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Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To studyExpression of serum Soluble Differentiation antigen 14 (sCD14), C-reactive protein (CRP), procalcitonin (PCT) in acute pancreatitis and their correlation with Acute physiological function and chronic health status scoring system Ⅱ (APACHEII), bedside acute pancreatitis severity index (BISAP). Methods: 150 patients with acute pancreatitis who were treated in our hospital from January 2019 to January 2021 were selected as the case group, and 50 healthy patients who were examined in our hospital during the same period were selected as the control group. The changes of serum sCD14, CRP and PCT levels and their correlation with APACHE Ⅱ and BISAP were analyzed. Results: The serum levels of sCD14, CRP, PCT, APACHE Ⅱ and BISAP in case group were significantly higher than those in control group, with significant differences (P<0.05); The serum levels of sCD14, CRP, PCT, APACHE Ⅱ and BISAP in mild patients were significantly lower than those in moderate and severe patients, and the serum levels of sCD14, CRP, PCT, APACHE Ⅱ and BISAP in moderate patients were significantly lower than those in severe patients, with significant differences (P<0.05). Correlation analysis results showed that serum sCD14, CRP and PCT and APACHE Ⅱ, there was a positive correlation between BISAP (r=0.449, 0.649, 0.584, 0.488, 0.674, 0.663, P<0.05). Conclusions: Serum sCD14, CRP and PCT were highly expressed in patients with acute pancreatitis, and were closely related to APACHE Ⅱ and BISAP. [ABSTRACT FROM AUTHOR]

To investigate the effects of carbetocin and Bakri balloon compression on ovarian function and coagulation function in patients with uterine asthenia postpartum hemorrhage. 86 patients with uterine asthenia postpartum hemorrhage who were treated in our hospital from February 2017 to March 2021 were selected, and they were randomly divided into control group and study group by random number table method. They were treated with Bakri balloon compression alone and carbetocin and Bakri balloon compression combined. Ovarian function indexes including luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2) were detected and compared. The changes of diastolic blood pressure (DBP), systolic blood pressure (SBP), heart rate, bleeding volume and hemostasis onset time in two groups were recorded. Fibrinogen (FIB), prothrombin time (PT) and activated partial thromboplastin time (APTT) were measured, the adverse reactions of the two groups were compared. The changes of DBP, SBP and heart rate in the two groups fluctuated little, and there was no significant difference after treatment (P>0.05). The bleeding volume at 2 h and 24 h after treatment in two groups decreased, and the bleeding volume and hemostasis onset time in the study group at 2 h and 24 h after treatment were shorter than those in the control group(P<0.05). 3 d after treatment, the level of FIB in the two groups decreased, and the levels of PT and APTT increased, and the level of FIB in the study group was lower than that in the control group, and the levels of PT and APPT were higher than those in the control group(P<0.05). 3 d after treatment, the levels of serum E2 in the two groups increased, and the levels of FSH and LH decreased, and the levels of serum E2, FSH and LH in the study group were better than those in the control group(P<0.05). The incidence of adverse reactions in the study group(8.89%) was higher than that in the control group (4.88%), but there was no significant difference (P>0.05). The combined treatment of carbetocin and Bakri balloon compression can effectively improve the ovarian function and coagulation function of patients with uterine asthenia postpartum hemorrhage, improve the postpartum hemostasis effect, and enhance the uterine contractility of patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of interleukin-17A (IL-17A) on lipopolysaccharide (LPS) -induced human bronchial epithelial cells (16-HBE) and their possible mechanisms. Methods: The 16-HBE cell line was cultured in vitro and intervened with LPS and IL-17A, and divided into blank control group, LPS group, IL-17A group and IL-17A+LPS group. The concentrations level of IL-4, IFN-γ, IL-6, IL-8 and other inflammatory factors in the supernatant of cell culture medium were determined by Enzyme linked immunosorbent assay(Elisa). The expression and activation of Mitogen-activated protein kinase(MAPKs) pathway related proteins: Phosphorylated extracellular regulated protein kinase (P-ERK), Extracellular regulated protein kinase (ERK), Phosphorylated P38 protein kinase (P-P38), P38 protein kinase (P38), Phosphorylated c-Jun N-terminal kinase (P-JNK), c-Jun N-terminal kinase (JNK) were detected byWestern Blotting (WB). The 16-HBE cell line was cultured in vitro and intervened with LPS, IL-17A, and ERK inhibitor(U0126), p38 inhibitor(SB203580), and JNK inhibitor (SP600125), and divided into blank control group, LPS + IL-17A group, IL-17A + LPS + UO126 group, IL-17A + LPS + SB203580 group, IL-17A + LPS + SP600125 group. Enzyme-linked immunosorbent assay was used to determine the levels of inflammatory factors such as IFN-γ, IL-4, IL-6, and IL-8 in the cell culture supernatant. Results: Compared with the blank control group, the concentration level of IL-6 and IL-8 were significantly increased in the cellular supernatant (P<0.01), while the concentration level of IL-4 was decreased (con vs LPS P<0.01, con vs IL-17A P<0.05) in the supernatant with either IL-17A or LPS stimulation. The expression of P-ERK, P-P38 and P-JNK protein was significantly increased (con vs LPS P<0.05, con vs IL-17A P<0.01). the concentration level of IL-6 and IL-8 were significantly increased (P<0.01). The levels of IL-6, IL-8, IL-4 and the expression of P-ERK, P-P38, and P-JNK in the cell supernatant of IL-17A + LPS group were higher than those in LPS and IL-17A group (P<0.05). After adding ERK, P38, and JNK inhibitors, compared with the LPS + IL-17A group, IL-17A + LPS + U0126 group, IL-17A + LPS + SB203580 group, and IL-17A + LPS + SP600125 group, the expression of IL-6, IL-8, IL-4 in cell supernatants has decreased (P<0.05). Conclusion: IL-17A might aggravate LPS-induced 16-HBE inflammatory injury by up-regulating IL-6 and IL-8 concentration level, and MAPKs may be an important signal transduction pathway in the process. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To evaluate the effect of ischemia preconditioning and ischemia preconditioning combination with selective inhibitor of NMDA recepter on the phosphorylation of Bcl-2 and the survival of CA1 subfield. Methods: Transient global brain ischemia was induced by 4-vessel occlusion in adult male Sprague-Dawley rats. The rats were pretreated with 3 min of ischemia preconditioning (IPC) alone or MK801 (selective inhibitor of NMDA) treatment before IPC, after reperfusion for 3 days, 6 min of ischemia was induced followed by different times of reperfusion. As brain ischemia reperfusion models, the rats was given six min of ischemia and followed by different times of reperfusion. We performed this experiment by using SDS-PAGE and Immunoblotting to examine the expression and phosphorylation of Bcl-2 protein. Cresyl violet staining was performed to examine the survival and apoptosis neurons in the pyramidal cell layer of the Hippocampal CA1 subfield. Results: Globle cerebral ischemia/reperfusion induced obvious phosphorylation of Bcl-2 and apoptosis of CA1 pyramidal neuron, which could be depressed by the use of IPC. However, MK801 treatment before IPC antagonized this effect of IPC. At the same time, there was no change in the expression level of Bcl-2. Conclusions: IPC could obviously depress the phosphorylation of Bcl-2 and apoptosis of CA1 pyramidal neuron induced by cerebral ischemia/reperfusion through NMDA recepter. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: The objective of this study is primarily to determine whether NMDA recepter affects GluR6 S-nitrosylation and the survival of CA1 subfield during the early stages of ischemia-reperfiision. Methods: Transient cerebral ischemia was induced by a four-vessel occluded (4-VO) method. Sprague-Dawley rats were treated intraperitoneally with MK801(3 mg kg. an selective inhibitor of NMDA recepter). We perform this study mainly by biotin switch assay. SDS-PAGE and western bloting to exam the S-nitrosylation and expression of GluR6. Cresyl violet staining was performed to examine the survival and apoptosis neurons in the pyramidal cell layer of the hippocamal C'Al sub field. Results: Here, we showed that S-nitrosylation of GluR6 and the apoptosis of CA1 pyramidal neuron was dramatically induced by cerebral ischemia-reperfiision. and that administration of MK801 observably diminished the increased S-nitrosylation of GluR6 and the apoptosis of CA1 pyramidal neuron. Conclusions: These data suggest that NMDA recepter facilitates GluR6 S-nitrosylation and the apoptosis of CA1 pyramidal neuron in the early stages of cerebral ischemia-reperfiision. In contrast. MK801 antagonizes the above action of cerebral ischemia-reperfiision. Unis, our results provide that NMDA recepter regulate GluR6 by S-nitrosylation and affect the CA1 pyramidal neuron during the early stages of ischemia-reperfiision. which can be a new approach for stroke therapy. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effect of cisplatin on the expression of PI3K/AKT and apoptosis related regulation factors in patients with ovarian cancer. Methods: 60 cases with ovarian cancer who were treated in our hospital were selected and randomly divided into the experiment and the control group, with 30 cases in each group. The patients in the control group were treated with cisplatin chemotherapy, while the patients in the experiment group were treated with the hyperthermia for 3 weeks. Then the changes of PI3 K, AKT and CA125 and the clinical efficacy of patients in the two groups were detected and compared before and after the treatment.Results: Compared with before treatment, the levels of PI3K, Akt and CA125 in the two groups decreased after the treatment, and the differences were statistically significant (P<0.05); Compared with the control group, the levels of PI3K, Akt and CA125 in the experiment group were lower after the treatment, and the differences were statistically significant (P<0.05); The total clinical efficiency of the experiment group was 80.0%, which was higher than 70.0%in the control group, and the difference was statistically significant (P<0.05).Conclusion: Compared with the simple application of cisplatin, the combination of the cisplatin chemotherapy and hyperthermia can reduce the levels of PI3 K, AKT and CA125 in patients with ovarian cancer, and improve the clinical efficacy, which is worthy of clinical significance. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of ulinastatin on the serum level of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and phospholipase A2 (PLA2) in the patients with chronic obstructive pulmonary disease (COPD) combined with respiratory failure. Methods: 80 patients with COPD were randomly selected in our hospital from January 2014 to January 2015 and divided into two groups that 40 cases in the experimental group and 40 cases in the control group. The control group was given routine treatment, and the experimental group was given ulinastatin treatment. Then the levels of COX-2, PGE2 and PLA2 in the two groups were detected and compared before and after the treatment. Results: After treatment, the levels of COX-2, PGE2 and PLA2 in the two groups were significantly lower than before treatment (P<0.05), and the experimental group was significantly lower than that of the control group (P<0.05). After the treatment, the FEV1 and FVC were significantly better in the experimental group than those of the control group (P<0.05). Conclusions: Ulinastatin can significantly reduce the serum levels of COX-2, PGE2 and PLA2 in the patients with COPD combined with respiratory failure, and effectively improve inflammatory reaction, cell damage and clinical symptoms of the patients, which can provide a new idea for efficient treatment of COPD in clinic. [ABSTRACT FROM AUTHOR]