Transient second-degree type 2 atrioventricular block after infliximab infusion in a patient with Crohn's disease and heterozygous familial hypercholesterolemia.

Current treatments for patients in the active phase of Crohn's disease (CD) include conventional treatments and biological treatments. Infliximab (IFX), a TNF-α antagonist, is recommended to induce remission in patients with moderate-to-severe CD who have not responded to conventional therapy. IFX terminates the inflammatory cascade by inhibiting the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and caspase signaling pathways and increases the apoptosis of activated T cells in inflamed tissues.

Transient second-degree type 2 atrioventricular block after infliximab infusion in a patient with Crohn’s disease and heterozygous familial hypercholesterolemia

Current treatments for patients in the active phase of Crohn's disease (CD) include conventional treatments and biological treatments. Infliximab (IFX), a TNF-α antagonist, is recommended to induce remission in patients with moderate-to-severe CD who have not responded to conventional therapy. IFX terminates the inflammatory cascade by inhibiting the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and caspase signaling pathways and increases the apoptosis of activated T cells in inflamed tissues. (AU)

ABCA12 Promotes Proliferation and Migration and Inhibits Apoptosis of Pancreatic Cancer Cells Through the AKT Signaling Pathway.

Background: As a malignant tumor, pancreatic cancer is difficult to detect in its early stage. Pancreatic cancer progresses rapidly and has a short survival time. Most cases have metastasized to distant organs before diagnosis. The mechanism of induction of pancreatic cancer is not fully understood. Methods: In this study, bioinformatics predicted ATP binding cassette subfamily A member 12 (ABCA12) expression in pancreatic tissues and performed survival analysis, risk assessment, and enrichment analysis. The expression of ABCA12 in 30 pairs of clinical samples was detected by immunohistochemistry and we analyzed its correlation with clinical information. Both reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect mRNA and protein expression in cell lines. Two different siRNAs and SW1990 cell line were used to construct pancreatic cancer cell models with ABCA12 knockdown. Cell viability was evaluated by cell counting kit-8 (CCK-8) and EdU proliferation assays. Wound healing assays and Transwell assays were used to measure the ability of cell migration and invasion. Flow cytometry was used to investigate the effect of ABCA12 on the proliferation cycle and apoptosis of pancreatic cancer. Western blot analysis detected changes in apoptosis, migration, and other pathway proteins in SW1990 cells after transfection. Results: ABCA12 is highly expressed in pancreatic cancer tissues and cells. After ABCA12 was knocked down, the proliferation, invasion, and migration of SW1990 cells were significantly reduced, and apoptosis was increased. The changes in pathway proteins suggested that ABCA12 may regulate the progression of pancreatic cancer through the AKT pathway. Conclusion: We found that ABCA12 is differentially expressed in pancreatic tissues and cells. ABCA12 can also affect the biological behavior of pancreatic cancer cells effectively, which may serve as a new target for pancreatic cancer diagnosis and treatment.