Effects of cerebral ischemia and postconditioning on signaling molecules PERK and GRP78 in hippocampus tissue of tree shrew during endoplasmic reticulum stress

AIM: To investigate the effects of cerebral ischemia and postconditioning on protein kinase R-like endoplasmic reticulum kinase (PERK) and glucose-regulated protein 78 (GRP78) in the hippocampus tissue of tree shrew during endoplasmic reticulum stress and the mechanism of post-conditioning protecting the brain from damage. METHODS: The focal cerebral ischemic model was duplicated by photochemical reaction in tree shrew and the postconditioning was induced by alternatively occluding and opening the carotid artery of ischemic side for 3 cycles (5 min each cycle) at 3.5 h after ischemia. The damage and ultrastructural changes of the hippocampal neurons were observed by HE staining. The expression of PERK and GRP78 at mRNA and protein levels in the hippocampal tissue at different time points after cerebral ischemia and postconditioning was determined by RT-PCR, immunohistochemistry and Western blot. RESULTS: The injuries of hippocampal neurons were aggravated with prolonged cerebral ischemia, which was most severe at 24 h after ischemia while the postconditioning alleviated these damages correspondingly. The expression of PERK at mRNA and protein levels was upregulated at 4 h, 24 h and 72 h after ischemia (P<0.05), while postconditioning downregulated the expressions of PERK at ischemia and postconditioning 4 h (IP4 h) gruop and IP24 h group (P<0.05). The expression of GRP78 at mRNA and protein levels was not changed at 4 h, 24 h and 72 h after ischemia, while postconditioning upregulated the expressions of GRP78 at IP24 h group (P<0.05). CONCLUSION: The focal thrombotic cerebral ischemia activates the endoplasmic reticulum stress in ischemic hippocampus of tree shrews, leading to the changes in mRNA and protein expression of PERK in the PERK/eIF2α signal transduction pathway. The postconditioning treatment alleviates endoplasmic reticulum stress and neuronal damages by downregulating PERK and upregulating GRP78, thereby protecting the brain from injury.     

Determination of lactate concentrations in blood plasma and peritoneal fluid in horses with colic by an Accusport analyzer

BACKGROUND: Intestinal hypoperfusion can lead to increased lactate concentrations in plasma and peritoneal fluid of horses with colic. HYPOTHESIS: The purposes of this study were to (1) evaluate the reliability of the Accusport analyzer to assess peritoneal fluid lactate (PFL) concentrations in healthy horses and those with colic, (2) identify clinical features associated with abnormal blood plasma lactate (BPL) and PFL concentrations, and (3) evaluate the prognostic value of BPL and PFL. ANIMALS: BPL and PFL were determined in 20 healthy horses and in 106 horses with colic. RESULTS: The Accusport was reliable for determining BPL concentrations < 13 mM and PFL concentrations < 20 mM. Multivariate analysis indicated that PCV and the need for intestinal resection were independently associated with the BPL; pulse, PCV, venous pO2, the presence of necrotic intestine, an increased amount of peritoneal fluid, and fluid total protein content were independently associated with PFL. With a 1 mM increase in BPL or PFL, the respective odds ratios for required abdominal surgery increase to 1.23 (BPL) and 1.58 (PFL), odds ratios for a required intestinal resection increase to 1.20 (BPL) and 1.41 (PFL), and odds ratios for developing ileus increase by 1.33 (BPL) and 1.36 (PFL). PFL concentrations of 1, 6, 12, and 16 mM correspond to a probability of death of 11, 29, 63, and 82%, respectively, in horses without strangulating obstruction and of 25, 52, 82, and 92%, respectively, in horses with strangulating obstruction. CONCLUSION: PFL is more useful and sensitive than BPL for prognostic purposes in horses with colic.     

缺血预处理对兔脊髓缺血再灌注损伤的保护作用

目的：观察缺血处理对脊髓缺血再灌注损伤的影响。方法：夹闭左肾动脉起点以下腹主脉３５ｍｉｎ，制作脊髓缺血损伤模型。在制作上述模型前预处理组动物夹闭腹主动脉５ｍｉｎ，松夹１０ｍｉｎ，松夹１０ｍｉｎ，反复３次进行缺血预处理，术后进行神经功能评分和观察组织病理学变化。结果：与对照组相比，预处理组神经功能恢复评玢明显增加（术后２４ｈ，ｐ０．０１；４８ｈ，ｐ〈０．０５），组织病理学变化明显减轻或消失。结论：缺     

ZFP580, a novel transcription factor,is involved in cardioprotection of hypoxic preconditioning against hypoxia-reoxygenation injury in myocardial cells

AIM：To elucidate whether ZFP580 is involved in the cardioprotective effects of hypoxic preconditioning (HPC) against hypoxia-reoxygenation (H/R) injury in H9c2 myocardial cells. METHODS：Rat heart-derived H9c2 cells were cultured in DMEM. H/R was induced by incubation under ischemic hypoxia for 3 h and reoxygenation for 2 h. HPC was induced by exposing the H9c2 cells to 10 min of hypoxia and 20 min of reoxygenation for 3 cycles before H/R treatment. MTT staining and LDH leakage detection were used to evaluate the effects of HPC. Western blotting was used to detect the protein levels of ZFP580, phosphorylated ERK1/2 and cleaved caspased-3. The effects of ZFP580 overexpre-ssion or knockdown on H/R induced apoptosis were determined. RESULTS：The results of MTT staining and LDH leakage detection showed evidence of HPC cytoprotection against H/R-induced cell death in H9c2 cells. ZFP580 protein level and ERK1/2 phosphorylation were significantly increased in the HPC group compared with control group and H/R group. PD98059, an inhibitor of ERK1/2 phosphorylation, significantly suppressed the HPC-induced up-regulation of ZFP580 protein expression. ZFP580 overexpression significantly inhibited apoptosis and caspase-3 activation in H9c2 cells. CONCLUSION：HPC exhibits cytoprotection against H/R and leads to high level of ZFP580 protein in H9c2 cells. ZFP580 is regulated by ERK1/2 activation and mediates the anti-apoptotic effect of the ERK1/2 signaling pathway in HPC cytoprotection.     

三维弹性力学问题中有限元方程的预处理方法

针对三维弹性问题中有限元方程的数值求解，建立了一类简单且实用的代数多重网格预处理共轭梯度法(AMG-CG法)，详细描述了相应代数多重网格方法的粗化技术及网格转移算子的构造．由于该预处理方法能有效地降低刚度矩阵的条件数，使刚度矩阵的谱分布更集中，从而大大提高了计算效率．数值结果表明，AMGCG法对求解三维弹性问题有限元方程是十分有效和健壮的。     

Ischemic preconditioning protects against hepatic ischemia-reperfusion injury by attenuating leukotriene C4 production

AIM：To investigate the effect of ischemic preconditioning (IP) on leukotriene C4 (LTC4) generation during hepatic ischemia-reperfusion(I/R) injury.METHODS：Adult male Sprague-Dawley rats were randomly divided into sham (control) group, I/R group and IP+I/R group. The rat liver was subject to 60 min of partial hepatic ischemia followed by 5 h of reperfusion. LTC4 content was measured by reversed-phase high-performance liquid chromatography (RP-HPLC). The activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was determined, and the changes of histological structures were observed to assess the tissue injury. The reduced glutathione (GSH) level in the liver tissues was also examined by biochemical methods.RESULTS：IP markedly decreased LTC4 content in rat livers compared with I/R group. The activity of serum ALT and AST in I/R group and IP+I/R group was higher than that in control group. Compared with I/R group, the levels of serum ALT and AST were markedly decreased, and the level of GSH in hepatic tissues was elevated in IP+I/R group. In addition, the structural damage of the rat liver tissues in IP+I/R group displayed slighter than that in I/R group.CONCLUSION：IP treatment reduces LTC4 production accompanied with improving the liver function and histological structure during I/R injury, suggesting that the beneficial effects of IP may be involved in its repressing LTC4 generation during hepatic I/R injury.     

The influence of experimental acidification on needle litter decomposition in a Picea abies L. forest

The effect on litter decomposition rates was studied after annual additions for four years to the forest floor of sulfuric acid (64 kg S.ha^?1), sulfur powder (64 kg S.ha^?1), and in the first year limestone (dolomite) powder (412 kg Ca+230 kg Mg.ha^?1). The litter was Norway spruce needles which were incubated in the field in litter‐bags. Drastic reductions in decomposition rates were observed and the addition of diluted acid caused a rate reduction to 66% of that in control and the additions of sulfur powder a reduction to 80%. The effect of the sulfur powder on litter mass‐loss rate appeared to be delayed and could not be noted until one year after the first addition. No effect could be seen of the limestone powder.     

Cardiac protective effect of granulocyte colony-stimulating factor combined with ischemic postconditioning on acute myocardial infarction in rabbits

AIM: To investigate the protective effect of granulocyte colony-stimulating factor (G-CSF) combined with ischemic postconditioning (IP) on acute myocardial infarction (AMI). METHODS: Male New Zealand rabbits were randomly divided into 4 groups (n=15) after 30 min of left ventricular artery (LVA) occlusion: the rabbits in ischemia-reperfusion (IR) group were directly given reperfusion|the rabbits in G-CSF group were subsequently treated with G-CSF (10 μg·kg^-1·d^-1) by subcutaneous injection after direct reperfusion|the rabbits in IP group received 4 episodes of 30 s reperfusion and 30 s occlusion before total reperfusion|the rabbits in IP combined with G-CSF (IP+G-CSF) group were treated with both IP and G-CSF. Electrocardiogram (ECG) monitoring was performed during the operation. Blood was drawn to evaluate white blood cell count (WBC) and cardiac troponin I (cTnI) before operation and 7 d later. Ultrasound cardiography was performed to evaluate left ventricular remodeling and functions 4 weeks after operation. The sizes of infarcted myocardium were determined by triphenyltetrazolium chloride (TTC) staining. Apoptosis of cardiomyocytes was measured by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) staining. RESULTS: ST-segment resolutions were significantly decreased in IP group and IP+G-CSF group compared with direct reperfusion groups (P<0.05). WBC significantly increased in the groups treated with G-CSF for 1 week. The values of cTnI after operation were significantly lowered in G-CSF group, IP group and IP+G-CSF group as compared with IR group (P<0.05). Left ventricular ejection fraction, the size of infarcted myocardium and apoptosis of cardiomyocytes were better in IP group, G-CSF group and IP+G-CSF group than those in IR group. CONCLUSION: G-CSF combined with IP is a promising strategy against cardiac reperfusion injury and accelerates cardiac repair in AMI.