Moreover, tumor-grade dependent groups were heterogeneous with regard to Ki67 expression. This study also provides information that will be useful in the future in order to study or Sipeimine target KLF8-activated gene-specific cellular functions in brain tumors. Abdominal obesity has been shown to be strongly related to systemic inflammatory state, including the development of vascular diseases and metabolic complications such as dyslipidemia, hypertension, and diabetes mellitus. Recent studies have provided ample evidence to support the importance of low-grade but sustained inflammation in this process. Usaramine adipose tissue produces a wide variety of pro-inflammatory cytokines and chemokines, including IL-6 and monocyte chemoattractant protein-1. These locally produced cytokines recruit immune cells such as monocytes/macrophages, lymphocytes, and dendritic cells toward adipose tissues, which aggravate systemic inflammation. Simultaneously, macrophages recruited to adipose tissues then produce pro-inflammatory cytokines or chemokines to further develop and sustain the inflammatory status. This inflammatory cascade in turn may advance atherosclerosis in the large artery. As previously reported, the phenotypic variety of macrophages is quite diverse, and dependent upon the properties of inflammation and activation in situ. Given the close connection between adipose tissue and inflammation, it is critical to assess the role of adipose inflammation in vascular dysfunctions such as atherosclerosis. However, it is not known whether a direct link between inflammation in adipose tissue and that in vasculature is present in the context of atherosclerosis. In the present study, we used a real-time imaging device to visualize vascular inflammation in mice and were able to document that inflammatory adipose tissue directly induces vascular inflammation, as manifested by leukocyte recruitment to the femoral artery. Our in vivo findings provide critically important evidence of a mechanistic link between obesity and atherosclerosis. Leukocyte adhesion is a multi-step complex cascade induced by various factors, including activation of adhesion molecules, production of oxidative stress, and secretion of inflammatory cytokines or chemokines from pro-inflammatory cells, and a crucial mechanism for vascular inflammation and following atherosclerosis.