AIM: To study the effects of QHF-cisplatin on H22 hepatocellular carcinoma(HCC) and their mechanisms of action.METHODS: Sixty BALB/c mice were randomly divided into a model group(n = 48) and a normal control group(n =...AIM: To study the effects of QHF-cisplatin on H22 hepatocellular carcinoma(HCC) and their mechanisms of action.METHODS: Sixty BALB/c mice were randomly divided into a model group(n = 48) and a normal control group(n = 12). An HCC xenograft tumor was created by injecting H22 cells directly into the liver parenchyma of the mice. The 48 BALB/c mice in the model group were randomly divided into four groups: QHF, DDP(cisplatin), QHF plus DDP, and model control. The inhibitory effects of these drugs on tumor growth were evaluated by calculating the rate of tumor growth inhibition. The mice were examined by observing their general condition, body weight and survival time. Changes in tumor tissue were observed under anoptical microscope. Aspartate aminotransferase(AST), alanine aminotransferase(ALT) and α-fetoprotein(AFP) levels in serum were measured. Hepatocyte growth factor(HGF), c-mesenchymal-epithelial transition(c-Met) factor, phosphorylated(p)-c-Met, p38, p-p38, extracellular signal-regulated kinase(ERK), p-ERK and vascular endothelial growth factor(VEGF) levels were evaluated in tumor and liver tissues using western blotting. RESULTS: Compared with the DDP group, a lower incidence of toxic reactions and a higher survival time were observed in the QHF plus DDP group. Tumor weight was significantly lower in the QHF, DDP and QHF plus DDP groups than in the model control group(0.24 ± 0.07, 0.18 ± 0.03 and 0.14 ± 0.01 g vs 0.38 ± 0.05 g, respectively), and the differences were statistically significant(P < 0.01). The rate of tumor growth inhibition in the QHF, DDP and QHF plus DDP groups was 38.7%, 52.6% and 63.5%, respectively. AST, ALT and AFP levels in serum were significantly lower in the QHF, DDP and QHF plus DDP groups compared to the model control group(P < 0.05). Similarly, HGF, p-c-Met, p-p38, p-ERK and VEGF levels in tumor tissue were significantly lower in the QHF, DDP and QHF plus DDP groups(P < 0.05).CONCLUSION: QHF and DDP have an antiangiogenic effect on H22 HCC in mice. QHF inhibits tumor growth v展开更多
Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver fibrosis.Methods:In vivo experiments were conducted usin...Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver fibrosis.Methods:In vivo experiments were conducted using 8-week-old multidrug resistance protein 2 knockout(Mdr2-/-)mice as an animal model of cholestatic liver fibrosis.DHQ was administered orally for 8 weeks,and its impact on cholestatic liver fibrosis was evaluated by assessing liver function,liver histopathology,and the expression of liver fibrosis-related proteins.Real-time polymerase chain reaction,Western blot,immunohistochemistry and other methods were used to observe the effects of DHQ on long non-coding RNA H19(H19)and signal transducer and activator of transcription 3(STAT3)phosphorylation in the liver tissue of Mdr2-/-mice.In addition,cholangiocytes and hepatic stellate cells(HSCs)were cultured in vitro to measure the effects of bile acids on cholangiocyte injury and H19 expression.Cholangiocytes overexpressing H19 were constructed,and a conditioned medium containing H19 was collected to measure its effects on STAT3 protein expression and cell activation.The intervention effect of DHQ on these processes was also investigated.HSCs overexpressing H19 were constructed to measure the impact of H19 on cell activation and assess the intervention effect of DHQ.Results:DHQ alleviated liver injury,ductular reaction,and fibrosis in Mdr2-/-mice,and inhibited H19expression,STAT3 expression and STAT3 phosphorylation.This formula also reduced hydrophobic bile acid-induced cholangiocyte injury and the upregulation of H19,inhibited the activation of HSCs induced by cholangiocyte-derived conditioned medium,and decreased the expression of activation markers in HSCs.The overexpression of H19 in a human HSC line confirmed that H19 promoted STAT3 phosphorylation and HSC activation,and DHQ was able to successfully inhibit these effects.Conclusion:DHQ effectively alleviated spontaneous cholestatic liver fibrosis in Mdr2-/-mice by inhibiting H19 upregulation in chol展开更多
The Hilbert boundary value problem Re{λ（t） p√ψ＋（t）} = c（t）, t∈L of normal type with Holder continuous coefficients is discussed, where L is the unit circle ｜t｜ = 1,p ≥2 is any definite integer,ψ^＋（t）...The Hilbert boundary value problem Re{λ（t） p√ψ＋（t）} = c（t）, t∈L of normal type with Holder continuous coefficients is discussed, where L is the unit circle ｜t｜ = 1,p ≥2 is any definite integer,ψ^＋（t） is the boundary value of the unknown function ψ（z） holomorphic in ｜z｜ 〈 1 with single-valued continuous p√ψ＋（t） on L.展开更多
In the present paper, the authors introduce a new integral transform which yields a number of potentially useful （known or new） integral transfoms as its special cases. Many fundamental results about this new integr...In the present paper, the authors introduce a new integral transform which yields a number of potentially useful （known or new） integral transfoms as its special cases. Many fundamental results about this new integral transform, which are established in this paper, in- clude （for example） existence theorem, Parseval-type relationship and inversion formula. The relationship between the new integral transform with the H-function and the H-transform are characterized by means of some integral identities. The introduced transform is also used to find solution to a certain differential equation. Some illustrative examples are also given.展开更多
The ability to identify patients with risk of mortality in the initial stages allows us to introduce a more aggressive treatment in order to improve patients’ survival. In this study, we used systemic inflammatory re...The ability to identify patients with risk of mortality in the initial stages allows us to introduce a more aggressive treatment in order to improve patients’ survival. In this study, we used systemic inflammatory response syndrome (SIRS) criteria, respiratory and heart rate per minute, and consciousness level [(Glasgow coma scale (GCS)] to develop a formula to predict death in patients admitted to the Infectious Diseases ward of Imam Reza hospital. Methods: This descriptive study was a cross sectional study done in the Infectious Diseases ward of Imam Reza hospital, Mashhad University of Medical Sciences, Iran. Alive and dead patients between the dates September 1, 2006 to September 1, 2007 were studied. In this study, data such as past medical history, prescribed drugs and their administration by nursing and medical staff was extracted from patients’ files. Also, the time of death, the first vital signs recorded in the hospital and the formula H = (PR + RR) - GCS (respiratory rate per minute plus heart rate per minute minus Glasgow coma scale (GCS)) was calculated for both alive and dead patients. Data was analyzed by SPSS software. Mann-Whitney test, Roc Curve, and logistic regression model were used for data analysis. Results: The total number of admitted patients was 1007 of whom 90 (10.82%) died. One patient was excluded from the study. Out of 90 dead patients, 51 (56.6%) were male and 39 (43.3%) were female. There was no significant difference between the two groups regarding the gender (P > 0.05). The mean age of the study group (deceased) was 59 ± 21 and the mean age of the control group (alive) was 58 ± 21. The Mann-Whitney test showed that the result of H Formula was significantly different between the two groups, (126 ± 26 for the study group and 111 ± 22 for the control group). The cutoff for H Formula was equal to 112.5. Negative and positive predictive values, specificity and sensitivity were 0.85, 0.35, 0.57, and 0.70 respectively. Logistic regression results show that the H index contents展开更多
基金Supported by Grants from the Natural Science Foundation of Hubei Province,China,No.2011CAD039
文摘AIM: To study the effects of QHF-cisplatin on H22 hepatocellular carcinoma(HCC) and their mechanisms of action.METHODS: Sixty BALB/c mice were randomly divided into a model group(n = 48) and a normal control group(n = 12). An HCC xenograft tumor was created by injecting H22 cells directly into the liver parenchyma of the mice. The 48 BALB/c mice in the model group were randomly divided into four groups: QHF, DDP(cisplatin), QHF plus DDP, and model control. The inhibitory effects of these drugs on tumor growth were evaluated by calculating the rate of tumor growth inhibition. The mice were examined by observing their general condition, body weight and survival time. Changes in tumor tissue were observed under anoptical microscope. Aspartate aminotransferase(AST), alanine aminotransferase(ALT) and α-fetoprotein(AFP) levels in serum were measured. Hepatocyte growth factor(HGF), c-mesenchymal-epithelial transition(c-Met) factor, phosphorylated(p)-c-Met, p38, p-p38, extracellular signal-regulated kinase(ERK), p-ERK and vascular endothelial growth factor(VEGF) levels were evaluated in tumor and liver tissues using western blotting. RESULTS: Compared with the DDP group, a lower incidence of toxic reactions and a higher survival time were observed in the QHF plus DDP group. Tumor weight was significantly lower in the QHF, DDP and QHF plus DDP groups than in the model control group(0.24 ± 0.07, 0.18 ± 0.03 and 0.14 ± 0.01 g vs 0.38 ± 0.05 g, respectively), and the differences were statistically significant(P < 0.01). The rate of tumor growth inhibition in the QHF, DDP and QHF plus DDP groups was 38.7%, 52.6% and 63.5%, respectively. AST, ALT and AFP levels in serum were significantly lower in the QHF, DDP and QHF plus DDP groups compared to the model control group(P < 0.05). Similarly, HGF, p-c-Met, p-p38, p-ERK and VEGF levels in tumor tissue were significantly lower in the QHF, DDP and QHF plus DDP groups(P < 0.05).CONCLUSION: QHF and DDP have an antiangiogenic effect on H22 HCC in mice. QHF inhibits tumor growth v
基金supported by grants from the National Natural Science Foundation of China(No.81773980)Project of Science and Technology Commission of Shanghai Municipality(No.15401902600)。
文摘Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver fibrosis.Methods:In vivo experiments were conducted using 8-week-old multidrug resistance protein 2 knockout(Mdr2-/-)mice as an animal model of cholestatic liver fibrosis.DHQ was administered orally for 8 weeks,and its impact on cholestatic liver fibrosis was evaluated by assessing liver function,liver histopathology,and the expression of liver fibrosis-related proteins.Real-time polymerase chain reaction,Western blot,immunohistochemistry and other methods were used to observe the effects of DHQ on long non-coding RNA H19(H19)and signal transducer and activator of transcription 3(STAT3)phosphorylation in the liver tissue of Mdr2-/-mice.In addition,cholangiocytes and hepatic stellate cells(HSCs)were cultured in vitro to measure the effects of bile acids on cholangiocyte injury and H19 expression.Cholangiocytes overexpressing H19 were constructed,and a conditioned medium containing H19 was collected to measure its effects on STAT3 protein expression and cell activation.The intervention effect of DHQ on these processes was also investigated.HSCs overexpressing H19 were constructed to measure the impact of H19 on cell activation and assess the intervention effect of DHQ.Results:DHQ alleviated liver injury,ductular reaction,and fibrosis in Mdr2-/-mice,and inhibited H19expression,STAT3 expression and STAT3 phosphorylation.This formula also reduced hydrophobic bile acid-induced cholangiocyte injury and the upregulation of H19,inhibited the activation of HSCs induced by cholangiocyte-derived conditioned medium,and decreased the expression of activation markers in HSCs.The overexpression of H19 in a human HSC line confirmed that H19 promoted STAT3 phosphorylation and HSC activation,and DHQ was able to successfully inhibit these effects.Conclusion:DHQ effectively alleviated spontaneous cholestatic liver fibrosis in Mdr2-/-mice by inhibiting H19 upregulation in chol
文摘The Hilbert boundary value problem Re{λ（t） p√ψ＋（t）} = c（t）, t∈L of normal type with Holder continuous coefficients is discussed, where L is the unit circle ｜t｜ = 1,p ≥2 is any definite integer,ψ^＋（t） is the boundary value of the unknown function ψ（z） holomorphic in ｜z｜ 〈 1 with single-valued continuous p√ψ＋（t） on L.
文摘In the present paper, the authors introduce a new integral transform which yields a number of potentially useful （known or new） integral transfoms as its special cases. Many fundamental results about this new integral transform, which are established in this paper, in- clude （for example） existence theorem, Parseval-type relationship and inversion formula. The relationship between the new integral transform with the H-function and the H-transform are characterized by means of some integral identities. The introduced transform is also used to find solution to a certain differential equation. Some illustrative examples are also given.
文摘The ability to identify patients with risk of mortality in the initial stages allows us to introduce a more aggressive treatment in order to improve patients’ survival. In this study, we used systemic inflammatory response syndrome (SIRS) criteria, respiratory and heart rate per minute, and consciousness level [(Glasgow coma scale (GCS)] to develop a formula to predict death in patients admitted to the Infectious Diseases ward of Imam Reza hospital. Methods: This descriptive study was a cross sectional study done in the Infectious Diseases ward of Imam Reza hospital, Mashhad University of Medical Sciences, Iran. Alive and dead patients between the dates September 1, 2006 to September 1, 2007 were studied. In this study, data such as past medical history, prescribed drugs and their administration by nursing and medical staff was extracted from patients’ files. Also, the time of death, the first vital signs recorded in the hospital and the formula H = (PR + RR) - GCS (respiratory rate per minute plus heart rate per minute minus Glasgow coma scale (GCS)) was calculated for both alive and dead patients. Data was analyzed by SPSS software. Mann-Whitney test, Roc Curve, and logistic regression model were used for data analysis. Results: The total number of admitted patients was 1007 of whom 90 (10.82%) died. One patient was excluded from the study. Out of 90 dead patients, 51 (56.6%) were male and 39 (43.3%) were female. There was no significant difference between the two groups regarding the gender (P > 0.05). The mean age of the study group (deceased) was 59 ± 21 and the mean age of the control group (alive) was 58 ± 21. The Mann-Whitney test showed that the result of H Formula was significantly different between the two groups, (126 ± 26 for the study group and 111 ± 22 for the control group). The cutoff for H Formula was equal to 112.5. Negative and positive predictive values, specificity and sensitivity were 0.85, 0.35, 0.57, and 0.70 respectively. Logistic regression results show that the H index contents
