Formation of Atomic Carbon Chains from Graphene Nanoribbons

The formation of one-dimensional carbon chains from graphene nanoribbons is investigated using it ab initio molecular dynamics. We show under what conditions it is possible to obtain a linear atomic chain via pulling of the graphene nanoribbons. The presence of dimers composed of two-coordinated carbon atoms at the edge of the ribbons is necessary for the formation of the linear chains, otherwise there is simply the full rupture of the structure. The presence of Stone-Wales defects close to these dimers may lead to the formation of longer chains. The local atomic configuration of the suspended atoms indicates the formation of single and triple bonds, which is a characteristic of polyynes.Comment: 4 pages, 5 figure

V(D)J recombination frequency is affected by the sequence interposed between a pair of recombination signals: sequence comparison reveals a putative recombinational enhancer element

The immunoglobulin heavy chain intron enhancer (Eμ) not only stimulates transcription but also V(D)J recombination of chromosomally integrated recombination substrates. We aimed at reproducing this effect in recombination competent cells by transient transfection of extrachromosomal substrates. These we prepared by interposing between the recombination signal sequences (RSS) of the plasmid pBlueRec various fragments, including Eμ, possibly affecting V(D)J recombination. Our work shows that sequences inserted between RSS 23 and RSS 12, with distances from their proximal ends of 26 and 284 bp respectively, can markedly affect the frequency of V(D)J recombination. We report that the entire Eμ, the Eμ core as well as its flanking 5′ and 3′ matrix associated regions (5′ and 3′ MARs) upregulate V(D)J recombination while the downstream section of the 3′ MAR of Eμ does not. Also, prokaryotic sequences markedly suppress V(D)J recombination. This confirms previous results obtained with chromosomally integrated substrates, except for the finding that the full length 3′ MAR of Eμ stimulates V(D)J recombination in an episomal but not in a chromosomal context. The fact that other MARs do not share this activity suggests that the effect is not mediated through attachment of the recombination substrate to a nuclear matrix-associated recombination complex but through cis-activation. The presence of a 26 bp A-T-rich sequence motif in the 5′ and 3′ MARs of Eµ and in all of the other upregulating fragments investigated, leads us to propose that the motif represents a novel recombinational enhancer element distinct from those constituting the Eµ cor

Motivational training improves self-efficacy but not short-term adherence with asthma self-management: a randomized controlled trial

Background: Adherence to self-management in asthma is poor. Aim: To investigate the effect of disease-unspecific motivational training on self-management adherence in addition to asthma-specific patient education. Methods: We randomized patients with partly controlled asthma to asthma education, with or without the Zurich Resource Model (ZRM) training. Main elements of the ZRM training are development of action-oriented personal goals and activation of resources to achieve and practice them in daily life. The primary outcome was adherence to self-monitoring and to a written personal action plan during three months. Secondary outcomes included patient-reported self-efficacy. Results: As control patients (n=30) were younger, mostly male and had better asthma control compared with the intervention group (n=30), we adjusted the analyses for these imbalances. Both groups showed excellent adherence to self-monitoring over three months [27 patients (90.0%) in intervention and 25 patients (83.3%) in control group, adjusted odds ratio: 1.28 (0.24-6.78), P=0.78)]. Patients in the ZRM group tended to adjust their medication more often [median 36% days with action (IQR 11-62%)] than control patients [9% (0-43), P=0.18]. In both groups, actions were rarely in accordance with the action plan [median 20% of actions appropriate (IQR 0-37) in intervention and 11% (IQR 0-56) in control group, P=0.92]. After three months, self-efficacy was significantly better with ZRM (adjusted difference on self-efficacy scale 2.31, 95% CI 0.31-4.31, P=0.02). Conclusion: Unspecific self-management training had no short-term effect on self-management adherence in asthma patients. Self-efficacy improved, but it is uncertain whether this translates into better long-term outcome

Surfactant secretion in LRRK2 knock-out rats : changes in lamellar body morphology and rate of exocytosis

Leucine-rich repeat kinase 2 (LRRK2) is known to play a role in the pathogenesis of various diseases including Parkinson disease, morbus Crohn, leprosy and cancer. LRRK2 is suggested to be involved in a number of cell biological processes such as vesicular trafficking, transcription, autophagy and lysosomal pathways. Recent histological studies of lungs of LRRK2 knock-out (LRRK2 -/-) mice revealed significantly enlarged lamellar bodies (LBs) in alveolar type II (ATII) epithelial cells. LBs are large, lysosome-related storage organelles for pulmonary surfactant, which is released into the alveolar lumen upon LB exocytosis. In this study we used high-resolution, subcellular live-cell imaging assays to investigate whether similar morphological changes can be observed in primary ATII cells from LRRK2 -/- rats and whether such changes result in altered LB exocytosis. Similarly to the report in mice, ATII cells from LRRK2 -/- rats contained significantly enlarged LBs resulting in a >50% increase in LB volume. Stimulation of ATII cells with ATP elicited LB exocytosis in a significantly increased proportion of cells from LRRK2 -/- animals. LRRK2 -/- cells also displayed increased intracellular Ca2+ release upon ATP treatment and significant triggering of LB exocytosis. These findings are in line with the strong Ca2+-dependence of LB fusion activity and suggest that LRRK2 -/- affects exocytic response in ATII cells via modulating intracellular Ca2+ signaling. Post-fusion regulation of surfactant secretion was unaltered. Actin coating of fused vesicles and subsequent vesicle compression to promote surfactant expulsion were comparable in cells from LRRK2 -/- and wt animals. Surprisingly, surfactant (phospholipid) release from LRRK2 -/- cells was reduced following stimulation of LB exocytosis possibly due to impaired LB maturation and surfactant loading of LBs. In summary our results suggest that LRRK2 -/- affects LB size, modulates intracellular Ca2+ signaling and promotes LB exocytosis upon stimulation of ATII cells with ATP