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3D modeling-based surgical planning in transsphenoidal pituitary surgery--preliminary results.

https://arctichealth.org/en/permalink/ahliterature90794
Source
Acta Otolaryngol. 2008 Sep;128(9):1011-8
Publication Type
Article
Date
Sep-2008
Author
Raappana Antti
Koivukangas John
Pirilä Tapio
Author Affiliation
Department of Otorhinolaryngology, Head and Neck Surgery, Oulu University Hospital, Oulu, Finland. antti.raappana@oulu.fi
Source
Acta Otolaryngol. 2008 Sep;128(9):1011-8
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Adenoma - pathology - radiography - surgery
Adolescent
Adult
Aged
Endoscopy - methods
Feasibility Studies
Female
Humans
Imaging, Three-Dimensional
Magnetic Resonance Imaging
Male
Middle Aged
Models, Neurological
Pituitary Neoplasms - pathology - radiography - surgery
Prospective Studies
Surgery, Computer-Assisted - methods
Tomography, X-Ray Computed
Young Adult
Abstract
CONCLUSION: The preoperative three-dimensional (3D) modeling of the pituitary adenoma together with pituitary gland, optic nerves, carotid arteries, and the sphenoid sinuses was adopted for routine use in our institution for all pituitary surgery patients. It gave the surgeon a more profound orientation to the individual surgical field compared with the use of conventional 2D images only. OBJECTIVE: To demonstrate the feasibility of 3D surgical planning for pituitary adenoma surgery using readily available resources. SUBJECTS AND METHODS: The computed tomography (CT) and magnetic resonance imaging (MRI) data of 40 consecutive patients with pituitary adenoma were used to construct 3D models to be used in preoperative planning and during the surgery. A freely available, open source program (3D Slicer) downloaded to a conventional personal computer (PC) was applied. RESULTS: The authors present a brief description of the 3D reconstruction-based surgical planning workflow. In addition to the preoperative planning the 3D model was used as a 'road map' during the operation. With the 3D model the surgeon was more confident when opening the sellar wall and when evacuating the tumor from areas in contact with vital structures than when using only conventional 2D images.
PubMed ID
19086197 View in PubMed
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Advancing care for traumatic brain injury: findings from the IMPACT studies and perspectives on future research.

https://arctichealth.org/en/permalink/ahliterature106604
Source
Lancet Neurol. 2013 Dec;12(12):1200-10
Publication Type
Article
Date
Dec-2013
Author
Andrew I R Maas
Gordon D Murray
Bob Roozenbeek
Hester F Lingsma
Isabella Butcher
Gillian S McHugh
James Weir
Juan Lu
Ewout W Steyerberg
Author Affiliation
Department of Neurosurgery, Antwerp University Hospital and University of Antwerp, Edegem, Belgium. Electronic address: andrew.maas@uza.be.
Source
Lancet Neurol. 2013 Dec;12(12):1200-10
Date
Dec-2013
Language
English
Publication Type
Article
Keywords
Adult
Blood pressure
Brain Injuries - epidemiology - therapy
Canada
Data Collection - standards
Disease Management
Europe
Forecasting
Glasgow Coma Scale
Humans
International Cooperation
Middle Aged
Models, Neurological
Multicenter Studies as Topic - methods - standards
National Institute of Neurological Disorders and Stroke
National Institutes of Health (U.S.)
Prognosis
Randomized Controlled Trials as Topic - methods - standards
Research Design
Symptom Assessment - standards
Trauma Severity Indices
Treatment Outcome
United States
Abstract
Research in traumatic brain injury (TBI) is challenging for several reasons; in particular, the heterogeneity between patients regarding causes, pathophysiology, treatment, and outcome. Advances in basic science have failed to translate into successful clinical treatments, and the evidence underpinning guideline recommendations is weak. Because clinical research has been hampered by non-standardised data collection, restricted multidisciplinary collaboration, and the lack of sensitivity of classification and efficacy analyses, multidisciplinary collaborations are now being fostered. Approaches to deal with heterogeneity have been developed by the IMPACT study group. These approaches can increase statistical power in clinical trials by up to 50% and are also relevant to other heterogeneous neurological diseases, such as stroke and subarachnoid haemorrhage. Rather than trying to limit heterogeneity, we might also be able to exploit it by analysing differences in treatment and outcome between countries and centres in comparative effectiveness research. This approach has great potential to advance care in patients with TBI.
Notes
Comment In: Lancet Neurol. 2013 Dec;12(12):1132-324139679
PubMed ID
24139680 View in PubMed
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Chromosome 13 dementia syndromes as models of neurodegeneration.

https://arctichealth.org/en/permalink/ahliterature191925
Source
Amyloid. 2001 Dec;8(4):277-84
Publication Type
Article
Date
Dec-2001
Author
J. Ghiso
T. Révész
J. Holton
A. Rostagno
T. Lashley
H. Houlden
G. Gibb
B. Anderton
T. Bek
M. Bojsen-Møller
N. Wood
R. Vidal
H. Braendgaard
G. Plant
B. Frangione
Author Affiliation
Department of Pathology, New York University School of Medicine, New York 10016, USA.). ghisoj0101@popmail.med.nyu.edu
Source
Amyloid. 2001 Dec;8(4):277-84
Date
Dec-2001
Language
English
Publication Type
Article
Keywords
Amino Acid Sequence
Amyloid - genetics - metabolism
Chromosomes, Human, Pair 13 - genetics
Dementia - genetics - metabolism - pathology
Denmark
Great Britain
Heredodegenerative Disorders, Nervous System - genetics - metabolism - pathology
Humans
Models, Genetic
Models, Neurological
Molecular Sequence Data
Mutation
Neurofibrillary Tangles - metabolism - pathology
Syndrome
Abstract
Two hereditary conditions, familial British dementia (FBD) and familial Danish dementia (FDD), are associated with amyloid deposition in the central nervous system and neurodegeneration. The two amyloid proteins, ABri and ADan, are degradation products of the same precursor molecule BriPP bearing different genetic defects, namely a Stop-to-Arg mutation in FBD and a ten-nucleotide duplication-insertion immediately before the stop codon in FDD. Both de novo created amyloid peptides have the same length (34 amino acids) and the same post-translational modification (pyroglutamate) at their N-terminus. Neurofibrillary tangles containing the classical paired helical filaments as well as neuritic components in many instances co-localize with the amyloid deposits. In both disorders, the pattern of hyperphosphorylated tau immunoreactivity is almost indistinguishable from that seen in Alzheimer's disease. These issues argue for the primary importance of the amyloid deposits in the mechanism(s) of neuronal cell loss. We propose FBD and FDD, the chromosome 13 dementia syndromes, as models to study the molecular basis of neurofibrillary degeneration, cell death and amyloid formation in the brain.
PubMed ID
11791622 View in PubMed
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CNS dopamine oxidation and catechol-O-methyltransferase: importance in the etiology, pharmacotherapy, and dietary prevention of Parkinson's disease.

https://arctichealth.org/en/permalink/ahliterature181611
Source
Int J Mol Med. 2004 Mar;13(3):343-53
Publication Type
Article
Date
Mar-2004
Author
Bao Ting Zhu
Author Affiliation
Department of Basic Pharmaceutical Sciences, College of Pharmacy, University of South Carolina, Columbia, SC 29208, USA. BTZhu@cop.sc.edu
Source
Int J Mol Med. 2004 Mar;13(3):343-53
Date
Mar-2004
Language
English
Publication Type
Article
Keywords
Animals
Catechol O-Methyltransferase - antagonists & inhibitors - metabolism
Central Nervous System - metabolism
Diet
Dopamine - metabolism
Dopamine Agonists - therapeutic use
Enzyme Inhibitors - therapeutic use
Humans
Levodopa - therapeutic use
Models, Neurological
Oxidation-Reduction
Parkinson Disease - drug therapy - etiology - metabolism - prevention & control
Abstract
In this article, a particular emphasis has been placed on the conceptual development and understanding of the unique pathogenic changes that are indigenous to the striatal dopaminergic neurons as an important etiological factor in human Parkinson's disease (PD) as well as on the understanding of their clinical implications. Specifically, I have discussed the etiological roles of central nervous system dopamine oxidation in PD, along with a critical review of the available evidence in support of the proposed hypotheses. The chemically-reactive dopamine quinone/semiquinone intermediates are known to be highly neurotoxic and potentially genotoxic. There is considerable evidence for the suggestion that the long-term use of levodopa accelerates the progression of PD. In comparison, centrally-acting non-catechol dopamine receptor agonists would be an excellent alternative to levodopa for the treatment of PD (particularly for late-stage PD) because these agents would not undergo redox cycling to cause oxidative neuronal damage. Catechol-O-methyltransferase (COMT)-mediated methylation metabolism of catecholamine neurotransmitters is a crucial first-line detoxification pathway, and its role in the causation and prevention of PD is also discussed. On the basis of the modulation of COMT-mediated methylation of catecholamines, it is mechanistically explained that hyperhomocysteinemia would be a pathogenic factor in PD whereas vitamins B6, B12, and folate would be a protective factor. Lastly, according to the mechanistic understanding developed here, a novel dietary strategy is proposed that is specifically tailored toward lowering the risk of human PD, which includes eating a nutritionally-balanced diet that contains adequate (but not excessive) amounts of fruits and vegetables, along with adequate dietary supplementation of S-adenosyl-L-methionine, vitamins C, B6, B12, and folate. It is believed that these conceptual developments would also aid in our better understanding of other age-related neurodegenerative disorders, such as Alzheimer's and Huntington's diseases.
PubMed ID
14767563 View in PubMed
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[Data on the standardization of a lubricant F-11 in the air of the work area].

https://arctichealth.org/en/permalink/ahliterature224847
Source
Gig Tr Prof Zabol. 1992;(6):26-8
Publication Type
Article
Date
1992
Author
N G Shubenkin
T V Suchkova
V V Zhukova
G A Volchkova
I V Nikiforova
G A Smirnova
Source
Gig Tr Prof Zabol. 1992;(6):26-8
Date
1992
Language
Russian
Publication Type
Article
Keywords
Air Pollutants, Occupational - toxicity
Animals
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Combinations
Exploratory Behavior - drug effects - physiology
Guinea Pigs
Humans
Male
Maximum Allowable Concentration
Models, Neurological
Models, Psychological
Nylons
Oleic Acids - administration & dosage - toxicity
Polyethylene Glycols - administration & dosage - toxicity
Rabbits
Rats
Reflex, Abnormal - drug effects - physiology
Russia
Textile Industry - standards
Abstract
F-11 lubricant is used in synthetic fibers industry for the polyamide fibers processing. LD50 in intragastric administration is over 11,000 mg/kg. Acute action threshold (limac) is 180 mg/m3 (as evidenced by changes of the investigatory reflex). Chronic action threshold (limch) is 100 mg/m3. MAC in the air is 5 mg/m3, hazard class III. F-11 lubricant is a moderately hazardous chemical compound.
PubMed ID
1478520 View in PubMed
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Deep dyslexia in the two languages of an Arabic/French bilingual patient.

https://arctichealth.org/en/permalink/ahliterature192475
Source
Cognition. 2001 Dec;82(2):77-126
Publication Type
Article
Date
Dec-2001
Author
R. Béland
Z. Mimouni
Author Affiliation
Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Montréal, Canada. renee.beland@umontreal.ca
Source
Cognition. 2001 Dec;82(2):77-126
Date
Dec-2001
Language
English
Publication Type
Article
Keywords
Adult
Dyslexia - pathology - psychology
Humans
Language
Lebanon - ethnology
Male
Models, Neurological
Psycholinguistics
Quebec
Stroke
Abstract
We present a single case study of an Arabic/French bilingual patient, ZT, who, at the age of 32, suffered a cerebral vascular accident that resulted in a massive infarct in the left peri-sylvian region. ZT's reading displays the characteristics of the deep dyslexia syndrome in both languages, that is, production of semantic, visual, and morphological errors, and concreteness effect in reading aloud and impossibility of reading nonwords. In the first part of this paper, using a three-route model of reading, we account for the patient's performance by positing functional lesions, which affect the non-lexical, the semantic lexical and the non-semantic lexical routes of reading. Phonological priming observed in a cross-language visual lexical decision task indicates that implicit assembled phonological recoding is possible. The above lesions and implicit nonword reading characterize the output form of deep dyslexia. However, error distribution reveals dissociations across languages (e.g. the semantic error rate is higher in French whereas translations are more frequent in the Arabic testing) that cannot be accounted for within a three-route model. In the second part, extensions to Plaut and Shallice's connectionist model (Cognitive Neuropsychology, 10 (5) (1993) 377) are proposed to account for the translinguistic errors observed. ZT's error distribution is compared to that obtained by Plaut and Shallice after lesions had been applied at different locations through the 40-60 network. The overall syndrome of deep dyslexia found in both languages is explained as resulting from lesions along the direct (O-->I) and output (S-->Ip, Ip-->P) pathways of reading. Lesions along the output pathway mostly affecting S-->Ip connections in French and Ip-->P connections in Arabic account for discrepancies in ZT's error pattern across tasks and languages. This case study demonstrates the superiority of a connectionist approach for predicting the error pattern in deep dyslexia.
PubMed ID
11716831 View in PubMed
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Development and validation of prognostic survival models in newly diagnosed Parkinson's disease.

https://arctichealth.org/en/permalink/ahliterature299943
Source
Mov Disord. 2018 01; 33(1):108-116
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
01-2018
Author
Angus D Macleod
Ingvild Dalen
Ole-Bjørn Tysnes
Jan Petter Larsen
Carl E Counsell
Author Affiliation
Division of Applied Health Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
Source
Mov Disord. 2018 01; 33(1):108-116
Date
01-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aged
Aged, 80 and over
Cohort Studies
England
Female
Humans
Incidence
Kaplan-Meier Estimate
Male
Models, Neurological
Norway
Parkinson Disease - diagnosis - epidemiology - mortality
Predictive value of tests
Prognosis
Reproducibility of Results
Scotland
Abstract
The objective of this study was to develop valid prognostic models to predict mortality, dependency, and "death or dependency" for use in newly diagnosed Parkinson's disease (PD).
The models were developed in the Parkinsonism Incidence in North-East Scotland study (UK, 198 patients) and validated in the ParkWest study (Norway, 192 patients), cohorts that attempted to identify and follow-up all new PD cases in the study area. Dependency was defined using the Schwab & England scale. We selected variables measured at time of diagnosis to include in the models. Internal validation and external validation were performed by calculating C-statistics (discrimination) and plotting observed versus predicted risk in quantiles of predicted risk (calibration).
Older age, male sex, increased severity of axial features, and Charlson comorbidity index were independent prognostic factors in the mortality model. Increasing age, higher smoking history, increased severity of axial features, and lower MMSE score were independent predictors in the models of dependency and "death or dependency." Each model had very good internal calibration and very good or good discrimination (internal and external C-statistics for the models were 0.73-0.75 and 0.68-0.78, respectively). Although each model clearly separated patients into groups according to risk, they tended to overestimate risk in ParkWest. The models were recalibrated to the baseline risk in the ParkWest study and then calibrated well in this cohort.
We have developed prognostic models for predicting medium-term risk of important clinical outcomes in newly diagnosed PD. These models have validity for use for stratification of randomization, confounder adjustment, and case-mix correction, but they are inadequate for individualized prognostication. © 2017. The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
PubMed ID
28976022 View in PubMed
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Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1.

https://arctichealth.org/en/permalink/ahliterature165971
Source
Hum Mol Genet. 2007 Mar 1;16(5):453-62
Publication Type
Article
Date
Mar-1-2007
Author
William Hennah
Liisa Tomppo
Tero Hiekkalinna
Outi M Palo
Helena Kilpinen
Jesper Ekelund
Annamari Tuulio-Henriksson
Kaisa Silander
Timo Partonen
Tiina Paunio
Joseph D Terwilliger
Jouko Lönnqvist
Leena Peltonen
Author Affiliation
Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland.
Source
Hum Mol Genet. 2007 Mar 1;16(5):453-62
Date
Mar-1-2007
Language
English
Publication Type
Article
Keywords
Alleles
Carrier Proteins - genetics
Exons - genetics
Family
Female
Finland
Genes, Dominant
Genes, Recessive
Genetic markers
Genetic Predisposition to Disease
Genome, Human - genetics
Haplotypes
Humans
Linkage Disequilibrium
Lod Score
Male
Models, Neurological
Nerve Tissue Proteins - genetics
Polymorphism, Single Nucleotide - genetics
Schizophrenia - genetics
Abstract
We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. Our finding would support the concept that initial gene findings in multifactorial diseases will assist in the identification of other components of complex genetic etiology. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia.
PubMed ID
17185386 View in PubMed
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[Hallucinations and dementia. Prevalence, clinical presentation and pathophysiology].

https://arctichealth.org/en/permalink/ahliterature180316
Source
Rev Neurol (Paris). 2004 Apr;160(4 Pt 2):S31-43
Publication Type
Article
Date
Apr-2004
Author
G. Fénelon
F. Mahieux
Author Affiliation
Service de neurologie, Hôpital Henri Mondor, Créteil, France. gilles.fenelon@hmn.ap-hop-paris.fr
Source
Rev Neurol (Paris). 2004 Apr;160(4 Pt 2):S31-43
Date
Apr-2004
Language
French
Publication Type
Article
Keywords
Cognition Disorders - etiology
Dementia - complications
Hallucinations - diagnosis - epidemiology - etiology - physiopathology
Humans
Models, Neurological
Prevalence
Abstract
Hallucinations are a common feature of certain degenerative diseases with a risk of dementia such as Alzheimer's disease, Lewy body dementia, and Parkinson's disease. Obtaining valid epidemiological data is nevertheless quite difficult because of methodological problems. As a rule, hallucinations are more prevalent in Lewy body disease than Parkinson's disease or Alzheimer's disease. The prevalence in parkinsonian dementia is about the same as in Lewy body disease. Complex visual hallucinations predominate, auditory or tactile hallucinations are more exceptional. Minor forms (illusions, sensation of presence) are also observed. Recurrence is common, mainly in the evening or at night. Patients with advanced mental impairment generally take the hallucinations for reality. The hallucinations can be associated with psychological and behavioral disorders such as delusionnal idea or identification disorders. It is important to search for other causes of hallucinations such as drugs, ocular disorders, or depression, but many of these disorders are common comorbidities in elderly patients with degenerative disease. There is no unique model fitting all the hypothesized pathogenic mechanisms. Complex visual hallucinations most likely arise from abnormal activation of the extra-striat temporal associative regions, but only hypothetical mechanisms have been proposed. Genetic studies and functional imaging have not provided convincing evidence. Current focus is placed on an imbalance between deficient cholinergic transmission and preserved or augmented monoaminergic transmission at the cortical level, but other neurotransmission systems could be involved. The dream dysregulation mechanism proposed in Parkinson's disease cannot be generalized. The link between cognitive disorders and hallucination is also poorly understood: hallucinations are associated with more severe cognitive impairments or more rapid cognitive deline in Parkinson's disease and Alzheimer's disease, but the association with specific cognitive disorders remains to be fully explored.
PubMed ID
15118551 View in PubMed
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K+ channels and their modulation by 5-HT in Drosophila photoreceptors: a modelling study.

https://arctichealth.org/en/permalink/ahliterature50595
Source
Ann Biomed Eng. 2004 Nov;32(11):1580-95
Publication Type
Article
Date
Nov-2004
Author
Mika Kauranen
Matti Weckström
Author Affiliation
Department of Physiology, Division of Biophysics, University of Oulu, Finland.
Source
Ann Biomed Eng. 2004 Nov;32(11):1580-95
Date
Nov-2004
Language
English
Publication Type
Article
Keywords
Animals
Drosophila Proteins
Drosophila melanogaster
Membrane Potentials - physiology
Models, Neurological
Photoreceptors - physiology
Potassium Channels - physiology
Serotonin - physiology
Shaker Superfamily of Potassium Channels
Abstract
In order to clarify the role of inactivating and noninactivating K+ conductances in nonspiking neurons, we developed an isopotential model of the Drosophila photoreceptor membrane based on Hodgkin-Huxley-type equations. The model includes voltage dependent potassium conductances, the shaker (gKA) and the delayed rectifier (gKs). The model parameters were derived from published results by Hardie and coworkers and nearly identical model was used also in our previous work (J. E. Niven, M. Vähäsöyrinki, M. Kauranen, R. C. Hardie, M. Juusola, and M. Weckström. The Contribution of shaker K+ channels to the information capacity of Drosophila photoreceptors. Nature. 421:630-634, 2003). The model explains how the two types of channels function together to define the voltage dependent properties of the photoreceptor membrane. Additionally the model enables us to run simulations of conditions which are difficult to achieve in patch clamp, like prolonged membrane depolarizations by light adaptation. Effects of the activation of the delayed rectifier type conductance were found to be in accordance with published experimental work but the inactivation of the shaker channels, in addition to its importance in the determination of the resting potential, produced voltage amplification over equivalent passive membrane under dark adapted conditions. This phenomenon was not present in light adapted conditions. The modulation of the voltage dependence of the conductances as reported by serotonin (5-HT) caused the shaker to act essentially like the delayed rectifier conductance.
PubMed ID
15636117 View in PubMed
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22 records – page 1 of 3.