A standard interface for debugger access to message queue information in MPI

Abstract. This paper discusses the design and implementation of an interface that allows a debugger to obtain the information necessary to display the contents of the MPI message queues. The design has been implemented in the TotalView debugger, and dynamic libraries that conform to the interface exist for MPICH, as well as the proprietary MPI implementations from Compaq, IBM, and SGI.

A Standard Interface for Debugger Access to Message Queue Information in MPI

. This paper discusses the design and implementation of an interface that allows a debugger to obtain the information necessary to display the contents of the MPI message queues. The design has been implemented in the TotalView debugger, and dynamic libraries that conform to the interface exist for MPICH, as well as the proprietary MPI implementations from Compaq, IBM, and SGI. 1 Introduction In any debugging task one of the debugger's main objectives is to make visible information about the state of the executing program. Debuggers for sequential processes provide easy access to the state of the process, allowing the user to observe the values of variables, machine registers, stack backtraces, and so on. When debugging message-passing programs all of this information is still required; however, additional information specic to the message passing model is also needed if the user is to be able to debug the problems, such as deadlock that are specic to this new environment. Un..

Gratitude stimulates word-of-mouth more than words of thanks

This study examines the impact of feelings and expressions of gratitude on word-of-mouth communication applying a quantitative method and PLS-SEM. It is the first study evidencing the power of feelings of gratitude as a driver of positive word-of-mouth within the context of students’ experience of Higher Education in ASEAN and UK contexts. The study finds that feelings of gratitude are more likely to result in positive conversations with others than in thanks to the benefactor. Feelings of gratitude may also reduce silent endurance. However, expressions of gratitude appear to have no influence on a sender’s conversations about H

Transforming legal education through emotions

Law has traditionally viewed emotions as the enemies of rationality and reason, irrational and potentially dangerous forces which must be suppressed or disregarded. This separation and enmity has been mirrored within undergraduate legal education in England and Wales, with its rigid focus on seemingly impartial and objective analysis and notions such as the ubiquitous ‘thinking like a lawyer’. This paper will argue that attempts to disregard or suppress emotions within the law school are both misguided and destined to fail. It will explore the integral part emotions play within effective legal learning, the development of legal skills, and the well-being of both law students and legal academics. It will also consider how developments in legal scholarship and the evolving climate of higher education generally offer some potential, but also pitfalls, for the future acknowledgment and incorporation of emotions within undergraduate legal education in England and Wales. Bodies of literature relating to not only legal education, but also education generally, psychology and philosophy will be drawn on to demonstrate that emotions have a potentially transformative power within legal education, requiring them to be acknowledged and utilised within a more holistic, integrated form of law degree

Abstract B169: Neratinib has clinical activity in HER2-amplified breast cancer patients with tumors that have acquired activating mutations in HER2

Abstract Overexpression/amplification of HER2/ERBB2 occurs in 20% of breast cancers. Thanks to specific anti-HER2 agents, the prognosis of HER2-positive breast cancer has improved considerably. However, acquired resistance inevitably emerges over time and tumors escape pharmacologic pressure. In this work, we propose that acquisition of activating somatic mutations in HER2 upon anti-HER2 therapy may be more frequent than commonly reported and can reduce sensitivity to these agents. Moreover, we tested whether neratinib, an irreversible pan-HER inhibitor, is effective in tumors bearing both amplification and mutations of ERBB2. By targeted exome sequencing, we found that samples from metastatic breast cancer (MBC) patients relapsing to multiple lines of anti-HER2 therapy presented the acquisition of HER2 mutations. These mutations spanned from the extracellular domain (L313I, R456C) to the kinase domain (L755S, D769Y) of the receptor. To investigate the role of these mutations in drug resistance, we conducted functional studies by stably transducing the L755S HER2 mutation (the most frequent HER2 mutation in breast cancer) in two ERBB2-amplified breast cancer cell lines intrinsically sensitive to HER2 inhibition. In both models, we found that expression of L755S mutant-HER2 was sufficient to limit sensitivity to trastuzumab, lapatinib, or the combination of both agents. Consistently, neither trastuzumab nor lapatinib was effective in inhibiting tumor growth of patient-derived xenografts established from a patient with ERBB2-amplified/mutant (D769Y) breast cancer. However, neratinib treatment demonstrated marked sensitivity in this tumor model, resulting in significant tumor growth inhibition. The antitumor activity of neratinib was also explored in breast cancer patients with coexisting ERBB2 amplification and mutation, either by compassionate use after failure of standard-of-care therapy or as part of a “basket” trial (NCT01953926) enrolling ERBB2-mutant patients. In both settings, we observed durable clinical response to neratinib. MBC case #HER2 co-mutationResponse to neratinibDurability of response (mo)1D769YSD62L313ISD93Y772_A775dupSD44L755SSD55V777LPR6 Our findings indicate that acquired HER2 mutations may reduce the effectiveness of therapeutic agents commonly used for the management of ERBB2-amplified MBC. Moreover, we propose neratinib as an effective treatment option for patients whose tumors harbor both ERBB2 amplifications and mutations. Citation Format: Emiliano Cocco, F. Javier Carmona, Helen H. Won, Michael F. Berger, David M. Hyman, Valentina Rossi, Carmen Chan, Alyssa Moriarty, Kyriakos P. Papadopoulos, Michael J. Wick, James Cownie, Ivana Sarotto, Richard E. Cutler, Francesca Avogadri-Connors, Peter Savas, Alshad S. Lalani, Valentina Boni, Sherene Loi, Jose Baselga, Filippo Montemurro, Maurizio Scaltriti. Neratinib has clinical activity in HER2-amplified breast cancer patients with tumors that have acquired activating mutations in HER2 [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2017 Oct 26-30; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2018;17(1 Suppl):Abstract nr B169