rudyvdbrink/CitationDatabase huggingface dataset:
Stop testing for autoantibodies to the VGKC-complex: only request LGI1 and CASPR2.
Practical neurology, 2020

Autoantibodies to leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein like-2 (CASPR2) are associated with clinically distinctive syndromes that are highly immunotherapy responsive, such as limbic encephalitis, faciobrachial dystonic seizures, Morvan's syndrome and neuromyotonia. These autoantibodies target surface-exposed domains of LGI1 or CASPR2, and appear to be directly pathogenic. In contrast, voltage-gated potassium channel (VGKC) antibodies that lack LGI1 or CASPR2 reactivities ('double-negative') are common in healthy controls and have no consistent associations with distinct syndromes. These antibodies target intracellular epitopes and lack pathogenic potential. Moreover, the clinically important LGI1 and CASPR2 antibodies comprise only ~15% of VGKC-positive results, meaning that most VGKC-antibody positive results mislead rather than help. Further, initial VGKC testing misses some cases that have LGI1 and CASPR2 antibodies. These collective observations confirm that laboratories should stop testing for VGKC antibodies and instead, test only for LGI1 and CASPR2 antibodies. This change in practice will lead to significant patient benefit.
High Sensitivity In Vivo Imaging of Cancer Metastasis Using a Near-Infrared Luciferin Analogue seMpai.
International journal of molecular sciences, 2020

Bioluminescence imaging (BLI) is useful to monitor cell movement and gene expression in live animals. However, D-luciferin has a short wavelength (560 nm) which is absorbed by tissues and the use of near-infrared (NIR) luciferin analogues enable high sensitivity in vivo BLI. The AkaLumine-AkaLuc BLI system (Aka-BLI) can detect resolution at the single-cell level; however, it has a clear hepatic background signal. Here, to enable the highly sensitive detection of bioluminescence from the surrounding liver tissues, we focused on seMpai (C
Serum Amyloid A is Expressed in the Brain After Traumatic Brain Injury in a Sex-Dependent Manner.
Cellular and molecular neurobiology, 2020

Serum amyloid A (SAA) is an acute phase protein upregulated in the liver after traumatic brain injury (TBI). So far, it has not been investigated whether SAA expression also occurs in the brain in response to TBI. For this, we performed a moderate controlled cortical impact injury in adult male and female mice and analyzed brain, blood, and liver samples at 6 h, 1, 3, and 10 days post-injury (dpi). We measured the levels of SAA in serum, brain and liver by western blot. We also used immunohistochemical techniques combined with in situ hybridization to determine SAA mRNA and protein expression in the brain. Our results revealed higher levels of SAA in the bloodstream in males compared to females at 6 h post-TBI. Liver and serum SAA protein showed a peak of expression at 1 dpi followed by a decrease at 3 to 10 dpi in both sexes. Both SAA mRNA and protein expression colocalize with astrocytes and macrophages/microglia in the cortex, corpus callosum, thalamus, and hippocampus after TBI. For the first time, here we show that SAA is expressed in the brain in response to TBI. Collectively, SAA expression was higher in males compared to females, and in association with the sex-dependent neuroinflammatory response after brain injury. We suggest that SAA could be a crucial protein associated to the acute neuroinflammation following TBI, not only for its hepatic upregulation but also for its expression in the injured brain.
Neonatal opioid exposure: public health crisis and novel neuroinflammatory disease.
Neural regeneration research, 2021

Substance use, specifically the use of prescription and non-prescription opioids among pregnant women, is a major public health issue and chief contributor to the opioid crisis. The prevalence of Neonatal Opioid Withdrawal Syndrome has risen 5-fold in the past decade, and is a well-recognized consequence of perinatal opioid exposure. By contrast, the long-term damage to the developing brain from opioid medications is just beginning to be recognized as a serious concern. Published data suggest that opioid exposure commencing in utero negatively affects the maturation of the neural-immune system, and trajectory of central nervous system development. Methadone induces peripheral immune hyper-reactivity, lasting structural and microstructural brain injury, and significant deficits in executive function and cognitive control in adult animals following in utero exposure. Thus, to address the cascading public health crisis stemming from the multitude of infants with in utero opioid exposure who will grow up with altered neurodevelopmental trajectories, rigorous preclinical, mechanistic studies are required. Such studies will define the long-term sequelae of prenatal opioid exposure in an effort to develop appropriate and targeted interventions. Specifically, the development of novel fluid, neuroimaging and biobehavioral biomarkers will be the most useful to aid in early identification and treatment of opioid exposed infants with the greatest risk of poor clinical outcomes. These studies will be essential to understand how in utero insults determine brain structure and function in adulthood, and what targeted interventions will be required to improve long-term outcomes in the countless children being born exposed to opioids each year.
Romantic Partner Alcohol Misuse Interacts with 
Journal of contemporary criminal justice, 2019

Previous research has identified the importance of romantic partners-including spouses, significant others, and dating partners-for influencing the engagement in health-risking behaviors, such as alcohol misuse during emerging adulthood. Although genetic factors are known to play a role in the development of young adult alcohol misuse, little research has examined whether genetic factors affect young adults' susceptibility to their romantic partners' alcohol misusing behaviors. The current study tests whether a single nucleotide polymorphism in the
Quantitative differences in neuronal subpopulations between mouse and human dorsal root ganglia demonstrated with RNAscope in situ hybridization.
Pain, 2020

Next-generation transcriptomics in combination with imaging-based approaches have emerged as powerful tools for the characterization of dorsal root ganglion (DRG) neuronal subpopulations. The mouse DRG has been well characterized by many independently conducted studies with convergent findings, but few studies have directly compared expression of population markers between mouse and human. This is important because of our increasing reliance on the mouse as a preclinical model for translational studies. Although calcitonin gene-related peptide (CGRP) and P2X purinergic ion channel type 3 receptor (P2X3R) have been used to define peptidergic and nonpeptidergic nociceptor subpopulations, respectively, in mouse DRG, these populations may be different in other species. To directly test this, as well as a host of other markers, we used multiplex RNAscope in situ hybridization to elucidate the distribution of a multitude of unique and classic neuronal mRNAs in peptidergic (CGRP-expressing) and nonpeptidergic (P2X3R-expressing) nociceptor subpopulations in mouse and human DRG. We found a large overlapping CGRP and P2X3R neuronal subpopulation in human, lumbar DRG that was not present in mouse. We also found differential expression in a variety of mRNAs for transient receptor potential channels, cholinergic receptors, potassium channels, sodium channels, and other markers/targets. These data offer insights into the spatial and functional organization of neuronal cell subpopulations in the rodent and human DRG and support the idea that sensory system organizational principles are likely different between both species.
The R-line: A New Imaging Index for Decision Making Regarding C2 Lamina Decompression in Cervical Ossification of the Posterior Longitudinal Ligament.
Korean journal of neurotrauma, 2020

The optimal treatment modality for cervical ossification of the posterior longitudinal ligament (OPLL) including the C2 level remains controversial. Cervical laminoplasty is a widely accepted considering of advantages such as development of few postoperative complications, including kyphosis or neck pain. We encountered seven patients with postoperative disabilities resulting from incomplete decompression after undercutting of the C2 lamina. Based on this experience, we developed a new index to determine the degree of decompression in cervical OPLL-the rostral line (R-line).
Plasma membrane localization of the GFL receptor components: a nexus for receptor crosstalk.
Cell and tissue research, 2020

The glial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs) comprise a group of four homologous and potent growth factors that includes GDNF, neurturin (NRTN), artemin (ARTN), and persephin (PSPN). The survival, growth, and mitotic activities of the GFLs are conveyed by a single receptor tyrosine kinase, Ret. The GFLs do not bind directly to Ret in order to activate it, and instead bind with high affinity to glycerophosphatidylinositol (GPI)-anchored coreceptors called the GDNF family receptor-αs (GFRαs). Several mechanisms have recently been identified that influence the trafficking of Ret and GFRαs in and out of the plasma membrane, thereby affecting their availability for ligand binding, as well as their levels by targeting to degradative pathways. This review describes these mechanisms and their powerful effects on GFL signaling and function. We also describe the recent discovery that p75 and Ret form a signaling complex, also regulated by plasma membrane shuttling, that either enhances GFL survival signals or p75 pro-apoptotic signals, dependent on the cellular context.
Inter and intra-generational phenotypic variability in a Portuguese family with DYT-GCH1.
Parkinsonism & related disorders, 2021

DYT-GCH1 is the most common form of Dopa-responsive dystonia. We analysed a three-generation Portuguese family with the same variant of DYT-GCH1. Dystonia and parkinsonism were found, along with non-motor symptoms. There was a wide array of phenotypic manifestations. Further studies are needed to explain the wide clinical expression of this entity.
The Child & Youth CompreHensIve Longitudinal Database for Deep Brain Stimulation (CHILD-DBS).
Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2021

Deep brain stimulation (DBS) is a common tool for the treatment of movement disorders in adults; however, it remains an emerging treatment modality in children with a growing number of indications, including epilepsy and dystonia. The Child & Youth CompreHensIve Longitudinal Database of DBS (CHILD-DBS) study aims to prospectively collect relevant data on quality of life (QoL), safety, efficacy, and long-term neurodevelopmental outcomes following DBS in children.
Elucidating risk mechanisms of gene-environment interactions on pediatric anxiety: integrating findings from neuroscience.
European archives of psychiatry and clinical neuroscience, 2008

Recent findings of gene-environment interaction on child and adolescent anxiety generate interest in mechanisms through which genetic risks are expressed. Current findings from neuroscience suggest avenues for exploring putative mechanisms. Specifically recent documentations of abnormality in brain function among anxious adolescents may reflect the end-result of gene expression. In turn these inherited predispositions may increase the likelihood of psychopathology in the presence of stress. The aim of the current article is to consider putative mechanisms reflecting genetic sensitivity to the environment (G x E). Thus we review data implicating biased processing of threat information and anomalies in brain circuitry in the expression of pediatric anxiety. These data suggest that links across development among genes, brain, psychological processes, and behavior are far from established. Accordingly, the article proposes strategies for examining these links. Exploring these relationships during development is crucial, given that these early life processes may potentially shape longer-term patterns of emotional behavior, and therefore life-long trajectories of anxiety.
Complement protein 6 deficiency in PVG/c rats does not lead to neuroprotection against seizure induced cell death.
Neuroscience, 2011

Since the membrane attack complex (MAC), an end product of the activated complement cascade, has been shown to play a role in neurodegeneration, we investigated to which extent MAC contributes to structural reorganization, neuronal cell death, and seizure development in two rat models for temporal lobe epilepsy. We used the electrically-induced status epilepticus (SE) model and the kindling model in C6-deficient rats (that are unable to form MAC) and wild-type (WT) PVG/c rats. Structural reorganization was investigated using hilar cell counts and mossy fiber sprouting. Seizure development was monitored using electroencephalographic (EEG) recordings. 4 weeks after electrically stimulated SE, hilar cell counts in C6-deficient and WT post-SE rats were significantly decreased compared to an unstimulated control group, but not different between C6-deficient and WT post-SE. Since seizure development was unexpectedly absent in most post-SE rats we assessed epileptogenesis using the kindling rate as main parameter. Kindling development was slightly delayed in C6-deficient rats compared to WT rats. The lack of effect of C6 deficiency on hilar cell death and mossy fiber sprouting after electrically-induced SE or kindling argues against a role of the terminal complement complex in neuronal cell death induced by SE or seizures. A small but significant delay of kindling epileptogenesis suggests a subtle role of MAC in seizure spread. Whether complement components upstream of MAC play a crucial role in neuronal death and/or epileptogenesis needs to be further investigated.
Oxygen therapy for cerebral malaria.
Travel medicine and infectious disease, 2011

Malaria is an important global health issue, killing nearly one million people worldwide each year. There is a disproportionate disease burden, since 89% of cases are of African origin, and 85% of deaths worldwide occur in children under 5 years of age of age.(1) Cerebral malaria (CM) is the most serious complication of infection. Despite prompt anti-malarial treatment, fatalities remain high - mortality rates while undergoing treatment with Artemisinin or quinine-based therapy reach 15% and 22% respectively.(2) There is, therefore, a need to develop an adjunct therapy to preserve neurological function during the treatment period. Recent experimental research has indicated hyperbaric oxygenation (HBO) to be a rational and effective adjunct therapy.(3) This article examines the current understanding of CM, and the possible benefits provided by HBO therapy.
Prenatal exposure to methanol as a dopamine system sensitization model in C57BL/6J mice.
Life sciences, 2012

In this study, the effects of prenatal exposure to methanol (MeOH) on the nigrostriatal dopamine (NSDA) system were examined to determine if the interaction could sensitize this system, and serve as an underpinning for Parkinson's disease (PD) like changes that occur later in life. Methanol was studied because its toxicity resembles the symptoms of PD and the symptoms are relieved by L-dopa meaning that MeOH targets the NSDA system. Since fermentation and wood combustion are major sources for MeOH, the incidence of human encounters with MeOH is high. As a superior solvent and the precursor for formaldehyde, MeOH has a powerful and sometimes, irreversible impact on chemical processes, such as cross-linking proteins and nucleic acids. It may cause subthreshold changes that sensitizes the NSDA system to PD, that occur during aging.
Beneficial Effects of Ibuprofen on Pentylenetetrazol-induced Convulsion.
Neurochemical research, 2020

Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) that is commonly used as an anti-inflammatory, anti-pyretic, and analgesic. Although some studies have focused on the anti-inflammatory and anti-pyretic properties of ibuprofen during febrile convulsions, only one has investigated its antiepileptic effects. In the present study, we aimed to investigate the effects of ibuprofen in rats exposed to pentylenetetrazol (PTZ)-induced seizures. In total, 48 rats were randomly divided in two groups: Group A for electroencephalography (EEG) recordings and Group B for behavioral assessment. All EEG recordings and behavioral assessment protocols were performed. In addition, groups were compared in terms of prostaglandin F2 alfa (PGF2α) levels in the brain. We demonstrated the beneficial effects of the administration of ibuprofen in PTZ-induced seizures in rats via the following findings: spike percentages and Racine convulsion scale values were significantly lower and first myoclonic jerk (FMJ) onset times were significantly higher in the ibuprofen-administered groups. Moreover, PGF2α levels in the brain were significantly higher in the saline and PTZ 70 mg/kg group than in the control and PTZ 70 mg/kg and 400 mg/kg ibuprofen groups. Our study is the first to demonstrate the beneficial effects of ibuprofen on seizures through behavioral, EEG, and PGF2α brain assessments. Ibuprofen can be used for epilepsy and febrile seizures safely and without inducing seizures. However, further experimental and clinical studies are needed to confirm our results.
Drosophila ortholog of succinyl-CoA synthetase {beta} subunit: a novel modulator of Drosophila KCNQ channels.
Journal of neurophysiology, 2008

Voltage-gated KCNQ potassium channels are responsible for slowly activating potassium currents in heart, brain, and other tissues. Functional defects of KCNQ channels are linked with many diseases, including epilepsy and cardiac arrhythmias. Therefore KCNQ potassium channels have been widely studied, especially in the CNS. We have identified Drosophila CG11963, which encodes a protein orthologous to the beta subunit of mammalian succinyl-CoA synthetase (SCS, also known as succinate thiokinase), as a novel modulator of Drosophila KCNQ channels. Direct interaction of CG11963 and dKCNQ was demonstrated by yeast two-hybrid screen and coimmunoprecipitation. Cell surface biotinylation experiments further confirmed that CG11963 resides on the plasma membrane of tsA-201 cells. Coexpression of CG11963 with dKCNQ shifts the conductance-voltage (G-V) relationship of dKCNQ channels to more positive membrane potentials in Chinese hamster ovary (CHO) cells. Moreover, directly dialyzing glutathione S-transferase fusion CG11963 protein into CHO cells also shifts the dKCNQ G-V curve rightward. The effect of CG11963 persists in the presence of 1 mM adenosine triphosphate (ATP), a substrate of SCS. Taken together, our data define CG11963 as a new dKCNQ-binding protein capable of modulating the properties of the channel. Our evidence suggests that this modulation is mediated by direct interaction of CG11963 with the channel and is not dependent on ATP.
Distinct Expression of Inflammatory Features in T Helper 17 Cells from Multiple Sclerosis Patients.
Cells, 2019

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). T helper (Th) 17 lymphocytes play a role in the pathogenesis of MS. Indeed, Th17 cells are abundant in the cerebrospinal fluid and peripheral blood of MS patients and promote pathogenesis in the mouse model of MS. To gain insight into the function of Th17 cells in MS, we tested whether Th17 cells polarized from naïve CD4 T cells of healthy donors and MS patients display different features. To this end, we analysed several parameters that typify the Th17 profile during the differentiation process of naïve CD4 T cells obtained from relapsing-remitting (RR)-MS patients (n = 31) and healthy donors (HD) (n = 28). Analysis of an array of cytokines produced by Th17 cells revealed that expression of interleukin (IL)-21, tumour necrosis factor (TNF)-β, IL-2 and IL-1R1 is significantly increased in Th17 cells derived from MS patients compared to healthy donor-derived cells. Interestingly, IL-1R1 expression is also increased in Th17 cells circulating in the blood of MS patients compared to healthy donors. Since IL-2, IL-21, TNF-β, and IL-1R1 play a crucial role in the activation of immune cells, our data indicate that high expression of these molecules in Th17 cells from MS patients could be related to their high inflammatory status.
A novel digital health intervention to improve patient engagement to stimulants in adult ADHD in the primary care setting: Preliminary findings from an open label study.
Psychiatry research, 2020

We piloted the effectiveness and acceptability of a novel text messaging-based (SMS) digital health intervention aimed at addressing the previously documented poor rate of patient engagement in stimulant treatment in the primary care setting.
Cross-camera comparison of ROI-based semi-quantitative ¹²³I-IBZM SPECT data in healthy volunteers using an anthropomorphic phantom for calibration.
Acta radiologica (Stockholm, Sweden : 1987), 2013

In (123)I-Iolopride (IBZM) SPECT reference values may diverge between camera systems. If multicenter pooling of normal material databases is needed, differences in measured semi-quantitative data due to equipment performance and reconstruction parameters have to be investigated in each instance to determine the comparability.
Facilitation of dopamine-dependent long-term potentiation in the medial prefrontal cortex of male rats follows the behavioral effects of stress.
Journal of neuroscience research, 2021

The effect of stress on animal behavior and brain activity has been attracting growing attention in the last decades. Stress dramatically affects several aspects of animal behavior, including motivation and cognitive functioning, and has been used to model human pathologies such as post-traumatic stress disorder. A key question is whether stress alters the plastic potential of synaptic circuits. In this work, we evaluated if stress affects dopamine (DA)-dependent synaptic plasticity in the medial prefrontal cortex (mPFC). On male adolescent rats, we characterized anxiety- and depressive-like behaviors using behavioral testing before and after exposure to a mild stress (elevated platform, EP). After the behavioral protocols, we investigated DA-dependent long-term potentiation (DA-LTP) and depression (DA-LTD) on acute slices of mPFC and evaluated the activation of DA-producing brain regions by western and dot blot analysis. We show that exposure to the EP stress enhances DA-LTP and that desipramine (DMI) treatment abolishes this effect. We also found that DA-LTD is not affected by EP stress unless when this is followed by DMI treatment. In addition, EP stress reduces anxiety, an effect abolished by both DMI and ketamine, while motivation is promoted by previous exposure to EP stress independently of pharmacological treatments. Finally, this form of stress reduces the expression of the early gene cFOS in the ventral tegmental area. These findings support the idea that mild stressors can promote synaptic plasticity in PFC through a dopaminergic mechanism, an effect that might increase the sensitivity of mPFC to subsequent stressful experiences.