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2. Time resolved imaging of the non-linear bullet mode within an injection-locked nano-contact spin Hall nano-oscillator

Author

Spicer, Timothy M, Keatley, Paul S, Dvornik, Mykola, Loughran, Thomas H J, Awad, A. A., Dürrenfeld, Philipp, Houshang, Afshin, Ranjbar, Mojtaba, Åkerman, Johan, Kruglyak, Volodymyr V., and Hicken, Robert J

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics, Condensed Matter - Materials Science
Abstract

Injection of a radio frequency (RF) current was used to phase lock the SHNO to the TRSKM. The out of plane magnetization was detected by means of the polar magneto optical Kerr effect (MOKE). However, longitudinal MOKE images were dominated by an artifact arising from the edges of the Au NCs. Time resolved imaging revealed the simultaneous excitation of a non-linear `bullet' mode at the centre of the device, once the DC current exceeded a threshold value, and ferromagnetic resonance (FMR) induced by the RF current. However, the FMR response observed for sub-critical DC current values exhibits an amplitude minimum at the centre, which is attributed to spreading of the RF spin current due to the reactance of the device structure. This FMR response can be subtracted to yield images of the bullet mode. As the DC current is increased above threshold, the bullet mode appears to increase in size, suggesting increased translational motion. The reduced spatial overlap of the bullet and FMR modes, and this putative translational motion, may impede the injection locking and contribute to the reduced locking range observed within NC-SHNO devices. This illustrates a more general need to control the geometry of an injection-locked oscillator so that the autonomous dynamics of the oscillator exhibit strong spatial overlap with those resulting from the injected signal.

Published
2018
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3. Spatial Mapping of Torques within a Spin Hall Nano-oscillator

Author

Spicer, Timothy M, Keatley, Paul S, Loughran, Thomas H J, Dvornik, Mykola, Awad, A. A., Dürrenfeld, Philipp, Houshang, Afshin, Ranjbar, Mojtaba, Åkerman, Johan, Kruglyak, Volodymyr V., and Hicken, Robert J

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics, Condensed Matter - Materials Science
Abstract

Time-resolved scanning Kerr microscopy (TRSKM) was used to study precessional magnetization dynamics induced by a radio frequency (RF) current within a Al$_2$O$_3$/Py(5 nm)/Pt(6 nm)/Au(150 nm) spin Hall nano-oscillator structure. The Au layer was formed into two needle-shaped electrical contacts that concentrated the current in the centre of a Py/Pt mesa of 4 $\mu$m diameter. Due to the spin Hall effect, current within the Pt layer drives a spin current into the Py layer, exerting a spin transfer torque (STT). By injecting RF current, and exploiting the phase-sensitivity of TRSKM and the symmetry of the device structure, the STT and Oersted field torques have been separated and spatially mapped. The STT and torque due to the in-plane Oersted field are observed to exhibit minima at the device centre that is ascribed to spreading of RF current that is not observed for DC current. Torques associated with the RF current may destabilise the position of the self-localised bullet mode excited by the DC current, and inhibit injection locking. The present study demonstrates the need to characterise both DC and RF current distributions carefully.

Published
2018
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4. A platform for time-resolved scanning Kerr microscopy in the near-field

Author

Keatley, Paul S., Loughran, Thomas H. J., Hendry, Euan, Barnes, William L., Hicken, Robert J., Childress, Jeffrey R., and Katine, Jordan A.

Subjects
Condensed Matter - Materials Science
Abstract

Time-resolved scanning Kerr microscopy (TRSKM) is a powerful technique for the investigation of picosecond magnetization dynamics at sub-micron length scales by means of the magneto-optical Kerr effect (MOKE). The spatial resolution of conventional (focused) Kerr microscopy using a microscope objective lens is determined by the optical diffraction limit so that the nanoscale character of the magnetization dynamics is lost. Here we present a platform to overcome this limitation by means of a near-field TRSKM that incorporates an atomic force microscope (AFM) with optical access to a metallic AFM probe with a nanoscale aperture at its tip. We demonstrate the near-field capability of the instrument through the comparison of time-resolved polar Kerr images of magnetization dynamics within a microscale NiFe rectangle acquired using both near-field and focused TRSKM techniques at a wavelength of 800 nm. The flux-closure domain state of the in-plane equilibrium magnetization provided the maximum possible dynamic polar Kerr contrast across the central domain wall, and enabled an assessment of the magneto-optical spatial resolution of each technique. Line profiles extracted from the Kerr images demonstrate that the near-field spatial resolution was enhanced with respect to that of the focused Kerr images. Furthermore, the near-field polar Kerr signal (~1 mdeg) was more than half that of the focused Kerr signal, despite the potential loss of probe light due to internal reflections within the AFM tip. We have confirmed the near-field operation by exploring the influence of the tip-sample separation, and have determined the spatial resolution to be ~550 nm for an aperture with a sub-wavelength diameter of 400 nm. The spatial resolution of the near-field TRSKM was in good agreement with finite element modelling of the aperture..., Comment: Abstract cut due to character limit, see PDF for full abstract

Published
2017
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5. Impaired spatial memory in adult vitamin D deficient BALB/c mice is associated with reductions in spine density, nitric oxide, and neural nitric oxide synthase in the hippocampus

Author

Md. Mamun Al-Amin, Robert K. P. Sullivan, Suzy Alexander, David A. Carter, DanaKai Bradford, and Thomas H. J. Burne

Subjects
vitamin d, hippocampus, spatial learning, ca1, mushroom spine, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Vitamin D deficiency is prevalent in adults and is associated with cognitive impairment. However, the mechanism by which adult vitamin D (AVD) deficiency affects cognitive function remains unclear. We examined spatial memory impairment in AVD-deficient BALB/c mice and its underlying mechanism by measuring spine density, long term potentiation (LTP), nitric oxide (NO), neuronal nitric oxide synthase (nNOS), and endothelial NOS (eNOS) in the hippocampus. Adult male BALB/c mice were fed a control or vitamin D deficient diet for 20 weeks. Spatial memory performance was measured using an active place avoidance (APA) task, where AVD-deficient mice had reduced latency entering the shock zone compared to controls. We characterised hippocampal spine morphology in the CA1 and dentate gyrus (DG) and made electrophysiological recordings in the hippocampus of behaviourally naïve mice to measure LTP. We next measured NO, as well as glutathione, lipid peroxidation and oxidation of protein products and quantified hippocampal immunoreactivity for nNOS and eNOS. Spine morphology analysis revealed a significant reduction in the number of mushroom spines in the CA1 dendrites but not in the DG. There was no effect of diet on LTP. However, hippocampal NO levels were depleted whereas other oxidation markers were unaltered by AVD deficiency. We also showed a reduced nNOS, but not eNOS, immunoreactivity. Finally, vitamin D supplementation for 10 weeks to AVD-deficient mice restored nNOS immunoreactivity to that seen in in control mice. Our results suggest that lower levels of NO and reduced nNOS immunostaining contribute to hippocampal-dependent spatial learning deficits in AVD-deficient mice.

Published
2022
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7. Elp2 mutations perturb the epitranscriptome and lead to a complex neurodevelopmental phenotype

Author

Marija Kojic, Tomasz Gawda, Monika Gaik, Alexander Begg, Anna Salerno-Kochan, Nyoman D. Kurniawan, Alun Jones, Katarzyna Drożdżyk, Anna Kościelniak, Andrzej Chramiec-Głąbik, Soroor Hediyeh-Zadeh, Maria Kasherman, Woo Jun Shim, Enakshi Sinniah, Laura A. Genovesi, Rannvá K. Abrahamsen, Christina D. Fenger, Camilla G. Madsen, Julie S. Cohen, Ali Fatemi, Zornitza Stark, Sebastian Lunke, Joy Lee, Jonas K. Hansen, Martin F. Boxill, Boris Keren, Isabelle Marey, Margarita S. Saenz, Kathleen Brown, Suzanne A. Alexander, Sergey Mureev, Alina Batzilla, Melissa J. Davis, Michael Piper, Mikael Bodén, Thomas H. J. Burne, Nathan J. Palpant, Rikke S. Møller, Sebastian Glatt, and Brandon J. Wainwright

Subjects
Science
Abstract

Subunits of the Elongator complex have been implicated in several nervous system pathologies. Here, the authors identify ELP2 variants in six patients with neurodevelopmental anomalies and show in mouse models that these variants impact protein stability and the activity of the complex during brain development.

Published
2021
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8. Genome-wide association study identifies 143 loci associated with 25 hydroxyvitamin D concentration

Author

Joana A. Revez, Tian Lin, Zhen Qiao, Angli Xue, Yan Holtz, Zhihong Zhu, Jian Zeng, Huanwei Wang, Julia Sidorenko, Kathryn E. Kemper, Anna A. E. Vinkhuyzen, Julanne Frater, Darryl Eyles, Thomas H. J. Burne, Brittany Mitchell, Nicholas G. Martin, Gu Zhu, Peter M. Visscher, Jian Yang, Naomi R. Wray, and John J. McGrath

Subjects
Science
Abstract

Vitamin D is a precursor of the steroid hormone 1,25-dihydroxyvitamin D3, and its deficiency is associated with many adverse health outcomes. Here, Revez et al. perform a genome-wide association study for circulating 25-hydroxyvitamin D in 417,580 individuals and test for potential causal relationships with other traits using Mendelian randomization.

Published
2020
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10. Elp2 mutations perturb the epitranscriptome and lead to a complex neurodevelopmental phenotype

Author

Kojic, Marija, Gawda, Tomasz, Gaik, Monika, Begg, Alexander, Salerno-Kochan, Anna, Kurniawan, Nyoman D., Jones, Alun, Drożdżyk, Katarzyna, Kościelniak, Anna, Chramiec-Głąbik, Andrzej, Hediyeh-Zadeh, Soroor, Kasherman, Maria, Shim, Woo Jun, Sinniah, Enakshi, Genovesi, Laura A., Abrahamsen, Rannvá K., Fenger, Christina D., Madsen, Camilla G., Cohen, Julie S., Fatemi, Ali, Stark, Zornitza, Lunke, Sebastian, Lee, Joy, Hansen, Jonas K., Boxill, Martin F., Keren, Boris, Marey, Isabelle, Saenz, Margarita S., Brown, Kathleen, Alexander, Suzanne A., Mureev, Sergey, Batzilla, Alina, Davis, Melissa J., Piper, Michael, Bodén, Mikael, Burne, Thomas H. J., Palpant, Nathan J., Møller, Rikke S., Glatt, Sebastian, and Wainwright, Brandon J.

Published
2021
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13. Subcortical Dopamine and Cognition in Schizophrenia: Looking Beyond Psychosis in Preclinical Models

Author

Kyna-Anne Conn, Thomas H. J. Burne, and James P. Kesby

Subjects
operant tasks, goal-directed behavior, reversal learning, rodent, translation, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Schizophrenia is characterized by positive, negative and cognitive symptoms. All current antipsychotic treatments feature dopamine-receptor antagonism that is relatively effective at addressing the psychotic (positive) symptoms of schizophrenia. However, there is no clear evidence that these medications improve the negative or cognitive symptoms, which are the greatest predictors of functional outcomes. One of the most robust pathophysiological observations in patients with schizophrenia is increased subcortical dopamine neurotransmission, primarily in the associative striatum. This brain area has an important role in a range of cognitive processes. Dopamine is also known to play a major part in regulating a number of cognitive functions impaired in schizophrenia but much of this research has been focused on cortical dopamine. Emerging research highlights the strong influence subcortical dopamine has on a range of cognitive domains, including attention, reward learning, goal-directed action and decision-making. Nonetheless, the precise role of the associative striatum in the cognitive impairments observed in schizophrenia remains poorly understood, presenting an opportunity to revisit its contribution to schizophrenia. Without a better understanding of the mechanisms underlying cognitive dysfunction, treatment development remains at a standstill. For this reason, improved preclinical animal models are needed if we are to understand the complex relationship between subcortical dopamine and cognition. A range of new techniques are facillitating the discrete manipulation of dopaminergic neurotransmission and measurements of cognitive performance, which can be investigated using a variety of sensitive translatable tasks. This has the potential to aid the successful incorporation of recent clinical research to address the lack of treatment strategies for cognitive symptoms in schizophrenia. This review will give an overview on the current state of research focused on subcortical dopamine and cognition in the context of schizophrenia research. We also discuss future strategies and approaches aimed at improving the translational outcomes for the treatment of cognitive deficits in schizophrenia.

Published
2020
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14. Analysis of hippocampal-dependent learning and memory behaviour in mice lacking Nfix from adult neural stem cells

Author

Oressia Zalucki, Danyon Harkins, Lachlan Harris, Thomas H. J. Burne, Richard M. Gronostajski, and Michael Piper

Subjects
NFIX, Active place avoidance, Hippocampus, Learning and memory, Medicine, Biology (General), QH301-705.5, Science (General), Q1-390
Abstract

Abstract Objective The active place avoidance task (APA) is a behavioural task used to assess learning and memory in rodents. This task relies on the hippocampus, a region of the cerebral cortex capable of generating new neurons from neural stem cells. In this study, to gain further insight into the behavioural phenotype of mice deficient in the transcription factor Nfix, a gene expressed by adult neural stem cells, we examined learning and memory parameters from the APA task that were not published in our original investigation. We analysed time to first and second shock, maximum path and time of shock avoidance, number of entries into the shock zone and time spent in the shock zone. We also assessed performance in the APA task based on sex. Results We found mice deficient in Nfix displayed decreased latency to second shock compared to the control mice. Nfix deficient mice entered the shock zone more frequently and also spent more time in the shock zone. Our data provides further insights into the memory deficits evident in Nfix mutant mice, indicating these mice have a memory retrieval problem and may employ a different navigation strategy in the APA task.

Published
2018
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20. Global plant trait relationships extend to the climatic extremes of the tundra biome

Author

Thomas, H. J. D., Bjorkman, A. D., Myers-Smith, I. H., Elmendorf, S. C., Kattge, J., Diaz, S., Vellend, M., Blok, D., Cornelissen, J. H. C., Forbes, B. C., Henry, G. H. R., Hollister, R. D., Normand, S., Prevéy, J. S., Rixen, C., Schaepman-Strub, G., Wilmking, M., Wipf, S., Cornwell, W. K., Beck, P. S. A., Georges, D., Goetz, S. J., Guay, K. C., Rüger, N., Soudzilovskaia, N. A., Spasojevic, M. J., Alatalo, J. M., Alexander, H. D., Anadon-Rosell, A., Angers-Blondin, S., te Beest, M., Berner, L. T., Björk, R. G., Buchwal, A., Buras, A., Carbognani, M., Christie, K. S., Collier, L. S., Cooper, E. J., Elberling, B., Eskelinen, A., Frei, E. R., Grau, O., Grogan, P., Hallinger, M., Heijmans, M. M. P. D., Hermanutz, L., Hudson, J. M. G., Johnstone, J. F., Hülber, K., Iturrate-Garcia, M., Iversen, C. M., Jaroszynska, F., Kaarlejarvi, E., Kulonen, A., Lamarque, L. J., Lantz, T. C., Lévesque, E., Little, C. J., Michelsen, A., Milbau, A., Nabe-Nielsen, J., Nielsen, S. S., Ninot, J. M., Oberbauer, S. F., Olofsson, J., Onipchenko, V. G., Petraglia, A., Rumpf, S. B., Shetti, R., Speed, J. D. M., Suding, K. N., Tape, K. D., Tomaselli, M., Trant, A. J., Treier, U. A., Tremblay, M., Venn, S. E., Vowles, T., Weijers, S., Wookey, P. A., Zamin, T. J., Bahn, M., Blonder, B., van Bodegom, P. M., Bond-Lamberty, B., Campetella, G., Cerabolini, B. E. L., Chapin, III, F. S., Craine, J. M., Dainese, M., Green, W. A., Jansen, S., Kleyer, M., Manning, P., Niinemets, Ü., Onoda, Y., Ozinga, W. A., Peñuelas, J., Poschlod, P., Reich, P. B., Sandel, B., Schamp, B. S., Sheremetiev, S. N., and de Vries, F. T.

Published
2020
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21. Gestational vitamin D deficiency and autism spectrum disorder

Author

Anna A. E. Vinkhuyzen, Darryl W. Eyles, Thomas H. J. Burne, Laura M. E. Blanken, Claudia J. Kruithof, Frank Verhulst, Tonya White, Vincent W. Jaddoe, Henning Tiemeier, and John J. McGrath

Subjects
Psychiatry, RC435-571
Abstract

Background There is growing interest in linking vitamin D deficiency with autism spectrum disorders (ASDs). The association between vitamin D deficiency during gestation, a critical period in neurodevelopment, and ASD is not well understood. Aims To determine the association between gestational vitamin D status and ASD. Method Based on a birth cohort (n=4334), we examined the association between 25-hydroxyvitamin D (25OHD), assessed from both maternal mid-gestation sera and neonatal sera, and ASD (defined by clinical records; n=68 cases). Results Individuals in the 25OHD-deficient group at mid-gestation had more than twofold increased risk of ASD (odds ratio (OR)=2.42, 95% confidence interval (CI) 1.09 to 5.07, P=0.03) compared with the sufficient group. The findings persisted in analyses including children of European ethnicity only. Conclusions Mid-gestational vitamin D deficiency was associated with an increased risk of ASD. Because gestational vitamin D deficiency is readily preventable with safe, inexpensive and readily available supplementation, this risk factor warrants closer scrutiny.

Published
2017
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22. Baseline-dependent effects of amphetamine on attention are associated with striatal dopamine metabolism

Author

Karly M. Turner, James Peak, and Thomas H. J. Burne

Subjects
Medicine, Science
Abstract

Abstract Psychostimulants, such as amphetamine, are widely used to treat attentional deficits. In humans, response to dopaminergic medications is complex with improvement often dependent on baseline performance. Our goal was to determine if attention in rats could be improved by low dose amphetamine in a baseline-dependent manner by examining the relationship between task performance, drug response and monoamine levels in corticostriatal tissue. Firstly, rats performed a signal detection task with varying signal durations before administration of saline, 0.1 or 0.25 mg/kg amphetamine. Following 0.1 mg/kg amphetamine, accuracy in poor performing individuals increased to that of high performing rats. Furthermore, baseline accuracy correlated with the magnitude of improvement after amphetamine. Secondly, neurochemical analysis of monoamine content and gene expression levels in the prefrontal cortex (PFC) and dorsal striatum (CPU) was conducted. CPU homovanillic acid and 5-hydroxyindoleacetic acid levels were increased in poor performers with a significant correlation between the expression of the dopamine transporter gene and baseline accuracy. No changes were found in the PFC. These results indicated poor performance was associated with greater response to amphetamine and altered DA and 5-HT neurotransmitter systems in CPU. These results suggest striatal monoamine function may be fundamental to explaining individual differences in psychostimulant response.

Published
2017
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27. Serum sulfate level and Slc13a1 mRNA expression remain unaltered in a mouse model of moderate vitamin D deficiency.

Author

Atcheson, Ranita J., Burne, Thomas H. J., and Dawson, Paul A.

Abstract

Sulfate is essential for healthy foetal growth and neurodevelopment. The SLC13A1 sulfate transporter is primarily expressed in the kidney where it mediates sulfate reabsorption and maintains circulating sulfate levels. To meet foetal demands, maternal sulfate levels increase by twofold in pregnancy via upregulated SLC13A1 expression. Previous studies found hyposulfataemia and reduced renal Slc13a1 mRNA expression in rodent models with either severe vitamin D deficiency or perturbed vitamin D signalling. Here we investigated a mouse model of moderate vitamin D deficiency. However, serum sulfate level and renal Slc13a1 mRNA expression was not decreased by a moderate reduction in circulating vitamin D level. We confirmed that the mouse Slc13a1 5'-flanking region was upregulated by 1,25(OH)2D3 using luciferase assays in a cultured renal OK cell line. These results support the presence of a functional VDRE in the mouse Slc13a1 but suggests that moderate vitamin D deficiency does not impact on sulfate homeostasis. As sulfate biology is highly conserved between rodents and humans, we proposed that human SLC13A1 would be under similar transcriptional regulation by 1,25(OH)2D3. Using an online prediction tool we identified a putative VDRE in the SLC13A1 5'-flanking region but unlike the mouse Slc13a1 sequence, the human sequence did not confer a significant response to 1,25(OH)2D3 in vitro. Overall, this study suggests that moderate vitamin D deficiency may not alter sulfate homeostasis. This needs to be confirmed in humans, particularly during pregnancy when vitamin D and sulfate levels need to be maintained at high levels for healthy maternal and child outcomes. [ABSTRACT FROM AUTHOR]

Published
2023
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28. The association between neonatal vitamin D status and risk of schizophrenia

Author

Eyles, Darryl W., Trzaskowski, Maciej, Vinkhuyzen, Anna A. E., Mattheisen, Manuel, Meier, Sandra, Gooch, Helen, Anggono, Victor, Cui, Xiaoying, Tan, Men Chee, Burne, Thomas H. J., Jang, Se Eun, Kvaskoff, David, Hougaard, David M., Nørgaard-Pedersen, Bent, Cohen, Arieh, Agerbo, Esben, Pedersen, Carsten B., Børglum, Anders D., Mors, Ole, Sah, Pankaj, Wray, Naomi R., Mortensen, Preben B., and McGrath, John J.

Published
2018
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30. Touchscreen-based Visual Discrimination and Reversal Tasks for Mice to Test Cognitive Flexibility

Author

Karly Turner, Christopher Simpson, and Thomas H. J. Burne

Subjects
Biology (General), QH301-705.5
Abstract

Reversal learning can be used to examine deficits in cognitive flexibility, which have been linked to a number of neuropsychiatric disorders including schizophrenia and addiction. However, methods of examining reversal learning have varied substantially between species. Touchscreen technology has allowed researchers to explore cognitive deficits with a platform that is translatable across rodents, non-human primates and human subjects. Here we describe a method for measuring visual discrimination and reversal learning in mice using automated touchscreen-based operant chambers.

Published
2017
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31. Effect of the glucocorticoid receptor antagonist RU486 on MK-801 induced behavioural sensitisation.

Author

Emilia M Lefevre, Gregory A Medley, Timothy Reeks, Suzy Alexander, Thomas H J Burne, and Darryl W Eyles

Subjects
Medicine, Science
Abstract

Stress is known to modulate sensitisation to repeated psychostimulant exposure. However, there is no direct evidence linking glucocorticoids and sensitisation achieved by repeated administration of the NMDA receptor antagonist MK-801. We tested the hypothesis that co-administration of RU486, a glucocorticoid receptor (GR) antagonist, prior to repeated daily MK-801 injections would block the expression of locomotor sensitisation due to its dual effects on corticosterone and dopamine. We employed a repeated MK-801 administration locomotor sensitisation paradigm in male Sprague Dawley rats. RU486 or a dimethyl sulfoxide (DMSO) vehicle was co-administered with MK-801 or saline during the induction phase. Subsequent to withdrawal, rats were challenged with MK-801 alone to test for the expression of sensitisation. In a separate cohort of rats, plasma corticosterone levels were quantified from blood samples taken on the 1st, 4th and 7th day of induction and at expression. One day after challenge, nucleus accumbens tissue levels of dopamine and its metabolites DOPAC and HVA were measured. During the induction phase, RU486 progressively enhanced locomotor sensitisation to MK-801. RU486 and MK-801 both showed stimulatory effects on corticosterone levels and this was further augmented when given in combination. Contrary to our hypothesis, RU486 did not block the expression of locomotor sensitisation to MK-801 and actually increased levels of dopamine, DOPAC and HVA in nucleus accumbens tissue. Our results showed that RU486 has augmentative rather than inhibitory effects on MK-801-induced sensitisation. This study indicates a divergent role for glucocorticoids in sensitisation to MK-801 compared to sensitisation with other psychostimulants.

Published
2017
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33. Elp2 mutations perturb the epitranscriptome and lead to a complex neurodevelopmental phenotype

Author

Nyoman D. Kurniawan, Margarita Saenz, Melissa J. Davis, Anna Salerno-Kochan, Julie S. Cohen, Sebastian Glatt, Anna Kościelniak, Ali Fatemi, Mikael Bodén, Martin F. Boxill, Joy Lee, Woo Jun Shim, Nathan J. Palpant, Tomasz Gawda, Jonas K. Hansen, Katarzyna Drożdżyk, Alexander Begg, Rikke S. Møller, Michael Piper, Marija Kojic, Soroor Hediyeh-Zadeh, Thomas H. J. Burne, Brandon J. Wainwright, Kathleen Brown, Isabelle Marey, Sergey Mureev, Rannvá K. Abrahamsen, Enakshi Sinniah, Zornitza Stark, Laura A. Genovesi, Monika Gaik, Andrzej Chramiec-Głąbik, Suzanne Alexander, Alun Jones, Alina Batzilla, Christina Fenger, Camilla Gøbel Madsen, Maria Kasherman, Boris Keren, and Sebastian Lunke

Subjects
0301 basic medicine, Microcephaly, TRNA modification, Autism Spectrum Disorder, Science, General Physics and Astronomy, Spodoptera, Biology, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Epigenesis, Genetic, 03 medical and health sciences, 0302 clinical medicine, Intellectual Disability, Intellectual disability, Sf9 Cells, medicine, Animals, Humans, Mice, Knockout, Mutation, Multidisciplinary, Neurodegeneration, Intracellular Signaling Peptides and Proteins, Translation (biology), General Chemistry, medicine.disease, Grooming, Phenotype, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Mice, Inbred DBA, Neurodevelopmental Disorders, Autism spectrum disorder, Transcriptome, Neuroscience, 030217 neurology & neurosurgery
Abstract

Intellectual disability (ID) and autism spectrum disorder (ASD) are the most common neurodevelopmental disorders and are characterized by substantial impairment in intellectual and adaptive functioning, with their genetic and molecular basis remaining largely unknown. Here, we identify biallelic variants in the gene encoding one of the Elongator complex subunits, ELP2, in patients with ID and ASD. Modelling the variants in mice recapitulates the patient features, with brain imaging and tractography analysis revealing microcephaly, loss of white matter tract integrity and an aberrant functional connectome. We show that the Elp2 mutations negatively impact the activity of the complex and its function in translation via tRNA modification. Further, we elucidate that the mutations perturb protein homeostasis leading to impaired neurogenesis, myelin loss and neurodegeneration. Collectively, our data demonstrate an unexpected role for tRNA modification in the pathogenesis of monogenic ID and ASD and define Elp2 as a key regulator of brain development.

Published
2021
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34. Substance use confounds associations between peer victimization and aggression in adolescence with mental disorders in adulthood:a prospective birth cohort study

Author

Sarala, M. (Marian), Miettunen, J. (Jouko), Alakokkare, A.-E. (Anni-Emilia), Mustonen, A. (Antti), Scott, J. G. (James G.), Thomas, H. J. (Hannah J.), Hurtig, T. (Tuula), Niemelä, S. (Solja), Sarala, M. (Marian), Miettunen, J. (Jouko), Alakokkare, A.-E. (Anni-Emilia), Mustonen, A. (Antti), Scott, J. G. (James G.), Thomas, H. J. (Hannah J.), Hurtig, T. (Tuula), and Niemelä, S. (Solja)

Abstract

Introduction: Peer victimization and aggression in adolescence are associated with later mental health morbidity. However, studies examining this association have not controlled for adolescent substance use. We aimed to study the associations between peer victimization, peer aggression, and mental disorders in adulthood, adjusting for substance use in adolescence. Methods: Participants were from the prospective Northern Finland Birth Cohort 1986. Data were available for 6682 individuals (70.8% of the original sample). Peer victimization and peer aggression were assessed with items from the Achenbach Youth Self Report at ages 15−16 years. Outcomes were nonorganic psychosis, anxiety disorder, mood disorder, substance use disorder, and any mental disorder (a none-vs-any indicator) at age 33 years collected from nationwide health care, insurance, and pension registers. Family structure, alcohol intoxication frequency, daily smoking, illicit drug use, and baseline psychopathology using Youth Self-Report total score, and parental mental disorders were considered as confounding factors. Results: In multivariable analyses, the association between peer victimization and psychosis (Hazard ratio [HR]: 2.9, 95% confidence interval [CI]: 1.2−6.9, p = .020) and mood disorder (HR: 1.7, 95% CI: 1.2−2.4, p = .012) in females remained significant after adjusting for confounders. Other associations between female and male peer victimization or aggression and the studied outcomes attenuated after adjustments. Conclusions: Some associations between peer victimization and aggression and later mental health morbidity are explained by adolescent substance use. For females, substance use does not account for the increased risk of psychosis and mood disorder in those who experience peer victimization.

Published
2022

35. Global maps of soil temperature

Author

Lembrechts, J. J. (Jonas J.), van den Hoogen, J. (Johan), Aalto, J. (Juha), Ashcroft, M. B. (Michael B.), De Frenne, P. (Pieter), Kemppinen, J. (Julia), Kopecky, M. (Martin), Luoto, M. (Miska), Maclean, I. M. (Ilya M. D.), Crowther, T. W. (Thomas W.), Bailey, J. J. (Joseph J.), Haesen, S. (Stef), Klinges, D. H. (David H.), Niittynen, P. (Pekka), Scheffers, B. R. (Brett R.), Van Meerbeek, K. (Koenraad), Aartsma, P. (Peter), Abdalaze, O. (Otar), Abedi, M. (Mehdi), Aerts, R. (Rien), Ahmadian, N. (Negar), Ahrends, A. (Antje), Alatalo, J. M. (Juha M.), Alexander, J. M. (Jake M.), Allonsius, C. N. (Camille Nina), Altman, J. (Jan), Ammann, C. (Christof), Andres, C. (Christian), Andrews, C. (Christopher), Ardo, J. (Jonas), Arriga, N. (Nicola), Arzac, A. (Alberto), Aschero, V. (Valeria), Assis, R. L. (Rafael L.), Assmann, J. J. (Jakob Johann), Bader, M. Y. (Maaike Y.), Bahalkeh, K. (Khadijeh), Barancok, P. (Peter), Barrio, I. C. (Isabel C.), Barros, A. (Agustina), Barthel, M. (Matti), Basham, E. W. (Edmund W.), Bauters, M. (Marijn), Bazzichetto, M. (Manuele), Marchesini, L. B. (Luca Belelli), Bell, M. C. (Michael C.), Benavides, J. C. (Juan C.), Benito Alonso, J. L. (Jose Luis), Berauer, B. J. (Bernd J.), Bjerke, J. W. (Jarle W.), Bjork, R. G. (Robert G.), Bjorkman, M. P. (Mats P.), Bjornsdottir, K. (Katrin), Blonder, B. (Benjamin), Boeckx, P. (Pascal), Boike, J. (Julia), Bokhorst, S. (Stef), Brum, B. N. (Barbara N. S.), Bruna, J. (Josef), Buchmann, N. (Nina), Buysse, P. (Pauline), Camargo, J. L. (Jose Luis), Campoe, O. C. (Otavio C.), Candan, O. (Onur), Canessa, R. (Rafaella), Cannone, N. (Nicoletta), Carbognani, M. (Michele), Carnicer, J. (Jofre), Casanova-Katny, A. (Angelica), Cesarz, S. (Simone), Chojnicki, B. (Bogdan), Choler, P. (Philippe), Chown, S. L. (Steven L.), Cifuentes, E. F. (Edgar F.), Ciliak, M. (Marek), Contador, T. (Tamara), Convey, P. (Peter), Cooper, E. J. (Elisabeth J.), Cremonese, E. (Edoardo), Curasi, S. R. (Salvatore R.), Curtis, R. (Robin), Cutini, M. (Maurizio), Dahlberg, C. J. (C. Johan), Daskalova, G. N. (Gergana N.), Angel de Pablo, M. (Miguel), Della Chiesa, S. (Stefano), Dengler, J. (Juergen), Deronde, B. (Bart), Descombes, P. (Patrice), Di Cecco, V. (Valter), Di Musciano, M. (Michele), Dick, J. (Jan), Dimarco, R. D. (Romina D.), Dolezal, J. (Jiri), Dorrepaal, E. (Ellen), Dusek, J. (Jiri), Eisenhauer, N. (Nico), Eklundh, L. (Lars), Erickson, T. E. (Todd E.), Erschbamer, B. (Brigitta), Eugster, W. (Werner), Ewers, R. M. (Robert M.), Exton, D. A. (Dan A.), Fanin, N. (Nicolas), Fazlioglu, F. (Fatih), Feigenwinter, I. (Iris), Fenu, G. (Giuseppe), Ferlian, O. (Olga), Fernandez Calzado, M. R. (M. Rosa), Fernandez-Pascual, E. (Eduardo), Finckh, M. (Manfred), Higgens, R. F. (Rebecca Finger), Forte, T. G. (T'ai G. W.), Freeman, E. C. (Erika C.), Frei, E. R. (Esther R.), Fuentes-Lillo, E. (Eduardo), Garcia, R. A. (Rafael A.), Garcia, M. B. (Maria B.), Geron, C. (Charly), Gharun, M. (Mana), Ghosn, D. (Dany), Gigauri, K. (Khatuna), Gobin, A. (Anne), Goded, I. (Ignacio), Goeckede, M. (Mathias), Gottschall, F. (Felix), Goulding, K. (Keith), Govaert, S. (Sanne), Graae, B. J. (Bente Jessen), Greenwood, S. (Sarah), Greiser, C. (Caroline), Grelle, A. (Achim), Guenard, B. (Benoit), Guglielmin, M. (Mauro), Guillemot, J. (Joannes), Haase, P. (Peter), Haider, S. (Sylvia), Halbritter, A. H. (Aud H.), Hamid, M. (Maroof), Hammerle, A. (Albin), Hampe, A. (Arndt), Haugum, S. V. (Siri, V), Hederova, L. (Lucia), Heinesch, B. (Bernard), Helfter, C. (Carole), Hepenstrick, D. (Daniel), Herberich, M. (Maximiliane), Herbst, M. (Mathias), Hermanutz, L. (Luise), Hik, D. S. (David S.), Hoffren, R. (Raul), Homeier, J. (Juergen), Hörtnagl, L. (Lukas), Hoye, T. T. (Toke T.), Hrbacek, F. (Filip), Hylander, K. (Kristoffer), Iwata, H. (Hiroki), Jackowicz-Korczynski, M. A. (Marcin Antoni), Jactel, H. (Herve), Jarveoja, J. (Jarvi), Jastrzebowski, S. (Szymon), Jentsch, A. (Anke), Jimenez, J. J. (Juan J.), Jonsdottir, I. S. (Ingibjorg S.), Jucker, T. (Tommaso), Jump, A. S. (Alistair S.), Juszczak, R. (Radoslaw), Kanka, R. (Robert), Kaspar, V. (Vit), Kazakis, G. (George), Kelly, J. (Julia), Khuroo, A. A. (Anzar A.), Klemedtsson, L. (Leif), Klisz, M. (Marcin), Kljun, N. (Natascha), Knohl, A. (Alexander), Kobler, J. (Johannes), Kollar, J. (Jozef), Kotowska, M. M. (Martyna M.), Kovacs, B. (Bence), Kreyling, J. (Juergen), Lamprecht, A. (Andrea), Lang, S. I. (Simone, I), Larson, C. (Christian), Larson, K. (Keith), Laska, K. (Kamil), Maire, G. I. (Guerric Ie), Leihy, R. I. (Rachel, I), Lens, L. (Luc), Liljebladh, B. (Bengt), Lohila, A. (Annalea), Lorite, J. (Juan), Loubet, B. (Benjamin), Lynn, J. (Joshua), Macek, M. (Martin), Mackenzie, R. (Roy), Magliulo, E. (Enzo), Maier, R. (Regine), Malfasi, F. (Francesco), Malis, F. (Frantisek), Man, M. (Matej), Manca, G. (Giovanni), Manco, A. (Antonio), Manise, T. (Tanguy), Manolaki, P. (Paraskevi), Marciniak, F. (Felipe), Matula, R. (Radim), Clara Mazzolari, A. (Ana), Medinets, S. (Sergiy), Medinets, V. (Volodymyr), Meeussen, C. (Camille), Merinero, S. (Sonia), Guimaraes Mesquita, R. d. (Rita de Cassia), Meusburger, K. (Katrin), Meysman, F. J. (Filip J. R.), Michaletz, S. T. (Sean T.), Milbau, A. (Ann), Moiseev, D. (Dmitry), Moiseev, P. (Pavel), Mondoni, A. (Andrea), Monfries, R. (Ruth), Montagnani, L. (Leonardo), Moriana-Armendariz, M. (Mikel), di Cella, U. M. (Umberto Morra), Moersdorf, M. (Martin), Mosedale, J. R. (Jonathan R.), Muffler, L. (Lena), Munoz-Rojas, M. (Miriam), Myers, J. A. (Jonathan A.), Myers-Smith, I. H. (Isla H.), Nagy, L. (Laszlo), Nardino, M. (Marianna), Naujokaitis-Lewis, I. (Ilona), Newling, E. (Emily), Nicklas, L. (Lena), Niedrist, G. (Georg), Niessner, A. (Armin), Nilsson, M. B. (Mats B.), Normand, S. (Signe), Nosetto, M. D. (Marcelo D.), Nouvellon, Y. (Yann), Nunez, M. A. (Martin A.), Ogaya, R. (Roma), Ogee, J. (Jerome), Okello, J. (Joseph), Olejnik, J. (Janusz), Olesen, J. E. (Jorgen Eivind), Opedal, O. H. (Oystein H.), Orsenigo, S. (Simone), Palaj, A. (Andrej), Pampuch, T. (Timo), Panov, A. V. (Alexey V.), Pärtel, M. (Meelis), Pastor, A. (Ada), Pauchard, A. (Aníbal), Pauli, H. (Harald), Pavelka, M. (Marian), Pearse, W. D. (William D.), Peichl, M. (Matthias), Pellissier, L. (Loïc), Penczykowski, R. M. (Rachel M.), Penuelas, J. (Josep), Petit Bon, M. (Matteo), Petraglia, A. (Alessandro), Phartyal, S. S. (Shyam S.), Phoenix, G. K. (Gareth K.), Pio, C. (Casimiro), Pitacco, A. (Andrea), Pitteloud, C. (Camille), Plichta, R. (Roman), Porro, F. (Francesco), Portillo-Estrada, M. (Miguel), Poulenard, J. (Jérôme), Poyatos, R. (Rafael), Prokushkin, A. S. (Anatoly S.), Puchalka, R. (Radoslaw), Pușcaș, M. (Mihai), Radujković, D. (Dajana), Randall, K. (Krystal), Ratier Backes, A. (Amanda), Remmele, S. (Sabine), Remmers, W. (Wolfram), Renault, D. (David), Risch, A. C. (Anita C.), Rixen, C. (Christian), Robinson, S. A. (Sharon A.), Robroek, B. J. (Bjorn J. M.), Rocha, A. V. (Adrian V.), Rossi, C. (Christian), Rossi, G. (Graziano), Roupsard, O. (Olivier), Rubtsov, A. V. (Alexey V.), Saccone, P. (Patrick), Sagot, C. (Clotilde), Sallo Bravo, J. (Jhonatan), Santos, C. C. (Cinthya C.), Sarneel, J. M. (Judith M.), Scharnweber, T. (Tobias), Schmeddes, J. (Jonas), Schmidt, M. (Marius), Scholten, T. (Thomas), Schuchardt, M. (Max), Schwartz, N. (Naomi), Scott, T. (Tony), Seeber, J. (Julia), Segalin De Andrade, A. C. (Ana Cristina), Seipel, T. (Tim), Semenchuk, P. (Philipp), Senior, R. A. (Rebecca A.), Serra-Diaz, J. M. (Josep M.), Sewerniak, P. (Piotr), Shekhar, A. (Ankit), Sidenko, N. V. (Nikita V.), Siebicke, L. (Lukas), Siegwart Collier, L. (Laura), Simpson, E. (Elizabeth), Siqueira, D. P. (David P.), Sitková, Z. (Zuzana), Six, J. (Johan), Smiljanic, M. (Marko), Smith, S. W. (Stuart W.), Smith-Tripp, S. (Sarah), Somers, B. (Ben), Sørensen, M. V. (Mia Vedel), Souza, J. J. (José João L. L.), Souza, B. I. (Bartolomeu Israel), Dias, A. S. (Arildo Souza), Spasojevic, M. J. (Marko J.), Speed, J. D. (James D. M.), Spicher, F. (Fabien), Stanisci, A. (Angela), Steinbauer, K. (Klaus), Steinbrecher, R. (Rainer), Steinwandter, M. (Michael), Stemkovski, M. (Michael), Stephan, J. G. (Jörg G.), Stiegler, C. (Christian), Stoll, S. (Stefan), Svátek, M. (Martin), Svoboda, M. (Miroslav), Tagesson, T. (Torbern), Tanentzap, A. J. (Andrew J.), Tanneberger, F. (Franziska), Theurillat, J.-P. (Jean-Paul), Thomas, H. J. (Haydn J. D.), Thomas, A. D. (Andrew D.), Tielbörger, K. (Katja), Tomaselli, M. (Marcello), Treier, U. A. (Urs Albert), Trouillier, M. (Mario), Turtureanu, P. D. (Pavel Dan), Tutton, R. (Rosamond), Tyystjärvi, V. A. (Vilna A.), Ueyama, M. (Masahito), Ujházy, K. (Karol), Ujházyová, M. (Mariana), Uogintas, D. (Domas), Urban, A. V. (Anastasiya V.), Urban, J. (Josef), Urbaniak, M. (Marek), Ursu, T.-M. (Tudor-Mihai), Vaccari, F. P. (Francesco Primo), Van De Vondel, S. (Stijn), Van Den Brink, L. (Liesbeth), Van Geel, M. (Maarten), Vandvik, V. (Vigdis), Vangansbeke, P. (Pieter), Varlagin, A. (Andrej), Veen, G. F. (G. F.), Veenendaal, E. (Elmar), Venn, S. E. (Susanna E.), Verbeeck, H. (Hans), Verbrugggen, E. (Erik), Verheijen, F. G. (Frank G. A.), Villar, L. (Luis), Vitale, L. (Luca), Vittoz, P. (Pascal), Vives-Ingla, M. (Maria), Von Oppen, J. (Jonathan), Walz, J. (Josefine), Wang, R. (Runxi), Wang, Y. (Yifeng), Way, R. G. (Robert G.), Wedegärtner, R. E. (Ronja E. M.), Weigel, R. (Robert), Wild, J. (Jan), Wilkinson, M. (Matthew), Wilmking, M. (Martin), Wingate, L. (Lisa), Winkler, M. (Manuela), Wipf, S. (Sonja), Wohlfahrt, G. (Georg), Xenakis, G. (Georgios), Yang, Y. (Yan), Yu, Z. (Zicheng), Yu, K. (Kailiang), Zellweger, F. (Florian), Zhang, J. (Jian), Zhang, Z. (Zhaochen), Zhao, P. (Peng), Ziemblińska, K. (Klaudia), Zimmermann, R. (Reiner), Zong, S. (Shengwei), Zyryanov, V. I. (Viacheslav I.), Nijs, I. (Ivan), Lenoir, J. (Jonathan), Lembrechts, J. J. (Jonas J.), van den Hoogen, J. (Johan), Aalto, J. (Juha), Ashcroft, M. B. (Michael B.), De Frenne, P. (Pieter), Kemppinen, J. (Julia), Kopecky, M. (Martin), Luoto, M. (Miska), Maclean, I. M. (Ilya M. D.), Crowther, T. W. (Thomas W.), Bailey, J. J. (Joseph J.), Haesen, S. (Stef), Klinges, D. H. (David H.), Niittynen, P. (Pekka), Scheffers, B. R. (Brett R.), Van Meerbeek, K. (Koenraad), Aartsma, P. (Peter), Abdalaze, O. (Otar), Abedi, M. (Mehdi), Aerts, R. (Rien), Ahmadian, N. (Negar), Ahrends, A. (Antje), Alatalo, J. M. (Juha M.), Alexander, J. M. (Jake M.), Allonsius, C. N. (Camille Nina), Altman, J. (Jan), Ammann, C. (Christof), Andres, C. (Christian), Andrews, C. (Christopher), Ardo, J. (Jonas), Arriga, N. (Nicola), Arzac, A. (Alberto), Aschero, V. (Valeria), Assis, R. L. (Rafael L.), Assmann, J. J. (Jakob Johann), Bader, M. Y. (Maaike Y.), Bahalkeh, K. (Khadijeh), Barancok, P. (Peter), Barrio, I. C. (Isabel C.), Barros, A. (Agustina), Barthel, M. (Matti), Basham, E. W. (Edmund W.), Bauters, M. (Marijn), Bazzichetto, M. (Manuele), Marchesini, L. B. (Luca Belelli), Bell, M. C. (Michael C.), Benavides, J. C. (Juan C.), Benito Alonso, J. L. (Jose Luis), Berauer, B. J. (Bernd J.), Bjerke, J. W. (Jarle W.), Bjork, R. G. (Robert G.), Bjorkman, M. P. (Mats P.), Bjornsdottir, K. (Katrin), Blonder, B. (Benjamin), Boeckx, P. (Pascal), Boike, J. (Julia), Bokhorst, S. (Stef), Brum, B. N. (Barbara N. S.), Bruna, J. (Josef), Buchmann, N. (Nina), Buysse, P. (Pauline), Camargo, J. L. (Jose Luis), Campoe, O. C. (Otavio C.), Candan, O. (Onur), Canessa, R. (Rafaella), Cannone, N. (Nicoletta), Carbognani, M. (Michele), Carnicer, J. (Jofre), Casanova-Katny, A. (Angelica), Cesarz, S. (Simone), Chojnicki, B. (Bogdan), Choler, P. (Philippe), Chown, S. L. (Steven L.), Cifuentes, E. F. (Edgar F.), Ciliak, M. (Marek), Contador, T. (Tamara), Convey, P. (Peter), Cooper, E. J. (Elisabeth J.), Cremonese, E. (Edoardo), Curasi, S. R. (Salvatore R.), Curtis, R. (Robin), Cutini, M. (Maurizio), Dahlberg, C. J. (C. Johan), Daskalova, G. N. (Gergana N.), Angel de Pablo, M. (Miguel), Della Chiesa, S. (Stefano), Dengler, J. (Juergen), Deronde, B. (Bart), Descombes, P. (Patrice), Di Cecco, V. (Valter), Di Musciano, M. (Michele), Dick, J. (Jan), Dimarco, R. D. (Romina D.), Dolezal, J. (Jiri), Dorrepaal, E. (Ellen), Dusek, J. (Jiri), Eisenhauer, N. (Nico), Eklundh, L. (Lars), Erickson, T. E. (Todd E.), Erschbamer, B. (Brigitta), Eugster, W. (Werner), Ewers, R. M. (Robert M.), Exton, D. A. (Dan A.), Fanin, N. (Nicolas), Fazlioglu, F. (Fatih), Feigenwinter, I. (Iris), Fenu, G. (Giuseppe), Ferlian, O. (Olga), Fernandez Calzado, M. R. (M. Rosa), Fernandez-Pascual, E. (Eduardo), Finckh, M. (Manfred), Higgens, R. F. (Rebecca Finger), Forte, T. G. (T'ai G. W.), Freeman, E. C. (Erika C.), Frei, E. R. (Esther R.), Fuentes-Lillo, E. (Eduardo), Garcia, R. A. (Rafael A.), Garcia, M. B. (Maria B.), Geron, C. (Charly), Gharun, M. (Mana), Ghosn, D. (Dany), Gigauri, K. (Khatuna), Gobin, A. (Anne), Goded, I. (Ignacio), Goeckede, M. (Mathias), Gottschall, F. (Felix), Goulding, K. (Keith), Govaert, S. (Sanne), Graae, B. J. (Bente Jessen), Greenwood, S. (Sarah), Greiser, C. (Caroline), Grelle, A. (Achim), Guenard, B. (Benoit), Guglielmin, M. (Mauro), Guillemot, J. (Joannes), Haase, P. (Peter), Haider, S. (Sylvia), Halbritter, A. H. (Aud H.), Hamid, M. (Maroof), Hammerle, A. (Albin), Hampe, A. (Arndt), Haugum, S. V. (Siri, V), Hederova, L. (Lucia), Heinesch, B. (Bernard), Helfter, C. (Carole), Hepenstrick, D. (Daniel), Herberich, M. (Maximiliane), Herbst, M. (Mathias), Hermanutz, L. (Luise), Hik, D. S. (David S.), Hoffren, R. (Raul), Homeier, J. (Juergen), Hörtnagl, L. (Lukas), Hoye, T. T. (Toke T.), Hrbacek, F. (Filip), Hylander, K. (Kristoffer), Iwata, H. (Hiroki), Jackowicz-Korczynski, M. A. (Marcin Antoni), Jactel, H. (Herve), Jarveoja, J. (Jarvi), Jastrzebowski, S. (Szymon), Jentsch, A. (Anke), Jimenez, J. J. (Juan J.), Jonsdottir, I. S. (Ingibjorg S.), Jucker, T. (Tommaso), Jump, A. S. (Alistair S.), Juszczak, R. (Radoslaw), Kanka, R. (Robert), Kaspar, V. (Vit), Kazakis, G. (George), Kelly, J. (Julia), Khuroo, A. A. (Anzar A.), Klemedtsson, L. (Leif), Klisz, M. (Marcin), Kljun, N. (Natascha), Knohl, A. (Alexander), Kobler, J. (Johannes), Kollar, J. (Jozef), Kotowska, M. M. (Martyna M.), Kovacs, B. (Bence), Kreyling, J. (Juergen), Lamprecht, A. (Andrea), Lang, S. I. (Simone, I), Larson, C. (Christian), Larson, K. (Keith), Laska, K. (Kamil), Maire, G. I. (Guerric Ie), Leihy, R. I. (Rachel, I), Lens, L. (Luc), Liljebladh, B. (Bengt), Lohila, A. (Annalea), Lorite, J. (Juan), Loubet, B. (Benjamin), Lynn, J. (Joshua), Macek, M. (Martin), Mackenzie, R. (Roy), Magliulo, E. (Enzo), Maier, R. (Regine), Malfasi, F. (Francesco), Malis, F. (Frantisek), Man, M. (Matej), Manca, G. (Giovanni), Manco, A. (Antonio), Manise, T. (Tanguy), Manolaki, P. (Paraskevi), Marciniak, F. (Felipe), Matula, R. (Radim), Clara Mazzolari, A. (Ana), Medinets, S. (Sergiy), Medinets, V. (Volodymyr), Meeussen, C. (Camille), Merinero, S. (Sonia), Guimaraes Mesquita, R. d. (Rita de Cassia), Meusburger, K. (Katrin), Meysman, F. J. (Filip J. R.), Michaletz, S. T. (Sean T.), Milbau, A. (Ann), Moiseev, D. (Dmitry), Moiseev, P. (Pavel), Mondoni, A. (Andrea), Monfries, R. (Ruth), Montagnani, L. (Leonardo), Moriana-Armendariz, M. (Mikel), di Cella, U. M. (Umberto Morra), Moersdorf, M. (Martin), Mosedale, J. R. (Jonathan R.), Muffler, L. (Lena), Munoz-Rojas, M. (Miriam), Myers, J. A. (Jonathan A.), Myers-Smith, I. H. (Isla H.), Nagy, L. (Laszlo), Nardino, M. (Marianna), Naujokaitis-Lewis, I. (Ilona), Newling, E. (Emily), Nicklas, L. (Lena), Niedrist, G. (Georg), Niessner, A. (Armin), Nilsson, M. B. (Mats B.), Normand, S. (Signe), Nosetto, M. D. (Marcelo D.), Nouvellon, Y. (Yann), Nunez, M. A. (Martin A.), Ogaya, R. (Roma), Ogee, J. (Jerome), Okello, J. (Joseph), Olejnik, J. (Janusz), Olesen, J. E. (Jorgen Eivind), Opedal, O. H. (Oystein H.), Orsenigo, S. (Simone), Palaj, A. (Andrej), Pampuch, T. (Timo), Panov, A. V. (Alexey V.), Pärtel, M. (Meelis), Pastor, A. (Ada), Pauchard, A. (Aníbal), Pauli, H. (Harald), Pavelka, M. (Marian), Pearse, W. D. (William D.), Peichl, M. (Matthias), Pellissier, L. (Loïc), Penczykowski, R. M. (Rachel M.), Penuelas, J. (Josep), Petit Bon, M. (Matteo), Petraglia, A. (Alessandro), Phartyal, S. S. (Shyam S.), Phoenix, G. K. (Gareth K.), Pio, C. (Casimiro), Pitacco, A. (Andrea), Pitteloud, C. (Camille), Plichta, R. (Roman), Porro, F. (Francesco), Portillo-Estrada, M. (Miguel), Poulenard, J. (Jérôme), Poyatos, R. (Rafael), Prokushkin, A. S. (Anatoly S.), Puchalka, R. (Radoslaw), Pușcaș, M. (Mihai), Radujković, D. (Dajana), Randall, K. (Krystal), Ratier Backes, A. (Amanda), Remmele, S. (Sabine), Remmers, W. (Wolfram), Renault, D. (David), Risch, A. C. (Anita C.), Rixen, C. (Christian), Robinson, S. A. (Sharon A.), Robroek, B. J. (Bjorn J. M.), Rocha, A. V. (Adrian V.), Rossi, C. (Christian), Rossi, G. (Graziano), Roupsard, O. (Olivier), Rubtsov, A. V. (Alexey V.), Saccone, P. (Patrick), Sagot, C. (Clotilde), Sallo Bravo, J. (Jhonatan), Santos, C. C. (Cinthya C.), Sarneel, J. M. (Judith M.), Scharnweber, T. (Tobias), Schmeddes, J. (Jonas), Schmidt, M. (Marius), Scholten, T. (Thomas), Schuchardt, M. (Max), Schwartz, N. (Naomi), Scott, T. (Tony), Seeber, J. (Julia), Segalin De Andrade, A. C. (Ana Cristina), Seipel, T. (Tim), Semenchuk, P. (Philipp), Senior, R. A. (Rebecca A.), Serra-Diaz, J. M. (Josep M.), Sewerniak, P. (Piotr), Shekhar, A. (Ankit), Sidenko, N. V. (Nikita V.), Siebicke, L. (Lukas), Siegwart Collier, L. (Laura), Simpson, E. (Elizabeth), Siqueira, D. P. (David P.), Sitková, Z. (Zuzana), Six, J. (Johan), Smiljanic, M. (Marko), Smith, S. W. (Stuart W.), Smith-Tripp, S. (Sarah), Somers, B. (Ben), Sørensen, M. V. (Mia Vedel), Souza, J. J. (José João L. L.), Souza, B. I. (Bartolomeu Israel), Dias, A. S. (Arildo Souza), Spasojevic, M. J. (Marko J.), Speed, J. D. (James D. M.), Spicher, F. (Fabien), Stanisci, A. (Angela), Steinbauer, K. (Klaus), Steinbrecher, R. (Rainer), Steinwandter, M. (Michael), Stemkovski, M. (Michael), Stephan, J. G. (Jörg G.), Stiegler, C. (Christian), Stoll, S. (Stefan), Svátek, M. (Martin), Svoboda, M. (Miroslav), Tagesson, T. (Torbern), Tanentzap, A. J. (Andrew J.), Tanneberger, F. (Franziska), Theurillat, J.-P. (Jean-Paul), Thomas, H. J. (Haydn J. D.), Thomas, A. D. (Andrew D.), Tielbörger, K. (Katja), Tomaselli, M. (Marcello), Treier, U. A. (Urs Albert), Trouillier, M. (Mario), Turtureanu, P. D. (Pavel Dan), Tutton, R. (Rosamond), Tyystjärvi, V. A. (Vilna A.), Ueyama, M. (Masahito), Ujházy, K. (Karol), Ujházyová, M. (Mariana), Uogintas, D. (Domas), Urban, A. V. (Anastasiya V.), Urban, J. (Josef), Urbaniak, M. (Marek), Ursu, T.-M. (Tudor-Mihai), Vaccari, F. P. (Francesco Primo), Van De Vondel, S. (Stijn), Van Den Brink, L. (Liesbeth), Van Geel, M. (Maarten), Vandvik, V. (Vigdis), Vangansbeke, P. (Pieter), Varlagin, A. (Andrej), Veen, G. F. (G. F.), Veenendaal, E. (Elmar), Venn, S. E. (Susanna E.), Verbeeck, H. (Hans), Verbrugggen, E. (Erik), Verheijen, F. G. (Frank G. A.), Villar, L. (Luis), Vitale, L. (Luca), Vittoz, P. (Pascal), Vives-Ingla, M. (Maria), Von Oppen, J. (Jonathan), Walz, J. (Josefine), Wang, R. (Runxi), Wang, Y. (Yifeng), Way, R. G. (Robert G.), Wedegärtner, R. E. (Ronja E. M.), Weigel, R. (Robert), Wild, J. (Jan), Wilkinson, M. (Matthew), Wilmking, M. (Martin), Wingate, L. (Lisa), Winkler, M. (Manuela), Wipf, S. (Sonja), Wohlfahrt, G. (Georg), Xenakis, G. (Georgios), Yang, Y. (Yan), Yu, Z. (Zicheng), Yu, K. (Kailiang), Zellweger, F. (Florian), Zhang, J. (Jian), Zhang, Z. (Zhaochen), Zhao, P. (Peng), Ziemblińska, K. (Klaudia), Zimmermann, R. (Reiner), Zong, S. (Shengwei), Zyryanov, V. I. (Viacheslav I.), Nijs, I. (Ivan), and Lenoir, J. (Jonathan)

Abstract

Research in global change ecology relies heavily on global climatic grids derived from estimates of air temperature in open areas at around 2 m above the ground. These climatic grids do not reflect conditions below vegetation canopies and near the ground surface, where critical ecosystem functions occur and most terrestrial species reside. Here, we provide global maps of soil temperature and bioclimatic variables at a 1-km² resolution for 0‐5 and 5‐15 cm soil depth. These maps were created by calculating the difference (i.e. offset) between in situ soil temperature measurements, based on time series from over 1200 1‐km² pixels (summarized from 8519 unique temperature sensors) across all the world’s major terrestrial biomes, and coarse-grained air temperature estimates from ERA5-Land (an atmospheric reanalysis by the European Centre for Medium-Range Weather Forecasts). We show that mean annual soil temperature differs markedly from the corresponding gridded air temperature, by up to 10° degrees C (mean = 3.0 +/‐ 2.1° degrees C), with substantial variation across biomes and seasons. Over the year, soils in cold and/or dry biomes are substantially warmer (+3.6 +/‐2.3° degrees C) than gridded air temperature, whereas soils in warm and humid environments are on average slightly cooler (‐0.7 +/‐ 2.3° degrees C). The observed substantial and biome-specific offsets emphasize that the projected impacts of climate and climate change on near-surface biodiversity and ecosystem functioning are inaccurately assessed when air rather than soil temperature is used, especially in cold environments. The global soil-related bioclimatic variables provided here are an important step forward for any application in ecology and related disciplines. Nevertheless, we highlight the need to fill remaining geographic gaps by collecting more in situ measurements of microclimate conditions to further enhance the spatiotemporal resolution of global soil temperature products for ecological

Published
2022

37. Behavioural Effects of Adult Vitamin D Deficiency in BALB/c Mice Are not Associated with Proliferation or Survival of Neurons in the Adult Hippocampus.

Author

Natalie J Groves, DanaKai Bradford, Robert K P Sullivan, Kyna-Anne Conn, Rasha Fahad Aljelaify, John J McGrath, and Thomas H J Burne

Subjects
Medicine, Science
Abstract

Epidemiological studies have shown that up to one third of adults have insufficient levels of vitamin D and there is an association between low vitamin D concentrations and adverse brain outcomes, such as depression. Vitamin D has been shown to be involved in processes associated with neurogenesis during development. Therefore, the aim of this study was to test the hypothesis that adult vitamin D (AVD) deficiency in BALB/c mice was associated with (a) adult hippocampal neurogenesis at baseline, b) following 6 weeks of voluntary wheel running and (c) a depressive-like phenotype on the forced swim test (FST), which may be linked to alterations in hippocampal neurogenesis. We assessed proliferation and survival of adult born hippocampal neurons by counting the number of cells positive for Ki67 and doublecortin (DCX), and incorporation of 5-Bromo-2'-Deoxyuridine (BrdU) within newly born mature neurons using immunohistochemistry. There were no significant effects of diet on number of Ki67+, DCX+ or BrdU+ cells in the dentate gyrus. All mice showed significantly increased number of Ki67+ cells and BrdU incorporation, and decreased immobility time in the FST, after voluntary wheel running. A significant correlation was found in control mice between immobility time in the FST and level of hippocampal neurogenesis, however, no such correlation was found for AVD-deficient mice. We conclude that AVD deficiency was not associated with impaired proliferation or survival of adult born neurons in BALB/c mice and that the impact on rodent behaviour may not be due to altered neurogenesis per se, but to altered function of new hippocampal neurons or processes independent of adult neurogenesis.

Published
2016
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38. The Ubiquitin System: a Regulatory Hub for Intellectual Disability and Autism Spectrum Disorder

Author

Michael Piper, Stephen A. Wood, Susitha Premarathne, Thomas H. J. Burne, and Maria Kasherman

Subjects
0301 basic medicine, biology, Neuroscience (miscellaneous), Wnt signaling pathway, medicine.disease, System a, 03 medical and health sciences, Cellular and Molecular Neuroscience, 030104 developmental biology, 0302 clinical medicine, USP9X, Neurology, Ubiquitin, Autism spectrum disorder, Intellectual disability, biology.protein, medicine, Signal transduction, Neuroscience, 030217 neurology & neurosurgery, PI3K/AKT/mTOR pathway
Abstract

Intellectual disability (ID) and autism spectrum disorder (ASD) are two of the most common neurodevelopmental disorders. Both disorders are extremely heterogenous, and only ~ 40% of reported cases have so far been attributed to genetic mutations. Of the many cellular processes that are affected, the ubiquitin system (UbS) is of particular relevance in that it can rapidly regulate multiple signaling cascades simultaneously. The UbS is a post-translational modification process that revolves around the covalent attachment of a ubiquitin moiety to a substrate, thereby influencing different elements of protein biology, including trafficking, signal transduction, and degradation. Importantly, the UbS has been implicated in regulating multiple pathophysiological pathways related to ASD and ID. This review will discuss how the UbS acts as major signaling hub in the pathogenesis of ASD and ID, raising the prospect of treating broader patient cohorts by targeting the UbS as a common point of convergence of various mutations.

Published
2020
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42. Impaired spatial memory in adult vitamin D deficient BALB/c mice is associated with reductions in spine density, nitric oxide, and neural nitric oxide synthase in the hippocampus

Author

Md Mamun, Al-Amin, Robert K P, Sullivan, Suzy, Alexander, David A, Carter, DanaKai, Bradford, and Thomas H J, Burne

Subjects
nervous system, General Neuroscience
Abstract

Vitamin D deficiency is prevalent in adults and is associated with cognitive impairment. However, the mechanism by which adult vitamin D (AVD) deficiency affects cognitive function remains unclear. We examined spatial memory impairment in AVD-deficient BALB/c mice and its underlying mechanism by measuring spine density, long term potentiation (LTP), nitric oxide (NO), neuronal nitric oxide synthase (nNOS), and endothelial NOS (eNOS) in the hippocampus. Adult male BALB/c mice were fed a control or vitamin D deficient diet for 20 weeks. Spatial memory performance was measured using an active place avoidance (APA) task, where AVD-deficient mice had reduced latency entering the shock zone compared to controls. We characterised hippocampal spine morphology in the CA1 and dentate gyrus (DG) and made electrophysiological recordings in the hippocampus of behaviourally naïve mice to measure LTP. We next measured NO, as well as glutathione, lipid peroxidation and oxidation of protein products and quantified hippocampal immunoreactivity for nNOS and eNOS. Spine morphology analysis revealed a significant reduction in the number of mushroom spines in the CA1 dendrites but not in the DG. There was no effect of diet on LTP. However, hippocampal NO levels were depleted whereas other oxidation markers were unaltered by AVD deficiency. We also showed a reduced nNOS, but not eNOS, immunoreactivity. Finally, vitamin D supplementation for 10 weeks to AVD-deficient mice restored nNOS immunoreactivity to that seen in in control mice. Our results suggest that lower levels of NO and reduced nNOS immunostaining contribute to hippocampal-dependent spatial learning deficits in AVD-deficient mice.

Published
2021

44. Global plant trait relationships extend to the climatic extremes of the tundra biome

Author

Thomas, H J D, Bjorkman, A D, Myers-Smith, I H, et al, Rixen, C, Schaepman-Strub, Gabriela, Wipf, Sonja, Frei, E R, Little, C J, Rumpf, S B, University of Zurich, and Thomas, H J D

Subjects
10127 Institute of Evolutionary Biology and Environmental Studies, UFSP13-8 Global Change and Biodiversity, 1300 General Biochemistry, Genetics and Molecular Biology, General Biochemistry, 570 Life sciences, biology, 590 Animals (Zoology), General Physics and Astronomy, 1600 General Chemistry, Genetics and Molecular Biology, General Chemistry, 3100 General Physics and Astronomy
Published
2020

45. Treating cognitive impairment in schizophrenia with GLP-1RAs: an overview of their therapeutic potential

Author

Dan Siskind, Jonathan Flintoff, Thomas H. J. Burne, and James P. Kesby

Subjects
endocrine system, medicine.medical_treatment, Rodentia, Affect (psychology), Glucagon-Like Peptide-1 Receptor, Preclinical research, medicine, Animals, Humans, Pharmacology (medical), Cognitive Dysfunction, Antipsychotic, Cognitive impairment, Pharmacology, business.industry, digestive, oral, and skin physiology, Cognition, General Medicine, medicine.disease, Patient population, Disease Models, Animal, Neuropsychiatric disorder, Schizophrenia, business, Clinical psychology
Abstract

Schizophrenia is a neuropsychiatric disorder that affects approximately 1% of individuals worldwide. There are no available medications to treat cognitive impairment in this patient population currently. Preclinical evidence suggests that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) improve cognitive function. There is a need to evaluate how GLP-1 RAs alter specific domains of cognition and whether they will be of therapeutic benefit in individuals with schizophrenia.This paper summarizes the effects of GLP-1 RAs on metabolic processes in the brain and how these mechanisms relate to improved cognitive function. We provide an overview of preclinical studies that demonstrate GLP-1 RAs improve cognition and comment on their potential therapeutic benefit in individuals with schizophrenia.To understand the benefits of GLP-1 RAs in individuals with schizophrenia, further preclinical research with rodent models relevant to schizophrenia symptomology are needed. Moreover, preclinical studies must focus on using a wider range of behavioral assays to understand whether important aspects of cognition such as executive function, attention, and goal-directed behavior are improved using GLP-1 RAs. Further research into the specific mechanisms of how GLP-1 RAs affect cognitive function and their interactions with antipsychotic medication commonly prescribed is necessary.

Published
2021

46. Vitamin D and schizophrenia:20 years on

Author

Thomas H. J. Burne, John J. McGrath, Xiangyang Cui, and Darryl W. Eyles

Subjects
0301 basic medicine, BRAIN-DEVELOPMENT, Psychosis, medicine.medical_specialty, D DVD DEFICIENCY, D SUPPLEMENTATION, Physiology, Dopamine, Bioinformatics, vitamin D deficiency, 03 medical and health sciences, Cellular and Molecular Neuroscience, Cognition, 0302 clinical medicine, Neurochemical, ADULT-RAT, D-RECEPTOR, Epidemiology, Vitamin D and neurology, Animals, Humans, Medicine, Vitamin D, Molecular Biology, 1,25-DIHYDROXYVITAMIN D-3, TYROSINE-HYDROXYLASE EXPRESSION, SUBSTANTIA-NIGRA, business.industry, NERVE GROWTH-FACTOR, Glutamate receptor, Vitamin D Deficiency, medicine.disease, Psychiatry and Mental health, 030104 developmental biology, D DEFICIENCY ALTERS, Schizophrenia, Expert Review, business, 030217 neurology & neurosurgery, Neuroscience
Abstract

Many epidemiological studies have highlighted the link between vitamin D deficiency and schizophrenia. In particular, two prominent studies report an association between neonatal vitamin D deficiency and an increased risk of schizophrenia. In parallel, much has been learnt about the role of vitamin D in the developing central nervous system over the last two decades. Studies in rodent models of developmental vitamin D (DVD)-deficiency describe how brain development is altered leading to a range of neurobiological and behavioral phenotypes of interest to schizophrenia. While glutamate and gamma aminobutyric acid (GABA) systems have been little investigated in these models, alterations in developing dopamine systems are frequently reported. There have been far more studies reporting patients with schizophrenia have an increased risk of vitamin D deficiency compared to well controls. Here we have conducted a systematic review and meta-analysis that basically confirms this association and extends this to first-episode psychosis. However, patients with schizophrenia also have poorer general health, poorer diets, are frequently less active and also have an increased risk of other medical conditions, all factors which reduce circulating vitamin D levels. Therefore, we would urge caution in any causal interpretation of this association. We also summarize the inconsistent results from existing vitamin D supplementation trials in patients with schizophrenia. In respect to animal models of adult vitamin D deficiency, such exposures produce subtle neurochemical alterations and effects on cognition but do not appear to produce behavioral phenotypes of relevance to schizophrenia. We conclude, the hypothesis that vitamin D deficiency during early life may increase the risk of schizophrenia remains plausible and warrants ongoing research.

Published
2021
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47. Adult vitamin D deficiency disrupts hippocampal-dependent learning and structural brain connectivity in BALB/c mice

Author

Md. Mamun Al-Amin, Thomas H. J. Burne, Robert K. P. Sullivan, and Nyoman D. Kurniawan

Subjects
Male, Vitamin, Receptors, N-Acetylglucosamine, medicine.medical_specialty, Histology, Hippocampus, Hippocampal formation, Biology, 050105 experimental psychology, vitamin D deficiency, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, Neural Pathways, Avoidance Learning, Connectome, medicine, Vitamin D and neurology, Animals, 0501 psychology and cognitive sciences, Muscle, Skeletal, Decision Making, Computer-Assisted, Analysis of Variance, Mice, Inbred BALB C, Learning Disabilities, General Neuroscience, Perineuronal net, 05 social sciences, medicine.disease, Magnetic Resonance Imaging, Motor coordination, Disease Models, Animal, Parvalbumins, Endocrinology, chemistry, Ascorbic Acid Deficiency, biology.protein, Plant Lectins, Psychomotor Disorders, Anatomy, 030217 neurology & neurosurgery, Parvalbumin
Abstract

Converging evidence from human and animal studies support an association between vitamin D deficiency and cognitive impairment. Previous studies have shown that hippocampal volume is reduced in adults with vitamin D deficiency as well as in a range of disorders, such as schizophrenia. The aim of the current study was to examine the effect of adult vitamin D (AVD) deficiency on hippocampal-dependent spatial learning, and hippocampal volume and connectivity in healthy adult mice. Ten-week-old male BALB/c mice were fed a control (vitamin D 1500 IU/kg) or vitamin D-depleted (vitamin D 0 IU/kg) diet for a minimum of 10 weeks. The mice were then tested for hippocampal-dependent spatial learning using active place avoidance (APA) and on tests of muscle and motor coordination (rotarod and grip strength). The mice were perfused and brains collected to acquire ex vivo structural and diffusion-weighted images using a 16.4 T MRI scanner. We also performed immunohistochemistry to quantify perineuronal nets (PNNs) and parvalbumin (PV) interneurons in various brain regions. AVD-deficient mice had a lower latency to enter the shock zone on APA, compared to control mice, suggesting impaired hippocampal-dependent spatial learning. There were no differences in rotarod or grip strength, indicating that AVD deficiency did not have an impact on muscle or motor coordination. AVD deficiency did not have an impact on hippocampal volume. However, AVD-deficient mice displayed a disrupted network centred on the right hippocampus with abnormal connectomes among 29 nodes. We found a reduction in PNN positive cells, but no change in PV, centred on the hippocampus. Our results provide compelling evidence to show that AVD deficiency in otherwise healthy adult mice may play a key role in hippocampal-dependent learning and memory formation. We suggest that the spatial learning deficits could be due to the disruption of right hippocampal structural connectivity.

Published
2019
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48. Improving the energy efficiency of industrial drying processes: a computational fluid dynamics approach

Author

Julian Praß, Thomas H.-J. Uhlemann, Christoph T. Hoffmann, and Jörg Franke

Subjects
business.industry, Process (engineering), media_common.quotation_subject, Flow (psychology), Energy balance, Energy consumption, Computational fluid dynamics, Industrial and Manufacturing Engineering, Artificial Intelligence, Component (UML), Environmental science, Quality (business), business, Process engineering, media_common, Efficient energy use
Abstract

In order to reach the United Nation’s Sustainable Development Goals, increasing the efficiency of industrial processes is one of the core components. As value adding processes in manufacturing determine the quality of the product significantly and are more difficult to adapt, non-value adding processes are primarily in the focus of efficiency measures. Especially when considering the energy balance of a component over its entire lifecycle, processes such as drying play a decisive role. This paper discusses an approach to increase energy efficiency during the drying process of metal parts in electroplating processes by improving the air guidance inside industrial drying chambers. In addition to a numerically investigation using a computational fluid dynamics approach, in-situ measurements of the energy consumption of a dryer were carried out. In order to measure the positive effects of the improved flow, a prototype of such a dryer will be developed and energetically measured next step.

Published
2019
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49. Heterozygosity for Nuclear Factor One X in mice models features of Malan syndrome

Author

Danyon Harkins, Richard M. Gronostajski, Maria Kasherman, Michael Piper, Thomas H. J. Burne, Lachlan Harris, Sabrina Oishi, Nyoman D. Kurniawan, and Oressia Zalucki

Subjects
Male, 0301 basic medicine, Research paper, NFIX, Spatial Learning, Intellectual disability, Anterior commissure, Haploinsufficiency, Biology, Corpus callosum, General Biochemistry, Genetics and Molecular Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, Fractional anisotropy, Connectome, medicine, Animals, Humans, Macrocephaly, Megalencephaly, Malan syndrome, Cerebral Cortex, Organ Size, General Medicine, medicine.disease, Magnetic Resonance Imaging, Disease Models, Animal, NFI Transcription Factors, 030104 developmental biology, 030220 oncology & carcinogenesis, Brain size, biology.protein, Female, Neuroscience, Tractography
Abstract

Background Nuclear Factor One X (NFIX) haploinsufficiency in humans results in Malan syndrome, a disorder characterized by overgrowth, macrocephaly and intellectual disability. Although clinical assessments have determined the underlying symptomology of Malan syndrome, the fundamental mechanisms contributing to the enlarged head circumference and intellectual disability in these patients remains undefined. Methods Here, we used Nfix heterozygous mice as a model to investigate these aspects of Malan syndrome. Volumetric magnetic resonance imaging (MRI) was used to calculate the volumes of 20 brain sub regions. Diffusion tensor MRI was used to perform tractography-based analyses of the corpus callosum, hippocampal commissure, and anterior commissure, as well as structural connectome mapping of the whole brain. Immunohistochemistry examined the neocortical cellular populations. Two behavioral assays were performed, including the active place avoidance task to assess spatial navigation and learning and memory function, and the 3-chambered sociability task to examine social behaviour. Findings Adult Nfix+/− mice exhibit significantly increased brain volume (megalencephaly) compared to wildtypes, with the cerebral cortex showing the highest increase. Moreover, all three forebrain commissures, in particular the anterior commissure, revealed significantly reduced fractional anisotropy, axial and radial diffusivity, and tract density intensity. Structural connectome analyses revealed aberrant connectivity between many crucial brain regions. Finally, Nfix+/− mice exhibit behavioral deficits that model intellectual disability. Interpretation Collectively, these data provide a significant conceptual advance in our understanding of Malan syndrome by suggesting that megalencephaly underlies the enlarged head size of these patients, and that disrupted cortical connectivity may contribute to the intellectual disability these patients exhibit. Fund Australian Research Council (ARC) Discovery Project Grants, ARC Fellowship, NYSTEM and Australian Postgraduate Fellowships.

Published
2019
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50. Comprehensive behavioural analysis of Long Evans and Sprague-Dawley rats reveals differential effects of housing conditions on tests relevant to neuropsychiatric disorders.

Author

Karly M Turner and Thomas H J Burne

Subjects
Medicine, Science
Abstract

Genetic (G) and environmental (E) manipulations are known to alter behavioural outcomes in rodents, however many animal models of neuropsychiatric disorders only use a restricted selection of strain and housing conditions. The aim of this study was to examine GxE interactions comparing two outbred rat strains, which were housed in either standard or enriched cages. The strains selected were the albino Sprague-Dawley rat, commonly used for animal models, and the other was the pigmented Long Evans rat, which is frequently used in cognitive studies. Rats were assessed using a comprehensive behavioural test battery and included well-established tests frequently employed to examine animal models of neuropsychiatric diseases, measuring aspects of anxiety, exploration, sensorimotor gating and cognition. Selective strain and housing effects were observed on a number of tests. These included increased locomotion and reduced pre-pulse inhibition in Long Evans rats compared to Sprague Dawley rats; and rats housed in enriched cages had reduced anxiety-like behaviour compared to standard housed rats. Long Evans rats required fewer sessions than Sprague Dawley rats to learn operant tasks, including a signal detection task and reversal learning. Furthermore, Long Evans rats housed in enriched cages acquired simple operant tasks faster than standard housed Long Evans rats. Cognitive phenotypes in animal models of neuropsychiatric disorders would benefit from using strain and housing conditions where there is greater potential for both enhancement and deficits in performance.

Published
2014
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