Independent mesh method-based prediction of local and volume average fields in textile composites

An independent mesh method (IMM) for three-dimensional stress analysis in composites with complex fiber architectures is proposed. The method represents a combination of direct meshing and voxel-based methodology and allows the modeling of complex tow geometries not readily amenable to traditional finite element meshing. Each fiber tow is meshed independently, while the matrix is meshed throughout the volume of interest. The matrix approximation is then truncated by disregarding the shape functions, whose support is completely inside a tow or completely covered by more than one tow in regions such as tow intersections. The calculation of average stiffness properties of both an oblong fiber-matrix representative volume element (RVE) and a plain weave composite RVE is performed for verification and convergence evaluation purposes. The digital chain technique was used to model fiber architecture in the tri-axial braided composite with high fidelity including the effects of nesting and compaction of plies. Local deformations of the digital architecture due to relief of residual processing stress following a saw cut were predicted by using IMM. These deformations in the tri-axial braided composite were then measured experimentally using Moiré interferometry. The degree of agreement between the predicted strain fields and those measured experimentally was shown to correlate with the degree of accuracy of digital architecture and varied from agreement in average behavior to practically point wise agreement across the entire field of measurement.     

mTOR Activity and Autophagy in Senescent Cells,a Complex Partnership

Cellular senescence is a form of proliferative arrest triggered in response to a wide variety of stimuli and characterized by unique changes in cell morphology and function. Although unable to divide, senescent cells remain metabolically active and acquire the ability to produce and secrete bioactive molecules, some of which have recognized pro-inflammatory and/or pro-tumorigenic actions. As expected, this “senescence-associated secretory phenotype (SASP)” accounts for most of the non-cell-autonomous effects of senescent cells, which can be beneficial or detrimental for tissue homeostasis, depending on the context. It is now evident that many features linked to cellular senescence, including the SASP, reflect complex changes in the activities of mTOR and other metabolic pathways. Indeed, the available evidence indicates that mTOR-dependent signaling is required for the maintenance or implementation of different aspects of cellular senescence. Thus, depending on the cell type and biological context, inhibiting mTOR in cells undergoing senescence can reverse senescence, induce quiescence or cell death, or exacerbate some features of senescent cells while inhibiting others. Interestingly, autophagy—a highly regulated catabolic process—is also commonly upregulated in senescent cells. As mTOR activation leads to repression of autophagy in non-senescent cells (mTOR as an upstream regulator of autophagy), the upregulation of autophagy observed in senescent cells must take place in an mTOR-independent manner. Notably, there is evidence that autophagy provides free amino acids that feed the mTOR complex 1 (mTORC1), which in turn is required to initiate the synthesis of SASP components. Therefore, mTOR activation can follow the induction of autophagy in senescent cells (mTOR as a downstream effector of autophagy). These functional connections suggest the existence of autophagy regulatory pathways in senescent cells that differ from those activated in non-senescence contexts. We envision that untangling these functional connections will be key for the generation of combinatorial anti-cancer therapies involving pro-senescence drugs, mTOR inhibitors, and/or autophagy inhibitors.     

Serogroup Y meningococcal disease in Chicago, 1991-1997

CONTEXT: In 1994, surveillance by the Chicago Department of Public Health detected a growing trend in the proportion of invasive meningococcal infections caused by serogroup Y. OBJECTIVE: To examine the emergence of serogroup Y meningococcal disease and compare its clinical characteristics with those of other meningococcal serogroups. DESIGN: Population-based retrospective review of surveillance records; medical record review and cohort analysis of serogroup Y vs non-serogroup Y case patients. SETTING: Chicago, III. PARTICIPANTS: City residents with Neisseria meningitidis isolated from a normally sterile site from January 1, 1991, through December 31, 1997; cohort analysis included those identified through March 31, 1996. MAIN OUTCOME MEASURES: Serogroup-specific incidence, demographics, and clinical outcomes. RESULTS: We identified 214 case patients; 53 (25%) had serogroup Y. The attack rate of serogroup Y meningococcal disease increased from 0.04 cases per 100000 in 1991 to a peak of 0.82 cases per 100000 in 1995 and subsequently decreased to 0.26 cases per 100000 and 0.34 cases per 100000 in 1996 and 1997, respectively. Compared with patients infected by other serogroups, patients with serogroup Y were older (median age, 16 years vs 1 year; P = .001) and more likely to have a chronic underlying illness (prevalence ratio, 2.3; 95% confidence interval, 1.2-4.4). Outcome did not differ significantly between the 2 groups. Multilocus enzyme electrophoresis typing of isolates from 19 case patients identified 5 different types. We found no clustering among the enzyme types by age, race/ethnicity, community area, or time. CONCLUSIONS: Serogroup Y emerged as the most frequent cause of meningococcal disease in Chicago in 1995 and accounted for a substantial proportion of cases in 1996 and 1997. Current data suggest that the magnitude of serogroup Y meningococcal disease is sufficient for vaccine developers to incorporate serogroup Y into new vaccines.     

Photoluminescence, Raman, and infrared diagnosis of GaAs-AlGaAssuperlattices for intersubband infrared detection

We present optical diagnosis of GaAs-AlGaAs superlattices grown by molecular beam epitaxy for use as 8-20 μm infrared detectors, that combines photoluminescence, Raman, and Fourier transform infrared spectroscopies. Various structural and physical parameters were obtained by theoretical analysis of the optical results. The use of multiple optical techniques offers comprehensive characterization and further understanding of the physics of long wavelength infrared detectors     

Cell-permeant caged InsP3 ester shows that Ca2+ spike frequency can optimize gene expression

Inositol 1,4,5-trisphosphate (InsP3) releases calcium from intracellular stores and triggers complex waves and oscillations in levels of cytosolic free calcium. To determine which longer-term responses are controlled by oscillations in InsP3 and cytosolic free calcium, it would be useful to deliver exogenous InsP3, under spatial and temporal control, into populations of unpermeabilized cells. Here we report the 15-step synthesis of a membrane-permeant, caged InsP3 derivative from myo-inositol This derivative diffused into intact cells and was hydrolysed to produce a caged, metabolically stable InsP3 derivative. This latter derivative accumulated in the cytosol at concentrations of hundreds of micromolar, without activating the InsP3 receptor. Ultraviolet illumination uncaged an InsP3 analogue nearly as potent as real InsP3, and generated spikes of cytosolic free calcium, and stimulated gene expression via the nuclear factor of activated T cells. The same total amount of InsP3 analogue elicited much more gene expression when released by repetitive flashes at 1-minute intervals than when released at 0.5- or > or = 2-minute intervals, as a single pulse, or as a slow sustained plateau. Thus, oscillations in cytosolic free calcium levels at roughly physiological rates maximize gene expression for a given amount of InsP3.     

Adding value in product development by creating information and reducing risk

Many firms expend a great amount of effort to increase the customer value of their product development (PD) processes. Yet, in PD, determining how and when value is added is problematic. The goal of a PD process is to produce a product "recipe" that satisfies requirements. Design work is done both to specify the recipe in increasing detail and to verify that it does in fact conform to requirements. As design work proceeds, certainty increases surrounding the ability of the evolving product design (including its production process) to be the final product recipe (i.e., technical performance risk decreases). The goal of this paper is to advance the theory and practice of evaluating progress and added customer value in PD. The paper proposes that making progress and adding customer value in PD equate with producing useful information that reduces performance risk. The paper also contributes a methodology-the risk value method-that integrates current approaches such as technical performance measure tracking charts and risk reduction profiles. The methods are demonstrated with an industrial example of an uninhabited combat aerial vehicle.