Serum visfatin levels may be related to visceral obesity in men, and the visfatin gene may account for variation of glucose and lipid parameters in Chinese subjects.
BackgroundPlatelets play a fundamental role in maintaining hemostasis and have been shown to participate in hematogenous dissemination of tumor cells. Abundant platelets were detected in the tumor microenvironment outside of the blood vessel, thus, platelet -tumor cell interaction outside of the bloodstream may play a role in regulating primary tumor growth and metastasis initiation. However, it is unclear that platelet depletion affects tumor vessel structure and dynamics.MethodsUsing thrombocytopenia induction in two different tumor-bearing mouse models, tumor tissues were performed by Westernblotting and immunohistochemical staining. Vascular permeability was evaluated by determination of intratumoral Evans blue and Miles vascular permeability assay. Furthermore, microdialysis was used to examining the intratumoral extracellular angiogenic growth factors (VEGF, TGF-β) by ELISA.ResultsPlatelet depletion showed no change in tumor growth and reduced lung metastasis. Platelet depletion led to reduced tumor hypoxia and Met receptor activation and was associated with a decreased release of MMP-2, 9, PAI-1, VEGF, and TGF-β. Tumor vessels in platelet-depleted mice showed impaired vessel density and maturation.ConclusionsOur findings demonstrate that platelets within the primary tumor microenvironment play a critical role in the induction of vascular permeability and initiation of tumor metastasis.
Oncogenic KRAS, an important target for antitumor therapy, contributes to pancreatic cancer tumorigenesis, progression and maintenance. However, intracellular compensation regulation can help cells to resist the targeted therapy. Gene knockdown method such as RNAi may help to understand this intracellular regulatory system and discover novel therapeutic approach. In this study, two stable transfected cell lines were constructed through lentivirus-mediated shRNA targeting KRAS of PANC-1 cells, to investigate cell response to the knockdown of KRAS. Human whole genome microarray was then used to compare the gene expression profile. As a result, ribosomal proteins L26 and L29 (RPL26 and RPL29) were dramatically upregulated by KRAS-shRNA specifically. To identify whether RPL26 or RPL29 was critical for PANC-1 cells, siRNAs against RPL26 and RPL29 were designed and transfected in vitro. The results showed that knockdown of RPL26 or RPL29 expression significantly suppressed cell proliferation, induced cell arrest at G0/G1 phase and enhanced cell apoptosis. Reactive oxygen species (ROS) assay indicated that silencing of RPL26 or RPL29 markedly decreased the intracellular ROS generation. Our findings imply that siRNA interference against RPL26 and RPL29 is of potential value for intervention of pancreatic cancer.
A hydro-mechanic model was put forward to study the fundamental nature of acupuncture meridians. The basic state of low hydraulic resistance was tested on humans and mini pigs using three methods. The first, a modified Guyton's method, proved that there was lower hydraulic resistance on meridians compared with nonmeridians. The second scanning method involved a single pressure transducer that can find the lowest resistance point in tissue, and the third method used two transducers and provided a more stable measurement. Using the latter method, low hydraulic resistance points were found very close to low impedance points along meridians. The transmission of artificial interstitial fluid pressure waves was measured to examine their connection to the low resistance points, with the result that a good connection between the points was confirmed. This means the points form channels along the meridians that we refer to as low hydraulic resistance channels. The channel was imaged through isotopic tracing and a migration of isotope (99m)Te could be found along the channel. The layer of the channel was detected by injecting Alcian blue and the track was found beneath the skin. All of the above experiments suggest the existence of a new type of channel in living tissues that has not yet been described in modern science, but coincides quite well with the Qi channel theory of traditional Chinese medicine.
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