Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Access to Information: Individual's rights to obtain and use information collected or generated by others.Stem Cells: Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.Journal Impact Factor: A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.Bibliometrics: The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Peer Review, Research: The evaluation by experts of the quality and pertinence of research or research proposals of other experts in the same field. Peer review is used by editors in deciding which submissions warrant publication, by granting agencies to determine which proposals should be funded, and by academic institutions in tenure decisions.Alphavirus: A genus of TOGAVIRIDAE, also known as Group A arboviruses, serologically related to each other but not to other Togaviridae. The viruses are transmitted by mosquitoes. The type species is the SINDBIS VIRUS.Alphavirus Infections: Virus diseases caused by members of the ALPHAVIRUS genus of the family TOGAVIRIDAE.Sindbis Virus: The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of TOGAVIRIDAE INFECTIONS; HERPESVIRIDAE INFECTIONS; ADENOVIRIDAE INFECTIONS; FLAVIVIRIDAE INFECTIONS; BUNYAVIRIDAE INFECTIONS; PICORNAVIRIDAE INFECTIONS; PARAMYXOVIRIDAE INFECTIONS; ORTHOMYXOVIRIDAE INFECTIONS; RETROVIRIDAE INFECTIONS; and ARENAVIRIDAE INFECTIONS.Startle Reaction: A complex involuntary response to an unexpected strong stimulus usually auditory in nature.Sensory Gating: The ability of the BRAIN to suppress neuronal responses to external sensory inputs, such as auditory and visual stimuli. Sensory filtering (or gating) allows humans to block out irrelevant, meaningless, or redundant stimuli.Encephalitis Virus, Venezuelan Equine: A species of ALPHAVIRUS that is the etiologic agent of encephalomyelitis in humans and equines. It is seen most commonly in parts of Central and South America.Glycine-tRNA Ligase: An enzyme that activates glycine with its specific transfer RNA. EC Ligase: An enzyme that activates alanine with its specific transfer RNA. EC Ligase: An enzyme that activates tyrosine with its specific transfer RNA. EC Disease: A hereditary motor and sensory neuropathy transmitted most often as an autosomal dominant trait and characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life. This condition has been divided into two subtypes, hereditary motor and sensory neuropathy (HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. (Adams et al., Principles of Neurology, 6th ed, p1343)RNA, Transfer, Gly: A transfer RNA which is specific for carrying glycine to sites on the ribosomes in preparation for protein synthesis.Amino Acyl-tRNA Synthetases: A subclass of enzymes that aminoacylate AMINO ACID-SPECIFIC TRANSFER RNA with their corresponding AMINO ACIDS.Political Systems: The units based on political theory and chosen by countries under which their governmental power is organized and administered to their citizens.Induced Pluripotent Stem Cells: Cells from adult organisms that have been reprogrammed into a pluripotential state similar to that of EMBRYONIC STEM CELLS.Pluripotent Stem Cells: Cells that can give rise to cells of the three different GERM LAYERS.Nervous System Diseases: Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.Embryonic Stem Cells: Cells derived from the BLASTOCYST INNER CELL MASS which forms before implantation in the uterine wall. They retain the ability to divide, proliferate and provide progenitor cells that can differentiate into specialized cells.Nuclear Reprogramming: The process that reverts CELL NUCLEI of fully differentiated somatic cells to a pluripotent or totipotent state. This process can be achieved to a certain extent by NUCLEAR TRANSFER TECHNIQUES, such as fusing somatic cell nuclei with enucleated pluripotent embryonic stem cells or enucleated totipotent oocytes. GENE EXPRESSION PROFILING of the fused hybrid cells is used to determine the degree of reprogramming. Dramatic results of nuclear reprogramming include the generation of cloned mammals, such as Dolly the sheep in 1997.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.ArchivesBiological Science Disciplines: All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from BIOLOGY, one of its subdivisions, concerned specifically with the origin and life processes of living organisms.PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Directories as Topic: Lists of persons or organizations, systematically arranged, usually in alphabetic or classed order, giving address, affiliations, etc., for individuals, and giving address, officers, functions, and similar data for organizations. (ALA Glossary of Library and Information Science, 1983)Euphoria: An exaggerated feeling of physical and emotional well-being not consonant with apparent stimuli or events; usually of psychologic origin, but also seen in organic brain disease and toxic states.Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.Cocaine-Related Disorders: Disorders related or resulting from use of cocaine.MissouriCommodification: The social process by which something or someone comes to be regarded and treated as an article of trade or commerce.Alcoholics: Persons who have a history of physical or psychological dependence on ETHANOL.Self Administration: Administration of a drug or chemical by the individual under the direction of a physician. It includes administration clinically or experimentally, by human or animal.Levocardia: Congenital abnormalities in which the HEART is in the normal position (levocardia) in the left side of the chest but some or all of the THORAX or ABDOMEN viscera are transposed laterally (SITUS INVERSUS). It is also known as situs inversus with levocardia, or isolated levocardia. This condition is often associated with severe heart defects and splenic abnormalities such as asplenia or polysplenia.Models, Neurological: Theoretical representations that simulate the behavior or activity of the neurological system, processes or phenomena; includes the use of mathematical equations, computers, and other electronic equipment.Neurosciences: The scientific disciplines concerned with the embryology, anatomy, physiology, biochemistry, pharmacology, etc., of the nervous system.Functional Laterality: Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.Theory of Mind: The ability to attribute mental states (e.g., beliefs, desires, feelings, intentions, thoughts, etc.) to self and to others, allowing an individual to understand and infer behavior on the basis of the mental states. Difference or deficit in theory of mind is associated with ASPERGER SYNDROME; AUTISTIC DISORDER; and SCHIZOPHRENIA, etc.Brain Mapping: Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Schizophrenia: A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.Pseudobulbar Palsy: A syndrome characterized by DYSARTHRIA, dysphagia, dysphonia, impairment of voluntary movements of tongue and facial muscles, and emotional lability. This condition is caused by diseases that affect the motor fibers that travel from the cerebral cortex to the lower BRAIN STEM (i.e., corticobulbar tracts); including MULTIPLE SCLEROSIS; MOTOR NEURON DISEASE; and CEREBROVASCULAR DISORDERS. (From Adams et al., Principles of Neurology, 6th ed, p489)Laughter: An involuntary expression of merriment and pleasure; it includes the patterned motor responses as well as the inarticulate vocalization.Psychotic Disorders: Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)Schizophrenic Psychology: Study of mental processes and behavior of schizophrenics.REM Sleep Parasomnias: Abnormal behavioral or physiologic events that are associated with REM sleep, including REM SLEEP BEHAVIOR DISORDER.

Vision: modular analysis--or not? (1/10314)

It has commonly been assumed that the many separate areas of the visual system perform modular analyses, each restricted to a single attribute of the image. A recent paper advocates a radically different approach, where all areas in the hierarchy analyse all attributes of the image to extract perceptually relevant decisions.  (+info)

Somatic recording of GABAergic autoreceptor current in cerebellar stellate and basket cells. (2/10314)

Patch-clamp recordings were performed from stellate and basket cells in rat cerebellar slices. Under somatic voltage clamp, short depolarizing pulses were applied to elicit action potentials in the axon. After the action potential, a bicuculline- and Cd2+-sensitive current transient was observed. A similar response was obtained when eliciting axonal firing by extracellular stimulation. With an isotonic internal Cl- solution, the peak amplitude of this current varied linearly with the holding potential, yielding an extrapolated reversal potential of -20 to 0 mV. Unlike synaptic or autaptic GABAergic currents obtained in the same preparation, the current transient had a slow rise-time and a low variability between trials. This current was blocked when 10 mM BAPTA was included in the recording solution. In some experiments, the current transient elicited axonal action potentials. The current transient was reliably observed in animals aged 12-15 d, with a mean amplitude of 82 pA at -70 mV, but was small and rare in the age group 29-49 d. Numerical simulations could account for all properties of the current transient by assuming that an action potential activates a distributed GABAergic conductance in the axon. The actual conductance is probably restricted to release sites, with an estimated mean presynaptic current response of 10 pA per site (-70 mV, age 12-15 d). We conclude that in developing rats, stellate and basket cell axons have a high density of GABAergic autoreceptors and that a sizable fraction of the corresponding current can be measured from the soma.  (+info)

Competitive mechanisms subserve attention in macaque areas V2 and V4. (3/10314)

It is well established that attention modulates visual processing in extrastriate cortex. However, the underlying neural mechanisms are unknown. A consistent observation is that attention has its greatest impact on neuronal responses when multiple stimuli appear together within a cell's receptive field. One way to explain this is to assume that multiple stimuli activate competing populations of neurons and that attention biases this competition in favor of the attended stimulus. In the absence of competing stimuli, there is no competition to be resolved. Accordingly, attention has a more limited effect on the neuronal response to a single stimulus. To test this interpretation, we measured the responses of neurons in macaque areas V2 and V4 using a behavioral paradigm that allowed us to isolate automatic sensory processing mechanisms from attentional effects. First, we measured each cell's response to a single stimulus presented alone inside the receptive field or paired with a second receptive field stimulus, while the monkey attended to a location outside the receptive field. Adding the second stimulus typically caused the neuron's response to move toward the response that was elicited by the second stimulus alone. Then, we directed the monkey's attention to one element of the pair. This drove the neuron's response toward the response elicited when the attended stimulus appeared alone. These findings are consistent with the idea that attention biases competitive interactions among neurons, causing them to respond primarily to the attended stimulus. A quantitative neural model of attention is proposed to account for these results.  (+info)

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. (4/10314)

We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both alpha amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid- and N-methyl-D-aspartate-like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.  (+info)

Simultaneous measurement of evoked release and [Ca2+]i in a crayfish release bouton reveals high affinity of release to Ca2+. (5/10314)

The opener neuromuscular junction of crayfish was used to determine the affinity of the putative Ca2+ receptor(s) responsible for evoked release. Evoked, asynchronous release, and steady-state intracellular Ca2+ concentration, [Ca2+]ss, were measured concomitantly in single release boutons. It was found that, as expected, asynchronous release is highly correlated with [Ca2+]ss. Surprisingly, evoked release was also found to be highly correlated with [Ca2+]ss. The quantal content (m) and the rate of asynchronous release (S) showed sigmoidal dependence on [Ca2+]ss. The slope log m/log [Ca2+]ss varied between 1.6 and 3.3; the higher slope observed at the lower [Ca2+]o. The slope log S/log [Ca2+]ss varied between 3 and 4 and was independent of [Ca2+]o. These results are consistent with the assumption that evoked release is controlled by the sum of [Ca2+]ss and the local elevation of Ca2+ concentration near the release sites resulting from Ca2+ influx through voltage-gated Ca2+ channels (Y). On the basis of the above, we were able to estimate Y. We found Y to be significantly <10 microM even for [Ca2+]o = 13.5 mM. The dissociation constant (Kd) of the Ca2+ receptor(s) associated with evoked release was calculated to be in the range of 4-5 microM. This value of Kd is similar to that found previously for asynchronous release.  (+info)

Small conductance potassium channels cause an activity-dependent spike frequency adaptation and make the transfer function of neurons logarithmic. (6/10314)

We made a computational model of a single neuron to study the effect of the small conductance (SK) Ca2+-dependent K+ channel on spike frequency adaptation. The model neuron comprised a Na+ conductance, a Ca2+ conductance, and two Ca2+-independent K+ conductances, as well as a small and a large (BK) Ca2+-activated K+ conductance, a Ca2+ pump, and mechanisms for Ca2+ buffering and diffusion. Sustained current injection that simulated synaptic input resulted in a train of action potentials (APs) which in the absence of the SK conductance showed very little adaptation with time. The transfer function of the neuron was nearly linear, i.e., both asymptotic spike rate as well as the intracellular free Ca2+ concentration ([Ca2+]i) were approximately linear functions of the input current. Adding an SK conductance with a steep nonlinear dependence on [Ca2+]i (. Pflugers Arch. 422:223-232; Kohler, Hirschberg, Bond, Kinzie, Marrion, Maylie, and Adelman. 1996. Science. 273:1709-1714) caused a marked time-dependent spike frequency adaptation and changed the transfer function of the neuron from linear to logarithmic. Moreover, the input range the neuron responded to with regular spiking increased by a factor of 2.2. These results can be explained by a shunt of the cell resistance caused by the activation of the SK conductance. It might turn out that the logarithmic relationships between the stimuli of some modalities (e.g., sound or light) and the perception of the stimulus intensity (Fechner's law) have a cellular basis in the involvement of SK conductances in the processing of these stimuli.  (+info)

Transient potassium currents regulate the discharge patterns of dorsal cochlear nucleus pyramidal cells. (7/10314)

Pyramidal cells in the dorsal cochlear nucleus (DCN) show three distinct temporal discharge patterns in response to sound: "pauser," "buildup," and "chopper." Similar discharge patterns are seen in vitro and depend on the voltage from which the cell is depolarized. It has been proposed that an inactivating A-type K+ current (IKI) might play a critical role in generating the three different patterns. In this study we examined the characteristics of transient currents in DCN pyramidal cells to evaluate this hypothesis. Morphologically identified pyramidal cells in rat brain slices (P11-P17) exhibited the three voltage-dependent discharge patterns. Two inactivating currents were present in outside-out patches from pyramidal cells: a rapidly inactivating (IKIF, tau approximately 11 msec) current insensitive to block by tetraethylammonium (TEA) and variably blocked by 4-aminopyridine (4-AP) with half-inactivation near -85 mV, and a slowly inactivating TEA- and 4-AP-sensitive current (IKIS, tau approximately 145 msec) with half-inactivation near -35 mV. Recovery from inactivation at 34 degrees C was described by a single exponential with a time constant of 10-30 msec, similar to the rate at which first spike latency increases with the duration of a hyperpolarizing prepulse. Acutely isolated cells also possessed a rapidly activating (<1 msec at 22 degrees C) transient current that activated near -45 mV and showed half-inactivation near -80 mV. A model demonstrated that the deinactivation of IKIF was correlated with the discharge patterns. Overall, the properties of the fast inactivating K+ current were consistent with their proposed role in shaping the discharge pattern of DCN pyramidal cells.  (+info)

Passive electrotonic properties of rat hippocampal CA3 interneurones. (8/10314)

1. The linear membrane responses of CA3 interneurones were determined with the use of whole-cell patch recording methods. The mean input resistance (RN) for all cells in this study was 526 +/- 16 MOmega and the slowest membrane time constant (tau0) was 73 +/- 3 ms. 2. The three-dimensional morphology of 63 biocytin-labelled neurones was used to construct compartmental models. Specific membrane resistivity (Rm) and specific membrane capacitance (Cm) were estimated by fitting the linear membrane response. Acceptable fits were obtained for 24 CA3 interneurones. The mean Rm was 61.9 +/- 34.2 Omega cm2 and the mean Cm was 0.9 +/- 0.3 microF cm-2. Intracellular resistance (Ri) could not be resolved in this study. 3. Examination of voltage attenuation revealed a significantly low synaptic efficiency from most dendritic synaptic input locations to the soma. 4. Simulations of excitatory postsynaptic potentials (EPSPs) were analysed at both the site of synaptic input and at the soma. There was little variability in the depolarization at the soma from synaptic inputs placed at different locations along the dendritic tree. The EPSP amplitude at the site of synaptic input was progressively larger with distance from the soma, consistent with a progressive increase in input impedance. 5. The 'iso-efficiency' of spatially different synaptic inputs arose from two opposing factors: an increase in EPSP amplitude at the synapse with distance from the soma was opposed by a nearly equivalent increase in voltage attenuation. These simulations suggest that, in these particular neurones, the amplitude of EPSPs measured at the soma will not be significantly affected by the location of synaptic inputs.  (+info)

  • Unfortunately, by the time the symptoms are evident, the neurological damage is already severe, with a massive loss of dopaminergic neurons in the substantia nigra ( Double, 2012 ). (
  • Now, University of Missouri researchers Ashwin Mohan and Sandeep Pendyam, doctoral students in the Department of Electrical and Computer Engineering , are utilizing computational models to study how the brain's chemicals and synaptic mechanisms, or connections between neurons, react to cocaine addiction and what this could mean for future therapies. (
  • A study describing the characterization and validation of two neural progenitor cell models and their ability to differentiate into multiple types of neurons. (
  • Considering the sensitivity of neurons to hypoxic insult, the most beneficial therapeutic window for minimizing neurological deficit from stroke is the hyperacute period. (
  • Gait analysis as a method for assessing neurological outcome in a mouse model of stroke. (
  • In order to improve stroke outcome, novel treatment approaches as well as animal stroke models predictive for the clinical setting are of urgent need. (
  • One of the main obstacles in experimental stroke research is measuring long-term outcome, in particular in mouse models of stroke. (
  • After completing a PhD in the physics department of the University of Cologne and the Max-Planck-Institute for Neurological Research in Cologne, he transferred to the Experimental Neurology Department and the Center for Stroke Research at the Charité in Berlin to offer his expertise in small animal MRI and quickly became the scientific lead of the imaging core facility. (
  • Monoclonal antibody to the ICAM-1 adhesion site reduces neurological damage in a rabbit cerebral embolism stroke model. (
  • We evaluated the effect of antibodies directed against a leukocyte adhesion molecule (ICAM-1) in an embolic model of stroke followed by thrombolysis with tissue plasminogen activator (tPA). (
  • In an animal model for stroke, delta opioid peptide reduced by as much as 75 percent the damage to the brain's striatum, the deeper region of the brain and a major target for strokes, according to researchers. (
  • Recent animal experiments demonstrated that basic fibroblast growth factor-2 (FGF-2) can improve neurological function after stroke by the neuroprotective effect or vasodilating effect. (
  • Test DDFPe as neuroprotective agent in permanent occlusion rat stroke models in Sprague Dawley (SD) and Spontaneously Hypertensive Rats (SHR) measuring both %SV and neurological assessment scores (NAS). (
  • The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes. (
  • Upon low-dose infection of wild-type C57B/6 mice, asymptomatic and symptomatic groups were established and compared to mock-infected mice to measure general health and baseline neurological function, including the acoustic startle response and prepulse inhibition paradigm. (
  • Each disease model was crossed to mice ubiquitously overexpressing wild-type GARS in order to determine whether the disease phenotype is caused by a loss of function in GARS. (
  • Rapamycin treatment also resulted in prolonged healthspan in KO mice, as indicated by the offset of neurological damage, maintenance of weight and body fat, and the improvement of deleterious behavioral phenotypes. (
  • We developed separate models of respiratory and neurological disease following EV-D68 infection in AG129 mice that respond to antiviral treatment with guanidine. (
  • In 10-day-old mice infected intraperitoneally, EV-D68 causes a neurological disease with weight-loss, paralysis, and mortality. (
  • In our neurological model, guanidine treatment protects mice from weight-loss, paralysis, and mortality. (
  • Further studies on the mutant mice already prove the model to be very powerful. (
  • The usefulness of these mice as translational models is discussed, with focus on their construct and face validity. (
  • In mouse models of myotonic dystrophy, the researchers found that treating newborn mice with a virus carrying the dCas9 enzyme reduced the prevalence of myotonia, prolonged muscle contractions commonly experienced by myotonic dystrophy patients. (
  • Because of underlying differences in the aging of mice and humans, useful mouse models have been difficult to obtain and study. (
  • Performance of the handheld PA system was tested in an animal ischemia model, which revealed that cerebral blood volume (CBV) changes at the cortical surface could be monitored immediately after ischemia induction. (
  • Background Survival with good neurological function post out-of-hospital cardiac arrest (OHCA), defined as cerebral performance category (CPC) 1-2, ranges from 1.6% to 3% in Asia. (
  • Morbidity following SAH are commonly defined in terms of neurological repercussions, including aneurysm rebleeding, intracranial hypertension, cerebral vasospasm, brain edema, cerebral infarction, and hydrocephalus [ 3 ]. (
  • In the present study, we examined the effects of neurological improvement after transient middle cerebral artery occlusion (MCAO) in rats by a novel therapeutic strategy with FGF-2 gene-transferred MSCs by the herpes simplex virus type 1 (HSV-1) vector. (
  • In addition, we demonstrated that drugs known to activate HIF-1 in cultured cells as well as in vivo had neuroprotective properties in this model of cerebral ischemia. (
  • 6 Environmental construct validity Environmental construct validity considers the effects of environmental factors known to confer increased risk for mental illness, and whether these factors are associated with the altered behavioral phenotype in the animal model. (
  • Human disease modeling with iPSCs has enabled researchers to study the disease phenotypes of patient-derived cells directly in the lab. (
  • An international team of scientists, led by University of California San Diego School of Medicine researchers, has created a human stem cell-based model of a rare, but devastating, inherited neurological autoimmune condition called Aicardi-Goutieres Syndrome (AGS). (
  • Deeper probing into the pathogenesis of AGS has been difficult because animal models do not accurately mimic the human version of the disease. (
  • Chapter 1 begins with a brief review of the ethics of animal use in neuro- biological research, inc1uding a discussion of the criteria that may be used to evaluate animal models of human disease and extrapolate from the model to appropriate questions regarding humans. (
  • While they have very different levels of severity, they are both reliable models of the human disease. (
  • This review seeks to discuss the reasons for these difficulties by considering the differences between human and animal cells (including isolation, handling and transplantation) and between the human disease model and the animal disease model. (
  • Here, we see evidence that the zebrafish's central nervous system is suitable for modeling human neurological disease and we review and evaluate natural product research using zebrafish as a vertebrate model platform to systematically identify bioactive natural products. (
  • Mature neuronal and glial cells derived from human pluripotent stem cells have emerged as a physiologically relevant model for the study of neurological development and disease. (
  • Building-associated neurological damage modeled in human cells: a mechanism of neurotoxic effects by exposure to mycotoxins in the indoor environment. (
  • Damage to human neurological system cells resulting from exposure to mycotoxins confirms a previously controversial public health threat for occupants of water-damaged buildings. (
  • Our results demonstrate that this new fucosidosis mouse model resembles the human disease and thus will help to unravel underlying pathological processes. (
  • Due to the close resemblance of the clinical and histological picture of human psoriasis, the new disease-model is ideally suited to study in detail all aspects of pathogenesis. (
  • The Reeler Mouse: A Translational Model of Human Neurological Conditions or Simply a Good Tool for Better Understanding Neurodevelopment? (
  • An effective human cellular model of AD would use the appropriate cell types and ideally neural circuits affected by the disease, would develop relevant pathology and would do so in a reproducible manner over a timescale short enough for practical use. (
  • We review here current progress in applying this approach to generating human models of AD and the potential for such models in the AD field. (
  • The PMFE is an anatomy-based inverse dynamic-static optimisation model aiming to fulfil the requirements for controlling a human-inspired rehabilitation robot via muscle forces. (
  • We believe that the future of brain research will include less reliance on animals, more reliance on human, cell-based models. (
  • To answer important questions about human brain development, animal scientists Rod Johnson and Ryan Dilger have developed a model of the pig brain. (
  • Now, a group of University of Florida Health researchers has found a way to block the transcription of those dysfunctional genetic sequences into RNA, in human cells and mouse models. (
  • Background: Progressive neurological dysfunction is a key aspect of human aging. (
  • We have used gene-expression analysis and polymorphism screening to study molecular senescence of the retina and hippocampus in two rare inbred mouse models of accelerated neurological senescence (SAMP8 and SAMP10) that closely mimic human neurological aging, and in a related normal strain (SAMR1) and an unrelated normal strain (C57BL/6J). (
  • Although kindling is a widely used model, its applicability to human epilepsy is controversial. (
  • However, in both human epilepsy and in some animal models, evidence suggests that a process like that found in kindling does occur. (
  • Further research by Goddard on the characteristics of the kindling phenomenon led to his conclusion that kindling can be used to model human epileptogenesis, learning and memory. (
  • The publication of these results opened a completely new niche for epilepsy research and has stimulated a significant amount of studies on the subject of kindling and its relevance to human epilepsy Kindling (sedative-hypnotic withdrawal) Epileptogenesis Racine Stages (a method by which seizure severity is quantified in animal models of epilepsy) Bertram E (2007). (
  • Since the publication of Reflections on the Dawn of Consciousness , a number of new studies have been published that also show bilateral temporal lobe ('bicameral') activation during auditory hallucinations, providing further support for Jaynes's neurological model specifically and his bicameral mind theory in general. (
  • Beginning in 1999, research began to emerge confirming Julian Jaynes's neurological model for the bicameral mind: fMRI studies showing a right/left temporal lobe interaction during auditory verbal hallucinations. (
  • In my chapter in Reflections on the Dawn of Consciousness , "Consciousness, Hallucinations, and the Bicameral Mind: Three Decades of New Research," I discuss a number of neuroimaging studies that emerged over the past decade that provide support for Jaynes's neurological model. (
  • While it certainly does not 'prove' Jaynes's theory, research supportive of his neurological model is important evidence. (
  • Among the mouse models of FRDA, the liver conditional mouse model pointed to a tumor suppressor activity of frataxin leading to the hypothesis that individuals with FRDA might be predisposed to cancer. (
  • These findings suggest an active inflammation in neurofibromas and partly explain why mast cell removal alone is not sufficient to relieve tumor burden in this experimental neurofibroma model. (
  • Neuroscience applicants using invertebrate model systems have successfully competed for NINDS grant funding in peer review in recent years. (
  • Indeed, the NIH BRAIN Initiative supports the use of invertebrate model systems in research to understand neural functions and recognizes that this is an important part of the neuroscience ecosystem. (
  • When Jaynes’s neurological model for the bicameral mind was first proposed, both he and his critics conceded that it would be decades before progress in neuroscience could validate or disprove it. (
  • The landmark publication Neurological, Psychiatric and Developmental Disorder: Meeting the Needs in the Developing World 1 was an early driver of the growth of global mental health as a discipline. (
  • We performed a pilot study using heterogeneous ataxias as a model neurogenetic disorder to assess the introduction of next-generation sequencing into clinical practice. (
  • As they analyzed the correlation of 663 neuronal phenotypes with genotypic data from 243 patients and 214 controls - and examined research practices and reporting bias in neurological disease models - they found that there is no established standard for the reporting of methods nor a defined minimal number of cell lines. (
  • Our phenogenetic map can be used to build new hypotheses in the field of neurological disease modeling, and to identify potential new opportunities to design novel drug strategies," said first author Ethan W. Hollingsworth, a neural stem cell research assistant at Ohio State's Wexner Medical Center and a hematology/oncology clinical research intern at Nationwide Children's Hospital. (
  • NINDS' mission is impartial to the model system employed, but is advanced by the neuroscientific impact of each research project. (
  • Within the biomedical research community, there is little doubt about the utility of such models. (
  • The long-term objective of our research is to find out how some rehabilitative drugs work by devising a model of the fundamental workings of an addict's brain," said Mohan, who will attend Washington University in St. Louis for his postdoctoral fellowship. (
  • We've created a model that tests the ability to do sensory integration, which should be extremely useful for pharmaceutical research . (
  • Here, we report a systematic analysis of research practices and reporting bias in neurological disease models from 93 published articles. (
  • This booklet contains a comprehensive suite of solutions to support your research using neurological mouse models. (
  • To assess whether gait analysis is applicable to assess improvements by neuroprotective compounds, we applied a model calculation and approached common statistical problems. (
  • In contemporary biomedicine, the growing need to develop experimental models to obtain a detailed understanding of malady conditions and to portray pioneering treatments has resulted in the application of zebrafish to close the gap between in vitro and in vivo assays. (
  • Dong Ys, Wang Jl, Feng Dy, Qin Hz, Wen H, Yin Zm, Gao Gd, Li C. Protective Effect of Quercetin against Oxidative Stress and Brain Edema in an Experimental Rat Model of Subarachnoid Hemorrhage. (
  • Kindling: An experimental model of epilepsy" (PDF). (
  • Our models enable fine stratification into phenotypes enabling more focussed analysis to identify subgroups that respond to putative treatments. (
  • The researchers found that with TREX1 not functioning normally, all of the cell models displayed excess extra-chromosomal DNA and that a major source of the excess DNA came from LINE1 (L1) retroelements. (
  • The first thing to understand is the scale of the problem that researchers face when trying to dissect the processes that lead to neurodegeneration and neurological disease. (
  • have been shown to promote remyelination in mouse models of demyelination by promoting proliferation or differentiation of oligodendrocyte progenitor cells (OPCs) directly or indirectly. (
  • The models offer innovation potential by underpinning support systems for clinical and drug-development applications. (
  • Efficacy studies performed by JAX® In Vivo Services for ALS typically feature clinical observations, body weights, progressive neurological scoring, electrophysiological assessment of motor neuropathy, survival, tissue/blood collection and histological assessment of neuromuscular junctions and femoral nerves. (
  • We strongly believe that this model will be highly suitable for future pre-clinical studies ultimately aimed at understanding and curing this widespread disease. (
  • Overall, these data suggest that in hamsters hE16 can ameliorate neurological disease after significant viral replication has occurred, although there is a time window that limits therapeutic efficacy. (
  • The findings suggest that the early administration of optimal dose of quercetin may ameliorate brain damage and provide neuroprotection in the SAH model, potentially by enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation. (
  • Results suggest that CMT2D can be modeled in fly, that the toxicity of the mutant protein is tissue autonomous, and that mutations in CARS and YARS have similar effects in Drosophila, hinting at a shared mechanism. (
  • There are two murine models of CMT2D with different mutations in the Cars gene. (
  • Many neurological conditions are caused by immensely heterogeneous gene mutations. (
  • This study aims to characterize the neurological basis of obesity and response to surgical and medical treatment by inducing adult pluripotent stem cells into neuronal cells from subjects that have demonstrated extreme response to bariatric surgery or pharmacological treatment for obesity. (
  • This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. (
  • We aim to study the influence of comorbidities and peri-OHCA event factors on neurological recovery and develop a model that can help clinicians predict neurological function among patients with post-OHCA admitted to the hospital. (
  • An interactive graphics-based model of the lower extremity to study orthopaedic surgical procedures. (
  • Latent class modeling of US Food and Drug Administration Adverse Event Reporting System (FAERS) data was performed using indicators defined by the Medical Dictionary for Regulatory Activities neurologic and psychiatric high-level group terms, in a study dataset of FAERS reports ( n = 5332) of reactions to common antimalarial drugs. (
  • We will use the information obtained from this study information to develop a biopsychosocial prospective surveillance model, a method for early detection, intervention, and moderation of shoulder pain. (
  • Transcription profiling of hippocampus and retina from two rare inbred mouse models of accelerated neurological senescence ( SAMP8 and SAMP10) and a related wild type strain SAMR1 to study molecular senescence of the retina and hippocampus. (
  • In these models, mitochondrial electron transport chain complex I activity is reduced but results in distinct patterns of neuronal pathology. (
  • Thus far, comparison of these studies suggests that rapamycin treatment has both overlapping and distinct effects that contribute to attenuation of neural pathology of NDUFS4 and MPTP mouse models. (
  • This webinar provides an overview of the features and applications of induced pluripotent stem cells with respect to neurological disease modeling. (
  • Modeling Neurological Disease with iPS Cells? (
  • Disease modeling with induced pluripotent stem cells (i PSC s) is creating an abundance of phenotypic information that has become difficult to follow and interpret. (
  • Thus, undifferentiated high-passage SH-SY5Y cells could be a good noradrenergic model for in vivo studies. (
  • These cells take up DA and NE more efficiently than undifferentiated cells suggesting they could be used either as partial noradrenergic or dopaminergic models. (
  • Another common model, MN9D cells, store high levels of DA under normal growth conditions, but do not convert it to NE. (
  • They show poor catecholamine uptake characteristics compared to SH-SY5Y cells, however n-butyric acid differentiated MN9D cells show more efficient DA uptake similar to undifferentiated SH-SY5Y, suggesting that they could be used as a reasonable dopaminergic model. (
  • During the past ten years, the development of mouse models of FRDA has allowed better understanding of the pathophysiology of the disease. (
  • In addition to existing mouse models, several major programmes have been set up to generate new mouse models of disease. (