Structure Collisions between Interacting Proteins

Protein-protein interactions take place at defined binding interfaces. One protein may bind two or more proteins at different interfaces at the same time. So far it has been commonly accepted that non-overlapping interfaces allow a given protein to bind other proteins simultaneously while no collisions occur between the binding protein structures. To test this assumption, we performed a comprehensive analysis of structural protein interactions to detect potential collisions. Our results did not indicate cases of biologically relevant collisions in the Protein Data Bank of protein structures. However, we discovered a number of collisions that originate from alternative protein conformations or quaternary structures due to different experimental conditions

Measurement of the branching fraction and CP content for the decay B(0) -> D(*+)D(*-)

This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APS.We report a measurement of the branching fraction of the decay B0→D*+D*- and of the CP-odd component of its final state using the BABAR detector. With data corresponding to an integrated luminosity of 20.4  fb-1 collected at the Υ(4S) resonance during 1999–2000, we have reconstructed 38 candidate signal events in the mode B0→D*+D*- with an estimated background of 6.2±0.5 events. From these events, we determine the branching fraction to be B(B0→D*+D*-)=[8.3±1.6(stat)±1.2(syst)]×10-4. The measured CP-odd fraction of the final state is 0.22±0.18(stat)±0.03(syst).This work is supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the A.P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation

Anesthesia advanced circulatory life support

The constellation of advanced cardiac life support (ACLS) events, such as gas embolism, local anesthetic overdose, and spinal bradycardia, in the perioperative setting differs from events in the pre-hospital arena. As a result, modification of traditional ACLS protocols allows for more specific etiology-based resuscitation. Perioperative arrests are both uncommon and heterogeneous and have not been described or studied to the same extent as cardiac arrest in the community. These crises are usually witnessed, frequently anticipated, and involve a rescuer physician with knowledge of the patient's comorbidities and coexisting anesthetic or surgically related pathophysiology. When the health care provider identifies the probable cause of arrest, the practitioner has the ability to initiate medical management rapidly. Recommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community. Adapting ACLS algorithms and considering the differential diagnoses of these perioperative events may prevent cardiac arrest

Measurement of B-0 -> D-s(*)D+*(-) branching fractions and B-0 -> D-s*D+*(-) polarization with a partial reconstruction technique

We present a study of the decays B-0 --> D-s((*)) D*-, using 20.8 fb(-1) of e(+)e(-) annihilation data recorded with the BABAR detector. The analysis is conducted with a partial reconstruction technique, in which only the D-s((*)+) and the soft pion from the D*- decay are reconstructed. We measure the branching fractions B(B-0 --> Ds+D*-) = (1.03 +/- 0.14 +/- 0.13 +/- 0.26)% and B(B-0 --> D-s(*+) D*-) = (1.97 +/- 0.15 +/- 0.30+/- 0.49)%, where the first error is statistical, the second is systematic, and the third is the error due to the D-s(+) --> phipi(+) branching fraction uncertainty. From the B-0 --> D-s(*+) D*- angular distributions, we measure the fraction of longitudinal polarization Gamma(L)/Gamma = (51.9 +/- 5.0 +/- 2.8)%, which is consistent with theoretical predictions based on factorization

Geodesign:A Tale of Three Cities

In this paper we discuss the application of the Steinitz (A framework for geodesign: changing geography by design. ESRI, Redlands, CA, 2012) Geodesign Framework in the context of three cities including (i) South East Sydney, (ii) the emerging Western City of Sydney and (iii) Canberra. In all three of these case studies we have used the Geodesign Hub platform to develop a series of future city scenarios. A common theme with each of these cities is they are all experiencing population growth. Another common theme is that each city required integrated land use transport planning given new transformational infrastructure including light rail, mass transit and in the case of the Western City of Sydney a new airport being built. The research conducted is reflective and based on case studies in the context of studio work undertaken by three different Geodesign classes run across two universities. The research reflects on the strengths and opportunities of the Geodesign Framework in supporting the planning and design of future cities in the context of (i) data and technology, (ii) process, and (iii) outputs. Future work will examine the pedagogical experiences of students in working with Geodesign methods and software as we train the next generation of city planners and designers.</p

Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation

Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle