In the forward end-cap of the Belle II spectrometer, particle identification is provided by a proximity focusing RICH detector with an aerogel radiator (ARICH). The ARICH’s primary function is to ...effectively distinguish between pions and kaons in the momentum range of 0.5GeV/c to about 4GeV/c, as well as to contribute to identification of low-momentum leptons. Since its operation began, Belle II has collected over 420fb−1 of data. Based on this large data sample, studies of several effects that impact the performance of the ARICH detector were carried out. In this paper, we present a comparison of the observed Cherenkov ring image and detector particle identification performance in the measured data and detector simulation. Furthermore, we highlight recent efforts aimed at enhancing the ARICH’s performance by taking into account the effects of particle decay in flight and scattering in materials before the detector, as well as by refining the probability density function used for particle identification likelihood evaluation.
In the Belle II experiment, an aerogel-based proximity focusing ring-imaging Cherenkov (ARICH) counter is used for charged particle identification (PID) in the forward end-cap region. The goal is to ...separate kaons from pions at above 4σ significance level for momenta up to 4 GeV/c, which is critical for the measurements of rare B decays and CP violation in B decays. Chrerenkov photons are emitted in aerogel tiles and 144-channel Hybrid Avalanche Photo Detector (HAPDs) are used as the photo-detectors. We utilize a two-layer aerogel design with different refractive indexes in a focusing configuration. In Phase 3 of the Belle II operation (from Apr. 2019), the ARICH system has been operating smoothly. The performance of particle identification with ARICH has been well validated and is in agreement with simulation.
We have previously reported increased expression of matrix metalloproteinase‐2 (MMP‐2) using a rat model of liver fibrosis. However we did not clarify how the precursor of MMP‐2 (proMMP‐2) was ...activated. Therefore, we used human liver specimens with chronic hepatitis (CH) and liver cirrhosis (LC) to examine expression of membrane‐type‐1‐MMP (MT1‐MMP), which has recently been determined to activate proMMP‐2. Northern hybridization studies showed a 5.4‐ and 1.4‐ fold increase in MMP‐2 expression in CH and LC, respectively, as compared with normal liver. MT1‐MMP gene expression simultaneously increased 4.0‐ and 1.4‐fold in CH and LC, respectively. In situ hybridization using 35S‐cRNA probes of MMP‐2 and MT1‐MMP showed prominent silver granules in elongated cells found in the lobules, periportal areas, and fibrous septa of CH and LC samples. These elongated cells expressed α‐smooth muscle actin by immunohistochemistry. Immunoelectron microscopic examination localized MMP‐2 and MT1‐MMP to the rough endoplasmic reticulum of stellate cells located in the lobules and periportal areas, or to fibroblasts in the fibrous septa, suggesting that MMP‐2 and MT1‐MMP were produced by these cells. In addition, cytoplasmic and membranous immunodeposits of both MMPs were found in endothelial cells, Kupffer cells, capillary endothelial cells, and lymphocytes, indicating that activation of proMMP‐2 occurs locally. Increased expression of MMP‐2 and MT1‐MMP was detected in CH and LC, while dual over‐expression was found in stellate cells and fibroblasts, possibly resulting in the increase of active MMP‐2 in and around these cells. These findings suggest that activated MMP‐2 may remodel liver parenchyma during the process of liver fibrosis.
To analyze the structure of LH in three patients with immunologically anomalous LH, the whole coding region of the LH beta-subunit gene was examined. These patients were infertile, and their serum LH ...levels could not be measured with an immunoassay kit. Immunoblotting of the LH beta-subunit showed no marked changes in the molecular size of LH beta. Genomic DNA was extracted from peripheral lymphocytes of the patients and normal controls, and LH beta genes were amplified by the polymerase chain reaction technique, using primer pairs that are capable of specifically amplifying only the LH beta gene without interference by the CG beta genes. No deletions were observed in the coding regions of the LH beta gene of the patients. Nucleotide sequencing revealed two nucleotide substitutions in the LH beta gene of the patients, which cause amino acid replacements from Trp8 (TGG) to Arg8 (CGG) and Ile15 (ATC) to Thr15 (ACC). Restriction fragment length polymorphism analysis in three families indicated that the affected probands were homozygous, and their family members were heterozygous, except for their husbands. The heterozygotes showed reduced detectability with the LH immunoassay kit. These results suggest that these amino acid replacements are responsible for this immunologically anomalous variant.
Abstract
Background
Sick sinus syndrome (SSS) and atrial fibrillation (AF) frequently coexist and interact to initiate and perpetuate each other. Several retrospective or small cohort studies have ...suggested that successful catheter ablation of AF may help to waive device implantations in patients with paroxysmal AF plus SSS, however, no prospective large studies are so far available on this scenario.
Purpose
We aimed to elucidate the device implantation-free survival after catheter ablation of paroxysmal AF with coexisting SSS in a prospective large-scale registry. We also determined the risk factors for device implantations after catheter ablation of paroxysmal AF.
Methods
The Kansai Plus Atrial Fibrillation (KPAF) study is a multi-center prospective registry that enrolled 5,019 consecutive patients that underwent an initial pulmonary vein isolation-based radiofrequency catheter ablation of AF. This study was comprised of 3,226 patients with paroxysmal AF registered in the KPAF study (age, 64.8±10.5 years old; female, n=999 31.0%; left atrial diameter LAD, 37.5±8.0 mm; left ventricular ejection fraction LVEF, 65.3±8.4%, CHADS2 score, 1.09±1.05). The atrial tachyarrhythmia-free and device-free survivals after catheter ablation were compared between patients with SSS (n=368; tachy-brady syndrome, 88%) and without SSS (control; n=2,858).
Results
The atrial tachyarrhythmia-free survival was almost identical between the two groups both after the first ablation session (Fig.1A) and after the last procedure with an average of 1.3±0.5 sessions. At baseline, the devices had already been implanted in 53 (14.4%) SSS and 36 (1.3%) control patients. In the remaining patients, devices were newly implanted in 54 (17.1%) SSS and 62 (2.2%) control patients during the follow-up of 3 years after the catheter ablation (Figure 1B). In the SSS group, devices were implanted predominantly within 6 months after the catheter ablation, and atrial tachyarrhythmia recurrence preceded the device implantation in 48 (89%) patients. Multivariate predictors of device implantations after the paroxysmal AF ablation included: SSS (hazard ratio HR 6.85, 95% confidence interval CI 4.61–10.19, p<0.001), an age>75 years old (HR 1.69, 95% CI 1.08–2.64, p=0.019), a female gender (HR 2.16, 95% CI 1.44–3.24, p<0.001), the LAD (mm) (HR 1.05, 95% CI 1.02–1.08, p=0.006), and the LVEF (%) (95% CI 0.96, 95% CI 0.94–0.98, p<0.001).
Figure 1
Conclusions
Device implantations could be waived in >80% of patients with SSS at 3 years of follow-up after the catheter ablation of paroxysmal AF in this real world all comer prospective registry. In addition to coexisting SSS, predictors of device implantations after paroxysmal AF ablation included: the elderly, a female gender, a large LA, and a reduced LVEF.
Acknowledgement/Funding
None
PDF
