Impact of IT Multisourcing on vendor opportunistic behaviour - A research framework

IT Multisourcing (ITM), the provision of IT services by multiple interdependent vendors to a single client, is widely prevalent now. ITM, in principle, is believed to mitigate both strategic and operational risks of IT outsourcing for client organizations. Yet an in-depth inquiry into the association of ITM with these risks is largely missing in literature. There is limited research which systematically investigates the effects of ITM on different forms of risk. This paper develops a theoretical framework to understand the implications of ITM for the specific risk of vendor opportunistic behaviour, also termed ‘strategic risks’ of outsourcing. The fundamental attributes of ITM are identified and mechanisms through which they influence vendor opportunistic behaviour are explained. The advantages and limitations of the framework are discussed and future research directions are laid out

IS discipline in the IT services land : an exploratory study of IS in India

Information Systems (IS) research is characterized by plurality of methodologies, perspectives and contexts giving rise to various communities within the discipline. Studies of IS communities in North America, Europe and Asia-Pacific highlight the cognitive diversity, institutional distribution and research themes based on geography. While regional variations have been acknowledged, the debate on the identity and status of IS is on-going. In this paper we conduct an exploratory study of the IS research paradigm in India and contribute to IS discipline studies by bringing in the India perspective. We analyse the &lsquo;cognitive&rsquo; and &lsquo;behavioural&rsquo; legitimacy of IS discipline in India based on interviews conducted with Indian business school professors from IS and non-IS disciplines. The focus of the study is to understand the current state of IS research community in India. We find a need to establish a &lsquo;collective identity&rsquo; of IS research in India, which will benefit both the Indian and larger IS community to work on unique research possibilities presented by the socioeconomic context of India.<br /

Construction of an instant structured illumination microscope

A challenge in biological imaging is to capture high-resolution images at fast frame rates in live cells. The “instant structured illumination microscope” (iSIM) is a system designed for this purpose. Similarly to standard structured illumination microscopy (SIM), an iSIM provides a twofold improvement over widefield microscopy, in x, y and z, but also allows much faster image acquisition, with real-time display of super-resolution images. The assembly of an iSIM is reasonably complex, involving the combination and alignment of many optical components, including three micro-optics arrays (two lenslet arrays and an array of pinholes, all with a pitch of 222 μm) and a double-sided scanning mirror. In addition, a number of electronic components must be correctly controlled. Construction of the system is therefore not trivial, but is highly desirable, particularly for live-cell imaging. We report, and provide instructions for, the construction of an iSIM, including minor modifications to a previous design in both hardware and software. The final instrument allows us to rapidly acquire fluorescence images at rates faster than 100 fps, with approximately twofold improvement in resolution in both x-y and z; sub-diffractive biological features have an apparent size (full width at half maximum) of 145 nm (lateral) and 320 nm (axial), using a 1.49 NA objective and 488 nm excitation

GGN repeat length and GGN/CAG haplotype variations in the androgen receptor gene and prostrate cancer risk in south Indian men

The ethnic variation in the GGN and CAG microsatellites of the androgen receptor (AR) gene suggests their role in the substantial racial difference in prostate cancer risk. Hence, we performed a casecontrol study to assess whether GGN repeats independently or in combination with CAG repeats were associated with prostate cancer risk in South Indian men. The repeat lengths of the AR gene determined by Gene scan analysis, revealed that men with GGN repeats £21 had no significant risk compared to those with >21 repeats (OR 0.91 at 95% CI-0.52–1.58). However, when CAG repeats of our earlier study was combined with the GGN repeat data, the cases exhibited significantly higher frequency of the haplotypes CAG £19/GGN £21 (OR-5.2 at 95% CI-2.17– 12.48, P 21(OR-6.9 at 95%CI-2.85–17.01, P < 0.001) compared to the controls. No significant association was observed between GGN repeats and prostate-specific antigen levels and the age at diagnosis. Although a trend of short GGN repeats length in high-grade was observed, it was not significant (P = 0.09). Overall, our data reveals that specific GGN/CAG haplotypes (CAG £19/GGN £21 and CAG £19/GGN > 21) of AR gene increase the risk of prostate cancer and thus could serve as susceptibility marker for prostate cancer in South Indian men

The EPICS Software Framework Moves from Controls to Physics

The Experimental Physics and Industrial Control System (EPICS), is an open-source software framework for high-performance distributed control, and is at the heart of many of the world’s large accelerators and telescopes. Recently, EPICS has undergone a major revision, with the aim of better computing supporting for the next generation of machines and analytical tools. Many new data types, such as matrices, tables, images, and statistical descriptions, plus users’ own data types, now supplement the simple scalar and waveform types of the former EPICS. New computational architectures for scientific computing have been added for high-performance data processing services and pipelining. Python and Java bindings have enabled powerful new user interfaces. The result has been that controls are now being integrated with modelling and simulation, machine learning, enterprise databases, and experiment DAQs. We introduce this new EPICS (version 7) from the perspective of accelerator physics and review early adoption cases in accelerators around the world

Enabling remote design and troubleshooting experiments using the ilab shared architecture

12th Biennial International Conference on Engineering, Construction, and Operations in Challenging Environments; and Fourth NASA/ARO/ASCE Workshop on Granular Materials in Lunar and Martian Exploration Honolulu, Hawaii, United States March 14-17, 2010The MIT iLab Project is dedicated to the goal of increasing laboratory experimentation opportunities for engineering students worldwide. Since its inception in 1998, the project has furthered this goal through the development of individual remote laboratories, or iLabs, as well as a distributed software infrastructure designed to streamline the implementation and sharing of remote laboratories. iLabs are designed to complement traditional, hands-on laboratories by providing practical educational experiences where they would not otherwise be available. Such remote labs, developed and hosted by MIT and other institutions within the iLab Consortium, have been successfully used by instructors at schools across the educational spectrum and around the world. While certainly valuable, many of the original experiments available through the iLab platform provide a limited experience in that they are observational in nature. They only provide students the ability to study the behavior of a pre-defined system under test. Such labs have proven to be valuable additions to engineering curricula, but do not have the flexibility that is inherent in a traditional laboratory experience. To address this, the MIT iLab Project has begun focusing on the development of iLabs that provide students with the ability to design or troubleshoot experimental systems. Through two particular remote labs, focusing on electronic control system analysis and basic electronics test and measurement respectively, the project is designing remote labs that provide a more flexible learning experience for students and are more attractive to instructors in a broad set of disciplines.National Science Foundation (U.S.) (award 0702735)Singapore-MIT Alliance for Research and Technology CenterMicrosoft CorporationCarnegie Corporation of New YorkMaricopa County Community College District. Maricopa Advanced Technology Education Cente

The role of cardiac troponin T quantity and function in cardiac development and dilated cardiomyopathy

Background: Hypertrophic (HCM) and dilated (DCM) cardiomyopathies results from sarcomeric protein mutations, including cardiac troponin T (cTnT, TNNT2). We determined whether TNNT2 mutations cause cardiomyopathies by altering cTnT function or quantity; whether the severity of DCM is related to the ratio of mutant to wildtype cTnT; whether Ca2+ desensitization occurs in DCM; and whether absence of cTnT impairs early embryonic cardiogenesis. Methods and Findings: We ablated Tnnt2 to produce heterozygous Tnnt2+/ mice, and crossbreeding produced homozygous null Tnnt2-/-embryos. We also generated transgenic mice overexpressing wildtype (TGWT) or DCM mutant (TGK210Δ) Tnnt2. Crossbreeding produced mice lacking one allele of Tnnt2, but carrying wildtype (Tnnt2+/-/TGWT) or mutant (Tnnt2+/-/TGK210Δ) transgenes. Tnnt2+/-mice relative to wildtype had significantly reduced transcript (0.82 ± 0.06 [SD] vs. 1.00 ± 0.12 arbitrary units; p = 0.025), but not protein (1.01 ± 0.20 vs. 1.00 ± 0.13 arbitrary units; p = 0.44). Tnnt2+/-mice had normal hearts (histology, mass, left ventricular end diastolic diameter [LVEDD], fractional shortening [FS]). Moreover, whereas Tnnt2+/-/ TGK210Δ mice had severe DCM, TGK210Δ mice had only mild DCM (FS 18 ± 4 vs. 29 ± 7%; p < 0.01). The difference in severity of DCM may be attributable to a greater ratio of mutant to wildtype Tnnt2 transcript in Tnnt2+/-/TGK210Δ relative to TGK210Δ mice (2.42±0.08, p = 0.03). Tnnt2+/-/TGK210Δ muscle showed Ca2+ desensitization (pCa50 = 5.34 ± 0.08 vs. 5.58 ± 0.03 at sarcomere length 1.9 μm. p<0.01), but no difference in maximum force generation. Day 9.5 Tnnt2-/-embryos had normally looped hearts, but thin ventricular walls, large pericardial effusions, noncontractile hearts, and severely disorganized sarcomeres. Conclusions: Absence of one Tnnt2 allele leads to a mild deficit in transcript but not protein, leading to a normal cardiac phenotype. DCM results from abnormal function of a mutant protein, which is associated with myocyte Ca2+ desensitization. The severity of DCM depends on the ratio of mutant to wildtype Tnnt2 transcript. cTnT is essential for sarcomere formation, but normal embryonic heart looping occurs without contractile activity. © 2008 Ahmad et al

Uremic serum-induced calcification of human aortic smooth muscle cells is a regulated process involving Klotho and RUNX2

© 2019 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).Vascular calcification (VC) is common in subjects with chronic kidney disease (CKD) and is associated with increased cardiovascular risk. It is an active process involving transdifferentiation of arterial smooth muscle cells (SMCs) into osteogenic phenotype. We investigated the ability of serum from CKD subjects to induce calcification in human SMCs in vitro (calcific potential of sera: CP), and associated changes in expression of Runt-related transcription factor 2 (RUNX2), SM22a, and Klotho. Sera from subjects with CKD (18 stage 3, 17 stage 4/5, and 29 stage 5D) and 20 controls were added to human cultured SMCs and CP quantified. The CP of CKD sera was greater (P>0.01) than that of controls, though not influenced by CKD stage. Modification of diet in renal disease estimated glomerular filtration rate (MDRD-4 eGFR) (P>0.001), serum phosphate (P=0.042), receptor activator of nuclear factor ?appa-B ligand (RANKL) (P=0.001), parathyroid hormone (PTH) (P=0.014), and high-density lipoprotein (HDL)/cholesterol ratio (P=0.026) were independent predictors of CP accounting for 45% of variation. Adding calcification buffer (CB: calcium chloride [7 mM] and β-glycerophosphate [7 mM]) increased the CP of control sera to approximate that of CKD sera. CP of CKD sera was unchanged. CKD sera increased RUNX2 expression (P>0.01) in human SMCs and decreased SM22a expression (P>0.05). Co-incubating control but not CKD serum with CB further increased RUNX2 expression (P>0.01). Both SM22a and Klotho expression decreased significantly (P>0.01) in the presence of CKD serum, and were virtually abolished with stage 5D sera. These findings support active regulation by CKD serum of in vitro VC by induction of RUNX2 and suppression of SM22a and Klotho.Peer reviewe