Serum metabolomics analysis of biomarkers and metabolic pathways in patients with colorectal cancer associated with spleen-deficiency and qi-stagnation syndrome or damp-heat syndrome: a prospective cohort study.

Objective: To profile the serum metabolites and metabolic pathways in colorectal cancer (CRC) patients associated with spleen-deficiency and qi-stagnation syndrome (SDQSS) or damp-heat syndrome (DHS).

Methods: From May 2020 to January 2021, CRC patients diagnosed with traditional Chinese medicine (TCM) syndromes of SDQSS or DHS were enrolled. The clinicopathological data of the SDQSS and DHS groups were compared.

Deficiency of neuropeptide Y attenuates neointima formation after vascular injury in mice.

Background: Restenosis after percutaneous coronary intervention (PCI) limits therapeutic revascularization. Neuropeptide Y (NPY), co-stored and co-released with the sympathetic nervous system, is involved in this process, but its exact role and underlying mechanisms remain to be fully understood. This study aimed to investigate the role of NPY in neointima formation after vascular injury.

Physical exercise inhibits atherosclerosis development by regulating the expression of neuropeptide Y in apolipoprotein E-deficient mice.

Aims: Population-based studies have shown that exercise has anti-atherosclerotic effects, but the mechanisms underlying this cardiac protection are poorly understood. The aim of this study was to investigate if the anti-atherosclerotic effects of exercise are associated with changes in neuropeptide Y (NPY) expression in apolipoprotein E-deficient (ApoE) mice.

Main Methods: Thirty-one male ApoE mice were randomly divided into regular exercise (5 days/week), occasional exercise (1-2 days/week), and sedentary groups.

Collagen biomaterial for the treatment of myocardial infarction: an update on cardiac tissue engineering and myocardial regeneration.

Myocardial infarction (MI) remains one of the leading cause of mortality over the world. However, current treatments are more palliative than curative, which only stall the progression of the disease, but not reverse the disease. While stem cells or bioactive molecules therapy is promising, the limited survival and engraftment of bioactive agent due to a hostile environment is a bottleneck for MI treatment.

Single nucleotide polymorphism in the SEPS1 gene may contribute to the risk of various human diseases: a meta-analysis.

Background: Recently the G-105A promoter polymorphism in SEPS1 has been shown to increase pro-inflammatory cytokine expression and, thus, to be correlated with various types of human cancers and diseases.

Aims: This study examined whether this functional polymorphism was related to the risks of several human diseases by performing a meta-analysis.

Subjects And Methods: This study identified all published studies in MEDLINE, Science Citation Index, the Cochrane Library, PubMed, Embase, Current Contents Index and three Chinese databases.

5-Aminoisoquinolinone reduces the expression of vascular endothelial growth factor-C via the nuclear factor-κB signaling pathway in CT26 cells.

Objective: VEGF-C has recently been identified as a key molecule which is involved in tumor lymphangiogenesis. The aim of this research was to investigate the role of PARP-1 inhibition in the regulation of VEGF-C expression in CT26 cells.

Methods: CT26 cells were treated with or without the PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ).

[Inhibition of hepatitis C virus gene expression by antisense nucleotide in vitro].

Objective: To study the mechanism of hepatitis C virus (HCV) gene regulation and the inhibitory effect of antisense RNA on HCV gene expression in vitro.

Methods: The hepatoblastoma cell line (HepG2) was co-transfected by recombinant plasmid of antisense RNA complementary to HCV 5' untranslated region (5'UTR)and HCV 5' UTR Directed luciferase (luc) gene expression recombinant plasmid. Meanwhile a reversed HCV 5'UTR recombinant plasmid which can not transcribe as antisense RNA in the cell and a recombinant plasmid in which the luc was regulated by simian virus 40 (sv40) 5'UTR were used as controls respectively.