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To determine the separate and interactive effects of fetal inflammation and neonatal hyperoxia on the developing lung, we hypothesized that: 1) antenatal endotoxin (ETX) causes sustained abnormalities of infant lung structure; and 2) postnatal hyperoxia augments the adverse effects of antenatal ETX on infant lung growth. Escherichia coli ETX or saline (SA) was injected into amniotic sacs in pregnant Sprague-Dawley rats at 20 days of gestation. Pups were delivered 2 days later and raised in room air (RA) or moderate hyperoxia ([O.sub.2], 80% [O.sub.2] at Denver's altitude, ~65% [O.sub.2] at sea level) from birth through 14 days of age. Heart and lung tissues were harvested for measurements. Intraamniotic ETX caused right ventricular hypertrophy (RVH) and decreased lung vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) protein contents at birth. In ETX-exposed rats (ETX-RA), alveolarization and vessel density were decreased, pulmonary vascular wall thickness percentage was increased, and RVH was persistent throughout the study period compared with controls (SA-RA). After antenatal ETX, moderate hyperoxia increased lung VEGF and VEGFR-2 protein contents in ETX-[O.sub.2] rats and improved their alveolar and vascular structure and RVH compared with ETX-RA rats. In contrast, severe hyperoxia ([greater than or equal to]95% [O.sub.2] at Denver's altitude) further reduced lung vessel density after intra-amniotic ETX exposure. We conclude that intra-amniotic ETX induces fetal pulmonary hypertension and causes persistent abnormalities of lung structure with sustained pulmonary hypertension in infant rats. Moreover, moderate postnatal hyperoxia after antenatal ETX restores lung growth and prevents pulmonary hypertension during infancy. antenatal inflammation: vascular endothelial growth factor; bronchopulmonary dysplasia; persistent pulmonary hypertension of the newborn doi: 10.1152/ajplung.00153.2010.

Vascular endothelial growth factor (VEGF) receptor blockade impairs lung growth and decreases nitric oxide (NO) production in neonatal rat lungs. Inhaled NO (iNO) treatment after VEGF inhibition preserves lung growth in infant rats by unknown mechanisms. We hypothesized that neonatal VEGF inhibition disrupts lung growth by causing apoptosis in endothelial cells, which is attenuated by early iNO treatment. Three-day-old rats received SU-5416, an inhibitor of VEGF receptor, or its vehicle and were raised in room air with or without iNO (10 ppm). SU-5416 reduced alveolar counts and lung vessel density by 28% (P < 0.005) and 21% (P < 0.05), respectively, as early as at 7 days of age. SU-5416 increased lung active caspase-3 protein by 60% at 5 days of age (P < 0.05), which subsided by 7 days of age, suggesting a transient increase in lung apoptosis after VEGF blockade. Apoptosis primarily colocalized to lung vascular endothelial cells, and SU-5416 increased endothelial cell apoptotic index by eightfold at 5 days of age (P vascular growth; alveolar growth; developing lung; bronchopulmonary dysplasia

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejor.2006.01.038 Byline: Sunantha Teyarachakul (a), Suresh Chand (b), Jen Tang (b) Keywords: Control limits; Statistical process control; Bootstrap; Simulation Abstract: This paper considers the problem of finding limits for a statistical process control (SPC) chart for the process mean, when the process distribution is unknown. The bootstrap method estimates these limits relying on Monte Carlo methods, which are subject to simulation errors. Therefore this paper develops a computationally efficient enumeration method for exact calculations of the control limits. Author Affiliation: (a) College of Business and Industry, Minnesota State University Moorhead, Moorhead, MN 56563, USA (b) Krannert School of Management, Purdue University, West Lafayette, IN 47907, USA Article History: Received 8 March 2005; Accepted 11 January 2006

Calculation of statistical process control chart limits, using bootstrap method, is presented.

Inhaled nitric oxide attenuates pulmonary hypertension and improves lung growth in infant rats after neonatal treatment with a VEGF receptor inhibitor. Am J Physiol Lung Cell Mol Physiol 287: L344-L351, 2004. First published April 2, 2004; 10.1152/ajplung.00291. 2003.--VEGF plays a critical role during lung development and is decreased in human infants with bronchopulmonary dysplasia. Inhibition of VEGF receptors in the newborn rat decreases vascular growth and alveolarization and causes pulmonary hypertension (PH). Nitric oxide (NO) is a downstream mediator of VEGF, but whether the effects of impaired VEGF signaling are due to decreased NO production is unknown. Therefore, we sought to determine whether impaired VEGF signaling downregulates endothelial NO synthase (eNOS) expression in the developing lung and whether inhaled NO (iNO) decreases PH and improves lung growth after VEGF inhibition. Newborn rats received a single dose of SU-5416 (a VEGF receptor inhibitor) or vehicle by subcutaneous injection and were killed up to 3 wk of age for assessments of right ventricular hypertrophy (RVH), radial alveolar counts (RAC), lung eNOS protein, and NOx production in isolated perfused lungs (IPL). Neonatal treatment with SU-5416 increased RVH in infant rats and reduced RAC. Compared with controls, SU-5416 reduced lung eNOS protein expression by 89% at 5 days (P < 0.01). IPL studies from day 14 rats demonstrated increased baseline pulmonary artery pressure and lower perfusate NOx concentration after SU-5416 treatment. Importantly, iNO treatment prevented the increase in RVH and improved RAC after SU-5416 treatment. We conclude that treatment of neonatal rats with SU-5416 downregulates lung eNOS expression and that iNO therapy decreases PH and improves lung growth after SU-5416 treatment. We speculate that decreased NO production contributes to PH and decreases distal lung growth caused by impaired VEGF signaling. vascular endothelial growth factor; bronchopulmonary dysplasia; lung development; alveolarization

In addition to its vasodilator properties, nitric oxide (NO) promotes angiogenesis in the systemic circulation and tumors. However, the role of NO in promoting normal lung vascular growth and its impact on alveolarization during development or in response to perinatal stress is unknown. We hypothesized that NO modulates lung vascular and alveolar growth and that decreased NO production impairs distal lung growth in response to mild hypoxia. Litters of 1-day-old mouse pups from parents that were heterozygous for endothelial nitric oxide synthase (eNOS) deficiency were placed in a hypobaric chamber at a simulated altitude of 12,300 ft ([FI.sub.O2] = 0.16). After 10 days, the mice were killed, and lungs were fixed for morphometric and molecular analysis. Compared with wild-type controls, mean linear intercept (MLI), which is inversely proportional to alveolar surface area, was increased in the eNOS-deficient (eNOS -/-) mice [51 [+ or -] 2 [micro]m (eNOS -/-) vs. 41 [+ or -] 1 [micro]m (wild type); P < 0.01]. MLI was also increased in the eNOS heterozygote (+/-) mice (44 [+ or -] 1 [micro]m; P < 0.03 vs. wild type). Vascular volume density was decreased in the eNOS -/- mice compared with wild-type controls (P < 0.03). Lung vascular endothelial growth factor (VEGF) protein and VEGF receptor-1 (VEGFR-1) protein content were not different between the study groups. In contrast, lung VEGFR-2 protein content was decreased from control values by 63 and 34% in the eNOS -/- and eNOS +/- mice, respectively (P 0.03). We conclude that exposure to mild hypoxia during a critical period of lung development impairs alveolarization and reduces vessel density in the eNOS-deficient mouse. We speculate that NO preserves normal distal lung growth during hypoxic stress, perhaps through preservation of VEGFR-2 signaling. pulmonary hypertension; persistent pulmonary hypertension of the newborn; lung hypoplasia; congenital diaphragmatic hernia; angiogenesis

The concept of Shewhart charts is generalized to include other kinds of data usually encountered in practice. Specifically, valid control charts for dependent data and for independent data that are not necessarily nearly normal are constructed. The proposed charts are developed from the moving blocks bootstrap and the standard bootstrap techniques. Their construction is completely parametric and no distributional assumptions are needed., 1. INTRODUCTION The control chart, first developed by W. A. Shewhart, is a useful tool in statistical process control. It is an on-line process control technique used to detect the [...]

A procedure is proposed for screening applications in quality control that eliminates overselection (namely, the condition where the proportion of accepted screened items is greater than the proportion of conforming [...]

A Nafion/ruthenium oxide pyrochlore ([Pb.sub.2][Ru.sub.2-x] [Pb.sub.x][O7.sub.-y]) chemically modified electrode (CME) for the determination of uric acid by Osteryoung square-wave voltammetry (OSWV) is described. Compared to the glassy carbon electrode, the CME exhibits a 150 mV shift of the oxidation potential of uric acid in the cathodic direction and a marked enhancement of the current response. The best instrumental settings for OSWV are 50 Hz modulation frequency, 20 mV modulation amplitude, and 2 mV step height. Linear calibration curves are obtained over the 7.5 X [10.sup.-5]-5 X [10.sup.-7] M range in pH 1 buffer solution. The detection limit (3[Sigma]) is 1.1 X [10.sup.-7] M. Ascorbic acid in less than 10-fold excess does not interfere. The practical analytical utility is illustrated by selective measurements of uric acid in human urine and serum without any preliminary treatment.

A Nafion/ruthenium oxide pyrochlore (Pb2Ru2-xPbxO7-y)-modified glassy carbon electrode exhibits excellent electrocatalytic activity in the oxidation of hydrazine in neutral media. The catalyst is synthesized directly inside the Nation thin film matrix, which is spin coated onto a glassy carbon electrode. Hydrazine is detected by flow injection analysis at the modified electrode with excellent sensitivity. Linear calibration curves are obtained over the 5 X 10[superscript -5]-6 X 10[superscript -7] M range with pH 8.0 ammonia-ammonium chloride buffer solution as the carrier. The detection limit is 0.048 ng. The practical analytical utility is illustrated by selective flow injection measurements of hydrazine in the presence of oxalic acid and surface-active materials.

An asymptotic expansion, used to calculate Bayes credibility intervals, was obtained for the posterior Cdf of the reliability of series systems containing very reliable components. Bayes credibility intervals were calculated when the infinite series expansion was truncated. The asymptotic expansion was used to determine the magnitude of error when the infinite series expansion was eliminated.

Stochastic elements of additive multiattribute utility models were used in distribution of aggregate utility.

DOGAN A. SEREL [1] HERBERT MOSKOWITZ [2] JEN TANG [2] The early work on multivariate statistical process control was built upon Hotelling's [T.sup.2] control chart which was developed to simultaneously [...]

William J. Kolarik WCB/McGraw-Hill, 641 pp., ISBN 0-07-036309-9 With growing global competition, quality management is becoming increasingly important to the leadership and management of all organizations. There are widely accepted [...]

Tang, Jen-Ruey, Timothy D. Le Cras, Kenneth G. Morris, Jr., and Steven H. Abman. Brief perinatal hypoxia increases severity of pulmonary hypertension after reexposure to hypoxia in infant rats. Am. J. Physiol. Lung Cell. Mol. Physiol. 278: L356-L364, 2000.--We hypothesized that disrupted alveolarization and lung vascular growth caused by brief perinatal hypoxia would predispose infant rats to higher risk for developing pulmonary hypertension when reexposed to hypoxia. Pregnant rats were exposed to 11% inspired oxygen fraction (barometric pressure, 410 mmHg; inspired oxygen pressure, 76 mmHg) for 3 days before birth and were maintained in hypoxia for 3 days after birth. Control rats were born and raised in room air. At 2 wk of age, rats from both groups were exposed to hypoxia for 1 wk or kept in room air. We found that brief perinatal hypoxia resulted in a greater increase in right ventricular systolic pressure and higher ratio of right ventricle to left ventricle plus septum weights after reexposure to hypoxia after 2 wk of age. Moreover, perinatal hypoxic rats had decreased radial alveolar counts and reduced pulmonary artery density. We conclude that brief perinatal hypoxia increases the severity of pulmonary hypertension when rats are reexposed to hypoxia. We speculate that disrupted alveolarization and lung vascular growth following brief perinatal hypoxia may increase the risk for severe pulmonary hypertension with exposure to adverse stimuli later in life. pulmonary circulation; persistent pulmonary hypertension of the newborn; lung development; alveolarization; lung vascular growth

Krannert Graduate School of Management, Purdue University, 1310 Krannert Building, West Lafayette, Indiana 47907-1310 The relentless pursuit of increased product quality via continuous improvement is an important long-term strategy for [...]

Multi-characteristic, complete inspection screening models are developed which are capable of evaluating the interactions between quality characteristics in a unit. One model features separate screening specifications and joint evaluation of the inspection results in order to determine overall conformance. The other model direct tradeoffs among the quality of characteristics is achieved by using a joint screening rule based on an collection of the characteristics. The cost performance of the multi-characteristic models is evaluated and compared to the cost performance of independently-determine single characteristic models.

There are different approaches for studying linear models (and multivariate statistical analysis in general); for example, decision analytic approach, algebraic approach, and geometric approach. Quite a few books on linear [...]