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Introduction: Designation and Mechanical properties of Engineering Materials, design considerations, basic design concept (strength consideration), Failure of brittle materials, Failure of ductile materials, factor of safety, criteria for selection of factor of safety, design of simple machine members subjected to static loading (including eccentric load) [limited to biaxial stresses (normal, shear, bending, torsional, crushing/bearing, principal stresses)].
Design of Shaft: Introduction, types of shafts, shafts subjected to combine bending and twisting, shaft design (including hollow shafts) based on strength, shaft design based on torsional rigidity, ASME code for shaft design.
Threaded Joints: Introduction, basic terminology of screw threads, types of screw threads, types of screw fastenings, designations of screw threads, Stresses in threaded fasteners due to static loading, Effect of initial tension, threaded joints for cylinder covers, design of eccentrically loaded bolted joints.
Mechanisms of CAF activation have been thoroughly studied over the recent decades, where multiple cytokines have been shown to activate PSCs (e.g., PDGF, TGFß, IL1) . TGFß is a well-known fibrosis-inducing factor that has been previously well studied in CAF activation [34,35]. TGFß family ligands bind to type 2 TGFß receptor (TGFBR2), which then recruits and phosphorylates TGFBR1 (also known as ALK5) . The resulting heterotetrameric receptor complex then initiates downstream signaling. Canonical signaling is mediated by SMAD2/3 phosphorylation and SMAD4 recruitment. The phosphorylated SMAD complex can translocate to the nucleus and induce target gene expression, due to the presence of SMAD binding elements in promotor regions [37,38]. Non-canonical TGFß signaling, on the other hand, can be independent of SMADs and involves PI3K, ERK, JNK, and RHOA pathways . In PDAC, TGFß signaling has been associated with CAF activation, as TGFß induces alpha-SMA expression and collagen deposition, most probably through a combination of canonical and non-canonical pathways [8,40]. Multiple studies, using GEMMs and human biopsies, link myCAF differentiation and activity to TGFß signaling [15,25,29,32], suggesting that TGFß signaling is crucial for the myCAF subtype. However, it is important to note that several other stimuli have been shown to induce myCAF differentiation in PDAC.
The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. 2b1af7f3a8