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Institution

University of Münster

EducationMünster, Germany
About: University of Münster is a education organization based out in Münster, Germany. It is known for research contribution in the topics: Population & Catalysis. The organization has 35609 authors who have published 69059 publications receiving 2278534 citations. The organization is also known as: University of Munster & University of Muenster.


Papers
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Journal ArticleDOI
TL;DR: In this article, vertical impacts of 0.3-g cylindrical plastic projectiles into noncohesive quartz sand in which vertical and horizontal reference strate were employed by using layers of colored sand were performed at velocities of 5.9-6.9 km/sec.
Abstract: Results are presented for vertical impacts of 0.3-g cylindrical plastic projectiles into noncohesive quartz sand in which vertical and horizontal reference strate were employed by using layers of colored sand. The impacts were performed at velocities of 5.9-6.9 km/sec with a vertical gun ballistic range. The craters, 30-33 cm in diameter, reveal a radial decay of the ejecta mass per unit area with a power of -2.8 to -3.5. Material displaced from the upper 15% of the crater depth d is represented within the whole ejecta blanked, material from deeper than 28% of d is deposited inside 2 crater radii, and no material from deeper than 33% of d was ejected beyond the crater rim. Shock-metamorphosed particles (glassy agglutinates, cataclastic breccias, and comminuted quartz) amount to some 4% of the total displaced mass and indicate progressive zones of decay of shock intensity from a peak pressure of 300 kbar. The shock-metamorphosed particles and the shock-induced change in the grain size distribution of ejected samples have close analogies to the basic characteristics of the lunar regolith. Possible applications to regolith formation and to ejecta formations of large-scale impact craters are discussed.

305 citations

Journal ArticleDOI
TL;DR: The study shows that an adenosine receptor gene polymorphism that has been associated with Panic Disorder is also associated with anxiogenic responses to an acute dose of caffeine.

305 citations

Journal ArticleDOI
TL;DR: A novel pathophysiological role is established for CMNLRP3 inflammasome signaling, with a mechanistic link to the pathogenesis of AF, and the inhibition of NLRP3 is established as a potential novel AF therapy approach.
Abstract: Background —Atrial fibrillation (AF) is frequently associated with enhanced inflammatory response. The "NACHT, LRR and PYD domain containing protein 3" (NLRP3)-inflammasome mediates caspase-1 activation and interleukin-1β release in immune cells, but is not known to play a role in cardiomyocytes (CMs). Here, we assessed the role of CM NLRP3-inflammasome in AF. Methods —NLRP3-inflammasome activation was assessed by immunoblot in atrial whole-tissue lysates and CMs from patients with paroxysmal (pAF) or long-standing persistent (chronic) AF (cAF). To determine whether CM-specific activation of NLPR3 is sufficient to promote AF, a CM-specific knock-in mouse model expressing constitutively active NLRP3 (CM-KI) was established. In vivo electrophysiology was used to assess atrial arrhythmia vulnerability. To evaluate the mechanism of AF, electrical activation pattern, Ca 2+ spark frequency (CaSF), atrial effective refractory period (AERP), and morphology of atria were evaluated in CM-KI mice and WT littermates. Results —NLRP3-inflammasome activity was increased in atrial CMs of pAF and cAF patients. CM-KI mice developed spontaneous premature atrial contractions and inducible AF, which was attenuated by a specific NLRP3-inflammasome inhibitor, MCC950. CM-KI mice exhibited ectopic activity, abnormal sarcoplasmic-reticulum Ca 2+ -release, AERP shortening and atrial hypertrophy. Adeno-associated virus subtype-9 mediated CM-specific knockdown of Nlrp3 suppressed AF development in CM-KI mice. Finally, genetic inhibition of Nlrp3 prevented AF development in CREM transgenic mice, a well-characterized mouse model of spontaneous AF. Conclusions —Our study establishes a novel pathophysiological role for CM NLRP3-inflammasome signaling with a mechanistic link to the pathogenesis of AF, and establishes inhibition of NLRP3 as a potential novel AF-therapy approach.

305 citations

Journal ArticleDOI
TL;DR: In multiple sclerosis, the choroid plexus could represent a site for lymphocyte entry in the CSF and brain, and for presentation of antigens, as well as new diagnostic markers and potential molecular targets for choroids papilloma and carcinoma.
Abstract: The choroid plexus is an epithelial–endothelial vascular convolute within the ventricular system of the vertebrate brain. It consists of epithelial cells, fenestrated blood vessels, and the stroma, dependent on various physiological or pathological conditions, which may contain fibroblasts, mast cells, macrophages, granulocytes or other infiltrates, and a rich extracellular matrix. The choroid plexus is mainly involved in the production of cerebrospinal fluid (CSF) by using the free access to the blood compartment of the leaky vessels. In order to separate blood and CSF compartments, choroid plexus epithelial cells and tanycytes of circumventricular organs constitute the blood–CSF–brain barrier. As non-neuronal cells in the brain and derived from neuroectoderm, choroid plexus epithelia are defined as a subtype of macroglia. The choroid plexus is involved in a variety of neurological disorders, including neurodegenerative, inflammatory, infectious, traumatic, neoplastic, and systemic diseases. Aβ and Biondi ring tangles accumulate in the Alzheimer’s disease choroid plexus. In multiple sclerosis, the choroid plexus could represent a site for lymphocyte entry in the CSF and brain, and for presentation of antigens. Recent studies have provided new diagnostic markers and potential molecular targets for choroid plexus papilloma and carcinoma, which represent the most common brain tumors in the first year of life. We here revive some of the classical studies and review recent insight into the biology and pathology of the choroid plexus.

305 citations

Journal ArticleDOI
TL;DR: The frequency, sequence, and efficacy of therapies used for NMO attacks are analyzed and it is shown that certain therapies are more effective than others in cases of severe N MO attacks.
Abstract: ObjectiveNeuromyelitis optica (NMO) attacks often are severe, are difficult to treat, and leave residual deficits. Here, we analyzed the frequency, sequence, and efficacy of therapies used for NMO attacks. MethodsA retrospective review was made of patient records to assess demographic/diagnostic data, attack characteristics, therapies, and the short-term remission status (complete remission [CR], partial remission [PR], no remission [NR]). Inclusion criteria were NMO according to Wingerchuk's 2006 criteria or aquaporin-4 antibody-positive NMO spectrum disorder (NMOSD). Remission status was analyzed with generalized estimating equations (GEEs), a patient-based statistical approach. ResultsA total of 871 attacks in 185 patients (142 NMO/43 NMOSD, 82% female) were analyzed. The 1,153 treatment courses comprised high-dose intravenous steroids (HD-S;n=810), plasma exchange (PE;n=192), immunoadsorption (IA;n=38), other (n=80), and unknown (n=33) therapies. The first treatment course led to CR in 19.1%, PR in 64.5%, and NR in 16.4% of attacks. Second, third, fourth, and fifth treatment courses were given in 28.2%, 7.1%, 1.4%, and 0.5% of attacks, respectively. This escalation of attack therapy significantly improved outcome (p<0.001, Bowker test). Remission rates were higher for isolated optic neuritis versus isolated myelitis (p<0.001), and for unilateral versus bilateral optic neuritis (p=0.020). Isolated myelitis responded better to PE/IA than to HD-S as first treatment course (p=0.037). Predictors of CR in multivariate GEE analysis were age (odds ratio [OR]=0.97, p=0.011), presence of myelitis (OR=0.38, p=0.002), CR from previous attack (OR=6.85, p<0.001), and first-line PE/IA versus HD-S (OR=4.38, p=0.006). InterpretationParticularly myelitis and bilateral optic neuritis have poor remission rates. Escalation of attack therapy improves outcome. PE/IA may increase recovery in isolated myelitis. Ann Neurol 2016;79:206-216

305 citations


Authors

Showing all 36075 results

NameH-indexPapersCitations
Hyun-Chul Kim1764076183227
Klaus Müllen1642125140748
Giacomo Bruno1581687124368
Anders M. Dale156823133891
Holger J. Schünemann141810113169
Joachim Heinrich136130976887
Markus Merschmeyer132118884975
Klaus Ley12949557964
Robert W. Mahley12836360774
Robert J. Kurman12739760277
Bart Barlogie12677957803
Thomas Schwarz12370154560
Carlos Caldas12254773840
Klaus Weber12152460346
Andrey L. Rogach11757646820
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023253
2022831
20213,683
20203,499
20193,236
20182,918