bluuebunny/crossref_metadata_2025_split huggingface dataset:
Supported Lipid Bilayers
Authors: Kiessling Volker , Domanska Marta K. , Murray David , Wan Chen , Tamm Lukas K. 
Published: August 2008

AbstractLipid bilayers supported on solid substrates were developed almost a quarter century ago as a new model membrane system to study fundamental properties of biological membranes and their constituent lipid and protein molecules, as well as for numerous practical applications. In this review, we summarize the development of supported bilayer‐based model membrane systems of increasing complexity while always keeping in mind their primary purpose, which is to reproduce the complex fluid structure of biological membranes to mimic cell membrane‐based molecular processes as close to physiological reality as possible. This process must include maintaining the structure and fluidity of the lipid bilayer, as well as the structure and function of reconstituted membrane proteins. We start the review with a general description of a contemporary picture of a generic biological membrane and proceed with an account of how supported membranes recapture different physiological aspects of biological membranes, such as membrane fusion, cell adhesion, or membrane permeability. Supported membranes are particularly good models for reproducing the fluidity of cell membranes even when different liquid lipid phases coexist. They are also superb models for measuring ligand‐receptor interactions between membrane‐bound receptors and soluble or membrane‐bound ligands. The chemical biology of these and many other lipid–lipid, lipid–protein, and protein–protein interactions that have been investigated in supported bilayers are summarized in several sections that form the main body of this review. The article closes with summaries of practical procedures to prepare and characterize supported bilayers.
Anxiety Disorders: Macromolecular Pathways and Interactions
Authors: Toth Miklos 
Published: August 2008

AbstractFear and anxiety can be a normal adaptive reaction to help cope with stress in the short term, but when the emotional, cognitive, and physical manifestations are long lasting, extreme, and disproportionate to threat, whether real or preceived, anxiety is maladaptive and has become a disabling disorder. Anxiety disorders may be deconstructed to elementary behaviors/symptoms that can be conceptualized as quantitative characters determined by the combined effects of several risk genes and nongenetic factors (e.g., early‐life adversity). Progress in neurogenetics, molecular and cellular neuroscience, and neuroimaging is beginning to yield significant insights of how genetic and nongenetic factors contribute to specific manifestations of anxiety disorders. The aim of this overview is to summarize and integrate the current knowledge on anxiety‐related macromolecular pathways and mechanisms initiated by genetic risk and envionmental factors. These pathways interact with each other, often during specific periods of development, and could lead to alterations in the formation and function of neuronal circuits that encode emotional behavior.
Protein Trafficking Diseases: Small Molecule Approaches
Authors: Sampson Heidi M. , Thomas David Y. 
Published: August 2008

Abstract
Many diseases are caused by defects in protein trafficking. Protein trafficking diseases occur when a mutant protein is recognized by the endoplasmic reticulum (ER) quality control system (ERQC), retained in the ER, and degraded in the cytosol by the proteasome rather than being trafficked to its correct site of action. Among these diseases are cystic fibrosis, lysosomal storage diseases (Fabry, Gaucher, and Tay‐Sachs), nephrogenic diabetes insipidus, oculocutaneous albinism, protein C deficiency, and many others. A characteristic of many of these diseases is that the mutant protein remains functional, but it cannot escape the stringent ER quality‐control machinery, and it is retained in the ER. This characteristic suggests that pharmacological interventions that promote the correct folding of the mutant protein would enable its escape from the ER and ameliorate the symptoms of the disease. In this review, we focus on specific examples of protein trafficking diseases in pharmacological or chemical chaperones have been shown to rescue trafficking of the mutant protein.
Electron Paramagnetic Resonance (EPR) in Enzymology
Authors: Liu Aimin 
Published: August 2008

AbstractElectron paramagnetic resonance (EPR) is a versatile tool for chemical biology research. A remarkable wealth of information about the mechanistic enzymology has been obtained by EPR experiments. As an analytical method, EPR can obtain these two useful pieces of information in a study of enzymatic reaction mechanisms: 1) detection and complete description of free radicals and 2) characterization of the electronic structures of paramagnetic metal ions and their response to changes of the protein environment or substrate binding. The first feature has spurred the development of the new field known as radical enzymology; the second has enhanced the understanding of the mechanisms of metalloenzyme action. The potential of EPR spectroscopy to serve as an important biophysical tool for the future development of enzymology is highlighted by several selected examples.
Schizophrenia: Biological Mechanisms
Authors: Perrone‐Bizzozero Nora I. , Bullock W. Michael 
Published: August 2008

AbstractSchizophrenia is a chronic and severely debilitating mental disorder that affects approximately 1% of the world's population. Although schizophrenia has been recognized for over 100 years, the causes and pathophysiological mechanisms of this illness remained rather elusive until recently. Evidence obtained during the last 3 decades suggests that schizophrenia is a neurodevelopmental disorder that affects the structure and function of distributed brain regions. Multiple neurotransmitter systems have been implicated, as have both gray and white matter abnormalities. These structural alterations result in synaptic miscommunication at local neuronal circuits and long‐distance functional disconnectivity, with both genetic and environmental factors contributing to these deficits. This article will discuss our current understanding of the biological and neurochemical bases of schizophrenia and will describe new pharmacological, genetic, and lesion models used for testing the mechanisms that underlie this devastating disease.
Chronic Obstructive Pulmonary Disease (
COPD
): Biological Mechanisms
Authors: Barnes Peter J. 
Published: August 2008

Abstract

Airway obstruction in chronic obstructive pulmonary disease (COPD) is caused by narrowing of small airways as a result of inflammation and fibrosis and the disruption of their alveolar attachments as a result of emphysema. COPD is characterized by a complex inflammatory disease process that increases as the disease progresses, which leads to increasing airflow limitation. Many inflammatory cells and mediators have now been implicated in the pathogenesis of COPD. Increased numbers of macrophages, neutrophils, T‐lymphocytes (particularly CD8
+
cells) and B‐lymphocytes have been observed, as well as the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). Macrophages seem to play an important role in orchestrating the inflammatory process, which includes the recruitment of neutrophils and T‐cells into small airways and lung parenchyma and the secretion of proteinases that lead to emphysema. A high level of oxidative and nitrative stress may amplify this inflammation through the reduction in histone deacetylase‐2, which also results in corticosteroid resistance.
Depression: Chemical Mechanisms
Authors: Baker Glen B. , Mitchell Nicholas D. 
Published: August 2008

Abstract
Although the etiology of depression remains to be elucidated, our knowledge of the neurobiology and biochemistry of this mental disorder has been updated increasingly. Early research focused on the biogenic amines norepinephrine (NE; noradrenaline) and 5‐hydroxytryptamine (5‐HT; serotonin). The biogenic amine (monoamine) hypothesis of depression states that depression is the result of a functional deficiency of NE and/or 5‐HT at central synapses. However, it soon became obvious that other factors were also important in the neurobiology of depression. Dopamine is thought to be involved in various aspects, which include reward and locomotion. The amino acids gamma‐aminobutyric acid (GABA) and glutamate, their receptors, and various neuroactive steroids that act as allosteric modulators at GABA‐A and/or NMDA glutamate receptors have been proposed to have an important role. Stress and the hypothalamic‐pituitary‐adrenal (HPA) axis play a central role, and it has been proposed that increased secretion of corticotropin releasing factor (CRF) may be critical in producing the symptoms of depression. Various other neurochemicals have also been implicated in depression, and in several cases they have links to the HPA axis. Abnormal levels of Substance P have been reported in depression, which led to development of potential antidepressants that interact with neurokinin receptors. Abnormalities in the immune system, which presumably involve cytokines, have been reported in depression. Cell loss seems to occur in some brain areas (e.g., hippocampus) in depression, and such loss can be produced by stress and prevented by antidepressants (which also increase expression of various neurotrophic and transcription factors). Agonists at melatonin receptors have been proposed in recent years as effective antidepressants. The possible involvement of the various neurochemicals mentioned above in depression will be reviewed, and some other neurochemicals that are being examined will also be mentioned.
A stochastic Hammerstein model for control of oxygen uptake during robotics‐assisted gait
Authors: Hunt K. J. , Allan D. B. 
Published: August 2008

AbstractRobotics‐assisted gait devices have been introduced as part of rehabilitation therapy for people with neurological impairment. The scope of application has recently been expanded to encompass cardiopulmonary training and assessment, but the response of oxygen uptake to progressively increasing work rate while walking with robotics assistance can be strongly nonlinear. This hampers efforts to estimate cardiopulmonary performance parameters.We hypothesized that a linear increase in oxygen uptake can be achieved by employing feedback control. We aimed to develop a nonlinear stochastic model of oxygen uptake response to work rate during robotics‐assisted gait, and to employ this model to design and test feedback strategies for control of oxygen uptake during incremental exercise testing.A new model structure was developed consisting of a Hammerstein component, i.e. a static nonlinear gain combined with a linear time‐invariant transfer function, and a stochastic approximation of regularized breath‐by‐breath fluctuations in oxygen uptake.Simulation results using the model and a range of control design parameters confirmed the ability of feedback to achieve a linear increase in work rate in the face of strong plant nonlinearity.This new approach could be applied during incremental exercise tests and may lead to improved understanding and estimates of the sub‐maximal gas exchange threshold and peak cardiorespiratory performance parameters. Copyright © 2008 John Wiley & Sons, Ltd.
Cover Picture: Texture Evolution During Bending of a Single Crystal Copper Nanowire Studied by EBSD and Crystal Plasticity Finite Element Simulations (Adv. Eng. Mater. 8/2008)
Authors: Weber F. , Schestakow I. , Roters F. , Raabe D. 
Published: August 2008

AbstractThe cover shows a bending test on a Cu single crystal nanowire. The distribution of the geometrically necessry dislocations in the bent wire was determined using high resolution electron back scatter diffraction and predicted using a crystal plasticity finite element method which uses a dislocation based constitutive law. More details can be found in the article of F. Weber, I. Schestakow, F. Roters, D. Raabe on page 737.
State of the art in developmental toxicity screening methods and a way forward: a meeting report addressing embryonic stem cells, whole embryo culture, and zebrafish
Authors: Chapin Robert , Augustine‐Rauch Karen , Beyer Bruce , Daston George , Finnell Richard , Flynn Thomas , Hunter Sidney , Mirkes Phillip , Sue O'Shea K. , Piersma Aldert , Sandler David , Vanparys Philippe , Van Maele‐Fabry Geneviève 
Published: August 2008

AbstractA meeting was convened so that users of three models for in vitro developmental toxicity (embryonic stem cells, whole embryo culture, and zebrafish) could share their experiences with each model, and explore the areas for improvement. We present a summary of this meeting and the recommendations of the group. Birth Defects Res (Part B) 83:446–456, 2008. Published 2008 Wiley‐Liss, Inc.
Sensory‐dependent asymmetry for a urine‐responsive olfactory bulb glomerulus
Authors: Oliva Anthony M. , Jones Kevin R. , Restrepo Diego 
Published: August 2008

AbstractAn unusual property of the olfactory system is that sensory input at the level of the first synapse in the olfactory bulb takes place at two mirror‐image glomerular maps that appear identical across the axis of symmetry. It is puzzling how two identical odor maps would contribute to sensory function. The functional units in these maps are the glomeruli, ovoid neuropil structures formed by axons from olfactory sensory neurons expressing the same olfactory receptor. Here we find that the genetically identified P2 glomeruli are asymmetric across the axis of symmetry in terms of responsiveness to urine volatiles and neuroanatomical structure. Furthermore, P2 asymmetry is modified by sensory deprivation and abolished by decreased BDNF levels. Thus, while mirror odor maps show symmetry at the macroscopic level in maps encompassing the entire surface of the olfactory bulb, they display asymmetry at the level of the single glomerulus. J. Comp. Neurol. 510:475–483, 2008. © 2008 Wiley‐Liss, Inc.
Muscarinic‐2 and orexin‐2 receptors on GABAergic and other neurons in the rat mesopontine tegmentum and their potential role in sleep–wake state control
Authors: Brischoux Frédéric , Mainville Lynda , Jones Barbara E. 
Published: August 2008

AbstractAcetylcholine (ACh) plays an important role in the promotion of paradoxical sleep (PS) with muscle atonia through the muscarinic‐2 receptor (M2R) in the mesopontine tegmentum. Conversely, orexin (Orx or hypocretin) appears to be critical for the maintenance of waking with muscle tone through the orexin‐2 (or hypocretin‐B) receptor (Orx2R), which is lacking in dogs having narcolepsy with cataplexy. In dual‐immunostained material viewed under fluorescence microscopy, we examined the presence and distribution of M2R or Orx2R labeling on all neuronal nuclei (NeuN)‐stained neurons or on glutamic acid decarboxylase (GAD)‐stained neurons through the mesopontine tegmentum. Applying stereological analysis, we determined that many neurons bear M2Rs on their membrane (≈6,300), including relatively large, non‐GABAergic cells, which predominate (>75%) in the oral and caudal pontine (PnO and PnC) reticular fields, and small, GABAergic cells (≈2,800), which predominate (>80%) in the mesencephalic (Mes) reticular formation. Many neurons bear Orx2Rs on their membrane (≈6,800), including relatively large, non‐GABAergic cells, which predominate (>70%) through all reticular fields, and comparatively few GABAergic cells (≈700). In triple‐immunostained material viewed by confocal microscopy, many large neurons in PnO and PnC appear to bear both M2Rs and Orx2Rs on their membrane, indicating that ACh and Orx could exert opposing influences of inhibition vs. excitation on putative reticulo‐spinal neurons and thus attenuate vs. facilitate activity and muscle tone. A few GABAergic cells bear both receptors and could as PS inhibitor neurons serve under these different influences to control PS effector neurons and accordingly gate PS and muscle atonia appropriately across sleep–wake states. J. Comp. Neurol. 510:607–630, 2008. © 2008 Wiley‐Liss, Inc.
Probing neurochemical structure and function of retinal ON bipolar cells with a transgenic mouse
Authors: Dhingra Anuradha , Sulaiman Pyroja , Xu Ying , Fina Marie E. , Veh Rüdiger W. , Vardi Noga 
Published: August 2008

AbstractRetinal ON bipolar cells make up about 70% of all bipolar cells. Glutamate hyperpolarizes these cells by binding to the metabotropic glutamate receptor mGluR6, activating the G‐protein Go1, and closing an unidentified cation channel. To facilitate investigation of ON bipolar cells, we here report on the production of a transgenic mouse (Grm6‐GFP) in which enhanced green fluorescent protein (EGFP), under control of mGluR6 promoter, was expressed in all and only ON bipolar cells. We used the mouse to determine density of ON bipolar cells, which in central retina was 29,600 cells/mm2. We further sorted the fluorescent cells and created a pure ON bipolar cDNA library that was negative for photoreceptor unique genes. With this library, we determined expression of 27 genes of interest. We obtained positive transcripts for Go interactors: regulators of G‐protein signaling (RGS), Ret‐RGS1 (a variant of RGS20), RGS16, RGS7, purkinje cell protein 2 (PCP2, also called L7 or GPSM4), synembryn (RIC‐8), LGN (GPSM2), RAP1GAP, and Gβ5; cGMP modulators: guanylyl cyclase (GC) 1α1, GC1β1, phosphodiesterase (PDE) 1C, and PDE9A; and channels: inwardly rectifying potassium channel Kir2.4, transient receptor potential TRPC2, and sperm‐specific cation channels CatSper 2–4. The following transcripts were not found in our library: AGS3 (GPSM1), RGS10, RGS19 (GAIP), calbindin, GC1α2, GC1β2, PDE5, PDE2A, amiloride‐sensitive sodium channel ACCN4, and CatSper1. We then localized Kir2.4 to several cell types and showed that, in ON bipolar cells, the channel concentrates in their dendritic tips. The channels and modulators found in ON bipolar cells likely shape their light response. Additional uses of the Grm6‐GFP mouse are also discussed. J. Comp. Neurol. 510:484–496, 2008. © 2008 Wiley‐Liss, Inc.
The ventral nucleus of the lateral lemniscus of the gerbil (Meriones unguiculatus): Organization of connections with the cochlear nucleus and the inferior colliculus
Authors: Benson Christina G. , Cant Nell B. 
Published: August 2008

AbstractThe spatial organization of projections from the ventral cochlear nucleus (VCN) to the ventral nucleus of the lateral lemniscus (VNLL) and from the VNLL to the central nucleus of the inferior colliculus (CNIC) was investigated by using neuroanatomical tracing methods in the gerbil. In order to label cells in the VNLL that project to the CNIC, focal injections of biotinylated dextran amine (BDA) were made into different CNIC regions. Retrogradely labeled cells were distributed throughout the dorsal‐to‐ventral axis of the VNLL in all cases. In contrast, the distribution of labeled cells across the lateral‐to‐medial dimension of the VNLL was related to the location of the injection site along the dorsolateral to ventromedial (frequency) axis of the CNIC. Cells projecting to dorsolateral (low‐frequency) regions of the CNIC were located peripherally in the VNLL, mainly laterally and caudally, whereas those projecting to ventromedial (high‐frequency) regions of the CNIC tended to be clustered centrally. Projections to the VNLL were labeled anterogradely following injections of BDA in the VCN. The distribution of terminal fields in the VNLL closely paralleled the topographic arrangement of cells projecting to the CNIC; projections from ventrolateral (low‐frequency) areas of the VCN terminated mainly along the lateral and caudal borders of the VNLL, whereas projections from dorsomedial (high‐frequency) areas terminated in more central regions. The results demonstrate a topographic organization of the major afferent and efferent connections of the gerbil VNLL. J. Comp. Neurol. 510:673–690, 2008. © 2008 Wiley‐Liss, Inc.
Serine racemase is predominantly localized in neurons in mouse brain
Authors: Miya Kazushi , Inoue Ran , Takata Yoshimi , Abe Manabu , Natsume Rie , Sakimura Kenji , Hongou Kazuhisa , Miyawaki Toshio , Mori Hisashi 
Published: August 2008

AbstractD‐Serine is the endogenous ligand for the glycine binding site of the N‐methyl‐D‐aspartate (NMDA)‐type glutamate receptor (GluR) channel and is involved in the regulation of synaptic plasticity, neural network formation, and neurodegenerative disorders. D‐Serine is synthesized from L‐serine by serine racemase (SR), which was first reported to be localized in astrocytes. However, recently, SR mRNA and its protein have been detected in neurons. In this study, we examined the SR distribution in the brain during postnatal development and in cultured cells by using novel SR knockout mice as negative controls. We found that SR is predominantly localized in pyramidal neurons in the cerebral cortex and hippocampal CA1 region. Double immunofluorescence staining revealed that SR signals colocalized with those of the neuron‐specific nuclear protein, but not with the astrocytic markers glial fibrillary acid protein and 3‐phosphoglycerate dehydrogenase. In the striatum, we observed SR expression in γ‐aminobutyric acid (GABA)ergic medium‐spiny neurons. Furthermore, in the adult cerebellum, we detected weak but significant SR signals in GABAergic Purkinje cells. From these findings, we conclude that SR is expressed predominantly in many types of neuron in the brain and plays a key role in the regulation of brain functions under physiological and pathological conditions via the production of the neuromodulator D‐serine. J. Comp. Neurol. 510:641–654, 2008. © 2008 Wiley‐Liss, Inc.
Dynamic modeling of cable system using a new nodal position finite element method
Authors: Zhu Z. H. 
Published: August 2008

AbstractThe handling of cable systems onboard surface ships and submarines presents a significant technical challenge to design engineers in defense and ocean industries. The current approaches rely heavily on empirical methods and time‐consuming/expensive prototype testing. Computer simulation provides a cost effective way to reduce the high risks associated with the design of the cable‐towed system. This paper presents a new nodal position finite element method (FEM) to effectively simulate the dynamics of cable system experiencing large rigid body rotation coupled with small elastic deformation. The existing FEM deals with the large rigid body rotation by linearized incremental approximation that is prone to numerical inaccuracies resulting from large 3D rotations. By solving for the position directly instead of indirectly via the displacement, the new FEM does not need to decouple the elastic deformation from the rigid body rotation and thus eliminates the error source arising from the linearized incremental approximation in existing FEM. Analysis results demonstrate that the new FEM algorithm is simple and robust by comparing with numerical benchmark test and experiments including sea trial data. Copyright © 2008 John Wiley & Sons, Ltd.
A novel key management scheme for dynamic multicast communications
Authors: Chang Chin‐Chen , Cheng Yi‐Fang , Lin Iuon‐Chang 
Published: August 2008

AbstractSecure multicasting allows the sender to deliver an identical secret to an arbitrary set of recipients through an insecure broadcasting channel, whereas the unintended recipients cannot obtain the secret. A practical approach for securing multicast communications is to apply a session key to encrypt the transmitted data. However, the challenges of secure multicast are to manage the session keys possessed by a dynamic group of recipients and to reduce the overhead of computation and transmission when the membership is changed. In this paper, we propose a new key management scheme for dynamic multicast communication, which is based on privacy homomorphism and Chinese remainder theorem. Our scheme can efficiently and securely deliver an identical message to multiple recipients. In particular, the complexity of the key update process in our scheme isO(1). Copyright © 2008 John Wiley & Sons, Ltd.