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An einem Beispiel wird demonstriert, dass es oft vom Erfassungsaufwand abhängt, ob ein Merkmal als qualitativ oder quantitativ (zähl- bzw. messbar) einzustufen ist. Es folgt ein Überblick über quantitative Merkmale, die von 1820 bis heute in der Literatur über mitteleuropäische Wildrosenarten (Rosaceae: Rosa) behandelt werden. Bei vielen dieser Merkmale erscheint eine Erfassung in Ordinalskalen sinnvoller als eine metrische. Zu 8 Merkmalen, bei denen das Sammeln von Messwerten und ihre statistische Aufbereitung Erfolg verheißt, werden eigene Beobachtungen und Untersuchungen mitgeteilt. Bei ihrer Erfassung gilt es, eine Reihe von Fehlerquellen zu beachten, die meist in den Objekten, in einem Fall im Beobachter liegen. Bei der Erfassung von Hagebuttenmerkmalen muss ein Dimorphismus zwischen End- und Seitenblüten der Blütenstände berücksichtigt werden. Die Beschränkung von Messungen auf solitäre Blüten verringert die Streuung der Messwerte ebenso wie die Ermittlung der Standardabweichung anstelle der von älteren Autoren verwendeten Variationsbreite. Aufgrund einer optischen Täuschung wird die relative Länge des Fruchtstiels in Bezug zur Hagebuttenlänge meist zu hoch eingeschätzt. Merkmale, deren quantitative Erfassung diagnostisch brauchbare Daten liefern kann, sind in erster Linie die relative Fruchtstiellänge und der Griffelkanaldurchmesser, in zweiter Linie die Endfiederlänge, der Längen-Breiten index der Endfiedern und die Kronblattlänge.
Die Nelke Dianthus carthusianorum wurde nach dem Kartäuserorden benannt. Nach den derzeit geltenden deutschen Rechtschreibregeln ist nur die Schreibweise „Kartäusernelke“ ohne h korrekt. Der tatsächliche Gebrauch (Literatur, Internet) ist jedoch nicht einheitlich. Für die Form ohne h sprechen die etymologische Herkunft und die Übereinstimmung mit anderen europäischen Sprachen, für die Form mit h eine mehr als 500jährige Tradition im deutschen Sprachraum.
Objective: Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with an overall 5-year survival rate of 9%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC; however, subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumour biology. It is clear that hyperactivation of MYC generates dependencies that can be exploited therapeutically. The aim of the study was to find and to target MYC-associated dependencies.
Design: We analysed human PDAC gene expression datasets. Results were corroborated by the analysis of the small ubiquitin-like modifier (SUMO) pathway in a large PDAC cohort using immunohistochemistry. A SUMO inhibitor was used and characterised using human and murine two-dimensional, organoid and in vivo models of PDAC.
Results: We observed that MYC is connected to the SUMOylation machinery in PDAC. Components of the SUMO pathway characterise a PDAC subtype with a dismal prognosis and we provide evidence that hyperactivation of MYC is connected to an increased sensitivity to pharmacological SUMO inhibition.
Conclusion: SUMO inhibitor-based therapies should be further developed for an aggressive PDAC subtype.
The title compound, [FeZr2(C5H5)4Cl2(C13H18B2)], is a heteronuclear complex that consists of a [3]ferrocenophane moiety substituted at each cyclopentadienyl (Cp) ring by a BH3 group; the BH3 group is bonded via two H atoms to the Zr atom of the zirconocene chloride moiety in a bidentate fashion. The two Cp rings of the [3]ferrocenophane moiety are aligned at a dihedral angle of 8.9 (4)° arising from the strain of the propane-1,3-diyl bridge linking the two Cp rings. [One methylene group is disordered over two positions with a site-occupation factor of 0.552 (18) for the major occupied site.] The dihedral angles between the Cp rings at the two Zr atoms are 50.0 (3) and 51.7 (3)°. The bonding Zr(...)H distances are in the range 1.89 (7)–2.14 (7) Å. As the two Cp rings of the ferrocene unit are connected by an ansa bridge, the two Zr atoms approach each other at 6.485 (1) Å. The crystal packing features C—H(...)Cl interactions.
Sleep is regulated in a time-of-day dependent manner and profits working memory. However, the impact of the circadian timing system as well as contributions of specific sleep properties to this beneficial effect remains largely unexplored. Moreover, it is unclear to which extent inter-individual differences in sleep-wake regulation depend on circadian phase and modulate the association between sleep and working memory. Here, sleep electroencephalography (EEG) was recorded during a 40-h multiple nap protocol, and working memory performance was assessed by the n-back task 10 times before and after each scheduled nap sleep episode. Twenty-four participants were genotyped regarding a functional polymorphism in adenosine deaminase (rs73598374, 12 G/A-, 12 G/G-allele carriers), previously associated with differences in sleep-wake regulation. Our results indicate that genotype-driven differences in sleep depend on circadian phase: heterozygous participants were awake longer and slept less at the end of the biological day, while they exhibited longer non rapid eye movement (NREM) sleep and slow wave sleep concomitant with reduced power between 8–16 Hz at the end of the biological night. Slow wave sleep and NREM sleep delta EEG activity covaried positively with overall working memory performance, independent of circadian phase and genotype. Moreover, REM sleep duration benefitted working memory particularly when occurring in the early morning hours and specifically in heterozygous individuals. Even though based on a small sample size and thus requiring replication, our results suggest genotype-dependent differences in circadian sleep regulation. They further indicate that REM sleep, being under strong circadian control, boosts working memory performance according to genotype in a time-of-day dependent manner. Finally, our data provide first evidence that slow wave sleep and NREM sleep delta activity, majorly regulated by sleep homeostatic mechanisms, is linked to working memory independent of the timing of the sleep episode within the 24-h cycle.
Background Parkinson's disease (PD) is an adult-onset movement disorder of largely unknown etiology. We have previously shown that loss-of-function mutations of the mitochondrial protein kinase PINK1 (PTEN induced putative kinase 1) cause the recessive PARK6 variant of PD. Methodology/Principal Findings Now we generated a PINK1 deficient mouse and observed several novel phenotypes: A progressive reduction of weight and of locomotor activity selectively for spontaneous movements occurred at old age. As in PD, abnormal dopamine levels in the aged nigrostriatal projection accompanied the reduced movements. Possibly in line with the PARK6 syndrome but in contrast to sporadic PD, a reduced lifespan, dysfunction of brainstem and sympathetic nerves, visible aggregates of alpha-synuclein within Lewy bodies or nigrostriatal neurodegeneration were not present in aged PINK1-deficient mice. However, we demonstrate PINK1 mutant mice to exhibit a progressive reduction in mitochondrial preprotein import correlating with defects of core mitochondrial functions like ATP-generation and respiration. In contrast to the strong effect of PINK1 on mitochondrial dynamics in Drosophila melanogaster and in spite of reduced expression of fission factor Mtp18, we show reduced fission and increased aggregation of mitochondria only under stress in PINK1-deficient mouse neurons. Conclusion Thus, aging Pink1 -/- mice show increasing mitochondrial dysfunction resulting in impaired neural activity similar to PD, in absence of overt neuronal death.