Effects of Sodium-Glucose Cotransporter-2 (SGLT-2) Inhibitors on Health-Related Quality of Life and Exercise Capacity in Heart Failure Patients With a Preserved Ejection Fraction: A Scoping Review.

This scoping review examines the effects of sodium-glucose cotransporter-2 (SGLT-2) inhibitors on health-related quality of life (HRQoL) and exercise capacity in heart failure patients with preserved ejection fraction (HFpEF). Five randomized controlled trials were analyzed, revealing consistent improvements in HRQoL metrics, such as the Kansas City Cardiomyopathy Questionnaire (KCCQ) scores and exercise capacity, measured by the six-minute walk distance (6MWD). The findings suggest that SGLT-2 inhibitors significantly enhance physical functioning and overall well-being in HFpEF patients.

Corrigendum to "Hypoxia Impairs NK Cell Cytotoxicity through SHP-1-Mediated Attenuation of STAT3 and ERK Signaling Pathways".

[This corrects the article DOI: 10.1155/2020/4598476.].

Resistance of osteosarcoma cells to the proapoptotic effects of carfilzomib involves activation of mitogen activated protein kinase pathways.

New Findings: What is the central question of this study? Carfilzomib, a second-generation proteasome inhibitor approved for the treatment of multiple myeloma, shows efficacy against osteosarcoma. However, drug resistance remains a major challenge. What is the role of carfilzomib-induced changes in mitogen-activated protein kinase (MAPK) pathways in the sensitivity of osteosarcoma cells to the proapoptotic effects of the drug? What is the main finding and its importance? The dose-dependent antiapoptotic effects in osteosarcoma are associated with activation of MAPK signalling.

ER stress arm XBP1s plays a pivotal role in proteasome inhibition-induced bone formation.

Background: Bone destruction is a hallmark of multiple myeloma (MM). It has been reported that proteasome inhibitors (PIs) can reduce bone resorption and increase bone formation in MM patients, but the underlying mechanisms remain unclear.

Methods: Mesenchymal stem cells (MSCs) were treated with various doses of PIs, and the effects of bortezomib or carfilzomib on endoplasmic reticulum (ER) stress signaling pathways were analyzed by western blotting and real-time PCR.

Hypoxia Impairs NK Cell Cytotoxicity through SHP-1-Mediated Attenuation of STAT3 and ERK Signaling Pathways.

Natural killer (NK) cells are innate immune effectors with potent antitumor activity. However, tumor cells can create an immunosuppressive microenvironment to escape immune surveillance. Although accumulating evidence indicates that microenvironmental hypoxia plays an important role in favoring tumor development and immune evasion, it remains unclear by what means hypoxia directly impairs NK cell antitumor activity.

A novel CD2 staining-based flow cytometric assay for assessment of natural killer cell cytotoxicity.

Background: Assessing cytotoxicity is fundamental to studying natural killer (NK) cell function. Various radioactive and non-radioactive cytotoxicity assays measuring target cell death have been developed. Among these methods, the most commonly used Chromium-release assay (CRA) and flow cytometry-based cytotoxicity assays (FCCs) are the major representatives.

Cell cycle exit during bortezomib-induced osteogenic differentiation of mesenchymal stem cells was mediated by Xbp1s-upregulated p21 and p27.

Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiating into a variety of cell types. Bortezomib, the first approved proteasome inhibitor used for the treatment of multiple myeloma (MM), has been shown to induce osteoblast differentiation, making it beneficial for myeloma bone disease. In the present study, we aimed to investigate the effects and underlying mechanisms of bortezomib on the cell cycle during osteogenic differentiation.

Identification of a Five-CpG Signature with Diagnostic Value in Thyroid Cancer.

Thyroid cancer (TC) ranks as the most common endocrine malignancy, and its incidence and mortality rates continue to rise annually. Increasing evidence have shown that DNA methylation, a kind of stable epigenetic modification, is associated with carcinogenesis, suggesting its potential as biomarkers for the early detection of tumors. With the aim of exploring likely DNA methylation biomarkers for TC diagnosis, we conducted a synthetic analysis of DNA methylation profiles based on 789 samples from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases.

Tetrandrine induces apoptosis in human neuroblastoma through regulating the Hippo/YAP signaling pathway.

Tetrandrine (TET), a bis-benzylisoquinoline alkaloid, shows cytotoxicity against several different types of tumors. However, the mechanism by which TET exerts its anti-cancer capabilities remains unclear. In this study, we confirmed that TET inhibits proliferation and induces apoptosis in neuroblastoma (NB) in vitro and in vivo.

Hypoxia promotes osteosarcoma cell proliferation and migration through enhancing platelet-derived growth factor-BB/platelet-derived growth factor receptor-β axis.

Osteosarcoma is a primary malignant bone tumor, characterized by high therapeutic resistance and poor outcomes, due to unclear pathological mechanisms. It has been shown recently that the platelet-derived growth factor (PDGF)/platelet-derived growth factor receptor (PDGFR) pathway is closely associated with the pathogenesis of osteosarcoma. Hypoxia is a critical hallmark of tumor microenvironment that promotes the malignant phenotype in many solid tumors and a fundamental impediment to effective tumor therapy.