bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation Between Beat‐to‐Beat QT Interval Variability and Impaired Left Ventricular Function in Patients with Previous Myocardial Infarction
Authors: Hiromoto Kenji , Shimizu Hiroki , Mine Takanao , Masuyama Tohru , Ohyanagi Mitsumasa 
Published: October 2006

Background: Beat‐to‐beat QT interval variability (QTV) is associated with sudden cardiac death and New York Heat Association functional class severity. We sought to evaluate the relationship between QTV and left ventricular (LV) function in patients with previous myocardial infarction (MI). Methods: Fifty‐nine patients with previous anterior MI were enrolled. LV ejection fraction (EF), LV end‐systolic volume index (LVESVI), and LV end‐diastolic volume index (LVEDVI) were measured by LV contrast angiography. QT interval was measured by automated analysis of 512‐beat records of 12‐lead electrocardiogram. The mean interval, standard deviation and variance in RR and QT intervals, and the QT variability index (QTVI) were calculated for each patient using two leads that corresponded with and without the infarction site. High‐frequency power, low‐frequency power, total‐frequency power, and the ratio of low‐frequency to high‐frequency power in RR and QT intervals were calculated. Results: While measured indices of RR intervals and indices of QT intervals, which did not correspond with the infarction site, did not correlate with differences in LV function, measured indices of QT intervals, which corresponded with the infarction site, did correlate with differences in LV function. However, there were no correlations between the ratio of low‐frequency to high‐frequency power in QT intervals and EF or LVEDVI. Correlations between QTVI and LV function were observed, particularly between QTVI and LVESVI (r = 0.712, P < 0.0001). Conclusion: In patients with previous anterior MI, there was variability in temporal dispersion of QT interval and a strong correlation between QTV corresponded with the infarcted site and LV function.
Heart Rate Variability in Young Women with Polycystic Ovary Syndrome
Authors: Yildirir Aylin , Aybar Funda , Kabakci Giray , Yarali Hakan , Oto Ali 
Published: October 2006

Background: Limited data are available related to the effects of sex hormones on cardiac autonomic function. Few studies investigated the heart rate variability (HRV) parameters during regular menstrual cycle or in postmenopausal women using hormone replacement therapy, but the results were contradictory. The aim of the study was to compare the characteristics of the autonomic innervation of the heart in polycystic ovary syndrome (PCOS) patients with regularly cycling controls. Methods: Thirty PCOS patients and 30 healthy regularly cycling controls were included in the study. Groups were compared with respect to age and various cardiovascular risk factors. Characteristics of autonomic innervation of the heart were evaluated with HRV. Power spectral analysis of HRV was performed to calculate the low frequency peak (LF 0.04–0.15 Hz), high‐frequency peak (HF 0.15–0.40 Hz), LF in normalized unit (LF nu), HF in normalized unit (HF nu) and LF/HF ratio. Results: PCOS patients had adverse cardiovascular risk profile than controls. As the HRV parameters, PCOS patients had significantly higher LF nu (P = 0.005) and LF/HF ratio (P = 0.001) and significantly lower HF (P = 0.006) and HF nu (P < 0.001) compared to controls. Conclusion: Autonomic innervation of the heart can be affected in PCOS with increased sympathetic and decreased parasympathetic components of HRV. As a result, sympathetic to parasympathetic ratio may increase in PCOS. This finding should be confirmed with larger studies also evaluating the clinical implications of altered HRV parameters.
Reproducibility of Computerized Measurements of QT Interval from Multiple Leads at Rest and During Exercise
Authors: Hekkala Anna‐Mari , Väänänen Heikki , Swan Heikki , Oikarinen Lasse , Viitasalo Matti , Toivonen Lauri 
Published: October 2006

Background: Accurate measurement of the QT interval is important for diagnosing long QT syndrome (LQTS), and in research on determinants of ventricular repolarization time. We tested automatic analysis of QT intervals from multiple ECG leads on chest. Methods: Eleven healthy volunteers and 10 genotyped LQTS patients were tested at rest and during exercise with a bicycle ergometer twice 1–31 months apart. Electrocardiograms were recorded with the body surface potential mapping system, and 12 precordial channels were selected for analysis. Averaged QT peak and QT end intervals were determined with an automated algorithm, and the difference QT end minus QT peak (Tp‐e) was calculated. Repeatability was assessed by coefficient of variation (CV) between measurements. Results: Within one test at rest the QT end intervals were highly repeatable with CV 0.6%. In repeated tests CV was 4.4% for QT end interval and 3.5% when the QT interval was corrected for heart rate. In exercise test at specified heart rates, mean CV was 3.0% for QT end and 2.9% for QT peak interval. The CV of Tp‐e interval was 10.2% at rest, and 9.3% in exercise test. Reproducibility was comparable between healthy subjects and LQTS patients. Conclusions: The BSPM system with automated analysis produced accurate and highly repeatable QT interval measurements. Reproducibility was adequate also over prolonged time periods both at rest and in exercise stress test. The method can be applied in studying duration of ventricular repolarization time in different physiologic and pharmacologic interventions.
Characterization of novel M‐superfamily conotoxins with new disulfide linkage
Authors: Han Yu‐Hong , Wang Qi , Jiang Hui , Liu Li , Xiao Cai , Yuan Duo‐Duo , Shao Xiao‐Xia , Dai Qiu‐Yun , Cheng Ji‐Sheng , Chi Cheng‐Wu 
Published: October 2006

The M‐superfamily with the typical Cys framework (–CC–C–C–CC–) is one of the seven major superfamilies of conotoxins found in the venom of cone snails. Based on the number of residues in the last Cys loop (between C4 and C5), M‐superfamily conotoxins can be provisionally categorized into four branches (M‐1, M‐2, M‐3, M‐4) [Corpuz GP, Jacobsen RB, Jimenez EC, Watkins M, Walker C, Colledge C, Garrett JE, McDougal O, Li W, Gray WR, et al. (2005) Biochemistry44, 8176–8186]. Here we report the purification of seven M‐superfamily conotoxins from Conus marmoreus (five are novel and two are known as mr3a and mr3b) and one known M‐1 toxin tx3a from Conus textile. In addition, six novel cDNA sequences of M‐superfamily conotoxins have been identified from C. marmoreus, Conus leopardus and Conus quercinus. Most of the above novel conotoxins belong to M‐1 and M‐2 and only one to M‐3. The disulfide analyses of two M‐1 conotoxins, mr3e and tx3a, revealed that they possess a new disulfide bond arrangement (C1–C5, C2–C4, C3–C6) which is different from those of the M‐4 branch (C1–C4, C2–C5, C3–C6) and M‐2 branch (C1–C6, C2–C4, C3–C5). This newly characterized disulfide connectivity was confirmed by comparing the HPLC profiles of native mr3e and its two regioselectively folded isoforms. This is the first report of three different patterns of disulfide connectivity in conotoxins with the same cysteine framework.
Manufacturing and Service Supply Chain Performance: A Comparative Analysis
Authors: Sengupta Kaushik , Heiser Daniel R. , Cook Lori S. 
Published: October 2006

SUMMARYAs the economy evolves from manufacturing to services, it is important to understand whether the lessons learned in the manufacturing sector can be directly extrapolated to service supply chains. Unfortunately, the majority of existing supply chain research focuses exclusively on the manufacturing sector. To address this deficiency, this article compares the effect of traditional manufacturing‐oriented supply chain strategies on the operational and financial performance of firms in both service and manufacturing sectors. The results highlight similarities and differences between the two sectors — demonstrating that effective supply chain strategies in one sector may not be appropriate in the other sector. This suggests that practicing managers should identify appropriate benchmarks and competitive priorities before pursuing specific supply chain strategies. The insights provided by this research should help guide companies toward strategies that may positively affect their specific organization's operational and financial performance.
Supplier Diversity Effectiveness: Does Organizational Culture Really Matter?
Authors: Whitfield Gwendolyn , Landeros Robert 
Published: October 2006

SUMMARYThis study empirically examines the influence of organizational culture on supplier diversity. It examines the relationship between buyer behavior and culture using the Organizational Culture for Diversity Inventory (OCDI). The research assesses 12 business units within a heavy equipment manufacturer and uses confirmatory factor analysis to test an explanatory model of supplier diversity effectiveness. Results indicate achievement and affiliative culture styles are important to the effectiveness of supplier diversity. Moreover, in business units characterized by defensive or passive–defensive cultures, minority sourcing was lower. Conversely, the business units with constructive cultures for diversity had higher minority sourcing.
Molecular Epidemiology of Tuberculosis: Current Insights
Authors: Mathema Barun , Kurepina Natalia E. , Bifani Pablo J. , Kreiswirth Barry N. 
Published: October 2006

SUMMARYMolecular epidemiologic studies of tuberculosis (TB) have focused largely on utilizing molecular techniques to address short- and long-term epidemiologic questions, such as in outbreak investigations and in assessing the global dissemination of strains, respectively. This is done primarily by examining the extent of genetic diversity of clinical strains ofMycobacterium tuberculosis. When molecular methods are used in conjunction with classical epidemiology, their utility for TB control has been realized. For instance, molecular epidemiologic studies have added much-needed accuracy and precision in describing transmission dynamics, and they have facilitated investigation of previously unresolved issues, such as estimates of recent-versus-reactive disease and the extent of exogenous reinfection. In addition, there is mounting evidence to suggest that specific strains ofM. tuberculosisbelonging to discrete phylogenetic clusters (lineages) may differ in virulence, pathogenesis, and epidemiologic characteristics, all of which may significantly impact TB control and vaccine development strategies. Here, we review the current methods, concepts, and applications of molecular approaches used to better understand the epidemiology of TB.
Updated Review of Blood Culture Contamination
Authors: Hall Keri K. , Lyman Jason A. 
Published: October 2006

SUMMARY
Blood culture contamination represents an ongoing source of frustration for clinicians and microbiologists alike. Ambiguous culture results often lead to diagnostic uncertainty in clinical management and are associated with increased health care costs due to unnecessary treatment and testing. A variety of strategies have been investigated and employed to decrease contamination rates. In addition, numerous approaches to increase our ability to distinguish between clinically significant bacteremia and contamination have been explored. In recent years, there has been an increase in the application of computer-based tools to support infection control activities as well as provide clinical decision support related to the management of infectious diseases. Finally, new approaches for estimating bacteremia risk which have the potential to decrease unnecessary blood culture utilization have been developed and evaluated. In this review, we provide an overview of blood culture contamination and describe the potential utility of a variety of approaches to improve both detection and prevention. While it is clear that progress is being made, fundamental challenges remain.
ON q-EXTENSIONS OF MEHTA'S EIGENVECTORS OF THE FINITE FOURIER TRANSFORM
Authors: ATAKISHIYEV NATIG M. 
Published: October 2006

Mehta has shown that eigenvectors [Formula: see text] of the finite Fourier transform with the matrix [Formula: see text], 0 ≤ j, k ≤ N-1, can be defined in terms of the classical Hermite functions [Formula: see text] as [Formula: see text], where [Formula: see text]. We argue that the finite Fourier transform [Formula: see text] does actually govern also some q-extensions of Mehta's eigenvectors [Formula: see text], associated with certain well-known orthogonal q-polynomial families. For the pairs of the continuous q-Hermite and q-1-Hermite polynomials, the Rogers–Szegő and Stieltjes–Wigert polynomials, and the discrete q-Hermite polynomials of types I and II such links are explicitly derived. In the limit when the base q → 1 these q-extensions coincide with Mehta's eigenvectors [Formula: see text], whereas in the continuous limit (i.e. when the parameter N → ∞) they correspond to the classical Fourier integral transforms between the above-mentioned pairs of q-polynomial families.
Signaling interactions of rapamycin combined with erlotinib in cervical carcinoma xenografts
Authors: Birle Diana C. , Hedley David W. 
Published: October 2006

Abstract
Clinical trials using rapamycin analogues or HER1/epidermal growth factor receptor (EGFR) inhibitors show that each class of agent has activity against a range of human solid tumors. Because blockade of mitogen-activated protein kinase signaling occurs following HER1/EGFR inhibition in some cell types, we tested the combination of rapamycin and erlotinib in SiHa, Me180, and CaSki human cervical carcinomas xenografts in severe combined immunodeficient mice. In tissue culture, all three cell lines showed decreased phosphorylated S6 ribosomal protein and decreased phosphorylated extracellular signal-regulated kinase (ERK) following treatment with rapamycin and erlotinib, respectively. In SiHa tumors, suppression of phosphorylated S6 was induced by either drug alone, whereas phosphorylated ERK decreased with erlotinib, and enhancement of these effects was obtained with the combination. Continuous treatment of xenografts for 3 weeks led to significant tumor growth delay compared with vehicle control for rapamycin as single agent (P = 0.003) and greater for the combination (P = 0.04 versus rapamycin). Significant antiangiogenic effect was obtained in SiHa xenografts using the drugs together (measured by microvascular density and vascular endothelial growth factor plasma levels) but not for the single agents. Me180 and CaSki xenografts showed significant growth delay with rapamycin but not with erlotinib. Erlotinib treatment resulted in decreased phosphorylated ERK, associated with enhanced suppression of phosphorylated S6 and improved growth delay in Me180 but not in CaSki tumors. These results support the further clinical investigation of rapamycin and EGFR inhibitor combinations in anticancer therapy but highlight the problem of intertumoral heterogeneity in the prediction of in vivo response. [Mol Cancer Ther 2006;5(10):2494–502]
Quantitative analysis of O6-alkylguanine-DNA alkyltransferase in malignant glioma
Authors: Maxwell Jill A. , Johnson Stewart P. , Quinn Jennifer A. , McLendon Roger E. , Ali-Osman Francis , Friedman Allan H. , Herndon James E. , Bierau Katja , Bigley Joseph , Bigner Darell D. , Friedman Henry S. 
Published: October 2006

Abstract
Promoter hypermethylation of the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) has been associated with an enhanced response to chloroethylating and methylating agents in patients with malignant glioma. The purpose of this study was to compare three distinct yet related indices for measuring AGT to determine if these assays could be used interchangeably when AGT status is to be used to guide chemotherapeutic decisions. Real-time methylation-specific PCR (MSP), assessed as the ratio of methylated AGT copies to internal β-actin control, was used to quantitate AGT hypermethylation in 32 glioma samples. Data were compared with AGT enzyme activity as well as immunohistochemical detection of AGT protein from the same samples. Hypermethylation of the AGT promoter was detected in 19 of 31 (61%) samples evaluable by MSP. Low-level AGT, defined as &lt;20% nuclear AGT staining by immunohistochemistry, was found in 10 of 32 samples (31%), whereas 12 of 32 (38%) had low levels of AGT activity. Correlation of immunohistochemistry to AGT activity was statistically significant (P = 0.014) as was the correlation of immunohistochemistry to MSP (P = 0.043), whereas MSP compared with AGT activity (P = 0.246) was not significant. Cross-tabulation of immunohistochemistry and MSP data based on prognostic groups, where good prognosis was represented by an immunohistochemistry of &lt;20% and an MSP ratio &gt;12, showed no significant relationship (P = 0.214), suggesting that one assay cannot be used interchangeably for another. The observed discordance between respective measures of AGT based on prognosis supports further standardization of AGT assays designed to guide therapeutic practice. The data also suggest that consideration be given to the large population of AGT-expressing cells within samples when therapeutic strategies based on tumor methylation are used. [Mol Cancer Ther 2006;5(10):2531–9]
Inhibition of cell growth and nuclear factor-κB activity in pancreatic cancer cell lines by a tylophorine analogue, DCB-3503
Authors: Shiah Her-Shyong , Gao Wenli , Baker David C. , Cheng Yung-Chi 
Published: October 2006

Abstract
A tylophorine analogue, DCB-3503, has been shown to have potent activity against tumor growth in vitro and in vivo, as well as activity in an autoimmune disease model in vivo. This study focuses on investigating the mechanisms responsible for antitumor activity of DCB-3503. The concentrations for inhibiting 50% growth/colony formation ability are 50/162 and 40/149 nmol/L for PANC-1 and HPAC cells, respectively. The growth inhibition effects are associated with DCB-3503-induced reprogramming of tumor cells. DCB-3503 could interfere with cell cycle progression. Several cell cycle regulatory proteins, including cyclin D1, are down-regulated by DCB-3503. Using several different transcription elements coupled with a reporter gene, it was found that the nuclear factor-κB (NF-κB) signaling pathway is the most sensitive pathway mediator affected by DCB-3503. The inhibition of NF-κB activity is dependent on the down-regulation of nuclear phosphorylated p65, a component of the active form of the NF-κB complex. Such a decrease in nuclear phosphorylated p65 can be reversed by a proteosome inhibitor. Furthermore, the activity and protein expression of nuclear IκB kinase α, which is responsible for p65 phosphorylation, is suppressed and down-regulated in cells treated with DCB-3503. In summary, DCB-3503 could affect cell cycle regulatory proteins and is a potent modulator of NF-κB function. It is a potentially useful compound in the management of cancers in which cyclin D1 overexpression and high NF-κB activity play a pivotal role. [Mol Cancer Ther 2006;5(10):2484–93]
Expression of a suicidal gene under control of the human secreted protein acidic and rich in cysteine (SPARC) promoter in tumor or stromal cells led to the inhibition of tumor cell growth
Authors: Lopez María V. , Blanco Patricia , Viale Diego L. , Cafferata Eduardo G. , Carbone Cecilia , Gould David , Chernajovsky Yuti , Podhajcer Osvaldo L. 
Published: October 2006

Abstract
The successful use of transcriptional targeting for cancer therapy depends on the activity of a given promoter inside the malignant cell. Because solid human tumors evolve as a “cross-talk” between the different cell types within the tumor, we hypothesized that targeting the entire tumor mass might have better therapeutic effect. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein overexpressed in different human cancers malignant melanomas both in the malignant cells compartment as in the stromal one (fibroblasts and endothelial cells). We have shown that expression of the herpes simplex virus–thymidine kinase (TK) gene driven by the SPARC promoter in combination with ganciclovir inhibited human melanoma cell growth in monolayer as well as in multicellular spheroids. This inhibitory effect was observed both in homotypic spheroids composed of melanoma cells alone as well as in spheroids made of melanoma cells and stromal cells. Expression of the TK gene was also efficient to inhibit the in vivo tumor growth of established melanomas when TK was expressed either by the malignant cells themselves or by coadministered endothelial cells. Our data suggest that the use of therapeutic genes driven by SPARC promoter could be a valuable strategy for cancer therapy aiming to target all the cellular components of the tumor mass. [Mol Cancer Ther 2006;5(10):2503–11]
A urokinase-activated recombinant anthrax toxin is selectively cytotoxic to many human tumor cell types
Authors: Abi-Habib Ralph J. , Singh Ravibhushan , Liu Shihui , Bugge Thomas H. , Leppla Stephen H. , Frankel Arthur E. 
Published: October 2006

Abstract
Urokinase plasminogen activator (uPA) is a tumor-specific protease highly expressed in several types of solid tumors and rarely present on normal cells under physiologic conditions. Due to its high expression on metastatic tumors, several different strategies have been used to target the urokinase system. These have mostly led to tumor growth inhibition rather than tumor regression. A different approach was adopted by replacing the furin activation site on a recombinant anthrax toxin with a urokinase activation site. The resulting toxin, PrAgU2/FP59, was highly potent against tumors both in vitro and in vivo. In this study, we show that PrAgU2/FP59 is toxic to a wide range of tumor cell lines, including non–small cell lung cancer, pancreatic cancer, and basal-like breast cancer cell lines. Of the few cell lines found to be resistant to PrAgU2/FP59, most became sensitive upon addition of exogenous pro-uPA. PrAgU2/FP59 was much less toxic to normal human cells. The potency of PrAgU2/FP59 was dependent on anthrax toxin receptor, uPA receptor, and uPA levels but not on total plasminogen activator inhibitor-1 levels. In this study, we show that PrAgU2/FP59 is a wide-range, highly potent, and highly selective toxin that is capable of specifically targeting uPA-expressing tumor cells, independently of the tissue of origin of these cells. Furthermore, we identify three molecular markers, anthrax toxin receptor, uPA, and uPA receptor, which can be used as predictors of tumor cell sensitivity to PrAgU2/FP59. [Mol Cancer Ther 2006;5(10):2556–62]