Role of mast cells in estrogen-mediated experimental endometriosis in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the role of mast cells in the pathogenesis of estrogen-mediated experimental endometriosis in rats.</p><p><b>METHODS</b>Endometriosis model was established by transplanting autologous fragments of uterus to the inner surface of the abdominal wall in 24 un-pregnant female Sprague Dawley rats. The rats were divided randomly into three groups (n=8 in each group), and were injected with different doses of estrogen: high-dose group (200 μg·kg⁻¹·d⁻¹), low-dose group (100 μg·kg⁻¹·d⁻¹) and the control group (0 μg·kg⁻¹·d⁻¹). The ovaries were surgically removed in high-dose and low-dose groups. Four rats were sacrificed in each group at 2 and 4 weeks after surgery. Their serum estradiol levels, size of lesions, total number of mast cells and degranulations, serum TNF-α levels, expression of tryptase and NGF in tissues were analyzed and compared among groups.</p><p><b>RESULTS</b>The mean levels of serum estradiol 2 weeks and 4 weeks after model established and serum TNF-α at 4 weeks in estrogen-treated groups were significantly higher than those in control group (all P<0.05). The mean size of endometriotic lesions in the estrogen-treated groups was also significantly larger than that in the control group 2 weeks and 4 weeks after model established (all P<0.05). Meanwhile, both at week 2 and week 4, the mean ratio of degranulation/total number of mast cells by toluidine blue staining in low-dose estrogen group was significantly higher than that in the control group (P<0.05). The expression of NGF in high-dose estrogen group was significantly higher than that in the control group at week 4(P<0.05).</p><p><b>CONCLUSION</b>Estrogen can promote the growth of endometriotic lesions and may mediate the pathogenesis of endometriosis by activating mast cells, which may be associated with increasing TNF-α and NGF levels.</p>

Sodium cromoglycate attenuates experimental endometriosis in rats by regulating mast cells / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of sodium cromoglycate on experimental endometriosis in rats.</p><p><b>METHODS</b>Endometriosis model was established in 36 unpregnant female SD rats by transplanting autologous fragments of endometrium to the inner surface of the abdominal wall. The endometriotic lesions were measured by a second laparotomy 2 weeks after surgery. Then the rats were randomly divided into four groups (n=8 in each group) to receive intraperitoneal injection of different doses of sodium cromoglycate for 2 weeks: high-dose group (20 mg·kg⁻¹·d⁻¹); low-dose group (10 mg·kg⁻¹·d⁻¹); the negative control group and the blank control group. The animals were sacrificed and the size of the lesions were measured. The endometriosis model of SD rats was identified by HE staining and immunohistochemical staining of keratin and vimentin. The total number of mast cells and their degranulation were measured by Toluidine blue staining; the concentrations of TNF-α in serum were measured by enzyme linked immunosorbent assay; the concentrations of estradiol in serum were measured by enzyme immunoassay; the expression of tryptase and nerve growth factor (NGF) were measured by immunohistochemical staining.</p><p><b>RESULTS</b>The number of activated mast cells (MC) by Toluidine blue staining in high-dose group was significantly lower than that in negative control group (P<0.05), and its ratio of degranulation/total number of MC was significantly lower than that in negative control group or blank control group (P<0.05). The serum TNF-α levels and tryptase expression in tissues in high-dose group were significantly lower than those in negative control group or blank control group (P<0.05). However, no significant difference in the size of endometriotic lesions and expression of NGF was found among groups (P>0.05).</p><p><b>CONCLUSION</b>Sodium cromoglycate can stabilize mast cells from degranulation, which may relieve the clinical symptoms of endometriosis by reducing TNF-α and tryptase levels.</p>

Liraglutide prevents high glucose level induced insulinoma cells apoptosis by targeting autophagy / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells. Recently more attention has been paid to the effect of autophagy in type 2 diabetes. The regulatory pathway of autophagy in controlling pancreatic beta cells is still not clear. The aim of our study was to evaluate whether liraglutide can inhibit apoptosis and modulate autophagy in vitro in insulinoma cells (INS-1 cells).</p><p><b>METHODS</b>INS-1 cells were incubated for 24 hours in the presence or absence of high levels of glucose, liraglutide (a long-acting human glucagon-like peptide-1 analogue), or 3-methyadenine (3-MA). Cell viability was measured using the Cell Counting Kit-8 (CCK8) viability assay. Autophagy of INS-1 cells was tested by monodansylcadaverine (MDC) staining, an autophagy fluorescent compound used for the labeling of autophagic vacuoles, and by Western blotting of microtubule-associated protein I light chain 3 (LC3), a biochemical markers of autophagic initiation.</p><p><b>RESULTS</b>The viability of INS-1 cells was reduced after treatment with high levels of glucose. The viability of INS-1 cells was reduced and apoptosis was increased when autophagy was inhibited. The viability of INS-1 cells was significantly increased by adding liraglutide to supplement high glucose level medium compared with the cells treated with high glucose levels alone.</p><p><b>CONCLUSIONS</b>Apoptosis and autophagy were increased in rat INS-1 cells when treated with high level of glucose, and the viability of INS-1 cells was significantly reduced by inhibiting autophagy. Liraglutide protected INS-1 cells from high glucose level-induced apoptosis that is accompanied by a significant increase of autophagy, suggesting that liraglutide plays a role in beta cell apoptosis by targeting autophagy. Thus, autophagy may be a new target for the prevention or treatment of diabetes.</p>

Failure of internal fixation on displaced femoral neck fractures in adults under fifty-five years old / 中国骨伤

<p><b>OBJECTIVE</b>To investigate the failure of internal fixation on displaced femoral neck fractures in adults under fifty-five years old retrospectively inorder to pay more attention to the treatment of these fractures.</p><p><b>METHODS</b>From Junary 2007 to June 2010,18 failed cases of internal fixation on displaced femoral neck fractures in adults under fifty-five years old were treated,there were 13 males and 5 females with an average age of (48.0 +/- 6.0) years old ranging from 27 to 55. Among them, 17 patients were treated with cannulated screws and 1 patient was treated with intramedullary nail; 16 patients were diagnosed as osteonecrosis and 2 patients as osteonecrosis associated with nonunion.</p><p><b>RESULTS</b>The average time from internal fixation to failure was 23 months (ranged, 8 to 32 months). The quality of fracture reduction in Garden index was poor. The Harris Hip Score was (56.0 +/- 12.5) (ranged,33 to 80). Eight cases of osteonecrosis and 2 cases of nonunion combinated osteonecrosis were received total hip arthroplasty. Hip resurfacing arthroplasty were performed for other 5 osteonecrosis. Because of no evident clinical symptoms,the other 3 cases received conservative treatment. The patients with total hip arthroplasty and hip resurfacing arthroplasty were followed-up for 34 months ranging from 12 to 53 months. After operation,the Harris score was (94.0 +/- 3.0) ranged 89 to 96.</p><p><b>CONCLUSION</b>Osteonecrosis is a common complication after internal fixation on displaced femoral neck fracture in adults under fifty-five years old. More attention should be paid to the treatment of displaced femoral neck fracture in those patients.</p>

Investigation of Microcystins Pollution in Two Drinking Water Sources in Ningbo City / 环境与健康杂志

Objective To know the microcystins pollution caused by cyanobactcria bloom in two drinking water sources in Ningbo city.Methods Water samples were collected at four sampling sites in Yaojiang River and three sampling sites in Miehu reservoir from 20 July,2007 to 31 August,2007.The algae in these water samples were classified and counted,and Microcystin-LR (MC-LR),MC-RR were determined by UPLC-MS-MS.Results The Cyanobacteria cell concentration in Yaojiang River and Meihu reservoir ranged from 0.8?10~6 to 6.7?10~7,and from 1.21?10~7 to 9.928?10~8 cells/L respectively.The MC-LR and MC-RR in Yaojiang River weren't detected,and neither was the MC-RR in MeiHu reservoir.However,the MC-LR was detected at sometimes,and the maximum concentration of MC-LR was 0.84?g/L.Conclusion There is no microcystins pollution in Yaojiang River,but there existed MC-LR pollution in MeiHu Reservoir,and the MC-LR concentration in it was below national standard limit of 1.0?g/L after the treatment of controlling alage and microsystins.