The relationship between ENSO and Indian Ocean Dipole was discussed by using the data set of sea temperature from Scripps Institute of Oceanography, the air temperature at 1000hPa from the NCEP reanalysis data and the...The relationship between ENSO and Indian Ocean Dipole was discussed by using the data set of sea temperature from Scripps Institute of Oceanography, the air temperature at 1000hPa from the NCEP reanalysis data and the Nino3 index from the Climate Prediction Center （CPC） of U.S.A. during the period from 1955 to 2001. The results show that there exists a Dipole on the maximum temperature anomalous level （MTAL） in the Indian Ocean, which close relates to ENSO in the Pacific Ocean. During El Nino periods there are good relationships between ENSO and Indian Ocean Dipole which maximum correlation occurring when ENSO leads by one month, but in La Nina periods the relationship is not so good. The distribution of Dipole in Indian Ocean is from northeast to southwest, which one （west） pole in 65°E - 75°E, 6°S - 10°S and the other in 85°E - 95°E, 2°N - 6°N, which is different from that defined by Saij. The correlation coefficients of Nino3 index with temperature anomalies in the west/east poles on the MTAL are over 0.4 - 0.15, respectively. It is a main sea temperature system in the tropical Indian Ocean. However, in the surface layer from sea surface to the depth of 20 m - 30 m there is no such a dipole with opposite sea temperature anomalies in the NE and SW of tropical Indian Ocean. The SSTA in the NE might be influenced by the sensible exchange process because the evolution of sea and 1 000 hPa air temperature anomaly time series of the NE of tropical Indian Ocean is quite similar except those during 1962 - 1963 and 1986. The periods of Indian Ocean Dipole are shorter than that of ENSO, and about 1 to 6-year.展开更多
AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the ...AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.展开更多
基金supported by the National Natural Science Foundation of China, (No. 40976015)National Basic Research Program of China under Grant No. (2010CB950302)
文摘The relationship between ENSO and Indian Ocean Dipole was discussed by using the data set of sea temperature from Scripps Institute of Oceanography, the air temperature at 1000hPa from the NCEP reanalysis data and the Nino3 index from the Climate Prediction Center （CPC） of U.S.A. during the period from 1955 to 2001. The results show that there exists a Dipole on the maximum temperature anomalous level （MTAL） in the Indian Ocean, which close relates to ENSO in the Pacific Ocean. During El Nino periods there are good relationships between ENSO and Indian Ocean Dipole which maximum correlation occurring when ENSO leads by one month, but in La Nina periods the relationship is not so good. The distribution of Dipole in Indian Ocean is from northeast to southwest, which one （west） pole in 65°E - 75°E, 6°S - 10°S and the other in 85°E - 95°E, 2°N - 6°N, which is different from that defined by Saij. The correlation coefficients of Nino3 index with temperature anomalies in the west/east poles on the MTAL are over 0.4 - 0.15, respectively. It is a main sea temperature system in the tropical Indian Ocean. However, in the surface layer from sea surface to the depth of 20 m - 30 m there is no such a dipole with opposite sea temperature anomalies in the NE and SW of tropical Indian Ocean. The SSTA in the NE might be influenced by the sensible exchange process because the evolution of sea and 1 000 hPa air temperature anomaly time series of the NE of tropical Indian Ocean is quite similar except those during 1962 - 1963 and 1986. The periods of Indian Ocean Dipole are shorter than that of ENSO, and about 1 to 6-year.
文摘AIM:To investigate the correlation of hyperlipemia(HL) and acute cerebral ischemia/reperfusion(I/R) injury on liver damage and its mechanism.METHODS:Rats were divided into 4 groups:control,HL,I/R and HL+I/R.After the induction of HL via a high-fat diet for 18 wk,middle cerebral artery occlusion was followed by 24 h of reperfusion to capture I/R.Serum alanine transaminase(ALT) and aspartate aminotransferase(AST) were analyzed as part of liver function tests and liver damage was further assessed by histological examination.Hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) assay.The expression of genes related to apoptosis(caspase-3,bcl-2) was assayed by immunohistochemistry and Western blotting.Serum tumor necrosis factor-(TNF-),interleukin-1(IL-1) and liver mitochondrial superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA) and Ca 2+ levels were measured to determine inflammatory and oxidative/antioxidative status respectively.Microsomal hydroxylase activity of the cytochrome P450 2E1(CYP2E1)-containing enzyme was measured with aniline as the substrate,and CYP2E1 expression in the liver tissue and microsome was determined by immunohistochemistry and Western blotting respectively.RESULTS:HL alone induced by high-fat diet for 18 wk resulted in liver damage,indicated by histopathological analysis,and a considerable increase in serum ALT(25.13 ± 16.90 vs 9.56 ± 1.99,P < 0.01) and AST levels(18.01 ± 10.00 vs 11.33 ± 4.17,P < 0.05) compared with control.Moreover,HL alone induced hepatocyte apoptosis,which was determined by increased TUNEL-positive cells(4.47 ± 0.45 vs 1.5 ± 0.22,P < 0.01),higher caspase-3 and lower bcl-2 expression.Interestingly,compared with those in control,HL or I/R groups,massive increases of serum ALT(93.62 ± 24.00 vs 9.56 ± 1.99,25.13 ± 16.90 or 12.93 ± 6.14,P < 0.01) and AST(82.32 ± 26.92 vs 11.33 ± 4.17,18.01 ± 10.00 or 14.00 ± 6.19,P < 0.01) levels in HL+I/R group were observed suggesting severe liver damage,which was confirmed by liver histology.In addition,HL combined with I/R also caused significantly increased hepatocyte apoptosis,as evidenced by increased TUNEL-positive cells(6.20 ± 0.29 vs 1.5 ± 0.22,4.47 ± 0.45 or 1.97 ± 0.47,P < 0.01),elevated expression of caspase-3 and lower expression of bcl-2.Furthermore,when compared to HL or I/R alone,HL plus I/R enhanced serum TNF-,IL-1,liver mitochondrial MDA and Ca 2+ levels,suppressed SOD and GSH-Px in liver mitochondria,and markedly up-regulated the activity(11.76 ± 2.36 vs 4.77 ± 2.31 or 3.11 ± 1.35,P < 0.01) and expression(3.24 ± 0.38 vs 1.98 ± 0.88 or 1.72 ± 0.58,P < 0.01) of CYP2E1 in liver.CONCLUSION:The coexistence of HL and acute cerebral I/R induces severe liver damage,suggesting that cerebral ischemic stroke would exaggerate the damage of liver caused by HL.This effect is possibly due to en-hanced CYP2E1 induction which further promotes oxidative damage,inflammation and hepatocyte apoptosis.
