Abstract. We present the results from a detailed deprojection analysis of Abell 1835 as observed by XMM-Newton. If we fit the spectra with an isothermal plasma model, the deprojected temperature profile is flat in the outer region around 7.6 keV and decreases to ∼5.6 keV in the center, which may be connected with the gas cooling. In the central part, a two-component thermal plasma model can fit the spectrum significantly better. Moreover, the cool component (T ∼ 1.8 keV) has a much lower metal abundance than the hot component (T ∼ 8 keV), which may be due to the longer cooling time for the cool gas with lower abundance. In addition, it was found that without a main isothermal component, the standard cooling flow model cannot fit the spectrum satisfactorily. From the isothermal model fitting results we also derived the electron density n e , and fitted its radial distribution with a double-β model. The n e profile inferred with the double-β model and the deprojected X-ray gas temperature profile were then combined to derive the total mass and the total projected mass of the cluster. The projected mass is lower than that derived from the weak lensing method. However, assuming that the cluster extends to a larger radius ∼15 as found by Clowe & Schneider (2002), the two results are consistent within the error bars. Furthermore, we calculated the projected mass within the radius of ∼153 kpc implied by the presence of a gravitational lensing arc, which is about half of the mass determined from the optical lensing.

Pancreatic cancer is one of the most aggressive and lethal malignancies with extremely poor prognosis, and KLK7 was considered as a potential therapeutic target. In this study, we analyzed the expression of KLK7 in TCGA and GTEx databases and found that KLK7 had a negative correlation to long-term survival rate (>1.5 years) of pancreatic cancer patients. Compound 42 is a coumarinic derivative, a suicide substrate inhibitor of KLK7, which has been proved to inhibit the proliferation of PANC-1 cells in vitro effectively in our previous study. In this study, we further investigated the inhibition ability of Compound 42 in tumor formation and development in CDX and PDX tumor models of pancreatic cancer subsequently. Besides, we studied the inhibitory mechanism of Compound 42 and the result showed that Compound 42 arrested the pancreatic cancer cell cycle in G0/G1 phase and induced ferroptosis through down-regulation of GPX4 protein level and accumulation of iron ion. Thus, these experiments demonstrate that Compound 42, suppressing pancreatic cancer in vivo, is expected to become a novel drug for pancreatic cancer treatment.