Mechanical & Industrial Engineering
Permanent URI for this communityhttps://scholarworks.montana.edu/handle/1/33
The mission of the Mechanical & Industrial Engineering Department is to serve the State of Montana, the region, and the nation by providing outstanding leadership and contributions in knowledge discovery, student learning, innovation and entrepreneurship, and service to community and profession.
Browse
3 results
Search Results
Item Reducing Rework by Applying Set-Based Practices Early in the Systems Engineering Process(2013-05) Kennedy, Brian; Sobek, Durward; Kennedy, MichaelRework that occurs late in the product life cycle is dramatically more expensive than design work performed early in the cycle. However, shifting traditional design work earlier in the design process so as to avoid rework later is difficult. A number of product development practices that have been characterized as a shift from developing a single-point design to developing a set of possible designs have proven effective at reducing development rework. This paper refines the definitions of such “set-based” development practices, which are aimed at early development phases, and shows how they can be applied to the systems engineering process in order to reduce or eliminate the root causes of rework. Examples from the Wright Brothers, Toyota, and several other companies are presented.Item Selective Activation of Intrinsic Cohesive Elements.(2014-12) Kyeongsik, W.; Peterson, William Matthew; Cairns, Douglas S.In this paper, a selective activation strategy is studied in order to alleviate the issue of added compliance in the intrinsic cohesive zone model applied to arbitrary crack propagation. This strategy proceeds by first inserting cohesive elements between bulk elements and subsequently tying the duplicated nodes across the interface using controllable multi-point constraints before the analysis begins. Then, during the analysis, a part of the multi-point constraints are selectively released, thereby reactivating the corresponding cohesive elements and allowing cracks to initiate and propagate along the bulk element boundaries. The strategy is implemented in Abaqus/Standard using a user-defined multi-point constraint subroutine. Analysis results indicate that the strategy significantly alleviates the added compliance problem and reduces the computation time.Item Linked decreases in liver kinase B1 and AMP-activated protein kinase activity modulatematrix catabolic responses to biomechanical injury in chondrocytes(2013-07) Petursson, F.; Husa, M.; June, Ronald K.; Lotz, Martin K.; Terkeltaub, R.; Liu-Bryan, R.Introduction: AMP-activated protein kinase (AMPK) maintains cultured chondrocyte matrix homeostasis in response to inflammatory cytokines. AMPK activity is decreased in human knee osteoarthritis (OA) chondrocytes. Liver kinase B1 (LKB1) is one of the upstream activators of AMPK. Hence, we examined the relationship between LKB1 and AMPK activity in OA and aging cartilages, and in chondrocytes subjected to inflammatory cytokine treatment and biomechanical compression injury, and performed translational studies of AMPK pharmacologic activation. Methods: We assessed activity (phosphorylation) of LKB1 and AMPKα in mouse knee OA cartilage, in aging mouse cartilage (6 to 24 months), and in chondrocytes after mechanical injury by dynamic compression, via immunohistochemistry or western blot. We knocked down LKB1 by siRNA transfection. Nitric oxide, matrix metalloproteinase (MMP)-3, and MMP-13 release were measured by Griess reaction and ELISA, respectively. Results Knockdown of LKB1 attenuated chondrocyte AMPK activity, and increased nitric oxide, MMP-3 and MMP-13 release (P <0.05) in response to IL-1β and TNFα. Both LKB1 and AMPK activity were decreased in mouse knee OA and aged knee cartilage, and in bovine chondrocytes after biomechanical injury. Pretreatment of bovine chondrocytes with AMPK activators AICAR and A-769662 inhibited both AMPKα dephosphorylation and catabolic responses after biomechanical injury. Conclusion: LKB1 is required for chondrocyte AMPK activity, thereby inhibiting matrix catabolic responses to inflammatory cytokines. Concurrent loss of LKB1 and AMPK activity in articular chondrocytes is associated with OA, aging and biomechanical injury. Conversely, pharmacologic AMPK activation attenuates catabolic responses to biomechanical injury, suggesting a potentially novel approach to inhibit OA development and progression.