辅酶Q10软胶囊的急性毒性和遗传毒性研究

目的:研究辅酶Q10软胶囊的急性毒性和遗传毒性,为辅酶Q10的进一步开发利用提供安全依据。方法:应用小鼠急性经口毒性试验、Ames试验、小鼠骨髓嗜多染红细胞微核试验和小鼠精子畸形试验对某种辅酶Q10软胶囊的毒性进行试验观察。结果:该辅酶Q10软胶囊对雌雄小鼠LD50均大于10 000mg/kg.bw,属实际无毒物质;Ames试验中受试物各剂量组回变菌落数均未超过自发回变菌落数的2倍,亦无剂量-反应关系,结果为阴性;小鼠骨髓嗜多染红细胞微核试验和小鼠精子畸形试验中各剂量组微核率、精子畸形率与阴性对照组之间无显著性差异(P0.05),而环磷酰胺阳性对照组与阴性对照组之间有极显著性差异(P0.01),证明试验结果均为阴性。结论:本次试验条件下,该辅酶Q10软胶囊属实际无毒级,未显示有急性毒性和遗传毒性作用。     

The Effect of Minimally Invasive Hematoma Aspiration on the JNK Signal Transduction Pathway after Experimental Intracerebral Hemorrhage in Rats

Objective: To explore the effect of minimally invasive hematoma aspiration (MIHA) on the c-Jun NH₂-terminal kinase (JNK) signal transduction pathway after intracerebral hemorrhage (ICH). Methods: In this experiment, 300 adult male Wistar rats were randomly and averagely divided into sham-operated group, ICH group and MIHA group. In each group, 60 rats were used in the detection of indexes in this experiment, while the other 40 rats were used to replace rats which reached the exclusion criteria (accidental death or operation failure). In ICH group and MIHA group, ICH was induced by injection of 70 µL of autologous arterial blood into rat brain, while only the rats in MIHA group were treated by MIHA 6 h after ICH. Rats in sham-operated group were injected nothing into brains, and they were not treated either, like rats in ICH group. In each group, six rats were randomly selected to observe their Bederson’s scales persistently (6, 24, 48, 72, 96, 120 h after ICH). According to the time they were sacrificed, the remaining rats in each group were divided into 3 subgroups (24, 72, 120 h). The change of brain water content (BWC) was measured by the wet weight to dry weight ratio method. The morphology of neurons in cortex was observed by the hematoxylin–eosin (HE) staining. The expressions of phospho-c-Jun NH₂-terminal kinase (pJNK) and JNK in peri-hematomal brain tissue were determined by the immunohistochemistry (IHC) and Western blotting (WB). Results: At all time points, compared with the ICH groups, the expression of pJNK decreased obviously in MIHA groups (p < 0.05), while their Bederson’s scales and BWC declined, and neuron injury in the cortex was relieved. The expression level of JNK was not altered at different groups. The data obtained by IHC and WB indicated a high-level of consistency, which provided a certain dependability of the test results. Conclusion: The JNK signal transduction pathway could be activated after intracerebral hemorrhage, with the expressions of pJNK increasing. MIHA could relieve the histo-pathological damage of nerve cells, reducing brain edema and neurological deficits, and these neuroprotective effects might be associated with suppression of JNK signal transduction pathway.     

脑出血后肺组织炎症损伤情况的研究

目的研究脑出血后肺组织炎症损伤的发病机制。方法用病理学常规HE染色法观察脑出血组和对照组肺标本的出血、渗出和炎症细胞浸润改变情况,在光镜下对白细胞、巨噬细胞进行记数。结果与对照组比较,脑出血组肺组织存在明显渗出、出血及大量白细胞、巨噬细胞浸润,炎症细胞记数有显著意义P<0.05。结论脑出血可以通过引发炎症反应导致急性肺损伤;炎症反应在3~5d时最明显。     

早期CT环池形态变化与急性颅脑损伤病人预后关系的研究

目的前瞻性研究急性颅脑损伤患者早期CT扫描征象的环池形态和中脑变形程度与病人预后的关系,以指导临床的治疗。方法对132例病人早期CT扫描,在中脑水平准确测量环池宽度,分6个组记录数据。同时观测中脑有无变形及测量其前后径与横径之比。治疗后按GOS标准,随访3个月,评定疗效。结果通过比较,环池宽度>1mm者有较佳的预后;中脑无变形及前后径与横径之比为0.9∶1.1者的预后较佳。结论研究得出,环池形态、中脑受压变形能作为急性颅脑损伤患者预后判断的指标,并为临床医师治疗方案提供重要依据。     

ERK介导的AQP4对脑出血后早期脑水肿的影响

目的探讨大鼠实验性脑出血后细胞外信号调节激酶（ERK）介导的水通道蛋白4（AQP4）的不同表达对早期脑水肿的影响。方法72只健康雄性大鼠随机分为出血组、PD98029组、截体溶液对照组和假手术组,每组各18只。采用大鼠缓慢注射自体血出血模型,测定脑组织含水量及伊文斯蓝含量,并采用免疫组织化学、Western blot检测AQP4的表达,测定预先经尾静脉给予PD98059后的丝裂原活化蛋白激酶（MAPKs）信号通路关键蛋白酶ERK1／2磷酸化水平,同时观察PD98059对AQP4和脑水肿的影响。结果假手术组AQP4表达较低;在出血组AQP4表达升高,脑组织含水量及伊文斯蓝含量增加;给予PD98059后AQP4的表达和脑组织含水量降低,同时ERK1／2磷酸化水平降低。结论出血性损伤后AQP4表达上升,脑水肿明显,早期预先给予PD98059可抑制AQP4的表达,降低BBB通透性,减轻脑水肿。     

冰冻灾害及其他心理因素对脑出血发病的影响

目的探讨冰冻灾害及其他社会心理因素对脑出血患者发病的影响。方法应用自制一般情况量表、生活事件量表、社会支持量表、特质应对方式问卷、A型行为类型评定量表对60例脑出血患者及60例健康体检者进行病例对照研究。结果冰冻灾害、文化、职业、高血压病史、糖尿病病史、卒中家族史、正性事件刺激量、负性事件刺激量、事件刺激总量、主观支持、对支持的利用度、消极应对、积极应对,脑出血患者与健康体检者比较差异有统计学意义（P〈0.05或P〈0.01）。多元逐步Logistic回归分析发现：冰冻灾害、高血压病史、负性事件刺激量与脑出血呈正相关（P〈0.05或P〈0.01）,主观支持与脑出血呈负相关（P〈0.05）。结论冰冻灾害作为社会环境因素对脑出血患者发病有明显影响。     

Neuroelectric Mechanisms of Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

Delayed cerebral ischemia (DCI) remains a challenging but very important condition, because DCI is preventable and treatable for improving functional outcomes after aneurysmal subarachnoid hemorrhage (SAH). The pathologies underlying DCI are multifactorial. Classical approaches to DCI focus exclusively on preventing and treating the reduction of blood flow supply. However, recently, glutamate-mediated neuroelectric disruptions, such as excitotoxicity, cortical spreading depolarization and seizures, and epileptiform discharges, have been reported to occur in high frequencies in association with DCI development after SAH. Each of the neuroelectric disruptions can trigger the other, which augments metabolic demand. If increased metabolic demand exceeds the impaired blood supply, the mismatch leads to relative ischemia, resulting in DCI. The neuroelectric disruption also induces inverted vasoconstrictive neurovascular coupling in compromised brain tissues after SAH, causing DCI. Although glutamates and the receptors may play central roles in the development of excitotoxicity, cortical spreading ischemia and epileptic activity-related events, more studies are needed to clarify the pathophysiology and to develop novel therapeutic strategies for preventing or treating neuroelectric disruption-related DCI after SAH. This article reviews the recent advancement in research on neuroelectric disruption after SAH.     

Photo-Fenton-like treatment of BPA: Effect of UV light source and water matrix on toxicity and transformation products

UV-A (near-UV), UV-C (short-UV) and visible-light assisted Fenton-like treatment of Bisphenol A (BPA) was investigated in pure water and raw freshwater samples spiked with BPA. Treatment performances were evaluated in terms of BPA degradation, dissolved organic carbon (DOC) removal and H₂O₂ consumption rates. Complete BPA degradation accompanied with significant DOC removal was achieved for all studied processes. Increasing the initial solution pH only exhibited a negative effect on treatment efficiencies when bicarbonate alkalinity was used for pH adjustment, whereas the raw freshwater matrix and irradiation type also influenced oxidation rates appreciably. Acute toxicity analysis employing Vibrio fischeri revealed that the inhibitory effect of BPA decreased significantly during the course of Photo-Fenton-like treatment. Several transformation products could be identified via HPLC and GC–MS analyses including hydroxylated phenolic compounds (hydroquinone; 2-methoxy, 1-4-benzenediol; 4-isopropenylphenol; 4′-hydroxy-acetophenone; 1-(4-cyclohexylphenyl) ethanone; 4-isopropylenecatechol; 4-4′-dihydroxybenzophenone; 4-ethyl,1,3-benzenediol), as well as the ring opening products hexanoic acid methyl ester, fumaric, succinic and oxalic acids. A reaction pathway featuring hydroxylation, dimerization and ring opening steps is proposed.     

Effect of Ultrasonic Irradiation on the Treatment of Poly-Aromatic Substances (PAHs) from a Petrochemical Industry Wastewater

The effects of sonication time, nitrogen, N₂(g), increasing temperature, dissolved oxygen (DO) and titanium dioxide (TiO₂) concentrations on the sonodegradation of polyaromatic hydrocarbons (PAHs) in petrochemical wastewaters were investigated. Sonication alone without N₂(g), DO and TiO₂ provided 80% maximum PAH yields at 2 5°C after 150 min. This PAH yield increased to 89–95% at 60 °C after 150 min sonication. The contribution of DO, N₂(g) and TiO₂ on the PAH removal was not significant compared to the control. In the presence of HCO₃ ^?, the degradation of hydrophobic PAH dibenz[a,h]anthracene (DahA)was suppressed in the acceleration step of the sonication. Maximum acute toxicity removal was reached by 30 min N₂(g) sparging, 4 mg/L DO and by 0.1 mg/L TiO₂ after 150 min sonication.     

Adaptive disturbance rejection control for compartmental systems with application to intraoperative anesthesia influenced by hemorrhage and hemodilution effects

Compartmental system models involve dynamic states whose values are nonnegative. These models are widespread in biological and physiological sciences and play a key role in understanding these processes. In this paper, we develop a direct adaptive disturbance rejection control framework for compartmental dynamical systems with exogenous bounded disturbances. The proposed framework is Lyapunov based and guarantees partial asymptotic stability of the closed‐loop system, that is, asymptotic stability with respect to part of the closed‐loop system states associated with the plant dynamics. The remainder of the states associated with the adaptive controller gains are shown to be Lyapunov stable. In the case of bounded energy ??₂ disturbances, the proposed approach guarantees a nonexpansivity constraint on the closed‐loop input–output map between the plant disturbances and performance variables. Finally, a numerical example involving the infusion of the anesthetic drug propofol for maintaining a desired constant level of depth of anesthesia for surgery in the face of continuing hemorrhage and hemodilution is provided. Copyright © 2008 John Wiley & Sons, Ltd.