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Objective:To study the effects of trioxygen pretreatment on cerebral ischemia/reperfusion (I/R) injury in rats.Methods:A total of 24 clean grade male Sprague-Dawley (SD) rats were randomly divided into Sham group, brain I/R group (I/R group) and Ozone pretreatment group (Ozone group), with 8 rats in each group. The animals were routinely fed, and the operation was performed 5 days after the intervention of Ozone group by intraperitoneal injection of trioxygen water (concentration 80 mg/L, 0.01 mL/g), and the Sham group and I/R group were injected with equal volume normal saline. The Sham group only separated the arteries without ligation, and the I/R group and Ozone group established the rat cerebral I/R model. Neurological deficit score (NDS) was performed 2 hours after ischemia and modified neurological deficit score (mNSS) was performed 24 hours after reperfusion. Brain tissue was collected after anesthesia. Cerebral infarction was observed by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining and the percentage of cerebral infarction volume was calculated. Protein expression of metabolic glutamate receptor 5 (mGluR5) and ionic glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) subunit GluA2 in cerebral ischemic penumbra was determined by Western blotting.Results:Compared with the Sham group, NDS score, mNSS score and percentage of cerebral infarction volume in I/R group were increased [NDS score: 2.63±0.52 vs. 0, mNSS score: 9.63±1.19 vs. 1.13±0.64, cerebral infarction volume: (41.25±2.93)% vs. 0%, all P < 0.05], and expressions of mGluR5 and GluA2 in penumbra area of cerebral ischemia were decreased [mGluR5 protein (mGluR5/β-actin): 0.44±0.14 vs. 1.00±0.10, GluA2 protein (GluA2/β-actin): 0.23±0.08 vs. 1.00±0.25, both P < 0.05]. Compared with the I/R group, mNSS score and percentage of cerebral infarction volume in the Ozone group were decreased [mNSS score: 7.00±1.20 vs. 9.63±1.19, cerebral infarction volume: (27.23±6.21)% vs. (41.25±2.93)%, both P < 0.05], and mGluR5 and GluA2 expressions in the penumbra of cerebral ischemia were up-regulated [mGluR5 protein (mGluR5/β-actin): 0.81±0.10 vs. 0.44±0.14, GluA2 protein (GluA2/β-actin): 0.76±0.13 vs. 0.23±0.08, both P < 0.05]. Conclusion:Trioxygen preconditioning can alleviate cerebral I/R injury in rats, and its mechanism may be related to the upregulation of GluR5 and GluA2 in the ischemic penumbra.
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Preeclampsia is a unique complication in the second and third trimesters of pregnancy, but its pathogenesis remains unclear and the early diagnosis and treatment methods are yet to be perfect. Termination of pregnancy at the right time is the only way to prevent its deterioration and avoid adverse pregnancy outcomes. In recent years, with the in-depth research, non-coding RNAs has been found to be involved in many important physiological and pathological processes such as proliferation and apoptosis of trophoblast cells and these non-coding RNAs can regulate each other to form an intricate and competitive endogenous RNA regulatory network. This article will introduce the biological roles of non-coding RNAs in regulating the invasion and proliferation of trophoblast cells in patients with preeclampsia and possible regulatory relationship between non-coding RNAs. Furthermore, the potential clinical value of non-coding RNAs as diagnostic biomarkers for preeclampsia and therapeutic targets are also elaborated.
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Objective To execute quality control of OLYMPUS-PK7300 automated blood grouping analyzer to enhance the quality and efficiency in blood grouping.Methods Measures were proposed from the aspects of specimen quality,reagent quality,instrument maintenance,test parameters setup,internal quality control and external quality assessment,personnel and etc.Results Quality control was carried out at each link of the test by automated blood grouping analyzer to facilitate blood-related clinical operation.Conclusion Whole-course quality control of the analyzer has to be performed to improve blood grouping.
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Objective To investigate the effects of interleukin-34 (IL-34) on prostaglandin E2 (PGE2)/cyclo-oxygenase-2 (COX-2) expression on fibroblast-like synoviocytes (FLS) in patients with rheumatoid arthritis (RA). Methods FLS was isolated from 6 RA patients and stimulated with IL-34 (50 ng/ml), IL-34 receptor antagonist (25 ng/ml) and IL-34 (50 ng/ml), inhibitors of signaling pathway (10 μmol/L) and IL-34 (50 ng/ml) in vitro respectively. The expression of COX-2 mRNA was detected by reverse transcription polymerase chain reac-tion (RT-PCR). The level of PGE2 in the supernatant of RA FLS culture was measured by Enzyme linked immunosorbent assay (ELISA). Statistical analysis between groups were performed by t test. Results Com-pared to unstimulated FLS, COX-2 and PGE2 expression was increased dramatically on IL-34-stimulated FLS, most evidently in 48 hours [(139±24) pg/ml vs (201±8) pg/ml, t=-6.177, P<0.01]; Moreover, the level of PGE2 was decreased when anti-IL-34 antibody was added to the IL-34-stimulated RA FLS at 24 hours, 48 hours, 72 hours [(250 ±58) pg/ml vs (100 ±28) pg/ml, t=5.742, P<0.01; (375 ±24) pg/ml vs (97 ±23) pg/ml, t=20.564, P<0.001; (357 ±21) pg/ml vs (94 ±18) pg/ml, t=22.353, P<0.01]; In the presence of SB203580 and IKK-16, PGE2 level produced by IL-34-stimulated FLS was obviously decreased [(279 ±37) pg/ml vs (63 ±17) pg/ml, t=12.806, P<0.01;(279±37) pg/ml vs (77±16) pg/ml, t=6.177, P<0.01]. Conclusion Binding of IL-34 with its receptor may promote the secretion of PGE2 via NF-κB and P38 MAPK signaling pathway in RA FLS, suggesting that it might be involved in the pathogenesis of RA.
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Objective To preliminarily investigate the levels of interleukin (IL)-1 family and IL-34 in serum of patients with ankylosing spondylitis (AS) and their roles.Methods Serum IL-1 family levels were detected from 6 AS patients and 4 healthy controls by using protein-chip technique.Enzyme-linked immunosorbent assay (ELISA) method was used to detect the levels of serum IL-34 from 65 AS patients and 85 healthy controls and the relationships of serum IL-34 levels and clinical or laboratory features were analyzed.T test and Spearman correlation were used for statistical analysis.Results IL-1Ra [(3302±1352) pg/ml vs (10778±2764) pg/ml]and IL-36Ra [(1363±194) pg/ml vs (3875±996) pg/ml] levels were significantly down-regulated in AS patients compared with that of healthy controls (t=5.363 and 4.289 respectively,both P＜0.05).The levels of IL-1α,IL-18,IL-36α and IL-37 were increased more remarkable in AS patients than in healthy controls (t=-2.532,-5.400,-5.023 and-5.783 respectively,both P＜0.05).Moreover,serum IL-34 levels were elevated more significantly in AS patients than in healthy controls [(169±153) pg/ml vs (54±31) pg/ml,t=6.722,P＜0.01] and were positively correlated with the levels of CRP and ESR.Serum IL-34 levels were markedly up-regulated in human leukocyte antigen (HLA)-B27 positive patients than in HLA-B27 negative patients(P＜0.05).Conclusion Part of IL-1 family and IL-34 may be involved in inflammatory or immunological process of AS.