Objective Experimental research demonstrated that oxidative damage leads to formation of cataract in rats and its machanism is the decline of activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-PX) and catalase(CAT) . Aaspirin can improve the antioxidative ability of lens. The purpose of this study was to observe the inhibition of aspirin on D-Galactose-induced cataractous lenses of rats. Methods Galactose cataract model was established in 40 cleaning Wistar rals by intraperitoneal injection of 20 mL/kg 80% D-Galactose for 10 days. The models were divided into model group (20 rats) and aspirin group(20 rats). 150 mg/kg of aspirin was administered immediately by gastrogavaging in aspirin group for 20 days. Other 20 normal Wistar rats were as control group. At day 3, 6, 10, 14, 20, the transparency of rat lenses was observed under the slit lamp microscopy. At day 5 after experiment, the ultrastructure of the lenses was examined and evaluated under the scanning electron microscopy. The activities of SOD, GSH-PX and CAT were detected by Coomassie Brilliant Blue color comparator, respectively. The use of experimental animal followed the Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results All lenses were transparent in the rats of control group. The degree of lens opacity was more mild in asprin group compared with model group. 25. 00%, 41. 67%, 58. 33%, 83. 33% of lenses in aspirin group showed swelling at day 6, 10, 14, 20, respectively, but 65% lenses were opacity in model group on day 3 and 100% lenses were nuclear cataracts in 6 days. The structure of lenses was normal in control group, but the process number, fiber thickness and fiber density of lens were significantly increased in model group compared with control group (P ＜0. 05), and only process number was increased in asprin group. The activities of SOD, GSH-PX and CAT in lens of model group were obviously lower than in normal control group(P＜0. 05), but those in asprin group were significantly increased in comparison with model group(P ＜0. 05). Conclusion Aspirin could protect lenses of rats against oxidative damage by elevating activities of SOD, GSH-PX and CAT in lens and inhibiting the generation and development of galactose-induced cataract at early stage of cataract.

Background and purpose:Traditional Chinese medicine with notable effect and little adverse reaction is increasingly concerned about the medical profession because of its great potential and advantage in treating pancreatic carcinoma. In this experiment, we studied the effects of oridonin on apoptosis and cytoskeletal protein F-actin in human pancreatic carcinoma SW1990 cells. Methods:SW1990 cells in culture medium were treated with different concentrations of oridonin. The inhibitory rate of the cells was measured by MTT assay. Morphology of cell apoptosis was observed by DAPI stain and cell apoptotic rate was detected by lfow cytometry (FCM). The morphological changes of F-actin were observed by laser confocal microscopy. Results:The growth of human pancreatic carcinoma SW1990 cells was signiifcantly inhibited by oridonin. Apoptosis morphological changes including condensation of chromatin and nuclear fragmentation were observed clearly by DAPI stain. The early apoptotic rate of SW1990 cells treated with 25, 50μmol/L oridonin was signiifcantly higher than that of the control group (3.78±0.46, 9.51±0.63 vs 0.73±0.06, P<0.05), and the late apoptotic rate and cell necrosis rate were also signiifcantly higher than that of the control group (14.40±1.78, 20.53±2.54 vs 4.16±0.31, P<0.05). F-actin was showed from polymerization to depolymerization after oridonin treatment. Conclusion:Oridonin can obviously inhibit the proliferation and induce apoptosis of SW1990 cells. The mechanisms may involve the depolymerization of F-actin after treatment with oridonin.

Objective To establish thyrotropin( TSH) and thyroid hormones reference ranges during the neonatal period for the healthy term newborns in Suqian. Methods Blood samples from a heel-prick were collected from 500 healthy newborns 72 hours after birth to determine the level of TSH. 200 healthy newborns were chosen to determine the levels of serum TSH and thyroid hormones on the 14th day of life, and then compared with the results from 120 healthy adults. Results The reference range of TSH at 72 hours after birth was 0. 46-6. 59 mIU/ L. The reference ranges of TT3 , TT4 , TSH, FT3 , FT4 on the 14th day of life were 1. 10-2. 62 nmol/ L, 81. 10-158. 28 nmol/ L, 0. 83-6. 39 mIU/ L, 3. 76-6. 66 pmol/ L, and 10. 67-22. 27 pmol/ L, respectively. There was no significant difference in the interval of TSH between newborns and adluts, whereas there were significant difference in the intervals of TT3 , TT4 , FT3 , and FT4 between the two groups. Conclusions The establishment of TSH and thyroid hormone reference ranges during the neonatal period for the healthy term newborns could improve our understanding of the thyroid function during the neonatal period for the healthy term newborns, and our data suggests lowing the initiatory screening cut-off point of congential hypothyroidism.

Esophageal squamous cell carcinoma(ESCC)is a major histological subtype of esopha-geal cancer with a poor prognosis.Although several serum metabolomic investigations have been reported,ESCC tumor-associated metabolic alterations and predictive biomarkers in sera have not been defined.Here,we enrolled 34 treatment-naive patients with ESCC and collected their pre-and post-esophagectomy sera together with the sera from 34 healthy volunteers for a metabo-lomic survey.Our comprehensive analysis identified ESCC tumor-associated metabolic alterations as represented by a panel of 12 serum metabolites.Notably,postoperative abrosia and parenteral nutrition substantially perturbed the serum metabolome.Furthermore,we performed an examina-tion using sera from carcinogen-induced mice at the dysplasia and ESCC stages and identified three ESCC tumor-associated metabolites conserved between mice and humans.Notably,among these metabolites,the level of pipecolic acid was observed to be progressively increased in mouse sera from dysplasia to cancerization,and it could be used to accurately discriminate between mice at the dysplasia stage and healthy control mice.Furthermore,this metabolite is essential for ESCC cells to restrain oxidative stress-induced DNA damage and cell proliferation arrest.Together,this study revealed a panel of 12 ESCC tumor-associated serum metabolites with potential for monitor-ing therapeutic efficacy and disease relapse,presented evidence for refining parenteral nutrition composition,and highlighted serum pipecolic acid as an attractive biomarker for predicting ESCC tumorigenesis.