The Impact of Performance Funding on Community College Degree Completion, Certificate Completion, and Transfer Rate: A Difference-in-Differences Approach

Historically, state funding of higher education institutions has been allocated through enrollment, but there has been a recent trend towards a different model, performance funding. Performance funding is a model based on the attainment of designated metrics with the intent on improving student outcomes. The metrics used for these programs have often not aligned with the mission and characteristics of different institutions, especially that of community colleges. Although, several past performance funding models failed to improve student outcomes, much has been learned regarding program improvement. Texas implemented a performance funding model in 2013 which included a focus on community colleges and metrics specifically related to their institutional mission. Using a difference-in-differences approach, the impact Texas’ performance funding model had on associate degree completion, certificate completion, and transfer-out rates was evaluated. The study utilized IPEDS data from 2010 to 2017 and compared the pre- to post- differences in Texas to California. The results of the study found performance funding had no statistically significant impact on associate degree completion, certificate completion, or transfer-out rates, even after controlling for race/ethnicity, gender, age, enrollment, degree of urbanization, tuition and fees, and financial aid. The study recommends further research on programs with 50% or more of appropriations based on performance. If this research confirms that performance funding does not improve student outcomes, state legislatures need to consider the evidence from the results of this study and previous research and no longer pursue performance funding models

Loss of CMAH during Human Evolution Primed the Monocyte–Macrophage Lineage toward a More Inflammatory and Phagocytic State

Humans and chimpanzees are more sensitive to endotoxin than are mice or monkeys, but any underlying differences in inflammatory physiology have not been fully described or understood. We studied innate immune responses in Cmah-/- mice, emulating human loss of the gene encoding production of Neu5Gc, a major cell surface sialic acid. CMP-N-acetylneuraminic acid hydroxylase (CMAH) loss occurred ∼2-3 million years ago, after the common ancestor of humans and chimpanzees, perhaps contributing to speciation of the genus HomoCmah-/- mice manifested a decreased survival in endotoxemia following bacterial LPS injection. Macrophages from Cmah-/- mice secreted more inflammatory cytokines with LPS stimulation and showed more phagocytic activity. Macrophages and whole blood from Cmah-/- mice also killed bacteria more effectively. Metabolic reintroduction of Neu5Gc into Cmah-/- macrophages suppressed these differences. Cmah-/- mice also showed enhanced bacterial clearance during sublethal lung infection. Although monocytes and monocyte-derived macrophages from humans and chimpanzees exhibited marginal differences in LPS responses, human monocyte-derived macrophages killed Escherichia coli and ingested E. coli BioParticles better. Metabolic reintroduction of Neu5Gc into human macrophages suppressed these differences. Although multiple mechanisms are likely involved, one cause is altered expression of C/EBPβ, a transcription factor affecting macrophage function. Loss of Neu5Gc in Homo likely had complex effects on immunity, providing greater capabilities to clear sublethal bacterial challenges, possibly at the cost of endotoxic shock risk. This trade-off may have provided a selective advantage when Homo transitioned to butchery using stone tools. The findings may also explain why the Cmah-/- state alters severity in mouse models of human disease

Computational prediction of out-of-plane welding distortion and experimental investigation - Awarded Central Electricity Generating Board Prize

The main aim of the work was to investigate a simplified finite element simulation of the out-of-plane distortion caused by fusion butt welding. The thermal transient part of the simulation made use of a finite element analysis of the two-dimensional cross-section of the weld joint and the thermoelastic-plastic treatment was based on analytical algorithms describing transverse and longitudinal deformations, leading to predictions of transverse angular deformation and longitudinal contraction force. These results were then applied to a non-linear elastic finite element model to provide predictions of the final angular and overall deformations of the butt-welded plates. The validity of the simulation was investigated via full-scale tests on 4m x 1.4m x 5 mm steel plates, butt welded using a flux-cored Ar-CO2 metal-inert gas process. Thermography and thermocouple arrays were used to validate the thermal transient computations and out-of-plane deformations were measured using displacement transducers for transient deformations and a laser scanning system to measure the profiles of the whole plates before and after welding. The results of six full-scale tests are given and comparison with the simulations shows that the procedure provides good prediction of the angular and overall out-of-plane deformations. Prediction accuracy requires account to be taken of initial shape, gravity loading, and support conditions

The determination of residual strains and stresses in a TIG-welded sheet of IN718 superalloy using neutron diffraction

The residual stress state in a tungsten inert gas (TIG) welded sheet of IN718, a high-strength nickel-based superalloy, has been characterized using neutron diffraction. The measurements were performed using a time-of-flight diffractometer, which allowed lattice strains from the \u3b3-\u3b3\u2032 {111} and \u3b3-\u3b3\u2032 {311} composite peaks to be compared with the Reitveld-refined spectra. Residual stresses were estimated using plane-specific values of Young's modulus and Poisson's ratio for the {311} and {111} peaks, and the macroscopic material response for the Reitveld-refined data. These values were obtained from a theoretical analysis of existing data after Kr\uf6ner.The weld considered was an autogenous TIG weld 180mm long placed centrally on to a 2mm x 100mm x 200mm solution heat-treated sheet of IN718. The strain was mapped over the central 140mm of the plate; within this region, the measured strains were almost constant along the length, with the peak bulk longitudinal strain of 1700 x 10-6 detected 4mm from the weld centre, in the heat-affected zone. The corresponding peak longitudinal stress was 270 MPa, and the tensile region 11 mm wide, with the longitudinal residual stresses typically up to 2.5 times greater than those in the transverse direction. It was also found that, while in-weld stresses derived from analysis of single peaks may be incorrect due to textural and compositional effects, those derived from Reitveld refinement of the entire spectrum showed reasonable agreement with those obtained from incremental hole drilling measurements made with the Matthar-Soete method.Peer reviewed: YesNRC publication: N

Loss of CMAH during Human Evolution Primed the Monocyte–Macrophage Lineage toward a More Inflammatory and Phagocytic State

Humans and chimpanzees are more sensitive to endotoxin than mice or monkeys, but any underlying differences in inflammatory physiology have not been fully described or understood. We studied innate immune responses in Cmah(−/−) mice, emulating human loss of the gene encoding production of Neu5Gc, a major cell surface sialic acid. CMAH loss occurred ~2-3 million years ago, after the common ancestor of humans and chimpanzees, perhaps contributing to speciation of the genus Homo. Cmah(−/−) mice manifested a decreased survival in endotoxemia following bacterial lipopolysaccharide (LPS) injection. Macrophages from Cmah(−/−) mice secreted more inflammatory cytokines with LPS-stimulation and showed more phagocytic activity. Macrophages and whole blood from Cmah(−/−) mice also killed bacteria more effectively. Metabolic re-introduction of Neu5Gc into Cmah(−/−) macrophages suppressed these differences. Cmah(−/−) mice also showed enhanced bacterial clearance during sub-lethal lung infection. Although monocytes and monocyte-derived macrophages from humans and chimpanzees exhibited marginal differences in LPS responses, human monocyte-derived macrophages killed E. coli and ingested E. coli bioparticles better. Metabolic re-introduction of Neu5Gc into human macrophages suppressed these differences. While multiple mechanisms are likely involved, one cause is altered expression of C/EBPβ, a transcription factor affecting macrophage function. Loss of Neu5Gc in Homo likely had complex effects on immunity, providing greater capabilities to clear sub-lethal bacterial challenges, possibly at the cost of endotoxic shock risk. This trade-off may have provided a selective advantage when Homo transitioned to butchery using stone tools. The findings may also explain why the Cmah(−/−) state alters severity in mouse models of human disease