Systems and Methods for Structurally Interrelating Components Using Inserts Made from Metallic Glass-Based Materials

Systems and methods in accordance with embodiments of the invention operate to structurally interrelate two components using inserts made from metallic glass-based materials. In one embodiment, a method of structurally interrelating two components includes: forming an insert from a metallic glass-based composition; where the formed insert includes a metallic glass-based material; affixing the insert to a first component; and structurally interrelating the second component to the first component using the insert

Propagating waves in the steel, moment-frame factor building recorded during earthquakes

Wave-propagation effects can be useful in determining the system identification of buildings such as the densely instrumented University of California, Los Angeles, Factor building. Waveform data from the 72-channel array in the 17-story moment-resisting steel frame Factor building are used in comparison with finiteelement calculations for predictive behavior. The high dynamic range of the 24-bit digitizers allows both strong motions and ambient vibrations to be recorded with reasonable signal-to-noise ratios. A three-dimensional model of the Factor building has been developed based on structural drawings. Observed displacements for 20 small and moderate, local and regional earthquakes were used to compute the impulse response functions of the building by deconvolving the subbasement records as representative input motions at its base. The impulse response functions were then stacked to bring out wave-propagation effects more clearly. The stacked data are used as input into theoretical dynamic analysis simulations of the building’s response

Correcting Thermal Deformations in an Active Composite Reflector

Large, high-precision composite reflectors for future space missions are costly to manufacture, and heavy. An active composite reflector capable of adjusting shape in situ to maintain required tolerances can be lighter and cheaper to manufacture. An active composite reflector testbed was developed that uses an array of piezoelectric composite actuators embedded in the back face sheet of a 0.8-m reflector panel. Each individually addressable actuator can be commanded from 500 to +1,500 V, and the flatness of the panel can be controlled to tolerances of 100 nm. Measuring the surface flatness at this resolution required the use of a speckle holography interferometer system in the Precision Environmental Test Enclosure (PETE) at JPL. The existing testbed combines the PETE for test environment stability, the speckle holography system for measuring out-of-plane deformations, the active panel including an array of individually addressable actuators, a FLIR thermal camera to measure thermal profiles across the reflector, and a heat source. Use of an array of flat piezoelectric actuators to correct thermal deformations is a promising new application for these actuators, as is the use of this actuator technology for surface flatness and wavefront control. An isogrid of these actuators is moving one step closer to a fully active face sheet, with the significant advantage of ease in manufacturing. No extensive rib structure or other actuation backing structure is required, as these actuators can be applied directly to an easy-to-manufacture flat surface. Any mission with a surface flatness requirement for a panel or reflector structure could adopt this actuator array concept to create lighter structures and enable improved performance on orbit. The thermal environment on orbit tends to include variations in temperature during shadowing or changes in angle. Because of this, a purely passive system is not an effective way to maintain flatness at the scale of microns over several meters. This technology is specifically referring to correcting thermal deformations of a large, flat structure to a specified tolerance. However, the underlying concept (an array of actuators on the back face of a panel for correcting the flatness of the front face) could be extended to many applications, including energy harvesting, changing the wavefront of an optical system, and correcting the flatness of an array of segmented deployable panels

A well-defined magnesium complex of C706-

Funding: The authors are grateful to the EPSRC DTG (EP/N509759/1, EP/T518062/1), the School of Chemistry and the University of St Andrews for support. The computations were enabled by resources provided by the National Academic Infrastructure for Supercomputing in Sweden (NAISS), partially funded by the Swedish Research Council through grant agreement no. 2022-06725.Controlling and understanding charge state and metal coordination in carbon nanomaterials is crucial to harnessing their unique properties. Here we describe the synthesis of the well-defined fulleride complex [{(Mesnacnac)Mg}6C70], 2, (Mesnacnac) = HC(MeCNMes)2, Mes = 2,4,6-Me3C6H2, from the reaction of the β-diketiminate magnesium(I) complex [{(Mesnacnac)Mg}2] with C70 in aromatic solvents. The molecular structure of complex 2 was determined, providing the first high-quality structural study of a complex with the C706- ion. In combination with solution state NMR spectroscopic and DFT computational studies, the changes in geometry and charge distribution in the various atom and bond types of the fulleride unit were investigated. Additionally, the influence of the (Mesnacnac)Mg+ cations on the global and local fulleride coordination environment was examined.Peer reviewe

P-rex1 cooperates with PDGFRβ to drive cellular migration in 3D microenvironments

Expression of the Rac-guanine nucleotide exchange factor (RacGEF), P-Rex1 is a key determinant of progression to metastasis in a number of human cancers. In accordance with this proposed role in cancer cell invasion and metastasis, we find that ectopic expression of P-Rex1 in an immortalised human fibroblast cell line is sufficient to drive multiple migratory and invasive phenotypes. The invasive phenotype is greatly enhanced by the presence of a gradient of serum or platelet-derived growth factor, and is dependent upon the expression of functional PDGF receptor β. Consistently, the invasiveness of WM852 melanoma cells, which endogenously express P-Rex1 and PDGFRβ, is opposed by siRNA of either of these proteins. Furthermore, the current model of P-Rex1 activation is advanced through demonstration of P-Rex1 and PDGFRβ as components of the same macromolecular complex. These data suggest that P-Rex1 has an influence on physiological migratory processes, such as invasion of cancer cells, both through effects upon classical Rac1-driven motility and a novel association with RTK signalling complexes

Integrating team science into interdisciplinary graduate education: an exploration of the SESYNC Graduate Pursuit

Complex socio-environmental challenges require interdisciplinary, team-based research capacity. Graduate students are fundamental to building such capacity, yet formal opportunities for graduate students to develop these capacities and skills are uncommon. This paper presents an assessment of the Graduate Pursuit (GP) program, a formal interdisciplinary team science graduate research and training program administered by the National Socio-Environmental Synthesis Center (SESYNC). Quantitative and qualitative assessment of the program’s first cohort revealed that participants became significantly more comfortable with interdisciplinary research and team science approaches, increased their capacity to work across disciplines, and were enabled to produce tangible research outcomes. Qualitative analysis of four themes—(1) discipline, specialization, and shared purpose, (2) interpersonal skills and personality, (3) communication and teamwork, and (4) perceived costs and benefits—encompass participants’ positive and negative experiences and support findings from past assessments. The findings also identify challenges and benefits related to individual personality traits and team personality orientation, the importance of perceiving a sense of autonomy and independence, and the benefit of graduate training programs independent of the university and graduate program environment

Emergence of Microglia Bearing Senescence Markers During Paralysis Progression in a Rat Model of Inherited ALS

Age is a recognized risk factor for amyotrophic lateral sclerosis (ALS), a paralytic disease characterized by progressive loss of motor neurons and neuroinflammation. A hallmark of aging is the accumulation of senescent cells. Yet, the pathogenic role of cellular senescence in ALS remains poorly understood. In rats bearing the ALS-linked SOD1(G93A) mutation, microgliosis contribute to motor neuron death, and its pharmacologic downregulation results in increased survival. Here, we have explored whether gliosis and motor neuron loss were associated with cellular senescence in the spinal cord during paralysis progression. In the lumbar spinal cord of symptomatic SOD1(G93A) rats, numerous cells displayed nuclear p16(INK4a) as well as loss of nuclear Lamin B1 expression, two recognized senescence-associated markers. The number of p16(INK4a)-positive nuclei increased by four-fold while Lamin B1-negative nuclei increased by 1,2-fold, respect to non-transgenic or asymptomatic transgenic rats. p16(INK4a)-positive nuclei and Lamin B1-negative nuclei were typically localized in a subset of hypertrophic Iba1-positive microglia, occasionally exhibiting nuclear giant multinucleated cell aggregates and abnormal nuclear morphology. Next, we analyzed senescence markers in cell cultures of microglia obtained from the spinal cord of symptomatic SOD1(G93A) rats. Although microglia actively proliferated in cultures, a subset of them developed senescence markers after few days in vitro and subsequent passages. Senescent SOD1(G93A) microglia in culture conditions were characterized by large and flat morphology, senescence-associated beta-Galactosidase (SA-beta-Gal) activity as well as positive labeling for p16(INK4a), p53, matrix metalloproteinase-1 (MMP-1) and nitrotyrosine, suggesting a senescent-associated secretory phenotype (SASP). Remarkably, in the degenerating lumbar spinal cord other cell types, including ChAT-positive motor neurons and GFAP-expressing astrocytes, also displayed nuclear p16(INK4a) staining. These results suggest that cellular senescence is closely associated with inflammation and motor neuron loss occurring after paralysis onset in SOD1(G93A) rats. The emergence of senescent cells could mediate key pathogenic mechanisms in ALS

DNA and Inflammatory Mediators in Bronchoalveolar Lavage Fluid From Children With Acute Inhalational Injuries:

Assess the feasibility of using serial bronchoalveolar lavage fluids (BALF) to characterize the course of cell damage and inflammation in airways of pediatric patients with acute burn or inhalation injury

Emergence of Microglia Bearing Senescence Markers During Paralysis Progression in a Rat Model of Inherited ALS

Age is a recognized risk factor for amyotrophic lateral sclerosis (ALS), a paralytic disease characterized by progressive loss of motor neurons and neuroinflammation. A hallmark of aging is the accumulation of senescent cells. Yet, the pathogenic role of cellular senescence in ALS remains poorly understood. In rats bearing the ALS-linked SOD1G93A mutation, microgliosis contribute to motor neuron death, and its pharmacologic downregulation results in increased survival. Here, we have explored whether gliosis and motor neuron loss were associated with cellular senescence in the spinal cord during paralysis progression. In the lumbar spinal cord of symptomatic SOD1G93A rats, numerous cells displayed nuclear p16INK4a as well as loss of nuclear Lamin B1 expression, two recognized senescence-associated markers. The number of p16INK4a-positive nuclei increased by four-fold while Lamin B1-negative nuclei increased by 1,2-fold, respect to non-transgenic or asymptomatic transgenic rats. p16INK4a-positive nuclei and Lamin B1-negative nuclei were typically localized in a subset of hypertrophic Iba1-positive microglia, occasionally exhibiting nuclear giant multinucleated cell aggregates and abnormal nuclear morphology. Next, we analyzed senescence markers in cell cultures of microglia obtained from the spinal cord of symptomatic SOD1G93A rats. Although microglia actively proliferated in cultures, a subset of them developed senescence markers after few days in vitro and subsequent passages. Senescent SOD1G93A microglia in culture conditions were characterized by large and flat morphology, senescence-associated beta-Galactosidase (SA-β-Gal) activity as well as positive labeling for p16INK4a, p53, matrix metalloproteinase-1 (MMP-1) and nitrotyrosine, suggesting a senescent-associated secretory phenotype (SASP). Remarkably, in the degenerating lumbar spinal cord other cell types, including ChAT-positive motor neurons and GFAP-expressing astrocytes, also displayed nuclear p16INK4a staining. These results suggest that cellular senescence is closely associated with inflammation and motor neuron loss occurring after paralysis onset in SOD1G93A rats. The emergence of senescent cells could mediate key pathogenic mechanisms in ALS