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Aim To investigate the effect of forkhead transcription factors of O classl (FoxO1) on lipopolysaccharide (LPS) -induced acute lung injury and its regulatory mechanism. Methods The model of acute lung injury (ALI) was simulated by LPS. HE staining was used to observe the pathological changes of lung tissues. The contents of tumor necrosis factor a (TNF-a) and interleukin-6 (IL-6) in lung tissues were determined by ELISA. The expression of FoxOl in mouse lung tissues was observed by immunohistochemical staining. The phosphorylation levels of FoxOl, DNA methyltransferase and p38 MAPK were detected by Western blot. The mRNA levels of FoxOl, IL-6, TNF-a and DNA methyltransferase were detected by qRT-PCR. DNA methylation in FoxOl promoter region in lung tissues was detected by nested methylation specific PCR (nMS-PCR). Pulmonary vascular endothelial cells (PVECs) were cultured and transfected with FoxOl siRNA, and the phosphorylation of p38 MAPK was detected by Western blot. The correlation between FoxOl methylation level and inflammatory factors was analyzed by Pearson method. Results Compared with control group, alveolar inflammatory cells increased significantly in LPS group, and pulmonary edema and hyperemia were obvious. TNF-α and IL-6 levels increased by 52. 2% and 150. 4% (P < 0. 05), respectively. The phosphorylation level of p38 MAPK and FoxOl expression increased by 134. 1% and 61. 8% (P < 0. 05), respectively, while the DNA methylation level of Fox0l promoter region decreased by 17. 2% (P < 0. 05). After transfection of FoxOl siRNA in vitro, the phosphorylation level of p38 decreased. Pearson analysis showed that FoxOl methylation level was negatively correlated with inflammatory factors. Conclusion The regulation of FoxOl/p3 8 MAPK signaling pathway by hypomethylation of FoxOl promoter is an important mechanism of LPS-induced acute lung injury.
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Objective:To construct a geriatric comprehensive health evaluation system, and establish the norm of corresponding score.Methods:The methods of Delphi survey was implemented to develop the geriatric comprehensive health evaluation system.The weight coefficients of the items were calculated and assigned according to the expert-graded importance score and Saaty analytic hierarchy process.Reliability and validity of the system were examined.Goodness of fit was evaluated by confirmatory factor analysis.The demarcation norm of geriatric comprehensive health score was established based on an empirical study of 2, 118 non-hospitalized elderly population.Results:During the process of Delphi expert consultation and item analysis, nine items were deleted and two items were added.In the end, the 29-item comprehensive geriatric health evaluation system was developed, which included three dimensions of physiology, psychology, as well as social support and environment.The Cronbach's α coefficient of the evaluation system was 0.709.The exploratory factor analysis-extracted ten common factors meet ten second-level items.Confirmatory factor analysis indicated that the goodness of fit of the system was good.Geriatric health status was divided into five grades of very poor, poor, general, good and excellent by 0.5 to 1 standard deviation.The demarcation norm of geriatric comprehensive health score for different age and gender was established accordingly.Conclusions:The reliability and validity of the geriatric comprehensive health evaluation system are satisfactory.The construction of comprehensive health evaluation system and the establishment of the norm can facilitate the quantitative assessment of geriatric health status, and provide a reference for the screening and grading of individual health status in the elderly.
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Colorectal cancer is a kind of cancer with high incidence in the world, and its etiology has not been completely understood yet. Gut bacteria take part in the occurrence and the progression of colorectal cancer in a number of ways, and thereinto, the enrichment of specific bacteria have been proved to be closely correlated with colorectal cancer. This article summarizes the changes of intestinal flora in patients with colorectal cancer and the bacteria related to colorectal cancer; and also discusses the strategies in treatment and prevention of colorectal cancer through regulating the intestinal flora.
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Objective:To investigate the balance in young adult with scoliosis. Methods:From June to December, 2020, 30 college students with scoliosis in the outpatient department of Rehabilitation Department of Kunming Medical University Hospital were as the patients, and 30 normal peers were as the controls. They were measured with Pro-Kin balance test system to assess the static stability of both feet standing with eyes opened and closed, and the static and dynamic limit of stability (LOS) of both feet standing. Results:The moving distance of center of pressure (COP) on the Y-axis was longer in the patients than in the controls with both eye-opened and eye-closed (t > 2.022, P < 0.05). The static and dynamic LOS was less in the patients than in the controls (t > 3.365, P < 0.01). For static LOS, it was less in all the directions except left-forward and backward (t > 2.410, P < 0.05); for dynamic LOS, it was less in the directions of forward, right, left and left-forward (t > 2.446, P < 0.05). Conclusion:Both static and dynamic balance is deficient for yong adults with scoliosis, which may result in risk of fall.
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Notoginsenosides, the saponins extracted from Panax notoginseng, have many pharmacological effects, such as anti-inflammation, anti-oxidation, anti-tumor, nervous system and cardiovascular system protection, microcirculation improvement and calcium overload inhibition. At present, notoginsenosides are widely used clinically for treating many diseases with good efficacy, especially for nervous system diseases such as stroke, stroke sequelae and Alzheimer's disease. In recent years, the mechanism underlying their neuroprotective effect has been continuously explored. To advance the applied research on notoginsenosides in the prevention and treatment of central nervous system diseases, this paper, combined with the latest reports, summarizes their neuroprotective effect and mechanisms in terms of regulating voltage-gated ion channels, protecting nerve cells and neurovascular unit, inhibiting oxidative stress and inflammatory reaction, promoting angiogenesis and reducing excitatory neurotoxicity. Although the protective mechanism of notoginsenosides for the nervous system mainly involves the above several aspects, some of them still remain to be fully elucidated, which necessitates the further exploration of neuroprotective effect of notoginsenosides with molecular biology, metabolomics, proteomics and other technologies.
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Many recent studies have shown that the gut microbiome plays important roles in human physiology and pathology. Also, microbiome-based therapies have been used to improve health status and treat diseases. In addition, aging and neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, have become topics of intense interest in biomedical research. Several researchers have explored the links between these topics to study the potential pathogenic or therapeutic effects of intestinal microbiota in disease. But the exact relationship between neurodegenerative diseases and gut microbiota remains unclear. As technology advances, new techniques for studying the microbiome will be developed and refined, and the relationship between diseases and gut microbiota will be revealed. This article summarizes the known interactions between the gut microbiome and neurodegenerative diseases, highlighting assay techniques for the gut microbiome, and we also discuss the potential therapeutic role of microbiome-based therapies in diseases.
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Many recent studies have shown that the gut microbiome plays important roles in human physiology and pathology. Also, microbiome-based therapies have been used to improve health status and treat diseases. In addition, aging and neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, have become topics of intense interest in biomedical research. Several researchers have explored the links between these topics to study the potential pathogenic or therapeutic effects of intestinal microbiota in disease. But the exact relationship between neurodegenerative diseases and gut microbiota remains unclear. As technology advances, new techniques for studying the microbiome will be developed and refined, and the relationship between diseases and gut microbiota will be revealed. This article summarizes the known interactions between the gut microbiome and neurodegenerative diseases, highlighting assay techniques for the gut microbiome, and we also discuss the potential therapeutic role of microbiome-based therapies in diseases.
الموضوعات
Humans , Alzheimer Disease/therapy , Gastrointestinal Microbiome , Microbiota , Neurodegenerative Diseases/therapy , Parkinson Disease/therapyالملخص
OBJECTIVE:To investigate the effects of Buyang huanwu decoction on lipid metabolism and hepatic tissue in hyperlipemia model rats. METHODS :Male SD rats were randomly divided into blank control group ,model group ,positive control group (simvastatin 0.004 g/kg),Buyang huanwu decoction low-dose and high-dose groups (3.5,14.0 g/kg,by crude drugs),with 10 rats in each group. Except that blank control group was given water intragastrically ,hyperlipidemia mode of other groups was established by intragastric administration of fat emulsion according to the body weight. From the 21st day after modeling,the rats in each group were given water or fat emulsion in the morning and water or corresponding drugs in the afternoon for consecutive 20 days. After last medication ,the contents of TG ,TC,LDL-C,ALT,AST,LCAT,PLTP and HL in plasma were determined in each group ;the contents of LPL ,MTP and HMG-CoA redutase in liver tissue were also determined. The pathological changes of liver tissue were observed in each group. RESULTS :Compared with blank control group ,the contents of TG ,TC,LDL-C,ALT and HMG-CoA reductase were increased significantly in model group (P<0.05 or P<0.01),while the contents of HL ,LPL and MTP were decreased significantly (P<0.01). Compared with model group ,the contents of TG ,TC, LDL-C and HMG-CoA reductase in administration groups as well as the contents of ALT ,AST in Buyang huanwu decoction low-dose and high-dose groups were decreased significantly (P<0.05 or P<0.01);the contents of HL and MTP in administration groups as well as the content of LPL in positive control group were increased significantly (P<0.05 or P<0.01). Pathological sections showed that the hepatocytes of model group were arranged irregularly ,and there was obvious cell steatosis. The hepatocytes in positive control group and Buyang Huanwu decoction high-dose group had almost no abnormal change compared with blank control gr oup,and there was a small amount of slight cell steatosis in Buyang Huanwu decoction low-dose group. CONCLUSIONS : Buyang huanwu decoction has a 础。E-mail:zhang520-888@163.com significant lipid-lowering effect on hyperlipemia model rats ,which may be related to the regulation of lipid absorptiontransport and metabolism by regulating the expression of lipid 126.com metabolism related enzymes and transporter.
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@#【Objective】 To investigate whether the dedifferented human umbilical cord mesenchymal stem cells(hMSC)modified by IDO gene can get improved ability to survive oxidative stress as well as to induce regulatory T(Treg) lymphocytes.【Methods】The dedifferentiated hMSC(De- hMSC)were obtained by a transient adipogenic induction and subsequent recovery culture in normal medium. The IDO gene modified De-hMSC (IDO/De-hMSC)were prepared by retroviral infection using recombinant retrovirus harboring IDO gene. The De- hMSC infected by retrovirus containing ZsGreen1 gene,the non- infected De- hMSC and hMSC were set as controls. Exogenous expression of IDO protein was confirmed by Western blot. Flow cytometry analysis was performed to detect the immunophenotype of IDO/De- hMSC , and their osteogenic/adipogenic differentiation abilities were also assessed. Cell survival rates under the oxidative stress of 300 μmol/L t- BHP were determined by Annexin V- FITC/PI double staining flow cytometry. Human peripheral blood mononuclear cells (PBMC) were isolated and treated with conditioned medium containing the culture supernatant of hMSC,De-hMSC,Mock/De-hMSC and IDO/De-hMSC,respectively. Changes in the proportion of CD4+ CD25+ CD127low Treg cells in PBMC were determined by triple fluorescent labeling flow cytometry.【Results】The De-hMSC modified by IDO gene still have the immunophenotype as well as the osteogenic/adipogenic differentiation abilities that are typical of mesenchymal stem cells. When challenged by 300 μmol/L t-BHP,the number of viable cells in De-hMSC significantly elevated compared with hMSC(P<0.05),and the survival advantage of De-hMSC was not obviously affected by IDO gene modification(P>0.05). Conditioned medium containing the supernatant from IDO/De- hMSC dramatically up- regulated the percentage of CD4+CD25+CD127low Treg cells in PBMC in contrast to the control groups(P<0.05).【Conclusions】IDO/ De- hMSC have the same immunophenotype and differentiation capacity as the native hMSC ,and can simultaneously enhance the ability of hMSC to survive against oxidative stress and to induce Treg cells ,which may be a potential modification strategy of mesenchymal stem cells for immunosuppressive therapy.
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Objective To evaluate the role of phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/Akt) signaling pathway in propofol-induced inhibition of migration and invasion ability of human nonsmall cell lung cancer H1975 cells.Methods H1975 cells were divided into 4 groups (n=36 each) using a random number table method:control group (group C),20 μg/ml propofol group (group P),0.5 ng/ml PI3K/Akt signaling pathway activator insulin-like growth factor 1 (IGF-1) group (group IGF-1),and 20 μg/ml propofol plus 0.5 ng/ml IGF-I group (group P+IGF-1).The migration and invasion ability of H1975 cells was determined by wound healing assay and Transwell invasion assay,respectively.The expression of phosphorylated Akt (p-Akt) and matrix metalloproteinase-9 (MMP-9) was assessed by Western blot.Results Compared with group C,and the ability of migration and invasion was significantly reduced,and the expression of p-Akt and MMP-9 was down-regulated in group P,and the ability of migration and invasion was significantly enhanced,and the expression of p-Akt and MMP-9 was up-regulated in group IGF-1 (P<0.05).Compared with group P,the ability of migration and invasion was significantly enhanced,and the expression of p-Akt and MMP-9 was up-regulated in group P+IGF-1 (P<0.05).Compared with group IGF-1,the ability of migration and invasion was significantly reduced,and the expression of p-Akt and MMP-9 was down-regulated in group P+IGF-1 (P<0.05).Conclusion The mechanism by which propofol inhibits migration and invasion ability of human non-small cell lung cancer H1975 cells is related to blocking PI3K/Akt signaling pathway.
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BACKGROUND@#Lung cancer is a malignant tumor disease with high morbidity and high mortality. The non-small cell lung cancer (NSCLC) is the most common type, among them, lung squamous cell carcinoma own special pathological type and specific treatment, is a subtype of non-small cell lung cancer and can be divided into peripheral type and central type according to clinical phenotype. This study explores the differences in gene levels and their potential values based on clinical differences between central and peripheral in lung squamous cell carcinoma.@*METHODS@#The lung squamous cell carcinoma dataset was collected from The Cancer Genome Atlas (TCGA) database, clinical information and the corresponding gene expression profiles were downloaded. Then we further sort and analyze all these data.@*RESULTS@#In clinical characteristics analysis, result showed that central lung squamous cell carcinoma was more likely to metastasis with lymph node than peripheral lung squamous cell carcinoma (46.2%, 67/145 vs 28.9%, 26/90; P=0.019), while there were no significant differences in gender, age, tumor size, distant metastasis, tumor node metastasis (TNM) stage, and EGFR mutation. Gene expression analysis showed 1,031 differentially expressed genes between central and peripheral lung squamous cell carcinoma, of which 629 genes were up-regulated and 402 genes were down-regulated (peripheral vs central). Further enrichment analysis showed differentially expressed genes were mainly riched in 6 signaling pathways. Among them, the neuroactive ligand-receptor interaction pathway was the main enrichment pathway of differentially expressed genes, and other differential expressed genes were mainly involved in lipid metabolism and glucose metabolism. The analysis of interaction network showed that hepatocyte nuclear factor 1 homeobox A (HNF1A) and cytochrome p450 family, Cytochrome P450 3A4 (CYP3A4) own widely effect in up-regulated genes, while ALB and APOA1 at the key positions of the network in down-regulated genes were CONCLUSIONS: Central and peripheral lung squamous cell carcinoma showed clinical phenotype difference not only reflected in the incidence of lymph node metastasis, but also in gene expression profiles. Among them, HNF1A, CYP3A4, ALB, APOA1 at the key position of the differential gene interaction network and maybe as regulatory factors in the phenotypic difference.
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Aged , Female , Humans , Male , Middle Aged , Carcinoma, Squamous Cell , Genetics , Databases, Genetic , Gene Expression Profiling , Gene Regulatory Networks , Kaplan-Meier Estimate , Lung Neoplasms , Genetics , Smoking , Geneticsالملخص
BACKGROUND@#Lung cancer is one of the most deadly cancers in the world for human. In recent years, the effect of targeted therapy has become increasingly significant. Apatinib is a multi-target anti-tumor drug that is currently under study. The purpose of this study is to investigate the effects of Apatinib on the biological characteristics of lung cancer cells and its possible mechanism.@*METHODS@#Lung cancer cell lines H1299 and H3255 were cultured in vitro. The effects of Apatinib on proliferation, migration and invasion of H1299 and H3255 cells were detected by cell proliferation assays wound healing assays and Transwell assays. The protein expression related to cancer angiogenesis and invasion was detected by Western blot.@*RESULTS@#Apatinib significantly inhibited the proliferation, migration and invasion of H1299 and H3255 in a concentration-dependent manner. Western blot showed that with the increasing of drug concentration, VEGF, VEGFR2, N-cadherin, MMP9, MMP2 and Vimentin were down-regulated, and E-cadherin were up-regulated.@*CONCLUSIONS@#Apatinib can inhibit the invasion and migration of lung adenocarcinoma cells H1299 and H3255. By regulation of epithelial-mesenchymal transition and the expression of matrix metalloproteinase-related proteins.
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Humans , Antineoplastic Agents , Pharmacology , Cell Line, Tumor , Cell Movement , Lung Neoplasms , Pathology , Neoplasm Invasiveness , Pyridines , Pharmacologyالملخص
BACKGROUND@#Lung cancer is one of the common malignant tumors that impair human health. With the development of epigenetics, the researchers found that enhancer of Zeste homolog 2 (EZH2) is highly expressed in lung cancer tissue and its expression is closely related to the prognosis. EZH2 inhibitor can also enhance the sensitivity of tumor cells to a variety of anti-tumor drugs. The purpose of this study is to investigate the effect of combination of EZH2 inhibitor and gefitinib on the proliferation, apoptosis and migration of Gefitinib-resistant lung cancer cells.@*METHODS@#PC9 and PC9/AB2 cells were used for this study. CCK-8 and EdU experiment were used to detect combined treatment on cell viability and proliferation activity; Wound healing assay and Transwell chamber experiment were used to determine the effects of combination therapy on cell migration ability; Flow cytometry was used to detect the effect of combination therapy on EZH2 and apoptosis; Western blot was used to observe the effect of combination therapy on epidermal growth factor receptor (EGFR) signaling pathway-related proteins expression.@*RESULTS@#In gefitinib-resistant cell line PC9/AB2, gefitinib combined with EZH2 inhibitor GSK343 can significantly inhibit cell viability, reduce cell migration and increase cell apoptosis. At the same time, combination therapy can significantly inhibit the expression of EZH2 and phosphorylation EGFR proteins.@*CONCLUSIONS@#The combination of EZH2 inhibitor GSK343 and gefitinib sensitize PC9/AB2 cell to gefitinib response. This study also suggests that synergistic therapy plays a role in the reversal of EGFR-tyrosine kinase inhibitor (EGFR-TKIs) resistance in lung cancer.
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Humans , Antineoplastic Agents , Pharmacology , Cell Line, Tumor , Cell Movement , Cell Proliferation , Cell Survival , Drug Resistance, Neoplasm , Drug Synergism , Enhancer of Zeste Homolog 2 Protein , ErbB Receptors , Gefitinib , Pharmacology , Lung Neoplasms , Pathology , Protein Kinase Inhibitors , Pharmacologyالملخص
BACKGROUND@#Angiogenesis is an important process in the development of tumor. PD 0332991, a cell cycle inhibitor, can specifically inhibit CD4/6 phosphorylation and cell cycle progression. In xeongraft mice models, PD 0332991 treated mice had significantly decreased angiogenesis and vascular density compared with the control group, but the mechanism remains unknown. The purpose of this study is to investigate the role and molecular mechanism of PD 0332991 on vascular endothelial cells.@*METHODS@#EA.hy926 cells, a kind of vascular endothelial cell, were used as the research model. The effects of PD 0332991 on the activity and proliferation of EA.hy926 cells were detected by the MTT, EdU assays. Wound-healing assays and transwell assays were used to determine the effects of PD 0332991 on the mobility of EA.hy926. The influence of PD 0332991 on cell cycle and apoptosis of endothelial cells was tested by flow cytometry, and the Western blot was applied to observe the expression of cell cycle related proteins in EA.hy926 cells treated by PD 0332991.@*RESULTS@#PD 0332991 significantly inhibited the proliferation and mobility of EA.hy926 cells, caused cell cycle arrest and apoptosis. At the same time, PD 0332991 inhibited the expression of CDK4/6 and phosphorylation of Rb, and thus inhibited the cell cycle progression of EA.hy926 cells.@*CONCLUSIONS@#PD 0332991 can inhibit the proliferation and activity of endothelial cells and induces apoptosis.
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Animals , Humans , Mice , Angiogenesis Inhibitors , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Proliferation , Cell Survival , Cyclin-Dependent Kinase 4 , Genetics , Metabolism , Cyclin-Dependent Kinase 6 , Genetics , Metabolism , Endothelial Cells , Cell Biology , Metabolism , Lung Neoplasms , Drug Therapy , Genetics , Metabolism , Piperazines , Pharmacology , Pyridines , Pharmacologyالملخص
BACKGROUND@#LC-3 and P62, two of important autophagy-related proteins, were reported highly expressed in many kinds of human malignancies and associated with outcomes of the patients. The purpose of this study was to investigate the expression status of LC-3 and P62 in non-small cell lung cancer patients and define the clinical-pathologic features.@*METHODS@#66 cases of non-small cell lung cancer patients were employed. The expression of LC-3 and P62 were detected by immunohistochemistry.@*RESULTS@#LC-3 was positive stained in 27 out of 66 cases (40.9%) and P62 was positive stained in 43 out of 66 cases (65.2%). LC-3 positive staining was more frequently in squamous cell carcinoma patients (P<0.05); while P62 positive staining was more frequently in late-stage adenocarcinoma patients with metastasis (P<0.05). There was a significant negative correlation between LC-3 and P62 expressions in non-small cell lung cancer tissues (rs=-0.065, P<0.001). Kaplan-Meier analysis showed that patients with positive LC-3 expression had favorable clinical outcomes compared with the patients with negative LC-3 expression (P<0.05).@*CONCLUSIONS@#LC-3 and P62 showed abnormal expression in non-small cell lung cancer tissues, suggesting that autophagy is involved in the occurrence and development of NSCLC.
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Female , Humans , Male , Middle Aged , Carcinoma, Non-Small-Cell Lung , Diagnosis , Metabolism , Gene Expression Regulation, Neoplastic , Kaplan-Meier Estimate , Lung Neoplasms , Diagnosis , Metabolism , Microtubule-Associated Proteins , Metabolism , Prognosis , Proto-Oncogene Proteins c-myc , Metabolismالملخص
Objective To evaluate the effect of high-frequency oscillatory ventilation (HFOV) on lung injury in the piglets with acute respiratory distress syndrome (ARDS).Methods Twelve male piglets,aged 6-8 weeks,weighing 14-16 kg,were randomly divided into 2 groups (n=6 each) using a random number table:conventional mechanical ventilation with low tidal volume group (CMV group) and HFOV group.ARDS was induced by bilateral pulmonary lavages with isotonic saline (38 ℃),repeated every 10 min until the oxygenation index<200 mmHg.After successful establishment of the model,CMV group was ventilated using conventional mechanical ventilation with low tidal volumes.After successful establishment of the model,HFOV group was ventilated using HFOV,lung recruitment was performed,the airway pressure was set at 25 cmH2O and maintained at this level for 30 s,and the airway pressure was then adjusted 5 cmH2O higher than that after successful establishment of the model,with bias flow 25 L/min,inspiratory time ratio 33%,frequency 8 Hz,amplitude 40-80 cmH2O,and inspiratory oxygen fraction 1.0.In both groups,carbon dioxide partial pressure was maintained between 35 and 50 mmHg.Before establishment of the model (baseline),after successful establishment of the model (T1),and at 0.5,1.0,2.0 and 4.0 h after beginning of mechanical ventilation (T2-5),blood samples were collected from the femoral artery and central vein for blood gas analysis,arterial oxygen partial pressure and carbon dioxide partial pressure were recorded,oxygen delivery index,oxygen consumption index,oxygenation index and intrapulmonary shunt were calculated,and the improvement in pulmonary function (oxygenation index ≥ 200 mmHg) was recorded.At T0,T1 and T5,venous blood samples were collected for determination of the concentrations of serum Clara cell secretory protein 16,soluble intercellular adhesion molecule-1,and high-mobility group box 1.Results Compared with CMV group,the arterial oxygen partial pressure at T35 and oxygenation index at T4.5 were significantly increased (P < 0.05),and no significant change was found in the other parameters in HFOV group (P>0.05).Conclusion Compared with conventional mechanical ventilation with low tidal volumes,although HFOV improves lung oxygenation,the degree is small in the piglets with ARDS.
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Objective To observe the intervention effect of Ginkgo biloba extract EGb761 on tert-butyl hydroperoxide ( t-BHP)-induced injury in human umbilical cord-derived mesenchymal stem cells ( hUC-MSCs) . Methods Proliferation of hUC-MSCs after primary culture was detected by methyl thiazolyl tetrazolium (MTT) assay, and then the optimal concentrations of t-BHP and EGb761 for oxidative stress injured MSC model were screened. Cell apoptosis was assessed by flow cytometry after Annexin V-fluorescein isothiocyanatel propidium iodide ( Annexin V-FITC/PI) staining. Content of malondialdehyde ( MDA) and superoxide dismutase (SOD) activity in hUC-MSCs were evaluated, and the expression levels of p53 and p21Cip1/Waf1 were analyzed by real-time fluorescence PCR. Results Pretreatment with 10~200 mg/L of EGb761 for 3 hours reduced the sensitivity of hUC-MSCs to t-BHP ( 100 μmol/L) induced proliferation inhibition, while EGb761 over 100 mg/L had no significant effect on enhancing the protection of hUC-MSCs . EGb761 at 100 mg/L prohibited hUC-MSCs apoptosis and MDA accumulation in hUC-MSCs induced by 100μmol/L of t-BHP acting for 6 hours, maintained the enzymatic activity of SOD, and decreased the expression of p53 and p21Cip1/Waf1 in hUC-MSCs with t-BHP-induced injury. Conclusion EGb761 is capable of protecting hUC-MSCs against oxidative stress injury, and its mechanism is probably related with the modulation of p53/p21 signal pathway.
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The effect of high frequency oscillatory ventilation (HFOV) at early stage on hemodynamic parameters, extravascular lung water (EVLW), lung capillary permeability, CC16 and sICAM-1 in piglets with pulmonary or extrapulmonary acute respiratory distress syndrome (ARDS) was explored. Central vein pressure (CVP) and pulse indicator continuous cardiac output (PiCCO) were monitored in 12 anesthetized and intubated healthy piglets. Pulmonary ARDS (ARDSp) and extrapulmonary ARDS (ARDSexp) models were respectively established by lung lavage of saline solution and intravenous injection of oleic acid. Then the piglets received HFOV for 4 h. EVLW index (EVLWI), EVLW/intratroracic blood volume (ITBV) and pulmonary vascular permeability index (PVPI) were measured before and after modeling (T0 and T1), and T2 (1 h), T3 (2 h), T4 (3 h) and T5 (4 h) after HFOV. CC16 and sICAM-1 were also detected at T1 and T5. Results showed at T1, T3, T4 and T5, EVLWI was increased more significantly in ARDSp group than in ARDSexp group (P<0.05). The EVLWI in ARDSp group was increased at T1 (P=0.008), and sustained continuously within 2 h (P=0.679, P=0.216), but decreased at T4 (P=0.007) and T5 (P=0.037). The EVLWI in ARDSexp group was also increased at T1 (P=0.003), but significantly decreased at T3 (P=0.002) and T4 (P=0.019). PVPI was increased after modeling in both two groups (P=0.004, P=0.012), but there was no significant change within 4 h (T5) under HFOV in ARDSp group, while PVPI showed the increasing trends at first, then decreased in ARDSexp group after HFOV. The changes of EVLW/ITBV were similar to those of PVPI. No significant differences were found in ΔEVLWI (P=0.13), ΔPVPI (P=0.28) and ΔEVLW/ITBV between the two groups (P=0.63). The significant decreases in both CC16 and sICAM-1 were found in both two groups 4 h after HFOV, but there was no significant difference between the two groups. It was concluded that EVLWI and lung capillary permeability were markedly increased in ARDSp and ARDSexp groups. EVLW could be decreased 4 h after the HFOV treatment. HFOV, EVLW/ITBV and PVPI were increased slightly at first, and then decreased in ARDSexp group, while in ARDSp group no significant difference was found after modeling. No significant differences were found in the decreases in EVLW and lung capillary permeability 4 h after HFOV.
الموضوعات
Animals , Capillaries , High-Frequency Ventilation , Lung , Respiratory Distress Syndrome , Swineالملخص
The effect of high frequency oscillatory ventilation (HFOV) at early stage on hemodynamic parameters, extravascular lung water (EVLW), lung capillary permeability, CC16 and sICAM-1 in piglets with pulmonary or extrapulmonary acute respiratory distress syndrome (ARDS) was explored. Central vein pressure (CVP) and pulse indicator continuous cardiac output (PiCCO) were monitored in 12 anesthetized and intubated healthy piglets. Pulmonary ARDS (ARDSp) and extrapulmonary ARDS (ARDSexp) models were respectively established by lung lavage of saline solution and intravenous injection of oleic acid. Then the piglets received HFOV for 4 h. EVLW index (EVLWI), EVLW/intratroracic blood volume (ITBV) and pulmonary vascular permeability index (PVPI) were measured before and after modeling (T0 and T1), and T2 (1 h), T3 (2 h), T4 (3 h) and T5 (4 h) after HFOV. CC16 and sICAM-1 were also detected at T1 and T5. Results showed at T1, T3, T4 and T5, EVLWI was increased more significantly in ARDSp group than in ARDSexp group (P<0.05). The EVLWI in ARDSp group was increased at T1 (P=0.008), and sustained continuously within 2 h (P=0.679, P=0.216), but decreased at T4 (P=0.007) and T5 (P=0.037). The EVLWI in ARDSexp group was also increased at T1 (P=0.003), but significantly decreased at T3 (P=0.002) and T4 (P=0.019). PVPI was increased after modeling in both two groups (P=0.004, P=0.012), but there was no significant change within 4 h (T5) under HFOV in ARDSp group, while PVPI showed the increasing trends at first, then decreased in ARDSexp group after HFOV. The changes of EVLW/ITBV were similar to those of PVPI. No significant differences were found in ΔEVLWI (P=0.13), ΔPVPI (P=0.28) and ΔEVLW/ITBV between the two groups (P=0.63). The significant decreases in both CC16 and sICAM-1 were found in both two groups 4 h after HFOV, but there was no significant difference between the two groups. It was concluded that EVLWI and lung capillary permeability were markedly increased in ARDSp and ARDSexp groups. EVLW could be decreased 4 h after the HFOV treatment. HFOV, EVLW/ITBV and PVPI were increased slightly at first, and then decreased in ARDSexp group, while in ARDSp group no significant difference was found after modeling. No significant differences were found in the decreases in EVLW and lung capillary permeability 4 h after HFOV.
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Objective:To explore changes of central retinal vascular caliber and fractal dimension (Df) and their cor‐relation with blood pressure in hypertensive population .Methods :A total of 2169 subjects>30 years old were en‐rolled in this cross‐sectional study .They were divided into hypertension group (n=819) and non‐hypertension group (n=1350) .Fundus photos were collected in all subjects ,and semi‐automatic software was used to quantitatively ana‐lyze central retinal vascular caliber and Df ,and they were compared between two groups .Results:Compared with non- hypertension group ,there were significant reductions in central retinal arteriolar equivalent [CRAE ,(135.2 ± 10.72) μm vs .(132.25 ± 11.56) μm] ,central retinal venular equivalent [CRVE ,(184.95 ± 16.29) μm vs . (182.52 ± 17.07)μm] and Df [ (1.38 ± 0.05) vs .(1.34 ± 0.05)] in hypertension group , P5 years group was significantly lower than that of ≤5 years group [ (1.33 ± 0.05) vs .(1.35 ± 0.05)] , P<0.01. Conclusion:CARE ,Df are significantly in‐versely correlated to SBP ,DBP and PP in hypertensive population ,while correlation of Df is most .