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Objective:To observe the efficacy and safety of the combination of agomelatine and low-dose olanzapine (AO) in the treatment of postprandial distress syndrome (PDS) with depression, anxiety and sleep disorders.Methods:From April 2019 to September 2020, PDS patients with depression, anxiety and sleep disorders in Tianjin Medical University General Hospital were selected and divided into AO group and flupentixol-melitracen (FM) group. Patients of the AO group were given oral agomelatine 25 mg and AO 1.70 mg (both once per day), and the patients of FM group were given oral FM 10.5 mg (once per day), and all patients took itopride 50 mg (three times per day) at the same time. The total treatment course was eight weeks. Nepean dyspepsia index-symptom (NDIS), patient health questionnaire-9 (PHQ-9), generalized anxiety disorder-7 (GAD-7) and Pittsburgh sleep quality index (PSQI) were used to evaluate the gastrointestinal symptoms, depression, anxiety and sleep disorders before treatment and two, four and eight weeks after treatment, respectively. The efficacy was evaluated according to the changes of scores of gastrointestinal symptoms before and after treatment. The adverse effects after medication were recorded. Independent sample t test and chi-square test were used for statistical analysis. Results:A total of 184 PDS patients with depression, anxiety and sleep disorders were enrolled, including 98 patients in AO group and 86 patients in FM group. At two, four and eight weeks after treatment, NDIS, PHQ-9, GAD-7 and PSQI scores of AO group and FM group were all lower than those of each group before treatment (AO group: 13.73±0.53, 10.13±0.44 and 7.87±0.31 vs. 27.08±0.84; 6.04±0.35, 4.70±0.31 and 3.81±0.22 vs. 10.04±0.50; 6.36±0.30, 5.29±0.28 and 4.21±0.19 vs. 10.71±0.51; 6.64±0.37, 5.27±0.35 and 4.09±0.30 vs. 11.14±0.42; FM group: 15.33±0.58, 11.58±0.50 and 9.80±0.35 vs. 25.10±0.79; 6.79±0.35, 5.71±0.32 and 4.86±0.30 vs. 9.11±0.46; 7.27±0.31, 6.51±0.32 and 5.21±0.27 vs. 9.79±0.44; 8.01±0.33, 6.76±0.32 and 5.78±0.32 vs. 10.44±0.32), and the differences were statistically significant (AO group: tNDIS=13.470, 17.930 and 21.530, tPHQ-9=6.488, 8.991 and 11.300, tGAD-7=7.361, 9.315 and 11.031, tPSQI=7.088, 9.736 and 12.550. FM group: tNDIS=9.921, 14.400 and 17.640, tPHQ-9=4.032, 6.106 and 7.781, tGAD-7=4.638, 5.993 and 8.840, tPSQI=5.289, 8.199 and 10.310, all P<0.05). At two, four and eight weeks after treatment, NDIS, GAD-7 and PSQI scores of AO group were all lower than those of the FM group during the same period (NDIS: 13.73±0.53 vs. 15.33±0.58, 10.13±0.44 vs. 11.58±0.50, 7.87±0.31 vs. 9.80±0.35; GAD-7: 6.36±0.30 vs. 7.27±0.31, 5.29±0.28 vs. 6.51±0.32, 4.21±0.19 vs. 5.21±0.27; PSQI: 6.64±0.37 vs. 8.01±0.33, 5.27±0.35 vs. 6.76±0.32, 4.09±0.30 vs. 5.78±0.32), and the differences were statistically significant ( tNDIS=2.018, 2.225 and 4.156, tGAD-7=2.097, 2.869 and 2.536, tPSQI=1.951, 2.359 and 3.099, all P<0.05). At eight weeks after treatment, the total effective rate of the AO group was higher than that of the FM group (94.9%, 93/98 vs. 84.9%, 73/86), and the difference was statistically significant ( χ2=5.205, P=0.026). The incidence of adverse reactions of constipation and somnolence of the AO group were both lower than those of the FM group (2.0%, 2/98 vs. 9.3%, 8/86 and 1.0%, 1/98 vs. 8.1%, 7/86, respectively), and the differences were statistically significant ( χ2=4.699 and 5.582, P=0.047 and 0.027). Conclusion:AO may be a treatment option for PDS with depression, anxiety and sleep disorders.
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Objective To evaluate the anti-platelet aggregation effect of ergosterol in vitro and explore the preliminary mechanism. Methods The anti-platelet aggregation activity of ergosterol was assessed in vitro on rabbit platelet aggregation. Different inducers, ADP ( 4 μmol?L-1 ) , collagen ( 4 μg?mL-1 ) , arachidonic acid ( AA, 1 mmol?L-1 ) and thrombin (0.5 U?mL-1), and blockers (ozagrel, dipyridamole, clopidogrel and aspirin) were applied to observe the potential targets of ergosterol, platelet aggregation induced by ADP (0, 1, 2, 4, 6μmol?L-1) or fibrinogen (0, 1, 2, 4, 6, 10 mg?mL-1). Results Ergosterol exhibited an obvious anti-platelet aggregation effect in vitro with IC50 values on different inducers ( ADP, collagen, AA and thrombin) of (19.3±0.8), (23.4±1.2), (26.7±0.7), (32.9±1.5) μmol?L-1, respectively. Conclusion Ergosterol can significantly inhibit aggregation and activation of platelet. It provides experimental basis for full exploration of ergosterol and development of novel anti-platelet aggregation drugs.
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Objective@#To investigate the effects and mechanism of allogeneic platelet rich plasma (PRP) on collagen in wound surface at different time.@*Methods@#A total of 50 clean 7-week rats were selected for this study, including 10 rats for platelet-rich blood plasma preparation, 20 rats for PRP group and 20 rats for control group, 0.1 ml allogenic PRP and 0.1 ml saline were smeared respectively on wound surfaces of PRP and control group, wound regeneration and healing were examined. Cellular and histological morphology alteration was observed via Masson staining, type Ⅰ and type Ⅲ collagen protein and mRNA expression level were detected by Western blot and real-time PCR. T test was applied for comparison between two samples and one-way ANOVA was utilized for comparison between two groups.@*Results@#The wound healing rate of PRP group was higher than that of control group on 3rd, 6th, 10th and 15th day (30.33±3.35 vs.18.35±2.04, 55.51±2.74 vs.36.83±2.34, 79.64±1.40 vs.56.92±1.44, 86.88±2.12 vs.65.80±1.76) after wound surface formation, there were statistic differences (t=13.66-50.48, all P<0.05). The wound collagen of PRP group form faster and coarser, and the fibers arrayed more densely in Masson staining. The protein expression of type Ⅰ collagen(1.92±0.09 vs.1.18±0.11) and type Ⅲ collagen(1.16±0.05 vs.0.74±0.11) of PRP group were higher than that of control group (t=22.99, P<0.01; t=17.62, P<0.05); the mRNA expression of type Ⅰ collagen(5.17±0.11 vs.1.79±0.18, 6.97±0.09 vs.1.96±0.08, 6.00±0.26 vs.2.10±0.05, 4.95±0.11 vs.3.58±0.09)and type Ⅲ collagen(2.35±0.08 vs.1.44±0.05, 3.08±0.05 vs.1.84±0.06, 3.48±0.07 vs.2.36±0.09, 4.42±0.07 vs.2.77±0.10) were higher than that of control group on 3rd, 6th, 10th and 15th day after wound surface formation, there were significant differences (t=43.37-188.37, all P<0.05).@*Conclusion@#The allogeneic platelet rich plasma may promote fibroblasts secreted collagen by activated and releasing all kinds of growth factors, especially type Ⅰ and type Ⅲ collagen to accelerate the wound healing.
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Objective To evaluate the anti-platelet aggregation effect of ergosterol in vitro and explore the preliminary mechanism. Methods The anti-platelet aggregation activity of ergosterol was assessed in vitro on rabbit platelet aggregation. Different inducers, ADP ( 4 μmol?L-1 ) , collagen ( 4 μg?mL-1 ) , arachidonic acid ( AA, 1 mmol?L-1 ) and thrombin (0.5 U?mL-1), and blockers (ozagrel, dipyridamole, clopidogrel and aspirin) were applied to observe the potential targets of ergosterol, platelet aggregation induced by ADP (0, 1, 2, 4, 6μmol?L-1) or fibrinogen (0, 1, 2, 4, 6, 10 mg?mL-1). Results Ergosterol exhibited an obvious anti-platelet aggregation effect in vitro with IC50 values on different inducers ( ADP, collagen, AA and thrombin) of (19.3±0.8), (23.4±1.2), (26.7±0.7), (32.9±1.5) μmol?L-1, respectively. Conclusion Ergosterol can significantly inhibit aggregation and activation of platelet. It provides experimental basis for full exploration of ergosterol and development of novel anti-platelet aggregation drugs.
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Objective To explore the new way of administration and clinical effect of botulinum toxin A in the treatment of focal hyperhidrosis.Methods The clinical efficacy was observed in 132 sites of 28 patients with focal hyperhidrosis,and the degree and range of focal hyperhidrosis were determined by the minor iodine-starch test.50 U of botulinum toxin A was injected in unilateral axillary,palms and soles with BellaVita instrument and 30 U for forehead.Each patient was followed-up in 1 week,2 weeks and every month after injection for 8 months.According to the results of the minor iodine-starch test the objective effect and evaluation score were obtained,and the comprehensive effect evaluation score was calculated with the objective effect evaluation score and the subjective effect evaluation score in each follow-up.Results The comprehensive effect evaluation score before injection of botulinum toxin A was 1.34±3.94,and that after injection was 23.21±9.44 for 1 week,92.41±11.95 for 1 month,98.21±5.60 for 2 months,95.98±5.94 for 3 months,and 86.61±10.17 for 4 months,respectively.Compared with that before injection,the difference was statistically significant (P ＜0.05).The effect decreased slowly after 4 months of injection,and the efficacy was maintained for 8 months (4.46±6.98);compared with that before injection,the difference of the clinical efficacy was not statistically significant (P ＞0.05).Based on the comprehensive effect evaluation scores,the differ ence of the clinical efficacy was not statistically significant between 1 week and 6 months after injection (P＞0.05).Conclusions The clinical effect of botulinum toxin A injected by BellaVita is prompt and effective for focal hyperhidrosis.
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Objective:To observe the adverse reactions of killer cytokine-induced (CIK) in the treatment of malignant tumor and to analyze the possible mechanism ,and to develop the targeted prevention and treatment measures .Methods: The clinical data, including various adverse reactions , laboratory tests and the corresponding preventive measures against adverse reactions .In 1 240 patients with malignant tumor after treated with CIK cells from May 2013 to September 2015 were retrospectively analyzed .Results:The main adverse reactions after the first infusion of CIK cells were weak (10%),fever(7.25%),shiver (4%),arthralgia (3%),systemic in flammatory response syndrome reaction ( 3%) , digestive tract discomfort ( 0.96%) , acute allergic reaction ( 0.08%) , rash (0.08%),angina pectoris (0.08%),tumor lysis syndrome(0%),infection(0%).With the increase of the treatment ,the incidence of adverse reactions increased and the fever was the main performance ,after the fourth course into the platform .The combination of blood pressure increased or decreased and severe allergic reaction and systemic inflammatory response syndrome was needed to be treated .The CIK cells were pretreated before treatment could reduce the incidence of these reactions .Conclusion:CIK cells therapy is a safe and effective adoptive immunotherapy for malignant tumor and its adverse reactions can be treated expectantly , but rare adverse reactions may have potential risks .
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<p><b>OBJECTIVE</b>To explore the effect of 20 (S)-ginsenoside Rg3 [20 (S)-Rg3] on the proliferation inhibition and secretion of vascular endothelial growth factor (VEGF) of multiple myeloma (MM) cell line U266.</p><p><b>METHODS</b>The proliferation inhibition rate of U266 cells after treatment with different doses of 20 (S)-Rg3 was detected by MTT method, the cell cycle and apoptosis by flow cytometry, the expression of apoptosis related proteins of caspase-3, 8 and 9 by Western blot, VEGF concentration in the culture supernatant by ELISA.</p><p><b>RESULTS</b>It showed that 20 (S)-Rg3 could inhibit the proliferation of U266 in a dose-dependent manner (P<0.05) with IC50 of (71.07 ± 2.63)μmol/L and (44.06 ± 3.98) μmol/L at 24 h and 48 h, respectively. VEGF concentration in the culture supernatant showed a dosedependent reduction (P<0.05), decreased from (419.93 ± 36.76) pg/106 cells in the control group to (314.82 ± 27.05) pg/106 cells in 80 μmol/L 20 (S)-Rg3 treated group by ELISA assay. Flow cytometry with Annexin-V/PI double staining revealed that 20(S)-Rg3 may induce U266 cells apoptosis in a concentration-dependent manner from (0.51 ± 0.05)% at control group to (8.32 ± 0.83)%, (10.72 ± 1.29)% and (15.27 ± 2.26)% at 20, 40 and 80 μmol/L treatment groups, respectively (P<0.05). Flow cytometry with PI staining showed that the ratio of cells in G0/G1 phase increased from (49.11 ± 1.71)% to (52.72 ± 7.75)%, (60.29 ± 5.76)% and (61.81 ± 3.46)%, respectively (P<0.05). Western blot analysis indicated that the expression of caspase-3, 8 and 9 declined, and that of cleaved-caspase-3, 8 and 9 significantly increased (P<0.05) with 20 (S)-Rg3 concentration increased.</p><p><b>CONCLUSION</b>20(S)-Rg3 can inhibit the proliferation of U266 cells by cell cycle arrest in G1 phase and induce cell apoptosis by increasing the expressions of cleaved-caspase-3, -8 and -9. It can also inhibit VEGF secretion of U266 cells, which makes it a potential agent for multiple myeloma therapy.</p>
Subject(s)
Humans , Apoptosis , Caspases , Metabolism , Cell Cycle Checkpoints , Cell Line, Tumor , Cell Proliferation , Ginsenosides , Pharmacology , Multiple Myeloma , Metabolism , Pathology , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
0.05) in the maimed group, indignation score was high, depression score was low and self-esteem score was high ( P