COMPARISON OF HEPATIC ULTRASONOGRAHIC CHANGES WITH ENZYMATIC HISTOCHEMICAL CHANGES IN OBSTRUCTION OF BILE DUCT

ＣＯＭＰＡＲＩＳＯＮＯＦＨＥＰＡＴＩＣＵＬＴＲＡＳＯＮＯＧＲＡＨＩＣＣＨＡＮＧＥＳＷＩＴＨＥＮＺＹＭＡＴＩＣＨＩＳＴＯＣＨＥＭＩＣＡＬＣＨＡＮＧＥＳＩＮＯＢＳＴＲＵＣＴＩＯＮＯＦＢＩＬＥＤＵＣＴＣＯＭＰＡＲＩＳＯＮＯＦＨＥＰＡＴＩＣＵＬＴＲＡＳＯＮＯ...     

中国伞滑刃线虫属─新纪录（真滑刃目：寄生滑刃科）

中国伞滑刃线虫属─新纪录（真滑刃目：寄生滑刃科）ＴＨＥＮＥＷＲＥＣＯＲＤＯＦＢＵＲＳＡＰＨＥＬＥＮＣＨＵＳＦＲＯＭＣＨＩＮＡ（ＡＰＨＥＬＥＮＣＨＩＤＡ：ＰＡＲＡＳＩＴＡＰＨＥＬＥＮＣＨＩＤＡＥ）￥ＹＩＮＧａｎ－ｌｉｕ;ＦＡＮＧＹｕ－ｓｈｅｎｇ（Ｄｅｐ...     

TWO NEW SPECIES FROM TRICHOSANTHES（CUCURBITACEAE）

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中国果瓣螺属─新纪录（肺螺亚纲：基眼目：耳螺科）ＡＮＥＷＲＥＣＯＲＤＯＦＣＡＲＹＣＨＩＵＭＦＲＯＭＣＨＩＮＡ（ＰＵＬＭＯＮＡＴＡ：ＢＡＳＯＭＭＡＴＯＰＨＯＲＡ：ＥＬＬＯＢＩＩＤＡＥ）￥ＣＨＥＮＤｅ－ｎｉｕ（ＩｎｓｔｉｔｕｔｅｏｆＺｏｏｌｏｇｙ,Ａｃａ...     

多叶猴耳环──猴耳环属一新种

多叶猴耳环──猴耳环属一新种文和群（广西植物研究所分类研究室,桂林５４１００６）ＰＩＴＨＥＣＥＬＬＯＢＩＵＭＭＵＬＴＩＦＯＬＩＯＬＡＴＵＭ－ＡＮＥＷＳＰＥＣＩＥＳＯＦＰＩＴＨＥＣＥＬＬＯＢＩＵＭＦＲＯＭＧＵＡＮＧＸＩ,ＣＨＩＮＡＷｅｎＨｅｑｕｎ（Ｇｕ...     

拟南芥：植物分子生物学研究的模式物种

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青海棘豆属三新种

青海棘豆属三新种吴玉虎（中国科学院西北高原生物研究所，西宁８１０００１）ＴＨＲＥＥＮＥＷＳＰＥＣＩＥＳＯＦＴＨＥＧＥＮＵＳＯＸＹＴＲＯＰＩＳＦＲＯＭＱＩＮＧＨＡＩＷｕＹｕｈｕ（ＮｏｒｔｈｗｅｓｔＰｌａｔｅａｕＩｎｓｔｉｔｕｔｅｏｆＢｉｏｌｏｇｙ，Ｃｈ...     

鱖属鱼类一新亚种（鲤科：雅罗鱼亚科）

鱖属鱼类一新亚种（鲤科：雅罗鱼亚科）罗云林（中国科学院水生生物研究所,武汉４３００７２）关键词新亚种,属ＡＮＥＷＳＵＢＳＰＥＣＩＥＳＯＦＦＩＳＨＥＳＯＦＰＨＯＸＩＮＵＳ（ＣＹＰＲＩＮＩＤＡＥ：ＬＥＵＣＩＳＣＩＮＡＥ）￥ＬｕｏＹｕｎｌｉｎ（Ｉｎｓｔｉｔ...     

GENUS ANTROPHYUM KAULF.FROM CHINA AND NEIGHBORING REGIONS

ＧＥＮＵＳＡＮＴＲＯＰＨＹＵＭＫＡＵＬＦ．ＦＲＯＭＣＨＩＮＡＡＮＤＮＥＩＧＨＢＯＲＩＮＧＲＥＧＩＯＮＳＸ．Ｃ．ＺＨＡＮＧ（Ｔｈｅｈｅｒｂａｒｉｕｍ（ＰＥ）,ＩｎｓｔｉｔｕｔｅｏｆＢｏｔａｎｙ,ＣｈｉｎｅｓｅＡｃａｄｅｍｙｏｆＳｃｉｅｎｃｅｓ,Ｂｅｉ...     

国产多榔菊属两新种

国产多榔菊属两新种陈艺林（中国科学院植物研究所北京１０００９３）ＴＷＯＮＥＷＳＰＥＣＩＥＳＯＦＤＯＲＯＮＩＣＵＭＬＩＮＮ．（ＣＯＭＰＯＳＩＴＡＥ）ＦＲＯＭＣＨＩＮＡＣＨＥＮＹｉＬｉｎｇ（ＩｎｓｔｉｔｕｔｅｏｆＢｏｔａｎｙ,ｔｈｅＣｈｉｎｅｓｅＡｃ...     

大鼠脑血管痉挛时NO和ET—1变化及尼莫地平的影响

目的探讨蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)时脑组织一氧化氮(NO)和内皮素-1(ET-1)含量变化及尼莫地平(ND)对其影响。方法将135只Wistar大鼠随机均分为SAH组、ND处理组和假手术组,观察手术前后基底动脉管径,及24h内局部脑血流量(rCBF)、脑组织NO和ET-1含量动态改变,并行海马病理检查。结果SAH后rCBF明显而持续降低,基底动脉管径显著缩小;海马CAl区锥体细胞严重受损;脑组织NO和ET-1含量均在SAH后1～24h显著增加(P＜0．05～0．01)。ND处理后使上述异常变化均减轻。结论SAH后脑组织NO、ET-1增多可能参与了CVS所致脑损害过程,ND通过减轻CVS和拮抗脑组织NO及ET-1的病理性改变而发挥脑保护作用。     

Effect of ischemic preconditioning on cerebral blood flow after subsequent lethal ischemia in gerbils

Ischemic tolerance, the phenomenon where a sublethal ischemic preconditioning protects the brain against a subsequent lethal ischemia, has been widely studied. Studies have been done on cerebral blood flow levels prior to the lethal ischemia, but the hemodynamic pattern after global ischemia with ischemic preconditioning has not been reported. Sequential changes in regional cerebral blood flow (rCBF) in gerbil hippocampus after 5 min global ischemia with or without 2 min ischemic preconditioning were studied to determine if ischemic preconditioning affects rCBF. Four different treatments were given: (1) sham-operated, (2) 2 min ischemia, (3) non-preconditioned, and (4) preconditioned. Groups (1) and (2) (both groups n = 5) were given a 24-h recovery period and the rCBF was measured for baseline values. 24 h after sham-operation (3) and 2 min ischemia (4), gerbils were subjected to 5 min ischemia followed by 1 h, 6 h, 1-day or 7-day reperfusion periods (all groups n = 5). Although no regional difference was observed in the recovery pattern of rCBF, the values of rCBF were significantly higher in the preconditioned group throughout whole brain regions including hippocampus. These results indicate that ischemic preconditioning facilitated the recovery of rCBF after 5 min global ischemia. It needs further study to determine whether the protecting effects of preconditioning relate to the early recovery of rCBF or not. However, our results could be interpreted that the early recovery of rCBF may lead to benefits for cell survival in the CA1 neuron, probably facilitating other protecting mechanisms.     

Intervention effect of total flavonoids of ilex pubesceus on tolerant rat models under cerebral anoxia

Objective: To observe the intervention effect of total flavonoid of ilex pubesceus on animal models of cerebral ischemic tolerance. Methods: A rat model of global-focal cerebral ischemic tolerance was established by blocking bilateral common carotid artery blood flow and occluding left middle cerebral artery using thread-occlusion method. After the first operation, the Ginaton group and large-dosage, medium-dosage and small-dosage groups of total flavonoid of ilex pubesceus were given intragastric administration of corresponding drugs. The sham-operated group, pretreatment model group and ischemia-reperfusion group were given intragastric administration of the same volume of normal saline, 1 time a day, and administrated for 4d. At 24 h after the second operation, the neurological deficit was assessed, the whole blood viscosity, plasma viscosity, iNOS activity as well as NO level, IL-1β content and TNF-α content in the brain tissue of the rats were determined, and the morphological changes of brain tissue of the rats were observed by HE staining. Results: All the rat models of cerebral ischemic tolerance were established successfully. The total flavonoid of ilex pubesceus can obviously or significantly reduce the neurological deficit score, whole blood viscosity and plasma viscosity, obviously or significantly increase the NO level in the brain tissue of the rats, and significantly reduce the pathological damage of brain tissue of the rats. But compared with the ischemia-reperfusion group, the total flavonoid of ilex pubesceus can significantly or obviously increase the iNOS activity, IL-1β content and TNF-α content in the brain tissue of the rats.     

诱发电位评价脑组织血流量的实验研究

目的：观察实验性大鼠脑损伤后不同时相点大脑皮层体感诱发电位（sensorysomaticevoked potentials,ssep)和局部血流量（regional cerebral blood flow,rCBF)的变化。方法：用流体冲击装置制作中度脑损伤模型SYD4200型神经诱发电位诊断系统监测皮层体感诱发电位,氢清除测定大脑局部血流量。结果：中度脑损伤后rCBF明显低于伤前和正常对照组;大脑皮层体感诱发电位的潜伏期明显延长。结论：SEP的变化与脑血流量有着一定的关系,一定程度上SEP的变化可反映脑损伤后血流量的变化。     

Melatonin Ameliorates Cerebral Vasospasm After Experimental Subarachnoidal Haemorrhage Correcting Imbalance of Nitric Oxide Levels in Rats

In the present study, we investigated the in vivo effects of melatonin on SAH-induced cerebral vasospasm and oxidative stress, resulting from SAH in an experimental rat model. Twenty-eight rats (225–250 g) were divided into four groups equally: group 1; control, group 2; SAH, group 3; SAH plus placebo, and group 4; SAH plus melatonin. We used double haemorrhage method for SAH groups. Beginning 6 h after SAH, 20 mg/kg melatonin or equal volume of 0.9% saline was administered intraperitoneally twice daily for 5 days to groups 3 and 4, respectively. Melatonin or 0.9% saline injections were continued up to fifth day after SAH and rats were sacrificed at the end of this period. Brain sections at the level of the pons were examined by light microscopy. The lumen diameter and the vessel wall thickness of basilar artery were measured using a micrometer. The serum levels of cerebral vasodilator nitric oxide (NO), the brain levels of an intrinsic antioxidant superoxide dismutase (SOD) and a NO regulator arginase activities were measured. The brain levels of inducible nitric oxide (iNOS) and nitrotyrosine, a nitrosative stress parameter immunohistochemiacally determined. In conclusion, melatonin administration ameliorated cerebral vasospasm by increasing serum NO level and decreasing the brain the levels of arginase and oxidative stress. It is therefore possible that increased brain arginase activity after SAH may also have a significant role in the pathogenesis of vasospasm by limiting the availability of arginine for NO production.     

Hyperbaric Oxygen Reduces Cerebral Blood Flow by Inactivating Nitric Oxide

Based on recent evidence that nitric oxide (NO(.)) is involved in hyperoxic vasoconstriction, we tested the hypothesis that decreases in NO(.) availability in brain tissue during hyperbaric oxygen (HBO(2)) exposure contribute to decreases in regional cerebral blood flow (rCBF). rCBF was measured in rats exposed to HBO(2) at 5 atmospheres (ATA) and correlated with interstitial brain levels of NO(.) metabolites (NO(X)) and production of hydroxyl radical ((.)OH). Changes in rCBF were also correlated with the effects of NO(.) synthase inhibitor (l-NAME), NO(.) donor PAPANONOate, and intravascular superoxide dismutase (MnSOD) during HBO(2). After 30 min of O(2) exposure at 5 ATA, rCBF had decreased in the substantia nigra, caudate putamen, hippocampus, and parietal cortex by 23 to 37%. These reductions in rCBF were not augmented by exposure to HBO(2) in animals pre-treated with l-NAME. After 30 min at 5 ATA, brain NO(X) levels had decreased by 31 +/- 9% and correlated with the decrease in rCBF, while estimated (.)OH production increased by 56 +/- 8%. The decrease in rCBF at 5 ATA was completely abolished by MnSOD administration into the circulation before HBO(2) exposure. Doses of NO(.) donor that significantly increased rCBF in animals breathing air had no effect at 5 ATA of HBO(2). These results indicate that decreases in rCBF with HBO(2) are associated with a decrease in effective NO(.) concentration and an increase in ROS production in the brain. The data support the hypothesis that inactivation of NO(.) antagonizes basal relaxation of cerebral vessels during HBO(2) exposure, although an effect of HBO(2) on NO(.) synthesis has not been excluded.     

Nitric oxide and cerebral ischemic preconditioning

Nitric oxide (NO) is an important mediator of cerebral blood flow and metabolism. As a vasodilator, NO regulates cerebral blood flow, and couples regional brain perfusion with metabolic activity. Following cerebral ischemia, NO levels rise significantly due to activation of neuronal nitric oxide synthase by NMDA receptor mediated calcium entry. Depending on its tissue and enzymatic source, NO may be protective or toxic. This article reviews the effects of NO following cerebral ischemia, the signaling pathways through which NO acts, and its potential roles in cerebral ischemic preconditioning.     

Experimental Subarachnoid Hemorrhage in Rats: Comparison of Two Endovascular Perforation Techniques with Respect to Success Rate,Confounding Pathologies and Early Hippocampal Tissue Lesion Pattern

Recently aside from the “classic” endovascular monofilament perforation technique to induce experimental subarachnoid hemorrhage (SAH) a modification using a tungsten wire advanced through a guide tube has been described. We aim to assess both techniques for their success rate (induction of SAH without confounding pathologies) as primary endpoint. Further, the early tissue lesion pattern as evidence for early brain injury will be analyzed as secondary endpoint. Sprague Dawley rats (n=39) were randomly assigned to receive either Sham surgery (n=4), SAH using the “classic” technique (n=18) or using a modified technique (n=17). Course of intracranial pressure (ICP) and regional cerebral blood flow (rCBF) was analyzed; subsequent pathologies were documented either 6 or 24 h after SAH. Hippocampal tissue samples were analyzed via immunohistochemistry and western blotting. SAH-induction, regardless of confounding pathologies, was independent from type of technique (p=0.679). There was no significant difference concerning case fatality rate (classic: 40%; modified: 20%; p=0.213). Successful induction of SAH without collateral ICH or SDH was possible in 40% with the classic and in 86.7% with the modified technique (p=0.008). Peak ICP levels differed significantly between the two groups (classic: 94 +/- 23 mmHg; modified: 68 +/- 19 mmHg; p=0.003). Evidence of early cellular stress response and activation of apoptotic pathways 6 h after SAH was demonstrated. The extent of stress response is not dependent on type of technique. Both tested techniques successfully produce SAH including activation of an early stress response and apoptotic pathways in the hippocampal tissue. However, the induction of SAH with less confounding pathologies was more frequently achieved with the modified tungsten wire technique.     

Effects of interrupted and uninterrupted occlusion of the basilar artery on cerebral blood flow, and on neurological and histological outcome in rats with subarachnoid hemorrhage.

Most neurosurgeons consider temporary vessel occlusion for aneurysmal clipping an effective technique that facilitates dissection between the aneurysm and the parent vessel. It is generally believed that repeated short periods of cerebral ischemia are safer for the brain than a single long episode. The aim of this study was to identify whether interrupted and uninterrupted vessel occlusion differs with regard to changes in brain tissue and cerebral hemodynamics after subarachnoid hemorrhage (SAH). Fifty Spraque Dawley rats (300-350 g) were placed under general anaesthesia and ventilated. The basilar artery was exposed through a transclival approach. Baseline local cerebral blood flow (LCBF) values was measured, and then the basilar artery was punctured, causing subarachnoid hemorrhage (SAH). Group I (n = 24) was subjected to 60 min of interrupted basilar artery occlusion, defined as 5 min of reperfusion after every 10 min of occlusion, group II (n = 26) 60 min of uninterrupted artery occlusion. Three days after completion of the experiment, each rat was neurologically evaluated and decapitated. Coronal brain slices were obtained and stained to assess infarct volume. Immediately after SAH, LCBF fell by 58% in group I, and by 52% in group II. In group I, each ischemic insult brought a similar reduction in LCBF, and after each release of the occlusion there was a rapid rise in flow. In group II, the LCBF values dropped initially and remained at low levels until the end of the study. The 2,3,5 triphenyltetrazolium chloride stained sections showed similar volumes of brainstem infarction in both groups (38.3 +/- 9.2 mm3 vs. 34.3 +/- 8.7 mm3, respectively; p > 0.05). The results suggest that there is no neuroprotective advantage to either interrupted or uninterrupted temporary blockage of blood flow during neurovascular procedures after SAH in the basilar artery region.     

20-HETE contributes to the acute fall in cerebral blood flow after subarachnoid hemorrhage in the rat

This study examined the effects of blocking the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) on the acute fall in cerebral blood flow after subarachnoid hemorrhage (SAH) in the rat. In vehicle-treated rats, regional cerebral blood flow (rCBF) measured with laser-Doppler flowmetry fell by 30% 10 min after the injection of 0.3 ml of arterial blood into the cisterna magna, and it remained at this level for 2 h. Pretreatment with inhibitors of the formation of 20-HETE, 17-octadecynoic acid (17-ODYA; 1.5 nmol intrathecally) and N-hydroxy-N'-(4-butyl-2-methylphenyl)formamidine (HET0016; 10 mg/kg iv), reduced the initial fall in rCBF by 40%, and rCBF fully recovered 1 h after induction of SAH. The concentration of 20-HETE in the cerebrospinal fluid rose from 12 +/- 2 to 199 +/- 17 ng/ml after SAH in vehicle-treated rats. 20-HETE levels averaged only 15 +/- 11 and 39 +/- 13 ng/ml in rats pretreated with 17-ODYA or HET0016, respectively. HET0016 selectively inhibited the formation of 20-HETE in rat renal microsomes with an IC(50) of <15 nM and human recombinant CYP4A11, CYP4F2, and CYP4F3 enzymes with an IC(50) of 42, 125, and 100 nM, respectively. These results indicate that 20-HETE contributes to the acute fall in rCBF after SAH in rats.