Using Campylobacter ieiuni, strain of CJ-S131 to infect KM mice. Three months after infection, we examined the function of T and B cells in infected mice. We found that(l) there were higher, level antibodies against ds-DNA, ss-DNA.(2) ConAinduced suppressor cell activity was decreased and the ratio of Th/Ts was increased (3) The formation of PFC and lymphocyte transformation induced by LPS.PHA and ConA were increased. (4) The DTH reaction also was increased. The results mentioned above indicated that chronic infection of CJ-S131 would induce autoimmunity in KM mice.The ineffitiency of Ts cell function could be related to the hyperactivity of Th and B cells.

S-phase kinase associated protein (Skp2) assumes the high expression in the most of malignant tumors, with its occurrence, and the development and the prognosis is closely related with a latent diagnose and treat went value. This review will focus on unique feature, biology activity, the function mechanism and with malignant tumor relations of the Skp2.

Autoimmune disease is a condition arisen from an abnormal immune response to the tissue cells itself, its precise mechanism remains unknown, and the failure to distinguish self from non-self is often termed a breach of tolerance and is the basis for autoimmune illness. The tumor necrosis factor-α (TNF-α) induced protein 8 like-2 (TIPE2) is a newly discovered member of TNF-α induced protein 8 (TNFAIP8) family which is an essential negative controller of both innate and adaptive immunity. It has been documented that marked expressions of TIPE2 are evident in various autoimmune diseases, including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), myasthenia gravis (MG) and systemic lupus erythematosus (SLE), which appear to be closely related to the severity, progression as well as prognosis of the illness, thereby contribute to the pathogenesis of autoimmune diseases. Deficient expression of TIPE2 might contribute to the hyper-reactivity of auto-reactive lymphocytes and macrophages, or aggregate inflammatory reaction by prompting high concentration of pro-inflammatory cytokines in peripheral blood, thus, trigger the development and progression of autoimmune diseases. In addition, dysregulation of immune homeostasis could be another latent target involved into the mechanism of autoimmune diseases. The present paper summarized the potential role and its mechanism of TIPE2 in the development of autoimmune diseases.

Objective: To analyze the cause of prosthesis loosening by observing the interface membranes harvested during the hip restoration operation. Methods: A total of 28 specimens of interface membrane around the loose prosthesis were harvested from 28 patients undergoing the restoration of total hip replacement. All the specimens underwent the observation of appearance, light microscopy and scanning electronic microscopy(SEM). Results: All the gaps around the loose prosthesis were filled with interface membrane of different thickness. The color of the most interface membrane was madder red, and the other one third of membrane was black. The comparatively thicker membrane was similar to scar connective tissue while the thinner was similar to fiber membrane. A large number of wear debris, macrophages and foreign-body giant cells were found under light microscope. With SEM observation a large number of different diameter collagen fibra structures that looked like scar tissues were arranged disorderly in a great mass, foreign particles and bone debris of different size were distributed unevenly, and the fibroblast was distributed in the collagen fiber. Conclusion: Wear debris is related to inflammatory cell response around the interface membrane of the loose prosthesis. The wear debris engulfed by macrophage stimulates the interface membrane to release bone resorption factors (such as TNF) which lead to osteolysis, and this is one of the most important causes of the prosthesis loosening.

Objective: To analyze the cause of prosthesis loosening by observing the interface membranes harvested during the hip restoration operation. Methods: A total of 28 specimens of interface membrane around the loose prosthesis were harvested from 28 patients undergoing the restoration of total hip replacement. All the specimens underwent the observation of appearance, light microscopy and scanning electronic microscopy(SEM). Results: All the gaps around the loose prosthesis were filled with interface membrane of different thickness. The color of the most interface membrane was madder red, and the other one third of membrane was black. The comparatively thicker membrane was similar to scar connective tissue while the thinner was similar to fiber membrane. A large number of wear debris, macrophages and foreign-body giant cells were found under light microscope. With SEM observation a large number of different diameter collagen fibra structures that looked like scar tissues were arranged disorderly in a great mass, foreign particles and bone debris of different size were distributed unevenly, and the fibroblast was distributed in the collagen fiber. Conclusion: Wear debris is related to inflammatory cell response around the interface membrane of the loose prosthesis. The wear debris engulfed by macrophage stimulates the interface membrane to release bone resorption factors (such as TNF) which lead to osteolysis, and this is one of the most important causes of the prosthesis loosening.

Fracture healing has long been a major concern for orthopedists.Currently,about 10% of fracture patients still have poor fracture healing or bone nonunion.In recent years,research has found that nerve growth factor(NGF)can promote fracture healing.This article reviews the mechanism and research progress of NGF in promoting fracture healing.NGF can promote vascular regeneration and nerve growth at callus and plays an important role in the proliferation and migration of bone cells.New animal experiments and clinical trials have confirmed the role of NGF in promoting fracture healing and further revealed its possible mechanism of action.Further research on NGF can provide new ideas for promoting fracture healing,especially for treating nonunion.
Animals ; Fracture Healing ; Humans ; Nerve Growth Factor

Lung cancer is the main cause of cancer-related death worldwide. Non-small cell lung cancer (NSCLC) accounts for about 80% of lung cancer cases, but only 25%-30% of initially diagnosed patients have the option of radical surgery because of the lack of effective measures for early diagnosis. For locally advanced and advanced NSCLC, radiotherapy alone or comprehensive treatment with chemoradiotherapy is the main treatment method; however, the curative effect is unsatisfactory. Recently, increasing evidence sug-gests that targeted drugs, such as epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), combined with radiotherapy/chemoradiotherapy represent a promising treatment modality for NSCLC. This review will discuss the research status of EGFR-TKIs and radiotherapy for locally advanced and advanced NSCLC.

Objective:To set up a eukaryotic system for high expressing human CD137 and to investigate the role of CD137 and CD137L on signals transduction of cells.Methods:The pCDNA3 plasmid containing full length of human CD137 cDNA sequence(CMV ILA SEN,CIS) and pSV2 dhfr plasmid were cotransfected into dhfr CHO cells by lipoid mediating method. The positive clone was selected with G418. Expression of CD137 on dhfr CHO cells were induced by MTX and detected by RT PCR, immunocytochemistry and flow cytometry.It's activity study was done by method of incorporating 3H TdR.Results:CD137 expressed on the surface of dhfr CHO, expression rate was 96.07%, it's activity study indicated that CD137 increase the proliferation of PBMC stimulated by anti CD3 monoclonal antibody.Conclusion:dhfr CHO cells that highly express CD137 were established. CD137 can increase the proliferation of PBMC stimulated by anti CD3 monoclonal antibody.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; Male ; Middle Aged ; Young Adult