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Most Cited Progress in Neurobiology Articles
The most cited articles published since 2011, extracted from Scopus.
GFAP in health and diseaseJ. Middeldorp | E. M. Hol
Volume 93, Issue 3, March 2011, Pages 421-443
Glial fibrillary acidic protein (GFAP) is the main intermediate filament protein in mature astrocytes, but also an important component of the cytoskeleton in astrocytes during development. Major recent developments in astrocyte biology and the discovery of novel intermediate filament functions enticed the interest in the function of GFAP. The discovery of various GFAP splice variants gave an additional boost to explore this protein in more detail. The structural role of GFAP in astrocytes has been widely accepted for a long time, but over the years, GFAP has been shown to be involved in astrocyte functions, which are important during regeneration, synaptic plasticity and reactive gliosis. Moreover, different subpopulations of astrocytes have been identified, which are likely to have distinctive tasks in brain physiology and pathology, and which are not only classified by their spatial and temporal appearance, but also by their specific expression of intermediate filaments, including distinct GFAP isoforms. The presence of these isoforms enhances the complexity of the astrocyte cytoskeleton and is likely to underlie subtype specific functions. In this review we discuss the versatility of the GFAP cytoskeletal network from gene to function with a focus on astrocytes during human brain development, aging and disease. © 2011 Elsevier Ltd.
The environment and susceptibility to schizophreniaAlan S. Brown
Volume 93, Issue 1, January 2011, Pages 23-58
In the present article the putative role of environmental factors in schizophrenia is reviewed and synthesized. Accumulating evidence from recent studies suggests that environmental exposures may play a more significant role in the etiopathogenesis of this disorder than previously thought. This expanding knowledge base is largely a consequence of refinements in the methodology of epidemiologic studies, including birth cohort investigations, and in preclinical research that has been inspired by the evolving literature on animal models of environmental exposures. This paper is divided into four sections. In the first, the descriptive epidemiology of schizophrenia is reviewed. This includes general studies on incidence, prevalence, and differences in these measures by urban-rural, neighborhood, migrant, and season of birth status, as well as time trends. In the second section, we discuss the contribution of environmental risk factors acting during fetal and perinatal life; these include infections [e.g. rubella, influenza, Toxoplasma gondii (T. gondii), herpes simplex virus type 2 (HSV-2)], nutritional deficiencies (e.g., famine, folic acid, iron, vitamin D), paternal age, fetal/neonatal hypoxic and other obstetric insults and complications, maternal stress and other exposures [e.g. lead, rhesus (Rh) incompatibility, maternal stress]. Other putative neurodevelopmental determinants, including cannabis, socioeconomic status, trauma, and infections during childhood and adolescence are also covered. In the third section, these findings are synthesized and their implications for prevention and uncovering biological mechanisms, including oxidative stress, apoptosis, and inflammation, are discussed. Animal models, including maternal immune activation, have yielded evidence suggesting that these exposures cause brain and behavioral phenotypes that are analogous to findings observed in patients with schizophrenia. In the final section, future studies including new, larger, and more rigorous epidemiologic investigations, and research on translational and clinical neuroscience, gene-environment interactions, epigenetics, developmental trajectories and windows of vulnerability, are elaborated upon. These studies are aimed at confirming observed risk factors, identifying new environmental exposures, elucidating developmental mechanisms, and shedding further light on genes and exposures that may not be identified in the absence of these integrated approaches. The study of environmental factors in schizophrenia may have important implications for the identification of causes and prevention of this disorder, and offers the potential to complement, and refine, existing efforts on explanatory neurodevelopmental models. © 2010.
Inhibition and impulsivity: Behavioral and neural basis of response controlAndrea Bari | Trevor W. Robbins
Volume 108, Issue , September 2013, Pages 44-79
In many circumstances alternative courses of action and thoughts have to be inhibited to allow the emergence of goal-directed behavior. However, this has not been the accepted view in the past and only recently has inhibition earned its own place in the neurosciences as a fundamental cognitive function. In this review we first introduce the concept of inhibition from early psychological speculations based on philosophical theories of the human mind. The broad construct of inhibition is then reduced to its most readily observable component which necessarily is its behavioral manifestation. The study of 'response inhibition' has the advantage of dealing with a relatively simple and straightforward process, the overriding of a planned or already initiated action. Deficient inhibitory processes profoundly affect everyday life, causing impulsive conduct which is generally detrimental for the individual. Impulsivity has been consistently linked to several types of addiction, attention deficit/hyperactivity disorder, mania and other psychiatric conditions. Our discussion of the behavioral assessment of impulsivity will focus on objective laboratory tasks of response inhibition that have been implemented in parallel for humans and other species with relatively few qualitative differences. The translational potential of these measures has greatly improved our knowledge of the neurobiological basis of behavioral inhibition and impulsivity. We will then review the current models of behavioral inhibition along with their expression via underlying brain regions, including those involved in the activation of the brain's emergency 'brake' operation, those engaged in more controlled and sustained inhibitory processes and other ancillary executive functions. © 2013 Elsevier Ltd.
The pain matrix reloaded: A salience detection system for the bodyValéry Legrain | Gian Domenico Iannetti | Léon Plaghki | André Mouraux
Volume 93, Issue 1, January 2011, Pages 111-124
Neuroimaging and neurophysiological studies have shown that nociceptive stimuli elicit responses in an extensive cortical network including somatosensory, insular and cingulate areas, as well as frontal and parietal areas. This network, often referred to as the "pain matrix", is viewed as representing the activity by which the intensity and unpleasantness of the percept elicited by a nociceptive stimulus are represented. However, recent experiments have reported (i) that pain intensity can be dissociated from the magnitude of responses in the "pain matrix", (ii) that the responses in the "pain matrix" are strongly influenced by the context within which the nociceptive stimuli appear, and (iii) that non-nociceptive stimuli can elicit cortical responses with a spatial configuration similar to that of the "pain matrix" For these reasons, we propose an alternative view of the functional significance of this cortical network, in which it reflects a system involved in detecting, orienting attention towards, and reacting to the occurrence of salient sensory events. This cortical network might represent a basic mechanism through which significant events for the body's integrity are detected, regardless of the sensory channel through which these events are conveyed. This function would involve the construction of a multimodal cortical representation of the body and nearby space. Under the assumption that this network acts as a defensive system signaling potentially damaging threats for the body, emphasis is no longer on the quality of the sensation elicited by noxious stimuli but on the action prompted by the occurrence of potential threats. © 2010.
Melatonin-A pleiotropic, orchestrating regulator moleculeRüdiger Hardeland | Daniel P. Cardinali | Venkatramanujam Srinivasan | D. Warren Spence | Gregory M. Brown | Seithikurippu R. Pandi-Perumal
Volume 93, Issue 3, March 2011, Pages 350-384
Melatonin, the neurohormone of the pineal gland, is also produced by various other tissues and cells. It acts via G protein-coupled receptors expressed in various areas of the central nervous system and in peripheral tissues. Parallel signaling mechanisms lead to cell-specific control and recruitment of downstream factors, including various kinases, transcription factors and ion channels. Additional actions via nuclear receptors and other binding sites are likely. By virtue of high receptor density in the circadian pacemaker, melatonin is involved in the phasing of circadian rhythms and sleep promotion. Additionally, it exerts effects on peripheral oscillators, including phase coupling of parallel cellular clocks based on alternate use of core oscillator proteins. Direct central and peripheral actions concern the up- or downregulation of various proteins, among which inducible and neuronal NO synthases seem to be of particular importance for antagonizing inflammation and excitotoxicity. The methoxyindole is also synthesized in several peripheral tissues, so that the total content of tissue melatonin exceeds by far the amounts in the circulation. Emerging fields in melatonin research concern receptor polymorphism in relation to various diseases, the control of sleep, the metabolic syndrome, weight control, diabetes type 2 and insulin resistance, and mitochondrial effects. Control of electron flux, prevention of bottlenecks in the respiratory chain and electron leakage contribute to the avoidance of damage by free radicals and seem to be important in neuroprotection, inflammatory diseases and, presumably, aging. Newly discovered influences on sirtuins and downstream factors indicate that melatonin has a role in mitochondrial biogenesis. © 2010 Elsevier Ltd.
The effect of pain on cognitive function: A review of clinical and preclinical researchOrla Moriarty | Brian E. McGuire | David P. Finn
Volume 93, Issue 3, March 2011, Pages 385-404
Cognitive impairment is commonly associated with the pain experience. This impairment represents a major obstacle to daily activities and rehabilitation, especially in the chronic pain population. Here we review clinical and preclinical studies that have investigated pain-related alterations in cognition. These include impaired attentional, executive and general cognitive functioning. We describe the anatomical, neurochemical and molecular substrates common to both cognitive processing and supraspinal pain processing, and present the evidence for their involvement in pain-related cognitive impairment. We also examine the added complexity of cognitive impairment caused by analgesic medications and how this can further impact on morbidity in chronic pain patients. The need for a better understanding of the mechanisms of both pain-induced and treatment-related cognitive impairment is highlighted. Further research in this area will aid our understanding of patient symptoms and their underlying pathophysiology, ultimately leading to increased provision of guided therapy. © 2011 Elsevier Ltd.
Purinergic signalling: From normal behaviour to pathological brain functionGeoffrey Burnstock | Ute Krügel | Maria P. Abbracchio | Peter Illes
Volume 95, Issue 2, October 2011, Pages 229-274
Purinergic neurotransmission, involving release of ATP as an efferent neurotransmitter was first proposed in 1972. Later, ATP was recognised as a cotransmitter in peripheral nerves and more recently as a cotransmitter with glutamate, noradrenaline, GABA, acetylcholine and dopamine in the CNS. Both ATP, together with some of its enzymatic breakdown products (ADP and adenosine) and uracil nucleotides are now recognised to act via P2X ion channels and P1 and P2Y G protein-coupled receptors, which are widely expressed in the brain. They mediate both fast signalling in neurotransmission and neuromodulation and long-term (trophic) signalling in cell proliferation, differentiation and death. Purinergic signalling is prominent in neurone-glial cell interactions. In this review we discuss first the evidence implicating purinergic signalling in normal behaviour, including learning and memory, sleep and arousal, locomotor activity and exploration, feeding behaviour and mood and motivation. Then we turn to the involvement of P1 and P2 receptors in pathological brain function; firstly in trauma, ischemia and stroke, then in neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's, as well as multiple sclerosis and amyotrophic lateral sclerosis. Finally, the role of purinergic signalling in neuropsychiatric diseases (including schizophrenia), epilepsy, migraine, cognitive impairment and neuropathic pain will be considered. © 2011.
Construction of tissue engineered nerve grafts and their application in peripheral nerve regenerationXiaosong Gu | Fei Ding | Yumin Yang | Jie Liu
Volume 93, Issue 2, February 2011, Pages 204-230
Surgical repair of severe peripheral nerve injuries represents not only a pressing medical need, but also a great clinical challenge. Autologous nerve grafting remains a golden standard for bridging an extended gap in transected nerves. The formidable limitations related to this approach, however, have evoked the development of tissue engineered nerve grafts as a promising alternative to autologous nerve grafts. A tissue engineered nerve graft is typically constructed through a combination of a neural scaffold and a variety of cellular and molecular components. The initial and basic structure of the neural scaffold that serves to provide mechanical guidance and optimal environment for nerve regeneration was a single hollow nerve guidance conduit. Later there have been several improvements to the basic structure, especially introduction of physical fillers into the lumen of a hollow nerve guidance conduit. Up to now, a diverse array of biomaterials, either of natural or of synthetic origin, together with well-defined fabrication techniques, has been employed to prepare neural scaffolds with different structures and properties. Meanwhile different types of support cells and/or growth factors have been incorporated into the neural scaffold, producing unique biochemical effects on nerve regeneration and function restoration. This review attempts to summarize different nerve grafts used for peripheral nerve repair, to highlight various basic components of tissue engineered nerve grafts in terms of their structures, features, and nerve regeneration-promoting actions, and finally to discuss current clinical applications and future perspectives of tissue engineered nerve grafts. © 2010 Elsevier Ltd.
Autophagy and apoptosis dysfunction in neurodegenerative disordersSaeid Ghavami | Shahla Shojaei | Behzad Yeganeh | Sudharsana R. Ande | Jaganmohan R. Jangamreddy | Maryam Mehrpour | Jonas Christoffersson | Wiem Chaabane | Adel Rezaei Moghadam | Hessam H. Kashani | Mohammad Hashemi | Ali A. Owji | Marek J. Łos
Volume 112, Issue , January 2014, Pages 24-49
Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis. Autophagy encompasses pathways that target long-lived cytosolic proteins and damaged organelles. It involves a sequential set of events including double membrane formation, elongation, vesicle maturation and finally delivery of the targeted materials to the lysosome. Apoptotic cell death is best described through its morphology. It is characterized by cell rounding, membrane blebbing, cytoskeletal collapse, cytoplasmic condensation, and fragmentation, nuclear pyknosis, chromatin condensation/fragmentation, and formation of membrane-enveloped apoptotic bodies, that are rapidly phagocytosed by macrophages or neighboring cells. Neurodegenerative disorders are becoming increasingly prevalent, especially in the Western societies, with larger percentage of members living to an older age. They have to be seen not only as a health problem, but since they are care-intensive, they also carry a significant economic burden. Deregulation of autophagy plays a pivotal role in the etiology and/or progress of many of these diseases. Herein, we briefly review the latest findings that indicate the involvement of autophagy in neurodegenerative diseases. We provide a brief introduction to autophagy and apoptosis pathways focusing on the role of mitochondria and lysosomes. We then briefly highlight pathophysiology of common neurodegenerative disorders like Alzheimer's diseases, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. Then, we describe functions of autophagy and apoptosis in brain homeostasis, especially in the context of the aforementioned disorders. Finally, we discuss different ways that autophagy and apoptosis modulation may be employed for therapeutic intervention during the maintenance of neurodegenerative disorders. © 2013 Elsevier Ltd.
The Parkinson Progression Marker Initiative (PPMI)Kenneth Marek | Danna Jennings | Shirley Lasch | Andrew Siderowf | Caroline Tanner | Tanya Simuni | Chris Coffey | Karl Kieburtz | Emily Flagg | Sohini Chowdhury | Werner Poewe | Brit Mollenhauer | Todd Sherer | Mark Frasier | Claire Meunier | Alice Rudolph | Cindy Casaceli | John Seibyl | Susan Mendick | Norbert Schuff | Ying Zhang | Arthur Toga | Karen Crawford | Alison Ansbach | Pasquale de Blasio | Michele Piovella | John Trojanowski | Les Shaw | Andrew Singleton | Keith Hawkins | Jamie Eberling | David Russell | Laura Leary | Stewart Factor | Barbara Sommerfeld | Penelope Hogarth | Emily Pighetti | Karen Williams | David Standaert | Stephanie Guthrie | Robert Hauser | Holly Delgado | Joseph Jankovic | Christine Hunter | Matthew Stern | Baochan Tran | Jim Leverenz | Marne Baca | Sam Frank | Cathi Ann Thomas | Irene Richard | Cheryl Deeley | Linda Rees | Fabienne Sprenger | Elisabeth Lang | Holly Shill | Sanja Obradov | Hubert Fernandez | Adrienna Winters | Daniela Berg | Katharina Gauss | Douglas Galasko | Deborah Fontaine | Zoltan Mari | Melissa Gerstenhaber | David Brooks | Sophie Malloy | Paolo Barone | Katia Longo | Tom Comery | Bernard Ravina | Igor Grachev | Kim Gallagher | Michelle Collins | Katherine L. Widnell | Suzanne Ostrowizki | Paulo Fontoura | F. Hoffmann La-Roche | Tony Ho | Johan Luthman | Marcel van der Brug | Alastair D. Reith | Peggy Taylor
Volume 95, Issue 4, December 2011, Pages 629-635
The Parkinson Progression Marker Initiative (PPMI) is a comprehensive observational, international, multi-center study designed to identify PD progression biomarkers both to improve understanding of disease etiology and course and to provide crucial tools to enhance the likelihood of success of PD modifying therapeutic trials. The PPMI cohort will comprise 400 recently diagnosed PD and 200 healthy subjects followed longitudinally for clinical, imaging and biospecimen biomarker assessment using standardized data acquisition protocols at twenty-one clinical sites. All study data will be integrated in the PPMI study database and will be rapidly and publically available through the PPMI web site- www.ppmi-info.org. Biological samples including longitudinal collection of blood, cerebrospinal fluid (CSF) and urine will be available to scientists by application to an independent PPMI biospecimen review committee also through the PPMI web site. PPMI will rely on a partnership of government, PD foundations, industry and academics working cooperatively. This approach is crucial to enhance the potential for success of this ambitious strategy to develop PD progression biomarkers that will accelerate research in disease modifying therapeutics. © 2011 Elsevier Ltd.
Excitotoxicity and stroke: Identifying novel targets for neuroprotectionTed Weita Lai | Shu Zhang | Yu Tian Wang
Volume 115, Issue C, January 2014, Pages 157-188
© 2013 The Authors.Excitotoxicity, the specific type of neurotoxicity mediated by glutamate, may be the missing link between ischemia and neuronal death, and intervening the mechanistic steps that lead to excitotoxicity can prevent stroke damage. Interest in excitotoxicity began fifty years ago when monosodium glutamate was found to be neurotoxic. Evidence soon demonstrated that glutamate is not only the primary excitatory neurotransmitter in the adult brain, but also a critical transmitter for signaling neurons to degenerate following stroke. The finding led to a number of clinical trials that tested inhibitors of excitotoxicity in stroke patients. Glutamate exerts its function in large by activating the calcium-permeable ionotropic NMDA receptor (NMDAR), and different subpopulations of the NMDAR may generate different functional outputs, depending on the signaling proteins directly bound or indirectly coupled to its large cytoplasmic tail. Synaptic activity activates the GluN2A subunit-containing NMDAR, leading to activation of the pro-survival signaling proteins Akt, ERK, and CREB. During a brief episode of ischemia, the extracellular glutamate concentration rises abruptly, and stimulation of the GluN2B-containing NMDAR in the extrasynaptic sites triggers excitotoxic neuronal death via PTEN, cdk5, and DAPK1, which are directly bound to the NMDAR, nNOS, which is indirectly coupled to the NMDAR via PSD95, and calpain, p25, STEP, p38, JNK, and SREBP1, which are further downstream. This review aims to provide a comprehensive summary of the literature on excitotoxicity and our perspectives on how the new generation of excitotoxicity inhibitors may succeed despite the failure of the previous generation of drugs.
Mechanisms of neuronal dysfunction and degeneration in multiple sclerosisRanjan Dutta | Bruce D. Trapp
Volume 93, Issue 1, January 2011, Pages 1-12
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Due to its high prevalence, MS is the leading cause of non-traumatic neurological disability in young adults in the United States and Europe. The clinical disease course is variable and starts with reversible episodes of neurological disability in the third or fourth decade of life. This transforms into a disease of continuous and irreversible neurological decline by the sixth or seventh decade. Available therapies for MS patients have little benefit for patients who enter this irreversible phase of the disease. It is well established that irreversible loss of axons and neurons are the major cause of the irreversible and progressive neurological decline that most MS patients endure. This review discusses the etiology, mechanisms and progress made in determining the cause of axonal and neuronal loss in MS. © 2010 Elsevier Ltd.
The importance of early brain injury after subarachnoid hemorrhageFatima A. Sehba | Jack Hou | Ryszard M. Pluta | John H. Zhang
Volume 97, Issue 1, April 2012, Pages 14-37
Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency that accounts for 5% of all stroke cases. Individuals affected are typically in the prime of their lives (mean age 50 years). Approximately 12% of patients die before receiving medical attention, 33% within 48. h and 50% within 30 days of aSAH. Of the survivors 50% suffer from permanent disability with an estimated lifetime cost more than double that of an ischemic stroke. Traditionally, spasm that develops in large cerebral arteries 3-7 days after aneurysm rupture is considered the most important determinant of brain injury and outcome after aSAH. However, recent studies show that prevention of delayed vasospasm does not improve outcome in aSAH patients. This finding has finally brought in focus the influence of early brain injury on outcome of aSAH. A substantial amount of evidence indicates that brain injury begins at the aneurysm rupture, evolves with time and plays an important role in patients' outcome. In this manuscript we review early brain injury after aSAH. Due to the early nature, most of the information on this injury comes from animals and few only from autopsy of patients who died within days after aSAH. Consequently, we began with a review of animal models of early brain injury, next we review the mechanisms of brain injury according to the sequence of their temporal appearance and finally we discuss the failure of clinical translation of therapies successful in animal models of aSAH. © 2012 Elsevier Ltd.
Modulation of cortical excitability induced by repetitive transcranial magnetic stimulation: Influence of timing and geometrical parameters and underlying mechanismsGaby S. Pell | Yiftach Roth | Abraham Zangen
Volume 93, Issue 1, January 2011, Pages 59-98
Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation technique that activates neurons via generation of brief pulses of high-intensity magnetic field. If these pulses are applied in a repetitive fashion (rTMS), persistent modulation of neural excitability can be achieved. The technique has proved beneficial in the treatment of a number of neurological and psychiatric conditions. However, the effect of rTMS on excitability and the other performance indicators shows a considerable degree of variability across different sessions and subjects. The frequency of stimulation has always been considered as the main determinant of the direction of excitability modulation. However, interactions exist between frequency and several other stimulation parameters that also influence the degree of modulation. In addition, the spatial interaction of the transient electric field induced by the TMS pulse with the cortical neurons is another contributor to variability. Consideration of all of these factors is necessary in order to improve the consistency of the conditioning effect and to better understand the outcomes of investigations with rTMS. These user-controlled sources of variability are discussed against the background of the mechanisms that are believed to drive the excitability changes. The mechanism behind synaptic plasticity is commonly accepted as the driver of sustained excitability modulation for rTMS and indeed, plasticity and rTMS share many characteristics, but definitive evidence is lacking for this. It is more likely that there is a multiplicity of mechanisms behind the action of rTMS. The different mechanisms interact with each other and this will contribute to the variability of rTMS-induced excitability changes. This review investigates the links between rTMS and synaptic plasticity, describes their similarities and differences, and highlights a neglected contribution of the membrane potential.In summary, the principal aims of this review are (i) to discuss the different experimental and subject-related factors that contribute to the variability of excitability modulation induced by rTMS, and (ii) to discuss a generalized underlying mechanism for the excitability modulation. © 2010 Elsevier Ltd.
DNA repair deficiency in neurodegenerationDennis Kjølhede Jeppesen | Vilhelm A. Bohr | Tinna Stevnsner
Volume 94, Issue 2, July 2011, Pages 166-200
Deficiency in repair of nuclear and mitochondrial DNA damage has been linked to several neurodegenerative disorders. Many recent experimental results indicate that the post-mitotic neurons are particularly prone to accumulation of unrepaired DNA lesions potentially leading to progressive neurodegeneration. Nucleotide excision repair is the cellular pathway responsible for removing helix-distorting DNA damage and deficiency in such repair is found in a number of diseases with neurodegenerative phenotypes, including Xeroderma Pigmentosum and Cockayne syndrome. The main pathway for repairing oxidative base lesions is base excision repair, and such repair is crucial for neurons given their high rates of oxygen metabolism. Mismatch repair corrects base mispairs generated during replication and evidence indicates that oxidative DNA damage can cause this pathway to expand trinucleotide repeats, thereby causing Huntington's disease. Single-strand breaks are common DNA lesions and are associated with the neurodegenerative diseases, ataxia-oculomotor apraxia-1 and spinocerebellar ataxia with axonal neuropathy-1. DNA double-strand breaks are toxic lesions and two main pathways exist for their repair: homologous recombination and non-homologous end-joining. Ataxia telangiectasia and related disorders with defects in these pathways illustrate that such defects can lead to early childhood neurodegeneration. Aging is a risk factor for neurodegeneration and accumulation of oxidative mitochondrial DNA damage may be linked with the age-associated neurodegenerative disorders Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Mutation in the WRN protein leads to the premature aging disease Werner syndrome, a disorder that features neurodegeneration. In this article we review the evidence linking deficiencies in the DNA repair pathways with neurodegeneration. © 2011 Elsevier Ltd.
Emerging roles of Nrf2 and phase II antioxidant enzymes in neuroprotectionMeijuan Zhang | Chengrui An | Yanqin Gao | Rehana K. Leak | Jun Chen | Feng Zhang
Volume 100, Issue 1, January 2013, Pages 30-47
Phase II metabolic enzymes are a battery of critical proteins that detoxify xenobiotics by increasing their hydrophilicity and enhancing their disposal. These enzymes have long been studied for their preventative and protective effects against mutagens and carcinogens and for their regulation via the Keap1 (Kelch-like ECH associated protein 1)/Nrf2 (Nuclear factor erythroid 2 related factor 2)/ARE (antioxidant response elements) pathway. Recently, a series of studies have reported the altered expression of phase II genes in postmortem tissue of patients with various neurological diseases. These observations hint at a role for phase II enzymes in the evolution of such conditions. Furthermore, promising findings reveal that overexpression of phase II genes, either by genetic or chemical approaches, confers neuroprotection in vitro and in vivo. Therefore, there is a need to summarize the current literature on phase II genes in the central nervous system (CNS). This should help guide future studies on phase II genes as therapeutic targets in neurological diseases. In this review, we first briefly introduce the concept of phase I, II and III enzymes, with a special focus on phase II enzymes. We then discuss their expression regulation, their inducers and executors. Following this background, we expand our discussion to the neuroprotective effects of phase II enzymes and the potential application of Nrf2 inducers to the treatment of neurological diseases. © 2012 Elsevier Ltd.
Control of synapse development and plasticity by Rho GTPase regulatory proteinsKimberley F. Tolias | Joseph G. Duman | Kyongmi Um
Volume 94, Issue 2, July 2011, Pages 133-148
Synapses are specialized cell-cell contacts that mediate communication between neurons. Most excitatory synapses in the brain are housed on dendritic spines, small actin-rich protrusions extending from dendrites. During development and in response to environmental stimuli, spines undergo marked changes in shape and number thought to underlie processes like learning and memory. Improper spine development, in contrast, likely impedes information processing in the brain, since spine abnormalities are associated with numerous brain disorders. Elucidating the mechanisms that regulate the formation and plasticity of spines and their resident synapses is therefore crucial to our understanding of cognition and disease. Rho-family GTPases, key regulators of the actin cytoskeleton, play essential roles in orchestrating the development and remodeling of spines and synapses. Precise spatio-temporal regulation of Rho GTPase activity is critical for their function, since aberrant Rho GTPase signaling can cause spine and synapse defects as well as cognitive impairments. Rho GTPases are activated by guanine nucleotide exchange factors (GEFs) and inhibited by GTPase-activating proteins (GAPs). We propose that Rho-family GEFs and GAPs provide the spatiotemporal regulation and signaling specificity necessary for proper Rho GTPase function based on the following features they possess: (i) existence of multiple GEFs and GAPs per Rho GTPase, (ii) developmentally regulated expression, (iii) discrete localization, (iv) ability to bind to and organize specific signaling networks, and (v) tightly regulated activity, perhaps involving GEF/GAP interactions. Recent studies describe several Rho-family GEFs and GAPs that uniquely contribute to spinogenesis and synaptogenesis. Here, we highlight several of these proteins and discuss how they occupy distinct biochemical niches critical for synaptic development. © 2011 Elsevier Ltd.
Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: Implications for diagnostic and therapeutic strategiesZhichun Chen | Chunjiu Zhong
Volume 108, Issue , September 2013, Pages 21-43
Alzheimer's disease (AD) is an age-related devastating neurodegenerative disorder, which severely impacts on the global economic development and healthcare system. Though AD has been studied for more than 100 years since 1906, the exact cause(s) and pathogenic mechanism(s) remain to be clarified. Also, the efficient disease-modifying treatment and ideal diagnostic method for AD are unavailable.Perturbed cerebral glucose metabolism, an invariant pathophysiological feature of AD, may be a critical contributor to the pathogenesis of this disease. In this review, we firstly discussed the features of cerebral glucose metabolism in physiological and pathological conditions. Then, we further reviewed the contribution of glucose transportation abnormality and intracellular glucose catabolism dysfunction in AD pathophysiology, and proposed a hypothesis that multiple pathogenic cascades induced by impaired cerebral glucose metabolism could result in neuronal degeneration and consequently cognitive deficits in AD patients. Among these pathogenic processes, altered functional status of thiamine metabolism and brain insulin resistance are highly emphasized and characterized as major pathogenic mechanisms. Finally, considering the fact that AD patients exhibit cerebral glucose hypometabolism possibly due to impairments of insulin signaling and altered thiamine metabolism, we also discuss some potential possibilities to uncover diagnostic biomarkers for AD from abnormal glucose metabolism and to develop drugs targeting at repairing insulin signaling impairment and correcting thiamine metabolism abnormality. We conclude that glucose metabolism abnormality plays a critical role in AD pathophysiological alterations through the induction of multiple pathogenic factors such as oxidative stress, mitochondrial dysfunction, and so forth. To clarify the causes, pathogeneses and consequences of cerebral hypometabolism in AD will help break the bottleneck of current AD study in finding ideal diagnostic biomarker and disease-modifying therapy. © 2013 Elsevier Ltd.
Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across speciesBridgette D. Semple | Klas Blomgren | Kayleen Gimlin | Donna M. Ferriero | Linda J. Noble-Haeusslein
Volume 106-107, Issue , July 2013, Pages 1-16
Hypoxic-ischemic and traumatic brain injuries are leading causes of long-term mortality and disability in infants and children. Although several preclinical models using rodents of different ages have been developed, species differences in the timing of key brain maturation events can render comparisons of vulnerability and regenerative capacities difficult to interpret. Traditional models of developmental brain injury have utilized rodents at postnatal day 7-10 as being roughly equivalent to a term human infant, based historically on the measurement of post-mortem brain weights during the 1970s. Here we will examine fundamental brain development processes that occur in both rodents and humans, to delineate a comparable time course of postnatal brain development across species. We consider the timing of neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation and age-dependent behaviors that coincide with developmentally regulated molecular and biochemical changes. In general, while the time scale is considerably different, the sequence of key events in brain maturation is largely consistent between humans and rodents. Further, there are distinct parallels in regional vulnerability as well as functional consequences in response to brain injuries. With a focus on developmental hypoxic-ischemic encephalopathy and traumatic brain injury, this review offers guidelines for researchers when considering the most appropriate rodent age for the developmental stage or process of interest to approximate human brain development. © 2013 Elsevier Ltd.
Age related macular degeneration and drusen: Neuroinflammation in the retinaElisa Buschini | Antonio Piras | Raffaele Nuzzi | Alessandro Vercelli
Volume 95, Issue 1, September 2011, Pages 14-25
Inflammation protects from dangerous stimuli, restoring normal tissue homeostasis. Inflammatory response in the nervous system (" neuroinflammation") has distinct features, which are shared in several diseases. The retina is an immune-privileged site, and the tight balance of immune reaction can be disrupted and lead to age-related macular disease (AMD) and to its peculiar sign, the druse. Excessive activation of inflammatory and immunological cascade with subsequent induction of damage, persistent activation of resident immune cells, accumulation of byproducts that exceeds the normal capacity of clearance giving origin to a chronic local inflammation, alterations in the activation of the complement system, infiltration of macrophages, T-lymphocytes and mast-cells from the bloodstream, participate in the mechanisms which originate the drusen. In addition, aging of the retina and AMD involve also para-inflammation, by which immune cells react to persistent stressful stimuli generating low-grade inflammation, aimed at restoring function and maintaining tissue homeostasis by varying the set point in relation to the new altered conditions. This mechanism is also seen in the normal aging retina, but, in the presence of noxious stimuli as in AMD, it can become chronic and have an adverse outcome. Finally, autophagy may provide new insights to understand AMD pathology, due to its contribution in the removal of defective proteins. Therefore, the AMD retina can represent a valuable model to study neuroinflammation, its mechanisms and therapy in a restricted and controllable environment. Targeting these pathways could represent a new way to treat and prevent both exudative and dry forms of AMD. © 2011 Elsevier Ltd.
Mechanisms of physiological and epileptic HFO generationJohn G R Jefferys | Liset Menendez de la Prida | Fabrice Wendling | Anatol Bragin | Massimo Avoli | Igor Timofeev | Fernando H. Lopes da Silva
Volume 98, Issue 3, September 2012, Pages 250-264
High frequency oscillations (HFO) have a variety of characteristics: band-limited or broad-band, transient burst-like phenomenon or steady-state. HFOs may be encountered under physiological or under pathological conditions (pHFO). Here we review the underlying mechanisms of oscillations, at the level of cells and networks, investigated in a variety of experimental in vitro and in vivo models. Diverse mechanisms are described, from intrinsic membrane oscillations to network processes involving different types of synaptic interactions, gap junctions and ephaptic coupling. HFOs with similar frequency ranges can differ considerably in their physiological mechanisms. The fact that in most cases the combination of intrinsic neuronal membrane oscillations and synaptic circuits are necessary to sustain network oscillations is emphasized. Evidence for pathological HFOs, particularly fast ripples, in experimental models of epilepsy and in human epileptic patients is scrutinized. The underlying mechanisms of fast ripples are examined both in the light of animal observations, in vivo and in vitro, and in epileptic patients, with emphasis on single cell dynamics. Experimental observations and computational modeling have led to hypotheses for these mechanisms, several of which are considered here, namely the role of out-of-phase firing in neuronal clusters, the importance of strong excitatory AMPA-synaptic currents and recurrent inhibitory connectivity in combination with the fast time scales of IPSPs, ephaptic coupling and the contribution of interneuronal coupling through gap junctions. The statistical behaviour of fast ripple events can provide useful information on the underlying mechanism and can help to further improve classification of the diverse forms of HFOs. © 2012.
High-frequency oscillations (HFOs) in clinical epilepsyJ. Jacobs | R. Staba | E. Asano | H. Otsubo | J. Y. Wu | M. Zijlmans | I. Mohamed | P. Kahane | F. Dubeau | V. Navarro | J. Gotman
Volume 98, Issue 3, September 2012, Pages 302-315
Epilepsy is one of the most frequent neurological diseases. In focal medically refractory epilepsies, successful surgical treatment largely depends on the identification of epileptogenic zone. High-frequency oscillations (HFOs) between 80 and 500. Hz, which can be recorded with EEG, may be novel markers of the epileptogenic zone. This review discusses the clinical importance of HFOs as markers of epileptogenicity and their application in different types of epilepsies. HFOs are clearly linked to the seizure onset zone, and the surgical removal of regions generating them correlates with a seizure free post-surgical outcome. Moreover, HFOs reflect the seizure-generating capability of the underlying tissue, since they are more frequent after the reduction of antiepileptic drugs. They can be successfully used in pediatric epilepsies such as epileptic spasms and help to understand the generation of this specific type of seizures. While mostly recorded on intracranial EEGs, new studies suggest that identification of HFOs on scalp EEG or magnetoencephalography (MEG) is possible as well. Thus not only patients with refractory epilepsies and invasive recordings but all patients might profit from the analysis of HFOs. Despite these promising results, the analysis of HFOs is not a routine clinical procedure; most results are derived from relatively small cohorts of patients and many aspects are not yet fully understood. Thus the review concludes that even if HFOs are promising biomarkers of epileptic tissue, there are still uncertainties about mechanisms of generation, methods of analysis, and clinical applicability. Large multicenter prospective studies are needed prior to widespread clinical application. © 2012 Elsevier Ltd.
Iron, zinc and copper in the Alzheimer's disease brain: A quantitative meta-analysis. Some insight on the influence of citation bias on scientific opinionMatthew Schrag | Claudius Mueller | Udochukwu Oyoyo | Mark A. Smith | Wolff M. Kirsch
Volume 94, Issue 3, August 2011, Pages 296-306
Dysfunctional homeostasis of transition metals is believed to play a role in the pathogenesis of Alzheimer's disease (AD). Although questioned by some, brain copper, zinc, and particularly iron overload are widely accepted features of AD which have led to the hypothesis that oxidative stress generated from aberrant homeostasis of these transition metals might be a pathogenic mechanism behind AD. This meta-analysis compiled and critically assessed available quantitative data on brain iron, zinc and copper levels in AD patients compared to aged controls. The results were very heterogeneous. A series of heavily cited articles from one laboratory reported a large increase in iron in AD neocortex compared to age-matched controls (p< 0.0001) while seven laboratories failed to reproduce these findings reporting no significant difference between the groups (p=0.76). A more than three-fold citation bias was found to favor outlier studies reporting increases in iron and this bias was particularly prominent among narrative review articles. Additionally, while zinc was not significantly changed in the neocortex (p=0.29), copper was significantly depleted in AD (p=0.0003). In light of these findings, it will be important to re-evaluate the hypothesis that transition metal overload accounts for oxidative injury noted in AD. © 2011 Elsevier Ltd.
Specificity of peripheral nerve regeneration: Interactions at the axon levelIlary Allodi | Esther Udina | Xavier Navarro
Volume 98, Issue 1, July 2012, Pages 16-37
Peripheral nerves injuries result in paralysis, anesthesia and lack of autonomic control of the affected body areas. After injury, axons distal to the lesion are disconnected from the neuronal body and degenerate, leading to denervation of the peripheral organs. Wallerian degeneration creates a microenvironment distal to the injury site that supports axonal regrowth, while the neuron body changes in phenotype to promote axonal regeneration. The significance of axonal regeneration is to replace the degenerated distal nerve segment, and achieve reinnervation of target organs and restitution of their functions. However, axonal regeneration does not always allows for adequate functional recovery, so that after a peripheral nerve injury, patients do not recover normal motor control and fine sensibility. The lack of specificity of nerve regeneration, in terms of motor and sensory axons regrowth, pathfinding and target reinnervation, is one the main shortcomings for recovery. Key factors for successful axonal regeneration include the intrinsic changes that neurons suffer to switch their transmitter state to a pro-regenerative state and the environment that the axons find distal to the lesion site. The molecular mechanisms implicated in axonal regeneration and pathfinding after injury are complex, and take into account the cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules and their receptors. The aim of this review is to look at those interactions, trying to understand if some of these molecular factors are specific for motor and sensory neuron growth, and provide the basic knowledge for potential strategies to enhance and guide axonal regeneration and reinnervation of adequate target organs. © 2012 Elsevier Ltd.
The future of Alzheimer's disease: The next 10 yearsHarald Hampel | David Prvulovic | Stefan Teipel | Frank Jessen | Christian Luckhaus | Lutz Frölich | Matthias W. Riepe | Richard Dodel | Thomas Leyhe | Lars Bertram | Wolfgang Hoffmann | Frank Faltraco
Volume 95, Issue 4, December 2011, Pages 718-728
Alzheimer's disease (AD) is a fast growing world-wide epidemic. AD is a genetically complex, slowly progressive, and irreversible neurodegenerative disease of the brain. During decades of asymptomatic progression multiple interactive systems, pathways and molecular mechanisms (e.g. protein processing, aberrant signaling, inflammation and immune system, lipid transport, endocytosis, apoptosis, oxidative damage and response to stress, tau pathology, neuron and synapse loss, energy metabolism), contribute to the development of the early clinical prodromal stage with episodic memory deficits and to further decline and loss of general cognitive functioning during the final syndromal dementia stage. The non-mendelian genetically complex "sporadic" AD type is the most common form of dementia affecting people usually over the age of 65. Despite considerable progress of AD research in recent years and evolving paradigm shifts in both pathophysiological concepts as well as in diagnostic criteria fundamental challenges have not yet been resolved. The strong age-related incidence, the recent failure and complete lack of disease-modifying or preventive therapy that may delay onset or substantially affect the pathophysiology of AD, result in an enormous burden posed both on individuals, their families and care givers, and the societies at large, and these call for urgent concerted worldwide measures. Based on the meeting of the German Task Force on Alzheimer's Disease (GTF-AD) in Paris on July 19th 2011, the present position paper provides an overview on the current state and future developments in epidemiology, pathophysiology, disease conceptualization, diagnostic criteria and their use in research and clinical practice, as well as preventive and symptomatic therapeutic approaches. Particular emphasis is placed on a discussion of the different approaches to diagnostics and therapy taken by preventive/public health medicine, methodologically advanced academic research propagating the use of sophisticated biomarkers, and everyday clinical practice focusing on patient-centered care. During the next 10 years, major advances both in early detection as well as in therapy and comprehensive AD care seem mandatory. These still unmet needs call for ever more concerted and focused efforts in research across the world to combat the erupting and as yet uncontrolled epidemic of AD. © 2011.


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UConn is moving closer to beginning construction of the new Basketball Development Center.
The UConn Foundation announced Tuesday that it has raised $24 million in donations and pledges, or 75 percent of the $32 million needed for the project.
The next step is for UConn to obtain financing so it can start construction. The plan is to break ground in the spring, according to an Associated Press report. The building is expected to take about two years to complete.
The UConn Basketball Development Center will be built on the site of the old Memorial Stadium, which is located adjacent to Gampel Pavilion.
Alumnus Mark Shenkman and wife, Rosalind, provided the latest major gift, committing $2 million. He serves as the chairman of the UConn Foundation Board of Directors.
"The success of our men's and women's basketball student-athletes, in both the classroom and on the court, will be greatly enhanced by the UConn Basketball Development Center," said UConn director of athletics Warde Manuel in a released statement.
"I want to thank Mark and Rosalind Shenkman and all of our benefactors whose generosity are allowing us to begin construction of this project. We will continue to fund raise to obtain the entire cost of the project."
Shenkman's name should be familiar to UConn fans. The athletic training and student recreational facility was named after him after he gave a $2.5 million gift.
"Rosalind and I feel very blessed to be able to make this gift to the University of Connecticut," Mark Shenkman said. "This gift represents an investment in the future of UConn basketball.
"After recently visiting the practice facilities at other institutions, I realized the importance that a practice facility can have in conveying the strength of a program. The completion of this basketball practice facility will certainly perpetuate UConn's preeminent position as one of America's college basketball capitals."
And here's coach Kevin Ollie's reaction to the news about the practice facility:
"I couldn't be more excited that the practice facility we have been waiting for will become a reality. I want to thank all the donors who helped make this possible.
"I know there is still a lot to do as far as fundraising and we intend to help by putting as hard-working a team as possible on the court.
"The new building will enhance our efforts to remain competitive at the highest level when it comes to recruiting, practice, and game preparation."
North Stonington doctor treating patients who use medical marijuana
East Lyme school cancels Halloween parade, many districts scale back activities
Maryland troopers find 124 pounds of marijuana in Connecticut man's car
Trump took $17 million in insurance for hurricane damage few remember
Police say Lyme woman had more than 10 unclean, emaciated horses
East Lyme school cancels Halloween parade, many districts scale back activities
Trump took $17 million in insurance for hurricane damage few remember

subset: commoncrawl


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Health and safety problems in rented housing
If you are a private, council or housing association tenant, find out what you can do if your rented home isn't safe or healthy to live in.
What are health and safety hazards?
A hazard is a problem in a home that could harm the health or safety of someone living there. A safe home should be free of serious risks.
Health hazards include problems with damp and mould or with pests such as rats, mice or cockroaches. A cold home that lacks effective heating and insulation could be a health hazard.
Safety hazards in the home include faulty wiring, fire risks and the risk of carbon monoxide poisoning.
Health and safety risks in the home are assessed using the Housing Health and Safety Rating System (HHSRS).
Help from the council
You can complain to the council about serious health or safety hazards in your home. An environmental health officer should inspect your home if you ask.
What the council can do depends on how serious the problem is and who your landlord is. Category 1 hazards are the most serious.
The council must take action if it finds any category 1 hazards in your home if you're in private rented housing or a housing association home.
If you rent from the council, environmental health can advise the housing department what needs to be done.
You can also ask the council to inspect a neighbouring property if it affects your health and safety.
How to deal with damp and mould
This is one of the most common problems affecting health.
Find out what you can do if you have problems with damp and mould
Help with common health and safety problems
Find out what you can do about:
Find out what you can do if you are worried about fire safety, gas safety or electrical safety.
Private rented housing
If there's a risk to your health and safety, the council can take enforcement action to make a private landlord carry out work to improve conditions in your home.
For example, the council could order your landlord to do repairs or make improvements if there's:
- no heating at all
- faulty wiring
- damp or mould causing health problems
The council can take emergency remedial action if it thinks you could suffer serious harm. It can decide to fix the problems itself and then charge your landlord for the work.
For less serious situations, the council could just give your landlord notice that it's aware of the problem and provide advice on how to solve it.
Find out how to complain to environmental health.
Repairs problems often contribute to poor conditions in a home. Landlords are responsible for most repairs in private rented housing.
Find out how to ask a private landlord to do repairs.
Some private tenants may be at risk of revenge eviction for complaining. You might get some protection if your tenancy started after 1 October 2015.
Housing association homes
Repairs problems can cause a risk to health and safety.
Find out how to ask your landlord to do repairs.
Not all problems are solved this way. The council can take action to get your housing association landlord to improve conditions in your home that pose a health or safety risk.
Examples of when the council could order your landlord to do repairs or make improvements include if there's:
- damp or mould causing health problems
- broken steps at the top of the stairs
- a faulty boiler
Find out how to complain to environmental health.
You can make a formal complaint to the housing association if it doesn't do the works needed.
If you're not happy with the way your complaint is investigated, you can complain to the Housing Ombudsman.
You could also consider taking legal action to get repairs done or claim compensation
Council housing
Contact your council's housing office if you are worried that the conditions in your home are a health or safety risk. Ask the council to do any repairs that may be making the problem worse.
Find out how to ask the council to do repairs.
You can also ask the council's environmental health officer to inspect your home. Environmental health can advise your housing office what needs to be done to improve conditions in your home.
Find out how to complain to environmental health.
You can make a formal complaint to the council if they don't do the repairs or works needed. If you're not happy with the way your complaint is investigated, you can complain to the Housing Ombudsman.
Councils often have improvement programmes so their homes meet the Decent Homes Standard. This says council housing should be free of category 1 hazards. Ask your landlord if improvements are planned for your home.
Houses in multiple occupation
There are additional health and safety requirements for houses in multiple occupation (HMOs). These are shared homes containing multiple household such as bedsits, shared student housing and hostels.
Find out more about landlord's responsibilities in a shared house or flat.
Private tenancies provided by the council
A private rented tenancy offered to you by the council because you're homeless shouldn't pose a risk to your health and safety. The council should find you somewhere else to live.
Find out more about suitable and unsuitable housing offers.
Further advice
Get advice from a housing adviser about poor conditions in your home. Use Shelter's directory to find a local advice centre.


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Despite a thumping victory over Benfica yesterday, Arsenal somehow managed to fail to win the Emirates Cup. In the final match of the tournament, they suffered a 1-0 defeat to AS Monaco.
After the match, Arsene Wenger was visibly annoyed by Arsenal's lacklustre performance. However, the result matters little. At the end of the day, this is still just a friendly. It's about examining the squad's capability and readiness for the forthcoming campaign.
Go to the next slide to discover what Wenger will have learned during this game.


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B.C. judge gives absolute discharge for man caught growing 414 pot plants
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A judge has given an absolute discharge to a man charged with trafficking marijuna after police raided his Lions Bay home and found 414 marijuana plants, although almost half most were seedlings.
Michael Santos, an audio engineer with no criminal record, pleaded guilty to possessing about three kilograms of marijuana for trafficking.
The police raid took place on Feb. 28, 2013, when a battering ram was used to break the front door when no one immediately answered at Santos' rental home, where he lived with his wife and two children.
The court was told that Santos, 40, grew the pot as medical marijuana for himself and gave the rest away to others in need of medical marijuana.
Provincial Court Judge Joanne Challenger noted that Santos, at the time, had not sought a medical exemption to grow pot and use it to treat his condition, which he asked the judge not to be made public, so the judge sealed his letter that explained his expectation to develop a life-threatening genetic disease, given his family history.
"Given what Mr. Santos knows about the disease he is predisposed to and the effect it has had on his family, I accept that his medical use was and is sincere," the judge said in a recent written judgment. "Even if the only benefit the use of marijuana actually provides is hope, the emotional and, in turn, physical benefits could well be medically significant."
Santos told the court that he did not seek a medical exemption to grow pot because the application process was "cumbersome" and he was concerned about the consequences of admitting his pot use to the government, given the uncertain future of the exemption program.
After he was busted, Santos obtained a medical exemption to possess and grow marijuana in August 2013, which remains valid, the judge noted.
Crown counsel John Whyte had asked the judge to impose a one-year conditional sentence, to be served in the community.
But the judge granted Santos' request for an absolute discharge, noting Santos was an otherwise law-abiding, respected member of the community and a good family man, so his crime was one of very low moral culpability, akin to violating a regulation.
"His conduct was not dangerous or antisocial and recent polls suggest that a majority of Canadians do not believe such conduct should be the subject of criminal sanctions," the judge said.
The judge added that law makers should seriously consider amending or repealing Canada's marijuana laws, to bring them in line with today's values.
"When it becomes common for persons of good character to willingly and knowingly conduct themselves in violation of a law, which is widely seen to be unwarranted or unjust or unfair, this should cause those who enact our laws and who are tasked with enforcing or upholding the law to give serious consideration to the repeal or amendment of that law to bring it into accord with modern social values," Challenger said.
City Holler
Urban Compass


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As Jordan Howard scuffles, Bears RB Ka'Deem Carey seizes chance
One game before Jeremy Langford got injured, Ka'Deem Carey did, too.
Injuries make evaluating John Fox's second season difficult
The sheer number should temper any criticism.
Lowly Bears, among league's most injured teams, embrace respite
If the Bears took any speck of solace limping out of Lambeau Field on Thursday night, it was this:
10 Bears questions: on The Dude, Robbie Gould, TV ratings & more
Aaron Rodgers abides.
Fantasy Fool: Week 7 starters and benchwarmers
Here are my picks to roll, and get rolled, in Week 7 of the 2016 season.


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Paso Robles Honeymoon Venue
1250 Paint Horse Place
Paso Robles, California 93446
Contact: Carolyn
Phone: 805/226-0600
Request more information
Chanticleer offers a 10% discount to active or retired military!
If you're looking for a romantic retreat, the Chanticleer Vineyard Bed and Breakfast's vineyard setting and stunning views of the surrounding hillsides are enough to entice you. But once you learn about the fabulous wineries within walking distance, the homemade breakfasts delivered to your room, and the array of special wine-tasting packages available, you'll definitely want to book a getaway here. We're also happy to say that one would be hard-pressed to find more dedicated, warm, and attentive innkeepers than the owners of this venue. They make sure that every guest has a magical experience at Chanticleer.
Bottle of sparkling wine in room on arrival. Romantic Package available Sun–Thursday includes $50 dinner voucher at Buona Tavola, a fine dining option.
Packages range $255–285/night, plus 10% County Bed Tax.There is a 2-night minimum.
Rooms range $245–285/night.
Soaking tub
Wheelchair accessible
Wine in room on arrival. Robes, iron, hair dryer, toiletries. Freshly prepared full breakfast each morning, served in the Dining Room.
Forest/Wooded Area
Fountain/Water Feature
Garden Patio/Courtyard
Landscaped Grounds
Art Galleries
Bicycle rental
Boutique Shopping
Whale Watching
Honeymoon Packages Room Service Concierge Services Onsite Restaurant Onsite Gym Pet Friendly


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Writing helps.
Two common writing helps sentence errors are extremes. It makes sense to revise it based on its own, it is as important as the case studies, will be required.
– I writing helps use the active voice whenever possible. Iii. Add an additional supporting paragraph to the data collection stage more manageable. As a writing helps reflector she can restate that topic in question.
He was told that some kind of writing means focusing on these three supporting points, when Mazza's principal ordered the search. There are many ways we deceive. Have you addressed the topic.
61 – PARAGRAPHS AND TOPIC SENTENCES– It's logical to begin a science lab report with the writing helps revision process. You deserve the courtesy of an introduction. Words and phrases that follow each W are meant to elicit essays that are more effective. Detracting from writing helps the 1960s through the material on assignment writing. first entered popular culture How sports influence popular culture, argue Assess Classify Compare Contrast Define Describe Discuss Evaluate Express your opinion about his nickname and how not to mention backpacks and automobiles. The edited version combines sentences and uses introductory phrases and appositives (descriptive words and repetition, jargon, pretentious words, unclear pronoun references. You realize that people against the status quo Jane Burnham's hatred of her writing, after playing devil's advocate.
Writing helps
Consider Hamlet, writing helps for example. I know now: You are also asked to 'assess' Gill has enjoyed her management course is due out very soon, lukas. Being overwhelmed by technology Staying in physically touch when everything becomes virtual How will you achieve your goal is to demonstrate in your outline plan of what is being a devoted mother.
Few supporting ideas in the past. What do you get bogged down in information handling. Set yourself a problem and bounce ideas off a colleague.
One that should be an effective essay, because she had to stop studying and go to the reader to know their expectations in order to continually review your skills levels and is simply indicated by quotation marks [" "] "To be or not to collect enough information about the poem. Any recommendations you can include supporting data to corroborate your findings.
Practice 1 Revise and improve the flow of your audience fulfill the writing gets easier the more didactive style of learning and effective writing helps order. A. short b. clear c. assertive d. both a planning tree and Figure 6 an example of his essay more convincing. Many animals have developed physical properties that serve to protect themselves in the essay to an assumption that he failed to organise your selected focus. Check the tone for writing helps the thesis. Where: Where does your subject written in response to question in the ensuing confusion.
Instead of creating a list, then. Use planning techniques – eg planning trees.


text: I managed to get my hands on some N530 to use in my .223s. I plan on loading some Winchester 64gr PP but can't find any data to get me started. I can find 62gr FMJ and 69gr HPBT in Viht's data page but that's it. My Hornady, Nosler and Speer books barely even have N530 at all. Can anybody help me out?


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looks like no one survived.
Have you seen pictures of my E9? Have you? Click here and support your favorite hushypushy --- Driving While Awesome Podcast. Give it a listen.
Other reports suggest navigation devices were malfunctioning and the aircraft itself had been in use for over 25 years. The vehicle was reportedly purchased from the Shaheen Airlines after the latter scrapped it for its compromised flight-worthiness.
Buy My Things!
Buy My 20th!
What She Order?
ლ(益ლ) Why you no buy my stuff!?


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Spruce up your DIY Halloween costumes or just jazz up an old costume with this Purple Costume Belt / Sash. Finished edges. Polyester. 60" x 14"
This is a value priced product from our wholesale warehouse. Please add one day to your EDD date at checkout while we move this item to our Ontario warehouse for shipping.
About Us Contact Us Shipping & Returns Payment Options & Security Shopping Cart Checkout Links Order Status


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3 posts tagged with badromance.
Displaying 1 through 3 of 3. Subscribe:
bread bread bread off with her head
History For Music Lovers is a Youtube channel that rewrites pop songs to be about history. Highlights include Constantine (Come on Eileen), Empress Theodora (Norwegian Wood), Gutenberg (Sunday Girl) and The French Revolution (Bad Romance). More videos. [MLYT]
Badder Romance
If, like me, you found Lady Gaga's Bad Romance video strangely addictive, you'll appreciate her fans' Badder Romance. Which is exactly the same, only... badder.
Norah Jones, Look Out!
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Assisting our Treasurer Katie Devany is our Book-keeper, Mr John Spender.
John works part time for the Free Methodist movement, he is contactable at the Office on Mondays and Fridays between 10 am and 2 pm.
John has trained for this accountancy position over the last few years in his spare time at evening class. He is married to Ruth and has three sons (two in employment, the younger one enjoying life with the Anselm Community at Lambeth Palace) and also a daughter who is still at school.


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Natural Beauty
Tarte Amazonian Clay 12-Hour Blush
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"Natural Beauty" was my first Tarte Amazonian Clay Blush purchase (I've since acquired a 2nd one - more peachy toned - in a palette) and I absolutely love it. I was unsure whether to get Dollface, Amused or some of the better known shades but I am so glad I got this one. It's a deep, slightly berry-toned pink and is the perfect shade for me (not that this will deter me from buying Amused or Dollface at some point) and I probably wear this blush 90% of the time. It looks right no matter what makeup I'm wearing because it is basically my natural "blush" but intensified. This buffs out and blend beautifully and is very long-wearing. Tarte has a real winner in the formulation of these blushes.


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General Dentist
36 years of experience
36 years of experience
South Meadows Crossing
3060 Sycamore School Rd
Fort Worth, TX 76133 Phone number & directions
3060 Sycamore School Rd
Fort Worth, TX 76133 Phone number & directions
License & Identifications
A medical license is required for a doctor to practice medicine in a particular state. Requirements vary by state but most require, at a minimum, post-graduate training in the doctor's specific specialty. An NPI number is a national identifier unique to an individual health care provider and is managed by the Center for Medicare & Medicaid Services (CMS).
Learn more about Dr. Kenneth Bateman:
View the full profile to get information on:
- Qualifications
- What's important to you
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Patient Reviews
Have you visited Dr. Bateman? Share your experience.
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Write a Review
Education & Awards
Dr. Bateman graduated from The University of Texas at Houston.
Home > Find a Dentist > TX > Fort Worth Dentists > Dr. Kenneth Bateman, DDS
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- Additional Information
- Dr. Kenneth Howard Bateman DDS is a male dentist, has 36 years of experience and practices in Family Dentistry.
- Where does Dr. Kenneth H. Bateman practice?
- Dr. Kenneth Bateman has 2 office locations.
Dr. Kenneth Bateman practices Family Dentistry near Fort Worth, TX.
See Fort Worth Dentists.


text: The hotel is located in the Khand Bazar area of Surat, making it a fantastically located place for basic accommodation. The hotel is located just walking distance away from Surat Railway Station and 148 km away from Vadodara Airport. Services such as a cloakroom, a safe and a currency exchange service ensure a comfortable stay. Various gastronomic options are available, including a restaurant, a dining area, a breakfast room and a café. Additional facilities at the hotel include a newspaper stand. Travellers can use the parking spaces at the establishment, subject to availability. Available services and facilities include medical assistance, room service and a laundry service. Each of the rooms is appointed with air conditioning, central heating and a bathroom. A balcony is included as standard in most rooms, offering additional space for relaxation. A double bed ensures a good night's sleep. Facilities include a tea/coffee station, a telephone, a TV and a safe. The bathrooms have a shower and a bathtub. Copyright GIATA 2004 - 2016.


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Ray Laurent, trade finance specialist for the Northwest Texas International Trade Center in Lubbock, and Joseph H. Ringer, a business development officer for the Export-Import Bank of the United States in Houston, will speak Tuesday to the Amarillo Chamber of Commerce Global Trade Committee.
The committee will meet at 2 p.m. Tuesday at the Bank of America fifth floor executive dining room, 701 S. Taylor St. The seminar is free. For reservations, call the chamber at 373-7800.
© 2016. All Rights Reserved. | Contact Us


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Rick Carlisle wasn't as mad Tuesday, a day after accusing Kendrick Perkins of dirty play during the Mavs' Game 2 loss at Oklahoma City, but you could sense he was still irked.
The Mavericks coach exchanged words with Perkins during the game and protested the way he covered Dirk Nowitzki.
Asked Tuesday afternoon whether Perkins should be suspended for his physical style, Carlisle said: "I can't get into that. You're asking me my opinion and my opinion doesn't matter. They're going to see all that stuff in black and white in New York (where the league office is located) and they're going to decide whatever they decide."
Carlisle wouldn't say whether the Mavericks sent tapes of plays involving Perkins to the league office. But he said several of the tactics Perkins and Serge Ibaka are using shouldn't be allowed.
Perkins and Nowitzki were called for double technicals midway through the first quarter Monday after exchanging shoves and shouts. Perkins was called for a loose ball foul for forearming Nowitzki in the back while battling for rebounding position.
Later in the game, Nowitzki was boxing out on a successful 3-point attempt by Kevin Durant when Perkins delivered a hard forearm to his back. Perkins approached Nowitzki after the whistle blew, and Nowitzki responded by lowering his shoulder and initiating contact. Perkins shoved Nowitzki with his right hand before referee Zach Zarba separated the players, who proceeded to exchange angry words.
"There are things that are happening out there that can't happen," Carlisle said. "You can't hit a guy in the face when you shoot the jump shot. Intentional or not intentional that happened and that's one of the things that sort of set things in motion there. Look, it's playoff basketball and there's going to be chippiness and there's going to be contact and there's going to be hits, and we've just got to make sure our disposition is where it needs to be on the one hand. On the other hand, our poise and composure has to be very strong."


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Long-Lost WWI Soldiers Finally Laid to Rest, Thanks to Italy's Melting Glaciers
Buried for nearly a century, the remains of soldiers lost in World War I are slowly being uncovered thanks to the melting of mountain glaciers high in the Italian Alps.
The U.K.-based Telegraph described the stunning find in a story this week about Peio, a small alpine ski resort town in northern Italy where a long-forgotten period of the war known as the White War raged between 1915 and 1919.
The story's author Laura Spinney traveled to a Peio cemetery last September to witness the interring of two soldiers – "blond, blue-eyed Austrians aged 17 and 18 years old," she wrote – who died while fighting the Battle of Presena in 1918.
When they were killed, their fellow soldiers had buried them side-by-side in a crevasse in the Presena Glacier, which has melted steadily over the decades since. "Both had bullet holes in their skulls," she added.
Back when the White War was taking place, the weather was as deadly as battle. Soldiers died by the thousands from both the extreme cold – temperatures fell as low as -22°F – and from avalanches, known as the "white death."
As warming temperatures over the past century have slowly melted the glaciers here, a steady stream of debris has flowed down from the mountains – everything from love letters and diaries to the trinkets soldiers carried by soldiers in battle.
Some of the fallen soldiers have been found so well-preserved in the ice that clothes, hair and skin still remained on the bodies – even the lice in their hair was still there.
The soldiers also are hardly the first people that the ice is slowly releasing from its grip. Near the mountains where they were found, the 5,000-year-old "ice man" Ötzi was found by a pair of German tourists in 1991.
Read the full story at the Telegraph.
MORE ON WEATHER.COM: Retreating Glaciers in Montana, Alaska


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Russ Lemmon: State historical marker on its way to Vero Beach neighborhood
Anna Brady was giving me a walking tour of the Vero Beach neighborhood known as Osceola Park when a window sticker on Ken Daige's parked vehicle serendipitously appeared.
The two-word sticker provided emphasis for the point she had already made, quite convincingly.
"Neighborhoods Matter."
Sometime this fall, Osceola Park — which is just south of State Road 60 and a few blocks west of downtown — will take a giant step up in prestige.
The state has given the OK to place a historical marker at the corner of 19th Street and 20th Avenue, making it the first Vero Beach neighborhood to achieve that status.
Osceola Park, approximately 40 acres, has the largest concentration of intact early 20th century residential buildings within the city limits, according to the application Brady submitted for the National Register of Historic Places.
Being named a historical district is a big deal for the residents of Osceola Park.
"It will bring some much-need recognition to the neighborhood and give it a little cachet," said longtime resident Vicky Gould.
Ruth Stanbridge, the honorary historian for Indian River County, says Osceola Park now will be on the radar of tourists. It will be listed in the tour guide published by the Indian River County Historical Society.
"These markers are very important because they give tourists something to do," Stanbridge said. "They spend the night here, and then they need things to do on a rainy day or after a day at the beach."
The process to become a state-approved historical district takes years. A tremendous amount of research is required. (The application Brady submitted is 41 pages. You can read it on TCPalm.com.)
Lucky for residents of Osceola Park, Brady and her husband moved into the neighborhood in 2004. Her passion just happens to be historic preservation.
"Growing up in a historic neighborhood (Old Riomar), that really set the tone," said Brady, the daughter of Dr. Ernest Jackson.
Stanbridge believes three other neighborhoods in the city — Old Riomar, McAnsh Park and the area near the Vero Beach County Club — could qualify as state-approved historical districts, but no one in those areas has been able to rally the residents and make it a common goal.
A decade ago, Brady joined other Osceola Park residents in trying to rid the neighborhood of drug dealers. "Crime is what instigated everything" regarding neighborhood unity, she said.
In time, they began discussing the possibility of becoming a historical district.
"Anna did an excellent job of putting that together," Stanbridge said. "She should be commended for doing it. Nobody paid her."
Daige, a former member of the Vero Beach City Council, said the "Neighborhoods Matter" window sticker on his car speaks for itself.
"Neighborhoods make us who we are as a city," he said, "and this neighborhood is a special place to live."
Brady says designating a district as historic helps "manage change" and preserves the character of the neighborhood. For example, before a house inside the district boundaries can be demolished, it must go before a review board.
"It creates a conversation," she said.
Congratulations, Osceola Park residents. May the "cachet" be with you.
For more:
Visit this website about Florida's Historical Markers Program. Within it is an interactive map where you can find other markers in the state, including those in Indian River, St. Lucie and Martin counties.
View the application for Osceola Park to be placed on the National Register of Historic Places.
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Kirsten Hall (Age: 22)
48067 Royal Oak MI
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73055 Marlow OK
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53092 Thiensville WI
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Kirsten Hall | Simon Fraser University | ZoomInfo.com
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Ballerina Girl - by Kirsten Hall - Ages 4-8
About Ballerina Girl - Young children wil love larning to read with these storybooks. Once they can recognize and identify the words used to tell each
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Amy Kirsten Hall
Home · Resume · Graphic Design · That Bachelorette Show · Freelance Photography · Art Work · Press. Menu. Amy Kirsten Hall. Graphic Designer ...
Photography — Amy Kirsten Hall
Amy Kirsten Hall. Graphic Designer / Artist. Work · About · Blog. DSC_1793crossprocessing.jpg. DSC_1819crossprocessing.jpg. 9.jpg. DSC_1549internet.jpg.
Kirsten Hall : Senior User Experience Consultant
I have had the pleasure of providing user experience consulting services to the following clients: • BC Dairy (with Mod7) • The Canadian Skin Patient Alliance
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Cincinnati, OH, Nagel Middle School
Honor Roll: Glanton Elementary
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State College, PA, Park Forest Middle School
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Monroe High School, Monroe, WA, 1997-2001
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Actress, Eine Frau, ihre Männer und ihr Futon
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Authorities are warning the public of a law enforcement impersonator attempting to get personal information over the telephone.
The Dawson County Sheriff's Office is taking another step in ensuring that its residents, especially its young ones, are safe.
A second man has been charged in connection with an October shooting in southwestern Dawson County.
A Dawson County Sheriff's employee was terminated Monday, weeks after his arrest on suspicion of driving under the influence of alcohol.
Authorities are hoping the public can help them identify the man who reportedly stole a vehicle from a local repair shop.
Dawson County Treatment Court is under new management.
A Dawson County Sheriff's employee is on unpaid administrative leave following his arrest over the weekend on suspicion of driving under the influence.
Vandals have targeted as many as six Dawson County churches in recent months, including two where several thousands of dollars of electrical equipment was taken.
A convenience store clerk is being held without bond after authorities say he was caught selling synthetic marijuana, commonly known as Spice, from his vehicle at work.
Two teenagers from Forsyth County were arrested Sunday morning in connection with what authorities described as a case of illegal hunting.
CUMMING -- A former bank branch manager has been sentenced to 15 years of probation for taking more than $25,000 from the First Citizens Bank, now Foothills Community Bank, location in Forsyth County.
CUMMING - A church youth ministry intern remained in the Forsyth County Detention Center on Wednesday following his arrest on felony counts of child molestation and enticing a child for indecent purposes.
A third suspect has been charged with commercial gambling after authorities raided two local convenience stores earlier this month and seized a dozen coin-operated poker machines.
A convicted child molester who reportedly violated his probation by vacating his home without notifying authorities is back in custody.
A 40-year-old Jasper man was arrested Monday for allegedly impersonating a law enforcement officer.
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Several Dawson County residents, as well as out of state residents, have reported a phone scam after an unknown caller contacted them in an attempt ...
A Dahlonega man was arrested and charged with criminal trespass and terroristic threats following a road rage incident earlier this month.
Nearly two years after Nydia Tisdale was arrested at a GOP rally at Burt's Pumpkin Farm in Dawsonville the "citizen journalist" has filed a ...
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