Isoflurane preserves energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation

AIM: To investigate the protective effect of isoflurane on energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation, and to compare isoflurane with halothane. METHODS: Hepatocytes freshly isolated from fed rats were suspended in Krebs-Henseleit buffer, and incubated in sealed flasks under O2/CO2 or N2/CO2 (95%/5%, V/V) for 30 or 60 min, followed by 5 or 10 min of reoxygenation, with an added volatile anesthetic or not. ATP, ADP, and adenosine monophosphate in hepatocytes were determined by high performance liquid chromatography, and energy charge was calculated. RESULTS: During 30 min of anoxia, the energy charge and total adenine nudeotide steadily increased with the isoflurane dose from 0 to 2 minimum alveolar anesthetic concentration (MAC), then decreased from 2 to 3 MAC. In short incubations (30-35 min) at 1 MAC isoflurane, energy charge modestly decreased during anoxia, which was partially prevented by isoflurane and completely reversed by reoxygenation, and total adenine nudeotide did not decrease. In long incubations (60-70 min), both energy charge and total adenine nudeotide greatly decreased during anoxia, with partial and no reversal by reoxygenation, respectively. Isoflurane partly prevented decreases in both energy charge and total adenine nudeotide during anoxia and reoxygenation. In addition, 1 MAC isoflurane obviously increased ATP/ADP, which could not be changed by 1 MAC halothane. CONCLUSION: Isoflurane partially protects isolated hepatocytes against decreases in both energy charge and total adenine nudeotide during short (reversible) or long (irreversible) anoxia.

Effect of emulsified isoflurane on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytes

Objective:To explore the effect of emulsified isoflurane(EI)on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytea and relevant protein expression.Methods:Cardiac muscle anoxiareoxygenation damage model was established with culture in vitro neonatal rat cardiomyocytes.The cardiomyocytes were divided into control group,model group,fat emulsion group and EI group.The cardiomyocytes apoptosis rates and lactic dehydrogenase(LDH),superoxide dismutase(SOD)and malondialdehyde(MDA)index standardization were detected after relevant treatment The expression of apoptosis-related proteins Bel-2,Bax and Caspase-3 were detected with Western blot approach.Results:After hypoxia/reoxygenation(H/R)model was treated by EI,the cells apoptosis rate decreased and was dramatically below the fat emulsion group(P<0.05),Cardiomyocytes biochemical index detection presented that,compared with the control group that the LDH activity and MDA content dramatically increased(P<0.05),while the SOD activity notably decreased(P<0.05);compared with the H/R group,the SOD activity of the fat emulsion group and EI group increased(P<0.05);while the LDH activity and MDA content decreased(P<0.05).And the change of the EI group was more remarkable than the fat emulsion group(P<0.05).The Western blot analysis presented that,compared with the control group,the Bcl-2 protein expression of the other groups significantly decreased(P<0.05),the expressions of Bax protein and Caspase-3protein increased significantly(P<0.05);compared with H/R group,cardiomyocytes Bc1-2protein expression of EI group increased significantly(P<0.05),the expressions of Bax protein and Caspase-3 protein decreased significantly(P<0.05),and the change of EI group was more remarkable than the fat emulsion group(P<0.05).Conclusions:EI can inhabit the apoptosis of anoxia-reoxygenation damage model cardiomyocytes,and may he related to the up-regulation of expression of Bcl-2 and down-regulation of expression of Caspase-3 protein.

Rapamycin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury by Inducing Autophagy through the PI3k/Akt Pathway

The purpose of this study was to investigate the potential cardioprotection roles of Rapamycin in anoxia/reoxygenation（A/R） injury of cardiomyocytes through inducing autophagy, and the involvement of PI3k/Akt pathway. We employed simulated A/R of neonatal rat ventricular myocytes（NRVM） as an in vitro model of ischemial/reperfusion（I/R） injury to the heart. NRVM were pretreated with four different concentrations of Rapamycin（20, 50, 100, 150 μmol/L）, and pretreated with 10 mmol/L 3-methyladenine（3MA） for inhibiting autophagy during A/R. Then, Western blot analysis was used to examine variation in the expression of LC3-Ⅱ, LC3-Ⅰ, Bim, caspase-3, p-PI3KⅠ, PI3KⅠ, p-Akt and Akt. In our model, Rapamycin had a preferential action on autophagy, increasing the expression of LC3-Ⅱ/ LC3-Ⅰ, whereas decreasing the expression of Bim and caspase-3. Moreover, our results also demonstrated that Rapamycin inhibited the activation of p-PI3KⅠ and enhanced the activation of p-Akt. It is concluded that Rapamycin has a cardioprotection effect by inducing autophagy in a concentration-dependent manner against apopotosis through PI3K/Akt signaling pathway during A/R in NRVM.

The antiapoptotic effect of insulin against anoxia/reoxygenation injury in cultured cardiomyocyte of neonatal rat

Objective： To study protective effect of insulin against cardiomyocyte apoptosis in anoxia/reoxygenation （A/R） injury of neonatal rat. Methods： The model of A/R injury was finished through receiving anoxia for 2h and reoxygenation for 4h in cultured cardiomyocytes of neonatal rat. The cardiomyocytes were divided randomly into 3 groups： control group （CON）, anoxia/reoxygenation group （A/R） and insulin-treated group （INS）. At the end of reoxygenation of 4 hours, activities of lactate dehydrogenase （LDH）, contents of malondiaidehyde （MDA）, were assessed through spectrophotometric procedures, myocyte apoptosis were detected through TUNEL and DNA Ladder. Results： MDA, LDH, and Apoptosis Index were significantly decreased in INS group compared with A/R group （P〈0.01）. Conclusion： Insulin has a protective effect against A/R injury in cultured cardiomyocyte of neonatal rat; the protective mechanism may contribute to antiapoptosis of insulin.

Ecological Devastation in Lake Victoria: Part A: Thermal Structure and Anoxia

Lake Victoria is the second (excl. Caspian Sea) largest lake in the world by surface area and 7th by Volume. The lake and catchment territories are shared between three countries, Kenya, Uganda and Tanzania. A research was carried out during 1990-1992 exploring the changes of the thermo-chemical structure occurred after the invasion of Nile Perch. Results of changes of physico-chemical (Temperature, DO and pH) conditions are summarized in this paper. The anoxic conditions by space and time were enhanced. Enhancement of pollutant supply from anthropogenic developments of terrestrial sources and atmospheric dust deposition accompanied by the deleterious effects of the Nile Perch invasion caused enhancement of anoxia in the lake in space and time. The combination of bottom-up nutrient supply and strong mixing conditions, expressed as low RTR values accelerate phytoplankton growth rate and production. The surplus of organic matter originated from algal biomass, enhanced anoxia.

Comparative insights into mitochondrial adaptations to anoxia in brain

Numerous diseases and pathologies impair the delivery of oxygen to brain, with rapid and deleterious consequences. For example, diseases related to systemic hypoxemia （e.g., chronic pulmonary disorders, cystic fibrosis）, decreased oxygen carrying capacity of blood （e.g., anemia）, or decreased transport （e.g., heart attack, stroke） can all reduce or entirely prevent the delivery of oxygen to brain cells, resulting in the initiation of programmed cell death pathways, necrosis, or excitotoxic cell death in brain （Pamenter, 2014）. However, oxygen-limited environments are common on earth and many organisms naturally experience periods of intermit- tent or prolonged hypoxia or anoxia in their daily and/or annual life cycles （Bickler and Buck, 2007）.

Epidemio-Clinical Characteristics of Perinatal Anoxia and Immediate Outcome of Patients at Hospital Teaching Gabriel Toure of Bamako

Introduction: Neonatal asphyxia (NA) is one of the most likely causes of neuro-developmental abnormalities in children. In Mali it is responsible for half of the early deaths and the third of neonatal mortality. Updated data would help understand and improve intervention strategies to reduce mortality. Objective: It is the study of epidemiological and clinical characteristics, the immediate outcome and the factors associated with newborn (NB) mortality with NA. Material and Methods: This was a prospective cross-sectional study from June 27th to September 3rd 2016 about the NBs admitted for NA in the Hospital Teaching Gabriel Touré of Bamako. The clinical and biological data including the prognosis were collected from the health records of women, the liaison sheets and the medical file. The analysis was done using the software Epi info version 3.5.1. Results: 76 NBs were included which represented 23.45% of hospitalizations. The majority (89.5%, n = 68) were admitted to less than 24 hours of life for NA grade III according to the Sarnat classification (43.4%, n = 33). The average age of mothers was 24.17 ± 5.5 years. Almost half (41.3%, n = 31) were primigravida. The most common obstetrical event was dystocia (64.5%, n = 49). The prognosis was poor in grade III anoxia in our patients (56%) of deaths. Conclusion: The périnatal anoxia (PA) is a major health issue in Mali because of its frequency and severity. Monitoring of pregnancies, delivery assisted by skillful and qualified personnel, mastery of neonatal resuscitation techniques are good means of prevention.

红景天苷防治眼科疾病的研究进展

红景天苷是从红景天分离得到的一种苯丙素苷,具有耐缺氧、抗氧化、抗炎、保护神经、抗疲劳、抗衰老及调节免疫等广谱药理特性。红景天苷具有多靶点—多途径的整体调节特征,通过激活磷脂酰肌醇-3-激酶/蛋白激酶B信号通路和单磷酸腺苷活化蛋白激酶途径、B淋巴细胞瘤-2基因/B淋巴细胞瘤-2基因相关X蛋白通路和内源性抗氧化酶的活性及环氧合酶/前列腺素E2信号通路保护糖尿病性视网膜病变视网膜血管内皮细胞、视网膜色素上皮细胞及Müller细胞;激活调控转化生长因子信号通路、磷脂酰肌醇-3-激酶/蛋白激酶B信号通路和分泌性糖蛋白/β-连环蛋白通路,从而抑制青光眼小梁网细胞和神经节细胞凋亡,并调节眼内压的稳定;激活蛋白激酶B/糖原合成酶激酶-3信号通路抑制年龄相关性黄斑变性视网膜色素上皮细胞氧化损伤,降低血管内皮生长因子和缺氧诱导因子-1的表达水平抑制脉络膜新生血管的形成;发挥抗氧化活性,保护白内障晶状体上皮细胞免受氧化损伤;改善近视所致的巩膜缺氧;以及通过激活单磷酸腺苷活化蛋白激酶—沉默信息调节因子1信号通路促进自噬等来抑制机体氧化应激,缓解干眼症引起的角膜上皮细胞氧化损伤等。红景天苷在眼科应用研究涉及的范围越来越广,本文就国内、外红景天苷治疗相关眼科疾病的最新研究进展予以综述。

槲芪方加减对肝癌化疗栓塞术后大鼠一氧化氮合酶、血管内皮生长因子、乏氧及免疫功能的影响

目的:研究槲芪方加减对肝癌化疗栓塞术后大鼠一氧化氮合酶(iNOS)、血管内皮生长因子(VEGF)、乏氧及免疫功能的影响。方法:50只大鼠中随机抽取12只作为健康组进行对照,37只大鼠建立肝癌模型。建模过程中意外死亡1只大鼠,剩余36只大鼠建模成功,随机分为模型组、肝动脉化疗栓塞术组以及联合组,每组12只。肝动脉化疗栓塞术组给予肝动脉化疗栓塞术(TACE)治疗;联合组在肝动脉化疗栓塞术组基础上给予模型大鼠27 ml/kg槲芪方灌胃,2次/d,共24周。运用全自动生化分析仪检测各组大鼠肝功能指标水平,流式细胞仪检测各组大鼠免疫功能指标水平,苏木精-伊红(HE)染色观察各组大鼠肝组织病理变化,原位末端标记法(TUNEL)检测各组大鼠肝癌细胞凋亡,免疫印迹检测各组大鼠VEGF、iNOS、缺氧诱导因子1α(HIF-1α)蛋白表达。结果:与健康组比较,模型组丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)水平均升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组ALT、AST、ALP水平均降低(P<0.05),肝动脉化疗栓塞术组ALT、AST、ALP水平均高于联合组(P<0.05)。与健康组比较,模型组CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)降低,CD8^(+)升高(P<0.05),模型组与联合组比较差异无统计学意义(P>0.05),与模型组及联合组比较,肝动脉化疗栓塞术组CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)降低,CD8^(+)升高(P<0.05)。与健康组比较,模型组细胞凋亡率升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组细胞凋亡率降低(P<0.05),肝动脉化疗栓塞术组细胞凋亡率低于联合组(P<0.05)。与健康组比较,模型组VEGF、iNOS、HIF-1α表达均升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组VEGF、iNOS、HIF-1α表达均升高(P<0.05),与肝动脉化疗栓塞术组比较,联合组VEGF、iNOS、HIF-1α表达均降低(P<0.05)。结论:槲芪方加减可提高肝癌TACE术后大鼠的免疫功能,通过抑制肝癌大鼠乏氧微环境中HIF-1α、iNOS及VEGF水平,改善乏氧微环境,促进肿瘤细胞凋亡。

Terminal Ediacaran anoxia in deep-ocean: Trace element evidence from cherts of the Liuchapo Formation, South China

Here we report a detailed trace element study of the cherts from Liuchapo Formation, which is a terminal Ediacaran (551-542 Ma) succession in South China deposited in deep-water basinal setting. The REE of Liuchapo cherts shows similar features as observed for anoxic modern seawater (but not for hydrothermal fluids), characterized by positive La anomaly (LaN/CeN = 0.83–1.91, average 1.37), moderately negative Ce anomaly (0.53–1.1, average 0.73), positive Gd anomaly (average 1.08), positive Y anomaly (average 1.21), and depleted LREE and MREE. In addition, the Liuchapo cherts have low ΣREE (3.36–56.13 ppm, average 20.6 ppm), low Al2O3, Ti, Th and Zr concentrations, and high Y/Ho ratios (up to 43.9). The redox-sensitive trace elements concentrations in the cherts do not correlate with detrital input proxies. All of these features suggest that the redox-sensitive trace elements in the cherts were authigenically concentrated in water column and their concentrations thus are excellent indicators of ancient redox conditions. Very low Th/U ratios, high V/(V+Ni) and Fe?/Al ratios, enrichments of redox-sensitive trace elements (U, V, Mo), and low concentration of Mn in the cherts imply anoxia in the deep seawater. Our data reveal that the terminal Ediacaran ocean was not completely oxidized and the deep ocean was still anoxic, at least in South China. We propose that although the oxidative events existed in the terminal Ediacaran oceans, decomposition of organic matter prolonged anoxia in the deep ocean.

Anti-apoptotic effect of morphine-induced delayed preconditioning on pulmonary artery endothelial cells with anoxia/reoxygenation injury

Background Opioid preconditioning （PC） reduces anoxia/reoxygenation （A/R） injury to various cells. However, it remains unclear whether opioid-induced delayed PC would show anti-apoptotic effects on pulmonary artery endothelial cells （PAECs） suffering from A/R injury. The present study was conducted to elucidate this issue and to investigate the potential mechanism of opioid-induced delayed PC. Methods Cultured porcine PAECs underwent 16-hour anoxia followed by 1-hour reoxygenation 24 hours after pretreatment with saline （NaCI; 0.9%） or morphine （1 μmol/L）. To determine the underlying mechanism, a non-selective KATe channel inhibitor glibenclamide （Glib; 10 μmol/L）, a nitric oxide （NO） synthase blocker NG-nitro-L-arginine methyl ester （L-NAME; 100 μmol/L）, and an opioid receptor antagonist naloxone （Nal; 10μmol/L） were given 30 minutes before the A/R load. The percentage of apoptotic cells was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） staining, eNOS mRNA level was measured by real-time polymerase chain reaction （PCR）. NO content of PAECs supernatants was measured with the Griess reagent. Results Compared to the A/R PAECs, morphine-induced delayed PC significantly reduced PAECs apoptosis （（18.1±1.9）% vs （5.5±0.3）%; P 〈0.05）, increased NO release （（11.4±1.3） μmol/L vs （20.5±2.1） μmol/L, P 〈0.05）, and up-regulated eNOS gene expression nearly 9 times （P 〈0.05）. The anti-apoptosis effect of morphine was abolished by pretreatment with Glib, L-NAME and Nal, but the three agent-selves did not aggravate the A/R injury. Furthermore, L-NAME and Nal offset the enhanced release of NO caused by pretreatment with morphine. Conclusions Morphine-induced delayed PC prevents A/R injury of PAECs. This effect may be mediated by activation of KATe channel via opioid receptor and NO signaling pathways.

An Efficient and Reliable Assay for Investigating the Effects of Hypoxia/Anoxia on Drosophila

Stroke is a leading cause of death worldwide. Up to one thousand potential drugs or interventions have been developed to treat stroke, out of which;60 have gone on to clinical trials. However, none of them has been successful. New insights into the molecular and cellular mechanisms of ischemia-induced injury are needed for discovering new therapeutic targets. Recently, Drosophila has been used to uncover new hypoxia-related genes. In this study, we describe an efficient and reliable assay with a sophisticated apparatus for studying the effects of oxygen deprivation on flies. Using this assay, wild-type flies were exposed to an anoxic environment for varying lengths of time, then the cumulative death rate and mobility recovery were systematically analyzed. We found that anoxia for over one hour caused lethality. The cumulative death rate on day 5 after anoxia was linearly and positively correlatedwith the duration of anoxia, and reached 50% when the duration was 2.5 h–3 h. We also found that the mobility recovery in normoxia was slow, as the climbing ability remained largely unchanged 4 h–6 h after 2.5-h of anoxia.We suggest that 2.5 h–3 h of anoxia and 4 h–6 h of recovery before mobility analysis are appropriate for future use of the anoxia assay.

Extract of Paris polyphylla Simth Protects Cardiomyocytes from Anoxia-Reoxia Injury through Inhibition of Calcium Overload

Objective：To assess any direct effect of extract of Paris polyphylla Simth（EPPS）,a Chinese plant,on a cardiomyocyte subject to ischemia-reperfusion injury and to further elucidate its protective effect against myocardium ischemia on the cellular level.Methods：Neonatal rat cardiomyocytes were isolated and subjected to an anoxia-reoxia injury simulating the ischemia-reperfusion injury in vivo in the presence or absence of EPPS or diltizem,a positive control.The lactate dehydrogenase（LDH） activities in culture supematants and cell viabilities were analyzed using the enzymatic reaction kinetics monitoring-method and MTT method, respectively.Free intracellular calcium concentrations and activities of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase in cells were also measured with laser confocal microscopy and the inorganic phosphorus-transformation method,respectively.Results：In cardiomyocytes subject to anoxia-reoxia injury,EPPS at 50-400 mg/L showed a concentration-dependent inhibition on LDH leakage and maintenance of cell viability,and the effect was significant at 275 and 400 mg/L（both P0.01）.In addition,EPPS at 275 and 400 mg/L significantly inhibited the increase in intracellular free calcium（both P0.01） as well as decreased the activities of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase（P0.01,P0.05）.Conclusions：EPPS prevents anoxia-reoxia injury in neonatal rat cardiomyocytes in vitro by preservation of Na~＋-K~＋ ATPase and Ca^（2＋） ATPase activities and inhibition of calcium overload.The direct protective effect on cardiomyocytes may be one of the key mechanisms that underlie the potential therapeutic benefit of EPPS against myocardium ischemia.

Changes of summating potentials and morphology in theguinea pig cochlea during anoxia

The dynamic changes in CAP, and EP in the scale media were examined with single micropipet during anoxia and reventilation with oxygen. Also, the morphologic changes in IHC, OHC and synapse were observed in this experiment. It was found that the amplitude of SP and EP values declined with alteration in polarity of these value. The changes in polarity and amplitude of SP followed the changes of CAP threshold induced by anoxia. The histologic examinations revcaled no cvidence of acetylcholinesterase (AChE) alteration in the synapse and no succinict dehydrogenase (SDH) changes in IHC appeared. However, the activity of SDH in the OHC decreased. The results suggest that the polarity and amplitude of SP were influenced passively by the changes of EP value. In addition, the change of SP polarity from positive tonegative during anoxia is due to the loss of mudulation process of OHC to IHC, while the SP polarity from negative to positive during the supply of oxygen is caused by regain of the modulation process of OHC.

Heat shock protein 70 gene transfection protects rat myocardium cell against anoxia-reoxygeneration injury

Background A number of studies suggest that the expression of heat shock protein 70 （HSP70） induced by heat stress are associated with protection against ischemia-reperfusion injury. But the protective effects may be contaminated by other factors in the same stress. This study was conducted to explore the protective role of HSP70 expression in acute myocardial anoxia/reoxygeneration （A/R） injury with a liposome-mediated gene transfer technique for the introduction of pCDNA HSP70 into the neonatal rat myocardial cells. In addition, heat shock stress cytoprotection was also investigated for comparison. Methods The cultured primary neonatal rat myocardiocytes with an acute myocardial A/R injury model and the HS-treated rat myocardiocyte model were used. Three-day cultured myocardiocytes were randomly divided into four groups （n=8）： control group, A/R group, HS＋A/R group and pCDNA HSP70 ＋A/R group. A liposome-coated HSP70 pCDNA plasmid was transfected into the primary neonatal rat myocardiocytes; HSP70 mRNA and its protein were confirmed by reverse transcriptase polymerase chain reaction （RT-PCR） and Western blotting. The cell viability was assayed by monotetrazolium （MTT） and the lactate dehydrogenase （LDH） and creatine phosphokinase （CPK） activity of cells during incubation and the changes in cells ultrastructure were examined. NF-κB activity in the primary neonatal rat myocardiocytes was measured with flow cytometry. Results Compared with viability in the A/R group （（35.4±6.9）%） the cell viability in the HS＋A/R group （（72.8±11.6）%） and the pCDNA HSP70 ＋ A/R group （（76.3±12.2）%） was improved significantly （P〈0.05）. The activity of LDH and CPK was significantly elevated in the A/R group. However, in the HS＋A/R group and pCDNA HSP70 ＋A/R group, significant decreases in activity were observed. The cell ultrastructure of the A/R group cells was abnormal, whereas nearly normal ultrastructure was observed in HS＋A/R group and pCDNA HSP70＋A/R group. HSP70 mRNA and protein were slightly expressed in the myocardiocytes of the A/R group. However, obvious overexpression was observed in the HS＋A/R group and in the pCDNA HSP70＋A/R group （P〈0.01）. And there was a significant difference between the HS＋A/R group and the pCDNA HSP70＋A/R group in the expression of HSP70 mRNA and protein （P〈0.01）. A high activity of NF-κB （5.76±0.64） was detected in the A/R group. But in the HS＋A/R group there was a statistically significant decrease in the activity of N F-KB compared with the A/R group （3.11±0.52 vs 5.76±0.64, P〈0.01 ）. The same statistically significant difference was also observed in the pCDNA HSP70 ＋ A/R group and A/R group （2.83±0.49 vs 5.76±0.64, P〈0.01 ）. Conclusions Overexpression of HSP70 alone by gene transfection leads to protection for cardiac myocyte against anoxia-reoxygeneration. These cardioprotective effects were related to the reduction in activation of NF-κB.

Protective effect of cardiomyopeptidin on cultured rat hippocampal neurons injured by anoxia reoxygenation

Cardiomyopeptidin (CMP), a small molecular polypeptide, is a new drug extracted from pig myocardium. Recently, evidence of its protective effect on myocardium injured by ischemia or anoxia has appeared.^(1,2) Neurons are also vulnerable to ischemia/anoxia. The aim of this study was to evaluate the neuroprotection of CMP in an anoxic model, which was the cultured hippocampal neurons in vitro, and to determine the relationship between CMP and expression of Bcl-2.

牛磺酸生产废水处理工程案例

湖北某牛磺酸生产企业废水处理工程,从企业生产工艺和废水水质特点出发,有针对性地采用“水解酸化+前缺氧+好氧生化+后缺氧+二沉”工艺处理该企业生产废水。进水平均COD、氨氮、总氮分别为956.8、50.6、99.1mg/L时,出水平均COD、氨氮、总氮分别为73.6、1.6、12.2 mg/L,COD、氨氮、总氮平均去除率可分别达到92.3%、96.9%、87.7%,出水水质稳定,达到《化学合成类制药工业水污染物排放标准》(GB 21904—2008)中新建企业水污染物排放浓度限值。采用渐减曝气和风机变频控制,能耗显著降低,单位水量运行费用为1.60元/m~3。

CircACAP2靶向miR-29a-3p/CCNT2轴对缺氧/复氧诱导的心肌细胞损伤的影响

目的:探讨CircACAP2靶向miR-29a-3p/细胞周期蛋白T2(CCNT2)轴对缺氧/复氧(H/R)诱导的心肌细胞损伤的影响。方法:将H9c2细胞分为Control组(正常培养)、si-NC组(转染si-NC)、Model组(建立H/R模型)、si-CircACAP2组(转染si-CircACAP2)、si-CircACAP2+inhibitor-NC组(si-CircACAP2和inhibitor-NC共转染)、si-CircACAP2+miR-29a-3p inhibitor组(si-CircACAP2和miR-29a-3p inhibitor共转染);实时荧光定量聚合酶链式反应(qRT-PCR)检测H9c2细胞中CircACAP2、miR-29a-3p的表达水平;四唑盐(MTT)法检测H9c2细胞活力;流式细胞仪检测H9c2细胞凋亡;单丹磺酰尸胺(MDC)染色法检测H9c2细胞自噬;乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)试剂盒检测H9c2细胞上清中LDH、MDA、SOD水平,DCFH-DA荧光探针法检测细胞内活性氧(ROS)水平;蛋白质免疫印迹法(Western Blot)检测增殖细胞核抗原(PCNA)、细胞凋亡蛋白[B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)]、自噬相关蛋白(Beclin-1、P62)及CCNT2的表达;双荧光素酶报告检测CircACAP2对miR-29a-3p的靶向关系和miR-29a-3p对CCNT2的靶向关系。结果:与Control组比较,Model组H9c2细胞中CircACAP2表达、凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达升高,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达降低(P<0.05);与Model组比较,si-CircACAP2组H9c2细胞中CircACAP2表达、凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达降低,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达升高(P<0.05);与si-CircACAP2组比较,si-CircACAP2+miR-29a-3p inhibitor组H9c2细胞中CircACAP2表达差异无统计学意义(P>0.05),凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达升高,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达降低(P<0.05);CircACAP2靶向调控miR-29a-3p的表达,miR-29a-3p靶向负调控CCNT2的表达。结论:敲低CircACAP2可能通过靶向miR-29a-3p来下调CCNT2表达,进而抑制H/R诱导的H9c2细胞凋亡、自噬能力及氧化应激,促进细胞增殖,发挥保护作用。

Effects of catalase and endothelin on anoxia-induced vasoconstriction of porcine basilar artery in vitro

目的：研究缺氧引起的血管收缩是否与血管内皮细胞释放内皮素（ＥＴ）有关．方法：９５％Ｏ２＋５％ＣＯ２混合气体换成９５％Ｎ２＋５％ＣＯ２引起急性缺氧，描记猪基底动脉环的张力变化．结果：在基础张力条件下和由ＥＴ３ｎｍｏｌ·Ｌ－１引起收缩时，缺氧分别使基底动脉张力增加０２１ｇ±００８ｇ和０２４ｇ±００９ｇ．当ＥＴ浓度从１００ｎｍｏｌ·Ｌ－１增加到３００ｎｍｏｌ·Ｌ－１时，动脉的张力不进一步增加，此时急性缺氧仍使张力进一步增加０１６ｇ±０１０ｇ．过氧化氢酶８００，２４００ｋＵ·Ｌ－１明显降低缺氧引起的收缩，抑制率分别为３３％±７％和４７％±９％．

MRI扩散加权成像对急性脑梗死患者神经损伤程度的评估价值

目的:探究磁共振成像(magnetic resonance imaging,MRI)扩散加权成像(diffusion weighted imaging,DWI)对急性脑梗死患者神经损伤程度的评估价值。方法:回顾性选取2021年9月—2023年8月苏州市相城人民医院收治的150例急性脑梗死患者。根据NIHSS评分将其分为轻-中度组(65例)和重度组(85例)。两组均进行常规MRI检查和DWI检查。比较两组表观弥散系数(apparent diffusion coefficient,ADC)和相对表观扩散系数(relative apparent diffusion coefficient,rADC)、梗死病灶梗死体积和FLAIR血管高信号(FLAIR vascular hyperintensity,FVH)征评分。分析梗死体积、FVH征评分、ADC和rADC与急性脑梗死严重程度的相关性。分析梗死体积、FVH征评分、ADC对急性脑梗死患者病情严重程度的诊断价值。结果:重度组ADC与rADC均高于轻-中度组,差异有统计学意义(P<0.05)。重度组FVH征评分和梗死体积均高于轻-中度组,差异有统计学意义(P<0.05)。梗死体积、FVH征评分、ADC及rADC均与疾病严重程度呈正相关(P<0.001)。结论:MRI DWI对急性脑梗死患者神经损伤程度评估的准确度和敏感度高,具有较高诊断价值。