Rheumatoid arthritis ( RA) is a chronic inflammatory disease involving progressive articular damage cause by inflam-matory cells and synoviocytes.Stat3 gene, which is confirmed to play a role in the pathogenesis of RA, regulates the metabolism and apoptosis of the fibroblast-like synoviocytes ( FLS) .SirT1 gene relating to the bone formation was indicated to play a role in the patho-genesis of RA in recent years.This review introduces the pathogenesis and targeted treatment of RA and makes a prediction about the relation between Stat3 and SirT1 gene.We hope it will provide a new direction for the research of RA.

Thyroid hormone is an important hormone for regulating cell differentiation,growth and metabolism.Many studies have shown that thyroid hormone can induce turmor angiogenesis after binding with the integrin ανβ3 receptor at cell surface.Tetraiodothyroacetic acid is the analogue of thyroid hormone,and can inhibit tumor angiogenesis by inhibiting the binding of thyroid hormone with integrin ανβ3.Studying the role of thyroid hormone in promoting tumor angiogenesis may provide a new approach for molecular targeted therapy of tumor.

Rheumatoid arthritis (RA) is a systemic autoimmune disease with unknown etiology.The main feature of RA is chronic,symmetrical and invasive arthritis.RA may present with severe joint deformity and functional loss,which has higher disability and fatality rates.At present,no effective measures can reverse bone damage associated with RA clinically.Therefore,early diagnosis of RA is critical to improve prognosis.In recent years,imaging increasingly plays an important role in the early diagnosis of RA.This article reviews recent advances in imaging methods for early diagnosis of RA.

AIM To investigate the effect of tamoxifen on the proliferation of the anterior pituitary cell of rats and its mechanism. METHODS Primary culture of the anterior pituitary cell of rats and 3H TdR incorporation method were applied. The changes of cell morphology were observed directly by electric microscope. RESULTS Tamoxifen could inhibit the proliferation of the anterior pituitary cell of rats. The inhibitory effect of tamoxifen (0 1 ?mol?L -1 ) could be reversed by estrogen.The classical apoptotic changes appeared in the cells after tamoxifen incubation for 48 h. CONCLUSION Tamoxifen can inhibit the proliferation of the anterior pituitary cell of rats and resultin the cell apoptosis.

As the human population ages and the life expectancy increases,tendon injuries will become more prevalent,especially among young individuals.Though the traditional operative therapy for tendon lesion can relieve the suffering of patients,the functional reconstruction is usually not optimistic.Tissue engineering is an advancing field,as the technology of construction in vitro and application in vivo matures,that can provide a more promising approach for tendon repair without tendon autograft.Challenges and future directions in the field of tendon tissue engineering focusing on four key parameters:seed cells,novel scaffolds,and mechanical stimulation.Recently,the discovery of TDSCs (tendon-derived stem cells) provides new ideas for the selection of seed cells and effect of mechanical stimulation on the tendon tissue engineering has become a hot spot.This article provides a review of recent progress in research about seed cells,scaffolds and mechanical stimulation for tendon engineering,and also speculates on the development in the future.

ObjectiveTo identify the differences between acetylcholine(Ach)-induced increase and adenosine triphosphate(ATP)-induced increase in cytosolic free Ca2+ concentration ([Ca2+]c) in mouse pancreatic β-cells. MethodsMouse pancreatic β-cells were primarily cultured and divided into two groups,one group was stimulated by Ach and another by ATP.[Ca2+]c was recorded with Fura-2 in normal condition, chelation of extracellular Ca2+ by EGTA and depletion of intracellular Ca2+ stores by Thapsigargin.ResultsAch induced a transient peak increase and sustained increase in [Ca2+]c. ATP induced a transient peak increase and no sustained increase. Chelation of extracellular Ca2+ by EGTA eliminated the sustained increase induced by Ach, and did not eliminate the transient peak increase induced by Ach and ATP. Depletion of intracellular Ca2+ stores by Thapsigargin eliminated the transient peak increase induced by Ach and ATP and the sustained increase induced by Ach. ConclusionsAch induces intracellular Ca2+ release and the following Ca2+ release-activated Ca2+ influx, and ATP induces intracellular Ca2+ release, but blocks the following Ca2+ release-activated Ca2+ influx.

ObjectiveTo identify the influence of cholesterol on insulin-secreting cells.Methods MIN6 mouse insulin cells were cultured in vitro. After confluence of cells, on one hand, free cholesterol in series concentrations was added to cultu re medium to act for 24 hours, and on the other hand, free cholesterol in same c oncentration was added to culture medium to act for different periods. MTT test was used to evaluate the viability of MIN6 cells.Results25μmol/L free cholesterol significantly decreased the viability of MIN6 c ells after 24 hours and 100μmol/L free cholesterol significantly decreased the viability of MIN6 cells after 12 hours and induced cells death after 24 hours.Conclusions Free cholesterol decreases viability of MIN6 cells in a dose-dependent and time-dependent manner, and it is indicated that elevated free cholesterol concentration in blood may be one factor involved in the dysfunction of pancreatic β-cells.

BACKGROUND:Semaphorin7A (Sema7A) is a kind of cel surface protein, which can promote the fusion of osteoclasts and the migration of osteoblasts at the same time, affecting the dynamic balance of the bone. It is speculated that Sema7A siRNA may inhibit osteoblast apoptosis induced by titanium particles. OBJECTIVE:To study the effect of Sema7A on the preosteoblast activity inhibited by titanium particles. METHODS:Mouse MC3T3-E1 preosteoblasts at passages 6 and 7 were divided into four groups: in blank control group, MC3T3-E1 cels were cultured alone; in standard control group, cel were cultured with titanium particles; in experimental groups 1 and 2, the cels were cultured with titanium particles+Sema7A overexpression plasmids and titanium particles+Sema7A siRNA, respectively. Apoptotic rate of MC3T3-E1 cels was detected by flow cytometry; the mRNA expression of bone sialoprotein, osteocalcin and type I colagen was detected by Q-PCR; western blot assay was adopted to detect the protein expression of bone sialoprotein, osteocalcin and type I colagen; alizarin red calcium nodule staining was taken to detect the degree of osteoblast mineralization. RESULTS AND CONCLUSION:The expressions of bone sialoprotein, osteocalcin and type I colagen were decreased in the standard control group and experimental group 1, but these expression were significantly increased in the experimental group 2 compared with the standard control group (P < 0.05). Flow cytometry results suggested that the apoptotic rate of osteoblasts in the experimental group 1 was significantly higher than that in the other groups (P < 0.05), and the apoptotic rate in the experimental group 2 was lower than that in the standard control group (P < 0.05). Alizarin red staining showed that there were no obvious mineralized nodules in the experimental group 1, but mineralized nodules formed in the experimental group 2. In brief, the genetic interference technique that inhibits the activity of Sema7A can interfere the process of mouse MC3T3-E1 preosteoblast differentiation inhibited by titanium particles, and thus provide a feasible way for the clinical treatment of wear particles-induced osteolysis using biotechnology.

BACKGROUND:Sema7A is a kind of cel surface protein, which can promote the fusion of osteoclasts and the migration of osteoblast at the same time, affecting the dynamic balance of bone. OBJECTIVE:To investigate whether Sema7A siRNA has ainhibitory effect on the osteoclast activation in the process of osteolysis which induced by titanium particles. METHODS:The precursor osteoclasts with the concentration of 4×109 RESULTS AND CONCLUSION:At 7 days of culture, the expression levels of interleukin-1, interleukin-1β, tumor necrosis factor α, matrix metaloproteinase-9 and the receptor activator of nuclear factor-κB in the positive control, /L were seeded on 96-wel plates containing glass cover slips, and divided into four groups: blank control, positive control, experiment and negative control groups. The cel culture medium was added into the control group. 20 μL un-transfected siRNA supernatant was added into the positive control group. 20 μL transfected Sema7A siRNA supernatant was added into the experiment group. 20 μL transfected control siRNA supernatant was added into the negative control group. The supernatant was obtained through the co-culture between titanium particles solution and monocyte-macrophage cel line RAW264.7of mouse for 24 hours. siRNA was transfected into mononuclear macrophage cel lines RAW264.7 of mice. negative control and experiment groups were higher than those in the control group (P < 0.05). The expression level of each factor in the experiment group was lower than that in the positive control and negative control groups (P < 0.05). At 8 days of culture, the proliferation activity of osteoclasts and the number of positive cels stained by tartrate-resistant acid phosphatase in the positive control, negative control and experiment groups were higher than those in the control group (P < 0.05). The proliferation activity of osteoclasts and the number of positive cels stained by tartrate-resistant acid phosphatase in the experiment group were lower than those in the control and negative groups (P < 0.05). These results demonstrate that Sema7A siRNA has a certain inhibitory effect on the osteoclast activation induced by titanium particles.

BACKGROUND:Present studies mainly focused on in vitro culture of bone marrow mesenchymal stem cells(BMSCs)and cell transplantation for treating intracalvarium diseases.However,the understanding of survival,differentiation,migration and structure of transplanted cells in the damaged spinal cord is limited.OBJECTIVE:To explore effects of local BMSC transplantation in repair of spinal cord damage and feasibility of replacement therapy of BMSCs.METHODS:Adult healthy female Sprague-Dawley rats were randomly assigned to cell transplantation and control groups.Rat models of spinal cord transection damage were established.Rat BMSC suspension or calcium and magnesium phosphate buffer were transplanted immediately after injury to the damage zone.At 1 day,1,2,3,4 and 8 weeks before and after transplantation,BBB score motor function was observed in rats,and at 1 week after transplantation,immunohistochemical staining was utilized to observe BrdU-labeled BMSC survival in the spinal cord damaged site.At 4 weeks after transplantation,the general observation and histological detection were observed.RESULTS AND CONCLUSION:At 1-8 weeks after transplantation,BBB scores were higher in the cell transplantation group than in the control group.At 1 week following surgery,immunohistochemical staining showed that BrdU-positive cells were detected in the distal end of rat spinal cord in the cell transplantation group.At 4 weeks following surgery,nerve fibers were found in the damaged spinal cord.These verified that BMSCs were transplanted into rat damaged spinal cord immediately following damage,and the transplanted cells could survive.Living BMSCs can differentiate into neurons,and formed neuron pathway in the local region of damage,which will promote the recovery of conduction function of spinal nerve fibers,and contribute to the recovery of rat hindlimb motor function following high-level spinal cord injury.