rudyvdbrink/CitationDatabase huggingface dataset:
[A case of bronchial mucous gland adenoma: A rare diagnosis that should not be mistaken!].
Annales de pathologie, 2021

We report the case of a 32-year-old man, who was admitted for a recurrent pneumopathy. The thoracic computed tomography revealed a small well-circumscribed lesion of the lower right lobe of the lung. Microscopic examination from the biopsy material of the endoscopy concluded a mucoepidermoid carcinoma. A lobectomy was realized. Microscopic examination revealed the presence of a well-delineated lesion composed of glands and cysts containing mucous and limited by mucous and cylindric and ciliated cells without atypia. The proliferation index was very low. A diagnosis of mucous gland adenoma was made. It is an exceptional tumor and is very difficult to diagnose on biopsy material but should be known by pathologists. It is associated with a good prognosis. The aims of our observation are to present the macroscopic and microscopic features of this tumor and data from recent literature review to better diagnose it. This is also the second observation with molecular details for this entity.
Microscopy and chemical analyses reveal flavone-based woolly fibres extrude from micron-sized holes in glandular trichomes of Dionysia tapetodes.
BMC plant biology, 2021

Dionysia tapetodes, a small cushion-forming mountainous evergreen in the Primulaceae, possesses a vast surface-covering of long silky fibres forming the characteristic "woolly" farina. This contrasts with some related Primula which instead form a fine powder. Farina is formed by specialized cellular factories, a type of glandular trichome, but the precise composition of the fibres and how it exits the cell is poorly understood. Here, using a combination of cell biology (electron and light microscopy) and analytical chemical techniques, we present the principal chemical components of the wool and its mechanism of exit from the glandular trichome.
Dopamine Modulates Adaptive Prediction Error Coding in the Human Midbrain and Striatum.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017

Learning to optimally predict rewards requires agents to account for fluctuations in reward value. Recent work suggests that individuals can efficiently learn about variable rewards through adaptation of the learning rate, and coding of prediction errors relative to reward variability. Such adaptive coding has been linked to midbrain dopamine neurons in nonhuman primates, and evidence in support for a similar role of the dopaminergic system in humans is emerging from fMRI data. Here, we sought to investigate the effect of dopaminergic perturbations on adaptive prediction error coding in humans, using a between-subject, placebo-controlled pharmacological fMRI study with a dopaminergic agonist (bromocriptine) and antagonist (sulpiride). Participants performed a previously validated task in which they predicted the magnitude of upcoming rewards drawn from distributions with varying SDs. After each prediction, participants received a reward, yielding trial-by-trial prediction errors. Under placebo, we replicated previous observations of adaptive coding in the midbrain and ventral striatum. Treatment with sulpiride attenuated adaptive coding in both midbrain and ventral striatum, and was associated with a decrease in performance, whereas bromocriptine did not have a significant impact. Although we observed no differential effect of SD on performance between the groups, computational modeling suggested decreased behavioral adaptation in the sulpiride group. These results suggest that normal dopaminergic function is critical for adaptive prediction error coding, a key property of the brain thought to facilitate efficient learning in variable environments. Crucially, these results also offer potential insights for understanding the impact of disrupted dopamine function in mental illness.
3D neural tissue models: From spheroids to bioprinting.
Biomaterials, 2018

Three-dimensional (3D) in vitro neural tissue models provide a better recapitulation of in vivo cell-cell and cell-extracellular matrix interactions than conventional two-dimensional (2D) cultures. Therefore, the former is believed to have great potential for both mechanistic and translational studies. In this paper, we review the recent developments in 3D in vitro neural tissue models, with a particular focus on the emerging bioprinted tissue structures. We draw on specific examples to describe the merits and limitations of each model, in terms of different applications. Bioprinting offers a revolutionary approach for constructing repeatable and controllable 3D in vitro neural tissues with diverse cell types, complex microscale features and tissue level responses. Further advances in bioprinting research would likely consolidate existing models and generate complex neural tissue structures bearing higher fidelity, which is ultimately useful for probing disease-specific mechanisms, facilitating development of novel therapeutics and promoting neural regeneration.
Screening for blunt cerebrovascular injury: selection criteria for use of angiography.
Journal of neurosurgery, 2010

Blunt cerebrovascular injury (BCI) to the carotid and vertebral arteries is being recognized with increasing frequency in trauma victims. Yet, only broadly defined criteria exist for the use of screening angiography. In this study, the authors systematically identified the associated injuries that predict BCI and provide guidelines for the types of injuries best evaluated by angiography.
Cloninger's Temperament Dimensions and Longitudinal Alcohol Use in Early Midlife: A Northern Finland Birth Cohort 1966 Study.
Alcoholism, clinical and experimental research, 2018

Temperament is theorized to be an important factor contributing to the development of alcohol use disorder, but longitudinal studies on how temperament is related to alcohol use among general population in midlife are scarce. Our aims were to investigate potentially reciprocal associations between temperament and changes in alcohol use from age 31 to 46 using prospective birth cohort data.
The BAF (BRG1/BRM-Associated Factor) chromatin-remodeling complex exhibits ethanol sensitivity in fetal neural progenitor cells and regulates transcription at the miR-9-2 encoding gene locus.
Alcohol (Fayetteville, N.Y.), 2017

Fetal alcohol spectrum disorders are a leading cause of intellectual disability worldwide. Previous studies have shown that developmental ethanol exposure results in loss of microRNAs (miRNAs), including miR-9, and loss of these miRNAs, in turn, mediates some of ethanol's teratogenic effects in the developing brain. We previously found that ethanol increased methylation at the miR-9-2 encoding gene locus in mouse fetal neural stem cells (NSC), advancing a mechanism for epigenetic silencing of this locus and consequently, miR-9 loss in NSCs. Therefore, we assessed the role of the BAF (BRG1/BRM-Associated Factor) complex, which disassembles nucleosomes to facilitate access to chromatin, as an epigenetic mediator of ethanol's effects on miR-9. Chromatin immunoprecipitation and DNAse I-hypersensitivity analyses showed that the BAF complex was associated with both transcriptionally accessible and heterochromatic regions of the miR-9-2 locus, and that disintegration of the BAF complex by combined knockdown of BAF170 and BAF155 resulted in a significant decrease in miR-9. We hypothesized that ethanol exposure would result in loss of BAF-complex function at the miR-9-2 locus. However, ethanol exposure significantly increased mRNA transcripts for maturation-associated BAF-complex members BAF170, SS18, ARID2, BAF60a, BRM/BAF190b, and BAF53b. Ethanol also significantly increased BAF-complex binding within an intron containing a CpG island and in the terminal exon encoding precursor (pre)-miR-9-2. These data suggest that the BAF complex may adaptively respond to ethanol exposure to protect against a complete loss of miR-9-2 in fetal NSCs. Chromatin remodeling factors may adapt to the presence of a teratogen, to maintain transcription of critical miRNA regulatory pathways.
Decreased anterior cingulate activation in a motor task in youths with bipolar disorder.
Journal of child psychology and psychiatry, and allied disciplines, 2018

Bipolar disorder (BP) is characterized by abnormal shifts in mood between episodes of mania and severe depression, both of which have been linked with psychomotor disturbances. This study compares brain activation patterns in motor networks between euthymic youths with BP and healthy controls (HC) during the completion of a simple motor task.
The protein tyrosine phosphatase Shp2 is required for the generation of oligodendrocyte progenitor cells and myelination in the mouse telencephalon.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014

The protein tyrosine phosphatase Shp2 (PTPN11) is crucial for normal brain development and has been implicated in dorsal telencephalic neuronal and astroglia cell fate decisions. However, its roles in the ventral telencephalon and during oligodendrogenesis in the telencephalon remain largely unknown. Shp2 gain-of-function (GOF) mutations are observed in Noonan syndrome, a type of RASopathy associated with multiple phenotypes, including cardiovascular, craniofacial, and neurocognitive abnormalities. To gain insight into requirements for Shp2 (LOF) and the impact of abnormal Shp2 GOF mutations, we used a Shp2 conditional mutant allele (LOF) and a cre inducible Shp2-Q79R GOF transgenic mouse in combination with Olig2(cre/+) mice to target embryonic ventral telencephalic progenitors and the oligodendrocyte lineage. In the absence of Shp2 (LOF), neuronal cell types originating from progenitors in the ventral telencephalon were generated, but oligodendrocyte progenitor cell (OPC) generation was severely impaired. Late embryonic and postnatal Shp2 cKOs showed defects in the generation of OPCs throughout the telencephalon and subsequent reductions in white matter myelination. Conversely, transgenic expression of the Shp2 GOF Noonan syndrome mutation resulted in elevated OPC numbers in the embryo and postnatal brain. Interestingly, expression of this mutation negatively influenced myelination as mice displayed abnormal myelination and fewer myelinated axons in the white matter despite elevated OPC numbers. Increased proliferating OPCs and elevated MAPK activity were also observed during oligodendrogenesis after expression of Shp2 GOF mutation. These results support the notion that appropriate Shp2 activity levels control the number as well as the differentiation of oligodendrocytes during development.
CYP17A1 Maintains the Survival of Glioblastomas by Regulating SAR1-Mediated Endoplasmic Reticulum Health and Redox Homeostasis.
Cancers, 2019

Cytochrome P450 (CYP) 17A1 is an important steroidogenic enzyme harboring 17α-hydroxylase and performing 17,20 lyase activities in multiple steps of steroid hormone synthesis, including dehydroepiandrosterone (DHEA) biosynthesis. Previously, we showed that CYP17A1-mediated DHEA production clearly protects glioblastomas from temozolomide-induced apoptosis, leading to drug resistance. Herein, we attempt to clarify whether the inhibition of CYP17A1 has a tumor-suppressive effect, and to determine the steroidogenesis-independent functions of CYP17A1 in glioblastomas. Abiraterone, an inhibitor of CYP17A1, significantly inhibits the proliferation of A172, T98G, and PT#3 (the primary glioblastoma cells) by inducing apoptosis. In parallel, abiraterone potently suppresses tumor growth in mouse models through transplantation of PT#3 cells to the back or to the brain. Based on evidence that abiraterone induces endoplasmic reticulum (ER) stress, followed by the accumulation of reactive oxygen species (ROS), CYP17A1 is important for ER health and redox homeostasis. To confirm our hypothesis, we showed that CYP17A1 overexpression prevents the initiation of ER stress and attenuates ROS production by regulating SAR1a/b expression. Abiraterone dissociates SAR1a/b from ER-localized CYP17A1, and induces SAR1a/b ubiquitination, leading to degradation. Furthermore, SAR1 overexpression rescues abiraterone-induced apoptosis and impairs redox homeostasis. In addition to steroid hormone synthesis, CYP17A1 associates with SAR1a/b to regulate protein processing and maintain ER health in glioblastomas.
Interplay between sniffing and odorant sorptive properties in the rat.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012

For decades it has been known that the olfactory sensory epithelium can act like a chromatograph, separating odorants based on their air-mucus sorptive properties (Mozell and Jagodowicz, 1973). It has been hypothesized that animals could take advantage of this property, modulating sniffing behavior to manipulate airflow and thereby directing odorant molecules to the portions of the olfactory epithelium where they are best detected (Schoenfeld and Cleland, 2005). We report here a test of this hypothesis in behaving rats, monitoring respiratory activity through diaphragm electromyogram, which allowed us to estimate nasal airflow. In our test rats had to detect either low-sorption (LS) or high-sorption (HS) monomolecular odorant targets from the same stimulus set of six binary odor mixtures. We found that it is more difficult for rats to detect LS than HS targets. Although sniffing bouts are the same duration for each group (∼500 ms), sniffing longer and using more inhalations results in better performance for rats assigned to detect LS targets. LS-detecting rats also increase the duration of individual inhalations (81 ms for LS- vs 69 ms for HS-detecting rats) and sniff at lower frequencies (7.8 Hz for LS- vs 8.6 Hz for HS-detecting rats) when learning to sense the target. When LS-detecting rats do discriminate well, they do so with lower airflow, more sniffs, and lower frequency of sniffing than HS-detecting counterparts. These data show that rats adjust sniff strategies as a function of odorant sorptiveness and provide support for the chromatographic and zonation hypotheses.
Conditioned saccharin avoidance induced by infusion of amphetamine in the nucleus accumbens shell and morphine in the ventral tegmental area: behavioral and biochemical study.
Behavioural brain research, 2014

Drugs of abuse possess the seemingly paradoxical property of conditioning rats to avoid from drinking a saccharin solution that had been predictively paired with their systemic administration (conditioned saccharin avoidance, CSA). CSA is dependent upon an intact dopamine (DA) transmission but the locus, central or peripheral, and eventually the brain area from which this effect originates and its relationship with the rewarding properties of the drug is debated. In order to clarify this issue we tested the ability of amphetamine and morphine to induce CSA after infusion at the same dose-range and in the same areas from which these drugs induce conditioned place preference (CPP). Drugs were infused intracerebrally immediately after saccharin drinking in two acquisition trials and CSA was tested on a two bottle saccharin/water choice. Amphetamine (10 and 20 μg/0.5 μl) induced CSA after infusion in the NAc shell but was ineffective in the NAc core. Morphine (0.5 and 1 μg/0.5 μl) induced CSA from the VTA at both doses tested. Amphetamine (20 μg/0.5 μl) and morphine (1 μg/0.5 μl) failed to induce CSA after infusion 1.2mm dorsal the NAc shell and the VTA respectively. Finally, morphine (1 μg/0.5 μl), infused in the VTA, elicited a selective increase in dialysate DA in the NAc shell. These results indicate that drugs of abuse induce CSA from the same intracerebral sites and at the same doses at which they induce CPP. These observations are consistent with the existence of a strong relationship between CSA and drug reward related to their ability to stimulate DA transmission in the NAc shell.
Gene-network analysis identifies susceptibility genes related to glycobiology in autism.
PloS one, 2009

The recent identification of copy-number variation in the human genome has opened up new avenues for the discovery of positional candidate genes underlying complex genetic disorders, especially in the field of psychiatric disease. One major challenge that remains is pinpointing the susceptibility genes in the multitude of disease-associated loci. This challenge may be tackled by reconstruction of functional gene-networks from the genes residing in these loci. We applied this approach to autism spectrum disorder (ASD), and identified the copy-number changes in the DNA of 105 ASD patients and 267 healthy individuals with Illumina Humanhap300 Beadchips. Subsequently, we used a human reconstructed gene-network, Prioritizer, to rank candidate genes in the segmental gains and losses in our autism cohort. This analysis highlighted several candidate genes already known to be mutated in cognitive and neuropsychiatric disorders, including RAI1, BRD1, and LARGE. In addition, the LARGE gene was part of a sub-network of seven genes functioning in glycobiology, present in seven copy-number changes specifically identified in autism patients with limited co-morbidity. Three of these seven copy-number changes were de novo in the patients. In autism patients with a complex phenotype and healthy controls no such sub-network was identified. An independent systematic analysis of 13 published autism susceptibility loci supports the involvement of genes related to glycobiology as we also identified the same or similar genes from those loci. Our findings suggest that the occurrence of genomic gains and losses of genes associated with glycobiology are important contributors to the development of ASD.
Hippocampal Subgranular Zone FosB Expression Is Critical for Neurogenesis and Learning.
Neuroscience, 2019

Neural proliferation in the dentate gyrus (DG) is closely linked with learning and memory, but the transcriptional programming that drives adult proliferation remains incompletely understood. Our lab previously elucidated the critical role of the transcription factor ΔFosB in the dorsal hippocampus (dHPC) in learning and memory, and the FosB gene has been suggested to play a role in neuronal proliferation. However, the subregion-specific and potentially cell-autonomous role of dHPC ΔFosB in neurogenesis-dependent learning has not been studied. Here, we crossed neurotensin receptor-2 (NtsR2) Cre mice, which express Cre within the subgranular zone (SGZ) of dHPC DG, with floxed FosB mice to show that knockout of ΔFosB in hippocampal SGZ neurons reduces antidepressant-induced neurogenesis and impedes hippocampus-dependent learning in the novel object recognition task. Taken together, these data indicate that FosB gene expression in SGZ is necessary for both hippocampal neurogenesis and memory formation.
Cranioplasty and Duraplasty with Transcranial Color-Coded Duplex Sonography after Aneurysmal Subarachnoid Hemorrhage.
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association, 2015

Transcranial color-coded duplex sonography (TCCS) is a noninvasive technique for monitoring of cerebral vasospasm after neurosurgery for aneurismal subarachnoid hemorrhage. In this surgery, surgical materials are used. The goal of the study was to identify materials that can be used with ultrasound and to propose methods for cranioplasty and duraplasty using materials that permit TCCS.
Adaptation to Leftward Shifting Prisms Alters Motor Interhemispheric Inhibition.
Cerebral cortex (New York, N.Y. : 1991), 2018

Adaptation to rightward shifting prisms (rightward prism adaptation, RPA) ameliorates neglect symptoms in patients while adaptation to leftward shifting prisms (leftward prism adaptation, LPA) induces neglect-like behaviors in healthy subjects. It has been hypothesized that prism adaptation (PA) modulates interhemispheric balance between the parietal cortices by inhibiting the posterior parietal cortex (PPC) contralateral to the prismatic deviation, but PA's effects on interhemispheric inhibition (IHI) have not been directly investigated. Since there are hyper-excitable connections between the PPC and primary motor cortex (M1) in the left hemisphere of neglect patients, we reasoned that LPA might mimic right hemisphere lesions by reducing parietal IHI, hyper-exciting the left PPC and PPC-M1 connections, and in turn altering IHI at the motor level. Namely, we hypothesized that LPA would increase IHI from the left to the right M1. We examined changes in left-to-right and right-to-left IHI between the 2 M1s using the ipsilateral silent period (iSP) (Meyer et al. 1995) before and after either LPA or RPA. The iSP was significantly longer after LPA but only from left-to-right and it did not change at all after RPA. This is the first physiological demonstration that LPA alters IHI in the healthy brain.
The clinical course of late-life bipolar disorder, looking back and forward.
Bipolar disorders, 2017

Little is known about the course of late-life bipolar disorder (LLBD). First, we studied patients with LLBD retrospectively with regard to age at first mood episode, onset polarity, predominant polarity and episode density and its associations with other clinical variables. Next, we examined prospectively the clinical course and its associated factors.
Different clinicopathological features between Japanese siblings with facioscapulohumeral muscular dystrophy 2 with a novel nonsense SMCHD1 mutation (Arg552
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 2018

Facioscapulohumeral muscular dystrophy (FSHD) 2 is caused by a combination of heterozygous structural maintenance of chromosomes flexible hinge domain containing 1 (SMCHD1) mutation plus DNA hypomethylation on D4Z4. Here we report two Japanese FSHD2 siblings (brother and sister) with a new SMCHD1 nonsense mutation (a heterogeneous c. 1654C > T substitution, leading to a stop codon Arg552
Differential Impact of Obesity on CD69 Expression in Individuals with Bipolar Disorder and Healthy Controls.
Molecular neuropsychiatry, 2018

Preliminary evidence suggests that premature immunosenescence is involved in bipolar disorder (BD) pathophysiology. The cellular marker CD69 is expressed in T lymphocyte surface during their activation and its expression is negatively correlated with age. The objective of this study was to assess the moderating effects of obesity on the reduction of expression of CD69, a marker of immunosenescence. Forty euthymic patients with BD type I, aged 18-65 years, were included in this study. The healthy comparison group consisted of 39 volunteers who had no current or lifetime history of mental disorders, no use of psychotropic medications, and no known family history of mood disorders or psychosis. Peripheral blood mononuclear cells from BD patients and healthy controls were collected and isolated. The cells were allowed to grow in culture and stimulated for 3 days. CD69 was marked and read in flow cytometry. We found that the lower expression of CD69 in BD patients was moderated by body mass index (BMI) in both CD4+ (RR = 0.977, 95% CI 0.960-0.995,
mTOR-related neuropathology in mutant tsc2 zebrafish: Phenotypic, transcriptomic and pharmacological analysis.
Neurobiology of disease, 2017

Tuberous sclerosis complex (TSC) is a rare, genetic disease caused by loss-of-function mutations in either TSC1 or TSC2. Patients with TSC are neurologically characterized by the presence of abnormal brain structure, intractable epilepsy and TSC-associated neuropsychiatric disorders. Given the lack of effective long-term treatments for TSC, there is a need to gain greater insight into TSC-related pathophysiology and to identify and develop new treatments. In this work we show that homozygous tsc2