Abstract
Background
The visually guided laser balloon ablation is a balloon-based catheter ablation technology used for atrial fibrillation (AF) ablation in recent years. This balloon catheter ...consists of a compliant balloon that has the capability of real-time endoscopic visualization of the targeted pulmonary vein (PV). The sizeable balloon is usually inflated to obtain optimal PV occlusion. The isolation area after laser balloon (LB) ablation was reported to be smaller than that after cryoballoon ablation. However, when LB is inflated with its maximum pressure, it can visualize wide-area PV antrum. Thereby, we suspected that larger-size LB can create wider isolation area.
Purpose
The aim of this study is to quantitatively evaluate the isolation area after LB ablation at the size larger than appropriate size for ablation in the pulmonary vein carina region.
Methods
We assessed 66 patients with AF who underwent LB ablation at the larger inflation size in our hospital during the period from July 2018 to July 2019. After LB ablation, we created voltage maps with a circular mapping catheter and calculated isolation areas with CARTO system.
Results
Figure shows a larger LB with its maximum pressure. PV antrum isolation was extended to the posterior wall in all patients. The left- and right-sided pulmonary vein antrum isolation area were 15.1±3.9 and 19.4±4.3 cm2, respectively.
Conclusion
LB at the larger inflation size with its maximum pressure can isolate wider-area circumferential PV antrum than previously reported. This method may be a new way of pulmonary vein antrum isolation.
Left atrial voltage mapping after PVI.
Funding Acknowledgement
Type of funding source: None
The extinct p-process nuclide 146Sm (t1/2=103±5Myr) is known to have been present in the Early-Solar System and has been proposed as an astrophysical chronometer. 146Sm is also intensely used to date ...meteorite and planetary differentiation processes, enhancing the importance of an accurate knowledge of the 146Sm half-life. We are engaged in a new determination of the 146Sm half-life in which the 146Sm/147Sm atom ratio is determined by accelerator mass spectrometry at the ATLAS facility of Argonne National Laboratory. In order to reduce systematic errors in the AMS determination of the 146Sm/147Sm ratios (in the range of 10−7–10−9), 146Sm and 147Sm ions were alternately counted in the same detector in the focal plane of a gas-filled magnet, respectively in continuous-wave and attenuated mode. Quantitative attenuation is obtained with the 12MHz pulsed and ns-bunched ATLAS beam by chopping beam pulses with an RF sweeper in a ratio (digitally determined) down to 1:106. The experiments and preliminary results are discussed.
We investigated the effects of interleukin-1 beta (IL-1 beta), administered directly into the rat anterior hypothalamus (AHY), on monoamine release in the same region by using a brain microdialysis ...technique and an HPLC-electrochemical detection system. First, to study the local effects of IL-1 beta, we used a microdialysis probe equipped with a microinjection tube for administering IL-1 beta in the same region into which the probe had been inserted. IL-1 beta (1 ng) injected directly into the AHY elicited release of norepinephrine (NE), dopamine (DA), and 5-HT, as well as increases in their metabolites, 4-hydroxy-3-methoxyphenylglycol, 3,4-dihydroxyphenylacetic acid, 4-hydroxy-3-methoxyphenylacetic acid, and 5-hydroxyindole-3-acetic acid, in the AHY. Vehicle alone exerted no effect on monoamine release. Although the elevated levels of NE and DA persisted for more than 6 hr after injection of IL-1 beta, the elevated levels of 5-HT were transient. Second, in order to investigate whether this effect of IL-1 beta is a direct action in the AHY, we performed in vitro experiments using hypothalamus slices. IL-1 beta (0.1 and 1 nM) increased the levels of each monoamine released from hypothalamic slices in a dose-dependent manner. These findings suggest that IL-1 beta acts directly on the hypothalamus to induce release of NE, DA, and 5-HT. Third, the roles of prostaglandins (PGs) in NE release in the AHY elicited by direct injection of IL-1 beta were examined.
Retraction Kinoshita, N.; Paul, M.; Kashiv, Y. ...
Science (American Association for the Advancement of Science),
03/2023, Letnik:
379, Številka:
6639
Journal Article
Retraction Kinoshita, N; Paul, M; Kashiv, Y ...
Science (American Association for the Advancement of Science),
03/2023, Letnik:
379, Številka:
6639
Journal Article
Plants have evolved protective mechanisms to ensure their survival when threatened by adverse environmental conditions during their transition to autotrophic growth. During germination, there is a 2- ...to 3-d period during which a plant can execute growth arrest when challenged by water deficit. This postgermination developmental checkpoint is signaled by the stress hormone abscisic acid (ABA), which induces the expression of the bZIP transcription activator ABI5. The growth arrest efficiency depends on ABI5 levels, and abi5 mutants are ABA-insensitive and unable to execute the ABA-mediated growth arrest. Here we show that a novel ABI5-interacting protein, designated as AFP, can form high molecular weight (Mr) complexes with ABI5 in embryo-derived extracts. Like ABI5, ABI five binding protein (AFP) mRNA and protein levels are induced by ABA during seed germination. Two different afp mutant alleles (afp-1 and afp-2) are hypersensitive to ABA, whereas transgenic plants overexpressing AFP are resistant; in these plants, AFP and ABI5 protein levels are inversely correlated. Genetic analysis shows that abi5-4 is epistatic to afp-1, indicating the ABA hypersensitivity of afp mutants requires ABI5. Proteasome inhibitor studies show that ABI5 stability is regulated by ABA through ubiquitin-related events. When expressed together, AFP and ABI5 are colocalized in nuclear bodies, which also contain COP1, a RING motif protein. Our results suggest that AFP attenuates ABA signals by targeting ABI5 for ubiquitin-mediated degradation in nuclear bodies.
N-(2-hydroxyethyl)-nicotinamide nitrate (nicorandil) is a unique anti-anginal agent, reported to act as both an ATP-sensitive K(+) channel opener (PCO) and a nitric oxide donor. It also has an ...anti-oxidant action. We examined the effects of nicorandil on streptozotocin (STZ)-induced islet beta-cell damage both in vivo and in vitro.
STZ-induced diabetic Brown Norway rats (STZ-DM) were fed with nicorandil-containing chow from day 2 (STZ-DM-N48), 3 (STZ-DM-N72), and 4 (STZ-DM-N96) to day 30. Body weight, blood glucose, and plasma insulin were measured every week. For the in vitro assay, neonatal rat islet-rich cultures were performed and cells were treated with nicorandil from 1 h before to 2 h after exposure to STZ for 30 min. Insulin secretion from islet cells was assayed after an additional 24 h of culture. We also observed the effect of nicorandil on the generation of reactive oxygen species (ROS) from rat inslinoma cells (RINm5F).
Body weight loss and blood glucose levels of STZ-DM-N48 rats were significantly lower than those of STZ-DM rats. Immunohistochemical staining of insulin showed preservation of insulin-secreting islet beta-cells in STZ-DM-N48 rats. Nicorandil also dose-dependently recovered the insulin release from neonatal rat islet cells treated with STZ in in vitro experiments. Nicorandil did not act as a PCO on neonatal rat islet beta-cells or RINm5F cells, and did not show an inhibitory effect on poly(ADP-ribose) polymerase-1. However, the drug inhibited the production of ROS stimulated by high glucose (22.0 mmol/l) in RINm5F cells.
These results suggested that nicorandil improves diabetes and rat islet beta-cell damage induced by STZ in vivo and in vitro. It protects islet beta-cells, at least partly, via a radical scavenging effect.
Protein kinase C (PKC) has been implicated in the Wnt signaling pathway; however, its molecular role is poorly understood. We identified novel genes encoding delta-type PKC in the Xenopus EST ...databases. Loss of PKC delta function revealed that it was essential for convergent extension during gastrulation. We then examined the relationship between PKC delta and the Wnt pathway. PKC delta was translocated to the plasma membrane in response to Frizzled signaling. In addition, loss of PKC delta function inhibited the translocation of Dishevelled and the activation of c-Jun N-terminal kinase (JNK) by Frizzled. Furthermore, PKC delta formed a complex with Dishevelled, and the activation of PKC delta by phorbol ester was sufficient for Dishevelled translocation and JNK activation. Thus, PKC delta plays an essential role in the Wnt/JNK pathway by regulating the localization and activity of Dishevelled.
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