bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of roughskin newt medullary vasotocin target neurons with a fluorescent vasotocin conjugate
Authors: Lewis Christine M. , Dolence E. Kurt , Hubbard Catherine S. , Rose James D. 
Published: September 2005

AbstractArginine8 vasotocin (AVT), a neurohypophyseal peptide in nonmammalian vertebrates, plays a key role in the regulation of social behaviors related to reproduction. In male roughskin newts (Taricha granulosa), AVT is an important facilitator of several reproductive behaviors, including courtship clasping of females. Although AVT is known to act in certain brain regions and AVT receptors have been localized to some extent, specific target neurons for this peptide have not been identified in any species. Internalization of a receptor‐specific conjugate of AVT and the fluorescent dye Oregon green was used to identify AVT target cells in the medulla of male roughskin newts. Medullary neurons are of interest because they appear to mediate facilitation of clasping by AVT. Direct application of AVT‐Oregon green to the fourth ventricular surface of the medulla in vivo resulted in conjugate internalization by a widespread population of medullary neurons, particularly in the medial reticular formation and nuclei of cranial nerves V, VII, VIII, IX, and X. Some fourth‐ventricle ependymal cells were also labeled. Reticulospinal neurons, which play an important role in clasping, were identified by retrograde labeling with tetramethylrhodamine dextran amine. AVT‐Oregon green was internalized by 72% of these neurons. These results show that AVT can directly affect a very large and diverse medullary neuronal population, which may underlie the peptide's role in multiple neuroendocrinological processes, including autonomic and behavioral regulation. Selectivity of the AVT action may arise through interactions between AVT and steroids such as corticosterone. J. Comp. Neurol. 491:381–389, 2005. © 2005 Wiley‐Liss, Inc.
Performance analysis of multiroute packet combining scheme for real‐time communications in wireless multihop networks
Authors: Hirayama Yasuhiro , Nakagawa Nobuyuki , Okada Hiraku , Yamazato Takaya , Katayama Masaaki 
Published: September 2005

AbstractIn this research, real‐time packet communications on wireless multihop networks is considered. Since the communications quality is substantially degraded by packet delay in real‐time packet communications, packet retransmission is not usually used. In order to suppress the effect of packet errors in the communications channel on communications quality in such cases, this paper proposes an application of a multiroute packet combining scheme on a wireless multihop network. The performance of the proposed scheme depends on the time required for transmission of a packet on each route and the start time of packet combining at the destination node, in addition to the number of transmitted duplicate packets at the source node. In order to evaluate the constantly changing system performance from the viewpoint of the quality of service (QoS) required in real‐time communications, the distribution function of the time needed for attaining a certain required packet error rate and the average packet error rate attainable at a certain time are analytically derived. From numerical examples, it is proven that there exists a number of transmitted duplicate packets minimizing the required time for attaining the required packet error rate, and also a number of transmitted duplicate packets minimizing the average packet rate attainable within an allowed delay time. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 89(1): 34–44, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.20238
A study on multibeam pulse chasing for bistatic radar
Authors: Matsuda Shoji , Hashiguchi Hiroyuki , Fukao Shoichiro 
Published: September 2005

AbstractTo improve the volume search efficiency of a bistatic radar with the transmitting antenna and the receiving antenna positioned apart, a known beam scanning method is pulse chasing that scans the receive beam at high speed in response to the propagation of the transmitted pulses. However, in normal pulse chasing, the receive beam width cannot be narrower than some value in order to receive all of the transmitted pulses without losses. In other words, a limit is the antenna gain cannot be increased. The problem is the receive signal‐to‐noise ratio (SNR) decreases compared to when pulse chasing is not performed. In this paper, we propose multibeam pulse chasing, a beam scanning technique using multiple receive beams based on digital beam forming, as the solution. We show that even if the transmitted pulse width is relatively long, if the number of multibeams is increased, the received SNR does not exhibit a decrease. Furthermore, we study a method to decrease the number of multibeams by dropping a portion of the receive pulses when pulse compression is applied as the transmission and reception methods, and present the computational result of the relationship between the number of multibeams and the received SNR when the Taylor window is applied. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 89(1): 11–21, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.20240
Evaluation method of small anechoic chamber by site attenuation distribution using spherical dipole antenna
Authors: Kitani Atsuto , Kuwabara Nobuo , Kawabata Masato , Amemiya Fujio 
Published: September 2005

AbstractSite attenuation has been evaluated by means of a half‐wave dipole antenna. Since this antenna type requires a size on the order of a half wavelength, it is not suitable for evaluation of small anechoic chambers. In this paper, a method of evaluation of small anechoic chambers using a spherical dipole antenna with a diameter of 15 cm is discussed. First, the spherical dipole antenna is modeled by wire grids and the site attenuation and antenna factor are derived. It is found that in the range of 30 MHz through 1000 MHz the discrepancy between the analytical values and the measured values of the site attenuation is less than ±4 dB, while that of the antenna factor is less than ±2 dB. Next, the site attenuation taking account of the reflection characteristics of the anechoic chamber is analyzed by the ray tracing method. As parameters, the antenna factor and the radiation pattern derived from the wire grid model are used for the antenna characteristics, and the reflection coefficient derived from the multilayer plane approximation method is used for the reflection characteristics of the absorber. It is found that the discrepancy between the analytical values and the measured values for the site attenuation distribution at a frequency of 600 MHz is less than ±3 dB, and the ray tracing method is found useful for the analysis of the site attenuation distribution using a spherical dipole antenna. Further, when the new approach is applied to a small anechoic chamber in which absorbers with different characteristics are included, the present method is found effective for evaluation of the areas with good properties and of the effect of the absorbers. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 89(1): 1–10, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.20255
The introduction of social adaptation within evacuation modelling
Authors: Gwynne S. , Galea E. R. , Lawrence P. J. 
Published: September 2005

AbstractIn recent history, a number of tragic events have borne a consistent message; the social structures that existed prior to and during the evacuation significantly affected the decisions made and the actions adopted by the evacuating population in response to the emergency. This type of influence over behaviour has long been neglected in the modelling community. This paper is an attempt to introduce some of these considerations into evacuation models and to demonstrate their impact. To represent this type of behaviour within evacuation models a mechanism to represent the membership and position within social hierarchies is established. In addition, individuals within the social groupings are given the capacity to communicate relevant pieces of data such as the need to evacuate—impacting the response time—and the location of viable exits—impacting route selection. Furthermore, the perception and response to this information is also affected by the social circumstances in which individuals find themselves. Copyright © 2005 John Wiley & Sons, Ltd.
A role for endogenous reverse transcriptase in tumorigenesis and as a target in differentiating cancer therapy
Authors: Sinibaldi‐Vallebona Paola , Lavia Patrizia , Garaci Enrico , Spadafora Corrado 
Published: September 2005

AbstractAn unexpected result emerging from completion of the genome sequencing project is that a large portion of mammalian genomes is constituted by retrotransposons. A large body of published data supports the conclusion that retrotransposons are biologically active elements and indicates that retrotransposition is an ongoing process in mammalian genomes. Retroelements can act as insertional mutagens altering the coding integrity of genes and, recently, have been found to also affect the expression of cellular genes at the epigenetic level: in this light, they are a potential threat in that these events can trigger the onset of several pathologies including cancer. Retroelement genes, and particularly the gene coding for reverse transcriptase (RT), are typically expressed at high levels in transformed cells and tumors. In recent work, we have found that drug‐mediated inhibition of the endogenous RT activity, or silencing of expression of active retrotransposons of the LINE‐1 family by RNA interference, down‐regulate cell growth and induce the activation of differentiating functions in several cancer cell lines. Moreover, the inhibition of endogenous RT activity in vivo antagonizes the growth of human tumors in animal models. In this review, we discuss newly emerging concepts on the role of retrotransposons and suggest that an abnormally high level of the RT activity that they encode may contribute to the loss of control in the proliferation and differentiation programs typical of transformed cells. In this light, RT‐coding elements may be regarded as promising targets in the development of novel, differentiation‐inducing approaches to cancer therapy. © 2005 Wiley‐Liss, Inc.
Genome-Wide Response of the Human Hep3B Hepatoma Cell to Proinflammatory Cytokines, From Transcription to Translation *
Authors: Coulouarn Cédric , Lefebvre Grégory , Daveau Romain , Letellier Franck , Hiron Martine , Drouot Laurent , Daveau Maryvonne , Salier Jean-Philippe 
Published: September 2005

Abstract

Given the unknown timing of the onset of an acute systemic inflammation in humans, the fine tuning of cascades and pathways involved in the associated hepatocyte response cannot be appraised

in vivo

. Therefore, the authors used a genome-wide and kinetic analysis in the human Hep3B hepatoma cell line challenged with a conditioned medium from bacterial lipopolysaccharide-stimulated macrophages. A complete coverage of the liver transcriptome disclosed 648 mRNAs whose change in abundance allowed for their clustering in mRNA subsets with an early, intermediate, or late regulation. The contribution of transcription, stability, or translation was appraised with genome-wide studies of the changes in nuclear primary transcripts, mRNA decay, or polysome-associated mRNAs. A predominance of mRNAs with decreased stability and the fact that translation alone controls a significant number of acute phase–associated proteins are prominent findings. Transcription and stability act independently or, more rarely, cooperate or even counteract in a gene-by-gene manner, which results in a unidirectional change in mRNA abundance. Waves of mRNAs for groups of functionally related proteins are up- or downregulated in an ordered fashion. This includes an early regulation of transcription-associated proteins, an intermediate repression of detoxication and metabolism proteins, and finally an enhanced translation and transport of a number of membranous or secreted proteins along with an enhanced protein degradation.
In conclusion
, this study provides a comprehensive and simultaneous overview of events in the human hepatocyte during the inflammatory acute phase.

Supplementary material for this article can be found on the H

epatology

website

(
http://www.interscience.wiley.com/jpages/0270-9139/suppmat/index.html
). (Hepatology 2005;42:946–955.)
Hepatitis C Virus Inhibits Intracellular Interferon Alpha Expression in Human Hepatic Cell Lines *
Authors: Zhang Ting , Lin Rong-Tuan , Li Yuan , Douglas Steven D. , Maxcey Catherine , Ho Chun , Lai Jian-Ping , Wang Yan-Jian , Wan Qi , Ho Wen-Zhe 
Published: September 2005

Abstract

The chronicity of hepatitis C virus (HCV) infection raises the question of how HCV is able to persist in hepatic cells. We show that human primary hepatocytes and human hepatic cell lines (Huh7 and HepG2) spontaneously produce interferon (IFN)-α that is inhibited in the HCV replicon cells (Huh.8 and FCA-1). Silencing IFN-α gene expression by IFN-α small interfering RNA (siRNA) in the HCV replicon cells resulted in increased HCV replicon expression. The activation of IFN-α expression by interferon regulatory factor (IRF-7) led to the inhibition of HCV replicon expression, whereas the anti–IFN-α receptor antibody could partially block IRF-7–mediated HCV replicon inhibition. In addition, the blockade of IFN-α receptor by anti–IFN-α receptor antibody on the replicon cells increased HCV replicon expression. Among the HCV nonstructural (NS) proteins tested, NS5A is the most potent inhibitor of IFN-α expression by the hepatic cells. Investigation of the mechanism of HCV action on IFN-α showed that IRF-7–induced IFN-α promoter activation was inhibited in the HCV replicon cells. Furthermore, IRF-7 expression was restricted in the HCV replicon cells.
In conclusion
, we provide direct evidence that HCV undermines the intracellular innate immunity of the target cells, which may account for HCV persistence in hepatic cells. (Hepatology 2005;42:00–00.) (Hepatology 2005;42:819–827.)
Intrahepatic CD8+ T-Cell Failure During Chronic Hepatitis C Virus Infection *
Authors: Spangenberg Hans Christian , Viazov Sergei , Kersting Nadine , Neumann-Haefelin Christoph , McKinney Denise , Roggendorf Michael , von Weizsäcker Fritz , Blum Hubert E. , Thimme Robert 
Published: September 2005

Abstract

The precise mechanisms responsible for the failure of intrahepatic hepatitis C virus (HCV)-specific CD8+ T cells to control the virus during persistent infection have not been fully defined. We therefore studied the CD8+ T-cell response in 27 HLA-A2–positive patients using four previously well-defined HLA-A2–restricted HCV epitopes. The corresponding HCV sequences were determined in several patients and compared with the intrahepatic HCV-specific CD8+ T-cell response. The results of the study indicate: (1) intrahepatic HCV-specific CD8+ T cells are present in the majority of patients with chronic HCV infection and overlap significantly with the response present in the peripheral blood. (2) A large fraction of intrahepatic HCV-specific CD8+ T cells are impaired in their ability to secrete interferon γ (IFN-γ). This dysfunction is specific for HCV-specific CD8+ T cells, since intrahepatic Flu-specific CD8+ T cells readily secrete this cytokine. (3) T-cell selection of epitope variants may have occurred in some patients. However, it is not an inevitable consequence of a functional virus-specific CD8+ T-cell response, since several patients with IFN-γ–producing CD8+ T-cell responses harbored HCV sequences identical or cross-reactive with the prototype sequence. (4) The failure of intrahepatic virus–specific CD8+ T cells to sufficiently control the virus occurs despite the presence of virus-specific CD4+ T cells at the site of disease.
In conclusion
, different mechanisms contribute to the failure of intrahepatic CD8+ T cells to eliminate HCV infection, despite their persistence and accumulation in the liver. (Hepatology 2005;42:828–837.)
Antioxidative Function of L-FABP in L-FABP Stably Transfected Chang Liver Cells *
Authors: Wang Guqi , Gong Yuewen , Anderson Judy , Sun Dongfeng , Minuk Gerald , Roberts Michael S. , Burczynski Frank J. 
Published: September 2005

Abstract

Liver fatty acid binding protein (L-FABP) contains amino acids that are known to possess antioxidant function. In this study, we tested the hypothesis that L-FABP may serve as an effective endogenous cytoprotectant against oxidative stress. Chang liver cells were selected as the experimental model because of their undetectable L-FABP mRNA level. Full-length L-FABP cDNA was subcloned into the mammalian expression vector pcDNA3.1 (pcDNA-FABP). Chang cells were stably transfected with pc-DNA-FABP or vector (pcDNA3.1) alone. Oxidative stress was induced by incubating cells with 400 μmol/L H2O2 or by subjecting cells to hypoxia/reoxygenation. Total cellular reactive oxygen species (ROS) was determined using the fluorescent probe DCF. Cellular damage induced by hypoxia/reoxygenation was assayed by lactate dehydrogenase (LDH) release. Expression of L-FABP was documented by regular reverse transcription polymerase chain reaction (RT-PCR), real-time RT-PCR, and Western blot. The pcDNA-FABP–transfected cells expressed full-length L-FABP mRNA, which was absent from vector-transfected control cells. Western blot showed expression of 14-kd L-FABP protein in pcDNA-FABP–transfected cells, but not in vector-transfected cells. Transfected cells showed decreased DCF fluorescence intensity under oxidative stress (H2O2 and hypoxia/reoxygenation) conditions versus control in inverse proportion to the level of L-FABP expression. Lower LDH release was observed in the higher L-FABP–expressed cells in hypoxia/reoxygenation experiments.
In conclusion
, we successfully transfected and cloned a Chang liver cell line that expressed the L-FABP gene. The L-FABP–expressing cell line had a reduced intracellular ROS level versus control. This finding implies that L-FABP has a significant role in oxidative stress. (Hepatology 2005;42:871–879.)
Altered Monocyte Responses to Defined TLR Ligands in Patients With Primary Biliary Cirrhosis *
Authors: Mao Tin Ky , Lian Zhe-Xiong , Selmi Carlo , Ichiki Yasunori , Ashwood Paul , Ansari Aftab A. , Coppel Ross L. , Shimoda Shinji , Ishibashi Hiromi , Gershwin Eric M. 
Published: September 2005

Abstract

The role of the adaptive immune response, with regard to the development of autoantibodies, has been extensively studied in primary biliary cirrhosis (PBC). However, the importance of innate immunity has been noted only recently. Based on the proposed role of microorganisms in the pathogenesis of the disease, we hypothesize that patients with PBC possess a hyper-responsive innate immune system to pathogen-associated stimuli that may facilitate the loss of tolerance. To address this issue, we isolated peripheral blood monocytes from 33 patients with PBC and 26 age-matched healthy controls and stimulated such cells

in vitro

with defined ligands for toll-like receptor (TLR) 2 (lipoteichoic acid; LTA), TLR3 (polyIC), TLR4 (lipopolysaccharide; LPS), TLR5 (flagellin), and TLR9 (CpG-B). Supernatant fluids from the cultures were analyzed for levels of 5 different pro-inflammatory cytokines, interleukin (IL)-1β, IL-6, IL-8, IL-12p70, and TNF-α. After

in vitro

challenge with TLR ligands, PBC monocytes produced higher relative levels of pro-inflammatory cytokines, particularly IL-1β, IL-6, IL-8, and TNF-α, compared with controls.
In conclusion
, monocytes from patients with PBC appear more sensitive to signaling via select TLRs, resulting in secretion of selective pro-inflammatory cytokines integral to the inflammatory response that may be critical in the breakdown of self-tolerance. (Hepatology 2005;42:802–808.)
Large-Scale Search of Single Nucleotide Polymorphisms for Hepatocellular Carcinoma Susceptibility Genes in Patients With Hepatitis C *
Authors: Kato Naoya , Ji Guijin , Wang Yue , Baba Masanori , Hoshida Yujin , Otsuka Motoyuki , Taniguchi Hiroyoshi , Moriyama Masaru , Dharel Narayan , Goto Tadashi , Shao Run-Xuan , Matsuura Tadashi , Ishii Keisuke , Shiina Shuichiro , Kawabe Takao , Muramatsu Masaaki , Omata Masao 
Published: September 2005

Abstract

Hepatitis C virus (HCV) infection is a major risk factor for developing hepatocellular carcinoma (HCC). The host genetic factors that are involved in the development of HCC in patients with HCV infection remain to be investigated. To search for single nucleotide polymorphisms (SNPs) in HCC susceptibility genes, 393 SNPs in 171 candidate genes were examined in 188 Japanese patients with chronic HCV infection, including 77 patients with HCC. HCC-related SNPs were then examined in another 188 patients (including 93 patients with HCC) with chronic HCV infection. Haplotype analyses of HCC-related genes were performed in a total of 376 patients. Of the 393 SNPs, 31 SNPs in 29 genes were significantly associated with HCC based on an initial screening (

P

< .05). Of these 31 SNPs, 3 SNPs of 3 genes (SCYB14, GFRA1, and CRHR2) were significantly associated with HCC in a secondary screening. Haplotype analyses of these 3 genes identified 2 haplotype blocks associated with HCC.
In conclusion
, these SNPs and haplotypes located in the SCBY14, CRHR2, and GFRA1 genes will be used as markers to identify a subgroup of Japanese patients with chronic HCV infection who are at high risk of developing HCC.

Supplementary material for this article can be found on the Hepatology website

(
http://www.interscience.wiley.com/jpages/0270-9139/suppmat/index.html
). (Hepatology 2005;42:846–853.)
Alendronate Improves Bone Mineral Density in Primary Biliary Cirrhosis: A Randomized Placebo-Controlled Trial * #
Authors: Zein Claudia O. , Jorgensen Roberta A. , Clarke Bart , Wenger Doris E. , Keach Jill C. , Angulo Paul , Lindor Keith D. 
Published: September 2005

Abstract

Bone loss is a well-recognized complication of primary biliary cirrhosis (PBC). Although it has been suggested that alendronate might improve bone mineral density (BMD) in PBC, no randomized placebo-controlled trial has been conducted. The primary aim of this study was to compare the effects of alendronate versus placebo on BMD and biochemical measurements of bone turnover in patients with PBC-associated bone loss. We conducted a double-blinded, randomized, placebo-controlled trial. Patients with a PBC and BMD

t

score of less than −1.5 were randomized to receive 70 mg per week of alendronate or placebo over 1 year. BMD of the lumbar spine and proximal femur were measured at entry and at 1 year. Changes from baseline in BMD and biochemical measurements of bone turnover were assessed. Thirty-four patients were enrolled. Seventeen patients were randomized to each arm. After 1 year, a significantly larger improvement (

P

= .005) in spine BMD was observed in the alendronate group (0.09 ± 0.03 g/cm2 SD from baseline) compared with the placebo group (−0.003 ± 0.02 g/cm2 SD from baseline). A larger improvement (

P

= .046) was also observed in the femoral BMD of alendronate patients versus placebo. BMD changes were independent of concomitant estrogen therapy. The rate of adverse effects was similar in both groups.
In conclusion
, in patients with PBC-related bone loss, alendronate significantly improves BMD compared with placebo. Although in this study oral alendronate appears to be well tolerated in patients with PBC, larger studies are needed to formally evaluate safety. (Hepatology 2005;42:762–771.)