[Inhibition of Combination of Icaritin and Doxorubicin on Human Osteosarcoma MG-63 Cells in vitro].

Objective: To explore the inhibition and molecular mechanism of icaritin (ICT) combined doxorubicin (DOX) on human osteosarcoma MG-63 cells in vitro.

Methods: The control group, ICT groups (10, 20, 40, 80, and 160 µmol/L), DOX groups (1, 2, 4, 8, and 16 µg/mL), and combination groups (20 µmol/ L ICT +1 µg/mL DOX, 20 µmol/L ICT +2 µg/mL DOX, 20 µmol/L ICT +4 µg/mL DOX, 40 µmol/L ICT +1 µg/mL DOX, 40 µmol/L ICT +2 µg/mL DOX, 40 µmol/L ICT +4 µg/mL DOX, 80 µmol/L ICT +1 µg/mL DOX, 80 µmol/L ICT +2 µg/mL DOX, 80 µmol/L ICT +4 µg/mL DOX) were set up. Human osteosarcoma MG-63 cells were respectively cultured and their effects on morphological changes were observed using inverted phase contrast microscope after 24-and 48-h intervention.

Nicotine-induced ICAM-1 and VCAM-1 expression in mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway.

Objective: To explore the link between cigarette smoking and thromboembolic events and to investigate cigarette smoking as a major risk factor in the etiology of atherosclerosis.

Study Design: We determined the effect of nicotine on the expression of adhesion molecules, intercellular adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1) in mouse cardiac vascular endothelial cells and the involvement of important known intermediaries, namely p38 mitogen-activated protein kinase (MAPK) signaling pathway.

Results: Our results indicate that nicotine can enhance the expression of ICAM-1 and VCAM-1 on mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway, resulting in increased expression of the cellular adhesion molecules ICAM-1 and VCAM-1.

Compound danshen dripping pill pretreatment to prevent contrast-induced nephropathy in patients with acute coronary syndrome undergoing percutaneous coronary intervention.

Background. Contrast-induced nephropathy (CIN) limits the outcome of percutaneous coronary intervention (PCI). Objective.

[Clinical characteristics and antimicrobial resistance of invasive pneumococcal disease in children].

Objective: Streptococcus pneumoniae (SP) is a major causative agent of community-acquired pneumonia. In children older than 2 months, SP is also the most common cause of invasive bacterial infections. Invasive pneumococcal diseases (IPD) have become a severe problem of public health worldwide.

A comparison in association and linkage genome-wide scans for alcoholism susceptibility genes using single-nucleotide polymorphisms.

We conducted genome-wide linkage scans using both microsatellite and single-nucleotide polymorphism (SNP) markers. Regions showing the strongest evidence of linkage to alcoholism susceptibility genes were identified. Haplotype analyses using a sliding-window approach for SNPs in these regions were performed.

Crosstalk between ERK1/2 and STAT3 in the modulation of cardiomyocyte hypertrophy induced by cardiotrophin-1.

Background: The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway and the extracellular signal-regulated kinases 1/2 (ERK1/2) pathway are the two major independent signal transduction pathways. However, it has recently been found that STAT3 may be negatively regulated by ERK1/2 in gp130-dependent signaling. Cardiotrophin-1 (CT-1), a potent novel hypertrophic cytokine, depends on gp130 to induce signaling and depends on STAT3 to exert hypertrophic effect.

Different contributions of STAT3, ERK1/2, and PI3-K signaling to cardiomyocyte hypertrophy by cardiotrophin-1.

Aim: To assess the contribution of signal transducer and activator of transcription 3 (JAK-STAT3) pathway, extracellular signal-regulated kinases1/2 (ERK1/2) pathway, and phosphatidylinositol 3-kinase (PI3-K) pathway to cardiomyocytes hypertrophy induced by cardiotrophin-1 (CT-1), a new member of interleukin-6 (IL-6) family of cytokines.

Methods: STAT3, ERK1/2, and PI3-K were assessed by Western blot analysis. Activity of ERK1/2 was also confirmed by in-gel kinase assay.