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ObjectiveTo explore the synergetic effect of temperature and PM2.5 on cardiovascular and cerebrovascular diseases. MethodWe collected cardiovascular and cerebrovascular death cases，air pollution and meteorological data during the same period in Pudong New Area from 2013 to 2018.We used generalized additive models （GAMs） with poisson regression including non-stratification model， nonparametric bivariate response model and pollution-stratified parametric model， to assess the interaction between temperature and PM2.5 and on the number of cardiovascular cerebrovascular and cerebrovascular disease deaths. ResultsThe exposure-response relationship between temperature and the number of cardiovascular and cerebrovascular deaths exhibited "U" type and the most comfortable temperature was 18.9 ℃. When the concentrations of PM2.5 increased by 10 μg·m-3， the deaths of total， male， female， ≤75 years and >75 years increased， respectively， by 0.60%（95%CI： 0.30%‒0.91%）， 0.77%（95%CI：0.34%‒1.20%）， 0.46%（95%CI：0.05%‒0.86%）， 0.66%（95%CI：0.03%‒1.30%） and 0.59%（95%CI：0.26%‒0.92%）. With the increase of PM2.5 concentration level， the impact of temperature on cardiovascular and cerebrovascular diseases gradually increased， and the impact was the most significant when the concentration of PM2.5 was more than 150 µg·m-3. There were different sensitive people in different seasons. ConclusionPM2.5 concentration levels of mild pollution and above can exacerbate the negative effects of temperature on cardiovascular and cerebrovascular diseases.
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Aim To examine weather fructo-oligosaccharides(FOS) and silybin(Sil) could exhibit synergetic effect on treating obesity-associated non-alcoholic fatty liver disease(NAFLD).Methods Seventy mice were randomly divided into two groups:control group (NCD,fed with normal chow diet),the other sixty mice were fed with high-fat diet (HFD) to establish NAFLD model.Seventy days after the establishment of experimental model,the latter group was then randomly subdivided into six groups:model (HFD),Sil (30mg· kg-1),FOS (2 000 mg · kg-1),Sil (30 mg ·kg-1) combined with FOS of high,medium and low dose respectively.The NCD and HFD group were given 0.5％ CMC,and the other groups were fed with high-fat diet and given 10 mL · kg-1 by gavage daily,then body weight and food intake were recorded.Fasting blood glucose,insulin,homeostasis model of assessment for insulin resistence index (HOMA-IR) and oral glucose tolerance tests(OGTT) were measured after 120 days.All mice were sacrificed after 130 days,and blood and liver were collected.Levels of TC,TG,ALT,AST in serum were detected,and liver index and pathology were also examined.Results FOS (2 000 mg · kg-1) showed obvious synergism for Sil-mediated attenuation of levels of TC,TG,ALT,AST in serum,fasting blood glucose,insulin,HOMA-IR,OGTI curve,liver index and pathology,but FOS (4 000 mg · kg-1) could not bring superiority with a double dose,except for its improvement in body weight of mice with NAFLD.Conclusions In the treatment of NAFLD,FOS exhibits synergetic effect with Sil.This agent might be a potent candidate for obesity and NAFLD prevention,through modulating the composition of gut microbiota.
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Objective To investigate the synergetic effect of combined astaxanthin ( AST) and lith-ium chloride ( LiCl) treatment on cognitive dysfunction of chronic omethoate poisoned mice. Methods 8 mice were selected randomly as control group from 55 healthy adult male Kunming mice,and the rest were used to establish chronic organophosphate poisoning cognitive impairment models by injecting omethoate 5 mg/kg subcutaneously every day for 4 weeks. Totally 40 successfully established models were randomly divid-ed into model group,AST group,edaravone group,LiCl group and AST+LiCl group with 8 in each. Morris wa-ter maze test was used to examine the learning and memory ability of mice. Contents of reactive oxygen spe-cies (ROS) in hippocampus were measured by enzyme-linked immunosorbent assay (ELISA). Activity of superoxide dismutase ( SOD) in hippocampus was measured by colorimetric assay. Morphology of hippocam-pus area was observed by HE staining. The distribution and expression of p-PI3K,p-Akt,p-GSK3β and p-CREB were determined by immunohistochemical staining ( IHC staining) and Western blot. Results The average escape latency of 5 days in each group was statistically significant (F=1662.147, P<0.05) . The av-erage escape latency of 5 days in AST+LiCl group was significantly lower than that in model group ( all P<0.05) and was lower than other treatment groups. Compared with the control group (0.087±0.007,0.084± 0.009,0.097±0.002,0.076±0.012),the hippocampal neuronal injury in model group was serious,the expres-sions of p-PI3K (0.032±0.008),p-Akt (0.03±0.006),p-GSK3β (0.028±0.007) and p-CREB (0.020± 0.008) was significantly lower ( all P<0.05) . The injuries of hippocampal neurons in AST+LiCl group were slightly lighter than that in model group,and the expression of p-PI3K (0.067±0.008),p-Akt (0.065± 0.005),p-GSK3β (0.068±0.009) and p-CREB (0.062±0.008) in hippocampus was significantly higher than that in model group ( all P<0.05) . Conclusion Combined AST and LiCL treatment exerts neuroprotec-tive effect on cognitive dysfunction induced by chronic organophosphate poisoning via up-regulating the ex-pression of Akt/GSK3β/CREB.
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Objective To investigate the effects of curcumin on proliferation and apoptosis of CD34+CD38-KG1a cells and its synergetic effect with busulfan on CD34+CD38-KG1a cells.Methods The expressions of CD34 and CD38 on the surface of KG1a cells and the effect of curcumin on the cell cycle and apoptosis in CD34+CD38-KG1a cells were detected by flow cytometry.MTT assay was used to analyze curcumin’s inhibitory effects on proliferation and synergistic effect with busulfan on CD34+CD38-KG1a.Clone formation rate was measured by methylcellulose colony-formation assay.Morphological changes of apoptotic cells were observed with the inverted optical microscope.The expression of Bcl-2 at the protein level was detected by Western blot.Results The percentage of CD34+CD38-KG1a was (98.2±3.2)% in KG1a cells.Curcumin could inhibit the proliferation in time-and dose-dependent manners and reduce the colony-formation ability of CD34+CD38-KG1a.The coefficient of drug interaction between curcumin and busulfan was less than 1.CD34+CD38-KG1a cells were arrested in the G0/G1 phase by decreasing S phase cells.Meanwhile,curcumin induced the apoptosis of CD34+CD38-KG1a cells. Apoptotic cells became bigger than normal ones,with unclear cell structure and rough edge of cell membrane.The expression of Bcl-2 at the protein level was down-regulated by curcumin.Conclusion Curcumin inhibited the proliferation of CD34+CD38-KG1a cells by reducing colony-formation ability,arresting cells in the G0/G1 phase and inducing apoptosis.Besides,there was a synergistic effect between curcumin and busulfan in CD34+CD38-KG1a cells.The down-regulated expression of Bcl-2 at the protein level may be associated with curcumin-induced apoptosis of CD34+CD38-KG1a cells.
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OBJECTIVE: To observe the synergetic effect of Xuebijing injection and Cefoperazone Sodium/Sulbactam Sodium for the treatment of patients with sepsis.METHODS: Patients with sepsis were randomly assigned to receive Cefoperazone Sodium/Sulbactam Sodium 3 g bid alone by iv drip(Control Group,75 cases) or in combination with Xuebijing injection(100 mL bid,79 cases) for 7 days.RESULTS: The total efficective rate after 7-day treatment had significant difference between two groups(86.67% in control group versus 94.94% in treatment group,(P