bluuebunny/crossref_metadata_2025_split huggingface dataset:
Computation of GPS continuity with consideration of progress of time
Authors: Sakai Takeyasu , Koremura Kazunobu 
Published: November 2002

AbstractThe international civil aviation organization (ICAO) has defined the international standard for the global navigation satellite system (GNSS) based on GPS for aviation use. Navigation systems for aviation must ensure not only the specific positioning accuracy but also the required reliability performance. Continuity is one of the measures of system reliability, and is defined as the probability that the system operates without nonscheduled interruptions over a certain period of time. We have already proposed a method of computing the continuity of GPS for the approach and landing flight phase. However, the method cannot be applied to flight phases such as enroute or terminal airspace because of the longer periods for such phases, for example 1 hour, over which the continuity requirements are defined. This paper describes a method of computing continuity with consideration of the progress of time, taking into account the movement of the aircraft relative to navigation satellites. Some computation examples are also presented. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 86(3): 26–34, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.10044
Traffic characteristics of Go‐back‐N ARQ scheme with selective repeat in intra‐block
Authors: Maeda Akiko , Sugimachi Nobuyuki , Hayashida Yukuo , Fujii Shumji 
Published: November 2002

AbstractThis paper discusses the traffic characteristics of the Go‐back‐N (GBN)_SR scheme, in which the receiver returns the acknowledge signal blockwise and selective repeat is performed within the retransmission block. First the strict expression for the throughput and the strict expression for the average transmission delay of the blockwise bulk arrival model are derived. Then, the throughput of the GBN_SR scheme and the average transmission delay of the blockwise bulk arrival model are examined by numerical calculation. The average transmission delay of the packetwise bulk arrival model is investigated by simulation. It is shown that the throughput is improved with increasing block size, and that the average transmission delay can be minimized by using the optimal block size, depending on the average packet error rate and the block arrival rate. It is also shown for the packetwise bulk arrival model that there exists a block size which minimizes the average transmission delay, and that the minimum average transmission delay is smaller than in the blockwise bulk arrival model. © 2002 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 86(3): 9–16, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ ecja.10052
The influence of gender‐stereotyped perfumes on leadership attribution
Authors: Sczesny Sabine , Stahlberg Dagmar 
Published: November 2002

AbstractThe classification of perfumes as ‘women's’ and ‘men's’ fragrances is based on certain gender stereotypes. In two experiments, female and male participants were asked to assume the role of a manager. In Experiment 1, they read an application for the position of a junior manager written by a male or female job applicant. Application papers were prepared with a typically masculine perfume, a typically feminine perfume or no perfume at all (control group). In Experiment 2, participants conducted a job interview with a female or male applicant (a confederate) who had applied the respective perfume or no perfume. Persons with a typically masculine perfume were ‘employed’ with a higher degree of certainty compared to persons with a typically feminine perfume. Copyright © 2002 John Wiley & Sons, Ltd.
Regressive threshold model for familial analysis of complex diseases with variable age of onset
Authors: Briollais L. , Demenais F. 
Published: November 2002

AbstractFew models for segregation (or combined segregation‐linkage) analysis have been developed to account for variable age of onset. The unified model (UM) can only take into account age at examination. In the logistic hazard model (LHM), Abel and Bonney ([1990] Genet. Epidemiol. 7:391–407) incorporated survival analysis concepts into the regressive logistic model of Bonney ([1986] Am. J. Med. Genet. 18:731–749), but interpretation of familial dependence parameters is difficult. In this article, we extended the regressive threshold model (RTM) proposed by Demenais ([1991] Am. J. Hum. Genet. 49:773–785) to account for a variable age of onset of complex diseases. This model assumes an underlying liability to disease and is more general than the original logistic formulation, since the phenotypes of each individual's antecedents can be adjusted for their own genotypes and covariate effects. The variation of risk with age can be expressed as a general step function, and variants of the model have been proposed by imposing different types of constraints among the time‐dependent thresholds. The performances of the three models (UM, LHM, and RTM) were compared in the context of segregation analysis of family data generated with variable age of onset. All analysis models were robust with respect to false conclusion of a major gene, and the best results were obtained under RTM. The power to detect the major gene was higher under LHM than RTM, but the best fit of the estimated cumulative age‐dependent penetrance with respect to the true value was obtained under RTM. This new model may thus prove helpful in contributing to identification of genes underlying complex diseases, since it can easily include linked marker loci and linkage disequilibrium. Genet. Epidemiol. 23:375–397, 2002. © 2002 Wiley‐Liss, Inc.
Score test for mapping quantitative‐trait loci with sibships of arbitrary size when the dominance effect is not negligible
Authors: Wang Kai , Huang Jian 
Published: November 2002

AbstractIn the linakge analysis of quantitative traits, an additive model that assumes no dominance effect is often adopted. Intuitively, when the no‐dominance‐effect assumption does not hold, such a practice does not make efficient use of the data, and its power to detect linkage can be improved. Here we introduce a score statistic for detecting quantitative trait loci when the dominance effect is not neglible or the dominance effect is a concern. This statistic is derived from a normal likelihood function for sibships of arbitrary size. In the derivation, the inherent genetic constraints on model parameters are fully taken into consideration. This score statistic is asymptotically equivalent to the corresponding likelihood ratio statistic, but it is much easier to compute. The asymptotic distribution of this statistic is derived, which is a mixture of χ02, χ12, and χ22. Weights for distribution components are functions of the informativeness of the marker data. The type I error rate and the power of the proposed statistic in finite sample are evaluated via simulations. Genet. Epidemiol. 23:398–412, 2002. © 2002 Wiley‐Liss, Inc.
Palaeomagnetic evidence for the Gondwanian origin of the Taurides and rotation of the Isparta Angle, southern Turkey
Authors: Piper John D. A. , Gürsoy Hali̇l , Tatar Orhan , İşseven Turgay , Koçyi̇ği̇t Ali̇ 
Published: November 2002

AbstractThe Taurides, the southernmost of the three major tectonic domains that constitute present‐day Turkey, were emplaced following consumption of the Tethyan Ocean in Late Mesozoic to mid‐Tertiary times. They are generally assigned an origin at the northern perimeter of Gondwana. To refine palaeogeographic control we have investigated the palaeomagnetism of a range of Jurassic rocks. Forty‐nine samples of Upper Jurassic limestones preserve a dual polarity remanence (D/I=303/−9°, α95=6°) interpreted as a primary magnetization acquired close to the equator and rotated during emplacement of the Taurides. Result from mid‐Jurassic dolerites confirm a low palaeolatitude for the Tauride Platform during Jurassic times at the Afro–Arabian sector of Gondwana. Approximately 4000 km of Tethyan closure subsequently occurred between Late Jurassic and Eocene times. Although related Upper Jurassic limestones and Liassic redbeds preserve a sporadic record of similar remanence, the dominant signature in these latter rocks is an overprint of probable mid‐Miocene age, probably acquired during a single polarity chron and imparted by migration of a fluid front during nappe loading. This is now rotated consistently anticlockwise by c. 30° and conforms to results of previous studies recording bulk Neogene rotation of the Isparta region following Lycian nappe emplacement. The regional distribution of this overprint implies that the Isparta Angle (IA) has been subject to only small additional closure (<10°) since Late Miocene time. A smaller amount (c. 6°) of clockwise rotation within the IA since Early Pliocene times is associated with an ongoing extensional regime and reflects an expanding curvature of the Tauride arc produced by southwestward extrusion of the Anatolian collage as a result of continuing northward motion of Afro–Arabia. Copyright © 2002 John Wiley & Sons, Ltd.
The green tea polyphenol, epigallocatechin‐3‐gallate, protects against the oxidative cellular and genotoxic damage of UVA radiation
Authors: Tobi Simon E. , Gilbert Mileka , Paul Nigel , McMillan Trevor J. 
Published: November 2002

AbstractA number of biological activities have been ascribed to the major green tea polyphenol epigallocatechin‐3‐gallate (EGCG) to explain its chemopreventive properties. Its antioxidant properties emerge as a potentially important mode of action. We have examined the effect of EGCG treatment on the damaging oxidative effects of UVA radiation in a human keratinocyte line (HaCaT). Using the ROS‐sensitive probes dihydrorhodamine 123 (DHR) and 2′,7′‐dichlorodihydrofluorescein diacetate (DCFH‐DA), we detected a reduction in fluorescence in UVA‐irradiated (100 kJ/m2) cells in the case of the former but not the latter probe after a 24‐hr treatment with EGCG (e.g., 14%, [p < 0.05] after 10 μM EGCG). In the absence of UVA, however, both DHR and DCFH detected a pro‐oxidant effect of EGCG at the highest concentration used of 50 μM. Measurements of DNA damage in UVA‐exposed cells using the single cell gel electrophoresis assay (comet assay) also showed the protective effects of EGCG. A concentration of 10 μM EGCG decreased the level of DNA single strand breaks and alkali‐labile sites to 62% of the level observed in non‐EGCG, irradiated cells (p < 0.001) with a 5‐fold higher concentration producing little further effect. Correspondingly, EGCG ablated the mutagenic effects of UVA (500 kJ/m2) reducing an induced hypoxanthine‐guanine phosphoribosyl transferase (HPRT) mutant frequency of (3.39 ± 0.73) × 10−6 to spontaneous levels (1.09 ± 0.19) × 10−6. Despite having an antiproliferative effect in the absence of UVA, EGCG also served to protect against the cytotoxic effects of UVA radiation. Our data demonstrate the ability of EGCG to modify endpoints directly relevant to the carcinogenic process in skin. © 2002 Wiley‐Liss, Inc.
HER2 overexpression in muscle‐invasive urothelial carcinoma of the bladder: Prognostic implications
Authors: Krüger Stefan , Weitsch Georg , Büttner Hartwig , Matthiensen Arne , Böhmer Torsten , Marquardt Tim , Sayk Friedhelm , Feller Alfred C. , Böhle Andreas 
Published: November 2002

AbstractThe HER2 (c‐erbB‐2) receptor is overexpressed in a variety of human malignant tumors and, in breast carcinoma, has been identified as a target for anti‐HER2–directed therapy with the monoclonal antibody (MAb) trastuzumab. The aim of this retrospective study was to evaluate immunohistochemic HER2 expression in a large cohort of muscle‐invasive urothelial cell carcinomas of the urinary bladder and to compare the results to pathologic characteristics and survival. Paraffin‐embedded tumor specimens from 138 patients undergoing radical cystectomy for muscle‐invasive bladder carcinoma were studied immunohistochemically with the Food and Drug Administration (FDA)‐approved HercepTest (Dako, Glostrup, Denmark). HER2 overexpression was observed in 57 of 138 tumors (41%) and occurred more frequently in high‐grade carcinomas than in low‐grade carcinomas (p = 0.036). No significant relationship with HER2 overexpression was registered for tumor staging and lymph node status. Kaplan‐Meier curves showed a significantly worse disease‐related survival (p = 0.034) in patients with HER2‐overexpressing tumors compared to those without HER2 overexpression. In addition to lymph node status (p = 0.0001; relative risk [RR] = 2.93), HER2 status (p = 0.020; RR = 2.22) was identified as an independent predictor for disease‐related survival in a multivariate analysis. These results suggest that HER2 expression might provide additional prognostic information in patients with muscle‐invasive bladder carcinomas. Because many of these patients harbor HER2‐overexpressing tumors, clinical trials evaluating the efficacy of trastuzumab in bladder carcinoma are warranted. © 2002 Wiley‐Liss, Inc.
Recurrent human papillomavirus infection detected with the hybrid capture II assay selects women with normal cervical smears at risk for developing high grade cervical lesions: A longitudinal study of 3,091 women
Authors: Bory Jean‐Paul , Cucherousset Joël , Lorenzato Marianne , Gabriel René , Quereux Christian , Birembaut Philippe , Clavel Christine 
Published: November 2002

AbstractTo test the reliability of the Hybrid Capture II (HC‐II) assay detecting 13 high‐risk human papillomavirus (HR‐HPV) types for the screening of cervical lesions, we monitored by cytology, HR‐HPV testing, colposcopy and biopsy, 3,091 women with normal smears at the first entry. Our primary endpoint was clinical progression defined as the presence of a high‐grade lesion (HGSIL) at the biopsy. In our population of 659 HR‐HPV‐infected women, 241 (36.6%) had a positive HR‐HPV test at 2 to 4 examinations with a final histological diagnosis of HGSIL in 51 cases (21.2%) within 4 to 36 months, while women with regressive HPV infection did not develop any lesion during the same period. In the cohort of 2,432 women testing negative for HR‐HPV infection, only 2 women (0.08%) developed a HGSIL. Both were HR‐HPV positive 18 and 24 months after the first entry, at the time of diagnosis of disease. The RR of incident HGSIL when a HR‐HPV was detected at enrollment in women with normal smears was 96.7 (95% CI, 95.8–97.7). The RR increased to 237.3 (95% CI, 222.8–251.8) when the HR‐HPV test remained positive at 2 controls, and to 314.3 (95% CI, 260.7–367.9) when the HR‐HPV test was positive at 3 controls. The evaluation of the viral load of HR‐HPV by the HC‐II did not represent a sensitive approach to predict the recurrence of HR‐HPV infection and/or the apparition of HGSIL. Nevertheless, a recurrent HR‐HPV infection detected with HC‐II represents a reliable tool to select populations at risk for the development of HGSIL. © 2002 Wiley‐Liss, Inc.
Nuclear factor‐κB, induced in human carcinoma cell line A2780 by the new anthracycline men 10755, is devoid of transcriptional activity
Authors: Camarda Grazia , Binaschi Monica , Maggi Carlo A. , Goso Cristina 
Published: November 2002

AbstractThe new disaccharide anthracycline MEN 10755 induces activation of both NF‐κB and p53 transcription factors in A2780 cells. Nevertheless, pharmacologic inhibition of NF‐κB activation does not modify the sensitivity of A2780 cells to MEN 10755 treatment. To better characterize the role of NF‐κB in MEN 10755–induced cytotoxicity, we analyzed the expression of a number of genes that are known to be regulated by NF‐κB. None of these genes is modified by MEN 10755 treatment. On the contrary, our results suggest that the p53 DNA damage‐responsive pathway is fully activated in A2780 cells, several genes controlled by p53 being up‐ or downregulated according to the described action of p53 on their promoters. Thus, in the A2780 cell line, the role of p53 in transducing the DNA‐damage signal appears to be relevant, whereas NF‐κB, although activated, appears to be nonfunctional. Other human carcinoma cell lines besides A2780 activate NF‐κB DNA binding in response to MEN 10755 treatment, but again, this binding does not always lead to target gene activation. These results suggest that other factors, tumor type‐specific and different from mere activation, could influence NF‐κB transcriptional activity. Therefore, care should be taken when considering the pharmacologic inhibition of NF‐κB as a means to improve anticancer therapy efficacy. © 2002 Wiley‐Liss, Inc.
Expression of mitogen‐activated protein kinase phosphatase‐1 (MKP‐1) in primary human ovarian carcinoma
Authors: Denkert Carsten , Schmitt Wolfgang D. , Berger Stefan , Reles Angela , Pest Sören , Siegert Antje , Lichtenegger Werner , Dietel Manfred , Hauptmann Steffen 
Published: November 2002

AbstractThe mitogen‐activated protein kinase phosphatase‐1, MKP‐1 (CL100) is involved in inactivation of MAP‐kinase pathways, regulation of stress‐responses and suppression of apoptosis. We investigated expression of MKP‐1 in 90 cases of primary ovarian tumors, 11 normal ovaries as well as 4 ovarian carcinoma cell lines. Immunohistochemical expression of MKP‐1 protein was reduced in tissue from LMP tumors and invasive ovarian carcinomas compared to normal ovaries and cystadenomas. A moderate to strong expression of MKP‐1 was detected in 57.6% of invasive ovarian carcinomas. In a descriptive univariate survival analysis, MKP‐1 expression was a prognostic marker for shorter progression‐free survival of patients with invasive ovarian carcinomas. Patients with carcinomas positive for MKP‐1 had a median progression‐free survival of only 18.3 months compared to 40.6 months for patients with carcinomas negative for MKP‐1 (log‐rank test, p = 0.019). Other prognostic parameters for progression‐free survival were FIGO stage, grade and pT stage. In an exploratory multivariate analysis, we found that MKP‐1 expression as well as FIGO stage and grade were independent prognostic factors for progression‐free survival. In contrast to progression‐free survival, we did not find any influence of MKP‐1 expression on patient overall survival. We investigated expression and regulation of MKP‐1 mRNA by Northern Blot in vitro using 4 ovarian carcinoma cell lines (SKOV‐3, OVCAR‐3, CAOV‐3, OAW‐42). MKP‐1 mRNA was inducible by interleukin‐1β and tumor necrosis factor‐α in SKOV‐3 and OVCAR‐3 cells, whereas CAOV‐3 and OAW‐42 expressed MKP‐1 mRNA constitutively. In OVCAR‐3 cells MKP‐1 mRNA levels were strongly inducible upon treatment of cells with cisplatin. Our data indicate that MKP‐1 is expressed in a subset of ovarian carcinomas and regulated by inflammatory mediators. Expression of MKP‐1 may be associated with shorter progression‐free survival times. Further studies are needed to determine whether MKP‐1 expression is a clinically useful marker to estimate patient prognosis as well as the response to chemotherapy. © 2002 Wiley‐Liss, Inc.
Protein arginine methyltransferase I: Substrate specificity and role in hnRNP assembly
Authors: Pawlak Maciej R. , Banik‐Maiti Sarbani , Pietenpol Jennifer A. , Ruley H. Earl 
Published: November 2002

AbstractPrmt1, the major protein arginine methyltransferase in mammalian cells, has been implicated in signal transduction, transcriptional control, and protein trafficking. In the present study, mouse embryonic stem cells homozygous for an essentially null mutation in the Prmt1 gene were used to examine Prmt1 activity and substrate specificity, which by several criteria appeared to be highly specific. First, other methyltransferases did not substitute for the loss of Prmt1 activity. Second, almost all proteins modified by recombinant Prmt1 in vitro were authentic substrates, i.e., proteins rendered hypomethylated by Prmt1 gene disruption. Finally, Prmt1 did not modify the substrates of other methyltransferases from cells treated with methyltransferase inhibitors. Recombinant proteins corresponding to two splice‐variants, Prmt1353 and Prmt1371, methylated different, proteins in vitro, providing the first evidence for functional differences between the two isoforms. However, the differences in substrate specificity were lost by the addition of an N‐terminal His6 tag. Loss of Prmt1 activity (and hypomethylation of hnRNPs) has no obvious effect on the formation or composition of hnRNP complexes. Finally, methylation of the most abundant Prmt1 substrates appeared to be extensive and constitutive throughout the cell cycle, suggesting the modification does not modulate protein function under normal growth conditions. J. Cell. Biochem. 87: 394–407, 2002. © 2002 Wiley‐Liss, Inc.
Expression pattern of alternatively spliced PECAM‐1 isoforms in hematopoietic cells and platelets
Authors: Wang Yongji , Sheibani Nader 
Published: November 2002

AbstractPECAM‐1 (CD31) is a cell adhesion molecule that is highly expressed in the endothelium. Hematopoietic cells including platelets, monocytes, neutrophils, and some T cells also express moderate levels of PECAM‐1. PECAM‐1 undergoes alternative splicing generating a number of isoforms in the endothelium. However, the expression of PECAM‐1 isoforms in hematopoietic cells and platelets has not been determined. Here, we examined the expression pattern of PECAM‐1 isoforms in human and rodent hematopoietic cells and platelets by RT‐PCR and DNA sequencing analysis. Our results showed that multiple PECAM‐1 isoforms are expressed in a cell‐type and species‐specific pattern. We identified seven human PECAM‐1 isoforms, six murine PECAM‐1 isoforms, and four rat PECAM‐1 isoforms. The full‐length PECAM‐1 was the predominant isoform detected in human cells. The PECAM‐1 isoforms that lack exon 14 and 15 (Δ14&15) or Δ12,14&15 were the predominant isoform in rodent cells. In addition, we identified a novel PECAM‐1 isoform, Δ13&14, in human hematopoietic cells. Thus, hematopoietic cells express multiple isoforms of PECAM‐1 in a pattern similar to that observed in the endothelium of the same species. The regulated expression of these isoforms may be important during hematopoiesis and transendothelial migration. J. Cell. Biochem. 87: 424–438, 2002. © 2002 Wiley‐Liss, Inc.
Stress‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) plays a part in endothelin‐1‐induced vascular endothelial growth factor synthesis in osteoblasts
Authors: Wang Xiaodan , Tokuda Haruhiko , Hirade Kouseki , Kozawa Osamu 
Published: November 2002

AbstractWe previously reported that endothelin‐1 (ET‐1) activates both p44/p42 mitogen‐activated protein (MAP) kinase and p38 MAP kinase in osteoblast‐like MC3T3‐E1 cells, and that not p44/p42 MAP kinase but p38 MAP kinase participates in the ET‐1‐induced vascular endothelial growth factor (VEGF) synthesis. In the present study, we investigated the involvement of stress‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) in ET‐1‐induced VEGF synthesis in these cells. ET‐1 significantly induced the phosphorylation of JNK in a dose‐dependent manner in the range between 0.1 and 100 nM. SP600125, an inhibitor of JNK, markedly reduced the ET‐1‐induced VEGF synthesis. A combination of SP600125 and SB203580 additively reduced the ET‐1‐stimulated VEGF synthesis. SP600125 suppressed the ET‐1‐induced phosphorylation of JNK, while having no effect on the phosphorylation of p38 MAP kinase elicited by ET‐1. SB203580, an inhibitor of p38 MAP kinase, hardly affected the ET‐1‐induced phosphorylation of JNK. These results strongly suggest that JNK plays a role in ET‐1‐induced VEGF synthesis in addition to p38 MAP kinase in osteoblasts. J. Cell. Biochem. 87: 417–423, 2002. © 2002 Wiley‐Liss, Inc.