Quality and inspection of machining operations: Review of condition monitoring and CMM inspection techniques 2000 to present

In order to consistently produce quality parts, many aspects of the manufacturing process must be carefully monitored, controlled, and measured. The methods and techniques by which to accomplish these tasks has been the focus of numerous studies in recent years. With the rapid advances in computing technology, the complexity and overhead that can be feasibly incorporated in any developed technique has dramatically improved. Thus, techniques that would have been impractical for implementation just a few years ago can now be realistically applied. This rapid growth has resulted in a wealth of new capabilities for improving part and process quality and reliability. In this paper, overviews of recent advances that apply to machining are presented. Moreover, due to the relative significance of two particular machining aspects, this review focuses specifically on research publications pertaining to using tool condition monitoring and coordinate measurement machines to improve the machining process. Tool condition has a direct effect on part quality and is discussed first. The application of tool condition monitoring as it applies to turning, drilling, milling, and grinding is presented. The subsequent section provides recommendations for future research opportunities. The ensuing section focuses on the use of coordinate measuring machines in conjunction with machining and is subdivided with respect to integration with machining tools, inspection planning and efficiency, advanced controller feedback, machine error compensation, and on-line tool calibration, in that specific order and concludes with recommendations regarding where future needs remain

Antibiotic Prophylaxis with Trimethoprim-Sulfamethoxazole versus No Treatment after Mid-to-Distal Hypospadias Repair: A Prospective, Randomized Study

Purpose. To evaluate the impact of prophylactic antibiotics after distal hypospadias repair on postoperative bacteriuria, symptomatic urinary tract infection, and postoperative complications in a prospective, randomized trial. Materials and Methods. Consecutive patients aged 6 months to 2 years were enrolled at our institution between June 2013 and May 2017. Consenting patients were randomized to antibiotic prophylaxis with trimethoprim-sulfamethoxazole versus no antibiotic. Patients had catheterized urine samples obtained at surgery and 6–10 days postoperatively. The primary outcome was bacteriuria and pyuria at postoperative urine collection. Secondary outcomes included symptomatic urinary tract infection and postoperative complications. Results. 70 patients consented to the study, of which 35 were randomized to receive antibiotics compared to 32 who did not. Demographics, severity of hypospadias, and type of repair were similar between the groups. Patients in the treatment group had significantly less pyuria (18%) and bacteriuria (11%) present at stent removal compared to the nontreatment group (55% and 63%; p=0.01 and p<0.001, resp.). No patient had a symptomatic urinary tract infection. There were 11 postoperative complications. Conclusions. Routine antibiotic prophylaxis appears to significantly decrease bacteriuria and pyuria in the immediate postoperative period; however, no difference was observed in symptomatic urinary tract infection or postoperative complications. Clinical Trial Registration Number NCT02593903

The AP-2 adaptor β2 appendage scaffolds alternate cargo endocytosis

The independently folded appendages of the large α and β2 subunits of the endocytic adaptor protein (AP)-2 complex coordinate proper assembly and operation of endocytic components during clathrin-mediated endocytosis. The β2 subunit appendage contains a common binding site for β-arrestin or the autosomal recessive hypercholesterolemia (ARH) protein. To determine the importance of this interaction surface in living cells, we used small interfering RNA-based gene silencing. The effect of extinguishing β2 subunit expression on the internalization of transferrin is considerably weaker than an AP-2 α subunit knockdown. We show the mild sorting defect is due to fortuitous substitution of the β2 chain with the closely related endogenous β1 subunit of the AP-1 adaptor complex. Simultaneous silencing of both β1 and β2 subunit transcripts recapitulates the strong α subunit RNA interference (RNAi) phenotype and results in loss of ARH from endocytic clathrin coats. An RNAi-insensitive β2-yellow fluorescent protein (YFP) expressed in the β1 + β2-silenced background restores cellular AP-2 levels, robust transferrin internalization, and ARH colocalization with cell surface clathrin. The importance of the β appendage platform subdomain over clathrin for precise deposition of ARH at clathrin assembly zones is revealed by a β2-YFP with a disrupted ARH binding interface, which does not restore ARH colocalization with clathrin. We also show a β-arrestin 1 mutant, which engages coated structures in the absence of any G protein-coupled receptor stimulation, colocalizes with β2-YFP and clathrin even in the absence of an operational clathrin binding sequence. These findings argue against ARH and β-arrestin binding to a site upon the β2 appendage platform that is later obstructed by polymerized clathrin. We conclude that ARH and β-arrestin depend on a privileged β2 appendage site for proper cargo recruitment to clathrin bud sites

How chemistry controls electron localization in 3d1 perovskites: A Wannier-function study

In the series of 3d1 t2g perovskites, SrVO3--CaVO3--LaTiO3--YTiO3 the transition-metal d electron becomes increasingly localized and undergoes a Mott transition between CaVO3 and LaTiO3. By defining a low-energy Hubbard Hamiltonian in the basis of Wannier functions for the t2g LDA band and solving it in the single-site DMFT approximation, it was recently shown[1] that simultaneously with the Mott transition there occurs a strong suppression of orbital fluctuations due to splitting of the t2g levels. The present paper reviews and expands this work, in particular in the direction of exposing the underlying chemical mechanisms by means of ab initio LDA Wannier functions generated with the NMTO method. The Wannier functions for the t2g band exhibit covalency between the transition-metal t2g, the large cation-d, and the oxygen-p states; this covalency, which increases along the series, turns out to be responsible not only for the splittings of the t2g levels, but also for non-cubic perturbations of the hopping integrals, both of which are decisive for the Mott transition. We find good agreement with the optical and photoemission spectra, with the crystal-field splittings and orbital polarizations recently measured for the titanates, and with the metallization volume for LaTiO3. The metallization volume for YTiO3 is predicted. Using super-exchange theory, we reproduce the observed magnetic orders in LaTiO3 and YTiO3, but the results are sensitive to detail, in particular for YTiO3 which, without the Jahn-Teller distortion, would be AFM C- or A-type, rather than FM. Finally, we show that it possible to unfold the orthorhombic t2g LDA bandstructure to a pseudocubic zone. In this zone, the lowest band is separated from the two others by a direct gap and has a width, W_I, which is significantly smaller than that, W, of the entire t2g band. The progressive GdFeO3-type distortion favours electron localization by decreasing W, by increasing the splitting of the t2g levels and by decreasing W_I. Our conclusions concerning the roles of GdFeO3-type and JT distortions agree with those of Mochizuki and Imada [2].Comment: Published version, final. For high resolution figures see http://www.fkf.mpg.de/andersen/docs/pub/abstract2004+/pavarini_02.pd

p90 Ribosomal S6 Kinase 2, a Novel GPCR Kinase, Is Required for Growth Factor-Mediated Attenuation of GPCR Signaling

The 5-hydroxytryptamine 2A (5-HT2A) receptor is a member of the G protein-coupled receptor superfamily (GPCR) and plays a key role in transducing a variety of cellular signals elicited by serotonin (5-HT; 5-hydroxytryptamine) in both peripheral and central tissues. Recently, we discovered that the ERK/MAPK effector p90 ribosomal S6 kinase 2 (RSK2) phosphorylates the 5-HT2A receptor and attenuates 5-HT2A receptor signaling. This raised the intriguing possibility of a regulatory paradigm whereby receptor tyrosine kinases (RTKs) attenuate GPCR signaling (i.e., ‘inhibitory cross-talk’) by activating RSK2 [Strachan et al. (2009) J. Biol. Chem. 284, 5557-5573]. We report here that activation of multiple endogenous RTKs such as the epidermal growth factor receptor (EGFR), the platelet-derived growth factor receptor (PDGFR), and ErbB4 significantly attenuates 5-HT2A receptor signaling in a variety of cell types including mouse embryonic fibroblasts (MEFs), mouse vascular smooth muscle cells (mVSMCs), and primary cortical neurons. Importantly, genetic deletion of RSK2 completely prevented signal attenuation, thereby suggesting that RSK2 is a critical mediator of inhibitory cross-talk between RTKs and 5-HT2A receptors. We also discovered that P2Y purinergic receptor signaling was similarly attenuated following EGFR activation. By directly testing multiple endogenous growth factors/RTK pathways and multiple Gq-coupled GPCRs, we have now established a cellular mechanism whereby RTK signaling cascades act via RSK2 to attenuate GPCR signaling. Given the pervasiveness of growth factor signaling, this novel regulatory mechanism has the potential to explain how 5-HT2A receptors are regulated in vivo, with potential implications for human diseases in which 5-HT2A or RTK activity is altered (e.g. neuropsychiatric and neurodevelopmental disorders)

SMaRT: A Science-based Tiered Framework for Common Ravens

Large-scale increases and expansion of common raven (Corvus corax; raven) populations are occurring across much of North America, leading to increased negative consequences for livestock and agriculture, human health and safety, and sensitive species conservation. We describe a science-based adaptive management framework that incorporates recent quantitative analyses and mapping products for addressing areas with elevated raven numbers and minimizing potential adverse impacts to sensitive species, agricultural damage, and human safety. The framework comprises 5 steps: (1) desktop analysis; (2) field assessments; (3) comparison of raven density estimates to an ecological threshold (in terms of either density or density plus distance to nearest active or previous nest); (4) prescribing management options using a 3-tiered process (i.e., habitat improvements, subsidy reductions, and direct actions using StallPOPd.V4 software); and (5) post-management monitoring. The framework is integrated within the Science-based Management of Ravens Tool (SMaRT), a web-based application outfitted with a user-friendly interface that guides managers through each step to develop a fully customized adaptive plan for raven management. In the SMaRT interface, users can: (1) interact with pre-loaded maps of raven occurrence and density and define their own areas of interest within the Great Basin to delineate proposed survey or treatment sites; (2) enter site-level density estimates from distance sampling methods or perform estimation of raven densities using the rapid assessment protocol that we provide; (3) compare site-level density estimates to an identified ecological threshold; and (4) produce a list of potential management options for their consideration. The SMaRT supports decision-making by operationalizing scientific products for raven management and facilitates realization of diverse management goals including sensitive species conservation, protection of livestock and agriculture, safeguarding human health, and addressing raven overabundance and expansion. We illustrate the use of the framework through SMaRT using an example of greater sage-grouse (Centrocercus urophasianus) conservation efforts within the Great Basin, USA

Structural and functional insight into human O-GlcNAcase

O-GlcNAc hydrolase (OGA) removes O-linked N-acetylglucosamine (O-GlcNAc) from a myriad of nucleocytoplasmic proteins. Through co-expression and assembly of OGA fragments, we determined the three-dimensional structure of human OGA, revealing an unusual helix-exchanged dimer that lays a structural foundation for an improved understanding of substrate recognition and regulation of OGA. Structures of OGA in complex with a series of inhibitors define a precise blueprint for the design of inhibitors that have clinical value