西非加蓬盆地深水区复杂盐下圈闭落实关键技术探索与实践

近年来,以西非、墨西哥湾等为代表的全球深水盐下油气勘探日趋活跃,而构造落实一直是盐下勘探面临的主要难题,亟需形成一套有效的盐下圈闭落实技术方法。以加蓬某区为研究靶区,基于盐下地震成像特点,剖析盐下圈闭落实难点,再从盐岩形变机制分析入手,探索形成了一套复杂盐下圈闭落实关键技术组合,主要包括:①基于盐岩形变机制建立构造解释模型;②以脏盐体精细识别技术为核心的盐下层位解释技术;③利用重-磁-震资料联合,开展盐下断裂多尺度综合解释;④基于波动方程正演的构造假象识别技术。通过实践应用,在研究区内有效落实多个盐下圈闭,其中的M圈闭钻探证实为盐下大气田。形成的技术体系能够辅助解决盐下构造落实难题,可为西非及其他区域类似问题提供参考。

南大西洋两岸被动陆缘盆地地质特征及其对勘探的影响

南大西洋两岸发育近20个被动陆缘盆地,虽然已在深水区获得多个油气重大发现,但对于被动陆缘盆地地质特征认识不清,导致深水区勘探程度依然很低,待发现油气资源量巨大。为此,在综合分析大量资料及案例的基础上,充分结合近年的研究成果及认识,系统地总结了南大西洋两岸中段及南段被动陆缘盆地的关键地质特征,并深入分析地质特征对油气勘探的影响。研究表明:南大西洋两岸盆地群在整个裂陷期广泛发育3种成因类型、3个活动期次的火成岩;南段火山型被动陆缘盆地广泛发育厚度较大、向海倾斜反射楔形体;中段盐岩发育型盆地群盐岩平面分布与厚度变化规律在两岸既有相似性又有差异性,且可能出现盐下砂岩储层盐胶结现象;加蓬盆地、桑托斯盆地、坎波斯盆地、下刚果盆地均发育脏盐;西非中段宽扎盆地因旋回性蒸发模式使其成为南大西洋两岸唯一一个盐岩—硬石膏—碳酸盐岩互层沉积盆地,盐间较薄碳酸盐岩层既是烃源岩又是储层。上述地质特征对盐下地震成像、盐下储层与烃源岩及盐间碳酸盐岩预测带来较大影响,增加了地震勘探的多解性。该研究可为被动陆缘盆地未来技术攻关方向的精准定位提供依据。

Sodium butyrate attenuates high-fat diet-induced steatohepatitis in mice by improving gut microbiota and gastrointestinal barrier

AIM To investigate whether gut microbiota metabolite sodium butyrate (NaB) is an effective substance for attenuating non-alcoholic fatty liver disease (NAFLD) and the internal mechanisms. METHODS Male C57BL/6J mice were divided into three groups, normal control were fed standard chow and model group were fed a high-fat diet (HFD) for 16 wk, the intervention group were fed HFD for 16 wk and treated with NaB for 8 wk. Gut microbiota from each group were detected at baseline and at 16 wk, liver histology were evaluated and gastrointestinal barrier indicator such as zonula occluden-1 (ZO-1) were detected by immunohistochemistry and realtime-PCR, further serum or liver endotoxin were determined by ELISA and inflammation-or metabolism-associated genes were quantified by real-time PCR. RESULTS NaB corrected the HFD-induced gut microbiota imbalance in mice, while it considerably elevated the abundances of the beneficial bacteria Christensenellaceae, Blautia and Lactobacillus. These bacteria can produce butyric acid in what seems like a virtuous circle. And butyrate restored HFD induced intestinal mucosa damage, increased the expression of ZO-1 in small intestine, further decreased the levels of gut endotoxin in serum and liver compared with HF group. Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention. Liver inflammation and fat accumulation were ameliorated, the levels of TG and cholesterol in liver were decreased after NaB intervention, NAS score was significantly decreased, metabolic indices such as FBG and HOMA-IR and liver function indicators ALT and AST were improved compared with HF group. CONCLUSION NaB may restore the dysbiosis of gut microbiota to attenuate steatohepatitis, which is suggested to be a potential gut microbiota modulator and therapeutic substance for NAFLD.

Sphingosine 1 phosphate receptor-1 （S1PR1） signaling protects cardiac function by inhibiting cardiomyocyte autophagy

Objective To investigate the role of sphingosine-l-phosphate （S1P） and its receptors in cardiomyocyte autophagy, cardiomyocyte hypertrophy and cardiac function. Methods Cardiomyocytes were isolated from neonatal Vista rats. Autophagy and hypertrophy of car- diomyocytes were induced via starvation culture and phenylephrine （PE）, respectively, and S 1 P was used to treat the cardiomyocytes. The effect of S1P on cardiomyocyte autophagy was evaluated by the number of autophagosomes, the expression of autophagy-related proteins and autophagic marker genes in cardiomyocytes. The effect of S1P on cardiomyocyte hypertrophy was evaluated by examining the surface area of cardiomyoeytes and the expression of hypertrophic genes. Subsequently, different small interfering RNAs （siRNAs） were used to knockdown the expression of the three types of S 1P receptors on cardiomyocytes and to analyze the type of receptor that mediates S 1P sig- naling in cardiomyocytes. Finally, sphingosine 1 phosphate receptor-1 （S1PR1） was knockout in the mouse cardiomyocytes using the Cas9 technique. The effect of S 1PR1 on cardiac autophagy and cardiac hypertrophy was examined by assessing cardiomyocyte autophagy, car- diomyocyte hypertrophy and cardiac function. Results Starvation-induced cardiomyocyte autophagy and PE -induced cardiomyocyte hy- pertrophy were significantly attenuated by SIP. The results showed that the formation of autophagosomes was decreased, the auto- phagy-associated protein LC3 II/I and the expression of autophagic marker genes Atg5, Atgl2, Beclinl and LC3B decreased after SIP treatment. The surface area of the cardiomyocytes was decreased, and the expression of hypertrophic genes, including atrial natriuretic factor （ANF）, skeletal muscle and cardiac actin （SKA）, myosin heavy chain （β-MHC） and brain natriuretic peptide （BNP） were all decreased after S 1 P treatment. The autophagy and hypertrophy of cardiomyocytes in the S 1PR 1 knocked-down group were significantly increased compared to those in the control group, the SIPR2 and the S1PR3 knocked-down groups. In vivo, the knockout of S1PR1 in cardiomyocytes exacer- bated stress-induced cardiac autophagy, cardiac hypertrophy and the impairment of cardiac function. Conclusion SIP could inhibit car- diomyocyte autophagy, thereby inhibiting cardiomyocyte hypertrophy and protecting cardiac function by activating S1PR1 in pres- sure-overloaded cardiomyocytes in mice.

Expression and function of renal and hepatic organic anion transporters in extrahepatic cholestasis

Obstructive jaundice occurs in patients suffering from cholelithiasis and from neoplasms affecting the pancreas and the common bile duct.The absorption,distribution and elimination of drugs are impaired during this pathology.Prolonged cholestasis may alter both liver and kidney function.Lactam antibiotics,diuretics,non-steroidal anti-inflammatory drugs,several antiviral drugs as well as endogenous compounds are classified as organic anions.The hepatic and renal organic anion transport pathways play a key role in the pharmacokinetics of these compounds.It has been demonstrated that acute extrahepatic cholestasis is associated with increased renal elimination of organic anions.The present work describes the molecular mechanisms involved in the regulation of the expression and function of the renal and hepatic organic anion transporters in extrahepatic cholestasis,such as multidrug resistanceassociated protein 2,organic anion transporting polypeptide 1,organic anion transporter 3,bilitranslocase,bromosulfophthalein/bilirubin binding protein,organic anion transporter 1 and sodium dependent bile salt transporter.The modulation in the expression of renal organic anion transporters constitutes a compensatory mechanism to overcome the hepatic dysfunction in the elimination of organic anions.

Alanyl-glutamine dipeptide inhibits hepatic ischemiareperfusion injury in rats

AIM： To investigate the protective effect and mechanism of alanyl-glutamine dipeptide （Ala-GIn） against hepatic ischemia-reperfusion injury in rats. METHODS： Rats were divided into group C as normal control Group （/7=16） and group G as alanyl-glutamine pretreatment 07=16）. Rats were intravenously infused with 0.9% saline solution in group C and Ala-GIn -enriched （2% glutamine） 0.9% saline solution in group G via central venous catheter for three days. Then all rats underwent hepatic warm ischemia for 30 min followed by different periods of reperfusion. Changes in biochemical parameters, the content of glutathione （GSH） and the activity of superoxide dismutase （SOD） in liver tissue, Bcl-2 and Bax protein expression and morphological changes of liver tissue were compared between both groups. RESULTS： One hour after reperfusion, the levels of liver enzymes in group G were significantly lower than those in group C （P〈0.05）. Twenty-four hours after reperfusion, the levels of liver enzymes in both groups were markedly recovered and the levels of liver enzyme in group G were also significantly lower than those in group C （P〈0.01）. One and 24 h after reperfusion, GSH content in group G was significantly higher than that in group C （P 〈0.05）. There was no statistical difference in activities of SOD between the two groups. One and 24 h after reperfusion, the positive expression rate of Bcl-2 protein was higher in group G than in group C （P〈0.05） and the positive expression rate of Bax protein was lower in group G than in group C （P〈0.05）. Histological and ultrastructural changes of liver tissue were inhibited in group C compared to group G. CONCLUSION： Our results suggest that Ala-GIn pretreatment provides the rat liver with significant tolerance to warm ischemia-reperfusion injury, which may be mediated partially by enhancing GSH content and regulating the expression of Bcl-2 and Bax proteins in the liver tissue.

Effect of implanting fibrin sealant with ropivacaine on pain after laparoscopic cholecystectomy

AIM:To investigate the safety and efficacy of implant-ing fibrin sealant with sustained-release ropivacaine in the gallbladder bed for pain after laparoscopic chole-cystectomy(LC).METHODS:Sixty patients(American Society of Anes-thesiologists physical status wasⅠorⅡand underwent LC)were randomly divided into three equal groups:group A(implantation of fibrin sealant in the gallbladder bed),group B(implantation of fibrin sealant carrying ropivacaine in the gallbladder bed),and group C(normal saline in the gallbladder bed).Postoperative pain was evaluated,and pain relief was assessed by visual analog scale(VAS)scoring.RESULTS:The findings showed that 81.7%of patients had visceral pain,50%experienced parietal,and 26.7% reported shoulder pain after LC.Visceral pain was significantly less in group B patients than in the other groups(P<0.05),and only one patient in this group experienced shoulder pain.The mean VAS score in group B patients was lower than that in the other groups.CONCLUSION:Visceral pain is prominent after LC and can be effectively controlled by implanting fibrin sealant combined with ropivacaine in the gallbladder bed.

Alverine citrate induced acute hepatitis

Alverine dtrate is a commonly used smooth muscle relaxant agent.A MEDLINE search on January 2004 revealed only 1 report implicating the hepatotoxicity of this agent.A 34- year-old woman was investigated because of the finding of elevated liver function tests on biochemical screening.Other etiologies of hepatitis were appropriately ruled out and elevated enzymes were ascribed to alverine citrate treatment. Although alverine citrate hepatotoxicity was related to an immune mechanism in the first case,several features such as absence of predictable dose-dependent toxicity of alverine citrate in a previous study and absence of hypersensitivity manifestations in our patient are suggestive of a metabolic type of idiosyncratic toxicity.

TypeⅠinositol 1, 4, 5-triphosphate receptors increase in kidney of mice with fulminant hepatic failure

AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant hepatic failure （FHF）. METHODS： FHF was induced by lipopolysaccharide （LPS） in D-galactosamine （GAIN） sensitized BALB/c mice. There were 20 mice in normal saline （NS）-treated group, 20 mice in LPS-treated group, 20 mice in GaIN- treated group, and 60 mice in GalN/LPS-treated group （FHF group）. Liver and kidney tissues were obtained at 2, 6, and 9 h after administration. The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope. The expression of IP3R I in kidney tissue was tested by immunohistochemistry, Western blot and reverse transcription （RT）-PCR. RESULTS： Kidney tissues were morphologically normal at all time points in all groups. IP3R I proteins were found localized in the plasma region of glomerular mesangial cells （GMC） and vascular smooth muscle cells （VSMC） in kidney by immunohistochemical staining. In kidney of mice with FHF at 6 h and 9 h IP3R I staining was upregulated. Results from Western blot demonstrated consistent and significant increment of IP3R I expression in mice with FHF at 6 h and 9 h （t = 3.16, P 〈 0.05; t = 5.43, P 〈 0.01）. Furthermore, we evaluated IP3R I mRNA expression by RT-PCR and observed marked upregulation of IP3R I mRNA in FHF samples at 2 h, 6 h and 9 h compared to controls （t = 2.97, P 〈 0.05; t = 4.42, P 〈 0.01; t = 3.81, P 〈 0.01）. CONCLUSION： The expression of IP3R I protein increased in GMC and renal VSMC of mice with FHF, possibly caused by up-regulation of IP3R I mRNA.

The effect of body weight on the induction of mild hypothermia in a rabbit model of asphyxia cardiac arrest

Objective To investigate the effect of body weight on the induction of mild hypothermia in a rabbit model of asphyxia cardiac arrest. Methods Twenty-four rabbits were randomized into two groups： the ice bag group and the intravenous 4℃ saline group. Cardiac arrest was induced and after 3 minutes of cardiac arrest, cardiopulmonary resuscitation was begun. Simultaneously, mild hypothermia was induced by putting an ice bag over the abdomen or infusion of 4℃ saline via an ear vein. A 2℃ decrease of rectal temperature was considered as the completion of hypothermia induction. Induction times were recorded, compared, and analyzed with respect to body weight. Results All rabbits had restoration of spontaneous circulation （ROSC） and ROSC lasted during the experiment. Induction time in the ice bag group was significantly shorter than that in the intravenous 4℃ saline group （22.8 ± 4.7 min VS 42.5 ± 4.0 min, P〈 0.001）. Induction time significantly correlated with body weight in the ice bag group （Pearson Correlation： r = 0.725, P = 0.029）, but not in the intravenous 4℃ saline group （Pearson Correlation： P = 0.418）. Conclusions In a rabbit model, induction of mild hypothermia with an ice bag is faster than with intravenous 4~C saline; induction time positively correlates with body weight when an ice bag is used, but not when intravenous 4℃ saline used. The effect of body weight should be considered when choosing an appropriate method to achieve early induction of mild hypothermia

Effect of hypertonic saline solution on the left ventricular functions of isolated hearts from burned rats

Objective: To study the effect of hypertonic saline solution on the left ventricular functions of isolated hearts from burned rats. Methods: Thirty six Wistar rats were used and divided into 4 groups: (1) normal hearts perfused with isotonic Krebs Henseleit solution; (2) normal hearts perfused with Krebs Henseleit solution which contained 215 mmol/L Na +; (3) hearts of rats suffered from 25% TBSA third degree burn and perfused with isotonic Krebs Henseleit solution; (4) hearts of the burned rats perfused with Krebs Henseleit solution which contained 215 mmol/L Na +. The systolic and diastolic functions of the left ventricle were observed.Results: During perfusion, there were very short periods of decrease in heart systolic and diastolic functions at first, but they recovered very soon and even became stronger than normal both in the normal and burned rats. The systolic and diastolic functions of the hearts increased very significantly when the perfusion solution was changed to isotonic solution from the hypertonic solutions. The effect of the hypertonic saline solution on the ventricular systolic and diastolic improvements was stronger in the hearts of the burned rats than that in the normal hearts. Conclusions: Hypertonic saline solution can directly affect myocardium and significantly improve the ventricular systolic and diastolic functions, especially in the hearts of the burned rats.