Distributed computing system with dual independent communications paths between computers and employing split tokens

This is a distributed computing system providing flexible fault tolerance; ease of software design and concurrency specification; and dynamic balance of the loads. The system comprises a plurality of computers each having a first input/output interface and a second input/output interface for interfacing to communications networks each second input/output interface including a bypass for bypassing the associated computer. A global communications network interconnects the first input/output interfaces for providing each computer the ability to broadcast messages simultaneously to the remainder of the computers. A meshwork communications network interconnects the second input/output interfaces providing each computer with the ability to establish a communications link with another of the computers bypassing the remainder of computers. Each computer is controlled by a resident copy of a common operating system. Communications between respective ones of computers is by means of split tokens each having a moving first portion which is sent from computer to computer and a resident second portion which is disposed in the memory of at least one of computer and wherein the location of the second portion is part of the first portion. The split tokens represent both functions to be executed by the computers and data to be employed in the execution of the functions. The first input/output interfaces each include logic for detecting a collision between messages and for terminating the broadcasting of a message whereby collisions between messages are detected and avoided

Thioxoethenylidene (CCS) as a bridging ligand

The reaction of [Mo(≡CBr)(CO)2(Tp*)] (Tp* = hydrotris(3,5-dimethylpyrazol-1-yl)borate) with [Fe2(μ-SLi)2(CO)6] affords, inter alia, the unsymmetrical binuclear thioxoethenylidene complex [Mo2(μ,σ(C):η2(C′S)-CCS)(CO)4(Tp*)2], which may be more directly obtained from [Mo(≡CBr)(CO)2(Tp*)] and Li2S. The reaction presumably proceeds via the intermediacy of the bis(alkylidynyl)thioether complex S{C≡Mo(CO)2(Tp*)}2, which was, however, not directly observed but explored computationally and found to lie 78.6 kJ mol–1 higher in energy than the final thioxoethenylidene product. Computational interrogation of the molecules [M2(μ-C2S)(CO)2(Tp*)2] (M = Mo, W, Re, Os) reveals three plausible coordination modes for a thioxoethenylidene bridge which involve a progressive strengthening of the C–C bond and weakening of the M–C and M–S bonds, as might be expected from simple effective atomic number considerations.This work was supported by the Australian Research Council (DP130102598 and DP110101611)

Systemic central venous oxygen saturation is associated with clot strength during traumatic hemorrhagic shock: A preclinical observational model

<p>Abstract</p> <p>Background</p> <p>Clot strength by Thrombelastography (TEG) is associated with mortality during trauma and has been linked to severity of tissue hypoperfusion. However, the optimal method for monitoring this important relationship remains undefined. We hypothesize that oxygen transport measurements will be associated with clot strength during traumatic shock, and test this hypothesis using a swine model of controlled traumatic shock.</p> <p>Methods</p> <p>N = 33 swine were subjected to femur fracture and hemorrhagic shock by controlled arterial bleeding to a predetermined level of oxygen debt measured by continuous indirect calorimetry. Hemodynamics, oxygen consumption, systemic central venous oxygenation (ScvO₂), base excess, lactate, and clot maximal amplitude by TEG (TEG-MA) as clot strength were measured at baseline and again when oxygen debt = 80 ml/kg during shock. Oxygen transport and metabolic markers of tissue perfusion were then evaluated for significant associations with TEG-MA. Forward stepwise selection was then used to create regression models identifying the strongest associations between oxygen transport and TEG-MA independent of other known determinants of clot strength.</p> <p>Results</p> <p>Multiple markers of tissue perfusion, oxygen transport, and TEG-MA were all significantly altered during shock compared to baseline measurements (p < 0.05). However, only ScvO₂demonstrated a strong bivariate association with TEG-MA measured during shock (R = 0.7, p < 0.001). ScvO₂measured during shock was also selected by forward stepwise selection as an important covariate in linear regression models of TEG-MA after adjusting for the covariates fibrinogen, pH, platelet count, and hematocrit (Whole model R²= 0.99, p ≤ 0.032).</p> <p>Conclusions</p> <p>Among multiple measurements of oxygen transport, only ScvO₂was found to retain a significant association with TEG-MA during shock after adjusting for multiple covariates. ScvO₂should be further studied for its utility as a clinical marker of both tissue hypoxia and clot formation during traumatic shock.</p

Optimal growth ofLactobacillus casei in a Cheddar cheese ripening model system requires exogenous fatty acids

Flavor development in ripening Cheddar cheese depends on complex microbial and biochemical processes that are difficult to study in natural cheese. Thus, our group has developed Cheddar cheese extract (CCE) as a model system to study these processes. In previous work, we found that CCE supported growth of Lactobacillus casei, one of the most prominent nonstarter lactic acid bacteria (NSLAB) species found in ripening Cheddar cheese, to a final cell density of 108 cfu/mL at 37°C. However, when similar growth experiments were performed at 8°C in CCE derived from 4-mo-old cheese (4mCCE), the final cell densities obtained were only about 106 cfu/mL, which is at the lower end of the range of the NSLAB population expected in ripening Cheddar cheese. Here, we report that addition of Tween 80 to CCE resulted in a significant increase in the final cell density of L. casei during growth at 8°C and produced concomitant changes in cytoplasmic membrane fatty acid (CMFA) composition. Although the effect was not as dramatic, addition of milk fat or a monoacylglycerol (MAG) mixture based on the MAG profile of milk fat to 4mCCE also led to an increased final cell density of L. casei in CCE at 8°C and changes in CMFA composition. These observations suggest that optimal growth of L. casei in CCE at low temperature requires supplementation with a source of fatty acids (FA). We hypothesize that L. casei incorporates environmental FA into its CMFA, thereby reducing its energy requirement for growth. The exogenous FA may then be modified or supplemented with FA from de novo synthesis to arrive at a CMFA composition that yields the functionality (i.e., viscosity) required for growth in specific conditions. Additional studies utilizing the CCE model to investigate microbial contributions to cheese ripening should be conducted in CCE supplemented with 1% milk fat

Experimental design of complement component 5a‐induced acute lung injury (C5a‐ALI): a role of CC‐chemokine receptor type 5 during immune activation by anaphylatoxin

Excessive activation of the complement system is detrimental in acute inflammatory disorders. In this study, we analyzed the role of complement‐derived anaphylatoxins in the pathogenesis of experimental acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in C57BL/6J mice. Intratracheal administration of recombinant mouse complement component (C5a) caused alveolar inflammation with abundant recruitment of Ly6‐G+CD11b+ leukocytes to the alveolar spaces and severe alveolar‐capillary barrier dysfunction (C5a‐ALI; EC50[C5a] = 20 ng/g body weight). Equimolar concentrations of C3a or desarginated C5a (C5adesArg) did not induce alveolar inflammation. The severity of C5a‐ALI was aggravated in C5‐deficient mice. Depletion of Ly6‐G+ cells and use of C5aR1‐/‐ bone marrow chimeras suggested an essential role of C5aR1+ hematopoietic cells in C5a‐ALI. Blockade of PI3K/Akt and MEK1/2 kinase pathways completely abrogated lung injury. The mechanistic description is that C5a altered the alveolar cytokine milieu and caused significant release of CC‐chemokines. Mice with genetic deficiency of CC‐chemokine receptor (CCR) type 5, the common receptor of chemokine (C‐C motif) ligand (CCL) 3, CCL4, and CCL5, displayed reduced lung damage. Moreover, treatment with a CCR5 antagonist, maraviroc, was protective against C5a‐ALI. In summary, our results suggest that the detrimental effects of C5a in this model are partly mediated through CCR5 activation downstream of C5aR1, which may be evaluated for potential therapeutic exploitation in ALI/ARDS.—Russkamp, N. F., Ruemmler, R., Roewe, J., Moore, B. B., Ward, P. A., Bosmann, M. Experimental design of complement component 5a‐induced acute lung injury (C5a‐ALI): a role of CC‐chemokine receptor type 5 during immune activation by anaphylatoxin. FASEB J. 29, 3762‐3772 (2015). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154372/1/fsb2029009014.pd

Control-Flow Integrity for Real-Time Embedded Systems

Attacks on real-time embedded systems can endanger lives and critical infrastructure. Despite this, techniques for securing embedded systems software have not been widely studied. Many existing security techniques for general-purpose computers rely on assumptions that do not hold in the embedded case. This paper focuses on one such technique, control-flow integrity (CFI), that has been vetted as an effective countermeasure against control-flow hijacking attacks on general-purpose computing systems. Without the process isolation and fine-grained memory protections provided by a general-purpose computer with a rich operating system, CFI cannot provide any security guarantees. This work proposes RECFISH, a system for providing CFI guarantees on ARM Cortex-R devices running minimal real-time operating systems. We provide techniques for protecting runtime structures, isolating processes, and instrumenting compiled ARM binaries with CFI protection. We empirically evaluate RECFISH and its performance implications for real-time systems. Our results suggest RECFISH can be directly applied to binaries without compromising real-time performance; in a test of over six million realistic task systems running FreeRTOS, 85% were still schedulable after adding RECFISH

A Review of Current Standards and the Evolution of Histopathology Nomenclature for Laboratory Animals.

The need for international collaboration in rodent pathology has evolved since the 1970s and was initially driven by the new field of toxicologic pathology. First initiated by the World Health Organization's International Agency for Research on Cancer for rodents, it has evolved to include pathology of the major species (rats, mice, guinea pigs, nonhuman primates, pigs, dogs, fish, rabbits) used in medical research, safety assessment, and mouse pathology. The collaborative effort today is driven by the needs of the regulatory agencies in multiple countries, and by needs of research involving genetically engineered animals, for "basic" research and for more translational preclinical models of human disease. These efforts led to the establishment of an international rodent pathology nomenclature program. Since that time, multiple collaborations for standardization of laboratory animal pathology nomenclature and diagnostic criteria have been developed, and just a few are described herein. Recently, approaches to a nomenclature that is amenable to sophisticated computation have been made available and implemented for large-scale programs in functional genomics and aging. Most terminologies continue to evolve as the science of human and veterinary pathology continues to develop, but standardization and successful implementation remain critical for scientific communication now as ever in the history of veterinary nosology

Process of discovery: A fourth-year translational science course

The Liaison Committee on Medical Education notes the importance of educating medical students on clinical and translational research principles.To describe a fourth-year course, &#x201C;Process of discovery,&#x201D; which addresses teaching these principles, and to discuss students&#x2019; perceptions of the course.Core components and pedagogical methods of this course are presented. Course assessment was performed with specific pre- and post-course assessments.During academic years 2004 to 2009, 562 students were enrolled, with assessment response rate of 94% pre-course and 85% post-course. The students&#x2019; self-assessment of their current understanding of clinical and translation research significantly increased, as well as their understanding of how clinical advances will take place over the next decade.A fourth-year course teaching clinical and translational research is successful, is seen as a positive experience and can meet the requirements for including clinical and translational research in the medical school curriculum

Extracellular histones are essential effectors of C5aR‐ and C5L2‐mediated tissue damage and inflammation in acute lung injury

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154331/1/fsb2027012034.pd