network that wire FliMM to the FliGC C-terminal, four-helix motor module (C3-6). FliG C3-6 coevolution is organized around the torque helix, differently from other ARM domains. The nodes form separated, surface-proximal patches that are targeted by deleterious mutations as in other allosteric systems. The dominant node is formed by the EHPQ motif at the FliMMFliGM contact interface and adjacent helix residues at a central location within FliGM. The node interacts with nodes in the N-terminal FliGc α-helix triad (ARM-C) and FliGN. ARM-C, separated from C3-6 by the MFVF motif, has poor intra-network connectivity consistent with its variable orientation revealed by structural data. ARM-C could be the convertor element that provides mechanistic and species diversity.JK was supported by Medical Research Council grant U117581331. SK was supported by seed funds from Lahore University of Managment Sciences (LUMS) and the Molecular Biology Consortium

The assessment of information technology maturity in emergency response organizations

[EN] In emergency response organizations, information technologies are not adequately explored. Sometimes, the mere adoption of new information technologies is not productive, as their efficient use depends on other interrelated technologies and the environment where they are installed. This work describes a model to help organizations understand their capability in respect to the adoption of these technologies. The model also helps the performing of the evaluation from different perspectives, making it suitable to collaborative evaluation. Using the proposed model, an organization can measure its maturity level in different aspects of the evaluation and guide the investment on its capabilities. Part of the model has been developed for emergency response organizations and the information technology dimension of the model has been applied to two fire department installations.Marcos R. S. Borges was partially supported by grants No. 560223/2010-2 and 480461/2009-0 from CNPq (Brazil). Work of José H. Canós is partially funded by the Spanish Ministerio. de Educación y Ciencia (MEC) under grant TIPEX (TIN2010–19859-C03-03). The cooperation between the Brazilian and the Spanish research groups was partially sponsored by the CAPES/MECD Cooperation Program, Project #169/ PHB2007-0064-PC.Santos, RS.; Borges, MRS.; Canos Cerda, JH.; Gomes, JO. (2011). The assessment of information technology maturity in emergency response organizations. Group Decision and Negotiation. 20(5):593-613. doi:10.1007/s10726-011-9232-zS593613205Bigley G, Roberts KH (2001) The incident command system: high reliability organizing for complex and volatile task environments. Acad Manag J 44(6): 1281–1299Chinowsky P, Molenaar K, Realph A (2007) Learning organizations in construction. J Manag Eng 23(1): 27–34Diniz VB, Borges MRS, Gomes JO, Canós JH (2008) Decision making support in emergency response. In: Encyclopedia of decision making, Information Science Reference (an imprint of IGI Global), New York, pp 184–191Dörner R, Grimm P, Seiler C (2001) ETOILE—an environment for team, organizational and individual learning. CG Top 13(3): 5–6Dykstra E (2003) Concept paper: toward an international system model in emergency management. In: Proceedings of toward an international system model in emergency management, Public Entity Risk InstituteFederal Emergency Management Agency (FEMA) (1998) Emergency management guide for business and industry: a step-by-step approach to emergency planning, response and recovery for companies of all sizesGu Q, Mendonça D (2005) Patterns of group information seeking in a simulated emergency response environment. In: Proceedings of the 2nd international ISCRAM conference, Brussels, BelgiumHale J (1997) A layered communication architecture for the support of crisis response. J Manag Inf Syst 14(1): 235–255King W, Teo T (1997) Integration between business planning and information systems planning: validating a stage hypothesis. Decis Sci 28(2): 279–307Lachner J, Hellwagner H (2008) Information and communication systems for mobile emergency response. Lecture notes in business information processing, vol 5. pp 213–224Lavoie D, Culbert A (1978) Stages in organization and development. Human Relat 31(5): 417–438Lindel MK, Prater C, Perry RW (2007) Emergency management. Wiley, New YorkLlavador M, Letelier P, Penadés MC, Borges MRS, Solís C (2006) Precise yet flexible specification of emergency resolution procedures. In: Proceedings of the information systems for crisis response and management (ISCRAM), pp 110–120Meissner A, Wang Z, Putz W, Grimmer J (2006) MIKoBOS: a mobile information and communication system for emergency response. In: Proceedings of the 3rd international ISCRAM conference, Newark, New JerseyNonaka I, Takeuchi H (1995) The knowledge creating company: how Japanese companies create the dynamics of innovation. Oxford University Press, OxfordOchoa S, Neyem A, Pino JA, Borges MRS (2007) Supporting group decision making and coordination in urban disasters relief efforts. J Decis Syst 16(2): 143–172Paton D, Flin R (1999) Disaster stress: an emergency management perspective. Disaster Prev Manag 8(4): 261–267Paulk MC, Weber C, Curtis B, Chrissis M (1995) The capability maturity model: guidelines for improving the software process. Addison-Wesley, ReadingQuarantelli EL (1997) Problematical aspects of the information/communication revolution for disaster planning and research: ten non-technical issues and questions. Disaster Prev Manag 6(2): 94–106Santos RS, Borges MRS, Gomes JO, Canós JH (2008) Maturity levels of information technologies in emergency response organizations. In: Proceedings of the international workshop on groupware, Omaha, Nebraska, USA. Groupware: design, implementation and use. Lecture notes in computer science, vol 5411. Springer, Berlin, pp 135–150Schoenharl T, Szabo G, Madey G, Barabasi AL (2006) WIPER: a multi-agent system for emergency response. In: Proceedings of the 3rd international ISCRAM conference, Newark, New JerseyTuroff M (2002) Past and future emergency response information systems. Commun ACM 45(4): 29–33Turoff M, Chumer M, Hiltz R, Clasher R, Alles M, Vasarhelyi M, Kogan A (2004a) Assuring homeland security: continuous monitoring, control and assurance of emergency preparedness. J Inf Technol Theor Appl (JITTA) 6(3): 1–24Turoff M, Chumer M, Vande Walle B, Yao X (2004b) The design of a dynamic emergency response management information system (DERMIS). J Inf Technol Theor Appl (JITTA) 5(4): 1–35Van der Lee MDE, Van Vugt M (2004) IMI—An information system for effective multidisciplinary incident management. 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A mitotic function for the high-mobility group protein HMG20b regulated by its interaction with the BRC repeats of the BRCA2 tumor suppressor.

The inactivation of BRCA2, a suppressor of breast, ovarian and other epithelial cancers, triggers instability in chromosome structure and number, which are thought to arise from defects in DNA recombination and mitotic cell division, respectively. Human BRCA2 controls DNA recombination via eight BRC repeats, evolutionarily conserved motifs of ∼35 residues, that interact directly with the recombinase RAD51. How BRCA2 controls mitotic cell division is debated. Several studies by different groups report that BRCA2 deficiency affects cytokinesis. Moreover, its interaction with HMG20b, a protein of uncertain function containing a promiscuous DNA-binding domain and kinesin-like coiled coils, has been implicated in the G2-M transition. We show here that HMG20b depletion by RNA interference disturbs the completion of cell division, suggesting a novel function for HMG20b. In vitro, HMG20b binds directly to the BRC repeats of BRCA2, and exhibits the highest affinity for BRC5, a motif that binds poorly to RAD51. Conversely, the BRC4 repeat binds strongly to RAD51, but not to HMG20b. In vivo, BRC5 overexpression inhibits the BRCA2-HMG20b interaction, recapitulating defects in the completion of cell division provoked by HMG20b depletion. In contrast, BRC4 inhibits the BRCA2-RAD51 interaction and the assembly of RAD51 at sites of DNA damage, but not the completion of cell division. Our findings suggest that a novel function for HMG20b in cytokinesis is regulated by its interaction with the BRC repeats of BRCA2, and separate this unexpected function for the BRC repeats from their known activity in DNA recombination. We propose that divergent tumor-suppressive pathways regulating chromosome segregation as well as chromosome structure may be governed by the conserved BRC motifs in BRCA2

Genome wide analysis of gene expression changes in skin from patients with type 2 diabetes

Non-healing chronic ulcers are a serious complication of diabetes and are a major healthcare problem. While a host of treatments have been explored to heal or prevent these ulcers from forming, these treatments have not been found to be consistently effective in clinical trials. An understanding of the changes in gene expression in the skin of diabetic patients may provide insight into the processes and mechanisms that precede the formation of non-healing ulcers. In this study, we investigated genome wide changes in gene expression in skin between patients with type 2 diabetes and non-diabetic patients using next generation sequencing. We compared the gene expression in skin samples taken from 27 patients (13 with type 2 diabetes and 14 non-diabetic). This information may be useful in identifying the causal factors and potential therapeutic targets for the prevention and treatment of diabetic related diseases

A Novel Checkpoint and RPA Inhibitory Pathway Regulated by Rif1

Cells accumulate single-stranded DNA (ssDNA) when telomere capping, DNA replication, or DNA repair is impeded. This accumulation leads to cell cycle arrest through activating the DNA–damage checkpoints involved in cancer protection. Hence, ssDNA accumulation could be an anti-cancer mechanism. However, ssDNA has to accumulate above a certain threshold to activate checkpoints. What determines this checkpoint-activation threshold is an important, yet unanswered question. Here we identify Rif1 (Rap1-Interacting Factor 1) as a threshold-setter. Following telomere uncapping, we show that budding yeast Rif1 has unprecedented effects for a protein, inhibiting the recruitment of checkpoint proteins and RPA (Replication Protein A) to damaged chromosome regions, without significantly affecting the accumulation of ssDNA at those regions. Using chromatin immuno-precipitation, we provide evidence that Rif1 acts as a molecular “band-aid” for ssDNA lesions, associating with DNA damage independently of Rap1. In consequence, small or incipient lesions are protected from RPA and checkpoint proteins. When longer stretches of ssDNA are generated, they extend beyond the junction-proximal Rif1-protected regions. In consequence, the damage is detected and checkpoint signals are fired, resulting in cell cycle arrest. However, increased Rif1 expression raises the checkpoint-activation threshold to the point it simulates a checkpoint knockout and can also terminate a checkpoint arrest, despite persistent telomere deficiency. Our work has important implications for understanding the checkpoint and RPA–dependent DNA–damage responses in eukaryotic cells

PP1A-Mediated Dephosphorylation Positively Regulates YAP2 Activity

Background: The Hippo/MST1 signaling pathway plays an important role in the regulation of cell proliferation and apoptosis. As a major downstream target of the Hippo/MST1 pathway, YAP2 (Yes-associated protein 2) functions as a transcriptional cofactor that has been implicated in many biological processes, including organ size control and cancer development. MST1/Lats kinase inhibits YAP2’s nuclear accumulation and transcriptional activity through inducing the phosphorylation at serine 127 and the sequential association with 14-3-3 proteins. However, the dephosphorylation of YAP2 is not fully appreciated. Methodology/Principal Findings: In the present study, we demonstrate that PP1A (catalytic subunit of protein phosphatase-1) interacts with and dephosphorylates YAP2 in vitro and in vivo, and PP1A-mediated dephosphorylation induces the nuclear accumulation and transcriptional activation of YAP2. Inhibition of PP1 by okadiac acid (OA) increases the phosphorylation at serine 127 and cytoplasmic translocation of YAP2 proteins, thereby mitigating its transcription activity. PP1A expression enhances YAP2’s pro-survival capability and YAP2 knockdown sensitizes ovarian cancer cells to cisplatin treatment. Conclusions/Significance: Our findings define a novel molecular mechanism that YAP2 is positively regulated by PP1mediate