Three-dimensional distinct element modeling of fault reactivation and induced seismicity due to hydraulic fracturing injection and backflow

This paper presents a three-dimensional fully hydro-mechanical coupled distinct element study on fault reactivation and induced seismicity due to hydraulic fracturing injection and subsequent backflow process,based on the geological data in Horn River Basin,Northeast British Columbia,Canada.The modeling results indicate that the maximum magnitude of seismic events appears at the fracturing stage.The increment of fluid volume in the fault determines the cumulative moment and maximum fault slippage,both of which are essentially proportional to the fluid volume.After backflow starts,the fluid near the joint intersection keeps flowing into the critically stressed fault,rather than backflows to the wellbore.Although fault slippage is affected by the changes of both pore pressure and ambient rock stress,their contributions are different at fracturing and backflow stages.At fracturing stage,pore pressure change shows a dominant effect on induced fault slippage.While at backflow stage,because the fault plane is under a critical stress state,any minor disturbance would trigger a fault slippage.The energy analysis indicates that aseismic deformation takes up a majority of the total deformation energy during hydraulic fracturing.A common regularity is found in both fracturing-and backflow-induced seismicity that the cumulative moment and maximum fault slippage are nearly proportional to the injected fluid volume.This study shows some novel insights into interpreting fracturing-and backflowinduced seismicity,and provides useful information for controlling and mitigating seismic hazards due to hydraulic fracturing.

Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension

Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS),hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.

DI-3-n-butylphthalide exerts neuroprotective effects by modulating hypoxia-inducible factor 1-alpha ubiquitination to attenuate oxidative stress-induced apoptosis

DI-3-n-butylphthalide is used to treat mild and moderate acute ischemic stroke.However,the precise underlying mechanism requires further investigation.In this study,we investigated the molecular mechanism of DI-3-n-butylphthalide action by various means.We used hydrogen peroxide to induce injury to PC12cells and RAW264.7 cells to mimic neuronal oxidative stress injury in stroke in vitro and examined the effects of DI-3-n-butylphthalide.We found that DI-3-nbutylphthalide pretreatment markedly inhibited the reduction in viability and reactive oxygen species production in PC12 cells caused by hydrogen peroxide and inhibited cell apoptosis.Furthermore,DI-3-n-butylphthalide pretreatment inhibited the expression of the pro-apoptotic genes Bax and Bnip3.DI-3-nbutylphthalide also promoted ubiquitination and degradation of hypoxia inducible factor 1α,the key transcription factor that regulates Bax and Bnip3 genes.These findings suggest that DI-3-n-butylphthalide exhibits a neuroprotective effect on stroke by promoting hypoxia inducible factor-1α ubiquitination and degradation and inhibiting cell apoptosis.

A synthetical geoengineering approach to evaluate the largest hydraulic fracturing-induced earthquake in the East Shale Basin, Alberta

On 2019-03-04,the largest induced earthquake(ML4.18)occurred in the East Shale Basin,Alberta,and the underlying physical mechanisms have not been fully understood.This paper proposes a synthetical geoengineering methodology to comprehensively characterize this earthquake caused by hydraulic fracturing.Based on 3D structural,petrophysical,and geomechanical models,an unconventional fracture model is constructed by considering the stress shadow between adjacent hydraulic fractures and the interactions between hydraulic and natural fractures.Coupled poroelastic simulations are conducted to reveal the triggering mechanisms of induced seismicity.It is found that four vertical basement-rooted faults were identified via focal mechanisms analysis.The brittleness index(BI)along two horizontal wells has a high magnitude(BI>0.5),indicating the potential susceptibility of rock brittleness.Due to the presence of overpressure,pre-existing faults in the Duvernay Formation are highly susceptible to fault reactivation.The occurrence of the earthquake clusters has been attributed to the fracturing fluid injection during the west 38^(th)-39^(th) stage and east 38^(th) stage completions.Rock brittleness,formation overpressure,and large fracturing job size account for the nucleation of earthquake clusters,and unconventional natural-hydraulic fracture networks provide fluid flow pathways to cause fault reactivation.This workflow can be used to mitigate potential seismic risks in unconventional reservoirs in other fields.

Dissecting the molecular pathophysiology of drug-induced liver injury

Drug-induced liver injury(DILI) has become a major topic in the field of Hepatology and Gastroenterology. DILI can be clinically divided into three phenotypes: hepatocytic, cholestatic and mixed. Although the clinical manifestations of DILI are variable and the pathogenesis complicated, recent insights using improved preclinical models, have allowed a better understanding of the mechanisms that trigger liver damage. In this review, we will discuss the pathophysiological mechanisms underlying DILI. The toxicity of the drug eventually induces hepatocellular damage through multiple molecular pathways, including direct hepatic toxicity and innate and adaptive immune responses. Drugs or their metabolites, such as the common analgesic, acetaminophen, can cause direct hepatic toxicity through accumulation of reactive oxygen species and mitochondrial dysfunction. The innate and adaptive immune responses play also a very important role in the occurrence of idiosyncratic DILI. Furthermore, we examine common forms of hepatocyte death and their association with the activation of specific signaling pathways.

Production of reactive oxygen species and expression of inducible nitric oxide synthase in rat isolated Kupffer cells stimulated by Leptospira interrogans and Borrelia burgdorfen

AIM： To evaluate the production of reactive oxygen species （ROS） and the expression of inducible nitric oxide synthase （iNOS） in rat isolated Kupffer cells （KCs） stimulated by Leptospira interrogans and Borrelia burgdorferi. METHODS： Rat Kupffer cells were separated by perfusion of the liver with 0.05% collagenase, and purified by Percoll gradients. Pudfied Kupffer cells were tested in vitro with alive L.interogans and B. burgdorferi preparations. The production of ROS was determined by chemiluminescence, whereas iNOS protein expression was evaluated by Western blot assay using anti-iNOS antibodies. RESULTS： B. burgdorferi and to a less extent L. interrogans induced ROS production with a peak 35 min after infection. The chemiluminescence signal progressively diminished and was undetectable by 180 min of incubation. Leptospirae and borreliae induced an increased iNOS expression in Kupffer cells that peaked at 6 hours and was still evident 22 h after infection. CONCLUSION： Both genera of spirochetes induced ROS and iNOS production in rat Kupffer cells. Since the cause of liver damage both in leptospiral as well as in borrelial infections are still unknown, we suggest that leptospira and borrelia damage of the liver can be initially mediated by oxygen radicals, and is then maintained at least in part by nitric oxide.

Sirtuin1 attenuates acute liver failure by reducing reactive oxygen species via hypoxia inducible factor 1α

BACKGROUND The occurrence and development of acute liver failure(ALF)is closely related to a series of inflammatory reactions,such as the production of reactive oxygen species(ROS).Hypoxia inducible factor 1α(HIF-1α)is a key factor that regulates oxygen homeostasis and redox,and the stability of HIF-1αis related to the ROS level regulated by Sirtuin(Sirt)family.The activation of Sirt1 will lead to a powerful antioxidant defense system and therapeutic effects in liver disease.However,little is known about the relationship between HIF-1αand Sirt1 in the process of ALF and the molecular mechanism.AIM To investigate whether HIF-1αmay be a target of Sirt1 deacetylation and what the effects on ALF are.METHODS Mice were administrated lipopolysaccharide(LPS)/D-gal and exposed to hypoxic conditions as animal model,and resveratrol was used as an activator of Sirt1.The cellular model was established with L02 cells stimulated by LPS.N-acetyl-Lcysteine was used to remove ROS,and the expression of Sirt1 was inhibited by nicotinamide.Western blotting was used to detect Sirt1 and HIF-1αactivity and related protein expression.The possible signaling pathways involved were analyzed by immunofluorescent staining,co-immunoprecipitation,dihydroethidium staining,and Western blotting.RESULTS Compared with mice stimulated with LPS alone,the expression of Sirt1 decreased,the level of HIF-1αacetylation increased in hypoxic mice,and the levels of carbonic anhydrase 9 and Bcl-2-adenovirus E1B interacting protein 3 increased significantly,which was regulated by HIF-1α,indicating an increase of HIF-1αactivity.Under hypoxia,the down-regulation of Sirt1 activated and acetylated HIF-1αin L02 cells.The inhibition of Sirt1 significantly aggravated this effect and the massive production of ROS.The regulation of ROS was partly through peroxisome proliferatoractivated receptor alpha or AMP-activated protein kinase.Resveratrol,a Sirt1 activator,effectively relieved ALF aggravated by hypoxia,the production of ROS,and cell apoptosis.It also induced the deacetylation of HIF-1αand inhibited the activity of HIF-1α.CONCLUSION Sirt1 may have a protective effect on ALF by inducing HIF-1α deacetylation to reduce ROS.

Change of hs-CRP,sVCAM-1,NT-proBNP levels in patients with pregnancy-induced hypertension after therapy with magnesium sulfate and nifudipine

Objective:To investigate the change of the hs-CRP,sVC AM-1,NT-proBNP levels of the patients with pregnancy-induced hypertension(PIH) syndrome.Methods:A total of 200 patients with PIH were divided into mild,moderate and severe group,and 50 healthy pregnancy patients served as the control group.The serum sVCAM-1 levels were detected by enzyme-linked immunosorbent assay,hs-CRP were detected by immunity transmission turbidity,and NT-proBNP levels were determined by the colloidal gold method.Patients were treated with magnesium sulfate and nifudipine and the contrastive analysis was performed before and after treatment.And the pathological changes in placental of PIH patients were delected by hematoxylin-eosin staining at the same time.Results:The hs-CRP,sVCAM-l,NT-proBNP levels of patients in the mild, moderate and severe PHI group were significantly higher than that in the control group(P<0.05). The hs-CKP,sVCAM-l,NT-proBNP levels in the severe group were significantly higher than the mild group and the moderate group,the difference was statistically significant(P<0.05).The hsCRP,sVCAM-l,NT-proBNP of the moderate group were significantly higher than the mild group(P<0.05).There was a positive correlation between hs-CRP,sVCAM-1,NT-proBNP expression levels and the degree of the PIH.The expression of hs-CRP,sVCAM-1,NT-proBNP levels of the moderate and the severe group were significantly decreased(P<0.05).The number of placental villi and interstitial blood vessel in the moderate and severe PIH group were significantly less than the control group(P<0.05).Conclusions:The increased levels of serum hs-CRP,sVCAM-1, NT-proBNP may be involved in the process of vascular endothelial cell injury of the PIH,and the hs-CRP,sVCAM-1,NT-proBNP can be used as the auxiliary index for diagnosis of PIH and determination of PIH severity.

Reservoir-induced landslides and risk control in Three Gorges Project on Yangtze River,China

The Three Gorges region in China was basically a geohazard-prone area prior to construction of the Three Gorges Reservoir （TGR）. After construction of the TGR, the water level was raised from 70 m to 175 m above sea level （ASL）, and annual reservoir regulation has caused a 30-m water level difference after impoundment of the TGR since September 2008. This paper first presents the spatiotemporal distribution of landslides in six periods of 175 m ASL trial impoundments from 2008 to 2014. The results show that the number of landslides sharply decreased from 273 at the initial stage to less than ten at the second stage of impoundment. Based on this, the reservoir-induced landslides in the TGR region can be roughly classified into five failure patterns, i.e. accumulation landslide, dip-slope landslide, reversed bedding landslide, rockfall, and karst breccia landslide. The accumulation landslides and dip-slope landslides account for more than 90%. Taking the Shuping accumulation landslide （a sliding mass volume of 20.7 × 106 m^3） in Zigui County and the Outang dip-slope landslide （a sliding mass volume of about 90 × 106 m^3） in Fengjie County as two typical cases, the mechanisms of reactivation of the two landslides are analyzed. The monitoring data and factor of safety （FOS） calculation show that the accumulation landslide is dominated by water level variation in the reservoir as most part of the mass body is under 175 m ASL, and the dip-slope landslide is controlled by the coupling effect of reservoir water level variation and precipitation as an extensive recharge area of rainfall from the rear and the front mass is below 175 m ASL. The characteristics of landslide-induced impulsive wave hazards after and before reservoir impoundment are studied, and the probability of occurrence of a landslide-induced impulsive wave hazard has increased in the reservoir region. Simulation results of the Ganjingzi landslide in Wushan County indicate the strong relationship between landslide-induced surge and water variation with high potential risk to shipping and residential areas. Regarding reservoir regulation in TGR when using a single index, i.e. 1-d water level variation, water resources are not well utilized, and there is also potential risk of disasters since 2008. In addition, various indices such as 1-d, 5-d, and 10-d water level variations are proposed for reservoir regulation. Finally, taking reservoir-induced landslides in June 2015 for example, the feasibility of the optimizing indices of water level variations is verified.

Pigment epithelium-derived factor protects retinal ganglion cells from hypoxia-induced apoptosis by preventing mitochondrial dysfunction

AIM： To investigate the potential of pigment epitheliumderived factor（PEDF） to protect the immortalized rat retinal ganglion cells-5（RGC-5） exposed to Co Cl2-induced chemical hypoxia. METHODS： After being differentiated with staurosporine（SS）, RGC-5 cells were cultured in four conditions： control group cells cultured in Dulbecco ＇s modified eagle medium（DMEM） supplemented with 10% fetal bovine serum, 100 μmol/m L streptomycin and penicillin（named as normal conditions）; hypoxia group cells cultured in DMEM containing 300 μmol/m L Co Cl2; cells in the group protected by PEDF were first pretreated with 100 ng/m L PEDF for 2h and then cultured in the same condition as hypoxia group cells; and PEDF group cells that were cultured in the presence of 100 ng/m L PEDF under normal conditions. The cell viability was assessed by MTT assay, the percentage of apoptotic cells was quantified using Annexin V-FITC apoptosis kit, and intra-cellar reactive oxygen species（ROS） was measured by dichloro-dihydro-fluorescein diacetate（DCFH-DA） probe. The mitochondria-mediated apoptosis was also examined to further study the underlying mechanism of the protective effect of PEDF. The opening of mitochondrial permeability transition pores（m PTPs） and membrane potential（Δψm） were tested as cellular adenosine triphosphate（ATP） level and glutathione（GSH）. Also, the expression and distribution of Cyt C and apoptosis inducing factor（AIF） were observed.RESULTS： SS induced differentiation of RGC-5 cells resulting in elongation of their neurites and establishing contacts between outgrowths. Exposure to 300 μmol/m L Co Cl2 triggered death of 30% of the total cells in cultures within 24 h. At the same time, pretreatment with 100 ng/m L PEDF significantly suppressed the cell death induced by hypoxia（P〈0.05）. The apoptosis induced by treatment of Co Cl2 was that induced cell death accompanied with increasing intracellar ROS and decreasing GSH and ATP level. PEDF pretreatment suppressed these effects（P〈0.05）. Additionally, PEDF treatment inhibited the opening of m PTPs and suppressed decreasing of Δψm in RGC-5 cells, resulting in blocking of the mitochondrial apoptotic pathway.CONCLUSION： Pretreatment of RGC-5 cells with 100 ng/m L PEDF significantly decreases the extent of apoptosis. PEDF inhibits the opening of m PTPs and suppresses decreasing of Δψm. Moreover, PEDF also reduces ROS production and inhibits cellular ATP level＇s reduction. Cyt C and AIF activation in PEDF-pretreated cultures are also reduced. These results demonstrate the potential for PEDF to protect RGCs against hypoxic damage in vitro by preventing mitochondrial dysfunction.

Factors Predicting the Relapse of Radiation-Induced Organizing Pneumonia after Breast-Conserving Therapy

We investigated the factors predicting radiation-induced organizing pneumonia (RIOP) relapse after tangential breast irradiation. The participants included 23 patients diagnosed with RIOP at the St. Marianna University School of Medicine Hospital between January 2008 and March 2015. Relapse was defined as the appearance of new lesions on diagnostic images during follow-up or after commencing treatment. The relapse-free survival rate and the following 9 parameters were compared between patients with and without RIOP relapse: 1) age (less than vs. equal to or more than the median);2) white blood cell count (less than vs. equal to or more than the median);3) C-reactive protein (CRP) level at the time of RIOP diagnosis (less than normal, more than normal/ less than borderline, and more than borderline);4) boost irradiation (yes vs. no);5) maximum lung depth on linacgraphy (less than vs. equal to or more than the median);6) hormone therapy (yes vs. no);7) chemotherapy (yes vs. no);8) RIOP ratio in the whole lung (less than vs. equal to or more than the median) at the time of RIOP diagnosis;and 9) use of corticosteroids (yes vs. no). The Kaplan-Meier method was used for statistical analysis, with relapse as the cutoff. The follow-up period spanned the date of RIOP onset to May 30, 2015. The level of significance for 2-sided tests was p < 0.05. Relapse was evident in 14 patients (60.8%). The relapse-free survival rate was significantly greater in the normal CRP group (less than 0.30 mg/dl) than in the abnormal CRP group (more than 0.36 mg/dl) (p = 0.044) and in the normal/borderline CRP group (less than 0.36 mg/dl) than in the high CRP group (more than 0.70 mg/dl) (p < 0.01). The CRP level at RIOP onset may be a useful predictor of relapse after breast-conserving therapy.We investigated the factors predicting radiation-induced organizing pneumonia (RIOP) relapse after tangential breast irradiation. The participants included 23 patients diagnosed with RIOP at the St. Marianna University School of Medicine Hospital between January 2008 and March 2015. Relapse was defined as the appearance of new lesions on diagnostic images during follow-up or after commencing treatment. The relapse-free survival rate and the following 9 parameters were compared between patients with and without RIOP relapse: 1) age (less than vs. equal to or more than the median);2) white blood cell count (less than vs. equal to or more than the median);3) C-reactive protein (CRP) level at the time of RIOP diagnosis (less than normal, more than normal/ less than borderline, and more than borderline);4) boost irradiation (yes vs. no);5) maximum lung depth on linacgraphy (less than vs. equal to or more than the median);6) hormone therapy (yes vs. no);7) chemotherapy (yes vs. no);8) RIOP ratio in the whole lung (less than vs. equal to or more than the median) at the time of RIOP diagnosis;and 9) use of corticosteroids (yes vs. no). The Kaplan-Meier method was used for statistical analysis, with relapse as the cutoff. The follow-up period spanned the date of RIOP onset to May 30, 2015. The level of significance for 2-sided tests was p < 0.05. Relapse was evident in 14 patients (60.8%). The relapse-free survival rate was significantly greater in the normal CRP group (less than 0.30 mg/dl) than in the abnormal CRP group (more than 0.36 mg/dl) (p = 0.044) and in the normal/borderline CRP group (less than 0.36 mg/dl) than in the high CRP group (more than 0.70 mg/dl) (p < 0.01). The CRP level at RIOP onset may be a useful predictor of relapse after breast-conserving therapy.

Efficient stabilization of dredged sludge with high water content using an improved bio-carbonation of reactive magnesia cement method

This study proposed an improved bio-carbonation of reactive magnesia cement(RMC)method for dredged sludge stabilization using the urea pre-hydrolysis strategy.Based on unconfined compression strength(UCS),pickling-drainage,and scanning electron microscopy(SEM)tests,the effects of prehydrolysis duration(T),urease activity(UA)and curing age(CA)on the mechanical properties and microstructural characteristics of bio-carbonized samples were systematically investigated and analyzed.The results demonstrated that the proposed method could significantly enhance urea hydrolysis and RMC bio-carbonation to achieve efficient stabilization of dredged sludge with 80%high water content.A significant strength increment of up to about 1063.36 kPa was obtained for the bio-carbonized samples after just 7 d of curing,which was 2.64 times higher than that of the 28-day cured ordinary Portland cement-reinforced samples.Both elevated T and UA could notably increase urea utilization ratio and carbonate ion yield,but the resulting surge in supersaturation also affected the precipitation patterns of hydrated magnesia carbonates(HMCs),which weakened the cementation effect of HMCs on soil particles and further inhibited strength enhancement of bio-carbonized samples.The optimum formula was determined to be the case of T?24 h and UA?10 U/mL for dredged sludge stabilization.A 7-day CA was enough for bio-carbonized samples to obtain stable strength,albeit slightly affected by UA.The benefits of high efficiency and water stability presented the potential of this method in achieving dredged sludge stabilization and resource utilization.This investigation provides informative ideas and valuable insights on implementing advanced bio-geotechnical techniques to achieve efficient stabilization of soft soil,such as dredged sludge.

Prednisolone inhibits SaOS2 osteosarcoma cell proliferation by activating inducible nitric oxide synthase

AIM:To investigate the effect of prednisolone,a synthetic glucocorticoid used in inflammatory diseases,on the growth of cultured osteosarcoma cells.METHODS:Two osteosarcoma cell lines with different degree of differentiation were used.SaOS2 show a rather mature phenotype,while U2 OS are negative for almost all osteoblastic markers.The cells were exposed to different concentrations of prednisolone(1-9 μmol/L) with or without antioxidants or the inhibitor of inducible nitric oxide synthase(i NOS) l-N6-(iminoethyl)-lysine-HCl(L-NIL).Cell growth was assessed by counting viable cells.The production of nitric oxide(NO) was measured in the conditioned media by the Griess method.The production of reactive oxygen species was quantified using 2'-7'-dichlorofluorescein diacetate.Western blot with specific antibodies against NOSs was performed on cell extracts.RESULTS:Prednisolone inhibited SaOS2 cell growth in a dose dependent manner.No significant effects were observed in U2OS.The inhibition of SaOS2 growth is not due to oxidative stress,because antioxidants do not rescue cell proliferation.Since high concentrations of NO inhibit bone formation,we also measured NO and found it induced in SaOS2,but not in U2 OS,exposed to prednisolone,because of the upregulation of i NOS as detected by western blot.Therefore,we treated SaOS2 with prednisolone in the presence or in the absence of L-NIL.L-NIL prevented NO release induced by prednisolone at all the concentrations apart from 9 μmol/L.At the same concentrations,we found that L-NIL rescued SaOS2 growth after exposure to prednisolone.In U2 OS cells,prednisolone did not induce NO production nor affected cell growth.All together,these data indicate that a link exists between increased amounts of NO and growth inhibition in response to prednisolone in SaOS2.CONCLUSION:Prednisolone inhibited SaOS2 proliferation by increasing the release of NO through the upregulation of i NOS,while no effect was exerted on U2OS.

高空电磁脉冲晚期成分作用下500 kV变压器无功损耗仿真研究

高空电磁脉冲晚期成分(HEMP E3)效应会在变压器中性点与大地构成的回路中产生地磁感应电流(GIC),严重时会使变压器铁心半波饱和,进而导致励磁电流严重畸变、无功损耗急剧增加、局部过热和振动加剧等后果。为准确地分析电力变压器在HEMPE3作用下的无功损耗特性,该文搭建了HEMP E3对500 kV电力变压器作用的电磁暂态仿真模型,基于IEC 61000-2-9给出的标准HEMP E3波形,定量分析了感应电场幅值、上升时间、下降时间以及变压器带负载情况等对电力变压器的影响规律。分析结果表明,HEMP E3作用下500 kV变压器无功损耗与GIC呈正相关性,且无功损耗波形滞后于感应电场的变化;HEMP E3感应电场的下降时间对500 kV变压器无功损耗的影响远超上升时间;负载阻抗的阻值相同时,容性负载下的励磁电流和无功损耗幅值最大,感性负载下幅值最小。研究结果可为进一步评估HEMPE3对电力系统稳定性的影响提供重要依据。

Reactive Arthritis: From Clinical Features to Pathogenesis

Reactive arthritis (ReA) is a sterile synovitis which occurs after a gastrointestinal or urogenital infection. ReA belongs to Spondyloarthritis (SpA), a group of diseases that share several clinical and radiological features including familiar clustering, absence of rheumatoid factor and association with HLA-B27. Clinically, ReA is characterized by an asymmetric arthritis predominantly affecting the lower limbs, often associated with urethritis, conjunctivitis and other extraarticular symptoms. The ReA prevalence depends on the incidence of causative pathogens. The ReA diagnosis is based on clinical features and serological tests to evidence previous infection. Different treatment including antibiotics, disease modifying antirheumatic drugs (DMARs) and biologic agents has been recommended. Even though knowing that infections trigger the joint inflammation, the ReA pathogenesis remains to be poorly understood. Several animal models and in vitro studies have been used to elucidate the mechanisms involved in ReA development. In this sense, HLA-B27 transgenic rat or mice have been used to explain the role of this molecule in SpA aetiopathogenesis. Moreover, the infectious model of Yersinia-induced ReA in rodents has shed some lights on the relationship between host genetic susceptibility to infection and abnormal immune response in ReA development. Understanding the immune mediators triggering ReA will contribute to find a specific treatment for this arthritis. In this review, we focus on clinical features, epidemiology, treatment, and the different attempts to understand the pathogenesis of ReA.

Hypoxia regulates reactive oxygen species levels in SHG-44 glioma cells

In the present study, cultured human SHG-44 glioma cells were subjected to a hypoxic environment simulated using the CoOl2 method. Flow cytometry showed increased reactive oxygen species production in these cells. Real-time reverse transcription-PCR showed significantly increased hypoxia-inducible factor-la mRNA expression in cells exposed to the hypoxic condition. The antioxidant N-acetylcysteine significantly inhibited reactive oxygen species production and reduced hypoxia-inducible factor-la mRNA expression in normoxic and hypoxic groups, especially in the latter group. These findings indicate that hypoxia induces reactive oxygen species production and hypoxia-inducible factor-la mRNA expression in human SHG-44 glioma cells, and that the antioxidant N-acetylcysteine can inhibit these changes.

近红外低能量激光调节血小板活性氧水平对防止冷藏损伤的研究

目的探究近红外低能量激光(Low Level Laser,LLL)照射处理对冷藏血小板保存期间活性氧的调节作用,进而对减少被巨噬细胞和肝细胞识别吞噬的影响。方法将白膜来源的浓缩血小板分为室温保存组(RTP)、冷藏保存组(CSP)和LLL照射组(CSP-L)。LLL照射组为血小板冷藏12 h后,采用1 J、5 J、10 J不同辐照强度的LLL单次照射并继续冷藏保存。各组保存5 d后,流式细胞仪检测血小板ROS生成、活化指标表达、糖基蛋白及其残基的暴露情况并进行比较。佛波酯诱导的THP-1细胞和HepG2肝细胞用于检测对各组血小板的吞噬作用。结果保存5 d后,CSP组血小板胞内ROS(cyto-ROS)水平较RTP组显著升高(RTP vs.CSP,3960±259.6 vs.5846±757.4,P<0.01),而线粒体ROS(mito-ROS)水平则低于RTP组(RTP vs.CSP,595±47.1 vs.416±50.2,P<0.05)。经低强度LLL(1 J)照射后,CSP-L1组血小板较CSP组显著降低了cyto-ROS水平(5846±757.4 vs.3945±459.4,P<0.01),CD62P、PS表达和GPⅠb/ɑ糖蛋白残基的暴露程度均显著减少(P<0.05),且与RTP组均无显著性差异。THP-1和HepG2对CSP-L1组血小板的吞噬率也显著低于CSP组(P<0.05)。同时,LLL照射对冷藏血小板的计数、pH值和MPV均无明显影响。结论低强度LLL照射处理可显著降低冷藏血小板胞内ROS水平并维持线粒体ROS的低水平生成,并能有效的抑制血小板活化和GPⅠb/ɑ去唾液酸化,减轻冷藏损伤,进而减少冷藏血小板被巨噬细胞和肝细胞识别吞噬。

幽门螺杆菌感染与胃癌患者血清缺氧诱导因子-1α及活性氧水平的相关性

目的探讨幽门螺杆菌(Hp)感染与胃癌患者血清缺氧诱导因子-1α(HIF-1α)、活性氧水平的相关性。方法回顾性选取2019年9月至2023年9月大庆油田总医院胃炎及胃癌患者60例,依据疾病类型方法分为胃癌组、慢性萎缩性胃炎组、慢性非萎缩性胃炎3组,每组各20例。统计分析3组患者的血清HIF-1α、活性氧水平,并统计分析3组不同临床特征患者的血清HIF-1α、活性氧水平及其相关性。结果胃癌组患者的血清HIF-1α、活性氧水平分别为(248.04±41.36)、(3361.50±512.23)μmol/L,慢性萎缩性胃炎组患者的血清HIF-1α、活性氧水平分别为(231.25±36.21)、(3079.76±502.12)μmol/L,均高于慢性非萎缩性胃炎组[(180.45±30.41)、(2599.07±412.63)μmol/L],差异均有统计学意义(P<0.05)。不同年龄、性别患者的血清HIF-1α、活性氧水平比较,差异均无统计学意义(P>0.05);胃癌组、慢性萎缩性胃炎组Hp阳性患者的血清HIF-1α、活性氧水平均高于Hp阴性患者,差异均有统计学意义(P<0.05);慢性非萎缩性胃炎组中Hp阳性患者的血清HIF-1α、活性氧水平与Hp阴性患者比较,差异均无统计学意义(P>0.05)。胃癌组、慢性萎缩性胃炎组患者的血清HIF-1α与活性氧水平呈显著正相关(r=0.712,P<0.05)。结论胃癌患者Hp感染与血清HIF-1α、活性氧水平的相关性显著,Hp感染可能通过上调血清HIF-1α、活性氧水平促进胃癌的发生、发展,可为临床诊疗提供有效依据。

地磁感应电流作用下三相五柱变压器无功功率定量分析

无功功率作为电力系统运行重要指标,其波动影响电力设备的安全稳定运行以及整个系统的电压稳定。为分析三相五柱变压器在地磁感应电流作用下的无功功率分布,根据变压器的实际参数,通过串联电阻及电压补偿的办法,建立三相五柱变压器磁场-电路耦合有限元计算模型,对不同大小地磁感应电流下的变压器无功功率进行定量分析。通过计算三相五柱空载及额定负载下无功功率的分布以及单相自耦变压器无功功率,发现随着地磁感应电流的增大,三相五柱空载及负载无功功率特性曲线均大体呈线性增加,且单相自耦变压器相较于三相五柱变压器无功曲线对于地磁感应电流更为敏感。并结合不同芯柱结构变压器的磁路特点,分析了无功差异变化的原因。研究结果可为地磁感应电流作用下三相五柱变压器稳定运行提供参考依据。