A framework for analysis of data quality research

Organizational databases are pervaded with data of poor quality. However, there has not been an analysis of the data quality literature that provides an overall understanding of the state-of-art research in this area. Using an analogy between product manufacturing and data manufacturing, this paper develops a framework for analyzing data quality research, and uses it as the basis for organizing the data quality literature. This framework consists of seven elements: management responsibilities, operation and assurance costs, research and development, production, distribution, personnel management, and legal function. The analysis reveals that most research efforts focus on operation and assurance costs, research and development, and production of data products. Unexplored research topics and unresolved issues are identified and directions for future research provided     

High PCO does not alter pHi, but raises [Ca2+]i in cultured rat carotid body glomus cells in the absence and presence of CdC12

We measured the effect of high PCO (500-550 Torr) on the pHi and [Ca2+]i in cultured glomus cells of adult rat carotid body (CB) as a test of the two models currently proposed for the mechanism of CB chemoreception. The metabolic model postulates that the rise in glomus cell [Ca2+]i, the initiating reaction in the signalling pathway leading to chemosensory neural discharge, is due to [Ca2+] release from intracellular Ca2+ stores. The membrane potential model postulates that the rise in [Ca2+]i comes from influx of extracellular Ca2+ through voltage-dependent Ca2+ channels (VDCC) of the L-type. High PCO did not change pHi at PO2 of 120-135 Torr, showing that CO-induced changes in [Ca2+]i are not due to changes in pHi. High PCO caused a highly significant rise in [Ca2+]i from 90+/-12 nM to 675+/-65 nM, both in the absence and in the presence of 200 microM CdCl2, a potent blocker of L-type VDCCs. This result is fully consistent with release of Ca2+ from glomus cell intracellular stores according to metabolic model, but inconsistent with influx of extracellular Ca2+ through VDCCs according to the membrane potential model.     

Advanced pain & symptom management (a case study-workshop discussion)

Coexpression of the rat beta 1 subunit with rat brain and skeletal muscle sodium channel alpha subunits in Xenopus oocytes normalizes currents by accelerating sodium current decay kinetics, shifting steady state availability relationships, and accelerating recovery from inactivation. Unlike brain and skeletal muscle, the heart alpha subunit expressed without beta 1 has native-like decay kinetics in oocytes. Messenger RNA for beta 1 has been found in heart, but whether and how it affects cardiac sodium channel function are unclear. We studied coexpression of human heart alpha subunit with beta 1 in Xenopus oocytes using two microelectrode voltage-clamp and macropatch techniques. Coexpression with beta 1 caused a significant positive shift of 3-7 mV in the midpoint of the steady state inactivation relationship but did not affect single-channel conductance, activation, current decay, or recovery from inactivation. Sensitivity to lidocaine block, however, was decreased for both resting state block (Kd = 0.5-1.3 mM) and phasic block in response to pulse trains, but inactivated state block was not affected (Kd = approximately 10 microM). Coexpression with beta 1 increased the rate of recovery from lidocaine block, which accounted for the major part of the observed differences in tonic and phasic block. A beta 1 construct with the cytoplasmic tail removed also produced these effects, demonstrating that the beta 1 cytoplasmic tail was not involved in altering lidocaine block. We conclude that the beta 1 subunit is capable of affecting function of the cardiac sodium channel in oocytes by decreasing tonic and phasic lidocaine block with small effects on gating.     

Review of Psychological Testing (3rd ed.).

Reviews the book, Psychological Testing (3rd ed.) by Anne Anastasi (1968). The many admirers and followers Anastasi incurred through the first two editions of this book along with her other writing will not be disappointed with this third edition. All of the testing knowledge apparently adequately updated, is still there, along with the familiar clarity and authority of expression. The third edition contains more useful-to-the-testing-purpose material than did either of the earlier editions. This feat has been accomplished in spite of the fact that the book is no longer than the others, containing 665 pages as opposed to 681 and 657 for the first and second editions respectively. This content improvement seems to have been brought about through the curtailment of less valuable data on the one hand and the inclusion of more recent and better material on the other. This edition of Anastasi's text contains enough new material in measurement to recommend that it be read by both students of and experts in the field. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fatigue crack propagation in aluminium alloy NP8 determined from tests on 12.5 mm nominal thickness specimens

Fatigue crack growth tests were carried out on aluminium alloy BS1477 NP8 which has a 0.1% proof stress of 120 MN/m². The tests were performed in air at room temperature using centrecrack fracture toughness specimens of 12.5 mm nominal thickness. Crack growth rates were found to depend on the stress ratio σ_min/σ_max (the R ratio) and probably on specimen thickness, but not on net section yield. The results were similar to those reported by Frost using high strength aluminium alloys of 3–4 mm thickness, and this has been attributed to the increased thickness of the NP8 specimens. The individual da/dN vs Δ K results formed into bands depending on R; crack growth rates at each R value could be correlated in terms of the linear elastic fracture mechanics parameter ΔK, in the form da/dN=C(ΔK)ⁿ suggested by Paris. Crack growth rates were greater than predicted by expressions due to Frost based on thin low strength aluminium specimens and due to Pearson based on 12.7 mm thickness high strength aluminium specimens. A modified Pearson equation has been deduced which is in good agreement with the test results. Used in conjunction with an approximate expression for ΔK, the modified equation leads to conservative estimates of the number of cycles for a crack to reach a given length, which is a safe result of value in engineering practice.