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Objective:To explore the influence of ulinastatin combined with thymosinα1 on the immune function of patients with a-cute brain injury. Methods:Sixty-eight cases of patients with acute brain injury were divided into the control group and the observation group randomly with thirty-four ones in each. The control group was given the routine treatment, and the observation group was given ulinastatin combined with thymosinα1 additionally. After the 1-day, 3-day, 7-day and 14-day treatment, transforming growth factor-β1 (TGF-β1), interleukin-6(IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α) and the other serum inflammatory cyto-kine levels, and CD4 +, CD8 +, CD4 + /CD8 +, HLA-DR and cellular immune index levels were detected in the two groups. The prog-nosis effects were evaluated by the prognostic classification of brain injury, and the adverse reactions were analyzed in the two groups as well. Results:After the 1-day treatment, there were no significant differences in the serum inflammatory cytokines and immune param-eters between the groups (P>0. 05). After the 3-day, 7-day and 14-day treatment, serum TGF-β1, IL-6, IL-10 and TNF- α levels were higher than those on the first day after the treatment, and TGF-β1 showed an increasing trend with time extension, while IL-6, IL-10, TNF-α and CD4 + and CD4 + /CD8 +rose first and then decreased. After the 3-day, 7-day and 14-day treatment, serum IL-10 and CD4 +levels in the observation group were significantly higher than those in the control group, and IL-6 and TNF-αlevels were signifi-cantly lower than those in the control group (P<0. 05). After the 3-day and 14-day treatment, CD4 + and CD8 + levels in the observa-tion were significantly higher than those in the control group, and after the 7-day and 14-day treatment, HLA-DR levels were signifi-cantly higher than those in the control group (P<0. 05). The prognosis effect of the observation group was better than that of the con-trol group with statistically significant difference (P<0. 05). Conclusion:Ulinastatin combined with thymosin α1 is used to treat the patients with acute brain injury with better cellular immune function improvement and prognosis effect, which is worthy of clinical popu-larization and application.
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Cerebral ischemia represents one of the leading causes of death and disability in modern time, but only few options exist for the treatment of ischemia-related disease. Neural cell replacement can reconstruct the nerve conduction circuit unit and lead to functional recovery partly in patients. The mechanism lies in: the stem cells transplanted into the lesion can differentiate into functional glial cells or neurons, and they can substitute the functions of dead neurons; to activate the endogenous neural stem cells; to excrete cytokines and improve the local environments, such as inflammatory reactions, tissue necrosis and glial scar formation. Transplantation of bone marrow mesenchymal stem cells, umbilical cord blood, embryonic stem cells and adipose mesenchymal cells have been used for stem cells transplantation in treatment of cerebral ischemia in animal models. So far, the underlying mechanisms of the cell replacement therapy for stroke lesions have remained unknown, and this therapy faces predominantly two major problems: one is how cell grafts survive in an ischemic environment; the other is how cell grafts substitute or rescue neural cells with many different phenotypes.
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Pubmed Database was undertaken to identify relevant articles of brain tumor stem cells published from January 2000 to January 2008. Books on stem cells and brain tumor stem cells were retrieved. The data were selected primarily, 39 articles related to brain tumor stem cells were selected. Of the 39 inclusive articles, 8 were on review of the brain tumor stem cells theory, 31 were about the research and experiment of brain tumor stem cells. Data synthesis shows that the CD133+ cells isolated from brain tumor have the stem cell-like properties of endless cell proliferation, uncontrolled self-renewal and multi-directional differentiation, but brain tumor stem cells have more vigorous capacity to increase than normal neural stem cells. The brain tumor stem cells express the same gene product as the normal neural stem cells, but the nuclear type of the brain tumor stem cells is abnormal. Brain tumor stem cells maybe the products of gene mutation from the normal neural stem cells. Brain tumor stem cells are the bad seeds of brain cancer, and play a key role in the progress of tumorigenesis, growth, invasion, metastasis, drug resistance and recurrence. Thus, studies on brain cancer stem cells have crucial effects on analyzing the mechanism of occurrence and development, as well as radical cure of brain tumor.