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| 1 | 老年人缺血性肠病诊治中国专家建议(2011)显示文摘缺血性肠病分为急性肠系膜缺血 ( acute mesenteric ischemia, AMI ) 、慢性肠系膜缺血(chronic mesenteric ischemia,CMI)和缺血性结肠炎(ischemic colitis,IC)。本建议拟通过介绍缺血性肠病的临床特点、诊断标准、治疗原则,为临床医师提供诊断和防治依据,本建议不包括门静脉高压所致肠系膜静脉血栓形成引起的肠缺血。 | | 2011 | 中华老年医学杂志2011，30，1： | 154 |
| 2 | Angiogenesis and neuronal remodeling after ischemic stroke显示文摘Increased microvessel density in the peri-infarct region has been reported and has been correlated with longer survival times in ischemic stroke patients and has improved outcomes in ischemic animal models.This raises the possibility that enhancement of angiogenesis is one of the strategies to facilitate functional recovery after ischemic stroke.Blood vessels and neuronal cells communicate with each other using various mediators and contribute to the pathophysiology of cerebral ischemia as a unit.In this mini-review,we discuss how angiogenesis might couple with axonal outgrowth/neurogenesis and work for functional recovery after cerebral ischemia.Angiogenesis occurs within 4 to 7 days after cerebral ischemia in the border of the ischemic core and periphery.Post-ischemic angiogenesis may contribute to neuronal remodeling in at least two ways and is thought to contribute to functional recovery.First,new blood vessels that are formed after ischemia are thought to have a role in the guidance of sprouting axons by vascular endothelial growth factor and laminin/β1-integrin signaling.Second,blood vessels are thought to enhance neurogenesis in three stages:1)Blood vessels enhance proliferation of neural stem/progenitor cells by expression of several extracellular signals,2)microvessels support the migration of neural stem/progenitor cells toward the peri-infarct region by supplying oxygen,nutrients,and soluble factors as well as serving as a scaffold for migration,and 3)oxygenation induced by angiogenesis in the ischemic core is thought to facilitate the differentiation of migrated neural stem/progenitor cells into mature neurons.Thus,the regions of angiogenesis and surrounding tissue may be coupled,representing novel treatment targets. | Masahiro Hatakeyama Itaru Ninomiya Masato Kanazawa | 2020 | Neural Regeneration Research2020，15，1： | 63 |
| 3 | Hyperbaric oxygen preconditioning induces neuroprotection against ischemia in transient not permanent middle cerebral artery occlusion rat model显示文摘This study was designed to determine if repeated hyperbaric oxygen (HBO) exposure induces ischemic tolerance in focal cerebral ischemia Methods Sixty male SD rats were used in this study Thirty animals underwent transient middle cerebral artery occlusion (MCAO) and the other thirty permanent MCAO model The rats were randomly allocated to 3 sub-groups: control group (n=10), HBO-3 group (n=10), and HBO-5 group (n=10) The animals in HBO-3 and HBO-5 groups received 1*!hour hyperbaric oxygenation at 2 5 atmosphere absolute (ATA) in 100% oxygen every day for 3 and 5 days, respectively The animals in the control group received sham treatments 24*!hours after the last HBO, transient MCAO (120 min) and permanent MCAO were induced by introducing a 3-0 nylon monofilament suture through internal carotid artery based on the Koizumi technique The neurological outcome was evaluated until 24*!hours after reperfusion in transient MCAO rats and ischemia in permanent MCAO rats The infarct volume was then assessed by TTC staining Results In transient MCAO rats, the neurological outcome in both the HBO-3 and HBO-5 groups was better than that of the control group ( P <0 05 and 0 001) The infarct volume decreased from 171 5±113*!mm 3 to 40 6±49 9*!mm 3 ( P <0 05) in the HBO-3 group and 16 2±28 8*!mm 3 ( P <0 01) in the HBO-5 group There were no significant differences in neurological outcome and infarct volume among the three groups in permanent MCAO rats Conclusions The present study demonstrated that HBO preconditioning can induce ischemic tolerance in transient not permanent MCAO rats in a “dose-dependent' | 熊利泽 朱正华 董海龙 胡文能 候立朝 陈绍洋 | 2000 | Chinese Medical Journal2000，，9： | 60 |
| 4 | 后循环缺血概念的提出及神经耳科的对策显示文摘 | 吴子明 张素珍 杨伟炎 韩东一 | 2008 | 听力学及言语疾病杂志2008，16，1： | 36 |
| 5 | Challenges in diagnosing mesenteric ischemia显示文摘Early identification of acute mesenteric ischemia (AMI) is challenging. The wide variability in clinical presentation challenges providers to make an early accurate diagnosis. Despite major diagnostic and treatment advances over the past decades, mortality remains high. Arterial embolus and superior mesenteric artery thrombosis are common causes of AMI. Non-occlusive causes are less common, but vasculitis may be important, especially in younger people. Because of the unclear clinical presentation and non-specific laboratory findings, low clinical suspicion may lead to loss of valuable time. During this diagnostic delay, progression of ischemia to transmural bowel infarction with peritonitis and septicemia may further worsen patient outcomes. Several diagnostic modalities are used to assess possible AMI. Multi-detector row computed tomographic angiography is the current gold standard. Although computed tomographic angiography leads to an accurate diagnosis in many cases, early detection is a persistent problem. Because early diagnosis is vital to commence treatment, new diagnostic strategies are needed. A non-invasive simple biochemical test would be ideal to increase clinical suspicion of AMI and would improve patient selection for radiographic evaluation. Thus, AMI could be diagnosed earlier with follow-up computed tomographic angiography or high spatial magnetic resonance imaging. Experimental in vitro and in vivo studies show promise for alpha glutathione S transferase and intestinal fatty acid binding protein as markers for AMI. Future research must confirm the clinical utility of these biochemical markers in the diagnosis of mesenteric ischemia. | Teun C van den Heijkant Bart AC Aerts Joep A Teijink Wim A Buurman Misha DP Luyer | 2013 | World Journal of Gastroenterology2013，19，9： | 31 |
| 6 | Susceptibility weighted imaging: Clinical applications and future directions显示文摘Susceptibility weighted imaging(SWI) is a recently developed magnetic resonance imaging(MRI) technique that is increasingly being used to narrow the differential diagnosis of many neurologic disorders. It exploits the magnetic susceptibility differences of various compounds including deoxygenated blood, blood products, iron and calcium, thus enabling a new source of contrast in MR. In this review, we illustrate its basic clinical applications in neuroimaging. SWI is based on a fully velocity-compensated, high-resolution, three dimensional gradientecho sequence using magnitude and phase images either separately or in combination with each other, in order to characterize brain tissue. SWI is particularly useful in the setting of trauma and acute neurologic presentations suggestive of stroke, but can also characterize occult low-flow vascular malformations, cerebral microbleeds, intracranial calcifications, neurodegenerative diseases and brain tumors. Furthermore, advanced MRI post-processing technique with quantitative susceptibility mapping, enables detailed anatomical differentiation based on quantification of brain iron from SWI raw data. | Ahmet Mesrur Halefoglu David Mark Yousem | 2018 | World Journal of Radiology2018，10，4： | 32 |
| 7 | 心理应激导致稳定性冠心病患者心肌缺血的诊断与治疗专家共识显示文摘大量证据表明,1/3以上的冠心病患者可在心理应激的状态下发生心肌缺血,该类型缺血称之为心理应激性心肌缺血( mental stress-induced myocardial ischemia, MSIMI)。MSIMI除影响患者生活质量外,还会导致临床预后恶化,死亡风险增加。 | | 2016 | 中华心血管病杂志2016，44，1： | 29 |
| 8 | 2020年中国急性肠系膜缺血诊断与治疗专家共识显示文摘急性肠系膜缺血(acute mesenteric ischemia, AMI)常被定义为小肠部分血液供应的突然中断,引起的局部缺血、细胞损伤和肠道病变。如果未经及时治疗,该过程将迅速进展为危及生命的肠坏死。AMI有非闭塞性(acute non-occlusive mesenteric ischemia, NOMI)和闭塞性两种类型,闭塞性肠系膜缺血又可进一步细分为肠系膜动脉栓塞(acute mesenteric artery embolism, EAMI),肠系膜动脉血栓形成(acute mesenteric arterial thrombosis, TAMI)及肠系膜静脉血栓形成(mesenteric venous thrombosis, VAMI)。该病总体发病率较低,但在全部急诊就诊患者中,其比例仍能达到0.09%~0.2% 。 | 无 金红旭 赵晓东 吕传柱 于学忠 戴晶 姜宏 | 2020 | 中华急诊医学杂志2020，29，10： | 30 |
| 9 | Biliary tract injury caused by different relative warm ischemia time in liver transplantation in rats显示文摘BACKGROUND:There is a controversy over the degree of liver and biliary injury caused by the period of secondary warm ischemia.A liver autotransplantation model was adopted because it excludes the effects of infection and immunological rejection on bile duct injury.This study was undertaken to assess biliary tract injury caused by relative warm ischemia(secondary warm ischemia time in the biliary tract)and reperfusion. METHODS:One hundred and two rats were randomly divided into 5 groups:groupⅠ(control);groupsⅡtoⅤ, relative warm ischemia times of 0 minute,30 minutes,1 hour and 2 hours.In addition to the levels of serum alkaline phosphatase,and total bilirubin,pathomorphology assessment and TUNEL assay were performed to evaluate biliary tract damage. RESULTS:Under the conditions that there were no significant differences in warm ischemia time,cold perfusion time and anhepatic phase,group comparisons showed statistically significant differences.The least injury occurred in groupⅡ(portal vein and hepatic artery reperfused simultaneously)but the most severe injury occurred in groupⅤ(biliary tract relative warm ischemia time 2 hours). CONCLUSIONS:Relative warm ischemia is one of the factors that result in bile duct injury,and the relationship between relative warm ischemia time the bile injury degree is time-dependent.Simultaneous arterial and portal reperfusion is the best choice to avoid the bile duct injury caused by relative warm ischemia. | Zhao, Hong-Feng Zhang, Guo-Wei Zhou, Jie Lin, Jian-Hua Cui, Zhong-Lin Li, Xiang-Hong | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，3： | 24 |
| 10 | Calpain system and its involvement in myocardial ischemia and reperfusion injury显示文摘Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction. | Christiane Neuhof Heinz Neuhof | 2014 | World Journal of Cardiology2014，6，7： | 23 |
| 11 | Mesenteric ischemia:Pathogenesis and challengingdiagnostic and therapeutic modalities显示文摘Mesenteric ischemia(MI) is an uncommon medical condition with high mortality rates. ΜΙ includes inadequate blood supply, inflammatory injury and eventually necrosis of the bowel wall. The disease can be divided into acute and chronic MI(CMI), with the first being subdivided into four categories. Therefore, acute MI(AMI) can occur as a result of arterial embolism, arterial thrombosis, mesenteric venous thrombosis and nonocclusive causes. Bowel damage is in proportion to the mesenteric blood flow decrease and may vary from minimum lesions, due to reversible ischemia, to transmural injury, with subsequent necrosis and perforation. CMI is associated to diffuse atherosclerotic disease in more than 95% of cases, with all major mesenteric arteries presenting stenosis or occlusion. Because of a lack of specific signs or due to its sometime quiet presentation, this condition is frequently diagnosed only at an advanced stage. Computed tomography(CT) imaging and CT angiography contribute to differential diagnosis and management of AMI. Angiography is also the criterion standard for CMI, with mesenteric duplex ultrasonography and magnetic resonance angiography also being of great importance. Therapeutic approach of MI includes both medical and surgical treatment. Surgical procedures include restoration of the blood flow with arteriotomy, endarterectomy or anterograde bypass, while resection of necrotic bowel is always implemented. The aim of this review was to evaluate the results of surgical treatment for MI and to present the recent literature in order to provide an update on the current concepts of surgical management of the disease. Mesh words selected include MI, diagnostic approach and therapeutic management. | Aikaterini Mastoraki Sotiria Mastoraki Evgenia Tziava Stavroula Touloumi Nikolaos Krinos Nikolaos Danias Andreas Lazaris Nikolaos Arkadopoulos | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，1： | 23 |
| 12 | Inhibition of FOXO3a/BIM signaling pathway contributes to the protective effect of salvianolic acid A against cerebral ischemia/reperfusion injury显示文摘Salvianolic acid A(SalA) is an effective compound extracted from traditional Chinese medicine Salvia miltiorrhiza Bunge. The Forkhead box O3a(FOXO3a) signaling pathway plays crucial roles in the modulation of ischemia-induced cell apoptosis. However, no information about the regulatory effect of SalA on FoxO3a is available. To explore the anti-cerebral ischemia effect and clarify the therapeutic mechanism of SalA, SH-SY5Y cells and Sprague–Dawley rats were applied, which were exposed to oxygen glucose deprivation/reoxygenation(OGD/R) and middle cerebral artery occlusion/reperfusion(MCAO/R) injuries, respectively. The involved pathway was identified using the specific inhibitor LY294002. Results showed that SalA concentration-dependently inhibited OGD/R injury triggered cell viability loss. SalA reduced cerebral infarction, lowered brain edema, improved neurological function, and inhibited neuron apoptosis in MCAO/R rats, which were attenuated by the treatment of phosphatidylinositol-4,5-bisphosphate 3-kinase(PI3K) specific inhibitor LY294002. SalA time-and concentration-dependently upregulated the phosphorylation levels of protein kinase B(AKT) and its downstream protein FOXO3a. Moreover, the nuclear translocation of FOXO3a was inhibited by SalA both in vivo and in vitro, which was also reversed by LY294002. The above results indicated that SalA fought against ischemia/reperfusion damage at least partially via the AKT/FOXO3a/BIM pathway. | Junke Song Wen Zhang Jinhua Wang Haiguang Yang Qimeng Zhou Haigang Wang Li Li Guanhua Du | 2019 | Acta Pharmaceutica Sinica B2019，9，3： | 20 |
| 13 | Mechanism of TLR-4/NF-κB pathway in myocardial ischemia reperfusion injury of mouse显示文摘Objective: To detect the expression of Toll-like receptor 4(TLR-4) and NF-κB and to discuss the mechanism of TLR-4/NF-κB pathway in the myocardial ischemia reperfusion injury of mouse. Methods: TLR-4 mutant mice and wild homozygous mice were divided into the model group and sham group. Mice in the model group were given the ligation of left anterior descending coronary artery for the modeling, while mice in the sham group were not given the ligation after threading. The cardiac muscle tissues were collected for the morphological observation. The immuno histochemistry was employed to detect the expression of NF-κB, Western blot was used to detect the expression of TLR-4 and ELISA to detect the expression of serum inflammatory factors. Results: The expression of NF-κB in TLR-4 null mice after the myocardial ischemia reperfusion was significantly lower than that in wild homozygous mice. For the model group and sham group, the expression of TLR-4 in wild homozygous mice was all significantly higher than that in TLR-4 null mice, while the expression of TLR-4 in TLR-4 null mice in the model group was significantly higher than that in sham group, with the statistical difference(P<0.05). The expression of inflammatory factors in TLR-4 null mice and wild homozygous mice in the model group was significantly higher than that in sham group. The expression of all factors in group A with TLR-4 null was significantly lower than that in group B with wild homozygous type, with the statistical difference(P<0.05). Conclusions: TLR-4/NF-κB pathway is closely related to the myocardial ischemia reperfusion injury, which plays its role through the release of inflammatory cytokines. | Hao Chen Ruo-Qing Zhang Xiao-Gang Wei Xiao-Min Ren Xiao-Qian Gao | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，5： | 19 |
| 14 | Metabonomic phenotype and identification of “heart blood stasis obstruction pattern” and “qi and yin deficiency pattern” of myocardial ischemia rat models显示文摘The traditional Chinese medicine concepts of 'Xinxueyuzuzheng (heart blood stasis obstruction pattern)' and 'Qiyinliangxuzheng (qi and yin deficiency pattern)' for myocardial ischemia rat models were constructed in the present study. Endogenous metabolites in rat plasma were analyzed using the GC/TOF-MS-based metabonomic method. Significant metabolic differences were observed between the control and two model groups, and the three groups were distinguished clearly by pattern recognition. Compared with those of the control, the levels of hydroxyproline, threonic acid, glutamine and citric acid were strikingly up or down-regulated in model rats. The metabolites contributing most to the classification between the two 'pattern' rats were identified, such as valine, serine, threonine, ornithine, hydroxyproline, lysine, 2-hydroxybutanoic acid, 3-hydroxybutanoic acid, galactofuranose and inositol. These compounds were indicated as the potential biomarkers. The results suggested that the two 'patterns' are involved in dysfunction in oxidative stress, energy metabolism and amino acid metabolism. These findings also provided the substantial foundation for exploring the scientific connotation of these two 'Zhengxing (pattern types)' of myocardial ischemia, and 'Bianzheng (pattern identification)'. | YAN Bei1, A JiYe1, HAO HaiPing1, WANG GuangJi1, ZHU XuanXuan2, 3, ZHA WeiBin1, LIU LinSheng1, GUAN EnZe3, ZHANG Ying1, GU ShengHua1, HUANG Qing1 & ZHENG YuanTing1 1Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China 2Pharmacological Laboratory of Clinical Research Institute, Jiangsu Provincial Hospital of Traditional Chinese Medicine, Nanjing 210029, China 3College of Pharmacy, Nanjing University of Traditional Chinese Medicine, Nanjing 210029, China | 2009 | Science China(Life Sciences)2009，52，11： | 19 |
| 15 | 人重复肢体缺血对血压、心率及组织氧饱和度的影响显示文摘 | 党莎 罗玉敏 吉训明 吕国蔚 刘佑琴 钮伟真 丁海曙 | 2008 | 基础医学与临床2008，28，11： | 18 |
| 16 | Adipose tissue-derived stem cells as a therapeutic tool for cardiovascular disease显示文摘Adipose tissue-deried stem cells( ADSCs) are adult stem cells that can be easily harvested from subcutaneous adipose tissue. Many studies have demonstrated that ADSCs differentiate into vascular endothelial cells(VECs), vascular smooth muscle cells(VSMCs), and cardiomyocytes in vitro and in vivo. However, ADSCs may fuse with tissue-resident cells and obtain the corresponding characteristics of those cells. If fusion occurs, ADSCs may express markers of VECs, VSMCs, and cardiomyocytes without direct differentiation into these cell types. ADSCs also produce a variety of paracrine factors such as vascular endothelial growth factor, hepatocyte growth factor, and insulin-like growth factor-1 that have proangiogenic and/or antiapoptotic activities. Thus, ADSCs have the potential to regenerate the cardiovascular system via direct differentiation into VECs, VSMCs, and cardiomyocytes, fusion with tissueresident cells, and the production of paracrine factors. Numerous animal studies have demonstrated the efficacy of ADSC implantation in the treatment of acute myocardial infarction(AMI), ischemic cardiomyopathy(ICM), dilated cardiomyopathy, hindlimb ischemia, and stroke. Clinical studies regarding the use of autologous ADSCs for treating patients with AMI and ICM have recently been initiated. ADSC implantation has been reported as safe and effective so far. Therefore, ADSCs appear to be useful for the treatment of cardiovascular disease. However, the tumorigenic potential of ADSCs requires careful evaluation before their safe clinical application. | Etsu Suzuki Daishi Fujita Masao Takahashi Shigeyoshi Oba Hiroaki Nishimatsu | 2015 | World Journal of Cardiology2015，7，8： | 17 |
| 17 | Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury显示文摘The activation of heme oxygenase-1(HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide(CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection.In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload(with signs of a chronic hepatitis) and iron deficiency anemia(with paradoxical increased levels of ferritin).Hypoxia induces HO-1 expression in multiple rodent,bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types(endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury. | Clarice Silvia Taemi Origassa Niels Olsen Saraiva Cmara | 2013 | World Journal of Hepatology2013，5，10： | 17 |
| 18 | Neuroprotective effect of Notch pathway inhibitor DAPT against focal cerebral ischemia/reperfusion 3 hours before model establishment显示文摘As an inhibitor of the Notch signaling pathway, N-[N-(3,5-difluorohenacetyl)-l-alanyl]-S-phenylglycine tert-butyl ester(DAPT) may protect brain tissue from serious ischemic injury. This study aimed to explore neuroprotection by DAPT after cerebral ischemia/reperfusion(I/R) injury. DAPT was intraperitoneally injected 3 hours before the establishment of a focal cerebral I/R model in the right middle cerebral artery of obstructed mice. Longa scores were used to assess neurological changes of mice. Nissl staining and TdT-mediated dUTP-biotin nick-end labeling staining were used to examine neuronal damage and cell apoptosis in the right prefrontal cortex, while immunofluorescence staining was used to detect glial fibrillary acidic protein-and Notch1-positive cells. Protein expression levels of Hes1 and Hes5 were detected by western blot assay in the right prefrontal cortex. Our results demonstrated that DAPT significantly improved neurobehavioral scores and relieved neuronal morphological damage. DAPT decreased the number of glial fibrillary acidic protein-and Notch1-positive cells in the right prefrontal cortex, while also reducing the number of apoptotic cells and decreasing interleukin-6 and tumor necrosis factor-α contents, and simultaneously downregulating Hes1 and Hes5 protein expression. These findings verify that DAPT alleviates pathological lesions and strengthens the anti-inflammatory response after cerebral I/R injury. Thus, DAPT might be developed as an effective drug for the prevention of cerebral I/R injury. | Jun-Jie Wang Jun-De Zhu Xian-Hu Zhang Ting-Ting Long Guo Ge Yan Yu | 2019 | Neural Regeneration Research2019，14，3： | 17 |
| 19 | Combined bone marrow stromal cells and oxiracetam treatments ameliorates acute cerebral ischemia/reperfusion injury through TRPC6显示文摘Ischemic stroke has become one of the leading causes of deaths and disabilities all over the world.In this study,we investigated the therapeutic effects of combined bone marrow stromal cells(BMSCs)and oxiracetam treatments on acute cerebral ischemia/reperfusion(I/R)injury.A rat model of middle cerebral artery occlusion(MCAO)followed by complete reperfusion,as well as a cortex neuron oxygen-glucose deprivation(OGD)model was established.When compared with BMSCs or oxiracetam monotherapy,combination therapy significantly improved functional restoration with decreased infarct volume in observed ischemic brain.We propose that it may occur through the transient receptor potential canonical(TRPC)6 neuron survival pathway.The increased expression of TRPC6 along with the reduction of neuronal cell death in the OGD cortex neurons and combination therapy group indicated that the TRPC6 neuron survival pathway plays an important role in the combined BMSCs and oxiracetam treatments.We further tested the activity of the calpain proteolytic system,and the results suggested that oxiracetam could protect the integrity of TRPC6 neuron survival pathway by inhibiting TRPC6 degradation.The protein levels of phospho-cAMP response element binding protein(p-CREB)were tested.It was found that BMSCs play a role in the activation of the TRPC6 pathway.Our study suggests that the TRPC6 neuron survival pathway plays a significant role in the protective effect of combined BMSCs and oxiracetam treatments on acute cerebral I/R injury.Combined therapy could inhibit the abnormal degradation of TRPC6 via decreasing the activity of calpain and increasing the activation of TRPC6 neuron survival pathway. | Jing Wang Ruohan Sun Zhenzhu Li Yujun Pan | 2019 | Acta Biochimica et Biophysica Sinica2019，51，8： | 17 |
| 20 | Computed tomography findings of pneumatosis and portomesenteric venous gas in acute bowel ischemia显示文摘AIM:To use more representative sample size to evaluate whether computed tomography(CT)scan evidence of the concomitant presence of pneumatosis and portomesenteric venous gas is a predictor of transmural bowel necrosis.METHODS:Data from 208 patients who were referred for a diagnosis of bowel ischemia were retrospectively reviewed.Only patients who underwent a surgical intervention following a diagnosis of bowel ischemia who also had a post-operative histological confirmation of such a diagnosis were included.Patients were split into two groups according to the presence of histological evidence of transmural bowel ischemia(case group)or partial bowel ischemia(control group).CT images were reviewed for findings of ischemia,including mural thickening,pneumatosis,bowel distension,portomesenteric venous gas and arterial or venous thrombi.RESULTS:A total of 248 subjects who underwent surgery for bowel ischemia were identified.Among the208 subjects enrolled in our study,transmural bowel necrosis was identified in 121 subjects(case group),and partial bowel necrosis was identified in 87 subjects(control group).Based on CT findings,including mural thickening,bowel distension,pneumatosis,pneumatosis plus portomesenteric venous gas and presence of thrombi or emboli,there were no significant differences between the case and control groups.The concomitant presence of pneumatosis and porto-mesenteric venous gas showed an odds ratio of 1.95(95%CI:0.491-7.775,P=0.342)for the presence of transmural necrosis.The presence of pneumatosis plus porto-mesenteric venous gas exhibited good specificity(83%)but low sensitivity(17%)in the identification of transmural bowel infarction.Accordingly,the positive and negative predictive values were 60% and 17%,respectively.CONCLUSION:Although pneumatosis plus porto-mesenteric venous gas is associated with bowel ischemia,we have demonstrated that their co-occurrence cannot be used as diagnostic signs of transmural necrosis. | Marco Milone Matteo Nicola Dario Di Minno Mario Musella Paola Maietta Vittorio Iaccarino Giovanni Barone Francesco Milone | 2013 | World Journal of Gastroenterology2013，19，39： | 15 |
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