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Objective:To investigate the relationship of swallowing experience to frailty and nutrition in old stroke inpatients. Methods:From March to July, 2019, 174 stroke inpatients aged above 60 were investigated with Dysphagia Handicap Index (DHI), FRAIL Scale and Mini Nutritional Assessment Short Form (MNA-SF). The correlation of DHI score to scores of FRAIL Scale and MNA-SF was analyzed with Pearson correaltion analysis. Multiple regression was analyzed using the scores of dimensions and total score of DHI as dependent variables, and the scores of FRAIL Scale and MNA-SF as independent variables. Results:The inpatients aged (76.16±9.908) years. The DHI score was (50.34±28.325), in which the body score was (17.68±10.254), the function score was (20.31±11.085) and the emotion score was (12.36±9.193). The FRAIL Scale score was (3.16±1.301), and the MNA-SF score was (8.95±2.529). The DHI scores positively correlated with the FRAIL Scale score (r = 0.575, P < 0.001) and negatively correlated with the MNA-SF score (r = -0.544, P < 0.001). The scores of FRAIL Scale and MNA-SF explained the 34.4% of variable for body, 38.7% for function, 36.1% for emotion and 42.4% for DHI total score. Conclusion:Improving the frailty and nutrition may reduce the poor swallowing experience for old stroke inpatients.
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Objective:To test the reliability and validity of Work-ability Support Scale (WSS) in stroke patients. Methods:WSS was translated into Chinese with the standard translation-retroversion. From December, 2018 to March, 2019, 193 middle-aged and young stroke patients from two community health service centers in Zhengzhou were conveniently selected, and investigated with Chinese WSS by two nurses. The data were analyzed with item analysis, content validity, exploratory factor analysis, internal consistency reliability and inter-rater reliability. Results:The content validity was 0.94 in WSS A and 0.90 in WSS B. Three factors were extracted from 16 items in WSS A, with cumulative variance contribution of 67.747%; while three factors were extracted from 12 items in WSS B, with cumulative variance contribution of 56.056%. Cronbach's α was 0.933 and 0.778 in WSS A and WSS B, respectively. The kappa coefficient was above 0.6 between two raters in every item, except items B8 and B10. Conclusion:Chinese WSS is satisfactory in validity and reliability for using in young and middle-aged stroke patients during their return to work.
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Home environment assessment tools for people with disabilities can be classfied into those based on classical test theory and item response theory. This paper reviewed the content, methods, target population, reliability and validity of the two types of home environment assessment tools and summarized their advantages and disadvantages.
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Objective:To construct a nursing grading evaluation indicator system for patients with stroke at home to provide a basis for graded care. Methods:Based on literature analysis, qualitative interviews and panel meeting, an evaluation indicator system was preliminarily drafted. June to September, 2018, the indicator system was consulted to experts three times. It was used to evaluate 210 patients with stroke at home from September to December, 2018 to test its reliability and validity. Results:The effective recovery rates of the three times of consultation were 85.00%, 89.47% and 100%, and the authority coefficient were 0.878, 0.879 and 0.879. The indicator system included four first-level indicators, 30 second-level indicators and 120 items. The scale-level content validity index (CVI) universal agreement was 0.733, average CVI was 0.927; the item-level CVIs were 0.83 to 1.00. For the overall level, the Cronbach's α coefficient was 0.928, and the Guttman Spilt half-factor coefficient was 0.794. For the dimensions, the Cronbach's α coefficient and the Guttman Spilt half-factor coefficients were all above 0.700. The correlated coefficients inter-evaluator of each indicators were 0.492 to 0.963 (P< 0.05). Conclusion:The nursing grading evaluation indicator system for patients with stroke at home is simple and operable, with satisfactory reliability and validity to grade the level of care for patients with stroke at home.
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Objective:To develop and evaluate the effect of Professional Care APP for stroke patients at home. Methods:Professional Care APP 1.0 was developed by reviewing literature, analyzing APP function and consulting expert, and combined with the findings at the early stage. And then it was upgraded to APP 2.0 after a 4-week trial in 10 stroke patients at home, which included two parts: patient-side and medical-side. The patient-side provided health education, rehabilitation guidance, medication reminder, online consultation and so on. From December, 2017 to June, 2018, 77 stroke patients in a community in Zhengzhou, China were conveniently selected and randomly divided into control group (n = 39) and intervention group (n = 38). The control group received routine community follow-up, and the intervention group received Professional Care APP 2.0, for 12 weeks. Results:After a 12-week intervention, the level of knowledge and medication compliance was significantly higher in the intervention group than in the control group (t > 4.205, P < 0.001). The score of demand for professional care was significantly lower in the intervention group than in the control group (t = -18.183, P < 0.001). The intervention group made a good evaluation for APP in usefulness, ease of learning, usability, credibility, acceptability and satisfaction. Conclusion:Professional Care APP can meet the professional care needs, and improve the level of knowledge on disease and medication compliance for stroke patients at home. The patients' evaluation for APP is ideal.
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OBJECTIVE@#To compare the clinical effects of total hip arthroplasty(THA) with non-osteotomy and subtrochanteric osteotomy in the treatment of Crowe type IV hip dysplasia (DDH) in adults.@*METHODS@#Data of 35 Crowe type IV DDH patients who underwent THA were analyzed retrospectively, the patients were divided into two groups:15 cases of non-osteotomy and 20 cases of subtrochanteric osteotomy. There was no significant difference in age, gender, body mass index between two groups (>0.05). The operative time, bleeding volume, hospitalization duration, Harris hip score and the limb length discrepancy (LLD) were evaluated.@*RESULTS@#All of the patients were followed up for 12 to 48 months, no prosthesis loosening or infection occurred by the end of follow-up. In non-osteotomy group, 1 case had occurred by sciatic nerve injury and 1 case developed cutaneous branch injury of the femoral nerve, both of which were spontaneously recovered completely without treatment after 3 months. One case of dislocation occurred in subtrochanteric osteotomy group, after closed reduction, dislocation did not recur; three cases had proximal femoral crack fractures and received steel plate fixation; no reoperation was needed. There was significant difference in operation duration, bleeding volume, and hospitalization days between two groups(0.05). The postoperative discrepancy of bilateral lower limbs had significant difference(<0.05).@*CONCLUSIONS@#THA with no femoral shortening osteotomy can achieve good clinical results in patients with unilateral Crowe IV developmental dysplasia of hip. Comparing with subtrochanteric osteotomy, the procedure of no femoral shortening osteotomy is easier technically. For unilateral high dislocation DDH patients with limb lengthening <=4 cm and good tissue conditions, THA without femoral osteotomy may be considered.
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Adult , Humans , Arthroplasty, Replacement, Hip , Femur , Hip Dislocation, Congenital , General Surgery , Osteotomy , Retrospective StudiesABSTRACT
BACKGROUND: Some studies have found that zinc ions have pro-osteogenic activity, while zinc ions at high levels are also reported to inhibit the differentiation of osteoblasts instead of the pro-osteogenic activity. In some studies, zinc ions that are injected into the surface of titanium have ineffective antibacterial effects. Therefore, further investigations on zinc ion's effects as a controversial topic are required. OBJECTIVE: To observe the effects of zinc ion content on the pro-osteogenic and antibacterial activities of micro-arc oxidation coatings. METHODS: The coating was made on the surface of titanium by micro-arc oxidation method. The zinc ion content (atomic percentage) in the coating was set to 0.199%, 0.574%, and 1.995%, respectively, as low, medium and high dose groups. Untreated titanium plates were used as controls. MG63 cells were seeded on the surface of four groups of materials and tested for cell proliferation, morphological changes, and alkaline phosphatase activity.Staphylococcus aureus was inoculated on the surface of four groups of materials and the antibacterial rate was detected at 48 hours after inoculation. Bacterial adhesion was observed at 24 hours after inoculation. RESULTS AND CONCLUSION: Within 7 days of culture, the number of MG63 cells on the material surface gradually increased with time. The proliferative ability of cells was highest in the low-dose group, followed by the middle-dose and control group, and it was lowest in the high-dose group. After 48 hours of culture, the cells in the control, low-dose and middle-dose groups showed normal morphology and expanded pseudopodia, and some pseudopodia penetrated into the cell surface, while normal or intact cells were undetected in the high-dose group. Within 13 days of culture, the activity of alkaline phosphatase was the highest in the low-dose group, followed by the middle-dose and control groups, and the lowest in the high-dose group. There were significant differences in the activity of alkaline phoshatase between groups (P < 0.05). The antibacterial rate of the materials was 62.54% in the low-dose group, 69.84% in the middle-dose group, and 79.19% in the high-dose group, respectively. Findings from this study reveal that with the increase of zinc ion contents, the pro-osteogenic activity of micro-arc oxidation coatings decreased, while the antibacterial property improved.
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The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas. The population of this study was the males above 15 years old from 6 villages in rural areas. The villages were randomly assigned to intervention group or control group (3 villages in each group). Self-designed smoking questionnaire was applied. The intervention group received the village-based health education of tobacco control for one year. The primary outcome measurement was the male current smoking rate. In the baseline investigation, completed surveys were returned by 814 male residents from the control group and 831 male residents from the intervention group. The male current smoking rate in the control group and the intervention group was 61.2% and 58.5%, respectively, before intervention. There was no significant difference between these two groups (P>0.05). After one-year intervention, the current smoking rate in the intervention group (51.2%) was significantly lower than that in the control group (62.8%) (P<0.001). Our study suggested that the village-based health education of tobacco control was effective in lowering the male current smoking rate in rural areas, which could be a suitable and feasible way for tobacco control in the Chinese rural areas.
Subject(s)
Adolescent , Adult , Humans , Male , Middle Aged , Case-Control Studies , China , Delivery of Health Care , Methods , Health Education , Methods , Rural Population , Smoking Prevention , Tobacco Use CessationABSTRACT
The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas. The population of this study was the males above 15 years old from 6 villages in rural areas. The villages were randomly assigned to intervention group or control group (3 villages in each group). Self-designed smoking questionnaire was applied. The intervention group received the village-based health education of tobacco control for one year. The primary outcome measurement was the male current smoking rate. In the baseline investigation, completed surveys were returned by 814 male residents from the control group and 831 male residents from the intervention group. The male current smoking rate in the control group and the intervention group was 61.2% and 58.5%, respectively, before intervention. There was no significant difference between these two groups (P>0.05). After one-year intervention, the current smoking rate in the intervention group (51.2%) was significantly lower than that in the control group (62.8%) (P<0.001). Our study suggested that the village-based health education of tobacco control was effective in lowering the male current smoking rate in rural areas, which could be a suitable and feasible way for tobacco control in the Chinese rural areas.
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To compare the effectiveness and safety of posterior-substituting [PS] with cruciate-retaining [CR] total knee prostheses after the elimination of confounding variables. Between January 2008 and June 2012, a total of 32 subjects who had bilateral arthritis of the knees agreed to have one knee replaced with a PS total knee design and the other with a CR design. In addition to postoperative complications, clinical outcomes [Knee Society Score, Range of Motion, Western Ontario and McMaster Universities Arthritis Index, as well as radiographic findings] were evaluated preoperatively, and at 2-week, 3-month, 12-month, and 24-month follow-up. At the 24-month follow-up interval, no benefit of CR design was observed over PS design regarding functional assessment, patient satisfaction, or postoperative complication. However, the PS total knee design did display statistically significant improvements in range of motion as compared with the CR design. While comparable regarding supporting good clinical outcomes, the PS design does appear to support significantly improved postoperative range of motion when compared with the CR design
Subject(s)
Humans , Male , Female , Prostheses and Implants , Treatment OutcomeABSTRACT
Alveolar epithelial type II (AT II) cells are essential for lung development and remodeling, as they are precursors for type I cells and also produce other non-repair cells (fibroblasts). Progenitor cells are believed to possess capability of multi-potent transdifferentiation, which is closely related to the niche, suggesting the importance of establishment of a lung progenitor cell niche model. We hypothesized that pulmonary surfactant-associated protein A (SPA) suicide gene system would cause AT II cell to kill itself through apoptosis and leave its niche. In vitro, the recombinant adeno-associated virus vectors-SPA-thymidine kinase (rAAV-SPA-TK) system was established to get targeted apoptotic AT II cells. The apoptosis of AT II cells was detected by using MTT. The results showed that cloned SPA gene promoter had specific transcriptional activity in SPA high expression cells, and SPA high expression cells (H441) transfected with TK gene had higher sensitivity to ganciclovir (GCV) than SPA low expression cells (A549). In vivo, increased apoptosis of AT II cells induced by GCV in rAAV-SPA-TK system was observed by TUNEL. Finally, the successful packaging and application of rAAV-SPA-TK system provide experimental basis to get specific lung progenitor cell (AT II) niche in vitro and in vivo.
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Alveolar epithelial type II (AT II) cells are essential for lung development and remodeling, as they are precursors for type I cells and also produce other non-repair cells (fibroblasts). Progenitor cells are believed to possess capability of multi-potent transdifferentiation, which is closely related to the niche, suggesting the importance of establishment of a lung progenitor cell niche model. We hypothesized that pulmonary surfactant-associated protein A (SPA) suicide gene system would cause AT II cell to kill itself through apoptosis and leave its niche. In vitro, the recombinant adeno-associated virus vectors-SPA-thymidine kinase (rAAV-SPA-TK) system was established to get targeted apoptotic AT II cells. The apoptosis of AT II cells was detected by using MTT. The results showed that cloned SPA gene promoter had specific transcriptional activity in SPA high expression cells, and SPA high expression cells (H441) transfected with TK gene had higher sensitivity to ganciclovir (GCV) than SPA low expression cells (A549). In vivo, increased apoptosis of AT II cells induced by GCV in rAAV-SPA-TK system was observed by TUNEL. Finally, the successful packaging and application of rAAV-SPA-TK system provide experimental basis to get specific lung progenitor cell (AT II) niche in vitro and in vivo.
Subject(s)
Humans , Antiviral Agents , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Survival , Cells, Cultured , Dependovirus , Genetics , Dose-Response Relationship, Drug , Electrophoresis, Polyacrylamide Gel , Epithelial Cells , Cell Biology , Metabolism , Ganciclovir , Pharmacology , Gene Expression Regulation, Neoplastic , Genes, Transgenic, Suicide , Genetics , Genetic Vectors , Genetics , In Situ Nick-End Labeling , Luciferases , Genetics , Metabolism , Promoter Regions, Genetic , Genetics , Pulmonary Alveoli , Cell Biology , Metabolism , Pulmonary Surfactant-Associated Protein A , Genetics , Metabolism , Thymidine Kinase , Genetics , MetabolismABSTRACT
<p><b>BACKGROUND</b>Expression of murine calcium-activated chloride channel family member 3 (mCLCA3) has been reported to be increased in the airway epithelium of asthmatic mice challenged with ovalbumin (OVA). However, its role in asthmatic airway inflammation under no OVA exposure has not yet been clarified.</p><p><b>METHODS</b>mCLCA3 plasmids were transfected into the airways of normal BALB/c mice. mCLCA3 expression and airway inflammation in mouse lung tissue were evaluated. Cell differentials and cytokines in bronchoalveolar lavage fluid (BALF) were analyzed. The expression of mCLCA3 protein and mucus protein mucin-5 subtype AC (MUC5AC) were analyzed by Western blotting. The mRNA levels of mCLCA3, MUC5AC and interleukin-13 (IL-13) were determined quantitatively.</p><p><b>RESULTS</b>mCLCA3 expression was not detected in the control group while strong immunoreactivity was detected in the OVA and mCLCA3 plasmid groups, and was strictly localized to the airway epithelium. The numbers of inflammatory cells in lung tissue and BALF were increased in both mCLCA3 plasmid and OVA groups. The protein and mRNA levels of mCLCA3 and MUC5AC in the lung tissue were significantly increased in the mCLCA3 plasmid and OVA groups compared to the control group. The level of IL-13, but not IL-4, IL-5, IFN-γ, CCL2, CCL5 or CCL11, was significantly increased compared with control group in BALF in the mCLCA3 plasmid and OVA groups. The level of IL-13 in the BALF in the mCLCA3 plasmid group was much higher than that in the OVA group (P < 0.05). The level of mCLCA3 mRNA in lung tissue was positively correlated with the levels of MUC5AC mRNA in lung tissue, IL-13 mRNA in lung tissue, the number of eosinophils in BALF, and the content of IL-13 protein in BALF. The level of IL-13 mRNA in lung tissue was positively correlated with the number of eosinophils in BALF and the level of MUC5AC mRNA in lung tissue.</p><p><b>CONCLUSION</b>These findings suggest that increased expression of a single-gene, mCLCA3, could simulate an asthma attack, and its mechanism may involve mCLCA3 overexpression up-regulating IL-13 expression.</p>
Subject(s)
Animals , Female , Mice , Allergens , Asthma , Chloride Channels , Inflammation , Metabolism , Interleukin-13 , Metabolism , Interleukin-4 , Genetics , Metabolism , Interleukin-5 , Genetics , Metabolism , Mice, Inbred BALB C , Mucin 5AC , Genetics , Metabolism , Ovalbumin , PharmacologyABSTRACT
<p><b>BACKGROUND</b>Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis. This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.</p><p><b>METHODS</b>Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group, the model group, the magnesium sulfate group and the anisodamine group. The rabbit model of infusion phlebitis, induced by intravenous administration, was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline. We evaluated expression by histopathology, immunohistochemistry, reverse transcription-polymerase chain reaction, and Western blotting assay.</p><p><b>RESULTS</b>Pathohistological changes of the model group were observed, such as loss of venous endothelial cells, inflammatory cell infiltration, edema and thrombus. The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion, inflammatory cell infiltration, proliferation, swelling of endothelium and perivascular hemorrhage. The model group showed the highest expressions of VEGF and ICAM-1 of the four groups (P < 0.01). On the contrary, anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group (P < 0.01). There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group (P > 0.05).</p><p><b>CONCLUSION</b>Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1, and shows significant protective effects in an animal model of infusion phlebitis.</p>
Subject(s)
Animals , Male , Rabbits , Blotting, Western , Immunohistochemistry , Intercellular Adhesion Molecule-1 , Metabolism , Phlebitis , Drug Therapy , Random Allocation , Reverse Transcriptase Polymerase Chain Reaction , Solanaceous Alkaloids , Therapeutic Uses , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
<p><b>BACKGROUND</b>Increased proliferation of airway smooth muscle cells (ASMCs) are observed in asthmatic patients and smoking can accelerate proliferation of ASMCs in asthma. To elucidate the molecular mechanisms leading to these changes, we studied in vitro the effect of cigarette smoke extract (CSE) on the proliferation of ASMCs and the expression of cyclin D1, an important regulatory protein implicated in cell cycle.</p><p><b>METHODS</b>ASMCs cultured from 8 asthmatic Brown Norway rats were studied. Cells between passage 3 and 6 were used in the study and were divided into control group, pcDNA3.1 group, pcDNA3.1-antisense cyclin D1 (ascyclin D1) group, CSE group, CSE + pcDNA3.1 group and CSE + pcDNA3.1-ascyclin D1 group based on the conditions for intervention. The proliferation of ASMCs was examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. The expression of cyclin D1 was detected by reverse transcriptase-PCR (RT-PCR) and Western blotting.</p><p><b>RESULTS</b>(1) The percentage of S + G2M phase, absorbance value at 490 nm wavelength (A(490)) and the expression rate of PCNA protein in CSE group were (31.22 +/- 1.17)%, 0.782 +/- 0.221, (90.2 +/- 7.0)% respectively, which were significantly increased compared with those of control group ((18.36 +/- 1.02)%, 0.521 +/- 0.109, and (54.1 +/- 3.5)%, respectively) (P < 0.01). After the transfection with antisense cyclin D1 plasmid for 30 hours, the percentage of S + G2M phase, A(490) and the expression rate of PCNA protein in ASMCs were much lower than in untreated cells (P < 0.01). (2) The ratios of A(490) of cyclin D1 mRNA in CSE group was 0.288 +/- 0.034, which was significantly increased compared with that of control group (0.158 +/- 0.006) (P < 0.01). After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A(490) of cyclin D1 mRNA in ASMCs was much lower than in untreated cells (P < 0.01). (3) The ratios of A(490) of cyclin D1 protein expression in CSE group was 0.375 +/- 0.008, which was significantly increased compared with that of control group (0.268 +/- 0.004) (P < 0.01). After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A(490) of cyclin D1 protein expression in ASMCs was much lower than in untreated cells (P < 0.01).</p><p><b>CONCLUSION</b>CSE may increase the proliferation of ASMCs in asthmatic rats via regulating cyclin D1 expression.</p>
Subject(s)
Animals , Female , Rats , Asthma , Metabolism , Blotting, Western , Cell Cycle , Cell Proliferation , Cells, Cultured , Cyclin D1 , Genetics , Metabolism , Disease Models, Animal , Flow Cytometry , Immunohistochemistry , Microscopy, Phase-Contrast , Myocytes, Smooth Muscle , Cell Biology , Metabolism , Plant Extracts , Toxicity , Respiratory System , Cell Biology , Reverse Transcriptase Polymerase Chain Reaction , Smoking , Nicotiana , ChemistryABSTRACT
<p><b>BACKGROUND</b>Cigarette-smoke induced DNA damage can cause airway cell apoptosis and death, which may be associated with the development of chronic obstructive pulmonary disease (COPD). However, only 20% - 30% of smokers develop COPD, suggesting that different degrees of DNA repair produce different outcomes in smokers, i.e., part of them develop COPD. We investigated the association between polymorphisms in DNA repair genes hOGG1 (Ser326Cys) and XRCC1 (Arg399Gln), alone or in combination, and susceptibility of COPD.</p><p><b>METHODS</b>Altogether 201 COPD patients and 309 controls were recruited and frequency-matched on age and sex. hOGG1 and XRCC1 genotypes were determined by PCR-restriction fragment length polymorphism analysis.</p><p><b>RESULTS</b>The risk of COPD was not significantly different among individuals with Ser/Cys and Cys/Cys genotypes compared with those with hOGG1 Ser/Ser genotype. The risk of COPD was not significantly different among individuals with Gln/Gln genotype compared with those with XRCC1 Arg/Arg genotype, but it was significantly elevated among individuals with Arg/Gln genotype (adjusted odds ratios (OR) = 1.55, 95% confidence intervals (CI) 1.05 - 2.29, P = 0.029). Assessment of smoking status in current smokers compared with those with hOGG1 Ser/Ser genotype revealed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR = 5.07, 95% CI 1.84 - 13.95, P = 0.002). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Arg/Gln genotype (adjusted OR = 2.77, 95% CI 1.52 - 5.07, P = 0.001). Assessment of smoking exposure in light smokers compared with those with hOGG1 Ser/Ser genotype showed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR = 4.02, 95% CI 1.05 - 16.80, P = 0.042). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Gln/Gln genotype (adjusted OR = 4.48, 95% CI 1.35 - 14.90, P = 0.014). In heavy smokers compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Arg/Gln genotype (adjusted OR = 2.55, 95% CI 1.42 - 4.58, P = 0.002). When hOGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms were evaluated together, compared with those with 0 - 1 of hOGG1 326Cys and XRCC1 399Gln alleles, the risk of COPD was significantly elevated among individuals with 3 - 4 of hOGG1 326Cys and XRCC1 399Gln alleles (adjusted OR = 3.18, 95% CI 1.86 - 5.43, P = 0.000). Assessment of smoking status and smoking exposure in current/light/heavy smokers showed that the risk of COPD was significantly elevated among individuals with 3 - 4 of hOGG1 326Cys and XRCC1 399Gln alleles (adjusted OR = 8.32, 95% CI 3.59 - 19.27, P = 0.000; OR = 5.46, 95% CI 2.06 - 14.42, P = 0.001; OR = 2.93, 95% CI 1.43 - 6.02, P = 0.003; respectively).</p><p><b>CONCLUSIONS</b>hOGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms are associated with the susceptibility to COPD. The risk of COPD is significantly elevated among current/light smokers with hOGG1 326Cys and XRCC1 399Gln.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , DNA Glycosylases , Genetics , DNA-Binding Proteins , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Polymerase Chain Reaction , Polymorphism, Genetic , Polymorphism, Restriction Fragment Length , Pulmonary Disease, Chronic Obstructive , Genetics , X-ray Repair Cross Complementing Protein 1ABSTRACT
<p><b>BACKGROUND</b>The decrease of surfactant protein (SP) secreted by the alveolar type II cell is one of the important causes of limiting air of pulmonary emphysema. However, the SP-A gene and protein changes in this disease are rarely studied. This study was undertaken to investigate alterations in SP-A gene activity and protein, and to explore their roles in the pathogenesis of emphysematous changes.</p><p><b>METHODS</b>Twenty Wistar rats were divided randomly into a normal control group (n = 10) and a cigarette smoking (CS) + lipopolysaccharide (LPS) group (n = 10). Ultra-structural changes were observed under an electron microscope. The number of cells positive for SP-A was measured by immunohistochemistry. The mRNA expression and protein level of SP-A in the lung tissues were determined by quantitative polymerase chain reaction (qPCR) and Western blot separately. The protein level of SP-A in lavage fluid was determined by Western blot.</p><p><b>RESULTS</b>The number of cells positive for SP-A of the CS + LPS group (0.35 +/- 0.03) was lower than that of the blank control group (0.72 +/- 0.06, P < 0.05). The level of SP-A in the lung tissues of rats in the CS + LPS group (0.2765 +/- 0.0890) was lower than that in the blank control group (0.6875 +/- 0.1578, P < 0.05). The level of SP-A in the lavage fluid of rats in the CS + LPS group (0.8567 +/- 0.1458) was lower than that in the blank control group (1.3541 +/- 0.2475, P < 0.05). The lung tissues of rats in the CS + LPS group showed an approximate increase (0.4-fold) in SP-A mRNA levels relative to beta-actin mRNA (P < 0.05).</p><p><b>CONCLUSIONS</b>The changes of SP-A may be related to emphysematous changes in the lung. And cigarette smoke and LPS alter lung SP-A gene activity and protein homeostasis.</p>
Subject(s)
Animals , Male , Rats , Blotting, Western , Emphysema , Metabolism , Pathology , Homeostasis , Immunohistochemistry , Microscopy, Electron , Polymerase Chain Reaction , Pulmonary Surfactant-Associated Protein A , Genetics , RNA, Messenger , Rats, WistarABSTRACT
<p><b>BACKGROUND</b>Although it is recognized that bronchial smooth muscle cells (BSMCs) play a key role in airway remodeling during chronic asthma, it is not well understood how BSMCs exert their inflammatory functions. The extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is an important signaling pathway in chronic asthma, but its influence on secretion by BSMCs has not been well-studied. We investigated the impact of ERK1/2 signaling pathway on secretion by BSMCs in a rat model of chronic asthma in this study.</p><p><b>METHODS</b>To create a rat model of chronic asthma, Wistar rats underwent ovalbumim (OVA) injection and eight weeks of inhalation. BSMCs were isolated and cultured in vitro. Epidermal growth factor, PD98059 and ERK1/2 antisense oligonucleotide were used to explore the role of ERK1/2 signaling pathway. The expression of P-ERK1/2 (phospho-ERK1/2) in BSMCs was analyzed by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). Secretion of BSMCs was detected by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>Phospho-ERK1/2 expression was increased in BSMCs of chronic asthmatic rats compared with the controls. PD98059 inhibited expression of phospho-ERK1/2 protein, while treatment with an antisense oligonucleotide inhibited the expression of P-ERK1/2 mRNA and protein. BSMCs obtained from the chronic asthma group secreted significantly greater quantities of growth factors (transforming growth factor (TGF)-beta(1), vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF)), cytokines (regulated upon activation, normal T cell-expressed and secreted (RANTES) and eotaxin), and extracellular matrix (fibronectin and collagen I) compared with normal controls. Epidermal growth factor stimulated secretion in both groups, but the response of the chronic asthma group was more intense. Both PD98059 and antisense oligonucleotide suppressed secretion by BSMCs in chronic ashmatic rats. Antisense oligonucleotide reduced the level of RANTES nearly to that of normal controls, while PD98059 could not.</p><p><b>CONCLUSION</b>These results suggest that ERK1/2 signaling pathway may play an important role in the augmented secretion of BSMCs in chronic asthmatic rats, and ERK1/2 antisense oligonucleotide effectively inhibits the process.</p>
Subject(s)
Animals , Male , Rats , Asthma , Metabolism , Bronchi , Bodily Secretions , Chemokine CCL5 , Bodily Secretions , Chronic Disease , Disease Models, Animal , MAP Kinase Signaling System , Physiology , Mitogen-Activated Protein Kinase 1 , Physiology , Mitogen-Activated Protein Kinase 3 , Physiology , Myocytes, Smooth Muscle , Bodily Secretions , Rats, Wistar , Transforming Growth Factor beta1 , Bodily Secretions , Vascular Endothelial Growth Factor A , Bodily SecretionsABSTRACT
<p><b>AIM</b>To study the effects of bone marrow MSCs transplantation on the apoptosis of alveolar wall cells and the expression of Bcl-2 and Bax of lung tissue in papain and Co60-induced pulmonary emphysema rats.</p><p><b>METHODS</b>Female Lewis rats were randomly divided into three groups: control group, emphysema group, emphysema + MSCs transplantation group. Rats were sacrificed at days 14 and 28 after treatment. Morphologic analysis of the lung tissue was performed. The apoptosis of the lung cells was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The expression of Bcl-2 and Bax were determined by immunohistochemical staining.</p><p><b>RESULTS</b>Emphysematous changes of the lung tissue were observed in emphysema group and emphysema + MSCs transplantation group. However, the emphysematous change in emphysema + MSCs transplantation group was improved compared with the emphysema group. There was significant difference in the number of alveolar counted per unit area (MAN), mean alveoli area (MAA) and mean linear interval(MLI) between emphysema group and emphysema + MSCs transplantation group. The apoptotic index of the alveolar wall cells in emphysema + MSCs transplantation group was less than that in the emphysema group. The percentage of Bcl-2 positive cells in emphysema + MSCs transplantation group was significantly higher than that in the emphysema group. The percentage of Bax positive cells in emphysema + MSCs transplantation group was significantly lower than that in the emphysema group. The ratio of Bcl-2/Bax of emphysema + MSCs transplantation group was significantly higher than that in the emphysema group.</p><p><b>CONCLUSION</b>Bone marrow MSCs transplantation inhibits the apoptosis of alveolar wall cells, upregulates the expression of Bcl-2 and downregulates the expression of Bax. This may be part of the reason that bone marrow MSCs transplantation improves the papain and Co60-induced pulmonary emphysema.</p>
Subject(s)
Animals , Female , Rats , Apoptosis , Bone Marrow Transplantation , Cells, Cultured , Cobalt Isotopes , Lung , Cell Biology , Mesenchymal Stem Cell Transplantation , Papain , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Pulmonary Alveoli , Pathology , Radiation Effects , Pulmonary Emphysema , Metabolism , Pathology , General Surgery , bcl-2-Associated X Protein , MetabolismABSTRACT
<p><b>BACKGROUND</b>Increased proliferation of pulmonary vascular cells and muscularisation of pulmonary vessels are frequently observed in human smokers and in animals exposed to cigarette smoke. To elucidate the molecular mechanisms leading to these changes, we studied the in vitro effect of cigarette smoke extract (CSE) on proliferation of pulmonary artery smooth muscle cells (PASMCs) and activation of protein kinase C (PKC), an important kinase implicated in cell proliferation.</p><p><b>METHODS</b>PASMCs cultured from 12 normal Wistar rats were studied in the following conditions: (1) PASMCs were exposed to different concentrations of CSE for 24 hours, then MTT colorimetric assay was used for detection of cell proliferation. Cell viability was assessed by trypan blue exclusion. (2) PASMCs were pre-incubated with phorbol 12-myristate 13-acetate (PMA) for 24 hours or Ro31-8220 for 30 minutes before exposure to 5% CSE for 24 hours. Cell proliferation was examined by MTT colorimetric assay, cell cycle analysis and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. (3) PASMCs were exposed to 5% CSE for 24 hours. Then PKC-alpha mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR) and protein expression by Western blotting, while PKC-alpha translocation was observed by immunofluorescence staining and confocal microscopy. (4) PASMCs were transfected with specific antisense oligodeoxynucleotides against PKC-alpha 6 hours before exposure to 5% CSE for 24 hours. PKC-alpha protein expression and cell proliferation were detected by methods described previously.</p><p><b>RESULTS</b>(1) Low concentration of CSE (5%) increased proliferation of PASMCs, whereas high concentrations (20%, 30%) were inhibitory as a result of cytotoxicity. (2) The value of absorbance (Value A), proliferation index (PI), S-phase cell fraction (SPF) and average optical density of PCNA staining in PASMCs from 5% CSE exposure group (0.306 +/- 0.033, 0.339 +/- 0.033, 0.175 +/- 0.021, 0.315 +/- 0.038, respectively) were significantly increased compared with those of control group (0.249 +/- 0.018, 0.177 +/- 0.055, 0.092 +/- 0.023, 0.187 +/- 0.022, respectively) (P < 0.05). PKC down-regulation by PMA pretreatment or PKC inhibition by Ro31-8220 pre-incubation abolished the effect of 5% CSE on PASMCs proliferation. (3) After exposure to 5% CSE for 24 hours, PKC-alpha mRNA and protein expression in PASMCs (1.054 +/- 0.078, 1.185 +/- 0.041, respectively) were much higher than in untreated cells (0.573 +/- 0.054, 0.671 +/- 0.055, respectively) (P < 0.01). Moreover, 5% CSE induced a translocation of PKC-alpha from cytoplasm toward the perinuclear area and into the nucleus. (4) Specific antisense oligodeoxynucleotides against PKC-alpha reduced 5% CSE-induced expression of PKC-alpha protein (0.713 +/- 0.047 vs 1.180 +/- 0.056), also abolished the effect of 5% CSE on PASMCs proliferation significantly.</p><p><b>CONCLUSIONS</b>CSE can be cytotoxic at high concentrations. But at low concentrations, it makes a mitogenic effect on cultured PASMCs. PKC, especially its alpha isozyme, seems to play an important role in CSE-induced proliferation of PASMC.</p>