Oxidative Stress and Free Radical Damage in Patients With Acute Dipterex Poisoning

Objective To investigate whether acute dipterex poisoning (ADP) may cause oxidative stress and free radical damage in the bodies of acute dipterex poisoning patients (ADPPs), and to explore the mechanisms by which ADP may cause oxidative stress and free radical damage. Methods Fifty ADPPs and fifty healthy adult volunteers (HAVs) whose ages, gender and others were matched with the ADPPs were enrolled in a randomized controlled study, in which concentrations of nitric oxide (NO), vitamin C (VC), vitamin E (VE) and P-carotene (P-CAR) in plasma as well as concentration of lipoperoxide (LPO), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric analytical methods. Results Compared with the average values of experimental parameters in the HAVs group, the average values of plasma NO and erythrocyte LPO in the ADPPs group were significantly increased (P<0.0001), while those of plasma VC, VE and P-CAR as well as erythrocyte SOD, CAT, GPX and AChE in the ADPPs group were significantly decreased (P<0.0001). Bivariate correlation analysis and partial correlation analysis suggested that when NO and LPO values were increased, and VC, VE, β-CAR, SOD, CAT and GPX values were decreased in the ADPPs, AChE value was decreased gradually in the ADPPs (P<0.001-0.0001). Reliability analysis of experimental parameters reflecting oxidative stress and free radical damage in the ADPPs showed that the reliability coefficient (8 items) alpha=0.6909, and the standardized item alpha=0.8574. Conclusion The findings in the present study suggest that ADP can cause oxidative stress and free radical damage, and inhibit markedly erythrocyte acetylcholinesterase activity in ADPPs.

Abnormal Reactions of Free Radicals and Oxidative Damages in the Bodies of Patients With Chronic Glomerulonephritis

Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.

May Chronic Childhood Constipation Cause Oxidative Stress and Potential Free Radical Damage to Children?

Objective To investigate whether chronic childhood constipation (CCC) may cause oxidative stress and potential free radical damage to children, and to explore the mechanisms by which CCC may cause oxidative stress and potential free radical damage to chronic constipation patients (CCPs). Methods Sixty CCPs and sixty healthy child volunteers (HCVs) whose ages, gender and others were matched for the CCPs were enrolled in a randomized controlled study, in which levels of vitamin C (VC) and vitamin E (VE) in plasma as well as activities of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes were determined by spectrophotometric analytical methods. Results Compared with average values of the above biochemical parameters in the HCVs group, the average values of VC and VE in plasma as well as those of SOD and CAT in erythrocytes in the CCPs group were significantly decreased (P<0.0001). Linear regression and bivariate correlation analysis showed that with prolonged course of the CCPs, the levels of VC and VE in plasma as well as the activities of SOD and CAT in erythrocytes in the CCPs were decreased gradually (P<0.0001). Conclusion The findings in the present study suggest that chronic childhood constipation causes oxidative stress and potential free radical damage to children with chronic constipation.

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy

Objective: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies. Methods: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and β-carotene (β-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric mothods. Results: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P＜0.0001), while those ofVC, VE and β-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgANP group were significantly decreased (P＜0.0001). Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those ofVC, VE, β-CAR,SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually (P＜0.0001); and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, β-CAR, SOD, CAT and GPX were decreased gradually (P＜0.005). The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgAN patients were 73.8%-92.5%, and the correct rates for the HAV were 70.0%-91.3% when independent discriminant analysis was used; and the correct rate for the IgAN patients was increased to 98.8%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. The above biochemical parameters' reliability coefficient (alpha) were used to estimate the oxidative damage of the IgAN patients as 0.8145, the standardized item alpha=0.9730, F=53273.5681, P＜0.0001. Conclusions: A series of free radical chain reactions caused serious pathological aggravation in the IgANP' bodies, thus resulting in oxidative damage in their bodies. In treating IgANP, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Oxygen Radical Generation as an Index of Neurotoxic Damage

Biochemical, anatomical, and physiological characteristics of the brain make it especially vulnerable to insult. Specifically, some of these characteristics such as myelin and a high energy requirement provide for the introduction of free radical-induced insult. Recently, the biochemistry of free radicals has received considerable attention. It also has become increasingly suggestive that many drug and chemical-induced toxicities may be evoked via free radicals and oxidative stress. Major points addressed in this work are the regulation of neural-free radical generation by antioxidants and protective enzymes, xenobiotic-induced disruption of cerebral redox status, and specific examples of neurotoxic agent-induced alterations in free radicals as measured by the fluorescent probe dichlorofluorescein. This article considers that free radical mechanisms may contribute significantly to the properties of several diverse neurotoxic agents and proposes that free radicals may be common phenomena of neurotoxicity.

Transitional metal ions induced damage to biomolecules:role of ferryl and perferryl radicals

Objective:To investigate the effect of oxidized transitional metal（ferric and cupric） ions on the amino acids.Methods:25 mmol/L hydroxyproline and 25 mmol/L histidine were incubated with 50μL Fe3+ and Cu2+ ions at pH 7.4 and 37℃for 30 mins in separate test tubes.Then 500μL of 1% thiobarbituricacid（TBA） was added to the incubated amino acids followed by addition of 500μL of glacial acetic acid.The resultant mixture was vortexed and heated at 100℃for 30 min.Absorbance readings were noted after cooling to room temperature.The experiment was repeated in the presence of various reagents,like hydroxyl radical scavengers,antioxidant enzymes,and reducing agents and metal ion chelators.Results:The pink chromogen formed with the absorbance maxima at 524 nm,AND shifted to 560 nm in alkaline pH.The absorbance was expressed as TBAadduct in MDA units.The TBA-adduct decreased in the presence of reducing agents and metal ion chelators.Antioxidant enzymes and hydroxyl radical scavengers did not show any effect. Conclusion:Transitional metal ions in their oxidized state showed significant damage to amino acids,hydroxyproline and histidine.The results indicate the possible role played by high-valent oxo-iron species,ferryl and perferry radicals in damaging biomolecules.

Computational mechanistic investigation of radiation damage of adenine induced by hydroxyl radicals

The radiation damage of adenine base was studied by B3LYP and MP2 methods in the presence of hydroxyl radicals to probe the reactivities of five possible sites of an isolated adenine molecule. Both methods predict that the C8 site is the more vulnerable than the other sites. For its bonding covalently with the hydroxyl radicals, B3LYP predicts a barrierless pathway, while MP2 finds a transition state with an energy of 106.1 kJ/mol. For the hydroxylation at the C2 site, the barrier was calculated to be 165.3 kJ/mol using MP2 method. For the dehydrogenation reactions at five sites of adenine, B3LYP method predicts that the free energy barrier decreases in the order of H8 〉 H2 〉 HN62 〉 HN61 〉 HN9.

Sister chromatid exchange and DNA damage in human lymphocytes induced by air-dust in Lanzhou City: involvement in free radicals

The air-dust samples collected from petro-chemical industrial region in the suburb of Lanzhou and from a certain rural region 64 km away from the city were extracted, with a mixed solvent (benzene: hexane: isopropanol=7:2:1) for 8 hours. A strong free radical signal at g= 2.00 of air-dust itself and a hyperfine splitting EPR signal of extract from air-dust have been detected. The sister chromatid exchange frequency (SCE) was increased by extracts of both dusts from the industrial region and from the rural region. If a chemical is able to increase SCE up to twice as high as the control, this chemical is considered to be mutagenic and/or carcinogenic. The double SCE frequency concentration is 23 μg/ml for the dust extract obtained from the industrial region and 47μg/ml for that from the rural region. Extracts were able to damage to DNA template. Results indicated that the mutagenicity and/or carcinogenicity of the extracts obtained from the petro-chemical industrial region were stronger than that of the extracts from the rural region.

3,4-Methylenedioxymethamphetamine(MDMA)Abuse Markedly Inhibits Acetylcholinesterase Activity and Induces Severe Oxidative Damage and Liperoxidative Damage

Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. Methods 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. Results Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P<0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P<0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P<0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P<0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453. Conclusion The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.

Oxidative damage of primary cultured hippocampal neurons Does androgen have an antagonistic effect?

BACKGROUND： Evidence illustrates that androgen has a neuroprotective role. However, whether androgen also has the protective effect on hippocampal neurons during free radical mediated injury remains unclear. OBJECTIVE： To investigate the neuroprotective effect of androgen on hippocampal neurons during free radical damage. DESIGN, TIME AND SETTING： A controlled in vitro experiment was performed at the Department of Human Anatomy, Cell Culture Lab, and Neuroendocrinology Lab, Basic Medical School, Hebei Medical University from February to June 2009. MATERIALS： Testosterone was provided by Tianjin Jinyao Amino Acid Company, China. METHODS： Primary cultured neurons from 24 Sprague Dawley rats were randomly assigned into four groups： control, H202, testosterone, and testosterone （pre-added） plus H2O2 groups. MAIN OUTCOME MEASURES： The positive cell ratio of microtubule associated protein-Ⅱ and neuron specific enolase was determined by immunocytochemistry. Neuronal morphology was observed by hematoxylin-eosin staining and Nissl staining. Cell vitality and viability were determined using an inverted phase contrast microscope. The content of nitric oxide synthase, malondialdehyde, and superoxide dismutase were measured with a spectrophotometer. RESULTS： As compared with the control group, cell vitality and viability, and superoxide dismutase level were significantly decreased in the H202 group （P 〈 0.05）, while nitric oxide synthase and malondialdehyde levels were significantly increased （P 〈 0.05）. Neuronal vitality and viability as well as superoxide dismutase level in the testosterone plus H2O2 group were significantly greater than in the H2O2 group （P 〈 0.05）, and nitric oxide synthase and malondialdehyde levels were significantly less than in the H2O2 group （P〈 0.05）. CONCLUSION： Androgen partially reversed H2O2-induced neuronal damage and protected neurons.

Increased Oxidative Stress and Damage in Patients With Chronic Bacterial Prostatitis

Objective To investigate whether chronic bacterial prostatitis （CBP） increases oxidative stress and damage in patients with CBP, and to explore its possible mechanism. Methods Eighty patients with CBP and 80 healthy adults as controls were enrolled in a case-control study, in which levels of nitric oxide （NO）, vitamin C （VC）, and vitamin E （VE） in plasma, as well as malondialdehyde （MDA）, activities of superoxide dismutase （SOD）, and eatalase （CAT） in erythrocytes were determined by spectrophotometry. Results Compared with the average values of NO, VC, VE, MDA, SOD, and CAT in the healthy control group, those of plasma N O and erythrocyte MDA in the CBP group were significantly increased （P〈0.00 1）, and those of plasma VC and VE as well as erythrocyte SOD and CAT in the CBP group were significantly decreased （P〈0.001）. Findings from partial correlation analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in 80 patients with CBP, adjusted for age, suggested that with prolonged course of the disease, values of NO and MDA were gradually increased （P〈0.001）, and those of VC, VE, SOD, and CAT were gradually decreased （P〈0.05-0.001）. The findings from stepwise regression analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in CBP group suggested that the model of stepwise regression was Y = -19.1160 ＋0.3112MDA ＋ 0.0337NO, F = 22.1734, P〈0.001, r = 0.6045, P〈0.001. The findings from the reliability analysis for VC, VE, SOD, CAT, NO, and MDA in the CBP group showed that the reliability coefficients＇ alpha （6 items） was 0.7195, P〈0.0001, and the standardized item alpha was 0.9307, P〈0.0001. Conclusion There exist increased oxidative stress and damage induced by chronic bacterial prostatitis in patients, and such a phenomenon is closely related to the course of disease.

Radical scavenging and antibacterial activity of Arnebia benthamii methanol extract

Objective:To evaluate in vitro antioxidant and antibacterial activity of methanolic extract of Arnebia benthamii（A.benthamii） whole plant.Methods:Plasmid damage was analyzed by agarose gell electrophoresis.Calf thymus DNA was monitored by TBARS formation.DPPH, reducing power and lipid peroxidation was evaluated by using standard procedures.Antibacterial assay was monitored by disc diffusion method.Results:DPPH radical scavenging and hydroxyl radical scavenging potential of the plant revealed that the extract to be active radical scavenger.Reducing(Fe3+-Fe2+) power and lipid peroxidation inhibition efficiency（TBARS assay） of the extract was also evaluated and the extract showed promising activity in preventing lipid peroxidation and might prevent oxidative damages to biomolecules.The extract offered a significant protection against plasmid and calf thymus UNA damage induced by hydroxyl radicals. The extract was also evaluated on different bacterial strains and the maximum antibacterial activity was exhibited against Escherichia coli（E.coli） when compared with standard drug. Conclusions:These findings demonstrate that the methanol extract of A.benthamii has excellent anti-oxidant activities and could be considered as a potential source of lead molecules for pharmaceutical industries.

Non-peptidyl low molecular weight radical scavenger IAC attenuates DSS-induced colitis in rats

AIM:To investigate the effects of the free radical scavenger bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl) decandioate(IAC) in the dextran sodium sulphate(DSS) experimental model of ulcerative colitis.METHODS:Colitis was induced in Sprague Dawley male rats by administration of 5% DSS in drinking water.IAC(30 mg/kg,lipophilic or hydrophilic form) was administered daily(orally or ip) for 6 d until sacrifice.Colonic damage was assessed by means of indirect(Disease Activity Index score) and direct measures(macroscopic and microscopic scores) and myeloperoxidase(MPO)activity.Neutrophil infiltration within the tissue and glutathione S-transferase activity were also investigated.RESULTS:DSS-induced colitis impaired body weight gain and markedly increased all inflammatory parameters.Six-day treatment with lipophilic IAC significantly reduced intestinal damage caused by inflammation,induced a down-regulation in MPO activity(0.72 ± 0.12 and 0.45 ± 0.12 with lipophilic IAC po and ip,respectively,vs 1.10 ± 0.27 in untreated DSS colitis animals) and minimized DSS-induced neutrophil infiltration,while hydrophilic IAC administered orally did not ameliorate DSS-induced damage.CONCLUSION:These results support the hypothesis that reactive oxygen metabolites contribute to inflammation and that the radical scavenger IAC has therapeutic potential in inflammatory bowel disease.

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.

水液相下羟自由基与谷氨酸分子反应机理的量子化学研究

采用密度泛函理论的M06-2X和MN15方法,结合自洽反应场理论的SMD模型方法,研究了水液相下羟自由基(OH)与谷氨酸分子(Glu)反应的机理。研究发现:Glu的损伤可通过OH抽取其不同位置的H原子、OH加成到羧基和去质子羧基C以及单电子从Glu分子向OH转移3个途径实现。势能面计算表明:OH加成到羧基和去质子羧基C的反应通道最具优势,反应无势垒;OH抽取质子化氨基H、α-H、β-H、γ-H和羧基H的最低能垒分别是28.7、17.6、8.0、18.3和29.0 kJ/mol;电子从Glu分子向OH转移为劣势通道,反应能垒是255.2 kJ/mol。结果表明,水液相下OH加成和抽H均可诱导Glu分子损伤,损伤的Glu绝大多数难以修复,Glu具有清除羟自由基的能力。

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim:To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients(CBPP),and to explore its possible mechanism.Methods:Enrolled in a case- control study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers(HAV),on whom plasma nitric oxide(NO),vitamin C(VC),vitamin E(VE)and β-carotene(β-CAR)level,erythrocyte malondialdehyde (MDA)level,as well as erythrocyte superoxide dismutase(SOD),catalase(CAT)and glutathione peroxidase(GPX) activities were determined by spectrophotometry.Results:Compared with the HAV group,values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased(P<0,001);those of plasma VC,VE and β-CAR as well as erythrocyte SOD,CAT and GPX activities in the CBPP group were significantly decreased(P<0.001).Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease,values of NO and MDA were gradually increased(P<0.001),and those of VC,VE,β-CAR,SOD,CAT and GPX were gradually decreased(P<0.05- 0.001).The findings from stepwise regression for the 70 CBPP suggested that the model was Y=-13.2077 + 0.1894MDA + 0.0415NO-0.1999GPX.F=18.2047,P<0.001,r=0.6729,P<0.001.Conclusion:The findings suggest that there exist increased oxidative stress and oxidative damage reduced by chronic bacterial prostatitis in the patients,and such phenomenon was closely related to the course of disease.

THE EXPERIMENTAL RESEARCH ON CARDIOPLEGIC SOLU-TION CONTAINING SELENIUM AND MAGNESIUM AGAINST MYOCARDIAL ISCHEMIA REPERFUSION DAMAGE

The model of this test was set up according to Langendoff isolated heart reperfusion mechanics. The experimental research was designed to observe the protective effects on ischemic andreperfuslon myocardial tissue by using ST. Thomas cardioplegic solution containing selenium andmagnesium. We conclude that using cold crystallold cardioplegic solution containing Se'+, Mg' 4 canobviously reduce ischemic and reperfusion myocardlal injury and bas an advantage of recovering myocardial runctlon after operation by observing the content or lactic dehydrogenase (LDH); creatineI,kasphoklnase CK in the coronary vessel's sinus reflux solutlonl glutatblone peroxldase (GPX); suI,eroxlde dismutase (SOD); maloydladehyde (MDA ) I Se4+ .Mg'+ .Ca'+ and cia-nging or myocardialultrastructure.

根治性膀胱切除术后患者发生尿路造口周围潮湿相关性皮肤损伤的影响因素

目的探讨根治性膀胱切除术后患者发生尿路造口周围潮湿相关性皮肤损伤(PMASD)的影响因素。方法选取100例行根治性膀胱切除术治疗的膀胱癌患者作为研究对象,根据术后3个月是否发生PMASD分为发生组与未发生组。收集两组患者的一般资料和临床资料,分析根治性膀胱切除术后患者发生PMASD的影响因素,并绘制受试者工作特征(ROC)曲线评估影响因素的预测价值。结果根治性膀胱切除术后患者PMASD的发生率为32.00%(32/100)。相比于未发生组,发生组的体质指数、造口渗漏次数更高,自我护理能力测定(ESCA)量表评分更低(P<0.05)。多因素Logistic回归分析结果显示,体质指数、造口渗漏次数、ESCA量表评分是根治性膀胱切除术后患者发生PMASD的影响因素(P<0.05)。ROC曲线结果显示,体质指数、造口渗漏次数、ESCA量表评分预测根治性膀胱切除术后患者发生PMASD的曲线下面积分别为0.921、0.622、0.855,体质指数和ESCA量表评分的曲线下面积大于造口渗漏次数的曲线下面积(P<0.05)。结论根治性膀胱切除术后患者PMASD的发生率较高,体质指数、造口渗漏次数、ESCA量表评分为根治性膀胱切除术后患者发生PMASD的影响因素,应针对肥胖及自护能力较弱的根治性膀胱切除术后患者采取针对性措施,以降低PMASD的发生率。

根治性膀胱切除术后患者肾功能损害发生率及影响因素的系统评价与Meta分析

目的系统评价根治性膀胱切除术患者术后肾功能损害的发生率及影响因素。方法检索维普、万方、中国知网、中国生物医学文献数据库、The Cochrane Library、PubMed、Web of Science和Embase数据库中与根治性膀胱切除术患者术后肾功能损害有关的队列研究与病例对照研究。检索时限为建库至2023年9月30日。由2名研究者按照纳入与排除标准独立进行文献筛选、文章质量评价并数据进行提取。采用Stata14.0软件对文献进行Meta分析。结果共纳入11篇文献,Meta分析显示,纳入研究的异质性较大(I^(2)=92.5%,P<0.001),基于随机效应模型得出根治性膀胱切除术后患者肾功能损害发生率为32%[95%CI(0.25,0.35),P<0.001],亚组分析显示,研究时长在5 a及其以上30%[95%CI(0.24,0.37),P<0.001]、研究地区为亚洲35%[95%CI(0.28,0.42),P<0.001]、以术后估计肾小球滤过率<45 mL/(min·1.73 m^(2))为评价肾功能损害的标准33%[95%CI(0.29,0.36),P<0.001]、队列研究39%[95%CI(0.26,0.52),P<0.001]肾功能损害发生率更高。术后发生肾功能损害的影响因素为年龄[HR=1.03,95%CI(1.02,1.04)]、高血压[HR=2.14,95%CI(1.32,3.40)]、肾积水[HR=1.89,95%CI(1.50,2.36)]、尿路感染[HR=1.35,95%CI(1.13,1.61)]和吻合口狭窄[HR=2.53,95%CI(1.77,3.61)]。结论根治性膀胱切除术后肾功能损害发生率较高,且与年龄、高血压病史、术后肾积水、尿路感染及吻合口狭窄密切相关,医护人员应加强对此类患者术后肾功能的监测,针对相关影响因素制定有效措施,以降低肾功能损害的发生率。