rudyvdbrink/CitationDatabase huggingface dataset:
Astrocytic Expression of CTMP Following an Excitotoxic Lesion in the Mouse Hippocampus.
Experimental neurobiology, 2017

Akt (also known as protein kinase B, PKB) has been seen to play a role in astrocyte activation of neuroprotection; however, the underlying mechanism on deregulation of Akt signaling in brain injuries is not fully understood. We investigated the role of carboxy-terminal modulator protein (CTMP), an endogenous Akt inhibitor, in brain injury following kainic acid (KA)-induced neurodegeneration of mouse hippocampus. In control mice, there was a weak signal for CTMP in the hippocampus, but CTMP was markedly increased in the astrocytes 3 days after KA treatment. To further investigate the effectiveness of Akt signaling, the phosphorylation of CTMP was examined. KA treatment induced an increased p-CTMP expression in the astrocytes of hippocampus at 1 day. LPS/IFN-γ-treatment on primary astrocytes promoted the p-CTMP was followed by phosphorylation of Akt and finally upregulation of CTMP and p-CREB. Time-dependent expression of p-CTMP, p-Akt, p-CREB, and CTMP indicate that LPS/IFN-γ-induced phosphorylation of CTMP can activate Akt/CREB signaling, whereas lately emerging enhancement of CTMP can inhibit it. These results suggest that elevation of CTMP in the astrocytes may suppress Akt activity and ultimately negatively affect the outcome of astrocyte activation (astroglisiois). Early time point enhancers of phosphorylation of CTMP and/or late time inhibitors specifically targeting CTMP may be beneficial in astrocyte activation for neuroprotection within treatment in neuroinflammatory conditions.
Individual factors influencing the duration of untreated psychosis.
Early intervention in psychiatry, 2019

Duration of untreated psychosis (DUP), or the time between onset of psychosis and treatment initiation, is a prognostic factor of schizophrenia. However, few studies evaluated the relative influence of individual-related factors on this duration. The objective of this study was to evaluate the influence of socio-demographic, clinical and cannabis use on DUP.
Dopamine D₂ and acetylcholine α7 nicotinic receptors have subcellular distributions favoring mediation of convergent signaling in the mouse ventral tegmental area.
Neuroscience, 2013

Alpha7 nicotinic acetylcholine receptors (α7nAChRs) mediate nicotine-induced burst-firing of dopamine neurons in the ventral tegmental area (VTA), a limbic brain region critically involved in reward and in dopamine D2 receptor (D2R)-related cortical dysfunctions associated with psychosis. The known presence of α7nAChRs and Gi-coupled D2Rs in dopamine neurons of the VTA suggests that these receptors are targeted to at least some of the same neurons in this brain region. To test this hypothesis, we used electron microscopic immunolabeling of antisera against peptide sequences of α7nACh and D2 receptors in the mouse VTA. Dual D2R and α7nAChR labeling was seen in many of the same somata (co-localization over 97%) and dendrites (co-localization over 49%), where immunoreactivity for each of the receptors was localized to endomembranes as well as to non-synaptic or synaptic plasma membranes often near excitatory-type synapses. In comparison with somata and dendrites, many more small axons and axon terminals were separately labeled for each of the receptors. Thus, single-labeled axon terminals were predominant for both α7nAChR (57.9%) and D2R (89.0%). The majority of the immunolabeled axonal profiles contained D2R-immunoreactivity (81.6%) and formed either symmetric or asymmetric synapses consistent with involvement in the release of both inhibitory and excitatory transmitters. Of 160 D2R-labeled terminals, 81.2% were presynaptic to dendrites that expressed α7nAChR alone or together with the D2R. Numerous glial processes inclusive of those enveloping either excitatory- or inhibitory-type synapses also contained single labeling for D2R (n=152) and α7nAChR (n=561). These results suggest that classic antipsychotic drugs, all of which block the D2R, may facilitate α7nAChR-mediated burst-firing by elimination of D2R-dependent inhibition in neurons expressing both receptors as well as by indirect pre-synaptic and glial mechanisms.
Inhibition of ubiquitin proteasome system rescues the defective sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA1) protein causing Chianina cattle pseudomyotonia.
The Journal of biological chemistry, 2014

A missense mutation in ATP2A1 gene, encoding sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA1) protein, causes Chianina cattle congenital pseudomyotonia, an exercise-induced impairment of muscle relaxation. Skeletal muscles of affected cattle are characterized by a selective reduction of SERCA1 in sarcoplasmic reticulum membranes. In this study, we provide evidence that the ubiquitin proteasome system is involved in the reduced density of mutated SERCA1. The treatment with MG132, an inhibitor of ubiquitin proteasome system, rescues the expression level and membrane localization of the SERCA1 mutant in a heterologous cellular model. Cells co-transfected with the Ca(2+)-sensitive probe aequorin show that the rescued SERCA1 mutant exhibits the same ability of wild type to maintain Ca(2+) homeostasis within cells. These data have been confirmed by those obtained ex vivo on adult skeletal muscle fibers from a biopsy from a pseudomyotonia-affected subject. Our data show that the mutation generates a protein most likely corrupted in proper folding but not in catalytic activity. Rescue of mutated SERCA1 to sarcoplasmic reticulum membrane can re-establish resting cytosolic Ca(2+) concentration and prevent the appearance of pathological signs of cattle pseudomyotonia.
Behavioral Neuroscience: Who's Afraid of the C57BL/6 Mouse?
Current biology : CB, 2016

Behavioral paradigms in which laboratory rodents express behaviors that their wild counterparts presumably need every day are rare: a novel prey-capture model for laboratory mice has been developed for examining the neurophysiological underpinnings of prey capture in mice.
Identification of gene regions regulating inflammatory microglial response in the rat CNS after nerve injury.
Journal of neuroimmunology, 2009

Local CNS inflammation takes place in many neurological disorders and is important for autoimmune neuroinflammation. Microglial activation is strain-dependent in rats and differential MHC class II expression is influenced by variations in the Mhc2ta gene. Despite sharing Mhc2ta and MHC class II alleles, BN and LEW.1N rats differ in MHC class II expression after ventral root avulsion (VRA). We studied MHC class II expression and glial activation markers in BN rats after VRA. Our results demonstrate that MHC class II expression originates from a subpopulation of IBA1(+), ED1(-), and ED2(-) microglia. We subsequently performed a genome-wide linkage scan in an F2(BNxLEW.1N) population, to investigate gene regions regulating this inflammatory response. Alongside MHC class II, we studied the expression of MHC class I, co-stimulatory molecules, complement components, microglial markers and Il1b. MHC class II and other transcripts were commonly regulated by gene regions on chromosomes 1 and 7. Furthermore, a common region on chromosome 10 regulated expression of complement and co-stimulatory molecules, while a region on chromosome 11 regulated MHC class I. We also detected epistatic interactions in the regulation of the inflammatory process. These results reveal the complex regulation of CNS inflammation by several gene regions, which may have relevance for disease.
Longitudinal brain MRI study in a mouse model of Rett Syndrome and the effects of choline.
Neurobiology of disease, 2008

Rett Syndrome (RTT), the second most common cause of mental retardation in girls, is associated with mutations of an X-linked gene encoding the transcriptional repressor protein MeCP2. Mecp2(1lox) mutant mice express no functional MeCP2 protein and exhibit behavioral abnormalities similar to those seen in RTT patients. Here we monitor the development of both whole brain and regional volumes between 21 and 42 days of age in this model of RTT using MRI. We see decreases in whole brain volumes in both male and female mutant mice. Cerebellar and ventricular volumes are also decreased in RTT males. Previous work has suggested that perinatal choline supplementation alleviates some of the behavioral deficits in both male and female Mecp2(1lox) mutant mice. Here we show that perinatal choline supplementation also positively affects whole brain volume in heterozygous females, and cerebellar volume in male RTT mice.
Impact of Patient and Family Involvement in Long-Term Outcomes.
Critical care nursing clinics of North America, 2020

Surviving a critical illness can have long-term effects on both patients and families. These effects can be physical, emotional, cognitive, and social, and they affect both the patient and the family. Family members play a key role in helping their loved one recover, and this recovery process can take considerable time. Transferring out of an intensive care unit, and discharging home from a hospital, are important milestones, but they represent only the beginning of recovery and healing after a critical illness. Recognizing that these challenges exist both for patients and families is important to improve critical illness outcomes.
Nineteen-year follow-up of Waldenström's-associated neuropathy and Bing-Neel syndrome.
Muscle & nerve, 2009

We describe the follow-up of a patient with Waldenström's macroglobulinemia who developed mild predominantly sensory peripheral neuropathy, Bing-Neel syndrome, and, after 17 years, acute mononeuropathy multiplex associated with increasing paraprotein levels. Nerve biopsy demonstrated deposition of IgM in the endoneurium and perineurium. Magnetic resonance imaging showed extension of the cerebral white-matter abnormality. We suggest that the pathogenetic mechanism of the mononeuropathy multiplex may include direct IgM deposition. Late peripheral nerve complications appeared to be related to the paraprotein level.
Acetylated α-Tubulin Regulated by N-Acetyl-Seryl-Aspartyl-Lysyl-Proline(Ac-SDKP) Exerts the Anti-fibrotic Effect in Rat Lung Fibrosis Induced by Silica.
Scientific reports, 2016

Silicosis is the most serious occupational disease in China. The objective of this study was to screen various proteins related to mechanisms of the pathogenesis of silicosis underlying the anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) using proteomic profile analysis. We also aimed to explore a potential mechanism of acetylated α-tubulin (α-Ac-Tub) regulation by Ac-SDKP. Two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF/TOF MS) were used to assess the different protein expression profiles between control and silicosis rats treated with or without Ac-SDKP. Twenty-nine proteins were identified to be potentially involved in the progression of silicosis and the anti-fibrotic effect of Ac-SDKP. Our current study finds that 1) the lost expression of Ac-Tub-α may be a new mechanism in rat silicosis; 2) treatment of silicotic rats with N-acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits myofibroblast differentiation and collagen deposition accompanied by stabilizing the expression of α-Ac-Tub in vivo and in vitro, which is related with deacetylase family member 6 (HDAC6) and α-tubulin acetyl transferase (α-TAT1). Our data suggest that α-Ac-Tub regulation by Ac-SDKP may potentially be a new anti-fibrosis mechanism.
Biomarker for Ischemic Stroke Using Metabolome: A Clinician Perspective.
Journal of stroke, 2019

Finding ischemic stroke biomarker is highly desirable because it can improve diagnosis even before a patient arrives to the hospital. Metabolome is one of new technologies that help to find biomarkers. Most metabolome-related ischemic stroke studies were done in Asia and had exploratory designs. Although failed to find specific biomarkers, they discovered several important metabolite-stroke associations which belong to three pathophysiological mechanisms: Excitotoxicity with activation of glutamate, resulting in the increase of glutamate derivatives proline and pyroglutamate; Oxidative stress with production of free radicals and perturbed concentrations of uric acid, matrix metalloproteinase-9, branch-chained amino acids, sphingolipids, homocysteine, asymmetric dimethylarginine, nitric oxide and folate cycle metabolites; and Stroke mediated inflammation, affecting phospholipid metabolism with perturbed levels of lysophosphatidylethanolamine and lysophosphatidylcholine. The discovered metabolite-stroke associations need further evaluation in prospective, high-quality studies with patients matched for age, risk factors, and medications.
Bone morphogenetic protein 4 stimulates attachment of neurospheres and astrogenesis of neural stem cells in neurospheres via phosphatidylinositol 3 kinase-mediated upregulation of N-cadherin.
Neuroscience, 2010

The neurosphere culture system is useful for expanding neural stem cells (NSCs) without affecting self-renewal potential and multipotency. However, the extrinsic signals that affect the formation or dissociation of neurospheres are poorly understood. Here, we found that bone morphogenetic protein 4 (BMP4) induced the attachment of neurospheres, astrocytic differentiation, and migration of neurosphere NSCs. These outcomes were accompanied by Akt activation and upregulation of the adhesion molecule, N-cadherin. A phosphatidylinositol 3 kinase (PI3 kinase) inhibitor (LY294002) blocked attachment of neurosphere, astrocytic differentiation, migration, and N-cadherin upregulation of neurosphre NSCs. The PI3 kinase-Akt pathway appeared to selectively mediate the effects of BMP4, as neurosphere attachment was unaffected by MEK inhibitors (PD98059 and U0126). Importantly, a neutralizing N-cadherin antibody inhibited BMP4-induced neurosphere attachment, astrocytic differentiation, and migration of neurosphere NSCs. Together, these findings show that BMP4-induced attachment of neurospheres is related to the astrocytic differentiation of these cells and that these effects are attributable, at least in part, to PI3 kinase-Akt pathway-dependent induction of N-cadherin.
Evoked potentials recorded during routine EEG predict outcome after perinatal asphyxia.
Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology, 2017

To evaluate the added value of somatosensory (SEPs) and visual evoked potentials (VEPs) recorded simultaneously with routine EEG in early outcome prediction of newborns with hypoxic-ischemic encephalopathy under modern intensive care.
Perturbation of male sexual behavior in mice (Mus musculus) within a discrete range of perinatal bisphenol-A doses in the context of a high- or low-phytoestrogen diet.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013

Differentiation of masculine and feminine behavior in mammals depends on perinatal sex steroids. As bisphenol-A (BPA) can be estrogenic and anti-androgenic, we examined impacts of perinatal exposure upon adult sexual behavior and morphology of male mice. In Experiment 1, dams were fed either a high- or low-phytoestrogen diet and received daily oral doses of 0, 0.175, 1.75, or 17.5μg BPA from gestation day 10 through post-partum day 9. Male offspring from the high-phytoestrogen plus 17.5μg BPA condition showed reduced mass of vesicular-coagulating but not other male glands, and showed increased latency to insemination when paired with females. In Experiment 2, these procedures were replicated but with all animals fed the high-phytoestrogen diet and perinatal BPA doses of 0, 17.5, 175, or 1750μg/day. Adult masses of testes and male-accessory glands and levels of urinary steroids were not significantly affected. When males each encountered a sexually receptive female, there were fewer intromissions among those given 17.5 or 175μg and fewer ejaculations among those given 17.5μg, but the 1750μg dose had no effect. Perinatal BPA dosages thus influenced male sexual behavior non-monotonically, with impairment evident in a discrete dose range among males on a high-phytoestrogen diet.
Assessing apathy in everyday clinical practice with the short-form Lille Apathy Rating Scale.
Movement disorders : official journal of the Movement Disorder Society, 2013

Apathy is an invalidating behavioral disorder that must always be screened for and assessed in patients with Parkinson's disease (PD). The Lille Apathy Rating Scale (LARS) has been validated in several different contexts, but the lengthy administration time means that it is mostly recommended for research use. The aim of the present study was to validate a short form of the LARS for use in everyday practice.
Wi-Fi (2.4 GHz) affects anti-oxidant capacity, DNA repair genes expression and, apoptosis in pregnant mouse placenta.
Iranian journal of basic medical sciences, 2020

The placenta provides nutrients and oxygen to embryo and removes waste products from embryo's blood. As far as we know, the effects of exposure to Wi-Fi (2.4 GHz) signals on placenta have not been evaluated. Hence, we examined the effect of prenatal exposure to Wi-Fi signals on anti-oxidant capacity, expressions of CDKNA1, and GADD45a as well as apoptosis in placenta and pregnancy outcome.
Striatal sensitivity to reward deliveries and omissions in substance dependent patients.
NeuroImage, 2008

Some motivational theories of substance dependence (SD) posit either pathologically increased or decreased ventral striatum (VS) recruitment by cues for nondrug rewards. The incentive-sensitization hypothesis, alternatively, attributes SD to enhanced incentive salience of drug-predictive cues specifically, with no requirement for altered nondrug incentive processing. We assessed whether individuals undergoing inpatient therapy for SD are characterized by altered recruitment of mesolimbic incentive neurocircuitry by cues and deliveries of nondrug rewards. During functional magnetic resonance imaging, substance-dependent patients (SDP) and controls performed a modified monetary incentive delay task featuring: a) anticipatory cues that signaled opportunities to respond to a target to either win money or avoid losing money, b) notifications of wins and losses, and c) unexpected replacement of reward trial outcomes with a demand to repeat the trial. Both anticipatory reward cues and loss cues elicited similar mood responses and VS activation between SDP and controls. However, in SDP (but not controls), reward notifications also activated VS and mesial frontal cortex, and loss notifications activated anterior insula. Finally, substitution of expected outcomes in reward trials with notifications to repeat the trial deactivated the VS in SDP but not in controls. These data do not suggest that SD is characterized by altered recruitment of VS circuitry by cues for nondrug incentives. Rather, SDP may instead have increased limbic system sensitivity to reward and loss delivery, consistent with the role of impulsivity in SD.
Intra-parenchymal ferrous iron infusion causes neuronal atrophy, cell death and progressive tissue loss: implications for intracerebral hemorrhage.
Experimental neurology, 2012

Intracerebral hemorrhage (ICH) is a devastating stroke causing considerable tissue destruction from mechanical trauma and secondary degeneration. Free iron, released over days from degrading erythrocytes, causes free radicals that likely contribute to delayed injury. Indeed, an intracerebral injection of iron rapidly kills cells and causes cerebral edema. We expanded upon these observations by: determining a dose-response relationship of iron infusion, examining the structural appearance of surviving striatal neurons, and evaluating injury over months. First, we measured 24-h edema in rats given 3.8, 19.0 or 38.0 μg infusions of FeCl₂ (i.e., 30 μL of a 1, 5 or 10 mmol/L solution). Second, rats were given these infusions (vs. saline controls) followed by behavioral assessment and histology at 7 days. Third, dendritic structure was measured in Golgi-Cox stained neurons at 7 days after a 0.95-μg dose (30 μL of a 0.25 mmol/L solution). Last, rats survived 7 or 60 days post-injection (19.0 μg) for histological assessment. Larger doses of iron caused greater injury, but this was generally not reflected in behavior that indicated similar deficits among the 3.8-38.0 μg groups. Similarly, edema occurred but was not linearly related to dose. Even after a low iron dose the surviving neurons in the peri-injury zone were considerably atrophied (vs. contralateral side and controls). Finally, continuing tissue loss occurred over weeks with prominent neuronal death and iron-positive cells (e.g., macrophages) at 60 days. Iron alone may account for the chronic degeneration found after ICH in rodent models.
Rethinking Extinction.
Neuron, 2015

Extinction serves as the leading theoretical framework and experimental model to describe how learned behaviors diminish through absence of anticipated reinforcement. In the past decade, extinction has moved beyond the realm of associative learning theory and behavioral experimentation in animals and has become a topic of considerable interest in the neuroscience of learning, memory, and emotion. Here, we review research and theories of extinction, both as a learning process and as a behavioral technique, and consider whether traditional understandings warrant a re-examination. We discuss the neurobiology, cognitive factors, and major computational theories, and revisit the predominant view that extinction results in new learning that interferes with expression of the original memory. Additionally, we reconsider the limitations of extinction as a technique to prevent the relapse of maladaptive behavior and discuss novel approaches, informed by contemporary theoretical advances, that augment traditional extinction methods to target and potentially alter maladaptive memories.
Shame-proneness in attempted suicide patients.
BMC psychiatry, 2012

It has been suggested that shame may be an important feature in suicidal behaviors. The disposition to react with shame, "shame-proneness", has previously not been investigated in groups of attempted suicide patients. We examined shame-proneness in two groups of attempted suicide patients, one group of non-suicidal patients and one group of healthy controls. We hypothesized that the attempted suicide patients would be more shame-prone than non-suicidal patients and healthy controls.
Testing the disgust conditioning theory of food-avoidance in adolescents with recent onset anorexia nervosa.
Behaviour research and therapy, 2015

Anorexia nervosa is characterized by chronic food avoidance that is resistant to change. Disgust conditioning offers one potential unexplored mechanism for explaining this behavioral disturbance because of its specific role in facilitating food avoidance in adaptive situations. A food based reversal learning paradigm was used to study response flexibility in 14 adolescent females with restricting subtype anorexia nervosa (AN-R) and 15 healthy control (HC) participants. Expectancy ratings were coded as a behavioral measure of flexibility and electromyography recordings from the levator labii (disgust), zygomaticus major (pleasure), and corrugator (general negative affect) provided psychophysiological measures of emotion. Response inflexibility was higher for participants with AN-R, as evidenced by lower extinction and updated expectancy ratings during reversal. EMG responses to food stimuli were predictive of both extinction and new learning. Among AN-R patients, disgust specific responses to food were associated with impaired extinction, as were elevated pleasure responses to the cued absence of food. Disgust conditioning appears to influence food learning in acutely ill patients with AN-R and may be maintained by counter-regulatory acquisition of a pleasure response to food avoidance and an aversive response to food presence. Developing strategies to target disgust may improve existing interventions for patients with AN.