Diaqua­bis­{4-[(pyridin-2-yl)methyl­idene­amino]­benzene­sulfonato-κ2 N,N′}nickel(II) tetra­hydrate

In the title complex, [Ni(C12H9N2O3S)2(H2O)2]·4H2O, the NiII ion is coordinated by four N atoms from two bidentate chelating 4-[(pyridin-2-yl)methyl­idene­amino]­benzene­sulfonate ligands and two O atoms from cis-related water mol­ecules in a slightly distorted octa­hedral environment [Ni—N = 2.071 (3)–2.121 (3) Å and Ni—O = 2.071 (2) and 2.073 (3) Å]. In the crystal, the coordinated water mol­ecules and the four water mol­ecules of solvation are involved in inter­molecular O—H⋯O hydrogen-bonding inter­actions with water and sulfon­ate O-atom acceptors, giving a three-dimensional framework structure

Interpretable CNN-Multilevel Attention Transformer for Rapid Recognition of Pneumonia from Chest X-Ray Images

Chest imaging plays an essential role in diagnosing and predicting patients with COVID-19 with evidence of worsening respiratory status. Many deep learning-based approaches for pneumonia recognition have been developed to enable computer-aided diagnosis. However, the long training and inference time makes them inflexible, and the lack of interpretability reduces their credibility in clinical medical practice. This paper aims to develop a pneumonia recognition framework with interpretability, which can understand the complex relationship between lung features and related diseases in chest X-ray (CXR) images to provide high-speed analytics support for medical practice. To reduce the computational complexity to accelerate the recognition process, a novel multi-level self-attention mechanism within Transformer has been proposed to accelerate convergence and emphasize the task-related feature regions. Moreover, a practical CXR image data augmentation has been adopted to address the scarcity of medical image data problems to boost the model's performance. The effectiveness of the proposed method has been demonstrated on the classic COVID-19 recognition task using the widespread pneumonia CXR image dataset. In addition, abundant ablation experiments validate the effectiveness and necessity of all of the components of the proposed method.Comment: Accepted by the IEEE Journal of Biomedical and Health Informatic, doi: 10.1109/JBHI.2023.324794

The antitumor activity of umbelliferone in human renal cell carcinoma via regulation of the p110γ catalytic subunit of PI3Kγ

Umbelliferone exhibits extensive pharmacological activity, including anti-immunomodulatory, anti-inflammatory and antigenotoxicity activities. However, its antitumor properties still remain unclear in human renal cell carcinoma (RCC) cells. Our results have revealed that treatment of human RCC cells (786-O, OS-RC-2, and ACHN) with umbelliferone reduced cell proliferation in a concentration-dependent manner and induced dose-dependent apoptotic events. In addition, cell cycle analysis determined that umbelliferone treatment induced cell cycle arrest in the G1 phase in a dose-dependent manner. Furthermore, western blotting analysis showed a dose-dependent decrease in Ki67, MCM2, Bcl-2, CDK2, CyclinE1, CDK4, and CyclinD1 and a dose-dependent increase in Bax in RCC cells cultured with umbelliferone. Similarly, umbelliferone exhibited a dose-dependent reduction of p110γ when using western blotting analyses. Taken together, these results provide an insight into the pharmacology regarding the potential application of umbelliferone, which contributes to cell death by decreasing p110γ protein expression

Norcantharidin induces G2/M arrest and apoptosis via activation of ERK and JNK, but not p38 signaling in human renal cell carcinoma ACHN cells

Renal cell carcinoma (RCC) is generally acknowledged as the most resistant primary malignancy unresponsive to conventional radiotherapy and chemotherapy treatments. Norcantharidin (NCTD), a therapeutic compound derived from medicinal plants, has been shown to trigger apoptosis, as well as antimetastatic and antioxidant activities in several tumor cells. However, NCTD’s mechanism of antitumor activity in the RCC cell line remains unclear. In this study, we report that NCTD led to a time- and dose-dependent inhibition of cell proliferation. It had also markedly induced apoptosis and G2/M phase cell cycle arrest in a dose-dependent manner by decreasing the expressions of pro-caspase-3, pro-caspase-9, cyclin B1, and pCDC25C while increasing active caspase-3, cleaved-PARP, P21, and pCDC2 levels. Interestingly, NCTD treatment provoked the phosphorylation of extracellular-regulated protein kinase (ERK) and c-Jun-N-terminal kinase (JNK), but not of p38 MAPK. Moreover, SCH772984 and SP600125, ERK and JNK inhibitors, respectively, could partially abolish NCTD-induced apoptosis and G2/M phase cell cycle arrest. Collectively, these findings suggest that NCTD might activate JNK and ERK signaling pathways, consequently inducing apoptosis and G2/M arrest through the modulation of related proteins. This study provided evidence that NCTD is a promising therapeutic drug for the treatment of RCC

The transcription factor CREB is involved in sorafenib-inhibited renal cancer cell proliferation, migration and invasion

Our previous reports showed that the cyclic-AMP-response element-binding protein (CREB) served as a proto-oncogene in the process of tumorigenesis and mediated the growth and metastatic activity of renal cancer cells. Our study, therefore, explored the role of CREB in sorafenib-inhibited cell proliferation, migration and invasion. Renal cancer cells were cultured in medium containing sorafenib for 12, 24, 48 and 72 h. The MTT assay was used to study the cytotoxic effects of sorafenib. Cell invasion and migration were assayed in wound healing and transwell experiments, respectively. Protein expression levels were evaluated by western blotting. The results show that sorafenib treatment decreased cell viability in a dose- and time-dependent manner. Sorafenib inhibited cell migration and invasion and decreased the expression of MMP-2 and MMP-9. Moreover, addition of the recombinant plasmid pCI-neo/CREB (PN) reversed the sorafenib-induced inhibition of cell proliferation, migration and invasion. These results show that CREB is associated with the sorafenib-induced inhibition of proliferation, migration and invasion

Bis[2-(2-pyridylmethyl­eneamino)benzene­sulfonato-κ3 N,N′,O]cadmium(II) dihydrate

The title complex, [Cd(Paba)2]·2H2O or [Cd(C12H9N2O3S)2]·2H2O, was synthesized by the reaction of the potassium salt of 2-(2-pyridylmethyl­eneamino)benzene­sulfonic acid (PabaK) with CdCl2·2.5H2O in methanol. The CdII atom lies on a crystallographic twofold axis and is coordinated by four N atoms and two O atoms from two deprotonated tridentate 2-(2-pyridylmethyl­eneamino)benzene­sulfonate ligands in a slightly distorted octa­hedral environment. There are extensive hydrogen bonds of the type O—H⋯O between the uncoordinated water molecules and the sulfonate O atoms, through which the complex forms a layered structure parallel to (001)

Bis[2-(2-pyridylmethyl­eneamino)benzene­sulfonato-κ3 N,N′,O]cobalt(II) dihydrate

The title complex, [Co(C12H9N2O3S)2]·2H2O, has site symmetry 2 with the CoII cation located on a twofold rotation axis. Two tridentate 2-(2-pyridylmethyl­eneamino)benzene­sulfonate (paba) ligands chelate to the CoII cation in a distorted octa­hedral geometry. The pyridine and benzene rings in the paba ligand are oriented at a dihedral angle of 42.86 (13)°. Inter­molecular O—H⋯O and C—H⋯O hydrogen bonding is present in the crystal structure