bluuebunny/crossref_metadata_2025_split huggingface dataset:
Toxicokinetic variation in 15 freshwater arthropod species exposed to the insecticide chlorpyrifos
Authors: Rubach Mascha N. , Ashauer Roman , Maund Stephen J. , Baird Donald J. , Van den Brink Paul J. 
Published: June 2010

Abstract
Recent advances in modeling the processes of the toxicity of chemicals—toxicokinetics (TK) and toxicodynamics (TD)—are improving environmental risk assessment (ERA) through prediction of effects from time-varying exposure. This has been achieved by linking chemical fate and toxicological effects mechanistically, based on internal concentrations, through the tissue residue approach. However, certain questions remain: for example, how do TK and TD differ among species and how does this relate to differences in species sensitivity? In a series of experiments, we studied the TK of [14C]chlorpyrifos in 15 freshwater arthropod species, two of which were studied in juvenile and adult life stages. Uptake (kin) and elimination (kout) rate constants were fitted using a one-compartment single first-order kinetic model. The application of two complementary parameter estimation methods facilitated the calculation of bioconcentration factors (BCF) with prediction intervals and 95% depuration times (t95) for all tested species. Extremely slow elimination was observed in some species as well as high overall variation in kin, kout, BCF, and t95 across the tested aquatic arthropod species. This variation has implications for the development of TKTD approaches in ERA, including assessing fluctuating exposure concentrations and the interpretation of observed toxicity responses in the laboratory and in the field. Environ. Toxicol. Chem. 2010;29:2225–2234. © 2010 SETAC
The synergistic performance of multiwalled carbon nanotubes and sepiolite nanoclays as flame retardants for unsaturated polyester
Authors: Hapuarachchi T. D. , Bilotti E. , Reynolds C. T. , Peijs T. 
Published: June 2010

AbstractThe synergistic effect on the thermal decomposition and heat release rate (HRR) in particular the peak heat release rate (PHRR) of unsaturated polyester (UP) resin blended with multiwalled carbon nanotubes (MWNTs) and sepiolite nanoclay was investigated using thermal gravimetric analysis (TGA), pyrolysis combustion flow calorimetery (PCFC) and the cone calorimetery. Initial microcalorimeter findings established a synergistic effect for ternary system comprising a 10:0.5 wt% mixture of sepiolite:MWNT, respectively, which resulted in a 40% reduction in heat release capacity (HRC). This result was also confirmed within the well‐established cone calorimeter by a 50% reduction in PHRR in contrast to unfilled UP. The mechanism behind this reduction is thought to be due to the bridging of the MWNTs between the sepiolite clay needles, creating a tight protective surface layer that reduces the MLR. TGA also confirmed the advantage of such a ternary system through a 36∘C shift in the onset decomposition temperature and an 11% increase in residual char. Copyright © 2010 John Wiley & Sons, Ltd.
11q21.1‐11q23.3 Is a site of intrinsic genomic instability triggered by irradiation
Authors: Du Nga , Baker Pamela M. , Do To Uyen , Bien Christine , Bier‐Laning Carol M. , Singh Sheetal , Shih Shyh‐Jen , Diaz Manual O. , Vaughan Andrew T. 
Published: June 2010

AbstractThe chromosome location, 11q21‐23, is linked to loss of heterozygosity (LOH) in multiple tumors including those of breast, lung, and head and neck. To examine the process of LOH induction, the H292 cell line (human muco‐epidermoid carcinoma) was irradiated or treated with anti‐CD95 antibody, and individual clones isolated through two rounds of cloning. Regions of LOH were determined by screening a suite of eight polymorphic microsatellite markers covering 11p15‐11q24 using fluorescent primers and genetic analyzer peak discrimination. LOH induction was observed extending through 11q21.1‐11q23.3 in 6/49 of clones surviving 4 Gy and 8/50 after 8 Gy. Analysis of selected clones by Affymetrix 6.0 single nucleotide polymorphism (SNP) arrays confirmed the initial assessment indicating a consistent 27.3–27.7 Mbp deletion in multiple clones. The telomeric border of LOH mapped to a 1 Mbp region of elevated recombination. Whole genome analysis of SNP data indicated that site‐restricted LOH also occurred across multiple additional genomic locations. These data indicate that 11q21.1‐11q23.3, and potentially other regions of this cell line are sites of intrinsic cell‐specific instability leading to LOH after irradiation. Such deletions may subsequently be propagated by genetic selection and clonal expansion. © 2010 Wiley‐Liss, Inc.
Lateral differences in the default mode network in healthy controls and patients with schizophrenia
Authors: Swanson Nathan , Eichele Tom , Pearlson Godfrey , Kiehl Kent , Yu Qingbao , Calhoun Vince D. 
Published: June 2010

AbstractWe investigate lateral differences in the intrinsic fluctuations comprising the default mode network (DMN) for healthy controls (HCs) and patients with schizophrenia (SZ), both during rest and during an auditory oddball (AOD) task. Our motivation for this study comes from multiple prior hypotheses of disturbed hemispheric asymmetry in SZ and more recently observed lateral abnormalities in the DMN for SZ during AOD. We hypothesized that significant lateral differences would be found in HCs during both rest and AOD, and SZ would show differences from HCs due to hemispheric dysfunction. Our study examined 28 HCs and 28 outpatients with schizophrenia. The scans were conducted on a Siemens Allegra 3T dedicated head scanner. There were numerous crossgroup lateral fluctuations that were found in both AOD and rest. During the resting state, within‐group results showed the largest functional asymmetries in the inferior parietal lobule for HCs, whereas functional asymmetries were seen in posterior cingulate gyrus for SZ. Comparing asymmetries between groups, in resting state and/or performing AOD, areas showing significant differences between group (HC > SZ) included inferior parietal lobule and posterior cingulate. Our results support the hypothesis that schizophrenia is characterized by abnormal hemispheric asymmetry. Secondly, the number of similarities in crossgroup AOD and rest data suggests that neurological disruptions in SZ that may cause evoked symptoms are also detectable in SZ during resting conditions. Furthermore, the results suggest a reduction in activity in language‐related areas for SZ compared to HCs during rest. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Cortical representation of tympanic membrane movements due to pressure variation: An fMRI study
Authors: Job Agnès , Paucod Jean‐Charles , O'Beirne Greg A. , Delon‐Martin Chantal 
Published: June 2010

AbstractMiddle ear sensory information has never been localized in the homunculus of the somatosensory cortex (S1). We investigated the somatosensory representation of the middle ear in 15 normal hearing subjects. We applied small air pressure variations to the tympanic membrane while performing a 3T‐fMRI study. Unilateral stimulations of the right ear triggered bilateral activations in the caudal part of the postcentral gyrus in Brodmann area 43 (BA 43) and in the auditory associative areas 42 (BA 42) and 22 (BA 22). BA 43 has been found to be involved in activities accompanying oral intake and could be more largely involved in pressure activities in the oropharynx area. The tympanic membrane is indirectly related to the pharynx area through the action of tensor tympani, which is a Eustachian tube muscle. The Eustachian tube muscles have a role in pressure equalization in the middle ear and also have a role in the pharyngeal phase of swallowing. Activation of BA 42 and BA 22 could reflect activations associated with the bilateral acoustic reflex triggered prior to self‐vocalization to adjust air pressure in the oropharynx during speech. We propose that BA 43, 42, and 22 are the cortical areas associated with middle ear function. We did not find representation of tympanic membrane movements due to pressure in S1, but its representation in the postcentral gyrus in BA 43 seems to suggest that at least part of this area conveys pure somatosensory information. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Peripheral glutamate signaling in head and neck areas
Authors: Haas Helga Susanne , Linecker Alexander , Pfragner Roswitha , Sadjak Anton 
Published: June 2010

AbstractThe major excitatory neurotransmitter glutamate is also found in the periphery in an increasing number of nonexcitable cells. In line with this it became apparent that glutamate can regulate a broad array of peripheral biological responses, as well. Of particular interest is the discovery that glutamate receptor reactive reagents can influence tumor biology. However, the knowledge of glutamate signaling in peripheral tissues is still incomplete and, in the case of head and neck areas, is almost lacking. The roles of glutamate signaling pathways in these regions are manifold and include orofacial pain, periodontal bone production, skin and airway inflammation, as well as salivation. Furthermore, the interrelations between glutamate and cancers in the oral cavity, thyroid gland, and other regions are discussed. In summary, this review shall strengthen the view that glutamate receptor reagents may also be promising targets for novel therapeutic concepts suitable for a number of diseases in peripheral tissues. The contents of this review cover the following sections: Introduction; The “Glutamate System”; The Taste of Glutamate; Glutamate Signaling in Dental Regions; Glutamate Signaling in Head and Neck Areas; Glutamate Signaling in Head and Neck Cancer; A Brief Overview of Glutamate Signaling in Other Cancers; and Conclusion. © 2010 Wiley Periodicals, Inc. Head Neck, 2010
Ethics of Frey syndrome: Ensuring that consent is truly informed
Authors: Shuman Andrew G. , Bradford Carol R. 
Published: June 2010

AbstractFrey syndrome is a widely recognized sequela of parotidectomy with a variable prevalence dependent upon diagnostic criteria. There exists a multitude of strategies for both prevention and treatment. Surgeons are obligated to engage patients in a frank and open discussion of the operative risks, benefits, and alternatives. Due to uncertainty regarding the significance of Frey syndrome postoperatively, the process of informed consent and preoperative decision‐making pose a potential ethical quandary. This commentary is designed to heighten the awareness of the preoperative informed consent process by dissecting the ethical tenets underlying these patient encounters using Frey syndrome as an example, ensuring that patients are granted the opportunity to participate in their own care in accordance with the concept of individual autonomy. © 2010 Wiley Periodicals, Inc. Head Neck, 2010
Biliary Apotopes and Anti-Mitochondrial Antibodies Activate Innate Immune Responses in Primary Biliary Cirrhosis†
Authors: Lleo Ana , Bowlus Christopher L. , Yang Guo-Xiang , Invernizzi Pietro , Podda Mauro , Van de Water Judy , Ansari Aftab A. , Coppel Ross L. , Worman Howard J. , Gores Gregory J. , Gershwin Eric M. 
Published: June 2010

Abstract

Our understanding of primary biliary cirrhosis (PBC) has been significantly enhanced by the rigorous dissection of the multilineage T and B cell response against the immunodominant mitochondrial autoantigen, the E2 component of the pyruvate dehydrogenase complex (PDC-E2). PDC-E2 is a ubiquitous protein present in mitochondria of nucleated cells. However, the damage of PBC is confined to small biliary epithelial cells (BECs). We have previously demonstrated that BECs translocate immunologically intact PDC-E2 to apoptotic bodies and create an apotope. To define the significance of this observation, we have studied the ability of biliary or control epithelial apotopes to induce cytokine secretion from mature monocyte-derived macrophages (MDMΦs) from either patients with PBC or controls in the presence or absence of anti-mitochondrial antibodies (AMAs). We demonstrate that there is intense inflammatory cytokine production in the presence of the unique triad of BEC apotopes, macrophages from patients with PBC, and AMAs. The cytokine secretion is inhibited by anti-CD16 and is not due to differences in apotope uptake. Moreover, MDMΦs from PBC patients cultured with BEC apoptotic bodies in the presence of AMAs markedly increase tumor necrosis factor–related apoptosis-inducing ligand expression.

Conclusion:

These results provide a mechanism for the biliary specificity of PBC, the recurrence of disease after liver transplantation, and the success of ursodiol in treatment. They further emphasize the critical role of the innate immune system in the perpetuation of this autoimmune disease.
Clinical, Laboratory and Histological Associations in Adults with Nonalcoholic Fatty Liver Disease†
Authors: Neuschwander-Tetri Brent A. , Clark Jeanne M. , Bass Nathan M. , Van Natta Mark L. , Unalp-Arida Aynur , Tonascia James , Zein Claudia O. , Brunt Elizabeth M. , Kleiner David E. , McCullough Arthur J. , Sanyal Arun J. , Diehl Anna Mae , Lavine Joel E. , Chalasani Naga , Kowdley Kris V. 
Published: June 2010

Abstract

The Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) was formed to conduct multicenter studies on the etiology, contributing factors, natural history, and treatment of nonalcoholic steatohepatitis (NASH). The aim of this study was to determine the associations of readily available demographic, clinical, and laboratory variables with the diagnosis of NASH and its key histological features, and determine the ability of these variables to predict the severity of nonalcoholic fatty liver disease (NAFLD). A total of 1266 adults were enrolled in NASH CRN studies between October 2004 and February 2008, of whom 1101 had available liver histology. The median age was 50 years; 82% were white and 12% Hispanic. The median body mass index was 33 kg/m2; 49% had hypertension and 31% had type 2 diabetes. On liver biopsy, 57% were judged to have definite NASH and 31% bridging fibrosis or cirrhosis. Using data from the 698 patients with liver biopsies within 6 months of clinical data, patients with definite NASH were more likely to be female and have diabetes, higher levels of aspartate and alanine aminotransferases, alkaline phosphatase, gamma glutamyl transpeptidase, and homeostasis model assessment of insulin resistance (HOMA-IR). Progressive models for predicting histological diagnoses performed modestly for predicting steatohepatitis or ballooning (area under receiver operating characteristic curves [AUROC] ranged from 0.70-0.79), and better for advanced fibrosis (AUROC 0.73-0.85).

Conclusion:

Readily available clinical and laboratory variables can predict advanced fibrosis in adults with NAFLD, but additional information is needed to reliably predict the presence and severity of NASH. Prospective studies of this well-characterized population and associated tissue bank samples offer a unique opportunity to better understand the cause and natural history of NAFLD and develop more precise means for noninvasive diagnosis.
HFE Cys282Tyr Homozygotes With Serum Ferritin Concentrations Below 1000 μg/L Are at Low Risk of Hemochromatosis†,‡
Authors: Allen Katrina J. , Bertalli Nadine A. , Osborne Nicholas J. , Constantine Clare C. , Delatycki Martin B. , Nisselle Amy E. , Nicoll Amanda J. , Gertig Dorota M. , McLaren Christine E. , Giles Graham G. , Hopper John L. , Anderson Gregory J. , Olynyk John K. , Powell Lawrie W. , Gurrin Lyle C. 
Published: June 2010

Abstract

Hemochromatosis gene (

HFE

)-associated hereditary hemochromatosis (HH) is a genetic predisposition to iron overload and subsequent signs and symptoms of disease that potentially affects approximately 80,000 persons in Australia and almost 1 million persons in the United States. Most clinical cases are homozygous for the Cys282Tyr (C282Y) mutation in the

HFE

gene, with serum ferritin (SF) concentration >1000 μg/L as the strongest predictor of cirrhosis. The optimal treatment regimen for those with SF concentrations above the normal range but <1000 μg/L is unknown. We assessed

HFE

mutations in a prospective cohort of 31,192 participants of northern European descent, aged 40-69 years. An

HFE

-stratified random sample of 1438 participants including all C282Y homozygotes with iron studies 12 years apart were examined by physicians blinded to participants'

HFE

genotype. All previously undiagnosed C282Y homozygotes (35 male, 67 female) and all

HFE

wild-types (131 male, 160 female) with baseline and follow-up SF concentrations <1000 μg/L were assessed for HH-associated signs and symptoms including abnormal second/third metacarpophalangeal joints (MCP2/3), raised liver enzymes, hepatomegaly, and self-reported liver disease, fatigue, diabetes mellitus, and use of arthritis medication. The prevalence of HH-associated signs and symptoms was similar for C282Y homozygotes and

HFE

wild-types for both normal and moderately elevated SF concentrations. The maximum prevalence difference between

HFE

genotype groups with moderately elevated SF was 11% (MCP2/3, 95% confidence interval = −6%, 29%;

P

= 0.22) and for normal SF was 6% (arthritis medicine use, 95% confidence interval = −3%, 16%;

P

= 0.11).

Conclusion:

Previously undiagnosed C282Y homozygotes with SF concentrations that remain below 1000 μg/L are at low risk of developing HH-associated signs and symptoms at an age when disease would be expected to have developed. These observations have implications for the management of C282Y homozygotes.
Cholinergic hypofunction impairs memory acquisition possibly through hippocampal Arc and BDNF downregulation
Authors: Gil‐Bea Francisco J. , Solas Maite , Mateos Laura , Winblad Bengt , Ramírez María J. , Cedazo‐Mínguez Angel 
Published: June 2010

AbstractRecent evidence suggests that activity‐regulated cytoskeleton associated protein (Arc) and brain‐derived neurotrophic factor (BDNF) are key players in the cellular mechanisms that trigger synaptic changes and memory consolidation. Cholinergic deafferentiation of hippocampus has been largely shown to induce memory impairments in different behavioral tasks. However, the mechanisms underlying cholinergic‐induced memory formation remain unclear. The role of hippocampal cholinergic denervation on synaptic consolidation and further acquisition of spatial memory was hereby examined by analyzing Arc and BDNF in standard environment and after behavioral training in Morris water maze (MWM). In standard environment, a cholinergic hypofunction induced by the toxin 192IgG‐saporin led to significant decreases in Arc protein and mRNA as well as in BDNF. Lesioned rats subjected to MWM showed a worse acquisition performance that was reversed after galantamine treatment. Recovery of memory acquisition was accompanied by normalization of Arc and BDNF levels in hippocampus. Stimulation of muscarinic, but not nicotinic receptors, in hippocampal primary neurons caused a rapid induction of Arc production. These data suggest that cholinergic denervation of hippocampus leads to deficits in muscarinic‐dependent induction of Arc and a subsequent impairment of spatial memory acquisition. © 2010 Wiley‐Liss, Inc.
Kappa opioid receptor activation blocks progressive neurodegeneration after kainic acid injection
Authors: Schunk Eduard , Aigner Cornelia , Stefanova Nadia , Wenning Gregor , Herzog Herbert , Schwarzer Christoph 
Published: June 2010

AbstractWe recently demonstrated that endogenous prodynorphin‐derived peptides mediate anticonvulsant, antiepileptogenic and neuroprotective effects via kappa opioid receptors (KOP). Here we show acute and delayed neurodegeneration and its pharmacology after local kainic acid injection in prodynorphin knockout and wild‐type mice and neuroprotective effect(s) of KOP activation in wild‐type mice. Prodynorphin knockout and wild‐type mice were injected with kainic acid (3 nmoles in 50 nl saline) into the stratum radiatum of CA1 of the right dorsal hippocampus. Knockout mice displayed significantly more neurodegeneration of pyramidal cells and interneurons than wild‐type mice 2 days after treatment. This phenotype could be mimicked in wild‐type animals by treatment with the KOP antagonist GNTI and rescued in knockout animals by the KOP agonist U‐50488. Minor differences in neurodegeneration remained 3 weeks after treatment, mostly because of higher progressive neurodegeneration in wild‐type mice compared with prodynorphin‐deficient animals. In wild‐type mice progressive neurodegeneration, but not acute neuronal loss, could be mostly blocked by U‐50488 treatment. Our data suggest that endogenous prodynorphin‐derived peptides sufficiently activate KOP receptors during acute seizures, and importantly in situations of reduced dynorphinergic signaling—like in epilepsy—the exogenous activation of KOP receptors might also have strong neuroprotective effects during excitotoxic events. © 2010 Wiley‐Liss, Inc.
Medial septal cholinergic neurons are necessary for context‐place memory but not episodic‐like memory
Authors: Easton Alexander , Fitchett Ann E. , Eacott Madeline J. , Baxter Mark G. 
Published: June 2010

AbstractLoss of cholinergic cortical input is associated with diseases in which episodic memory impairment is a prominent feature, but the degree to which this neurochemical lesion can account for memory impairment in humans with neurodegenerative diseases remains unclear. Removal of cholinergic input to hippocampus impairs some of its functions in memory, perhaps by reducing the plasticity of information representation within the hippocampus, but the role of cholinergic hippocampal input in episodic‐like memories has not been investigated. To address this question, we tested rats with selective lesions of basal forebrain neurons in the medial septum and vertical limb of the diagonal band (MS/VDB), which contains hippocampal‐projecting cholinergic neurons, on a task of integrated memory for objects, places, and contexts (“what–where–which” memory). This task serves as a rodent model of human episodic memory (episodic‐like memory) and is sensitive to damage to the hippocampal system. Rats with lesions of cholinergic MS/VDB neurons performed as well on the what–where–which task as controls, but were impaired in a task that simply required them to associate places with contexts (“where–which” memory). Thus, episodic‐like memories that rely on the hippocampus do not require cholinergic neuromodulation to be formed. Nevertheless, some more specific aspects of where–which memory, which may be more dependent on the plasticity of hippocampal spatial representations, require acetylcholine. These results suggest that cholinergic projections to hippocampus are not necessary for episodic memory and, furthermore, that hippocampal spatial representations may be to some extent dissociable from episodic memory function. © 2010 Wiley‐Liss, Inc.