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  • 1
    Online Resource
    Online Resource
    Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury
    Proceedings of the National Academy of Sciences ; 1998
    In:  Proceedings of the National Academy of Sciences Vol. 95, No. 8 ( 1998-04-14), p. 4760-4765
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 95, No. 8 ( 1998-04-14), p. 4760-4765
    Abstract: Substance P, acting via the neurokinin 1 receptor (NK1R), plays an important role in mediating a variety of inflammatory processes. However, its role in acute pancreatitis has not been previously described. We have found that, in normal mice, substance P levels in the pancreas and pancreatic acinar cell expression of NK1R are both increased during secretagogue-induced experimental pancreatitis. To evaluate the role of substance P, pancreatitis was induced in mice that genetically lack NK1R by administration of 12 hourly injections of a supramaximally stimulating dose of the secretagogue caerulein. During pancreatitis, the magnitude of hyperamylasemia, hyperlipasemia, neutrophil sequestration in the pancreas, and pancreatic acinar cell necrosis were significantly reduced in NK1R−/− mice when compared with wild-type NK1R+/+ animals. Similarly, pancreatitis-associated lung injury, as characterized by intrapulmonary sequestration of neutrophils and increased pulmonary microvascular permeability, was reduced in NK1R−/− animals. These effects of NK1R deletion indicate that substance P, acting via NK1R, plays an important proinflammatory role in regulating the severity of acute pancreatitis and pancreatitis-associated lung injury.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.95.8.4760
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1998
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  • 2
    Online Resource
    Online Resource
    Stroke outcomes are worse with larger leukoaraiosis volumes
    Oxford University Press (OUP) ; 2017
    In:  Brain Vol. 140, No. 1 ( 2017-01), p. 158-170
    Details
    In: Brain, Oxford University Press (OUP), Vol. 140, No. 1 ( 2017-01), p. 158-170
    Type of Medium: Online Resource
    ISSN: 0006-8950 , 1460-2156
    URL: Article
    DOI: 10.1093/brain/aww259
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 1474117-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Exploring continued online service usage behavior: The roles of self-image congruity and regret
    Elsevier BV ; 2009
    In:  Computers in Human Behavior Vol. 25, No. 1 ( 2009-1), p. 111-122
    Details
    In: Computers in Human Behavior, Elsevier BV, Vol. 25, No. 1 ( 2009-1), p. 111-122
    Type of Medium: Online Resource
    ISSN: 0747-5632
    URL: Article
    DOI: 10.1016/j.chb.2008.07.009
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 2001911-7
    SSG: 5,2
    SSG: 7,11
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  • 4
    Online Resource
    Online Resource
    Excitatory Actions of GABA in the Suprachiasmatic Nucleus
    Society for Neuroscience ; 2008
    In:  The Journal of Neuroscience Vol. 28, No. 21 ( 2008-05-21), p. 5450-5459
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 28, No. 21 ( 2008-05-21), p. 5450-5459
    Abstract: Neurons in the suprachiasmatic nucleus (SCN) are responsible for the generation of circadian oscillations, and understanding how these neurons communicate to form a functional circuit is a critical issue. The neurotransmitter GABA and its receptors are widely expressed in the SCN where they mediate cell-to-cell communication. Previous studies have raised the possibility that GABA can function as an excitatory transmitter in adult SCN neurons during the day, but this work is controversial. In the present study, we first tested the hypothesis that GABA can evoke excitatory responses during certain phases of the daily cycle by broadly sampling how SCN neurons respond to GABA using extracellular single-unit recording and gramicidin-perforated-patch recording techniques. We found that, although GABA inhibits most SCN neurons, some level of GABA-mediated excitation was present in both dorsal and ventral regions of the SCN, regardless of the time of day. These GABA-evoked excitatory responses were most common during the night in the dorsal SCN region. The Na + -K + -2Cl − cotransporter (NKCC) inhibitor, bumetanide, prevented these excitatory responses. In individual neurons, the application of bumetanide was sufficient to change GABA-evoked excitation to inhibition. Calcium-imaging experiments also indicated that GABA-elicited calcium transients in SCN cells are highly dependent on the NKCC isoform 1 (NKCC1). Finally, Western blot analysis indicated that NKCC1 expression in the dorsal SCN is higher in the night. Together, this work indicates that GABA can play an excitatory role in communication between adult SCN neurons and that this excitation is critically dependent on NKCC1.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.5750-07.2008
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2008
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Iodide management in formamidinium-lead-halide–based perovskite layers for efficient solar cells
    American Association for the Advancement of Science (AAAS) ; 2017
    In:  Science Vol. 356, No. 6345 ( 2017-06-30), p. 1376-1379
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 356, No. 6345 ( 2017-06-30), p. 1376-1379
    Abstract: The formation of a dense and uniform thin layer on the substrates is crucial for the fabrication of high-performance perovskite solar cells (PSCs) containing formamidinium with multiple cations and mixed halide anions. The concentration of defect states, which reduce a cell’s performance by decreasing the open-circuit voltage and short-circuit current density, needs to be as low as possible. We show that the introduction of additional iodide ions into the organic cation solution, which are used to form the perovskite layers through an intramolecular exchanging process, decreases the concentration of deep-level defects. The defect-engineered thin perovskite layers enable the fabrication of PSCs with a certified power conversion efficiency of 22.1% in small cells and 19.7% in 1-square-centimeter cells.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aan2301
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2017
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 6
    Online Resource
    Online Resource
    Substance P Plays a Critical Role in Photic Resetting of the Circadian Pacemaker in the Rat Hypothalamus
    Society for Neuroscience ; 2001
    In:  The Journal of Neuroscience Vol. 21, No. 11 ( 2001-06-01), p. 4026-4031
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 21, No. 11 ( 2001-06-01), p. 4026-4031
    Abstract: Glutamate is considered to be the primary neurotransmitter in the retinohypothalamic tract (RHT), which delivers photic information from the retina to the suprachiasmatic nucleus (SCN), the locus of the mammalian circadian pacemaker. However, substance P (SP) also has been suggested to play a role in retinohypothalamic transmission. In this study, we sought evidence that SP from the RHT contributes to photic resetting of the circadian pacemaker and further explored the possible interaction of SP with glutamate in this process. In rat hypothalamic slices cut parasagittally, electrical stimulation of the optic nerve in early and late subjective night produced a phase delay (2.4 ± 0.5 hr; mean ± SEM) and advance (2.6 ± 0.3 hr) of the circadian rhythm of SCN neuronal firing activity, respectively. The SP antagonist L-703,606 (10 μ m ) applied to the slices during the nerve stimulation completely blocked the phase shifts. Likewise, a cocktail of NMDA (2-amino-5-phosphonopentanoic acid, 50 μ m ) and non-NMDA (6,7-dinitroquinoxaline-2,3-dione, 10 μ m ) antagonists completely blocked the shifts. Exogenous application of SP (1 μ m ) or glutamate (100 μ m ) to the slices in early subjective night produced a phase delay (∼3 hr) of the circadian firing activity rhythm of SCN neurons. Coapplication of the NMDA and non-NMDA antagonist cocktail (as well as L-703,606) resulted in a complete blockade of the SP-induced phase delay, whereas L-703,606 (10 μ m ) had no effect on the glutamate-induced delay. These results suggest that SP, as well as glutamate, has a critical role in photic resetting. Furthermore, the results suggest that the two agonists act in series, SP working upstream of glutamate.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.21-11-04026.2001
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2001
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Fingerprint ridges allow primates to regulate grip
    Proceedings of the National Academy of Sciences ; 2020
    In:  Proceedings of the National Academy of Sciences Vol. 117, No. 50 ( 2020-12-15), p. 31665-31673
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 117, No. 50 ( 2020-12-15), p. 31665-31673
    Abstract: Fingerprints are unique to primates and koalas but what advantages do these features of our hands and feet provide us compared with the smooth pads of carnivorans, e.g., feline or ursine species? It has been argued that the epidermal ridges on finger pads decrease friction when in contact with smooth surfaces, promote interlocking with rough surfaces, channel excess water, prevent blistering, and enhance tactile sensitivity. Here, we found that they were at the origin of a moisture-regulating mechanism, which ensures an optimal hydration of the keratin layer of the skin for maximizing the friction and reducing the probability of catastrophic slip due to the hydrodynamic formation of a fluid layer. When in contact with impermeable surfaces, the occlusion of the sweat from the pores in the ridges promotes plasticization of the skin, dramatically increasing friction. Occlusion and external moisture could cause an excess of water that would defeat the natural hydration balance. However, we have demonstrated using femtosecond laser-based polarization-tunable terahertz wave spectroscopic imaging and infrared optical coherence tomography that the moisture regulation may be explained by a combination of a microfluidic capillary evaporation mechanism and a sweat pore blocking mechanism. This results in maintaining an optimal amount of moisture in the furrows that maximizes the friction irrespective of whether a finger pad is initially wet or dry. Thus, abundant low-flow sweat glands and epidermal furrows have provided primates with the evolutionary advantage in dry and wet conditions of manipulative and locomotive abilities not available to other animals.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2001055117
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2020
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Macrophage migration inhibitory factor mediates the antidepressant actions of voluntary exercise
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 32 ( 2012-08-07), p. 13094-13099
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 32 ( 2012-08-07), p. 13094-13099
    Abstract: Voluntary exercise is known to have an antidepressant effect. However, the underlying mechanism for this antidepressant action of exercise remains unclear, and little progress has been made in identifying genes that are directly involved. We have identified macrophage migration inhibitory factor (MIF) by analyzing existing mRNA microarray data and confirmed the augmented expression of selected genes under two experimental conditions: voluntary exercise and electroconvulsive seizure. A proinflammatory cytokine, MIF is expressed in the central nervous system and involved in innate and adaptive immune responses. A recent study reported that MIF is involved in antidepressant-induced hippocampal neurogenesis, but the mechanism remains elusive. In our data, tryptophan hydroxylase 2 ( Tph2 ) and brain-derived neurotrophic factor ( Bdnf ) expression were induced after MIF treatment in vitro, as well as during both exercise and electroconvulsive seizure in vivo. This increment of Tph2 was accompanied by increases in the levels of total serotonin in vitro. Moreover, the MIF receptor CD74 and the ERK1/2 pathway mediate the MIF-induced Tph2 and Bdnf gene expression as well as serotonin content. Experiments in Mif −/− mice revealed depression-like behaviors and a blunted antidepressant effect of exercise, as reflected by changes in Tph2 and Bdnf expression in the forced swim test. In addition, administration of recombinant MIF protein produced antidepressant-like behavior in rats in the forced swim test. Taken together, these results suggest a role of MIF in mediating the antidepressant action of exercise, probably by enhancing serotonin neurotransmission and neurotrophic factor-induced neurogenesis in the brain.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1205535109
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2012
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Ectopic Expression of the Catalytic Subunit of Telomerase Protects against Brain Injury Resulting from Ischemia and NMDA-Induced Neurotoxicity
    Society for Neuroscience ; 2004
    In:  The Journal of Neuroscience Vol. 24, No. 6 ( 2004-02-11), p. 1280-1287
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 24, No. 6 ( 2004-02-11), p. 1280-1287
    Abstract: The catalytic subunit of telomerase reverse transcriptase (TERT) protects dividing cells from replicative senescence in vitro . Here, we show that expression of TERT mRNA is induced in the ipsilateral cortical neurons after occlusion of the middle cerebral artery in adult mice. Transgenic mice that overexpress TERT showed significant resistance to ischemic brain injury. Among excitotoxicity, oxidative stress, and apoptosis comprising of routes of ischemic neuronal death, NMDA receptor-mediated excitotoxicity was reduced in forebrain cell cultures overexpressing TERT. NMDA-induced accumulation of cytosolic free Ca 2+ ([Ca 2+ ] c ) was reduced in forebrain neurons from TERT transgenic mice, which was attributable to the rapid flow of [Ca 2+ ] c into the mitochondria from the cytosol without change in Ca 2+ influx and efflux through the plasma membrane. The present study provides evidence that TERT is inducible in postmitotic neurons after ischemic brain injury and prevents NMDA neurotoxicity through shift of the cytosolic free Ca 2+ into the mitochondria, and thus plays a protective role in ameliorating ischemic neuronal cell death.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.4082-03.2004
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2004
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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