rudyvdbrink/CitationDatabase huggingface dataset:
An industry update: what is the latest news in therapeutic delivery?
Therapeutic delivery, 2017

This Industry Update covers the period from 1 through 30 April 2017, and is based on information sourced from company press releases, scientific literature, patents and various news websites. Biogen expanded its portfolio of developmental drugs targeting neurological diseases by licensing a drug from Bristol-Myers Squibb which is currently under investigation for the treatment of progressive supranuclear palsy. Takeda announced a deal with NuBiyota focused on developing treatments for gastrointestinal disorders, based on the manipulation of microbes living in the gut. Novartis announced an expansion of its neuroscience collaboration with Amgen as well as licensing of a developmental compound to treat dry eye. EmulateBio announced a collaboration with the US FDA to explore and evaluate its organs-on-chip technology in toxicological testing of food products, but which has wider opportunities in drug development. In the treatment of pulmonary hypertension, Vectura announced the commercial launch of its Fox nebulizer technology to deliver a Bayer drug and Respira announced a deal in which it exclusively licensed an inhaled drug-device product to United Therapeutics. Published research suggested that the benefit of pumps over multiple injections in the treatment of diabetes maybe more due to training than technology, and a group from the University of Pennsylvania showed that electrical stimulation of the brain can improve memory function but only when applied at the right time. Alzheon published work that explains the mechanism behind its developmental Alzheimer's drug.
A one-plasmid conditional color-switching transgenic system for multimodal bioimaging.
Transgenic research, 2008

We have developed a new construct to generate transgenic mice with one plasmid that offers: (1) Cre/loxP-mediated spatial and temporally-controlled tissue-specific transgene expression; (2) A color-switching mechanism that uses spectrum-complementary genetically-encoded red (mRFP) and green (eGFP) fluorescent markers to label the transgene-expressing cells; (3) A bioluminescent marker that turns-on in the transgene-expressing cells; (4) eGFP as a cell surface marker in the transgene-expressing cells that facilitates the isolation and targeting of these cells. This vector was tested in vitro by co-transfection of the transgenic plasmid and a plasmid containing Cre recombinase into cultured cells and by establishing a transgenic mouse line. We show that this method allows versatile transgene expression targeting and color-switching to facilitate fluorescent and bioluminescent imaging both in cultured cells and in vivo. Our strategy provides time-saving features in tissue-specific transgene expression, bioimaging and primary cell isolation and can be used for generation of gene-specific transgenic mice.
Severe neurological nicotine intoxication by e-cigarette liquids: Systematic literature review.
Acta neurologica Scandinavica, 2021

Electronic cigarettes are a popular, easily purchased, alternative source of nicotine that is considered safer than conventional tobacco. However, Intentional or accidental exposure to e-liquid substances, mainly nicotine, can lead to serious, potentially fatal toxicity. Emergency and critical care physicians should keep in mind acute intoxication of this poison with a biphasic toxic syndrome. We highlight its potentially fatal outcome and suggest monitoring the adverse effects of nicotine according to a multimodal protocol integrating somatosensory evoked potentials, electroencephalography and neuroimaging data with anamnestic report and toxicological and laboratory data.
Clinical tools used in young infants born very preterm to predict motor and cognitive delay (not cerebral palsy): a systematic review.
Developmental medicine and child neurology, 2021

This systematic review evaluates the accuracy of clinical tools used at a corrected age of 6 months or younger to predict motor and cognitive delay (not cerebral palsy) at 24 months' corrected age, in infants born very preterm.
An Evaluation of Complications in Femoral Arterial Sheaths Maintained Post-Neuroangiographic Procedures.
Cureus, 2018

Digital subtraction angiography (DSA) is a frequently used technique in the neuro-diagnosis and treatment of cerebrovascular diseases. The routine use of femoral arterial sheaths (FAS) peri-procedurally has become standard. The maintenance of a FAS post-procedure may be warranted while awaiting the normalization of coagulopathy or to reaccess emergently. We retrospectively reviewed our stroke dataset to evaluate for complications associated with the prolonged use of FAS post-procedure.
Social Media and Well-Being: Pitfalls, Progress, and Next Steps.
Trends in cognitive sciences, 2021

Within a relatively short time span, social media have transformed the way humans interact, leading many to wonder what, if any, implications this interactive revolution has had for people's emotional lives. Over the past 15 years, an explosion of research has examined this issue, generating countless studies and heated debate. Although early research generated inconclusive findings, several experiments have revealed small negative effects of social media use on well-being. These results mask, however, a deeper set of complexities. Accumulating evidence indicates that social media can enhance or diminish well-being depending on how people use them. Future research is needed to model these complexities using stronger methods to advance knowledge in this domain.
Genetic variation in APOE, GRN, and TP53 are phenotype modifiers in frontotemporal dementia.
Neurobiology of aging, 2021

Frontotemporal dementia (FTD) is a clinical, genetic, and pathologic heterogeneous group of neurodegenerative diseases. In this study, we investigated the role of APOƐ4, rs5848 in GRN, and rs1042522 in TP53 gene as disease risk factors and/or phenotype modifiers in 440 FTD patients, including 175 C9orf72 expansion carriers. We found that the C9orf72 expansion carriers showing an earlier age at onset (p < 0.001). Among the clinical groups, the FTD-MND (motoneuron disease) showed the lowest survival (hazard ratio [HR] = 4.12), and the progressive nonfluent aphasia group showed the highest onset age (p = 0.03). In our cohort, the rs1042522 in TP53 was associated with disease onset (p = 0.02) and survival (HR = 1.73) and rs5848 GRN with a significantly shorter survival in CC homozygous patients (HR = 1.98). The frequency of APOƐ4 carriers was significantly increased in the C9orf72 noncarriers (p = 0.022). Although validation of our findings is necessary, our results suggest that TP53, GRN, and APOE genes may act as phenotype modifiers in FTD and should be considered in future clinical trials.
Rostral cuneiform nucleus and the defence reaction: Direct and indirect midbrain-medullary 5-HT mechanisms in baroreflex inhibition.
British journal of pharmacology, 2021

Activation of the defence reaction inhibits the baroreflex response via the intermediate rostro-ventromedial medulla (B3 raphé) and nucleus tractus solitarius (NTS). Our aim was to determine whether and how baroreflex inhibition, induced by the disinhibition of the rostral cuneiform nucleus (part of the defence pathway), involves 5-HT neurons in B3 and 5-HT
Open science in psychophysiology: An overview of challenges and emerging solutions.
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 2021

The present review is the result of a one-day workshop on open science, held at the Annual Meeting of the Society for Psychophysiological Research in Washington, DC, September 2019. The contributors represent psychophysiological researchers at different career stages and from a wide spectrum of institutions. The state of open science in psychophysiology is discussed from different perspectives, highlighting key challenges, potential benefits, and emerging solutions that are intended to facilitate open science practices. Three domains are emphasized: data sharing, preregistration, and multi-site studies. In the context of these broader domains, we present potential implementations of specific open science procedures such as data format harmonization, power analysis, data, presentation code and analysis pipeline sharing, suitable for psychophysiological research. Practical steps are discussed that may be taken to facilitate the adoption of open science practices in psychophysiology. These steps include (1) promoting broad and accessible training in the skills needed to implement open science practices, such as collaborative research and computational reproducibility initiatives, (2) establishing mechanisms that provide practical assistance in sharing of processing pipelines, presentation code, and data in an efficient way, and (3) improving the incentive structure for open science approaches. Throughout the manuscript, we provide references and links to available resources for those interested in adopting open science practices in their research.
Sleep loss disrupts pericyte-brain endothelial cell interactions impairing blood-brain barrier function.
Brain, behavior, and immunity, 2020

Sleep loss in the rat increases blood-brain barrier permeability to circulating molecules by disrupting interendothelial tight junctions. Despite the description of the ultrastructure of cerebral microvessels and the evidence of an apparent pericyte detachment from capillary wall in sleep restricted rats the effect of sleep loss on pericytes is unknown. Here we characterized the interactions between pericytes and brain endothelial cells after sleep loss using male Wistar rats. Animals were sleep-restricted 20 h daily with 4 h sleep recovery for 10 days. At the end of the sleep restriction, brain microvessels (MVs) were isolated from cerebral cortex and hippocampus and processed for Western blot and immunocytochemistry to evaluate markers of pericyte-endothelial cell interaction (connexin 43, PDGFR-β), tight junction proteins, and proinflammatory mediator proteins (MMP9, A
Vestibular disorders: clinician ENT perspective on the need for research and innovation.
Journal of neurology, 2020

Vertigo and dizziness are a frequent reason for medical consultation. However, diagnostic and therapeutic management is sometimes limited, and clinicians are faced with many unmet needs. The purpose of this study was to identify and prioritize these needs.
Lithium modulates striatal reward anticipation and prediction error coding in healthy volunteers.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021

Lithium is one of the most effective mood-stabilizing medications in bipolar disorder. This study was designed to test whether lithium administration may stabilize mood via effects on reward processing. It was hypothesized that lithium administration would modulate reward processing in the striatum and affect both anticipation and outcome computations. Thirty-seven healthy human participants (18 males, 33 with suitable fMRI data) received 11 (±1) days of lithium carbonate or placebo intervention (double-blind), after which they completed the monetary incentive delay task while fMRI data were collected. The monetary incentive delay task is a robust task with excellent test-retest reliability and is well suited to investigate different phases of reward processing within the caudate and nucleus accumbens. To test for correlations with prediction error signals a Rescorla-Wagner reinforcement-learning model was applied. Lithium administration enhanced activity in the caudate during reward anticipation compared to placebo. In contrast, lithium administration reduced caudate and nucleus accumbens activity during reward outcome. This latter effect seems related to learning as reward prediction errors showed a positive correlation with caudate and nucleus accumbens activity during placebo, which was absent after lithium administration. Lithium differentially modulates the anticipation relative to the learning of rewards. This suggests that lithium might reverse dampened reward anticipation while reducing overactive reward updating in patients with bipolar disorder. This specific effect of lithium suggests that a targeted modulation of reward learning may be a viable approach for novel interventions in bipolar disorder.
Cross-reactive probes on Illumina DNA methylation arrays: a large study on ALS shows that a cautionary approach is warranted in interpreting epigenome-wide association studies.
NAR genomics and bioinformatics, 2020

Illumina DNA methylation arrays are a widely used tool for performing genome-wide DNA methylation analyses. However, measurements obtained from these arrays may be affected by technical artefacts that result in spurious associations if left unchecked. Cross-reactivity represents one of the major challenges, meaning that probes may map to multiple regions in the genome. Although several studies have reported on this issue, few studies have empirically examined the impact of cross-reactivity in an epigenome-wide association study (EWAS). In this paper, we report on cross-reactivity issues that we discovered in a large EWAS on the presence of the
Increased prolidase activity in Alzheimer's dementia: A case-control study.
Asian journal of psychiatry, 2020

Prolidase enzyme, which catalyzes the final step in collagen metabolism can influence the cognitive functions through changes in extracellular matrix (ECM) resulting in altered synaptic connectivity in Alzheimer's disease (AD). In this study, it was found that the prolidase activity was significantly higher (p = 0.0016) in AD subjects (5.62 ± 2.05 U/ mL) than control group (4.45 ± 0.92 U/ mL). The increase was significant beginning at mild AD (p = 0.006) with an inverse correlation with HMSE scores (p = 0.0344), thus implying that prolidase mediated alterations in ECM may be associated with the cognitive deficits seen in AD.
SAFER, an Analysis Method of Quantitative Proteomic Data, Reveals New Interactors of the C. elegans Autophagic Protein LGG-1.
Journal of proteome research, 2016

Affinity purifications followed by mass spectrometric analysis are used to identify protein-protein interactions. Because quantitative proteomic data are noisy, it is necessary to develop statistical methods to eliminate false-positives and identify true partners. We present here a novel approach for filtering false interactors, named "SAFER" for mass Spectrometry data Analysis by Filtering of Experimental Replicates, which is based on the reproducibility of the replicates and the fold-change of the protein intensities between bait and control. To identify regulators or targets of autophagy, we characterized the interactors of LGG1, a ubiquitin-like protein involved in autophagosome formation in C. elegans. LGG-1 partners were purified by affinity, analyzed by nanoLC-MS/MS mass spectrometry, and quantified by a label-free proteomic approach based on the mass spectrometric signal intensity of peptide precursor ions. Because the selection of confident interactions depends on the method used for statistical analysis, we compared SAFER with several statistical tests and different scoring algorithms on this set of data. We show that SAFER recovers high-confidence interactors that have been ignored by the other methods and identified new candidates involved in the autophagy process. We further validated our method on a public data set and conclude that SAFER notably improves the identification of protein interactors.
Fine-Tuning of GPCR-Chemokine Interactions. Design and Identification of Chemokine Analogues as Receptor Agonists, Biased Agonists, and Antagonists.
Biochemistry, 2019

Chemokines play important roles in immune defense by directing migration of leukocytes and serve as key promoters of tumorigenesis and metastasis. This study explores the molecular mechanisms of recognition and activation of two homologous chemokine receptors, CXCR1 and CXCR2, using CXCL8 analogues with residue substitutions in the conserved Glu4Leu5Arg6 (ELR) triad. Analysis of the binding of CXCL8 analogues to CXCR1 is consistent with the two-site model for signal recognition of CXCR1, whereas analysis of the binding of CXCL8 analogues to CXCR2 supported a single-site model for signal recognition of CXCR2. The CXCL8-Arg6His analogue stimulated calcium release, phosphorylation of ERK1/2, and chemotaxis in cells expressing CXCR1. However, CXCL8-Arg6His failed to stimulate calcium release and chemotaxis in cells expressing CXCR2, although it stimulated phosphorylation of ERK1/2, indicating that CXCL8-Arg6His operated as a classical CXCR2 biased agonist. The CXCL8-Glu4AlaLeu5AlaArg6His analogue was inactive in cells expressing CXCR1 and CXCR2. These findings suggest that the Glu4Leu5 motif in CXCL8 is essential for activation of CXCR1 and CXCR2. Importantly, CXCL8-Glu4AlaLeu5AlaArg6His blocked specifically the calcium release and chemotaxis of cells expressing CXCR1 but not of cells expressing CXCR2. CXCL8-Glu4AlaLeu5AlaArg6His was identified as the first specific CXCR1 antagonist. The binding of CXCL8-ELR6H to CXCR1 created a Zn
Real-life gait assessment in degenerative cerebellar ataxia: Toward ecologically valid biomarkers.
Neurology, 2020

With disease-modifying drugs on the horizon for degenerative ataxias, ecologically valid motor biomarkers are highly warranted. In this observational study, we aimed to unravel and validate markers of ataxic gait in real life by using wearable sensors.
Regulating the availability of transforming growth factor ß1 in B104 neuroblastoma cells.
Experimental neurology, 2010

Transforming growth factor (TGF) beta1 is a key player in early brain development, hence, its availability (i.e., synthesis and release) affects neuronogenesis. TGFbeta1 moves proliferating cells out of the cell cycle and promotes their subsequent migration. The present study tested the hypothesis that neural progenitors self-regulate TGFbeta1. B104 neuroblastoma cells which can grow in the absence of serum or growth factors were used in systematic studies of transcription, translation, release, and activation. These studies relied on quantitative enzyme-linked immunosorbent assays and real-time polymerase chain reactions. TGFbeta1 positively upregulated its own intracellular expression and promoted increased release of TGFbeta1 from cells. The induction of TGFbeta1 was independent of a change in transcription, but it depended on cycloheximide-inhibited translation. Signaling mediated by downstream Smad2/3 through the TGFbeta receptors and intracellular protein transport were also required for release of TGFbeta1 from B104 cells. Thus, TGFbeta1 production and release were mediated through a feed-forward mechanism and were pivotally regulated at the level of translation. These activities appear to be key for the role of TGFbeta1 in the proliferation and migration of young neurons.
Comparing the Role of the p53 Gene and Telomerase Enzyme in 'Accelerated Aging Due to Cancer': A Literature Review.
Cureus, 2020

Aging is defined as progressive physiological alterations in an organism that lead to senescence. In response to stress, when proliferative-competent cells undergo permanent, irreversible growth arrest (like replicative dividing limit, oncogene activation, oxidative stress, or deoxyribonucleic acid (DNA) damage), it is termed as cellular senescence. Biomarkers p53, telomerase, and other inflammatory cytokines have a vital link with senescence, and directed use of these markers might be useful in manipulating cancer and the aging process. We included studies related to topics ' accelerated aging due to cancer', telomerase's relation to Aging and Cancer, p53's relation to Aging and Cancer, Atherosclerosis and Cancer from Search databases like PubMed and Google Scholar. We relied on peer-reviewed articles and included literature from the last 10 years written in the English language. Degenerative diseases in humans are usually linked to atherosclerosis, and atherosclerosis is associated with short leukocyte telomere length. Cancer itself and its treatment are linked with accelerated aging by causing progressive shortening of telomeres during cell replication, resulting in cell death. Gene p53 is known to have a dual effect that works as a tumor suppressor and has pro-aging side effects. In experimental studies, when p53 overcomes multiple regulatory mechanisms controlling its activity, then only the pro-aging side effects of p53 manifested. This might be a potential key for treating cancer without causing the side-effects of aging. In this review, we aim to explain and summarize the interdependent nature of p53, telomeres, and other conventional mechanisms of aging and cancer like inflammation, oxidative stress, uncontrolled proliferation, angiogenesis, micro ribonucleic acids (RNAs), and apoptosis, with a more synergistic approach that can help in developing new therapeutics and play a potential role in shaping modern human lifespan and revolutionize cancer treatment.
Human plasma biomarker responses to inhalational general anaesthesia without surgery.
British journal of anaesthesia, 2020

Postoperative neurocognitive disorders may arise in part from adverse effects of general anaesthetics on the CNS, especially in older patients or individuals otherwise vulnerable to neurotoxicity because of systemic disease or the presence of pre-existing neuropathology. Previous studies have documented cytokine and injury biomarker responses to surgical procedures that included general anaesthesia, but it is not clear to what degree anaesthetics contribute to these responses.
Neural population dynamics in motor cortex are different for reach and grasp.
eLife, 2020

Low-dimensional linear dynamics are observed in neuronal population activity in primary motor cortex (M1) when monkeys make reaching movements. This population-level behavior is consistent with a role for M1 as an autonomous pattern generator that drives muscles to give rise to movement. In the present study, we examine whether similar dynamics are also observed during grasping movements, which involve fundamentally different patterns of kinematics and muscle activations. Using a variety of analytical approaches, we show that M1 does not exhibit such dynamics during grasping movements. Rather, the grasp-related neuronal dynamics in M1 are similar to their counterparts in somatosensory cortex, whose activity is driven primarily by afferent inputs rather than by intrinsic dynamics. The basic structure of the neuronal activity underlying hand control is thus fundamentally different from that underlying arm control.
Matrin 3 in neuromuscular disease: physiology and pathophysiology.
JCI insight, 2021

RNA-binding proteins (RBPs) are essential factors required for the physiological function of neurons, muscle, and other tissue types. In keeping with this, a growing body of genetic, clinical, and pathological evidence indicates that RBP dysfunction and/or gene mutation leads to neurodegeneration and myopathy. Here, we summarize the current understanding of matrin 3 (MATR3), a poorly understood RBP implicated not only in ALS and frontotemporal dementia but also in distal myopathy. We begin by reviewing MATR3's functions, its regulation, and how it may be involved in both sporadic and familial neuromuscular disease. We also discuss insights gleaned from cellular and animal models of MATR3 pathogenesis, the links between MATR3 and other disease-associated RBPs, and the mechanisms underlying RBP-mediated disorders.
The spectrum of muscle pathologies: Three decades of experience from a reference laboratory in Saudi Arabia.
Annals of diagnostic pathology, 2020

When investigating patients with a suspected neuromuscular disorder, a muscle biopsy is considered an instrumental tool to reach a definitive diagnosis. There is a paucity of publications that assess the diagnostic utilization and yield of muscle biopsies. We intend to present our experience in this regard over an extended period of more than three decades.