bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distribution of contacts from vestibulospinal axons on the dendrites of splenius motoneurons
Authors: Grande Giovanbattista , Armstrong Stacey , Neuber‐Hess Monica , Rose P.K. 
Published: September 2005

AbstractCurrent descriptions of the organization of synapses on the dendritic trees of spinal motoneurons indicate that the inputs are arranged in several patterns: some are widely distributed; some are distributed to proximal dendrites; others are distributed based on the trajectory of the dendrites. However, the principles governing the organization of synapses on spinal motoneurons remain poorly defined. Our goal was to extend the descriptions of the distribution of synapses, identified by their source, on the dendritic trees of spinal motoneurons. We combined anterograde and intracellular staining techniques in cats to determine the distribution of contacts between excitatory axons from the rostral aspect of the descending vestibular nucleus and the dendrites of motoneurons supplying a dorsal neck muscle, splenius. In five of five motoneurons, the contacts were preferentially distributed on dendrites medial to the soma. This qualitative observation was confirmed by using Monte Carlo methods. The results from this analysis showed that the distribution of contacts can be explained not by the overall distribution of the dendritic membrane area but rather by a systematic innervation of the medial regions of the dendritic trees (P < 0.02). Despite this selectivity, there was no additional bias in the distribution of contacts to proximal vs. distal dendrites. By concentrating excitatory synapses in a restricted region of the dendritic tree, the actions of vestibulospinal connections on neck motoneurons may be increased as a result of a greater probability of activating persistent inward currents on the dendrites. J. Comp. Neurol. 491:339–351, 2005. © 2005 Wiley‐Liss, Inc.
A message delivery method for highly mobile agents based on clustering
Authors: Ohta Tomoyuki , Masuda Yasuo , Inoue Shinji , Kakuda Yoshiaki , Ito Atsushi 
Published: September 2005

AbstractThis paper discusses methods of sending messages from a source that created a mobile agent (MA) to the MA, which has moved. These methods include the Home‐Proxy method and Broadcast method. However, with these techniques, it is possible that the transmitted messages may not be delivered to an MA that is frequently moving around on the network. A method for resolving this problem has been proposed by Murphy and Picco (hereafter termed the Murphy method). Although the Murphy method can reliably deliver messages to the MA, it does not take into consideration the time that elapses until the messages are delivered to the MA. The authors propose a method for delivering messages in the shortest possible time (hereafter termed the clustering method) by partitioning the entire network into multiple areas (clusters) to improve this Murphy method. This paper, proposes the clustering method precisely and in detail. In addition, the validity of this method is certified by performing a logical verification. Simulation experiments are performed to compare the method and Murphy method to prove the effectiveness of the method by verifying that the time required to deliver messages to the MA decreases if the time that an MA stays at a node is not short and that the number of messages decreases if the time that an MA stays at a node is short. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 89(1): 67–80, 2006; Published online in Wiley InterScience (www.interscience.wiley. com). DOI 10.1002/ecja.20184
Theoretical study on measurement accuracy of rotating element electric field vector (REV) method
Authors: Takahashi Toru , Miyashita Hiroaki , Konishi Yoshihiko , Makino Shigeru 
Published: September 2005

AbstractThe rotating element electric field vector (REV) method is an extremely effective measurement technique for calibration of a phased array. However, if there is any error in the excitation amplitude and phase of each element antenna, the measurements will contain an error. In this paper, the relationship between the error of the excitation amplitude and phase of each element and the measurement error of the REV method is obtained by means of probabilistic analysis theory. In the derivation of the theoretical equation, we study the error in the combined power of the array antenna (to be called the array combined power) when the excitation phase of the element is varied in accordance with the measurement principle of the REV method. Then, the error from the ideal condition without any error in the excitation amplitude and phase is expressed in terms of probability density profile. Next, the relationship between the error in the array combined power and the measurement error of the REV method is given by an approximate formula. As a result, it is clarified that the error of the excitation amplitude and phase of each element and the measurement error of the REV method can be related by a simple theoretical equation. The effectiveness of the derived theoretical formula is verified experimentally, indicating that the measurement accuracy of the REV method is amenable to analysis. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 1, 89(1): 22–33, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecja.20239
Methods for quantification of mass emissions from leaking process equipment when using optical imaging for leak detection
Authors: Lev‐On Miriam , Taback Hal , Epperson David , Siegell Jeffrey , Gilmer Lee , Ritter Karin 
Published: September 2005

AbstractA cost‐effective fugitive emission reduction program should focus on locating and repairing the very high leakers. Although these components (such as valves, pumps, compressors, flanges, etc.) represent <1% of the total component count, they are the major contributor to overall mass emissions of volatile organic compounds (VOCs). Optical imaging technologies allow greater efficiencies in simultaneously monitoring large numbers of process piping components. Therefore, locating very high leakers can be done more frequently at reasonable costs and quicker repair of these very high leakers will result in lower overall emissions.This new approach to leak detection and repair (LDAR), called “Smart‐LDAR,” will result in better emissions control when compared with current U.S. federal and state work practices. Under Smart LDAR, plants will have the flexibility to implement inspection and maintenance procedures that are based on combinations of leak definitions for repair, monitoring frequencies, and components included. With the adoption of a Smart LDAR emissions control strategy, new approaches for the quantification of fugitive emissions from process components are required. This paper discusses options for such mass emission quantification that could be used for reporting requirements. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Analysis of a robust reputation system for self‐organised networks
Authors: Mundinger Jochen , Boudec Jean‐Yves Le 
Published: September 2005

AbstractSelf‐organised networks require some mechanism to ensure cooperation and fairness. A promising approach is the use of decentralised reputation systems. However, their vulnerability to liars has not yet been analysed in detail. In this paper, we provide a first step to the robustness analysis of a reputation system based on a deviation test. Users accept second‐hand information only if this does not differ too much from their reputation values. We simplify the original system in order to obtain a one‐dimensional formulation and show that it exhibits a phase transition. In the subcritical regime, the reputation system is robust. In the supercritical regime, lying has an impact. We obtain the critical values via a mean‐field approach and verify the results by explicit computation. Thus, we provide conditions for the deviation test to make the reputation system robust as well as quantitative results on what goes wrong in the supercritical regime. Copyright © 2005 AEIT.
Dietary Factors Alter Hepatic Innate Immune System in Mice With Nonalcoholic Ratty Liver Disease * #
Authors: Li Zhiping , Soloski Mark J. , Diehl Anna Mae 
Published: September 2005

Abstract

Dietary factors promote obesity and obesity-related disorders, such as fatty liver disease. Natural killer T (NKT) cells are components of the innate immune system that regulate proinflammatory (Th-1) and anti-inflammatory (Th-2) immune responses. Previously, we noted that NKT cells are selectively reduced in the fatty livers of obese, leptin-deficient

ob

/

ob

mice and demonstrated that this promotes proinflammatory polarization of hepatic cytokine production, exacerbating lipopolysaccharide (LPS) liver injury in these animals. In the current study, we show that hepatic NKT cells are also depleted by diets that induce obesity and fatty livers in wild-type mice, promoting Th-1 polarization of hepatic cytokine production and sensitization to LPS liver injury despite persistent leptin. Adult male C57BL6 mice fed diets containing high amounts of either fat or sucrose, or combined high-fat, high-sucrose, develop increased hepatic NKT cell apoptosis and reduced liver NKT cells. The hepatic lymphocytes are more Th-1 polarized with increased intracellular interferon gamma and tumor necrosis factor alpha. Mice fed high-fat diets also exhibit more liver injury, reflected by 2-fold greater serum alanine aminotransferase (ALT) than control animals after receiving LPS.
In conclusion
, when otherwise normal mice are fed with high-fat or sucrose diet, they become obese, develop fatty livers, and acquire hepatic innate immune system abnormalities, including increased NKT cell apoptosis. The latter reduces liver NKT cell populations and promotes excessive hepatic production of Th-1 cytokines that promote hepatic inflammation. These diet-induced alterations in the hepatic innate immune system may contribute to obesity-related liver disease. (Hepatology 2005;42:880–885.)
Fibroblast Activation Protein Increases Apoptosis, Cell Adhesion, and Migration by the LX-2 Human Stellate Cell Line *
Authors: Wang Xin Maggie , Yu Denise Ming Tse , McCaughan Geoffrey W. , Gorrell Mark D. 
Published: September 2005

Abstract

Injury and repair in chronic liver disease involve cell adhesion, migration, apoptosis, proliferation, and a wound healing response. In liver, fibroblast activation protein (FAP) has both collagenase and dipeptidyl peptidase IV (DPIV) activities and is expressed only by activated hepatic stellate cells (HSC) and myofibroblasts, which produce and degrade extracellular matrix (ECM). FAP was colocalized with collagen fibers, fibronectin, and collagen type I in human liver. FAP function was examined

in vitro

by expressing green fluorescent protein FAP fusion protein in cell lines cultured on collagen-I, fibronectin, and Matrigel. Glutamates at 203 and 204 as well as serine624 of FAP were essential for peptidase activity. Human embryonic kidney 293T cells overexpressing FAP showed reduced adhesion and migration. FAP overexpression in the human HSC line LX-2 caused increased cell adhesion and migration on ECM proteins as well as invasion across transwells in the absence or presence of transforming growth factor beta-1. FAP overexpression enhanced staurosporine streptomyces–stimulated apoptosis in both cell lines. Interestingly, the enzyme activity of FAP was not required for these functions. Overexpressing FAP increased the expression of matrix metalloproteinase-2 and CD44 and reduced integrin-β1 expression in 293T cells, suggesting potential pathways of FAP-mediated impairment of cell adhesion and migration in this epithelial cell line.
In conclusion
, these findings further support a pro-fibrogenic role for FAP by indicating that, in addition to its enzymatic functions, FAP has important nonenzymatic functions that in chronic liver injury may facilitate tissue remodeling through FAP-mediated enhancement of HSC cell adhesion, migration, and apoptosis.

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;42:935–945.)
Immunohistochemical Analysis of Cytokeratin 7 Expression in Resting and Proliferating Biliary Structures of Rat Liver *
Authors: Paku Sándor , Dezső Katalin , Kopper László , Nagy Peter 
Published: September 2005

Abstract

Cytokeratins are the largest subfamily of intermediate filament proteins and include more than 20 different gene products, which are expressed in an epithelial tissue-specific manner. We studied by immunohistochemistry and confocal microscopy the distribution of cytokeratin subtypes in the biliary system of adult rat liver. A cytokeratin (CK)19+/7− cholangiocyte population was observed in the smaller branches of the biliary tree including the canals of Hering. They proliferated after 2-acetaminofluorene (AAF) administration, although later the typical oval cells expressed CK7. This observation suggests that cholangiocytes with this cytokeratin phenotype may harbor adult hepatic stem cells. The CK19+/7− cholangiocytes were not present in the rat liver at birth, but developed postnatally. Similar cell populations were not observed in human livers.
In conclusion
, we propose that the CK19+/7− phenotype may be characteristic for adult hepatic stem cells in rat liver and that these cells are generated

de novo

after birth.

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;42:863–870.)
Comparison of Indices of Vitamin A Status in Children With Chronic Liver Disease *
Authors: Feranchak Andrew P. , Gralla Jane , King Robert , Ramirez Rebecca O. , Corkill Mary , Narkewicz Michael R. , Sokol Ronald J. 
Published: September 2005

Abstract

Malabsorption of fat-soluble vitamins is a major complication of chronic cholestatic liver disease. The most accurate way to assess vitamin A status in children who have cholestasis is unknown. The goal of this study was to assess the accuracy of noninvasive tests to detect vitamin A deficiency. Children with chronic cholestatic liver disease (n = 23) and noncholestatic liver disease (n = 10) were studied. Ten cholestatic patients were identified as vitamin A–deficient based on the relative dose response (RDR). Compared with the RDR, the sensitivity and specificity to detect vitamin A deficiency for each test was, respectively: serum retinol, 90% and 78%; retinol-binding protein (RBP), 40% and 91%; retinol/RBP molar ratio, 60% and 74%; conjunctival impression cytology, 44% and 48%; slit-lamp examination, 20% and 66%; tear film break-up time, 40% and 69%; and Schirmer's test, 20% and 78%. We developed a modified oral RDR via oral coadministration of d-alpha tocopheryl polyethylene glycol-1000 succinate and retinyl palmitate. This test had a sensitivity of 80% and a specificity of 100% to detect vitamin A deficiency.
In conclusion
, vitamin A deficiency is relatively common in children who have chronic cholestatic liver disease. Our data suggest that serum retinol level as an initial screen followed by confirmation with a modified oral RDR test is the most effective means of identifying vitamin A deficiency in these subjects. (Hepatology 2005;42:782–792.)
CCR5 Deficiency Exacerbates T-Cell–Mediated Hepatitis in Mice *
Authors: Moreno Christophe , Gustot Thierry , Nicaise Charles , Quertinmont Eric , Nagy Nathalie , Parmentier Marc , Le Moine Olivier , Devière Jacques , Louis Hubert 
Published: September 2005

Abstract

Experimental T-cell–mediated hepatitis induced by concanavalin A (Con A) involves the production of different cytokines and chemokines and is characterized by leukocyte infiltration. Because the chemokine receptor CCR5 and its ligands (CCL3, CCL4, and CCL5) regulate leukocyte chemotaxis and activation, we investigated the role of CCR5 during Con A–induced liver injury. Serum levels of CCR5 ligands and their hepatic transcript levels were significantly increased after Con A injection, whereas CCR5+ liver mononuclear cells were recruited to the liver. CCR5-deficient (CCR5−/−) mice disclosed increased mortality and liver injury following Con A administration compared with wild-type mice. CCR5−/− mice also exhibited increased production of interleukin 4, tumor necrosis factor α, CCL3, CCL4, and CCL5, and a prominent liver mononuclear cell infiltrate, among which many cells were CCR1+.

In vivo

neutralization of CCR5 ligands in CCR5−/− mice afforded a protection against hepatitis only when CCL5 was neutralized.
In conclusion
, CCR5 deficiency exacerbates T-cell–mediated hepatitis, and leads to increased levels of CCR5 ligands and a more pronounced liver mononuclear infiltrate, suggesting that CCR5 expression can modulate severity of immunomediated liver injury. (Hepatology 2005;42:854–862.)
Reduced Susceptibility to Cholesterol Gallstone Formation in Mice That Do Not Produce Apolipoprotein B48 in the Intestine *
Authors: Wang Helen H. , Wang David Q.-H. 
Published: September 2005

Abstract

It has been found that polymorphisms in the apolipoprotein (APO)-B gene are associated with cholesterol gallstones in humans. We hypothesized that APO-B plays a major regulatory role in the response of biliary cholesterol secretion to high dietary cholesterol and contributes to cholesterol gallstone formation. In the present study, we investigated whether lack of expression of intestinal

Apob48

or

Apob100

reduces susceptibility to cholesterol gallstones by decreasing intestinal absorption and biliary secretion of cholesterol in male mice homozygous for an “APO-B48 only” allele (

Apob

48/48

), an “APO-B100 only” allele (

Apob

100/100

), or a wild-type APO-B allele (

Apob

+/+) before and during an 8-week lithogenic diet. We found that cholesterol absorption was significantly decreased as a result of the APO-B48 deficiency in

Apob

100/100

mice compared with wild-type and

Apob

48/48

mice, regardless of whether chow or the lithogenic diet was administered. Consequently, hepatic cholesterol synthesis was significantly increased in

Apob

100/100

mice compared with wild-type and

Apob

48/48

mice. On chow, the APO-B100 deficiency in

Apob

48/48

mice with reduced plasma levels of LDL/VLDL —but not HDL cholesterol—induced relative hyposecretion of biliary bile salts and phospholipids accompanying normal biliary cholesterol secretion. Compared with

Apob

48/48

and wild-type mice, lithogenic diet–fed

Apob

100/100

mice displayed significantly lower secretion rates of biliary cholesterol, but not phospholipid or bile salts, which results in significant decreases in prevalence rates, numbers, and sizes of gallstones.
In conclusion
, absence of expression of intestinal

Apob48

, but not

Apob100

, reduces biliary cholesterol secretion and cholelithogenesis, possibly by decreasing intestinal absorption and hepatic bioavailability. (Hepatology 2005;42:894–904.)
Cholesterol Accumulation and Liver Cell Death in Mice With Niemann-Pick Type C Disease *
Authors: Beltroy Eduardo P. , Richardson James A. , Horton Jay D. , Turley Stephen D. , Dietschy John M. 
Published: September 2005

Abstract

Niemann-Pick type C (NPC) disease develops as a result of mutations in the

NPC1

gene that encodes a protein involved in the net movement of unesterified cholesterol from the late endosomal/lysosomal compartment to the metabolically active pool of sterol in the cytosol of virtually every cell in the body. Although early publications emphasized the neurodegeneration occurring in children with this mutation, more recent clinical information suggests that serious liver disease also is an important part of this syndrome. These studies, therefore, were undertaken to characterize the liver dysfunction seen in mice with this same mutation. The NPC mouse develops significant hepatomegaly that reaches 8% of body weight at 5 to 6 weeks of age. This increase in liver size is associated with a linear increase in cholesterol content and with accumulation of amorphous cellular inclusions in both hepatocytes and macrophages. During the few weeks after birth, significant elevation of the plasma alkaline phosphatase level occurs, as also is seen in the human infant with this disease. At 4 to 5 weeks of age, plasma aminotransferase levels also rise abruptly. Histologically, at this time there is apoptosis, but no excess deposition of collagen or glycogen. mRNA expression is elevated for caspase 1, caspase 6, and several enzymes associated with sterol biosynthesis and bile acid formation.
In conclusion
, the NPC mouse has liver disease similar to that seen in the NPC infant and represents a relevant model for exploring the molecular events occurring in this form of liver disease. (Hepatology 2005;42:886–893.)
Influence of Hepatic Venous Pressure Gradient on the Prediction of Survival of Patients With Cirrhosis in the MELD Era *
Authors: Ripoll Cristina , Bañares Rafael , Rincón Diego , Catalina María-Vega , Lo Iacono Oreste , Salcedo Magdalena , Clemente Gerardo , Núñez Oscar , Matilla Ana , Molinero Luis-Miguel 
Published: September 2005

Abstract

Measurements of portal pressure, usually obtained via the hepatic venous pressure gradient (HVPG) may be a prognostic marker in cirrhosis. The aim of this study was to evaluate the impact of HVPG on survival in patients with cirrhosis in addition to the Model for End-Stage Liver Disease (MELD) score. We also examined whether inclusion of HVPG in a model with MELD variables improves its prognostic ability. Retrospective analyses of all patients who had HVPG measurements between January 1998 and December 2002 were considered. Proportional hazards Cox models were developed. Prognostic calibrative and discriminative ability of the model was evaluated. In this period, 693 patients had a hepatic hemodynamic study, and 393 patients were included. Survival was significantly worse in those patients with greater HVPG value (univariate HR, 1.05; 95% CI, 1.02-1.08;

P

= .001). HVPG remained as an independent variable in a model adjusted by MELD, ascites, encephalopathy, and age (multivariate HR, 1.03; 95% CI, 1.00-1.06;

P

= .05) so that each 1-mmHg increase in HVPG had a 3% increase in death risk. In addition, HVPG as well as MELD score variables and age, significantly contributes to the calibrative predictive capacity of the prognostic model; however, discriminative ability improved only slightly (overall C statistic [95% CI]; MELD score variables: 0.71 [0.62-0.80], MELD score variables, age, and HVPG 0.76: [0.69-0.83]).
In conclusion
, HVPG has an independent effect on survival in addition to the MELD score. Although inclusion of HVPG and age in a survival predicting model would improve the calibrative ability of MELD, its discriminative ability is not significantly improved. (Hepatology 2005;42:793–801.)