The Hα\alpha broadband photometric reverberation mapping of four Seyfert 1 galaxies

Broadband photometric reverberation mapping (PRM) have been investigated for AGNs in recent years, but mostly on accretion disk continuum RM. Due to the small fraction of broad emission lines in the broadband, PRM for emission lines is very challenging. Here we present an ICCF-Cut method for broadband PRM to obtain the H$\alpha$ broad line lag and apply it to four Seyfert 1 galaxies, MCG+08-11-011, NGC 2617, 3C 120 and NGC 5548. All of them have high quality broadband lightcurves with daily/sub-daily cadence, which enables us to extract H$\alpha$ lightcurves from the line band by subtracting the contributions from the continuum and host galaxy. Their extracted H$\alpha$ lightcurves are compared with the lagged continuum band lightcurves, as well as the lagged H$\beta$ lightcurves obtained by spectroscopic RM (SRM) at the same epochs. The consistency of these lightcurves and the comparison with the SRM H$\beta$ lags provide supports to the H$\alpha$ lags of these AGNs, in a range from 9 to 19 days, obtained by the ICCF-Cut, JAVELIN and $\chi^2$ methods. The simulations to evaluate the reliability of H$\alpha$ lags and the comparisons between SRM H$\beta$ and PRM H$\alpha$ lags indicate that the consistency of the ICCF-Cut, JAVELIN and $\chi^2$ results can ensure the reliability of the derived H$\alpha$ lags. These methods may be used to estimate the broad line region sizes and black hole masses of a large sample of AGNs in the large multi-epoch high cadence photometric surveys such as LSST in the future.Comment: 22 pages, 19 figures, accepted for publication in Ap

CatNorth: An Improved Gaia DR3 Quasar Candidate Catalog with Pan-STARRS1 and CatWISE

A complete and pure sample of quasars with accurate redshifts is crucial for quasar studies and cosmology. In this paper, we present CatNorth, an improved Gaia DR3 quasar candidate catalog with more than 1.5 million sources in the 3$\pi$ sky built with data from Gaia, Pan-STARRS1, and CatWISE2020. The XGBoost algorithm is used to reclassify the original Gaia DR3 quasar candidates as stars, galaxies, and quasars. To construct training/validation datasets for the classification, we carefully built two different master stellar samples in addition to the spectroscopic galaxy and quasar samples. An ensemble classification model is obtained by averaging two XGBoost classifiers trained with different master stellar samples. Using a probability threshold of $p_{\mathrm{QSO\_mean}}>0.95$ in our ensemble classification model and an additional cut on the logarithmic probability density of zero proper motion, we retrieved 1,545,514 reliable quasar candidates from the parent Gaia DR3 quasar candidate catalog. We provide photometric redshifts for all candidates with an ensemble regression model. For a subset of 89,100 candidates, accurate spectroscopic redshifts are estimated with the Convolutional Neural Network from the Gaia BP/RP spectra. The CatNorth catalog has a high purity of > 90% while maintaining high completeness, which is an ideal sample to understand the quasar population and its statistical properties. The CatNorth catalog is used as the main source of input catalog for the LAMOST phase III quasar survey, which is expected to build a highly complete sample of bright quasars with $i < 19.5$.Comment: 24 pages, 13 figures, submitted to AAS journals. Table 4 (The CatNorth quasar candidate catalog) is available at https://nadc.china-vo.org/res/r101313

Evidence for an Outer Component in the Continuum Reverberation Mapping of Active Galactic Nuclei

Continuum reverberation mapping is widely used in studying the accretion disks of active galactic nuclei (AGNs). Some indirect evidence and simulations have indicated that the diffuse continuum, especially the strong Balmer continuum from the broad-line region, may contribute to the continuum in the u / U band. Here, we present direct evidence for this contribution. In this work, we apply the ICCF-Cut method to continuum reverberation mapping to extract the possible diffuse continuum light curves of six AGNs, using high-cadence, high-quality, and multiband observations. We find the existence of an outer component out of the accretion disk for each of the six AGNs in the Swift U band. Meanwhile, similar results can be derived with the JAVELIN Photometric Reverberation Mapping Model for four of them. The lags of the outer components are consistent with the predicted Balmer continuum lags, which are about half of the H β lag values. Our result directly reinforces the understanding that an outer component, especially the Balmer continuum in the rest-frame u / U band, can contribute significantly to the continuum reverberation lags of AGNs

The Prognostic Significance of <i>FKBP1A</i> and Its Related Immune Infiltration in Liver Hepatocellular Carcinoma

Liver hepatocellular carcinoma (LIHC) remains a global health challenge with poor prognosis and high mortality. FKBP1A was first discovered as a receptor for the immunosuppressant drug FK506 in immune cells and is critical for various tumors and cancers. However, the relationships between FKBP1A expression, cellular distribution, tumor immunity, and prognosis in LIHC remain unclear. Here, we investigated the expression level of FKBP1A and its prognostic value in LIHC via multiple datasets including ONCOMINE, TIMER, GEPIA, UALCAN, HCCDB, Kaplan–Meier plotter, LinkedOmics, and STRING. Human liver tissue microarray was employed to analyze the characteristics of FKBP1A protein including the expression level and pathological alteration in cellular distribution. FKBP1A expression was significantly higher in LIHC and correlated with tumor stage, grade and metastasis. The expression level of the FKBP1A protein was also increased in LIHC patients along with its accumulation in endoplasmic reticulum (ER). High FKBP1A expression was correlated with a poor survival rate in LIHC patients. The analysis of gene co-expression and the regulatory pathway network suggested that FKBP1A is mainly involved in protein synthesis, metabolism and the immune-related pathway. FKBP1A expression had a significantly positive association with the infiltration of hematopoietic immune cells including B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells. Moreover, M2 macrophage infiltration was especially associated with a poor survival prognosis in LIHC. Furthermore, FKBP1A expression was significantly positively correlated with the expression of markers of M2 macrophages and immune checkpoint proteins such as PD-L1, CTLA-4, LAG3 and HAVCR2. Our study demonstrated that FKBP1A could be a potential prognostic target involved in tumor immune cell infiltration in LIHC

Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis

Transgenic expression of Cre recombinase driven by a specific promoter is normally used to conditionally knockout a gene in a tissue- or cell-type-specific manner. In &alpha;MHC-Cre transgenic mouse model, expression of Cre recombinase is controlled by the myocardial-specific &alpha;-myosin heavy chain (&alpha;MHC) promoter, which is commonly used to edit myocardial-specific genes. Toxic effects of Cre expression have been reported, including intro-chromosome rearrangements, micronuclei formation and other forms of DNA damage, and cardiomyopathy was observed in cardiac-specific Cre transgenic mice. However, mechanisms associated with Cardiotoxicity of Cre remain poorly understood. In our study, our data unveiled that &alpha;MHC-Cre mice developed arrhythmias and died after six months progressively, and none of them survived more than one year. Histopathological examination showed that &alpha;MHC-Cre mice had aberrant proliferation of tumor-like tissue in the atrial chamber extended from and vacuolation of ventricular myocytes. Furthermore, the &alpha;MHC-Cre mice developed severe cardiac interstitial and perivascular fibrosis, accompanied by significant increase of expression levels of MMP-2 and MMP-9 in the cardiac atrium and ventricular. Moreover, cardiac-specific expression of Cre led to disintegration of the intercalated disc, along with altered proteins expression of the disc and calcium-handling abnormality. Comprehensively, we identified that the ferroptosis signaling pathway is involved in heart failure caused by cardiac-specific expression of Cre, on which oxidative stress results in cytoplasmic vacuole accumulation of lipid peroxidation on the myocardial cell membrane. Taken together, these results revealed that cardiac-specific expression of Cre recombinase can lead to atrial mesenchymal tumor-like growth in the mice, which causes cardiac dysfunction, including cardiac fibrosis, reduction of the intercalated disc and cardiomyocytes ferroptosis at the age older than six months in mice. Our study suggests that &alpha;MHC-Cre mouse models are effective in young mice, but not in old mice. Researchers need to be particularly careful when using &alpha;MHC-Cre mouse model to interpret those phenotypic impacts of gene responses. As the Cre-associated cardiac pathology matched mostly to that of the patients, the model could also be employed for investigating age-related cardiac dysfunction

Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis

Transgenic expression of Cre recombinase driven by a specific promoter is normally used to conditionally knockout a gene in a tissue- or cell-type-specific manner. In αMHC-Cre transgenic mouse model, expression of Cre recombinase is controlled by the myocardial-specific α-myosin heavy chain (αMHC) promoter, which is commonly used to edit myocardial-specific genes. Toxic effects of Cre expression have been reported, including intro-chromosome rearrangements, micronuclei formation and other forms of DNA damage, and cardiomyopathy was observed in cardiac-specific Cre transgenic mice. However, mechanisms associated with Cardiotoxicity of Cre remain poorly understood. In our study, our data unveiled that αMHC-Cre mice developed arrhythmias and died after six months progressively, and none of them survived more than one year. Histopathological examination showed that αMHC-Cre mice had aberrant proliferation of tumor-like tissue in the atrial chamber extended from and vacuolation of ventricular myocytes. Furthermore, the αMHC-Cre mice developed severe cardiac interstitial and perivascular fibrosis, accompanied by significant increase of expression levels of MMP-2 and MMP-9 in the cardiac atrium and ventricular. Moreover, cardiac-specific expression of Cre led to disintegration of the intercalated disc, along with altered proteins expression of the disc and calcium-handling abnormality. Comprehensively, we identified that the ferroptosis signaling pathway is involved in heart failure caused by cardiac-specific expression of Cre, on which oxidative stress results in cytoplasmic vacuole accumulation of lipid peroxidation on the myocardial cell membrane. Taken together, these results revealed that cardiac-specific expression of Cre recombinase can lead to atrial mesenchymal tumor-like growth in the mice, which causes cardiac dysfunction, including cardiac fibrosis, reduction of the intercalated disc and cardiomyocytes ferroptosis at the age older than six months in mice. Our study suggests that αMHC-Cre mouse models are effective in young mice, but not in old mice. Researchers need to be particularly careful when using αMHC-Cre mouse model to interpret those phenotypic impacts of gene responses. As the Cre-associated cardiac pathology matched mostly to that of the patients, the model could also be employed for investigating age-related cardiac dysfunction