ABSTRACT
To evaluate the efficacy of changing grains on the prevention and treatment of Kashin-Beck Disease (KBD) in children, community-based trials were acquired from seven electronic databases (up to July 2014). As a result, the methodological quality of the six trials that have been included into our analysis was low. The pooled ORs favoring the prevention and treatment effects of changing grains were 0.15 (95% CI: 0.03-0.70) and 2.13 (95% CI: 1.44-3.16) respectively by meta-analysis. Subgroup analysis demonstrated the pooled OR favoring treatment effect of exchanging grains rather than drying grains both compared with endemic grains. The results showed that changing grains had obvious effects on the prevention and treatment of KBD in children. However, the evidences were limited by the potential biases and confounders. Large and well-designed trials are still needed.
Subject(s)
Adolescent , Child , Child, Preschool , Humans , Infant , Infant, Newborn , Community-Based Participatory Research , Edible Grain , Physiology , Kashin-Beck Disease , TherapeuticsABSTRACT
Objective To understand the effect of hyaluronic acid (HA) on the proliferation and apoptosis of chondrocytes cultured in vitro with Kashin-Beck disease(KBD) to provide the experimental evidences for treating KBD diseases with HA. Methods The articular cartilage samples collected from KBD patients were selected according to Diagnosis for Kaschin-Beck Disease(GB 16003-1995). And the normal cartilage samples were collected from victims of incidence (control). Chandrocytes were separated and cultured in vitro. Then varying dosages of HA were administered to chondrocytes and individed into 0,100,500 mg/L group, according to HA doages. The effect of HA on the proliferation and apoptosis of chondrocytes cultured/n vitro both KBD and the controls were investigated by methyl thiazolyl tetrazolium(MTT), Annexin V/PI staining on 2~(nd), 4~(th), 6~(th) day. Results In the control group, 500 mg/L group(0.140 ± 0.049) promoted chondrocyte proliferation significantly than 0 mg/L group (0.116 ± 0.021 ) at the 4~(th) day(P < 0.05), similar phenomenon was observed in KBD group in the 6~(th) day between 500 and 0 mg/L group(0.179 ± 0.081,0.128 ± 0.017, P< 0.05). In the KBD group, compared with 0 mg/L (12.860 ± 2.159), both 100 and 500 mg/L( 10.458 ± 1.143,7.877 ± 1.346) inhibited chondrocyte apoptosis rate (P < 0.05). In control, apoptosis rate of 500 mg/L group(4.045 ± 1.204) descreased compared with 0 mg/L group (7.128 ± 1.244, P < 0.05). Conclusion HA can promote the proliferation and inhibit the apoptosis of KBD chondrocytes cultured in vitro, and 500 mg/L HA play more effective role than that of 100 mg/L in promoting proliferation and inhibiting poptosis.
ABSTRACT
This study was purposed to investigate the serum levels of soluble intracellular adhesion molecule (sVCAM-1), interleukin 18 (IL-18) and vascular endothelial growth factor (VEGF) in patients with aplastic anemia (AA) and their clinical significance. Enzyme linked immunosorbent assay (ELISA) was used to detect sVCAM-1, IL-18 and VEGF in serums of 30 patients with AA and 25 normal controls. The results showed that the serum levels of sVCAM-1 and IL-18 in patients with AA [(839.08 +/- 173.97) ng/ml, (380.35 +/- 47.76) pg/ml] were significantly higher than those in normal controls [(538.16 +/- 91.21) ng/ml, (256.39 +/- 59.52) pg/ml] (p < 0.01; p < 0.01). The levels of sVCAM-1 and IL-18 in severe AA patients [(969.94 +/- 182.54) ng/ml, (388.96 +/- 46.06) pg/ml] were higher than those in chronic AA patients [(709.26 +/- 165.32) ng/ml, IL-18 (352.21 +/- 47.08) pg/ml] (p < 0.01; p < 0.05), but the level of VEGF in AA patients [(69.63 +/- 27.42) pg/ml] was lower than that in the normal controls [(125.62 +/- 32.15) pg/ml] (p < 0.01)]. The level of VEGF in severe AA patients [(51.30 +/- 29.86) pg/ml] was significantly lower than that in chronic AA patients [(80.02 +/- 25.14) pg/ml] (p < 0.01). The levels of sVCAM-1 and IL-18 in AA patients after treatment were lower than those before treatment (p < 0.01; p < 0.05), but the level of VEGF after treatment was significantly higher than that before treatment (p < 0.05). It is concluded that the high levels of sVCAM-1, IL-18 and low level of VEGF in serum may be involved in the pathogenesis and progress of AA.