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Whether soft sounds are effective in eliciting any reflexive body movements remains unknown. To detect the possible sound-induced changes of body movements in unconstrained rats, we had developed and tested a novel method of image analysis based on a modified optical flow algorithm. Data collection involved a digital camera that captured from above body images of an unrestrained rat, while a short-duration noise burst was presented unexpectedly at different intensities. Positive responses of acoustic perturbation of breathing were successfully detected over the chest or abdominal area in all 6 rats studied, and reported here for the first time. The reflex change was a relatively small sound-induced perturbation in the amplitude of breathing and/or in the inter-breath interval exceeding a statistical threshold of the pre-stimulus levels. Results showed that such acoustic perturbation of breathing could be elicited rather robustly (> 90%) even with very soft sounds (< 30 dB SPL, or Sound Pressure Level). We concluded that our method of image analysis was powerful enough to detect these subtle changes of breathing pattern in freely moving rats.

Background: Capsicum plant, especially for C. annuum, is an abundant resource for bioactive antioxidants, but few studies have examined the unripe fruit part of the Capsicum plant. Objective: MeOH extract of unripe fruits of C. annuum L. var. conoides (UFCA) was chromatographed over a silica gel column using a gradient of CH2Cl2/MeOH as eluent to produce 9 fractions. Antioxidant activities are evaluated along with cell viabilities of 9 fractions of UFCA. Method: The antioxidant properties were analyzed in terms of total phenol content (TPC), total flavonoid content (TFC), 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, 2,2-azinobis (3-ethyl-benzothiazoline-6- sulfonic acid) (ABTS) radical scavenging, ferric reducing, and ferrous ion-chelating ability. The cell viability of human oral cancer cells (Ca9-22) was measured by 3-(4,5-dimethylthiazol-2-yl)-(3-carboxymethoxyphenyl)-2- (4-sulphophenyl)-2H-tetrazolium (MTS) assay. Results: Except for TFC, fractions (Frs.) 1 and 2 showed the lowest level of these antioxidant properties. Frs. 3 to 9 showed dose-responsive induction for antioxidant effects. Fr. 8 and Fr. 5 respectively showed the highest levels of TPC and TFC for 1162 ± 11 gallic acid equivalents (GAE) (mg)/UFCA (g) and 1295 ± 32 quercetin equivalents (QCE) (mg)/UFCA (g). The cell viability of Fr. 3 was moderately decreased (78.2%) while those of Frs. 4, 5, and 9 were dramatically decreased (55.6, 57.8, and 46.8%, respectively) in oral cancer Ca9-22 cells. UFCA-derived 14 compounds/mixtures derived from Frs. 1, 2, 3, 4, and 8 displayed differential antioxidant performance for these analyses. Conclusion: Taken together, fractions of UFCA displayed diverse antioxidant and anticancer effects for oral cancer cells. Some fractions of UFCA may be potent natural antioxidant supplements for antioral cancer cell treatment.

Background:Pulmonary hypertension (PH) worsens clinical outcomes in former preterm infants with bronchopulmonary dysplasia (BPD). Oxidant stress disrupts alveolar and vascular development in models of BPD. Bleomycin causes oxidative stress and induces BPD and PAH in neonatal rats. Disruption in the vascular endothelial growth factor (VEGF) and nitric oxide signaling pathways contributes to BPD. We hypothesized that loss of EC-SOD would worsen PAH associated with BPD in a neonatal mouse model of bleomycin-induced BPD by disrupting the VEGF/NO signaling pathway.Methods:Neonatal wild-type mice (WT), and mice lacking EC-SOD (EC-SOD KO) received intraperitoneal bleomycin (2 units/kg) or phosphate-buffered saline (PBS) three times weekly and were evaluated at weeks 3 or 4.Results:Lack of EC-SOD impaired alveolar development and resulted in PH (elevated right ventricular systolic pressures, right ventricular hypertrophy (RVH)), decreased vessel density, and increased small vessel muscularization. Exposure to bleomycin further impaired alveolar development, worsened RVH and vascular remodeling. Lack of EC-SOD and bleomycin treatment decreased lung total and phosphorylated VEGFR2 and eNOS protein expression.Conclusion:EC-SOD is critical in preserving normal lung development and loss of EC-SOD results in disrupted alveolar development, PAH and vascular remodeling at baseline, which is further worsened with bleomycin and associated with decreased activation of VEGFR2.

Radiotherapy effectively destroys cancer cells in many sites of the body, but several limitations remain. This study investigated alternative splicing, which is a common mechanism of increased diversity in mRNAs and proteins. The relationships of alternative splicing to DNA damage and radiation such as UV and ionizing radiation were analyzed. The DNA damage responses of many genes involved in alternative splicing were compared between non-radiation and radiation treatments. Drugs that affect radioresistence or radiosensitization by modulating the effects of alternative splicing and radiation were also reviewed.

Isocitrate dehydrogenase (IDH) encodes a nicotinamide adenine dinucleotide phosphate+‐dependent enzyme for oxidative decarboxylation of isocitrate and has an essential role in the tricarboxylic acid cycle. Mutations of IDH1 and IDH2 have been identified in patients with glioma, leukemia, and other cancers. However, the incidence of IDH mutations in acute myeloid leukemia in Taiwan is much lower than that reported in Western countries. The reason for the difference is unknown and its clinical implications remain unclear. Acute lymphoblastic leukemia (ALL) is a heterogenous hematopoietic malignancy. Oral squamous cell carcinoma (OSCC) results from chronic carcinogen exposures and is highly prevalent in trucking workers, especially in southern Taiwan. Subtypes of both diseases require specific treatments, and molecular markers for developing tailored treatments are limited. High‐resolution melting (HRM) analysis is now a widely used methodology for rapid, accurate, and low‐cost mutation scanning. In this study, 90 adults with OSC and 31 children with ALL were scanned by HRM analysis for IDH1 and IDH2 mutation hot spots. In ALL, the allele frequency was 3.23% in both IDH1 and IDH2. In OSCC, the allele frequency was 2.22% in IDH2. A synonymous mutation over pG313 (c.939A > G) of IDH2 was found in both pediatric ALL and adult OSCC. Therefore, we concluded that mutations of IDH are uncommon in ALL and OSCC and are apparently not a major consideration when selecting treatment modalities.

Isocitrate dehydrogenase (IDH) encodes a nicotinamide adenine dinucleotide phosphate+-dependent enzyme for oxidative decarboxylation of isocitrate and has an essential role in the tricarboxylic acid cycle. Mutations of IDH1 and IDH2 have been identified in patients with glioma, leukemia, and other cancers. However, the incidence of IDH mutations in acute myeloid leukemia in Taiwan is much lower than that reported in Western countries. The reason for the difference is unknown and its clinical implications remain unclear. Acute lymphoblastic leukemia (ALL) is a heterogenous hematopoietic malignancy. Oral squamous cell carcinoma (OSCC) results from chronic carcinogen exposures and is highly prevalent in trucking workers, especially in southern Taiwan. Subtypes of both diseases require specific treatments, and molecular markers for developing tailored treatments are limited. High-resolution melting (HRM) analysis is now a widely used methodology for rapid, accurate, and low-cost mutation scanning. In this study, 90 adults with OSC and 31 children with ALL were scanned by HRM analysis for IDH1 and IDH2 mutation hot spots. In ALL, the allele frequency was 3.23% in both IDH1 and IDH2. In OSCC, the allele frequency was 2.22% in IDH2. A synonymous mutation over pG313 (c.939A > G) of IDH2 was found in both pediatric ALL and adult OSCC. Therefore, we concluded that mutations of IDH are uncommon in ALL and OSCC and are apparently not a major consideration when selecting treatment modalities.

This study aimed to investigate if zinc compound would have effects on body weight loss and bone marrow suppression induced by total body irradiation (TBI). ICR mice were divided randomly into two groups and treated with test or control compounds. The test compound contained zinc (amino acid chelated with bovine prostate extract), and the control was reverse osmosis pure water (RO water). One week after receiving the treatment, mice were unirradiated, or irradiated with 6 or 3 Gy by 6MV photon beams to the total body. Body weight changes were examined at regular intervals. Three and 5 weeks after the radiation, animals were sacrificed to examine the histologic changes in the bone marrow. Lower body weight in the period of 1‐5 weeks after radiation and poor survival rate were found after the 6 Gy TBI, as compared with the 3 Gy groups. The median survival time after 6 Gy and 3 Gy TBI for mice given the test compound were 26 and 76 days, respectively, and the corresponding figures were 14 and 70 days, respectively, for mice given the control compound (p < 0.00001). With zinc supplement, the mean body weight in mice which received the same dose of radiation was 7‐8 g heavier than in the water‐supplement groups during the second and third weeks (p < 0.05). Hence, there was no statistically significant difference in survival rate between zinc and water supplement in mice given the same dose of irradiation. Histopathologically there was less recovery of bone marrow cells in the 6Gy groups compared with the 3Gy groups. In the 3 Gy water‐supplement group, the nucleated cells and megakaryocytes were recovered in the fifth week when recovery was still not seen in the 6Gy group. With zinc supplement, these cells were recovered in the third week. In this study, we found that zinc is beneficial to body weight in mice treated with TBI. Histologic examination of bone marrow showed better recovery of bone marrow cells in groups of mice fed with zinc. This study suggests that zinc can be used as supplements in cancer patients receiving radiotherapy to reduce radiation‐induced complications.

Exposure of newborn rats to hyperoxia impairs alveolarization and vessel growth, causing abnormal lung structure that persists during infancy. Recent studies have shown that impaired angiogenesis due to inhibition of vascular endothelial growth factor (VEGF) signaling decreases alveolar and vessel growth in the developing lung, and that nitric oxide (NO) mediates VEGF-dependent angiogenesis. The purpose of this study was to determine whether hyperoxia causes sustained reduction of lung VEGF, VEGF receptor, or endothelial NO synthase (eNOS) expression during recovery, and whether inhaled NO improves lung structure in infant rats after neonatal exposure to hyperoxia. Newborn rat pups were randomized to hyperoxia [fraction of inspired oxygen (Fio2), 1.00] or room air exposure for 6 d, and then placed in room air with or without inhaled NO (10 ppm) for 2 wk. Rats were then killed for studies, which included measurements of body weight, lung weight, right ventricular hypertrophy (RVH), morphometric analysis of alveolarization (by mean linear intercept (MLI), radial alveolar counts (RAC), and vascular volume (Vv), and immunostaining and Western blot analysis. In comparison with controls, neonatal hyperoxia reduced body weight, increased MLI, and reduced RAC in infant rats. Lung VEGF, VEGFR-2, and eNOS protein expression were reduced after hyperoxia. Inhaled NO treatment after hyperoxia increased body weight and improved distal lung growth, as demonstrated by increased RAC and Vv and decreased MLI. We conclude that neonatal hyperoxia reduced lung VEGF expression, which persisted during recovery in room air, and that inhaled NO restored distal lung growth in infant rats after neonatal hyperoxia.

Exposure of newborn rats to hyperoxia impairs alveolarization and vessel growth, causing abnormal lung structure that persists during infancy. Recent studies have shown that impaired angiogenesis due to inhibition of vascular endothelial growth factor (VEGF) signaling decreases alveolar and vessel growth in the developing lung, and that nitric oxide (NO) mediates VEGF-dependent angiogenesis. The purpose of this study was to determine whether hyperoxia causes sustained reduction of lung VEGF, VEGF receptor, or endothelial NO synthase (eNOS) expression during recovery, and whether inhaled NO improves lung structure in infant rats after neonatal exposure to hyperoxia. Newborn rat pups were randomized to hyperoxia fraction of inspired oxygen (Fio2), 1.00 or room air exposure for 6 d, and then placed in room air with or without inhaled NO (10 ppm) for 2 wk. Rats were then killed for studies, which included measurements of body weight, lung weight, right ventricular hypertrophy (RVH), morphometric analysis of alveolarization (by mean linear intercept (MLI), radial alveolar counts (RAC), and vascular volume (Vv), and immunostaining and Western blot analysis. In comparison with controls, neonatal hyperoxia reduced body weight, increased MLI, and reduced RAC in infant rats. Lung VEGF, VEGFR-2, and eNOS protein expression were reduced after hyperoxia. Inhaled NO treatment after hyperoxia increased body weight and improved distal lung growth, as demonstrated by increased RAC and Vv and decreased MLI. We conclude that neonatal hyperoxia reduced lung VEGF expression, which persisted during recovery in room air, and that inhaled NO restored distal lung growth in infant rats after neonatal hyperoxia.

Today, many products are designed and manufactured to function for a long period of time before they fail. Determining product reliability is a great challenge to manufacturers of highly reliable products with only a relatively short period of time available for internal life testing. In particular, it may be difficult to determine optimal burn-in parameters and characterize the residual life distribution. A promising alternative is to use data on a quality characteristic (QC) whose degradation over time can be related to product failure. Typically, product failure corresponds to the first passage time of the degradation path beyond a critical value. If degradation paths can be modeled properly, one can predict failure time and determine the life distribution without actually observing failures. In this paper, we first use a Wiener process to describe the continuous degradation path of the quality characteristic of the product. A Wiener process allows nonconstant variance and nonzero correlation among data collected at different time points. We propose a decision rule for classifying a unit as normal or weak, and give an economic model for determining the optimal termination time and other parameters of a burn-in test. Next, we propose a method for assessing the product's lifetime distribution of the passed units. The proposed methodologies are all based only on the product's initial observed degradation data. Finally, an example of an electronic product, namely contact image scanner (CIS), is used to illustrate the proposed procedure. © 2002 Wiley Periodicals, Inc. Naval Research Logistics, 2003

Opening windows is frequently done to refresh the indoor air for the occupants. To maintain the cleanliness and freshness of the indoor air, more outdoor air is needed. But its high temperature and humidity are harmful to the thermal comfort of the indoor environment. Therefore, determining the amount of outdoor air allowed to enter the room is very important for the optimum conditioning of the indoor air. The ASHRAE comfort charts indicate the percentage of subjects feeling comfortable during various combinations of dry-bulb temperature, humidity, and air movement. A set of mathematical expressions were proposed to model the charts in order to calculate the comfort degree of the outdoor air automatically with its temperature and humidity. In this paper, the measurement of temperature and humidity was completed by a self-developed digital method. Besides, the comfort level of the sampled air was also simultaneously determined by this digital method based on the mathematical model of comfort charts. The system implemented based on our method is portable. This will let us make good use of the outdoor air and controll the ventilation machine more effectively.

Purchased materials often account for more than 50% of a manufacturer's product nonconformance cost. A common strategy for reducing such costs is to allocate periodic quality improvement targets to suppliers of such materials. Improvement target allocations are often accomplished via ad hoc methods such as prescribing a fixed, across-the-board percentage improvement for all suppliers, which, however, may not be the most effective or efficient approach for allocating improvement targets. We propose a formal modeling and optimization approach for assessing quality improvement targets for suppliers, based on process variance reduction. In our models, a manufacturer has multiple product performance measures that are linear functions of a common set of design variables (factors), each of which is an output from an independent supplier's process. We assume that a manufacturer's quality improvement is a result of reductions in supplier process variances, obtained through learning and experience, which require appropriate investments by both the manufacturer and suppliers. Three learning investment (cost) models for achieving a given learning rate are used to determine the allocations that minimize expected costs for both the supplier and manufacturer and to assess the sensitivity of investment in learning on the allocation of quality improvement targets. Solutions for determining optimal learning rates, and concomitant quality improvement targets are derived for each learning investment function. We also account for the risk that a supplier may not achieve a targeted learning rate for quality improvements. An extensive computational study is conducted to investigate the differences between optimal variance allocations and a fixed percentage allocation. These differences are examined with respect to (i) variance improvement targets and (ii) total expected cost. For certain types of learning investment models, the results suggest that orders of magnitude differences in variance allocations and expected total costs occur between optimal allocations and those arrived at via the commonly used rule of fixed percentage allocations. However, for learning investments characterized by a quadratic function, there is surprisingly close agreement with an “across-the-board” allocation of 20% quality improvement targets. © John Wiley & Sons, Inc. Naval Research Logistics 48: 684–709, 2001

Objectives:To estimate the cord blood levels of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in preterm infants and to study the relationship of these levels to pregnancy-induced hypertension (PIH) and absolute neutrophil counts. Study design:G-CSF and GM-CSF levels in the cord blood of preterm neonates (n = 74) either with or without maternal PIH were estimated by enzyme-linked immunosorbent assay. Results:Infants in the PIH group had lower white blood cell, absolute neutrophil, absolute lymphocyte, and monocyte counts. The levels of G-CSF in cord blood were significantly lower in infants whose mothers had PIH (P= .04) and in infants with neutropenia (P= .01). G-CSF levels were positively correlated with both absolute neutrophil count (P= .02) and total white blood cell count (P= .01). GM-CSF was undetectable in all subjects. According to logistic regression with neutropenia as the dependent variable, only maternal PIH (P< .001), gestational age (P< .001), and G-CSF (P= .01) were independently related. Conclusion:In this study maternal PIH and low gestational age were significantly associated with neutropenia in premature infants. Low G-CSF levels may contribute to the neutropenia that is commonly seen in infants born to mothers with PIH. (J Pediatr 1999;135:56-9)

System reliability is often estimated by the use of components' reliability test results when system test data are not available, or are very scarce. A method is proposed for computing the exact posterior probability density function, cumulative distribution function, and credible intervals for system reliability in a Bayesian setting, with the use of components' prior probability distributions and current test results. The method can be applied to series, parallel, and many mixed systems. Although in theory the method involves evaluating infinite series, numerical results show that a small number of terms from the infinite series are sufficient in practice to provide accurate estimates of system reliability. Furthermore, because the coefficients in the series follow some recurrence relations, our results allow us to calculate the reliability distribution of a large system from that of its subsystems. Error bounds associated with the proposed method are also given. Numerical comparisons with other existing approaches show that the proposed method is efficient and accurate. © 1997 John Wiley & Sons, Inc.

In this paper, WILKS'type-B integral equation is solved in the general form of a series of beta functions and a series of weighted gamma functions as proposed by WALD and BROOKNER 1941. The coefficients in both representations can be obtained by explicit recurrence relartions, therefore the results solve many distributional problems and have the fewest computational difficulties of any representation that has surfaced to date. The radius of convergence of the second series representation is given, whereas the convergence property of the first series representation is given, whereas the convergence property of the first series representation was studied by WALD and Brookner. The exact null distributions of WILKS' statistic A for testing the independence of several groups of variables and of V = -log A are given. The coefficients in all the series representration can be computed recursilvely and hence can be obtained easily with the help of modern computatinal facilities

The null distribution of Wilks' likelihood-ratio criterion for testing independence of several groups of variables in a multivariate normal population is derived. Percentage points are tabulated for various values of the sample sizeN and partitions of p, the number of variables. This paper extends Mathai and Katiya's (1979) "sphericity" results and tables.

No abstract.