bluuebunny/crossref_metadata_2025_split huggingface dataset:
Steatohepatitis Induced by Intragastric Overfeeding in Mice *
Authors: Deng Qing-gao , She Hongyun , Cheng Jason H. , French Samuel W. , Koop Dennis R. , Xiong Shigang , Tsukamoto Hidekazu 
Published: September 2005

Abstract

Nonalcoholic steatohepatitis is prevalent among obese individuals with excessive caloric intake, insulin resistance, and type II diabetes. However, no animal models exist that recapitulate this important association. This study produced and characterized steatohepatitis (SH) caused by intragastric overfeeding in mice. C57BL/6, tumor necrosis factor (TNF) type I receptor–deficient, and genetically matched wild type mice were fed via an implanted gastrostomy tube a high-fat diet for 9 weeks in the increasing amount up to 85% in excess of the standard intake. Animals were examined for weight gain, insulin sensitivity, and histology and biochemistry of liver and white adipose tissue (WAT). Overfed C57BL/6 mice progressively became obese, with 71% larger final body weights. They had increased visceral WAT, hyperglycemia, hyperinsulinemia, hyperleptinemia, glucose intolerance, and insulin resistance. Of these mice, 46% developed SH with increased plasma alanine aminotransferase (121 ± 27 vs. 13 ± 1 U/L), neutrophilic infiltration, and sinusoidal and pericellular fibrosis. Obese WAT showed increased TNFα and leptin expression and reciprocally reduced adiponectin expression. The expression of lipogenic transcription factors (SREBP-1c, PPARγ, LXRα) was increased, whereas that of a lipolytic nuclear factor PPARα was reduced in SH. SH was associated with reduced cytochrome P450 (Cyp)2e1 but increased Cyp4a. TNF type I receptor deficiency did not prevent obesity and SH.
In conclusion
, forced overfeeding with a high-fat diet in mice induces obesity, insulin resistance, and SH in the absence of TNF signaling or Cyp2e1 induction.

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;42:905–914.)
Efficacy and tolerability of quetiapine in patients with schizophrenia who switched from haloperidol, olanzapine or risperidone
Authors: Larmo Ilkka , Nayer André de , Windhager Elmar , Irmansyah  , Lindenbauer Bernhard , Rittmannsberger Hans , Platz Thomas , Jones A. Martin , Altman Charles 
Published: September 2005

AbstractA post hoc analysis of the SPECTRUM trial was carried out to evaluate whether the improvements in efficacy and tolerability gained on switching to quetiapine occurred consistently for patients previously treated with either: haloperidol (n = 43); olanzapine (n = 66); or risperidone (n = 55) monotherapy. Patients were initiated with quetiapine to 400 mg/day over 7 days, and then flexibly dosed (300–750 mg/day) for 11 weeks. The mean (SD) modal dose of quetiapine was 501 (138) mg/day in the haloperidol subgroup, 472 (147) mg/day in the olanzapine subgroup and 485 (141) mg/day in the risperidone subgroup at the study endpoint. Switching to quetiapine induced significant improvements from baseline in PANSS scores, with least square mean changes in total scores of −32.5, −15.4, and −18.5 for patients previously treated with haloperidol, olanzapine and risperidone, respectively, (all p < 0.001 vs baseline). Significant improvements were also noted in CDSS scores, particularly for patients clinically depressed at baseline (all p < 0.001 vs baseline). There were significant reductions in EPS on the SAS and BAS for all subgroups (all p < 0.001 vs baseline). Switching to quetiapine produced efficacy and tolerability benefits regardless of whether their previous antipsychotic was haloperidol, olanzapine or risperidone. Copyright © 2005 John Wiley & Sons, Ltd.
Framework‐based design of a new all‐purpose molecular simulation application: The Adun simulator
Authors: Johnston Michael A. , Galván Ignacio Fdez. , Villà‐Freixa Jordi 
Published: September 2005

AbstractHere we present Adun, a new molecular simulator that represents a paradigm shift in the way scientific programs are developed. The traditional algorithm centric methods of scientific programming can lead to major maintainability and productivity problems when developing large complex programs. These problems have long been recognized by computer scientists; however, the ideas and techniques developed to deal with them have not achieved widespread adoption in the scientific community. Adun is the result of the application of these ideas, including pervasive polymorphism, evolutionary frameworks, and refactoring, to the molecular simulation domain. The simulator itself is underpinned by the Adun Framework, which separates the structure of the program from any underlying algorithms, thus giving a completely reusable design. The aims are twofold. The first is to provide a platform for rapid development and implementation of different simulation types and algorithms. The second is to decrease the learning barrier for new developers by providing a rigorous and well‐defined structure. We present some examples on the use of Adun by performing simple free‐energy simulations for the adiabatic charging of a single ion, using both free‐energy perturbation and the Bennett's method. We also illustrate the power of the design by detailing the ease with which ASEP/MD, an elaborated mean field QM/MM method originally written in FORTRAN 90, was implemented into Adun. © 2005 Wiley Periodicals, Inc. J Comput Chem 26: 1647–1659, 2005
Rotational superposition and least squares: The SVD and quaternions approaches yield identical results. Reply to the preceding comment by G. Kneller
Authors: Coutsias Evangelos A. , Seok Chaok , Dill Ken A. 
Published: September 2005

AbstractWe clarify once again that Kabsch's method and the Quaternion method are mathematically equivalent methods, that is, that they contain identical information and, when properly understood and applied, lead to identical answers to any questions regarding least‐squares rotational superposition, either by proper rotations or by rotation‐reflections. We also provide the correct bounds for the eigenvalue spectrum. © 2005 Wiley Periodicals, Inc. J Comput Chem 26: 1663–1665, 2005
Lithium‐induced gene expression of inducible cyclic adenosine monophosphate early repressor in the rat adrenal gland
Authors: Spencer Corinne M. , Jahng Jeong Won , Ryu Vitaly , Houpt Thomas A. 
Published: September 2005

AbstractLithium has acute and chronic effects on the hypothalamic‐pituitary‐adrenal gland (HPA) axis that are important for both therapeutic (e.g., treatment of mood disorders) and experimental (e.g., as the toxin in conditioned taste aversion studies) applications. We visualized lithium‐induced activation of the HPA axis in rats by the adrenal expression of inducible cAMP early repressor (ICER), which is activated by elevated intracellular cAMP. We have shown that 1) intraperitoneal lithium chloride (LiCl) induces transient expression of ICER and c‐fos mRNAs in the rat adrenal cortex and increases plasma level of corticosterone; 2) the cortical expression of ICER mRNA by LiCl occurs in a dose‐dependent manner; 3) adrenal induction of ICER expression is delayed compared with c‐fos expression; 4) dexamethasone pretreatment (4 mg/kg) blocks corticosterone release and adrenocortical ICER induction either by systemic LiCl (76 mg/kg) or by restraint stress; and 5) intracerebroventricular LiCl (127 μg/5 μl) is sufficient for adrenocortical, but not medullary, ICER induction. These results suggest that adrenocortical ICER expression could serve as a reliable marker for lithium‐induced activation of the HPA axis. Understanding the activation of immediate‐early genes such as c‐fos or ICER in response to a single LiCl injection is an important first step in understanding the long‐term changes in gene expression elicited by lithium that are involved in its therapeutic and toxic effect. The pattern and mechanism by which lithium stimulates ICER transcription in the adrenal gland would serve as a useful model system in future studies of lithium. © 2005 Wiley‐Liss, Inc.
Subchronic haloperidol increases CB1 receptor binding and G protein coupling in discrete regions of the basal ganglia
Authors: Andersson Mikael , Terasmaa Anton , Fuxe Kjell , Strömberg Ingrid 
Published: September 2005

AbstractThe present study was designed to test whether chronic neuroleptic treatment, which is known to alter both expression and density of dopamine D2 receptors in striatal regions, has effects upon function and binding level of the cannabinoid CB1 receptor in the basal ganglia by using receptor autoradiography. As predicted, subchronic haloperidol treatment resulted in increased binding of 3H‐raclopride and quinpirole‐induced guanosine 5′‐O‐(γ‐[35S]thio)triphosphate ([35S]GTPγS) in the striatum when compared to that measured in control animals. This increased D2 receptor binding and function after 3 days washout was normalized after a 2‐week washout period. Effect of haloperidol treatment was studied for CB1 receptor binding and CP55,940‐stimulated [35S]GTPγS in the striatum, globus pallidus, and substantia nigra. 3[H]CP55,940 binding levels were found in rank order from highest to lowest in substantia nigra > globus pallidus > striatum. Furthermore, subchronic haloperidol treatment resulted in elevated binding levels of 3[H]CP55,940 in the striatum and the substantia nigra and CB1 receptor‐stimulated [35S]GTPγS bindings in the substantia nigra after 3 days washout. These increased binding levels were normalized at 1–4 weeks after termination of haloperidol treatment. Haloperidol treatment had no significant effect on CB1 receptor or [35S]GTPγS binding levels in globus pallidus. The results help to elucidate the underlying biochemical mechanism of CB1 receptor supersensitivity after haloperidol treatment. © 2005 Wiley‐Liss, Inc.
Disruption of endoplasmic reticulum calcium stores is involved in neuronal death induced by glycolysis inhibition in cultured hippocampal neurons
Authors: Hernández‐Fonseca Karla , Massieu Lourdes 
Published: September 2005

AbstractDisturbances in neuronal calcium homeostasis have been implicated in a variety of neuropathological conditions, including cerebral ischemia, hypoglycemia, and epilepsy, and possibly constitute part of the cell death process associated with chronic neurodegenerative disorders. We investigated if endoplasmic reticulum (ER) calcium stores participate in neuronal death triggered by moderate glycolysis inhibition induced by iodoacetate, an inhibitor of glyceraldehyde‐3‐phosphate dehydrogenase, in cultured hippocampal neurons. Results show that exposure to iodoacetate leads to a slow partial decrease in cell survival, which is significantly prevented in the absence of Ca2+ or in the presence of the calcium chelator BAPTA‐AM. Treatment with caffeine and a low (1 μM) concentration of ryanodine, which activates the ryanodine receptor (RyR), exacerbates neuronal death, whereas dantrolene and 25 μM ryanodine, which antagonizes RyR, prevents damage. Xestospongin C (XeC), an antagonist of the inositol‐3‐phosphate (IP3) receptor (IP3R) also prevents neuronal damage. Inhibitors of the ER calcium ATPase (sarcoendoplasmic reticulum Ca2+ ATPase; SERCA) have no effect. The decrease in ATP levels induced by iodoacetate is potentiated by caffeine and prevented by dantrolene. Although only a slight increase in glutamate extracellular levels is observed 3.5 hr after iodoacetate exposure, the N‐methyl‐D‐aspartate (NMDA) glutamate receptor antagonist, MK‐801, efficiently prevents neuronal damage. Taken together, the data suggest that neuronal death induced during moderate glycolysis inhibition involves calcium influx through NMDA receptors and calcium release from intracellular ER stores. These results might be relevant to the understanding the mechanisms involved in neuronal damage related to aging and chronic neurodegenerative diseases, which have been associated with decreased glucose metabolism. © 2005 Wiley‐Liss, Inc.
Kainate‐induced zinc translocation from presynaptic terminals causes neuronal and astroglial cell death and mRNA loss of BDNF receptors in the hippocampal formation and amygdala
Authors: Revuelta Mati , Castaño Angélica , Machado Alberto , Cano Josefina , Venero José L. 
Published: September 2005

AbstractTo evaluate the potential role of endogenous zinc in the pathophysiology of epilepsy, we injected kainic acid into the medial septum, which evokes seizure activity and delayed hippocampal degeneration. Different approaches were used. In the hippocampus, we found a movement of zinc from the synaptic compartment to CA1 pyramidal neurons and astrocytes after kainate. The same was true in the amygdala. We found that in those areas showing intense zinc bleaching there was also a loss of reactive astrocytes, which supports the view that release of synaptic zinc induces astrocytic cell death. We have also tested whether the kainate‐induced zinc movement from the synaptic compartment to neuronal or glial cells alters the expression of brain‐derived neurotrophic factor (BDNF) and its high‐affinity receptor, trkB. There was a prominent loss of expression of trkB mRNA in areas that coincided precisely with those displaying astrocyte loss and zinc bleaching. In the amygdala, these events were accompanied by a high upregulation of BDNF mRNA. To demonstrate further a role of synaptic zinc in hippocampal pathology, we used two different approaches. We first injected different doses of zinc chloride in the CA1 area. At lower doses (0.1–10 nmol), zinc chloride selectively induced apoptosis in CA1 pyramidal neurons and dentate granular neurons. In a second approach, we found that hippocampal zinc chelation was effective in protecting CA1 pyramidal neurons against kainate‐induced cell death. © 2005 Wiley‐Liss, Inc.
Complex‐environment rearing prevents prenatal hypoxia‐induced deficitsin hippocampal cellular mechanisms necessary for memory consolidationin the adult Wistar rat
Authors: Foley Andrew G. , Murphy Keith J. , Regan Ciaran M. 
Published: September 2005

AbstractHypoxic episodes in utero can result in enduring and debilitating neurological sequelae that include nonprogressive motor disorders and/or significant learning deficits. The extent of long‐term disruption of synaptic function following prenatal hypoxia and its subsequent effect on learning ability, however, remain to be established. Polysialylation of the neural cell adhesion molecule, a cellular event integral to the consolidation of diverse learning paradigms, was used to correlate cellular end points with learning deficits as a consequence of prenatal hypoxia. Pregnant Wistar dams exposed to hypobaric hypoxia during gestational days 10–20 had significantly reduced litter sizes, but the lack of effect on subsequent pup weight gain suggested no gross developmental deficit. By contrast, adult animals with prior in utero hypoxia exhibited significant learning difficulties in both acquisition of a water maze spatial learning task and recall of a passive avoidance paradigm. Learning deficits correlated with a significant reduction in the frequency of polysialylated neurons in the dentate infragranular zone and a blunting of their transient activation 12 hr following task acquisition. Rearing animals with prior prenatal hypoxia in a complex environment, however, eliminated the task acquisition and recall deficits and restored dentate polysialylated cell frequency and their transient posttraining increase. © 2005 Wiley‐Liss, Inc.
Single‐fiber EMG with a concentric needle electrode: Validation in myasthenia gravis
Authors: Sarrigiannis Ptolemaios G. , Kennett Robin P. , Read Simon , Farrugia Maria E. 
Published: September 2005

AbstractWe performed a retrospective study to validate whether a disposable concentric needle electrode (CNE) can be used in place of a single‐fiber (SF) electrode for jitter measurements in myasthenia gravis (MG). Normal values for voluntary contraction of orbicularis oculi (OO) and extensor digitorum communis (EDC) were collected from 20 healthy subjects. The method was validated by a retrospective analysis of 56 consecutive MG patients, the “gold standard” being a positive acetylcholine receptor (AChR) antibody titer at the time of the electrophysiological (electromyography) study and the clinical diagnosis. Receiver operating characteristic (ROC) curves were constructed to define maximal sensitivity and specificity of the technique. The sensitivity was 96.4% (95% confidence interval 87.5%–99.6%), with no false‐positive results, similar to traditional SF EMG and confirming that the disposable CNE is a justifiable alternative. Muscle Nerve, 2005
Randomized controlled trial of modafinil for the treatment of fatigue in postpolio patients
Authors: Chan K. Ming , Strohschein Fay J. , Rydz David , Allidina Amyn , Shuaib Ashfaq , Westbury Chris F. 
Published: September 2005

AbstractThe purpose of this study was to test whether modafinil is effective in alleviating the symptoms of fatigue in postpolio patients, because it has been helpful for such symptoms in other neurologic disorders. Using a double‐blind, randomized, placebo‐controlled cross‐over design, 14 postpolio patients with moderate to severe fatigue were assigned to receive modafinil or placebo first. Piper Fatigue Scale, Epworth Sleepiness Scale, digit span, and reaction time tests were done at baseline and then at weekly intervals. The Piper Fatigue Scale scores improved by 27 ± 40% (mean ± SD) following modafinil and by 43 ± 36% following placebo. Scores for most of the other tests did not change during the study. Therefore, we conclude that modafinil was not effective in alleviating the symptoms of fatigue in postpolio patients. Muscle Nerve, 2005
Poly(p‐phenylenevinylene) presenting pendent pentaphenylene dendron groups for light‐emitting diodes
Authors: Tseng Ya‐Hsien , Wu Fang‐Iy , Shih Ping‐I , Shu Ching‐Fong 
Published: September 2005

AbstractWe have synthesized, using the Gilch method, a novel poly(p‐phenylenevinylene) derivative (PPV‐PP) containing two pendent pentaphenylene dendritic wedges, and have characterized its structure and properties. The incorporated side chain pentaphenylene dendrons serve as solubilizing groups, prevent π‐stacking interactions from occurring between the polymer main chains, and suppress the formation of excimers in the solid state. Photoluminescence studies indicate that efficient intramolecular energy transfer occurred from the photoexcited pentaphenylene groups to the poly(p‐phenylenevinylene) backbone. The polymer film exhibits a maximum emission at 510 nm and had a photoluminescence efficiency of 46%, which is similar to that measured in dilute solution. The photoluminescence spectra remained almost unchanged after thermal annealing at 150 °C for 20 h, and displayed inhibited excimer formation. Polymer light‐emitting diodes that we fabricated in the configuration ITO/PEDOT/PPV‐PP/Mg:Ag/Ag exhibited a maximum emission peak at 513 nm, corresponding to the green region [x = 0.30 and y = 0.62 in the Commission Internationale de L'Eclairage (CIE) chromaticity coordinates]. The maximum brightness and maximum luminance efficiency were 1562 cd/m2 and 1.93 cd/A, respectively. © 2005 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 5147–5155, 2005
Synthesis and helical conformation of poly(N‐propargylamides) carrying L‐aspartic acid in the side chain
Authors: Zhao Haichao , Sanda Fumio , Masuda Toshio 
Published: September 2005

AbstractAspartic acid‐based novel poly(N‐propargylamides), i.e., poly[N‐(α‐tert‐butoxycarbonyl)‐L‐aspartic acid β‐benzyl ester N′‐propargylamide] [poly(1)] and poly[N‐(α‐tert‐butoxycarbonyl)‐L‐aspartic acid α‐benzyl ester N′‐propargylamide] [poly(2)] with moderate molecular weights were synthesized by the polymerization of the corresponding monomers 1 and 2 catalyzed with (nbd)Rh+[η6‐C6H5B−(C6H5)3] in CHCl3 at 30 °C for 2 h in high yields. The chiroptical studies revealed that poly(1) took a helical structure in DMF, while poly(2) did not in DMF but did in CH2Cl2, CHCl3, and toluene. The helicity of poly(1) and poly(2) could be tuned by temperature and solvents. Poly(2) underwent solvent‐driven switch of helical sense, accompanying the change of the tightness. © 2005 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 5168–5176, 2005
Organosoluble star polymers from a cyclodextrin core
Authors: Karaky Khaled , Reynaud Stéphanie , Billon Laurent , François Jeanne , Chreim Yamama 
Published: September 2005

AbstractWell‐defined star polymers were synthesized with a combination of the core‐first method and atom transfer radical polymerization. The control of the architecture of the macroinitiator based on β‐cyclodextrin bearing functional bromide groups was determined by 13C NMR, fast atom bombardment mass spectrometry, and elemental analysis. In a second step, the polymerization of the tert‐butyl acrylate monomer was optimized to avoid a star–star coupling reaction and allowed the synthesis of a well‐defined organosoluble polymer star. The determination of the macromolecular dimensions of these new star polymers by size exclusion chromatography/light scattering was in agreement with the structure of armed star polymers in a large range of predicted molecular weights. This article describes a new approach to polyelectrolyte star polymers by postmodification of poly(tert‐butyl acrylate) by acrylic arm hydrolysis in a water‐soluble system. © 2005 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 5186–5194, 2005
Experimental and theoretical analysis of electropolymerized PMeT thin films
Authors: Velumani S. , Ascencio J. A. , Canizal G. , Sebastián P. J. , García‐Serrano J. , Pal U. 
Published: September 2005

AbstractIt is reported that the physical analysis of poly(3‐methylthophene) (PMeT) thin films were doped with BF anions, which were deposited on tin oxide‐coated glass and stainless steel substrates using electropolymerization technique. The atomistic and electronic structures were evaluated to understand the main principles for the pure and doped PMeT polymers that give the photonic and conductivity properties for this kind of materials. It is found that galvanostatic method is more suitable for the electropolymerization of PMeT on conducting glass or flexible metal surfaces. The films were characterized using SEM, AFM, XRD, FTIR, Raman, and UV–vis absorption techniques. Raman and FTIR spectra of the samples revealed no signal related to the Li or the anion BF dopant, indicating that the optimum dopant concentration was well below the threshold value. Apart from the dopant influence, which is a well understood phenomenon, an attempt has been made to explain the influence of the lithium in the polymer matrix. The Li+ ions incorporated into the PMeT films form highly confined conjugational defects, neither dynamically nor electronically coupled with the host lattice. Using density function theory calculations, we could determine the optimum geometrical configurations of the cis and trans polymers and their corresponding electronic structure modification because of the presence of Li+ atoms controlling the electronic band gaps. © 2005 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 43: 3058–3068, 2005