Implementation of ACTS for STCF track reconstruction

With an electron-positron collider operating at center-of-mass-energy 2-7 GeV and a peak luminosity above $0.5\times10^{35} cm^{-2} s^{-1}$, the STCF physics program will provide an unique platform for in-depth studies of hadron structure and non-perturbative strong interaction as well as probing new physics beyond the Standard Model in the $\tau$-Charm sector, succeeding the present Beijing Electron-Positron Collider. To fulfill the physics targets and further maximize the physics potential at STCF, the STCF tracking software should have capability to reconstruct charged particles with high efficiency and excellent momentum resolution, especially for the charged particles with low transverse momentum down to 50 MeV. A Common Tracking Software (ACTS) providing a set of detector-independent tracking algorithms is adopted for reconstructing charged tracks with the information of two sub-detectors, a $\mu$RWELL-based inner tracker and a drift chamber, at STCF. This is the first demonstration of ACTS for a drift chamber. The implementation details and performance of track reconstruction are presented.Comment: 14 pages, 7 figure

Novel approach to investigate η\eta decays via η′→ππη\eta'\rightarrow\pi\pi\eta

To avoid the impact from the background events directly from $e^+e^-$ annihilations or $J/\psi$ decays, we propose a novel approach to investigate $\eta$ decays, in particular for its rare or forbidden decays, by using $\eta^\prime\rightarrow\pi\pi\eta$ produced in $J/\psi$ decays at the $\tau-$charm factories. Based on the MC studies of a few typical decays, $\eta\rightarrow \pi\pi$, $\gamma l^+l^- (l= e, \mu)$, $l^+l^-$, as well as $l^+l^-\pi^0$, the sensitivities could be obviously improved by taking advantage of the extra constraint of $\eta^\prime$. Using one trillion $J/\psi$ events accumulated at the Super $\tau$-Charm facility, the precision on the investigation of $\eta$ decays could be improved significantly and the observation of the rare decay $\eta\rightarrow e^+e^-$ is even accessable.Comment: 7 pages, 6 figure

Methylation-mediated silencing of PTPRD induces pulmonary hypertension by promoting pulmonary arterial smooth muscle cell migration via the PDGFRB/PLCγ1 axis

OBJECTIVE: Pulmonary hypertension is a lethal disease characterized by pulmonary vascular remodeling and is mediated by abnormal proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). Platelet-derived growth factor BB (PDGF-BB) is the most potent mitogen for PASMCs and is involved in vascular remodeling in pulmonary hypertension development. Therefore, the objective of our study is to identify novel mechanisms underlying vascular remodeling in pulmonary hypertension. METHODS: We explored the effects and mechanisms of PTPRD downregulation in PASMCs and PTPRD knockdown rats in pulmonary hypertension induced by hypoxia. RESULTS: We demonstrated that PTPRD is dramatically downregulated in PDGF-BB-treated PASMCs, pulmonary arteries from pulmonary hypertension rats, and blood and pulmonary arteries from lung specimens of patients with hypoxic pulmonary arterial hypertension (HPAH) and idiopathic PAH (iPAH). Subsequently, we found that PTPRD was downregulated by promoter methylation via DNMT1. Moreover, we found that PTPRD knockdown altered cell morphology and migration in PASMCs via modulating focal adhesion and cell cytoskeleton. We have demonstrated that the increase in cell migration is mediated by the PDGFRB/PLCγ1 pathway. Furthermore, under hypoxic condition, we observed significant pulmonary arterial remodeling and exacerbation of pulmonary hypertension in heterozygous PTPRD knock-out rats compared with the wild-type group. We also demonstrated that HET group treated with chronic hypoxia have higher expression and activity of PLCγ1 in the pulmonary arteries compared with wild-type group. CONCLUSION: We propose that PTPRD likely plays an important role in the process of pulmonary vascular remodeling and development of pulmonary hypertension in vivo

Inhalation of electronic cigarettes slightly affects lung function and inflammation in mice

Electronic cigarettes have become increasingly popular, but the results of previous studies on electronic cigarette exposure in animals have been equivocal. This study aimed to evaluate the effects of electronic cigarette smoke (ECS) and cigarette smoke (CS) on lung function and pulmonary inflammation in mice to investigate whether electronic cigarettes are safer when compared to cigarettes. 32 specific pathogen-free BALB/c male mice were randomly grouped and exposed to fresh air (control), mint-flavored ECS (ECS1, 6 mg/kg), cheese-flavored ECS (ECS2, 6 mg/kg), and CS (6 mg/kg). After 3 weeks exposure to ECS or CS, we measured lung function (PIF and Penh) and blood oxygen saturation. The levels of TNF-α and IL-6 in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. HE staining was performed to observe the pathological changes in the lung tissues. The levels of IL-6 in BALF and serum, and TNF-α in BALF, were elevated similarly in the ECS and CS groups compared to the control group. Significant elevation was observed in serum TNF-α levels in the CS group. The total count of cells in BALF were increased after ECS1 exposure and CS exposure. PIF and oxygen saturation decreased, and Penh increased markedly in the CS group but not in the ECS groups. Compared with the ECS groups, mice in the CS group had widened lung tissue septa and increased inflammatory cell infiltration. However, we did not detect significant differences between mint-flavored and cheese-flavored e-cigarettes in our study. Overall, our findings suggested that both ECS and CS impair lung function and histopathology while promoting inflammation. In contrast, ECS has a less negative impact than CS