By using an improved projective Riccati equation method, this paper obtains several types of exact travelling wave solutions to the Benjamin Ono equation which include multiple soliton solutions, periodic soliton solu...By using an improved projective Riccati equation method, this paper obtains several types of exact travelling wave solutions to the Benjamin Ono equation which include multiple soliton solutions, periodic soliton solutions and Weierstrass function solutions. Some of them are found for the first time. The method can be applied to other nonlinear evolution equations in mathematical physics.展开更多
In the paper, the homoclinic (hateroclinic) breather limit method (HBLM) is applied to seek rogue wave solution of the Benjamin Ono equation. We find that the rational breather wave solution is just a rogue wave solut...In the paper, the homoclinic (hateroclinic) breather limit method (HBLM) is applied to seek rogue wave solution of the Benjamin Ono equation. We find that the rational breather wave solution is just a rogue wave solution. This result shows that rogue wave can come from the extreme behavior of the breather solitary wave for (1+1)-dimensional nonlinear wave fields.展开更多
In this paper, we study a certain partition function a（n） defined by ∑n≥0 a（n）qn ：= ∏n=1（1- qn）-1（1 -2n）-1. We prove that given a positive integer j 〉 1 and a prime m _〉 5, there are infinitely many cong...In this paper, we study a certain partition function a（n） defined by ∑n≥0 a（n）qn ：= ∏n=1（1- qn）-1（1 -2n）-1. We prove that given a positive integer j 〉 1 and a prime m _〉 5, there are infinitely many congruences of the type a（An ＋ B） ≡ 0 （rood m3）. This work is inspired by Ono＇s ground breaking result in the study of the distribution of the partition function p（n）.展开更多
In the article, the nonlinear equation is reduced to an ordinary differential equation under the travelling wave transformation. Using trial equation method, the ODE is reduced to the elementary integral form. In the ...In the article, the nonlinear equation is reduced to an ordinary differential equation under the travelling wave transformation. Using trial equation method, the ODE is reduced to the elementary integral form. In the end, complete discrimination system for polynomial is used to solve the corresponding integrals and obtain the classification of all single travelling wave solutions to the equation.展开更多
AIM To determine whether ONO 1078 {pranlukast, 4 oxo 8 [p (4 phenylbutyloxy) benzoyl amino] 2 (tetrazol 5 yl) 4H 1 benzopyran hemihydrate}, a potent leukotriene antagonist, has protective effect on focal cerebral isch...AIM To determine whether ONO 1078 {pranlukast, 4 oxo 8 [p (4 phenylbutyloxy) benzoyl amino] 2 (tetrazol 5 yl) 4H 1 benzopyran hemihydrate}, a potent leukotriene antagonist, has protective effect on focal cerebral ischemia in mice. METHODS Focal cerebral ischemia was induced by permanent middle cerebral artery (MCA) occlusion in mice. ONO 1078 (0 01, 0 05, 0 10 mg·kg -1 ), dexamethasone (0 5 mg·kg -1 ), nimodipine (0 2 mg·kg -1 ) or saline (control) were injected ip once daily for 3 days, and 30 min before MCA occlusion. Twenty four hours after cerebral ischemia, the neurological scores were evaluated, infarct volumes and areas of the right and left cerebral hemispheres were measured by computer imaging analysis. RESULTS ONO 1078, dexamethasone and nimodipine reduced the neurological scores. ONO 1078 and dexamethasone reduced the ratio of right/left hemisphere area, indicating inhibition of brain edema, while nimodipine showed no effect. ONO 1078 dose dependently reduced infarct size, and dexamethasone and nimodipine showed the same effect. CONCLUSION ONO 1078 showed protective effect on focal cerebral ischemia. This may represent a novel approach to the treatment of acute cerebral ischemia.展开更多
We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death...We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death is unclear. By using Western blotting, flow cytometry （FACS） and confocal laser scanning microscopy （CLSM）, we investigated the cellular signal transduction pathways of the neutrophil death. The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3, caspase-8, and phosphorylation of p38-MAPK. However, impairment of mitochondria transmembrane potential has been found during the process of cell death. These findings suggested that ONO-AE-248 induced a non-apoptotic programmed cell death of neutrophils through partially mitochondria signaling transduction pathway. Cellular ＆ Molecular Immunology.展开更多
文摘By using an improved projective Riccati equation method, this paper obtains several types of exact travelling wave solutions to the Benjamin Ono equation which include multiple soliton solutions, periodic soliton solutions and Weierstrass function solutions. Some of them are found for the first time. The method can be applied to other nonlinear evolution equations in mathematical physics.
文摘In the paper, the homoclinic (hateroclinic) breather limit method (HBLM) is applied to seek rogue wave solution of the Benjamin Ono equation. We find that the rational breather wave solution is just a rogue wave solution. This result shows that rogue wave can come from the extreme behavior of the breather solitary wave for (1+1)-dimensional nonlinear wave fields.
文摘In this paper, we study a certain partition function a（n） defined by ∑n≥0 a（n）qn ：= ∏n=1（1- qn）-1（1 -2n）-1. We prove that given a positive integer j 〉 1 and a prime m _〉 5, there are infinitely many congruences of the type a（An ＋ B） ≡ 0 （rood m3）. This work is inspired by Ono＇s ground breaking result in the study of the distribution of the partition function p（n）.
文摘In the article, the nonlinear equation is reduced to an ordinary differential equation under the travelling wave transformation. Using trial equation method, the ODE is reduced to the elementary integral form. In the end, complete discrimination system for polynomial is used to solve the corresponding integrals and obtain the classification of all single travelling wave solutions to the equation.
文摘AIM To determine whether ONO 1078 {pranlukast, 4 oxo 8 [p (4 phenylbutyloxy) benzoyl amino] 2 (tetrazol 5 yl) 4H 1 benzopyran hemihydrate}, a potent leukotriene antagonist, has protective effect on focal cerebral ischemia in mice. METHODS Focal cerebral ischemia was induced by permanent middle cerebral artery (MCA) occlusion in mice. ONO 1078 (0 01, 0 05, 0 10 mg·kg -1 ), dexamethasone (0 5 mg·kg -1 ), nimodipine (0 2 mg·kg -1 ) or saline (control) were injected ip once daily for 3 days, and 30 min before MCA occlusion. Twenty four hours after cerebral ischemia, the neurological scores were evaluated, infarct volumes and areas of the right and left cerebral hemispheres were measured by computer imaging analysis. RESULTS ONO 1078, dexamethasone and nimodipine reduced the neurological scores. ONO 1078 and dexamethasone reduced the ratio of right/left hemisphere area, indicating inhibition of brain edema, while nimodipine showed no effect. ONO 1078 dose dependently reduced infarct size, and dexamethasone and nimodipine showed the same effect. CONCLUSION ONO 1078 showed protective effect on focal cerebral ischemia. This may represent a novel approach to the treatment of acute cerebral ischemia.
基金supported by grants from the National Natural Science Foundation of China(No.30371305).
文摘We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death is unclear. By using Western blotting, flow cytometry （FACS） and confocal laser scanning microscopy （CLSM）, we investigated the cellular signal transduction pathways of the neutrophil death. The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3, caspase-8, and phosphorylation of p38-MAPK. However, impairment of mitochondria transmembrane potential has been found during the process of cell death. These findings suggested that ONO-AE-248 induced a non-apoptotic programmed cell death of neutrophils through partially mitochondria signaling transduction pathway. Cellular ＆ Molecular Immunology.
