Hemolytic anemia after percutaneous coronary intervention (PCI): A case report.

Background: In clinical practice, intravascular hemolysis is not common after interventional cardiovascular procedures. Although diagnostic and treatment techniques have developed, with the increasing importance placed on people's own health and the popularity of cardiovascular intervention, there have been occasional reports of hemolysis after different cardiovascular interventions, mainly including cardiac pacemaker implantation, atrial-fibrillation radiofrequency ablation, transcatheter aortic-valve implantation (TAVI), transcatheter mitral valve replacement (TMVR) and percutaneous repair of Gerbode defect and percutaneous coronary intervention (PCI) with Impella. However, so far, there have been no relevant reports on postoperative hemolysis after percutaneous coronary intervention (PCI).

Race between virus and inflammasomes: inhibition or escape, intervention and therapy.

The inflammasome is a multiprotein complex that further regulates cell pyroptosis and inflammation by activating caspase-1. The assembly and activation of inflammasome are associated with a variety of diseases. Accumulative studies have shown that inflammasome is a key modulator of the host's defense response to viral infection.

Pseudogene TDGF1P3 regulates the proliferation and metastasis of colorectal cancer cells via the miR-338-3p-PKM2 axis.

Research in the past decade has revealed significant roles of pseudogenes in colorectal cancer (CRC). Here, the role of teratocarcinoma-derived growth factor 1 pseudogene 3 (TDGF1P3) in regulating the proliferation and invasion of CRC cells was investigated; in addition, its downstream targets were analyzed, and the underlying mechanisms were elucidated. TDGF1P3 was determined to be upregulated in CRC cells and tissues.

Functions of regulators of G protein signaling 16 in immunity, inflammation, and other diseases.

Regulators of G protein signaling (RGS) act as guanosine triphosphatase activating proteins to accelerate guanosine triphosphate hydrolysis of the G protein α subunit, leading to the termination of the G protein-coupled receptor (GPCR) downstream signaling pathway. RGS16, which is expressed in a number of cells and tissues, belongs to one of the small B/R4 subfamilies of RGS proteins and consists of a conserved RGS structural domain with short, disordered amino- and carboxy-terminal extensions and an α-helix that classically binds and de-activates heterotrimeric G proteins. However, with the deepening of research, it has been revealed that RGS16 protein not only regulates the classical GPCR pathway, but also affects immune, inflammatory, tumor and metabolic processes through other signaling pathways including the mitogen-activated protein kinase, phosphoinositide 3-kinase/protein kinase B, Ras homolog family member A and stromal cell-derived factor 1/C-X-C motif chemokine receptor 4 pathways.

Effects of Clostridium butyricum Capsules Combined with Rosuvastatin on Intestinal Flora, Lipid Metabolism, Liver Function and Inflammation in NAFLD Patients.

The objective of this study was to investigate the effects of Clostridium butyricum capsules combined with rosuvastatin on the intestinal flora, lipid metabolism, liver function and inflammation in patients with nonalcoholic fatty liver disease (NAFLD). For this purpose, a total of 96 patients with NAFLD were selected as research subjects and randomly divided into a control group (n=48) and an observation group (n=48). The Control group was treated with rosuvastatin, based on which observation group received Clostridium butyricum capsule treatment.

CCL2-mediated monocytes regulate immune checkpoint blockade resistance in pancreatic cancer.

The immunosuppressive microenvironment of pancreatic ductal adenocarcinoma (PDAC) contributes to resistance to immune checkpoint blockade. C-C motif chemokine ligand 2 (CCL2) is believed to participate in pancreatic tumorigenesis, but its role in PDAC progression and resistance to immune checkpoint blockade remains unclear. We hypothesized that CCL2 contributes to the pancreatic immunosuppressive microenvironment.

Inactivation of Pancreatic Stellate Cells by Exendin-4 Inhibits the Migration and Invasion of Pancreatic Cancer Cells.

Background: Pancreatic stellate cells (PSCs) are precursor cells of cancer-associated fibroblasts that promote tumor proliferation, invasion, and metastasis. The glucagon-like peptide-1 receptor agonist exendin-4 has been reported to exhibit anticancer effects against several tumor cells; however, the function and mechanism underlying the effects of exendin-4 on pancreatic cancer cells remain unclear.

Methods: Gene expression levels were determined using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay.

Exosome-mediated transfer of miR-1290 promotes cell proliferation and invasion in gastric cancer via NKD1.

Currently, exosomes rich in RNAs and proteins are regarded as vital mediators of intercellular communication. Here, we aimed to explore the effects of exosomal miR-1290 in gastric cancer (GC) and understand its mechanism of action on GC progression. We first isolated exosomes from serum samples of GC patients and healthy people and characterized them by transmission electron microscopy.

Raloxifene inhibits bone loss and improves bone strength through an Opg-independent mechanism.

The osteoblast-derived paracrine factor osteoprotegerin (OPG) is considered to play a key role in inhibition of osteoclast formation and activity. Recently, raloxifene, a nonsteroidal benzothiophene, was found to exert anti-resorptive effects via modulating OPG expression in osteoblasts. To explore whether raloxifene regulates bone metabolism via an OPG-dependant pathway in vivo, we investigated the effects of raloxifene on bone loss in Opg-deficient mice.