Microenvironment of liver regeneration in liver cancer / 中国结合医学杂志

The occurrence and development of liver cancer are essentially the most serious outcomes of uncontrolled liver regeneration. The progression of liver cancer is inevitably related to the abnormal microenvironment of liver regeneration. The deterioration observed in the microenvironment of liver regeneration is a necessary condition for the occurrence, development and metastasis of cancer. Therefore, the use of a technique to prevent and treat liver cancer via changes in the microenvironment of liver regeneration is a novel strategy. This strategy would be an effective way to delay, prevent or even reverse cancer occurrence, development and metastasis through an improvement in the liver regeneration microenvironment along with the integrated regulation of multiple components, targets, levels, channels and time sequences. In addition, the treatment of "tonifying Shen (Kidney) to regulate liver regeneration and repair by affecting stem cells and their microenvironment" can regulate "the dynamic imbalance between the normal liver regeneration and the abnormal liver regeneration"; this would improve the microenvironment of liver regeneration, which is also a mechanism by which liver cancer may be prevented or treated.

Microcirculation of liver cancer, microenvironment of liver regeneration, and the strategy of Chinese medicine / 中国结合医学杂志

Microcirculation of liver cancer is the micro-vascular system which comes from the tissue of liver cancer. It can offer the nutritional requirement for accelerating the cancer cell proliferation and metastasis. The intrinsic mechanism of angiogenesis is the key link in the formation of liver cancer microcirculation system. Liver regeneration microenvironment also plays an important role in the construction of liver cancer microcirculation, through the improvement of liver regeneration microenvironment affecting tumor microcirculation is the new strategy of prevention and treatment of liver cancer. In recent years, it is found that many kinds of Chinese medicine can inhibit angiogenesis, decrease the microvessel density, and delay or prevent the development of liver cancer.

Effect of static pressure on the expression of glial fibrillary acidic protein and heat shock protein 70 by the cultured retinal M?ller cells / 眼科

Objective To observe the effects of static pressure on the number of cultured retinal M?ller glial cells(RMGC)and expression of glial fibrillary acidic protein(GFAP)and heat shock protein(HSP)70 by these cells.Design Experimental study. Participants Cultured rat RMGC.Methods Rat RMGCs were cultured and identified according to previous method described by Reichenbach.These cells were treated with different static pressures and divided into 4 groups:A(1.33kPa),B(2.67kPa),C(5.33kPa)and D(10.67 kPa)while the cells without treatment was as control group(NC).The morphologies of RMGC in these groups were observed under inverted phased contrast microscope,the number of RMGC counted with conservative method and the viability were studied with trypan blue staining.The expressions of GFAP and HSP70 in RMGCs were detected with the method of western blot.Main Outcome Measures The morphologies of RMGC,cell number,cell viability.Results There were pressure-dependent changes of RMGC number. The cell number of group C and D was less than that of group NC,A and B(P＜0.01).High static pressure resulted directly in the decreased ratio of unstained RMGCs(P＜0.01).The ratio of unstained RMGCs in group C and D was less than that in group NC,A and B(P＜0.01).Many cells in group C and D were injured and the higher the pressure elevated,the more the degree of injury became.The expressions of GFAP and HSP70 in group NC were less than other pressure treated groups and the expression of GFAP in group C and D was higher than that in group A and B.There was no obvious difference between these pressure treated groups.Conclusions High static pressure could cause the injuries of RMGCs.The increased expression of GFAP and HSP70 in RMGC might be regarded as a sign of retinal injury response to high intraocular pressure.